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Towards a Better Understanding

of
Early Atraumatic Brain Injury and its Treatment

Alan Challoner MA MChS


Towards a Better Understanding of Early Atraumatic Brain Injury
and its Treatment

OUTLINE

A General Introduction to Early Brain Injury 4


ATRAUMATIC OR NON-TRAUMATIC BRAIN INJURY 5
THE AFTERMATH OF CONVULSIONS 6

The Nature of Brain Injury 6


‘FIRST AID’ FOR BRAIN INJURIES 6
FOCAL IDENTITY IN THE FUNCTIONAL BRAIN 11
ASSESSMENT AND THE MORE RECENT CHANGES 11
DISORDERS OF THE HORMONE AND METABOLIC SYSTEMS 18
THE HORMONAL PROCESS 19
EFFECTS OF STRESS ON THE BRAIN 20
THE RESPONSE OF THE BODY'S REACTION TO STRESS 20
HOMEOSTASIS 21
PARASYMPATHETIC AND SYMPATHETIC NERVOUS SYSTEM 21
THE EMOTIONAL BRAIN: THE LIMBIC SYSTEM 22
Distress Signals from the Brain 22
Getting Back to Normal 22
Not All Stress is Bad 22
Stress Compromises the Blood-Brain Barrier 22
STRESS AND NOISE 23
Stress and Memory 23
CORTISOL AFFECTS MEMORY FORMATION AND RETRIEVAL 23
CORTISOL AND TEMPORARY MEMORY LOSS-STUDY 23
CORTISOL AND THE DEGENERATIVE CASCADE 24
CORTISOL AND BRAIN DEGENERATION 24

NUTRITION AND METABOLIC DISTURBANCES 24

Sleep and dreaming following Brain Injury 26


Information Processing 30
Executive Functioning 32
Memory 39
Direct effect of brain injury on emotion 46
Ego Functions 54
Abnormal Brain Structure & Autism 56

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INTRODUCTION 56
AETIOLOGY OF AUTISM SPECTRUM DISORDERS 57
AUTISM AND ITS TREATMENT 64

Management Following Early Brain Injury 68


EARLY MANAGEMENT 68
LONG-TERM MANAGEMENT 68
COGNITIVE PROBLEMS 69
PSYCHIATRIC INTERVENTION FOLLOWING EARLY BRAIN INJURY 72

Some of the Physical and Cognitive Difficulties Encountered


following Atraumatic Brain Damage 74

FEEDING AND SWALLOWING DIFFICULTIES 74


DYSPRAXIA AND NON-FLUENCY 75
PRAGMATIC SKILLS 76
LANGUAGE IN CHILDREN WITH EARLY BRAIN DAMAGE 76
PROBLEMS OF GAIT AND MOVEMENT 80

Types of Emotional, Behavioural, Psychiatric and Social


Problems Seen After Brain Injury in Children 84
Post-traumatic stress disorder 88
PTSD AND EMOTIONAL RESPONSES 91

Rational Drug Interventions 96


DIAGNOSIS AND TREATMENT 96
DRUG INTERVENTIONS 98

Possible Effects of Specific Cognitive Deficits on Behaviour


and Social Functioning 103
BEHAVIOUR MANAGEMENT 108
SPECIAL PROVISION 111
INTERVENTIONS WITH PARENTS 112
EDUCATION OF THE FAMILY AND OF THE CARERS 113
FAMILY COUNSELLING AND FAMILY THERAPY 113

Summary and Conclusions 113

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Towards a Better Understanding

of

Early atraumatic brain injury and its treatment

___________

A General Introduction to Early Brain Injury


Acquired brain injury is common and may follow traumatic and non- or atrau-
matic insults. It has major individual patient and public health implications.
Although head trauma is the leading cause of an acquired brain injury, non-
traumatic injuries are also common. Importantly, the survival rate of children
who have suffered both types of brain injury continues to increase, in part
reflecting the improved (and still improving), acute and resuscitative medical
and surgical treatment given at the time of, and immediately following, the
injury.

However, the survival of these children is clearly at some cost — to both the
child and their family — and this includes a corresponding increase in the mor-
bidity rate, in which children are often left with significant difficulties. These
difficulties will obviously range from mild to severe and may be transient or
permanent. In addition, children may have difficulties that are limited to just
one area, or more typically, the difficulties and their problems are multiple and
complex and there will be major implications for physical and educational (and,
subsequently, career) achievements and social interaction.

Paediatric traumatic brain injury is a major cause for concern when considering
both the number of children sustaining injuries and the large number of
children incurring life-long difficulties that impact on quality of life. Research is
continuing to investigate outcomes and predictors of recovery in both cognitive
and behavioural domains. Findings have contributed to better identification of
children at high risk for neurobehavioral difficulties. The challenge is to
develop new intervention programs to prevent or lessen the impact of such
difficulties. 1

Some brain injuries have been caused by vaccines and generally that is the
result of the toxins in the vaccine passing the blood/brain barrier and causing
sporadic damage to the nerve cells of the brain. This process and some of its
results have been dealt with elsewhere.2

1
Catroppa, C. & Anderson, V. Neuro-developmental outcomes of
‌ ‌(2009)

pediatric traumatic brain injury. Future Neurology November 2009, Vol. 4, No. 6,
Pages 811-821.
2
Challoner, A. 2009. Brain Damage caused by Vaccination.
(http://www.scribd.com/oakwoodbank)

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ATRAUMATIC OR NON-TRAUMATIC BRAIN INJURY

It is important to realize that brain damage can be caused by non-traumatic or


atraumatic brain injury (ABI). This may be almost as common as TBI.3 These
injuries may be caused by a number of different disorders and of those the
ones that are significant are:

• as a complication of meningitis or encephalitis;

• prolonged convulsive status epilepticus (when an epileptic convulsion


lasts more than 60 minutes)

• as a complication of some other toxic (e.g. alcohol, drug), metabolic


or biochemical impairment

These non-traumatic brain injuries are relatively common

When a nerve cell is injured or diseased, it may stop functioning and the
circuits to which it contributed will then be disrupted. Some circuits may
eventually reactivate as damaged cells resume functioning or alternative
patterns involving different cell populations take over. When a circuit loses a
sufficiently great number of neurons, the broken circuit can neither be
reactivated nor replaced. In general, when a human neuron dies, it is not
replaced, except in the capacity of the dentate gyrus of the human
hippocampus to generate new neurons (Eriksson et aI, 1998)4. Evidence of the
generation of new neurons in response to injury or disease is still lacking.

The experience at Alder Hey Hospital suggests that when one considers all
causes of atraumatic brain injury together, the incidence and prevalence of
significant ABI may be as high, or even higher, than TBI. This pattern seems to
have been emerging over the past couple of years. 5

A great deal of the research into early brain injury has been involved with TBI.
Most cases of ABI occur very early in a child’s life and therefore it is less easy to
assess what changes have taken place as a result of the injury, particularly as
there will be little or no pre-morbid history to take into consideration. That
said, the results of insults to the brain tissue will often have the same
implications whether the origins of the damage are ABI or TBI. The summary
that follows will therefore include the research into TBI and will use that
similarity as a means to try and identify what the outcomes will be for those
who suffer ABI. Where the research involved ABI subjects then that can be
seen to support this method of analysis.

THE AFTERMATH OF CONVULSIONS 6

There is an increased incidence of convulsions following head injury.


Convulsions can cause a rise in inter-cranial pressure (ICP) which may

3
Appleton, R. & Baldwin, T. Management of Brain Injured Children. 2nd
Ed. OUP,2006.
4
Eriksson, P.S., Perfilieva, E., Bjork-Eriksson, T., et al. (1998). Neu-
rogenesis in the adult human hippocampus. Nature Medicine, 4, 1313-1317.
5
Appleton, R. et al. 2006 idem
6
Appleton, R. et al. 2006 idem

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adversely affect cerebral blood flow (CBF) and contribute to further neuronal
damage.

Acute brain injury results in death of a variable number of brain cells, both
neurons and neural connective tissue. At this time, cellular energy metabolism
can be restored over a period as short as 30 minutes but cell swelling still
occurs. In the 'latent' phase which follows, magnetic resonance spectroscopy
may indicate oxidative cerebral energy metabolism similar to normal, but the
electroencephalography (EEG) is depressed and CBF reduced.

It is believed that cellular ionic changes begin in the 'latent' phase and progress
to apoptosis (programmed cell death). The latent phase is followed by 'second-
ary' deterioration after the acute event and manifests as delayed convulsions,
cytotoxic oedema, extracellular accumulation of potential cytotoxins such as
excitatory neurotransmitters, failure of oxidative metabolism and neuronal
death. There is damage to the blood-brain barrier with escape of water and
plasma as components of the oedema. This may already have been damaged
in the first phase of vaccine damage to the brain when the toxins pass into the
brain.

Acute cell necrosis may result in the release of cellular ions, such as calcium,
which may induce vascular spasm of cerebrovascular smooth muscle. These
ions may damage other cells which were unaffected by the primary acute brain
insult. There are physical effects related to sluggish flow of blood in small
blood vessels, such as capillary sludging and platelet aggregation that may
progress to critical and irreversible ischaemia and cerebral infarction. The
acute changes in this late phase may take several days to resolve.

_______

The Nature of Brain Injury


Would that we could simply describe the results of brain
damage and say, "this is how it is.” But what we see, and
how we talk about it, is never based on pure, naive,
veridical perception; rather, it is inextricably bound to what
we already know, what we're looking for, what we're trying
to prove. Just as a proper appreciation of contemporary
art demands familiarity with the fashions and approaches
of earlier eras, so the study of brain damage is inseparable
from consideration of the hypotheses of earlier clinicians,
the categories and syndromes they devised and,
lamentably, the facts they distorted or overlooked. 7

‘FIRST AID’ FOR BRAIN INJURIES

When brain cells die, whether from head trauma, stroke or disease, a substance
called glutamate floods the surrounding areas, overloading the cells in its path
and setting off a chain reaction that damages whole swathes of tissue.
Glutamate is always present in the brain, where it carries nerve impulses across
the gaps between cells; but when this chemical is released by damaged or
dying brain cells, the result is a flood that overexcites nearby cells and kills
them.
7
Gardner, H. The Shattered Mind: The person after brain damage.
Routledge & Kegan Paul, London, 1974.

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A new method for ridding the brain of excess glutamate has been developed at
the Weizmann Institute of Science. This method takes a completely new
approach to the problem, compared with previous attempts based on drugs
that must enter the brain to prevent the deleterious action of glutamate. Many
drugs, however, can’t cross the blood-brain barrier into the brain, while other
promising treatments have proved ineffective in clinical trials.

Prof. Vivian Teichberg, of the Institute’s Neurobiology Department, working


together with Prof. Yoram Shapira and Dr. Alexander Zlotnik of the Soroka
Medical Center and Ben Gurion University of the Negev, has shown that in rats,
an enzyme in the blood can be activated to “mop up” toxic glutamate spills in
the brain and prevent much of the damage. This method may soon be entering
clinical trials to see if it can do the same for humans.

In the majority of cases, the extent of a learning difficulty resulting from a head
or other brain injury is related to the severity and nature of the head injury 8.
For instance, in a child whose brain injury has been complicated by severe
cerebral oedema (brain swelling) then blood and oxygen supply to the brain
may be severely compromised. This is often termed an 'hypoxic-ischaemic
encephalopathy', resulting in diffuse cerebral damage and on recovery, general
cognitive functioning can be impaired.

The mention of injury to the head or brain strikes a note of apprehension in


most people. Similarly, reports of any injury or debilitating tragedy to children
arouse widespread sympathy and feelings of indignation that the young should
suffer in any way. For the head-injured child, however, such public sympathy
appears to be rather short lived, despite persisting and long-term difficulties
stemming from the injuries. Head injury is never an all-or-nothing
phenomenon, irrespective of the cause; rather, it is a matter of degree,
producing relative changes in brain structure and function. Johnson et al make
it evident that the notion of greater plasticity and recovery of children who
suffer head injury is not generally supported. 9

There is little age differentiation in the published reports on children's head


injury: a paediatric population may range from birth to 19 years of age 10 . This
has generated much confusion, especially in relation to evaluating outcome.
Age demarcates stages or periods of development which reflect the underlying
neurological substrate, although age alone is not a sufficient index 11 .
Consequently, head-injured children as a population may reasonably be
expected to show quite different, within-group responses to trauma, relative to
their stage of development 12.

Much of the early literature, especially neurosurgical and psychological, implies


that the younger child is less vulnerable and shows a greater recovery from
8
Levin, H. S., Benton, A. L., & Grossman R. G. (1982).
Neurobehavioural Consequences of a Closed Head Injury. Oxford: Oxford
University Press.
9
Johnson, DA.; Uttley, D. & Wyke, M. (1989) Children’s Head Injury:
Who Cares? Taylor & Francis.
10
Ward, J.D. & Alberico, A.M. (1987) 'Paediatric head injuries', Brain
Injury, 1, pp. 21-25
11
Jeffery, R. (1980) 'The developing brain and child development', in
WITTROCK, M.C. (ed.) The Brain and Psychology, New York, Academic Press.
12
Luerssen, T.G., Klauber, M.R. & Marshall, L.F. (1988) 'Outcome from
head injury related to patient's age', Journal of Neurosurgery, 68, pp. 409-416.

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head injury than those who are older. There have been extensive
methodological criticisms of such work, however, which suggest that given
adequate evaluations, particularly of cognitive function, the young head-injured
child does not show a preferential recovery rate.

Relatively greater impairment appears in children younger than 8 years at the


time of injury, but there has been a general failure to institute longitudinal
studies of infants and toddlers with sufficiently sensitive outcome measures,
and parallel neuro-radiological confirmation. It appears that younger children
may also be more vulnerable to a wide range of secondary factors, including
nutrition and environmental stimulation.

Head injury to the child occurs in the context of development and incomplete
neurological maturation. Consequently, the general concepts of critical periods
and vulnerability are most pertinent to the younger child sustaining head-injury.
It remains speculative as to what extent normal development proceeds after
head injury but, given the greater vulnerability of immature neurones to insult
and their tendency for more rapid degeneration, it seems reasonable that
normal maturation must be at high risk in terms of either the sequence or rate
of development, or both. 13

The age at which a head injury occurs is therefore an important factor to be


taken into consideration. Infants may appear to recover but if the child has
been very severely brain-injured, then they may always require a great deal of
intensive support. Many assessment tools are not appropriate for very young
children and yet subtle deficits can be acquired in the informative years that
may affect the long-term potential.

Clearly, the question, 'does an early injury have a more serious effect on overall
mental development than a later one?', cannot be answered easily, as many
factors including the type of injury and size, extent and location of damage
must be considered, as well as the specific mental activity involved and its
cognitive complexity. It is within this context that complex skills may not be
expected of children in their formative years, and therefore deficits acquired
early on may not become apparent until much later in their lives.

It is very likely that aberrant development may result from secondary factors in
the recovery process, or from subsequent atrophy of damaged tissue.
Secondary neural degeneration in the head-injured child, for example, has not
been widely reported 14, 15, 16, 17, , but this often arises even in the presence of
relatively good physical ability and appearance.

The Central Nervous System (CNS) possesses a finite adaptive capacity to


13
Johnson, DA.; Uttley, D. & Wyke, M. (1989) Children’s Head Injury:
Who Cares? Taylor & Francis.
14
Lange-Cosack, H., Wider, B., Schlfsner, H.J., Frumme, T. &
Kubicki, S. (1979) 'Prognosis of brain injuries in young children (1 until 5 years
of age)" Neuropaediatrie, 10, pp. 105-127.
15
Cullum, C.M. & Bigler, E.D. (1985) 'Late effects of haematoma on
brain morphology and memory in closed head injury', International Journal of
Neurosdenu, 28, pp. 279-283.
16
Jellinger, K. (1983) 'The neuropathology of paediatric head injury', in
SHAPIRO, K. (ed.) Paediatric Head Traurna, New York, Futura.
17
Mortimer, J.A. & Pirozzolo, F.J. (1985) Remote effects of head trauma,
Developmental Neuropsychology, 1, pp. 215-229.

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withstand the effects of any cerebral insult. Head injury reduces that capacity
and, with increasing severity of trauma and subsequent atrophy, the remaining
capacity of the CNS to adapt to any further neurological insult becomes
relatively limited. With a decline in capacity, new signs and symptoms may
appear as critical thresholds are reached.

As brain development results from complex interactions between genetic and


environmental factors, it seems reasonable to suggest that the young head-
injured child may be in greater need of early rehabilitation than his adult
counterpart.

Rehabilitation must aim to facilitate as normal a pattern of development as


possible, hence the need for follow-ups throughout the period of the child's
remaining development.18 Similarly, there must be a development of inter-
disciplinary rehabilitation facilities specifically for the head-injured child, incor-
porating neurological, educational and social factors. Rehabilitation must
become more scientifically based and practised in a coherent and
neurologically meaningful way, rather than the haphazard, inconsistent
guesswork which characterizes rehabilitation in the UK.

When someone is injured it is assumed by both public and doctors that the best
treatment is provided, based on sound knowledge of the patho-physiological
response to trauma 19. Recent reports challenge this complacency 20. The
system of such care would be of far greater practical importance that any of its
constituent parts.

Trauma to the brain exerts perhaps the highest toll among all injuries, simply
because it may dramatically alter the quality of future life for its survivors and
their families 21, 22, 23 . Nonetheless society continually fails to see the full
implications of disability resulting from head injury in childhood 24 including
increased educational support, lost or diminished careers, poor social and
emotional adjustment, and later demands on mental health services.

The long-term effects of a brain injury on a child can therefore depend upon the
age at which the injury occurs and problems may not always be evident from
the early stages. Unlike adults, children's brains develop rapidly both in size
and complexity through the childhood years and into adolescence.

18
Kaiser, G., Rudeberg, L., Fankhauser, L. & Zumbuhl, C. (1986)
'Rehabilitation medicine following severe head injury in infants and children', in
Raimondi, A.J., Choux, M. & DiRocco, C. (eds.) Head Injury in the Newborn and
Infant, New York, Springer.
19
Yates, D.W. (1988) 'Action for accident victims', British Medical Journal,
297, pp. 1419-1420.
20
Cummins, B. (1987) 'A head injury polemic', British Journal of Neurosurgery, 1,
pp. 6-8.
21
Shapiro, K. (1985) 'Head injury in children', in Becker, D.P. & Povlishock,
J.T. (eds.) Central Nervous System Traurna Status Report, Maryland, NIH.
22
Lezak, M.D. (1988) 'Brain damage is a family affair', Journal of Clinical
and Experimental Neuropsychology, 10, pp. 111-123.
23
Waaland, P.K. & Kreutzer, J.S. (1988) 'Family responses to childhood
brain injury', Journal of Head Trauma Rehabilitation, 3, pp.51-63.
24
Haas, J.F., Cope, D.N. & Hall, K. (1987) 'Premorbid prevalence of poor
academic performance in severe head injury', Journal of Neurology,
Neurosurgery and Psychiatry, 50, pp. 52-56.

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Neurodevelopment is not uniform through the brain at anyone time, and areas,
particularly those in the frontal lobes, do not become fully operational until
adolescence and early adulthood. Making a positive long-term prognosis from
what may appear a rapidly sound recovery can therefore be misleading. More
subtle deficits, particularly those affecting frontal lobe functioning, may not
become apparent until many years later.

For a substantial number of years, there has been a strong belief that recovery
from head injury is better in children than adults, due to what has been termed
'cerebral plasticity', that is, damaged skills being compensated for by areas of
the brain that are not affected, and are able to take over the function of the
damaged areas, at least to some degree. However, this is often not the case,
and children who have a very early ABI can often have a poorer prognosis than
had they sustained a somewhat similar injury as an older child or adult.
Goodman 25 argued that there were limits to cerebral plasticity.

Generally, research has indicated that ABI has more significant effect on the
cognitive skills of young children. Typically, it is thought that children younger
than seven or eight years do not improve in intellectual functioning in the same
way that older children and adults do 26, 27 .

Brain functioning and development occur rapidly during a child's life. The
period of most rapid development occurs within the first couple of years of life,
but it remains incomplete well into the teenage years, and final myelinisation 28
does not occur until adolescence.

There is a sequential pattern of myelinisation, with the frontal lobes being the
final areas to mature, usually with the onset of adolescence. The later
implications that early impairment to the frontal lobes can have on the social,
behavioural and cognitive functioning of children in their later years is given in
two case studies reported by Williams and Mateer 29.

In very recent years, neuro-imaging research has yielded important information


concerning the structure, neurochemistry, and function of the amygdala,
medial prefrontal cortex, and hippocampus in posttraumatic stress disorder
(PTSD). A review of neuro-imaging research reveals heightened amygdala
responsivity in PTSD during symptomatic states and during the processing of
trauma-unrelated affective information. Importantly, amygdala responsivity is
positively associated with symptom severity in PTSD. In contrast, medial
prefrontal cortex appears to be volumetrically smaller and is hypo-responsive
during symptomatic states and the performance of emotional cognitive tasks in
PTSD. Medial prefrontal cortex responsivity is inversely associated with PTSD
25
Goodman, R. (1989). Limits to cerebral plasticity. In: Children's Head
Injury: Who Cares (eds. D. A. Johnson, D. Uttley & M. Wyke). London: Taylor and
Francis.
26
Stiles J. (2002). Neural plasticity and cognitive development.
Developmental Neuropsychology, 18,237-72.
27
Stiles, J., Reilly, J., Paul, B., & Moses, P. (2005). Cognitive
development following early brain injury: evidence for neural adaptation. Trends
in Cognitive Sciences. 9, 136-43.
28
Myelinisation. The change or maturation of certain nerve cells whereby
a layer of myelin forms around the axons which allows the nerve impulses to
travel faster.
29
Williams, D. & Mateer, C. (1992). Developmental impact of frontal lobe
injury in middle childhood. Brain and Cognition 20,196-204.

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symptom severity. The reviewed research suggests diminished volumes,
neuronal integrity, and functional integrity of the hippocampus in PTSD. 30 (See
PTSD below, p85)

FOCAL IDENTITY IN THE FUNCTIONAL BRAIN

Thought and knowledge about the localization of mental functions in the human
brain have a long and complicated history and are still evolving. There has
been uncertainty about what the concept means, debate about where
localization takes place and even denial that it exists. Ideas about cerebral
localization have been determined primarily by the knowledge of brain anatomy
existing at a particular time and by the availability of techniques for disclosing
the presence and locus of brain lesions. They have also been influenced by
concepts of the nature of disease and the prevailing state of psychological
analysis. 31

ASSESSMENT AND THE MORE RECENT CHANGES

It is often only in a neuropsychological assessment that the underlying deficits


of children who have sustained a brain injury become apparent. Deficits in
many cases are not global, especially in the milder cases 32 although subtle
deficits do remain and can affect academic performance 33 where they may be
misinterpreted or overlooked. Most neuropsychological assessments have an
intelligence test as their core. However, the concept of intelligence tests
(intelligence quotients [IQ]) is, in many respects, outdated as suggested by
Lezak 34 and certainly these tests must be used with caution when making any
assumptions about the brain injured child. Tests of 'intelligence' may be useful
as indicators of levels of functioning and can be used as a basis from which
further assessments can be undertaken, but a screening test in which a broader
and more detailed neuropsychological assessment can take place will be
essential and will provide a better understanding of the injury.

Possibly the best source of general information about neuropsychological


assessments is to be found in Lezak 35, although in recent years, a range of
neuropsychological tests have been developed for use in children. These tend
to be rarely used in their totality and, indeed, concern has been expressed that
many of the sub-tests are not specific in detecting distinct neuropsychological

30
Shin, Lisa M.; Rauch, Scott L. & Pitman, Roger K. Amygdala, Medial
Prefrontal Cortex, and Hippocampal Function in PTSD. Ann. N.Y. Acad. Sci. 1071:
67–79; 2006.
31
Benton, A. (2000). Historical aspects of cerebral localization. In
Localization of Brain Lesions and Developmental Functions, D. Riva & A. Benton
(eds.); John Libbey & Company Ltd, pp. 1-14.
32
Bawden, H. N., Knights, R. M., & Winogron, H. W. (1985). Speeded-
performance head injury in children. Journal of Clinical Neuropsychology 7, 39-
54.
33
Wrightson, P., McGinn, V., & Gronwall, D. (1995). Mild head injury in
pre-school children - evidence that can be associated with a persisting cognitive
defect. Journal of Neurology Neurosurgery and Psychiatry 59, 375-80.
34
Lezak, M. D. (1988). IQ. R.I.P. journal of Clinical and Experimental
Neuropsychology 10, 351-61.
35
Lezak, M. D. (2004). Neuropsychological Assessment (4th edn). Oxford:
Oxford University Press.

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processes, but rather 'g' or general cognitive ability. In addition, following ABI,
sub-tests requiring more fluid performance tend to be depressed greater than
those comprising what are termed 'crystallized skills', that is, verbal abilities.
During the recovery phase, the discrepancy between these quotients generally
decreases, and although there are a number of reasons why this may occur, it
tends to indicate a general recovery. It can, of course, relate to the heavy prac-
tice effects that are possible from repeated testing, and care therefore needs to
be exercised when gauging improvement through changes in test results. The
tests themselves do not always measure what they intend to measure and may
be significantly affected by other factors.

Lezak comments:

“IQ refers to a derived score used in many test batteries designed to measure a
hypothesized general ability — intelligence. Because of the multiplicity of
cognitive functions assessed in these batteries, IQ scores are not useful in
describing cognitive test performances. IQ scores obtained from such tests
represent a composite of performances on different kinds of items, on different
items in the same tests when administered at different levels of difficulty, on
different items in different editions of test batteries bearing the same name, or
on different batteries contributing different kinds of items. If nothing else, the
variability in sources from which the scores are derived should lead to serious
questioning of their meaningfulness.

In neuropsychological assessment in particular, IQ scores are often unreliable


indices of neuropathic deterioration. Specific defects restricted to certain test
modalities, for example, may give a totally erroneous impression of significant
intellectual impairment when actually many cognitive functions may be
relatively intact and lower total scores are a reflection of impairment of specific
functional modalities. Conversely, IQs may obscure selective defects in specific
tests .

In fact, any derived score based on a combination of scores from two or more
measures of different abilities results in loss of data. Should the levels of
performance for the combined measures differ, the composite score-which will
be somewhere between the highest and the lowest of the combined measures-
will be misleading. Averaged scores on a Weschler Intelligence Scale battery
provide just about as much information as do averaged scores on a school
report card. In the same way, it is impossible to predict specific disabilities and
areas of competency or dysfunction from averaged ability test scores (e.g., "IQ"
scores). Thus composite scores of any kind have no place in neuropsychological
assessment.

In sum, "IQ", as a score, is inherently meaningless and not infrequently


misleading as well. "IQ" — whether concept, score, or catchword-has outlived
whatever usefulness it may once have had and should be discarded.” (idem)

Both the Weschler Intelligence Scale for Children (WISC) and the Weschler Pre-
School and Primary Scale of Intelligence (WIPPSI) have been replaced by new
and updated versions. The third edition of the WIPPSI provides a much-needed
update of the original WIPPSI which was last revised in 1989. In addition to the
material being updated and made more contemporary and appealing to chil-
dren, the tests have been extensively revised. As well as providing the original
cognitive domains of verbal IQ, performance IQ and a full-scale IQ, it now
provides further analysis of the updated and additional sub-tests to provide a
global language score, a processing speed quotient, and a general language
composite score, in addition to the original cognitive domains. It is suitable for

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children from the age of two years, six months to seven years, three months.

The WISC Ill-UK has now been superseded by the new WISC IV-UK. This
updated version provides a broadly similar assessment of general ability; how-
ever, it also incorporates significant revisions that include updated normative
data, new sub-tests and an increased emphasis on composite scores which
assess more discrete domains of cognitive functioning. In total, there are now
15 sub-tests available, but once more, the general test framework evaluates
the four original composite indexes of verbal comprehension, perceptual
reasoning, working memory and processing speed.

The WISC IV is linked to the Wechsler Individual Achievement Test (second


edition) which provides a comprehensive measure of academic achievements in
a number of principal domains. The test can therefore be used to provide a
predictive score and actual score, thereby indicating the extent to which a child
may be under-functioning in a particular attribute. The child's basic educational
attainments and other core attributes can therefore be judged in comparison
with their general level of intellectual ability using the newer versions of
Weschler Objective Numerical Dimensions (WOND) and Weschler Objective
Reading Dimensions (WORD).

The basis of any treatment programme must also take into account the wider
range of neuropsychological deficits in children as these will influence the
learning style and specific learning difficulties. The assessment of brain-injured
children may therefore be more appropriately addressed using a hypothesis
testing and problem solving approach looking at functional deficits. Until
recently, there was a very limited range of neuropsychological tests available
for children. These were well described by Strauss and Spreen 36.
Unfortunately, many of the tests had been devised for adults and although
normative data are available for children, they tended to be derived from very
small samples, and the tests themselves may not hold an inherent interest for
children.

A number of assessment instruments have become available since 1988.


These not only provide a broader overview of a child's level of functioning, but
in many respects provide very valid and functional assessments for the child,
which can form the basis of an assessment upon which further
neuropsychological testing can be carried out as part of an overall rehabilitation
teaching strategy. Although a child's limitations can be obvious, sometimes
they can be more subtle and missed. A number of general developmental
scales have been used in this respect, the Vineland Social Adaptive Scales
being the most notable (Sparrow et al) 37 and these can provide a detailed
overview of a child's functional capabilities in a number of domains.

The new Adaptive Behaviour Assessment System (ABAS) was published in two
versions in 2000; one questionnaire being completed by the parents, and the
other by the child's teachers. It provides a diagnostic assessment of the child
who has difficulties with daily living skills and is therefore more functionally
oriented. According to the manual, it provides a comprehensive diagnostic
assessment for very young people with a variety of disabilities, disorders and

36
Strauss, E. & Spreen, O. (1991). A Compendium of Neuropsychological
Tests. Oxford: Oxford University Press.
37
Sparrow, S., Balla, D., & Cichetti, D. V. (1984). Vineland Adaptive
Behaviour Scales. Minnesota: American Guidance Service Inc.

Page 13 of 114
health problems and also provides a basis upon which a rehabilitation
programme can be focused. It is unfortunate that a number of the questions
are American and to date there is no 'anglicized' version.

It does, however, provide a standardized score which can be used in compari-


son with other intellectual measures, in addition to providing a profile of
'strengths and weakness'. The age range is also practical (5-21 years), and can
therefore provide many years of assessment continuity.

During 2004, a number of neuropsychological tests specifically devised for


children became available, with the Developmental Neuropsychological
Assessment ('NEPSY') being one example. This test is not often cited in the
literature, but is useful in that it evaluates a range of neuropsychological
functioning that provides useful insight into a child's neuropsychological status.

The NEPSY is most probably the most unique test for children, because it has
been specifically devised for the 3-12 years age range. It provides assessment
of six complex cognitive functions:

• attention;

• executive functioning;

• language;

• sensory motor functioning;

• visual-spatial processing;

• memory and learning.

One of its primary aims is to provide a comprehensive assessment of the


neuropsychological status of children with a range of difficulties. Consequently,
it is, for example, used for children who have cerebral palsy, epilepsy,
hydrocephalus or traumatic brain injury.

A number of sub-tests in the NEPSY are of particular value when assessing


functional problems that may occur following a head injury. For instance,
children can sometimes be left with an extremely short verbal memory. Simple
tests such as 'sentence repetition' can reveal the very real problems a child can
have when they are unable to retain sentences of increasing length and
complexity; for example, asking a child to, 'finish their work, put the book on
the table, the pencil in the drawer and line up by the door', is pointless if the
child can only retain one instruction at a time. It is therefore extremely useful
to provide some normalized information in order to provide an objective
assessment.

When considering the effects of an acquired brain injury, it must be


acknowledged that neuropsychological assessments offer only moderate cor-
relations with everyday functioning, and this is particularly relevant when
providing neuropsychological reports that include comments on prognosis. It is
essential that ecologically valid information is obtained and that very careful
consideration is given with regard to the child's pre-injury status; the level of
support that the child has received following the injury, including educational

Page 14 of 114
support; parental expectations and attitude etc.

These issues are well discussed by Silver 38, who examined the multiple issues
that exist when trying to predict functioning following traumatic brain injury
(TBI) in day-to-day, real-life situations, and especially when having to consider
developmental factors and the intervening variables that may increase or
decrease the child's adaptive functioning over the course of recovery. Ylvisaker
and Gioia 39 pointed out that children with TBI may perform poorly on unfamiliar
or unappealing tests, whereas functioning in the real world with a familiar
routine may exceed expectations suggested by these more formal test results.
Cripe 40 emphasized the necessity for using observations or check-lists and that
rating scales are needed in order to provide some valid appraisal of the child's
functioning in the real world.

A further point to consider is the rehabilitation of adults and how well


neuropsychological assessments relate to outcomes. Leahy and Lam 41 exam-
ined the relationship between performance and neuropsychological measures,
and the vocational and independent living functioning of individuals following
TBI. They reported that the correlations were generally poor, with only the
intelligence test and colour and word test scores differentiating individuals who
did or did not require assistance with activities of daily living.

Whereas neuropsychological assessments are extremely important in assessing


children's abilities along a number of dimensions and in helping to plan
remediation strategies, the translation between test scores and the skills
required in everyday life in the child's real environment must be made with
caution. When devising therapeutic and rehabilitative packages, great care
must be taken regarding making long-term predictions from test results that, at
present, would appear to be relatively poor predictors of long-term outcome; a
much broader based assessment of a child's functioning, taking all factors into
consideration, is essential before making important statements that may have
very long-term implications to a child's future needs (Rivara et al.) 42.

A broad-based assessment is therefore needed to provide an overall profile of


the child's deficits. Some of this information may be derived from specific
tests, but valuable information can be derived from detailed observation of the
child in normal situations. A comprehensive neuropsychological evaluation
should therefore sample the following range of attributes which may or may not
have been provided by other professionals:

38
Silver, C. H. (2000). Ecological validity of neuropsychological
assessment in childhood traumatic brain injury. Journal of Head Trauma
Rehabilitation 15,973-88.
39
Ylvisaker, M. & Gioia, G. A. (1998). Cognitive assessment. In:
Traumatic Brain Injury Rehabilitation: Children and Adolescents. 2nd edn. (ed. M.
Ylvisaker), pp. 159-79. Boston: Butterworth-Heinemann.
40
Cripe, L. I. (1996). The ecological validity of executive function testing.
In: Ecological Validity of Neuropsychological Testing (eds F. R. Sbordone & C. J.
Long), pp. 171-202. Delray Beach, FL: GR Press/St. Lucie.
41
Leahy, B. J. & Lam, C. S. (1998). Neuropsychological testing and
functional outcome for individuals with traumatic brain injury. Brain Injury 12,
1025-35
42
Rivara, J. B., Jaffe, K. M., Fay, G. C., Polissar, N. L., Martin, K. M.,
Shurtleff, H. A., & Liao, S. (1993). Family functioning and injury severity as
predictors of child functioning one year following traumatic brain injury. Archives
of Physical Medicine and Rehabilitation, 74, 1047-55.

Page 15 of 114
1. A consideration of the child's sensory and motor functioning; this
includes vision and hearing including auditory perception, visual acuity
and visual fields and depth perception. Whereas these will usually have
been completed by the relevant medical personnel, their functional
implications are not always evaluated in the child's normal environment.

2. The child's physical skills need to be considered. At a fine motor level


this includes an assessment of the child's functional living skills including
dressing, feeding and, of course, writing skills - including their speed of
writing. Evaluation of the child's gross motor skills includes the child's
functional mobility within the home and school, and their ability to take
part in recreational sports.

3. An assessment of the child's overall intellectual functioning using a


standardized assessment. This would usually include an assessment to
profile the child's skills, assessing areas of comparative strengths and
weaknesses.

4. An evaluation of the child's ability to solve problems in real-life situations


and make reasonable judgements given the information that would be
available to them.

5. An examination of the child's ability to think flexibly, that is, their ability
to cope with changing situations and problems. Problems with mental
flexibility can reveal themselves both in coping with specific academic
skills and also day-to-day living skills.

6. Memory can often be impaired following a brain injury and many tests of
short- and longer-term verbal, auditory and visual memory are available.
However, some formal assessment of the child's functional memory is
needed.

7. In order to organize them in day-today living, it is necessary to assess


the child's ability. Deficits in this skill can often be masked in children
because parents usually fulfil the role for many years. It is only usually
following their transfer to secondary school, that these deficits become
manifest.

8. An assessment of the child's basic educational skills is essential; this


includes not only reading accuracy and spelling skills, but also the child's
reading comprehension, as frequently it is their comprehension skills that
are impaired following a brain injury. Mathematical skills are also com-
monly impaired, because of difficulties in mental processing.

9. Some assessment is required of the child's ability to process information


efficiently and quickly. The brain-injured child may have difficulties in
the rate at which they can process many tasks. The full extent of these
difficulties can be judged at a functional level when comparing their
performance with that of their peers.

10. It is important to make some assessment of the child's ability to learn


from their environment; although testing a child's ability to learn in a
structured setting or teaching situation is important, it must be
remembered that a great deal of information and skills will be learned
incidentally from their day-to-day living.

Page 16 of 114
11. Communication is a crucial skill which can frequently be impaired follow-
ing a brain injury. Within the expressive (language) domain, it is
necessary to assess the child's functional communications skills,
including intelligibility of speech, pragmatics and word finding. Within
the area of receptive language, there is a need to evaluate their ability to
understand short instructions and longer, more complex conversation.

12. Some estimation should be made of the child's stamina. Fatigue is a


common problem following a brain injury, particularly in first few weeks
and months, and whereas a child may be capable of several hours of
home tuition, they may not have the ability to cope with the rigours and
demands of a full or even half a school day.

13. Emotional lability is common, and it is necessary to assess the child's


ability to cope with the ups and downs of everyday life, including the
frustration often encountered in the classroom and other learning
situations.

14. The child's ability to make valid and appropriate social judgements relat-
ing to the behaviour and intentions of others is often overlooked, and if
impaired can result in behavioural difficulties and a diminished quality of
life for the child. 43

There is no one overall test or method of assessment that can evaluate all
these aspects of functioning. Indeed, in some cases, tests are not appropriate.
Given the rapid progress some children can make, the timing of any formal
assessment can be variable and, in the early stages, assessments may best be
done in the form of structured observations, although some detailed
assessments will be required at some stage.

With the rapid development of neuropsychological tests that are available for
children, the question arises as to the nature of any assessment, and the
appropriateness of administering battery after battery of test with the aim of
identifying some deficits. This is not only wasting time, but it can put the child
through a stressful experience. 44 It has been assumed that a fixed battery of
assessments provides an assessment of all the relevant neuropsychological
domains (Lezak) 45, but, of course, this is far from true. With the wide variety of
tests that are now available and suitable for children, it is not possible or
appropriate to give serial assessments. It can also add little to our knowledge
of the child. Excess testing can often lead to fatigue and poor test performance
(Strauss 46). The assessment of children's disabilities should therefore follow a
hypothesis-testing approach. 47

This has long been advocated within educational psychology, but more recently
eloquently explained in the book School Neuropsychology (Hale and Fiorello
2004 48). Clearly, some form of basic assessment is required in the first
instance, but a considerable amount of information should be gathered relating
43
Appleton, R.; Baldwin, T. Management of Brain Injured Children. 2nd
Ed. OUP,2006.
44
idem
45
Lezak, M. D. (2004). Neuropsychological Assessm ent
(4th edn). Oxford:
Oxford University Press.
46
Strauss, E. & Spreen, O. (1991). A Compendium of Neuropsychological
Tests. Oxford: Oxford University Press.
47
Appleton, R et al 2006 idem.

