Alcoholic polyneuropathy is a neurological disorder in which peripheral nerves throughout the body malfunction simultaneously. It is defined by axonal degeneration in neurons of both the sensory and motor systems and initially occurs at the distal ends of the longest axons in the body. This nerve damage causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally. Alcoholic polyneuropathy is caused primarily by chronic alcoholism; however, vitamin deficiencies are also known to contribute to its development. This disease typically occurs in chronic alcoholics who have some sort of nutritional deficiency. Treatment may involve nutritional supplementation, pain management, and abstaining from alcohol. Signs and symptoms
An early warning sign (prodrome) of the possibility of developing alcoholic polyneuropathy, especially in a chronic alcoholic, would be weight loss because this usually signifies a nutritional deficiency that can lead to the development of the disease.Alcoholic polyneuropathy usually has a gradual onset over months or even years, although axonal degeneration often begins before an individual experiences any symptoms.The disease typically involves sensory issues and motor loss, as well as painful physical perceptions, though all sensory modalities may be involved. Symptoms that affect the sensory and motor systems seem to develop symmetrically. For example, if the right foot is affected, the left foot is affected simultaneously or soon becomes affected. In most cases, the legs are affected first, followed by the arms. The hands usually become involved when the symptoms reach above the ankle. This is called a stocking-and-glove pattern of sensory disturbances.
Loeys–Dietz syndrome (LDS) is an autosomal dominant genetic connective tissue disorder. It has features similar to Marfan syndrome and Ehlers–Danlos syndrome. The disorder is marked by aneurysms in the aorta, often in children, and the aorta may also undergo sudden dissection in the weakened layers of the wall of the aorta. Aneurysms and dissections also can occur in arteries other than the aorta. Because aneurysms in children tend to rupture early, children are at greater risk for dying if the syndrome is not identified. Surgery to repair aortic aneurysms is essential for treatment. There are five types of the syndrome, labelled types I through V, which are distinguished by their genetic cause. Type 1, Type 2, Type 3, Type 4 and Type 5 are caused by mutations in TGFBR1, TGFBR2, SMAD3, TGFB2, and TGFB3 respectively. These five genes encoding transforming growth factors play a role in cell signaling that promotes growth and development of the bodys tissues. Mutations of these genes cause production of proteins without function. The skin cells for individuals with Loeys–Dietz syndrome are not able to produce collagen, the protein that allows skin cells to be strong and elastic. This causes these individuals to be susceptible to different tears in the skin such as hernias. Although the disorder has an autosomal pattern of inheritance, this disorder results from a new gene mutation in 75% of cases and occurs in people with no history of the disorder in their family.