Geri psych and neuropsych

DEMENTIA

Acquired, progressive impairment of cognition that interferes w social functioning but w/o clouding
of consciousness. Cardinal feature = memory impairment (STM worse than LTM). Common features
are: Sx present for 6m (of sufficient severity) + personality/behavioural change + cortical
(dysphasias/dyspraxias)/FND +/- psychosis (50%) + lack of insight (unless early on).

ASSESSMENT OF DEMENTIA

 Hx + O/E; cognitive testing (MMSE most widely used

screening) + others (Hopkins verbal learning test, CLOX to
complement MMSE). ACE-III for more in-depth testing.
 Baseline bloods in 1o care (to R/O treatable causes of
cognitive impairment) = FBC, electrolytes (including Ca2+),
LFTs, TFTs, ESR, B12/folate, syphilis, HIV, ANA.
 CXR (bronchial CA w cerebral mets)
 Refer to secondary care: memory clinic  CT scan (SDH,
NPH) + further Ix (LP, MRI, EEG, genetics if needed esp. if <
65y).

GENERAL MANAGEMENT

 Tx any reversible cause

 Non-pharm methods should be 1st; simple interventions (regular exercise, raise door handle =
prevent wandering; toileting routine for incontinence).
 Avoid anti-Q if possible (as worsens cognitive impairment, increases stroke risk, and sudden
death) If used, should only be ST (q6wk review).
 MDT employed  formal care plan.
 Social services – discuss social support e.g. meals-on-wheel, day care, respite admissions for
carers to cope.
 Environment = familiar, calm, lit, routine, clocks
 Psych Tx = aromatherapy, massage, reality orientation, music/art therapy, memory training,
reality orientation.
 Pharm Tx (cholinesterase inhibitors or NMDA R antagonists)
 Pay attention to CV RF to prevent dertrioration
 Tx exacerbation = pain, constipation, infection, deH2O; especially if sudden deterioration.
 Geri psych and neuropsych

 Tx depression (SSRI better tolerated), disturbed sleep, aggression

 Medico-legal:
1. DVLA: Dx should be informed 1st then decide if they can drive; cautioned risk of driving
(if assessed able to drive  new license for fixed 1-3 yrs; most tend to stop within 3 y of
Dx)
2. Capacity: to make specific decision. Are there advanced directives and DOL safeguards?
3. Palliative: advanced dementia  next of kin involved in decisions

AD

 MCC dementia (50-70%)

 4 As = amnesia, apahsia (e.g. nominal), agnosia (e.g. anosognosia), and apraxia (topographical or
dressing)
1. Subtypes:
 Memory trace laid down weakly
= harder to access; can retrieve if
reminded
 Complete failure to encode new
events (less common)
 Both types over time relentlessly
progress = affect language +
behaviour
 Pathology
1. Senile neuritic plaques in GM =
extracellular (b-amyloid core = may
cause amyloid angiopathy = ICH);
amyloid-beta is synthetized by cleaving
APP
2. NTFs = paired helical strands of
intracellular, hyper-phosphorylated tau = insoluble cytoskeletal elements; number of
tangles correlates w degree w dementia
3. Widespread cortical atrophy esp. basal forebrain (Meynert nucleus basalis – subcortical
ACh projections) and HIPPOCAMPUS (medial and superior temporal gyri). Narrowing gyri
and widening sulci.
4. Reduced ACh
 Dx = clinical (early memory failure, slow progression, and R/O other cause); aided by CT (multiple
infarcts), cerebral flow studies = parietal hypometabolism
 Genetics
1. ApoE2 = decreased risk sporadic form
2. ApoE4 = increased risk of sporadic form (2X risk htz + earlier)
3. APP, presenilin-1/2 = PSEN1/2 (familial 10%)  early-onset familial AD
 Down’s (APP is on Ch21)  middle age AD
 Other RF = homocysteinaemia (neurotoxic), age, females (slightly higher), obesity/DM, head
trauma (2X), latent HSV infection in patients w apoE4, Hx depression, ?Aluminium exposure
 Protective factors = statins, NSAIDs, HRT, high education (cognitive reserve), physical and mental
health (use it or lose it).
 Neuropsych co-morbidity= depression, paranoid delusions esp. theft, visual hallucinations,
personality change. Behaviours = wander, altered sleep, excess vocalisation
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 Some role of vascular dz in AD (co-exist).