Page 17 of 114
the child's functioning in the real world from which it is possible to draw
inferences about their neuropsychological functioning and areas of likely deficit.
(Appleton, R. et al 2006 idem.)

Using a hypothesis-testing approach, the amount of testing can be limited and


focused on areas where deficits are identified. This obviously needs knowledge
of the tests and an understanding of neuropsychology. Of course, the danger
of such an approach is to risk a confirmation bias, that is, to seek only
information that supports one's hypothesis. It is therefore necessary not to
avoid information that may be contradictory to one's hypothesis, nor indeed to
be over-restrictive in the gathering of information, but to look for supporting
evidence from a number of sources.

It must be recalled that ecological validity should be the main goal of an


assessment, but it is not relevant just to describe a child's neuropsychological
functioning, but rather this should lead on to a positive intervention strategy,
generating a working hypothesis by which a teaching strategy can then evolve.
Changes can then be appropriately assessed, preferably using some form of
objective measure to evaluate whether or not the teaching strategies are
appropriate, as again it is the functional outcome which is especially important.

For these reasons, a hypothesis-testing approach has far more relevance,


providing it follows the cardinal rules of objectivity. A number of tests are now
available and suitable for children, many with well-produced norms, and there
may be considerable overlap in the periods of neuropsychological functioning
they are assessing. It must be appreciated that in the case of ABI, multiple
areas of functioning may or will have been affected, and a number of hypothe-
ses would therefore have to be generated and then evaluated. Information
should be sought from a number of different sources and it is often necessary
to provide a preferred hierarchy of intervention, depending upon the particular
needs of the child, so that subsequent stages of action can take place.

It is essential that all members of those working with a child, including the
family, should have a consistent approach to the child. When the child is dis-
oriented, they should say who they are, and what they are doing, talking them
through all movements, clearly, calmly and positively. If the child is being
taught, then they are told where and why, being careful not to overload them
with information which may be too much for them to process. It is essential to
keep all instructions simple.

DISORDERS OF THE HORMONE AND METABOLIC SYSTEMS

It is important that there is an understanding that those with the type of brain
injury caused by vaccines may be particularly prone to disorders of the
hormone and metabolic systems. They may also have a lack of capacity to
rationalise fear and anxiety whether real or imagined or perhaps as a result of
dreams. [See Cortisol and Dreams below, p27]
If these failings of the system are looked upon as mental illness then there is a
grave risk of causing more harm through inappropriate medication. Such
medication will not only fail to solve the problems but it will exacerbate the
original condition by causing more damage to the system.

48
Hale, J. B & Fiorello, C. A. (2004). School Neuropsychology.
Guildford:
Guildford Press.

Page 18 of 114
The Hormonal Process — Normally, cortisol levels rise during the early
morning hours and are highest about 7 am, so giving the energy that is needed
to begin the day. In the evening and during the early phase of sleep the
cortisol level should drop by approximately 90%. Evening is generally the time
when the stresses of the day are behind you, the time when you can relax and
unwind.
For those who are constantly under stress, the cortisol level can remain
elevated over long periods of time. Research now correlates chronically
elevated levels of cortisol with blood sugar problems, fat accumulation,
compromised immune function, exhaustion, bone loss, and even heart disease.
Memory loss has also been associated with high cortisol levels. Continual
stress can indeed have a negative impact on our health.

An additional problem of long-term elevations of cortisol is that the adrenal


gland may wear itself out and no longer be able to produce even normal levels
of cortisol. This is called "adrenal exhaustion" and is associated with many
other health problems.

Besides impacting the immune system, fertility, and bone health, the list of the
risks of high cortisol levels grows longer. New studies demonstrate that
elevated cortisol levels can lead to abdominal weight gain, loss of verbal
declarative memory (see Memory below, p39) words, names, and numbers),
insulin resistance, and Type 2 Diabetes.

Increasing scientific evidence suggests that prolonged psychological stress


takes its toll on the body, but the exact mechanisms by which stress influences
disease processes have remained elusive. Now, scientists report that
psychological stress may exact its toll, at least in part, by affecting molecules
believed to play a key role in cellular aging and, possibly, disease development.

In this study 49, the UCSF-led team determined that chronic stress, and the
perception of life stress, each had a significant impact on three biological
factors — the length of telomeres, the activity of telomerase, and levels of
oxidative stress — in immune system cells known as peripheral blood
mononucleocytes, in healthy premenopausal women.

Telomeres are DNA-protein complexes that cap the ends of chromosomes and
promote genetic stability. Each time a cell divides, a portion of telomeric DNA
dwindles away, and after many rounds of cell division, so much telomeric DNA
has diminished that the aged cell stops dividing. Thus, telomeres play a critical
role in determining the number of times a cell divides, its health, and its life
span. These factors, in turn, affect the health of the tissues that cells form.
Telomerase is an enzyme that replenishes a portion of telomeres with each
round of cell division, and protects telomeres. Oxidative stress, which causes
DNA damage, has been shown to hasten the shortening of telomeres in cell
culture.

"Numerous studies have solidly demonstrated a link between chronic


psychological stress and indices of impaired health, including cardiovascular
disease and weakened immune function," says lead author Elissa Epel, an
assistant professor of psychiatry. "The new findings suggest a cellular
49
Blackburn, Elizabeth; Herzstein, Morris & Epel, Elissa.
Psychological stress and disease. Proceedings of the National Academy of
Sciences. 30 November 2004.

Page 19 of 114
mechanism for how chronic stress may cause premature onset of disease.
Anecdotal evidence and scientific evidence has have suggested that chronic
stress can take years off your life; the implications of this study are that this is
true at the cellular level. Chronic stress appears to have the potential to
shorten the life of cells, at least immune cells."

Sweeping changes are needed in the organisation and ethos of the NHS’s
dedicated inpatient facilities and care homes for people with learning
disabilities, the health watchdog for England has said. Care at NHS facilities for
people with learning disabilities falls short of modern safety and quality
standards, says the Healthcare Commission in a new report, and many people
live in bleak accommodation far away from their families. 50

Institutional failings mean that many people are being deprived of their human
rights and dignity and have little access to advocacy services, few choices
about how they live their lives, and limited activities, the report says. Services
are too reliant on drug treatment to control behaviour, it says, when the
evidence that this is a reasonable response is limited.
Effects of Stress on the Brain — there is a need for providers and carers
to understanding about how stress is generated. For everyone, those
aggravating things that go wrong in the day and those irritating things that go
bump in the night — disrupting routines and interrupting sleep — all have a
cumulative effect on the brain, especially its ability to remember and learn.
As science gains greater insight into the consequences of stress on the brain,
the picture that emerges is not a pretty one. A chronic overreaction to stress
overloads the brain with powerful hormones that are intended only for short-
term duty in emergency situations. Their cumulative effect damages and kills
brain cells.

The Response of the Body's Reaction to Stress — This is sometimes


referred to as General Adaptation Syndrome (GAS). When a person
experiences stress, the brain responds by initiating 1,400 different responses
including the transmission of a variety of chemicals to our blood stream. This
gives momentary boost to do whatever needs to be done to survive. Hormones
rush to the adrenal glands to suppress the streaming cortisol on its way to the
brain. Other hormones rush to the brain to round up all the remnants of cortisol
that made it to the hippocampus. These hormones escort the cortisol remnants
back to the kidneys and then on to the bladder. The body at this stage has
reached metabolic equilibrium, also known as homeostasis. (see below p21)

There are three stages to GAS. In the first stage — called alarm reaction, the
body releases adrenaline and a variety of other psychological mechanisms to
combat the stress and to stay in control. This is called fight or flight response.
The muscles tense, the heart beats faster, breathing and perspiration increase,
the eyes dilate, the stomach may clench. This happens as a natural process in
order to protect you in case something bad happens. Once the cause of the
stress is removed, the body will go back to normal. If the cause for the stress is
not removed, go to a second stage called resistance or adaptation. This is the
body's response and provides long term protection. It causes the secretion of
more hormones that increase blood sugar levels to sustain energy and raise

50
Zosia Kmietowicz. People with learning disabilities are being let down
by NHS. BMJ 2007;335:1177 (8 December)

Page 20 of 114
blood pressure. The adrenal cortex (outer covering) produces hormones called
corticosteroids for this resistance reaction.

Overuse by the body's defence mechanism in this phase may eventually lead to
disease. If this adaptation phase continues for a prolonged period of time
without periods of relaxation and rest to counterbalance the stress response,
sufferers become prone to fatigue, concentration lapses, irritability and
lethargy as the effort to sustain arousal slides into negative stress.

The third stage of GPS is called exhaustion. In this stage, the body has run out
of its reserve of body energy and immunity. Mental, physical and emotional
resources suffer heavily. The body experiences "adrenal exhaustion". The
blood sugar levels decrease as the adrenals become depleted, leading to
decreased stress tolerance, progressive mental and physical exhaustion, illness
and possibly collapse.

The hypothalamus-pituitary-adrenal (HPA) chain of command has served


humans well as a means of survival for thousands of years. However, for those
suffering from chronic anxiety and depression this process malfunctions.
Continual stress early in life disrupts the cycle. Instead of shutting off once the
crisis is over, the process continues, with the hypothalamus continuing to signal
the adrenals to produce cortisol.
Homeostasis — When a danger finally passes or the perceived
threat is over, the normal brain initiates a reverse course of action that releases
a different type of biochemicals throughout the body. Attempting to bring you
back into balance; the brain seeks the holy grail of "homeostasis," that elusive
state of metabolic equilibrium between the stimulating and the tranquilizing
chemical forces in the body. When either one of the stimulating or tranquilizing
chemical forces dominates the other without relief, then you will experience an
on-going state of internal imbalance. This condition is known as stress; it can
have serious consequences for brain cells.

Parasympathetic and Sympathetic Nervous System — the


sympathetic nervous system (SNS) turns on the fight or flight response. In
contrast, the parasympathetic nervous system (PNS) promotes the relaxation
response. Like two tug-of-war teams skilfully supporting their rope with a
minimum of tension, the SNS and PNS carefully maintain metabolic equilibrium
by making adjustments whenever something disturbs this balance. The vital
elements in this process are the hormones, the chemical messengers produced
by endocrine glands. These hormones travel through the bloodstream to
accelerate or suppress metabolic functions.

The trouble is that some stress hormones are not completely regulated by the
body’s system. They remain active in the brain for too long – injuring and even
killing cells in the hippocampus, the area of the brain needed for memory and
learning. Because of this hierarchical dominance of the SNS over the PNS, it
often requires conscious effort to initiate the relaxation response and re-
establish metabolic equilibrium.

The Emotional Brain: The Limbic System — The primary area of


the brain that deals with stress is its limbic system. Because of its enormous
influence on emotions and memory, the limbic system is often referred to as
the ‘emotional brain’. It is also called the mammalian brain, because it

Page 21 of 114
emerged during evolution with our warm-blooded relatives, and marked the
beginning of social cooperation in the animal kingdom.

Whenever a threat is perceived, imminent or imagined, the limbic system


immediately responds via the autonomic nervous system — the complex
network of endocrine glands that automatically regulates metabolism.

The term "stress" is short for distress, a word evolved from Latin that means "to
draw or pull apart.” The Romans even used the term districtia to describe "a
being torn asunder.” When stressed-out, most of us can probably relate to this
description.

Distress Signals from the Brain — The sympathetic nervous


system does an excellent job of rapidly preparing to deal with what is perceived
as a threat to one’s safety. Its hormones initiate several metabolic processes
that allows one to cope in the best way with sudden danger.

The adrenal glands release adrenaline (also known as epinephrine) and other
hormones that increase breathing, heart rate, and blood pressure. This moves
more oxygen-rich blood faster to the brain and to the muscles needed for
fighting or fleeing — and, you have plenty of energy to do either, because
adrenaline causes a rapid release of glucose and fatty acids into your
bloodstream. Also, your senses become keener, your memory sharper, and you
are less sensitive to pain

Other hormones shut down functions unnecessary during the emergency.


Growth, reproduction, and the immune system all go on hold. Blood flow to the
skin is reduced. With the mind and body in this temporary state of metabolic
overdrive, you are now prepared to respond to a life-threatening situation.

Getting Back to Normal — After a perceived danger has


passed, the body then tries to return to normal. But this may not be so easy,
and becomes even more difficult with age. Although the hyper-activating
sympathetic nervous system jumps into action immediately, it is very slow to
shut down and allow the tranquilizing parasympathetic nervous system to calm
things down. Once the stress response has been activated, the (normal)
system wisely keeps the body in a state of readiness.

Not All Stress is Bad — Bear in mind that an appropriate stress


response is a healthy and necessary part of life. One of the things it does is to
release norepinephrine, one of the principal excitatory neurotransmitters.
Norepinephrine is needed to create new memories. It improves mood.
Problems feel more like challenges, which encourages creative thinking that
stimulates your brain to grow new connections within it.

Stress Compromises the Blood-Brain Barrier (BBB) — Stress


can dramatically increase the ability of chemicals to pass through the blood-
brain barrier. During the Gulf War, Israeli soldiers took a drug to protect
themselves from chemical and biological weapons. Normally, it should not
have crossed the BBB, but scientists learned that the stress of war had
somehow increased the permeability of the BBB. Nearly one-quarter of the
soldiers complained of headaches, nausea, and dizziness — symptoms which
occur only if the drug reaches the brain.

Page 22 of 114
Stress and Noise — sudden sound is an urgent wake-up call that
alerts and activates the stress response — a biological alarm that affects the
brain in powerful ways. Because loud noise often heralds bad news, animals
and humans have evolved a rapid response to audio stressors: the roar of a
carnivore, the crack of a falling tree, the scream of a child and more recently;
the explosion of a weapon, the wail of a siren, the crash of the stock market.
Sudden and unexpected noise for those under stress can increase the startle
response to noise.

Stress and Memory — chronic over-secretion of stress


hormones adversely affects brain function, especially memory. Too much
cortisol can prevent the brain from laying down a new memory, or from
accessing already existing memories.

The renowned brain researcher, Robert M. Sapolsky, has shown that sustained
stress can damage the hippocampus, the part of the limbic brain which is
central to learning and memory. 51 The ‘culprits’ are "glucocorticoids," a class
of steroid hormones secreted from the adrenal glands during stress. They are
more commonly known as corticosteroids or cortisol.

During a perceived threat, the adrenal glands immediately release adrenalin. If


the threat is severe or still persists after a couple of minutes, the adrenals then
release cortisol. Once in the brain cortisol remains much longer than adrenalin,
where it continues to affect brain cells.

Cortisol Affects Memory Formation and Retrieval — Cortisol also


interferes with the function of neurotransmitters, the chemicals that brain cells
use to communicate with each other. Excessive cortisol can make it difficult to
think or retrieve long-term memories. That's why people get befuddled and
confused in a severe crisis. Their mind goes blank because "the lines are
down.” They can't remember where the fire exit is, for example.

Cortisol and Temporary Memory Loss – a Study — in an animal


study, rats were stressed by an electrical shock, and then made to go through a
maze with which they were already familiar. When the shock was given either
four hours before or two minutes before navigating the maze, the rats had no
problem but, when they were stressed by a shock 30 minutes before, the rats
were unable to remember their way through the maze.

This time-dependent effect on memory performance correlates with the levels


of circulating cortisol, which are highest at 30 minutes. The same thing
happened when non-stressed rats were injected with cortisol. In contrast, when
cortisol production was chemically suppressed, then there were no stress-
induced effects on memory retrieval.

According to James McGaugh, director of the Centre for the Neurobiology of


Learning and Memory at the University of California, Irvine, "This effect only
lasts for a couple of hours, so that the impairing effect in this case is a
temporary impairment of retrieval. The memory is not lost. It is just
inaccessible or less accessible for a period of time."

51
Sapolsky, Robert M.; Krey, Lewis C.; & McEwen, Bruce S.
Glucocorticoid-sensitive hippocampal neurons are involved in terminating the
adreno-cortical stress response. Proc. Natl. Acad. Sci. USA. Vol. 81, pp. 6174-
6177, October 1984

Page 23 of 114
Cortisol and the Degenerative Cascade — normally, in response
to stress, the brain's hypothalamus secretes a hormone that causes the
pituitary gland to secrete another hormone that causes the adrenals to secrete
cortisol. When levels of cortisol rise to a certain level, several areas of the
brain, especially the hippocampus, tell the hypothalamus to turn off the
cortisol-producing mechanism. This is the proper feedback response.

The hippocampus, however, is the area most damaged by cortisol. In his book
Brain Longevity, Dharma Singh Khalsa, M.D., describes how older people often
have lost 20-25% of the cells in their hippocampus, so it cannot provide proper
feedback to the hypothalamus, so cortisol continues to be secreted.52 This, in
turn, causes more damage to the hippocampus, and even more cortisol
production. Thus, a Catch-22, "degenerative cascade" begins, which can be
very difficult to stop.

Cortisol and Brain Degeneration -— Studies done by Dr. Robert M.


Sapolsky, Professor of Neurology and Neurological Sciences at Stanford
University, showed that lots of stress or exposure to cortisol accelerates the
degeneration of the aging hippocampus.53 And, because the hippocampus is
part of the feedback mechanism that signals when to stop cortisol production, a
damaged hippocampus causes cortisol levels to get out of control — further
compromising memory and cognitive function. The cycle of degeneration then
continues.

NUTRITION AND METABOLIC DISTURBANCES

Children with head injuries present a number of complex inter-related


metabolic disturbances. The specific requirement for, and effects of nutritional
support cannot be separated from the child's nutritional condition or the pre-
injury environment and must be considered as only part of the total
environment for recovery. Superimposed on the normal requirements for
growth and development are the metabolic problems induced by trauma, the
changes in nutrition that may directly result from focal brain injury, and the
effects on neurotransmitter metabolism which are secondary to tissue damage
and nutritional insufficiency. 54
The optimal milieu for recovery after head injury has been poorly investigated,
and the conditions essential for maximizing further development in the head-
injured child remain ill-defined. From a functional viewpoint, the effects on
neurotransmitter metabolism may be considered crucial, but these are unlikely
to persist solely because of dietary factors rather, they may be compounded by
post-traumatic changes in sleep and behaviour, prophylactic drug use,
disruption of social development or on-going social relationships, general levels
of home stimulation and parental management55. A continuum of insufficiency

52
Khalsa, Dharma Singh; Stauth, Cameron. Brain Longevity. Century,
1997
53
Sapolsky, Robert M.; Uno, Hideo; Rebert, Charles S. & Finch,
Caleb E. Hippocampal Damage Associated with Prolonged Glucocorticoid
Exposure in Primates. The Journal of Neuroscience, September 1990, 10(9):
2897-2902
54
Dickerson, JWT.; Johnson, DA. & Maclean, A. Food for thought: a rôle
for nutrition in recovery. In Johnson, D., Uttley, D., & Wyke, M. A. (1989).
Children's Head Injury: Who Cares? London: Taylor and Francis.
55
Kraemer, G.W. (1985) 'The primate social environment, brain
neurochemical changes and psychopathology', Trends in Neuroscience, 8, pp.

Page 24 of 114
and impairment of brain growth, development and mental ability may exist for
the head-injured child.

Consistent with a rational approach to rehabilitation, adequate nutritional


intake may be necessary, but not of itself sufficient. Sensory activity may be
essential but nutritional support a necessity in order to obtain it56. Whilst
nutritional intervention may not provide a magic wand for the head-injured
child, it might be possible to increase the probability of positive change by
nutritional intervention.

Studies of single amino acids such as tryptophan, tyrosine and choline or


lecithin in relatively large doses may have little meaning in strictly nutritional
terms for they are not representative of how people eat. The effects of ordinary
meals on behaviour are usually smaller than those in studies of single nutrients,
so that sizeable numbers of subjects, adequately sensitive measures and tight
methodological controls are required57. Dose response parameters are largely
unknown in this sort of investigation, making it difficult to determine portion
sizes for experimental studies.

Whilst less dramatic responses to food than to the pharmacologically pure


forms could be expected, food effects upon brain function may still be of more
significance, at least in longer term maintenance of recovery achieved. It is
important to note that if the specific neurotransmitter receptors are damaged,
or other neuronal populations are also destroyed which contain converting
enzymes, for example, then increasing a particular class of neuro-chemical
activity is unlikely to be uniformly successful, particularly in cases of severe
diffuse head injury.

A great deal of research is necessary before nutritional and dietary factors are
implicated in recovery from paediatric head injury. If post-traumatic deficits in
nutritional status persist, compounded by social, cognitive and emotional
difficulties, then dietary evaluation and management may be one avenue to
explore, to help maximize progress and outcome. The effects of dietary stress
on an individual child will not simply be matters of nutritional pathophysiology,
but rather will be moulded and modified by his genetic endowment, stage of
development, home stimulation, social and emotional climates.

With increasing knowledge of neurotransmission and parallel concern about


subclinical nutritional deficiencies, the development of collaborative research
studies in this most complex field would soon help to delineate the validity of
nutritional factors in determining the optimal milieu for recovery in paediatric
head-injury. Head-injured children grow up to become relatively disabled
adults, with the added possibility that, in the presence of structural damage,
the normal ageing process may be exacerbated. Consequently, instilling good
dietary habits in childhood may at the very least be beneficial to long-term
mental function. (Dickerson et al, 1989 idem)

339-340.
56
Ricciuti, H.N. (1981) ‘Adverse environmental and nutritional influences
on mental development: a perspective’, Journal of the American Dietetic
Associatian, 79, pp. 115-120.
57
Spreen, O., Tupper, O., Risser, A., Tuokko, H. & Edgell, D. (1984)
Human Developmental Neuropsychology, Oxford, Oxford University Press.

Page 25 of 114
Cohen et al have researched neurological dysfunction caused by traumatic
brain injury and have found that this results in profound changes in net
synaptic efficacy, leading to impaired cognition. Because excitability is directly
controlled by the balance of excitatory and inhibitory activity, underlying
mechanisms causing these changes have been investigated using lateral fluid
percussion brain injury in mice.

Although injury-induced shifts in net synaptic efficacy were not accompanied by


changes in hippocampal glutamate and GABA levels, significant reductions
were seen in the concentration of branched chain amino acids58 (BCAAs), which
are key precursors to de novo glutamate synthesis. Dietary consumption of
BCAAs restored hippocampal BCAA concentrations to normal, reversed injury-
induced shifts in net synaptic efficacy, and led to reinstatement of cognitive
performance after concussive brain injury.

All brain-injured mice that consumed BCAAs demonstrated cognitive


improvement with a simultaneous restoration in net synaptic efficacy.
Posttraumatic changes in the expression of cytosolic branched chain
aminotransferase, branched chain ketoacid dehydrogenase, glutamate
dehydrogenase, and glutamic acid decarboxylase support a perturbation of
BCAA and neurotransmitter metabolism. Ex vivo application of BCAAs to
hippocampal slices from injured animals restored posttraumatic regional shifts
in net synaptic efficacy as measured by field excitatory postsynaptic potentials.
These results suggest that dietary BCAA intervention could promote cognitive
improvement by restoring hippocampal function after a traumatic brain injury.59

_______

Sleep and dreaming following Brain Injury


By measuring electrical activity, we are able to distinguish sleep from its
unconscious imitation by other behaviours. Thus, sleep is an active state of the
brain and its electrical activity continues throughout sleep and differs from that
during waking. Sleep is of the brain.

The research of Payne and Nadel briefly stated is that variations in cortisol (and
other neurotransmitters) determine the functional status of hippocampal ↔
neocortical circuits, thereby influencing the memory consolidation processes
that transpire during sleep. The status of these circuits largely determines the
phenomenology of dreams, providing an explanation for why we dream and of
what. As a corollary, dreams can be thought of as windows onto the inner
workings of our memory systems, at least those of which we can become
conscious.

58
Branched Chain Amino Acids are Leucine, Isoleucine and Valine. They
are available combined in a powder or as a tablet. Effectiveness of BCAAs can
be increased by consuming 10mg of Vitamin B6 with every 10g of BCAA.
59
Cohen, Akiva S.; Cole, Jeffrey T.; Mitala, Christina M.; Kundu,
Suhali; Verma, Ajay; Elkind, Jaclynn A.; & Nissim, Itzhak. Dietary
branched chain amino acids ameliorate injury-induced cognitive impairment.
Proceedings of the National Academy of Sciences. published online before print
December 7, 2009,

Page 26 of 114
In addition to exploring these ideas, their paper provides some background
concerning:

(1) the states of sleep and the role of various neurotransmitters in


switching from one sleep state to another,

(2) how the characteristics of dreams vary as a function of sleep state,

(3) the memory content typically associated with dreaming in different


dream states, and
60
(4) the role of sleep in the consolidation of memory.

We know also, that the normal brain controls itself so as to produce sleep. The
clocks that turn sleep on and off are composed of networks of brain cells.
These clocks not only time whether we sleep or wake but also program an
elaborate and orderly sequence of brain events within sleep. In one such
event, the continuously active brain becomes extraordinarily more active every
90 to 100 minutes during sleep and remains so as long as an hour. It is during
such periods that we dream. Thus, dreaming, like sleep, is of the brain and by
the brain. 61

The brain is the prime beneficiary of sleep, as is made obvious by the progres-
sive decline in our cerebral capacities when we are deprived of sleep. We first
have difficulty concentrating, attending, and performing coordinated motor acts
such as driving cars. Then we become irritable and suffer an almost painful
sleepiness.

After we go five to ten days without sleep, our brain loses its bearings
altogether and madness takes over: the trusting become paranoid; the rational,
irrational; and the sane begin to see and hear things that aren't there. All the
dysfunctions caused by sleep deprivation are rapidly reversed when lost sleep
is recovered. We don't yet know exactly how sleep ensures efficient brain func-
tion, but that it does so is beyond doubt. Thus, sleep is for the brain. Sleep is
of the brain, by the brain, and for the brain. (Hobson, 1989, idem)

Recognizing the connection between the brain and sleep we can better
appreciate why sleep science is so new. It was not until the second quarter of
our own century that a way was found to measure sleep objectively by
recording the brain electrical activity.

There are two combined factors that have helped to produce an observational
sleep science. First, the subjective experience of nightmares and dreams
shows that sleep cannot occur without intense brain activity. Secondly, while
animal sleep appears tranquil, in all mammals — including humans —
observable movements of the eyes, face, and fingers occur periodically during
sleep. It seems inconceivable to us that those who watched sleeping cats'
paws twitch, sleeping puppies' feet scamper, or sleeping babies' faces grimace
and smile did not suspect intense underlying brain activity. We can infer that
such outward signs of motion are related to the inward experience of dreams

60
Payne, Jessica D. & Nadell, Lynn. Sleep, dreams, and memory
consolidation: The role of the stress hormone cortisol. Learning and Memory;
2004. 11: 671-678.
61
Hobson, JA. Sleep. Scientific American Library; 1989; pp3.

Page 27 of 114
and therefore a strong presumptive evidence of brain activation. (Hobson,
1989, idem)

When there is a chronic lack of sleep it seems likely that structures behind the
medulla (see below, this page) might actively contribute to the slowing of non-
REM sleep. Studies by other researchers have implied that an area just next to
the hypothalamus, called the basal forebrain, may playa role in controlling non-
REM sleep. The generation of non-REM sleep was shown to be impeded by
damaging and enhanced by stimulating this area of the brain.

Liu et al 62 and Madan et al 63 suggest that conditioned fear causes REMS


alterations, including difficulty in initiating a REMS episode as indicated by the
diminution in the number of seq-REMS episodes. Another finding, the increase
in phasic activity, agrees with the inference from clinical investigations that
retrieval of fearful memories can be associated with the long-term REMS
disturbances characteristic of posttraumatic stress disorder.

Michel Jouvet is perhaps the world's leading sleep and dream researcher. He
discovered a dream state that he called paradoxical sleep. This third category
of brain activity (distinct from sleeping and waking) is a state of very deep
sleep with some specific motor events, including rapid eye movements (REM).
64

In 1959 Michel Jouvet conducted several experiments on cats regarding muscle


atonia (paralysis) during REM sleep. Jouvet demonstrated that the generation
of REM sleep depends on an intact pontine tegmentum65 and that REM atonia is
due to an inhibition of motor centres in the medulla oblongata. 66 Cats with
lesions around the locus coeruleus67 have less restricted muscle movement

62
Liu, Xianling; Tang, Xiangdong & Sanford, L D. Fear-conditioned
suppression of REM sleep: relationship to Fos expression patterns in limbic and
brainstem regions in BALB/cJ mice. Brain Research. Volume 991, Issues 1-2, 21
November 2003, Pages 1-17
63
Madan, Vibha; Brennan, Francis X.;.Mann, Graziella L.; Horbal,
Apryle A.; Dunn, Gregory A.; Ross, Richard J. & Morrison, Adrian R. Long-
term Effect of Cued Fear Conditioning on REM Sleep Micro-architecture in Rats.
Sleep. 2008 April 1; 31(4): 497–503.
64
Jouvet, Michel. The Paradox of Sleep: The Story of Dreaming. MIT
Press 1999.
65
The pontine tegmentum is a part of the pons of the brain involved in the
initiation of REM sleep. It includes the pedunculo-pontine nucleus and the latero-
dorsal tegmental nucleus, among others, and is located near the raphe nucleus
and the locus ceruleus . PET studies seem to indicate that there is a correlation
between blood flow in the pontine tegmentum, REM sleep, and dreaming .
66
The medulla oblongata is the lowest part of the brain, situated at the
top of the spinal cord and controlling activities such as heart beat, blood
pressure and breathing.
67
The Locus coeruleus is a nucleus in a dense cluster of neurons in the
dorso rostral pons of the brain stem involved with physiological responses to
stress and panic. This nucleus gained prominence in the 1960s when new
anatomical approaches revealed it to be the major source of norepinephrine in
brain with projections throughout most central nervous system regions,
including the cerebral cortex, hippocampus, thalamus, midbrain, brainstem,
cerebellum, and spinal cord (Foote et al., 1983; Aston-Jones et al., 1995). These
findings stimulated a great deal of research into this unusual system, resulting in
a wealth of knowledge at the cellular, systems, and behavioural levels.

Page 28 of 114
during REM sleep, and show a variety of complex behaviours including motor
patterns suggesting that they are dreaming of attack, defence and exploration.

Jouvet proposed the speculative theory that the purpose of dreaming is a kind
of iterative neurological programming that works to preserve an individual's
psychological heredity, the basis of personality. 68

A different brainstem structure, the pons, has been shown by Jouvet to be


critical for REM sleep generation. He transected the midbrain of a cat, and then
completely removed all the structures above the cut, except the hypothalamus.
The resulting "pontine" cats had a periodically recurrent phase of rapid eye
movements associated with a complete loss of muscle tone. This latter phe-
nomenon (called postural atonia) had been shown also to characterize REM
sleep in normal cats by Jouvet and Francois Michel in 1959 and was later shown
to be true also of human REM sleep (Michel Jouvet et al)69. This experiment
pointed to a timer and trigger for REM sleep in the pons.

Electromyogram (EMG) experiments show that movements are found to be


abolished in REM sleep. Because we do not move our muscles in REM sleep, we
cannot express the motor acts of our dreams. Of course, during their atonic-
REM periods Jouvet's cats could show no cortical EEG changes (because they
had no cortex), but they did have spiking EEG waves in the pons during these
periods that resembled those seen in normal cats. Jouvet proposed that there
was both a REM sleep clock and trigger mechanism in the pons. The clock was
reliable because the episodes occurred in the cat at regular intervals of 30
minutes as in normal sleep; the trigger was effective because the episodes
lasted for the normal duration of 6 to 8 minutes.

It should be clear therefore that many areas of the complex brainstem are
involved in the control of sleep and waking. Non-REM sleep mechanisms in the
basal forebrain interact with medullary and midbrain reticular systems to
produce EMG slow waves in the cortex; periodically interrupting this process is
the REM sleep generator in the pons, which reactivates the brain. This then
leads us to look at why brain injury can cause sleep disturbance and what parts
of the sleep cycle may be affected.

Glen Johnson, a Clinical Neuropsychologist of the Neuro-Recovery Head Injury


Program, Traverse City, USA writes that, “…all of my head-injured patients have
some form of a sleep disorder.” 70 It is enlightening to read of his experience
with brain injured patients.

“First, let's recognize what happens with a typical sleep disorder caused by a
head injury. Typically, you may go to sleep fairly easily, although sometimes
people can’t stop their thoughts in the evening and have difficulty getting to
sleep. Once you have fallen asleep, you may feel that you’re waking up as often
as every hour. By about 4 or 5 in the morning, you're wide awake, even though
you are dead tired. In addition, many people who have head injuries are easily

68
Jouvet, Michel. Paradoxical Sleep - A Study of its Nature and
Mechanisms.
Progress In Brain Research Vol. 18 Sleep Mechanisms 1965
69
Jouvet, M., Michel, F., & Courjon, J. (1959). Sur un stade d'activité
é]ectrique cérébrale rapide au cours du sommeil physiologique C.R. Soc. Biol.
(Paris), 153, 1024-1028.
70
Johnson, Glen. Traumatic Brain Injury: Survival Guide. Online edition at:
www.tbiguide.com

Page 29 of 114
awakened by small noises. I've had patients who would sleep though a fire
alarm prior to their head injuries, but who now wake up when a cat walks by.

Sleep is very important to the healing process. If you don't sleep, you're going
to be tired throughout the day. If you're tired throughout the day, your memory
will get worse and you'll be more cranky and irritable. Lack of sleep makes the
other head injury symptoms much worse. Sleep also has an important role in
physical healing.” (idem)

A wide-range study of victims of head injury often reveals disorders that are
neglected by less extensive examinations, and dispels the idea that there is
usually a benign outcome. Following head trauma, there is a marked increase
in dreams of threatening content, despite the fact that, contrary to repression
occurring in many post-traumatic victims, a comatose person with head injury
has no registration of the traumatic event. The loss of self-esteem and self-
confidence creates a permanent state of stress, which can be reflected in the
patients’ threatening, frightening and anxiety-provoking dream content. It is
reasonable to assume that dreaming is, in part, an expression of both
neurological control and feedback of intention and action. 71

_______

Information Processing
A common deficit arising from a brain injury, and more commonly from a head
injury, is the inability to process information at the normal rate. Whereas the
child may be able to carry out a variety of mental tasks, the speed at which
these are completed in a brain-injured child may be significantly slower than it
would be for a normal child (Brooks 1984). 72 The deficit may involve the
speed at which the child can understand the task involved, learn the material,
retrieve it from memory and then carry out the mental processes involved.

Deficits in this area can severely limit the ability of the child to function in many
everyday situations and such deficits can arise following even a mild head
injury (Wrightson et al.) 73 In specific detail, the child finds difficulty
comprehending information at the normal rate, formulating their thoughts and
then carrying out the required actions. They may find it difficult to understand
if too much information is presented at any one occasion. They may therefore
initially start off understanding what is going on but rapidly lose their way as
the amount of information accumulates. This is particularly the case if the level
of information becomes more complex and can occur in both the classroom and
in social situations.

Borod 74 found brain-injured children to be less competent at comprehending


emotional information. In the teaching situation this often shows itself in the

71
Parker, RS. (2000) Concussive brain trauma: neurobehavioral
impairment and maladaptation. Taylor & Francis Ltd.
72
Brooks, N. (1984). Cognitive deficits after head injury. In: Closed Head
Injury: Psychosocial Social and Family Consequences (ed. N. Brooks), pp. 44-73.
Oxford: Oxford Community Press.
73
Wrightson, P., McGinn, V., & Gronwall, D. (1995). Mild head injury in
pre-school children - evidence that can be associated with a persisting cognitive
defect. Journal of Neurology Neurosurgery and Psychiatry 59, 375-80.

Page 30 of 114
child's inability to complete written assignments or answer questions in the
allotted time, and therefore never being able to answer a question directed at
the class, because by the time they raise their hand someone else has already
answered before them.

Children who are significantly affected can find themselves severely


disadvantaged at a social level. Whereas adults will give a child a sympathetic
look and the necessary time to collect their thoughts, a more competitive
adolescent group will not be so kind or so tolerant. In the playground, the
conversation moves at the pace of the group and for those too slow to respond,
they frequently find themselves left far behind; sometimes it is easier not to
even try, and the child may find themselves becoming increasingly isolated
from their peers. 75

The ability to understand, learn and then retrieve information involves a range
of abilities, including attention, short-term memory and the ability to
manipulate the information in order to place it into a more permanent memory
system. Essential to this, is the ability to organize material into a meaningful
manner so that it can be recalled and subsequently placed within some existing
scheme or order. As Tromp and Mulder (1991)76 demonstrated, access to the
memory system affects the speed at which information is processed.
Information therefore has to be organized and categorized so that it can be
stored in some permanent memory system. To do this, it is also necessary for
the child to be able to distinguish the core information and main ideas from any
irrelevant information. It is apparent that a range of strategies can be used at a
simplistic level. The rate, amount and complexity of the material may,
however, exceed what the child can comfortably cope with at a simplistic level.
To help the child cope with such processing problems, it is important that par-
ents and teachers are aware that the child may have such difficulties.
If people are so aware, the problem can be partly resolved by altering the rate
at which work is presented. It is also very valuable if the child can be offered
some basic strategies and prompt him to say; 'can you please explain that
again?'; 'can you go through that a little slower, please?’ Or 'can you let me
think about that for a minute before I answer?’ These sorts of responses can
give the child a second opportunity to answer or resolve the problem and help
to prevent an anxiety-producing situation.

It is possible to give children more general strategies in order to help to speed


up the processing problem within its own right. The child can be encouraged to
use visual imagery, provided that they have intact visual and perceptual skills.
This visual imagery technique has been well explained by Buzan 77 using 'mind
maps' whereby the child can be encouraged to use diagrams as cues to help
prompt the memory process. This technique can also be used to enhance both
short-term and working memory. It can show how new learning can be
attached to older more established, and more intact areas of memory and
therefore the child can be shown which 'hooks' to hang the new information on.

74
Borod, J. C. (1992). Interhemispheric and intrahemispheric control of
emotion. Journal of Consulting and Clinical Psychology 60, 339-48.
75
Appleton, R et al 2006 idem.
76
Tromp, E. & Mulder, T. (1991). Neuropsychological slowness of
information processing after a traumatic head injury. Journal of Clinical and
Experimental Neuropsychology 13, 821-30.
77
Buzan, T. (1974). Use Your Head. London: BBC Publications.

