1. 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)

2. 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

3. Stroke mimics Migraine Epilepsy Structural brain lesions
SDH, Tumour, abscess
Metabolic/toxic disorders
hypoglycemia
Vestibular disorders
Psychological disorders
Demyelination
Mononeuropathy

4. What part of the brain is affected?

5. 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

6. Localising the lesion depends on a basic understanding of neuroanatomy
the cortex
the homunculus
deep white matter
the brainstem
the vascular supply

7. What part of the brain is affected?
Left or right
Carotid territory or vertebrobasilar territory
Cerebral hemispheres or brainstem
Cortex or deep white matter

8. 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

9. Neuroanatomy 2: the cortex

10. Neuroanatomy 3: The homunculus

11. Neuroanatomy 4: deep white matter
A small stroke
there
(or there)
will result in a major deficit as the fibres are packed close together

12. Neuroanatomy 5: the brainstem
Cranial nerve signs suggest localisation to (and within) the brainstem

13. 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

14. 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

15. Some clinical vignettes

16. 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

17. Sudden onset left leg weakness O/E:
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

18. Hypertension, diabetes mellitus
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

19. 2 days ago episode of right arm & leg weakness
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

20. What caused this stroke?

21. 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

22. 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

23. 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

24. 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

25. Old lacunar infarct of right putamen & internal capsule
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

26. 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

27. Features of an infarct depend on the blood vessel occluded
3 main cortical vessels: ACA, MCA, PCA

28. Features of an infarct depend on the blood vessel occluded

29. What was the cause in THIS patient?

30. 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

31. Brain Imaging Rationale: Plain CT is the imaging technique of choice
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

32. Intracerebral haemorrhage on CT
Is always seen
apparent immediately
lasts 1 week
then disappears and looks like an infarct

33. 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

34. Haemorrhagic Transformation
Haemorrhage seen at the margins of an infarct

35. MR in acute stroke Advantages: Disadvantages:
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

36. 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

37. 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

38. 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

39. 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

40. PICH - two types Basal ganglia bleed (from right caudate nucleus)
Lobar bleed (from cerebral amyloid)

41. What is the likely prognosis after stroke?

42. 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

43. 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

44. 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? +
(5) What can we do to treat this patient? (RIL)