III. Cerebrovascular diseases

- Cerebrovascular disease denotes brain disorders caused by pathologic processes involving the blood vessels. - The three main pathogenic mechanisms are: 1. Thrombotic occlusion of vessels 2. Embolic occlusion of vessels 3. Vascular rupture.

Thrombosis and embolism cause ischemic injury or infarction of specific regions of the brain, depending on the vessel involved.

- Rupture of blood vessels cause hemorrhage

Stroke :

- Is the clinical designation applied to a. Abrupt onset of focal or global neurological symptoms b. Caused by ischemia or hemorrhage c. and these symptoms must continue for more than 24 hours d. and there should be permanent damage to the brain

.

Transient ischemic attack(TIA):

a- Applied that the neurological symptoms resolve within 24 hours b. No irreversible tissue damage

From the standpoint of the pathophysiology and pathologic anatomy, it is convenient to consider cerebrovascular disease as two processes a. Hypoxia, ischemia and infarction b. Hemorrhage

A. Hypoxia, ischemia and infarction

- The brain may be deprived of oxygen by several mechanisms a. Functional hypoxia in a setting of a low partial pressure of oxygen or impaired oxygen-carrying capacity .

b. Global Ischemia; either transient or permanent c. Vascular obstruction

I. Global ischemia

- Widespread ischemic injury can occur in the setting of severe systemic hypotension, when systolic pressure fall below 50 mm Hg such as in cardiac arrest, and shock because of failure of autoregulation - The clinical outcome varies with the severity and duration of the insult

A. Mild transient Global Ischemia

- There may be only a transient postischemic confusional state, with eventual complete recovery.

- Neurons are more susceptible to mild ischemic injury than glial cells

-

B. Severe global ischemia

- Widespread neuronal death occurs irrespective of regional vulnerability.(pan necrosis) a. Persistent vegetative state ( awake but not aware) In severe global cerebral ischemia, individuals who survive in this state often remain severely impaired neurologically.

b:

b . Brain death 1. Other patients meet the clinical criteria for "brain death," including a. Evidence of diffuse cortical injury (isoelectric, or "flat," electroencephalogram b. And brain stem damage, including absent reflexes and respiratory drive

-

2. Focal Cerebral Ischemia

Cerebral arterial occlusion leads to focal ischemia and-if sustained-to infarction of CNS tissue in the distribution of the compromised vessel. - Occlusive vascular disease of severity sufficient to lead to cerebral infarction may be due to

1. In situ thrombosis

- The majority of thrombotic occlusions causing cerebral infarctions are due to atherosclerosis - The most common sites of primary thrombosis are a. The carotid bifurcation, b. The origin of the middle cerebral artery, c. And at either end of the basilar artery

2. Embolization from a distant source.

- Overall, embolic infarctions are more common than thrombosis. - Sources of emboli: a. Cardiac mural thrombi are a frequent source b. Thromboemboli also arise in arteries, most often from atheromatous plaques within the carotid arteries.

B. Intracranial Hemorrhage

.

- May occur at any site within the CNS either 1. Within the brain parenchyma 2. Outside the brain: a. Subarachnoid hemorrhage b. Epidural hematoma: Most common is trauma c. Subdural hematoma: Most common is trauma

1. Intraparenchymal hemorrhages - Rupture of a small intraparenchymal vessel can lead to intraparenchymal hemorrhage and this condition is called hemorrhagic stroke

- Spontaneous non traumatic brain hemorrhage occur most commonly in the middle to late adult life - The peak incidence is at about 60 years

- Is divided into i. Ganglionic hemorrhages - Occur basal ganglia and thalamus - Mainly caused by hypertension ii. Lobar hemorrhages - In the cerebral hemispheres - Main cause id cerebral amyloid angiopathy

Hypertensive hemorrhages

- Hypertension is the risk factor for deep brain parenchymal hemorrhages - Accounts for more than 50% of clinically significant hemorrhages - It accounts for about 15% of deaths among individuals with hypertension - Most commonly affect the basal ganglia

Mechanisms of massive hemorrhage in Hypertension: 1. Hyaline arteriolar sclerosis - Affects the deep penetrating arteries and arterioles that supply the basal ganglia and the brain stem - Affected arteriolar walls are weakened and are more vulnerable to rupture.

2. Chronic hypertension results in formation of minute aneurysms (Charcot-Bouchard

microaneurysms )

- Form in vessels less than 300 μm in diameter

Acute hypertensive encephalopathy : - Most often is associated with sudden sustained rises in diastolic blood pressure to greater than 130 mm Hg and characterized :

a. By increased intracranial pressure and b Global cerebral dysfunction, manifesting as headaches, confusion, vomiting, convulsions, and sometimes coma. - Rapid therapeutic intervention to reduce the intracranial pressure is essential .

