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Case 22 > Dementia and Movement Disorders > Flashcards

Dementia and Movement Disorders Flashcards

1
Q

what is dementia?

A

a syndrome in which there is a deterioration in memory, thinking, behaviour and the ability to perform everyday activities

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2
Q

what is Alzheimers disease?

A

commonest type of dementia

caused by ageing with a complex interaction of genetic and environmental risk factors

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3
Q

what is vascular dementia?

A

dementia associated with cerebral vascular disease
cerebral ischaemia leads to impaired neurological function
classically step wise decline in cognition- each step associated with a vascular event

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4
Q

what is dementia with lewy bodies?

A

dementia associated with the development of abnormal protein clumps in the brain

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5
Q

what is front-temporal dementia?

A

dementia caused by selective neurodegeneration of frontal and temporal lobes

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6
Q

how does front-tempotal dementia present?

A

personality change, social inhibition, loss of language

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7
Q

how does Alzheimers disease present?

A

initially problems with memory (recent/ new memories)

may develop- dysphasia, apraxia (difficulty with motor tasks), disorientation, impairment in planning/problem solving

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8
Q

what are the diagnostic features of Alzheimers?

A

meets criteria for dementia
insidious onset- months/years
clear history of worsening cognition
deficits in one or more of - learning and memory, language, visuospatial, executive function

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9
Q

what are the investigations used in Alzheimers?

A 
cognitive testing- verbal episodic memory  
structural brain imaging- CT/MRI may have patterns of cortical atrophy 
functional imaging (PET)
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10
Q

what are the core clinical features of Lewy body dementia?

A
  1. fluctuating cognition
  2. visual hallucinations
  3. parkonsinism
  4. REM sleep behaviour disorder
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11
Q

what are the investigations for dementia with Lewy bodies?

A
  1. cognitive testing- attentional and executive function, visuospatial/visual perception
  2. structural imaging- exclude other causes
  3. SPECT/PET scan- can show low dopamine uptake in basal ganglia (DaT scan)
  4. 123 iodine- MIBG myocardial scintigraphy- reduced cardiac uptake of 123iodine-MIBG in DLB
  5. polysomnography- REM sleep disorder
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12
Q

how can cognition be assessed?

A

mini mental state exam

addenbrookes cognitive examination

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13
Q

which brain pathway and brain areas are involved in object recognition?

A

the ventral visual pathway

temporal lobe

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14
Q

what are the neuropathological features of Alzheimers disease?

A

macroscopic- atrophy of brain, particularly in the medial temporal lobe
microscopic:
hyperphosphorylated Tau- forms neurofibrillary tangles in cell bodies and neuropil threads in axons
extracellular amyloid beta plaques

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15
Q

what are the neuropathological features of Lewy body diseases?

A

macroscopic changes- depigmentation of substantia nigra

microscopic changes- misfolded alpha-synuclein forms inclusions in cell bodies (Lewy bodies) and axons (lewy neurites)

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16
Q

what are the clinical features of Huntington’s disease?

A

triad of motor, behavioural and cognitive deficits

17
Q

what are the neuropathological features of huntigtons disease?

A

macroscopic- cerebral atrophy, atrophy of neostriatum, globus pallidus, thalamus s.nigra and cerebellum
microscopic- loss of neurones, neostriatal dark neurones, intracellular huntingtin protein inclusions

18
Q

what are the effects of damage to the basal ganglia?

A

tremors, involuntary muscle movements, abnormal increase in tone, difficulty initiating movements, abnormal posture

19
Q

what are the symptoms of Parkinson’s disease?

A

motor symptoms- pill rolling terror, increased muscle tone, Bradykinesia (slow movement), postural instability
non-motor symptoms- sleep disorders, dementia, depression, fatigue

20
Q

what are the cardinal pathological features of Parkinson’s disease?

A

formation of Lewy bodies and lewy neurites

progressive neuronal loss particularly in the substantia nigra pars compacta- decreased dopamine

21
Q

what are the investigations for Parkinson’s disease?

A

DaT scan- type of SPECT scan which shows the function of the dopamine terminals

22
Q

what are the main treatments for Parkinson’s disease?

A

dopamine replacement therapy- levodopa, dopamine agonists
reduction of dopamine/levodopa breakdown- catechol-O-methyltransferase (COMT) inhibitor, monoamine oxidase isoenzyme type B (MAO-B) inhibitor

23
Q

what is the mechanism of action and side effects of levodopa?

A

MOA- it is converted to dopamine and exerts its effects

side effects- nausea/vomiting, tiredness, dizziness

24
Q

what is the mechanism of action and side effects of dopamine agonists (pergolide)?

A

MOA- agonist at D2 receptor

side effects- nausea/vomiting, dizziness, tiredness

25
Q

what is the mechanism of action and clinical use of catechol-O- methyltransferase inhibitors?

A

MOA- reduces the breakdown of levodopa, extending its half life and prolonging its action
clinical use- given with levodopa

26
Q

what is the mechanism of action of monoamine oxidase-B inhibitors (selegiline)?

A

MOA- prevents the breakdown of dopamine leading to greater dopamine availability

27
Q

what are the movement disorders seen in Huntington’s disease?

A

chorea- non-rhythmic, brief, irregular movements
dystonia- sustained or repetitive muscle contractions resulting in repetitive twisting movements or abnormal fixed postures
myoclonus- brief jerking movement of muscle
dysarthria- difficulty speaking, poor articulation of words
dysphagia
abnormal eye movements

28
Q

what are the behavioural and cognitive problems associated with Huntington’s disease?

A

behavioural- apathy, dysphoria (dissatisfaction), irritability, agitation, aggression, poor self care, inflexibility
cognitive- affects planning, abstract thinking and inhibition of inappropriate actions

29
Q

how is Huntington’s diagnosed?

A

made by a specialist neurologist
mainly based on the presence of specific movement disorders (e.g. chorea), can then be confirmed by gentling testing
MRI/CT may show some changes in moderate-severe disease

30
Q

how is dementia treated?

A

non-pharmacological- structured group cognitive stimulation programme
pharmacological:
1st line- acetylcholinesterase inhibitor
alternative- mematine hydrochloride
both of these drugs only have licensed indication in Alzheimers but are used in DLB

31
Q

what is the mechanism of action of donepezil hydrochloride, rivastigmine and galantamine?

A

inhibits acetylcholinesterase and choline acetyl transferase activity to reduce cholingeric deficit

32
Q

what is the mechanism of action and side effects of memantine hydrochloride?

A

MOA- weak glutamate receptor antagonist (NMDA receptor), prevents excessive pathological NMDA receptor activation
side effects- headache, impaired balance, dizziness, drowsiness, dyspnoea, hypertension

Case 22 (3 decks)

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