CLINICAL DIAGNOSIS AND TREATMENT OF NEUROCOGNITIVE DISORDERS

Doc Wamcie Chua

DOMAINS OF COGNITION ETIOLOGY

 Memory  Post-operative delirium
 Language o CNS disease
 Orientation o Systemic disease
 Judgment o Intoxication or withdrawal from pharmacologic or
 Conducting interpersonal relationships toxic agents
 Performing actions o Stress of surgery
o Postoperative pain
 Problem solving
o Insomnia
o Pain medication
NEUROCOGNITIVE DISORDERS
o Electrolyte imbalance
 Disruption in one or more domains o Infection
 Patient may also present with Behavioral symptoms o Fever
o Blood loss
DELIRIUM
 Acute onset RISK FACTORS
o The patient could be okay this morning then all of a When consulting on an inpatient with any of the following
sudden would present with behavioral changes risk factors, it is clinically helpful to assume delirium is
during lunch time or in the afternoon present until proven otherwise, regardless of the presenting
 Fluctuating or waxing and waning course psychiatric complaint.
o MSE may be within normal limits in the morning but
in the afternoon would present with agitation, RISK FACTORS
hallucinations, nor oriented, etc  Advanced age (65 and older)
o Lucid intervals: there are times when the patient is  Pre-existing brain damage (e.g. dementia, schizophrenia)
devoid of any symptoms  History of delirium, depression
 Hallmark symptom - impairment of consciousness,  Alcohol dependence
usually occurring in association with global impairments  Diabetes, Cancer, Stroke, Renal/Hepatic Disease
of cognitive functions
 Functional dependence (immobility, falls, low level of
 Syndrome not a disease activity)
 Many causes, may be multifactorial  Sensory impairment (hearing, visual)
 Poor prognostic sign: “harbinger of death”  Dehydration, Malnutrition
o Medical management should be more aggressive
 Fever or hypothermia
 Hypoalbuminemia
ETIOLOGY  Azotemia
 Another Medical Condition  Treatment with psychoactive drugs/substance abuse
 Substance-Induced  Polypharmacy
 Multiple causes
 Delirium NOS (not otherwise specified) PREDISPOSING FACTORS (TABLE 21.2-3)
 Demographic characteristics
EPIDEMIOLOGY o Age 65 years and older
 10 – 30% of medically ill patients o Male sex
 Highest rate in post cardiotomy patients (>90%)  Cognitive status
 80% of terminally ill patients o Dementia
o Cognitive impairment
POPULATION PREVALENCE o History of delirium
RATE (%) o Depression
Institutionalized elderly 44  Functional status
General medical in-patients 10-30 o Functional dependence
Cardiac surgery patients 16-34 o Immobility
Orthopedic surgery 33 o History of falls
Terminally ill cancer patients 23-28 o Low level of activity
Critical care unit patients 16  Sensory impairment
Medical and surgical in-patients 5-15 o Hearing
o Visual
 Decreased oral intake
o Dehydration
o Malnutrition

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 Drugs PATHOPHYSIOLOGY
o Treatment with psychoactive drugs  Acetylcholine (RAS)
o Treatment with drugs with anticholinergic properties  Reticular formation
o Alcohol abuse  Dorsal tegmental area
 Coexisting medical conditions  Mesencephalic reticular formation -> tectum -> thalamus
o Severe medical diseases  Hyperactivity of the locus ceruleus
o Chronic renal or hepatic disease  Noradrenergic neurons
o Stroke  Serotonin
o Neurological disease
 Glutamate
o Metabolic derangements
o Infection with human immunodeficiency virus
DIAGNOSIS AND CLINICAL FEATURES
o Fractures or trauma
o Terminal diseases CORE FEATURES
 Altered consciousness
 Altered attention
 Impairment in other realms of cognitive function
 Decreased memory
 Rapid onset
 Brief duration
 Marked, unpredictable fluctuations
o There’s no particular pattern of when the lucid
intervals will occur

ASSOCIATED FEATURES
 Disorganized thought process
 Perceptual disturbances: usually visual
 Psychomotor hyperactivity (agitated) or hypoactivity
(mistaken for patients experiencing depression)
 Disruption of sleep-wake cycle
o Asleep in the morning, awake at night (sundowning)
o Most cases of delirium are referred at night
 Mood alterations: e.g. mood swings

 Delirium does not always present as blatant cognitive

deficits or agitation. It may be subtle and surreptitious in
onset
o E.g. in hypoactive type of delirium, the patient is
quiet, socially withdraw, w/ increased sleeping time
o However, unlike depression (unless with suicidal
tendencies), delirium is an emergency psychiatric
referral. The difference in time before they are
referred could also spell the difference in mortality,
morbidity, and the person staying alive.
