1. Neurology in Practice. Edited by YL Yu, JKY Fong, SL Ho. Second Edition, Hong Kong, University Press
2. Davison's Principles and Practice of Medicine. Edited by C Haslett, ER Chilvers, JAA, Hunter, NA Boon. Eighteenth Edition, Churchill Livingstone

Stroke is one of the most common neurological diseases in adults, 3rd leading cause of death, a major cause of morbidity and disability

Definitions of stroke and transient ischaemic attack (TIA)

Stroke = syndrome of rapidly developing clinical symptoms and signs of focal or global disturbances of cerebral functions due to non-traumatic vascular causes, with symptoms lasting > 24h or leading to death

TIA = "ISS - ischaemic stroke" but symptoms completely resolved within 24 hours

DIAG: cerebral arterial supply ® Cardiothrombotic stroke from aorta sending thrombi to circulation

Types and subtypes of stroke:

Ischaemic stroke (ISS, 70%; cortical, subcortical, posterior circulation, lacunar) - West 80-85%

Intracerebral haemorrhage (ICH, 25%; supratentorial, infratentorial) - West < 10%

Subarachnoid haemorrhage (SAH, 5%) - same in West

Mortality: SAH (50% die within 1m) > ICH (40% at 1m, 50% at 1yr w/ sig deficits) > cortical infarct (20% at 1m, 35% at 1y) > lacunar infarct (small size, therefore less mortality)

SLIDE: Ischaemic stroke

Clot in carotid artery extend s directly to middle cerebral artery

Clot fragment carried from heart or more proximal artery

Hypotension and poor cerebral perfusion, border zone infarcts, no vascular occlusion

SLIDE: Haemorrhagic stroke

SAH: ruptured aneurysm

Intracerebral haemorrhage: hypertensive

SLIDE: Arterial causes of stroke

Stenosis or occlusion of carotid artery

Atheroma with or without clot at bifurcation of internal carotid artery into anterior and middle cerebral arteries

At siphon within cavernous sinus

Dissecting aneurysm of internal carotid artery below vase of skull (string(?) sign radiographically)

Atheroma with or without clot at bifurcation of common carotid artery into internal and external carotid arteries (most common - esp. Caucasians)

At origin of common carotid artery from brachiocephalic trunk or aorta (uncommon)

Seeing more disease extracranially than intracranially (diet changes etc.)

Morbidity: SAH (50% survivors with severe morbidity) > cortical infarct > ICH > lacunar infarct

ISS (atherosclerosis, thromboembolism, small vessel disease - esp. HT + DM - tend to have lacunar stroke)

ICH (hypertension, aneurysm, vascular malformation 10%, bleeding tendency - eg. Haematological malignancy, marrow problem,, anti-coagulation Tx)

SAH (aneurysm 80-85%, vascular malformation 10%, remainder cause unknown)

SLIDE: AS

Atherosclerotic plaques

Plaque fissure/ cracking/ rupture

Thrombus formation

1. Thrombus incorporated into atheroma - stabilised plaque (chronic ischaemia)

2. Embolism (acute event)

3. Occlusion (acute event)

Risk factors

Unmodifiable: old age (longer exposure to risk factors); male sex (not protected by oestrogen, female and male more similar risk post-menopause); Hx of TIA or stroke, PVD

Modifiable: HT (measure BP), heart disease; atrial fibrillation; diabetes mellitus (measure bld gluc), hyperlipidaemia; cigarette smoking; alcohol abuse; carotid artery stenosis; use of oral contraceptives; high plasma fibrinogen; high blood viscosity; obesity; lack of exercise

SLIDE: Cardiac causes of stroke

Mitral stenosis: mural and valvular thrombi

Subacute bacterial endocarditis, vegetations

Valve replacement with thrombus formation

Myocardial infarction with mural thrombus (AS)

Ventricular aneurysm with intraluminal clot formation (AS)

