Paper B: Older Adult Psychiatry

PAPER III

Older Adult Psychiatry

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I. THE AGEING PROCESS

Biological theories of ageing

Organ- and system-based theories
The underlying rationale of these theories was the belief that the onset and progression of
senescence was determined by a reduction in the operational efficiency of a single organ
e.g. from the cardiovascular, immune or neuroendocrine systems. This ‘wear and tear’
theory is no longer thought to be tenable.
Stochastic damage
Theories in this category are based on the assumption that cumulative adverse random
changes occur through time, which result in reduced operational efficiency of the
organism and ultimately overwhelm its capacity to survive. To date, three basic theories
of this nature have been described.
▪ Rate-of-living theory is based on the demonstration of an inverse relationship
between basal metabolic rate and longevity.
▪ Accumulation theories ascribe ageing to the build-up of waste products within
cells. These waste products are thought to interfere with normal cellular
metabolism and function. The presence of lipofuscin, a highly insoluble compound
present in the cells of most tissues, may be due to an age-related decline in the
function of cellular catabolic processes.
▪ Cross-linkage theories hypothesize that, with increasing chronological age,
macromolecules of biological importance gradually develop cross-links which
distort their chemical and physical properties in a detrimental manner.
▪ Stochastic theories now largely concentrate on the role of free-radical damage as a
significant factor in ageing. Free radicals are compounds with an unpaired
electron in their outer orbital that renders them highly reactive, resulting in
autocatalytic attack on neighbouring compounds. An inverse correlation has been
demonstrated between the longevity of mammalian species and rates of
perioxidation (Cutler 1985).
Genome-based theories
Genome theories postulate that ageing is primarily associated with changes in the genetic
constitution of the organism i.e. ‘programmed ageing’. This theory was given weight by
the demonstration of the ‘Hayflick limit’. This phenomenon is observed in normal human
cells after a specific number of laboratory sub-cultivations that are characteristic of the cell
strain, the cells undergo irreversible cessation of mitosis and enter a non-dividing state
known as replicative senescence. This is thought to be because of progressive losses of
DNA sequences in the telomere - specialized structures located at the termini of
chromosomes and believed to be critical in the maintenance of DNA stability and
replication.

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Normal ageing is associated with a reduction in total sleep time, reduced slow wave sleep
and daytime fatigue. These changes are heightened in dementia and are often associated
with an increased frequency of night-time wakening. As dementia progresses there is a
reduction in REM sleep with an increase in daytime sleep and finally a complete
disorganisation of the sleep-wake cycle. The worsening of activity disturbances in the
latter part of the day (sundowning) and night-time disturbance may be related to
underlying disturbances of diurnal rhythm.
Ageing and drug prescribing:
There is altered pharmacokinetics in the elderly affecting drug treatment.
1. Absorption: There is reduced gut motility, leading to drugs being absorbed slowly
 slower onset of action. The amount of drugs absorbed is similar to young
adults.
2. Distribution: Half-life of drugs is generally increased in older people as they have
an increase in body fat, less body water and less albumin than young adults. This
also leads to increased concentration of drugs at site of action, and more free form
available (active form) necessitating use of lower dosages than younger adults.
3. Metabolism: Though the liver size is reduced, there is no significant reduction in
the metabolic capacity.
4. Excretion: Renal function is reduced by 35% by the age of 65; and 50% by the age
of 80. This leads to reduced capacity to excrete metabolites of the drugs, and in
some cases, the drugs itself (lithium & Sulpiride). A reduction in dosage is
required for this reason. Renal function is best measured by creatinine clearance.
The EEG in normal ageing shows increased theta and delta activity, slowing of alpha and
decreased beta activity (>80 years).
The genetic contribution to longevity has been assessed in studies of twins, which have
produced quite low heritability estimates of 0.26 for males and 0.23 for females.
II. DEMENTIA

2.1 Alzheimer’s disease (AD)

Epidemiology
Alzheimer’s disease (AD) is the most common form of dementia in the elderly. A meta-
analysis of the incidence of AD found that East Asian countries have a lower incidence of
AD than Europe, although variations in diagnostic practices may account for this 1.
However, vascular dementia is apparently a more prevalent cause in a number of
countries in the Far East. Age-specific prevalence rates of dementia rise steeply with age
and approximately double with every additional 5 years of age2 . Due to increasingly life
expectancy, the prevalence of dementia in Western Europe will more than double over the
next 50 years3 . In summary, the prevalence of AD is as follows;
• Approx. 4% in over 65

1 Jorm et al (1998) Neurology, 51(3), 728-33

2 MRC Cognitive Function and Aging Study Psychol Med 1998
3 2007 Dementia UK report

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• 20% in over 80
• 30-40% at 90
• AD is rare before age 60.
Prevalence is the same in men and women. However, as women are more likely to live in
to advanced old age, there are more women with dementia than there are men.
AD is more common in developed rather than developing countries and is apparently
more prevalent in urban settings 4. Average survival period for patient’s following
diagnosis is 8-10 years.
Aetiology:
Genetics
Genetics
Familial cases of AD have been well demonstrated. At least three different genetic sites
have been implicated in the development of early-onset forms of the disease which have
an autosomal dominant mode of inheritance:
▪ Presenelin 2 gene (chromosome 1)
▪ Presenelin 1 gene (chromosome 14)
▪ -amyloid precursor protein (APP) gene (chromosome 21)
Down’s syndrome;
The relationship between Down’s syndrome and the development of AD is well
established. Patients with Down’s syndrome (trisomy 21) develop neuropathological
features of AD due to an extra copy of the APP gene. This extra copy results in precocious
and excessive amyloid production which is postulated to be the cause of early onset AD.
Post mortem studies show changes consistent with AD by 40 years of age. The average
age of clinical diagnosis of dementia is about 50 years and prevalence may be as high as
75% in those over 60 years. Two factors that have been consistently found to be risk
factors for AD in Down’s syndrome are age and ApoE.
Apolipoprotein E gene (ApoE);
ApoE, located on chromosome 19, is associated with increased risk of developing late-
onset AD; it does not cause AD (c/w the mutations involved in early onset AD). There are
three alleles (2, 3, 4). 4 is the rarest form in the general population but is the
commonest in those with late onset AD.
Individuals homozygous for 4 (4/4) have a higher risk of developing AD. Those
heterozygous (4/3 or 4/2) have a slightly higher risk of developing AD. The 2/2 and
2/3 alleles are slightly protective relative to 3/3 (around 40% lower risk).
However, genetic testing and counselling for this gene is not used because there are many
individuals with AD who do not have the 4 genotype and many without AD who do.
The 4 allele is less common in East Asian individuals. The ApoE 4 allele also affects
stabilisation of membrane lipoproteins and is a risk factor for hypercholesterolaemia as
well as AD.

