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Phase 3a Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

What is essential tremor?

A

autosomal dominant tremor
affects both upper limbs

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2
Q

features of essential tremor

A

postural tremor : worse if arms outstretched. nothing on relaxed

improved by alcohol and rest

mc cause of titubation (head tremor)

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3
Q

management of essential tremor

A

1st line: propranolol

primidone sometimes

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4
Q

most common causes of dementia

A

1st: alzheimers
2nd: vascular and lewy body

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5
Q

assesment tools of dementia

A

delayed/difficult diagnosis

recommended assesment tool: 10-cs or 6CIT

non recommended but can do: AMTS, GPCOG, MMSE (24 or less/30 is dementia)

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6
Q

initial investigations in dementia

A

primary care: blood screen to exclude reversible causes eg hypothyroidism

fbc, u+e, lft, calcium, glucose , esr/crp, tft, vit b12, folate.

secondary care: neuroimaging - exclude subdural haematoma, normal pressure hydrocephalus.

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7
Q

Define Delirium

A

acute confusional state.
affects 30% of elderly admitted to hospital.

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8
Q

presdisposing factors to delirium

A

age>65
dementia background
significant injury eg hip fracture
polypharmacy
frailty/multimorbidity

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9
Q

precipitating factors for delirium

A

infection: uti
environmental change
severe pain
alcohol withdrawal
constipation
any significant cv, resp, neuro, endo condition
metabolic: hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration

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10
Q

features of delirium

A

memory disturbance (loss of short term>long term)
mood change
visual hallucination
disturbed sleep cycle
possibly agitated/withdrawn
poor attention
disoriented

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11
Q

how would you manage delirium?

A

tx underlying cause
change environment

haloperidol 0.5mg : 1st line sedative
possibly olanzapine

if parkinson patient, antipycotic worsen parkinsonism symptom - careful reduction of parkinson medication helpful.

if sx require urgent tx give atypical antipsychotic like quetiapine/clozapine

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12
Q

difference between delirium and dementia (favouring delirium)

A

acute onset
impaired conciousness
fluctuating symptoms - worse @ night, periods of normality

abnormal perception (illusions and hallucinations)

agitation, fear

delusions

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13
Q

depression vs dementia (favouring depression)

A

short history, rapid onset

patient worried about poor memory

reluctant taking tests, disappointed w/ results

MMSE: variable

global memory loss - dementia is recent memory loss

biological sx: wt loss, sleep disturbance

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14
Q

what is alzheimers?

A

progressive degenerative disease of the brain.

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15
Q

rf of alzheimers

A

increasing age
fhx of alzheimers
caucasian
downs syndrome
apoprotein E allele E4 - encodes a cholestrol transport protein

5% cases - inherited autosomal dominant trait. mutation in amyloid precursor protein (chr 21) , presenilin 1 (chr 14) and presenilin 2 (chr 1) genes - thought to cause inherited form

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16
Q

Pathological changes for alzheimers

A

macroscopic: widespread cerebral atrophy, particular involves cortex and hippocampus

microscopic: cortical plaques due to deposition of type A - beta - amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of tau protein
hyperphosphorylation of tau protein linked to AD

biochemical: deficit of acetylcholine from damage to an ascending forebrain projection

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17
Q

what are neurofibrillary tangles?

A

paired helical filaments made from tau protein.

in AD tau proteins excessively phosphorylated= impaired function

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18
Q

what is tau protein?

A

Alzhiemers

protein interacting with tubulin.
stabilises microtubules
promotes tubulin assembly into microtubules

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19
Q

how would you manage alzheimers? (non-pharmacological)

A

activities to promote wellbeing tailored to preference

group cognitive stimulation therapy - mild/moderate dementia

group reminiscence therapy , cognitive rehab

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20
Q

how would you manage alzheimers (pharmacological mx)

A

acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine) - mild/moderate

memantine - nmda receptor antagonist. - 2nd line or monotherapy in severe alzheimers

moderate to severe: acetylcholineesterase inhibitor + memantine

moderate alzheimers intolerant of/contraindication of acetylcholinesterase inhibitors: memantine

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21
Q

how would you manage non cognitive symptoms in alzheimers?