 Unpredictable, fluctuating alertness and clouded sensory
awareness sound more recognizable on paper than they
are at the bedside
 Obvious cognitive problems occur in only about 30% of
consultations
 Other presentations are the rule
o 20%, anxiety or depression is the main feature
o 20%, hallucinations or delusions
o 20%, inappropriate behavior (e.g. irascibility,
uncooperativeness, attempts to leave against
medical advice)

DIAGNOSIS
 In the elderly, regardless of the setting, the onset of
confusion should trigger concern about infection
o Rule out an organic cause first
 Urinary tract infections (UTIs) and pneumonias are
among the most common infections in older patients
 When bacteremia is associated with a UTI, confusion is
the presenting feature nearly one third (30%) of the time
 A psychiatric etiology may be proposed “by default”
when no medical cause is obvious (e.g. “psychotic
depression,” insomnia-induced psychosis, and
schizophrenia in Cases 1,2,3 respectively)

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 Maintain diagnostic vigilance when there is no straight-
forward explanation for the delirious state, particularly
when the etiology seems “a little of this, a little of that.”
For example, the combination of a urinary tract infection
and a low-grade fever may not be dramatic, but it can
devastate the brain functioning of a debilitated patient,
as in case 1
 Observe over time: monitor MSE every 1-2 hours
o “Hit and run” consultation if fraught with potential
mistakes
o One cross-sectional interview may coincide with a
lucid state, concealing the disordered sensorium.
Collection of longitudinal data from many sources
provides the best method for diagnosis
 The DRS-R-98 is probably the most widely used
instrument for bedside screening and research in
delirium
o This instrument is a 16-item clinician-rated scale
divided into two sections: 3 diagnostic items for
initial ratings and a 13-item severity scale for
repeated measurements
o The scores from both groups of questions are added
together to arrive at a total score
o Total scores in excess of 18 are highly suggestive of
the presence of delirium
 Neuro exam
 MSE
 MMSE/MoCA
 Laboratory work up
DIFFERENTIALS
DEMENTIA
 Time to develop the condition: chronic
 Fluctuation in the level of attention
 Beclouded dementia: patients that with dementia that
develop delirium when they are hospitalized
SCHIZOPHRENIA OR DEPRESSION
 No change in level of consciousness
 Hallucinations and delusions more constant and better
organized
o Schizophrenia: hallucinations are usually auditory
o Dementia: hallucinations usually match the theme of
their sadness
COURSE AND PROGNOSIS
 Prodromal symptoms may occur
 Symptoms persist as long as causally relevant factors are
present
o The key to the management of delirium is to address
whatever is causing the delirium aggressively
 Symptoms usually recede over a 3-7 day period (2 weeks)
 Older patient -> longer time delirious -> longer time to
resolve
 Recall is spotty
TREATMENT
 Treat the underlying cause
 Provide physical, sensory and environmental support
 Psychosis and insomnia -> pharmacotherapy
 Haloperidol IV -> oral
 Advance directives
 Health care proxy
 When agitation accompanies delirium in the medical
setting, short-term use of antipsychotics remains the
treatment of choice
 No clear guidelines exist for the specific choice of
antipsychotic agents. Haloperidol alone or in
combination with lorazepam remains the most widely
used treatment for the agitation of delirium
 However, the atypical antipsychotics have gained use for
delirium, particularly for patients at risk for
extrapyramidal side effects
 For delirium, the goal of psychiatric treatment is
twofold:
o To completely calm (not obtund) an agitated,
delirious patient at the outset (rather than partially
