?

Second most common cause of death world-wide exceeded only by coronary heart disease and cancer. Worldwide 3 million women and 2.5 million men die each year. Most significant risk factor is Hypertension. Even where advanced facilities are available, 60 % of sufferers die or become dependant. Second leading cause of death in those above 65 years.
CVD Atlas WHO 16

IN PAKISTAN

Disability Adjusted Life Years (DALYs) lost per 1000 population is 9. Mortality in 2002 was 78512.

World Data Table WHO

APOPLEXY STRUCK DOWN WITH VIOLENCE

AN MYB PRESENTATION
By:

Mirza Yousuf Baig

House Officer Medical Unit V

CEREBROVASCULAR ACCIDENT
Abrupt onset of a neurologic deficit that is attributable to a focal vascular cause. 1

1 = Harrisons principles of Internal Medicine 16th ed. p2372

STROKE
Rapid onset of cerebral deficit (usually focal) lasting more than 24 hours or leading to death with no apparent cause other than a vascular one. 1, 2 "Neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". 3
1 = PK p1209 2 = Harrisons principles of Internal Medicine 16th ed. P2372 3 = World Health Organization. Cerebrovascular Disorders (Offset Publications). Geneva: WHO. 1970

TRANSIENT ISCHAEMIC ATTACK (TIA)

Neurologic signs and symptoms only last for < 24 hours (usually 5 15 minutes, average 12 minutes). 1 There is complete recovery. 1 A TIA proceeds to stroke in 10 40 % of cases.

1 = PK p1209

STROKE IN EVOLUTION
Neurologic deficit progresses during the first 24 hours. 1 Also called Evolving stroke, Progressing stroke or Crescendo TIAs. 2

1 = PK p1209 2 = Swansons family practice review 5th ed. p682

COMPLETED STROKE

Neurologic deficit has become maximal, usually within 6 hours. 1

1 = PK p1209

MINOR STROKE

Patient recovers without significant neurologic deficit, usually within a week. 1

1 = PK p1209

PATHOPHYSIOLOGY
ISCHAEMIA (80 90 %) Global (Hypoxic ischaemic) causes hypoxic ischaemic encephalopathy. Focal (thrombotic or embolic) Causes infarction Anoxia, Ca influx, excitatory aa, free radicals

Harrisons principles of Internal Medicine 16th ed. P2372

PATHOPHYSIOLOGY
Decreasing order of vulnerability to ischemia
Neurons Support cells Astrocytes Endothelial cells

PATHOPHYSIOLOGY
Vulnerable regions
Decreasing order of sensitivity
1. 2. 3. 4. Hippocampus Cerebellum Stratum Neocortex

PATHOPHYSIOLOGY
HAEMORRHAGE Mass effect (Compression and ischaemia). Toxic effect.

Harrisons principles of Internal Medicine 16th ed. P2372

RISK FACTORS

RISK FACTORS (NON-MODIFIABLE)

Age Gender M > F (1.25 X) Heredity Previous vascular event such as MI, stroke, peripheral embolism or TIA. Blacks > Whites

Harrisons principles of Internal Medicine 16th ed. P2377

RISK FACTORS (MODIFIABLE)

Hypertension (2 5 X) Smoking (1.5) Diabetes mellitus (1.8 6 X) Hyperlipidemia i.e. Increased LDL or cholesterol, Decreased HDL (1.8 6 X) Heart failure
Harrisons principles of Internal Medicine 16th ed. P2377

Atrial fibrillation MI Alcoholism Oral contraceptives Polycythemia Carotid stenosis

CAUSES (ISCHAEMIC STROKE)

THROMBOSIS
Lacunar stroke (small vessel) Large vessel thrombosis Dehydration

EMBOLISM Artery-to-artery
Carotid bifurcation Aortic arch Arterial dissection Valvular lesions eg MS, BE, mechanical valve. Paradoxical emboli through ASD, patent foramen ovale Atrial septal aneurysm Spontaneous echo contrast

Cardioembolic
Atrial fibrillation Mural thrombus MI Dilated CMP

UNCOMMON CAUSES Hypercoagulable states

Protein C or S def. Antithrombin III def. Antiphospholipid syndrome Factor V Leiden mutation Prothrombin G20210 def. Systemic malignancy Sickle cell anaemia thalassaemia Polycythemia vera SLE Homocysteinemia TTP DIC Dysproteinemias NeS IBD Oral contraceptives

