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Parkinson's disease

Cerebrovascular Diseases
Prof Ahmed Deif
Prof. of Neurology
Neuropsychiatry Dept
Alexandria Univ.

Definitions
Stroke is defined as a clinical syndrome consisting of 'rapidly developing clinical signs
of focal (at times global) disturbance of cerebral function, lasting more than 24 h secondary
to disturbance of cerebral circulation. It is caused by either reduced blood flow to the brain
(ischemic stroke) or the rupture of blood vessels in the brain (hemorrhagic stroke.
Transient ischaemic attacks [TIA] is focal CNS disturbances caused by vascular
events such as microemboli and occlusion leading to ischaemia where the symptoms
last less than 24 hours and there are no permanent neurological sequelae.
Stroke in evolution refers to a neurologic deficit that progresses or fluctuates whilst
the patient is under observation.

Types
Strokes result from:
o

Cerebral infarction (84%):

secondary to thrombosis (53%); or

embolus (31%)

Primary intracerebral haemorrhage (10%)

Subarachnoid haemorrhage (6%)

Ischemic stroke
Pathophysiology
An ischemic stroke results when cerebral blood flow to an area of the brain is
interrupted. Ischemia produces impaired energy metabolism and depolarization of
cells that leads to an accumulation of calcium ions in the intracellular space, elevated
lactate levels, acidosis, and production of free radicals. If the disruption is severe
enough, cell death occurs.
Normal adult brain cerebral blood flow is 50 -60 mL/100g/minute. Cerebral blood flow
below 10 mL/100g/minute is considered compatible with infarction. Cerebral blood
flows of 5 mL/100g/minute result in infarction within 30 minutes, whereas those
between 5 - 15 mL/100g/min result in infarction after 1 to 3 hours

Epidemiology
Worldwide, 15 million people suffer strokes each year. Of these, five million die
and five million are left permanently disabled, placing a burden on family and
community.
Stroke is now the second leading cause of death worldwide, after ischemic
heart disease. Demographic projections to 2020 suggest that it will remain so,
given the aging of many populations. In the coming decades a marked increase
in the number of stroke events is expected worldwide, particularly in developing
countries
Stroke will be among the five most important causes of disability in developed
and developing countries.iv
Incidence increases exponentially with age, rising from about 3 per 10,000 in
the third and fourth decades to about 300 per 10,000 in the eighth and ninth
The cumulative risk of recurrence of a stroke is high. Between one third and one
half of survivors are likely to experience a second stroke within 5 years of the
first

Risk factors
Non-modifiable risk factors:

increasing age

male gender

positive family history of stroke

Modifiable risk factors:

hypertension

smoking

diabetes mellitus

diet:
o

high salt intake

high fat intake

low potassium intake

low vitamin intake

excess alcohol intake

morbid obesity

low physical exercise

cholesterol concentrations (in patients with coronary artery disease)

Causes
Vascular causes
o Cerebral atherosclerosis
o Cerebral vasculitis
o Fibromuscular dysplasia
o Migraine
o Carotid dissection
o Lacunar state
o Infections [AIDS syphilis]
Haematological causes
o Thrombocytosis
o Polycythemia
o Sickle cell disease
o Leucemia
o Hypercoagulable states [e.g.macrglobenemia postoperative
postpartum]
o Protein C, prtein S deficiency
Cardiogenic causes
o Rheumatic vavular heart dieseases
o Myocardial infarction
o Arrhythmias especially atrial fibrillation
o Bacterial endocarditis
o Atrial myxoma
o Atrial spetal defect with right to left shunt

Clinical manifestations
Distinguishing anterior (or carotid territory) from posterior (or vertebrobasilar
territory) circulation strokes is important when deciding on the necessity and
relevance of diagnostic testing (eg, carotid imaging). Approximately 80% of ischemic
strokes involve the anterior circulation, and 20% involve the posterior circulation.
o Clinical features suggestive of ischemia in the anterior circulation are
monocular visual loss, aphasia, and neglect.

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Posterior circulation infarction is suggested by diplopia, binocular
visual loss, vertigo, hearing loss, lower motor neuron facial weakness,
bilateral or alternating weakness, delirium or severely altered level of
consciousness, and visual hallucinations.
o Focal weakness, focal sensory disturbance, dysarthria, and dysphagia
are not helpful per se in distinguishing between anterior and posterior
circulation ischemia.
o Headache occurs in approximately one third of patients and is less
frequent in those with pure motor or sensory disturbance. The
combination of headache and vomiting is more likely to be associated
with intracerebral hemorrhage, especially when accompanied by
rapidly progressing neurologic deficits.
o

