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Neuro Flashcards

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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
what are focal seizures?
temporal - hearing loss, speech, memory, emotions - hallucinations, flash backs, strange behaviour, deja vu - use lamotrigine or carbamazepine then valproate or levetiracetam
26
what are absence seziures?
they occur in children for around 10-15 seconds and are managed with valproate or ethosuximide
27
what are atonic seizures?
drop attacks in Lennox Gastaut syndrome - valproate or lamotrigine
28
what are myoclonic seizures?
they are sudden, brief contractions - usually awake - part of juvenile epilepsy - valproate then lamotrigine, levetiracetam or topiramate
29
what are infantile spasms?
about 6m of age, part of West syndrome, most die by 25 managed with prednisolone or vagibatran - full body spasms
30
describe the side effects of drugs used in epilepsy?
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
31
what is status epilepticus?
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
32
what is MND?
it is when the motor neurons stop functioning - ALS, progressive bulbar palsy, PLS and PMA upper and lower motor neurons but sensory spared
33
what are risk factors for MND?
genetics, smoking, heavy metals, pesticides
34
how does MND present?
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
35
how is MND diagnosed and managed?
clinical diagnosis once ruled out other causes management - riluzole can slow progression, NIV, EoL care planning advanced directives
36
what is benign essential tremor?
it is a fine tremor affecting voluntary muscles
37
what is the presentation of benign essential tremor?
symmetrical fine tremor, more prominent on voluntary movements, worse with caffeine, stress, tiredness, and improved with alcohol
38
how is BET managed?
propanolol, primidone
39
what is the presentation of brain tumours?
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
how do acoustic neuromas present?
tinnitus, hearing loss, balance problems, facial nerve palsies
41
summarise gliomas?
glial cells - astrocytomas, oligodendrogliomas, ependymomas grades 1-4
42
how do pituitary tumours present?
bitemporal hemianopia, hormone deficiencies or excess - acromegaly, thyrotoxicosis, cushings, hyperprolactinaemia
43
how are brain tumours managed?
palliation, chemo, radio, surgery pituitary - transspenoidal surgery, RT, bromocriptine, somatostatin analogues
44
what is facial nerve palsy?
it is an isolated dysfunction of the facial nerve resulting in unilateral facial weakness
45
what are the causes of facial nerve palsy?
UMN - stroke, MND, bulbar, tumour - forehead is spared LMN - infection, systemic such as DM, tumours, trauma e.g. surgery
46
how does LMN present?
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
what is huntingtons?
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
how is huntingtons diagnosed and managed?
genetic testing and counselling mx - SALT, genetic counselling, advanced directives, antipsychotics, benzodiazepines, dopamine depleting agents, antidepressants
49
how does huntingtons present?
cognitive, psychiatric or mood problems, chorea, eye movement disorders, dysarthria, dysphagia
50
what is neuropathic pain?
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
what causes neuropathic pain?
infection such as shingles, MS, diabetic neuralgia, CRPS, surgery, trigeminal neuralgia
52
what is the management of neuropathic pain?
amitriptyline, duloxetine, gabapentin, pregabalin flares - tramadol localised - capsaicin cream strength - physio coping - psych input TN - carbamazepine
53
what is myasthenia gravis?
it is an autoimmune condition, with muscle weakness getting worse with activity and better with rest
54
how does MG present?
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
how is MG investigated?
Ach receptor antibodies and muscle specific kinase and low density lipoprotein receptor 4 antibodies CT or MRI thymus edrophonium tests
56
how is MG managed?
reversible acetylcholinesterase inhibitors such as neostigimine, immunosupression with aza or pred, thymectomy, monoclonal ABs - rituximab
57
what is a myasthenic crisis?
life threatening, often triggered by infection BiPAP or I+B, IVIg and plasma exchange are management options
58
what is guillan barre?
it is an acute paralytic polyneuropathy - acute symmetrical ascending weakness from infection eg EBV
59
what is the pathophysiology of GBS?
molecular mimicry - B cells make ABs to antigens and the proteins match those on nerve cell proteins so myelin sheath is also targetted
60
how does GBS present?
symmetrical, ascending weakness, reduced reflexes, peripheral loss of sensation, neuropathic pain, progress to cranial nerves and cause facial weakness
61
how is GBS investigated and managed?
Brighton criteria, nerve conduction studies, LP mx - IVIg, plasma exchange, supportive, VTE prophylaxis
62
what are the red flags for headaches?
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
what are some investigations for headache?
clinical, BP, fundoscopy, CT, MRI
64
summarise a tension headache?
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
summarise sinusitis?
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
summarise cervical spondylosis?
degenerative changes in cervical spine - worse with movement
67
summarise trigeminal neuralgia?
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
how is hormonal headache treated?
can be treated with COCP
69
what are the types of migraine?
with or without aura, hemiplegic, silent
70
how does migraine present?
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
what are the 5 stages of a migraine?
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
what are some triggers for migraines?
stress, bright lights, smells, foods, dehydration, menstruation, abnormal sleeping patterns, trauma
73
how are migraines prevented?
avoid triggers, propanolol, topiramate, amitriptyline
74
how are migraines treated?
paracetamol, triptans, NSAIDs, antiemetics, quiet, dark room
75
what are cluster headaches?
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
what is the typical patient with cluster headache?
male, smoker, triggered by alcohol, smells and exercise
77
how does a cluster headache present?
red, swollen, watering eye, miosis, ptosis, nasal discharge, facial sweating
78
how are cluster headaches prevented?
verapamil, lithium or prednisolone
79
how are cluster headaches managed?
triptans (sumatriptan 6mg SC) or 100% oxygen for 15-20 minutes
80
what is charcot marie tooth disease?
it is an autosomal dominant inherited dysfunction of myelin on the PNS - motor and sensory presents at less than 10y or over 40y
81
what causes CMT disease?
alcohol, B12 deficiency, cancer, CKD, DM, drugs, vasculitis
82
how does CMT disease present?
high foot arches, distal muscle wasting, LL weakness, hand weakness, reduced reflexes and muscle tone, and peripheral sensory loss
83
how is CMT managed?
physio, occupational therapy, podiatry, surgery to correct joints
84
what is lambert eaton myasthenic syndrome?
it is progressive muscle weakness with use due to damage at NMJ but less pronounced than MG
85
what is the usual pathophysiology of CMT?
it present typically due to SCLC - ABs against VG Ca channels - destroy channel so less Ach released into synapse
86
how does LEMS present?
proximal - leg muscle weakness, diplopia, ptosis, slurred speech, dysphagia, dry mouth, blurred vision, impotence, dizziness, reduced reflexes, post tetanic
87
what is the management of LEMS?
ix for SCLC amifampridine, block VG K channels - prolongs depolarisation and time for Ca channels to work IVIg plasmapheresis immunosuppressants
88
what is neurofibromatosis?
development of nerve tumours - they are benign but can cause structural damage
89
what is the pathophysiology for NF?
NF1 gene - Cr17 - mutation of neurofibrin gene which is a TSG - AD NF2 gene - Cr22 - merlin protein - TSG
90
how is NF diagnosed?
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
how does NF2 present?
acoustic neuromas, hearing loss, tinnitus, balance problems - bilateral
92
what is the management of NF?
control symptoms, monitor, treat complications NF2 - surgery to resect tumours
93
what are the complications of NF?
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
what is tuberous sclerosis?
mutation in TSC1 and TSC2 gene on Cr9 (hamartin) and Cr16 (tuberin) respectively - abnormal cell size and growth
95
how does tuberous sclerosis present?
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
how is tuberous sclerosis managed?
supportive, monitor and treat complications

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