Cerebral Infarction- Causes, Symptoms and Treatment

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Cerebral infarction accounts for about 90% of strokes in the United States. According to the Centers for Disease Control and Prevention, strokes kill 130,000 Americans every year. It is an ischemic stroke resulting in a lack of blood supplied to the brain. Cerebral infarction occurs when a blood vessel becomes blocked or leaks outside of the vessel walls. These occurrences vary in severity, and one third result in death. The risk factors for cerebral infarction include high blood pressure, diabetes, atherosclerosis, tobacco smoking, hyperlipoproteinemia, hypercholesterolemia and obesity.

Types of Cerebral Infarction

Arteriosclerotic cerebral infarction is caused by the cerebrovascular cavity blockage or narrowing. It is the result of ischemic necrosis due to an insufficient blood supply to the brain. Patients may suffer aphasia, hemiplegia or other cerebral damages. It is common in elderly people, and the death rate is higher for those who smoke, have a high-fat diet or suffer from diabetes. The cerebrovascular occlusion is often due to cerebral thrombosis or cerebral embolism. Cerebral thrombosis occurs when the inner membrane of the canal cavity and the canal cavity itself are narrowed. The cerebral blood vessels have blood platelet factors condensed in blocks that cause a blood stickiness, reduced blood flow and blood pressure drop. With cerebral thrombosis, thrombi from other parts of the body flow to the brain and cause blockage, such as tumor cells. It may take several days for symptoms to peak, but also can occur within minutes or seconds.

Hemorrhagic cerebral infarction is when thrombosis or embolism occur to a major cerebral artery or branch. Blood leaks out of the artery and enters cerebral tissues. Cerebral tissues suffer anoxia, diffuse ischemia and weakened vassal and blood capillary walls. Bleeding is intensified when the blood tries to enter the damaged or paralyzed blood vessels through the anastomosis branch. The chances of the arterial vessels reopening after cerebral infarction are high. Medical scholars report that up to 75 percent of hemorrhagic cerebral infarction patients incur another incident within seven days of the initial occurrence. The sooner the opening occurs, the quicker another hemorrhage will occur. Often, patients are treated with drugs for dissolution and anti-coagulation or may require surgery.

Lacunar cerebral infarction refers to old or new infarctions deep within the brain. When this occurs, lacunas or holes are formed. Depending on the infracted blood vessels, symptoms like limb numbness, dizziness, headache, aphasia and clumsiness may occur. This is due to the small arteries being blocked. Lacunar cerebral infarction may be caused by cerebral arteriosclerosis and hypertension. The diagnosis rate of lacunar cerebral infarction has improved greatly with the use of NMR and CT. Middle-aged and old people are at risk due to decreased blood flow as a result to body changes, including increased blood lipids, enhanced platelet aggregation and increased blood viscosity.

Current Treatment for Cerebral Infarction

The treatment for cerebral infarction varies depending on the type and severity. Thrombolytic drugs are often used in therapy of cerebral infarction. According to the American Heart Association, patients have a better chance of survival and recovery if thrombolytic drugs are taken within 12 hours of the incident. Most patients are administered these drugs within 90 minutes of hospital arrival. For those who are unable to tolerate thrombolytic drugs, mechanical embolectomy devices have been effective for restoring blood flow.

If cerebral infarction is due to a thrombus blocking blood flow to the brain, removal of the blockage may be done by a thrombectomy or thrombolysis. Many stroke centers implement pharmacological thrombolysis with the drug tissue plasminogen activator (tPA). This drug is a protein that helps the breakdown of blood clots. It is also used for embolic stroke but contraindicated in hemorrhagic cerebral infarction. Another intervention for cerebral infarction is the removal of the thrombus causing the blockage. This procedure is done by the insertion of a catheter into the femoral artery.

Stenting and angioplasty are currently to be looked at as possible options for the treatment of cerebral ischaemia. Reviews of center trials with 300 patients using stenting or angioplasty are favorable. Clinical trials with intra-cranial stenting ranged from 90 to 98 percent successful. However, larger controlled trials are needed for complete evaluation of the therapeutic advantages of both angioplasty and stenting.


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