Cerebrovascular Disease
Dr Mohamed Rizk Khodair
Lecturer of neurology
October 6 Universirty

Definition:
Stroke is a sudden onset focal
and or generalized neurological
deficit, lasting more than 24
hours. Strokes occur due to
either ischemia (about 85%) or
hemorrhage (15%).
Transient ischemic attack (TIA)
is defined as sudden onset
focal neurological deficit lasting
less than 24 hours.

Types:
A) Ischemic Stroke :
Most ischemic strokes
are due to thrombosis
or embolism
B) Hemorrhagic
stroke: Intracerebral
hemorrhage and
Subarachnoid
hemorrhage

Etiology of ischemic stroke
Thrombosis: The commonest cause is atherosclerosis
Predisposing (Risk) Factors
A stroke may happen to anybody at any age. However, if you have specific risk factors, your chances of having a stroke increase. Some stroke
risk factors are modifiable, while others are not.
Non-Modifiable Factors:
 Older age. Incidence doubles each decade past 55 years.
 Race. African American race has twofold increased risk than whites. This is partly because the African American population has a greater
incidence of high blood pressure.
 Gender. Strokes are more common in men. (1.25 times that of females).
 History of prior stroke. There is a higher risk for having a second stroke after you have already had a stroke.
 Heredity or genetics. People with a positive family history of stroke are more likely to have a stroke.
Modifiable Factors:
 Hypertension: 3-4 folds increase of stroke.
 Dyslipidemia: high total cholesterol and low-density lipoprotein (LDL) are related to atherosclerosis and increase risk.
 Diabetes mellitus (DM): 2-4, folds increase of stroke, pathogenetic factor in cerebral small vessel disease. DM produces rheological
abnormalities and aggravates atherosclerosis. DM increases morbidity and mortality after
 stroke.
 Heart diseases
 Smoking (2-3 times greater than non-smokers), heavy alcohol consumption.

Embolism: Embolism (from the heart is also a common cause) include valvular disease, artificial heart valves, recent myocardial
infarction, endocarditis and cardiac tumors. Also, paradoxical embolism as in a patient with an atrial septal defect or patent
foramen oval.
Other causes include:
1. Arterial (e.g., carotid or vertebral) dissection
2. Vasculitis
3. Hematological disorders: polycythemia, thrombocythemia, sickle cell disease, leukemia and antiphospholipid syndrome
4. Genetic disorders: as Cerebral autosomal dominant arteriopathy with subcortical infarcts and Leukoencephalopathy
(CADASIL) and Mitochondrial encephalomyopathy, lactic acidosis, and Stroke-like episodes (MELAS).
5. Recreational drug use: cocaine, amphetamine
6. Hypoperfusion of the brain leading to so-called watershed or border zone infarcts as in shock, excessive blood loss, excessive
hypotensive drugs, low cardiac output (as in myocardia infarction or arrhythmia),hemoconcentration( as in dehydration) .
7. Venous disease as due to cerebral venous sinus thrombosis.

Clinical Picture: Symptoms and signs depend upon the occluded blood vessel.

The carotid system
(Anterior circulation).
Blood Supply of the brain
The vertebral system
(Posterior circulation).
.

The carotid system (Anterior circulation):
Each internal carotid artery enters the cranial cavity
through the carotid foramen and canal to the
cavernous sinus where it lies lateral to optic chiasma.
The artery in the sinus gives off three small branches:
- The ophthalmic artery.
- The anterior choroidal artery.
- The posterior communicating artery.
The internal carotid artery then divides into its two
terminal branches → the middle and anterior
cerebral arteries.

A. The middle cerebral artery gives 2 branches:
Capsular branch, supplying dorsal half of internal
capsule (Lenticulostriate branch of middle cerebral artery).
Cortical branches:
Frontal branch supplying the lower part of the
motor area (face, U.L. and trunk), and the motor
speech areas.
Parietal branch supplying the lower part of the
sensory area, the angular and supramarginal and
the upper fibers of the optic radiation.
lower fibers of the optic
Temporal branches supplying the auditory
areas and the lower fibers of the optic radiation.

B. The anterior cerebral artery supplies:
The anterior cerebral artery runs medially on the medial surface of the cerebral
hemisphere, then around the corpus callosum as far as the parieto-occipital
sulcus. This artery supplies the medial aspect of the anterior 3/5 of the cerebral
hemisphere and the upper edge of the lateral surface.
It gives the following branches:
• Capsular branch (Heubner's artery) supplying the ventral half of the anterior
limb of the internal capsule.
• Cortical branches:
a) Frontal branch supplying the pre-frontal area (area of mentality and inhibition of primitive reflexes).
b) Paracentral branch supplying the motor and sensory areas of the L.L., and the paracentral lobule
(cortical bladder center).
c) Callosal branch supplying the corpus callosum.