UNCOMMON CAUSES
Meningitis (Syphilis, TB, fungal, bacterial, zoster) Cardiogenic Mitral valve calcification Systemic vasculitis Atrial myxoma (PAN, Wegeners, Takayasus, giant cell Intracardiac tumour arteritis) Marantic endocarditis Primary CNS vasculitis Libman-Sacks endocarditis

Venous sinus thrombosis Fibromuscular dysplasia Vasculitis

UNCOMMON CAUSES Subarachnoid haemorrhage vasospasm Drugs

Cocaine Amphetamine Moyamoya disease Eclampsia

CAUSES (HAEMORRHAGIC STROKE)

HAEMORRHAGIC STROKE
Hypertension (including hypertensive encephalopathy) Aneurysm (ruptured or unruptured) Saccular (berry) Fusiform (atherosclerotic) Mycotic Arteriovenous malformation, ruptured or unruptured Hemorrhagic disorders (e.g., thrombocytopenia, thrombocytosis, coagulopathy, disseminated intravascular coagulation, anticoagulant therapy) Intracranial trauma (e.g., acute extradural or subdural hematoma, intracerebral hemorrhage)

ANTERIOR CEREBRAL ARTERY SYNDROME

Paralysis of opposite leg and foot. A lesser degree of paresis of opposite arm. Cortical sensory loss over toes, foot and leg. Urinary incontinence. Contralateral grasp reflex, sucking reflex, gegenhalten (paratonic rigidity).

ANTERIOR CEREBRAL ARTERY SYNDROME

Abulla (akinetic mutism), slowness, delay, intermittent interruption, lacking of spontaneity, whispering, reflex distraction to sight and sounds. Impairment of gait and stance (Gait apraxia) Dyspraxia of left limbs.

MIDDLE CEREBRAL ARTERY SYNDROME

Paralysis of contralateral face, arm and leg; sensory impairment over the same area. Motor aphasia (dominant). Central aphasia, word deafness, anomia, jargon speech, sensory agraphia, acalculia, alexia, finger agnosia, right left confusion. Conduction aphasia. Homonymous hemianopia (often homnymous inferior quadrantanopia) Paralysis of conjugate gaze to the opposite side.

MIDDLE CEREBRAL ARTERY SYNDROME

Apractognosia of the the nondominant hemisphere, anosgnosia, hemiasomatognosia, unilateral neglect, agnosia of the left half of the external space, dressing apraxia, constructional apraxia, distortion of visual co-ordinates, inaccurate localisation in the half field, impaired ability to judge distance, upside down reading, visual illusions

POSTERIOR CEREBRAL ARTERY SYNDROME

PERIPHERAL TERRITORY Homonymous hemianopia (often upper quadrantic) Bilateral homonymous hemianopia, cortical blindness, awareness or denial of blindness, tactile naming, achromatopia, failure to see to-and-fro movements, Ocular apraxia, Inability to count or enumerate objects.

POSTERIOR CEREBRAL ARTERY SYNDROME

Memory defect Topographic disorientation and prosopagnosia Simultagnosia, hemivisual neglect Unformed visual hallucinations, Distortion of outlines, Central photophobia.

POSTERIOR CEREBRAL ARTERY SYNDROME

CENTRAL TERRITORY Thalamic syndrome: sensory loss, spontaneous pain and dysesthesias, choreoathetosis, intention tremor, spasms of hand, mild hemiparesis. Claudes syndrome: crossed cerebellar ataxia with ipsilateral third nerve palsy.

OTHER SYNDROMES

Medial medullary syndrome Lateral medullary syndrome Total unilateral medullary syndrome Lateral pontomedullary syndrome Basilar artery syndrome

OTHER SYNDROMES
Medial inferior pontine syndrome Lateral inferior pontine syndrome Medial midpontine syndrome Lateral midpontine syndrome Medial superior pontine syndrome Lateral superior pontine syndrome

DIFFERENTIAL DIAGNOSIS
Cerebral tumour Brain abscess Demyelination disorders Focal migraine Subdural haematoma Todds paresis (post-seizure) Hypoglycaemia Encephalitis

Oxford Handbook of Acute Medicine

WORKUP AND DIAGNOSIS

Complete description of the event and associated symptoms. Recent trauma or illness. Comorbids like DM, HTN, migraine, hypoglycaemia, vasculitis. History of use of OCPs.

WORKUP AND DIAGNOSIS

Past history of stroke, TIA, MI, atrial fibrillation, valvular heart disease. History of smoking. Assess for risk factors. Family history of renal disease or cancer. Hospitalization. Complete examination specially general physical exam, CNS, fundoscopy and CVS. Investigations should include an urgent CT scan of the head to differentiate the stroke type.

