Cerebrovascular diseases are the third most common cause of death in Western countries.

Arteriovenous malformations predispose to intracranial haemorrhage

Arteriovenous malformations (AVMs) are developmental abnormalities of blood vessels (both arteries and veins) in which leashes of unusually fragile vessels are formed.
They occur most commonly in relation to the cerebral hemispheres, but other sites (including the cord) are affected.
Macroscopically, lesions may involve the meninges, extend deep into the brain, or be mixed in pattern. They vary in size, but are typically 3-4 cm in diameter.
Lesions have several feeding arterial vessels and several draining channels, making surgical removal very difficult.

Clinically, AVMs are a cause of epilepsy and of other focal neurological signs.
The major problem is that the fragile vessels bleed, causing life-threatening intracranial haemorrhage.

Haemangiomas also occur in the brain as cavernous or capillary lesions.

Cerebral blood vessels are prone to atheroma, arteriolosclerosis and amyloid deposition

The cerebral arteries are prone to the general pathological processes that affect systemic arteries.

Atheroma principally affects the main named cerebral arteries. It is generally more severe in the basilar artery than in the anterior and middle cerebral vessels.
The main complications of atheroma are thrombosis and aneurysm formation.
Atheroma is particularly important in the extracranial cerebral arteries, the carotid and vertebral vessels in the neck.
It is now appreciated that a large proportion of cerebral ischaemic events are caused by disease in the extracranial vessels.

Arteriolosclerosis affects the small vessels that penetrate the brain and is caused by long-standing hypertension or diabetes.
Vessels show replacement of the muscular media by hyaline material, which weakens the walls and predisposes to intracerebral haemorrhage.
Reduction in the size of the lumen of small vessels also predisposes to very small cerebral infarcts (lacunar infarcts).

Amyloid derived from b(A4) protein is frequently deposited in the cerebral vessels of the elderly, causing amyloid angiopathy.
This predisposes to intracerebral haemorrhage in a peripheral distribution in the cerebral hemispheres; it is the cause of cerebral haemorrhage in about 10% of cases in patients over the age of 70 years.

Berry aneurysms are the most common type of aneurysm of cerebral arteries
Berry aneurysms are small saccular aneurysms that occur in about 2% of the population. Macroscopically they appear as rounded swellings arising from the cerebral arteries. Although they can be 0.2-3 cm in diameter, most are under 1 cm. Occurring particularly at the branch points of vessels around the circle of Willis, they are frequently multiple.

• 45% arise in the region of the anterior communicating cerebral artery.

• 30% arise from the middle cerebral artery as it divides deep in the Sylvian fissure.

• 20% arise in the region of the internal carotid arteries, usually at the origin of the posterior communicating artery. 

• 5% arise elsewhere in the cerebral circulation.

Aneurysms are prone to rupture, with consequent sub-arachnoid haemorrhage.

Berry aneurysms arise because of developmental defects in the internal elastic lamina of vessels.
The stress of the systolic waves causes herniation of the intima, with formation of saccular aneurysms.
This is accentuated by hypertension, and aneurysms are commonly seen in association with coarctation of the aorta and adult polycystic renal disease. 
Less common are atherosclerotic and infective (mycotic) aneurysms.
Atherosclerotic aneurysms are most common in the basilar artery, where they tend to be fusiform. Infective (mycotic) aneurysms arise in cases of infective endocarditis, when a small segment of arterial wall is acutely inflamed and dilates due to local bacterial infection from a small septic embolus.

Berry aneurysms are seen arising where the internal carotid bifurcates into middle and anterior cerebral vessels.

Fusiform atherosclerotic aneurysm.
The basilar artery is replaced by a large fusiform aneurysm caused by atherosclerosis.


Stroke is common in the general population

Stroke occurs in 2 per 1000 of the general population.

The clinical diagnosis of stroke is defined as a sudden onset of non-traumatic focal neurological deficit that causes death or lasts for over 24 hours. 

