Gullian Barre Syndrome

GBS (Guillain Barre syndrome) is an autoimmune disease where the immune system attacks part of the peripheral nervous system myelin (demielinasi) and axons (axonal degeneration). Axons are long, single protrusion that delivers information from the cell body. Myelin is the sheath that surrounds axons, is a protein-lipid complex is white. GBS characterized by an overall polyneuropathy: paralysis of limbs, upper body and face; disappearance of tendon reflexes, decreased sensory functions (pain and temperature) from the body to the brain; autonomous dysfunctions and respiratory depression. Symptoms usually slowly, starting from the bottom up.

All forms of Guillain–Barré syndrome are due to an immune response to foreign antigens (such as infectious agents) that are mistargeted at host nerve tissues instead. The targets of such immune attack are thought to be gangliosides, compounds naturally present in large quantities in human nerve tissues. The most common antecedent infection is the bacteria Campylobacter jejuni. However, 60% of cases do not have a known cause; one study suggests that some cases are triggered by the influenza virus, or by an immune reaction to the influenza virus

Many terms have been used for the disease include, infectious polyneuritis, acute demyelinating segmentally Polyradiculoneuropathy, acute facial diplegia with polyneuritis, acute polyradiculitis, or Guillain Barre Strohl Syndrome.

The end result of such autoimmune attack on the peripheral nerves is damage to the myelin, the fatty insulating layer of the nerve, and a nerve conduction block, leading to a muscle paralysis that may be accompanied by sensory or autonomic disturbances.

The exact cause of GBS is unknown. Incidence of GBS is often preceded by the following things: (1) respiratory tract infection or ganstrointestinal tract (in two thirds of cases), (2) vaccination. The mechanism underlying the emergence of GBS is an abnormal response of T cells due infection

Cellular and humoral immune mechanisms appear a role, early inflammatory lesions will cause infiltration of lymphocytes and macrophages in myelin components. At the electron microscope image shows that macrophages destroy the myelin sheath. Humoral immune factors such as antibodies, antimielin, and the complement is involved in the process oponisasi macrophages in Schwann cells. This process can be observed either on the nerve roots, peripheral nerves, and cranial nerves. Cytokines were also played, as shown by the correlation of clinical tumor necrotic factor (TNF) with weight disorders elektrofisiologik.

Since the reduction in disease poliomyelitis in the world, GBS becomes the most common acute paralytic disease, especially in Western countries with prevalence of 1.3 to 1.8 cases per 100,000 people. In the United States, the incidence of GBS ranges from 0.4 to 2.0 people per 100,000, but from the research at several hospitals in frequency estimates as many as 15%. Did not reveal any relationship with the incidence of GBS season in the United States second.

GBS immune response is believed to directly attack the components of aksolema glikolipid and myelin sheath. Antibody on peripheral nerve activates the complement system and macrophages, which would appear to depend on cellular cytotoxicity antibody against myelin components and aksolemma.

Damage to the myelin sheath will cause demielinasi segmental, which causes decreased nerve conductivity, and conduction velocity block. Axonal type of GBS is also known as SAFE, mainly characterized by axonal damage that nyata.5

In the first era of modern medicine, there is GBS disease similar to that found by Landry at the year 1859. Later, Osler in 1892 to develop in more detail the number of disease called acute febrile polyneuritis. In 1916, Guillan, Barre, and Strohl described more clinical symptoms and was first put forward about the picture on the state of cerebrospinal fluid, cytology dissociation of albumin (in normal cerebrospinal fluid protein elevation there).

Currently, the epidemic disease which resembles GBS is found every year in some areas of North China, mainly occurs in summer. This epidemic of Campylobacter jejuni associated with infection, and many antiglikolipid antibodies found in patients. Because this disease causes degeneration of peripheral motor axons without much inflammation, this syndrome is called Acute Motor Axonal Neuropathy (AMAN). SECURE contained in <10% of patients with GBS in Western countries and> 40% in China and Japan.

However, in mild cases, nerve axon (the long slender conducting portion of a nerve) function remains intact and recovery can be rapid if remyelination occurs. In severe cases, axonal damage occurs, and recovery depends on the regeneration of this important tissue. Recent studies on the disorder have demonstrated that approximately 80% of the patients have myelin loss, whereas, in the remaining 20%, the pathologic hallmark of the disorder is indeed axon loss

Currently research is being concentrated on anti-gangliosid antibodies contained in the strains of Campylobacter jejuni. These antibodies attack normal gangliosid located on peripheral nerve tissue.