 Treatment (sx, don’t cure) – NICE says:
1. Mild-moderate = acetylcholinesterase inhibitors e.g. Donepezil, Rivastigmine, and
Galntamine
 Roughly 6 month delay on cognitive decline
 S/E = N, dizziness, insomnia
2. Severe (or modeate if above C/I or intolerable)= NMDA receptor antagonist (prevents
Ca2+ excitotoxicity) = memantine
 S/E = dizziness, confusion, hallucinations
 Survival: 6-8 u.

VASCULAR

 2nd MCC (20-25%). Pure vascular 5-15% (over Dx); AD + vascular = 10-15%.
 Unequal distribution of deficits in higher cognitive functions w some affected and some
relatively spared. So memory can be markedly affected while thinking, reasoning, and
information processing may only show mild decline.
 Step-wise decline w late-onset memory impairment; early gait disturbance (small steps or
Parkinsonian), early urinary Sx, personality change/labile mood. Usually intact insight.
 Clinical evidence of focal brain damage – manifesting as at least 1 of:
1. Unilateral spastic weakness of limbs
2. Unilateral increased DTRs
3. Extensor plantar response
4. Pseudobulbar palsy.
 Hx (stroke profile), CV risk, tests.
 Dx: clinical
 Subtypes:
1. Post-stroke (20% within 6m), stroke-related
2. Single infarct v.s. multi-infarct (flea bitten appearance)
3. Subcortical = leukoariopathy = white matter changes = SMALL VSL DZ; middle of brain =
periventricular = shadows on MRI. Often due to metabolic (liver) and vascular causes 
disrupt communication  impairs cognition and memory. Neuro manifestations of poor
gait, balance, rigidity… all mental function LAGs
 Tx = maintain BP, reduce cholesterol (statins), ASA, cholinesterase inhibitors

LBD

 15% dementia of old age (3rd MCC). LBD is termed if dementia precede/concurrent motor Sx by
> 12 m.
 2 out of 3 to Dx:
1. Fluctuating cognition w pronounced variation in attention and alertness
2. Recurrent detailed visual hallucinations
3. Motor features of Parkinsonism
 Supporting features = repeated falls, syncope/TLOC, neuroleptic sensitivity (50%; and 2-3X
increased mortality), systematised delusions, hallucinations in other modalities
 Path: cerebral cortex deposited w Lewy bodies of a-synuclein; also Ub  lose ACh and DA
neurons  sensitive to neuroleptics
 Tx: cholinesterase inhibitors e.g. rivastigmine
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PARKINSON’S DEMENTIA

 PD triad = rigidity, rest tremor, and bradykinesia. Dx: if Parkinsonism Sx precede dementia by >
12 m. 1/3 of all PD patients.
 Cognitive decline can be from global dementia, focal deficit, drug-induced, or pseudo (depress)
 Higher risk of mood disorders (apathy, anxiety, dep), psychosis, and personality changes.
 Can have executive dysfunction (failure of attention and STM).
 Hx of REM sleep disturbance.
 MSA and PSP must be R/O.
 Avoid anti-Q if possible (but there is evidence for QUET and clozapine for psychotic Sx). L-DOPA
will not improve dementia, but cholinesterase inhibitors may.