Transient ischaemic attacks (TIA) are defined as episodes of non-traumatic focal loss of cerebral or visual function lasting no more than 24 hours.

The causes of stroke can be divided into two main groups:
 
{\A ischaemic} (85%), caused by cerebral infarction.

{\B haemorrhagic} (15%), caused by intracerebral and sub-arachnoid haemorrhage.

Regional cerebral infarction is caused by occlusion of named cerebral arteries.

Large cerebral infarcts may cause death by associated cerebral swelling, leading to herniation, and brain stem compression.
Infarcts in critical sites, particularly brain stem infarcts, may interfere with vital functions and lead to death.
Immobility and difficulty in swallowing lead to development of pneumonia in many patients.

Regional cerebral infarcts are caused by occlusion of main named arteries supplying the brain. The most common causes originate outside the cranial cavity, e.g. emboli from the heart, aorta or carotid vessels, and thrombosis in the carotid or vertebral arteries, predisposed by atheroma.
Less common causes of infarction are seen in younger stroke patients.

Cerebral infarcts correspond to the territory of supply of the occluded arteries.
It is difficult to see an infarct in the first 24 hours, as changes are limited to focal swelling and blurring of the normal demarcation between grey and white matter, termed a pale or anaemic infarct.} If there is lysis of an occlusive thrombus, the infarcted area may be re-perfused with blood, resulting in a haemorrhagic infarct By about 1 week the infarcted area becomes macroscopically soft and is infiltrated by macrophages, which remove dead tissue.
Proliferation of astrocytes occurs around the margins of the infarct, and these partly replace the dead tissue, usually being well established by about 2 weeks.
Larger regional areas of infarction invariably heal as fluid-filled cystic spaces bounded by gliosis.

Although a number of clinical syndromes related to occlusion of individual arteries are described, the most important practical distinction is between those affecting the carotid territory (frontal, temporal, parietal lobes or basal ganglia/internal capsule) and those affecting the vertebrobasilar territory (occipital lobe, cerebellum or brain stem).

Lacunar infarction is caused by arteriolosclerosis of small vessels

Lacunar infarcts are small, often slit-shaped, areas of infarction that are less than 1 cm in maximum diameter. They are an important form of cerebral infarct, particularly in patients with hypertension and diabetes, being caused by hyaline arteriolosclerosis.

Macroscopically, lesions are usually multiple and are seen in the sites normally supplied by fine perforating branches, such as the basal ganglia, internal capsule, thalamus and pons.

Clinically, lacunar infarcts can be asymptomatic or may cause very restricted neurological deficits such as monoparesis.
Multiple lacunar infarcts in the basal ganglia cause a syndrome of rigidity and abnormal gait, which superficially resembles Parkinson's disease, termed 'vascular pseudo-Parkinsonism'.
Lacunar infarction is also associated with ischaemic white-matter degeneration, an important cause of dementia.

Because hypertension and diabetes are risk factors for ischaemic heart disease and atheroma, lacunar infarcts are often seen in association with regional infarcts caused by large vessel disease.
Cortical laminar necrosis is caused by generalized failure of perfusion

Diffuse necrosis of cerebral cortical neurons is the pattern of infarction seen in generalized failure of blood flow or oxygenation as seen, for example, following cardiac arrest, with severe hypoglycaemia and after carbon monoxide poisoning. 

Changes develop 24 hours after resuscitation from the damaging episode.
There is widespread damage to the cerebral cortex, with death of the majority of cortical neurons. With time, there is phagocytosis of dead neurons with astrocytic gliosis. Macroscopically the cerebral cortex is shrunken and there is extensive loss of axons from the brain, causing white matter loss.

Patients who survive global laminar necrosis generally have severe brain damage, existing in a vegetative state devoid of higher cortical functions.
Lesser degrees of hypoxia or cerebral perfusion failure result in similar damage, limited to the particularly vulnerable areas of the hippocampus and cerebellar cortex.