Congestive heart failure, atrial fib

SLIDE: cerebral aneurysms

Distribution of congenital cerebral aneurysms

Anterior cerebral 30%; Distal anterior cerebral 5%; Anterior communicating 25%

Internal carotid 30%; Ophthalmic 4%; Posterior communicating 18%; Bifurcation 4%; Anterior choroidal 4%

Posterior communicating and distal posterior cerebral 2%

Basilar 10%; Bifurcation 7%; Basilar trunk 3%

Vertebral - posterior inferior cerebellar 3%

SLIDE: ruptured carotid artery plaque with thrombus

Symptoms and signs of stroke: location and extent of damage; negative features from loss of functions; sudden or rapid in onset

Carotid territory events: (frontal eye field, post-central gyrus - cortical sensation) 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

Vertebrobasilar territory events: cortical blindness; homonymous visual field defects; diplopia; nystagmus; vertigo; Horner's syndrome; dysarthria; dysphagia; crossed hemiparesis; tetraparesis (must be upper part cervical cord or BS lesion); crossed unilateral sensory loss; bilateral sensory loss; ataxia

Five most common warning symptoms: sudden weakness or numbness of the face, arm or leg on one side of the body; sudden dimness of loss of vision, particularly in one eye; loss of speech, or trouble talking or understanding speech; sudden, severe headaches with no apparent cause; unexpected dizziness, unsteadiness or sudden falls, especially along with any of the previous symptoms

Intracranial tumour (progressive, but sudden presentation due to seizure, complication, has focal deficit after recovery from seizure)

Chronic subdural haematoma

Encephalitis (probably also have neck stiffness, fever, seizures which usu. not common in stroke)

Multiple sclerosis (esp. Western, young female, inflam demyelination, sudden onset, can be focal)

Seizure

Hysteria (made up from Pt's mind, even without Pt knowing)

Cerebral complications of stroke:

Cerebral oedema

Increased ICP

Herniation

Haemorrhagic transformation of cerebral infarction

Seizures (8-12% of haemorrhagic strokes; 5% of ischaemic stroke)

Systemic complications of stroke:

Bronchopneumonia

Aspiration pneumonia

DVT

Pul embolism

Pressure sores

UTI

Contractures

Frozen shoulder

Cardiovascular disturbances

Fluid and electrolytes disturbances

Anxiety and depression

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 - 1-2min) or magnetic resonance imaging (MRI - 30min) of the head; routine blood tests (CBC); erythrocyte sedimentation rate; fasting blood sugar; fasting lipoprotein pattern (risk factors ID important); ECG (LV hypertrophy, atrial fib); CXR (aspiration pneum already occurred because Pt presented late, cardiomegaly?)

Note: acute infarct will not show initially (esp. CT)

SLIDE: CT

Grey matter whiter

White matter darker

Blood and bone white colour

Cortical infarct

Subcortical infarct: corona radiata

SLIDE: MRI

Better quality picture - can see gyri, sulci

Lacunar infarct: within BG within internal capsule (not visible on CT)

T2W = CSF (water) is white

CT scan: Intracerebral haemorrhage: haematoma occupying lateral part of BG, may have involvement of internal capsule (left hemiparesis b/c haematoma on R side, drowsy or semi-comatose b/c of SOL effect)

SLIDE; Subarachnoid haemorrhage

CSF-blood level (CSF whitish)

Blood obstructing CSF flow -> Hydrocephalus

Further investigations (if indicated):

Tests for prothrombotic states

ECG (transthoracic or transoesophageal) - cardiac prob causing embolism? Paroxysmal atrial fib

Holter monitoring

US Doppler study (extracranial, transcranial)

Cerebral angiography - AVM?