Page 31 of 114
_______

Executive Functioning
The term 'executive functioning' is used to describe the ability to maintain the
appropriate solving-set necessary for the attainment of a future goal. This act
can involve one or more of the following:

• the ability to inhibit normal or more usual responses and possible defer
them for a later, or more appropriate time;

• the ability to develop a strategic plan of action required to solve the


problem;

• the ability to develop a conceptual model of the problem and to use past
experiences and incorporate them into the problem-solving exercise.

Executive functioning can therefore be quite separate from other areas in


intellectual development, including perception and many aspects of language
and memory. It does, however, overlap with other areas including attention-
reasoning and problem-solving. The typical lists used to describe executive
functioning include:

• set-shifting and set maintenance;

• interference control;

• inhibition;

• integration of thought across space and time;

• planning;

• working memory. 78

Working memory tasks

Efficient planning entails decision making and developing strategies for


setting priorities. Atkinson and Shiffrin (1968)79 described working
memory as involving, among other processes, decision making. Using a
similar model, Baddeley and Hitch (1974)80 proposed that working
memory depends on an attentional controller, which they called the
central executive and later the supervisory attentional system (Baddeley,
1986 81; Norman and Shallice, 1986)82. In this model, the supervisory
78
Appleton, R et al 2006 idem.
79
Atkinson, R.C.; Shiffrin, R.M. (1968). Human memory: A proposed
system and its control process. In Spence, K.W.; Spence, J.T. [Eds.]. The
psychology of learning and motivation (Volume 2). New York: Academic Press.
80
Baddeley, A.D., & Hitch, G. (1974). Working memory. In G.H. Bower
(Ed.), The psychology of learning and motivation: Advances in research and
theory (Vol. 8). New York: Academic Press.
81
Baddeley, A. Working memory. Oxford: Clarendon Press, 1986.
82
Norman, D. A. & Shallice, T. (1986). Attention to action: Willed and
automatic control of behaviour. In Davidson, R. J., Schwartz, G. E., & Shapiro, D.,
editors, Consciousness and Self-Regulation: Advances in Research and Theory.

Page 32 of 114
attentional system selects and operates strategies for maintaining and
switching attention as needs arise.

Baddeley and Hitch first proposed this Model of Working Memory, in an


attempt to describe a more accurate model of short-term memory. Their
tripartite working memory model is an alternative to the short-term store
in Atkinson & Shiffrin's 'multi-store' memory model (1968 idem). This
model is later expanded upon by Baddeley and other co-workers and has
become the dominant view in the field of working memory.

Executive processes include various kinds of judgments made on stimuli


held in short-term memory (e.g., comparison of the relative recency of
stimuli, judgments of the relative saliency or novelty of stimuli, etc.) and
active (voluntary) retrieval of specific information held in long-term form.
(Petrides, 1994, p.73)83

Failure of this system produces the dysexecutive syndrome (Baddeley,


1986 idem; Baddeley and Wilson, 1988)84. The dorsal prefrontal cortex
appears critical for allocating attentional resources during working
memory tasks (Koechlin, Basso, et aI., 199985; Koechlin, Corrado, et aI.,
2000 86; Petrides, 1994 idem).
Damage to the frontal structures may lead to a diverse set of changes in
cognitive, behavioural, or emotional domains. While lesion studies have
demonstrated distinct impairments related to pathology in different
frontal regions, it is clear that the frontal lobe syndrome is not restricted
to damage to frontal regions. Therefore, the broad range of impairments
in executive functioning evident in neurologic disease is often referred to
as the dysexecutive syndrome. Hanna-Pladdy provides an overview of
how executive functioning has been traditionally defined and measured.
The components of executive function such as planning, cognitive
flexibility and set-shifting, initiation and self-generation, response
inhibition, serial ordering and sequencing, are discussed with respect to
traditional measures and neural substrates. 87 [See also Memory
below, p37]

These skills therefore describe a complex range of higher-order cognitive skills


that are crucial to independent-living. The types of deficits that can occur in
adults who have sustained frontal lobe damage has been well reported; Stuss
and Benson 88 and assessed Malloy and Richardson 89.

Plenum Press.
83
Petrides M. (1994). Frontal lobes and working memory: evidence from
investigations of the effects of cortical excisions in nonhuman primates. In:
Boller F, Grafman J, editors. Handbook of neuropsychology. (Vol. 9.) Elsevier;
Amsterdam.
84
Baddeley, A. & Wilson, B.A. (1988). Frontal amnesia and the dys-
executive syndrome. Brain and Cognition, 7, 212-230.
85
Koechlin, E., Basso, G., Pietrini, P., et al. (1999). The role of the an-
terior prefrontal cortex in human cognition. Nature, 399, 148-151.
86
Koechlin, E., Corrado, G., Pietrini, P., & Grafman, J. (2000). Dis-
sociating the role of the medial and lateral anterior prefrontal cortex in human
planning. Proceedings of the National Academy of Sciences of the United States
of America, 97, 7651-7656.
87
Hanna-Pladdy, B. Dysexecutive Syndromes in Neurologic Disease.
Journal of Neurologic Physical Therapy, Sep 2007.
88
Stuss D. T. & Benson F. D. (1984). Neuropsychological studies of the
frontal lobes. Psychological Bulletin 95, 3-28.
89
Malloy, P. E & Richardson, D. E. (1994). Assessment of frontal lobe
functions. Journal of Neuropsychiatry 6, 399-410.

Page 33 of 114
Until recently, however, less attention has been paid to the problems
associated with such damage in children, as this is an aspect of normal
developmental patterns and variance seen in children, and partly because of
the educational settings in which they are placed. A young child is not
expected to organize themselves or plan and execute complex tasks. The child
is, by virtue of being in school or a family, structured and focused in much of
their day-to-day living.

One of the most common, but also vulnerable, structures to be damaged in a


head injury are the frontal lobes, and yet within the paediatric literature, it is
only comparatively recently that interest is being re-expressed in this crucial
area of functioning. It was often assumed that frontal lobe functioning was not
particularly relevant to children's development but this view has now changed
dramatically, including the developmental assessment of 'executive
functioning' (Kelly et al. 1996) 90.

The consequences of early-onset brain damage for the development of


cognition and behaviour have recently been identified as top research priorities
by National Institute of Neurological Disorders and Stroke (NINDS). There have
been a series of new empirical studies that address this issue in depth, from
several different perspectives and in both human and animal participants. The
focus is on the development of personality, social behaviour, and related
executive functions, in subjects who suffered early damage to prefrontal brain
regions. A consistent theme throughout is that early-onset prefrontal lesions
can frequently lead to severe, intractable deficits in social behaviour and moral
reasoning and to impairments of executive functions, such as planning,
judgment, and decision making. 91

It has been known for over 100 years that frontal lobe injury in children is often
associated with considerably more functional recovery than after similar injury
in adulthood. Systematic study of frontal cortical injury in laboratory animals
has shown that this recovery is tightly tied to developmental age: There is a
brief window of time during cortical development during which the brain is able
to compensate. Simply being young is not sufficient because injury prior to this
critical period leads to miserable behavioural outcomes.

For humans, the least favourable time for cortical injury is likely at the end of
the gestational period, perhaps including the 1st month or so of life whereas
the most favourable time is around one to two years of age. In addition to age,
the extent of behavioural recovery is influenced by age at assessment, the
nature of the behavioural assessment, sex, and lesion size.

Anatomical studies have shown that functional recovery following early cortical
injury is correlated with a reorganization of remaining cortical circuitry,
including increased dendritic arborisation and increased spine density.
Recovery, and the compensatory anatomical changes, can also be potentiated
by application of different treatments including behavioural therapy, trophic
factors, and neuromodulators.

90
Kelly, T. P., Borrill, H. S., & Maddell, D. L. (1996). Development and
assessment of executive function in children. Child Psychology and Psychiatry
Review 1, 46-51.
91
Tranel, Daniel; & Eslinger, Paul J. [Eds.] Early Frontal Lobe Damage
and Development. A Special Issue of Developmental Neuorpsychology Volume
18, Number 3, Psychology Press 2001.

Page 34 of 114
There is also preliminary evidence in laboratory animals to suggest that it may
be possible to induce neural regeneration in the injured brain and that the
regenerated brain functions to support functional recovery. 92

One of the main issues has always been that, not uncommonly, young people
who have frontal lobe damage or deficits in executive functioning can perform
relatively well on normal IQ tests and the difficulties in executive functioning do
not become fully apparent until they have progressed through adolescence; as
a consequence, important skills that are required for later life do not develop.
(Appleton, R. et al 2006 idem.)

Frontal lobe development is crucial to many aspects of behaviour in early


childhood. The terms 'frontal lobe functioning' and 'executive functioning', are
frequently used interchangeably, although executive functioning skills are
dependent upon many areas of the brain. Executive functioning is inherent in
all purposeful behaviour, including the arousal of interest, intentional action
and attainment of rewards.

It is essential for a purposeful goal-directed activity, and in recent years great


interest has been paid towards the relationship between frontal lobe
functioning and some crucial and wide-ranging developmental disorders
including attention deficit disorder (ADD) and autistic spectrum disorder (ASD).
The implication of frontal lobe deficits in developmental disorders and
functional effects has been extensively explored by Pennington and Oznoff 93.

Many of the functions that the frontal lobes control may not be required at a
young age, although it is clear that many aspects of frontal lobe functioning can
become increasingly apparent as the child gets older 94.

Difficulties in attention and control can be less evident and less crucial early in
the child's life. Equally, in the more structured primary school environment, the
ability to plan and organize is not as crucial as it is when the child transfers to
secondary school. One pattern that is frequently faced is the child who has
become overly friendly and disinhibited with their general social behaviour
resembling that of a much younger child, which consequently puts them at
considerable risk and causes great anxiety to parents. Alternatively the child
may be over-impulsive, disinhibited and aggressive in their behaviour, causing
frequent disruptions both in home and in school. (Appleton, R. et al 2006
idem.)

Rigidity in thinking produces a child who has major difficulties coping with any
changes in their environment. Sometimes these children can find life tolerable
at primary school, but transfer to secondary school is usually met with
increasing difficulties, as they have problems with switching from one set of
tasks to another and having to move from one lesson to another; the need to
92
Kolb, Bryan; Gibb, Robbin & Gorny Grazyna. Cortical Plasticity and
the Development of Behaviour After Early Frontal Cortical Injury. Developmental
Neuropsychology, Volume 18, Issue 3 February 2000 , pages 423 – 444.
93
Pennington, B. F. & Oznoff, S. (1996). Executive functioning and
developmental psychopathology. Journal of Child Psychology and Psychiatry 37,
58-89.
94
Diamond,A. (1991). Neuropsychological insights into the meaning of
object concept development. In: The Epigenesis of Mind: Essays on Biology and
Cognition (eds S. Carey & R. Gelman). Hillsdale, NJ: Lawrence Erlbaum
Association.

Page 35 of 114
possibly move up to nine times a day can frequently prove too much for them
and can lead to loss of attention, frustration and fatigue. The child lacks the
ability to delay their responses and although this may be entirely normal (and
therefore acceptable) in an 18-month-old child, it is very difficult to deal with in
a school child. PassIer et al. 95 concluded that the development of executive
functioning in children occurs in a multi-stage process.

Since 1998 there has been rapid development and interest in the whole area of
deficits in executive functioning in children and young people. Whereas one
previously had to choose from a range of available tests, there are currently
several well-standardized and published tests that specifically evaluate this
area of cognition function. Anderson 96 quite clearly reported that the
assessment of children with dysexecutive disorders was difficult due to the lack
of appropriate assessment tools. It is notable that very few tests were suitable
for children and most were downward extrapolations of adult tests with few
child norms. The behavioural assessment of the dysexecutive syndrome or
behavioural assessment of the dysexecutive syndrome BADS-C, has been
adapted for children with an emphasis on more real-life situations and
scenarios. This is considered to be an ecologically valid and reliable battery of
tests of executive functioning for children and adolescents with a child-friendly
administration and comprehensive normative data. (Appleton, R et al 2006
idem.)

The Deliss Kaplin Executive Function System97 (D-KEFS) was published in 2001
and comprises of nine tests that assess both verbal and non-verbal executive
functioning. Fortunately, each of the nine tests is designed to stand alone and
can be administered individually when adopting a hypothesis-testing approach
towards a child's deficits; alternatively the whole test can be administered,
although this can be quite a lengthy exercise. The test does, however, provide
a valuable and much-needed way of assessing the principal domains of
executive functioning.

Whereas specific tests have become available in assessing children who have
executive functioning deficits, assessment methods using questionnaires have
been developed and published by Psychological Assessment Resources (PAR).

The Behaviour Rating Inventory of Executive Functioning98 (BRIEF), are


questionnaires for parents and teachers that allow the assessment of executive
functioning behaviours in different environments and are designed for children
aged 5-18 years. The questionnaires cover the principal domains of executive
functioning, including inhibitory control; the shifting of mental set; emotional
control, the abilities to modulate emotional responses; the ability to initiate
tasks independently and generate novel ideas; and working memory; i.e. the
ability to hold information in mind and to maintain an activity for a purpose and
the ability to plan and organize both within the daily life, and also in the use of
95
Passler, M. A., Issac, W., & Hynd. G. W. (1985). Neuropsychological
development of behaviour attributed to frontal lobe functioning in children.
Developmental Neuropsychology 1, 349-70.
96
Anderson, P. (2002). Assessment and development of executive
function (EF) during childhood. Neuropsychology Dev Cog C Child
Neuropsychology, 8, 71-82.
97
Delis, D. C., Kaplan, E., & Kramer, J. H. (2001). Delis-Kaplan
Executive Function System (D-KEFS). San Antonio, TX: The Psychological
Corporation.
98
http://www3.parinc.com/products/product.aspx?Productid=BRIEF-P:SP

Page 36 of 114
materials and the ability to monitor the behaviour and performance.

The screening questionnaires take account of the developmental course of


executive functioning and the fact that many of these skills are not evident in
the young child, but gradually develop during adolescence. The scores have
been validated recently and can be considered as both a valid and reliable
method of assessing executive functioning in different settings. They are also
valuable in providing a range of strategies that are robust and practical.

Problems associated with frontal lobe damage are often complex and on first
sight can be confusing and mistaken as signs of emotional disturbance or
'naughtiness'. In general terms they fall into the following patterns, although
the specific difficulties can vary for each child:

• Sometimes they have difficulties in initiating behaviour; they also


appear to have a superficial depressive sort of approach and as a
result may just be considered lazy or disinterested. This has been
termed 'pathological inertia'. The child may know what to do, but
appears to have major problems initiating the appropriate behaviour.

• They may have difficulties in making mental or behavioural shifts, and


therefore carry on a style of behaviour long past the point at which it
is productive. They do not readily respond to correction and do not
pick up on day-to-day learning experiences (as opposed to those in
which they have been directly instructed).

• The child may have problems in stopping or modulating ongoing


behaviour which shows itself as impulsivity, overreaction and
disinhibition. The problems appear in everyday life as loss of control,
an attentional deficit and lack of self-awareness. This results in an
inability to perceive performance errors, to appreciate the impact one
has on others, or to size up social situations accurately. They may
therefore be impulsive and unconcerned about the social conventions,
and can put themselves at serious risk — from isolation, ridicule or
even abuse.

• A concrete attitude or lack of abstract thinking is also common among


children with frontal lobe injuries. They appear to have a difficulty in
dissociating themselves from the immediate surroundings. They are
therefore driven by the here and now, and do not reflect or make use
of previous information in order to modify their behaviour.
(Appleton, R et al 2006 idem.)

It therefore follows that social competence can be severely affected following a


brain injury, particularly if there has been frontal lobe damage. Whereas the
range of social difficulty can be found using checklists such as the Vineland
Social Adaptation Scales or ABAS; these are a descriptive series of statements
that refer to normal behavioural competencies and do not identify the under-
lying neurological deficit. Similarly, IQ measurements are generally not sensit-
ive in picking up such deficits and many children who have sustained significant
frontal lobe damage may be able to perform competently on conventional
intelligence tests.

Children with acute brain injuries often do not generalize from the rules of

Page 37 of 114
interpersonal behaviour into actual social interchanges. The children appear to
be quite concerned about their social relationships and they are often
apologetic after making the mistake and yet they continually repeat the same
behaviours and mistakes. These can often be simple aspects of normal social
rules, such as remembering to say 'pardon' or 'please' without prompting, or
following the general school rules. Equally, more subtle problems such as
keeping secrets, knowing who and when to tell, may severely affect social rela-
tionships. Similarly, exercising self-control by not asking embarrassing or
inappropriate questions is crucial if the child is to cope within the social context
of a school environment.

To be able to cope socially at a competent level with their peer group, a child
must possess the insight and have the ability to read the subtleties in commun-
ication such as body language, facial expression, tone and pitch of voice etc.
The child who has experienced a brain injury often lacks these skills, as well as
the ability to process the information and respond within a reasonable time
span. As such, they may either avoid interaction, or if they do interact, their
approach and behaviour may be inappropriate. They may want to dominate
the conversation or not know when to complete it. Other children may there-
fore have difficulties understanding their intentions and may misinterpret their
behaviour and also their abilities. Strategies therefore have to be developed to
help these children to clarify, organize, remember and express information in
an appropriate manner. (Appleton, R et al 2006 idem.)

Rehabilitation — The rehabilitation of children with frontal lobe injuries


and dysfunction is generally difficult. To some extent it is possible to focus on
areas of specific skills; for example, children with attentional difficulties can be
helped with some intensive tuition or training on attention. It is also possible to
encourage a degree of internal control using verbal mediation techniques.
Similarly, some problem-solving behaviours can be helped using a 'talking
through' approach, having the child verbalize as they work through a problem.
In the same way with a developing child, it is possible to teach alternative
strategies and through a combination of modelling and guiding, more
appropriate codes of behaviour can be encouraged. In the middle and later
adolescent years, these children can frequently have difficulties at school, not
because of the educational demands being placed upon them, but because of
the social demands of their peer group. Other children may be able to 'sense'
or identify a child who has some of these higher-order reasoning difficulties and
they can tease or 'set them up'. Therefore the support for many children who
have suffered frontal lobe injuries requires a restructuring of the child's
environment. This means a readjustment of parental expectations and
demands that may include an alteration in the organization of the school day,
and the type of lifestyle that the parents (and family) may have previously led.
The child may have to readjust from living within an active outgoing family to
one that follows more structured and solitary pursuits. Similarly, the school
environment may have to be modified, in that the child may require individual
support or assistance or may need transfer to a special school; however, such a
transfer may itself be difficult and necessitate major readjustments. (Appleton,
R et al 2006 idem.)

Whereas it may be that children with frontal lobe dysfunction need a more
structured environment, to some extent they can be taught some basic strate-
gies to help them cope with day-to-day living. They can be taught sets of social
rules which can then be reinforced and over-learned to the point that they

Page 38 of 114
become drilled responses, for example, 'stop, look, listen, stop at the kerb, look
left, look right, look left again, before crossing'; 'look outside, check the
weather, is it raining? What do I need to wear?' these sorts of tasks and exer-
cises are often carried out with younger children, but may only be taught on a
casual basis.

Similarly, social behaviour can be taught and children can be given some cues
to help them cope, including 'do not talk to strangers'; 'do not take sweets from
someone that you do not know'; and 'wait for someone else to answer your
question before repeating yourself'. Constructive activities such as simple
board games can help in coaching the child to develop turn-taking tasks. This
can be used as a very positive teaching exercise to encourage them to cooper-
ate in a positive manner with other children. From simple board games, the
exercise can be further developed to include more children and also more
active exercises, including kicking and catching balls, and simple team games.
It is important to emphasize that this process is to be taught primarily as spe-
cific teaching rather than as a physical exercise.

_______

Memory
In normal parlance memory is not a differentiated term but in brain science it is
a requirement to know what type of memory is being addressed because there
are different parts of the brain which deal with each one. Thus in practical
scientific terms there is a functional duality of memory systems, so vividly
demonstrated in amnesic patients and patients with degenerative disorders. 99

These have provided the basis for conceptualizing memory functions in terms
of two long-term storage and retrieval systems: a declarative system, or
explicit memory which deals with facts and events and is available to
consciousness, and a non-declarative or implicit system which is "non-
conscious" 100. However, depending on one's perspective, the count of systems
or kinds of memory varies. In a clinical perspective, Mayes 101 divides
declarative memory into semantic (fact memory) and episodic (autobiographic
memory), and non-declarative memory into item-specific implicit memory
(ISIM) and procedural-also implicit-memory (see also Baddeley 102). Because
humans can usually tell someone else that they are experiencing explicit
memories, they are easier to assess on cognitive tests.

Semantic memory represents our knowledge of the world beyond any


context or temporal parameters, is automatically expressed and lives in the
99
Butters, N. & Stuss, D.T. (1989). Diencephalic amnesia. In F. Boller & J.
Grafman (Eds.), Handbook of neuropsychology (Vol. 3). Amsterdam: Elsevier.
100
Squire L. R., Knowlton B. J. (2000). The medial temporal lobe, the
hippocampus, and the memory systems of the brain. In Gazzaniga M. (Ed.), The
new cognitive neurosciences (2nd ed., pp. 756-776). Cambridge, MA: MIT Press.
101
Mayes, A.R. (2000). The neuropsychology of memory. In G.E. Berrios &
J.R. Hodges (Eds.), Memory disorders in psychiatric practice. Cambridge, UK:
Cambridge University Press.
102
Baddeley, A. (2002). The psychology of memory. In A.D. Baddeley, M.D.
Kopelman, & B.A. Wilson (Eds.), The handbook of memory disorders. Chichester,
UK: Wiley.

Page 39 of 114
present; episodic memory is based on facts/events occurring in a precise
temporal and spatial context in which the fundamental reference point is the
person remembering. Amnesia is therefore related to the long-term declarative
memory 103. Given the existence of different types of memory, it follows that
they are processed by different brain areas and based on different neuronal
circuits 104.

Implicit memory refers to acquired knowledge that we are not explicitly


able to recall but that influences our performance on a task. For example, if a
child repeatedly practises riding a bicycle, then their performance will improve
to the level that they can simply get on a bicycle, without the aid of stabilizers,
and ride, in other words, accurately perform the necessary motor sequences
and adjust their balance according to a changing environment. However, they
will not explicitly recall the information that informs their performance. Such
memories take time and practice to acquire. Implicit memories are tightly
connected to the original stimulus conditions under which the learning
occurred, whereas explicit memories are more flexible and involve the associa-
tion of multiple elements of information and events (Kandel et al.) 105.

Within explicit memory there is a further division between short-term


working memory and long-term memory. Each is measured by different cog-
nitive tasks and is associated with different neural systems. Everyday activities
require us to hold information in mind for short periods of time until we have
used the information to work out a problem or perform a task. Such activities
might include a child holding on to an instruction spoken by the teacher until
they have performed the task, or performing mental arithmetic on a mathe-
matics problem written in their textbook. Baddeley and Hitch 106 described this
type of memory processing as short-term 'working' memory because it is the
memory used to 'work out information there and then'. They proposed a model
which included three main subcomponents; the phonological loop which holds
on to auditory information; the visual-spatial sketch pad which holds visual
information; and the central executive which is used to manipulate either
verbal or visual information. This model has been developed over the past 30
years and its basic dissociations are known to be present in early childhood ,
Gathercole 107.

Long-term Memory: The amount of time necessary between


presentation and recall of an event or fact for a memory to be considered 'long
term' and dependent on different neural structures from short-term memory is
unclear. However, within neuropsychology it is generally accepted that once a
memory has gone from immediate attention (e.g. following a short delay of
minutes with the child concentrating on new information in between), retrieving
103
Baddeley, A. (1984): The human memory (1982). Italian edn. La
memoria umana. Bologna: Il Mulino.
104
Gabrieli, J.D.E., Brewer, J.B., Desmond, J.E. & Glover, G.H. (1997):
Separate neural bases of two fundamental memory processes in the human
medial temporal lobe. Science 276, 264-266.
105
Kandel, E. R., Kupfermann, I., & Iversen, S. (2000). Learning and
memory. In: Principles of Neural Science (eds E. R. Kandel, J. H. Schwartz & T. M.
Jessell), pp. 1227-46. New York: McGraw-Hill.
106
Baddeley,A. D., Hitch, G. J. (1974). Working memory. In:
RecentAdvances in Learning and Motivation (ed. G. A. Bower), pp. 47-90. New
York: Academic Press.
107
Gathercole, S. E. (1998). The development of memory. Journal of Child
Psychology and Psychiatry and Allied Disciplines, 39, 3-27.

Page 40 of 114
the original information would require the support of the long-term memory
system. Long-term memories are usually further classified as episodic (event-
like) or semantic (fact-like).

Long-term memory is sub-divided into implicit (or procedural) and explicit (or
declarative) memory 108, 109. Procedural memory is at most only partially
conscious and consists of a collection of different skills; it is expressed by
means of 'activities', does not respond to the criterion of true/false, and
progressively increases with experience, and generally represents a
predisposition to behave in a particular way on the basis of previous memories.
Declarative memory is conscious and expressed by means of words, concepts
and propositions; it is also expressed by means of images and the recall of
previously encountered facts and events.

Short-term memory is probably processed by the inferior parietal lobe


(although not everybody agrees on this point); declaratory long-term memory is
processed by the temporo-mesial structures, in particular, the hippocampus
and para-hippocampal regions, whereas procedural memory seems to be
processed by the striatum and the cerebellum.

Episodic memory is a neurocognitive (brain/mind) system, uniquely


different from other memory systems that enables human beings to remember
past experiences. The notion of episodic memory was first proposed some 30
years ago. At that time it was defined in terms of materials and tasks. It was
subsequently refined and elaborated in terms of ideas such as self, subjective
time, and autonoetic consciousness. Tulving provides a history of the concept
of episodic memory, describes how it has changed (indeed greatly changed)
since its inception, considers criticisms of it, and then discusses supporting
evidence provided by (a) neuropsychological studies of patterns of memory
impairment caused by brain damage, and (b) functional neuro-imaging studies
of patterns of brain activity of normal subjects engaged in various memory
tasks. 110

Episodic memory is also identified with autonoetic consciousness, which gives


rise to remembering in the sense of self-recollection in the mental re-
enactment of previous events at which one was present. Autonoetic
consciousness is distinguished from noetic consciousness, which gives rise to
awareness of the past that is limited to feelings of familiarity or knowing.
Noetic consciousness is identified not with episodic but with semantic memory,
which involves general knowledge. A recently developed approach to episodic
memory makes use of 'first-person' reports of remembering and knowing.
Studies using this approach have revealed many independent variables that
selectively affect remembering and others that selectively affect knowing.
These studies can also be interpreted in terms of distinctiveness and fluency of
processing. Remembering and knowing do not correspond with degrees of
confidence in memory. Nor does remembering always control the memory
response. There is evidence that remembering is selectively impaired in
various populations, including not only amnesic patients and older adults but

108
Tulving, E. (1972): Episodic and semantic memory. In: Organization of
memory, eds. E. Tulving & W. Donaldson. New York: Academic Press.
109
Tulving, E. (1983): In: Elements of episodic memory. Oxford: Oxford
University Press.
110
Tulving, E. (2002) Episodic Memory: From Mind to Brain. Annual Review
of Psychology. Vol. 53: 1-25.

Page 41 of 114
also adults with Asperger's syndrome. This first-person approach to episodic
memory represents one way in which that most elusive aspect of
consciousness, its subjectivity, can be investigated scientifically. The two kinds
of conscious experiences can be manipulated experimentally in ways that are
systematic, replicable and intelligible theoretically. 111

These classifications give four long-term storage systems plus one system for
short-term (what Mayes calls working) memory which is supported by neuro-
imaging studies 112. As of July 25, 2002, Tulving (idem) had counted "134
different named types of memory."

While the dual system classification remains at the core of most other ways of
conceptualizing memory systems and subsystems, some variations have been
offered. For example, in listing long-term storage systems by their neuro-
anatomic sites, "thought to be especially important for each form of declarative
and non-declarative memory”, Squire and Zola (1996)113 raise the count of
systems to six by adding classical conditioning (two systems, one for emotional
and one for skeletal responses) and reflex learning, while merging semantic
and episodic memory into one declarative system and not including short-term
memory in their count.

Memory deficits are commonly reported in paediatric populations that


have suffered brain injury (Catroppa and Anderson) 114. Memory is not a unitary
skill, but much more a complex set of interconnected skills. These skills are
dependent on different molecular processes taking place within the brain
(KandeI )115 and within different neuro-anatomical structures (Aggleton and
Pearce )116.

For clinical purposes, the dual system conceptualization into declarative


(explicit) and non-declarative (implicit) memory with its major subsystems-
provides a useful framework for observing and understanding patterns of
memory competence and deficits presented patients. [For a fuller
understanding of memory in all its relevancies to neuropsychological
assessment, see Lezak, M. D. (2004). Neuropsychological Assessment (4th
edn). Oxford: Oxford University Press.]

Given that different brain areas process different components of the memory
system, it follows that these components may be independently deficient
depending on the damaged area. Short-term memory deficits can therefore

111
Gardiner JM. (2001) Episodic memory and autonoetic consciousness: a
first-person approach. Philos Trans R Soc Lond B Biol Sci. Sep
29;356(1413):1351-61.
112
Schacter, D.L., Wagner, A.D., & Buckner, R.L. (2000). Memory
systems of 1999. In: E. Tulving & F.I.M. Craik (Eds.), The Oxford Handbook of
Memory (pp. 627-643). New York: Oxford University Press.
113
Squire, L R. & Zola, S M. (1996) Structure and function of declarative
and non-declarative memory systems. Proc. Natl. Acad. Sci. USA. Vol. 93, pp.
13515–13522, November 1996.
114
Catroppa, C. & Anderson, V. (2002). Recovery in memory function in
the first year following TBI in children. Brain Injury 16,369-84
115
Kandel, E. R. (2001). The molecular biology of memory storage: a
dialogue between genes and synapses. Science 294, 1030-8.
116
Aggleton, J. P. & Pearce, J. M. (2001). Neural systems underlying
episodic memory: insights from animal research. Philosophical Transactions of
the Royal Society of London. Series B: Biological Sciences 356, 1467-82.

Page 42 of 114
exist in the presence of a perfectly functioning long-term memory, and vice
versa; a deficient declaratory memory in the presence of an intact procedural
memory, and vice versa; and a deficient semantic memory in the presence of
an integral episodic memory and vice-versa (Baddeley, 1984 idem); Ellis &
Young, 1988 117).

A wealth of animal and human research has pointed to a significant


involvement of the temporal lobes in memory processing. Helmstaedter et al
have studied verbal declarative memory by using a word list paradigm that
differentiates among learning (immediate recall), memory (delayed recall), and
recognition, in epilepsy patients being considered for surgical resection of the
left temporal lobe.

Verbal memory was evaluated preoperatively and during the recording of


intracranial event related potentials and postoperatively after selective
hippocampectomy, temporal cortical lesionectomy, or anterior two-thirds en
bloc temporal lobe resection procedures.

Preoperative differences in verbal memory performance as a function of


differences in underlying neuropathology, concurrent event-related potentials,
and specific patterns of postoperative memory impairments lead to converging
evidence that verbal declarative memory relies on a synergistic interaction of at
least two functionally distinct brain systems. Material-specific data acquisition,
or working memory, is mediated by neocortical temporal structures, whereas
long-term consolidation/retrieval is particularly mediated by temporo-mesial
structures.

The temporal neocortex is part of the outermost layer of the brain (neocortex).
It is located on either side of the brain. Cup your hands around your ears. This
is approximately where they lie. They play a critical role in high level visual
processing and in the long-term storage of language, general knowledge, and
autobiographical memories.

Findings suggest that the left temporal neocortex contributes to verbal memory
consolidation 118 and that the right temporal area is specialized for retaining
auditory information over short time spans.119 In contrast the function of the
temporo-mesial system appears to be material nonspecific. Apparently, its
preferential involvement in verbal memory is due to its close interaction with
overlying neocortical structures that are specialized for language processing.
120

117
Ellis, W.A. & Young, A.W. (1988): Memory. In: Human cognitive
neuropsychology. Hove, London, Hillsdale: Lawrence Erlbaum.
118
Perrine K, Devinsky O, Uysal S, Luciano DJ, Dogali M. Left temporal
neocortex mediation of verbal memory: evidence from functional mapping with
cortical stimulation. Neurology. 1994 Oct;44(10):1845-50.
119
Zatorre RJ, & Samson S. Role of the right temporal neocortex in
retention of pitch in auditory short-term memory. Brain. 1991 Dec;114 ( Pt
6):2403-17.
120
Helmstaedter, C.; Grunwald, Th.; Lehnertz, K.; Gleißner U. &
Elger, C. E. Differential Involvement of Left Temporolateral and Temporomesial
Structures in Verbal Declarative Learning and Memory: Evidence from Temporal
Lobe Epilepsy. Brain and Cognition Volume 35, Issue 1, October 1997, Pages
110-131

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In Mishkin et al. (1997)121 and Eichenbaum's (1997)122 model of the anatomy of
the temporo-mesial structures, the memory is seen as being very flexible and
based on representations stored in the neocortex in a highly precise and
sophisticated manner.

The representations are grouped into semantic associations in the para-


hippocampal region, in which memories are faithfully coded in such a way that
they can be re-evoked particularly when they are contiguous (i.e. if they belong
to similar semantic categories), whereas the hippocampus is the anatomical
site in which the personal context is attached. The memory is positioned in
time and place, and it or some of its parts can be manipulated and associated
with other parts of other memories in order to create an infinity of rearranged
complex memories (Mishkin et al, 1998) 123.

Temporo-mesial 124 structures are critical for the organization of long term
declarative (explicit) memories particularly in the developmental period. This
means that the architecture of the anatomical structures is established very
early in life. Very early lesions can cause memory deficits of different severity
and typology and are age-related. Very early lesions (particularly of the
hippocampus) irreversibly compromise the capacity to acquire complex
modalities of verbal and social communication and to organize a personal and
unique cognitive map. Later lesions cause amnesia of different severity, with
impairment of episodic memory and preservation of semantic memory if the
lesion is localized to the hippocampus, or the impairment of both types of
memory in case of hippocampus and para-hippocampus localization. 125

This has been supported by a large number of experimental and clinical studies
which have demonstrated that temporo-mesial structures play a fundamental
role in the organization of memory. The clinical studies have been based on
descriptions of patients suffering from global amnesia after undergoing surgery
for bilateral temporo-mesial lesions or patients with more selective partial
verbal and non-verbal memory deficits due to either left or right unilateral
surgical lesions. 126, 127, 128, 129, 130

121
Mishkin, M., Suzuki, W., Gadian, D.G. & Vargha-Khadem, F.
(1997): Hierarchical organization of cognitive memory. Phil. Trans. Roy. Soc.
London (B) 352,1461-1467.
122
Eichenbaum, H. (1997): How does the brain organize memory? Science
277, 330-332.
123
Mishkin, M., Vargha-Khadem, F. & Gadian, D.G. (1998): Amnesia
and the organization of the hippocampal system. Hippocampus 8, 212-216.
124
The surface of the temporo-mesial region is subdivided into several
areas: anteriorly, the lateral olfactory gyrus is covered by prepiriform cortex;
dorsomedially, the semilunar gyrus and uncus hippocampi consist, respectively,
of cortical amygdaloid nucleus and hippocampal cytoarchitectonic fields; and
ventrolaterally, the anterior part of the parahippocampal gyrus is covered by
periamygdaloid cortex, entorhinal, and transentorhinal areas and its posterior
part is covered by Fields TH and TF per Von Economo and subicular complex.
[Huther G, Dörfl J, Van der Loos H, Jeanmonod D. Microanatomic and vascular
aspects of the temporomesial region. Neurosurgery. 1998 Nov; 43(5):1118-36.]
125
Riva, D.; Saletti, V. & Nichelli, F. (2000) The organization of memory
in temporo- mesial structures in developmental age. In Localization of Brain
Lesions and Developmental Functions, D. Riva & A. Benton (eds.) 2000 John
Libbey & Company Ltd, pp. 15-21.
126
Frisk, V. & Milner, B. (1990): The role of the left hippocampal region in
the acquisition and retention of story content. Neuropsychologia 28, 349-359.

Page 44 of 114
There are now increasing clinical reports and more formal research studies that
demonstrate how specific memory disorders in childhood have significant
implications for the development of other cognitive skills or academic
knowledge (for review see Hood and Rankin 2005) 131. For example, children
with early phonological memory deficits commonly present with both receptive
and expressive language problems, literacy difficulties and behavioural
difficulties resulting from an inability to follow verbal instructions in the
classroom. In contrast, children with visual-spatial memory deficits have far
greater difficulty with social communication as a significant amount of com-
munication is based on remembering subtle non-verbal body language and
facial expression. Such children also have difficulties in academic subjects that
rely less on verbal information stored by the phonological loop, and more on
subjects that require good visual-spatial memory such as art, graphic design
and aspects of geography and science where a good visual-spatial understand-
ing of shapes, diagrams or maps is useful.

Unless children have a neuropsychological assessment following brain injury,


then there can be much misunderstanding about a child's memory ability and
subsequent behaviour. Teachers and parents often complain that a child can
remember some things but not others, which can lead people to believe that
the child is deliberately pretending to be forgetful or not trying 'hard enough' to
remember certain things.

For example, when children suffer damage to the temporal lobes and in
particular the hippocampi, they can have severe difficulties remembering day-
to-day events or personal experiences. However, such children may still have
relatively intact semantic memory systems so that they are able to learn
factual information that is consistent and repeatable over time (Vargha-Khadem
et al. 2001 )132. In other cases, children with brain injuries may perform well
when asked to recall information that is presented to them but have specific
difficulties remembering when the information was presented to them. For
example, if such children are asked only to recall information presented to
them at time point 1 and deliberately not recall the information at time point 2,
they have great difficulty discriminating between the two types of information
presented at each time point.

This inability to identify the source of a memory can result in a number of

127
Jones-Gotman, M. (1986): Right hippocampal excision impairs learning
and recall of a list of abstract design. Neuropsychologia 24, 659-670.
128
Jones-Gotman, M., Zatorre, R.J., Olivier, A., Andermann, F.,
Cendes, F., Stauton, H., McMackin, D., Siegel, A.M. & Wieser, H.G.
(1997): Learning and retention of words and designs following excision from
medial or lateral temporal-lobe structures. Neuropsychologia 35, 963-973.
129
Press, A.G., Amaral, D.G. & Squire L.R. (1989): Hippocampal
abnormalities in amnesic patients revealed by high resolution magnetic
resonance imaging. Nature 341, 54-57.
130
Rausch, R. & Babb, T.L. (1993): Hippocampal neuron loss and memory
scores before and after temporal lobe surgery for epilepsy. Arch. Neural. 50,812-
817.
131
Hood, J. & Rankin, P. M. (2005). How do specific memory disorders
present in the school classroom? Pediatric Rehabilitation
8, 272-82.
132
Vargha-Khadem, F., Gadian, D. G., & Mishkin, M. (2001).
Dissociations in cognitive memory: the syndrome of developmental amnesia.
Philosophical Transactions of the Royal Society of London. Series B: Biological
Sciences 356: 1435-440.