A

NO to antidepressants for mild/moderate depression in patients with dementia

antipsycotics only for patient at risk of harming themselves or others/agitation/hallucination/delusions causing severe distress (increased risk of mortality)

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22
Q

which drug is contraindicated in alzheimers treatement in patients with bradycardia?

A

donepezil (Acetylcholine esterase inhibitor)

adverse effect: insomnia

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23
Q

causes of dementia

A

common : alzheimers,
lewy body (10-20%), cerebrovascular disease : multi-infarct dementia (10-20%)

rarer (5%) - huntingtons, CJD, picks disease (atrophy of frontal/temporal lobes), HIV (50% of AIDS pts)

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24
Q

important differentials for dementia

A

hypothyroid, addisons
b12/folate/thiamine def
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use: alcohol, barbiturates

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25
what is lewy body dementia?
20% of dementia cases. lewy bodies (alpha-synuclein cytoplasmic inclusions) in substantia nigra, paralimbic and neocortical areas.
26
where would you find lewy bodies
substantia nigra paralimbic neocortical areas
27
what percentage of alzherimers patients have lewy bodies?
40%
28
features of lewy body dementia
parkinsonism visual hallucination - delusion and non-visual hallucination too) progressive cognitive impairement - BEFORE PARKINSONISM. - parkinsons is motor symptoms a yr before cognitive. FLUCTUATING COGNITION COMPARED WITH DEMENTIA
29
HOW DOES LEWY BODY DEMENTIA COMPARE WITH ALZHEIMERS
IN LEWY BODY EARLY IMPAIREMENT IN ATTENTION AND EXECUTIVE FUNCTION RATHER THAN JUST MEMORY LOSS.
30
diagnosis of lewy body dementia
clinical single-photon emission computed tomography (SPECT) / DaTscan. isotope used: 123-I-FP-CIT - radioisotope.
31
what is the sensitivity and specifity of SPECT in diagnosing lewy body dementia
sensitivity: 90% specificity: 100%
32
how would you manage lewy body dementia?
acetylcholinesterase inhibitors - donepezil, rivastigmine) AVOID NEUROLEPTICS - pts could get irreversible parkinsonism.
33
what drug should lewy body dementia patients avoid?
NEUROLEPTICS - can develop irreversible parkinsonism.
34
causes of parkinsonisms
parkinson's drug-induced eg antipsychotics, metoclopramide progressive supranuclear palsy - neurological condition causes issue with balance, movement,vision,speech, swallowing. wilsons disease post-encephalitis toxins: carbon monoxide, MPTP
35
what is the first line anti-emetic ( used for parkinsons?
domperidone - doesnt cross blood brain barrier. no extra-pyramidal side effects (movement disorder, parkinonism, tremor)
36
what is vascular dementia?
group of syndromes of cognitive impairement caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease.
37
epidemiology of vascular dementia
17% of uk dementia. prevalence following first stroke depends on location/size of infarct, interval after stroke, age. overall stroke doubles risk. incidence increase with age
38
subtypes of vascular dementia
stroke related - multi-infarct or single-infarct dementia subcortical - caused by small vessel disease mixed - presence of both VD and Alzheimers
39
risk factors of Vascular dementia
hx of tia AF HTN DM SMOKING OBESITY CORONARY HEART DISEASE HYPERLIPIDEMIA FHX OF STROKE/CV
40
can vascular dementia be inherited?
rarely if so CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)
41
presentation of vascular dementia typically
several months/years of hx of a sudden or stepwise deterioration of cognitive function.
42
symptoms of vascular dementia
speed of progression and sx may vary : seizures gait disturbance emotional disturbance memory disturbance attention and concentration difficulty focal neurological abnormality: visual disturbance, sensory/motor sx.
43
how to make diagnosis of vascular dementia?
hx and physical exam formal screen for cognitive impairement medical review - exclude medication cause of cognitive decline MRI - show infarcts and extensive white matter changes
