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Guillain-Barré Syndrome PDF
Guillain-Barré Syndrome PDF
Guillain-Barré Syndrome PDF
Etiology: Research indicates that a common cause of food poisoning, the bacterium Campylobacter jejuni, may trigger many cases of GBS in the United States. Other pathogens that have been linked to GBS include Haemophilus influenzae, Mycoplasma pneumoniae, Borrelia burgdorferi, cytomegalovirus, Epstein-Barr virus, and HIV. Some GBS patients dont experience a preceding infection. This disorder has also been seen in conjunction with immune system changes brought about by pregnancy, surgery, and administration of certain vaccines, specifically the swine flu vaccine that was distributed in 1976. Regardless of what initiates the disease process, the end result is that the myelin sheaths on peripheral nerves are attacked and destroyed by macrophages and lymphocytes. The damage progresses proximally and may also affect cranial nerves. This can be life threatening if the nerves that control breathing are damaged; many GBS patients spend time on a ventilator before they recover. GBS is now recognized as several different subtypes of demyelinating diseases. The most common form in the United States is acute inflammatory demyelinating polyneuropathy; this accounts for 90% of GBS diagnoses. Other types include these: Acute motor axonal neuropathy affects motor neurons only. It is most common in children and has a good prognosis. Acute motor-sensory axonal neuropathy affects motor and sensory function. It is most common in adults and has a poorer recovery rate than other forms of GBS. Miller-Fisher syndrome is a rare variant of GBS that involves only the cranial nerves. It leads to poor control of the eyes and other facial muscles. The cause of GuillainBarr syndrome is unknown, but in about 50% of cases, the onset follows the infections: Causes Why Viral infection, bacterial infection, Pathogens in these infections, such as C. jejuni in common cold, mononucleosis, hepatitis, GI infection, are thought to alter the immune gastrointestinal (GI) infection, system, causing T-lymphocytes to be sensitized inoculations to myelin and to trigger demyelination
Signs and Symptoms GBS is notorious for being unpredictable, but it has a few features that distinguish it from other peripheral nerve disorders. Onset is typically fast and severe; a patient may go from being fully functional to being hospitalized within a matter of hours or a couple of days. GBS is usually symmetrical, affecting both legs equally. Also, myelin damage progresses proximally, moving up toward the trunk rather than distally; this pattern is unique among peripheral nerve problems. When GBS first appears, it often involves weakness or tingling in the affected limbs. Reflexes become dull or disappear altogether. Loss of sensation progresses proximally, although pain frequently develops in the hips and pelvis. If the GBS affects cranial nerves of the face, facial weakness, pain, and difficulty with speech and swallowing may develop. As the disease progresses, the nerves that supply respiratory muscles are affected, and problems with breathing develop. GBS symptoms usually peak 2 or 3 weeks after onset, and they may linger for several weeks before they begin to subside. The amount of damage that accrues while the nerves are inflamed depends on what treatments were introduced when and on how soon the patient can begin to use the affected muscles after the paralysis resolves. Weakness usually begins in the legs, then spreads to involve the arms and face. Respiratory muscles may be involved. Life-threatening complications can occur such as tachycardia, arrhythmias, and pulmonary dysfunction
The signs and symptoms and rationales associated with GuillainBarr syndrome:
Why
Nerve impulses slow down or cease Nerve impulses slow down or cease With denervation, muscles atrophy With denervation, muscles atrophy
Diagnosis GuillainBarr syndrome is difficult to diagnose because of the varied symptoms, but if symptoms occur uniformly across the body and progress rapidly, the diagnosis is made much easier. Lumbar puncture may be performed to look for elevated proteins in cerebrospinal fluid which is common. Nerve conduction test may be recommended to confirm that nerve transmission to the extremities is impaired.
Treatment Because GBS is an idiopathic disease, no specific cure has been developed. Two treatment options have been successfully used to shorten recovery time: 1. Plasmapheresis (blood cleansing). This removes autoimmune antibodies and reduces attacks against myelin. This procedure is most effective within 2 weeks of onset. 2. Injections of high concentrations of IV immunoglobulin (donated antibodies). Inhibit the patients antibody and cytokine activity, thus limiting the autoimmune attack against myelin sheaths on peripheral nerves. These options can shorten the recovery process by up to 50%. About one-third of patients require the use of a ventilator until the respiratory nerves regain full function. Anticoagulants may be used against the danger of blood clots in immobilized legs. Pain management is problematic because powerful pain medications can depress the nervous system; massage and other nondrug options are often recommended for this purpose. Once the acute inflammation has passed, occupational and physical therapy is used to help the patient regain as much muscle function as possible.
Prognosis The good news is most people who develop GBS have a full or nearly full recovery, although the process may take 18 months or longer. Many people live with permanent loss of some neurological function (foot drop or numbness in an area, for instance), but these are not considered disabling problems. A small number of patients (5%15%) have permanent serious disability as a result of the disease. About 10% of GBS patients have a relapse later in life. About 5% to 7% of GBS patients die, usually of respiratory failure, pulmonary embolism, or cardiac arrest. Complications Respiratory or cardiovascular collapse may cause death. Weakness of some muscles may persist.