Page 45 of 114
consequences. Some people tell persistent untruths (confabulate) because
they cannot distinguish between real and imagined events (Schnider) 133, while
others may experience hallucinatory type events because they misattribute
their own thoughts to external voices (Rankin and O'Carroll) 134. Thus, a
neuropsychological assessment is critical in explaining the nature of children's
behaviour following brain injury, and is far more relevant and important than
the often lay and uninformed explanations of the child's behaviour, which may
be misleading and result in misguided or unethical interventions.

In summary, it is possible for there to be a selective impairment of the memory


system and, consequently, this may have significant implications for behav-
ioural performance as well as the appropriate design of educational
interventions and behavioural management strategies for a child's difficulties.
An accurate diagnosis of the memory systems affected by head injury will have
implications for the type of intervention designed for each child (for a review of
adapting clinical interventions to specific memory deficits see Rankin and Hood
2005 idem).

_______

The Direct Effect of Brain Injury on Emotion


Although depression and anxiety following brain injury may result from the
losses the survivor has suffered, it may also be due to injury to the parts of the
brain involved in the experience of mood, particularly in the early stages fol-
lowing the injury (Max et al. 2005) 135.

Fear Conditioning Converging evidence now indicates that the


amygdala plays a crucial role in the development and expression of conditioned
fear. Conditioned fear is a hypothetical construct used to explain the cluster of
behavioural effects produced when an initially neutral stimulus is consistently
paired with an aversive stimulus. For example, when a light, which initially has
no behavioural effect, is paired with an aversive stimulus such as a foot shock,
the light alone can elicit a constellation of behaviours that are typically used to
define a state of fear in animals. 136 After fear conditioning, the CS elicits a
complex pattern of fear-related behavioural responses, including freezing and
potentiated startle (McAllister WR, McAllister DE. (1971) idem., 137 . Fear
extinction occurs when a fear CS is repeatedly experienced in the absence of
aversive consequences, resulting in a reduction of CS elicited fear.
133
Schnider,A. (2003). Spontaneous confabulation and the adaptation of
thought to ongoing reality. Nature Reviews Neuroscience 8, 662-71.
134
Rankin, P. M. & O'Carroll, P. J. (1995). Reality discrimination, reality
monitoring and disposition towards hallucination. British Journal of Clinical
Psychology 34, 517-28.
135
Max, J. E., Levin, H. S., Landis, J., Schachar, R., Saunders, A.,
Ewing-Cobbs, L., Chapman, S. B., & Dennis, M. (2005). Predictors of
personality change due to traumatic brain injury in children and adolescents in
the first six months after injury. Journal of the American Academy of Child and
Adolescent Psychiatry 44, 434-42.
136
Davis, M. The Role of the Amygdala in Fear and Anxiety. Annual Review
of Neuroscienc. Vol. 15: 353-375, 1992.
137
Fanselow MS. (1994). Neural organization of the defensive behaviour
system responsible for fear. Psychonom Bull Rev 1: 429–438.

Page 46 of 114
To explain these findings, it is generally assumed 138 that during light shock
pairings (training session), the shock elicits a variety of behaviours that can be
used to infer a central stale of fear. After pairing, the light can produce the
same central fear state and thus the same set of behaviours formerly produced
by the shock, Moreover, the behavioural effects that are produced in animals by
this formerly neutral stimulus are similar in many respects to the constellation
of behaviours that are used to diagnose generalized anxiety in humans. Thus
there is an assumption that this data supports the idea that the amygdala, and
its many efferent projections may represent a central fear system involved in
both the expression and acquisition of conditioned fear. (Davis M. 1992, idem)

Research on the neural systems underlying emotion in animal models over the
past two decades has implicated the amygdala in fear and other emotional
processes. This work has stimulated interest in pursuing the brain mechanisms
of emotion in humans. 139

Over this period of time, the amygdala has gone from a being an obscure
region of the brain to practically a household word. Although known to be
involved in emotion for some time 140, much of the recent scientific interest in
the amygdala has investigated its role in fear conditioning. 141, 142, 143, 144 .

This research, mostly conducted in rats, has not only identified the amygdala as
a central structure in the circuitry underlying fear conditioning but has also
implicated specific synaptic connections and molecular cascades in the
amygdala in the acquisition and storage of memories of fear conditioning. 145

Recent studies in humans have begun to search for parallels to the animal
work. 146, 147, 148, 149 ,150 The results have complemented but also extended the

138
McAllister WR, McAllister DE. (1971). Behavioral measurement of
conditioned fear. In: Brush FR (ed). Aversive Conditioning and Learning.
Academic Press: New York. pp 105–179.
139
Phelps, Elizabeth A. & LeDoux, Joseph E. Contributions of the
Amygdala to Emotion Processing: From Animal Models to Human Behaviour.
Neuron, Vol. 48, 175–187, October 20, 2005
140
Weiskrantz, L. (1956). Behavioural changes associated with ablation of
the amygdaloid complex in monkeys. J. Comp. Physiol. Psychol. 49, 381–391.
141
LeDoux, J.E. (1996). The Emotional Brain (New York: Simon and
Schuster).
142
LeDoux, J.E. (2000). Emotion circuits in the brain. Annu. Rev. Neurosci.
23, 155–184.
143
Maren, S. (2001). Neurobiology of Pavlovian fear conditioning. Annu.
Rev. Neurosci. 24, 897–931.
144
Davis, M., & Whalen, P.J. (2001). The amygdala: vigilance and
emotion. Mol. Psychiatry 6, 13–34.
145
Rodrigues, S.M., Schafe, G.E., & LeDoux, J.E. (2004). Molecular
mechanisms underlying emotional learning and memory in the lateral amygdala.
Neuron 44, 75–91.
146
LaBar, K.S., LeDoux, J.E., Spencer, D.D., & Phelps, E.A. (1995).
Impaired fear conditioning following unilateral temporal lobectomy in humans. J.
Neurosci. 15, 6846–6855.
147
Morris, J.S., Friston, K.J., Buchel, C., Frith, C.D., Young, A.W.,
Calder, A.J., & Dolan, R.J. (1998). A neuromodulatory role for the human
amygdala in processing emotional facial expressions. Brain 121, 47–57.
148
Morris, J.S., Ohman, A., & Dolan, R.J. (1998). Conscious and
unconscious emotional learning in the human amygdala. Nature 393, 467–470.

Page 47 of 114
basic findings from animals regarding the amygdala’s role in emotional
processing.

Animal studies have shown that the amygdala receives sensory information via
two routes: a rapid but crude input from the sensory thalamus and a slower but
more veridical representation from the sensory cortex [SC]. 151, 152 , 153, Either
the thalamic or cortical pathway can be used for simple sensory stimuli such as
those typically used in animal conditioning studies, but presumably more-
complex stimuli would require cortical processing. However, even for complex
stimuli it is possible that crude features of the stimulus might have emotional
potency due to innate wiring. For example, through the thalamic pathway, the
amygdala might be activated by features or fragments of stimuli. This could
lead to inappropriate activation— for example, when walking through the
woods, the amygdala might be activated by the curvature of a slender stick on
the ground, as if it were a snake. Alternatively, through past learning certain
stimulus features might acquire the ability to activate the amygdala
unwittingly.

Current techniques for examining human brain function do not allow the
exploration of neural systems with the same level of specificity as animal
models. Nevertheless, studies exploring the role of the human amygdala in
fear learning are consistent with these models. Fear conditioning in humans
results in an increased blood-oxygen-level-dependent (BOLD) signal in the
amygdala as assessed with functional magnetic resonance imaging (fMRI).
154 155
,

In addition, studies in patients with brain lesions are consistent with the animal
models. Although the interpretation of lesion studies in humans can be
problematic because these lesions almost always include damage to additional
structures and often occur years before experimental testing, allowing the
possibility for the development of compensatory mechanisms, these studies
can provide a hint into the critical function of structures in human brain.

As expected from previous studies with other techniques, patients whose


damage includes the amygdala fail to show physiological indications of
conditioned fear. However, if the hippocampus in these patients is relatively
149
Phelps, E.A., O’Connor, K.J., Cunningham, W.A., Funayama, E.S.,
Gatenby, J.C., Gore, J.C., & Banaji, M.R. (2000). Performance on indirect
measures of race evaluation predicts amygdala activation. J. Cogn. Neurosci. 12,
729–738.
150
Adolphs, R., Gosselin, F., Buchanan, T.W., Tranel, D., Schyns, P.,
& Damasio, A.R. (2005). A mechanism for impaired fear recognition after
amygdala damage. Nature 433, 68–72.
151
LeDoux, J.E., Sakaguchi, A., & Reis, D.J. (1984). Subcortical efferent
projections of the medial geniculate nucleus mediate emotional responses
conditioned to acoustic stimuli. J. Neurosci. 4, 683–698.
152
LeDoux, J.E. (1994). Emotion, memory and the brain. Sci. Am. 270, 50–
57.
153
LeDoux, J.E. (2002). Synaptic Self: How Our Brains Become Who We Are
(New York: Viking).
154
Buchel, C., Morris, J., Dolan, R.J., & Friston, K.J. (1998). Brain
systems mediating aversive conditioning: an event-related fMRI study. Neuron
20, 947–957.
155
LaBar, K.S., Gatenby, J.C., Gore, J.C., LeDoux, J.E., & Phelps, E.A.
(1998). Human amygdala activation during conditioned fear acquisition and
extinction: a mixed-trial fMRI study. Neuron 20, 937–945.

Page 48 of 114
intact, they are able to explicitly recollect and report the events of fear
conditioning procedures, such as the relation between the conditioned
stimulus(CS) and unconditioned stimulus (US)156 157 In contrast, damage that
includes the hippocampus bilaterally but spares the amygdala impairs the
ability to report consciously the events of fear conditioning, although there is
normal expression of conditioned fear as assessed through physiological
measures (Bechara et al., 1995 idem).

This dissociation following amygdala or hippocampal damage between indirect


physiological assessments of the conditioned fear response (amygdala
dependent) and awareness of the aversive properties of the CS (hippocampal
dependent) supports the conclusion that there are multiple systems for the
encoding and expression of emotional learning.

Research evolving from the Klüver-Bucy syndrome (Klüver-Bucy syndrome is a


neuro-behavioural syndrome associated with bilateral lesions in the anterior
temporal horn or amygdala. Heinrich Klüver and Paul Bucy first described the
syndrome in 1937 following experimental work where they removed rhesus
monkeys' temporal lobes.) 158 They first emphasized the importance of the
amygdala in social behaviour. 159, 160, 161

Amaral and colleagues have recently revisited this issue in both adult and
infant monkeys and concluded that damage to the amygdala in adult animals,
while reducing fear of toy snakes, fails to produce significant adverse
alterations in social and affiliative behaviour. 162 In contrast, damage in infants
alters later adult behaviour in such a way that fear of a toy snake is intact, but
fear in social situations is altered. This specific effect on social fear is
consistent with studies that have emphasized the importance of amygdala
alterations in autism. 163, 164, 165

156
Bechara, A., Tranel, D., Damasio, H., Adolphs, R., Rockland, C., &
Damasio, A.R. (1995). Double dissociation of conditioning and declarative
knowledge relative to the amygdala and hippocampus in humans. Science 269,
1115–1118.
157
LaBar, K.S., LeDoux, J.E., Spencer, D.D., & Phelps, E.A. (1995).
Impaired fear conditioning following unilateral temporal lobectomy in humans. J.
Neurosci. 15, 6846–6855.
158
Kluver H, Bucy PC. Psychic blindness and other symptoms following
bilateral temporal lobectomy in rhesus monkeys.; Am J Physiol 1937;119:352-3
159
Kling, A.S., & Brothers, L.A. (1992). The amygdala and social
behavior. In The Amygdala: Neurobiological Aspects of Emotion, Memory, and
Mental Dysfunction, J.P. Aggleton, ed. (New York: Wiley-Liss, Inc), pp. 353–377.
160
Meunier, M., Bachevalier, J., Murray, E.A., Malkova, L., & Mishkin,
M. (1999). Effects of aspiration versus neurotoxic lesions of the amygdala on
emotional responses in monkeys. Eur. J. Neurosci. 11, 4403–4418.
161
Meunier, M., & Bachevalier, J. (2002). Comparison of emotional
responses in monkeys with rhinal cortex or amygdala lesions. Emotion 2, 147–
161.
162
Amaral, D.G. (2003). The amygdala, social behavior, and danger
detection. Ann. N Y Acad. Sci. 1000, 337–347.
163
Bachevalier, J. (1994). Medial temporal lobe structures and autism: A
review of clinical and experimental findings. Neuropsychologia 32, 627–648.
164
Baron-Cohen, S., Ring, H.A., Bullmore, E.T., Wheelwright, S.,
Ashwin, C., & Williams, S.C. (2000). The amygdala theory of autism.
Neurosci. Biobehav. Rev. 24, 355–364.
165
Kemper, T.L., & Bauman, M.L. (1993). The contribution of
neuropathologic studies to the understanding of autism. Neurol. Clin. 11, 175–

Page 49 of 114
Sandor et al’s study examined the effects of fear conditioning on REM and on
PGO wave (PGOE). On conditioning days the number of REM episodes, the
average REM duration and the REM percentage were decreased while REM
latency was increased. These results suggest that fear, most likely involving
the amygdala; can influence REM and brainstem alerting mechanisms. 166

The amygdala plays a central rôle in fear conditioning, a model of anticipatory


anxiety. It has massive projections to the brainstem regions involved in rapid
eye movement sleep (REM) and ponto-geniculo-occipital (PGO) wave
generation. PGO waves occur spontaneously in REM or in response to stimuli.
Electrical stimulation of the central nucleus of the amygdala enhances
spontaneous PGO wave activity during REM and the amplitude of both the
acoustic startle response and the elicited PGO wave (PGOE), a neural marker of
alerting. Considerable evidence implicates the amygdala as a crucial
component of the neural circuitry that underlies the acquisition and storage of
fear conditioning167, 168 . Although fear extinction also involves the amygdala 169,
its role is less clear than in fear conditioning 170, 171 .

Fear Extinction Similar to fear conditioning, fear extinction


involves both learning and memory 172, 173 . Thus, during extinction training, the
subject learns that the CS is no longer predictive of the US, and as extinction
proceeds, the conditioned response decreases in magnitude. The memory of
this learning experience is then assessed some time later by again presenting
the CS without the US in a retrieval test to determine whether the decrease in
responding is retained.

Animal research on extinction has implicated the amygdala and medial


prefrontal cortex (mPFC). However, the mPFC was implicated in fear extinction
first. Damage to mPFC, especially the ventral-most portion of this region
(vmPFC), significantly alters the ability of rats to undergo extinction learning.
174
Furthermore, neural activity increases in the mPFC as extinction is learned

187.
166
Sanford, LD.; Silvestri, AJ.; Ross, RJ. & Morrison, AR. (2001)
Influence of fear conditioning on elicited ponto-geniculo-occipital waves and
Rapid Eye Movement Sleep. Archives Italiennes de Biologie, 139: 169-183,
2001.
167
LeDoux JE (2000). Emotion circuits in the brain. Annu Rev Neurosci 23:
155–184.
168
Maren S (2001). Neurobiology of Pavlovian fear conditioning. Annu Rev
Neurosci 24: 897–931.
169
Davis M, Walker DL, Myers KM (2003). Role of the amygdala in fear
extinction measured with potentiated startle. Ann NY Acad Sci 985: 218–232.
170
Maren S, Quirk GJ (2004). Neuronal signalling of fear memory. Nat Rev
Neurosci 5: 844–852.
171
Sotres-Bayon F, Cain CK, LeDoux JE (2006). Brain mechanisms of fear
extinction: historical perspectives on the contribution of the prefrontal cortex.
Biol Psychiatry 60: 329–336.
172
Bouton ME. (2002). Context, ambiguity, and unlearning: sources of
relapse after behavioral extinction. Biol Psychiatry 52: 976–986.
173
Myers KM, Davis M. (2002). Behavioral and neural analysis of
extinction. Neuron 36: 567–584.
174
Phelps, Elizabeth A. & LeDoux, Joseph E. Contributions of the
Amygdala to Emotion Processing: From Animal Models to Human Behavior.
Neuron, Vol. 48, 175–187, October 20, 2005

Page 50 of 114
175
, 176 and electrical stimulation of mPFC can facilitate extinction learning. 177
It appears that vmPFC may be particularly involved in the memory or retention
of extinction. 178

Much of the evidence implicating the amygdala in fear extinction has involved
studies showing that blockade of N-methyl-D-aspartate receptors (NMDARs) in
the lateral and basal amygdala, using APV (D,L-2-amino-5- phospho-novaleric
acid), prevents the decrease in responding that normally occurs during
extinction learning, as assessed in a later test 179, 180 . For technical reasons
related to the behavioural paradigm used in these studies (fear-potentiated
startle), it was not possible to assess the effects of NMDAR blockade during
extinction learning.

Given the role of NMDARs in the induction of synaptic plasticity 181, 182 , the most
likely interpretation of these results is that the synaptic plasticity required for
the acquisition of fear extinction was disrupted. However, two studies 183, 184 ,
using a different measure of fear (freezing rather than potentiated startle) and
systemic infusions of the non-subunit selective NMDAR antagonist CPP ((7)-3-(2-
carboxypiperazin-4-yl)-propyl-1-phosphonic acid), found that whereas the
retention of extinction was impaired, there was no apparent impairment during
the acquisition of extinction.

Taken together, these previous results suggested that NMDARs in the amygdala
are involved in the retention/consolidation of the long-term extinction memory,
but not its initial acquisition 185 . However, the results are inconclusive, because
side effects of the two drugs used to block NMDARs may have interfered with
assessment of extinction acquisition during the training session. APV disrupts

175
Milad, M.R., & Quirk, G.J. (2002). Neurons in medial prefrontal cortex
signal memory for fear extinction. Nature 420, 70–74.
176
Rosenkranz, J.A., Moore, H., & Grace, A.A. (2003). The prefrontal
cortex regulates lateral amygdala neuronal plasticity and responses to
previously conditioned stimuli. J. Neurosci. 23, 11054–11064.
177
Milad, M.R., Vidal-Gonzalez, I., & Quirk, G.J. (2004). Electrical
stimulation of medial prefrontal cortex reduces conditioned fear in a temporally
specific manner. Behav. Neurosci. 118, 389–394.
178
Quirk, G.J., & Gehlert, D.R. (2003). Inhibition of the amygdala: key to
pathological states? Ann. N Y Acad. Sci. 985, 263–272.
179
Falls WA, Miserendino MJ, Davis M (1992). Extinction of fear-
potentiated startle: blockade by infusion of an NMDA antagonist into the
amygdala. J Neurosci 12: 854–863.
180
Liu L, Wong TP, Pozza MF, Lingenhoehl K, Wang Y, Sheng M et al
(2004). Role of NMDA receptor subtypes in governing the direction of
hippocampal synaptic plasticity. Science 304: 1021–1024.
181
Martin SJ, Grimwood PD, Morris RG (2000). Synaptic plasticity and
memory: an evaluation of the hypothesis. Ann Rev Neurosci 23: 649–711.
182
Riedel G, Platt B, Micheau J (2003). Glutamate receptor function in
learning and memory. Behav Brain Res 140: 1–47.
183
Santini E, Muller RU, Quirk GJ (2001). Consolidation of extinction
learning involves transfer from NMDA-independent to NMDA-dependent
memory. J Neurosci 21: 9009–9017.
184
Suzuki A, Josselyn SA, Frankland PW, Masushige S, Silva AJ, Kida
S (2004). Memory reconsolidation and extinction have distinct temporal and
biochemical signatures. J Neurosci 24: 4787–4795.
185
Maren S, Quirk GJ (2004). Neuronal signalling of fear memory. Nat Rev
Neurosci 5: 844–852.

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synaptic transmission in the amygdala 186, 187, 188 , and APV and CPP both
interfere with the expression of conditioned freezing 189, 190, 191 .

Social Behaviour Even though patients with amygdala damage


do not have markedly impaired social behaviour, they do have deficits in social
responses in some circumstances. In spite of their ability to generate normal
facial expressions of emotion, they do not always interpret facial expression in
others correctly. This impairment is most apparent for fear expressions; thus
damage to the amygdala results in impairment in interpreting the intensity of
fear expressions in others. 192

Recent studies suggest that the amygdala primarily responds to the eyes in
fear faces 193, and amygdala lesions result in a deficit in appropriately focusing
on the eyes when interpreting facial expression. 194) This impairment in
decoding facial expressions also leads these patients to rate some faces as
more trustworthy and approachable than normal controls. 195 The deficit in
responding to facial expressions is subtle, but nonetheless reliable and
potentially important. Further, it is consistent with the results of the primate
mentioned studies above suggesting a role for the amygdala in social emotions.
196

Another deficit in social responding observed following amygdala damage is the


ability to read social interpretations into ambiguous circumstances. The
tendency to anthropomorphize, that is, to apply human traits to nonhuman
186
Li, X, Phillips, RG, LeDoux, JE (1995). NMDA and non-NMDA receptors
contribute to synaptic transmission between the medial geniculate body and the
lateral nucleus of the amygdala. Exp Brain Res 105: 87–100.
187
Maren S (1996). Synaptic transmission and plasticity in the amygdala.
An emerging physiology of fear conditioning circuits. Mol Neurobiol 13: 1–22.
188
Weisskopf MG, LeDoux JE (1999). Distinct populations of NMDA
receptors at subcortical and cortical inputs to principal cells of the lateral
amygdala. J Neurophysiol 81: 930–934.
189
Maren S, Aharonov G, Stote DL, Fanselow MS (1996). N-methyl-
Daspartate receptors in the basolateral amygdala are required for both
acquisition and expression of conditional fear in rats. Behav Neurosci 110: 1365–
1374.
190
Lee, H. & Kim JJ. (1998). Amygdalar NMDA receptors are critical for
new fear learning in previously fear-conditioned rats. J Neurosci 18: 8444–8454.
191
Lee, HJ; Choi JS; Brown TH & Kim JJ (2001). Amygdalar NMDA
receptors are critical for the expression of multiple conditioned fear responses. J
Neurosci 21: 4116–4124.
192
Adolphs, R., Tranel, D., Hamann, S., Young, A.W., Calder, A.J.,
Phelps, E.A., Anderson, A., Lee, G.P., & Damasio, A.R. (1999). Recognition
of facial emotion in nine individuals with bilateral amygdala damage.
Neuropsychologia 37, 1111–1117.
193
Whalen, P.J., Kagan, J., Cook, R.G., Davis, F.C., Kim, H., Polis, S.,
McLaren, D.G., Somerville, L.H., McLean, A.A., Maxwell, J.S., &
Johnstone, T. (2004). Human amygdala responsivity to masked fearful eye
whites. Science 306, 2061.
194
Adolphs, R., Gosselin, F., Buchanan, T.W., Tranel, D., Schyns, P.,
& Damasio, A.R. (2005). A mechanism for impaired fear recognition after
amygdala damage. Nature 433, 68–72.
195
Adolphs, R., Tranel, D., & Damasio, A.R. (1998). The human
amygdala in social judgment. Nature 393, 470–474.
196
Amaral, D.G. (2003). The amygdala, social behavior, and danger
detection. Ann. N Y Acad. Sci. 1000, 337–347.

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forms, occurs naturally without effort. For example, a classic video by Heider
and Simmel 197 shows triangles and a circle moving around a box. Although
these are simple geometric shapes, the nature of the movements result in most
people describing the shapes as characters engaging in a social interaction.
Patients with amygdala damage, however, fail to read any social intent and
simply describe the movement of the shapes when responding to this video. 198
It is suggested that this deficit in anthropomorphizing may be indicative of the
kind of implicit social signals that depend on the amygdala for normal
interpretation.

The impairments in social responses following amygdala damage in humans are


robust, but limited. In contrast brain-imaging studies in normal subjects have
reported amygdala activation to a range of social stimuli, from bodily
movements indicating fear, 199 to race group information, 200 to pictures of
individuals who have previously acted untrustworthy. 201 These imaging
studies suggest that the amygdala responds to a wide range of social cues and
indicate that the subtle deficits observed following amygdala lesions may
reflect compensatory mechanisms and may not be indicative of the extent of
the amygdala’s involvement in normal social behaviour. Across species, there
is evidence that the amygdala is an important component of the network of
neural systems that produce adaptive social interactions.

Emotional Regulation and Coping: In complex social and


emotional environments, it is often important to be able to control our
emotional reactions in order to behave in adaptive or appropriate ways. The
ability to regulate and cope with emotion is a fundamental skill for normal
social interaction. It is also an important component of mental health. A
characteristic difficulty in many psychological disorders, such as depression or
anxiety, is the maladaptive cognitive interpretation of situations or events.

A component of treatment for these disorders is to teach active coping skills,


consciously applied strategies that help assure adaptive interpretations or
reactions to emotional stimuli. In humans, a significant portion of our
emotional life is generated by our thoughts, interpretations, and imagination.
The habits and skills we develop to guide these internally generated emotional
events are critical. Recent research on the neural systems of emotion
regulation has explored the mechanisms underlying the ability to use cognitive
and active coping strategies to alter emotional reactions.

197
Heider, F., & Simmel, M. (1944). An experimental study of apparent
behavior. Am. J. Psychol. 57, 243–259.
198
Heberlein, A.S., & Adolphs, R. (2004). Impaired spontaneous
anthropomorphizing despite intact perception and social knowledge. Proc. Natl.
Acad. Sci. USA 101, 7487–7491.
199
de Gelder, B., Snyder, J., Greve, D., Gerard, G., & Hadjikhani, N.
(2004). Fear fosters flight: a mechanism for fear contagion when perceiving
emotion expressed by a whole body. Proc. Natl. Acad. Sci. USA 101, 16701–
16706.
200
Phelps, E.A., O’Connor, K.J., Cunningham, W.A., Funayama, E.S.,
Gatenby, J.C., Gore, J.C., & Banaji, M.R. (2000). Performance on indirect
measures of race evaluation predicts amygdala activation. J. Cogn. Neurosci. 12,
729–738.
201
Singer, T., Kiebel, S.J., Winston, J.S., Dolan, R.J., & Frith, C.D.
(2004). Brain responses to the acquired moral status of faces. Neuron 41, 653–
662.

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In animals, emotion regulation (coping) can be studied by examining the
manner in which fear-arousing stimuli are dealt with. Although rats initially
freeze to a CS associated with shock, they can, with training, learn to actively
control their exposure to the CS and thus reduce its aversive consequences
(Amorapanth et al., 2000)202. For example, rats can learn to cross to the other
side of a chamber to terminate or prevent the occurrence of a fear-arousing CS.
Damage to the central nucleus of the amygdala prevents freezing to the CS (a
passive form of coping) but does not interfere with the ability to learn
responses that terminate or prevent the CS (active coping). In contrast,
damage to the basal amygdala has no effect on freezing but prevents learning
of the active coping response. Damage to the lateral nucleus prevents both
forms of learning. This suggests that the lateral nucleus is essential for
processing the CS and that passive and active coping responses elicited by the
CS involve different outputs of the lateral nucleus within the amygdala. These
findings are relevant to understanding the benefits of active coping strategies
in anxiety disorders. 203

_______

Ego Functions
Some of the problems that follow brain injury, especially if the injury occurs
very early in life are to do with the affected person’s ego functions. Identifying
and assessing ego strength helps the assessment on a developmental
continuum and it therefore helps in the provision of understanding neurological
deficits and may suggest therapeutic goals.

Reality Testing One of the ego functions is Reality Testing.


This is the ego’s capacity to distinguish what is occurring in one’s own mind
from what is occurring in the external world. It is perhaps the single most
important ego function because it is necessary for negotiating with the outside
world. One must be able to perceive and understand stimuli accurately. Those
with autistic spectrum disorders usually have great difficulty in understanding
the external world both in terms of what is happening outside of one’s
immediate environment and what other people are thinking. This area of
mental activity is also subject to even more distortion or deterioration if the
subject is suffering stressful conditions.

Impulse Control Another area of ego function that may be lost


or impaired is Impulse Control. If a person does not understand the world
around them or the thoughts of others that causes their behaviour then it is
difficult for them to manage their own behaviour because they do not have
reference points that might impose control.

Affect Regulation The inability to modulate feelings without being


overwhelmed is known as Affect Regulation. To assess a child's outward
behaviour as an inability to regulate requires a grasp of Emotion Regulation
(ER) theory and the developmental line of emotional understanding. While
theories surrounding ER are quite complex, key concepts can be distilled and
202
Amorapanth P, LeDoux JE, Nader K. (2000) Different lateral amygdala
outputs mediate reactions and actions elicited by a fear-arousing stimulus. Nat
Neurosci. 2000;3:74–79.
203
LeDoux, J.E., & Gorman, J.M. (2001). A call to action: overcoming
anxiety through active coping. Am. J. Psychiatry 158, 1953–1955.

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are very useful to guide the assessment of emotion regulation difficulties. A
traditional definition of ER is the processes and characteristics involved in
coping with heightened levels of positive and negative emotions (such as joy,
sadness, distress, and anger) (Kopp, 1989). This seems a logical way to think
about ER; that is, to consider the means one uses to "simmer down" strong
emotions. 204

What are some of these regulation strategies? When a distressing affect is


experienced, a child begins to employ emotional coping skills. They may shift
attention away from the stimulus causing distress or alternately raise the
feeling to awareness and modulate the intensity by talking it out. These mental
operations, which tone down emotions, are acquired throughout the course of
development. Following early brain injury, these emotional regulation skills
may be unable to be learned. So it is very little value to ask an affected child to
modify their behaviour voluntarily. They need to be helped to get away from
the cause of the problem and to redirect their attention to other things.

A useful development theory of affect regulation is contained in the work of


Daniel Stern (1985) 205, a developmental who studied the role of infants' early
interactions in their subsequent affect regulation abilities. His work is quite
detailed, but several key concepts can be distilled to illustrate the
developmental line of emotion regulation.
Disturbances (e.g. abuse, trauma) that occur during sensitive periods and
thereby interfere with important developmental processes may have more
severe consequences than "insults" later in life. According to Stern, these
disturbances may become overt any point in time and the nature rather than
the time of the insult will determine the resulting conflict.

Other functions that may be impaired are:

Judgment: The capacity to act responsibly. This process includes


identifying possible courses of action, anticipating and evaluating likely
consequences, and making decisions as to what is appropriate in certain
circumstances.

Object Relations: The capacity for mutually satisfying relationship. The


individual can perceive himself and others as whole objects with three
dimensional qualities.

Thought Processes: The ability to have logical, coherent, and abstract


thoughts. In stressful situations, thought processes can become disorganized.
The presence of chronic or severe problems in conceptual thinking is frequently
associated with schizophrenia and manic episodes.

Defensive Functioning: A defense is an unconscious attempt to protect


the individual from some powerful identity threatening feeling. Initial defences
develop in infancy and involve the boundary between the self and the outer
world; they are considered primitive defences and include projection, denial,
and splitting. As the child grows up, more sophisticated defences that deal with
204
Delaney, Kathleen R. Following the Affect: Learning to Observe
Emotional Regulation. Journal of Child and Adolescent Psychiatric Nursing, Nov
2006.
205
Stern, D. The Interpersonal World of the Infant. A View from
Psychoanalysis and Developmental Psychology. N.Y: Basic Books; 1985.

Page 55 of 114
internal boundaries develop, such as those between ego and super ego or the
id; these defences include repression, regression, displacement, and reaction
formation. All adults have, and use, primitive defences, but most people also
have more mature ways of coping with reality and anxiety.

Synthesis: The synthetic function is the ego’s capacity to organize and


unify other functions within the personality. It enables the individual to think,
feel, and act in a coherent manner. It includes the capacity to integrate
potentially contradictory experiences, ideas, and feelings; for example, a child
loves his or her mother yet also has angry feelings toward her at times. The
ability to synthesize these feelings is a pivotal developmental achievement.

_______

Abnormal Brain Structure & Autism


INTRODUCTION

Researchers no longer consider autism to be a rare disorder. At one time, only


two to four children per 10,000 were considered autistic, but with milder cases
factored in, one in 500 children is now considered to be autistic to some
degree. However it is not infrequent that the subtle signs of the milder cases
are being missed by physicians and other early childhood workers, according to
the report published in the December 2002 issue of the Journal of Autism and
Developmental Disorders.

Autism also brings about abnormalities in the brain (other than those, which
cause it) by interfering with normal development, both cognitive and emotional.

We should also be very careful about the ways in which we treat children with
autism. Behavioural characteristics often are part of their coping strategy.
Their brain has adapted to the damage it has received, and their behaviour
reflects the reparation and tolerance of what has happened to them. It is
wrong that their behaviour should be stylised as pathological and treated with
psychotropic drugs.

AETIOLOGY OF AUTISM SPECTRUM DISORDERS

Professor Peter Szatmari in his Editorial206, misses an important aetiology of


autism spectrum disorders. Although he includes a brief note on environmental
risk factors, he omits toxic considerations. He goes on to write that the MMR
vaccine is not an environmental risk factor, but omits any reference to the DPT
(whole cell) vaccine. It is now accepted that constituents of the whole cell DPT
vaccine can pass the blood/brain barrier. If they do so, they then can cause
sporadic damage to the brain. Abnormal brain structure has been put forward
by researchers looking for a cause for autism. These have involved the
amygdala, the hippocampus, the cerebellum and the caudate nucleus. 207

206
Szatmari, P. The causes of autism spectrum disorders. Editorial, BMJ
2003;326:173-174

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Malone and Waheed also seem to make an omission when describing autism
and there does need to be a different approach in research to differentiate
between classical autism and autistic spectrum disorder. In their paper 208
Malone and Waheed indicate that, “Patients with autistic disorder typically
demonstrate repetitiveness and a restricted repertoire of behaviour.
Additionally, they also have a number of disruptive symptoms that may be
reduced by drug treatment, including severe tantrums, hyperactivity and
lability.”

Eric Courchesne et al have shown that neo-cerebellar damage impairs the


ability to change attentional maps rapidly and accurately during shifts of
attention between auditory and visual information as well as between
perceptual domains within the visual modality.

During recent studies they have attempted to reveal the underlying causes of
autism using a variety of techniques. Particular emphasis was placed on
techniques that have been used by a number of different laboratories, including
structural magnetic resonance imaging and post-mortem studies of neuro-
anatomy. Neuro-biological and neuropsychological data from individuals across
a wide age range were examined from a neuro-developmental perspective.
From these recent advances they have developed a growth dysregulation
hypothesis of autism. 209

In an earlier study, Courchesne et al, in reinforcing the view that autism


involves abnormal regulation of brain growth during early life, show that there
is an unusual developmental neuro-anatomic phenotype characterised by
hyperplasia of cerebellar white matter, neocortical grey matter, and cerebral
white matter at the youngest ages with slowed growth thereafter; slowed
growth in the cerebellar hemispheres; and a smaller vermis at all ages
examined.210

They hypothesised the genetic factors most likely underlie this growth
abnormality, and suggest that future genetic research might usefully explore
linkage between autism and genes that are known to alter white matter
development. One example of such a gene is p27, which regulates proliferation
of glial and neural cells and affects myelin formation by oligodendrocytes. Loss
of the p27 gene may lead to additional glial and neuronal cell divisions before
withdrawal from cell proliferation cycles. In mice with this gene knocked out,
there was a 250% increase in glial fibrillary acid protein–staining glia cells in the
cerebellum and a 30% increase in numbers of neurons in CA1 of the
hippocampus.211

207
Challoner, A. Brain Damage caused by Vaccination.
http://www.scribd.com/oakwoodbank
208
Malone RP, Waheed A. (2009) The role of antipsychotics in the
management of behavioural symptoms in children and adolescents with autism.
Drugs. 2009;69(5):535-48.
209
Akshoomoff N, Pierce K, Courchesne E. The neurobiological basis of
autism from a developmental perspective. Dev Psychopathol 2002 Summer
14:613-34
210
Courchesne, E.; Karns, C.M.; Davis, H.R.; Ziccardi, R.; Carper,
R.A.; Tigue, Z.D.; Chisum, H.J.; Moses, P.; Pierce, K.; Lord, C.; Lincoln,
A.J.; Pizzo, S.; Schreibman, L.; Haas, R.H.; Akshoomoff, N.A.; &
Courchesne, R.Y. Unusual brain growth patterns in early life in patients with
autistic disorder An MRI study. Neurology 2001;57:245–254.

Page 57 of 114
Another important aetiology is excitotoxicity, an involvement that may allow
the brain to discard useless connections or reduce poorly functioning neurons.
If neurons are stimulated by toxins, lack of oxygen or are affected by genetic
programmes, they release glutamate. This process may be involved in stroke,
Alzheimer’s disease, and other neuro-degenerative conditions, possibly
including schizophrenia.

Alternatively, one pathology could trigger the second; although it is unclear


how Purkinje neuron loss could trigger excessive axonal or glial/myelin growth
in cerebellar white matter, excessive proliferation of excitatory axonal
projections might be speculated to lead to pathologic excitotoxicity and
Purkinje death. Excitotoxicity as a patho-physiologic factor in autism has
previously been proposed.212

The coexistence of both cerebral and cerebellar maldevelopment may explain


why the impairments in higher cognitive functions in autism are pervasive and
persistent across the life span. A postnatal period of extreme maldevelopment
of these two major brain structures will almost certainly be manifest in aberrant
behavioural expression, and it is during this early period (typically 12 to 24
months) that parents most often first express concern about their child’s
development. 213 During this developmental period, the human brain
undergoes rapid synaptogenesis, expansion of dendritic and axon arbors, and
selection of which neuronal elements to keep or eliminate. 214, 215, 216, 217 In the
normally developing brain, shaping of neural architecture and connectivity is
theorised to be significantly influenced or directed by functional neural activity
driven by learning and experience. 218, 219 In the autistic brain, however, the
researchers speculated that growth and elaboration of neural architecture and
connectivity occurs prematurely and without being guided by functional

211
Casaccia-Bonnefil P, Tikoo R, Kiyokawa H, Friedrich J, Chao M,
Koff A. Oligodendrocite precurser differentiation is perturbed in the absence of
the cyclin-dependent kinase inhibitor p27kip1. Genes Dev 1997;11:2335–2346..
212
Gordon WP. Neurotoxic theory of autism. In: Naruse H, Ornitz EM, eds.
Neurobiology of infantile autism: proceedings of the International Symposium on
Neurobiology of Infantile Autism, Tokyo, 10–11 November 1990: satellite
meeting of the joint convention of the 5th International Child Neurology
Congress and the 3rd Asian and Oceanian Congress of Child Neurology.New
York: Elsevier Science, 1992:373–376
213
Cox A, Charman T, Baron-Cohen S, et al. Autism spectrum disorders
at 20 and 42 months of age: stability of clinical and ADI-R diagnosis. J Child
Psychol Psychiatry 1999;5:719–732.
214
Schade JP, van Groenigen WB. Structural organization of the human
cerebral cortex. I. Maturation of the middle frontal gyrus. Acta Anat 1961;47:72–
111.
215
Huttenlocher PR, Dabholkar AS. Regional differences in
synaptogenesis in human cerebral cortex. J Comp Neurol 1997; 387:167–178.
216
Quartz SR, Sejnowski TJ. The neural basis of cognitive development: a
constructivist manifesto. Behav Brain Sci 1998;20: 537–596.
217
Courchesne E, Chisum H, Townsend J. Neural activity-dependent
brain changes in development: implications for psychopathology. Dev
Psychopathol 1994;6:697–722.
218
Quartz SR, Sejnowski TJ. The neural basis of cognitive development: a
constructivist manifesto. Behav Brain Sci 1998;20: 537–596.
219
Courchesne E, Chisum H, Townsend J. Neural activitydependent brain
changes in development: implications for psychopathology. Dev Psychopathol
1994;6:697–722.

