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Sudden Hemiplegia and

Dysphagia: Strokes;
Neuro-imaging II
RTF Cheung (Neurology)
YW Fan (Neurosurgery)
FL Chan (Radiology)
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Definitions

Stroke = most common adult neurological


diseases, 2nd & 3rd leading cause of death in China
& HK, major cause of morbidity and disability

Stroke = rapid onset clinical symptoms and signs


of focal or global disturbances of cerebral
functions due to non-traumatic vascular causes,
symptoms lasting > 24 hours or leading to death

Transient ischaemic attack (TIA) = ischaemic


stroke but symptoms < 24 hours

Do not use CVA!


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New Proposed Definition


Stroke

(ischemic) =

- continuing symptoms >24hr, or


- fatal, or
- imaging evidence of acute infarction

TIA =
- focal neurologic sypmtoms <1hr without

evidence of acute infarction

Cerebral Arterial Supply

Types & Mortality

Ischaemic stroke (ISS, 80%; cortical, subcortical,


posterior circulation, lacunar)

Intracerebral haemorrhage (ICH, 20%;


supratentorial, infratentorial)

Subarachnoid haemorrhage (SAH, <5%)

Mortality: SAH (50% die at 1 month) > ICH (40%


die at 1 month and 50% at 1 year) > cortical
infarct (20% die at 1 month and 35% at 1 year) >
lacunar infarct
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Types of Stroke

Arterial Causes of Stroke

Disability & Pathogenesis

Disability: SAH (50% survivors with severe


morbidity) > cortical infarct > ICH > lacunar
infarct

Pathogenesis:
ISS (atherosclerosis, cardioembolism,

thromboembolism, small vessel disease),

ICH (hypertension, aneurysm, vascular

malformation, bleeding tendency, cerebral


amyloid angiopathy),

SAH (aneurysm, vascular malformation)


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Atherosclerosis

Atherosclerotic
Plaque

Plaque
Fissure/
Cracking/
Rupture

Chronic Ischemia

Thrombus
Formation

Stabilized
Plaque

Thrombus
Incorporated
into Atheroma

Embolism

Occlusion

Acute Event
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Risk Factors
Unmodifiable

Modifiable

old age
male sex
history of TIA or stroke
peripheral vascular disease

obesity
lack of exercise
cigarette smoking
alcohol abuse
use of oral contraceptives
hypertension
diabetes mellitus
hyperlipidaemia
high plasma fibrinogen
high blood viscosity
heart disease
atrial fibrillation
carotid artery stenosis
homocysteinaemia

Cardiac Causes of Stroke

Cerebral Aneurysms

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Clinical Features (1)

Symptoms and signs: location and extent of


damage; negative features from loss of
functions; sudden or rapid in onset

Carotid territory: hemiparesis hemifacial


weakness; hemisensory loss; language
disturbances (dominant hemisphere);
visuospatial disorientation (non-dominant
hemisphere); visual disturbances (retinal stroke
or amaurosis fugax); dysarthria; deviation of
head and eyes towards the lesion side;
dysarthria; dysphagia
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Clinical Features (2)

Vertebrobasilar territory: cortical blindness;


homonymous visual field defects; diplopia;
nystagmus; vertigo; Horners syndrome;
dysarthria; dysphagia; crossed hemiparesis;
tetraparesis; crossed unilateral sensory loss;
bilateral sensory loss; ataxia

DDx of stroke: intracranial tumour; chronic


subdural haematoma; encephalitis; multiple
sclerosis; seizure; hysteria

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Complications

Cerebral: cerebral oedema; increased intracranial


pressure; herniation; haemorrhagic transformation
of cerebral infarction; seizures

Systemic: bronchopneumonia; aspiration


pneumonia; deep vein thrombosis; pulmonary
embolism; pressure sores; urinary tract infection;
contractures; frozen shoulder; cardiovascular
disturbances; fluid and electrolytes disturbances;
anxiety and depression

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Basic Investigations

To confirm the clinical diagnosis, classify the


types of stroke, define the underlying causes and
risk factors, and reveal any complications