control or barely keep up with agitation over several
days) so that the etiology of the delirium can be
diagnosed and corrected
o To normalize sleep disruption (which is a
consequence of delirium, not a cause of it)
 The strategy for treating delirium is to calm the patient
completely during the first day, later slowly tapering the
medication as the delirium clears
 For highly agitated patients, the choice of medications
may be limited to those with intramuscular forms
 On day 1, medication is titrated against agitation in a
stepwise fashion. Avoid obtunding the patient
o Dose 1: titrate antipsychotic to severity of agitation
(wait 15-30 minutes)
o Dose 2: If patient is still agitated, repeat the
antipsychotic at ≥ dose 1 (wait another 15-30
minutes)
o Dose 3 and thereafter: Repeat antipsychotic at ≥
dose 2 over the next few hours, until the patient is
no longer agitated
 Standing medication: repeat day 1 grand total, in divided
doses, morning, afternoon, evening, with the largest at
bedtime (e.g. if day 1 grand total was 15mg, recommend
3mg three times during the day and 6mg at bedtime)
 Days 3-7: Goal is to slowly taper the antipsychotic
o Titrate to mental status findings (e.g. reduce dose by
50% every 24 hours)
 Benzodiazepines with active metabolites should be
avoided in the setting of delirium
o The slow progressive accumulation of active
metabolites occurring with long-acting agents like
diazepam (t1/2=20-100 hours) or chlordiazepoxide
(t1/2=30-100 hours) produces cumulative CNS
toxicity in delirious patients, especially the elderly
 Benzodiazepines without active metabolites (e.g.
lorazepam, clonazepam) may be used in combination
with antipsychotics to sedate agitated, delirious patients
 The non-benzodiazepine medication zolpidem
specifically target the receptors mediating sleep, so they
have fewer effects than the benzodiazepines on motor
and respiratory function. There are no controlled studies
on their use in delirious patients
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 Barbiturates cause both rapid eye movement (REM)
suppression and respiratory depression. Avoid using
them in delirious patients
 Anticholinergic and antihistaminic medications such as
diphenhydramine and phenothiazines such as
chlorpromazine (Thorazine) potentially worsen the
confusion of delirium. Avoid using them as hypnotics in
delirious patients.
 Risperidone: several cases reports of the use of
risperidone specifically with delirious patients have
shown few side effects and good efficacy with 0.5-1.0mg
of risperidone twice daily
 Olanzapine: one controlled study found that oral
olanzapine was as effective as haloperidol in controlling
delirium-associated agitation, with fewer extrapyramidal
side effects and less sedation. An open, prospective trail
of olanzapine for the treatment of delirium in a sample
of hospitalized cancer patients also showed it to be safe
and efficacious
 The most common side effect was sedation. No patients
on olanzapine therapy developed extrapyramidal side
effects. The most powerful predictor of poor response to
this medication was age over 70 years
 Quetiapine has been safely and effectively used at low
doses (25-50mg) for the management of delirium
 Management of sundowning:
o Normalizing sleep-wake cycle disturbances has high
therapeutic priority. No one agent has been proven
to be consistently superior to others in treating
insomnia in the medically ill
 Non-pharmacologic treatment
o Hospital rooms with windows, calendars, clocks, and
a few mementos from home on the walls
o Soft and low lighting at night helps sundowners
o Supportive family in attendance reassures and
reorients the patient
o Restraints are also quite useful to protect patients
from inflicting harm on themselves or staff.