Investigation
The goals for the diagnostic evaluation are to establish the diagnosis of ischemic
stroke as a cause of the patient's symptoms and to determine the underlying cause
of the event.
A basic evaluation that should be considered in all patients with ischemic stroke
includes a complete blood count with differential and platelet count, prothrombin time
with international normalized ratio, partial thromboplastin time, serum chemistries
including plasma glucose level, blood urea nitrogen, and serum creatinine; lipid
analysis; liver function tests; electrocardiography.
Brain imaging with CT or MRI; and vascular imaging with computed tomographic
angiography, Doppler, or magnetic resonance angiography.
o CT may not show the ischemic area up to 72 hrs after the onset. Initial CT
brain done immediately on presentation to exclude the presence of
hemorrhage,
o MRI can show the ischemic brain area within the 1 st hour after the onset. It
allow better visualization of the brain stem and cerebellum. MR angio allow
non-invasive visualization of the cerebral blood vessels.
Additional testing for cardiac sources of embolism includes transthoracic
echocardiography and transesophageal echocardiograph
Critical elements in the initial evaluation include
o identification of cerebral hemorrhage, which would preclude treatment
with antiplatelet agents and anticoagulants;
o identification of atrial fibrillation, which would be a strong indication for
anticoagulation;

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o identification of severe stenosis in the extracranial internal carotid
artery ipsilateral to hemispheric symptoms, which would be a strong
indication for invasive repair
Additional hematologic testing for protein C deficiency, protein S deficiency,
antithrombin III deficiency, factor V Leiden gene mutation, yperfibrinogenemia or
dysfibrinogenemia, cardiolipin antibodies, and lupus anticoagulant. If a collagen
vascular disease is suspected clinically, testing for erythrocyte sedimentation rate
and antinuclear antibody may be warranted

Management
Acute management
Hospitalization in ICU or better in a dedicated stroke unit.
The focuses of acute management are:
o recanalization of occluded vessels,
o preventing expansion of the ischemic tissue volume,
o

preventing secondary complications such as pneumonia and deep

venous thrombosis

o Enhancing recovery.
Proven acute medical treatment includes:
o Aspirin [300 mg] with 48 hours of stroke
o Intravenous recombinant tissue plasminogen activator (rt-PA) within
4.5 hours of stroke

Can be given up to 4.5 hrs from a clear stroke onset

The proven dose of rt-PA for ischemic stroke is 0.9 mg/kg with
the initial 10% delivered as a bolus, and the remaining 90%
delivered intravenously over 1 hour. The maximum dose is 90
mg.

the requirements for administering rt-PA include a CT scan of

the head, which is negative for hemorrhage; a serum glucose
level between 50 and 400 mg/dL; INR less than 1.7; platelet
count more than 100,000 per cubic mL; systolic blood pressure
less than 185 mmHg systolic; and no recent major procedures,
traumas, or stroke.

o Heparin is indicated only in; embolic stroke, stroke in evolution and

crescendo TIAs

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Rehabilitation after stroke begins as soon as the diagnosis of stroke is established
and as soon as any life-threatening neurologic or medical complications have been
stabilized
. Prevention of recurrence
Secondary stroke prevention consists of lifestyle modification, pharmacological
management, and surgical and revascularization procedures
o Lifestyle modification includes improving cardiovascular fitness, altering diet, and
smoking cessation.
o Pharmacological options for secondary stroke prevention include antiplatelet
therapy, anticoagulant therapy, antihypertensives, and medications to treat lipid
abnormalities.
o Antiplatelet choices in North America include aspirin, clopidogrel, dipyridamole or
combination of antiplatelets.
o Oral anticoagulant as warfarin is indicated for patients with cardiac source of
embolization; atrial fibrillation, vavular heart disease with a target INR 2-2.5.
Patients with mechanical mitral valves require anticoagulation with a higher target
INR of 2.5 to 3.5.
o
Stroke syndromes
Artery affected
Middle cerebral artery

Clinical manifestations
Hemiparesis (faciobrachiocrural
weakness)
Cortical sensory loss, global aphasia or
spatial neglect, hemianopsia,

Posterior cerebral artery--paramedian

contralateral gaze palsy

Hemiparesis (faciobrachiocrural

midbrain

weakness)
Ipsilateral 3rd nerve palsy (Weber
syndrome)
+/- Supranuclear vertical gaze palsy

Basilar artery--paramedian pontine

+/- Sensory deficit

Hemiparesis (faciobrachiocrural

perforators

weakness)
Ipsilateral 6th nerve palsy
+/- 7th nerve palsy (Millard-Gubler

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syndrome), internuclear ophthalmoplegia

Hemorrhagic strokes
Hemorrhagic strokes are responsible for roughly 30% of all strokes, more commonly
from intracerebral rather than subarachnoid etiologies. Patients present similarly to
those with ischemic stroke except that they tend to appear more ill with signs of
increased intracranial pressure. The most common etiologies are trauma, leakage
from small intracerebral arteries secondary to chronic hypertension, aneurysmal
rupture, iatrogenic anticoagulation, cocaine abuse, or cerebral amyloidosis.