Clinical assessment Aims (1) Is it a stroke? (MSD) (2) What part of the brain is affected? (3) What caused this stroke? Is it a haemorrhage or an infarct? Can we prevent a further stroke? (4) What are this patient’s problems? + (5) What can we do to treat this patient? (RIL)
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Clinical assessment Aims (1) Is it a stroke? (MSD) (2) What part of the brain is affected? (3) What caused this stroke? Is it a haemorrhage or an infarct?
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Clinical assessment
Aims
(1) Is it a stroke? (MSD)
(2) What part of the brain is affected?
(3) What caused this stroke?
Is it a haemorrhage or an infarct?
Can we prevent a further stroke?
(4) What are this patient’s problems?+
(5) What can we do to treat this patient? (RIL)
Is it a stroke?(a) The setting (or demographics)
• age• hypertension• smoking• diabetes• cholesterol• presence of other vascular disease
(b) The nature of the event• onset• course• focal vs general symptoms• “negative” symptoms (loss of function)• associated symptoms
Localising the lesion depends on a basic understanding of
neuroanatomy
• the cortex
• the homunculus
• deep white matter
• the brainstem
• the vascular supply
What part of the brain is affected?
• Left or right
• Carotid territory or vertebrobasilar
territory
• Cerebral hemispheres or brainstem
• Cortex or deep white matter
• Crossing of sensory and motor fibres– corticospinal tracts - lower medulla– spinothalamic fibres - spinal cord– dorsal columns - upper medulla
• Cerebellar lesions result in ipsilateral deficits
• The “dominant hemisphere”– Language function localises to left hemisphere– Awareness of body localises to right hemisphere
• Visual pathways– monocular vs homonymous deficits
Neuroanatomy 1: Left or Right?
Neuroanatomy 2: the cortex
Neuroanatomy 3: The homunculus
Neuroanatomy 4: deep white matter
A small strokethere
(or there) will result in a major deficit as the fibres are packed close
together
Neuroanatomy 5: the brainstem
Cranial nerve signs suggest localisation to
(and within) the brainstem
Neuroanatomy 6: the vascular supply
The carotid system supplies most of the hemispheres and
cortical deep white matter
The vertebro-basilar system supplies the brain stem,
cerebellum and occipital lobes
So, from the symptoms and signs you observe, you can tell:
• what side of the brain is affected• whether the lesion is in the brainstem (a
brainstem stroke)• whether the cortex is involved (a cortical
stroke) • or if the lesion is in the deep white matter
(a lacunar stroke)• what blood vessel is involved
Some clinical vignettes
• Male, 58 years• Headache for 4
weeks • 10 days of gradually
increasing right side weakness
• O/E:– poor concentration– slow speech, unable
to follow commands– right face & arm
weak, walking OK– papilloedema
Is it a stroke?
• 68 year old woman• On warfarin for AF• Previous mild stroke• Sudden onset left
leg weakness• O/E:
– unaware of problems– dense weakness of
left, loss of sensation– doesn’t look to left– mildly drowsy
• INR 2.9
• 75 year old man• Hypertension,
diabetes mellitus• sudden onset
dizziness & vomiting, unable to walk
• O/E:– constricted pupil on left– nystagmus in all
directions– ataxia of left arm & leg– loss of PP on right
• 69 year old woman• hypertension, smoker• 2 days ago episode of
right arm & leg weakness
• sudden onset worse right sided weakness
• O/E:– slurred speech only– equal weakness of face,
arm and leg; unable to walk; sensation OK
– alert
What caused this stroke?