Lumbar puncture - suspect other Dx or SAH but CT -ve

SLIDE: cerebral angiogram

Normal DSA

Left carotid stenosis (narrowed to hairline)

SLIDE: MR angiogram (MRA)

Can be used without contrast

Absent right MCA due to acute thrombosis of R internal carotid a

Aim to keep the patient comfortable and avoid complications: cerebral oedema; increased intracranial pressure; herniation; haemorrhagic transformation of cerebral infarction; seizures; 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

Regular neuro-observation (neuro-observation chard: BP, HR, O2 sat, GCS, pupil reflexes, limb power)

Monitor arterial blood pressure; treat severe hypertension but avoid rapid lowering of blood pressure (acute stage may be reactions)

Avoid electrolyte imbalance, hypovolaemia, and fluid overload by regular clinical assessment and monitoring of electrolytes

Need IV drip b/c Pt cannot eat at first

Refer to speech therapist for dysphagia or speech problems; Ryle's tube feeding for depressed conscious level or dysphagia

Monitor blood glucose level and maintain euglycaemia. Pt not on usual diet

Prevent pulmonary complications such as silent aspiration and pulmonary embolism by careful feeding practice, early mobilisation, and chest physiotherapy; low dose subcutaneous heparin (e.g., 5000 units twice daily) for prophylaxis of deep vein thrombosis and pulmonary embolism in immobilised patients (esp. Caucasians have high chance of DVT leading to pul embolism - therefore use heparin). If cannot tolerate heparin, use elastic stockings

Treat any infection vigorously and reduce the core and brain temperature in case of fever

Avoid bladder over-distension and genitourinary infection by condom catheter in incontinent man and indwelling catheter in both sexes if necessary; use intermittent catheterisation to measure post-void residual volume. UB overdistension: discomfort, increases BP.

Avoid constipation, faecal impaction, and soiling by providing high fibre diet and stool softeners but not laxatives. Very difficult to urinate/ open bowels in bed (b/c usu. upright posture)

Prevent pressure sores by repositioning of weak limbs, frequent (eg., 2 hourly) turning, and the use of cushions, egg-crater mattress and air mattress

Avoid contractures by 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). Do not need regular use of prophylactic anti-convulsants. But if seizure due to stroke, then chance of another seizure high, so use therapeutic anti-convulsants for prophylaxis

Psychiatric complications like depression and insomnia are common

Use medications cautiously and review them frequently to avoid iatrogenic complications

Recombinant Tissue Plasminogen Activator (tPA) within 3 hours of the onset of stroke is effective in highly selected patients; increased risk of haemorrhagic complications

Intravenous streptokinase was found to have unacceptable risk of haemorrhagic complications

AVOID if extensive infarct, haemorrhagic infarct, active or unidentified bleeding source, lack of monitoring, uncontrolled hypertension, infective endocarditis (IE = mainstay of Tx is ABX unless underlying cardiac prob requires anti-coagulation)

Clinical trials FAILED to show any beneficial effects of anticoagulation (heparin, low molecular- weight heparin) in acute stage (only useful in stroke if stroke due to cardioembolic mechanism)

LOGICAL in patients without severe neurological deficit when under the following circumstances: (i) definite or probable cardiac source of emboli, (ii) prophylaxis of thrombus propagation or embolisation distal to an occluded large cerebral artery (recommendation, without evidence), and (iii) prophylaxis of thrombotic occlusion or embolisation distal to a severely stenotic large cerebral artery (failing anti-platelet Tx)

In the International Stroke Trial, 2 different regimen of subcutaneous unfractionated heparin (5000 or 12500 IU twice daily) given in ischaemic strokes within 48 hours of onset did not reduce the risk of death or dependency at 6 months

In the International Stroke Trial, aspirin (300 mg/D) given in ischaemic strokes within 48 hours of onset achieved a non-significant trend of benefit

In the 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

The role of carotid endarterectomy is convincingly documented by the North American Carotid Endarterectomy Trial (1991, 1998) and European Carotid Surgery Trial (1991). For symptomatic patients, surgery is better than medical treatment for stenosis greater than 50%.

