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Neuro Flashcards

1
Q

what is MS?

A

it is the demyelination of the CNA due to activation of immune cels against myelin

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2
Q

what are the causes of MS and how is it investigated?

A

genetic, EBV, decreased vitamin D, smoking and obesity
diagnosis - clinical - over 1 year, MRI and LP (oligoclonal bands)

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3
Q

how does MS present?

A

develops over more than 24 hours and can last a few days or weeks - optic neuritis, eye movement abnormalities, focal weakness, focal sensory symptoms, sensory and cerebellar ataxia

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4
Q

what are some disease patterns of MS?

A

clinically isolated, relapsing remitting, secondary progressive and primary progressive

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5
Q

what are the complications of MS?

A

optic neuritis - unilateral loss of vision, central scotoma, pain on eye movements, impaired colour vision, RAPD
eye movement abnormalities - lesions in CNV1 - unilateral = internuclear ophthalmoplegia, bilateral = conjugate lateral gaze disorder
focal weakness - bells, horners, incontinence, limb paralysis
focal sensory - trigeminal neuralgia, numbness, paraesthesia, Lhermitte’s sign

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6
Q

how is MS managed?

A

disease modifying and biologic therapy
relapses with methylprednisolone
symptomatic - exercise, antidepressants, amitriptyline, anticholinergics, baclofen, physio, gabapentin

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7
Q

what is the difference between TIA and stroke?

A

TIA is ischaemia without infarction whereas stroke has infarction

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8
Q

what are the risk factors and presentation of stroke?

A

risk factors - CVD, previous stroke or TIA, AF, carotid artery disease, HTN, smoking, vasculitis, thrombophilia, COCP
presentation - weakness, visual or sensory loss, dysphagia

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9
Q

how is stroke investigated?

A

diffusion weighted MRI, CT, carotid USS

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10
Q

how is stroke managed?

A

r/o hypoglycaemia
CT brain to r/o haemorrhage
aspirin 300mg stat for 2 weeks
thrombolysis - alteplase within 4-5 hours
thrombectomy within 24 hours
TIA - aspirin 300mg OD and CVD prevention

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11
Q

what is the secondary prevention for stroke?

A

clopidogrel 75mg OD, atorvastatin 80mg, carotid endarterectomy, treat risk factors

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12
Q

what are the risk factors for intracranial bleeds?

A

head injury, HTN, aneurysms, ischaemic stroke, tumours, anticoagulants,

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13
Q

how does intracranial bleed present?

A

sudden onset headache, seizures, vomiting, weakness, decreased LOC, neuro sx

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14
Q

summarise extradural?

A

rupture of MMA - biconvex shape and limited by sutures
neuro sx, consciousness then LOC - younger with TBI

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15
Q

summarise intracerebral?

A

infarct, tumour or rupture and presents similarly to ischaemic

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16
Q

summarise subdural?

A

bridging veins between dura and arachnoid - crescent - not limited by sutures on CT - elderly and alcoholics

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17
Q

what is the management for intracranial bleeds?

A

CT, FBC, clotting, I+V, correct clotting, correct severe HTN, coiling, clipping

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18
Q

how does SAH present?

A

after strenuous activity - thunderclap headache in occipital region with neck stiffness, photophobia, visual changes, neuro sx

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19
Q

how is SAH investigated and managed?

A

ix - CT (hyperattenuation), LP (increased RCC, xanthochromia), angiography
mx - surgical coiling or clipping, nimodipine, LP or shunt insertion, antiepileptics

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20
Q

what is parkinsons?

A

it is a progressive decrease in dopamine in the BG resulting in disorders of movement
it is asymmetrical with resting tremor, rigidity, bradykinesia

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21
Q

what is the presentation of parkinsons?

A

typically a male in 70s
pin rolling, unilateral tremor that improves on voluntary movement, cogwheel rigidity, bradykinesia, depression, postural instability, sleep disturbance, anosmia, CI and memory issues

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22
Q

how is Parkinsons managed?

A

levodopa combined with carbidopa, COMTi, dopamine agonists, MAOis

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23
Q

what are some side effects of parkinson medications?

A

dopas - dyskinesias, athetosis, dystonia, chorea
dopamine agonists - PF

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24
Q

what is epilepsy?

