Cerebrovascular diseases

Cerebrovascular disease is the third leading cause of death (after heart disease and cancer) in the United States; it is also the most prevalent neurologic disorder in terms of both morbidity and mortality. The term cerebrovascular disease denotes any abnormality of the brain caused by a pathologic process of blood vessels. Includes: Hypoxic brain injury. Brain Infarction: caused by local vascular occlusion. Intracranial hemorrhages.

1. Hypoxic brain injury Although the brain accounts for only 1% to 2% of body weight, it receives 15% of the resting cardiac output and accounts for 20% of the total body oxygen consumption. Cerebral blood flow, normally about 50 mL per minute for each 100 gm of tissue (with considerable regional variations between white and gray matter and among different portions of the gray matter), remains constant over a wide range of blood pressure and intracranial pressure because of autoregulation of vascular resistance.

The brain is a highly aerobic tissue The brain is a highly aerobic tissue. The brain may be deprived of oxygen by any of several mechanisms: A. functional hypoxia: in cases of low partial pressure of oxygen (pO2), or impaired oxygen-carrying capacity of the blood. B. Ischemia: either transient or permanent, after interruption of the normal circulatory flow. Cessation of blood flow can result from a reduction in perfusion pressure, as in hypotension, or secondary to small- or large-vessel obstruction, or both.

Two principal types of acute ischemic injury are recognized: a. Global cerebral ischemia: occurs when there is a generalized reduction of cerebral perfusion, such as in cardiac arrest, shock, and severe hypotension. b. Focal cerebral ischemia: follows reduction or cessation of blood flow (such as embolic or thrombotic arterial occlusion.

2. BRAIN InfaRctION * Incidence: Represents 80% of cerebro-vascular diseases (stroke). Occur mostly in 7th decade. More common in male than female. * Causes: Thrombosis on top of cerebral atherosclerosis. Embolism (emboli originating from heart). Rarely: surgical ligation.

First 12 hours: No changes By 24 hours: * Gross picture: First 12 hours: No changes By 24 hours: The affected area is swollen and soft with loss of demarcation between grey and white matter due to edema. The infarct either pale (thrombotic) or red “hemorrhagic” (embolic). Heal by gliosis.

A thrombosis of the internal carotid artery

* Microscopic picture: First 12 hours, ischemic neuronal changes with neutrophil infiltration. By 24 hours: edema, necrotic neurons surrounded by macrophages which start to phogocytose this necrotic debris. Heal by gliosis.

The microscopic appearance of this acute cerebral infarction reveals marked edema (the pale areas).

The neurons are the most sensitive cells to anoxic injury The neurons are the most sensitive cells to anoxic injury. Seen here are red neurons which are dying as a result of hypoxia.

This cerebral infarction demonstrates the presence of many macrophages at the right which are cleaning up the lipid debris from the liquefactive necrosis.

Resolution of the liquefactive necrosis in a cerebral infarction leads to the formation of a cystic space.

3. Intracranial Hemorrhage * Classification: 1. According to the etiology: a. Spontaneous (Non-traumatic) hemorrhage (stroke): b. Traumatic. 2. According to the site of hemorrhage: a. Epidural hemorrhage. b. Subdural hemorrhage. c. Subarachnoid hemorrhage. d. Parenchymal hemorrhage. e. Intraventricular hemorrhage.

A blood clot is seen over the external surface of the dura A blood clot is seen over the external surface of the dura. Thus, this is an epidural hematoma. Such a location for hemorrhage is virtually always the result of trauma that causes a tear in the middle meningeal artery.

The dura has been reflected above to reveal the bridging veins that extend across to the superior aspect of the cerebral hemispheres. These can be torn with trauma, particularly if there is significant cerebral atrophy that exposes these veins even more.

The dura has been reflected back (with a small portion visible at the lower right) to reveal a subdural hematoma. Such a blood clot is usually the result of trauma with tearing of the bridging veins.

The subarachnoid hemorrhage from a ruptured aneurysm

Spontaneous intraparenchymal Brain Hemorrhage (hemorrhagic stroke) * Causes: 1. Hypertension (the most common cause of cerebral stroke) 2. Coagulation abnormalities. 3. Rupture of cerebral aneurysms. * Sites: Basal ganglia (65%). Pons (15%). Cerebellum (10%).

* Morphology of hypertensive hemorrhagic stroke: Hematoma and associated edema cause expansion of affected hemisphere. Cut surface show; well demarcated hematoma, which may dissect its way to ventricles or subarachnoid space. If the patient survives, the hematoma is absorbed leaving a fluid-filled cavity lined by gliotic tissue and hemosiderin-laden macrophages.

Hemorrhages involving the basal ganglia tend to be non-traumatic and caused by hypertension

CEREBRAL ANEURYSMS Congenital (Berry) aneurysms: - Small saccular aneurysms develop in and around the circle of Willis at the site of arterial bifurcation due congenital absence of the media. Rupture of these aneurysms lead to fatal subarachnoid and/ or intraparenchymal or intraventricular hemorrhage.

Congenital berry aneurysms

2. Atherosclerotic aneurysm: Intracerebral or extraparenchymal, usually asymptomatic, rarely rupture. 3. Hypertensive aneurysms (Charcot-Bouchard aneurysms): long standing hypertension leads to deposition of lipid-hyaline substances within the walls of small branches of penetrating arteries and arterioles which weaken the vessel walls and cause microscopic aneurysms.

4. Mycotic aneurysms: caused by inflammatory weakening of the wall of the artery by infection from impacted emboli of subacute bacterial endocarditis containing low virulent bacteria.