Computed tomography (CT) or magnetic


resonance imaging (MRI) of the head;

routine blood tests; erythrocyte sedimentation


rate; fasting blood sugar; fasting lipoprotein
pattern;

ECG; CXR
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Further Investigations

Tests for prothrombotic states

Echocardiography (transthoracic or
transoesophageal)

Holter monitoring

Ultrasound Doppler study (extracranial,


transcranial)

Cerebral angiography

Lumbar puncture
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General Management (1)

Keep the patient comfortable and avoid


complications

Regular neuro-observation

Monitor arterial blood pressure; avoid rapid


lowering of blood pressure

Avoid electrolyte imbalance, hypovolaemia, and


fluid overload

Refer to speech therapist for dysphagia or


speech/language problems
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General Management (2)

Ryles tube feeding for depressed conscious level


or dysphagia

Monitor blood glucose level and maintain


euglycaemia

Prevent pulmonary complications by careful


feeding practice, early mobilization, and chest
physiotherapy

Consider low dose subcutaneous heparin for


prophylaxis of deep vein thrombosis and
pulmonary embolism
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General Management (3)

Treat any infection vigorously and reduce the


core and brain temperature if fever

Avoid bladder over-distension and genitourinary


infection by condom catheter in incontinent man
and indwelling catheter in both sexes if
necessary; use intermittent catheterization to
measure post-void residual volume

Avoid constipation, faecal impaction, and soiling


by providing high fibre diet and stool softeners but
not laxatives

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General Management (4)

Prevent pressure sores by repositioning of weak


limbs, frequent turning, and the use of cushions,
egg-crater mattress and air mattress

Early physiotherapy and use of occupational


therapy devices

Control seizures with anticonvulsant therapy


(post-stroke seizure complicates 11% of stroke
patients without previous history of seizure)

Watch out for depression

Avoid iatrogenic complications


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General Management (5)

Initiate measures to prevent future strokes or


cardiovascular events

Risk factor identification and control

Antiplatelet agents for non-cardioembolic


ischemic stroke, e.g. aspirin, clopidogrel, slowrelease form of dipyridamole

Anticoagulation for cardioembolic ischemic


stroke

Healthy life styles

Regular exercise
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Acute Thrombolytic Therapy

Recombinant Tissue Plasminogen Activator


within 3(4.5) hours of the onset of stroke is
effective; more haemorrhagic complications

Intravenous streptokinase has


unacceptable risk of haemorrhagic
complications

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Merci
Retriever

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Mechanical Thrombectomy

Alligator retrieval device; chestnut medical technology;


FDA approved for peripheral and neurovasculature foreign
body removal in March 2005
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Anticoagulation in Acute Stage

AVOID if extensive or haemorrhagic infarct, active


or unidentified bleeding source, lack of monitoring,
uncontrolled hypertension, infective endocarditis

Clinical trials FAILED to show any beneficial effects


of anticoagulation in acute stage

LOGICAL but unproven: (i) definite or probable


cardiac emboli, (ii) prophylaxis of thrombus
formation/propagation or embolisation distal to an
occluded or severely stenotic large cerebral artery

INDICATED in cerebral venous thrombosis


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Antiplatelet Therapy in Acute Stage

International Stroke Trial: aspirin (300 mg/D)


given in ischaemic strokes within 48 hours of
onset achieved a non-significant trend of benefit

Chinese Acute Stroke Trial: aspirin at 160 mg/D


within 48 hours of the onset of suspected acute
ischaemic resulted in a significant 14%
proportional risk reduction in mortality at 4 weeks
and a non-significant 11% proportional risk
reduction in death and dependency upon
discharge when compared to placebo
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Neurosurgery in Stroke Management (1)

Carotid endarterectomy beneficial in symptomatic


patients with severe stenosis, but small benefit in
asymptomatic severe stenosis

Negative results of the EC-IC Co-operative study for


extracranial to intracranial bypass; in patients with
cerebral hypoperfusion?