Page 58 of 114
experiences and adaptive learning; that is, in early life the autistic brain
exhibits premature “growth without guidance.”

In addition, the cerebellum and certain cerebral regions may perform


analogous, possibly complementary, functions. For instance, in the normal
brain, cerebellar cortex is activated by tasks that commonly activate frontal
cortex, such as tasks involving working memory, attention, or semantic
association. 220, 221, 222 Adults with cerebellar lesions show impaired
performance on similar frontal lobe tasks, including tests of source memory and
executive functions (e.g., shifting attention, cognitive planning, and working
memory). 223, 224 So, the presence of both cerebral and cerebellar defects from
the earliest stages of cognitive development would likely result in severe and
persistent functional deficits.

Abnormally elevated brain neurotrophins and neuropeptides (brain-derived


neurotrophic factor, neurotrophin-4, vasoactive intestinal peptide, calcitonin-
related gene peptide) have been found in neonatal blood spots of individuals
who later developed autism and mental retardation. 225 These brain growth
factors play roles in neural proliferation, migration, differentiation, growth, and
circuit organisation, and it was hypothesised that abnormal elevations may
result in unusual regional growth abnormalities (e.g., overgrowth in the
cerebrum due to excessive sparing of neurons and stimulation of growth of
neural elements, but, paradoxically, loss of Purkinje cells in the cerebellum 226).
Eric Courchesne et al (idem), further hypothesise that in autism there is a
relationship between abnormally elevated brain growth factors at birth and the
abnormal brain growth patterns described above.

Pauline Filipek has said, as a member of a research panel convened by the


American Academy of Neurology, "By 12 months of age, most children should
be pointing as a non-verbal communication gesture and babbling. By 16
months of age they should have in their vocabulary words other than ‘mummy’
and ‘daddy’, and by 24 months of age, they should be using phrases." 227

Goldberg has told us that,

220
Allen G, Buxton RB, Wong EC, Courchesne E. Attentional activation
of the cerebellum independent of motor involvement. Science 1997;275:1940–
1943.
221
Desmond JE, Gabrieli JD, Wagner AD, Ginier BL, Glover GH. Lobular
patterns of cerebellar activation in verbal working memory and finger-tapping
tasks as revealed by functional MRI. J Neurosci 1997;17:9675–9685.
222
Raichle ME, Fiez JA, Videen TO, et al. Practice-related changes in
human brain functional anatomy during nonmotor learning. Cereb Cortex 1994;
4:8–26.
223
Akshoomoff NA. Intramodality shifting attention in children with
damage to the cerebellum. J Cogn Neurosci 1994; 6:388– 399.
224
Schmahmann JD, Sherman JC. The cerebellar cognitive affective
syndrome. Brain 1998; 121:561–579.
225
Nelson KB, Grether JK, Croen LA, et al. Neuropeptides and
neurotrophins in neonatal blood of children with autism or mental retardation.
Ann Neurol 2001;49:597–606.
226
Morrison ME, Mason CA. Granule neuron regulation of Purkinje cell
development: striking a balance between neurotrophin and glutamate signaling.
J Neurosci 1998;18:3563–3573.
227
Filipek, Pauline. Journal of Autism and Developmental Disorders (1999;
29:437-482)

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“In the past, autism was considered a "psychiatric" disorder. We now know that autism is
a "medical condition," not a mental disorder. Perhaps one of the reasons no one has
come up with an answer for autism is the way we have thought of it (or rather did not
think of it, in medicine).
Even though children with classic autism might be helped medically as our knowledge of
the brain’s physiology expands, for now it might be helpful to separate children afflicted
with autistic syndrome from those with classic autism. As children with autistic syndrome
increasingly become categorised as a "medical" problem, separating them from the many
negative connotations and hopelessness associated with "classic" autism could be
advantageous to promoting research and funding to help these children.
Increased frontal perfusion may be related to "hyperfrontality" disorder, and cerebellar
hypoperfusion to motility impairment. Temporal lobe hypoperfusion and other areas of
dysfunction remain in spite of multiple various therapies used by these children. We are
looking at anatomical markings, defining autism / PDD dysfunction, correlating to models
proposed by behavioural neurologists.
Past focus for autistic children has been on trainability, co-operation, and behaviour, NOT
on improving the cognitive processing. A shift to the idea of "rehabilitation" is already in
motion; a full review of techniques and goals is urgently needed.
Based on NeuroSPECT findings, implications are that medications or efforts to "calm" the
brain and child down, may further shut down the areas in which we want to improve
blood flow and function and down regulated blood flow.” 228

There are also indications that particular parts of the brain can be shown to be
damaged in the autistic person. Studies in animals have recorded symptoms
typical of autism in young animals with amygdala lesions. Amygdala
dysfunction has also been implicated in human disorders ranging from social
anxiety to depression and to autism.

Baron-Cohen suggests that the amygdala plays a role in social understanding.


229
If a monkey has a lesion in the amygdala, for example, its social behaviour
changes; it no longer knows where it fits into the social group, and doesn't
know whether another monkey is being friendly, or not. This idea of the "social
brain" was first written about in the 1980s by Lesley Brothers at the University
of California, Los Angeles. Baron-Cohen’s work in autism has added support to
this idea.

Valerie Stone has also contributed to this research. She has written that the
ability to infer others' mental states, such as their beliefs, knowledge and
desires — is a central cognitive faculty underlying our ability to engage in social
interaction.230 Children with the developmental disorder of autism suffer from a
deficit in theory of mind. Autistic children's problems with social behaviour may
result from their difficulty making inferences about others' mental states.
Certain kinds of neurological patients also show specific deficits in social
functioning. Her research involved looking for parallels between the social
deficits (particularly theory of mind deficits) exhibited by individuals with
autism and patients with frontal lobe or amygdala damage.

228
Goldberg, M. Frontal and Temporal Lobe Dysfunction in autism and
Other Related Disorders: ADHD and OCD. Alasbimn Journa1(4): July 1999.
http://www.alasbimnjournal.cl/revistas/4/goldberg.htm
229
Baron-Cohen, Simon; Tager-Flusberg, Helen & Cohen, Donald.
[Eds.] Understanding Other Minds - Perspectives from Developmental Cognitive
Neuroscience Second Edition. OUP, 1999.
230
Stone, V.E., Baron-Cohen, S., Calder, A.C., Keane, J. & Young, A.W. (in
press). Acquired theory of mind impairments in individuals with bilateral
amygdala lesions. Neuropsychologia.

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231, 232
Further studies exploring the relationships of anxiety with autism and the
amygdala in autism 233 led to the conclusions that:

(1) the amygdala is not essential for social behaviour;

(2) pathology of the amygdala may not be the basis for impaired functioning in
autism; and

(3) impairments of amygdala functioning in autism may produce effects


through influencing fear and anxiety that are commonly comorbid in autism,
and that in turn might exacerbate other causes of social impairment.

In another set of studies, 234, 235, 23610-12] in which primates had amygdala lesions
placed shortly after birth, (as opposed to studying lesions made in mature
animals), Dr. Amaral established that the amygdala was not necessary for
gaining or acquiring social knowledge in the first place.

Another study also suggests that brain damage may bring with it autistic
syndrome. More than one area of the brain is responsible for autistic behaviour
in children with tuberous sclerosis and brain lesions, according to an article
published in the October 9, 2001 issue of Neurology, the scientific journal of the
American Academy of Neurology.

In a study of 26 children with tuberous sclerosis complex (TSC), a genetic


disorder that causes benign lesions or tumours to form in many different
organs, including the brain where the lesions are called "tubers.” Autism is a
common occurrence in children with TSC.

Researchers used MRI and PET exams to study how brain lesions resulted in
common behaviours of autism including difficulties in social interaction and
communication, and narrow and repetitive stereotyped behaviour. "We wanted
to know if where the tuber was located or what it was 'doing' in the brain could
predict behaviours of autism," said Diane C. Chugani, PhD, a researcher at the
PET Center at Children's Hospital of Michigan, Detroit, Michigan. "We found
that in these children, autism results from a complex combination of events in
different parts of the brain, rather than from one single source."237
231
Muris P, Steerneman P, Merckelbach H, Holdrinet I, Meesters C.
Comorbid anxiety symptoms in children with pervasive developmental disorders.
J Anxiety Disord. 1998;12:387-393.
232
Gillott A, Furniss F, Walter A. Anxiety in high-functioning children with
autism. Autism. 2001;5:277-286.
233
Thomas KM, Drevets WC, Dahl RE, et al. Amygdala response to fearful
faces in anxious and depressed children. Arch Gen Psychiatry. 2001;58:1057-
1063.
234
Amaral DG. The primate amygdala and the neurobiology of social
behavior: implications for understanding social anxiety. Biol Psychiatry.
2002;51:11-17.
235
Prather MD, Levenex P, Mauldin-Jourdain ML, et al. Increased social
fear and decreased fear of objects in monkeys with neonatal amygdala lesions.
Neuroscience. 2001;106:653-658.
236
Emery NJ, Capitanio JP, Mason WA, Machado CJ, Mendoza SP,
Amaral DG. The effects of bilateral lesions of the amygdala on dyadic social
interactions in rhesus monkeys (Macaca mulatta). Behav Neurosci.
2001;115:515-544.
237
Chugani DC, Chugani HT, Muzik O, Shah JR, Shah AK, Canady A,
Mangner TJ, Chakraborty PK. Imaging epileptogenic tubers in children with

Page 61 of 114
Defects in the cerebellum, the part of the brain responsible for co-ordination,
have been induced in guinea pigs, and the result was the development of some
of the traits typical of autism. They were much less inclined to interact with
their fellow animals, they did far less sniffing, licking and mating attempts, and
showed a reluctance to explore or respond to their surroundings.238

In research by Sparkes et al,239 children with autism spectrum disorder (ASD)


were found to have significantly increased cerebral volumes compared with
typically developing (TD) and developmentally delayed (DD) children.
Cerebellar volume for the ASD group was increased in comparison with a TD
group, but this increase was proportional to overall increases in cerebral
volume.

Measurements of amygdalae and hippocampi in this group of young children


with ASD revealed enlargement bilaterally that was proportional to overall
increases in total cerebral volume. There were similar findings of cerebral
enlargement for both girls and boys with ASD. In a subgroup of children with
ASD with strictly defined autism, amygdala enlargement was in excess of
increased cerebral volume.

Geraldine Dawson reported particular findings in April 2001 at the annual


meeting of the Society for Research in Child Development in Minneapolis.
These suggest that impairment in face recognition may turn out to be one of
the earliest indicators of abnormal brain development in autism.

"We know that even new-born babies are drawn to face-like stimuli. This inborn
interest in faces is the start of social development," she said. "This new study
tells us something very fundamental about abnormalities in autism. It may be
an important clue to actual brain circuits that are not functioning properly.
Since all of the children in the study reacted similarly to toys and only the
children with autism had problems with face recognition, it tells us autism is not
a global problem. Rather, it indicates an abnormality in those brain circuits
responsible for social function. It highlights that autism is a disorder of the
social brain.” Dawson said the idea that face recognition may be hard-wired, or
something people are born with, is controversial.

Withdrawing from social interaction and communication is a hallmark of autism,


and researchers have identified structural differences in the brains of autism
patients that might explain the behaviour.240

Using computerised imaging, researchers have observed mini-columnar


abnormalities in the frontal and temporal lobes of autistic patients. 241 The
study by scientists at the Medical College of Georgia, the University of South

tuberous sclerosis complex using alpha-[11C]methyl-L-tryptophan positron


emission tomography. Ann Neurol. 1998 Dec;44(6):858-66.
238
Reported in European Journal of Neuroscience, Vol. 10 p2677.
239
Sparks BF, Friedman SD, Shaw DW,
Aylward EH, Echelard D, Artru AA, Maravilla KR, Giedd JN, Munson J,
Dawson G, Dager SR. Brain structural abnormalities in young children with
autism spectrum disorder. Neurology 2002 Jul 23;59(2):184-92
240
Casanova MF, Buxhoeveden DP, Switala AE, Roy E. Minicolumnar
pathology in autism. Neurology 2002 Feb 12; 58(3): 428-32.
241
The frontal lobe of the brain is involved with reasoning, planning, parts
of speech and movement, emotions and problem-solving. The temporal lobe is
involved with perception and recognition of sound and memory.

Page 62 of 114
Carolina, and the Downtown VA Medical Center in Augusta, Georgia, is reported
in Neurology, the scientific journal of the American Academy of Neurology.

A mini-column is a basic organisational unit of brain cells and connective wiring


allows an individual to take in information, process it, and respond. Thus, any
changes in size, shape or location of the mini-column will have an effect on the
processing capacity of the brain. For the study, scientists examined the brain
tissue of nine autistic patients and nine controls using five measures: columnar
width, peripheral neuropil space, mean inter-neuronal distance, compactness,
and grey level index.

According to study author, Manuel F. Casanova, MD, a neurologist and neuro-


pathologist at the Downtown VA Medical Center in Augusta, Georgia, the
examinations revealed that the cell mini-columns of autistic patients are
significantly smaller, but there are many more of them.

Casanova reports that evolution of the brain has kept mini-column size
essentially constant while increasing total cortical surface area, which in larger
brains has resulted in more columns per brain and thus more processing units
and increased complexity.

This would be consistent with an existing theory that autistic individuals suffer
a chronic state of over-arousal, and portray abnormal behaviours to diminish
the arousal. The lack of lateral inhibitors, contained in the cortex, would affect
an individual's ability to discriminate between competing sensory information,
(Casanova, idem). Researchers do not yet know whether the difference in the
number and size of the mini-columns is attributable to a gene mutation or some
other factor.

As mentioned above, Sparks et al 242 explored the specific gross neuro-


anatomic substrates of this brain developmental disorder. They examined
brain morphometric features in a large sample of carefully diagnosed 3- to 4-
year-old children with autism spectrum disorder (ASD) compared with age-
matched control groups of typically developing (TD) children and
developmentally delayed (DD) children.

Volumes of the cerebrum, cerebellum, amygdala, and hippocampus were


measured from three-dimensional coronal MR images acquired from 45 children
with ASD, 26 TD children, and 14 DD children. The volumes were analysed with
respect to age, sex, volume of the cerebrum, and clinical status.

Children with ASD were found to have significantly increased cerebral volumes
compared with TD and DD children. Cerebellar volume for the ASD group was
increased in comparison with the TD group, but this increase was proportional
to overall increases in cerebral volume. The DD group had smaller cerebellar
volumes compared with both of the other groups. Measurements of amygdalae
and hippocampi in this group of young children with ASD revealed enlargement
bilaterally that was proportional to overall increases in total cerebral volume.
There were similar findings of cerebral enlargement for both girls and boys with
ASD. For sub-region analyses, structural abnormalities were observed primarily

242
Sparks BF, Friedman SD, Shaw DW, Aylward EH, Echelard D,
Artru AA, Maravilla KR, Giedd JN, Munson J, Dawson G, Dager SR. Brain
structural abnormalities in young children with autism spectrum disorder.
Neurology 2002 Jul 23; 59(2): 184-92.

Page 63 of 114
in boys, although this may reflect low statistical power issues because of the
small sample (seven girls with ASD) studied.

Among the ASD group, structural findings were independent of non-verbal IQ.
In a subgroup of children with ASD with strictly defined autism, amygdala
enlargement was in excess of increased cerebral volume.

The authors believe that these structural findings suggest abnormal brain
developmental processes early in the clinical course of autism. Research
currently is underway to better elucidate mechanisms underlying these
structural abnormalities and their longitudinal progression.

AUTISM AND ITS TREATMENT

Psychiatrists and their predecessors, in the middle ages, picked up those who
were developmentally and intellectually disabled and they have been running
with them ever since.

General executive and administrative laziness brought this about and little has
been done to make any adequate change. Although many fewer of these
subjects are now in hospital, the transition to community care has not loosened
the hold which psychiatrists have on this group of people.

A lack of professional development and understanding, together with only a


fairly recent burgeoning of brain science may have aided this débâcle.
However it can only be a lack of common sense that allows psychiatrists to
conflate psychoses and brain damage.

Due to the problems associated with early brain damage, and the lack of neuro-
psychological knowledge, there seems to be a situation where the psychiatrist
is unable to understand the person or the person’s condition. However it is
often the case that the psychiatrist is the only available professional who can
attend the person concerned. Most psychiatric faculty members, however,
believe that there will always remain a specific role for clinicians within the field
of ‘learning disability’ (whatever the cause). This has existed in some guise
since the asylums and workhouses of the early 1800s. The fact that about 77%
of UK consultant posts and 74% of specialist registrar national training numbers
are filled, despite general recruitment problems in psychiatry bears reference
to this. 243

As Neville has written: “If a learning disability is to be regarded as the province


of psychiatry, people have to be trained to be able to manage this group of
disorders or set up collaborative arrangements which include input from
neurologists. When we are trying to define the medical needs of a group of
people with one form of brain impairment — that is, cognitive — it is not
surprising that this is found to coexist with several other major medical
impairments. I do not believe that without such comprehensive input the
mental health of disabled adults can be appropriately provided for”. 244

243
Middleton, Isla & Courtenay, Ken. Psychiatry of learning disability.
BMJ Classified; pp2-3, 13 May 2000.
244
Neville, BGR. Medical needs are important too. In Doody, G. Mental
health services for people with learning disabilities: People with comorbidity can
fall between two stools. BMJ. 2001 February 3; 322(7281): 301.

Page 64 of 114
In order to justify his interventions, the psychiatrist has to create the person in
the image of what he is able to understand and to treat. When the person
seems to respond favourably to some aspects of this treatment, the psychiatrist
does not attribute this to his good fortune, but for him it reinforces his view that
the image he has created, ‘will do’ as a clinical entity. When the person does
not respond favourably, the psychiatrist views this outcome as an indication of
the intractability of the condition he has ‘created’.

The past decade has seen a dramatic increase in the use of medications in
children and adolescents with psychiatric disorders. Despite a lack of clear
scientific evidence for their efficacy and long-term safety, at least to date,
psychotropic medications have been used quite widely in children and
adolescents. 245

Researchers discussed these issues in a series of presentations at the APA


meeting in 2000, reporting on novel antipsychotics and anti-seizure
medications, as well as medication use in incarcerated youth.

Antipsychotics are often used in this co-morbid population, yet few studies are
looking for efficacy and safety. In a study presented by Dr. Hussain, 246 of
Prince Albert, Canada, 50 children aged 6 to 14 (74% being male) with co-
morbid diagnosis of ADHD and conduct disorder who had not responded to
stimulants alone were randomly assigned to risperidone or olanzapine
augmentation.

The researchers compared the consensus diagnosis, which used all the
information from medical records and structured diagnostic interviews, to the
discharge diagnoses of the independent clinician. Overall, there was least
agreement for the diagnosis of bipolar disorder, where the clinician was over-
diagnosing bipolarity. The study showed the increased rate of diagnosis of
bipolar disorder by clinicians when the best estimate diagnosis by researchers
refuted it.

Koehler believes that bipolar disorder is a heavily genetic condition. 247 There
is no evidence of this condition in any members of her family. Koehler does
believe that sleep deprivation plays a part in mania-like symptoms. (idem) His
paper emphasizes that subjects who suffer from bipolar disorder seem to have
normal goal-intentioned capabilities.

A currently practicing psychiatrist, Joanna Moncrieff who is also a Senior


Lecturer in psychiatry at University College London has expressed her views
about psychiatric drug treatment. She has written articles critical of various
treatments, including lithium, antidepressants and neuroleptics. She has also
written about the adverse influence of the pharmaceutical industry on
psychiatry. She is a long-standing critic of psychiatric drug treatment and has
published numerous articles in medical journals. She was a founding member
245
Weller, Elizabeth B. Issues in Child and Adolescent
Psychopharmacology. American Psychiatric Association 153rd Annual Meeting.
Day 3 - May 16, 2000.
246
Hussain MZ. Novel antipsychotic in ADHD with conduct disorder.
Program and abstracts from the 153rd Annual American Psychiatric Association
Meeting, May 13-18, 2000; Chicago, Illinois. Abstract 35.
247
Koehler, B. International Society for the Psychological Treatments of
Schizophrenia and Other Psychoses. 6 March 2005.
http://www.isps-us.org/koehler/sociocultural_bipolar.htm

Page 65 of 114
and is the co-chair person of the Critical Psychiatry Network. Her book, ‘A Myth
of the Chemical Cure’ exposes as fraudulent the claims that psychiatric drugs
correct chemical imbalances.

Dr Moncrieff’s book explains how the notion of a chemical cure is fatally flawed,
because psychiatric drugs do not work by treating diseases of the brain. While
drugs developed for physical disease interact with a defined disease process, in
the case of psychiatry, there is no good evidence that drugs work in this way,
argues Dr Moncrieff.

Although psychiatrists commonly talk of psychiatric drugs correcting a


‘chemical imbalance’, there is in fact no proof that such an imbalance exists —
hence the notion of a drug ‘correcting’ such an imbalance is meaningless.

In fact, argues Dr Moncrieff, psychiatric drugs ‘work’ by creating abnormal brain


states, which are often unpleasant, and which impair normal intellectual and
emotional functions, along with other harmful consequences.

This misleading situation, says Dr Moncrieff, has arisen because it serves the
interests of the psychiatric profession, the pharmaceutical industry and the
modern state. Over time, these interests have led to a distortion of knowledge,
deluding society since the 1960s that a ‘chemical cure’ is possible in psychiatry.

Dr Moncrieff’s book explains the history of the power relations that have
influenced psychiatric drug development, covering the arrival of new
psychiatric drugs during the 20th century, the development of so-called
‘antipsychotic’ medications, and the introduction of the modern SSRI
medications that have come under fire recently.

She demonstrates how the research literature paints a far less positive picture
of the effectiveness of psychiatric drug treatment than is generally supposed.
Dr Moncrieff was a lead commentator in the widely reported stories about the
inefficiency of Prozac and other bestselling antidepressants – although the
stories about the overall lack of evidence for these drugs are no revelation to
her.

Dr Moncrieff proposes in her book that psychiatric drugs 'work' by creating


abnormal brain states, which are often unpleasant and impair normal
intellectual and emotional functions along with other harmful consequences.
She has examined research on antipsychotics, antidepressants and mood
stabilisers and demonstrates this thesis and it is suggested that acknowledging
the real nature of psychiatric drugs would lead to a more democratic practice of
psychiatry. She reports that most antidepressants are now off patent in Europe
and the US. Currently, drug companies are making bigger profits from atypical
antipsychotics and the fashionable diagnosis of the moment is no longer
depression but bipolar disorder.” 248

Another point to be aware of is that "brain-damaged" children may be much


more sensitive to side effects of drugs than normal children. Drugs normally
used to help anxiety or sleep sometimes have the opposite effect in susceptible
children. This is not to say that they must never be used, merely that it may be
a matter of trial and error to find something that suits the child. It may be that

248
Moncrieff, Joanna. The Myth of the Chemical Cure: A Critique of
Psychiatric Drug Treatment. Palgrave Macmillan. 4 Dec 2007.

Page 66 of 114
some children with brain damage are more susceptible to food additives or
colourings as well, although this has not been proved.

As with the use of any psychopharmacological agent, care should be taken in


the selection and administration of medications. The profile of side effects and
risk as well as potential benefits will of course vary depending on the agent
used and the target symptoms. Since individuals with autism/PDD are often
non-verbal, reliance typically is made on reports and observation of specific
behaviours. This can be an advantage in many ways in helping to document
the efficacy of the selected medication. However, it is important not to lose
sight of the overall goal of facilitating the child's adjustment and engagement
with educational intervention. For example, sedation might be misinterpreted
as a positive therapeutic response. Issues of informed consent should be
carefully considered, particularly as many medications have yet to be approved
for use in children; close follow-up is required.

Medications may be useful for symptoms which interfere with participation in


educational interventions or are a source of impairment or distress to the
individual. These medications are not specific to autism and do not treat core
aspects of the disorder, and their potential side effects should be carefully
considered. The neuroleptics, selective serotonin re-uptake inhibitors, tricyclic
antidepressants, lithium and mood stabilisers, and anxiolytics have been used
in these patients with only varying degrees of success.

_______

Management Following Early Brain Injury


EARLY MANAGEMENT

There is little evidence regarding estimates of the number of children who are
non-verbal following brain injury. However, Carlisle-Ladtkow and Culp 249 found
that 21 per cent of 138 adolescents and adults with brain injury were judged to
be non-verbal for a period of time in their recovery. While there is tremendous
variability in recovery observed within the brain injury population (DeRuyter
and Kennedy 250 ), there is the need to augment expressive communication at
some stage in the process of recovery following brain injury.
251
According to Body and Parker , communication in its broadest sense is the

249
Carlisle-Ladtkow, M. & Culp, D. M. (1992). Augmentative
communication with traumatic brain injury. In: Augmentative Communication in
the Medical Setting (ed. K. M. Yorkston). Tuscon,AZ: Communication Skill
Builders.
250
DeRuyter, F. & Kennedy, M. R. T. (l991). Augmentative
communication following traumatic brain injury. In: Communication Disorders
Following Traumatic Brain Injury: Management of Cognitive, Language and
Motor Impairments (eds. D. R. Beukelman & K. M. Yorkston). Austin, TX: Pro Ed.
251
Body, R. and Parker, M. (l999). The use of multiple informants in the
assessment of communication after traumatic brain injury. In: Communication
Disorders Following Traumatic Brain Injury: Brain Damage Behaviour and
Cognitive Series (eds. S. McDonald, L. & Togher C. Code), pp. 147-74 Hove,
Sussex: Psychology Press Ltd.

Page 67 of 114
responsibility of all involved in the management of the individual following brain
injury. A team approach should therefore be adopted to enable sharing of
information and to achieve mutually-agreed therapy goals. Such collaborative
working is essential to ensure that all therapy aims are appropriately reinforced
by all team members.

LONG-TERM MANAGEMENT

Over time, new problems may be revealed as the child's development following
TBI may fail to proceed normally (Johnson 2002 252). Such problems may affect
the child's ability to access the curriculum and may have a subtle effect on
interaction with their peers, thereby influencing reintegration into school. It is
therefore essential to liaise with and advise educational staff on the child's
return to education. In addition, onward referral to community speech and
language therapy services for the ongoing management of the child's
communication needs is required.

Any communication difficulties the child presents with must continue to be


viewed within the context of their abilities, particularly cognitive and physical
skills, in addition to their social and emotional needs.

COGNITIVE PROBLEMS

The purpose of this section is to outline the main cognitive and educational
difficulties that may follow an acquired brain injury and put them into the
context of their learning environment. As the research into very early toxic
brain damage is rare the focus here is on traumatic brain injuries (TBIs). These
tend to be more frequently associated with long-term educational problems,
although they may often be subtle and become apparent some months or years
following the injury. There is considerable overlap with additional problems —
including speech and language impairment and emotional and behavioural
difficulties — which again reinforce the need for a coordinated and
multidisciplinary approach for these children.

Cognition is a term used to describe all of our thinking skills and is comprised of
different cognitive domains including memory, language, visual-spatial
processes and motor planning — a group of organizational/planning skills
known collectively as 'executive function'. (See also General Introduction, P 2.)

All of these skills are dependent on the integrity of brain function, therefore, a
brain injury can adversely affect specific or general cognitive skills. In healthy
adults, cognitive skills are developed to the extent that they are specialized
functions which are dissociable on neuropsychological testing and each
cognitive domain is primarily associated with different brain regions. For
example, the region in the temporal lobe known as the hippocampus, is par-
ticularly important for certain types of memory function, whereas the prefrontal
cortex is fundamental to executive skills.

As we are not born with mature cognitive skills, they have to develop gradually
and become more specialized throughout childhood and adolescence. As we
learn from our interaction with the environment, cognition and behaviour
become more adult-like over time. This development is reflected in parallel
252
Johnson, D. A. (2002). Voices from the past. Introduction to 'The After
Effects of Head Injuries'. Pediatric Rehabilitation 5, 71-4.

Page 68 of 114
neurobiological processes occurring in the brain throughout development. It is
important to consider the neural and social developmental processes taking
place when a child suffers a brain injury, as the effects can be very different
from when an injury occurs in adulthood and it is often much more difficult to
predict future cognitive outcome. When a child suffers a brain injury, the
immediate outcome can range from mild to severe impairment. The longer-
term outcome can improve to leave subtle or no cognitive impairment, but it
can also deteriorate so that the adolescent presents with severe difficulties that
were not obvious during the early years following the injury.

Because the outcome for children can be so variable, professionals have


sometimes over-generalized about the likely prognosis following brain injury.
For example, for a long time it was assumed that it was 'better' to suffer a brain
injury during childhood rather than adulthood. This assumption was partly
based on early animal studies performed by Margaret Kennard in which it was
demonstrated that damage to young monkey brains has less severe effects on
motor function than in adult monkeys 253. In addition, human studies have
shown that damage to parts of the brain in adults cause specific difficulties,
such as the ability to produce speech, whereas similar damage occurring in the
same area in a neonate or infant, seems to have little effect, with other parts of
the brain being flexible enough to take over this function 254. The ability to re-
organize and take over a function is referred to as 'plasticity'; immature brains
are generally more plastic than adult brains 255. However, this research
probably applies more to TBI than ABI.

However, different brain regions may have different degrees of plasticity


available at different stages of development; this has implications as to which
cognitive skills may or may not recover. Other factors can prevent plasticity
from occurring; for example, if the same brain regions in both hemispheres are
injured then re-organization of function is much more difficult, such that if a
child suffers an injury to both hippocampi early in development, they are often
left with significant memory problems regardless of how early they suffered the
injury 256 .

In response to studies that show significant problems following childhood brain


injury, some professionals suggest that suffering a brain injury during childhood
is much worse than in adulthood 257 . Sometimes this can be the case, partly
because of the reasons noted above, but also for other reasons.

• First, if other parts of the brain try to compensate for areas that are
253
Kennard, M. (1942). Cortical reorganisation of motor function. Archives
of Neurology 48, 227-40.
254
Liegeois, E, Connelly, A., Cross, J. H., Boyd, S. G., Gadian, D. G.,
Vargha- Khadem, E, & Baldeweg, T. (2004). Language reorganization in
children with early-onset lesions of the left hemisphere: an fMRI study. Brain
127, 1229-36.
255
Kolb, B., Gibb, R., & Gorny, G. (2000). Cortical plasticity and the
development of behaviour after early prefrontal cortical injury. Developmental
Neuropsychology 18,423-44.
256
Isaacs, E. B., Vargha-Khadem, E, Watkins, K. E., Lucas, A.,
Mishkin, M. and Gadian, D. G. (2003). Developmental amnesia and its
relationship to degree and hippocampal atrophy. Proceedings of the National
Academy of Sciences, 100, 13060-63.
257
Johnson, D., Uttley, D., & Wyke, M. A. (1989). Children's Head Injury:
Who Cares? London: Taylor and Francis.

Page 69 of 114
no longer functioning, then their own ability to perform will be
reduced as they will have to take on extra cognitive work. So, for
example, when injuries occur early in life to brain regions commonly
associated with language, then other areas may take on these skills
because language is so fundamental to human function 258 . However,
this often comes at a 'cost' to other cognitive abilities that would
usually be subserved by the intact parts of the brain. Frequently
verbal reasoning skills are preserved in paediatric populations with
neurological disorders but this often compromises non-verbal
reasoning 259. This is sometimes referred to as the 'crowding
hypothesis', which, in simple terms, means the parts of the brain that
still function adequately become overcrowded trying to support too
many cognitive abilities.

• Second, when a healthy adult suffers a brain injury and loses a


particular skill or skills, they have, up until the time of injury,
developed all of their abilities normally. In contrast, if a child loses a
particular skill, they may require this skill before they can develop
many other, and possibly interrelated skills. So, for example, if a child
suffers a specific memory deficit, then the child will have to develop
all their other skills in life without the ability to consolidate certain
types of memories. There is now increasing evidence that specific
memory deficits early in life can have differentiating but significant
implications for a wide range of skills depending on the nature of the
memory deficit, including learning factual information in the academic
curriculum, literacy skills, social skills, artistic skills and independent
daily living skills 260. Therefore, a relatively specific deficit in
childhood could have far greater consequences than if it occurred in
adulthood.

• Third, some cognitive skills only become functional to a noticeable


degree later on in development. In particular, adult-like planning and
organizational skills (executive function) are known to develop during
adolescence and early adulthood. If you recall how different your
social behaviour was between the ages of 13 and 18 years of age you
can appreciate how much social development took place during
adolescence and early adulthood. These periods of development
correspond to periods of brain maturation, particularly in the
prefrontal cortex, and it is not until the brain undergoes this
maturation, that one will develop very complex skills in organization
and moral reasoning.

These skills are fundamental to developing responsible roles in the


complex social systems in which adults need to operate, and for
developing reciprocal social relationships and moral reasoning to an
adult level. Children may suffer injuries to these parts of the brain

258
Vargha- Khadem, F., O'Gorman, A. M., & Watters, G. V. (1985).
Aphasia and handedness in relation to hemispheric side, age at injury and
severity of cerebral lesion during childhood. Brain 108,677-96.
259
Vargha-Khadem, F., Isaacs, E., & Muter, V. (1994). A review of
cognitive outcome after unilateral lesions sustained during childhood. Journal of
Child Neurology 9 Supp!. 2, 67-73
260
Hood, J. & Rankin, P. M. (2005). How do specific memory disorders
present in the school classroom? Pediatric Rehabilitation 8, 272-82.

Page 70 of 114
and the difficulties associated with such injuries might then not
become apparent until the adolescent would normally start to develop
such skills. This is sometimes called the 'sleeper effect', because the
child can make what appears to be good recovery with no obvious
difficulties in the first few years following the injury and it may only be
at a later stage that the child demonstrates significant difficulties.
However, as the child grows older, the hidden difficulties become
apparent when a higher order of learning skills is required.

• Fourth, the social opportunities and obstacles are very different for
children's rehabilitation compared with that of adults 261 .

As the number of children surviving head injuries grows, there is an increasing


recognition of the complexity that acquired cognitive deficits can take, but
often parents and teachers are unsure as to the best way to help their child.

Children who suffer a brain injury in later childhood are frequently able to make
a good physical recovery and this can mask a range of cognitive deficits that
may severely interfere with functional living and educational skills. However,
for those who are affected in early infancy, new learning becomes ever more
difficult for them and their difficulties can be underestimated by those working
with them. The necessity for more systematic and long-term follow-up of brain
injured children for these reasons was made by Oddy 262, but this quite clearly
has significant resource implications and because of the available staffing-
levels, it may not be achieved. As far back as the middle of the last century,
Hebb 263 commented on the effects that brain damage may have on the ability
to learn new tasks.

The need for a greater understanding of head injuries in the educational system
has been well expressed by Johnson 264 who outlined the need for a greater
awareness of the nature of the learning difficulties faced by such children. If
their problems are misunderstood, children may start to lose self-esteem, which
further compounds their underlying difficulties.

PSYCHIATRIC INTERVENTION FOLLOWING EARLY BRAIN INJURY

It would be unthinkable in the 21st century to begin to use psychiatric treatment


as a prime medical input until all other avenues of intervention had been tried
or at least considered and weighed in the balance. The reason is that
psychiatry relies on theories and theories can be wrong. Neuropsychology
relies on scientific understanding of the brain and of its functions and what
happens where and when things go wrong.

The test of a good scientific theory, according to Karl Popper, a famous


twentieth century philosopher of science, is that it must be clear and concise.
This is known as the principle of parsimony, or 'Occam's Razor' — A good
theory generates a logical statement or hypothesis that is falsifiable.
261
Wright, I. & Limond, J. (2004). A developmental framework for memory
rehabilitation in children. Pediatric Rehabilitation 7, 85-96.
262
Oddy, M. (1993). Head injury during childhood. Neuropsychological
Rehabilitation 3, 301-20.
263
Hebb, D. O. (1949). The Organisation of Behaviour. New York: Wiley.
264
Johnson, D. A. (1992). Head injured children and education; a need for
greater delineation and understanding. British journal of Educational Psychology
62, 404-9.

Page 71 of 114
Occam's razor (entia non sunt multiplicanda praeter necessitatem), is the
principle that, entities must not be multiplied beyond necessity and the
conclusion thereof, that the simplest explanation or strategy tends to be the
best one. The principle is attributed to 14th-century English logician,
theologian and Franciscan friar, William of Ockham. Occam's razor may be
alternatively phrased as pluralitas non est ponenda sine necessitate (‘plurality
should not be posited without necessity’).

When competing hypotheses are equal in other respects, this principle


recommends selection of the hypothesis that introduces the fewest
assumptions and postulates the fewest entities while still sufficiently answering
the question. It is in this sense that Occam's razor is usually understood. To
quote Isaac Newton, "We are to admit no more causes of natural things than
such as are both true and sufficient to explain their appearances. Therefore, to
the same natural effects we must, so far as possible, assign the same causes."
265

When discussing Occam's razor in contemporary medicine, doctors and


philosophers of medicine speak of diagnostic parsimony. Diagnostic parsimony
advocates that when diagnosing a given injury, ailment, illness, or disease a
doctor should strive to look for the fewest possible causes that will account for
all the symptoms. Of course that requires a thorough investigation and it does
not assist reputations or the patient to try and use short-cuts.

This philosophy is one of several demonstrated in the popular medical adage


"when you hear hoof beats, think horses, not zebras" 266. It is often statistically
more likely that a patient has several conditions, rather than having a single
rarer one which explains their myriad symptoms. There is a well-accepted
likelihood that some patients do in fact turn out to have multiple conditions,
which by common sense nullifies the approach of insisting to explain any given
collection of symptoms with one condition. These misgivings emerge from
simple probability theory — which is already taken into account in many
modern variations of the razor. Misdiagnosis can result in the loss of a person's
health and potentially life. It is considered better to test and pursue all
reasonable theories even if there is some theory that appears the most likely.

Popper argued that no theory can ever be proved, but it can be disproved. He
used the example of white swans: it is possible to observe thousands of swans
over many years and record that they are all white. The logical deduction is
that all swans are white. However, it takes only one black swan to overturn the
theory that all swans are white. Therefore, even the best available theory
should not be treated as fact.

Psychiatric theory, as with all scientific theory, should be treated with caution.
Theories predict what is likely to happen, not what will happen to an individual.
People vary in their genetic make-up, experiences and circumstances, so no
theory or research evidence can ever tell us precisely what will apply to a
particular patient or client.

In spite of recent advances in brain technology, it is rarely possible to study the


265
Hawking, S [Ed.] (2003). On the Shoulders of Giants. Running Press.
p. 731. ISBN 076241698x.
266
‘Zebra’ is a medical slang term for an obscure and unlikely diagnosis
from ordinary symptoms.