DEMENTIA
 Major neurocognitive disorder
 Progressive
 Impairment in cognitive functions
 Clear consciousness
 Global impairment of intellect
o Memory
o Attention
o Thinking
o Comprehension
TYPES
 Alzheimer’s type
 Vascular
 Other medical conditions
 Substance induced
 Multiple etiologies
 NOS
EPIDEMIOLOGY
 50 – 60%: Alzheimer’s type (most common cause)
 2nd most common: Vascular dementia
o 60 – 70 y/o
o women>men
 >65 y/o
o Alzheimer’s
o Vascular
o Mixed vascular and Alzheimer’s dementia
ETIOLOGY
DEMENTIA OF THE ALZHEIMER’S TYPE
 Diagnosed when other causes have been excluded
 Hallmark: amyloid deposit
 Classic pathognomonic microscopic findings:
neurofibrillary tangles, senile plaques, neuronal loss
(cortex and hippocampus), synaptic loss, granulovascular
degeneration of neurons
 Hypoactivity of acetylcholine and norepinephrine
 Parietal-temporal distribution
VASCULAR DEMENTIA
 Multi-infarct dementia
 Pre-existing hypertension or cardiovascular risk factors
 Affects small to medium-sized cerebral vessels
PICK’S DISEASE
 Fronto-temporal atrophy
 Pick’s bodies in post-mortem specimens
 Behavioral and personality changes early on
 Otherwise, similar to Alzheimer’s
LEWY BODY DISEASE
 Similar to Alzheimer’s, with hallucinations, parkinsonian
features and EPS
HUNTINGTON’S DISEASE
 Is classically associated with the development of
dementia
 Subcortical type (more motor abnormalities)
 Psychomotor slowing and difficulty with complex tasks
PARKINSON’S DISEASE
 Disease of the basal ganglia
 Associated with dementia and depression
 20-30% have dementia
 Slowed movement paralleled with slow thinking:
bradyphrenia
HIV-RELATED DEMENTIA
 Encephalopathy in HIV infection
 AIDS dementia complex or HIV dementia
 Paralleled by the appearance of parenchymal
abnormalities in MRI scans
HEAD TRAUMA RELATED DEMENTIA
 punch-drunk syndrome (in boxers)
 AKA dementia pugilistica
 Emotional lability, dysarthria, impulsivity
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POSSIBLE ETIOLOGIES OF DEMENTIA (TABLE 21.3-1) PSYCHIATRIC AND NEUROLOGICAL CHANGES
 Personality – introverted, less concerned
 Hallucinations and delusions
 Mood
 Cognitive change – aphasia, apraxia, agnosia
 Catastrophic reaction – “abstract attitude”
o Difficulty generalizing from a single instance, forming
concepts, and grasping similarities and differences
among concepts
o Compromised ability to solve problems, to reason
logically, and to make sound judgments
 Sundowner syndrome
o Drowsiness, confusion, ataxia, and accidental falls
o When external stimuli, such as light and
Pseudodementia: Memory problems presenting in patients interpersonal orienting cues, are diminished
with major depressive disorder
COURSE AND PROGNOSIS
PSEUDODEMENTIA DEMENTIA  There is no cure for dementia
CLINICAL COURSE AND HISTORY  Gradual deterioration over 5 – 10 yrs -> death
 Family always aware of  Family often unaware  Subtle signs -> progress -> “empty shells” of their former
dysfxn & severity selves
 Onset can be dated with  Dated within broad limits
some precision DIAGNOSIS
 Sxs of short duration  Long duration before  Laboratory tests: complete blood count (CBC), electrolyte
before medical consult consult and metabolic panels, B12 and folate levels, rapid plasma
 Rapid progression after  Slow progression regain titer, urinalysis; urine toxicology, if indicated
onset  More specific tests depending on history and pattern of
 Hx of previous psychiatric  Hx of previous dysfxn cognitive deficits such as erythrocyte sedimentation rate,
dysfxn common unusual antinuclear antibodies test, Lyme titer, antiphospholipid
COMPLAINTS AND CLINICAL BEHAVIOR syndrome test, anti-Hu antibody test
 Complain of much  Little cognitive loss  Other tests: electrocardiogram, chest x-ray (if indicated),
cognitive loss test for human immunodeficiency virus, computed
 Complaints of cognitive  Complaints usually vague tomography (CT) of head-to rule out recent bleed or
dysfxn detailed mass lesion, normal-pressure hydrocephalus
 Emphasize disability  Conceal disability
 Highlight failures  Delight in TREATMENT
accomplishments  Verification of diagnosis