A

it is an umbrella term for the tendency to have seizures

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25
Q

what are focal seizures?

A

temporal - hearing loss, speech, memory, emotions - hallucinations, flash backs, strange behaviour, deja vu - use lamotrigine or carbamazepine then valproate or levetiracetam

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26
Q

what are absence seziures?

A

they occur in children for around 10-15 seconds and are managed with valproate or ethosuximide

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27
Q

what are atonic seizures?

A

drop attacks in Lennox Gastaut syndrome - valproate or lamotrigine

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28
Q

what are myoclonic seizures?

A

they are sudden, brief contractions - usually awake - part of juvenile epilepsy - valproate then lamotrigine, levetiracetam or topiramate

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29
Q

what are infantile spasms?

A

about 6m of age, part of West syndrome, most die by 25
managed with prednisolone or vagibatran - full body spasms

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30
Q

describe the side effects of drugs used in epilepsy?

A

valproate - increases GABA - teratogenic, hair loss, tremor, liver damage, hepatitis
carbamazepine - agranulocytosis, aplastic anaemia, lots of interactions
phenytoin - folate and vitamin D decrease, megaloblastic anaemia, osteomalacia
ethosuximide - night terrors and rash
lamotrigine - SJS, DRESS, leukopenia

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31
Q

what is status epilepticus?

A

it is a seizure over 5 minutes or over 3 in one hours - A-E including glucose levels, IV lorazepam 4mg, repeat after 10m, IV phenytoin, or phenobarbital

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32
Q

what is MND?

A

it is when the motor neurons stop functioning - ALS, progressive bulbar palsy, PLS and PMA
upper and lower motor neurons but sensory spared

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33
Q

what are risk factors for MND?

A

genetics, smoking, heavy metals, pesticides

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34
Q

how does MND present?

A

insidious onset - progressive weakness of limbs, trunk, face and speech
first upper limb clumsiness, tripping, dysarthria
LMN - muscle wasting, decreased tone, fasciculations, decreased reflexes
UMN - increased tone, spasticity, increased reflexes, upgoing plantars

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35
Q

how is MND diagnosed and managed?

A

clinical diagnosis once ruled out other causes
management - riluzole can slow progression, NIV, EoL care planning advanced directives

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36
Q

what is benign essential tremor?

A

it is a fine tremor affecting voluntary muscles

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37
Q

what is the presentation of benign essential tremor?

A

symmetrical fine tremor, more prominent on voluntary movements, worse with caffeine, stress, tiredness, and improved with alcohol

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38
Q

how is BET managed?

A

propanolol, primidone

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39
Q

what is the presentation of brain tumours?

A

focal neuro symptoms depending on location
signs of raised ICP - change in personality, papilloedema, headache
altered MS, visual field defects, seizures, ptosis, 3rd and 6th nerve palsies

40
Q

how do acoustic neuromas present?

A

tinnitus, hearing loss, balance problems, facial nerve palsies

41
Q

summarise gliomas?

A

glial cells - astrocytomas, oligodendrogliomas, ependymomas
grades 1-4

42
Q

how do pituitary tumours present?

A

bitemporal hemianopia, hormone deficiencies or excess - acromegaly, thyrotoxicosis, cushings, hyperprolactinaemia

43
Q

how are brain tumours managed?

A

palliation, chemo, radio, surgery
pituitary - transspenoidal surgery, RT, bromocriptine, somatostatin analogues

44
Q

what is facial nerve palsy?

A

it is an isolated dysfunction of the facial nerve resulting in unilateral facial weakness

45
Q

what are the causes of facial nerve palsy?

A

UMN - stroke, MND, bulbar, tumour - forehead is spared
LMN - infection, systemic such as DM, tumours, trauma e.g. surgery

46
Q

how does LMN present?

A

Bells - ptosis, loss of nasolabial fold, forehead included - prednisolone 50mg for 10 days or 60mg for 5 days then reduce by 10mg over 5 days, lubricating eye drops
Ramsay Hunt - VZV - tender and vesicular rash around ear canal - prednisolone, aciclovir and lubricating eye drops

47
Q

what is huntingtons?

A

it is a progressive deterioration of the nervous system - asymptomatic until around 30-50 years old - AD inheritance with anticipation resulting in earlier age of onset and increased severity as the trinucleotide repeats increase

48
Q

how is huntingtons diagnosed and managed?