2. Cerebral Amyloid Angiopathy (CAA) :

- Is the risk factor most commonly associated with lobar hemorrhages - In CAA, amyloidogenic peptides usally the same ones in Alzheimer diseases ((Aβ amyloid) are deposited in the walls of medium-small caiber menigeal and cortical vessel

- This deposition can weaken the vessel wall and lead to hemorrhage

Subarachnoid hemorrhage

CAUSES

1. Saccular aneurysms a. The most frequent cause of clinically significant subarachnoid hemorrhage is arupture of saccular (berry aneurysm) b. May be caused from extension of a traumatic hematoma

3. Rupture of a hypertensive intracerebral hematoma into the ventricyular system 4. Vascular malformations

1. Saccular (Berry ) aneurysm: - Is the most common type of intracranial aneurysms - About 90% of saccular aneurysms are found near major arterial branchpoints in the anterior circulation

Between 25% and 50% of individuals die with the first rupture, although those who survive typically improve and recover consciousness in minutes Recurring bleeding is common in survivors - It is currently not possible to predict which individuals will have recurrences of bleeding. - The prognosis worsens with each episode of bleeding. .

- The probability of rupture increases with the size of the lesion, - Aneurysms greater than 10 mm have a roughly 50% risk of bleeding per year

2. Hydrocephalus

Means accumulation of excessive CSF within the ventricular system as a result of disturbance in its secretion, circulation or absorption

Hydrocephalus

Causes a. Most commonly due to impaired flow or impaired resorption of CSF b. Overproduction of CSF, seen in choroid plexus tumors such as choroid plexus papilloma or carcinoma rarely causes hydrocephalus .

Types of hydrocephalus -

I. Non-communicating hydrocephalus

(obstructive) : It occurs when a lesion impedes the free passage of the CSF from the ventricles to the subarachnoid space, causing dilatation of the portion of the CSF pathway that lies proximal to the obstructions;

II. Communicating hydrocephalus, : - Refers to the abnormality in which there is free passage of CSF from within the ventricular system into the subarachnoid space -Causes a. Defects in the subarachnoid space such as fibrosis in leptomeningitis and hemorrhage from saccular aneurysms

B. Defects in absorption of CSF at the arachnoid granulations such as 1. congenital deficiency of arachnoids' granulation 2. Increased cerebral venous pressure C. Overproduction of CSF by choroid plexus papilloma D. Idiopathic

. Interstitial Edema: - It occurs in Patients with acute obstructive high pressure hydrocephalus - Due to damage to the ependymal lining by stretching

3. Brain herniations

- Results from increased in the intracranial pressure beyond the compensatory mechanisms

Herniations are named by . a. Either the part of the brain that is displaced or b. The structure across which it moves.

-

Types of herniations

1. Subfalcine (cingulate) herniation

- Caused by expansion of a mass (hematoma or tumor) in the frontal or parietal lobe - Means displacement of the ipsilateral cingulate gyrus under the free edge of the falx - It produces selective displacement of the pericallosal arteries (branches of the anterior cerebral artery ) away from the lesion and from the midline

This may compromise circulation through the pericallosal arteries ( branches of anterior cerebral artery) - This type of herniation results in infarction of the parietal parasaggital cortex , manifesting clinically as a weakness in the contralateral leg

2. Uncal or transtentorial herniations - Means herniation of the ipsilateral uncus (tip and medial part of parahippocampal gyrus)medially and downwards through the tentorial incisura - Its complications include:

• A. As the uncus herniates it compresses the oculomotor nerve between the free edge of the tentorium and th posterior cerebral artery 1. It results in compression of the parasympathetic input to the eye resulting in pupil dilatation ipsilateral to the lesion

NOTE: - Dilation of the pupil is the earliest consistent sign of uncal herniation and may occur before there is any loss of consciousness

B. Compression of the cerebral peduncle on the side of the mass lesion by direct pressure from the herniating brain will result in

contralateral limb weakness

D. The posterior cerebral artery may also be compressed, - This results in ischemic injury to the territory supplied by that vessel, including the primary visual cortex

E. Duret hemorrhages . Progression of uncal is often accompanied by hemorrhagic lesions in the in the tegmentum of the midbrain and the tegmental parts of the pons but NOT in the medulla - Are linear or flame-shaped lesions

The most likely mechanism of hemorrhage is stretching and tearing of the central perforating branches of the basilar artery that supply the rostral brainstem leading to infarction or hemorrhage - The presence of Duret hemorrhages implies a grim prognosis

Durett hemorrhage

.

4

.Tonsillar herniation

- Called (foramen impaction, cerebellar cone) - Refers to displacement of the cerebellar tonsils through the foramen magnum. - It occurs as an early complication of expanding masses in the posterior cranial fossa

The pathognomonic indication of this herniation is hemorrhagic necrosis at the tips of the cerebellar tonsils and a groove on the ventral surface of the medulla where it is compressed against the anterior border of foramen magnum - This pattern of herniation is life-threatening

Tonsillar herniation