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Y3 - CS - Neuro > Conditions Part 1 > Flashcards

Conditions Part 1 Flashcards

1
Q

defintion for Stroke and TIA

A

a cerebrovascular event is a clinical syndrome caused by disruption of blood supply to the brain characterised by rapidly developing signs of focal or global disturbance of cerebral functions lasting for more than 24 hours ore leading to deaths

A transient ischaemic attack refers to a similar presentation that resolves within 24 hours

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2
Q

how common is stroke or TIA

A

about 150 00 have a stroke in the UK every year
53 000 deaths each year
further 20 000 have a TIA

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3
Q

who is affected the most by stroke or TIA

A

uncommon if <40yrs, rates greater in Asian and black africans than white

M>F

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4
Q

causes for stroke

A

cerebral infraction

  • 70%
  • arterial thrombus in-situ atheromatous carotid, vertebral or cerebral arteries
  • cardiac embolus following AF, valvular disease, prosthetic valves, MI (>30% of stroke)

primary haemorrhage

  • 15%
  • high BP
  • trauma
  • aneurysm rupture

subarachnoid haemorrhage

  • 5%
  • arterious aneurysms
  • arterio-venous malformations

Uncertain type

  • 5%
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5
Q

causes for TIA

A

mainly due to

  • micro-emboli from heart or atheromatous plaques
  • fall in cerebral perfusion due to cardiac dysrhythmia, postural hypotension, dec flow due to atheroma
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6
Q

what are the different stages of stroke

A

minor stroke - stroke-in-evolution - completed stroke

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7
Q

pathogenesis of stroke

A

vessel obstruction –> brain ishaemia –> infract –> infracted area surrounded by a swollen area which is structurally intact but does not function (ischaemic penumbra) –> this can regain neurological function

within the ischaemia area –> hypoxia –> fall in ATP –> glutamate release –> Ca2+ channels open –> free radial release –> inflammation and necrosis

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8
Q

RF for stroke and TIA

A

hypertension, smoking, DM, heart disease (valvular, ischaemia, AF), peripheral vascular disease, polycythaemia vera (too much blood cells), past TIA, cortid bruit, the pill, hyperlipidaemia, alcohol, clotting disorder, syphilis

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9
Q

symptoms of stroke and TIA

A

either sudden onset or step-wise progression of symptoms

symptoms depends on whether ischaemic/haemorrhagic and which artery affected

cerebral hemisphere infarct -50%

  • contralateral hemiplegia (weakness of the body) initially flaccid then spastic
  • contralateral sensory loss
  • homonymous hemianopia (blindness of half visual field)
  • dysphasia

brainstem infarction - 25%

  • quadriplegia
  • disturbances of gaze/vision
  • locked-in syndrome

lacunar infarct - small infarct around the basal ganglia, internal capsule, thalamus, pons - 25%

  • pure motor/sensory or mixed signs
  • ataxia (lack of voluntary movement)
  • intact cognition/consciousness
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10
Q

differential diagnosis for stroke and TIA

A 
CNS tumour 
subdural haemorrhage
drug overdose 
hemiplegic migraine 
- hepatic encephalopathy
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11
Q

further investigation for stroke and TIA

A

Brain CT - often normal in ischaemic stroke for the first few hours

MRI - more accurate thatn CT

echocardiography - if suspected cardiac cause/origin

fundoscopy, bloods, carotid duplex ultrasound, BP, hypoglycaemia, hyperglycaemia, dyslipidaemia

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12
Q

management for stroke and TIA

A

immediate mangement

  • ABCDE
  • thrombolysis needed? if yes then imaging
  • brain imaging (CT - quick and easy)
  • cerebral infarction - CT exclude haemorrhag. give immediate thrombolytic therapy, or 300mg aspirine if contra-indicated
  • cerebral haemorrhage - do not give anto-coagulant and neurosurgery

later management

  • MR angiography (MRA) or CT angiography - to discover surgical location and confirmation of location of infarct
  • carotid dopplet and duplex scanning - carotid occlusion

low dose aspirin as primary prevent if 10-year risk of CHD >10%

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13
Q

treatment for stroke and TIA

A

RF identify and reduce
anti-hypertensive therapy
anti-platelet therapy (clopidogrel monotherapy)
anticoagulants - heparin and warfarin
surgery - internal carotid endarterectomy if carotid occlusion