4 Baker et al. International Journal of Geriatric Psychiatry 1993; 8, 379-385

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Neuropathology
Macroscopic
▪ Brain atrophy frequent but inconsistent. Usually diffuse and symmetrical,
although the frontoparietal region and the temporal lobes may be more severely
affected than the rest of the brain. (Dementia, third edition, page 394). Most severe
in early-onset (<65).
▪ Widened sulci
▪ Enlarged ventricles.
Histological
Neurofibrillary tangles (NFTs)
• Intracellular inclusions consisting of paired helical filaments twisted into a coil. A
major component of the NFT is a microtubule associated protein, tau, which is
involved in microtubule assembly and stabilisation. In AD, tau is present in an
ubiquinated and abnormal highly phosphorylated form. This form of tau is less
effective at stabilising microtubules and plays an important role in
neurodegeneration. The degree of cognitive impairment correlates with the
number of NFTs.
• NFTs are found in the dystrophic neurites of amyloid plaques.
• NFTs are found to a much lesser degree in normal aging. They are not specific to
AD, and occur in other neurodegenerative disorders, including Down’s syndrome,
post-encephalitic parkinsonism, dementia pugilistica, amyotrophic lateral
sclerosis-parkinsonism-dementia complex of Guam, subacute sclerosing
panencephalitis and in myotonic dystrophy 5.
• In AD, NFTs are common in the medial temporal structures, in the hippocampus,
amygdala and parahippocampal gyrus, as well as occurring throughout the
neocortex and the deep grey matter including the lentiform nucleus, mamillary
bodies and substantia nigra 6.
Amyloid Plaques:
• Extra cellular aggregates consisting of an amyloid core surrounded by dystrophic
neurites. The amyloid appears to be derived from peptides that arise from the
amyloid precursor protein (APP), a transmembrane protein which can be cleaved
by one of three enzymes, called secretases.
• Hardy and Higgins (1992) proposed the ‘amyloid cascade hypothesis’ – This
proposes that the central pathogenic event in AD is an increased formation and
deposition of -amyloid. APP is normally cleaved by ά-secretase and this does not
produce -amyloid. In AD more APP is processed via -secretase and γ-secretase,
leading to increased -amyloid production. -amyloid protein is directly or
indirectly neurotoxic and leads to development of NFTs and plaques, with

5 Kiuchi et al 1991
6 Dementia, Third Edition Page 398-399

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subsequent neuronal death. The presenilins are part of the γ-secretase complex.
The amyloid cascade hypothesis is the basis for much of the therapeutic research.
• Mutations in the tau gene do not cause plaques, only tangles. Plaques and NFTs
first occur in the hippocampus before involving other regions
Other histological findings in AD include:
• Hirano bodies – intracellular crystalline deposits most commonly seen in and
amongst the pyramidal cells of the hippocampus. Also occur in normal subjects,
Picks disease, MND and Kuru, among others.
• Granulovacuolar accumulation – holes within neurons. Virtually restricted to the
pyramidal neurones in the hippocampus.
• Vascular/ congophilic angiopathy – Amyloid deposits in blood vessel walls. The
parieto-occipital cortex is usually more affected than frontal or temporal lobes.
Neurochemical
There is an age-dependent decrease in acetylcholine. This decline in cholinergic activity is
more prominent in those with AD, suggesting this is a primary factor in its aetiology. This
hypothesis is supported by the fact that there are severe changes in the nucleus of
Meynert (a highly cholinergic area) during AD.
Other neurotransmitters have been implicated in AD, but their role in aetiology is less
clear. These include noradrenaline, 5HT and glutamate.
In summary, risk factors for AD include:

▪ Increasing age ▪ Organic solvents

▪ Family history (RR is 3.5 in first ▪ Smoking (although some studies
degree relatives) show it is protective!)
▪ Down’s syndrome ▪ Hypothyroidism
▪ Apolipoprotein E genotype ▪ Depression
▪ Other possible risk factors (where ▪ Family history of Down’s syndrome
evidence is not so clear) include: ▪ Family history of Parkinson’s
▪ Head injury (NFTs found in disease
dementia pugilistica, but some ▪ Increasing maternal and paternal
studies have failed to find an age at time of birth
association. ▪ Other conditions e.g. diabetes,
▪ Aluminium (one study showed infections, vascular dementia
association with level of aluminium
in drinking water)
Protective factors may include
▪ HRT (has been proposed, but the WHIST study showed this does not protect
against AD)
▪ Anti-inflammatory drugs
▪ Control of hypertension
▪ Fish consumption
▪ High premorbid verbal ability

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Clinical Features
The clinical features of AD consist of
▪Insidious onset
▪Amnesia, aphasia, apraxia and agnosia (the 4 As)
▪Behavioural and psychiatric symptoms of AD
o Disorders of thought content
o Disorders of perception
o Disorders of affect
o Behavioural disturbance
o Personality change
AD begins insidiously and the first evidence of the condition is often minor forgetfulness,
which may be difficult to distinguish from normal ageing. The disease is progressive and
gradual.
Cognitive deficits include:
Amnesia is universal and characteristically for recent memories initially before remote
memories are lost. Disorientation occurs with disorientation for time usually being more
obvious than place. Disorientation to person occurs late in the disease.
Aphasia usually supervenes later and is often a mixture of receptive and expressive
problems. Includes word-finding difficulties (Nominal dysphasia) and errors in syntax
(fragmented sentences). Word approximation or paraphasic speech develops as the
disease progresses. Language deficits are not as severe a Frontotemporal Dementia.
Apraxia leads to difficulties in complex motor tasks such as copying a design or
demonstrating a task. There may be evidence of an inability to put on clothes in the
correct sequence or inability to use a knife and fork to eat despite intact motor
functioning.
Agnosia may be demonstrated as an inability to recognise and name objects, parts of the
body, faces (prosopagnosia – may lead to delusional misidentification), or one’s own face
(autoprosopagnosia – the mirror sign).
Neuropsychiatric Symptoms:
Delusions have been found in rates varying from about 15% to 37% of patients 7. Many
sorts of false beliefs can occur, but the commonest are simple delusions of theft and
suspicion (such as being watched, ‘the phantom boarder’ or an unfaithful spouse). Unlike
functional illness, delusions are not usually systemised, but in contrast are often transient
and isolated.
10 – 15% will experience visual or auditory hallucinations. They may be a manifestation of
more severe illness and have been associated with a greater cognitive deterioration.
Roughly 50% will have disturbance of affect, with depressive symptoms requiring
treatment occurring in up to 20%.
Behavioural disturbances:

7 Berrios and Brook 1985

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Behavioural disorders (Behavioural and Psychological Symptoms of Dementia, BPSD)

often have the most clinical impact. These include physical aggression, wandering,
excessive eating, sexual disinhibition and misdemeanours, shouting and screaming, faecal
smearing and searching behaviour.
Personality changes:
Changes in personality are often difficult to define, and most information is gathered
from informant history. The observed changes vary from the negative or deficit, to the
positive or active. Negative changes are characterised by lack of decisiveness, activity,
initiative, and drive (organic abulia), with loss of sense of humour and emotional warmth.
Positive or active changes are the most concerning to carers, and are characterised by poor
attention to personal hygiene, social skills, emotional control and sensitivity to the
feelings of others.
Physical Symptoms
Weight loss and weakness, stooped posture and non specific or apraxic abnormalities of
gait are common. Physical deterioration is progressive, often resulting in gross wasting,
leading to bronchopneumonia, the commonest form of death8. A late feature of AD is
urinary incontinence. Physical problems such as urinary incontinence, decreased mobility
and balance problems are more commonly seen in people with vascular dementia than
with AD.
Diagnosis:

Full psychiatric history and informant history

Mode of onset, course of progression, pattern of cognitive impairment
Non cognitive symptoms i.e. behavioural disturbance, wandering, aggression
Presence of co-morbid depression.
Mental state examination
Family history
Other diagnostic possibilities e.g. vascular, rule out possible organic causes.
Investigations: blood tests to include FBC, U&Es, TFTs, B12 and folate, bone profile,
glucose. CT scan.
MMSE (See below)
Initial Cognitive Testing: The Mini-Mental State Examination was developed as a
screening tool and is widely used. However, its brevity can result in a somewhat
superficial assessment of language, memory impairment and visuospatial functioning.
Processing speed and executive functioning are not tested.
Initial testing can be improved by the use of screenings tools such as the MoCA (Montreal
Cognitive Assessment) which is a 30-point test (cut-off score of 26), and the ACE
(Addenbrooke’s Cognitive Examination; the original version incorporated the MMSE)

8 Burns et al 1990

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which is a 100-point test battery assessing six cognitive domains (cut-off score of 88 & 82).
The most recent version of the ACE (ACE-III) is a 100-point screening tool that does not
include the MMSE.