Page 72 of 114
human mind directly. We can never 'know' what someone is really thinking.
We can only find out by studying what people say, how people behave and,
more recently, how the electrical activity in their brains varies in different
situations. Therefore, psychiatry is not a body of 'facts', but a body of theories
that change over time in the light of new information, new research methods,
new technologies and new ways of thinking about conceptualizing things.

_______

Some of the Physical and Cognitive Difficulties Encountered


Following Atraumatic Brain Damage

FEEDING AND SWALLOWING DIFFICULTIES

The child with a brain injury is at significant risk of feeding and swallowing
difficulties. Such difficulties can include problems with the placement and
manipulation of food in the oral cavity or the physiology of swallowing, or both,
and are referred to as dysphagia.

Swallowing is a highly complex motor process, requiring neurological control


and coordination of breathing and swallowing. Cerebral damage may affect the
neurological control of swallowing 267 and consequently, the child is at increased
risk of fluids and food material entering the airway, termed aspiration.

According to Reilly et al. 268 the signs suggestive of aspiration include coughing,
choking or deterioration in respiratory status during a feed, noisy or wet
breathing, or excessive pharyngeal secretions; sneezing during drinking may
also indicate naso-pharyngeal incoordination and reflux. The child who has
sustained neurological damage, with associated motor deficits, is at significant
risk of aspiration due to the impairment in the timing and coordination of the
swallow. In addition, sensory deficits as a result of neurological damage may
result in diminished or ineffective cough reflexes, thereby impeding one of the
central mechanisms of airway cleansing and protection 269. Such sensory
deficits place the child at an increased risk of aspiration; in addition, as a result
of this reduced sensation, the child may not demonstrate overt signs and
awareness of aspiration. Aspiration is potentially very serious; it may lead to
sudden respiratory arrest, although more commonly, it presents as repeated
chest infections and pneumonia and, consequently, long-term lung damage,
including bronchiectasis.
267
Murdoch, B. E. & Theodoros, D. G. (2001). Language disorders
following traumatic brain injury in childhood. In: Traumatic Brain Injury:
Associated Speech Language and Swallowing Disorders (eds B. E. Murdoch and
D. G. Theodoros), pp. 247-71 San Diego, CA: Singular Publishing.
268
Reilly, S., Wisbeach, A., & Carr, L. (2000). Assessing feeding in
children with neurological problems. In: Feeding Problems in Children (A
Practical Guide) (eds. A. Southall & A. Schwartz). Oxford: Radcliffe Medical Press.
269
Bhattacharyya, N., Kotz, T., & Shapiro, M. D. (2002). Dysphagia and
aspiration with unilateral vocal cord immobility: incidence, characterisation and
response to surgical treatment. The Annals of Otology Rhinology and
Laryngology Ill, 672-9.

Page 73 of 114
The likelihood of dysphagia resulting from brain injury is understandably high
given the degree of neurological control required for efficient and accurate
execution of the swallowing mechanism. This will inevitably lead to functional
implications with regards to the child’s eating and drinking abilities.

Given the complex nature of coexisting deficits, an interdisciplinary team


approach, combining medical, speech and language therapy, physiotherapy,
occupational therapy, dietetics, nursing, psychology, social work services and
the family, is essential for achieving optimal swallowing and feeding outcomes
for the dysphagic patient 270.

DYSPRAXIA AND NON-FLUENCY

Dyspraxia is a motor speech programming disorder, characterized by


articulatory errors and concomitant changes in prosodic features such as
intonation and stress.271 The child may demonstrate groping of the articulators
(e.g. tongue) in an attempt to achieve sequences of articulatory postures when
producing sounds and words. The child’s resultant speech appears effortful and
is slower, with more pauses. Errors in articulation are inconsistent and more
evident in repetition than in spontaneous speech. There may also be hesitancy
or several attempts to start a sentence and this will involve repetition until the
child finds the correct articulation to complete the sentence. It is important not
to interrupt this process by prompting. Although the Nuffield Centre Dyspraxia
Programme (The Nuffield Hearing and Speech Centre 2004 272) is primarily
designed for children with developmental dyspraxia, it may be applied to the
assessment and treatment of children with acquired dyspraxia following brain
injury.

Impaired receptive and expressive language skills, including slow information


processing and word-retrieval difficulties, and/or motor speech disorders, may
result in disturbances in the fluency of speech production. In addition acquired
neurological non-fluency following brain injury has been reported in the
literature (e.g. Heuer et al. 1996 273). Bijleveld et al. (1994 274) consider that
such neurogenic non-fluency is not simply a secondary psychological
consequence of brain injury, but represents a primary effect of a cerebral
lesion.

Of the different types of acquired childhood aphasia which a speech therapist


may see, the most common and complex are presented by head-injured
children. Whilst the majority of these make good initial progress, very few can
be said to recover completely. Specific types of language disturbance can
occur after head injury in childhood, which frequently resolve into difficulties of
auditory processing and lexical recall. These, in turn, may significantly affect
270
Logemann, J. A. (1994). Multidisciplinary management of dysphagia.
Acta-Oto-RhinoLaryngologica-Belgica 48, 235-8.
271
Murdoch, B. E., Ozanne, A. E., & Cross, J. A. (1990). Acquired
childhood speech disorders: dysarthria and dyspraxia. In: Acquired Neurological
Speech/Language Disorders in Childhood (ed. B. E. Murdoch). London: Taylor &
Francis.
272
http://www.ndp3.org/documents/ndp3-sample-manual-chp2.pdf
273
Heuer, R. J., Sataloff, R. T., Mandel, S., & Travers, N. (1996).
Neurogenic stuttering: further corroboration of site of lesion. Ear Nose and
Throat Journal 75, 161-8.
274
Bijleveld, H., Lebrun, Y. & van Dongen, H. (l994). A case of acquired
stuttering. Folia Phoniatrica Logopedia 46, 250-3.

Page 74 of 114
educational needs. Other specific long term problems include dysarthria
(including swallowing and phonation) and spelling.

The view that younger children with head injury recover better cannot be
upheld. The speech therapy required by head-injured children will change
during the course of recovery and it is important to review continually these
changing needs. Investigations into the evaluation, treatment and recovery of
head-injured children of speech and language disorders are absent 275.

Although evaluations of post-traumatic cognition are just beginning, these are


far behind in the area of language. Yet this is an equally important area of
development and normal function for the child. Consequently, there should be
a far more scientific and methodologically rigorous approach adopted to this
research in this area. 276

PRAGMATIC SKILLS

Following brain injury, the child may demonstrate difficulties with the social
aspects of their communication (i.e. pragmatic skills; Yeates et al. 2004 277).
The child’s pragmatic skills most typically impaired following brain injury
include topic selection/maintenance and turn-taking skills. Poor social
interaction skills such as a lack of awareness of body proximity and social
inhibitions may also be affected, thus impacting upon their interaction with
others.

Furthermore, higher-level language difficulties such as literal interpretation of


ambiguous sentences, and impaired reasoning, inferencing and problem-solving
abilities have been reported to be more evident in the later stages of recovery
or non-recovery following brain injury 278. According to Jordan et al. (idem),
children with severe brain injury are also less able to describe social situations.
Future implications for the ongoing development of higher-level language
abilities have been documented in the literature 279 . Such higher-level
language difficulties will undoubtedly impact upon the child’s social use of
language and therefore may have implications for reintegration into
educational settings.

LANGUAGE IN CHILDREN WITH EARLY BRAIN DAMAGE

275
Jordan, F.M., Ozanne, A.E. & Murdoch, B.E. (1988), 'Longterm
speech and language disorders subsequent to closed head injury in children',
Brain Injury, 2, pp. 179-185.
276
Lees, JA. Recovery of Speech and Language Deficits after Head Injury in
Children. In Johnson, DA.; Uttley, D. & Wyke, M. (1989) Children’s Head Injury:
Who Cares? Taylor & Francis.
277
Yeates, K. 0., Swift, E., Taylor, H. G., Wade, S. L. Drotar, D.
Stancin, T., & Minich, N. (2004). Short and long term social outcomes
following pediatric traumatic brain injury. Journal of the International
Neuropsychological Society 10,412-26.
278
Jordan, F. M., Cremona-Meteyard, S., & King, A. (1996). High-level
linguistic disturbances subsequent to childhood closed head injury. Brain Injury
10, 729-38.
279
Didus, E., Anderson, V. A. & Catroppa, C. (1999). The development
of pragmatic communication skills in head-injured children. Pediatric
Rehabilitation 3,177-86.

Page 75 of 114
In the last thirty years or so, new technologies have permitted us to 'look' inside
the human brain to better understand its functioning. However, brain-
behaviour relationships have long been of interest to the scientific community.
In the domain of language, Paul Broca's discovery in the 1860s that the left
frontal cortex was implicated in productive language and Carl Wernicke's
subsequent studies revealing the left temporal lobe to be critical for language
comprehension were landmark events.

Interestingly, in the last 35 years or so, the right hemisphere has also been
implicated in aspects of linguistic processing, especially in discourse and non-
literal uses of language 280, 281, 282, 283,284 285 . At present there is an extensive body
of research on those structures mediating adult language functions, but we are
only beginning to understand how these relationships develop in children.

Whilst a large number of studies have contributed to the understanding of


language functions in children with neurological dysfunction, many have
included children who incurred damage at different ages, and these studies
have come to differing conclusions regarding the nature and role of the left
hemisphere in language development. The goal over the last twenty years has
been to understand the development of brain-language relations from the
beginning of life by following the course of language development in children
with early unilateral focal brain damage. All of these children in this group
suffered their cerebral insult before six months of age, that is, pre-linguistically.
By prospectively chronicling their language development from infancy to
adolescence, there is an opportunity created to address the following basic
questions:
a. Localization of function
To what degree is language specified early on?
Do behavioural patterns correlate with site of brain damage?
Are they comparable to those of adults with homologous injuries?
b. Neuroplasticity
Do behavioural deficits persist or is there recovery of function over time?
Does the deficit express itself differentially over time?
c. The nature of the language acquisition process
280
Brownell, H., Simpson, T., Bihrle, A., Potter, H. & Gardner, H.
(1990): Appreciation of metaphoric alternative word meanings by left and right
brain-damaged patients. Neuropsychologia 28, 375-384.
281
VanLancker, D. & Kempler, D. (1986): Comprehension of familiar
phrases by left- but not by righthemisphere-damaged patients. Brain Lang.
32,265-277.
282
Gardner, H., Brownell, H., Wapner, W. & Michelow, D. (1983):
Missing the point: the role of the right hemisphere in the processing of complex
linguistic materials. In: Cognitive processing in the right hemisphere, ed. E.
Perceman. New York: Academic Press.
283
Hough, M. (1990): Narrative comprehension in adults with right and left
hemisphere brain damage: theme organization. Brain Lang. 38, 253-277.
284
Joanette, Y., Goulet, P. & Hannequin, D. (1990): Right hemisphere
and verbal communication. New York: Springer-Verlag.
285
Kaplan, J., Brownell, H., Jacobs, J. & Gardner, H. (1990): The effects
of right hemisphere damage on the pragmatic interpretation of conversational
remarks. Brain Lang. 38,315-333.

Page 76 of 114
How flexible is the language acquisition process itself?
Is the process fairly rigid or are there many ways to approach learning a
language?

For the past thirty years, a broad base of studies has examined early language
development in children from a variety of languages and across a wide array of
language families. The findings are consistent: children acquire languages in
principled ways 286. Although specific features characterize the acquisition of
particular languages, researchers have identified a set of milestones that
children pass through as they grapple with learning their native tongue.

Early language development in children with focal brain injury Reilly 287
investigated a group of children that all suffered a unilateral focal cerebral
insult either pre- or peri-natally; the lesions had all been confirmed by CT scan
or MRI before the child reached six months of age, that is, before they had
acquired any language. Additionally, these children were free from other birth
complications that might suggest more diffuse brain damage.

With respect to their early language development, as a group, these children


were delayed in both comprehension and production of first words 288. That is,
regardless of side of lesion, the children with focal brain damage are delayed
when compared to their age and gender matched controls.

There was sufficient variability in the group that some children were within the
normal range of performance. Nonetheless, as a whole, children with either
right hemisphere damage (RHD) or left hemisphere damage (LHD) were
delayed in the onset of language. Within this overall delay, there were
interesting and unexpected site-specific behaviour patterns.

In studies using parental report as a means to assess early comprehension and


production skills, Bates and her colleagues presented cross-sectional data from
over 50 toddlers with unilateral brain damage (Bates et al., 1997 idem) which
confirmed the earlier findings of ThaI et al, (1991) 289 which included a smaller
cohort. Both studies showed that in children from 10-17 months, infants with
right posterior damage were more delayed in comprehension than the rest of
the focal lesion (FL) children. Bates also found that toddlers (from 19-31
months) with either left or right frontal damage were more delayed in
production than would be expected, but this was a transient effect. Finally,
looking at both parental report and spontaneous speech data in children from
20 to 44 months, children with left temporal damage evidenced more delays in
productive vocabularies and had shorter utterances than the rest of the FL
group, and the group as a whole continued to perform significantly below

286
Slobin, D.I. (1985): The cross-linguistic study of language acquisition.
Hillsdale, NJ: Lawrence Erlbaum Associates.
287
Reilly, JS. Language in children with early brain damage: the
development of brain-behaviour relations. In Localization of Brain Lesions and
Developmental Functions, D. Riva & A. Benton (eds.) 2000 John Libbey &
Company Ltd.
288
Bates, E.A., Thal, D., Trauner, D., Fenson, J., Aram, D., Eisele, J. &
Nass, R. (1997): From first words to grammar in children with focal brain injury.
Dev. Neuropsychol. 13,275-343.
289
ThaI, D.J., Marchman, V.A., Stiles, J., Aram, D., Trauner, D., Nass,
R. & Bates, E. (1991): Early lexical development in children with focal brain
injury. Brain Lang. 40,491-527.

Page 77 of 114
controls.

From these studies of early language development in this population, It was


seen that the children with early brain damage lagged behind their controls on
measures of comprehension, production, and mean length of utterance. In
addition to the delay for the group as a whole, an additional and unpredicted
lag was found in the younger children with right posterior damage for
comprehension. A persistent delay in vocabulary and then in morphology, as
measured by mean length of utterance (MLU) was found in children with left
temporal damage.

Neither of these patterns maps onto the adult profile for brain organization of
language which would have predicted that children with right hemisphere
damage would have shown normal language development; those with left
frontal damage would have evidenced production delays; and those with
posterior left damage would have demonstrated impaired comprehension.
Overall, the findings suggest that initially, at least, both hemispheres are
implicated in initiating the language acquisition process, and that rather than
being localized to the left hemisphere, as is true for the vast majority of adults,
language as it is being acquired is a rather broadly distributed function.

Reilly (idem) first looked at the degree to which language is localized from an
early point in development. She found that the language profiles of the
children with focal brain damage did not map onto those of adults with
comparable damage. In fact, irrespective of damage site, the children showed
initial delay, and subsequent development. Hence, although perhaps not opti-
mally suited for language, her data suggested that multiple areas of the brain
can subserve language functions. Additionally the data suggested that the
brain areas suited to acquire language may be more broadly distributed than
those necessary to maintain language functioning once it has been acquired.

Regarding the issue of neuroplasticity, the fairly rapid acquisition of the


morpho-syntax of English in the children with early brain damage regardless of
lesion site is strong evidence of the flexibility of the developing brain. In those
morpho-syntactic structures that were examined, she found that for the
mandatory grammatical functions, the children in the FL group were initially
delayed, but eventually performing within the normal range. However, she did
not know the extent of this plasticity, that is, she did not know whether they
would continue to expand their syntactic repertoire to acquire some of the
optional, but more adult-like morphological and syntactic forms.

Finally, with respect to the nature of the language acquisition process itself, the
finding that the morphological errors of all the groups of children were of the
same types, that is, the differences are in quantity rather than in quality. This
suggests that the language acquisition process itself is fairly rigid in nature.
Additionally, the slope of the trajectory for the FL children for morphology is
similar to younger developing pre-schoolers. It appears that once children
begin to acquire grammatical morphemes, the rate and nature of the
acquisition processes are similar; what differs is when they begin. In sum,
developmental differences appear to be in timing rather than in kind.

In summary, Reilly found that children with brain damage are delayed in the
acquisition of language, regardless of side of lesion, but eventually do go on to
acquire the lexicon and grammar and be competent speakers of English. From

Page 78 of 114
the children's cases studied it was clear that just as different aspects of
language develop at different points in time so, too, do the deficits change over
time. Thus, language development continues in the face of early unilateral
brain damage, and although recruiting alternative neural means, the children
with early focal brain damage follow a similar, but delayed, behavioural path to
their typically developing counterparts.

It can be seen therefore that an acquired language impairment may be


expressed in one or more modes of communication such as spoken and written
output. One of the significant issues surrounding very early brain injury is that
unless the particular areas of damage are known, the development of literacy
will also be an unknown factor. However, in the course of development it may
be possible to make an approximate appraisal of the areas that have been
damaged from the lacks that become evident.

In the present day situation scans may help this initiative and therefore
preclude delayed assessment. It is important to note that these steps should
be taken as early as possible.

When establishing the child’s literacy abilities, it is important to consider


prerequisites for literacy skills including phonological knowledge, such as the
ability to segment a word into its phonological constituents, memory and visuo-
spatial skills. Given the prerequisites for literacy skills, it is essential to have
collaborative working with other professionals including educational staff,
educational psychologists and occupational therapists.

PROBLEMS OF GAIT AND MOVEMENT

These problems are almost always a result of the effects of psychotropic


medication and often follow a regime of medication that has been prolonged
and persistent. As such medications are sometimes prescribed for brain injured
patients it seems appropriate that a section on this condition is included.

Akathisia (or acathisia), is a syndrome characterized by unpleasant


sensations of inner restlessness that manifests itself with an inability to sit still
or remain motionless.

Its most common cause is as a side effect of medications, mainly neuroleptic


antipsychotics especially the phenothiazines (such as perphenazine and
chlorpromazine), thioxanthenes (such as flupenthixol and zuclopenthixol) and
butyrophenones (such as haloperidol (Haldol)), piperazines (such as
ziprasidone), and antidepressants. Akathisia can also, to a lesser extent, be
caused by Parkinson's disease and related syndromes.290 However, most
antipsychotic psychotropic drugs cause Parkinsonian like symptoms due to
blockage of dopamine receptors in the nigrostriatal pathway of the brain.

Akathisia may range in intensity from a mild sense of disquiet or anxiety (which
may be easily overlooked) to a total inability to sit still, accompanied by
overwhelming anxiety, malaise, and severe dysphoria (manifesting as an
almost indescribable sense of terror and doom). The condition is difficult for the
patient to describe and is often misdiagnosed. When misdiagnosis occurs in
antipsychotic neuroleptic-induced akathisia, more antipsychotic neuroleptics
290
Szabadi E (1986). "Akathisia—or not sitting". British Medical Journal
(Clinical research ed.) 292 (6527): 1034–5.

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may be prescribed, potentially worsening the symptoms. 291 High-functioning
patients have described the feeling as a sense of inner tension and torment or
chemical torture. The presence and severity of akathisia can be measured
using the Barnes Akathisia Scale.292

Kane et al 293, provide a description of the pathophysiology of akathisia, the


challenges of diagnosing and treating this condition, and potential associated
clinical issues. Also, they provide a review of the literature on the incidence of
drug-induced akathisia associated with the use of second-generation
antipsychotics (SGAs) and first-generation antipsychotics (FGAs).

They concluded that akathisia remains a concern with the use of SGAs. More
accurate and standardized evaluations are required for a better understanding
of the nature and incidence of akathisia.

Healy, et al (2006), described the following regarding akathisia: tension,


insomnia, a sense of discomfort, motor restlessness, and marked anxiety and
panic. Increased labile affect can result, such as weepiness. Interestingly, in
some people the opposite response to SSRIs occurs, in the form of emotional
blunting; but sufficient clinical research has not yet been made in this area. 294

Antipsychotic-induced akathisia can be classified according to the time of onset


in the course of antipsychotic treatment (acute, tardive, withdrawal and chronic
akathisia). Reported prevalence rates vary widely between 5% and 36.8%.
Numerous risk factors for acute akathisia have been described and the exact
pathophysiology of akathisia is still unknown. Since akathisia is a drug-induced
adverse effect, optimal management involves its prevention rather than
treatment. Standardised titration and the use of novel antipsychotics are
successful measures of prevention. Evidence on the treatment of tardive
akathisia is unsatisfactory. 295
Gao et al 296 show that the newer atypical antipsychotics have been reported to
cause a lower incidence of extrapyramidal side effects (EPS) than conventional
agents. Their review compared antipsychotic-induced EPS relative to placebo
in bipolar disorder (BPD) and schizophrenia.
The results included eleven trials in mania, four in bipolar depression, and eight
in schizophrenia. Of these, haloperidol significantly increased the risk for
akathisia, overall EPS, and anticholinergic use in both mania and schizophrenia,

291
Szabadi E (1986). idem
292
The following website offers a test sheet.
http://www.medafile.com/zyweb/Barnes.htm
293
Kane JM; Fleischhacker WW; Hansen L; Perlis R; Pikalov A 3rd; &
Assunção-Talbott S. Akathisia an updated review focusing on second-
generation antipsychotics. J Clin Psychiatry. 2009 Apr 21.
294
Healy D; Herxheimer A; & Menkes DB. (2006). "Antidepressants and
violence: problems at the interface of medicine and law". PLoS Med. 3 (9): e372.
295
Miller CH; & Fleischhacker WW. Managing antipsychotic-induced
acute and chronic akathisia. Drug Saf 2000 Jan; 22(1):73-81.
296
Gao K; Kemp DE; Ganocy SJ; Gajwani P; Xia G; & Calabrese JR.
Antipsychotic induced extrapyramidal side effects in bipolar disorder and
schizophrenia: a systematic review. J Clin Psychopharmacol. 2008
Apr;28(2):203-9.

Page 80 of 114
with a larger magnitude in mania, an NNTH297 for akathisia of 4 versus 7, EPS of
3 versus 5, and anticholinergic use of 2 versus 4, respectively.
Among atypical antipsychotics, only ziprasidone significantly increased the risk
for overall EPS and anticholinergic use in both mania and schizophrenia, again
with larger differences in mania, an NNTH for overall EPS of 11 versus 19, and
anticholinergic use of 5 versus 9. In addition, risks were significantly increased
for overall EPS (NNTH = 5) and anticholinergic use (NNTH = 5) in risperidone-
treated mania, akathisia in aripiprazole-treated mania (NNTH = 9) and bipolar
depression (NNTH = 5), and overall EPS (NNTH = 19) in quetiapine-treated
bipolar depression.
They concluded that bipolar patients, especially in depression, were more
vulnerable to having acute antipsychotic-induced movement disorders than
those with schizophrenia.
In another study, Goa et al compared the sensitivity and tolerability of
antipsychotics in patients with bipolar disorder or schizophrenia.298 They used
English-language literature from January 1966 to December 2006 cited in
MEDLINE and where it was searched for the terms antipsychotics, typical
antipsychotics, atypical antipsychotic, generic and brand names of
antipsychotics, safety, tolerability, discontinuation due to adverse events,
somnolence, and bipolar mania, bipolar depression, bipolar disorder, manic-
depressive illness, or schizophrenia, randomized, double blind, and controlled
clinical trial. They included in their data randomized, double-blind, placebo-
controlled, monotherapy studies of anti-psychotics in both bipolar disorder and
schizophrenia were prioritized. The data extraction is shown as: absolute risk
increase (ARI) or reduction (ARR) and the numbers needed to treat to harm
(NNTH) or benefit (NNTB) for the discontinuation due to adverse events and
somnolence relative to placebo were estimated.
The results showed that ten acute trials in mania, 3 in bipolar depression, and 8
in schizophrenia were identified, along with 2 maintenance studies in bipolar
disorder and 2 in schizophrenia. In schizophrenia, ziprasidone caused
significantly more discontinuations due to adverse events than placebo, with an
NNTH of 19, while aripiprazole caused significantly fewer discontinuations due
to adverse events than placebo, with an NNTB of 12.
In mania, there was no statistically significant difference in discontinuation due
to adverse events between antipsychotics and placebo. However, in bipolar
depression, both quetiapine and olanzapine caused more discontinuations due
to adverse events than placebo, with NNTHs of 7 and 24, respectively.
All atypical antipsychotics caused a significantly greater incidence of
somnolence than placebo in mania and depression, with NNTHs from 5 to 8 for
mania and 2 to 6 for depression. In schizophrenia, only olanzapine,
ziprasidone, and aripiprazole (NNTHs from 5 to 14) caused a significantly higher
incidence of somnolence.

297
NNTH = Number needed to harm. An epidemiological measure that
indicates how many patients need to be exposed to a risk-factor to cause harm
in one patient that would not otherwise have been harmed. It is defined as the
inverse of the attributable risk. Intuitively, the lower the number needed to
harm, the worse the risk-factor.
298
Gao K; Ganocy SJ; Gajwani P; Muzina DJ; Kemp DE; & Calabrese
JR. A review of sensitivity and tolerability of antipsychotics in patients with
bipolar disorder or schizophrenia: focus on somnolence. J Clin Psychiatry. 2008
Feb;69(2):302-9.

Page 81 of 114
There was no significant difference between schizophrenia and mania in the
discontinuation due to adverse events or somnolence of all studied
antipsychotics. However, there was a significantly higher incidence of
discontinuation due to adverse events and somnolence caused by quetiapine in
bipolar depression than that in schizophrenia or mania.
The study shows that patients with bipolar disorder appear more sensitive to
antipsychotics, and depressed patients are less tolerant to somnolence than
those with either mania or schizophrenia.
Antipsychotics are widely used in geriatric psychiatric disorders. A growing
number of atypical antipsychotics are available, expanding clinical options but
complicating decision-making. Many questions about use of antipsychotics in
older patients remain unanswered by available clinical literature. Alexopoulos
et al 299 surveyed expert opinion on antipsychotic use in older patients (65
years of age or older) for recommendations concerning indications for
antipsychotics, choice of antipsychotics for different conditions (e.g., delirium,
dementia, schizophrenia, delusional disorder, psychotic mood disorders) and for
patients with comorbid conditions or history of side effects, dosing strategies,
duration of treatment, and medication combinations.
The expert panel reached consensus on 78% of options rated on a 9-point
scale. The experts did not recommend using antipsychotics in panic disorder,
generalized anxiety disorder, non-psychotic major depression, hypochondriasis,
neuropathic pain, severe nausea, motion sickness, or irritability, hostility, and
sleep disturbance in the absence of a major psychiatric syndrome. However,
antipsychotics were favoured in several other disorders.
For agitated dementia with delusions, the experts' first-line recommendation is
an antipsychotic drug alone; they would also consider adding a mood stabilizer.
Risperidone (0.5-2.0 mg/day) was first line followed by quetiapine (50-150
mg/day) and olanzapine (5.0-7.5 mg/day) as high second-line options. There
was no first-line recommendation for agitated dementia without delusions; an
antipsychotic alone was high second line (rated first line by 60% of the
experts).
The experts reached a high level of consensus on many of the key treatment
questions. Within the limits of expert opinion and with the expectation that
future research data will take precedence, these guidelines provide direction for
common clinical dilemmas in the use of antipsychotics in elderly patients.
Clinicians should keep in mind that no guidelines can address the complexities
of an individual patient and that sound clinical judgment based on clinical
experience should be used in applying these recommendations.

Hindmarsh compared cognitive impairment of medications used in social


anxiety disorder (SAD). 300 He used data from peer-reviewed publications
(1975-2007) of controlled, crossover design, pharmaco-dynamic studies on SAD
medications in healthy volunteers were analysed. The number of objective
psychometrics for each drug/dose level at all time points after dosing, and of
instances of statistically significant impairment of cognitive function, enabled
calculation of drug-induced cognitive impairment. The magnitude of
299
Alexopoulos GS; Streim J; Carpenter D; & Docherty JP. (Expert
Consensus Panel for Using Antipsychotic Drugs in Older Patients). Using
antipsychotic agents in older patients. J Clin Psychiatry. 2004;65 Suppl 2:5-99.
300
Hindmarch I. Cognitive toxicity of pharmacotherapeutic agents used in
social anxiety disorder. Int J Clin Pract. 2009 Jul;63(7):1085-94.

Page 82 of 114
impairment between drugs was compared using proportional impairment ratios
(PIRs).

He found that olanzapine, oxazepam, lorazepam and mianserin had twice the
average cognitive toxicity of other treatments. Selective serotonin reuptake
inhibitors (SSRIs) impaired cognition to a lesser extent than other
pharmacological groupings. There was extensive intra-class variation:
fluvoxamine (PIR = 0.08) possessed little detrimental cognitive activity,
whereas sertraline (PIR = 5.33) caused impairment over five times the SSRI
group average. Benzodiazepines caused noticeable cognitive impairment.

_______

Types of Emotional, Behavioural, Psychiatric and Social


Problems

Seen After Brain Injury in Children

These can be many and varied and include social disinhibition or acting in
socially inappropriate ways, irritability, increased emotionality, reduced judge-
ment and motivation, perseveration, lowered tolerance to frustration, and
egocentricity seen through insensitivity to others, unawareness of their impact
on others, and an increase in demanding behaviour (Lehr 1990)301 . Added to
this list can be impulsivity, fearfulness, depressive and anxiety symptoms,
verbal and physical aggression, discipline problems, sleep disturbance, eating
problems (over- and under-eating), over-activity, a tendency to make facile
jokes, and gullibility (Deaton and Waaland 1994) 302. Self-esteem may also be
affected following a head injury (Andrews et al. 1998) 303. In addition, sexually
inappropriate behaviour may also develop (Max et al. 2001) 304.

There may be a sufficient number of symptom clusters to warrant diagnosis of a


psychiatric disorder, although the spectrum of difficulties seen in a particular
child after brain injury may not fit easily into the current psychiatric diagnostic
categories (Geraldina et al. 305) . Post-injury psychiatric disorders that have

301
Lehr, E. (1990). Psychological Management of Traumatic Brain Injuries in
Children and Adolescents. Rockville, MD: Aspen Publishers Inc.
302
Deaton, A. V. & Waaland, P. (1994). Psychosocial effects of acquired
brain injury. In: Educational Dimensions of Acquired Brain Injury. (eds R. C.
Savage, & G. F. Wolcott), 239-55. Austin, TX: PRO- FD, Inc.
303
Andrews, T. K., Rose, F. D., & Johnson, D.A. (1998). Social and
behavioural effects of traumatic brain injury in children. Brain Injury 12,133-8.
304
Max, J. E., Robertson, B. A., & Lansing, A. E. (2001). The
phenomenology of personality change due to traumatic brain injury in children
and adolescents. Journal of Neuropsychiatry and Clinical Neuroscience 13,161-
70.
305
Geraldina, P., Mariarosaria, L., Annarita, A., Susanna, G.,
Michela, S., Alessandro, D., Sandra, S., & Enrico, C. (2003).
Neuropsychiatric sequelae in TBl: a comparison across different age groups.

Page 83 of 114
been identified include oppositional defiant disorder (ODD), conduct disorder
(CD), Post-traumatic stress disorder (PTSD – See below, p83), attention deficit
hyperactivity disorder (ADHD), obsessive compulsive disorder (OCD), and
various other mood and anxiety disorders (Bloom et al. 2001 306, Gerring et al.
1998 307, Luis and Mittenberg 2002 308, Max et al. 1997 309).

In some cases, a diagnosis of 'personality change disorder' may be made (Max


et al. 2001 310, 2005 311). ADHD that develops after a brain injury is usually
referred to as secondary ADHD (S-ADHD) as the diagnostic criteria require that
the symptoms of impulsivity, over-activity and inattention are present before
the age of seven years (American Psychiatric Association 1994)312 and this may
not be the case in acquired ADHD-type deficits (Max et al. 2004) 313. It has
been suggested that, only very rarely, traumatic brain injury (TBI) may be
associated with the development of a psychotic disorder (Fujii and Ahmed
2001) 314.

Many of the emotional and behavioural problems seen after brain injury are
similar to those that occur in the general population, the exception being pro-
found socially disinhibited behaviour such as the making of very personal
remarks (Brown et al. 1981) 315, although such behaviour is seen frequently in

Brain Injury 17, 835-46.


306
Bloom, D. R., Levin, H. S., Ewing-Cobbs, L., Saunders, A. E., Song,
J., Fletcher, J. M., & Kowatch, R.A. (2001). Lifetime and novel psychiatric
disorders after pediatric traumatic brain injury. Journal of the American Academy
of Child and Adolescent Psychiatry 40, 572-9.
307
Gerring, J. P., Brady, K. D., Chen, A., Vasa, R., Grados, M.,
Bandeen-Roche, K. J., Bryan, R. N., & Denckla, M. B. (1998). Premorbid
prevalence of ADHD and development of secondary ADHD after closed head
injury. journal of the American Academy of Child and Adolescent Psychiatry 37,
647-54.
308
Luis, C., A. & Mittenberg, W. (2002). Mood and anxiety disorders
following pediatric traumatic brain injury: a prospective study. Journal of Clinical
and Experimental Neuropsychology 24, 270-9.
309
Max, J. E., Robin, D. A., Lindgren, S. D., Smith, W. L. Jr., Sato, Y.,
Mattheis, P. J., Stierwalt, J . A., & Castillo, C. S. (1997). Traumatic brain
injury in children and adolescents: psychiatric disorders at two years. Journal of
the American Academy of Child and Adolescent Psychiatry 36,1278-85.
310
Max, J. E., Robertson, B. A., & Lansing, A. E. (2001). The
phenomenology of personality change due to traumatic brain injury in children
and adolescents. Journal of Neuropsychiatry and Clinical Neuroscience 13,161-
70.
311
Max, J. E., Levin, H. S., Landis, J., Schachar, R., Saunders, A.,
Ewing-Cobbs, 1., Chapman, S. B., & Dennis, M. (2005). Predictors of
personality change due to traumatic brain injury in children and adolescents in
the first six months after injury. Journal of the American Academy of Child and
Adolescent Psychiatry 44, 434-42.
312
American Psychiatric Association. (1994). Diagnostic and Statistical
Manual of Mental Disorders (4th edn). Washington, DC: American Psychiatric
Association.
313
Max, J.. E., Lansing, A. E., Koele, S. L., Castillo, C. S., Bokura, H.,
Schachar, R., Collings, N., & Williams, K. E. (2004). Attention deficit
hyperactivity disorder in children and adolescents following traumatic brain
injury. Developmental Neuropsychology 25,159-77.
314
Fujii, D. E. & Ahmed, I. (2001). Risk factors in psychosis secondary to
traumatic brain injury. journal of Neuropsychiatry and Clinical Neuroscience 13,
61-9.

Page 84 of 114
316
autistic spectrum disorders (ASD) (e.g. Temple 1996) .

Because of the wide variety of behavioural changes seen after brain injury and
concerns that instruments designed to detect problems in the general child
population (such as behaviour checklists) may not adequately capture such
changes, attempts have been made to devise specific instruments (e.g. Roberts
and Furuseth 1997) 317. Other ways of conceptualizing the changes seen after
brain injury (in terms of types of personality change) have also been suggested
(see Max et al. 2005) 318.

As the prefrontal cortex is vulnerable in brain injury, in particular in TBI, it


should not be surprising that early brain injuries can then manifest in severe
disorders of executive, social and emotional development which can result in a
range of behavioural difficulties.

There have been cases noted of impaired planning, behavioural difficulties,


social skill deficits, and abnormal emotion, despite having normal function on
most conventional cognitive domains such as memory, language and
perception. In some of these cases, detailed neuro-anatomical analysis of brain
scans revealed focal damage to the prefrontal regions, including areas known
as the ventro-medial and polar sectors. Damage to these regions in adults is
known to cause emotional and planning deficits (Damasio and Anderson 2003)
319
.

Investigation of the complex relationship between cognitive, social and


emotional processes is ongoing within both normal human populations (e.g.
Moll et al. 2005) 320, clinical populations of children and adults with brain injuries
(e.g. Coelho et al. 2005 321, Shamay-Tsoory et al. 2005 322) and animal studies

315
Brown, G., Chadwick, 0., Shaffer, D., Rutter, M., & Traub, M.
(1981). A prospective study of children with head injuries III: psychiatric
sequelae. Psychological Medicine 11, 63-78
316
Temple, C. E. (1996). Autism. In: The Blackwell Dictionary of
Neuropsychology. (eds J. G. Beaumont, P. M. Kenealy, & M. J. C. Rogers), 133-
137. Oxford Blackwell Publishers.
317
Roberts, M. A. & Furuseth, A. (1997). Eliciting parental report
following pediatric traumatic brain injury: preliminary findings on the Pediatric
Inventory of Neurobehavioral Symptoms. Archives of Clinical Neuropsychology
12,449-57.
318
Max, J. E., Levin, H. S., Landis, J., Schachar, R., Saunders, A.,
Ewing-Cobbs, 1., Chapman, S. B., & Dennis, M. (2005). Predictors of
personality change due to traumatic brain injury in children and adolescents in
the first six months after injury. Journal of the American Academy of Child and
Adolescent Psychiatry 44, 434-42.
319
Damasio, A. R. & Anderson, S. W. (2003). The frontal lobes. In:
Clinical Neuropsychology, 4th edn (eds K. M. Heilman & E. Valenstein), 404-46.
New York: Oxford University Press.
320
Moll, J., de Oliveira,-Souza, R., Moll, F., Ignacio, F. A., Bramati, I.
E., Caparelli-Daquer, E. M., & Eslinger P. J. (2005). The moral affiliations of
disgust: a functional MRI study. Cognitive Behavioural Neurology 18,66-76.
321
Coelho, S., Max, J., & Tranel, D. (2005). A matched lesion analysis of
childhood versus adult-onset brain injury due to unilateral stroke: another
perspective on neural plasticity and recovery of social functioning. Cognitive
Behavioural Neurology 18, 5-17.
322
Shamay-Tsoory, S. G., Tomer, R., Berger, B. D., Goldsher, D., &
Aharon-Peretz, J. (2005). Impaired 'affective theory of mind' is associated with
right ventromedial prefrontal damage. Cognitive Behavioural Neurology 18, 54-

Page 85 of 114
323 324
of brain injury (e.g. Malkova et al. 2000 ; Kolb et al. 2000 ).

Although there are obvious limitations to the generalizations we can make


about human brain injury from animal studies, many insightful findings about
brain development have been made with studies of early injuries to animals.
For example, Kolb et al. (2000 - idem) have demonstrated that interventions
following early brain injury, such as placing the animal in an enriched
environment and providing physical stimulation such as stroking the animal
three times per day, actually has physiological effects on the injured brain so
that additional rewiring in the brain occurs which supports behavioural
improvement in the injured animals compared with those who do not receive
such interventions.

While there is still a significant step between such well-controlled animal


studies and the effects of early brain injury in children, it is important that this
area of study is developed over the coming years. Understanding the
relationship between prefrontal damage and severe emotional, behavioural,
psychiatric and social difficulties is important as it has implications for the
interventions that one might attempt with such adolescents.

