‘Stroke’
Cerebrovascular diseases
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Vascular diseases of the nervous system
are amongst the most frequent causes of
admission to hospital.
Strokes of all types rank third as a cause
of death, surpassed only by heart disease
and cancer.
The annual incidence in the UK varies
between 150-200/100 000, with a
prevalence of 600/100 000 of which one
third are severely disabled.
Risk factors
Prevention of cerebrovascular disease is more likely to
reduce death and disability than any medical or surgical
advance in management. Prevention depends upon the
identification of risk factors and their correction.
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Hypertension (a major factor, no critical BP level).
Cardiac disease (cardiac enlargement, failure,
arryhthmias, rheumatic heart disease, patent foramen ovale)
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Diabetes (the risk of cerebral infarction is increased twice).
Heredity
Blood lipids, cholesterol, smoking,
diet/obesity
Haematocrit (a  Hb concentration,  fibrinolysis)
Oral contraceptives ?
Cerebrovascular diseases mechanisms

‘Stroke’ is a generic term, lacking pathological meaning.
Cerebrovascular diseases can be defined as those in which brain
disease occurs secondary to a pathological disorder of blood
vessels (usually arteries) or blood supply.
Whatever mechanism, the
resultant effect on the brain
is either:
ischemia/infarction, or
haemorrhagic disruption
Of all strokes:
- 85% are due to INFARCTION
- 15% are due to HAEMORRHAGE
Cerebrovascular diseases –
natural history
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Approximately 1/3 of all ‘strokes’ are fatal.
The age of the patient, the anatomical size of the
lesion, the degree of deficit and the underlying cause
all influence the outcome.
In cerebral haemorrhage, mortality approaches 50%.
Cerebral infarction fares better, with an immediate
mortality of less than 20%, fatal lesions being large
with associated oedema and brain shift.
Embolic infarction carries a better outcome than
thrombotic infarction.
The level of consciousnees on admission to hospital gives a good
indication to immediate outcome. The deeper the conscious level the
graver the prognosis.
Cerebrovascular diseases –
causes
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Occlusion (50%)
Atheromatous/thrombotic
1. Large vessel occlusion or stenosis (e.g. carotid artery)
2. Branch vessel occlusion or stenosis (e.g. MCA)
3. Perforating vessel occlusion (lacunar infarction)
Non-atheromatous diseases of the vessel wall
1. Collagen disease (e.g. systemic lupus erythematosis)
2. Vasculitis (e.g. polyarteritis nodosa)
3. Granulomatous vasculitis (e.g. Wegener’s granulomatosis)
4. Miscellaneous (e.g. syphilitic vasculitis, sarcoidosis, …)
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Embolisation (25%) mostly from atheromatous
plaque in the intracranial or extracranial arteries or from the heart.
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Haemorrhage (20%); parenchymal (15%), SAH (5%)
Transient ischemic attacks
(TIAs)
=
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episodes of focal neurological symptoms due to
inadequate blood supply to the brain. Attacks are sudden
in onset, resolve within 24 hours or less and have no
residual deficit. These attacks are important as warning
episodes or precursors of cerebral infarction.
The pathogenesis: A reduction of cerebral blood flow
below 20-30 ml/100 g/min produces neurological
symptoms. The development of infarction is a
consequence of the degree of reduced flow and the
duration of such a reduction. If flow is restored within the
critical period, ischemic symptoms will reverse.
Emboli are accepted as the cause of the majority of TIAs.
Occlusion of the internal
carotid artery
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The degree of deficit varies – it may be asymptomatic or a
catastrophic infarction may result.
In the most extreme cases there may be:
Unconsciousness, contralateral hemiplegia,
contralateral hemisensory disturbance, homonymous
hemianopia of the contralateral side and gaze palsy to
the opposite side (eyes are deviated to the side of the
lesion!). Occlusion of the dominant hemisphere side will
result in a global aphasia.
Prodromal symptoms prior to occlusion may take the form
of monocular blindness – AMAUROSIS FUGAX and
transient hemisensory or hemimotor disturbance.
Branch vessel occlusions or stenosis
Occlusion of the anterior
cerebral artery
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Cortical branches supply the medial surface of the
hemisphere: Orbital, frontal, and parietal ctx.
Deep branches pass to the anterior part of the internal
capsule and basal nuclei.
Clinical features depend on the site of occlusion
(especially in relation to the anterior communicating artery)
and anatomical variation.
