Hypertensive Encephalopathy

The internal carotid and vertebral arteries give rise to the brain's blood supply. The arterial branches lie in the subarachnoid space. The internal carotid arteries originate in the neck from the common carotid arteries, ascend to the skull base, and enter the middle cranial fossa through the carotid canals. The carotid arteries pass anteromedially toward the cavernous sinus on the sphenoid body. The anterior and middle cerebral arteries are the internal carotid arteries' terminal branches, comprising the brain's anterior circulation. The anterior communicating artery bridges the right and left anterior cerebral arteries. The vertebral arteries are the first branches of the first part of the subclavian arteries, arising from the root of the neck (see . Branches of the Aorta). The superior vertebral artery segments run through the C1 to C6 transverse foramina. Suboccipital branches enter the dura and arachnoid and traverse the foramen magnum (see . Vertebral Artery Anatomy in the Neck Region). The basilar artery arises from the fusion of the right and left vertebral arteries at the caudal pontine margin. This artery then ascends to the superior pontine border and bifurcates into 2 posterior cerebral arteries. The vertebrobasilar arterial system comprises the brain's posterior circulation. The posterior communicating arteries connect the internal carotid and posterior cerebral arteries. Connecting the anterior and posterior brain circulations completes the cerebral arterial circle of Willis (see . Arterial Circulation of the Brain). The dural venous sinuses drain the superficial and deep veins of the brain. These venous sinuses empty into the internal jugular veins. The veins on the brain's superolateral aspect drain into the superior sagittal sinus. Their posteroinferior counterparts empty into the straight, superior petrosal, and transverse sinuses. The blood-brain barrier (BBB) separates the peripheral and central nervous system (CNS) circulation. Endothelial cells connected by tight junctions are the main BBB components. The tight junctions hinder paracellular transport that can contaminate the cerebral vasculature. Other cells comprising the BBB include the astrocytes, pericytes, and microglia. Astrocyte endfeet (podocytes) form the glia limitans, a membrane that further hinders solute movement across the BBB. Without membrane transporters, only small or lipid-soluble particles can enter the CNS circulation.[38] Angiotensin receptors make the BBB sensitive to the effects of the renin-aldosterone-angiotensin system. These receptors mediate endocrine regulation of water and electrolyte balance, vascular resistance, oxidative stress, neuroinflammation, and brain homeostasis.[39] A hypertensive emergency is a life-threatening condition. Target-organ damage occurs due to markedly elevated blood pressure.[1] Hypertensive emergencies may arise in patients with or without a history of preexisting hypertension.[2] Pulmonary edema, cardiac ischemic events, acute renal failure, aortic dissection, eclampsia, retinopathy, encephalopathy, and intracranial hemorrhage may develop as a result of hypertension-related organ injury.[3] Hypertensive encephalopathy is an uncommon hypertensive emergency manifestation. Signs and symptoms include severe headaches, nausea, vomiting, visual disturbances, seizures, and mental status changes.[4] The condition is diagnosed after ruling out other CNS dysfunction etiologies. Lowering the blood pressure dramatically improves symptoms. Early recognition of hypertensive encephalopathy can result in favorable clinical outcomes as prompt treatment can reverse the symptoms of this condition.[5]