FTD

 Spectrum of disease. 5% of all dementia. Disease only affecting the fronto-temporal lobe.
 Three patterns
1. Behavioural variant: early changes in personality and behaviour = apathy, loss of drive,
loss social inhibition, increased appetite for sweets (frontal lobe atrophy)
2. Progressive non-fluent aphasia: progressively difficult to generate speech
spontaneously, loss verbal fluency, preserved understanding (dominant temporal lobe
atrophy)
3. Semantic dementia: lack of knowledge of words and knowledge of world (bilateral
temporal lobe atrophy)
 Early primitive reflexes; memory usually relatively preserved. Early loss of insight.
 Slowly progressive + FHx. More common in women. Onset < 70.
 Path: 40-50% due to Ch17 granulin (PGRN) or tau (MAPT)  hyper-phosphorylated inclusions =
Pick’s bodies; the rest associated w TDP-43 (Ub). Imaging: atrophy of frontal + temporal lobes.
 Sensitivity to psychotropic (used w caution to Tx depressive or psychotic Sx)

NPH

 Triad = wet (urge incontinence) + wacky (cognitive impairment) + wobbly (ataxic gait)
 Hydrocephalus but NORMAL CSF pressure.
 50% idiopathic, 50% secondary to another cause e.g. SAH, meningitis, XRT, trauma
 Prognosis: potentially reversible
 Mgt: brain scan + LP (Dx & Tx); may require VP shunt.

PRION

 CJD – can be transmitted by blood, contaminated surgical instruments, and diet.

 vCJD – (“mad cow disease”)  younger adults.
 Gerstmann Straussler  familial CJD
 Pt: 1st prominent psychiatric Sx (depression, anxiety, personality change)  myoclonus/ ataxia/
akinesis + seizures  dementia  death within 12 months
 Path: abnormal protein folding that spreads its motif  vacuolation of glial cells = spongiform
 EEG: 1-2 Hz triphasic sharp waves w protein complexes; CSF: 14-3-3 protein.
 Tx: none.

ALCOHOL-INDUCED DEMENTIA

 Rare. Pt: visuospatial deficits

 Geri psych and neuropsych

 Path: atrophy WM and frontal lobes (EtOH dependence  dementia usually AD or vascular
dementia rather than this dementia!)
 Doesn’t improve w abstinence.

OTHER CAUSES

 Trauma (e.g. dementia pugilisitca)

 AIDS-dementia complex (usually “subcortical” dementia = slowing)
 Tumours (frontal lobe, ventricles III, corpus callosum)
 HD (caudate atrophy 1st then frontal lobe, Ch4 triplet CAG expansion  chorea, schizo-like
psychosis, and depression + irritable)
 MND
 Whipple’s (tropical disease dementia)
 Syphilis
 Metabolic and nutritonal dementia
 CADASIL

Neuropsychometric testing if: early dementia, atypical dementia, R/O or separate depressive illness,
monitor therapies.
 Geri psych and neuropsych

MILD COGNITIVE IMPAIRMENT

 Pre-dementia state.
 Memory impairment, new learning difficulties, reduced concentration  lose ability to multi-
task, or engage in new things.
 None of the Sx meets “caseness” of disorder (social or occupational functioning)
 > 2 week duration
 Progression is NOT inevitable… only 1/3 progress (?ageing)

Montreal Cognitive Assessment (MOCA)

 Visuospatial/executive (1A  2…; copy cube; draw clock)
 Naming
 Memory (read list of 5 words repeat after 5 minutes)
 Attention (forward/backward numbers; serial “As”)
 Language (repeat sentence; max # words beginning with F = fluency)
 Abstraction (similarity between 2 objects)
 Delayed recall w no cue
 Orientation (time, place)

MOCA is more discerning than AMTS (more subtle elements for higher-order patients)
Dementia = 16; MCI = 22; normal > 26

AMTS screen must be done to all > 75 y (score of < 7- 8 = cognitive impairment at that time).

