Attempts to separate the causative agent of infectious unsuccessful and the cause is unknown. However it has been known that GBS is not hereditary or contagious diseases. Although there may be no precipitating event, a complete patient history often shows an unusual viral disease that occurs 1 to 3 weeks before the onset of motor weakness. Another type of illness that preceded the syndrome is a mild respiratory infection or GI infection. Surgery, immunization, Hodgkin's disease, or other lymphoma, and lupus erythematosus. The most frequently reported circumstances are Campylobacter jejuni infection which typically causes GI illness characterized by diarrhea, abdominal pain, and fever.
The most common result of this incident is that the events in the pathology of the originator (viral or inflammatory processes) change in the nervous system so that the immune system recognizes the system as foreign cells. After that, the sensitized T lymphocytes and macrophages to attack myelin. Besides lymphocytes induces B lymphocytes to produce antibodies that attack the myelin sheath certain legendary, causing damage to myelin (NINDS, 2000).
The result is a mild to severe demyelination injuries that interfere with nerve impulse conduction in peripheral attacked. (on the contrary, demyelination in MS is limited to the central nervous system). Pathological changes follow a precise pattern: infiltration of lymphocytes occurs in the perivascular space adjacent to the nerve and myelin degeneration into focus.
Demyelination of peripheral nerve axons causing positive and negative symptoms. Positive symptoms are pain and paresthesias were derived from abnormal impulse activity in sensory fibers or "cross-talk" between axons abnormal electrical damage. Negative symptoms are muscle weakness or paralysis, loss of tendon reflexes, and decreased sensation. The first two negative symptoms caused by damage to motor axons; the latter is caused by damage to sensory fibers.
In GBS, sensory symptoms tend to be mild and can include pain, tingling, numbness, and abnormal vibration and position. However, a motor dominant polyneuropathy and clinical findings can be at variance ranging from muscle weakness to paralysis of the respiratory muscles requiring ventilator treatment. Skeletal muscle weakness is often very acute so that no muscle atrophy, but lost muscle tone and areflexia easily detected. Sensitivity is usually stimulated by strong pressure and squeeze the muscles. The arm can be thin or weak arm muscles less than the leg muscles. Autonomic symptoms including postural hypotension, sinus tachycardia, and no ability to sweat. When cranial nerves are involved, paralysis of facial muscles will attack, ocular, and oropharyngeal muscles normally after the engagement arm. Symptoms of cranial nerve palsy is facial and speech difficulties, visual disturbances and difficulty swallowing. Bulbar palsy term is sometimes used specifically to paralysis of the jaw, pharynx, and tongue muscles caused by damage to cranial nerves IX, X, and XI, which originate from the medulla oblongata and the so-called bulb.
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