STROKE

Stroke or CVA is an acute disorder or syndrome of the blood vessel of the brain. The term stroke refers to the sudden death of brain tissue caused by a lack of oxygen resulting from an interupted blood supply.
There are two ways that brain tissue death can occur, (ischemic stroke) or (hemorrhagic stroke).

65 85% of first stroke were due to supplying the brain (ischemic stroke / non hemorrhagic stroke: cerebral thrombosis or embolism, and infarction). 15 35% were cause by (hemorrhagic stroke), mostly caused by . The risk of recurrent stroke within five years of a first stroke is between 30% and 43%.

Hypertension is the major cause of stroke. In hypertension, severely elevated blood pressure damages the blood vessels. If blood vessels are subjected to high blood pressure for an extended period of time, their response is the thicken, making them less flexible. This condition is called . Also, if excessive amounts of fat are found in the blood, the arteries can accumulate fatty deposits called . This build up, called

is a blockage or reduction of blood flow in an artery that feeds that area of the brain. This blockage may result from and . It is the most common cause of an infarct. An infarct is the area of the brain that has died because of this lack of oxygen.

result from bleeding within and ground the brain causing compression and tissue injury, the most common presentations are and .

DEFINITION: Clinical symptoms of acute developing focal (or global) cerebral dysfunction lasting 24 hours or longer, or lasting to death, without any apparent cause other than vascular origin (WHO, 1986)

TIA (Transient Ischemic Attack) has the same definition but last s less than 24 hours, often just for a few minute.
SAH (Subarachnoid hemorrage) is the exeption to this definition and usually present without focal neurological deficit.

STROKE
15% 85%

Primary Hemorrhage
Intraparenchymal. subarachnoid.

Ischemic stroke

20% Atherosclerotic Cerebrovascular disease

25% Penetrating Artery Disease (lacunae)

20% Cardiogenic Embolism Atrial fibrillation Valve disease Ventricular thrombi Many others

30% Cryptogenic Stroke

5% Other, unsual Causes Prothrombic states Dissections Arteritis Migraine/vasospasm Drug abuse Many more

hypoperfusion

Arteriogenic emboli

Classification of stroke by mechanism, with frequency estimates of the abnormalities. Note that about 30% of stroke is cryptogenic (From Albers GW. Et al: Chest 2001; 119:3005, with permission)

CLINICAL CLASIFICATION: I. ISCHEMIC/NON-HEMORRHAGIC STROKE 1. RIND (Reversible Ischemic Neurological Deficit) 2. Stroke in evolution/progressing stroke. 3. Completed stroke.
I. HEMORRHAGIC STROKE

OXFORDSHIRE CSP CLINICAL CLASIFICATION/BAMFORD 1. Partial Anterior Circulation Infarction (PACI) VARIABLE 2. Total Anterior Circulation Infarction (TACI) POOR 2. Lacunar Infarction (LACI) GOOD 4. Posterior Circulation Infarction (POCI) VARIABLE

A.A.B.N. Nuartha, 2007

I. Ischemic/non hemorrhagic stroke:

1. Reversible ischemic neurological deficit (RIND):

The sudden or rapid onset of a focal neurological deficit that is caused by a cerebrovascular disease, but the deficit lasts over 24 hours and regression completely to normal within about 1 3 weeks.

2. Stroke in evolution (progressing stroke):

Refer to the progression of a focal neurological deficit over 24 hours secondary to a stroke in the carotid artery distribution, or 72 hours in the vertebral basilar artery distribution.

3. Completed stroke:
Refer to a stable neurological deficit for more than 24 hours with infarcts in the carotid artery distribution, or 72 hours with infarcts in the vertebral basilar artery distribution.

II. Hemorrhagic stroke:

Usually presents with a sudden onset of focal neurologic deficit that may be accompanied by alteration in mental status, headache, and vomiting. 1. Intra cerebral hemorrhage: Present as a rapidly expanding mass lesion (hematoma) with sign of increased intracranial pressure.

2. Subarachnoid hemorrhage: A hemorrhage from cerebral blood pressure, aneurysm or vascular malformation (arterio venous malformation) in to the subarachnoid space, ie the space surroundings the brain where blood vessles lie between the arachnoid and pial layers.

RISK FACTORS FOR CEREBRAL INFARCTION (ISCHEMIC STROKE)

Unmodifiable risk factors Age Sex Low birth weight Race/ethnicity Genetic/family history Previous stroke Major modifiable risk factors Hypertension Atrial fibrillation Isolated systolic hypertension Myocardial infarction Other heart disease Diabetes mellitus dyslipidemia Transient ischemic attacks smoking

Questionable, rare, or weak modifiable risk factors AIDS Alcohol Fibrinogen and platelets Exercise/physical inactivity Obesity/poor diet Hematocrit Water supply Hypercoagulability Oral contraceptives Pregnancy Hyperhomocysteinemia Socioeconomic status Season claudication Post menopausal hormone therapy Carotid artery stenosis

Risk factors predominant in the young Mitral velve leaflet prolapse Sicle cell disease and other hemoglobinophathies Migraine Cocaine/drug abuse Obstructive sleep apnea Intercurrent infection and inflammation Patent foramen ovale Atrial septal aneurysm Systemic lupus erythematosus

Etiology of intracerebral hemorrhage

Hypertension (50% 60%).
Arteriovenous Malformation, aneurysm. Bleeding into a tumor. Anticoagulant use. Fibrinolytic agents. Sympathomimetic drugs. Vasculitis.

Cerebral amyloid angiopathy .