NICE (updated 2016) have advised the following criteria for diagnosis:

Type of dementia Diagnostic criteria

Alzheimer's disease Preferred criteria: NINCDS/ADRDA. Alternatives include ICD-10

and DSM-IV

Vascular dementia Preferred criteria: NINDS-AIREN. Alternatives include ICD-10

and DSM-IV

Dementia with Lewy bodies International Consensus criteria for dementia with Lewy bodies

Frontotemporal dementia Lund-Manchester criteria, NINDS criteria for frontotemporal

dementia

DSM-IV, Diagnostic and Statistical Manual of Mental Disorders, fourth edition; ICD-10, International
Classification of Diseases, 10th revision; NINCDS/ADRDA, National Institute of Neurological and
Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association; NINDS–
AIREN, Neuroepidemiology Branch of the National Institute of Neurological Disorders and Stroke–
Association Internationale pour la Recherche et l'Enseignement en Neurosciences.

Table 1: Diagnostic criteria for dementia

CSF examinations are not recommended as routine investigations for dementia. Even
though preliminary diagnostic studies have shown that reduced levels of CSF beta-
amyloid and increased levels of CSF tau can differentiate patients with AD from patients
with other dementias, there is insufficient evidence to support the use of CSF markers9.
There is evidence to support the limited use of EEGs in dementia diagnosis. The EEG in
AD shows slowing in alpha and beta activity with increased delta and theta waves (i.e.
can be confused with normal ageing, but changes can occur earlier). Wright et al (1984)
found that while pattern evoked responses were normal in dementia, the major positive
component (P2) to flash was considerably delayed.

9Sunderland T et al. Decreased beta-amyloid 1-42 and increased tau levels in cerebrospinal fluid of patients
with Alzheimer’s Disease. JAMA 2003;289:2094-103

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Factors associated with diminished survival include parietal lobe damage, male gender,
onset <65, prominent behavioural abnormalities, more severe cognitive impairment
(particularly apraxia), depression and the absence of misidentification phenomena.
Management
Pharmacological
The current NICE guidelines (November 2006, updated 2016)10 sets out clear guidance on
their use:
▪ The three acetylcholinesterase (AChE) inhibitors donepezil, galantamine and
rivastigmine are recommended as options for managing mild to moderate
Alzheimer's disease.

Cholinesterase inhibitors are the mainstay of treatment for AD. There are 3 such drugs
available for the treatment of moderate AD, namely donepezil, rivastigmine and
galantamine. These prevent the breakdown of acetylcholine by inhibiting
acetylcholinesterase (AchE) and butylcholinesterase (BuChE). Donepezil and galantamine
are reversible inhibitors of AchE and rivastigmine is pseudoreversible inhibitor of AChE
and BuChE. Galantamine also modulates nicotinic receptor function.
▪ Donepezil 5-10mg OD. Steady state reached in 14 days. Single dose (easier to take)
▪ Rivastigmine 3-6mg BD. Half-life 10 hours.
▪ Galantamine 8-12mg BD. Half-life 6 hours.

Approximately 30-50% of patients will derive some benefit from treatment. Cognition can
improve slightly and deterioration can be prevented for approximately 6-12 months. The
cholinesterase inhibitors can also improve global outcome, ADLs 11 and may lower
caregiver burden. AChEs appear to have a minimal effect on time to institutionalisation or
progression of disability 12. They may also affect non-cognitive aspects of AD, in particular
neuropsychiatric symptoms13. On stopping the drug, the patient will revert back to the
stage of the disease they would have reached if no treatment had been given, so these
drugs do not affect the disease process.
▪ Memantine, given at 10mg BD, is a NMDA receptor inhibitor, and is considered to
be neuroprotective and disease modifying. Memantine is recommended as an
option for managing Alzheimer's disease for people with:
o moderate Alzheimer's disease who are intolerant of or have a
contraindication to AChE inhibitors or

o severe Alzheimer's disease.

There has been some interest in the use of anti-oxidants such as gingko biloba, selegeline
and vitamin E in the treatment of AD, but data is scarce. Ginkgo-biloba is felt to be less

10 Dementia. Supporting people with dementia and their carers in health and social care. NICE 2006, updated
2016.
11 Neurology 1998; 50 135-145

12 Lancet 2004; 363: 2105-15

13 CNS Drugs 2000; 13: 385-95

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potent in establishing cognitive improvement than cholinesterase inhibitors, though it is

tolerated as well as placebo. In patients with advanced AD the differences between
Ginkgo and placebo were more pronounced14. Note: Ginkgo causes bleeding when
combined with warfarin or aspirin, raises BP when combined with thiazide diuretics and
possibly causes coma when combined with trazadone15.
Medical treatment of behavioural and psychiatric disorders related to AD includes the use
of SSRIs and antipsychotics. SSRIs are of doubtful efficacy in the treatment of
behavioural and psychiatric disorders associated with AD.
With regard to the use of antipsychotics, as per CSM guidance, risperidone and
olanzapine should not be used to treat behavioural problems in elderly patients with
dementia due to increased risk of CVA. However, evidence suggests such risks may be
shared by all antipsychotics (Gill et al, 2005). Current British guidelines recommend that
antipsychotics should not be used in dementia unless there are severe problems
associated with psychotic symptoms, serious distress or if the behaviour poses a danger of
physical harm. However risperidone and olanzapine can be used to treat acute psychotic
conditions and schizophrenia in the elderly. Monitoring for risk factors for stroke in this
population is advised and potential cardiovascular risks discussed.
People with mild to moderate Alzheimer's disease who have non-cognitive symptoms
and/or behaviour that challenges, causing significant distress or potential harm to the
individual, may be offered an acetylcholinesterase inhibitor provided:
non-pharmacological approach is inappropriate or has been ineffective, and antipsychotic
drugs are inappropriate or have been ineffective

Non-pharmacological
Specific psychological treatments for dementia have been developed to ensure that
behavioural disturbance and psychological symptoms are thoroughly explored. A person
centred approach to individual problems is important. Using bio-psycho-social
formulation templates (such as the New Castle Model) help in understanding and
managing challenging behaviour.
Psychotherapy people with dementia, who are in the early stages, can benefit from one-
to-one psychotherapy to deal with issues around loss of identity, grief (over impending
changes eventually leading to death), affective features (depression 16 & anxiety)and social
impact of the diagnosis.
Behaviour modification depends on operant conditioning techniques whereby the
desired behaviour is positively reinforced and the undesirable behaviour is negatively
reinforced. The basis of the technique is charting the behaviour using the ABC approach,
where A is the antecedent, B is the behaviour and C is the consequences of the behaviour.
Reality orientation aims to continuously stimulate and orientate patients using informal

14 Kurz et al. Dement Geriatr Cogn Disord 2004; 18(2): 217-26

15 Hu et al. Drugs 2005;65(9):1239-82

16Forstmeier, Maercker, Savaskan, & Roth. Cognitive behavioural treatment for mild alzheimer's
patients and their caregivers (cbtac): study protocol for a randomized controlled trial. Trials 2015;
16: 526

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(communicating individually) and formal (daily group sessions) techniques. ROT may
slow cognitive decline and delay NH placement17.
Validation therapy is more patient-centred and aims to validate the patient’s past and
present experiences and feelings in whatever time and place is real to them. Benefits
include restoration of self worth, reduction in anxiety and the promotion of
communication and interaction. There are no statistically significant or clinically relevant
effects however from using VT18.
Reminiscence therapy has its roots in psychodynamic theory and uses triggers such as
old photographs to trigger memory and discussion in an effort to resolve past conflict.
Evidence is lacking about its clinical effectiveness.
Expressive therapies include art, music and techniques involving physical contact (e.g.
massage) to provide interest and occupation as well as to aid self-expression and reduce
anxiety.
Aromatherapy- There is insufficient evidence for the efficacy of aromatherapy in reducing
core and associated symptoms of dementia. One RCT on Melissa officinalis (lemon balm)
reported it to have a positive effect on agitation, although patients continued to receive
neuroleptic medications19. Lavender oil has not been proven to reduce associated
symptoms of dementia.
Memory training uses techniques to aid the memory (such as visual associations or
prompts). Cognitive Stimulation Therapy20 is the only non-drug intervention to be
recommended by NICE guidelines for cognitive symptoms and maintenance of
function.

