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Nervous System > Neurological Diseases - Degenerative disorders - Dementia and Parkinson's > Flashcards

Neurological Diseases - Degenerative disorders - Dementia and Parkinson's Flashcards

1
Q

what are common features of neurodegenrative diseases?

A

Aetiology largely unknown
(Mendelian genetic cases rare, often younger onset)

Usually late onset

Gradual progression

Neuronal loss (specific neuropathology)

Structural imaging often normal (atrophy)

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2
Q

what is dementia?

A

Progressive impairment of multiple domains of cognitive function in alert patient leading to loss of acquired skills and interference in occupational and social role

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3
Q

what is the incidence and prevalence of dementia?

A

incidence 200 per 100,000

Prevalence 1,500 per 100,000

> 850,000 patients in UK ( 1.6M by 2040)

47M worldwide 2015 (131M by 2050)

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4
Q

what are causes of late onset dementia (65+ years)?

A

Alzheimer’s (55%)
Vascular (20%)
Lewy body (20%)
Others (5%)

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5
Q

what are the causes of young onset dementia?

A

Alzheimer’s (33%)
Vascular (15%)
Frontotemporal (15%)
Other (33%)

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6
Q

what are other causes of dementia?

A

Toxic (alcohol)
Genetic (Huntington’s)
Infection (HIV, CJD)
Inflammatory (MS)

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7
Q

what are treatable causes / mimics of dementia?

A

Vitamin deficiency - B12
Endocrine - thyroid disease (hypothyroidism)
Infective - HIV, syphilis

Mimics: Hydrocephalus
Tumour
Depression: “pseudodementia”

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8
Q

what should be asked in the history for dementia?

A

type of deficit, progression, risk factors, FH

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9
Q

what should be examined in diagnosis of dementia?

A

cognitive function, neurological, vascular

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10
Q

what investigations are done to diagnose dementia?

A

routine - bloods, CT / MRI

others - CSF, EEG, functional imaging, genetics

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11
Q

what various domains should be covered in examination of cognitive function?

A

Memory, attention, language, visuospatial,
Behaviour, emotion, executive function
Apraxias, agnosias

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12
Q

what screening tests can assess cognitive function?

A

Mini-mental (MMSE), Montreal (MOCA)

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13
Q

what is mini-mental test?

A

The mini mental state examination (MMSE) is a commonly used set of questions for screening cognitive function.[1] This examination is not suitable for making a diagnosis but can be used to indicate the presence of cognitive impairment, such as in a person with suspected dementia or following a head injury

The examination has been validated in a number of populations. Scores of 25-30 out of 30 are considered normal, 21-24 as mild, 10-20 as moderate and below 10 as severe impairment.

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14
Q

what assessment is used to examine cognitive function?

A

Neuropsychological assessment

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15
Q

what is Montreal (MOCA)?

A

The Montreal Cognitive Assessment (MoCA) was designed as a rapid screening instrument for mild cognitive dysfunction. It assesses different cognitive domains: attention and concentration, executive functions, memory, language, visuoconstructional skills, conceptual thinking, calculations, and orientation

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16
Q

what would rapid progression of disease suggest?

A

CJD

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17
Q

what is CJD?

A

Creutzfeldt-Jakob disease (CJD) is a rare and fatal condition that affects the brain. It causes brain damage that worsens rapidly over time.

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18
Q

what would stepwise progression of disease suggest?

A

vascular dementia

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19
Q

which disease is indicated from abnormal movements?

A

Huntington’s

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20
Q

which disease is indicated from parkinsonism?

A

Lewy body

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20
Q

which disease is indicated from myoclonus?

A

CJD

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21
Q

what is the commonest neurodegenerative condition?

A

Alzheimer’s disease

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22
Q

when is the mean age onset for alzheimers disease?

A

mean age onset 70 yr (25% <65yrs)

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23
Q

what is the pathology of alzeimers disease?

A

β-amyloid plaques and neurofibrillary tangles

24
Q

what increases risk of alzeimers disease?

A

smoking, obesity, diabetes, hypertension

25
Q

what decreases the risk of alzheimers disease?

A

cognitive reserve, exercise, diet (medditeranian)

26
Q

what genes increase risk of alzheimers disease?

A

APOE, APP, PSEN1, PSEN2

27
Q

how does temporo-parietal dementia present clinically?

A

Early memory disturbance
Language and visuospatial problems
Personality preserved until later

28
Q

how does frontotemporal dementia present clinically?

A

Tau pathology
Early change in personality / behaviour
Often change in eating habits
Early dysphasia
Memory / visuospatial relatively preserved

29
Q

what is the pathology of dementia wirh lewy bodies?

A

Lewy bodies (accumulations of abnormal α synuclein)

30
Q

what are the clinical features of dementia with lewy bodies?