Young patients with Moyamoya disease (rare) may


benefit from synangiosis: duro-arterioencephalosynangiosis, formal superficial temporal
artery to middle cerebral artery bypass
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Neurosurgery in Stroke Management (2)

Treatment of raised intracranial pressure is guided


by ICP monitoring

Surgical decompression of supratentorial infarct:


may not improve quality of life, consider in young
patients with non-dominant infarct

In cerebellar infarct, direct brain stem compression


from infarcted tissue and/or hydrocephalus may
lead to acute deterioration; consider prompt
drainage of hydrocephalus, infarctectomy and
posterior fossa decompression
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Neurosurgery in Stroke Management (3)

Cerebellar haemorrhages are neurosurgical


emergencies: prompt CSF drainage and clot
evacuation

Haemorrhage at basal ganglia is often related to


hypertension. Surgery improves mortality but
increases vegetative survival. Minimal invasive
techniques like endoscopy, stereotaxy and
chemical clot liquefaction have shown some
promise, but proper clinical trials are awaited

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Neurosurgery in Stroke Management (4)

Brain stem haemorrhage has very high mortality,


for conservative treatment

Diverse aetiologies for lobar hemorrhage;


evacuation and examination for haematoma
cavity under microscope recommended for most
cases except for amyloid angiopathy

Intraventricular haemorrhage and associated


hydrocephalus usually treated with ventricular
drainage and chemical clot lysis using
streptokinase, urokinase or tPA
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Neurosurgery in SAH

Subarachnoid haemorrhage is associated with


ruptured cerebral aneurysm in 75%

High index of suspicion is required for prompt


referral and early treatment

Early microsurgical clipping is the standard


treatment in good surgical candidate

Conservative treatment adopted for poor grade


patients

Angioplasty and intra-arterial papaverine for


treatment of vasopasm is becoming popular
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Neuro-imaging in Stroke

CT or MRI is mandatory

Able to delineate blood vessels and assess


brain perfusion

USG applicable for neonatal brain, intraoperative


imaging or extracranial vascular imaging

Conventional angiography invasive and reserved


for selected cases, or for andovascular
interventional therapy

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Evolution of CT Findings

Normal up to 12 hours; hyperdense artery or


decreased density of lentiform nucleus

12 to 24 hours: loss of gray-white differentiation


or insular ribbon, sulcal effacement

1 to 3 days: wedge-shaped hypodensity,


cytotoxic oedema, haemorrhagic transformation

4 to 7 days: maximal cytotoxic oedema, gyral


enhancement

1 to 8 weeks: subsiding oedema

>8 weeks: encephalomalacia


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Evolution of MRI Findings

Abnormal DWI or vascular enhancement

12 to 24 hours: T2W hyperintensity (oedema),


loss of gray-white differentiation or insular ribbon,
sulcal effacement, intravascular & meningeal
enhancement

1 to 3 days: wedge-shaped T2W hyperintensity,


cytotoxic oedema, haemorrhagic transformation

4 to 7 days: maximal cytotoxic oedema, gyral


enhancement

1 to 8 weeks: subsiding oedema

>8 weeks: encephalomalacia

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Interventional Neuroradiology

Transarterial thrombolysis

Embolotherapy for AVM and aneurysm

Angioplasty (+/- stenting) for arterial


stenosis

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Cortical Infarct

Subcortical Infarct

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Lacunar Infarct

Intracerebral Haemorrhage

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Subarachnoid Haemorrhage

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CT vs MRI in Acute stroke

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Evolution of infarct without


intervention
DWI

PWI

2 weeks later

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Cerebral haemodynamics in acute stroke

CT

CBF

CBV

MTT

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Normal DSA

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Absent Right MCA on MRA

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Top of Basilar Artery Giant Aneurysm

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Vasospasm following SAH:


Anterior Circulation

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Vasospasm following SAH:


Posterior Circulation

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Ruptured Carotid Artery Plaque


with Thrombus

Left Carotid Stenosis

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Severe LICA stenosis: Before stenting

Severe LICA stenosis:


After stenting & Angioplasty

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Colour-coded ultrasonography

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Surgical Decompression
CT Findings

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Surgical Decompression

Dural Opening

After Infarctectomy

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