44
criteria for diagnosing vascular dementia
NINDS-AIREN presence of cognitive decline interfering with ADLs, not due to secondary effects of cv event. (clinical exam and neuropsychological testing) cv disease - neurological signs/brain imaging relationship between the above 2 disorders: - fluctuating,stepwise deterioration of cognitive deficit - abrupt deterioration of cognitive function - onset of dementia within 3 months following recognised stroke
45
how would you manage vascular dementia?
symptomatic non pharma: cognitive stimulation programme multisensory stimulation music/art therapy, animal assisted therapy address pain, avoid overcrowding, clear communication pharma: only with AChE inhibitor/memantine if have VD and Alzheimers,Parkinsons dementia or dementia w/ Lewy Bodies. NO EVIDENCE OF ASPIRIN TREATING PTS WITH VD no trails showed statins good to tx of vd
46
what is normal pressure hydrocephalus?
reversible cause of dementia. elderly secondary to reduced CSF absorption at the arachnoid villi. could be due to head injury, subarachnoid haemorrhage or meningitis.
47
classic triad of features seen in normal pressure hydrocephalus
urinary incontinence dementia and bradyphrenia(slowness of thought) gait abnormality - similar to parkinsons sx typically develop over a few months
48
imaging for normal pressure hydrocephalus
MRI - ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement
49
how would you manage normal pressure hydrocephalus?
ventriculoperitoneal shunting
50
potential complications of ventriculoperitoneal shunting treatment?
10% of patients seizures infection intracerebral haemorrhages
51
what is parkinsons diseases
progressive neurodegenerative caused by degeneration of dopaminergic neurones in substantia nigra. reduction in dopaminergic output results in triad of features.
52
parkinson classic triad
bradykinesia - hypokinesia,short shuffling steps , reduced arm swing, difficulty initiating movement tremor - at rest, 3-5 hz, worse when stressed/tired, voluntary movement improves. - PIN-ROLLING rigidity - lead pipe. cogwheel: superimposed tremor
53
are parkinsons symtoms symmetrical or asymmetrical?
asymmetrical!!
54
epidemiology of parkinsons
twice as common in men mean age of diagnosis: 65
55
other features of parkinsons
mask-like facies flexed posture micrographia - small writing drooling of saliva rem sleep behaviour disorder fatigue autonomic disfunction: postural hypotension impaired olfaction psychiatric: depression - 40% , dementia, psychosis, sleep disturbed
56
drug-induced parkinsonism features:
motor symptoms bilateral and rapid onset. rigidity and rest tremor uncommon
57
how would you diagnosis parkinsons?
clinical. if hard to differentiate between essential tremor and parkinsons consider : SPECT single photon emission computed tomography 123 i - fp - cit
58
what colour stain is for lewy body?
brown - alpha synuclein
59
how would you manage parkinsons?
1st line: levodopa - if motor sx affect QoL non-ergot derived dopamine agonist (ropinirole,rotigotine,apomorphine), levodopa, monoamine oxidase B inhibitor - if motor sx dont affect QoL
60
give an example of a monoamine oxidase b inhibitor and tell us how it works?
selegelline inhibits breakdown of dopamine secreted by dopaminergic neurones
61
common adverse affects of levodopa
dry mouth anorexia palpitations postural hypotension psychosis
62
give an example of a catechol-o-methyl transferase inhibitor and how is works?
entacapone, tolcapone comt is enzyme involved in dopamine breakdown, could use as adjunct in levodopa therapy. esp with pts with established pd give with levodopa
63
give examples of antimuscarinics and tell us how they work
procyclidine, benzotropine, trihexyphenidyl (benzhexol) block cholinergic receptors treat drug-induced parkinsonism rather than idiopathic parkinsons disease help tremor and rigidity
64
what class of drug is amantadine and what is its function?