A

genetic testing and counselling
mx - SALT, genetic counselling, advanced directives, antipsychotics, benzodiazepines, dopamine depleting agents, antidepressants

49
Q

how does huntingtons present?

A

cognitive, psychiatric or mood problems, chorea, eye movement disorders, dysarthria, dysphagia

50
Q

what is neuropathic pain?

A

it is the abnormal functioning of sensory nerves delivering abnormal painful signs to brain - burning, tingling, pins and needles, electric shocks, loss of sensation

51
Q

what causes neuropathic pain?

A

infection such as shingles, MS, diabetic neuralgia, CRPS, surgery, trigeminal neuralgia

52
Q

what is the management of neuropathic pain?

A

amitriptyline, duloxetine, gabapentin, pregabalin
flares - tramadol
localised - capsaicin cream
strength - physio
coping - psych input
TN - carbamazepine

53
Q

what is myasthenia gravis?

A

it is an autoimmune condition, with muscle weakness getting worse with activity and better with rest

54
Q

how does MG present?

A

proximal muscle weakness, extraocular weakness, eyelid weakness, swallowing difficulty, slurred speech, jaw fatigue, progressive weakness
repeated blinking test, upward gazing test, repeated arm abduction test, thyectomy scar and FVC can point to diagnosis

55
Q

how is MG investigated?

A

Ach receptor antibodies and muscle specific kinase and low density lipoprotein receptor 4 antibodies
CT or MRI thymus
edrophonium tests

56
Q

how is MG managed?

A

reversible acetylcholinesterase inhibitors such as neostigimine, immunosupression with aza or pred, thymectomy, monoclonal ABs - rituximab

57
Q

what is a myasthenic crisis?

A

life threatening, often triggered by infection
BiPAP or I+B, IVIg and plasma exchange are management options

58
Q

what is guillan barre?

A

it is an acute paralytic polyneuropathy - acute symmetrical ascending weakness from infection eg EBV

59
Q

what is the pathophysiology of GBS?

A

molecular mimicry - B cells make ABs to antigens and the proteins match those on nerve cell proteins so myelin sheath is also targetted

60
Q

how does GBS present?

A

symmetrical, ascending weakness, reduced reflexes, peripheral loss of sensation, neuropathic pain, progress to cranial nerves and cause facial weakness

61
Q

how is GBS investigated and managed?

A

Brighton criteria, nerve conduction studies, LP
mx - IVIg, plasma exchange, supportive, VTE prophylaxis

62
Q

what are the red flags for headaches?

A

fever, photophobia, neck stiffness, new neuro sx, dizziness, pregnancy, visual disturbance, Hx trauma, vomiting, waking up from sleep, postural, worse on straining, sudden occipital

63
Q

what are some investigations for headache?

A

clinical, BP, fundoscopy, CT, MRI

64
Q

summarise a tension headache?

A

mild, band like, muscle aches cause, gradual onset and resolution, associated with stress, depression, alcohol, hunger, dehydration
mx - reassurance, relaxation, simple analgesia, hot compress

65
Q

summarise sinusitis?

A

inflammation in sinuses- facial pain, tenderness, mostly viral
self resolving in 2-3w
if required then nasal irrigation with saline, steroid spray and ABx if suspect bacterial

66
Q

summarise cervical spondylosis?

A

degenerative changes in cervical spine - worse with movement

67
Q

summarise trigeminal neuralgia?

A

associations with MS
spontaneous facial pain seconds to hours - electric shock shooting pain
triggers are cold, spice, caffeine, citrus fruits
management - carbamazepine, surgery to decompress or intentionally damage nerve

68
Q

how is hormonal headache treated?

A

can be treated with COCP

69
Q

what are the types of migraine?

A

with or without aura, hemiplegic, silent

70
Q

how does migraine present?

A

headaches of 4-72 hours, moderate to severe intensity, pounding, throbbing, uni or bilateral, photo or phonophobia, aura, N+V
aura - visual changes, loss of visual field, sparks, blurs, lines
hemiplegic - mimic stroke - sudden or gradual onset hemiplegia, ataxia and change in LOC

71
Q

what are the 5 stages of a migraine?