 Little effort to perform  Struggle to perform tasks o Order laboratory exams to rule out medical problems
even simple task  Rely on notes, calendars, that may cause dementia or dementia-like symptoms
etc to keep up (reversible dementia) such as neurosyphilis, normal
 Strong sense of distress  Often appear pressure hydrocephalus
unconcerned  Pharmacological agents
 Affective change often  Affect labile and shallow  Donepezil, rivastigmine, galantamine, and tacrine are
pervasive cholinesterase inhibitors used to treat mild to moderate
 Loss of social skills early  Social skills retained cognitive impairment in Alzheimer’s disease
and prominent o They reduce the inactivation of the neurotransmitter
 Behavior incongruent  Compatible with severity acetylcholine -> potentiate the cholinergic
with severity of cognitive of dysfxn neurotransmitter -> modest improvement in
dysfxn memory and goal-directed thought
CLINICAL FEATURES o These drugs are most useful for persons with mild to
 Attention & concentration  Attention and moderate memory loss who have sufficient
preserved concentration faulty preservation of their basal forebrain cholinergic
 “Don’t know”  Near-miss answers neurons to benefit from augmentation of cholinergic
frequent neurotransmission
 Memory loss for recent  Memory loss for recent o Donepezil is well tolerated and widely used
and remote events events > remote events o Tacrine is rarely used because of its potential for
usually severe hepatotoxicity
 Memory gaps for specific  Memory gaps unusual o Fewer clinical data are available for rivastigmine and
periods or events galantamine, which appear more likely to cause
common gastrointestinal (GI) and neuropsychiatric adverse
 Marked variability in  Consistently poor effects than does donepezil
o None of these medications prevents the progressive
performance of tasks of performance
neuronal degeneration of the disorder
similar difficulty
 Memantine protects neurons from excessive amounts of
 First type of memory affected in dementia:
glutamate, which may be neurotoxic
immediate memory
o The drug is sometimes combined with donepezil. It
has been known to improve dementia
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 Other drugs being tested for cognitive-enhancing activity
include general cerebral metabolic enhancers, calcium
channel inhibitors, and serotonergic agents
 Some studies have shown that selegiline, a selective type
B monoamine oxidase (MAO-B) inhibitor, may slow the
advance of this disease
 Ondansetron, a 5-HT3 receptor antagonist, is under
investigation
 Estrogen replacement therapy may reduce the risk of
neurocognitive decline in postmenopausal women;
however, more studies are needed to confirm this effect
 Complementary and alternative medicine studies of
ginkgo biloba and other phytomedicinals are required to
see if they have a positive effect on cognition
 Reports have appeared of patients using non-steroidal
anti-inflammatory agents having a lower risk of
developing Alzheimer’s disease
 Vitamin E has not been shown to be of value in
preventing the disease
TREATMENT OF DEMENTIA-RELATED BEHAVIORAL
PROBLEMS
 For symptom management in dementia, a multimodal
approach using behavioral and pharmacological
treatments ensures optimal results
o Many symptoms of dementia, including wandering,
perseverative behavior, and impaired social skills, do
not respond to medications and may even be
exacerbated by them
o When at all possible, use non-pharmacological
interventions to deal with symptoms, to avoid
unnecessary side effects form medications as well as
polypharmacy
 Agitation is not a diagnostic term, but rather is often
used to describe a cluster of behaviors including
repetitive verbal, vocal, or motor activity that is
disruptive to others
 Some behaviors are best managed with non-
pharmacological treatment
 Others-especially those that are distressing or
threatening harm to the patients and others-may
warrant pharmacological intervention
 Etiology of the above behaviors is often multifocal and
may include cognitive impairment, pre-existing
psychiatric illness, medical disorders and their treatment,
pain, and functional disability