Novel approaches to treatment

Targeting -amyloid; 1. Drugs preventing aggregation of -amyloid. 2. Drugs to inhibit
secretases by which -amyloid is formed from APP. 3. Immunisation strategies.
Other approaches include; hormone replacement therapy, NSAIDs, statins, and folate
supplementation. Other targets include tau and its phosphorylation.
2.2 VASCULAR DEMENTIA:

Epidemiology
The vascular dementias (VaD) are a clinically and pathologically heterogeneous group,
overlapping with other dementias. VaD is the second most common cause of dementia
after AD, accounting for approximately a quarter to one third of all dementias. It shows

17 Metiteri et al. Reality Orientation Therapy to delay outcomes of progression in patients with
dementia: A retrospective study. Clin Rehabil 2001; 15(5):471-8
18 Neal M.Validation therapy for dementia (Cochrane Review). Issue 3, 2003
19 Ballard et al. Aromatherapy as a safe and effective treatment for the managementof agitation in
severe dementia. J Clin Psychiatry 2002
20National Institute for Health and Clinical Excellence (2006). Dementia:
supporting people with dementia and their carers in health and social care. NICE
clinical guideline 42, November 2006.

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marked racial variation and is common in countries such as China and Japan, which have
a high incidence of vascular disease.
The prevalence of VaD is higher with increasing age (onset commonly in the seventh and
eighth decade) and in males.
Aetiology
Patients often have a family history of vascular disease. There are many medical
associations with VaD including:
Hypertension, diabetes, hyperlipidaemia (increased LDL and reduced HDL levels is a
known RF for CVD and therefore dementia, especially VaD21), polycythaemia,
homocysteinuria, sickle cell anaemia, coagulopathies and valvular heart disease. VaD is
more common in smokers.
CADASIL
In a few families there is an autosomal dominant pattern of inheritance, with onset
around the age of 45 years. This syndrome has been termed ‘cerebral autosomal dominant
arteriopathy with subcortical infarcts and leukoencephalopathy’ (CADASIL) and is
caused by a point mutation in the Notch3 gene on chromosome 19. CADASIL appears to
be the commonest genetic form of VaD. Rarely, it can be caused by cerebral vasculitis,
haemorrhage, chronic subdural haematoma and during severe hypotensive crises.
The clinical features of CADASIL are cognitive deterioration (50%), epilepsy (10%), mood
disorders (30%) and gait disorders and recurrent subcortical strokes (80%).
Clinical Features
VaD is differentiated from AD by history of onset, clinical features and subsequent
course. The dementia may follow a succession of acute CVAs or, less commonly, a single
stroke.
The NINDS-AIREN22 (International Work Group) diagnostic criteria for a diagnosis of
PROBABLE vascular dementia include all of the following:
1. Dementia – defined by cognitive decline from a previously higher level of functioning
and manifested by impairment of memory and of two or more cognitive domains.
2. Cerebrovascular disease: with clinical and CT/MRI evidence
3. A relationship between the above two disorders, manifested or inferred by one or
more of the following: a) Dementia within 3 months following a recognised stroke b)
abrupt deterioration in cognitive functions; or fluctuating stepwise decline of
cognitive deficits.
Clinical features are variable but include:
▪ Abrupt onset
▪ Stepwise deterioration
▪ Fluctuating course

21 Moroney et al. JAMA 1999

22Roman et al., Vascular Dementia. NEUROLOGY 1993;43:250

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▪ Focal neurological deficits (including mild motor or sensory deficits, decreased co-
ordination, brisk tendon reflexes, extensor plantar, visual field signs, bulbar signs
(pseudobulbar palsy), including dysarthria and dysphagia, extrapyramidal signs,
early presence of gait disturbance, unsteadiness, falls and urinary frequency and
urgency not explained by urologic disease).
▪ History of stroke
▪ Deficits in executive function rather than short-term memory or language
▪ Preservation of personality and insight
▪ Patchy preservation of some cortical functions

Multifocal disease presents with:

Gait disorders, Urinary incontinence, Rigidity, Bradyphrenia
Associated features include: Hypertension, Carotid bruits, Emotional lability, anxiety and
depression, transient clouding of consciousness
A number of subtypes have been described:
Vascular dementia of acute onset: new onset dementia develops rapidly after either a single
‘strategic’ stroke, or after a succession of strokes from cerebrovascular thrombosis,
embolism or haemorrhage.
Multi-infract dementia: this is more gradual in onset and follows a number of minor
ischaemic episodes which produce multiple infarcts in the cerebral cortex.
Subcortical vascular dementia: This term incorporates two entities – 1. ‘the lacunar state’ and
2. ‘Biswanger’s disease’. It is characterised by small vessel disease (lacunar infarcts, focal
and diffuse white matter lesions and incomplete ischaemic injury). There is usually a
history of severe hypertension, acute strokes and an accumulation of focal neurological
signs. Clinically, one would see deficits in executive functioning, pure motor hemiparesis,
bulbar signs and dysarthria, gait disorder, depression and emotional lability23. SIVD
tends to have a more insidious onset and more slowly progressive course. The memory
deficits may be milder than in AD and is specified by impaired recall, relative intact
recognition and less severe forgetting (Desmond et al 1999).
The Hachinski Ischaemic Score (HIS)24 is a widely used but not very reliable instrument
for distinguishing VaD from AD. It is based on 13 clinical features. A score of seven or
more is indicative of VaD, whereas a score of four or less is suggestive of AD.
Components of the HIS:
Abrupt onset 2
Stepwise deterioration 1
Fluctuating course 2
Nocturnal confusion 1
Relative preservation of the personality 1
Depression 1
Somatic complaints 1

23Dementia. Burns ed, 3rd Edition. Page533

24Moroney et al., Meta-analysis of the Hachinski Ischemic Score in pathologically verified
dementias1997, vol. 49, no4, pp. 1096-1105

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Emotional incontinence 1
History of hypertension 1
History of strokes 2
Associated atherosclerosis 1
Focal neurological symptoms 2
Focal neurological signs 2
Total 18
CT/ MRI show multiple, bilateral, dominant hemisphere vascular pathologies, especially
involving the limbic system.
The EEG can be normal in VaD, especially in the early stages of disease. The EEG may
show changes similar to AD but focal and paroxysmal abnormalities are more prominent,
with greater asymmetry of activity.
Leukoariosis –This term denotes diminution of white matter density in periventricular
regions as observed on brain imaging. It appears to represent a pathological process with
relevance to cognitive dysfunction in the elderly, and to be associated with vascular risk
factors. It is commoner and more severe in VaD than in AD but the overlap is too great
for it to be used as a diagnostic marker.
Management
Management of VaD relate to identifying and controlling any cardio-vascular risk factors.
For example maximising treatment for hypertension, hyperlipidaemia etc. Antiplatelet
drugs have been shown to prevent TIA’s and ischaemic stroke25 and a population based
study in 1996 26 showed that aspirin users had a slight protection against cognitive decline.
However a Cochrane review (Williams 2000) concluded that there is no evidence that
aspirin is effective in treating patients with VaD.
There is growing evidence to suggest that cholinesterase inhibitors may be of benefit in
VaD, but none of the currently available drugs are licenced for VaD. The overall effects
seem similar to those seen in AD, however many cases of dementia have mixed causation.
The use of nimodipine, memantine (early evidence suggests this is useful in mild-
moderate cases) and gingko are also under investigation.
2.3 DEMENTIA OF LEWY BODY TYPE