The vertebral system (Posterior circulation):
Vertebral Arteries
Course and branches:
The left and right vertebral arteries originate from their
respective subclavian arteries, on the posterosuperior aspect.
The vertebral arteries then proceed to enter the transverse foramina of
the spine at level C6 and continue superiorly.
After passing through the transverse foramen of C1, the arteries traverse
the foramen magnum.
The vertebral arteries give off the following branches once within the cranial
vault:
 Posterior inferior cerebellar artery (PICA) – this is the largest branch of
the vertebral artery and is one of three main arteries supplying the cerebellum
 Anterior and posterior meningeal arteries – supply the dura mater
 Anterior and posterior spinal arteries – supply the spinal cord along its
entire length
The vertebral arteries then converge to form one midline single artery,
basilar artery, at the base of the pons, inside the cranium.

Basilar Arteries
Course and branches:
The basilar artery runs superiorly within the central
groove of the pons, giving off several branches
including the pontine arteries, which supply
the pons.
The basilar artery anastomoses with the circle of
Willis via the posterior cerebral arteries and posterior
communicating arteries.
Branches of posterior cerebral artery :
Cortical branches supply occpital lobe and posterior
communicating artery to circle of willis
Capsular branche: thalamogeniculate artery ( ventral
aspect of genu and posterior limb of internal capsule)

Circle of Willis
The terminal branches of
the anterior and posterior circulation form
an anastomosis to create a ring-like vascular structure
known as the circle of Willis, located within the base of
the cranium.
The left and right internal carotid arteries continue as
the middle cerebral arteries (MCA), after each giving off
a branch to supply the anterior cerebral arteries (ACA).
The anterior communicating artery links the two anterior
cerebral arteries together.
The internal carotid arteries also give off
the posterior communicating arteries (PCoA), linking
the middle cerebral arteries (MCA) with
the posterior cerebral arteries (PCA).

The Internal capsule
It is a broad band of white fibers lying in the depth of the cerebral hemisphere.
It is formed of:
1. The anterior limb which is placed between the caudate nucleus medially and the lentiform nucleus
laterally.
2. The genu.
3. The posterior limb which is placed between the thalamus medially and the lentiform nucleus laterally.
Fibers passing through the internal capsule:
a) Pyramidal fibers descend in the genu, adjacent part of anterior limb and anterior 1/2 of posterior limb.
The fibers supplying the arm are followed by those supplying the head, trunk, and lastly the lower limb.
b) Sensory fibers from the thalamus ascend in the PL.
c) Auditory and optic radiations pass in the posterior part of PL.
d) Associative fibers pass in the anterior part of AL.

Blood supply of the internal capsule
• Upper part: MCA (lenticulostriate artery).
• Lower part:
Anterior limb; ACA (recurrent artery of Heubner).
Posterior limb: PCA (thalamogeniculate artery).

(1) Anterior circulation (carotid system) infarction
A) Middle cerebral artery occlusion:
Contralateral hemiparesis (face and arm > leg)
Contralateral hemisensory loss (face and arm > leg)
Homonymous hemianopia
Contralateral gaze palsy
Neglect
Aphasia (if dominant hemisphere is affected)

B) Anterior cerebral artery occlusion:
• Contralateral hemiparesis (leg > arm)
• Contralateral hemisensory loss (leg > arm)
• Mental changes
• Sphincteric disturbances in massive infarction

(2) Posterior circulation (vertebrobasilar territory) infarct
A) Posterior cerebral artery occlusion:
• Contralateral homonymous hemianopia
(which may be macular sparing, as this may
be supplied by the middle cerebral artery).
• Thalamic pain (spontaneous intractable and
persistent pain).
• Transient hemiparesis.
• Visual agnosia.

B) Posterior inferior cerebellar artery (Lateral medullary syndrome; Wallenberg syndrome) crossed
hemianesthesia
• Contralateral impairment of
pain/temperature sensation in the limb with
ipsilateral impairment of pain/temperature in
the face
• Ipsilateral Horner‘s syndrome
• Ipsilateral cerebellar signs (ataxia),
• Ipsilateral dysarthria, vertigo, vomiting,
dysphagia

C) Other brainstem stroke syndromes
• Apart from the lateral medullary syndrome, other brainstem stroke syndromes are rare, e.g., the medial
medullary syndrome which causes ipsilateral tongue weakness and contralateral hemiparesis in the arm
and leg. (crossed hemiplegia)
D) Lacunar strokes:
These infarcts are usually less than 1 cm in diameter and are caused by the occlusion of small penetrating
arteries supplying deep structures in the brain as basal ganglia, thalamus, pons. It include:
• Pure motor strokes (face, arm, and leg) in the posterior limb of internal capsule.
• Pure sensory stroke (thalamus).
• Ataxic hemiparesis (weakness and ataxia affecting the same side) due to a pontine lesion.
• Clumsy hand/dysarthria due to a lesion in the pons or internal capsule.

