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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
GENERAL MANAGEMENT
AD
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
Geri psych and neuropsych
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
ALCOHOL-INDUCED DEMENTIA
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
Neuropsychometric testing if: early dementia, atypical dementia, R/O or separate depressive illness,
monitor therapies.
Geri psych and neuropsych
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
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.
TYPES OF EPILEPSY
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
HEAD TRAUMA