Occlusion proximal to the AComA is normally well tolerated
because of the cross flow.
Distal occlusion results in weakness and cortical sensory
loss in the contralateral lower limb with associated
incontinence. Bilateral frontal lobe infarction may result in
akinetic mutism or deterioration in conscious level.
Occlusion of the middle
cerebral artery
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MCA is the largest branch of the ICA. It gives off deep
branches (perforating arteries) which supply the anterior
limb of the internal capsule and part of the basal nuclei. It
then passes out to the lateral surface of the hemisphere
and here it gives off cortical branches temporal, frontal,
and parietal.
Clinical features depend on the site of occlusion and
whether dominant or non-dominant hemisphere is
affected.
All cortical branches are involved – contralateral
hemiplegia (leg relatively spared), contralateral
hemianaesthesia and hemianopia, aphasia (dominant),
neglect syndrome (non-dominant hemisphere).
Vertebral artery occlusion
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The vertebral artery arises from the subclavian artery on
each side. Underdevelopment of one vessel occurs in
10%. VA and its branches supply the medulla and the
inferior surface of the cerebellum before forming the
basilar artery.
Clinical features variable. When low in the neck, it is
compensated by anastomotic channels. When one VA is
hypoplastic, occlusion of the other is equivalent to basilar
artery occlusion. Typical VA occlusion presents as a PICA
syndrome: dysarthria, ipsilateral limb ataxia, vertigo and
nystagmus, contralateral sensory loss (pain/temperature)
of limbs and trunk, ipsilateral sensory loss (pain/temp.) of
face, ipsilateral pharyngeal and laryngeal paralysis.
Basilar artery occlusion
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The basilar artery supplies the brainstem from medulla
upwards and divides eventually into posterior cerebral
arteries which run forward to join the anterior circulation
(circle of Willis).
Clinical features: Prodromal symptoms are common and
may take the form of diplopia, visual field loss,
intermitent memory disturbance and a whole
constellation of other brainstem symptoms: vertigo,
ataxia, paresis, paraesthesia.
The complete basilar syndrome following occlusion
consists of: Coma, bilateral motor and sensory
dysfunction, cerebellar signs and cranial nerve signs.
Very serious condition!
Lacunar stroke
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Occlusion of deep penetrating arteries produces
subcortical infarction characterised by preservation of
cortical function – language, other cognitive and visual
functions.
Clinical syndromes are distinctive and normally result from
long-standing hypertension. In 80%, infarcts occur in
periventricular white matter and basal ganglia, the rest in
cerebellum and brainstem. Areas of infarction are 0.5-1.5
cm in diameter and occluded vessels demonstrate
lipohyalinosis, microaneurysms and microatheromatous
changes.
Lacunar or subcortical infarction accounts for 17% of all
thromboembolic strokes and knowledge of commoner
syndromes is essential.
Lacunar stroke (cont’d)
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Pure motor hemiplegia (lesion in posterior limb of
internal capsule) – equal weakness of contralateral face,
arm, end leg with dysarthria.
Pure sensory stroke (lesion in VPLnucleus of thalamus)
– numbness and tingling of contralateral face and limbs.
Sensory examination may be normal!
Dysarthria/clumsy hand (lesion in dorsal pons) –
dysarthria due to weakness of ipsilateral face and tongue
associated with clumsy but strong contralateral arm.
Ataxic hemiparesis (lesion in ventral pons) – mild
hemiparesis with more marked ipsilateral limb ataxia
Severe dysarthria with facial weakness (lesion in
anterior limb of internal capsule) – dysarthria, dysfagia and
even mutism with mild facial and no limb weakness.
Stroke - investigations
CONFIRM THE DIAGNOSIS
Computerised tomography (CT scan)
1.
All patients should have a CT scan, urgently if
conscious level depressed
diagnosis uncertain
on anticoagulants
before commencing/resuming anthitrombotics
if thrombolysis is considered
Infarction is evident as a low density lesion which
conforms to a vascular teritory. Subtle changes
occur within 3 hours in some pts; most scans
become abnormal within 48 hours.
Early hypodensities
Blurring grey/white matter distinction
Dense artery sign
Hyperdense thrombosed middle
cerebral artery
16h 20min
Lacunar stroke
CT scan also identifies intracerebral haemorrhage or tumour
Stroke – investigations
(cont’d)
CONFIRM THE DIAGNOSIS
Magnetic resonance imaging
T2 prolongation (hyperintensity in relation to white and
grey matter) occurs within hours of onset of
ischemic symptoms.