Investigations
A) Imaging studies: Should be performed within 24 hours to exclude haemorrhagic stroke and other causes,
e.g., tumors.
1- CT: It is the first diagnostic tool to exclude hemorrhage , Ct is free in 1st 48 hours of onset of ischemic stroke.
2- MRI: Diffusion-weighted images (DWIs) show changes within minutes (most diagnostic tools). Useful to
distinguish acute from chronic changes.
3- Imaging of extracranial vessels should be performed in all patients with TIA or stroke for diagnosis of
partial or complete obstruction of the extracranial vessels as: Carotid and vertebral ultrasonography; MR or CT
angiography (MRA/CTA).
4- Imaging of intracranial vessels should be performed in all patients for diagnosis of partial or complete
obstruction of the intracranial vessels as: Trascranial color coded duplex; MR or CT angiography (MRA/CTA).
5- ECG and Echocardiography :for diagnosis of cardiac diseases as a cause for stroke.

Normal vs ischemic vs hemorrhagic

Treatment of acute ischemic stroke:
A) Specific treatment
1- Thrombolysis
Thrombolysis with IV rt-PA was used for the treatment of acute ischemic stroke
within 3,5 hours of onset to achieve early recanalization of a thrombosed artery.
2- Antiplatelet Therapy:
• Aspirin
All patients should be initially treated with aspirin; 150-325 mg/day; following
acute ischemic stroke unless they are being treated with thrombolytic therapy.
Beyond the initial treatment period following ischemic stroke, most patients should
be maintained on antiplatelet therapy to reduce the long-term risk of recurrent
stroke.
• Clopidogrel, Ticlopidine and combined aspirin and dipyridamole (
persantine) are acceptable alternative to aspirin.

3- Anticoagulant therapy :
The goal of anticoagulation in acute ischemic stroke is to prevent early recurrent
cerebral embolism as cardioembolic stroke due to atrial fibrillation or prevention of DVT due to recumbency.
4- Treatment of risk factors: as antihypertensive, control of diabetes, antiarrhythmic.
5- Dehydrating measures: especially in massive infarction. Mannitol 1-2 mg/kg/day used for 48 hours.
6- Nootropic drugs: as Piracetam (Nootropil). These drugs enhance the brain metabolism and brain
oxygenation.
B) General treatment: in comatose patients
1-Care of skin by changing the position of patient.
2- Care of respiration by maintaining patent airways, frequent suctions of secretions
3- Care of nutrition and fluids 4- Care of urinary bladder 5- physiotherapy

ΙΙ- Hemorrhagic :
It may be in the brain ‫״‬intracerebral hemorrhage or within the subarachnoid space ―subarachnoid
hemorrhage.

Spontaneous Intracerebral hemorrhage (ICH)
ICH is the second most common form of stroke (about 15–30% of all strokes).
Risk factors:
Risk factors for ICH are like those with ischemic stroke:
• Age;
• Male gender
• Hypertension
• Smoking
• Diabetes
• Excess alcohol use.

Causes of ICH:
1. Chronic hypertension.
2. Excess anticoagulant use, antiplatelet use, Thrombolytic therapy.
3. Rupture of intracranial aneurysms, arteriovenous malformations and cavernomas.
4. Hemorrhagic blood diseases as in purpura, leukemia
5. Moya Moya syndrome
6. Trauma to the head.
Common sites for ICH:
Basal ganglia., Thalamus, Pons, Cerebellum, Cerebrum (lobar hemorrhage) and Brainstem.

Clinical picture:
1- Prodromal symptoms are related to hypertension as severe headache, vomiting, and alterations in
level of consciousness as confusion may be more common.
2- The focal symptoms ad signs depend upon the site of hemorrhage.
3- Onset is usually very sudden.
4- Convulsions are common and may point to the onset of hemorrhagic stroke.

Investigations:
A) Imaging studies:
1. CT scan: Non contrast brain CT scan is the
usual initial imaging procedure of choice.
2. CT angiography (CTA): CTA is very
sensitive and specific in detecting vascular
lesions (e.g., AVM or aneurysm).
3. MRI with appropriate scanning
sequences.

Treatment:
A) Nonsurgical management:
1. Airway, breathing and circulation should be the initial focus.
2. Hypertension (HTN) should be controlled.
3. Intubate if GSC ≤ 8 as patient can‘t maintain his or her airways.
4. Monitoring of intracranial pressure and treatment of elevated ICP with dehydrating measures (as mannitol),
and hyperventilation.
5. Fluid management.
6. Anticonvulsants drugs.
7. Maintain body temperature.
B) Surgical treatment:
1. Evacuation of large, surfacing and manifesting ICH with imminent transtentorial herniation..
2. Endoventricular drainage for intraventricular hemorrhage.
3. large cerebellar hemorrhage >3cm.
3. Definitive treatment of the underlying cause as AVM or aneurysm

Thank you
Mohamedrizk.med@o6u.edu.eg