WORKUP AND DIAGNOSIS

MRI Contrast enhanced CT scan CT angiography EEG helps in localising lesion. Baseline laboratory studies include urinalysis, coagulation studies, complete blood cell count, serum osmolality, and electrolyte, glucose, triglyceride, creatinine, and blood urea nitrogen levels, syphilis serology.

COMPLICATIONS
CEREBRAL
Transtentorial herniation Haemorrhagic transformation Acute hydrocephalus Seizures SIADH Depression
Oxford Handbook of Acute Medicine

SYSTEMIC
Aspiration Infection Fever Pulmonary embolism Hypertension Pressure sores

COMPLICATIONS
CEREBRAL
Transtentorial herniation Haemorrhagic transformation Acute hydrocephalus Seizures SIADH Depression
Oxford Handbook of Acute Medicine

SYSTEMIC
Aspiration Infection Fever Pulmonary embolism Hypertension Pressure sores

MANAGEMENT
Maintain airway. Frequent assessment of neurologic status using NIH stroke scale. Monitoring of patients for signs of haemorrhage if treated with a fibrinolytic. Monitor BP. Do not treat SBP < 200 mm Hg or DBP < 120 mm Hg within 3 5 days of a stroke. Treat fever using acetaminophen and hypothermia blankets.

MANAGEMENT

Monitor blood glucose and ECG. Analgesic for headache. Watch for signs and symptoms of complications. Urinal or bed pan every 2 hours or catheterize if necessary. Ensure adequate nutrition. Upright lateral position and frequent turning. Exercise and physiotherapy. Occupational therapy and speech therapy.

MANAGEMENT
Psychological support. Devices to increase mobility. Patient education. Involve patients social support. Proper plan for discharge.

MANAGEMENT
THROMBOLYSIS:
NINDS recombinant tPA Stroke Study clearly shows a benefit for IV rtPA in selected patients with acute stroke.
tPA Prourokinase

MANAGEMENT
ANTIPLATELET AGENTS:
IST and CAST found use of aspirin within 48 hours of stroke onset reduced both stroke recurrence and mortality minimally. IV abciximab can be used safely within 6 hours of stroke onset.

MANAGEMENT
ANTICOAGULATION:
TOAST trial failed to show any benefit of heparin over aspirin. It also led to increased bleeding rates. Theoretically heparin may prevent propagation of clot.

MANAGEMENT
NEUROPROTECTION: Hypothermia Drugs that block excitatory amino acids have been found beneficial in animals. Various classes tested include CCBs, Kchannel openers, glu antagonists, antiadhesion molecules, NMDA receptor antagonists and modulators, AMPA receptor antagonists, membrane stabilizers, growth factors, glycine-site antagonists, and free radical scavengers.
EMEDICINE

PRIMARY PREVENTION
Regulate optimal BP, blood sugar and blood cholesterol. Low fat and salt diet. Lose weight. Avoid smoking and alcoholism. Regular exercise. Fish 2 3 times per week. Antiplatelets or anticoagulants in those at risk.

PRIMARY PREVENTION

For every ten people who die of stroke, 4 could have been saved if their BP was controlled. In under 65 year age, two fifths of deaths from stroke are linked to smoking.

CVD Atlas 16 WHO

SECONDARY PREVENTION
A 15% relative risk reduction in vascular events (stroke, death, and MI) has been documented for aspirin compared with placebo. A relative risk reduction of approximately 9% for stroke, death, and MI has been reported for ticlopidine compared with aspirin. Blood monitoring is required (a complete blood count assessed every 2 wk for 3 mo).

EMEDICINE

SECONDARY PREVENTION
A relative risk reduction of approximately 9% for stroke, death, and MI has been reported for clopidogrel compared with aspirin (an absolute risk reduction of about 0.25% per year). No blood monitoring is required with clopidogrel ESPS-2 and ESPRIT trial both showed that dipyridamole is more effective in combination with aspirin than aspirin alone. STATINS decrease the risk of future stroke in a patient with atherosclerosis.
EMEDICINE

SECONDARY PREVENTION
In HOPE study, the addition of the ACE inhibitor (ramipril) to all other medical therapy, including antiplatelet agents, reduced the relative risk of stroke, death, and MI by 32% compared with placebo. Relative risk reduction of warfarin in secondary stroke prevention is 70 % compared with placebo. Lifestyle modifications.

EMEDICINE

TIME IS BRAIN

CEREBELLAR INFARCT

HAEMORRHAGIC INFARCT

OLD CEREBRAL INFARCT

LACUNAR INFARCT IN PONS