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neuro > dementia (excluding alzheimers) > Flashcards

dementia (excluding alzheimers) Flashcards

-frontotemporal -vascular -demetia with lewey bodies -parkinsons -huntingtons

1
Q

what is frontotemporal dementia

A

specific degeneration/atrophy of the frontal and temporal lobes of the brain

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2
Q

cause of frontotemporal

A

-genetic
-may be part of MND-FTD spectrum

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3
Q

presentation of frontotemporal dementia

A

-disinhibition
-apathy
-loss of empathy
-stereotypes or compulsive behaviours
-hyperorality
-early loss of insight
-difficulty in planning, executive function and impulse control

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4
Q

what is the behavioural variant

A

-behavioural changes
-executive dyfunction
-disinhibition
-impulsivity
-loss of social skills
-apathy
-obsessions
-change in diet

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5
Q

what is primary progressive aphasia

A

-effortless non-fluent speech
-speech errors
-lack of grammar
-lack of words

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6
Q

what is semantic dementia

A

-impaired understanding of meaning of words
-fluent but empty speech
-difficulty retrieving names

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7
Q

what is seen on MRI of frontotemporal dementia

A

atrophy of frontotemporal lobes

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8
Q

what is seen on SPECT in frontotemporal dementia

A

reduced metabolism in frontotemporal

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9
Q

what is seen in the CSF in frontotemporal

A

increased tau and normal amyloid

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10
Q

what is the most useful for frontotemporal

A

SPECT

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11
Q

management of frontotemporal

A

-trial of trazadone/antipsychotics to help behavioural features
-safety management
-power of attorney

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12
Q

onset of vascular dementia

A

late but abrupt

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13
Q

what causes vascular dementia

A

Brain damage due to cerebrovascular disease: either major stroke, multiple smaller unrecognised strokes (multi-infarct) or chronic changes in smaller vessels (subcortical dementia)
-causes areas of cell death

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14
Q

who gets vascular dementia

A

men over 60 with hypertension

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15
Q

presentation of vascular dementia

A

• Dysphasia, dyscalculia, frontal lobe symptoms and affective symptoms more common than in Alzheimers
-decreased attention, executive dysfunction, slowed processing
• May have focal neurological signs
• May have vascular risk factors
• May have step wise decline
• Cognitive functions not fully regained after each step
-Impairments seen in the areas most affected by vascular injury

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16
Q

investigation for vascular dementia

A

evidence of stroke or small vessel disease may be seen on CT or MRI

17
Q

treatment of vascular dementia

A

-vascular risk factors
-secondary prevention to protect against further vascular injury
-only consider cholinesterase inhibitors if they have suspected comorbid Alzheimer’s, parkinson’s or lewy bodies

18
Q

what is dementia with lewey bodies

A

Deposition of abnormal protein (⍺-synuclein) within neurons in the brain stem and neocortex

19
Q

presentation of dementia with lewey bodies

A

dementia

two of:
○ Visual hallucinations
○ Fluctuating cognition (delirium-like)
○ REM sleep behaviour disorder
○ Extrapyramidal features (Parkinsonism)
- Not more than 1 year prior to onset of dementia
-Positive DAT scan

20
Q

investigation for dementia with lewey bodies

A

DaT scan (dopamine active transporter imaging)
-CT
-MRI

21
Q

treatment for dementia with lewey bodies

A

-small dose levodopa for movement problems
-trial cholinesterase inhibitors - donepezil or rivastigmine
-if they don’t work then galantamine which is an acetylcholinesterase inhibitor

22
Q

what needs to be done before prescribing/increasing dose of cholinesterase inhibitors

A

check pulse

23
Q

what is parkinson’s dementia

A

Late onset dementia
-progressive reduction of dopamine in the basal ganglia of the brain, leading to disorders of movement

24
Q

presentation of parkinson’s

A

-bradykinesia (movements get smaller and slower, handwriting gets smaller)
-rigidity (cogwheel, movement with small jerks)
-resting tremor
-symptoms are classically asymmetrical
-dementia
-decrease attention
-slow processing
-loss of memory
-forward tilt
-reduced arm swing
-facial masking
-stooped posture
-shuffling gait

25
Q

what is the parkinson’s tremor like

A

-asymmetrical
-4-6 Hz
-worse at rest
-improves with intentional movement
-no change with alcohol

26
Q

treatment options for parkinson’s

A

-levodopa (usually combined)
-COMT inhibitors (entacapone)
-dopamine agonists
-monoamine oxidase-B inhibitors

27
Q

pathophysiology of parkinsons

A

Part of the basal ganglia called the substantia nigra produces a neurotransmitter called dopamine. Dopamine is essential for the correct functioning of the basal ganglia. In Parkinson’s disease, there is a gradual but progressive fall in the production of dopamine

28
Q

what are some parkinson’s plus syndromes

A

-multiple system atrophy
-dementia with lewey bodies
-progressive supranuclear palsy
-corticobasal degeneration

29
Q

what is huntingon’s disease

A

early onset dementia
-progressive deterioration in the nervous system

30
Q

what is the huntington’s gene

A

HTT gene on chromosome 4
-CAG trinucleotide repeat

autosomal dominant

31
Q

pathophysiology of huntington’s

A

-cells are lost from the basal ganglia causing flattening of the normal convex curve of the lateral ventricles
-cells are lost from other brain areas including the cerebral cortex

32
Q

what is genetic anticipation of huntington’s

A

this is where successive genertations have more repeats in the gene resulting in:
-earlier age on onset
-increased severity of disease

33
Q

presentation of huntingtons

A

-dementia
-dysexecutive syndrome (frontal lobe damage leading to emotional, motivational and behavioural symptoms)
-involuntary movements
-slow processing
-changes in mood and personality
-anxiety, psychosis, compulsions, suicidality, aggression
-usually presents with the cognitive, psychiatric and mood problems first then movement disorders

34
Q

what are the late signs of huntington’s

A

-rigidity
-bradykinesia
-severe chorea (involuntary abnormal movements)
-serious weight loss
-inability to walk
-inability to speak
-swallowing problems

35
Q

investigations for huntington’s

A

-genetic tests
-CT scan

36
Q

treatment for huntingtons

A

there isnt really any
-support

37
Q

life expectancy of Huntington’s

A

15-20 yrs

neuro (26 decks)

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