The pathology
2 processes result in a stroke:
(1) Infarction– 85% of strokes– occlusion of a vessel by thrombosis or
embolus
(2) Haemorrhage– 15% of strokes– rupture of a vessel results in bleeding into
the substance of the brain
Intracerebral Haemorrhage
• Usually caused by hypertension
• thickening & weakening of walls of small arteries/arterioles
• formation of small aneurysms
• rupture produces a large blood filled cavity that acts as a SOL
• typically basal ganglia or thalamus
Cerebral Infarction
• Infarction is caused by failure of blood flow to a region
• damage to the brain is due to:– ischaemia– oedema surrounding the ischaemic area
• sources of occlusion of vessels:– thrombosis of small vessels - hypertensive
lipohyalinosis - lacunar infarcts– thrombosis of larger vessels– embolus from extracranial vessels or heart
Thrombo-embolism
• At least 1/3 of strokes are due to emboli from heart or ICA
• small clot breaks off from a larger thrombus
• it becomes lodged in a distal smaller vessel, producing an infarct
• Cardiac sources of embolus are common with conditions such as AF or prosthetic valves
Cerebral Infarction
A recent infarct in the right temporal lobe - loss of gray-white margin, swelling
Old lacunar infarct of right putamen & internal capsule
Old infarct of the right MCA - cystic formation & enlargement of the ventricle
Haemorrhagic infarction
• Usually infarcts are bland - necrosis only
• Occasionally there is haemorrhage seen in the infarct
• occurs in embolic infarcts
• due to spontaneous lysis of the clot reperfusion of damaged vessels
• often asymptomatic
The bleeding is petichial and confined to the cortex
Features of an infarct depend on the blood vessel occluded
3 main cortical vessels: ACA, MCA, PCA
Features of an infarct depend on the blood vessel occluded
What was the cause in THIS
patient?
• On history:• severe headache • vomiting within 2 hours of onset
• On examination:• marked hypertension• altered conscious state
• Increasing evidence to suggest that mild events may be due to PICH
• Scanning is the only acceptable method
Distinguishing haemorrhage from infarct clinically is difficult &
unreliable
Brain Imaging
• Rationale: – to exclude (rare) stroke mimics eg SDH– to distinguish between haemorrhage and
infarct
• Plain CT is the imaging technique of choice– available, rapid– reliably differentiates haemorrhage:
blood is white
Intracerebral haemorrhage on CT
• Is always seen• apparent immediately• lasts 1 week• then disappears and
looks like an infarct
Ischaemic stroke on CT
• Infarcts seen as areas of hypodensity
• become more obvious as time progresses
• small infarcts appear later than large ones
• overall, 40% strokes have normal CT
• posterior fossa difficult
Haemorrhagic Transformation
Haemorrhage seen at the margins of an infarct
MR in acute stroke
• Advantages:– much better at defining the anatomy– shows ischaemic changes earlier, and in a
greater proportion of patients– diffusion weighted imaging can show
ischaemia within minutes-hours, and differentiate between old and new lesions
– MRA allows imaging of blood vessels non-invasively
• Disadvantages:– expense, time, lack of access to the patient
MRI in acute stroke: an example
A 42 year old man with headache and left hemiparesis
CT brain (3 hours) ? R MCA hypodensity
DWI (24 hrs) obvious R MCA infarct
MRA (24 hrs) dissection R ICA with distal occlusion
What caused this infarct?
• The clinical assessment may provide clues to the likely cause– history - demographics atheroma– examination - carotid bruits atheroembolism,
heart abnormalities (AF, murmurs) cardioembolism
• Localisation provides the best clues: – cortical stroke cardiac or large artery embolus– lacunar stroke small vessel disease– brainstem stroke local atheroma
Knowing the likely cause tells you how to investigate further...
• If cortical stroke:– look closely at the heart (ECG, ?Echo)– look for carotid atheroma (Carotid duplex)– specialised tests if young
• If lacunar stroke:– look closely for risk factors, fewer tests
What caused this haemorrhage?
• According to age:<45 years AVM
45-69 years small vessel disease
>70 years cerebral amyloid
small vessel disease
• According to location:Lobar amyloid, AVM, small vessel
Deep white small vessel disease
PICH - two types
Basal ganglia bleed (from right caudate nucleus)
Lobar bleed (from cerebral amyloid)
What is the likely prognosis after stroke?
Prognosis after Intracerebral Haemorrhage
• 40% dead in first 7 days
• 50% dead in first 30 days
• 62% dead by 1 year
more likely to die early, but mortality reduces thereafter
of the 40% alive, 30% are independent
Prognosis after cerebral infarction
• For all: 5% dead by 7 days10% dead by 1 month23% dead by 1 year
• For large cortical strokes:60% dead, 35% disabled