Dementia of lewy body type (DLB) comprises 12-20% of cases of dementia. Lewy bodies
are intracellular inclusions which stain for ubiquitin and -synuclein in the cortex and in
some brainstem nuclei. They are also found in Parkinson’s disease, but mainly in the
substantia nigra; smaller numbers are found in the cortex.
Currently Lewy body related disorders are thought of as a spectrum of disease, with the
clinical presentation varying according to the site of Lewy body formation. Three patterns
of disease can be identified:
1. Nigrostriatal involvement producing motor features of parkinsonism

25 Easton. Cerebrovascular Diseases 16 (Suppl. 1):20-26 2003

26 Sturmer et al. Am J Epi 143: 683-691

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2. Cortical involvement producing cognitive impairment and neuropsychiatric

symptoms
3. Sympathetic nervous system involvement producing autonomic failure.
The consensus criteria for the clinical diagnosis of probable and possible DLB are:
A – Progressive cognitive decline
B – Two of the following core features are essential for a diagnosis of probable DLB,
one for possible DLB:
▪ Fluctuating cognition with pronounced variations in attention and alertness
▪ Recurrent visual hallucinations (typically well formed and detailed)
▪ Spontaneous parkinsonism
C – Features supportive of diagnosis are:
▪ Repeated falls
▪ Syncope
▪ Transient loss of consciousness
▪ Neuroleptic sensitivity
▪ Systematised delusions
▪ Hallucinations in other modalities

The early features of DLB are different from those of AD: Symptoms of persistent or
prominent memory impairment are not always present early in disease course and
language loss is less marked. There is visuospatial dysfunction and fluctuating loss of
attention over a 24-hour period. Prominent deficits on tests of executive function and
problem solving can help to discriminate between DLB and AD.
However, there is clinical and pathological overlap in these patients with AD and
idiopathic Parkinson's disease. Approximately three quarters of older people with
Parkinson’s disease develop dementia after 10 years 27.
Visual hallucinations are usually well formed and detailed and are present in 33% of DLB
cases at the time of presentation. They are associated with greater deficits in cortical
acetylcholine, and predict a better response to cholinesterase inhibitors. Extrapyramidal
signs are reported in 25-50% of DLB cases at diagnosis, and the majority of cases develop
some EPS during disease course.
CT/MRI show preservation of the medial temporal lobes compared to AD. Dopamine
transported loss in the caudate and putamen can be detected in DLB but not AD by
Dopaminergic SPECT. The EEG is diffusely abnormal in 90% of DLB patients. EEG shows
diffuse slowing, with focal delta transients in the temporal lobes in 50% of cases.
The range of pathologies is similar to AD and VaD. The cholinergic deficit is said to be
more marked than in AD.
Treatment consists of use of cholinesterase inhibitors (evidence supports the use of
rivastigmine and donepezil), low-dose atypical antipsychotics for delusions and
hallucinations (but these carry a high risk of adverse events and worsening of

27Aarsland et al. Prevalence and characteristics of dementia in Parkinson’s disease. Arch Neurol
2003;60(3):387-92

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parkinsonian symptoms) and L-dopa (this can lead to some benefit in motor symptoms,
but delirium is not uncommon).
2.4 FRONTOTEMPORAL DEMENTIA

Frontotemporal dementia (FTD) encompasses dementias caused by frontotemporal lobar

degeneration, including Pick’s disease, semantic dementia, frontal lobe degeneration of
the non-Alzheimer’s type and motor neurone disease with dementia. It constitutes 12% of
presenile dementias.
Onset is usually between the ages of 45 – 65 years (mean age is 50), gender distribution is
equal and there is a family history in more than a third of cases. Familial cases have been
linked to mutations on chromosome 17 (FTDP-17) which is caused by tau gene mutations.
Other familial frontotemporal dementias are linked to chromosome 3. The mean illness
duration is 8 years. There are no known geographical or environmental influences.
The Lund-Manchester consensus on clinical criteria for the disorder includes:
▪ Behavioural disorder:
o Insidious onset with slow progression early loss of insight
o Early loss of personal and social awareness (personal neglect, lack of
social tack)
o Early signs of disinhibition (inappropriate jocularity, unrestrained
sexuality etc)
o Mental rigidity, inflexibility
o Stereotyped, repetitive and imitative behaviour
o Utilisation behaviour, distractibility, impulsivity and impersistence.
▪ Affective symptoms:
o Depression, anxiety, excessive sentimentality, suicidal and fixed ideation
o Hypochondriasis, bizarre preoccupation
o Emotional unconcern
o Amimia (inertia, aspontaneity)
▪ Speech disorders:
o Progressive reduction of speech, stereotypies, perseveration, echolalia.
▪ Spatial orientation, receptive speech and praxis relatively preserved
▪ Physical signs:
o Early primitive reflexes
o Early incontinence
o Late akinesia, rigidity and tremor
o Low and labile blood pressure.
▪ Investigations:
o Usually normal EEG (even late into the disease)
o Predominant frontal or anterior temporal abnormality on MRI
o Profound frontal lobe deficits on neuropsychological testing in the
absence of severe amnesia or perceptual spatial disorder.
▪ Supportive features:
o Onset before 65
o Positive family history of similar disorder in first degree relative
o Bulbar palsy, muscular weakness and wasting, fasciculations

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CT scans show non-specific cerebral atrophy in the majority of cases. MRI is more
reliable. On post-mortem examination the pathological features are variable.
In the majority of cases of FTD there is marked frontal and temporal atrophy, with
neuronal loss, gliosis, spongiform change in superficial layers of the cortex, often
ballooned cells and neuronal inclusions which stain for ubiquitin, tau and phosphorylated
neurofilaments. FTD does not show the distinctive histopathological features such as
tangles and plaques. Atrophy is also seen in the amygdala and basal ganglia. The parietal
cortex and posterior cingulate are comparatively spared (unlike AD).
When frontal and temporal lobe atrophy is visible on neuroimaging this gives weight to
the diagnosis, but these findings may be lacking in up to 50% of those with FTD.
FTD is not associated with cholinergic deficits, and dopamine also appears unaffected.
However, 5HT receptors are lost from frontal and temporal cortex in FTD (c/w temporal
and parietal cortex in AD).
Pick’s disease is differentiated from other forms of FTD by pathological features such as
severe ‘knife-edge’ atrophy of the frontal and temporal lobes and the presence of
argyrophilic inclusion bodies (Pick bodies) in neurones. They are comprised of tau,
ubiquitin and other proteins. Swollen, achromatic neurones (also called ballooned
neurones or Pick cells) are present in other neurodegenerative diseases and do not
reliably identify Pick’s disease. The clinical features do not distinguish it from other
forms of FTD; it may present with features of a frontal lobe dementia, or less frequently,
with features of selective temporal lobe disease. Features of Alzheimer’s disease are
absent. Classical Pick’s disease is the cause for only a small minority of FTD. Male:female
preponderance is 1:2.
Semantic dementia is a form of FTD that arises from degeneration of the temporal lobes.
It is sporadic and onset is usually between 50 and 65 years. Clinically, speech is fluent
and spontaneous but relatively empty of meaning. As the disease progresses, there is loss
of word meaning, and semantic paraphasias (for example an ‘elephant’ is referred to as a
‘cat’). Object and face recognition are impaired (associative agnosia and prosopagnosia
respectively) while behaviour shows egocentricity, rituals and a narrowed repertoire.
Memory is better for recent rather than for remote events unlike AD, and there is a
striking preservation of the patients’ autobiographical memory. Patients can negotiate the
environment without getting lost. However they show a gross breakdown in impersonal,
factual knowledge about the world.
2.5 OTHER DEMENTIAS

