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Neurology > Dementia > Flashcards

Dementia Flashcards

1
Q

what is the prevalence of dementia in different age groups?

A
  • VERY RARE <55 YEARS
  • 5-10% PREVALENCE IN >65’S
  • 20% IN >80 YEARS
  • 80% IN >100 YEARS
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2
Q

what are the primary dementias?

A

ALZHEIMER’S DISEASE (60-75%)
LEWY BODY DEMENTIA (10-15%)
PICK’S DISEASE (FRONTO-TEMPORAL DEMENTIA) (<2%)
HUNTINGTON’S DISEASE

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3
Q

what are the secondary dementias?

A
  • MULTI-INFARCT (VASCULAR) DEMENTIA (20%)
  • INFECTION (HIV, SYPHILIS)
  • TRAUMA
  • METABOLIC
  • DRUGS AND TOXINS (ALCOHOL)
  • VITAMIN DEFICIENCIES (VITAMIN B1)
  • PARANEOPLASTIC SYNDROMES
  • INTRACRANIAL SPACE OCCUPYING LESIONS
  • CHRONIC HYDROCEPHALUS
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4
Q

what are the macroscopic features of Alzheimer’s?

A

o Decreased size and weight of brain (cortical atrophy)
o Location: frontal, temporal and parietal lobe atrophy
o Widening of sulci
o Narrowing of gyri
o Compensatory dilatation ventricles, 2° hydrocephalus ex vacuo
o Occipital lobe spared, brainstem and cerebellum normal

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5
Q

what are the microscopic features of Alzheimer’s?

A

Extensive neuronal loss with associated astrocyte proliferation - simple neuronal atrophy, gliosis
Neurofibrillary tangles
Neurotic Plaques
Amyloid Angiopathy

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6
Q

what are neurofibrillary tangles made of?

A

Tau protein associated with microtubules

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7
Q

where are neurofibrillary tangles found?

A

hippocampus and temporal lobe

Intracytoplasmic

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8
Q

what are neuritic plaques made of?

A

Aß amyloid plaques (dense amyloid oligomers)

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9
Q

where are neuritic plaques found?

A

Surrounding astrocytes and microglia

Found in hippocampus and parietal lobes

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10
Q

how are neuritic plaques?

A

excess intraneuronal amyloid peptides, due to overproduction or diminished clearance of beta-amyloid.
cause an inflammatory process through microglial activation, cytokine formation, and activation of the complement cascade. Inflammation leads to the formation of neurotic plaques, causing synaptic and neurotic injury and cell death.

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11
Q

what is amyloid angiopathy?

A

Polymerised beta pleated sheets formed by AB

leads to Extracellular eosinophillic accumulation

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12
Q

what is the consequence of amyloid angiopathy?

A 
Disrupts blood brain barrier:
•	Serum leaking
•	Oedema
•	Local hypoxia
•	exacerbating oxidative stress, excitotoxicity and neuronal injury
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13
Q

what are the causes of Alzhemier’s?

A

Sporadic
Familial - point mutation of apolipoprotein E – allele e4, Presenilin 1 – Chromosome 14 and Presenilin 2 – Chromosome 1
Trisomy 21

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14
Q

what are the risk factors to Alzhemier’s?

A 
o	smoking
o	midlife obesity
o	insulin resistance 
o	diet high in saturated fats 
o	???increased serum cholesterol and homocysteine levels, vitamin e and vitamin C
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15
Q

What is the summary steps of Alzheimer’s?

A

Abnormal production of AB results in AB oligomerisation and formation of plaques
which cause astrocyte, microglial activation, and possibly directly to excitotoxicity….
Main lesion = Abeta oligomer, they enter synaptic space and cause excitotoxicity = Ca2+ influx, mitochondrial dysregulation and cell death
Oligomers also cause Tau hyper-phosphorylation and mislocalisation of Tau which enhances the excitotoxicity affect of Abeta oligomers

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16
Q

what are the clinical features of Alzheimer’s?