For example, compared with young people who display anti-social behaviour
largely because of negative social influences, lack of social opportunities and/or
attentional deficits, young people with brain injuries may require significantly
different remedial approaches.

Damage to the prefrontal cortex seems to result in highly inflexible behaviour


and therefore it will be extremely important to exert significant external control
over the environment in which an individual learns and socializes.
Environments with little structure or predictability that are not designed to
stimulate the individual with sufficient one-to-one attention are most likely to
cause severe behavioural difficulties.

Thus, educational policies that may laudably promote social inclusion by


placing children with special needs in mainstream environments need to be
balanced against a consideration of the factors which will best suit the learning
and behavioural responses of each individual who has suffered a brain injury. It
could be the case that someone with a brain injury may not be able to adapt
their behaviour in the same way as someone who has developmental learning
difficulties and, therefore, they will require a more intensive support package
including adaptation of their whole educational environment.

In summary, a range of behavioural, emotional and social difficulties can result


from a brain injury sustained early in development. The degree or extent of
these difficulties is not adequately identified by traditional neuropsychological
tests alone. Such difficulties seem to occur because of problems with the
neural integration of cognitive, emotional and social processing. This
processing is dependent on multiple brain systems and the successful integra-
65.
323
Malkova, 1., Bachevalier, J., Webster, M., and Mishkin, M. (2000).
Effects of neonatal inferior prefrontal and medial temporal lesions on learning
the rule to delayed non-matching-to-sample. Developmental Neuropsychology
18, 399-421.
324
Kolb, B., Gibb, R., & Gorny, G. (2000). Cortical plasticity and the
development of behaviour after early prefrontal cortical injury. Developmental
Neuropsychology 18, 423-44.

Page 86 of 114
tion of these functions appears to be mediated by the prefrontal cortex, in par-
ticular the ventro-medial and polar sectors.

With the honourable exception of Rutter and colleagues the territory of


psychiatric disorder in the head-injured child and adolescent population has
barely been mapped. 325, 326, 327, 328, 329

From an examination of the issues covered, there would seem to be a particular


need to consider seriously the following problems.

1. Precise characterization of the disinhibition, amnesia, dysfunctional


attention syndrome which is widely recognized among very severely
head injured older children but not yet delineated. Neuro-
pathological correlates need exploration by means of modern imaging
techniques, especially NMR.

2. Development of effective treatment techniques for children and


adolescents with such a constellation of difficulties.

3. Long-term prospective controlled follow-up of mildly head-injured


young children in conjunction with documentation of life events, using
interviews with children, parents and teachers, as well as
neuropsychological assessment with contemporary instruments such
as the CHIPASAT 330. This would enable an examination of Boll's
(1983) 331 hypothesis that overtly normal behaviour may be
maintained only by extreme effort and will decompensate under
stress.

4. Further exploration of changes in family relationships and interactions


following head injury, so that these can be predicted from the point of
view of preventative counselling.

_______

Post-traumatic Stress Disorder (PTSD)


325
Rutter, M. (1981) 'Psychological sequelae of brain damage in children',
American Journal of Psychiatry, 138, pp. 1533-1544.
326
Rutter, M. (1984) 'Issues and prospects in developmental
neuropsychiatry, in Rutter, M. (ed.) Developmental Neuropsychiatry, Edinburgh,
Churchill Livingstone.
327
Rutter, M., Chadwick, O., Shaffer, D. & Brown, G. (1980) 'A
prospective study of children with head injuries I: design and methods',
Psychological Medicine, 10, pp. 633-645.
328
Rutter, M., Chadwick, O. & Shaffer, D. (1984) 'Head Injury', in Rutter,
M. (ed.) Developmental Neuropsychiatry, Edinburgh, Churchill Livingstone.
329
Rutter, M., Graham, P. & Yule, W. (1970) 'A Neuropsychiatric Study in
Childhood', Clinics in Developmental Medicine, Nos. 35-36. London, SIMP-
Heinemann.
330
Johnson, D.A., Roethig-Johnston, K. & Middleton,J. (1988)
'CHIPASAT: the development of an attentional test for head-injured children:
Information processing in a normal sample' ,journal of Child Psychology and
Psychiatry, 29, pp. 199-208.
331
Boll, T.J. (1983) 'Minor head injury in children — out of sight but not out
of mind'. Journal of Clinical Child Psychology, 12. pp. 74-80.

Page 87 of 114
Posttraumatic stress disorder is characterised by a traumatic event that results
in long-standing psychological, social, and biological sequelae. Because of the
occurrence of a defined external event(s) that initiated the disorder, PTSD
allows us to study the process by which the environment influences the
individual in dramatic ways. PTSD is therefore an ideal vehicle to study the
integrative process taking place between external and internal processes.
Several symposia at the 154th Annual Meeting of the American Psychiatric
Association were devoted to the integration of these perspectives.

The use of increasingly sophisticated imaging techniques including the positron


emission tomography scan, magnetic resonance imaging (MRI), and functional
MRI (fMRI) have allowed researchers to identify brain regions involved in the
traumatic response. Several studies have shown reduced hippocampal volume,
consistent with the memory disturbances characteristic of PTSD. 332

Van der Kolk 333 has suggested that the deficiencies in explicit or declarative
memory may result in a reorganisation of the trauma on a somato-sensory
level. The somato-sensory memories include visual and physical
representations, and they are processed in subcortical regions outside of the
hippocampal system and difficult to extinguish. Cortical activity may able to
modify these subcortical responses; however, the extent of physiologic arousal
and hormonal responsiveness may limit the ability of the cortex to carry out
this inhibitory process. Activation of the amygdala, a limbic structure involved
in emotional memories, such as fear responses, has been demonstrated by
Liberson and colleagues. 334 Using fMRI, Rauch and co-workers 335 were able to
link activation of the amygdala response to masked presentation of trauma-
related stimuli.

The expected emotional reactions to disaster are pretty much known and
include helplessness, anxiety, sleep disturbances, somatic symptoms. Almost
invariably there is a tremendous fear of recurrence, and the emotional upset
associated with the trauma.

Hall et al (idem) also tell us, “When you evaluate a child, you need to look at
the inventory of stressors: displacements; translocations; unemployment;
separation from loved ones, the closing of schools.” The most important thing
that a child needs is a return to the safety of the pre-event period, and to
resume the routines of family and community life as much as possible.

Research in basic science and functional neuro-imaging has helped to identify


three brain regions that may be involved in the pathophysiology of PTSD: the
amygdala, medial prefrontal cortex, and hippocampus. The amygdala is
involved in the assessment of threat-related stimuli and/or biologically relevant
ambiguity and is necessary for the process of fear conditioning. 336, 337 Given
that individuals with PTSD are hyper-vigilant concerning potential threat in the
332
Korn, Martin MD. Emerging Trends in Understanding Posttraumatic
Stress Disorder. 154th Annual Meeting of the American Psychiatric Association;
Day 3 - May 7, 2001.
333
van der Kolk BA. The body keeps the score: memory and the evolving
psychobiology of posttraumatic stress. Harv Rev Psychiatry. 1994; 1:253-265.
334
Liberzon I, Taylor SF, Amdur R, et al. Brain activation in PTSD in response
to trauma-related stimuli. Biol Psychiatry. 1999;45:817-826
335
Rauch SL, Whalen PJ, Shin LM, et al. Exaggerated amygdala
response to masked facial stimuli in posttraumatic stress disorder: a functional
MRI study. Biol Psychiatry. 2000; 47:769-776.

Page 88 of 114
environment and that they show relatively heightened acquisition of
conditioned fear in the laboratory many researchers have hypothesized that the
amygdala is hyper-responsive in this disorder. 338 ,339 Indeed, functional neuro-
imaging studies have provided evidence for amygdala hyper-responsivity in
PTSD.

A second region of interest is the medial prefrontal cortex, which includes the
anterior cingulate cortex, sub-callosal cortex, and medial frontal gyrus. Medial
prefrontal cortex is well connected to the amygdala in primates, 340, 341, 342, 343 and
is involved in the process of extinction of fear conditioning and the retention of
extinction 344, 345, 346. Extinction does not occur normally when medial prefrontal
cortex is damaged. 347, 348 Individuals with PTSD exhibit persistent
inappropriate fear responses in daily life and diminished extinction of
conditioned fear responses in the laboratory, 349, 350 leading to the hypothesis
that medial prefrontal cortex may be impaired in this disorder. Neuro-imaging
studies have reported reduced cortical volumes and neuronal integrity, as well
as decreased function in medial prefrontal structures in this disorder. 351
336
Davis, M. & Whalen, P.J.. 2001. The amygdala: vigilance and emotion.
Mol. Psychiatry 6: 13–34.
337
Ledoux, J.E. 2000. Emotion circuits in the brain. Annu. Rev. Neurosci.
23: 155–184.
338
Orr, S.P.; Metzger L.J.; Lasko N.B., et al. 2000. De novo conditioning
in trauma exposed individuals with and without posttraumatic stress disorder. J.
Abnorm. Psychol. 109: 290–298.
339
Peri, T., G. Ben-Shakhar, S.P. Orr, et al. 2000. Psychophysiologic
assessment of aversive conditioning in posttraumatic stress disorder. Biol.
Psychiatry 47: 512–519.
340
Aggleton, J.P.; Burton, M.J. & Passingham, R.E. 1980. Cortical and
subcortical afferents to the amygdala of the rhesus monkey (Macaca mulatta).
Brain Res. 190: 347–368.
341
Chiba, T.; Kayahara, T. & Nakano, K. 2001. Efferent projections of
infralimbic and prelimbic areas of the medial prefrontal cortex in the Japanese
monkey, Macaca fuscata. Brain Res. 888: 83–101.
342
Ghashghaei, H.T. & Barbas, H. 2002. Pathways for emotion:
interactions of prefrontal and anterior temporal pathways in the amygdala of
the rhesus monkey. Neuroscience 115: 1261–1279.
343
Stefanacci, L. & Amaral, D.G. 2002. Some observations on cortical
inputs to the macaque monkey amygdala: an anterograde tracing study. J.
Comp. Neurol. 451: 301–323.
344
Milad, M.R. & Quirk, G.J. 2002. Neurons in medial prefrontal cortex
signal memory for fear extinction. Nature 420: 70–74.
345
Morgan, M.A.; Romanski L.M. & Ledoux, J.E. 1993. Extinction of
emotional learning: contribution of medial prefrontal cortex. Neurosci. Lett. 163:
109–113.
346
Quirk, G.J.; Russo G.K.; Barron, J.L. et al. 2000. The role of
ventromedial prefrontal cortex in the recovery of extinguished fear. J. Neurosci.
20: 6225–6231.
347
Morgan et al; idem.
348
Quirk et al; idem
349
Orr et al; idem
350
Rothbaum, B.O.; Kozak M.J.; & Foa, E.B. et al. 2001. Posttraumatic
stress disorder in rape victims: autonomic habituation to auditory stimuli. J.
Trauma. Stress 14:283–293.
351
Shin, Lisa M.; Rauch, Scott L. & Pitman, Roger K. Amygdala, Medial
Prefrontal Cortex, and Hippocampal Function in PTSD. Ann. N.Y. Acad. Sci. 1071:
67–79; 2006.

Page 89 of 114
A third region of interest is the hippocampus, which is involved in explicit
memory processes and in the encoding of context during fear conditioning. 352,
353, 354
Importantly, the hippocampus appears to interact with the amygdala
during the encoding of emotional memories, 355, 356 a process that is highly
relevant to the study of trauma and PTSD. In animals, hippocampal cell
damage and memory impairment can result from extreme stressors and high
levels of stress-related hormones. 357, 358, 359 As we will show, PTSD has been
associated with memory impairment as well as reduced hippocampal volumes
and abnormal hippocampal function.

One neuro-circuitry model of PTSD posits that the amygdala is hyper-


responsive, medial prefrontal cortex is hypo-responsive, and medial prefrontal
cortex and the hippocampus fail to inhibit the amygdala. Other related models
have been described elsewhere. 360, 361, 362

The neuro-imaging research shown above provides evidence for heightened


responsivity of the amygdala, diminished responsivity of the medial prefrontal
cortex, as well as a functional relationship between these two regions. In
addition, there is evidence for diminished hippocampal volumes and neuronal
integrity, as well as impaired hippocampal function in PTSD. 363

PTSD AND EMOTIONAL RESPONSES

Psychological Responses to Trauma Many neuro-biological systems


are involved in mediating the response to trauma. The amygdala helps to
initiate the fight or flight response, and several systems — including the

352
Corcoran, K.A. & Maren, S. 2001. Hippocampal inactivation disrupts
contextual retrieval of fear memory after extinction. J. Neurosci. 21: 1720–1726.
353
Dolcos, F.; Labar, K.S. & Cabeza, R. 2004. Interaction between the
amygdala and the medial temporal lobe memory system predicts better memory
for emotional events. Neuron 42: 855–863.
354
Schacter, D.L. 1997. The cognitive neuroscience of memory:
perspectives from neuroimaging research. Philos. Trans. R. Soc. Lond. B. Biol.
Sci. 352: 1689–1695.
355
Dolcos et al, idem
356
McGaugh, J.L. 2004. The amygdala modulates the consolidation of
memories of emotionally arousing experiences. Annu. Rev. Neurosci. 27: 1–28.
357
Sapolsky, R.M.; Uno H. & Rebert, C.S et al. 1990. Hippocampal
damage associated with prolonged glucocorticoid exposure in primates. J.
Neurosci. 10:2897–2902.
358
Uno, H.; Tarara R. & Else J.G, et al. 1989. Hippocampal damage
associated with prolonged and fatal stress in primates. J. Neurosci. 9: 1705–
1711.
359
Watanabe, Y.; Gould E. & McEwen B.S. 1992. Stress induces atrophy
of apical dendrites of hippocampal CA3 pyramidal neurons. Brain Res. 588:
341–345.
360
Layton, B. & Krikorian, R. 2002. Memory mechanisms in posttraumatic
stress disorder. J. Neuropsychiatry Clin. Neurosci. 14: 254–261.
361
Elzinga, B.M. &. Bremner, J.D. 2002. Are the neural substrates of
memory the final common pathway in posttraumatic stress disorder (PTSD)? J.
Affect. Disord. 70: 1–17.
362
Hamner, M.B., Lorberbaum J.P. & George, M.S. 1999. Potential role
of the anterior cingulate cortex in PTSD: review and hypothesis. Depress.
Anxiety 9: 1–14.
363
Shin et al, idem

Page 90 of 114
sympathetic and parasympathetic systems and the hypothalamic-pituitary axis
(HPA) — are subsequently mobilised. The sympathetic nervous system
releases adrenaline, resulting in increases in heart rate, blood pressure, and
glucose levels. Corticotrophin-releasing factor (CRF) is released from the
hypothalamus, and adreno-corticotropic hormone (ACTH) is subsequently
secreted from the pituitary. Cortisol is then released from the adrenal gland.
Cortisol plays a central role in mobilising and mediating the stress response.

In a normal response to fear, the sympathetic nervous system,


parasympathetic nervous system, and HPA axis return to normal within several
hours. Long-term effects often occur if the individual has experienced a
previous serious stressor. That is, the brain has a memory for previous stress
that may sensitise the brain to subsequent trauma.

In a study by Orr and associates,364 individuals with PTSD manifested increased


acoustic startle responses as compared to trauma controls, anxious individuals,
and non-trauma controls. After 15 trials, the individuals with PTSD did not
habituate to the tone, while each of the other three groups did.

Utilising increasingly sophisticated brain-imaging techniques; the neuro-


circuitry involved in PTSD is being elucidated.365 Neuro-anatomical regions that
are thought to be involved in PTSD are the following:
• Amygdala. The amygdala is involved in intense emotional states
such as fear responses.
• Medial prefrontal cortex. This cortical prefrontal region plays a
modulating role, tempering or organising the emotional response to
trauma.
• Hippocampus. The hippocampus is involved in declarative
memory as well as spatial and contextual memory. (See Memory above,
p37) This structure serves as a context modulator and helps the
individual to identify places and events associated with past negative
experiences. Animal models have shown that chronic stress can cause
injury to this structure. 366

It is hypothesised that PTSD may be caused by increased activation of the


amygdala (i.e., a "bottom-up" response) or failure of the modulatory action of
the medial prefrontal cortex (i.e., a "top-down" deficiency). In PTSD, the fear
response is generalised to other situations and the individual becomes hyper-
stimulated when this is not warranted. 367

364
Orr SP, Solomon Z, Peri T, Pitman RK, Shalev AY. Physiologic
responses to loud tones in Israeli veterans of the 1973 Yom Kippur War. Biol
Psychiatry. 1997;41:319-326.
365
Rauch SL, Shin LM. Functional neuroimaging studies in posttraumatic
stress disorder. Ann N Y Acad Sci. 1997;821:83-98.
366
McEwen BS, Magarinos AM. Stress effects on morphology and function
of the hippocampus. Ann NY Acad Sci. 1997;821:271-284.
367
Korn, Martin L. Recent developments in the science and treatment of
PTSD. Meeting of the American Psychiatric Assn. 155th Annual Meeting, 2002.

Page 91 of 114
Several studies have found that hippocampal volumes are smaller in adults with
PTSD. 368, 369 However, in a prospective study, Bonne and associates 370 did not
show smaller hippocampal volumes at one week or at six months in individuals
developing PTSD after a traumatic event. De Bellis and associates 371 also
found no differences in hippocampal volumes of children at least two years
after follow-up.

Using 5-bromo-2'-deoxyuridine (BrdU) labelling, combined with cell type-


specific markers, recent studies have shown that several thousand new
neurons are produced every day in the dentate gyrus of adult rats. Gould and
colleagues372 speculated that the high rate of re-genesis of the neurons
implicates a high demand for the new neurons in the hippocampus, and the
late-generated cells play an important role in hippocampal function. This is also
because the neurons in the dentate gyrus are unusually sensitive to
experience-dependent structural changes and are easily damaged.

The generation and survival of the dentate gyrus neurons in the hippocampus
are regulated by many factors, including endocrine, neural, and experiential
factors. The factors facilitating regeneration are:
(1) ovarian steroid hormones,
(2) learning,
(3) environment complexity, and
(4) running.
The factors repressing the regeneration are:
(1) adrenal steroid hormones,
(2) stress, and
(3) deprivation.

Environmental complexity is especially important for survival of the neurons,


and often laboratory animals show low survival rate of the neurons because of
the lack of complexity in their environment.

Throughout postnatal life, glucocorticoids appear to exert suppressive effects


on cell proliferation in the dentate gyrus. Basal levels of adrenal steroids are
negatively correlated with the rate of cell proliferation in the dentate gyrus.
368
Gurvits TV, Shenton ME, Hokama H, et al. Magnetic resonance
imaging study of hippocampal volume in chronic, combat-related posttraumatic
stress disorder. Biol Psychiatry. 1996;40:1091-1099.
369
Bremner JD, Randall P, Vermetten E, et al. Magnetic resonance
imaging-based measurement of hippocampal volume in posttraumatic stress
disorder related to childhood physical and sexual abuse -- a preliminary report.
Biol Psychiatry. 1997;41:23-32.
370
Bonne O, Brandes D, Gilboa A, et al. Longitudinal MRI study of
hippocampal volume in trauma survivors with PTSD. Am J Psychiatry.
2001;158:1248-1251.
371
De Bellis MD, Hall J, Boring AM, Frustaci K, Moritz G. A pilot
longitudinal study of hippocampal volumes in pediatric maltreatment-related
posttraumatic stress disorder. Biol Psychiatry. 2001;50:305-309.
372
Gould E, Tanapat P, Rydel TA, Hastings NB. Hormones and
experience modulate adult neurogenesis. Int J Neuropsychopharmacol.
2000;3(suppl 1):S42. Abstract S.27.1.

Page 92 of 114
Treatment of adult rats with corticosterone also diminishes the proliferation of
granule cell precursors. The suppressive effects of glucocorticoids on cell
genesis suggest that stressful experiences, which are known to elevate levels
of circulating glucocorticoids and stimulate hippocampal glutamate release in
adulthood, naturally inhibit cell proliferation in the dentate gyrus. Previously, it
was shown that an acute stressful experience decreases the number of adult-
generated neurons produced in the adult dentate gyrus in a number of different
mammalian species.

Patterns of activation of the brain related to PTSD may be revealed using the
positron emission tomography (PET) scan and functional magnetic resonance
imaging (fMRI). 373 Symptom provocation studies designed to expose the
individual to reminders of the trauma have been utilised to stimulate involved
areas. Increases in activation of the amygdala, anterior cingulate, anterior
paralimbic regions, and visual cortex have been noted. Alternatively,
decreased activation in Broca's area has been observed. Broca's area is
involved in verbal output, and this may explain the problems some individuals
with PTSD have with verbalisation of issues related to the event. (Pitman et al ,
idem) In order to determine whether amygdala activation is present in PTSD
independent of deficiencies in "top-down" prefrontal inhibition, a "masked
faces" paradigm has been utilised. 374 Fearful and happy faces were briefly
shown embedded in a longer presentation of neutral faces. The individual is
consciously aware of seeing only a neutral face. Nevertheless, activation of the
amygdala occurs by the viewing of these unconsciously processed affectively
laden images. The magnitude of the amygdala activation on fMRI varied with
the severity of the PTSD symptoms. This suggests that exaggerated activation
of the amygdala is at least one of the factors involved in this disorder.
Activation of the amygdala was not seen in patients with obsessive-compulsive
disorder (OCD). (Pitman et al, idem)

The anterior cingulate area is one of the areas of the medial prefrontal cortex
that may also be involved in this disorder. The Stroop test is a cognitive
counting task that provides a measure of prefrontal or executive functioning.
The emotional version of the Stroop utilises emotionally laden words and
measures the subsequent reaction time of the individual. Utilising fMRI, it has
been shown that the affective division of the anterior cingulate becomes
activated when negative emotional words such as murder are processed. 375
Shin and colleagues 376 compared Vietnam combat veterans with and without
PTSD utilising the emotional Stroop test. The non-PTSD group demonstrated
fMRI blood oxygenation increases in the rostral anterior cingulated gyrus when
shown both combat- and non-combat-related words. The PTSD group did not
show these increases. This finding may reflect inadequate functioning of the

373
Pitman RK, Shin LM, Rauch SL. Investigating the pathogenesis of
posttraumatic stress disorder with neuroimaging. J Clin Psychiatry.
2001;62(suppl 17):47-54.
374
Rauch SL, Whalen PJ, Shin LM, et al. Exaggerated amygdala
response to masked facial stimulation in posttraumatic stress disorder: a
functional MRI study. Biol Psychiatry. 2000;47:769-776.
375
Whalen PJ, Bush G, McNally RJ, et al. The emotional counting Stroop
paradigm: a functional magnetic resonance imaging probe of the anterior
cingulate affective division. Biol Psychiatry. 1998;44:1219-1228.
376
Shin LM, Whalen PJ, Pitman RK, et al. An fMRI study of anterior
cingulate function in posttraumatic stress disorder. Biol Psychiatry. 2001;50:932-
942.

Page 93 of 114
prefrontal cortex, resulting in an inability to suppress salient emotional content
effectively. This demonstrates the lack of "top-down" prefrontal regulation in
PTSD sufferers. (Pitman et al, idem)

Thus, the triad of proposed structural deficiencies noted in PTSD is as follows:

• Amygdala hypersensitivity is present and may be assessed by the


masked faces test. This hypersensitivity results in increased fear and
emotional responses that may overwhelm the individuals' modulating
systems.

• The hippocampus may be smaller or less active. This may result in


deficient cognitive processing of memories and, therefore, the
individual is more inclined to act on emotional stimuli.

• The anterior cingulate is hypoactive. The decreased activity results in


failure of the cortex to modulate the responses of the amygdala and
less cognitive control. (Pitman et al , idem)

Hall et al, report the highlights of the psychological response of children and
adolescents to trauma. “Some of the data will be re-framed in terms of what
we know about adult responses, because there is little empirical data on the
psychological responses of children. We know that children are frequently
exposed to the same traumatic situations and trauma as adults. The difference
is that the traumagnomic event is processed by a developing child who is still
maturing psychologically, cognitively, physically, and socially, and very
frequently the trauma gets woven into the personality structure and character
of the individual.377

They go on, “These children, at the time they are traumatised, are often
struggling with issues of definition of self, definition of others. They are also
struggling with how to internalise mechanisms for regulating and modulating
intense emotional states, as well as trying to consolidate mechanisms in a
repertoire for adapting and coping in the process of growing up. (idem)

Hall et al , tell us that, “Disaster literally means "The stars are evil.” As we talk
about children, we will see that their cognitive perceptions are often quite
immature and "The stars are evil" represents pre-operational cognitive thinking,
a type of animism. Children often deal with egocentric theories of causality.
We define a disaster as a severe disruption, ecological and psychosocial, which
greatly exceeds the coping capacities of the altered community.” (idem)

Essentially she found the environment stressful. Hall et al defines stress as


being akin to beauty, it is in the eyes of the beholder. How you define a
situation determines your emotional response to it. He defines stress as an
incongruity between demands placed on an organism and the adaptive
capacity of the organism. (idem)

377
Hall, Judith G.; Armstrong, F. Daniel &; Shaw, Jon. Masters of
Pediatrics: Developmental and Behavioral Pediatrics Sessions. University of
Miami School of Medicine; based on transcripts and slides of presentations as
delivered by the faculty at the "Masters of Pediatrics" symposium held at the
Wyndham Miami Beach Resort in Miami, Florida, on January 16-21, 2002.

Page 94 of 114
Dr Jeffrey H Newcorn, a New York physician, reported to the 48th Annual
Meeting of the American Academy of Child and Adolescent Psychiatry, that
children who have been diagnosed with depression or anxiety may actually be
experiencing post-traumatic stress disorder. He said that we need to be aware
that children’s traumatic stressors differ from those of adults. Clinicians tend to
diagnose the mood and anxiety disorders, and miss the post-traumatic stress
disorder. If this error is being made in a psychiatric setting, it certainly must be
also missed in a paediatric setting. 378

There is a compelling need to avoid any traumatic reminders that bring


conscious awareness of the traumatic situation. These criteria are woven into
the PTSD DSM-IV diagnoses. As a result, in children, you look for disorganised,
agitated behaviour, not the affects of fear, helplessness, and horror. Children
have a tendency to relive and re-experience the trauma in play and in dreams.
It is this that, in part, interferes with sleep.

NOTE: It is important to understand that the research into PTSD here


reviewed only involves the response to the causative agent and not to the brain
damage that resulted from it. It is speculative perhaps to suggest that TBI
might damage the areas of the brain that are concerned with PTSD and
therefore compound the situation.

_______

Rational Drug Interventions


DIAGNOSIS AND TREATMENT

Cultural and professional models of illness influence decisions on individual


patients and delivery of health care. The biomedical model of illness, which has
dominated health care for the past century, cannot fully explain many forms of
illness. This failure stems partly from three assumptions: all illness has a single
underlying cause, disease (pathology) is always the single cause, and removal
or attenuation of the disease will result in a return to health. Evidence exists
that all three assumptions are wrong. 379 (See 'Occam's Razor' above, p70)

The model of illness adopted by society can have important consequences. In


the First World War, for example, soldiers complaining of symptoms after
experiencing severe stresses were sometimes shot as malingerers, but today
they are considered victims and eligible for financial settlements. Social
acceptance that a behaviour or reported symptom constitutes an illness
bestows privileges on an individual and formal duties on society. 380

Many patients present with symptoms that are not attributable to any
underlying pathology or disease. 381 Nevertheless, such patients are often
378
Pediatric PTSD underestimated, related to different stressors
than in adults. Reuter’s Professional Medical News 2001-10-29
379
Wade DT, Halligan P. New wine in old bottles: the WHO ICF as an
explanatory model of human behaviour. Clin Rehabil 2003;18: 349-54.
380
Parsons T. The social system. Glencoe, IL: Free Press, 1951.
381
Carson AJ, Ringbauer B, Stone J, McKenzie L, Warlow C, Sharpe
M. Do medically unexplained symptoms matter? A prospective cohort study of

Page 95 of 114
given a medical diagnosis, implying an underlying structural cause and
reflecting cultural expectations. On the other hand, some patients suffer from a
well-documented condition but its symptoms are misrepresented as a mental
illness. Such misrepresentation is not only poor (even negligent) medicine but
it puts the patient in a difficult situation and due to the extraordinary control
that is gained through placing a patient under the Mental Health Act, their lives
can become a nightmare and it takes enormous courage and resolution to fight
such a monstrous imposition.

It is clear therefore that the use of diagnostic labels has implications for the
patient, society, and ultimately for the credibility of medicine. Any illness
provided with a (medically validated) diagnostic label is widely assumed to be
secondary to defined pathology, to be capable of confirmation independently of
the symptoms, and to have a specific treatment that health services should
supply. If such a condition has been misrepresented as another then the
possibility of appropriate care becomes difficult to achieve.

The problems arising from illnesses without a definable cause have been well
documented. 382 They are most appropriately termed functional somatic
syndromes, 383 recognising that psychological and social factors strongly
influence the presentation of somatic symptoms.

Funding is determined by diagnosis (in health related groups or similar) and


ignores the initial cost associated with diagnosis (patients present with
problems, not diagnoses). It also fails to recognise that a major part of
healthcare cost relates to disability. 384 Resources are primarily allocated for
the diagnosis and specific treatment of disease. Little attention is paid to other
interventions despite good evidence of their effectiveness.

Finally, most biomedical models also seem strongly linked to primitive forms of
intuitive mind-body dualism. Health commissioners, budgetary systems,
healthcare professionals, and the public all act as if there is some clear,
inescapable separation between physical and mental health problems, ignoring
evidence that a person's emotional state always affects their function and
presentation of physical symptoms. 385

Weller has written, “In the case of schizophrenia many abnormalities of regional
brain activity have been reported...The precise site of dysfunction is
complicated because of the widespread consequences of disrupted or
malfunctioning pathways within a connectionist architecture...there are
corresponding morphological and cyto-architectural abnormalities, with
changes in the structure and organisation of neurons and their connections.”
He then adds: "A higher number of small neurons have been found in layers...of

300 new referrals to neurology outpatient clinics. J Neurol Neurosurg Psychiatry


2000;68: 207-10.
382
Malleson A. Whiplash and other useful illnesses. Kingston, ON: McGill-
Queen's University Press, 2002.
383
Barsky AJ, Borus JF. Functional somatic syndromes. Ann Intern Med
1999;130: 910-21
384
Evers S, Voss G, Nieman F, Ament A, Groot T, Lodder J, et al.
Predicting the cost of hospital stay for stroke patients: the use of diagnosis
related groups. Health Policy 2002;61: 21-42
385
Wade, Derick T. & Halligan, Peter W. Do biomedical models of
illness make for good healthcare systems? BMJ 2004;329:1398-
1401 (11 December)

Page 96 of 114
the prefrontal cortex in one study of schizophrenia and in all cortical layers in
another by the same team. There is a reduced synaptic spine density on
dendrites...these are the same brain regions in which functional activity is
abnormal, as referenced in my previous letter." 386

Even if all this were true and solidly and repeatedly demonstrated, would it not
then require rigorous proof of causation between mental states usually called
‘schizophrenia’ and these observed pathologies? Because not to demand such
rigorous proof would be like flippantly claiming (and seriously believing) that
the pattern of trains leaving Paddington are the cause of the pattern of those
arriving at King's Cross, or Victoria, even though no physical connection — and
hence no cause and effect relationship — can be shown to exist between what
are merely parallel events in the rail system of the same city. 387

Pointing out patterns is not enough to show causality. There must be rigorous
proof of the highly frequent presence of these pathologies with schizophrenia,
and for the hypothesis to really hold up, proof of their absence in non-
schizophrenia. Otherwise, people will rightly conclude that the only thing
holding up such an assumption of causality is the strong belief some have that
it exists. Belief alone is not generally regarded as very cast-iron or copper-
bottom proof in science. (idem)

History of research in psychiatry is replete with examples of claims for the


discovery of a biological basis for schizophrenia that have subsequently been
shown to be false. We will be able to look back to see if Weller’s contentions
survive. The problem is that even if Weller’s claims prove to be false or non-
specific, Double suspects he will not abandon his notion of schizophrenia as a
neurobiological disorder. He will just look for other alternative hypotheses from
the latest research. The neurobiological hypothesis, therefore, tends to be self-
perpetuating. 388

Double goes on to write that, “More seriously, misunderstanding of so-called


"anti-psychiatry" should not lead to an overstatement of the biomedical case.
Laing was not the only person who has pointed to the craziness of "normal"
society. Moreover, the psychoanalyst D.W. Winnicott can be cited in support of
the thesis that regression and psychosis can be mechanisms of healing and re-
adaptation. Although there were some excesses in Laing's work, in the sense
that he wanted to abandon the metaphor of pathology, he did quote favourably
from psychiatrists, for example Manfred Bleuler, who adopted a psychosocial
model, such as that restated by Wade & Halligan.389 Laing never minimised the
suffering of people diagnosed as schizophrenic. His emphasis on the role of the
family is welcome in a research area that has now essentially dried up. (Idem)

DRUG INTERVENTIONS

Studies of pharmacological interventions in adults with acquired brain injury are


limited 390, though the field is expanding rapidly. It is already apparent that
some drug treatments can be of help in a number of areas, which may be
386
Malcolm P Weller. Trying to knit fog? BMJ eLetters; 21 February 2005
http://www.bmj.com/cgi/eletters/330/7488/419-b#97775.
387
Morrell, Peter. Trying to knit fog? BMJ eLetters; 21 February 2005
(idem)
388
Double, D B. Trying to knit fog? BMJ eLetters; 21 February 2005 (idem)
389
Wade DT, Halligan PW. Do biomedical models make for good
healthcare systems? BMJ 2004; 329: 1398-401

Page 97 of 114
common to both head-injured children and adults, including attention, memory,
learning and social behaviour. Fundamental research, however, is still
desperately needed.

Pharmacology is the science concerned with the nature and mode of drug
effects. Therapeutics concerns the use of drugs in clinical conditions. Clearly,
pharmacology should be the main basic of therapeutics, but the teaching of
these subjects tends to happen at different stages in medical training and, as a
result, their relationship is often loosened.

Most commonly, pharmacology is taught pre-clinically as a basic science in a


coherent course. Subsequently, therapeutics is invariably taught piecemeal, as
different disorders are encountered during clinical training. Unless clinical
teachers actively encourage students to relate treatments to their previously
acquired knowledge of pharmacology, this science becomes relegated to the
past, along with botany and inorganic chemistry. Indeed, in ordinary medical
practice the commonest basis for drug prescription is an almost automatic
disorder-drug association, rather than the logical development of a therapeutic
solution from pharmacological knowledge 391; or indeed from good enough
diagnosis in the first place.

The great majority of treatments in medicine, both effective and irrelevant, are
empirical. This means that a drug has been found to be effective and, in the
best instances, the finding has been upheld after careful study using double
blind controlled conditions. It also implies that there is little knowledge of how
the effect is achieved.

Ideally, of course, all drug treatments should simply redress some specific
patho-physiological abnormality which underlies the clinical abnormality. This
ideal of rational drug intervention however, can be achieved only when some
clear patho-physiological disturbance is known to be the cause of the clinical
condition, and this is a rare occurrence.

Perhaps the best example involving the central nervous system (CNS) was the
use of L-dopa in the treatment of Parkinson's disease, although even this is not
as straightforward as it might seem. As far as the target symptom or disorder
is concerned, the empirical approach generally works quite well, but two
particular problems are associated with it. First, automatic disorder-drug
associations tend to be made so quickly that important aspects of the whole
context may be overlooked. For example, it requires a significant degree of
self-discipline to remember to enquire about a previous history of asthma
before prescribing propranalol for migraine prophylaxis. Secondly, the process
tends to focus attention on a desired effect of the drug, so that additional
effects may be overlooked. (Eames, 1989 idem)

The common expression used to describe these additional effects is ‘side


effects’, but this is a term which is in itself misleading. In normal circumstances
any drug has a range of effects; in the treatment of a particular symptom or
condition, some particular effect is desired, but the others will occur
nevertheless, and there is nothing truly ‘side’ about them. (Eames, 1989 idem)

390
Gualtieri, C. T. (1988) 'Pharmacotherapy and the neurobehavioural
sequelae of traumatic brain-injury', Brain Injury, 2, pp. 101-129.
391
Eames, P. Rational Drug Interventions in Johnson, DA.; Uttley, D. &
Wyke, M. (1989) Children’s Head Injury: Who Cares? Taylor & Francis.

Page 98 of 114
As an illustration, the drug orphenadrine is marketed by one pharmaceutical
company for the treatment of Parkinsonian disorders, but by another as a
skeletal muscle relaxant. In the promotional material neither company
mentions the other's use or indeed action, and these omissions result from a
marketing agreement between the companies. Which is the side effect?
(Eames, 1989 idem)

Context can be very important in predicting drug effects. For head-injured


children, a feature of obvious importance is age. For some drugs, different
effects can be expected in children from those seen in adults, though probably
the most important difference in most cases relates to dosage. Some drugs are
metabolized quite differently in two age groups. An example where this can
mislead is the anticonvulsant carbamazepine (Tegretol), for which the different
balances between its two major catabolic pathways require that much the same
dose levels be used in children as in adults.

A much greater distortion of standard drug effects is produced by severe


diffuse head injury, which presents an extremely complex, though nonetheless
broadly predictable special context. For example, whilst the use of
prochlorperazine (Stemetil) for the treatment of nausea and vomiting presents
few problems when the appropriate dose is used in otherwise normal subjects,
in the head-injured individual it may have two adverse effects; first, it is
epileptogenic, and this is of particular importance to the head-injured since
they already carry an increased risk of epilepsy and the onset of post-traumatic
epilepsy is known to have very serious effects on educational and occupational
outcomes, as well as on the general quality of life. Second, even quite low
doses of prochlorperazine may produce extrapyramidal movement disorders in
head-injured patients. This example highlights the fact that potential adverse
effects are most easily overlooked when drugs are prescribed for symptomatic
disorders unrelated to the primary problem; for example, trivial viral symptoms
in a person recovering from a severe head injury. The obvious solution for all
physicians dealing with the head-injured is to develop the habit of thinking
pharmacologically. (Eames, 1989 idem)

In many areas it is rare for the condition to be treated in special units wholly
devoted to it. The much wider development of ‘categorical’ head injury
rehabilitation units in the United States has not been attended by consistent or
committed medical interest in many cases. As a result, little is yet known about
specific aspects of drug treatments in the head-injured generally, and virtually
nothing is known about the special problems of head-injured children.

Inevitably, most problems are approached by comparison with superficially


similar ones in other pathological states, and trying out the appropriate drug
treatment. This sort of approach is inadequate in many ways. More creative
thinking is needed, based on actual knowledge of the brain disorders caused by
head injury.