Dementia associated with other neurological diseases

Many other neurological diseases, including motor neurone disease, progressive
supranuclear palsy and multiple sclerosis, are associated with dementia.
Progressive supranuclear palsy is characterised by supranuclear ophthalmoplegia,
pseudobulbar palsy, dysarthria, retrocollis, parkinsonism and dementia. Usually affects
patients in the 7 th decade. No significant difference between the sexes. Often
misdiagnosed. Presents with unsteadiness, falls, slurred speech and memory impairment.
As the disease progresses, rigidity and downgaze palsy develop.

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In multiple sclerosis, cognitive impairment occurs in approximately 40% of patients. In

most cases, cognitive impairment occurs later in the disease course, however it may be an
early manifestation of the disease and can result in a rapidly progressive dementia 28.
Deficits may be seen in abstraction, problem solving, memory and learning.
Metabolic and endocrine
Virtually any metabolic or endocrine derangement can cause cognitive problems, so it is
important to screen for conditions such as renal and liver disease and hypothyroidism.
Infective
Neurosyphilis is now a very rare cause of dementia, but should be considered as a cause,
especially if there is a relevant past history or if the clinical picture is atypical, as it is
treatable. Serological testing can confirm or exclude the diagnosis.
AIDS can produce dementia through direct invasion of the brain by the virus, or as a
result of a number of associated CNS infections. It presents with forgetfulness, slowness
and poor concentration, or sometimes atypically with affective or psychotic symptoms.
Motor features, from clumsiness to paraplegia and incontinence, can also occur. Progress
of the disease is usually rapid, leading to global dementia, mutism and death.
Vitamin deficiencies
Several vitamin deficiencies can cause cognitive decline including vitamin B12, folate,
nicotinic acid and thiamine.
Normal pressure hydrocephalus
This comprises 1-2% of cases of dementia. 80% of patients with this disorder are over 70
years old. It presents with cognitive impairment, incontinence and gait disturbance.
There are many psychiatric and behavioural features. CT shows periventricular
hypodensities and ventricular dilation with small sulci. Treatment is by shunting to
divert the CSF, but pre-selection of cases is necessary.
Toxins, drugs and neoplasms are also important causes of dementia.

III. AFFECTIVE DISORDERS IN OLD AGE

Depression
Epidemiology/risk factors/aetiology
Prevalence rates for depression in the elderly range from 3–15% in community samples.
Higher rates are found in those who attend general practitioners (15-20%), care home
residents (15–20%) and general hospital in-patients (approx. 20%). It is more common in
women than men.
Generally the aetiology of depression in the elderly resembles that of depression at a
younger age (bio-psycho-social influences). The genetic contribution is smaller than that
of depression of early onset. Other risk factors include:

28 Zarei et al 2003

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▪ Physical health problems, disability ▪ Past history of depression

▪ Sensory impairment ▪ Neuroticism
▪ Adverse life events – particularly ▪ Caring for ill relatives
losses e.g. bereavement
▪ Being widowed/divorced
▪ Poor social support
▪ Lack of confidante
There is now strong evidence, both epidemiological and biological, for a vascular basis of
depression - ‘vascular depression’ 29. In terms of neuropathology, white matter
hypertensities seen frequently on MRI scans of patients with late-life depression reflect
focal areas of ischaemia and infarction. Patients in this group are said to show more
cognitive impairment, psychomotor retardation, limited depressive ideation, poor insight,
apathy, greater disability and poorer response to treatment. SPECT may show frontal and
paralimbic hypoperfusion.
A subgroup of elderly patients with affective disorders show ventricular dilatation on CT
There are a number of organic factors that can lead to presentation of depressive
symptoms:
Drugs Beta-blockers, methyldopa, nifedipine, digoxin, clonidine steroids, opioids,
antipsychotics, benzodiazepines, antiparkinsonians
Metabolic Anaemia, hypothyroidism, B12/folate deficiency, occult carcinoma (lung,
pancreas), hypercalcaemia, Cushing’s
Infective Post-viral, ME, brucellosis, neurosyphilis, UTI
Inflammatory Temporal arteritis
Intracranial Post stroke, post head injury, subdural haematoma, Parkinson’s disease,
delirium, space-occupying lesion, dementia
Clinical presentation
Typical depressive symptoms occur but the elderly are more likely to present with
agitation, neuro-vegetative symptomatology, somatic preoccupation, delusions and
forgetfulness. Some studies have reported that a third of depressed elderly patients had
severe retardation and agitation. Depressed older adults are more likely to display
cognitive changes, somatic symptoms, and loss of interest than are younger adults 30.
Depressive delusions concerning poverty and physical illness are common, and
occasionally there are nihilistic delusions i.e. that the body is not functioning, empty or
non-existent. Hallucinations may occur and are often accusatory or obscene.
Standard depression rating scales are not very appropriate to older adult psychiatry, as
questions about biological symptoms will not clearly distinguish between depressive and
physical illness. The Geriatric Depression Scale and the Cornell Scale for depression and
dementia have been specifically developed for use in elderly and dementing populations
respectively.

29 Thomas et al 2004
30Fiske A, Wetherell JL, Gatz M. Depression in Older Adults. Annual review of clinical psychology.
2009;5:363-389. doi:10.1146/annurev.clinpsy.032408.153621.

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Good prognostic indicators include:

• Onset before the age of 70
• Short duration of illness
• Good previous adjustment
• Absence of disabling physical illness or frailty
• Good recovery from previous episodes
• Religiosity
DSH/Suicide
Suicide rates in the elderly are higher than in other age groups and although there is a
trend towards a reduction in suicide rates in older adults, suicide attempts in late life
were found to be 25 times more likely to be fatal than in younger adulthood 31. Successful
attempts were linked to age-related increases in planning and the lack of disclosure of
suicidal ideation [poor detection]. Countries with high rates of older adult suicide include
European Union countries, Canada, the U.S., and several Asian countries, including
Japan, Singapore, and Taiwan32; Older men were found to be at higher risk than women.
However, DSH declines with age. Most cases of DSH are failed suicide attempts in this
group and they will tend to have a significant mental illness.
Risk factors for suicide include:
▪ Mental illness, usually depressive disorder
▪ Physical illness
▪ Male gender
▪ Social isolation/ decreased social support
▪ Single/separated/divorced/widowed
▪ Bereavement
▪ Alcohol misuse
▪ Anankastic and anxious personality traits
Outcome
Statistics vary depending on the patient setting and treatment adequacy. For inpatients,
at 2 years 60% have intermittent or continuous periods of being well, but 20% develop
chronic symptoms. Evidence suggests, however, that outcomes in the elderly are at least
as good as for younger patients. Mortality is increased in later life depression.
Management
Management involves:
▪ Provision of education and diagnosis
▪ Addressing any concomitant medical illnesses
▪ Social management where needed to reduce isolation and ensure adequate care,
companionship and nutrition
▪ Assessment of risks, including self-neglect and suicide
▪ Specific treatments including psychological interventions