A
  • Insidious impairment of higher intellectual function
  • gradual, progressive onset
  • memory loss – affects short term memory more than autobiographical and political
  • language deficits
  • nominal dysphagia
  • apathy
  • with alterations in mood and behaviour
  • decline in ADLs
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17
Q

what are the late clinical features of Alzheimers?

A

Progressive disorientation, memory loss and aphasia = severe cortical dysfunction
• Can result in profound disability, muteness and immobility

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18
Q

What are the initial investigations for Alzheimer’s?

A

Cognitive testing
CT and MRI
Biochemical tests
Amyloid-PET

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19
Q

what are the biochemical tests for Alzheimer’s?

A

FBC, metabolic panel, serum TSH, serum Vit-B12, urine drug screen, neuropsychological testing, serum RPR/VDRL, serum HIV, CSF analysis, egnetic testing, FDG-PET, SPECT, electroencephalogram

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20
Q

what is the main management of Alzheimer’s?

A
  • supportive treatment – OT and support groups

* cholinesterase inhibitors – donepezil, rivastigmine, rivastigmine transdermal, galantamine

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21
Q

what is the additional management of Alzheimer’s?

A

o antidepressants – sertraline, citalopram, escitalopram, mirtazapine, trazodone
o antipsychotics – risperidone, olanzapine, quetiapine, aripiprazole, haloperidol, ziprasidone
o management of insomnia
o behavioural modification – citalopram, carbamazepine, lorazepam, trazodone
o Switch to or add Memantine if severe of cholinesterase inhibitors not effective

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22
Q

what are the complications of Alzheimer’s?

A

Death usually occurs due to a secondary cause – like bronchopneumonia

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23
Q

what is the characteristic feature of Lewy body dementia?

A

accumulation of Lewy bodies

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24
Q

what are Lewy Bodies composed of?

A

alpha-synuclein

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25
Q

what is the mechanism of Lewy Body damage in LB dementia?

A

synuclein aggregates = insoluble -> cell dysfunction -> cell damage, leads to disruption of cholinergic and dopaminergic pathways

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26
Q

what part of the brain is affected in LB dementia?

A

degeneration of the substantia nigra

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27
Q

what are the macroscopic features of LB dementia?

A

pallor in the substantia nigra, where pigmented dopaminergic neurons run

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28
Q

what are the microscopic features of LB dementia?

A

o Loss of pigmented neurons
o Reactive gliosis, microglial accumulation
o Remaining neurons may show Lewy bodies:
o Fewer cortical Lewy bodies

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29
Q

what are the microscopic features of lewy bodies in neurons?

A

 “Single / multiple intracytoplasmic, eosinophilic, round to elongated bodies that have a dense core and a surrounding pale halo”
 Aggregates of a-synuclein and ubiquitin

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30
Q

what are the causes of lewy body dementia?

A
  • unknown
  • most sporadic
  • some familial clusters - alpha-synuclein gene on chromosome 4, and apolipoprotein E e4 allele.
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31
Q

what are the clinical features of lewy body dementia?

A
  • progressive dementia
  • hallucinations
  • fluctuating levels of attention/cognition
  • memory affected later than AZ
  • parkinsons features
  • REM sleep disturbance
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32
Q

what are the additional clinical features of lewy body dementia?

A

depression, falls + syncope, orthostatic hypotension, urinary incontinence + constipation, delusions, hypersomnia, hyposmia

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33
Q

what is the association between Parkinson’s and LB Dementia?

A

Everyone with lewy body dementia will get parkinsonism, Not everyone with Parkinson’s disease get Lewy body dementia

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34
Q

how is LB dementia diagnosed?

A

Cognitive testing
CT and MRI
Biochemical Investigations
Amyloid PET

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35
Q

what is the management of LB dementia?

A

Cholinesterase Inhibitors – donepezil, rivastigmine, rivastigmine transdermal, galantamine

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36
Q

what is the management of psychotic symptoms of LB dementia?

A

risperidone, olanzapine, quetiapine, pimavanserin

37
Q

what is the management of acute behavioural disturbance symptoms of LB dementia?

A

short acting benzodiazepines – lorazepam, oxazepam

38
Q

what is the management of depression and anxiety symptoms of LB dementia?