 When called regarding an “agitated” patient, first
determine the disturbance in behavior and then begin to
investigate potential cause
 Potentially reversible common causes of agitation-such
as urinary tract infections, constipation, chronic pain,
initiation of new medications, a recent change in
environment or withdrawal from alcohol, and illicit drugs
or medications-must be appropriately evaluated and
treated first
 Sensory interventions include music therapy,
aromatherapy, bright-light therapy (in the evening for
sundowning, in the morning for agitation with sleep
dysregulation), examination of glasses, dentures, and
hearing aids, pain assessment, and light exercise to
promote regularity and a sense of well-being
 Environmental strategies include promoting personal
space for patients, reducing disruptive stimuli such as
noise from other patients, loudspeakers, and
equipment/machinery, providing safe venues for
wandering, and pet therapy
 Behavioral approaches include providing praise and
encouragement for positive behavior, redirecting
negative behavior, reality orientation, and approaching
the patient in a calm, soft-spoken manner rather than a
confrontational, seemingly punitive one
 Medication may be necessary when
o Non-pharmacologic treatments do not work
o Reversible causes for the behavioral disturbances
have not been found, and/or
o The symptoms are dangerous or distressing to the
patient or others
 Medicating the psychiatric symptoms of dementia
requires a delicate hand. Starting doses should be
reduced to ¼ to ½ of the starting dose to those given to
younger adults; each increase in dose should be small,
and longer periods should elapse between increases
 Avoid anticholinergic medications that can promote
confusion and worse preexisting symptoms such as
urinary retention or blurry vision
 All elderly patients, but particularly those with dementia,
are particularly prone to extrapyramidal side effects
 Psychosis: delusions, hallucinations, and other types of
psychosis may be treated with atypical antipsychotics
such as olanzapine, quetiapine. Watch for excessive
sedation, parkinsonism, and the tendency to fall
 Mood: in assessing possible depression, take note that
patients with dementia may be apathetic rather than
truly depressed
 Use antidepressants such as selective serotonin re-
uptake inhibitors (SSRIs), mirtazapine, or venlafaxine
for depression, with or without irritability and anxiety
 Common side effects of antidepressants include
gastrointestinal upset, headache, falls, sedation, or
activation and possible increased blood pressure,
hyponatremia, and tremor
 Lability and impulsivity: use mood stabilizers such as
valproic acid or carbamazepine. Side effects include
sedation, ataxia, tremor, thrombocytopenia/anemia and
liver function test abnormalities, and leukopenia.
Monitor CBC, liver function, and drug levels
 Use atypical antipsychotics such as olanzapine,
quetiapine, for in patients with mood lability and
concurrent psychosis
 Lithium is potentially problematic because of the
vulnerability of elderly patients to dehydration-induced
toxicity and drug-drug interactions
 Anxiety: same medications used for depression may be
used for anxiety
o If possible, avoid benzodiazepines which can worsen
confusion, cause paradoxical agitation, and increase
risk of falls and respiratory suppression
 Insomnia, nocturnal confusion, and interrupted sleep
commonly occur in dementia
 Simple sleep hygiene may suffice if sleep dysregulation is
mild or does not cause disruption to family/caregiver,
especially if the risk of medication side effects outweighs
the sleep problem
 Sleep hygiene includes regular sleep and waking times,
restricted caffeine intake, limited napping, regular
exercise and social stimulation during the day, avoidance
of fluids in the evening, and soothing bedtime rituals
 Occasionally, medical causes of sleep dysregulation-such
as sleep apnea-require attention
 Psychosocial therapies
o Psychoeducation
o Supportive psychotherapy
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 AMNESTIC DISORDER
 Major or minor neurocognitive disorder
 Impairment in memory as the major sign and symptom