31 Conwell, Orden, & Caine 2011; De Leo et al 2001

32 World Health organization Suicide Prevention 2011

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Antidepressants are a mainstay of treatment:

SSRIs are usually first-line treatment, due to better tolerated SE profile and a lower
propensity towards cardiotoxicity. There is also a risk of postural hypotension with TCAs
and MAOIs. The central anticholinergic effects of TCAs are undesirable in case there is a
subclinical dementing process. Low doses of antidepressants are preferred as older people
are more sensitive to side effects and interactions with other physical medications should
be considered. As with early-onset depression, antidepressant medication should
continue for at least a number of months after full recovery. There is some evidence to
suggest treatment should continue possibly permanently 33.
Psychotherapies can also be used. CBT and IPT are both supported by evidence.
Electroconvulsive therapy is well tolerated and commonly used in the elderly, and is
appropriate for depressive disorder with severe or distressing agitation, suicidal ideation,
life-threatening stupor, or failure of response to medications.
Mania
One-year community prevalence rates for mania in the over 65s are 0.1%. Mania
represents 12% of all affective disorders treated on specialised geriatric psychiatry units
and accounts for 5-10% of all psychiatric disorders in the over 65s. Female:male ratio is
2:1. The onset of affective disorder in elderly patients who present with mania is later
(late 40s) with onset of mania being at a mean age of 55. Genetic factors appear to be less
important in aetiology of late-onset mania with coarse neurological disorders playing a
more prominent role. It is more common for depression to follow mania in the elderly.
Lithium retains an important role in management and appears to be as effective as in
younger patients. Due to altered renal excretion and distribution it has a longer half-life
in elderly patients and they are therefore more prone to toxicity. Lower doses are
required with the aim of keeping plasma levels between 0.35-0.70 mmol/l.
Carbamazepine is also used but requires ECG monitoring due to cardiac side effects and
carries a risk of neurotoxicity. Valproate may be preferable but can also be neurotoxic in
the elderly.
Pseudodementia
This is not an ICD-10 diagnostic term, but it is widely used and serves as a reminder that
some patients with severe depression (especially those with severe psychomotor
retardation or agitation) can appear to be suffering from dementia. Those who present
with depression and cognitive impairment have a four-fold increase in the risk of
developing an irreversible dementia even though their initial cognitive deficit reverses
with treatment. Note however that depression without cognitive impairment does not
increase the risk of developing dementia. Clues to a diagnosis of pseudodementia include
a history of relatively rapid onset with a personal or family history of depression. The
episode tends to start with depressive symptoms rather than memory problems and
patients tend to give ‘don’t know’ answers on cognitive assessment. Higher cortical
dysfunction such as apraxia and aphasia is usually absent and memory loss tends to be
for both recent and remote events. A patient with pseudodementia will often complain of
having a memory problem and want help. Sleep deprivation improves cognitive

33 Old Age Depression Interest Group 1993

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functioning in those with affective disorder and worsens it in those with a dementing
illness.
IV. DELUSIONAL DISORDERS AND SCHIZOPHRENIA OF LATE ONSET

In ICD-10 and DSM-IV there are no separate codes for late-onset schizophrenia (aka
paraphrenia). Terms used include:
• Late onset schizophrenia (onset 40-59 years)
• Very late onset schizophrenia-like psychosis (>60 years)
The incidence is 17-24 per 100,000 per year and female outnumber males with this
preponderance becoming more pronounced with increasing age of onset. Patients with
late paraphrenia represent approx. 10% of the elderly population of psychiatric hospitals
and prevalence among the elderly living in the community ranges from 0.1-4%.
The core symptoms and overall clinical profile is similar to that of younger onset
schizophrenia, however the relative prominence of some features do differ:
Symptoms which are commoner
▪ Persecutory delusions often predominate, although other delusions can
commonly arise
▪ Partition delusions (i.e. believing that a person or object can pass through a
barrier)
▪ Visual, tactile and olfactory hallucinations
Symptoms which are less common
▪ First-rank symptoms and formal thought disorder
▪ Personality is better preserved with fewer negative symptoms
▪ Cognitive deficits are very mild, and progression is slow over time.
Factors associated with paraphrenia:
• Family history - although risk in first degree relatives is reduced compared with early
onset schizophrenia. While the lifetime risk of the more typical early-onset
schizophrenia for first-degree relatives of patients is around 10 per cent and does not
seem to reduce with increasing age at onset up to about 50 years, the first-degree
relatives of patients with very-late-onset (> 59 years) schizophrenia-like psychoses do
not have an elevated lifetime morbid risk compared to healthy, aged control subjects.
• Other features include:
▪ Female gender
▪ Hearing loss
▪ Visual impairment
▪ Social isolation
▪ Brain disease
▪ Not marrying (may be a weak factor)
▪ Schizoid and paranoid personalities
Rates of white matter hypertensities are not increased unlike late-onset depression.

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Paranoid and schizophrenia-like psychoses can complicate AD or DLB, but in such cases
disorders of memory and concentration can generally clearly be seen to have preceded the
emergence of persecutory symptoms. Many patients with psychoses that begin in old age
have subtle and apparently only slowly progressive cognitive deficits; these do not
constitute dementia and are not the same as schizophrenic negative symptoms, but seem
to be more significant than the cognitive symptoms that accompany early-onset
schizophrenia. Even the most cognitively intact of these patients appear to be impaired on
‘executive’ cognitive functions such as attention set-shifting ability and planning.
There tends to be a poorer response to antipsychotic treatment. Lower doses are required
(10-20% of general adult dose). The risk of tardive dyskinesia is significantly higher in the
elderly34.
V. NEUROTIC DISORDERS

Both prevalence and incidence of most anxiety disorders seem to be lower in old age. In
patients over 65 the prevalence is:
▪ Social phobia – 1%
▪ Simple phobia – 4%
▪ Generalised anxiety disorder – 4%
▪ OCD – 0.1-0.8%
▪ Agoraphobia – 1.4-7.9%
Panic disorder is unusual in old age, and a first onset presentation should always prompt
a search for an underlying physical or depressive disorder (Flint and Gagnon 2003).
Symptoms of anxiety in the elderly are often non-specific with features of both anxiety
and depression. Hypochondriacal symptoms may be prominent (Lindesay 2000).
Remember that in the elderly, anxiety symptoms are often associated with physical
disorders, and the assessment of an anxious patient should always include a thorough
physical examination. Symptoms of anxiety can also be caused by prescribed drugs such
as oral hypoglycaemics and corticosteroids.
The clinical features, aetiologies and treatments vary little as compared to those used in
younger adults, although cautious use of medication is recommended.
VI. SUBSTANCE MISUSE

About half of the over-65 age group drink alcohol and the prevalence of misuse and
dependence decreases with age. Elderly people with alcoholism who were dependent in
younger life have different characteristics to those who started drinking in later life.
Early-onset drinkers tend to have a family history of alcohol misuse, a history of smoking
and a higher alcohol intake. Late-onset drinkers are more likely to have an obvious
precipitant for their drinking e.g. bereavement or physical illness, a milder, more
circumscribed drinking problem and greater premorbid psychological stability.