A

sertraline, citalopram, alprazolam

39
Q

what is the management of REM sleep disorder symptoms of LB dementia?

A

clonazepam or melatonin

40
Q

what is the management of motor symptoms of LB dementia?

A

carbidopa/levodopa

41
Q

what part if the brain is affected in fronto-temporal dementia?

A

extreme atrophy of cerebral cortex in frontal, and later in temporal lobes

42
Q

what are the 3 histological subtypes of fronto-temporal dementia?

A

o FTLD-Tau
o FTD-ubiquitin
o FTLD-TDP

43
Q

what is the characteristic histological feature of FT dementia?

A

Picks bodies

44
Q

what are Picks Bodies?

A

Tau = get protein aggregation and this leads to cell damage = ballooned abnormal cells

45
Q

what is the mechanism of neuron damage in FT dementia?

A

neuronal loss and gliosis – most severe in the outer three layers of the cortex with remaining neurons frequently containing picks bodies

46
Q

what is the cause of FT dementia?

A

Genetics
o tau positive – MAPT gene on Chromosome 17
o FTLD-TDP – GRN gene on chromosome 17, VCP, C9ORF72

47
Q

what are the 3 patterns of presentation of FT dementia?

A

o Behavioural Variant
o progressive non-fluent aphasia
o Sematic Dementia

48
Q

what are the features of the behavioural variant of Ft dementia?

A

 frontal lobe atrophy
 change in personality, impaired judgement, stereotyped behaviours, loss of appropriate emotional response
 relatively preserved memory

49
Q

what are the features of the progressive non-fluent aphasia variant of Ft dementia?

A

 dominant temporal lobe atrophy

 loss of verbal fluency, relatively preserved understanding

50
Q

what are the features of the sematic dementia variant of Ft dementia?

A

 bilateral temporal lobe atrophy

 loss of knowledge of the meaning of words, and knowledge about the world

51
Q

what are the additional clinical features of FT dementia?

A

Personality and behavioural change, Speech and communication problems, Changes in eating habits, Reduced attention span

52
Q

what are the investigations for FT dementia?

A

cognitive testing, brain MRI, brain CT
Biochemical testing
Brain single photon emission computed tomography, brain (FDG)-PET

53
Q

what biochemical testing is done in FT dementia?

A

FBC, serum erythrocyte sedimentation rate, serum CRP, serum thyroid-stimulating hormone (TSH), free T4, metabolic panel, serum urea, serum creatinine, LFTs, serum vitamin B12 levels, serum folate levels, syphilis serology, HIV testing, serum enzyme-linked immunosorbent assay, brain biopsy, genetic testing, cerebrospinal fluid analysis

54
Q

what is the general management of FT dementia?

A

supportive

55
Q

what is the management of irritability in FT dementia?

A

benzodiazepine or neuroleptic

56
Q

what is the management of insomnia in FT dementia?

A

mirtazapine

57
Q

what is the management of distractibility in FT dementia?

A

amantadine

58
Q

what is the management of mood swings in FT dementia?

A

valproate semi sodium

59
Q

what is the management of gluttony in FT dementia?

A

topiramate

60
Q

what is the disease progression of FT dementia?

A

rapidly progressive

61
Q

what is the onset of vascular dementia?

A

Late onset

62
Q

what is vascular dementia?

A

Disorder involving a deterioration in mental functioning due to cumulative damage to the brain through hypoxia or anoxia as a result of multiple blood clots within the blood vessels supplying the brain.

63
Q

what are the different types of vascular pathologies associated with vascular dementia?

A

infarction
leukoaraisosis
haemorrhage

64
Q

how do large infarcts lead to vascular dementia?

A

when they reach a certain volume exhaust the brain’s compensatory mechanisms and lead to dementia

65
Q

what areas of the brain are often affected in vascular dementia?

A

basal ganglia, thalamus, pons, internal capsule, deep white matter areas

66
Q

what is leukoaraisosis?