 3 categories:
o Caused by Medical Condition
o Caused by Toxin or Medication (eg., marijuana,
diazepam)
o NOS
ANATOMY
 Dorsomedial and midline nuclei of the thalamus
 Hippocampus
 Mamillary bodies
 Amygdala
 Usually bilateral damage
 Left>right
DIAGNOSIS
 Inability to learn new information
 Inability to recall previously learned information
 Memory disturbance causes significant impairment
 Short term and recent memory are usually impaired
ETIOLOGY
KORSAKOFF’S SYNDROME
 Caused by thiamine deficiency
 Mostly associated with poor nutritional habits
 Often associated with Wernicke’s encephalopathy -
confusion, ataxia, and ophthalmoplegia
 Although delirium clears up within a month or so, the
amnestic syndrome either accompanies or follows
untrated Wernicke’s encephalopathy (85%)
 Symptoms: confabulation, apathy, passivity
 Associated symptoms: change in personality, executive
function deficits
 Onset is gradual
 Recent memory tends to be affected more than remote
memory
ECT (ELECTROCONVULSIVE THERAPY)
 Retrograde amnesia for a period of several minutes
before the treatment
 Anterograde amnesia after the treatment
 Anterograde amnesia usually resolves within 5 hours
 Mild memory deficits may remain for 1 to 2 months after
a course of ECT treatments
 Symptoms are completely resolved 6 to 9 months after
treatment
TRANSIENT GLOBAL AMNESIA
 Abrupt loss of the ability to recall recent events or to
remember new information
 Characterized by mild confusion and a lack of insight into
the problem; a clear sensorium; and, occasionally, the
inability to perform some well-learned complex tasks
 Episodes last from 6 to 24 hours
Doc: Review list and discussion on the book regarding more
causes. So here we go!
CEREBROVASCULAR DISEASES
 Involves posterior cerebral and basilar arteries and their
branches -> hippocampus infarct -> amnestic disorder
 Infractions are rarely limited to the hippocampus; they
often involve other parts such as:
o Occipital and parietal lobes -> focal neurological
signs involving vison and sensory modalities
o Bilateral medial thalamus, particularly the anterior
portion -> amnestic disorder
 May also be due to rupture of an aneurysm of the
anterior communicating artery resulting in the infarction
of the basal forebrain region
MULTIPLE SCLEROSIS
 Involves formation of plaques within the brain
parenchyma
 If these plaques occur in the temporal lobe and
diencephalic regions -> memory impairment
 Most common cognitive complaints in patients with MS
involve impaired memory (40-60%)
 Digit span memory is normal, but immediate recall and
delayed recall of information are impaired
 Memory impairment can affect both verbal and
nonverbal material
ALCOHOLIC BLACKOUTS
 In persons with severe alcohol abuse
 Awake in the morning with a conscious awareness of
being unable to remember a period the night before
during which they were intoxicated
HEAD INJURY
 Both closed and penetrating injuries
 Retrograde amnesia leading up to the traumatic incident
and amnesia for the traumatic incident itself
 Severity of injury correlates with duration and severity of
the amnestic syndrome
 Best correlate of eventual improvement is the degree of
clinical improvement in the amnesia during the first week
after the patient regains consciousness
MANAGEMENT
 Course and prognosis depend on underlying cause
 Little improvement seen over time, no progression
o Acute amnesias
o Associated with head trauma
 Treat underlying cause
 Serve as auxiliary ego
 Psychoeducation
END OF TRANSCRIPTION
“You’re not a monster, Shallan,” Wit whispered. “Oh, child. The
world is monstrous at times, and there are those who would have
you believe that you are terrible by association.”
“I am.”
“No. For you see, it flows the other direction. You are not worse for
your association with the world, but it is better for its association
with you.”
-Oathbringer by Brandon Sanderson
Transcription Team 2019
Transcribed by: Sharmaine Tablada
References: Lecture ppt, recordings
Kaplan
Remarks: Those underlined
were underlined in
the ppt itself. Must
knows!
Smple cases 1-3
weren’t given yet.

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