According to the over-regulation conception, brain vessels spasm in response to acute hypertension, which results in cerebral ischemia and cytotoxic edema. According to the autoregulation breakthrough conception, cerebral arterioles are forced to dilate, leading to vasogenic edema.Cerebral edema can be generalized or focal. Brain ventricles are compressed, cortical gyri flattened. Diagnosis
Diagnostic methods for hypertensive encephalopathy include physical examination, blood pressure measurement, blood sampling, ECG, EEG, chest X-ray, urinalysis, arterial blood gas analysis, and imaging of the head (CAT scan and/or MRI). Since decreasing blood pressure is essential, anti-hypertensive medication is administered without awaiting the results of the laboratory tests. Electroencephalographic examination detects the absence of alpha waves, signifying impaired consciousness. In people with visual disturbances, slow waves are detected in the occipital areas. Treatment
The initial aim of treatment in hypertensive crises is to rapidly lower the diastolic pressure to about 100 to 105 mmHg; this goal should be achieved within two to six hours, with the maximum initial fall in BP not exceeding 25 percent of the presenting value. This level of BP control will allow gradual healing of the necrotizing vascular lesions. More aggressive hypotensive therapy is both unnecessary and may reduce the blood pressure below the autoregulatory range, possibly leading to ischemic events (such as stroke or coronary disease).Once the BP is controlled, the person should be switched to medication by mouth, with the diastolic pressure being gradually reduced to 85 to 90 mmHg over two to three months.
With the development of methods for detection and treatment of hypertension, hypertensive encephalopathy has been becoming more rare.Symptoms of hypertensive encephalopathy typically start to occur 12–48 hours after a sudden and sustained increase in blood pressure. The first manifestation of these symptoms is a severe headache. Headache occurs in greater than 75% of patients. The patient becomes restless. Alterations in consciousness may follow several hours later, which include impaired judgement and memory, confusion, somnolence and stupor. If the condition is not treated, these neurological symptoms may worsen and ultimately turn into a coma. Other symptoms may include increased irritability, vomiting, diplopia, seizures, twitching and myoclonus of the limbs. Alterations in vision (vision blurring, hemivisual field defects, color blindness, cortical blindness) are common. They occur in  4 out of 11 cases (Jellinek et al. 1964). Hemiparesis, intracerebral hemorrhage, aphasia may also occur, but they are less common. Pathogenesis
Hypertensive encephalopathy is caused by an increase in blood pressure. Several conditions may evoke blood pressure elevation: acute nephritis, eclampsia, crises in chronic essential hypertension, sudden withdrawal of antihypertensive treatment. Additionally, hypertensive encephalopathy may occur in pheochromocytoma, Cushings syndrome, renal artery thrombosis.The impairment of cerebral blood flow that underlies hypertensive encephalopathy is still controversial. Normally, cerebral blood flow is maintained by an autoregulation mechanism that dilates arterioles in response to blood pressure decreases and constricts arterioles in response to blood pressure increases. This autoregulation falters when hypertension becomes excessive.