Small benefit in asymp severe stenosis

For asymptomatic patients, results from the Asymptomatic Carotid Atherosclerosis Study (1994) also support surgical treatment for stenosis greater than 60% if surgical morbidity can be maintained below 3%

The enthusiasm of EC-IC bypass of treatment of cerebral ischaemia was discouraged by the EC-IC Co-operative study. However, this procedure may have a role in patients with cerebral hypoperfusion. Pre-operative cerebral blood flow study may identify the patient who needs this procedure

Moya Moya disease is rare (progressive occlusive disease around Circle of Willis). Young patients may benefit from synangiosis: myoencephalosynangiosis, duro-arterio-encephalosynangiosis, formal STA-MCA (superior temporal artery to middle cerebral artery) bypass

Young: ischaemic events

Older: bleeding events

In patients with established infarction, treatment of raised intracranial pressure from brain swelling is guided by ICP monitoring

The decision of surgical decompression (reduce skull, remove necrotic brain tissue) of supratentorial infarct depends on the expected quality of life of patient (tends not to improve deficit). In general, one would only consider decompression for patient who is young and with non-dominant hemispheric infarct

In cerebellar infarction, direct brain stem compression from infarcted tissue in the small posterior fossa and associated hydrocephalus often leads to acute deterioration in conscious level. Prompt drainage of hydrocephalus, infarctectomy and posterior fossa decompression often yield satisfactory outcome

SLIDE: surgical decompression

Dural opening (skull bone removed)

After infarctectomy

Room inside skull for remaining brain tissue to swell (otherwise may press on normal brain tissue)

Cerebellar haemorrhages are neurosurgical emergencies. Similar to cerebellar infarct, hydrocephalus and posterior fossa mass effect often requires prompt CSF drainage and clot evacuation

Haemorrhage at basal ganglia is often related to hypertension. In general, result of surgical treatment does not compare favourably over medical treatment. Surgery may improve mortality but increases vegetative survival. Recent development of minimal invasive techniques like endoscopy, stereotaxy and chemical clot liquefaction had shown some promise, but their advantage over conventional technique requires a longer-term follow-up

Brain stem haemorrhage is associated with very high mortality. Conservative treatment is often recommended. Stereotactic aspiration and open evacuation are only mentioned for case reporting

Aetiologies for lobar haemorrhage are more diverse. Evacuation and examination for haematoma cavity under microscope is recommended for most cases except for amyloid angiopathy. However, if vascular abnormality was suspected, preoperative angiographic study is best performed for surgical planning

Intraventricular haemorrhage and associated hydrocephalus usually treated with ventricular drainage (endoscopic means) and chemical clot lysis using streptokinase, urokinase or tPA

Subarachnoid haemorrhage is associated with ruptured cerebral aneurysm in 75%. Becoming a neurosurgical condition. High index of suspicion is required for prompt referral and early treatment. For good grade patients, early microsurgical clipping is still the standard of treatment that endovascular coiling has to be compared with (without clipping cannot perform HHH therapy - hypotensive, haemodiltuion, hypovolaemia). A conservative attitude is often adopted for poor grade patients although there are more and more neurosurgeons advocating more aggressive treatment. Angioplasty and intra-arterial papaverine for treatment of vasopasm is gaining popularity with very encouraging result

Cross-sectional imaging with computed tomography (CT) or magnetic resonance imaging (MRI) are preferred modalities. These techniques are also able to delineate blood vessels and assess brain perfusion.

Ultrasonography is applicable for neonatal brain, intraoperative imaging or extracranial vascular (neck BV) imaging. Angiography is invasive and reserved for assessment of selective cases, or for endovascular interventional therapy (now have CT and MR angiogram). DSA = digital subtraction angiography

For detection of haemorrhage, evaluation of lesions requiring surgery or interventional therapy (eg. space-occupying haematoma, aneurysm, AV malformation), triage of patients for different therapeutic approaches, monitor progress.

Diagnosis or exclusion of haemorrhagic stroke is the primary role. Non-enhanced CT readily achieves this, since recent clots are hyperdense to the brain substance. MRI is used to solve specific clinical problems.

For ischaemic stroke, imaging may assess the age of the lesion for planning of thrombolytic therapy. Not so much to visualise infarct because it takes time to develop

Transarterial thrombolysis

Embolotherapy for AVM and aneurysm (deliberating introduce emboli into AVM)

Angioplasty (+/- stenting) for arterial stenosis

Therefore, role of neurosurgery may become less and less due to these methods