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The occurrence and extent of cerebral infarction is determined by three basic factors: i) site of arterial occlusion, ii) the rapidity of arterial occlusion, and iii) the presence or absence of collateral circulation. Grossly, infarcts are usually divided into pale (non-hemorrhagic) and hemorrhagic types. Infarcts evolve over time, thus their gross appearance gives a clue to when they occurred. The temporal evolution of an infarct occurs in three stages: i) acute (1 day – 1 week) – the involved area is soft and edematous and there is a blurring of anatomic detail; ii) subacute (1 week – 1 month) – there is obvious tissue destruction and liquefactive necrosis of the involved brain; iii) chronic (>1 month) – the damaged tissue has been phagocytized and there is cavition with surrounding gliosis. Microscopically there is also a temporal evolution of cerebral infarcts. During the earliest phase of infarction (0-48 hours) chromatolysis and swollen eosinophilic neurons are seen. Neuronal cell necrosis and an acute inflammatory response are usually seen from 24-72 hours. This response is typically followed by an influx of mononuclear cells which begin to phagocytize necrotic debris (3-5 days). From 1-2 weeks after the infarct there is vascular proliferation and reactive astrocytosis. Over time (>1 month) the necrotic tissue will be completely removed and a cystic cavity surrounded by a glial scar will be formed.
Bronchiolitis is a common lung infection in young children and infants. It causes inflammation and congestion in the small airways (bronchioles) of the lung. Bronchiolitis is almost always caused by a virus. Typically, the peak time for bronchiolitis is during the winter months. Bronchiolitis starts out with symptoms similar to those of a common cold but then progresses to coughing, wheezing and sometimes difficulty breathing. Symptoms of bronchiolitis can last for several days to weeks, even a month.
Cosmetic iris implants have not been evaluated by any U.S. regulatory agency or tested for safety in clinical trials. While the implants are not approved by the U.S. Food and Drug Administration, it has been reported in the media this month that the surgery is being performed overseas. During iris implant surgery, an artificial iris made of silicone is folded and inserted into a slit that has been cut into the cornea. Then the iris is unfolded and adjusted to cover the natural iris. Local anesthesia is used.
The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. Although many pathogenic processes have been implicated in the development of abdominal ascites, about 75% likely occur as a result of portal hypertension in the setting of liver cirrhosis, with the remainder due to infective, inflammatory, and infiltrative conditions. Three theories of ascites formation have been proposed: underfilling, overflow, and peripheral arterial vasodilation. The underfilling theory suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention. The overflow theory suggests that the primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. This theory was developed in accordance with the observation that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia. The most recent theory, the peripheral arterial vasodilation hypothesis, includes components of both of the other theories. It suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume. As the natural history of the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This leads to overflow of fluid into the peritoneal cavity. The vasodilation theory proposes that underfilling is operative early and overflow is operative late in the natural history of cirrhosis. Although the sequence of events that occurs between the development of portal hypertension and renal sodium retention is not entirely clear, portal hypertension apparently leads to an increase in nitric oxide levels. Nitric oxide mediates splanchnic and peripheral vasodilation. Hepatic artery nitric oxide synthase activity is greater in patients with ascites than in those without ascites. Regardless of the initiating event, a number of factors contribute to the accumulation of fluid in the abdominal cavity. Elevated levels of epinephrine and norepinephrine are well-documented factors. Hypoalbuminemia and reduced plasma oncotic pressure favor the extravasation of fluid from the plasma to the peritoneal fluid, and, thus, ascites is infrequent in patients with cirrhosis unless both portal hypertension and hypoalbuminemia are present.
X-linked adrenoleukodystrophy is a genetic disorder that occurs primarily in males. It mainly affects the nervous system and the adrenal glands, which are small glands located on top of each kidney. In this disorder, the fatty covering (myelin) that insulates nerves in the brain and spinal cord is prone to deterioration (demyelination), which reduces the ability of the nerves to relay information to the brain. In addition, damage to the outer layer of the adrenal glands (adrenal cortex) causes a shortage of certain hormones (adrenocortical insufficiency). Adrenocortical insufficiency may cause weakness, weight loss, skin changes, vomiting, and coma.
Ebstein anomaly is a congenital malformation of the heart that is characterized by apical displacement of the septal and posterior tricuspid valve leaflets, leading to atrialization of the right ventricle with a variable degree of malformation and displacement of the anterior leaflet.
Syringomyelia is a cystic cavitation of the spinal cord associated with Chiari I malformation (70%) or basilar invagination (10%) or tumor. It may be a post-traumatic condition. There are 2 main forms: communicating with the central canal or subarachnoid spaces (Chiari I malformation); non communicating (trauma, tumors).
There have been rapid and remarkable changes over the recent past in treating Parkinson's disease. The development of new drugs and an understanding of how best to use them and the older drugs have significantly improved the quality of life of people with the disease. There are two general approaches to the treatment of Parkinson's disease with medication. The first approach attempts to increase the levels of dopamine in the brain and the second approach attempts to improve the symptoms of Parkinson's disease by other means. Most patients with Parkinson's disease can initially be treated with drugs that adequately alleviate their symptoms. If or when medications are not sufficiently effective, new, highly effective and safe surgical treatments are also available.