A

premonitory or prodromal - yawning, fatigue, mood changes
aura up to 60m
headache of 4-72 hours
resolution through vomiting or sleep
post dromal or recovery

72
Q

what are some triggers for migraines?

A

stress, bright lights, smells, foods, dehydration, menstruation, abnormal sleeping patterns, trauma

73
Q

how are migraines prevented?

A

avoid triggers, propanolol, topiramate, amitriptyline

74
Q

how are migraines treated?

A

paracetamol, triptans, NSAIDs, antiemetics, quiet, dark room

75
Q

what are cluster headaches?

A

they are severe, unbearable unilateral headaches around the eyes that are usually in groups of 3-4 attacks per day for weeks to months and remission periods of years
attacks last 15m-3h

76
Q

what is the typical patient with cluster headache?

A

male, smoker, triggered by alcohol, smells and exercise

77
Q

how does a cluster headache present?

A

red, swollen, watering eye, miosis, ptosis, nasal discharge, facial sweating

78
Q

how are cluster headaches prevented?

A

verapamil, lithium or prednisolone

79
Q

how are cluster headaches managed?

A

triptans (sumatriptan 6mg SC) or 100% oxygen for 15-20 minutes

80
Q

what is charcot marie tooth disease?

A

it is an autosomal dominant inherited dysfunction of myelin on the PNS - motor and sensory
presents at less than 10y or over 40y

81
Q

what causes CMT disease?

A

alcohol, B12 deficiency, cancer, CKD, DM, drugs, vasculitis

82
Q

how does CMT disease present?

A

high foot arches, distal muscle wasting, LL weakness, hand weakness, reduced reflexes and muscle tone, and peripheral sensory loss

83
Q

how is CMT managed?

A

physio, occupational therapy, podiatry, surgery to correct joints

84
Q

what is lambert eaton myasthenic syndrome?

A

it is progressive muscle weakness with use due to damage at NMJ but less pronounced than MG

85
Q

what is the usual pathophysiology of CMT?

A

it present typically due to SCLC - ABs against VG Ca channels - destroy channel so less Ach released into synapse

86
Q

how does LEMS present?

A

proximal - leg muscle weakness, diplopia, ptosis, slurred speech, dysphagia, dry mouth, blurred vision, impotence, dizziness, reduced reflexes, post tetanic

87
Q

what is the management of LEMS?

A

ix for SCLC
amifampridine, block VG K channels - prolongs depolarisation and time for Ca channels to work
IVIg
plasmapheresis
immunosuppressants

88
Q

what is neurofibromatosis?

A

development of nerve tumours - they are benign but can cause structural damage

89
Q

what is the pathophysiology for NF?

A

NF1 gene - Cr17 - mutation of neurofibrin gene which is a TSG - AD
NF2 gene - Cr22 - merlin protein - TSG

90
Q

how is NF diagnosed?

A

2/7 features: cafe au lait spots, relative with NF, axillary or inguinal freckles, bony dysplasia, iris hamartomas, neurofibromas, glioma of optic nerve
clinical criteria, genetic testing, XR bone lesions, CT or MRI

91
Q

how does NF2 present?

A

acoustic neuromas, hearing loss, tinnitus, balance problems - bilateral

92
Q

what is the management of NF?

A

control symptoms, monitor, treat complications
NF2 - surgery to resect tumours

93
Q

what are the complications of NF?

A

migraines, epilepsy, RAS leading to HTN, learning and behavioural problems, scoliosis, visual loss, malignant peripheral nerve tumours, GI stromal tumours, brain tumours, spinal cord tumours, increased risk of cancer and leukaemia

94
Q

what is tuberous sclerosis?

A

mutation in TSC1 and TSC2 gene on Cr9 (hamartin) and Cr16 (tuberin) respectively - abnormal cell size and growth

95
Q

how does tuberous sclerosis present?

A

hamartomas - skin, brain, lung, heart, eyes, kidneys - abnormal growth of origin tissue
skin signs - ash leaf spots, angiofibromas, shagreen patches, subungal fibromata, cafe au lait, poliosis
neuro - epilepsy, learning disability, developmental delay
other - rhabdomyomas, gliomas, PCKD, lymphangioleiomyomatosis, retinal hamartomas

96
Q

how is tuberous sclerosis managed?

A

supportive, monitor and treat complications

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