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14
Q

definition for sub-arachnoid haemorrhage

A

bleeding into the subarachnoid space

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15
Q

how common is subarachnoid haemorrhage

A

constitutes about 6% of first stroke

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16
Q

causes for subarachnoid haemorrhage

A

intracranial arterial aneurysms - berry anerurysms
non-aneurysmal peri-mesencephalic haemorrhage
other vascular abnor - arteriovenous malformation

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17
Q

RF for subarachnoid haemorrhage

A

larger aneurysm - more likely to ruputre
hypertension
smoking
excessive alcohol intake
FH
genetic
adult polycystic kidney disease (around 10% have berry aneurysm)

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18
Q

symptoms of subarachnoid haemorrhage

A

sudden, severe, typically occipital headache lasting few seconds - ‘thought I had been kicked at the back of my head’ thunder clap headache ?

vomiting

collapse

seizures

coma/drowsiness

neck stiffness - due to meningeal irritation by blood

complete/partial palsy of oculomotor nerve

marked rise in BP

sentinel headache - resolve with no other symptoms - due to ‘warning leak’ from aneurysm

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19
Q

differential for subarachnoid headache

A

other causes of stroke
meningitis
trauma
idiopathic thunderclap headche

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20
Q

further investigations for subarachnoid haemorrhage

A

CT - detect 90% of SAH within first 48 hrs

lumbar puncture - if CT -ve, CSF is uniformly bloody early on and turn yeloow later on as blood is broken down into bilirubin like piss

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21
Q

management for SAH

A

refer all SAH to neurology team asap
re-exam CNS often to see any further development of the haemorrhage
repeat CT if deteriorating

nimodipine - Ca2+ antagonist which reduce vasospasm and consequent mobility from cerebral ischaemia

endovascular coiling

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22
Q

prognosis for SAH

A

up to 60% die within first 30 days, 10% die immediately with no symptoms

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23
Q

definition for peripheral neuropathy

A

damage or disease affecting the peripheral nerves which can be a mononeuropathy or polyneuropathy or mononeuritis multiplex (several separate mononeuropathies) and can be acute or chronic

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24
Q

what is mononeuropathy

A

a process affecting a single nerve (including CN)

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25
Q

what is mononeuritis multiplex

A

multiple mnoneuropathy and or multifocal neuroapthy affects several or multiple nerves

26
Q

what is polyneuropathy

A

diffuse, symmetrical disease, usually commencing peripherally

classed broadly into demyelinating and axonal types, depending upon which principal pathological process predominates, often impoosible to separate these clinically

27
Q

what is myelopathy

A

disease of the cord

28
Q

radiculopathy

A

disease affecting nerve roots and plexopathy, the brachial or lumbosacral plexus

29
Q

causes of mononeuropathy

A
  • nerve compression eg carpal tunnel
  • trauma eg ulnar elbow trauma
  • radiotherapy
  • tumours
  • fractures
30
Q

causes of mononeuritis multiplex

A 
DM 
vasculitides 
immune-mediatd disease eg RA, SLE 
infections eg leprosy, HIV, lyme disease 
sarcoidosis 
amyloidosis 
chemical agents
31
Q

causes of polyneuropathy

A

metabolic eg DM, RF, hypothyroid, hypoglycaemia
vasculitides
malignancy
inflammation
infection eg leprosy, HIV, syphilis, Lyme disease
nutritional eg vitamine B12, B1, E, B6 folate deficiency
inherited syndrome
toxins eg lead, arsenic
drugs
amyloidosis

32
Q

pathogenesis of nerve damage

A

demyelination - Schwann cell dmage - myelin sheath damage - slowing of conduction (Guillain-Barre Syndrome)

axonal damage - nerve fibre dies back from neuropathy, conduction velocity normal though as axon continuity is maintained by surviving fibre (eg in toxic neuropathies)

Wallerian degeneration - changes follwoing nerve section - axon and distal myelin sheath degenerate over weeks

compression

infarction - micoinfarction of vaso nervorum as in DM and arteritis

inflitration - by inflam cells (eg in leprosy and sarcoidosis and neoplastic granulomas)

