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Neurology > Stroke > Flashcards

Stroke Flashcards

1
Q

Stroke definition

A

Weakness, usually permanent, on one side, often with loss of speech.

Rapid onset of cerebral deficit (usually focal) lasting longer than 24 hours or resulting in death

No apparent cause other than a vascular one

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2
Q

TIA definition

A

Brief episode of neurological dysfunction due to temporary focal cerebral or retinal ischaemia without infarction

Lasts no longer than 24 hours

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3
Q

Treatment for TIA

A

Thrombolyse if still have symptoms but usually gone within 20mins

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4
Q

Causes of TIA

A

Microemboli, fall in cerebral perfusion, hyperviscosity (polycythaemia, sickle-cell, leukostasis - WCC raised)

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5
Q

DDX of TIA and why not TIA?

A

Epilepsy - no jerking (brief if present) or LOC in TIA and progression over a few mins in epilepsy not TIA

Migraine - not normally a headache or visual disturbances in TIA

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6
Q

Prognosis of TIA

A

30% have a stroke (1/3 within a year) 15% have MI

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7
Q

RIsk analysis in TIA

A

ABCD2 Score
6 = high risk within 7 days

A = age>60 - 1 point

B= BP >140 S and/or >90 D - 1 point

C= Clinical features

  • Unilateral weakness -2 points
  • Speech disturbance - 1 point
  • Other - 0 points

D= Duration of symptoms (mins)
>60 - 2 points
10-59 = 1 point

Diabetes - 1 point

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8
Q

Prevention following TIA (and stroke)

A

Conservative management - lower BP, statin, stop smoking and treat DM

Clopidogrel - 75mg/day (not according to NICE guidelines - clopidogrel only post-stroke according to them)

Aspirin - 300mg/day - after 2 weeks down to 75mg/day

Dipyridamole - 200mg/12 hr (BD) anti-platelet

Warfarin - if AF

High grade carotid stenosis >70% = endarterectomy (removal of inner lining and any endothelial deposits) or stenting

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9
Q

Driving post TIA

A

Avoid for 1month

Only inform DVLA if multiple attacks in short period or residual effects

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10
Q

Stroke and TIA incidence

A

1/1000 in UK for stroke

0.4/1000 for TIA

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11
Q

Stroke risk factors

A 
HTN 
Obesity
High cholesterol 
Sedentary lifestyle
Smoking 
DM 
Alcohol - >6-7 units/day
Heart disease 
PVD
Stress
Age
Male sex 
African-American ethnicity x2 risk
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12
Q

Region of medial cerebral artery and deficit

A

Lateral hemispheres - supplies head, neck and arms
Most commonly affected in stroke
If left sided (dominant) wernickes and brocas
If right sided - visuospatial problems

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13
Q

Region of anterior cerebral artery and deficit

A

Medial hemispheres - supplies legs and lower trunk
Motor leg signs and incontinence
Occasional loss of contralateral grasp

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14
Q

Region of posterior cerebral artery and deficits - proximal, cortical and bilateral

A

Occipital and temporal lobes and perforating branches to the thalamus and midbrain

Proximal - midbrain syndrome, 3rd nerve palsy contralateral hemiplegia, thalamic syndrome, chorea or hemiballismus

Cortical occlusion - homonymous hemianopia with macular sparing

Bilateral - cortical blindness

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15
Q

Internal capsule stroke

A

Optic tract runs through it therefore can affect vision

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16
Q

Which stroke more common

A

Ischaemic - 80-85%

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17
Q

Main pathology behind ischaemic stroke

A

Arterial disease and atherosclerosis - thromboembolic - particularly:

  • Origins of great vessels
  • Bifurcation of ICA and ECA
  • Origin of distal intracranial branches eg. bi/trifurcation of middle cerebral artery
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18
Q

What causes 25% of ischaemic strokes?