Don’t forget:
 Statins
 Low (postural) BP
 Anti-cholinergics
 DM medications = high chance dementia if hypos
 Be careful of morphine
 Will never return to baseline
 Falls

PSEUDODEMENTIA
 Mimics dementia, can occur in pt with primary psych diagnosis
 9% < 65 referred to neuro for suspected dementia
 Association bet ween late life depression and subsequent cognitive impairment = 1/3 persistent
cognitive impairment
 DEPRESSION MCC = Hx of acute onset w no evidence memory loss or intellectual decline before
onset, often previohs Hx of depression/premorbid personality. Disproportionate concern w
memory problems, inconsistent Hx, “don’t know” as opposed to giving wrong or vague answers!
Geri psych and neuropsych
 Geri psych and neuropsych

DELIRIUM (ACUTE CONFUSIONAL STATE)

 10 hospitalised patient (up to 50% elderly)  1.1% aged over 55

 ICD-10 criteria
1. Impairment of consciousness and attention (on a continuum from clouding to coma;
reduced ability to direct, focus, sustain, and reduced attention  “count down from 20
to 1”)
2. Global disturbance of cognition (perceptual distortions, illusions, and hallucinations –
mostly visual; impairment of abstract thinking and compression + delusions – usually
transient persecutory, but some incoherence; impairment of immediate recall and
recent memory w intact remote memory; disorientation for time as well as place and
person  “tell me how long the interview has been going on for?”)
3. Psychomotor disturbance (hypo- or hyperactivity and unpredictable shifts from 1 to the
other; increased reaction time; increased or decreased flow of speech; enhanced startle
reaction)
4. Disturbance of sleep-wake cycle (insomnia, or in severe cases – total sleep loss or
reversal of cycle; daytime drowsiness, nocturnal worsening = sun-downing; disturbing
dreams; hallucinations after awakening)
5. Emotional disturbances (depression, anxiety, or feat, irritability, euphoria, apathy, or
wondering perplexity)
6. That is transient and fluctuating (worse at night)
 DDx: dementia esp. LBD (but is insidious onset + constant + good attention + less common and
more stable delusions or hallucinations)
 Aetiology
1. Rx drugs: TCAs, BZDs/sedatives, digoxin, diuretics, Li+, steroids, opiates
2. Other drugs: EtOH intoxication, EtOH withdrawal & DTs, BZD withdrawal
3. Medical conditions: hypoxia e.g. post-op, infections (sepsis, UTIs and LRTIs), organ
failure (cardiac/renal/hepatic), hypos, dehydration/shock, constipation, burns, major
trauma, pain!
4. Neuro conditions: epilepsy (post-ictal), head injury, SOL, encephalitis
 Risk factors:
1. Elderly, male, frailty or immobility
2. Previous episode delirium, pre-existing dementia
3. Sensory impairment, environment
 CAM testing
1. Is there AMS?  no  no delirium
2. Yes  inattention (serial “As”; letter to pictures)  0-2 errors  no delirium
3. > 2 errors  altered level of consciousness  not 0 = DELIRIUM
 If LOC (RASS level) = 0  is there disorganised thinking (will stone float on water… or command
hold up X finger – no do same for other hand – now add 1 more finger to both)  >1 error 
DELIRIUM
 Management
1. Look for the reversible causes (anaemia, thyroid, LFTs, hypoNa+, dehydration, infection!)
2. Environment e.g. adequate lightening, avoid sensory overload or deprivation, clock
3. Clear simple communication, limit number of staff, family help
4. Monitor vitals
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5. Medication considered if agitation/ behavioural risk to self or others (NICE) 

antipsychotics e.g. haloperidol or olanzapine given < 1 wk, PO/IM @ lowest dose and
titrate up = best first-line
 But may worsen confusion… and should never be used in LBD due to EPSE and
worsening of Sx!
 2nd-line = benzos PO (e.g. lorazepam = quick onset). Lorazepam is safer than
anti-Q e.g. haloperidol. Lorazepam is also used for EtOH or sz-related
behavioural disturbance
 Capacity should be assessed each time. If delirium impairs capacity – cannot give
informed consent, so use MCA (or doctrine of necessity).
 If continuing interventions w/o consent anticipated – MHA.
 Prognosis: depends on cause (many recover in days or weeks). Can persist for months.
Associated w high mortality (>65y  45% survive 2-4 y).