33
Q

what are the symptoms of peripheral neuropathy

A

sensory
- -ve signs - numbeness, tremor, gait abnor

  • +ve signs - tingling, pain, itching, crawling, pins and needles

motor
- -ve signs - weakness, tiredness, heaviness, gait abnor, reduced reflexex

  • +ve signs - cramps/myalgia, tremor, fasciculations
34
Q

further investigation for peripheral neuropathy

A

usually clinical and detailed history and exam

can do bloods, genetic tests, lead levels and immuno tests

35
Q

management for peripheral neuropathy

A

treat the cause, involve phsyio and OT

treat neuopathic pain with amitriptyline or nortriptyline

36
Q

what is the most common type of mononeuropathy

A

median nerve (C6-T1) - carpal tunnel syndrome

37
Q

how does carpal tunnel syndrome present

A

at wrist - aching pain in hand/arm esp at night
parasethesiae in radial 3.5 fingers
relieved by dangling out of bed or shaking
sensory loss and weakness of abductor pollicis brevis +/- wasting of thenar eminence

tinel’s sign - tap flexor/anterior aspect of wrist = tingling and pain

phalen’s test -symptoms are reproducable on passive maximal wrist flexion

38
Q

treatment for carpal tunnel syndrome

A

local steroid injection +/- decompression surgery

39
Q

what is the syndrome caused by ulnar nerve mononeurpathy

A

ulnar (c7-T1) - cubital tunnel syndrome

40
Q

presentation for cubital tunnel syndrome

A

clawing of the hand due to weakness of medial wrist flexors etc

sensory loss over medial 1.5 fingers

41
Q

treatment for cubital tunnel snydrome

A

remove pressure over elbow for ulnar nerve

42
Q

what is the nerve root of radial nerve

A

C5-T1 , Saturday night palsy

43
Q

what is the presentation of radial nerve neuropathy

A

wrist drop and weakness of flexors

sensory loss to dorsal aspect of thumb

44
Q

treatment for radial nerve neuropathy

A

recovery within a few months usually (damage via compression against the humerus eg arm draped over a hard chair for hours)

45
Q

what are the different types of polyneuropathy

A

Guillain-barre syndrome & charcor-Marie-Tooth Syndrome

46
Q

presentation of guillain-barre syndrome

A

acute
weakness of distal limb muscles +/- numbness
this progresses proximally and may lead to paralysis
loss of tendon reflexes, respiratory and facial muscles may become weak
monophasic - does not recur
often caused due to minor infection as it induce AB response against nerves

47
Q

what is the treatment for Guillain-barre syndrome

A

diagnosis confirmed by nerve conduction studies - prolonged distal motor latency IV Ig

48
Q

presentation of charcot-marie-tooth syndrome

A

personal muscular atrophy, distal limb wasting and weakness that slowly progresses over years, legs might resemble inverted champaign bottles

in mild cases, pes cavus and clawing of toes

49
Q

what does MS stand for

A

Multiple Sclerosis

50
Q

what causes MS

A

cell-mediated autoimmune condition

51
Q

what does MS normally occur

A

discrete plaques of demyelination occur at multiple CNS sites - the demyelination heals poorly causing relapsing and remitting symptoms, prolonged demyelination causes axonal loss and clinically progressive symptoms

52
Q

who is affected the most by MS

A

commoner in temperate areas and less common in Black Africans/Asians

53
Q

what is the presentation of MS

A

unilateral optic neuritis, numbness or tingling in the limbs, leg weakness, brainstem or cerebellar symptoms, Bell’s palsy, relapses and remits –> secondary progression. Can be primarily progessive

54
Q

what test can be used to diagnose MS

A

usually clinical but MRI can be used to confirm or support diagnosis

55
Q

treatment for MS

A

disease modifying therapy, interferon beta, non-immunosuppressives, monoclonal antibodies, methylprednisolone for acute relapses

56
Q

what is proximal myopathy

A

symmetrical weakness of proximal upper and/or lower limbs

57
Q

causes of proximal myopathy

A

broad range of underlying causes including drugs, alcohol, thyroid disease, osteomalacia, idiopathic inflammatory myopathies, hereditary myopathies, malignancy, infections and sarcoidosis

58
Q

presentation for proximal myopathy

A

gradual onset, proximal not distal weakness, symmetrical, preserved tendon reflexes, normal sensation, muscle wasting but maybe muscle hypertrophy
fever with inflammatory myopathies
hypotonia is common in some myopathies

59
Q

further tests for proximal myopathy

A

urinalysis –> myoglobinuria

bloods –> raised CK

60
Q

complication of proximal myopathy

A

respiratory failure, aspiration pneumonia, rhaboymolysis, chest/spine/joint deformities

Y3 - CS - Neuro (2 decks)

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