antidyskinetic most likely increases dopamine release and inhibits uptake at dopaminergic synapses se: ataxia, slurred speech, confusion, dizziness, livedo reticularis (spasm of blood vessel near skin surface)
65
give examples of dopamine receptor agonists and potential side effects
bromocriptine, ropinirole, cabergoline, apomorphine ergot derived : pulmonary,retroperitoneal and cardiac fibrosis. DO ECHO, ESR, CREATININE AND CXR BEFORE AND DURING TX. INFORM PT POTENTIAL IMPULSE CONTROL DISORDER AND EXCESSIVE DAYTIME SOMNOLENCE(sleepy) hallucination (more likely than levodopa in elder patients) nasal congestion , postural hypotension.
66
what drug is nearly always combined with levodopa in PD tx and why?
decarboxylase inhibitor (carbidopa or benserazide) prevents peripheral metabolism of levodopa to dopamine outside of brain so reduce side effects
67
what do you give if patient has sx despite optimal levodopa or developed dyskinesia?
add dopamine agonist, MAO-B inhibitor or COMT inhibitor as adjunct.
68
in parkinsons, what can cause acute akinesia or neuroleptic malignant syndrome?
medication not taken/absorbed - gastroenteritis no drug holidays
69
causes of impulse control disorder
dopamine agonist therapy hx of previous impulse behaviours hx of alcohol consumption and/or smoking
70
patient develops excessive daytime sleepiness, he has pmh of parkinsons. how to treat?
do not drive. adjust med to control symptoms. give modafinil.
71
patient with parkinsons develops orthostatic hypotension. what to do?
medication review midodrine (acts on peripheral alpha-adrenergic receptors to increase arterial resistance)
72
patient with parkinsons develops drooling of sailva. how to treat?
glycopyrronium bromide
73
things to know about prescribing levodopa
adverse affects due to difficulty achieving steady dose: end of dose wearing off - sx worsen at end of dosage interval. decline in motor activity. on-off phenomenon - large variation in motor performance. normal function in on period. weakness/restricted mobility in off. dyskinesia at peak dose: dystonia (muscle contraction) , chorea(involuntary muscle movements) and athetosis(involuntary writhing movements)
74
rules for administering and stopping levodopa
dont acutely stop levodopa if pt with PD cant take levodopa orally, give dopamine agonist patch as rescue medication to prevent ACUTE DYSTONIA (muscle contraction)
75
what is MND and types??
neuro condition of unknown cause can present with both UMN,LMN signs. amyotrophic lateral sclerosis progressive muscular atrophy bulbar palsy primary lateral sclerosis rarely presents before 40.
76
clues pointing towards MND diagnosis
asymmetric limb weakness - MC ALS no sensory deficits mixed umn and lmn signs wasting of small hand muscles/ tibialis anterior fasciculations you might get vague sensory symptoms in early disease (limb pain) but never sensory signs
77
what muscles are spared in MND?
external ocular muscles - eyes are spared. no cerebellar signs abdominal reflexes preserved and sphincter dysfunction (late feature)
78
how would you diagnose MND?
clinical nerve conduction study - normal motor conduction - help exclude neuropathy. elelectromyography shows - reduced number of action potentials with increased amplitude. MRI - excludes differentials of cervical cord compression and myelopathy
79
mnd type - presentation - ALS - AMYOTROPHIC LATERAL SCLEROSIS
50% pts typically LMN signs in arms UMN signs in legs in familial cases, gene responsible lies on chr 21 and codes for superoxide dismutase
80
presentation of primary lateral sclerosis - MND
UMN signs only
81
presentation of MND - Progressive Muscular Atrophy
LMN signs only affects distal muscles before proximal carries best prognosis
82
presentation of progressive bulbar palsy - MND
palsy (paralysis) of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei carries worst prognosis
83
how to manage MND?
riluzole - prevents stimulation of glutamate receptors . used in ALS mainly - prolongs life by about 3 months respiratory care - non invasive ventilation (BIPAP) @ night. 7 months survival benefit PEG tube - nutrition
84
prognosis of mnd
