Stroke Flashcards
Stroke definition
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
TIA definition
Brief episode of neurological dysfunction due to temporary focal cerebral or retinal ischaemia without infarction
Lasts no longer than 24 hours
Treatment for TIA
Thrombolyse if still have symptoms but usually gone within 20mins
Causes of TIA
Microemboli, fall in cerebral perfusion, hyperviscosity (polycythaemia, sickle-cell, leukostasis - WCC raised)
DDX of TIA and why not TIA?
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
Prognosis of TIA
30% have a stroke (1/3 within a year) 15% have MI
RIsk analysis in TIA
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
Prevention following TIA (and stroke)
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
Driving post TIA
Avoid for 1month
Only inform DVLA if multiple attacks in short period or residual effects
Stroke and TIA incidence
1/1000 in UK for stroke
0.4/1000 for TIA
Stroke risk factors
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
Region of medial cerebral artery and deficit
Lateral hemispheres - supplies head, neck and arms
Most commonly affected in stroke
If left sided (dominant) wernickes and brocas
If right sided - visuospatial problems
Region of anterior cerebral artery and deficit
Medial hemispheres - supplies legs and lower trunk
Motor leg signs and incontinence
Occasional loss of contralateral grasp
Region of posterior cerebral artery and deficits - proximal, cortical and bilateral
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
Internal capsule stroke
Optic tract runs through it therefore can affect vision
Which stroke more common
Ischaemic - 80-85%
Main pathology behind ischaemic stroke
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
What causes 25% of ischaemic strokes?
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
5 other causes of stroke other than lacunes and large artery stenosis throwing off embolus
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
Brainstem infarction incidence and presentation
25%
Wide range of presentations
Including quadriplegia, disturbances of gaze and vision
Locked-in syndrome - upper brainstem infarction - conscious and can move eyes
Investigations in stroke
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
Acute treatment of stroke 5 points
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
Post-acute management of stroke
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
Treatment 24hours after stroke
Start aspirin 300mg - if not given thrombolysis then can give earlier than 24 hours
Treatment of motor side effects of stroke
Spasticity treated with splinting, physio or drugs: gapapentin, baclofen (SE - drowsiness etc), Botox to target muscles
Incidence, cause, location and prognosis of intracerebral haemorrhage
12-15%
Usually rupture of micro aneurysms (Charcot-Bouchard aneurysms) secondary to chronic hypertension
Often in basal ganglia, pons and cerebellum
Usually fatal
Cerebellar haemorrhage - signs
Headache, followed by stupor/coma
Signs of cerebellar/brainstem origin
Gaze deviates towards haemorrhage
Sometimes acute hydrocephalus
Cause, incidence, presentation (x5) and location of SAH
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)
Forewarning of SAH
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
Pathology of SAH - 70% of time
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
Other common pathology in SAH other than berry aneurysms
AVMS = 10%
- Haemorrhage risk 1-2% per year
- Can be ablated with endovascular treatment, surgery or stereotactic radiotherapy
Investigations in SAH
CT imaging immediately - 95% detectable within 24hours
Risk factors for SAH x6
Alcohol HTN Smoking Bleeding disorders Mycotic aneurysm (aneurysm arising from bacterial infection of vascular wall - eg. SBE) Relatives with SAH
Management of SAH
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
Complications of SAH
Rebleeding in 20%
Cause of SDH
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
Signs of SDH
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
Investigations in SDH
CT/MRI will show clot and shifting midline
Sickle shaped clot
Treatment of SDH
1st line = burr hole craniostomy
2nd line = craniotomy
Cause of extradural haematoma
Blood accumulating between scalp and meninges usually due to trauma to the temporal bone causing tearing of middle meningeal artery
Presentation of extradural haematoma
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
Management of extradural haematoma
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
Prognosis of extradural haematoma
Excellent if early treatment
Poor if coma, pupil abnormalities or decerebrate rigidity have developed already
What is Brocas aphasia
Difficulty expressing but can fully understand normal conversation
Where is Brocas area
Posterio-lateral aspect of frontal lobe - inferior frontal gyrus. Usually left side (dominant lobe)
What is Wernickes aphasia
Receptive aphasia. Word substitution and neologisms but speech remains fluent.
Where is Wernickes area
temporal lobe
Features of parietal lobe lesion
Sensory inattention, apraxia, tactile agnosia (astereognosis), inferior homonymous quadrantanopia, Gerstmanns syndrome
What is Gerstmanns syndrome?
Lesion of dominant parietal region - alexia, aclculia, finger agnosia and R-L disorientation
Occiptal lobe lesion features
Homonymous hemianopia with macula sparing.
Cortical blindness. Visual agnosia
Temporal lobe lesion features
Wenickes aphasia, superior homonymous quadrantanopia. Auditory agnosia. Prosopagnosia (difficulty recognising faces)
Frontal lobe lesion features
Disinhibition, perseveration, anosmia, brocas, inability to generate a list
What do you get with lesions of Subthalamic nucleus of the basal ganglia
Hemiballism
What do you get with lesions of Striatum (caudate nucleus) of the basal ganglia
Huntington chorea
What do you get with lesions of Amygdala
Kluver-Bucy syndrome (hypersexuality, hyperorality, hyperphagia, visual agnosia)
What do you get with lesions of Medial thalamus and mammillary bodies of the hypothalamus
Wernicke and Korsakoff syndrome