A major impediment to this is the ingrained attitude, particularly prevalent in


academic centres, which effectively demands that a drug treatment be already
described in the literature before it can be considered proper to use it. On
closer inspection, it is apparent that this attitude stems from rules which apply
more to therapeutics than to pharmacology. Ironically it seems much more
likely that what is needed is creative pharmacological thinking. (Eames, 1989
idem)

Page 99 of 114
There is a rapidly expanding literature on drug treatments for head injury
disorders. 392, and Gualtieri, 1988 idem. The bulk of this literature however,
consists of reports of studies of very small groups, or of single cases, the
motivation for which can be seen to come from traditional drug treatments of
conditions other than head injury. It is distressing to see how often the
conclusions of these studies lead to recommendations which clearly ignore
potential adverse effects which are predictable from current knowledge of the
drugs and of head injury disorders. (Eames, 1989 idem)

For example, Mysiw and Jackson 393 state that tricyclic antidepressants may
diminish aggressive behaviours and, “are rapidly gaining recognition as having
a major impact on the rehabilitation course of the TBI (traumatic brain injury)
patient”. No mention is made of the considerable and well established risk of
provoking epilepsy 394, 395 and, their confident statement is based on a single
study of one patient, by their own group 396 — a further study not then
published. The latter subsequently reported twenty patients with agitation (out
of a total of fifty-eight patients treated for head injury) of whom thirteen
showed ‘dramatic decrease in agitation’ one week after starting treatment with
amitriptyline (Amitrip) 397 .

The proportion of patients who responded to the drug, however, dropped


dramatically with decreasing degree of confusion, inviting the alternative in-
terpretation that their agitation resolved spontaneously as post-traumatic
confusion cleared. Given that these drugs increase the risk of epilepsy by only
a few per cent, it is not surprising that this problem did not make itself
apparent in their study. If, however, their recommendation were to be followed
by physicians around the world, one could confidently predict, on the basis of
the extensive literature on antidepressants, a significant increase in the
number of individuals developing posttraumatic epilepsy.

In his review, (Gualtieri, 1988 idem) mentions that one particular


antidepressant, maprotiline (Deprilept, Ludiomil, Psymion), ‘is known to lower
seizure threshold ... and is therefore probably contraindicated in TBI patients’.
He also states, ‘one advantage of amitriptyline is that it is the tricyclic
antidepressant least likely to lower seizure threshold’, but the study he quotes
in support of this 398 is in fact a study of the effects of drugs locally applied to
specific sites in animal preparations, and the findings are quite different from
those in man which show this drug to be the antidepressant most likely to

392
Journal of Head Trauma Rehabilitation (1987) Psychopharmacology, 2, pp.
1-76.
393
Mysiw, W.J. & Jackson, R.D. (1987) 'Tricyclic antidepressant therapy
after traumatic brain injury', Journal of Head Trauma Rehabilitation, 2, pp. 34-42.
394
Markowitz, J.C. and Brown, R.P. (1987) 'Seizures with neuroleptics
and antidepressants', General Hospital Psychiatry, 9, pp. 135-141.
395
Hayes, P.E. & Kristoff, C.A. (1986) 'Adverse reactions to five new
antidepressants', Clinical Pharmacology, 5, pp. 471-480.
396
Jackson, R.D., Corrigan, J.D. & Arnett, J .A. (1985) 'Amitriptyline for
agitation in head injury' , Archives of Physical Medicine and Rehabilitation, 66,
pp. 180-181.
397
Mysiw, W.J., Jackson, R.D. & Corrigan, J.D. (1988) 'Amitriptyline for
post-traumatic agitation' , American Journal of Physical Medicine Rehabilitation,
67, pp. 29-33.
398
Clifford, D.B., Rutherford, J.L., Hicks, F.G. and Zorumski, C.F.
(1985) 'Acute effects of antidepressants on hippocampal seizures'. Annals of
Neurology, 18, 692-697.

Page 100 of 114


provoke epilepsy.

Very similar considerations apply to the small literature, frequently overinflated


by reviewers, claiming beneficial effects from neuroleptic (antipsychotic) drugs
on behavioural disorders after head injury. Cardenas (1987) 399 quotes three
studies (with eighteen, twelve, and eleven patients respectively) and one report
containing a few case examples. She notes that most of the studies have
flawed methodological designs, yet concludes that it is a fact that antipsychotic
medications can alleviate symptoms following brain injury. In her review of
adverse effects she does not even mention the possible provocation of
epilepsy, and recommends diphenhydramine for treatment of neuroleptic-
induced extra-pyramidal disorders in the elderly, despite that fact that even the
American Physicians Desk Reference Book warns of the significant
epileptogenic actions of this drug. (Eames, 1989 idem)

An even more ominous point is that all antidepressant and neuroleptic drugs
have more or less marked anticholinergic activity, which is known to have
deleterious effects on cognition. A few of the published head injury studies
claim useful effects on behaviour without cognitive deterioration, but these
claims turn out to be based on screening procedures that assess well
established and static intellectual functions, rather than the often subtle kinds
of cognitive disorder, such as attention and learning, that characterize the
head-injured, and are particularly sensitive to the effects of these drugs.
(Eames, 1989 idem)

Similarly, there is a growing literature on the use of stimulant drugs for


behavioural and attentional disorders after head injury. Close scrutiny,
however, reveals that the claims are built upon alleged similarities between
these patients and children with Attention Deficit Disorder, coupled with just
three published studies, one well-designed 400, the others 'open' case reports 401,

402
. Each of these three studies concerns just one patient.

Knowing how antipsychotic drugs work at specific receptor sites on specific


neurons helps the clinician select the drug of choice for an individual patient.
Individualised strategies of treatment, the clinician's task, cannot be learned
from analysing results of large randomised clinical trials. Such trials tell us
about group effects but can give only limited information about what will work
for a particular individual.403 404

399
Cardenas, D.D. (1987) 'Antipsychotics and their use after traumatic
brain injury', Journal of Head Trauma Rehabilitation, 2, pp. 4-9.
400
Evans, R. W., Gualtieri, C. T. & Patterson, D .R. (1987) 'Treatment of
chronic closed head injury with psychostimulant drugs: a controlled case study
and appropriate evaluation procedure' ,Journal of Nervous and Mental Diseases,
175, pp. 106-110.
401
Weinstein, G.S. & Wells, C.E. (1981) 'Case studies in neuropsychiatry:
post-traumatic psychiatric dysfunction: diagnosis and treatment', Clinical
Psychiatry, 42, pp. 120-122.
402
Lipper, S. & Tuchman, M.M. (1976) 'Treatment of chronic post-
traumatic organic brain syndrome with dextroamphetamine: first reported case',
journal of Nervous and Mental Disease, 162, pp. 366-371.
403
Streiner DL. Thinking small. research designs appropriate for clinical
practice. Can J Psychiatry. 1998;43:737-741.
404
Seeman MV. Clinical trials in psychiatry: Do results apply to practice?
Can J Psychiatry. 2001;46:352-355.

Page 101 of 114


________

Possible Effects of Specific Cognitive Deficits on

Behaviour and Social Functioning 405

While executive difficulties are likely to be the most important cognitive factor
influencing behaviour, other deficits may also be significant. Deficits in atten-
tion, memory, and reasoning are likely to affect academic progress and conse-
quently self-esteem. Some difficulties may also have a more direct effect on
adjustment. A child with impaired verbal working memory may have difficulty
following instructions and be seen as disobedient. A child who has difficulty
placing information into longer-term memory may forget previous
conversations with peers and so appear to be uninterested, possibly resulting in
social rejection or social withdrawal. A child with prospective memory problems
may be seen as trying to avoid situations. Children's memory difficulties can be
a significant source of stress for their families (Rivara et al. 1992) 406.

Attentional problems may also have a direct impact on adjustment. A child who
has difficulty with divided auditory-visual attention may become frustrated if
they are spoken to while they are playing a computer game because their
performance deteriorates. In general, ADHD-type behaviours (inattention,
impulsivity, and high activity levels) cause strain to parents (Rivara et al. 1992
idem).

Pragmatic language difficulties can also be important and it has been noted
that some brain-injured children may be able to talk but not communicate
(Dennis 1991) 407. The child may have difficulty in knowing the alternative
meanings of words in context (e.g. the duck was ready to eat); getting the point
of figurative or metaphoric expressions (e.g. she was easily crushed); bridging
inferential gaps in interpersonal situations; and verbally describing the
apparent intention of others. Such difficulties are clearly likely to affect the
child's relationship with peers, but may also contribute to them being seen as
disobedient. Thus, most 14-year-olds know that when a teacher says, “Would
you like to come and see me after class”, a choice is not really being offered.
This may not be the case for some brain-injured children.

EMOTIONAL RESPONSES AND THEIR NEUROLOGICAL ORIGINS

Emotions have generally been tied in with behaviour. Although several


disciplines have contributed to an understanding of emotions, Linda Camras
believes that a lot of work is really now in neuroscience. The professor of

405
Appleton, R.; Baldwin, T. Management of Brain Injured Children. 2nd
Ed. OUP,2006.
406
Rivara, J. B., Fay, G., Jaffe, K., Polissar, N., Shurtleff, H., &
Martin, K. (1992). Predictors of family functioning one year following traumatic
brain injury in children. Archives of Physical Medicine and Rehabilitation 73, 899-
910.
407
Dennis, M. (1991). Frontal lobe function in childhood and adolescence: a
heuristic for assessing attention regulation, executive control, and the
intentional states important for social discourse. Developmental
Neuropsychology 7,327-58.

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psychology at DePaul University in Chicago sees neuroscience as probably the
fastest emerging area in the understanding of emotions. 408

At a conference organised by the New York Academy of Sciences. (See


footnote below) Camras presented new evidence that complicates an existing
debate about how infant emotional responses develop. Her results show that,
contrary to a popular theory in developmental psychology, 11-month old infants
still have undifferentiated negative emotions.

The "differential emotions theory" holds that humans develop distinct


expressions for different negative emotions very early in life. Anger and
sadness develop in the first few months, and fear by six months of age,
according to the theory.

But Camras and her colleagues found only partial differentiation of emotional
expression in their 11-month old subjects. Emotional expressions in infants are
tied to general states of distress, and are not yet linked to specific negative
emotions at that age, Camras told the conference. Camras believes that it is
not yet clear at what age emotions differentiate. However she does believe
that the timing is later than some people would expect. Research on emotions
has been limited by the selection of appropriate subjects, Camras says.
Because research with human subjects can be ethically problematic, much of
the evidence for functional associations between brain regions and emotions
has come from animal studies.

For example, the amygdala has been associated with a range of cognitive
functions, including emotion, learning, memory, attention and perception. Most
current views of amygdala function emphasise its role in negative emotions,
such as fear, and in linking negative emotions with other aspects of cognition,
such as learning and memory. However, recent evidence supports a role for
the amygdala in processing positive emotions as well as negative ones,
including learning about the beneficial biological value of stimuli. Indeed, the
amygdala's role in stimulus–reward learning might be just as important as its
role in processing negative affect and fear conditioning.409

Poremba & Gabriel have demonstrated, in research with rabbits, that there is a
reverse action to the well-known one of neurons of the medial geniculate (MG)
nucleus of the thalamus sending axonal projections to the amygdala. It has
been proposed that these projections supply information that supports
amygdala associative processes underlying acquisition of acoustically cued
conditioning and learning. They have now demonstrated the reverse direction
of influence. Temporary inactivation of the amygdala using the GABAA
receptor agonist muscimol just before the onset of discriminative avoidance
conditioning, permanently blocked the development of training-induced
discriminative neuronal activity in the MG nucleus of rabbits. No discriminative
activity developed when the amygdala was inactivated or during later training
to criterion without muscimol. Thus, amygdala processing at the outset of

408
Stated at a conference organised by the New York Academy of
Sciences in December 2002, and attended by experts in psychology,
neuroscience and animal behaviour. They pooled resources and shared
information.
409
Baxter, Mark G. & Murray, Elisabeth A. The Amygdala and Reward.
Neuroscience 3, 563 -573 (2002).

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training is necessary for the development of training-induced discriminative
activity of neurons in the MG nucleus.410

Baxter & Murray (idem) tell us that a number of types of behaviour that involve
reward processing are independent of the amygdala. These include visual-
discrimination learning, visuo-motor conditional learning, food-cup approach
(Pavlovian conditioning), and food and object preferences. These behaviours,
in the absence of stimulus–reward association mediated by the amygdala, could
rely on stimulus–response learning or cortical representations of the value of
stimuli.

Different divisions of the amygdala mediate different kinds of stimulus–value


association. Lesions of the baso-lateral nucleus of the amygdala impair
performance on tasks that require linking an object with a current (as opposed
to a consistent) stimulus value. Examples of paradigms that can expose this
effect include reinforcer devaluation (in which the value of a reinforcer
changes) and second-order conditioning (in which a previously neutral stimulus
comes to acquire the value of the reinforcer with which it has been paired).
Baxter & Murray (idem)

Neurons of the baso-lateral amygdala, like neurons in the prefrontal cortex,


show complex patterns of firing that include specific responses to particular
objects, such as foods. These patterns of firing can be modulated by reinforcer
devaluation. Lesions of the central nucleus of the amygdala, by contrast,
impair Pavlovian approach or avoidance responses to specific conditioned
stimuli. An example of Pavlovian approach is the increased rearing response of
rats to a light that is repeatedly paired with food delivery.

Patients with bilateral amygdala damage perform poorly on laboratory-based


gambling tasks. Unlike patients with damage to the prefrontal cortex, who are
also impaired on these tasks, patients with amygdala damage fail to generate
normal changes in skin-conductance response and other autonomic responses
when they 'win' or 'lose' money. Their inability to learn a winning strategy
might result from an inability to generate the appropriate affective state.
Future work should aim to integrate these functions of the amygdala with its
other functions, such as the production of fear responses and attentional
processing. Baxter & Murray (idem)

It will be seen that the role of the amygdala in social behaviour has been a
controversial topic in recent years. Research in animals and humans has
pointed to a role for the amygdala in emotion, particularly in fear. But based on
experiments in rats and primates, some scientists have also asked whether the
region is essential for normal social interactions.

"The answer from our research is clearly no," said David Amaral, professor of
psychiatry and neuroscience at the University of California in Davis. Instead,
the amygdala seems to have an indirect role in altering social behaviour,
through modulation of anxiety and fear, Amaral says. Damaging the region, he
adds, has the same effect as a few too many drinks at a cocktail party - it
makes monkeys socially uninhibited. 411

410
Poremba, Amy & Gabriel, Michael. Amygdala Efferents Initiate
Auditory Thalamic Discriminative Training-Induced Neuronal Activity. Journal of
Neuroscience, January 1, 2001, 21(1):270–278

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The amygdala has long been implicated in the mediation of emotional and
social behaviours. Amaral writes that because there are very few human
subjects with selective bilateral damage of the amygdala, much of the evidence
for these functional associations has come from studies employing animal
subjects. Macaque monkeys live in complex, highly organised social groups
that are characterised by stable and hierarchical relationships among
individuals who engage in complex forms of social communication, such as
facial expressions. Understanding the role of the amygdala in animals that
display a level of social sophistication approaching that of humans will help in
understanding the amygdala's role in human social behaviour and in
psychopathology such as social anxiety. Selective bilateral lesions of the
amygdala in mature macaque monkeys result in a lack of fear responses to
inanimate objects and a "socially uninhibited" pattern of behaviour. These
results imply that the amygdala functions as a protective "brake" on
engagement of objects or organisms while an evaluation of potential threat is
carried out. They also suggest that social anxiety may be a dysregulation or
hyperactivity of the amygdala's evaluative process. Finally, recent data from
developmental studies raise the possibility that, at least at some developmental
stages, fear in social contexts may be subserved by different brain regions than
fear of inanimate objects. (Amaral, idem)

However, Kennedy et al report that the amygdala is critical for processing


information about emotion, but they add that little is known about what role it
might play in human behavioural interactions. They found that a patient with
complete bilateral amygdala lesions lacks any sense of personal space and that
in healthy controls the amygdala is activated by close personal proximity.412

"What we're finding is that monkeys don't seem to need an amygdala either as
an adult or in the developing animal," Amaral said. The researchers have
published initial reports from a pilot study but have since replicated them in a
larger group of animals. The data is to be published in a special issue of
Neuropsychologia, titled "The Cognitive Neuroscience of Social Behaviour."

Damaging the amygdala does alter social behaviour, however. When


confronted with an unfamiliar monkey or an inanimate object, normal monkeys
typically are anxious or afraid, Amaral explains. "But our [adult] animals that
didn't have an amygdala have thrown their caution to the wind," Amaral said.
"They just simply start interacting with [others] socially." The lack of suitable
human subjects may be allowing Amaral to make presumptions that are not
valid in respect to humans. Infant monkeys also did not fear inanimate objects,
but unlike the adults, were anxious about novel social interactions. "We don't
have a good explanation for that," Amaral said. Perhaps, he suggests, fear of
inanimate objects is separate from social fear. There may also be redundant
systems for fear at an early age, which disappear in adulthood. "There's lots of
speculation at the moment, but no one has the data," he said.

Previous studies in animals have recorded symptoms typical of autism in young


animals with amygdala lesions. But the symptoms may be a result of rearing

411
Amaral D.G. The primate amygdala and the neurobiology of social
behaviour: implications for understanding social anxiety. Biol Psychiatry 2002
Jan 51:11-7.
412
Kennedy, DP; Gläscher, J; Tyszka, JM & Adolphs, R. Personal space
regulation by the human amygdala. Nature Neuroscience; October 2009 Volume
12, Issue 10, pp1226 – 1227.

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the animals in a nursery, Amaral says. In his study, animals were nursed by
mothers and exposed to "normal" social interactions, and did not exhibit any
autism-like symptoms.

"This is fascinating work for at least two reasons," said Adolphs. 413 414 The data
show that the consequences of damaging the amygdala vary with age, he
notes, and that the amygdala's role in fear behaviour is dissociable. "It is
essential for certain aspects of triggering a fear response, but not for others,"
he said.

"The findings may be especially important for understanding human diseases in


which there is compromised amygdala function early in life," he said, "as has,
for example, been speculated with respect to autism."

Amaral's results in animals, support Adolph's observations in humans, which


suggest that the amygdala is required for social judgments of other individuals
on the basis of their facial appearance.

For example, the amygdala is active when individuals interpret facial


expressions associated with negative emotions. S.M., a woman with a
damaged amygdala, had problems deciphering faces with negative emotions,
such as fear or anger, but had no difficulty with "positive" emotions such as
happiness. Together, the observations are consistent with the idea that the
amygdala is involved in the subjective evaluation of potential threats - a "fear
detector" of sorts.

In another piece of research Dolan et al found that in social environments,


multiple sensory channels are simultaneously engaged in the service of
communication. In this experiment, Dolan and colleagues were concerned with
defining the neuronal mechanisms for a perceptual bias in processing
simultaneously presented emotional voices and faces. Specifically, they were
interested in how bimodal presentation of a fearful voice facilitates recognition
of fearful facial expression. By using event-related functional MRI, that crossed
sensory modality (visual or auditory) with emotional expression (fearful or
happy), they showed that perceptual facilitation during face fear processing is
expressed through modulation of neuronal responses in the amygdala and the
fusiform cortex. These data suggest that the amygdala is important for
emotional cross-modal sensory convergence with the associated perceptual
bias during fear processing, being mediated by task-related modulation of face-
processing regions of fusiform cortex.415

The researchers are now engaged in detecting which brain regions, other than
the amygdala, are involved in mediating fear in baby monkeys. Amaral is
413
Adolphs, Ralph. Neural systems for recognising emotion. (Different
brain structures, including the amygdala and the basal ganglia, are involved in
the recognition of emotions.) Current Opinion in Neurobiology, 2002, 12:2:169-
177.
414
Kawasaki, Hiroto; Adolphs, Ralph; Kaufman, Olaf; Damasio,
Hanna; Damasio, Antonio R.; Granner, Mark; Bakken, Hans; Hori,
Tomokatsu & Howard III, Matthew A. Single-neuron responses to emotional
visual stimuli recorded in human ventral prefrontal cortex. Nat. Neurosci.
January 2001 Volume 4 Number 1 pp 15 – 16.
415
Dolan, R. J.; Morris, J. S. & de Gelder B. Crossmodal binding of fear in
voice and face. Proc. Natl. Acad. Sci. USA, Vol. 98, Issue 17, 10006-10010,
August 14, 2001.

Page 106 of 114


focusing his work on areas in the frontal lobe, including the orbital frontal
cortex. [See notes on page 8]

So, are there separate brain regions for processing each of the many human
emotions like happiness, fear, anger, sadness, guilt, and jealousy? "Probably
not," Adolphs said. Key questions need to be answered before researchers can
begin to understand how the brain processes emotion, he says. How should
emotions be categorised, for example? "What are the right ways of dividing up
the stimuli and behaviours?" he asked. "We don't presently have an answer to
that important question."

In his paper on neural systems involved with emotions, Adolphs believes that
recognition of emotion draws on a distributed set of structures that include the
occipito-temporal neocortex, amygdala, orbito-frontal cortex and right fronto-
parietal cortices. Recognition of fear may draw especially on the amygdala and
the detection of disgust may rely on the insula and basal ganglia. Two
important mechanisms for recognition of emotions are the construction of a
simulation of the observed emotion in the perceiver, and the modulation of
sensory cortices via top-down influences.

Similar results from his recent studies tell us that specific neural structures,
genes, and neurotransmitter systems also have a rôle to play in social
cognition. Cortical regions in the temporal lobe participate in perceiving
socially relevant stimuli, whereas the amygdala, right somato-sensory cortices,
orbito-frontal cortices, and cingulate cortices all participate in linking perception
of such stimuli to motivation, emotion, and cognition. Open questions remain
about the domain-specificity of social cognition, about its overlap with emotion
and with communication, and about the methods best suited for its
investigation.416

Prather et al 417 believe that the amygdala has been implicated in the
mediation of emotional and species-specific social behaviour. Their research
also shoes that humans with bilateral amygdala damage are impaired in
judging negative emotion in facial expressions and making accurate
judgements of trustworthiness. Todd and Anderson have also researched this
field and have shown that recent human imaging work has expanded the view
of amygdala function beyond early findings in animals and that two studies of
an individual with bilateral amygdala damage suggest that we should be
thinking even more broadly.418 Amygdala dysfunction has also been implicated
in human disorders ranging from social anxiety to depression and to autism.
They produced selective amygdala lesions in 2-week-old macaque monkeys
who were returned to their mothers for rearing. At 6-8 months of age, the
lesioned animals demonstrated less fear of novel objects such as rubber snakes
than age-matched controls. However, they displayed substantially more fear
behaviour than controls during dyadic social interactions. These results
suggest that neonatal amygdala lesions dissociate a system that mediates
416
Adolphs, Ralph. The neurobiology of social cognition. Current Opinion
in Neurobiology, 2001, 11:2:231-239.
417
Prather MD, Lavenex P, Mauldin-Jourdain ML, Mason WA,
Capitanio JP, Mendoza SP, Amaral DG. Increased social fear and decreased
fear of objects in monkeys with neonatal amygdala lesions. Neuroscience 2001
106:653-8.
418
Todd, RM. & Anderson, AK. Six degrees of separation: the amygdala
regulates social behavior and perception. Nature Neuroscience; October 2009
Volume 12, Issue 10, pp1217–1218

Page 107 of 114


social fear from one that mediates fear of inanimate objects. Furthermore,
much of the age-appropriate repertoire of social behaviour was present in
amygdala-lesioned infants indicating that these lesions do not produce autistic-
like behaviour in monkeys. Finally, amygdala lesions early in development
have different effects on social behaviour than lesions produced in adulthood.
(Prather et al, idem)

BEHAVIOUR MANAGEMENT

Behaviour management is likely to be the main approach taken with children


with brain injury and has been described by (Deaton 1994) 419. Such an
approach often needs to be implemented before other treatment strategies are
tried because children with severe behaviour problems are likely to drain the
parents' resources and result in deterioration in the relationship between the
child and their parents (Leichtman 1992) 420. The following stages in the imple-
mentation of a behavioural programme have been described (Deaton 1994
idem).

First, the problem (or target) behaviour must be defined. The people involved
in implementing the programme need to agree on a precise, detailed
description of the behaviour to be changed. There should be agreement
between the people implementing the programme (such as family members,
teachers and all rehabilitation staff) that the behaviour is a problem and should
be tackled. Where possible, the brain-injury survivor should be involved at this
and other stages and agree that the behaviour needs to change.

Second, a baseline assessment needs to be carried out to identify the function,


cause and rate of the target behaviour along with other salient characteristics
such as intensity and duration. During this stage, information obtained on the
events preceding (antecedents) and following (consequences) the target
behaviour will often indicate why the behaviour occurs. Antecedents can
include cognitions, emotions, settings, or behaviours. Increasingly, emphasis is
placed on analysis of the antecedents of inappropriate behaviour (Ylvisaker et
al, 2003 idem, Ylvisaker et al, 2005) 421.

Inappropriate or challenging behaviour is seen as a communication that the


person may be under some stress and analysis of the antecedents may make it
clear what the source of the stress is. For example, a child may behave
inappropriately in a particular lesson. It would be important in these
circumstances to try to understand the reasons for this. It may be that the
child finds particular aspects of the work in this lesson difficult and, if so, it may
be possible to change the way the topic is taught to better suit the child's
abilities or learning style. This may be sufficient to result in a reduction in the
challenging behaviour. Similarly, a child with attentional difficulties following
brain injury may find doing homework difficult and misbehave at such times. It
419
Deaton,A. V. (1994). Changing the behaviors of students with acquired
brain injury. In: Educational Dimensions of Acquired Brain Injury. (eds R. C.
Savage & G. F. Wolcott), 257-276. Austin, TX: PRO-FD, Inc.
420
Leichtman, M. (1992). Psychotherapeutic interventions with brain-
injured children and their families I: diagnosis and treatment planning. Bulletin
of the Menninger Clinic 56,321-37.
421
Ylvisaker, M., Adelson, D., Braga, L W., Burnett, S. M., GIang, A.,
Feeney, T., Moore, W., Rumney, P., & Todis, B. (2005). Rehabilitation and
ongoing support after TBI: twenty years of progress. Journal of Head Trauma
Rehabilitation 20, 95-109.

Page 108 of 114


may also be possible that some children may find a particular teacher not to
their liking and due to their lack of social ability and understanding the child
may not know how to handle the situation and this needs to be understood and
suitable intervention instituted to improve the situation for both child and
teacher.

Relatively simple methods such as breaking the work down into discrete
sections with small breaks in between may result in better cooperation.
Analysis of possible antecedents of challenging behaviour have also been
extended to include remote events, such as difficulty sleeping, and it may be
that concentrating on trying to address these difficulties results in an
improvement in behaviour. Ylvisaker et al, (2005) idem outline the difference
between a more traditional applied behaviour analysis approach and the
approach they use (referred to as positive behaviour supports).

Consequences can be viewed as being positive (which serve to reinforce the


behaviour and make it more likely it will occur in the future) or negative (and so
decease the likelihood of future occurrence). It is, however, the child's percep-
tion of the consequences that is most important.

Thus, the brain-injured child may be desperate to make friends and believe that
certain behaviours cause his peers enjoyment and increase his popularity. To
the outside observer, however, it may be clear that his peers use him as a
source of amusement. A particular behaviour may also be found to serve a
number of different functions. Thus, a child may hit peers both to obtain
desired toys and stop them teasing him. In addition, once a particular
behaviour is established, reinforcement may only need to be intermittent in
order for it to be maintained.

A baseline assessment may, therefore, need to be prolonged in order to identify


factors that serve to maintain the behaviour. This can be a source of frustration
to parents; however, premature intervention may lead to failure. During
baseline assessment it may also become clear that the behaviour is not as
great a problem as was initially thought, because there is a tendency to see
intense behaviours (such as temper outbursts) as being more frequent than is
actually the case.

In the third stage, the resources available for behavioural intervention need to
be identified. Resources may include the assets of the brain-injured child such
as memory, motivation, and learning ability. Assessment of the family's assets
such as knowledge of brain injury, the time and energy available from family
members, and their ability to be consistent in implementing any behavioural
programme is likely to be very important.

It is also important that any programme takes into account the child's cognitive
strengths and weaknesses (Ylvisaker et al. 2003) idem. Programmes can be
complicated and take a considerable time to be effective and, particularly with
brain-injury survivors, need to be very consistently applied — by all those
involved in caring for the child (e.g. see Gardner et al. 2003) 422. However, in
some cases, relatively simple interventions have proved effective (Mottram and

422
Gardner, R. M., Bird, F. L., Maguire, H., Carreiro, R., & Abenaim,
N. (2003). Intensive positive behavior supports for adolescents with acquired
brain injury: long-term outcomes in community settings. Journal of Head Trauma
Rehabilitation 18,52-74.

Page 109 of 114


423
Berger-Ross 2004) .

Parents can have strong feelings of guilt and sympathy for the injured child,
which may interfere with their ability to carry out a behavioural programme.
Such feelings therefore need to be addressed before the programme is
implemented. A programme that is begun but not carried through is likely to
result in feelings of frustration, helplessness and even failure on the part of the
parents; this can confuse the child, possibly resulting in deterioration in their
behaviour.

Fourth, there is often a tendency to concentrate on simply decreasing


undesirable behaviour such as hitting peers and pro-social alternatives to such
behaviour need to be developed and rewarded. Thus, a child may be taught
how to negotiate with peers/siblings when they want to use a particular toy,
rather than simply hit them. Rewards are likely to be highly individual to the
child, may change with time, and need to be given immediately after the
desired behaviour for maximum effectiveness (Mottram and Berger-Ross 2004)
idem.

Fifth, the chosen strategy must be implemented and evaluated via ongoing
collection of data. Parents need to be forewarned that in some cases the prob-
lem behaviour is likely to escalate before it diminishes. For instance, if temper
tantrums have been effective for the child in the past, these are likely to
become more prolonged and intense at the start of the programme. If parents
acquiesce to these tantrums, the child may learn that they should escalate this
behaviour in order to achieve what they want. Concrete feedback in the form
of graphs or charts may be needed for the child with memory problems.
Continual evaluation will help determine if the intervention is being successful
and, if not, help identify possible reasons for its failure such as inconsistent
implementation.

The sixth and final stage involves the maintenance and generalization of
desirable behaviours. This demands a gradual shift in control of the behaviour
back to the child and away from external sources, and a fading of reinforce-
ment. Rewards need, therefore, to become less concrete, less frequently given
and less artificial, but such changes need to be very gradual. Behaviours
taught in one setting to a child with brain injury may be less likely to generalize
to other settings (Ylvisaker et al. 2003) idem. Skills may, therefore, need to be
taught in a variety of settings.

Once parents and others have learned behaviour management techniques,


they can be applied to a variety of problems and so reduce the need for profes-
sional consultation. The time and effort (as well as support and encourage-
ment) needed by parents to learn to use such techniques should not, however,
be underestimated.

Although there has been relatively little research into the effectiveness of these
techniques with brain-injured children, existing research is promising (see
Gurdin et al. 2005) 424 and the techniques have been shown to be effective with

423
Mottram, L. & Berger-Gross, P. (2004). An intervention to reduce
disruptive behaviours in children with brain injury. Pediatric Rehabilitation 7,
133-43.
424
Gurdin, L. S., Huber, S. A., & Cochran, C. R. (2005). A critical
analysis of data-based studies examining behavioural interventions with children

Page 110 of 114


other client groups (Ylvisaker et al. 2003) idem.

SPECIAL PROVISION

Following a brain injury, it is often necessary for the child to attend a special
school. The child may have significant learning difficulties or behaviour prob-
lems that would render them disadvantaged within a mainstream setting, no
matter what type and level of support were provided.

It may be that these children would benefit from a small-group classroom


setting in which the presentation of work and the level of tasks can be
individually devised. In most circumstances, the special school offers a suitable
and secure environment for the brain-injured child, but unfortunately, the class
teachers will not be fully aware of their needs.

By virtue of its role, most special schools cater for children who have
developmental difficulties and not for children who have acquired difficulties.
Whereas there is a degree of similarity in the learning processes of both
groups, the cognitive deficits of a brain-injured child can be complex, subtle or
severe; the situation may be further compounded if the child also has
significant physical problems. The cognitive difficulties can be much more
specific than those usually encountered in children with developmental
problems and these differences are not always fully recognized. In addition,
the brain-injured child may feel ill at ease with children who have grown up with
their disability. There is a need for a greater understanding of the very specific
needs of the brain-injured child throughout the educational system.

INTERVENTIONS WITH PARENTS

Parents, children and may be some professionals need to know that PTSD is a
normal reaction to an abnormal event. Sufferers should be provided with a
safe, supportive environment in which to discuss and/or write and draw about
the traumatic event. Therapeutic sessions which are too brief may sensitize
rather than desensitize children to the trauma.

The main components of effective treatment are psycho-education about


trauma reactions; sustained exposure to trauma-related cues and memories
until habituation occurs; and the teaching of coping skills to children to help
them manage anxiety, coupled with parent training to equip parents with the
skills to help them facilitate their children's recovery (Carr 2004) 425.

Sleeping problems should be tackled early on as sleep deprivation is likely to


impair the child's ability to function in everyday situations and so compound
problems. If the child has difficulty getting to sleep, then the use of relaxing
routines before going to bed may help. Music may help mask or distract the
child from intrusive thoughts that prevent sleep onset. Nightmares linked to
trauma and accidents can be treated via relaxation and systematic
desensitization, coupled with teaching positive self-statements and storyline
alteration, that is, recounting the nightmare with a different, happy, ending
(Yule 1994)426. The effectiveness of PTSD treatment for children and
adolescents is now reasonably well established (Carr 2004 idem).

and adolescents with brain injuries. Behavioral Interventions 20, 3-16.


425
Carr A. (2004). Interventions for posttraumatic stress disorder in children
and adolescents. Pediatric Rehabilitation
7, 231-44.

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The main thrust of treatment interventions is likely to be aimed at parents
because it is they who have to deal with the child on a daily basis. Indeed, in
some cases, unfortunately, they may have to care for the child for the rest of
their lives. In addition, some interventions with the child are unlikely to be
successful without parental support. Thus, teaching a child anger management
skills is unlikely to be effective if temper outbursts continue to be rewarded at
home.

EDUCATION OF THE FAMILY AND OF THE CARERS

Educating parents and carers about brain injury and its effects is very
important. Parents and other family members also need to be educated about
the specific neuropsychological deficits shown by the brain-injured child. This
particularly applies to executive dysfunction which many parents/carers appear
to find confusing. In addition, because of the structured environment that is
usually provided for young children by their parents, the consequences of such
deficits may be minimal in this age group. As a result, parents may see little
reason to intervene to try to improve executive functioning.

However, in view of evidence that executive dysfunction appears to be linked to


a poor outcome, it is possible that early intervention may prevent future
problems developing. Possible strategies for improving executive functions
have been noted elsewhere (Ylvisaker and Feeney 2002) 427. Furthermore, the
way in which brain-injured children are managed generally by parents may
need to be altered to take into account the child's deficits by, for example,
providing more structure and routine.

FAMILY COUNSELLING AND FAMILY THERAPY

It is likely that when a child suffers a brain injury the whole family is affected.
Pre-morbid difficulties in family relationships may also contribute to behavioural
problems the child had prior to the injury and affect their post-injury
adjustment. For these reasons, work with the family as a whole may be neces-
sary if the brain-injured child's behaviour problems are to be successfully
addressed.
_______

SUMMARY AND CONCLUSIONS


An examination of the foregoing clearly indicates that there is a plethora of
information that should be of special interest to those who are treating or
caring for a brain-injured patient; especially those who have been injured in
childhood and even more importantly if the injury is sustained in infancy. None
426
Yule, W. (1994). Posttraumatic stress disorder. In: Child and Adolescent
Psychiatry: Modern Approaches. (eds M. Rutter, E. Taylor & L. Hersov), 392-406.
Oxford: Blackwell Scientific Publications.
427
Ylvisaker, Mo, Jacobs, H. E & Feeney, T. (2003). Positive supports for
people who experience behavioral and cognitive disability after brain injury: a
review. Journal of Head Trauma Rehabilitation 18, 7-32.

Page 112 of 114


of the foregoing material is to do with pre-natal conditions or peri-natal injuries
such as anoxia.

It is shown that the earlier a child has its brain damaged the more important it
is for that child to receive immediate attention and that attention should follow
it during the rest of its life unless there is a complete recovery.

When there is a serious trauma to the head that injures the brain it is almost
always possible to gain a realistic understanding of which areas have been
damaged from the nature of the injury. However, when the damage occurs
atraumatically — more often due to toxins that have passed the blood/brain
barrier — then it becomes difficult to be sure where the brain injuries lie. This
is especially so if the injury has occurred in the pre-development stage of a
child’s life. It is hoped that this paper will help that situation by having drawn
together much of the science that has been published to date.

The problems that occur from atraumatic brain damage are multiple and often
serious and long-lasting; indeed they will probably exist for the rest of the
sufferer’s life. It is so important therefore for a full understanding to be gained
about the nature of the injury, how it affects the patient’s behaviour and how
the professionals involved in his/her care can bring about a sustained
programme of rehabilitation in a safe and secure environment. It is also their
responsibility not only to educate the parents and carers in following
appropriate courses of action but also to give them optimum opportunity to
learn about the nature of the injury and how it will affect the patient’s life from
that time forward.

This not only involves pragmatic behaviour but the consequences of any
disorders that arise subsequent to the injury such as those to the hormone and
metabolic systems; language and speech; the sleep cycle; memory and the
possible evolution of an autistic syndrome and PTSD.

There also needs to be a demanding involvement of all the professionals as well


as the family and carers when consideration is given to the use of drug
intervention. This is vital, for any drug that is in contemplation to be used will
not have been tested in clinical trials in this population of patients. There will
probably be few anticipated responses, indeed some may be paradoxical.
When affected children are to be cared for it must only be after every aspect
has been considered that they are placed in the homogenous learning disabled
category. It is very convenient for children who have suffered very early ABI to
be written-off as simply being ‘learning disabled’. Such egregious professional
effrontery costs less financially and in personal effort and — what is clearly
understood by those who perpetrate this nefarious activity — the subjects know
nothing of what they are missing. This approach is undertaken by authorities in
the hope that they are not challenged as, unfortunately, they rarely are.

Any brain injured child should not be excluded from the very important and
needful care and treatment that would be given by neuropsychologists and
other specific dedicated consultants or it would be a travesty of their human
rights and a service that takes that course of action indiscriminately should be
deeply ashamed of its actions.

Now we are in the 21st Century we cannot allow treatment and care for the
brain injured child to follow courses that may have been acceptable in the

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1960s and even in the 1970s. There is absolutely no excuse for the deprivation
of an adequate medical and social care plan for all those so damaged. A lesser
course can only be one of negligence.
_______

OTHER REFERENCES
AT PAGE 25:
Aston-Jones G, Shipley MT, et al. (1995): The locus coeruleus, A5 and A7
noradrenergic cell groups. In: The Rat Nervous System, Paxinos G, ed. New
York: Academic Press, pp. 183-214

Foote SL, Bloom FE, et al. (1983): Nucleus locus coeruleus: new evidence of
anatomical and physiological specificity. Physiol Rev 63(3):844-914

Alan Challoner
oakwoodbank.ac@virgin.net
30 January 2010

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