PSYC20006 Lecture Notes - Lecture 12: Dementia, Mild Cognitive Impairment, Acalculia
10 May 2018
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Lecture 12
- Alzheimer (1907, 1911) → Commonest of primary dementing illnesses [directly
damages neuronal tissue rather than affect somewhere else causing secondary
impact on neurons]; autopsy studies report approximately 50% of all dementias are
AD
- Prevalence: ~2% (65-70), ~20% (>80); problem of ageing population → eventually
become dependent and enter supported accommodation
- Age is biggest risk factor for developing AD
- Definitive diagnosis of AD can only be made on pathology; need to biopsy someone’s
brain, usually done at autopsy if at all
- In life - can only diagnose Dementia of the Alzheimer Type (DAT) based on
syndrome
- Aetiology [cause] of AD: majority arise sporadically (ApoE [Apolipoprotein E gene
Epsilon 4 allele of that gene shown to increase risk late onset AD); rare early onset
autosomal dominant cases (mutations in 3 genes: amyloid precursor protein [APP],
presenilin 1 (PSEN1), presenilin 2 (PSEN2) → all alter production of amyloid β (Aβ)
peptide – principal component of senile plaques); individuals with Downs syndrome
are unusually prone to developing AD (typically occurs much earlier [~40s]; no
precipitating factors known [there is no something that happens to you → then have
AD; people who had head injuring in lifetime have slightly higher risk of AD later in
life slightly riskier for men than women]; can have sudden decompensation
- Clinical features of DAT: onset: insidious (slowly progresses, symptoms 1-2 years
prior to diagnosis); course: slow deterioration (years, occasionally see plateaus in
deterioration, death: M = 8.5 years after onset [range: 2-20 years])
- 3 main phases in disease progress:
- → Phase 1 lasts 2-3 years [some of the time is prediagnostic]: failing memory
(amnestic representation [driving symptom of concern]); muddled inefficiency in
Activities of Daily Living (ADL)s [shopping, cleaning, gardening, finances etc]; spatial
disorientation [losing their way]; mood disturbance can occur (agitated or apathetic)
- → Phase 2 more rapid progress of deterioration: intellect and personality deteriorate;
focal symptoms appear (dysphasia [problems with language, particularly anomia
{difficulties remembering particular nouns}], dyspraxia [normal ability to move body
and limbs but difficulty synchronising those movements into a goal-
directed/purposeful sequence of movement], agnosia [somebody sees a
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picture/diagram → cant tell you what it is, but if they touch/smell it they can say what
it is], and acalculia [lose understanding of arithmetical functions, can count forwards
and backwards, lost understanding of relationships of numbers to other numbers,
cant do multiplication and division → as disease progresses, cant do addition and
subtraction]); disturbance of posture and gait, increased muscle tone [muscles are
tighter, even at rest → tighter than normally would be]; delusions/hallucinations can
occur
- → Phase 3 terminal stage [need high level round the clock care]: profound apathy [no
desire to move or eat], become bed ridden; eventually lose neurological function;
bodily wasting occurs [normally die of pneumonia or chest infections because just
lying on bed daily]
- McKhann et al. criteria: working party developed operational criteria for making
diagnosis of AD (probable AD, possible AD, definite AD [only under pathological
condition, or brain under microscope])
- Probable AD: deficits in 2 or more areas of cognition (amnestic presentation: most
common, nonamnestic presentations: language, visuospatial, executive dysfunction);
progressive worsening of memory and/or other cognitive functions; no disturbance of
consciousness; onset between 40 and 90; in the absence of other causes [of the
cognitive difficulties]; biomarkers [blood test etc, presence of biomarkers increase
likelihood of it being AD, but absence doesn’t mean not probable AD]
- Possible AD: toned down version of probable; made on the basis of dementia
syndrome if have variations in onset, presentation or clinical course; can be made in
the presence of another disorder, which is not considered to be the cause of the
dementia
- Definite AD: histopathological evidence of AD obtained from biopsy or autopsy
- Pathology: grossly atrophied brain [brain looks shrunken because many neurons
have died] (affects frontal and temporal lobes > parieto-occipital regions); extensive
degeneration of neurons [most extensive in hippocampi and amygdala];
accompanying glial cell proliferation [fill in the space left by the dying neurons];
extensive amounts of senile plaques [most number in hippocampi and amygdala];
extensive amounts of neurofibrillary tangles [concentrated in hippocampi, must see
neurofibrillary tangles to diagnose AD]; intensity of neuropathological features
correlates closely with severity of dementia [the more the features, the worse the
symptoms]
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-
- Amyloid is found in core of senile plaque, large amount of amyloid placement in
pathology associated with AD
-
- Lies within neuron itself, can displace cell nucleus entirely, major part of
neurofibrillary tangle is tau protein in abnormal form (contains amyloid)
- Course of neuropathological changes (amnestic): commence in hippocampus/MTL
[neurofibrillary tangles and senile plaques start proliferating when rest of brain looks
fine]; spread posteriorly to parietal cortex [through posterior temporal lobe]; spreads
to involve frontal cortex; tells us order of brain damage → reflected in symptoms
- Clinical pattern of cognitive impairment in DAT - amnestic presentation:
- → Initially see MTL memory impairment, due to early predominance of
hippocampal/MTL involvement [inability to relate info together] (anterograde memory:
impaired new learning, impaired delayed recall, poor recognition memory [having
trouble encoding info and encoded info has been lost, no info to be accessed, not
retrieval difficulty, difficulty with fundamental memory system that are not retaining
the info for it to be accessed later]; retrograde memory: intact for remote memories,
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