THE AMNESIC SYNDROMES

Characterised by:

1. Retrograde amnesia (impairment of memory for events that antedate illness or injury);
2. Antegrade amnesia (inability to learn new verbal or non-verbal information from onset
of illness or injury;
3. Intact retrieval of old info (immediate recall, LTM intact); intact IQ and attention; intact
personality; tendency to confabulate.
 Korsakoff’s
o Alcoholism, encephalitis, head injury
o Lesions occur within thalamus and mamillary bodies. Commonly associated w
confabulation – a false rationalisation of events and circumstances
 Post-traumatic amnesia
o After trauma, retrograde amnesia may span several years, but w recovery, this gradually
diminishes. The duration of post-traumatic amnesia on the other hand remains fixed and
relates directly to severity of injury.
 Amnesic stroke
o Bilateral medial temporal lobe infarction from PCA stroke
o Usually associated w hemiplegia and visual disturbance or loss e.g. Anton’s/Balint’s
 Transient global amnesia (TGA)
o Attack witnessed by capable observer and reported as anterograde amnesia (recent
memory loss). Pt is bewildered and keep asking same questions.
o Key negatives = no epilepsy, no FND during or after attack, no clouding of
consciousness, or cognitive impairment (can perform complex tasks – drive/cook).
 DDx: strokes (thrombosis basilar artery, cardioembolic, lacunar, PCA), complex
partial seizures, frontal/temporal epilepsy, migraine variants, syncope
o Resolve in 24h (usually 1-10 h) associated w migraines. Triggers: stress or exercise.
 Transient epileptic amnesia (TEA) – due to temporal lobe epilepsy. Lasts 15 min – 1 h, often on
waking.
o Profound difficulty remembering events in past few minutes or of events in hours prior
to onset of attack (anterograde), or even cannot access memories of the past
(retrograde)
o May have olfactory hallucinations or gustatory taste hallucinations
 Geri psych and neuropsych

 Amnesia w tumours (that compress thalamic structures or fornix e.g. colloid cyst 3rd vent)
 Dissociative amnesia = psychogenic
o Affects overlearned and personally relevant memory e.g. “What is my name?”, while
less well learned memory unaffected.
o Clinically evident acute mental stress may ppt this
o This inadequate defence mechanism suggests serious psych/personality disorder.
 Temporal lobectomy
o Amnesia will occur if function in unoperated temporal lobe abnormal
o Pre-op assessment = Wada tests – minimises this.

EPILEPSY (BRIEF SUMMARY)

TYPES OF EPILEPSY

 Simple = no LOC; complex = LOC.

 Tonic-clonic (grand mal)
1. Tonic phase = LOC and generalised contractions (elbows flexed, legs extended), eyes are
open and sphincter control may be lost at end of this
2. Clonic phase = rhythmic jerking of extremities, tongue biting, autonomic activation.
Duration = 30-2 minutes.
3. Post-ictal = minutes – hours; stertor + unarousable + tired, confused, amnesia,
headache, myalgia.
 Absence (petit mal)
1. Brief staring and unresponsiveness.
2. Most common in childhood and can occur multiple times per day; impair school
performance. 80% childhood absence remit.
3. Hyperventilation, strobe lights, or sleep deprivation are triggers.
4. Generalised 3Hz spike and wave
 Atonic – rare, almost always occur wi other types of seizures. Loss of muscle tone + sudden fall.
 Myoclonic – sudden brief generalised mm contraction in morning = hard to eat/drink.
Commonest is JME (after puberty onset).
 Geri psych and neuropsych

 Focal or partial seizures.

