Transcript Undergraduate Symposium on STROKE

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?
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(5) What can we do to treat this patient? (RIL)
Is it a stroke?
(a) The setting (or demographics)
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age
hypertension
smoking
diabetes
cholesterol
presence of other vascular disease
(b) The nature of the event
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onset
course
focal vs general symptoms
“negative” symptoms (loss of function)
associated symptoms
Stroke mimics
• Migraine
• Epilepsy
• Structural brain lesions
– SDH, Tumour, abscess
• Metabolic/toxic disorders
– hypoglycemia
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Vestibular disorders
Psychological disorders
Demyelination
Mononeuropathy
What part of the brain is
affected?
Localisation: Why bother?
1. Confirms the diagnosis of stroke
2. Allows better selection of imaging
3. Gives an indication of cause
4. Gives an indication of prognosis
Localising the lesion depends
on a basic understanding of
neuroanatomy
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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
Neuroanatomy 1: Left or Right?
• 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 2: the cortex
Neuroanatomy 3: The homunculus
Neuroanatomy 4: deep white matter
A small stroke
there
(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
Is it a stroke?
• 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
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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?
Distinguishing haemorrhage from
infarct clinically is difficult &
unreliable
• 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
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
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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 noninvasively
• 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
45-69 years
>70 years
AVM
small vessel disease
cerebral amyloid
small vessel disease
• According to location:
Lobar
Deep white
amyloid, AVM, small vessel
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 days
10% dead by 1 month
23% dead by 1 year
• For large cortical strokes:
60% dead, 35% disabled
• For lacunar strokes:
11% dead, 26% disabled
Clinical assessment
Aims
(1) Is it a stroke? (MSD)
(2) What part of the brain is affected? (PJH)
(3) What caused this stroke? (PJH)
Is it a haemorrhage or an infarct?
Can we prevent a further stroke?
(4) What are this patient’s problems?
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(5) What can we do to treat this patient? (RIL)