Acute or sustained elevation of blood pressure (BP) may result in failure of cerebral autoregulatory mechanisms, with vasodilation, hyperperfusion, and exudation of fluid. Increased intracranial pressure (ICP), capillary compression, and decreased intraparenchymal blood flow may result in hypertensive encephalopathy.

Affected patients have malignant or uncontrolled hypertension from any of various causes, including chronic renal disease, pheochromocytoma, antihypertensive withdrawal syndrome, sympathomimetic drugs, acute toxemia of pregnancy, Cushing’s syndrome, aortic dissection, and polyarteritis nodosa. The diagnostic term should be reserved for the few patients who, in addition to extreme increases in BP (diastolic pressure usually >120 mm Hg), have severe hypertensive retinopathy (papilledema, retinal hemorrhages, or exudates, with or without optic nerve infarction) or severe retinal arteriolar spasm and altered consciousness.

The syndrome usually develops during a period of several minutes to several hours and is usually characterized by diffuse, moderate-to-severe headache; nausea; vomiting; and various visual symptoms such as visual blurring or dimming, scintillating scotoma, or cortical blindness, with or without vivid visual hallucinations. Generalized or focal seizures or altered consciousness or behavior (anxiety, agitation, disorientation, drowsiness, confusion, or coma) are common. On examination, generalized hyperreflexia is a common early feature. Focal neurologic findings (which may be postictal) are infrequent and may reflect an underlying intracerebral hemorrhage or infarction. Computed tomography may reveal evidence of cerebral edema or ischemia (widespread low attenuation primarily involving white matter). Magnetic resonance imaging (MRI) usually demonstrates white matter edema and punctate or confluent areas of increased T2-weighted signal bilaterally involving the occipital lobes, the parieto-occipital junction areas, or the superior frontal lobes.

Hypertensive encephalopathy may be complicated by acute congestive heart failure, pulmonary edema, acute anuria, or microangiopathic hemolytic anemia. Prompt reduction in BP is essential and is achieved with labetalol hydrochloride (10-20 mg intravenously for 1-2 minutes, repeated or doubled every 10-20 minutes until desired BP is achieved or until a cumulative dose of 300 mg is reached; or 2 mg per minute by intravenous infusion), nicardipine (starting at 5 mg per hour intravenously, titrated to the desired effect, with a maximum infusion rate of 30 mg per hour), or sodium nitroprusside (starting with 0.3-0.5 µg/kg/minute intravenously, titrated to the desired effect, with the usual dose of 1-3 µg/kg/minute).

The initial aim of antihypertensive therapy should be to reduce the patient’s mean arterial BP by approximately 20% within a few hours. Further control of BP
is achieved during the next 24 hours, with a goal of reducing the diastolic pressure toward but not less than 90 mm Hg. Reduction in BP reverses the pathophysiologic processes that are responsible for the clinical symptoms.

With the emergence of advanced MRI and other imaging technologies along with more detailed epidemiologic studies, it has become clear in recent years that cognitive disorders of vascular etiology constitute a very heterogeneous group of conditions with diverse clinical manifestations and underlying pathophysiologies. The continuum of vascular cognitive disorders (VCDs) includes the categories of mild VCD, and vascular dementia or major VCD. Although isolated vascular pathologies appear to account for a much smaller percentage of all cases of dementia, when vascular contributions to other forms of dementia are included, such vascular pathologies rise substantially in importance. In particular, the combination of Alzheimer’s disease (AD) and VCD may constitute the most common explanation for cognitive impairment among elderly patients.

The clinical profile of VCD has been broadened to include all forms of cognitive impairment related to vascular factors affecting the brain as opposed to the prior concept of vascular dementia requiring memory loss and more severe impairment. Clinical diagnosis is based upon the presence of cognitive and/or behavioral impairments sufficient enough to affect one’s social or occupational functioning, documentation of a temporal relationship between the vascular disorder or event(s) and the cognitive disorder, and radiologic evidence of structural damage to the brain resulting from vascular factors. Thus, the diagnosis involves a combination of the historical evaluation (see Chapter 2), examination (see Chapter 5), and diagnostic imaging findings.