1. Frontal (usually structural) – Jacksonian march; Complex partial seizure
clonic (shaking) movements usually in hand or face During
(largest homunculus). Other movements = Impaired consciousness
“fencing”, stereotypy, elaborate automatisms. Hallucinations and other distorted
Adversion = eyes and head move AWAY from side of perceptions (olfactory, somatic esp.
seizure foci. epigastric) .
 Post-ictal  Todd’s paresis Déjà vu
2. Parietal (usually structural) – vertigo, aphasia or Depersonalization and derealisation
hemi-neglect (if non-dominant). Limb is weak rather Automatisms and stereotyped behaviour.
than moving + sensory tingling/burning (post-
Rolandic sensory cortex). Post-ictal (h to days)
3. Temporal (e.g. hippocampus); MCC of complex Transient, florid psychosis
partial seizures.
 Medial: visceral disturbance (butterflies in Inter-ictal
stomach), autonomic (sweating etc.), vacant Schizo-like psychosis
staring, oro-alimentary e.g. lip smacking, Depression
swallowing, chewing. Sexual dysfunction and lack of libido
 Lateral: vertigo, auditory hallucinations or
Higher risk of developing schizophrenia.
impairment
 BG: contralateral dystonia and ipsilateral
automatisms (plucking, stroking)
 Post-ictal  amnesia, tiredness
4. Occipital – visual Sx (flashes, scotomas); C/L hemianopia; visual hallucination; nystagmus
and eye movements.

 Key DDx: syncope, panic attacks, hypos, schizo, pseudoseizures

 Pseudoseizures (non-epileptic seizures)

1. Psychogenic (e.g. Munchausen’s, conversion) but can have true organic substrate
(pseudo on top of real)
2. Hx: TOO LONG of a seizure + rapidly regaining consciousness after episode with no
post-ictal confusion; recent stressors
3. Dx: clinical
 Face looks relaxed, non-stereotyped movements, hip thrusting, tongue-biting on
the FRONT of tongue
 Talks about the experience as metaphors of space/place patients go through,
and its distress/impact on their life. Resistant to focus on the individual seizure
episodes, need repeated prompting to do so.
 Tilt test = no loss of head posture
 No EEG abnormality
4. Tx: CBT, address triggers. Do not give medications
 Geri psych and neuropsych

THE PSYCHIATRIC ASPECTS OF SEIZURES

 Psych Sx:
1. Shared aetiology – temporal lobe tumour
2. At start of sz – hallucinations during aura
3. During – non-convulsive status (usually temporal lobe epilepsy) pt as fugue state
4. After – post-ictal confusion/delirium
5. In between episodes – psychosis of complex partial epilepsy
 Psych disorder masquerading as epilepsy = pseudoseizures
 Psych disorders associated w epilepsy = depression (common) + suicide (5X increase) due to
persisting negative attitudes
 Psych problems of Tx
1. AEDs e.g. barbiturates (phenobarbitone)  depression (hyperactivity and irritability in
children; e.g. phentytoin = ataxia
2. Medications that cause Sz as S/E e.g. anti-Q and TCAs (3Cs).

DVLA

 1st unprovoked seizures  group 1 = 6 months, group 2 = 5 years

 Epilepsy  group 1 = 12 months, group 2 = 10 years w/o AEDs
 Epilepsy – AED withdrawal  group 1 = 6 months post-cessation
 Pseudoseizures  case-by-case
 Geri psych and neuropsych

HEAD TRAUMA

 ApoE4 allele are at greatest risk of persistent risk following HI.

 Amnesia (anterograde or retrograde) common after HI w LOC. Poor outcome if anterograde
amnesia lasts > 24 h (including persistent cognitive deficits). Impairment ranges from subtle
slowing of thoughts and distractibility through dementia. Tends to improve in 1st year then
permanent. No Tx.
 Personality change – frequent following HI due to frontal lobe damage. They cannot plan or they
persevere. There is mood lability, emotional shallowness, and impulsivity (including sexual
behaviour and speech). Co-morbid schizo, anxiety, mood disorders are common after HI.
1. Left frontal  depression; right frontal  mania
 Post-concussion = emotional, cognitive, bodily Sx after relatively minor HI. It is “psychological”
or even feigned (for compensation), but can reflect subtle brain injury.

OTHER ORGANIC DISEASE

 Organic brain syndromes = dementia, delirium, amnesic syndrome

 Organic delusional (psychotic) disorders = SLE
 Organic mood disorders = MS
 Organic anxiety = thyrotoxicosis
 Organic personality disorders = head injury.