Coagulopathy (deficiency of factors VII, VIII, IX, XIII, von Willebrands factors, afibrinogenemia, idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, disseminated intravascullar coagulation, uremia)

Myeloproliferative disorders (multiple myeloma, acute and chronic myelogenous leukemia, essential thrombocythemia).
Eclampsia. Moyamoya syndrome. Acute elevation of blood pressure or reperfusion of ischemic area (prolonged migraine, exposure to cold, dental pain, postendarterectomy).

LEFT- SIDE STROKE Right-sided hemiparesis/paralysis. Right-side hemihypesthesia/anesthesia. Hoonymous hemianopsia of right visual field. Right sided dysarthria. Motor and/or sensory aphasia.
RIGHT-SIDE STROKE Left-sided hemiparesis/paralysis. Left-sided hemihypesthesia/anethesia. Hemianopsia of left visual field. Left-side dysarthria.

 Monocular blindness (ipsilateral) Aphasia (motor and/or sensory in

OCCLUSION

dominant hemisphere)
Hemiparesis/paralysis (contralateral)
Hemihypesthesia/anesthesia (contralateral) Homonymous hemianopsia (contralateral) Motor paresis and/or sensory loss of face and
ICA
MCA

upper limb (contralateral)

Motor paresis and sensory loss of lower

limb (contralateral)
Transient hemiparesis (contralateral) Transient hemihypesthesia (contralateral) Homonymous hemianopsia (contralateral) Sensory aphasia (in dominant hemisphere)
PCA

ACA

Bilateral visual disturbance. Double vision (diplopia). Nistagmus. Tinnitus, Vertigo, Hearing disturbance. Circumoral paresthesia. Motor/sensory disturbance (bilateral, alternating, crossed). Ipsilateral cerebellar ataxia. Nausea, vomitus. Dysphasia. Dysarthria. Amnesia, confusion. Intermitten loss of consciousness. Drowsy tendency. Drop attacks (drop spells). Ipsilateral Horner syndrome. Internuclear opthalmoplegia.

Anatomic area of imvolvement Lobar 15% Frontal Parietal Temporal Occipital Deep Putaminal 55% Thalamic Cerebellum Pontine 10% 10% 10%

Clinical findings

Frontal headache, motor weakness arm> leg behavioral abnormalities. Unilateral headache, hemisensory deficit, spatial neglect (nondominant), visual field deficits. Unilateral headache, aphasia (dominat), visual field defect. Ipsilateral periorbital headache, visual field loss or blurring. Unilateral motor, sensory and visual field loss, aphasia (dominant), neglect (nondominat), coma. Hemisensory deficit > hemiparesis. Gaze deviation, pupil asymetry. Nausea, vomiting, ataxia, depressed level of consciousness. Coma, quadriplegia, decerebrate posturing, pinpoint pupils.

MEDICAL HISTORY (ANAMNESIS)

GENERAL EXAMINATION NEUROLOGICAL EXAMINATION

MULTIDICIPLINARY TEAM

INVESTIGATIONS CLINICAL LABORATORY TEST. DIAGNOSTIC RADIOLOGIC/IMAGING EXAMINATION: CHEST X-RAY. CT, CTA,MRI, MRA, MRS. DSA, CATHETER ANGIOGRAPHY PET, SPECT, CT-PET. TRANSCRANIAL DOPPLER AND DUPLEX CAROTID ULTRASONOGRAPHY. EEG. ECHOCARDIOGRAPHY (TTE, TEE). LUMBAR PUNCTURE.

ISCHEMIC STROKE

HEMORRHAGIC STROKE

MANAGEMENT

No treatment of stroke can be as successful as of the even from occuring. Prevention is the most effective way to avoid or suffering from stroke: I. Promotion. II. Primary prevention. III. Secondary prevention.

STROKE CONTROL STRATEGY

HEALTHY

RISK FACTOR

STROKE/TIA

PROMOTION

PRIMARY PREVENTION

SECONDARY REVENTION

MODIFY LIFE-STYLE

MODIFY LIFE-STYLE

MODIFY LIFE-STYLE

- CONTROL OF RISK FACTOR

- CONTROL OF RISK FACTOR - ANTI THROMBOTIC. - CAROTID THROMBECTOMY/ ENDARTERECTOMY. - CAROTID ANGIOPLASTY WITH OR WITHOUT STENTING

MODIFY LIFESTYLE

CONTROL OF RISK FACTORS

ANTI THROMBOTIC

CAROTID THROMBECTOMY/ ENDARTERECTOMY

CAROTID ANGIOPLASTY WITH OR WITHOUT STENTING

1. Patient with high risk symptomatic carotid stenosis or inoperable cases.

1. Diet 2. Physical exercise. 3. Cessation of smoking. 4. Alcohol reduction.

1. Inmodifiable. 2. Modifiable.

1. Anti platelet. 2. Anti coagulant.

1. Symptomatic stenosis (>70%). 2. Asymptomatic stenosis (>90%).

 Reducing body weight. Restricting dietary salt. Increasing fibers and decreasing fat in

your diet. Not smoking. Avoiding exess alcohol. Exercising regularly. Practicing relaxation techniques.

1. 2. 3.

Modify life style. Control of risk factor. Anti platelet agent:

Asetosal/ASA tab: 75 325 mg/day, 1 X I. ASA 25 mg/Dipyridamole 200 mg cap: 2 X I. Clopidogrel 75 mg tab: 1 X I. Ticlopidine 250 mg tab: 2 X I. Aspirin 75 mg tab + Clopidogrel 75 mg tab: 1 X I. Triflusal 300 mg tab: 1 X 2. Warfarin with AF, prosthetic heart valves and other cardio emboli

4. 5.

Oral anti coagulant:

Surgery-microsurgery/radiosurgery-intervention (e.g. carotid surgery, gamma-knife, carotid angioplasty with or without stenting, coils, glue, or ballons embolization).