A

Loss of axons, myelin, and oligodendrocytes is noted. There is perivascular tissue loss and dilation of the perivascular spaces. There is damage to the capillaries with breakdown of the blood-brain barrier and protein leakage

67
Q

how does haemorrhage cause vascular dementia?

A

are centred in the basal ganglia are often secondary to HTN, whereas multiple small haemorrhages occurring in the cortex and white matter are usually secondary to amyloid angiopathy. The angiopathy is due to amyloid beta protein, which is deposited in the small arteriolar walls and renders them prone to rupture.

68
Q

what is the morphological appearance of large vessel vascular dementia?

A

scattered throughout hemisphere, atheroma of large cerebral arteries provoke thromboembolism

69
Q

what is the morphological appearance of small vessel vascular dementia?

A

central subcortical distribution, particularly related to longstanding hypertension and arteriosclerosis of small vessels

70
Q

what are the causes of vascular dementia?

A

Vascular pathologies

Strokes

71
Q

what are the risk factors to developing vascular dementia?

A

obesity, hypertension, cigarette smoking, diabetes, hypercholestrolaemia, alcohol abuse

72
Q

what is the progression of vascular dementia?

A

Abrupt onset

stepwise progression

73
Q

what are the clinical features of vascular dementia?

A
  • apathy
  • disinhibition
  • poor attention
  • focal neurological signs
  • slowed processing of information, retrieval memory deficit
  • prone to depression and anxiety
  • may also have - pseudobulbar palsy, shuffling gait
74
Q

how is vascular dementia diagnosed?

A

Cognitive tests
Biochemical tests
Imaging - CT, MRI, carotid duplex, echocardiogram

75
Q

what biochemical tests are used in investigating vascular dementia?

A

FBC, erythrocyte sedimentation rate, blood glucose level, renal and LFTs, syphilis serology, vitamin B12, folate, thyroid function, lupus anticoagulant, antiphospholipid, and antinuclear testing

76
Q

what is the preventative management of vascular dementia?

A

Aspirin or warfarin therapy

Controlling BP Anticholinesterases and memantine

77
Q

what is the management of atherosclerotic ischaemic disease in the context of vascular dementia?

A

antiplatelet therapy + lifestyle modification + carotid endarterectomy or carotid angioplasty and stenting + cholinesterase inhibitors or memantine + BP control + statin therapy + optimisation of glycaemic control

78
Q

what is the management of cardioembolic disease in the context of vascular dementia?

A

anticoagulation or antiplatelet + lifestyle modification + cholinesterase inhibitors or memantine + BP control + statin therapy + glycaemic control

79
Q

when is the onset of posterior cortical atrophy?

A

50-60s (earlier than AD)

80
Q

what part of the brain is affected in posterior cortical atrophy?

A

posterior part of cerebral cortex

81
Q

what is the macroscopic feature of PCA?

A

loss of grey matter in posterior part of cerebral cortex

82
Q

what is the histological features of PCA?

A

like AD - senile plaques and neurofibrillary tangles

83
Q

what are the causes of PCA?

A

dementia with lewy bodies

Creutzfeldt-Jakob disease

84
Q

what are the clinical features of PCA?

A

Visual spatial and visuoperceptual disturbance
Progressive primary aphasia
Difficulties with: recognising faces, handwriting or reading, mental arithmetic, dealing with money, co-ordination

85
Q

how does Visual spatial and visuoperceptual disturbance present in PCA?

A

starts as difficulty reading, blurred vision, light sensitivity, depth perception

86
Q

what are the features of progressive primary aphasia in PCA?

A

o Semantic (naming)
o Logopenic aphasia (repeating)
o Non-fluent aphasia (effortful)

87
Q

how is PCA diagnosed?

A
  • History
  • MRI - atrophy of temporal and parietal lobes
  • SPECT: temporoparietal decreased metabolism (before atrophy so useful in scan normal)
  • CSF: decrease amyloid to tau reaction
88
Q

what is the management of PCA?

A 
Similar to Alzheimers
•	Address vascular RF's 
•	Ach boosting Rx: 
•	Chonesterase I's: Rivastigmine/galantamine 
•	NMDA R blocker Memantine

Neurology (18 decks)

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