34 Jeste et al 1995

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Risk factors for late-onset alcohol misuse include female gender and higher socio-
economic class. Older adults have an altered distribution and increased blood alcohol
levels for a given dose of alcohol and ageing organs are less able to withstand the toxic
effects of alcohol. Presentation can be with falls, drowsiness, delirium, depression, self-
neglect or poor control of comorbid conditions such as hypertension or diabetes.
Acute alcohol withdrawal is often more severe in the elderly compared with younger
patients. Increased caution is needed with benzodiazepine treatment for withdrawal and
out-patient detoxification may not be appropriate. With relapse prevention, it is
recommended that disulfiram should be used cautiously and only for short term usage
due to the risk of precipitating an acute confusional state. Compared with disulfiram,
acamprosate has a benign side-effect profile and is less likely to cause dangerous drug
interactions. It is also more effective for those with liver damage. As with younger adults,
psychological treatments include psychoeducation, counselling and motivational
interviewing.
In the ECA study in the USA, among participants over the age of 55, the prevalence of
alcohol use disorders was 1.5 times greater among people with mild and severe cognitive
impairment than those with no impairment (George et al, 1991). It has been reported that
there is increased occurrence of all types of dementia except Alzheimer’s disease in elderly
people with alcohol use disorders (Thomas & Rockwood, 2001).
Dependence on other substances tends to be more related to prescribed medication such
as benzodiazepines. However other ‘street’ drug misuse and dependence in the elderly
may be more of a problem in the future due to the cohort effect of its increasing
prevalence in younger adults.
VII PERSONALITY DISORDERS

A meta-analysis found the prevalence of personality disorders in the over 50s was 7-10%.
The prevalence of personality disorders decreases with increasing age (Abrams and
Horowitz, 1996). This appears to be largely due to a reduction in the cluster B group.
There are a number of reasons postulated for this pattern, including maturation of
personality and reduction in problematic behaviours associated with the personality
disorder. However, obsessive-compulsive and schizoid characteristics may become more
prominent (Engles et al 2003). Schizoid and paranoid traits may become more pronounced
due to isolation, and can be mistaken for delusional disorder or schizophrenia.
Personality disorder as a co morbid condition appears to be significantly more common in
patients hospitalised for depression than in those hospitalised for disorders of cognition
(Kunik et al 1994). As with younger patients, personality disorder is likely to be
associated with a poorer prognosis. Personality disorder may be a risk factor for late-life
depression.
Diogenes syndrome (aka senile squalor syndrome) is characterised by severe self neglect,
neglect of surroundings, social withdrawal and isolation. No medical or psychiatric illness
can account for this. Syllogomania also occurs (the hoarding of rubbish).
Diogene’s syndrome can be precipitated by stressful life events. It has also been suggested
that the syndrome represents the end-stage of a personality disorder or that there may be

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a degree of frontal lobe impairment. Dementia, psychosis and depression must be

excluded.
Management is notoriously difficult. Moreover, 46% of patients have a 5 year mortality rate.
Hospitalisation has to be avoided whenever possible, due to a high mortality rate following an
admission, and ambulatory treatment and social measures should be favoured. (Hanon et al.
Diogenes syndrome: a transnosographic approach35.

35 Encephale. 2004 Jul-Aug;30(4):315-22

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VIII. DELIRIUM

Delirium (acute confusional state) in the elderly is common but prevalence varies
depending on the situation.
▪ 10-20% in elderly medical admissions
▪ 5-15% in nursing homes
▪ 37% incidence post-operatively
Patients who develop delirium have high mortality, institutionalisation and complication
rates, and have longer lengths of hospital stays than non-delirious patients. Patients with
delirium are also three times more likely to develop dementia, even if they have no prior
cognitive or functional impairment36. This highlights the importance of early recognition
and management. Delirium may be unrecognised by doctors and nurses in up to two-
thirds of cases!37.
The National Guidelines38 on the prevention, diagnosis and management of delirium in
older people subdivide delirium into two types:
1. Hyperactive delirium – characterised by increased motor activity with agitation,
hallucinations and inappropriate behaviour
2. Hypoactive delirium – characterised by reduced motor activity and lethargy. This
is the commonest type and also carries a poorer prognosis.
It is important to differentiate delirium from dementia, as the presentation can be similar.
In summary the main features of delirium include:
▪ Clouding of consciousness
▪ Altered sleep-wake cycle
▪ Over-/underactivity
▪ Fluctuating consciousness level and symptoms (often worse at night)
▪ Muddled thinking with ideas of reference and poorly elaborated persecutory
beliefs
▪ Visual illusions, misinterpretations and hallucinations
▪ Impaired registration, retention and recall
▪ Impaired concentration
▪ Disorientation to time, then place, then person
▪ Early loss of insight
▪ Anxious/irritable/depressed/perplexed mood
Risk factors for delirium include
▪ Increasing age
▪ Dementia (patients with dementia are five times more likely to develop delirium)
▪ Admission with infection or dehydration
▪ Physical frailty

36 Rockwood et al. Ageing 1999;28:551-6

37 Foreman M et al. Primary Psychiatry 2004;11:46-50
38 The prevention, diagnosis and management of delirium in older people. National Guidelines (June 2006).
Clinical Effectiveness and Evaluation Unit. Royal College of Physicians

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▪ Surgery e.g. fractured neck of femur

▪ Visual impairment
▪ Pain
▪ Poly-pharmacy

There are many potential causes for delirium: infective, withdrawal, metabolic, trauma,
CNS pathology, hypoxia, vitamin deficiency, endocrine, vascular and toxic.

Patients at high risk should be identified on admission. Up to a third of delirium is

preventable. Many patients with delirium cannot provide an accurate history, therefore
wherever possible a collateral history should be sought. Do not forget to complete a
MMSE.

A full physical examination should be carried out and investigations should consist of the
following: FBC, CRP, U&Es, LFTs, TFTs, Bone profile, Glucose, MSU. Consider CXR/
blood cultures/ECG depending on findings of physical examination.

Other investigations may be indicated, again according to the history and examination.
These include:
CT head – Indications for the use of CT are:
• Focal neurological signs
• Confusion post head injury
• Confusion developing after a fall
• Evidence of raised ICP
EEG – Although EEG is frequently abnormal with delirium, routine use as a diagnostic
tool has not been fully investigated. EEG usually shows diffuse slowing. An EEG may be
useful for
• Differentiating delirium from dementia
• Differentiating delirium from non-convulsive status epilepticus and TLE
• Patients who may have a focal intracranial lesion presenting as delirium.

Lumbar puncture – routine LP is not useful in identifying cause for delirium. It should be
reserved for
• Meningism
• Headache and fever

Management should consist of

1. Treatment of the underlying cause, bearing in mind that this is often
multifactorial.
2. Management of confusion
a. Environment – appropriate lighting levels, use of clocks and calendars for
orientation, familiar nursing staff etc
b. Wandering – close observation, least restrictive option, identifying any
reasons for agitation (e.g. pain, thirst, need for toilet).
c. Sedation – Keep the use of sedatives and major tranquillisers to a
minimum.

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Paper B: Older Adult Psychiatry

3. Appropriate follow-up- Many patient with delirium have an underlying dementia

which may require F/U by the Older Adult Psychiatry services.
REFERENCES:

▪ Shorter Oxford Textbook of Psychiatry – fifth edition. Gelder, Mayou, Cowen.

Oxford University Press. 2006.
▪ Maudsley Prescribing Guidelines – 12th Edition
▪ Essential Revision Notes for the MRCPych. Fear. Pastest. 2004.
▪ Psychiatry in the Elderly – Third Edition. Jacoby, Oppenheimer. Oxford University
Press. 2002.
▪ New Oxford Textbook of Psychiatry. Gelder, Lopez-Iber Jr, Andreasson. Oxford
University Press. 2000.
▪ Companion to Psychiatric Studies – Eigth Edition. Churchill Livingstone. 2010.
▪ Dementia – Third Edition. Edited by Alistair Burns. 2005.
▪ The prevention, diagnosis and management of delirium in older people. National
Guidelines (June 2006). Clinical Effectiveness and Evaluation Unit. Royal College of
Physicians.

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