Deck 5b Flashcards
- Q. What occurs in fronto-temporal dementias? (FTD)
A. Damage to frontal lobe – voluntary and planned motor behaviours, motor
speech area (Broca’s), personality, planning
B. Personality and behavioural change followed by breakdown in attention and
executive function
C. Language variants: semantic dementia (SD), primary non fluent aphasia (PNFA)
D. Motor disorders plus dementia: cortico basal syndrome (CBS), progressive
supranuclear palsy (PSP), Parkinson’s disease dementia (PDD) and dementia with
lewy bodies (DLB)
- Q. What is the function of the temporal lobe?
A. Hearing (superior temporal lobe
B. Language comprehension (superior temporal lobe)
C. Semantic knowledge (anterior temporal lobe)
D. Memory (hippocampus)
E. Emotional/affective behaviour (limbic system)
- Q. What occurs if the hippocampus and medial temporal lobe are damaged?
A. Profound failure to create new memories, can’t remember new people, names,
tasks etc
Q. Where does the typical variant of Alzeheimer’s begin? What symptoms are seen?
Typical amnesia variant: Early degeneration of medial temporal love before spreading – results in selective amnesia
- Q. What is seen in preclinical AD “amnesic prodrome”?
Memory impairment is first cognitive marker of AD – poor performance on
episodic memory tests (new learning and retention) – no evidence of dementia-
normal general cognitive function and activities of daily living are intact – high
risk of developing AD
Q. How does semantic dementia present?
Primary progressive aphasia - Loss of semantic memory in both verbal and non-
verbal domains – e.g. difficulty finding the right word
- Q. What are the six parts of the six-item cognitive impairment test?
A. What year is it?
B. What month is it?
C. Give an address with 5 parts (John, Smith, 42, High, St, Bedford)
D. Count 20-1
E. Say months of year in reverse
F. Repeat address
Q. What is a functional memory disorder? (FMD)
A. Acquired (>6 months) dysfunction of memory that significantly affects their
professional and/or private life
B. Psychosocial burden/ significant psychological stress
C. Verbal memory and attentional capacity > -1.5SD
D. Absence of organic cause of cognitive impairment
E. Absence of major psychiatric disease, e.g. severe depression
Q. What is seen on autopsy of Alzheimer’s?
A. The cerebral cortex was thinner and senile plaque, previously only encountered in elderly people, were found along with neurofibrillary tangles. – dendritic/neuronal losses
Q. What imaging is used to stage Alzheimer’s?
A. MRI (T1)
B. Braak staging – amyloid imaging (pathology mismatch)
C. Functional MRI – brain networks
D. PET & SPECT – energy and blood supply
Q. What treatment is used in Alzheimer’s?
A. Acetylcholinesterase inhibitor: tacrine, rivastigmine, galantamine and donepezil
– reduce Ach breakdown rate, side effects: nausea, vomiting
B. NMDA receptor antagonist: memantine – inhibits overstimulation of NMDA receptors by glutamate (which is excessive in AD leading to cell death through excitotoxicity) –adverse effects: hallucinations, confusion, headache, fatigue,
dizziness
Q. What is apraxia?
A. Disorder of consciously organised patterns of movement of impaired ability to
recall acquired motor skills e.g. show me how you would light a match
Q. What is a motor unit?
LMN + axon + several supplied muscle fibres
Q. What system regulates muscle tone? What occurs in diseased states?
Muscle spindle: stretch receptor in muscle innervated by gamma motor neurons
B. Muscle stretched afferent impulses from muscle spindles which reflex
partial contraction of muscle
C. Disease states: e.g. spasticity and extrapyramidial rigidity
Q. Describe four features of LMN lesions
A. Muscle tone is normal or reduced (Flaccid)
B. Muscle wasting: predominantly distal bulbar, upper limb, lower limb, resp
muscles
C. Fasciculation: visible spontaneous contractions of motor units
D. Reflexes depressed or absent (everything goes down!)