A

Early visuospatial and executive dysfunction
Prominent fluctuation
Parkinsonism and visual hallucinations common

31
Q

how does vascular dementia present clinically?

A

Mixed picture
Stepwise decline

32
Q

what is non pharmacological symptomatic treatment for dementia?

A

Information & support, dementia services
Occupational therapy
Social work / support / respite / placement
Voluntary organisations

33
Q

what is pharmacological symptomatic treatment for dementia?

A

Insomnia
Behaviour (care with antipsychotics)
Depression

34
Q

what is specific treatment for alzheimers (+/- lewy body dementia)?

A

Cholinesterase inhibitors (cholinergic deficit)
Donepezil, rivastigmine, galantamine
Small symptomatic improvement in cognition (wash-out)
No delay in institutionalisation

NMDA antagonist (memantine)

35
Q

what are the effects of cholinesterase inhibitors on alzheimers?

A

Small symptomatic improvement in cognition (wash-out)

No delay in institutionalisation

36
Q

what are examples of cholinesterase inhibitors?

A

Donepezil, rivastigmine, galantamine

37
Q

what specific treatments are there for frontotemporal dementia?

A

none

38
Q

what are specific treatments for vascular dementia?

A

none

39
Q

what is parkonsonism?

A

A clinical syndrome with ≥ 2 of:

Bradykinesia (slowness of movement)
Rigidity (stiffness)
Tremor (shakiness)
Postural instability (unsteadiness / falls)

40
Q

what is the pathology of parkinosonism?

A

predominantly dopamine loss

Lewy bodies (α synuclein)

41
Q

what are four different causes of parkinsonism?

A

Idiopathic Parkinson’s disease
Dementia with Lewy bodies

Drug-induced (e.g. dopamine antagonists)

Vascular parkinsonism (lower-half)

Parkinson’s plus syndromes
Multiple system atrophy
Progressive supranuclear palsy / corticobasal degen

42
Q

what is the 2nd commonest neurodegenerative disease?

A

parkinsons disease

43
Q

what is the incidence of parkinsons disease?

A

Incidence: 15-20 per 100,000 per year

  • age dependent, 1.5 M : F

Crude prevalence: 150-300 per 100,000
~150,000 in UK

44
Q

what are risk factors for parkinsons disease?

A

Genetic (LRRK2, Parkin, GBA)

Environmental (pesticides, smoking, caffeine)

45
Q

how is parkinsons definitevly diagnosed?

A

post-mortem

46
Q

what is the clinical presentation of parkinsons disease?

A

Bradykinesia + ≥1 tremor, rigidity, postural instability

No other cause / atypical features

Slowly progressive (> 5-10 yrs)

Supported by asymmetric rest tremor

47
Q

what does parkinsons asymmetric rest tremor respond well to?

A

dopamine replacement treatment

48
Q

when does symptoms of parkinsons disease have a poor response to treatment?

A

Less likely if rapid progression, symmetrical, lack of rest tremor, poor response to treatment, early falls, early dementia, other abnormal neurological signs

49
Q

what are cardinal signs of parkinsonism?

A

Tremor
Unilateral
At rest

Bradykinesia
Progressive decrement
(asymmetry, expressionless face)

postural instability

50
Q

what are non-motor symptoms?

A

Anosmia
REM sleep behaviour disorder
Autonomic (constipation, urinary, bowel sexual)
Neuropsychiatric (hallucinations, cognitive)
Depression, fatigue, pain

51
Q

what functional imaging can be done for parkinsons disease?

A

Dopamine transporter SPECT

52
Q

what medical treatments are available for PD?

A

COMT inhibitor
MAO-B inhibitor
Dopamine agonists
Levadopa

53
Q

what are examples of COMT inhibitors?

A

entacapone
tolcapone
opicapone

54
Q

what are examples of dopamine agonists?

A

ropinirole
pramipexole
rotigotine

55
Q

what are examples of MAO-B inhibitors?

A

selegiline
rasagiline
safinamide

56
Q

what are later drug induced complications of PD?

A

Motor fluctuations - levodopa wears off

Dyskinesias - involuntary movements (levodopa)

Psychiatric - hallucinations, impulse control

57
Q

what are later complications of PD?

A

Balance/falls/fractures
Dementia (~50% after 10 yrs)
Speech, swallow
Gait freezing

58
Q

what pharmalogical treatment can be given late into PD?

A

Prolong levodopa half life:
MAO-B inhibitors
COMT inhibitor
slow release levodopa

Add oral dopamine agonist
Continuous infusion (apomorphine, Duodopa)

Functional neurosurgery (deep brain stimulation)

Allied health professionals +/- care package

Nervous System (40 decks)

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