Lack of oxygen causes neurons in the brain to die in several ways. Autolysis can occur, which results from the digestion of nerve tissues by enzymes. Cerebral infarction causes the death of neurons; transient cessation of the cerebral circulation for a few minutes causes selective areas of ischemic necrosis. This type of necrosis is especially evident in highly vulnerable neurons that are sensitive to abrupt oxygen deprivation. More prolonged periods of moderate-to-severe hypoxemia or carbon monoxide poisoning can cause a loss of the outer sheath of neurons.
In cases of severe ischemia to brain tissue, the tissue loses structural integrity within a few seconds or a few minutes. Soon after there is an abnormal exchange of ions in neurons through a process called depolarization; this is characterized by an influx of sodium and calcium ions inside the neuron, and a simultaneous efflux of potassium ions outside the neuron.
Cerebral edema refers to abnormal increases in water content in the brain and occurs with all types of cerebral ischemia and hemorrhagic stroke. Increased water retention in the brain causes an increase in intracranial pressure. This pressure causes the brain to be pushed against the skull, resulting in neurologic deterioration and death due to herniation. Cerebral edema and herniation of the brain is the cause of death for approximately 75% of all fatal stroke victims and 33% of fatalities for all ischemic events to the brain.
Symptoms vary depending on the severity of damage. Symptoms of mild cerebral hypoxia can include poor judgment, memory loss, inattentiveness, and a decrease in motor coordination. In more severe cases, there can be permanent neurologic deficits, coma, seizures, or death.
Treatment depends on the cause and availability of equipment. Treatment is urgent and includes basic and advanced life-support measures. It is important to maintain breathing, dispense intravenous fluids and medications, and maintain stability with blood products and medications that control blood pressure and seizures. The outlook depends on the extent of cerebral ischemia.
Goldman, Lee, et al. Cecil's Textbook of Medicine, 21st ed. Philadelphia: W. B. Saunders Company, 2000.
|
|
Author Info: Laith Farid Gulli MD, Robert Ramirez DO, The Gale Group Inc., Gale, Detroit, Gale Encyclopedia of Neurological Disorders, 2005 |