A

Small vessel cerebrovascular disease
Small penetrating arteries supplying deep brain parenchyma - basal ganglia, thalamus, IC and pons

Occlusive vasculopathy - lipohyalinosis - consequence of hypertension causing thickening of vessel wall

Small infarcts less than 1.5cm = lacunes - gradual accumulation of ischaemic changes in deep white matter

Causes: Ataxic hemiparesis, motor, sensory or sensorimotor and dysarthria/clumsy hand. If thalamic infarcts - affects cognition

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19
Q

5 other causes of stroke other than lacunes and large artery stenosis throwing off embolus

A

1) Cardiac embolus - AF, valve disease - simultaneous infarcts in different vascular territories indicative of proximal origin of embolus
2) Carotid embolus - bifurcation of ICA and ECA
3) Systemic hypoperfusion - shock, cardiac arrest - watershed areas between vessels affected - especially parieto-occiptal between middle and posterior CA
4) Carotid or verebral artery dissection - more common in the young

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20
Q

Brainstem infarction incidence and presentation

A

25%
Wide range of presentations
Including quadriplegia, disturbances of gaze and vision
Locked-in syndrome - upper brainstem infarction - conscious and can move eyes

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21
Q

Investigations in stroke

A

Non-contrast CT scan will show haemorrhagic but unlikely to show infarction

MRI (esp diffusion weighted) shows early infarction - clot will appear as white dot in vessel

Carotid doppler - carotid stenosis >70 = critical

FBC - need to know platelets if going to thombolyse

ECG - cardiac rhythm disturbances eg. AF

U&E - if patient has hypertension looking for long standing renal damage

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22
Q

Acute treatment of stroke 5 points

A

IV thrombolysis - recombinant tissue plasminogen activator - rtPA - alteplase

0.9mg/kg over 1 hour (max = 90mg) - 10% of dose given in 1minute

Only if within 4.5 hours of onset and CT performed to exclude haemorrhagic

Admit to ITU or stroke unit for monitoring

Follow up CT or MRI at 24 hours before starting anticoagulants or anti-platelet drugs

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23
Q

Post-acute management of stroke

A

Endovascular interventions - removable stents - remove clot with the stent - for recanalisation

Can do up to 6-8 hours after onset or if thrombolysis contraindicated or inaffective

24
Q

Treatment 24hours after stroke

A

Start aspirin 300mg - if not given thrombolysis then can give earlier than 24 hours

25
Q

Treatment of motor side effects of stroke

A

Spasticity treated with splinting, physio or drugs: gapapentin, baclofen (SE - drowsiness etc), Botox to target muscles

26
Q

Incidence, cause, location and prognosis of intracerebral haemorrhage

A

12-15%

Usually rupture of micro aneurysms (Charcot-Bouchard aneurysms) secondary to chronic hypertension

Often in basal ganglia, pons and cerebellum

Usually fatal

27
Q

Cerebellar haemorrhage - signs

A

Headache, followed by stupor/coma
Signs of cerebellar/brainstem origin
Gaze deviates towards haemorrhage
Sometimes acute hydrocephalus

28
Q

Cause, incidence, presentation (x5) and location of SAH

A

Haemorrhage of artery of circle of willis within SA space

5% of all strokes - often occipital

1) Thunderclap headache
2) Vomiting
3) Often coma and death or patient may remain comatose or drowsy for hours, days or longer
4) Neck stiffness
5) Positive Kernig’s sign = hamstring stiffness (takes 6hours to develop)

29
Q

Forewarning of SAH

A

Sentinel bleeds, leaking of aneurysm which precedes rupture by hours/days
May get sentinel headache - sudden pain that may be severe
Approx 17% of patients

30
Q

Pathology of SAH - 70% of time

A

Haemorrhage of saccular/berry aneurysms = 70%

Common sites:
1) Between posterior communicating artery and internal carotid artery

2) Between anterior communicating artery and anterior cerebral artery
3) At tri/bifurcation of middle cerebral artery

Associated with polycystic kidneys, coarctation of aorta, Ehlers-Danlos Syndrome

31
Q

Other common pathology in SAH other than berry aneurysms

A

AVMS = 10%

  • Haemorrhage risk 1-2% per year
  • Can be ablated with endovascular treatment, surgery or stereotactic radiotherapy
32
Q

