Brain And Hypertension

Brain And Hypertension

The risk of stroke is directly related to arterial pressure, and this graded relationship appears to be maintained even within the normal range of diastolic blood pressure. Meta-analysis of nine prospective observational studies confirmed that there is no convincing evidence of a ‘threshold’ level of diastolic blood pressure at which risk begins. In general, with sustained increases in diastolic blood pressure of 5, 7.5 and 10 mmHg, there are corresponding increases in stroke risk of 34, 46 and 56%, respectively. Of the factors that predict stroke, blood pressure is dominant, although other independent risk factors have been identified and these include smoking, obesity and plasma levels of fibrinogen.

The incidence of stroke remains particularly low in some lessdeveloped countries where the average diastolic blood pressure may be only 60 mmHg. In China, Japan and parts of Africa, high blood pressure and stroke are common but coronary artery disease is relatively infrequent. This discrepancy, at least in the Far East, is probably due to differences in prevailing levels of blood cholesterol and low-density lipoproteins (LDL).

Just over 10% of all clinical strokes are caused by cerebral hemorrhage. Hemorrhages in hypertension are caused by rupture of microaneurysms that develop on the short penetrating branches of the main cerebral arteries. Such small aneurysms have been identified on arteries 50–220 μm in diameter, principally at sites of branching, and are particularly frequently seen in the distribution of the lateral lenticulostriate artery. The density of lesions tends to be highest in the putamen, globus pallidus, caudate nucleus, thalamus, external capsule and basis pontis. Hemorrhage into the putamen is especially frequent , and presents as weakness of the contralateral face, arm and leg, sometimes with hyperreflexia at an early stage.


Large lesions cause hemisensory loss and hemianopia with conjugate deviation of the eyes, reduced consciousness and aphasia, or visuospatial . Another brain lesion associated with uncontrolled hypertension is a small infarct which evolves into a slit-like space or lacune 0.5–15.0 mm in diameter. These small deep
infarcts are often undetectable on computed tomography (CT), and are the result of occlusion of one of the same perforating arteries that rupture in hypertensive cerebral hemorrhage.

The arteries immediately proximal to small infarcts show segmental disorganization of the vessel wall, possibly resulting from mechanical disruption of the intima and insudation of plasma constituents. Such changes are seen in small arteries that are close to high-pressure arteries, but not in vessels of the same caliber at more remote sites.

The relative underdevelopment of the muscle and elastic tissue layers of these particular small brain arteries may contribute to their vulnerability. Intraluminal pressures may also be higher in these arteries immediately proximal to small infarcts show segmental disorganization of the vessel wall, possibly resulting from mechanical disruption of the intima and insudation of plasma constituents. Such changes are seen in small arteries that are close to high-pressure arteries, but not in vessels of the same caliber at more remote sites. The relative underdevelopment of the muscle and elastic tissue layers of these particular small brain arteries may contribute to their vulnerability. Intraluminal pressures may also be higher in these countries and most usually present as episodes of pure motor hemiparesis, pure sensory stroke or ataxic hemiparesis.




Symptoms may evolve progressively over a period of 24–48 hours. Because subcortical white matter is involved, there are no signs of cortical dysfunction such as dysphagia, neglect, agnosia, or apraxia. Transient ischemic attacks may also occur. It is not difficult to understand that the incidences of hemorrhage and lacunar infarction are greatly reduced by effective treatment of chronic hypertension.

Most strokes in Western populations are due to atheromatous disease, often affecting extracranial vessels, especially the origin of the internal carotid artery. This predilection to atheroma is probably explained by the turbulent blood flow at a point of arterial bifurcation causing alterations in endothelial function.

Atheroma within the proximal internal carotid artery most often causes cerebral infarction in the distribution of the middle cerebral artery. Vascular occlusion is initiated by rupture of the fibrous cap of an atherosclerotic plaque with superimposed thrombosis. Artery-to-artery embolism is the predominant mechanism of transient ischemic attacks (TIAs) in carotid artery stenosis. In some cases, the fragmented emboli can sometimes be

visualized as refractile cholesterol-rich deposits at points where the retinal arterioles branch.

The velocity of blood flow in narrowed vessels is increased, and this acceleration may be detected by Doppler ultrasonography in combination with a two-dimensional image of the structures referred to as the duplex method with color flow imaging. Because Doppler misclassifies a proportion of carotid artery lesions, computed tomographic angiography or magnetic resonance angiography is increasingly used to supplement or

replace ultrasonography. Most TIAs in the territory of a stenosed internal carotid artery are caused by either atheroembolism with resultant hemiparesis or amaurosis fugax.

Clinical trials have clearly shown that drug treatment of hypertension reduces the incidence of stroke by about 40% and benefit accrues after relatively short periods of reduction in blood pressure. Benefits are especially seen in men or women of African-American origin and in elderly patients with isolated systolic hypertension or diabetes. Monotherapy is not effective in about 40% of patients; these patients require more than one drug and sometimes several different drugs.

Treatment trials have not differentiated between hemorrhagic stroke, lacunar events and large artery disease and cardioembolism. In primary prevention, there is some evidence from the Hypertension Optimal Treatment (HOT) study that aspirin in patients with well-controlled arterial pressures reduces the risk of myocardial events but, if pressures are poorly controlled, then there is little evidence that aspirin is of benefit. In secondary prevention of stroke, results of the PROGRESS trial showed that treatment based on an angiotensin converting enzyme (ACE) inhibitor and thiazide diuretics were effective in reducing risk of re-occurrence of major vascular events, but treatment was not started until at least 2 weeks from the acute event. Benefits extended to patients with normal levels of blood pressure. There have been concerns about antihypertensive therapy immediately after stroke when cerebral autoregulation is impaired, but there is, as yet, little evidence from clinical trials about the safety (or otherwise) of early antihypertensive therapy.

Antiplatelet agents such as aspirin or clopidogrel are also routinely used for prevention of ischemic
strokes, and the combination of aspirin and dipyridamole may also be effective. In the presence of large artery atherosclerosis causing carotid or extracranial vertebral artery stenosis, antihypertensive drugs have the potential to cause ischemic events if the degree of narrowing is critical. In practice, such events seem to occur rather infrequently. Symptomatic carotid stenoses greater than 70% are treated by endarterectomy and trials of angioplasty and stent insertion are ongoing. There is less certainty about the role of surgery in asymptomatic patients and various algorithms have been proposed to quantify risk in individual patients.