Cerebrovascular Accident (CVA): Types, Causes, and Mechanisms
Cerebrovascular Accident (CVA)
A Cerebrovascular Accident (CVA), also known as a stroke, has an impact characterized by a sudden focal neurological deficit that persists for at least 24 hours. It normally occurs in the encephalic circulation due to a lack of blood flow, and cells die, causing permanent damage to structures.
Risk Factors: Hypertension, hypercholesterolemia, diabetes, smoking, heavy drinking, and the use of oral contraceptives.
Pathophysiology
Vascular supply is related to the signs and symptoms associated with the affected blood vessels.
Ischemic Event (88%)
Vascular occlusion disrupts blood flow to a specific region of the encephalon, producing focal ischemic neurological deficits. It results from embolic or thrombotic occlusion of brain vessels.
- Thrombosis affects the carotid, middle cerebral, or basilar artery.
- Emboli from the heart, aortic arch, or carotids can occlude the middle cerebral artery, travel in the vertebral and basilar arteries, and lodge at the top of the basilar artery or posterior cerebral artery.
The most frequently affected vessels are the lenticulostriate arteries, which supply the basal ganglia and the internal capsule. Occlusion of small arteries leads to lacunar infarctions in the putamen, caudate nucleus, thalamus, pons, and internal capsule. Vascular, cardiac, and hematic diseases can produce focal cerebral ischemia (e.g., atherosclerosis).
Hemorrhage (12%)
Hemorrhages are less predictable because they depend on the location of the bleeding and factors affecting the function of regions distant from the encephalic bleeding. They arise as a consequence of a cephalic injury.
Epidural Hemorrhage
Originates from a lesion in an artery (middle meningeal) that can be broken with a blow to the temporal bone. Blood dissects the dura and compresses the hemisphere located below. It causes a loss of consciousness, producing a contusion, which may be transient. Hours later, neurological symptoms appear, including herniation.
Subdural Hemorrhage
Originates from venous blood due to torn cortical veins in the subdural space. The blood is under low pressure, and symptoms can take several days to appear.
Subarachnoid Hemorrhage
May occur due to head trauma, the extension of blood from another compartment into the subarachnoid space, or the rupture of an arterial aneurysm. Brain dysfunction occurs due to increased intracranial pressure and the toxic effects of subarachnoid blood on brain tissue and vessels. The most common cause of spontaneous (non-traumatic) subarachnoid hemorrhage is an aneurysm (a congenital weakness in the walls of large vessels at the base of the brain). When an aneurysm ruptures, it increases intracranial pressure, interrupts blood flow, and produces widespread confusion and loss of consciousness. Focal ischemia is a consequence of vasospasm of the arteries near the rupture site, which can be fatal.
Intraparenchymal Hemorrhage
Caused by increased blood pressure or weakening of blood vessels. The hematoma produces a focal neurological deficit, and the metabolic effects of extravasated blood disturb the function of the surrounding brain tissue and compress vessels, producing local ischemia. Other causes include:
- Vascular malformations
- Brain tumors
- Platelet and coagulation disorders
- Cocaine and amphetamine use, which increase blood pressure and bleeding
Excitotoxicity
During ischemia, toxic concentrations of extracellular glutamate occur. Altered energy supplies inhibit the Na+/K+ ATPase pump, leading to:
- Accumulation of extracellular K+, which depolarizes nerve endings and releases glutamate.
- Decreased extracellular Na+, which reduces sodium-dependent glutamate uptake and enhances the effects of synaptic glutamate release.
A sustained increase in intracellular Ca2+ in postsynaptic cells provokes the activation of Ca2+-sensitive enzymes such as proteases, phospholipases, and endonucleases, causing cell death.