Investigations in SAH

A

CT imaging immediately - 95% detectable within 24hours

33
Q

Risk factors for SAH x6

A 
Alcohol
HTN
Smoking
Bleeding disorders
Mycotic aneurysm (aneurysm arising from bacterial infection of vascular wall - eg. SBE)
Relatives with SAH
34
Q

Management of SAH

A

Maintain cerebral perfusion

Nimodipine (calcium antagonist) reduces vasospasm and consequent morbidity from cerebral ischaemia

Surgical clipping or endovascular coiling (promote clotting around the coil)
Intracranial stents and balloon remodelling for wide necked aneurysms

35
Q

Complications of SAH

A

Rebleeding in 20%

36
Q

Cause of SDH

A

Rupture of bridging veins between cortex and venous sinuses

Haematoma accumulates between dura and arachnoid

Most are from trauma but trauma can be as long as 9 months previously

Spontaneous can occur in elderly because brain atrophy makes bridging veins more vulnerable

37
Q

Signs of SDH

A

Headaches, drowsiness and confusion - as SDH expands and raises ICP - shifting midline and can cause tentorial herniation and coning = coma

Fluctuating consciousness

Can also get focal deficits - motor or sensory

Seizures from raised ICP

38
Q

Investigations in SDH

A

CT/MRI will show clot and shifting midline

Sickle shaped clot

39
Q

Treatment of SDH

A

1st line = burr hole craniostomy

2nd line = craniotomy

40
Q

Cause of extradural haematoma

A

Blood accumulating between scalp and meninges usually due to trauma to the temporal bone causing tearing of middle meningeal artery

41
Q

Presentation of extradural haematoma

A

Deteriorating consciousness following no loss of consciousness after trauma or a lucid period following recovery of consciousness

This can last for up to a few days before raised ICP starts causing symptoms

Vomiting, severe headache, confusion and fits
Then stuporose with ipsilateral dilated pupil and contralateral hemiparesis, brisk reflexes and upgoing plantar

Further developement will cause brainstem compression and respiratory distress

42
Q

Management of extradural haematoma

A

Immediate CT - more localised (than SDH) biconvex/lens shaped haematoma

Surgery urgently to remove clot and ligate the bleeding vessel
If no neurosurgeon - burr holes can be life saving

43
Q

Prognosis of extradural haematoma

A

Excellent if early treatment

Poor if coma, pupil abnormalities or decerebrate rigidity have developed already

44
Q

What is Brocas aphasia

A

Difficulty expressing but can fully understand normal conversation

45
Q

Where is Brocas area

A

Posterio-lateral aspect of frontal lobe - inferior frontal gyrus. Usually left side (dominant lobe)

46
Q

What is Wernickes aphasia

A

Receptive aphasia. Word substitution and neologisms but speech remains fluent.

47
Q

Where is Wernickes area

A

temporal lobe

48
Q

Features of parietal lobe lesion

A

Sensory inattention, apraxia, tactile agnosia (astereognosis), inferior homonymous quadrantanopia, Gerstmanns syndrome

49
Q

What is Gerstmanns syndrome?

A

Lesion of dominant parietal region - alexia, aclculia, finger agnosia and R-L disorientation

50
Q

Occiptal lobe lesion features

A

Homonymous hemianopia with macula sparing.

Cortical blindness. Visual agnosia

51
Q

Temporal lobe lesion features

A

Wenickes aphasia, superior homonymous quadrantanopia. Auditory agnosia. Prosopagnosia (difficulty recognising faces)

52
Q

Frontal lobe lesion features

A

Disinhibition, perseveration, anosmia, brocas, inability to generate a list

53
Q

What do you get with lesions of Subthalamic nucleus of the basal ganglia

A

Hemiballism

54
Q

What do you get with lesions of Striatum (caudate nucleus) of the basal ganglia

A

Huntington chorea

55
Q

What do you get with lesions of Amygdala

A

Kluver-Bucy syndrome (hypersexuality, hyperorality, hyperphagia, visual agnosia)

56
Q

What do you get with lesions of Medial thalamus and mammillary bodies of the hypothalamus

A

Wernicke and Korsakoff syndrome

Neurology (10 decks)

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