50% of patients die within 3 years
85
what is multiple sclerosis?
chronic cell-mediated autoimmune disorder characterised by demyelination in the CNS.
86
epidemiology of MS - multiple sclerosis
3 times more common in women 20-40 much more common at higher latitudes (5 times more common than in tropics.
87
genetics with multiple sclerosis
monozygotic twin concordance = 30% dizygotic twin concordance = 2%
88
subtypes of multiple sclerosis
relapsing remitting - 85% mc - acute attacks (1-2mths) followed by remission periods secondary progressive - relapsing remitting pts with deteriorating w/ neurological signs and symptoms between relapses. (65% pts develop within 15 yrs) - gait and bladder disorders seen too primary progressive disease - 10% pts - progressive deterioration from onset. mc older ppl.
89
how would you investigate for multiple sclerosis?
YOU NEED TO SEE LESIONS DISSEMINATED IN TIME AND SPACE MRI CSF VISUAL EVOKED POTENTIALS
90
when you do an MRI in someone with multiple sclerosis what will you see?
high signal t2 lesions periventricular plaques dawson fingers : seen in FLAIR images - hyperintense lesions perpendicular to corpus callosum
91
when you do a lumbar puncture in a multiple sclerosis pt , what would you see?
csf: oligoclonal bands - not in serum increased intrathecal synthesis of IgG
92
when you do visual evoked potentials in a multiple sclerosis pt, what would you see?
delayed, but well preserved waveform
93
how could you diagnose multiple sclerosis?
2 or more relapses and either objective clinical evidence of 2 or more lesions or objective clinical evidence of 1 lesion + reasonable historical evidence of previous relapse
94
visual features of multiple sclerosis
optic neuritis : MC optic atrophy UHTHOFF'S PHENOMENON - worsening of vision following body temp rise internuclear opthalmoplegia
95
sensory features of multiple sclerosis
pins/needles numbness trigeminal neuralgia lhermitte's syndrome : paresthesia in limbs on neck flexion
96
motor features of multiple sclerosis
spastic weakness: mc legs
97
cerebellar features of multiple sclerosis
ataxia : more often in acute relapse than presenting symptom tremor
98
general features (non specific) of Multiple Sclerosis
LETHARGY (85%) urinary incontinence sexual dysfunction intellectual deterioration
99
is there a treatment for multiple sclerosis?
tx focused on reducing frequency and duration of relapse. NO CURE
100
what drug would you give in an acute relapse of multiple sclerosis and for how long?
high dose steroids - oral/iv methylprednisolone - 5 DAYS shortens length of acute relapse. but not degree of recovery
101
why would you give a disease modifying drug in multiple sclerosis , indications and examples?
reduce risk of relapse indications: relapse remitting disease + 2 relapses in past 2 yrs+ able to walk 100m unaided secondary progressive + 2 relapses in lasat 2 yrs + able to walk 10m (aided/unaided) natalizumab - iv - 1st line ocrelizumab - iv fingolimod - oral formulation beta-interferon - subcut/intramuscular (not as effective as others) qlatiramer acetate - subcut
102
MoA of natalizumab - MS 1st line DMD
recombinant monoclonal antibody - antagonises alpha 4 beta 1 integrin on surface of leucocytes. inhibits migration of leucocytes across endothelium across blood brain barrier strongest base for preventing relapse - 1st line give IV
103
class of drug - ocrelizumab - MS tx
humanized anti-cd20 monoclonal antibody high-efficacy drug - often 1st line like natalizumab GIVE IV
104
what type of drug is fingolimod , MoA ? MS TX
sphingosine 1 phosphate receptor modulator prevents lymphocytes from leaving lymph nodes ORAL FORMULATION
105
what type of drug is glatiramer acetate? MS TX
immunomodulating drug - acts as a immune decoy GIVE SUBCUT older drug - less effective like beta interferon - monoclonal antibodies and s1p receptor modulators more effective.
106
if a MS pt experiences fatigue, how could you treat?
trial AMANTADINE - if anaemia, thyroid, depression

Phase 3a Medicine (16 decks)

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