Advanced technique, diffusion weighted imaging (DWI)
and perfusion imaging (PWI) show respectively
early infarction (cytotoxic oedema) and ischaemic
tissue at risk (‘ischaemic penumbra’).
These advanced techniques are valuable predictors of
outcome and guide treatments directed as
thrombolysis.
1.
Stroke – investigations
(cont’d)
2.
DEMONSTRATE THE SITE OF PRIMARY
LESION
a) Non-invasive investigation
Ultrasound – Doppler/Duplex scanning: assesses
extra- and intracranial vessels.
Transcranial Doppler
(TCD)
A non invasive ultrasound
technology used to evaluate
blood flow velocity in the major
basal intracranial arteries.
Transcranial Color Coded Duplex
(TCCD)
TCCD sonography is a newer technique that permits the real-time visualization
of the intracranial vascular anatomy and blood flow dynamics.
Stroke – investigations
(cont’d)
2.
DEMONSTRATE THE SITE OF PRIMARY
LESION
a) Non-invasive investigation
Computed tomographic angiography (CTA) –
dynamic helical CT, following bolus injection of
non-ionic contrast, can be used to investigate both
intracranial and extracranial vasculature.
CTA compared with DSA correctly classifies the
degree of carotid stenosis in 96% of cases but is
insensitive to ulcerative plaques.
It is best used in conjunction with Doppler.
CT angiography (CTA)
Stroke – investigations
(cont’d)
2.
DEMONSTRATE THE SITE OF PRIMARY
LESION
a) Non-invasive investigation
Magnetic resonance angiography (MRA) – ‘Time of
flight’ or contrast enhanced techniques are used. It
tends to overestimate the severity of stenosis.
When assessing the carotid arteries it is best used
in combination with Doppler.
Its non-invasive nature makes it helpful in
investigating the intracranial circulation.
MRA
Stroke – investigations
(cont’d)
2.
DEMONSTRATE THE SITE OF PRIMARY
LESION
b) Digital intravenous subtraction angiography (DSA)
Stroke – investigations
(cont’d)
3.
IDENTIFY FACTORS WHICH MAY INFLUENCE
TREATMENT AND OUTCOME
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General investigation
Chest X-ray (cardiac enlargement, HT,…)
ECG (cardiac disease)
Blood glucose (diabetes)
Serum lipids and cholesterol (hyperlipidemia)
Full blood count (polycythaemia, thrombocytopenia)
Urine analysis (polyarteritis, thrombocytopenia)
Auto-antibodies
Prothrombin time and partial thromboplastin time (PTT)
Note drug history (oral contraceptives, amphetamines,…)
Selectively cardiac ultrasound, HIV screen, viscosity studies,
anticardiolipin antibodies, …
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Cerebral infarction –
management
The acute stroke
Treatment aims: 1/ prevent progression of present event
2/ prevent development of complication (e.g. aspiration
pneumonia, pressure sores, deep vein thrombosis)
3/ to rehabilitate the patient
4/ prevent the development of subsequent event
Ad 1/ Thrombolysis with tissue plasminogen activator (TPA)
TPA is approved for treatment of acute ischemic stroke. The key is
delivery within 3 hours of stroke onset. This agent is associated with
rapid recanalisation of occluded vessels. TPA is administered
intravenously, randomised clinical trials of other thrombolytics as
well as use of TPA after ‘3 hours window’ either i.v. or i.a.,
combination of TPA with mechanical recanalisation etc. are currently
under way.
General measures – hydratation, oxygenation, slow correction of blood
pressure, treatment of oedema
DB -- Mismatch
5:24
NIH 16
8 cc
71 cc
23 cc
5 cc
M1 occlusion
+4:23
+4:23hrs
hrs
NIH
NIH14
14
Recanalization
Cerebral infarction –
management (cont’d)
The acute stroke
Ad 4/ Prevention of further stroke
The recognition of risk factors and their correction to minimise the risk of
further events forms a necessary and important step in long-term
treatment.
Control hypertension
Emphasize the need to stop cigarette smoking
Correct lipid abnormality
Give platelet antiaggregation drugs (aspirin or in selected cases
Clopidogrel) to reduce the rate of reinfarction
Remove or treat embolic source (long-term anticoagulation in atrial
fibrillation)
Treat inflammatory or vascular inflammatory diseases
Stop thrombogenic drugs, e.g. oral contraceptives.