What are the symptoms of GBS? What happens in GBS? How does nerve damage occur? What disorders are related to GBS?
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What are the symptoms of GBS? What happens in GBS? How does nerve damage occur? What disorders are related to GBS? What research is being done? Where can I get more information? GBS can range from a very mild case with brief weakness to nearly devastating paralysis, leaving the person unable to breathe independently.
Fortunately, most people eventually recover from even the most severe cases of GBS. After recovery, some people will continue to have some degree of weakness.
It can strike at any age although it is more frequent in adults and older people and both sexes are equally prone to the disorder. GBS is estimated to affect about one person in , each year. The exact cause of GBS is not known. It is not contagious or inherited. What they do know is that the affected person's immune system begins to attack the body itself. It is thought that, at least in some cases, this immune attack is initiated to fight an infection and that some chemicals on infecting bacteria and viruses resemble those on nerve cells, which, in turn, also become targets of attack.
Normally the immune system uses antibodies molecules produced in an immune response and special white blood cells to protect us by attacking infecting microorganisms bacteria and viruses. Most cases usually start a few days or weeks following a respiratory or gastrointestinal viral infection. Occasionally surgery will trigger the syndrome. In rare cases vaccinations may increase the risk of GBS. Recently, some countries worldwide reported an increased incidence of GBS following infection with the Zika virus.
Unexplained sensations often occur first, such as tingling in the feet or hands, or even pain especially in children , often starting in the legs or back. Children will also show symptoms with difficulty walking and may refuse to walk. These sensations tend to disappear before the major, longer-term symptoms appear. Weakness on both sides of the body is the major symptom that prompts most people to seek medical attention. The weakness may first appear as difficulty climbing stairs or with walking.
Symptoms often affect the arms, breathing muscles, and even the face, reflecting more widespread nerve damage.
Occasionally symptoms start in the upper body and move down to the legs and feet. Most people reach the greatest stage of weakness within the first two weeks after symptoms appear; by the third week 90 percent of affected individuals are at their weakest.
These symptoms can increase in intensity over a period of hours, days, or weeks until certain muscles cannot be used at all and, when severe, the person is almost totally paralyzed. In these cases, the disorder is life-threatening—potentially interfering with breathing and, at times, with blood pressure or heart rate. There is a central conducting core in the nerves called the axon that carries an electric signal. The axon an extension of a nerve cell is surrounded by a covering, like insulation, called myelin.
The myelin sheath surrounding the axon speeds up the transmission of nerve signals and allows the transmission of signals over long distances. Weakness When we move, for example, an electric signal from the brain travels through and out of the spinal cord to peripheral nerves along muscles of the legs, arms, and elsewhere—called motor nerves. In most cases of GBS, the immune system damages the myelin sheath that surrounds the axons of many peripheral nerves; however, it also may also damage the axons themselves.
As a result, the nerves cannot transmit signals efficiently and the muscles begin to lose their ability to respond to the brain's commands. This causes weakness. The weakness seen in GBS usually comes on quickly and worsens over hours or days.
Symptoms are usually equal on both sides of the body called symmetric. In addition to weak limbs, muscles controlling breathing can weaken to the point that the person must be attached to a machine to help support breathing. Sensation changes Since nerves are damaged in GBS, the brain may receive abnormal sensory signals from the rest of the body. This results in unexplained, spontaneous sensations, called paresthesias, that may be experienced as tingling, a sense of insects crawling under the skin called formications , and pain.
Various ideas have been proposed to explain how GBS develops. According to this explanation, molecules on some nerves are very similar to or mimic molecules on some microorganisms. When those microbes infect someone, the immune system correctly attacks them. And if the microbe and myelin look similar, the immune system makes a mistake and attacks the myelin.
Different mechanisms may explain how the molecular mimicry concept may work. The immune system treats these nerves as foreign bodies and mistakenly attacks them. It is also possible that the virus makes the immune system itself less discriminating and no longer able to recognize its own nerves. Some parts of the immune system—special white blood cells called lymphocytes and macrophages—perceive myelin as foreign and attack it.
In some forms of GBS, antibodies made by the person to fight a Campylobacter jejuni bacterial infection attack axons in the motor nerves. This causes acute motor axonal neuropathy, which is a variant of GBS that includes acute paralysis and a loss of reflexes without sensory loss.
Campylobacter infections can be caused by ingesting contaminated food or from other exposures. This slows nerve conduction and causes paralysis. Scientists are investigating various GBS subtypes to find why the immune system reacts abnormally in this syndrome and other autoimmune diseases. While GBS comes on rapidly over days to weeks, and the person usually recovers, other disorders develop slowly and can linger or recur.
In AIDP, the immune response damages the myelin coating and interferes with the transmission of nerve signals. It is characterized by abnormal muscle coordination with poor balance and clumsy walking, weakness or paralysis of the eye muscles, and absence of the tendon reflexes.
Like GBS, symptoms may follow a viral illness. Additional symptoms include generalized muscle weakness and respiratory failure. Most individuals with Miller Fisher syndrome have a unique antibody that characterizes the disorder. Related peripheral nerve disorders with slow onset and persisting or recurrent symptoms include chronic inflammatory demyelinating polyneuropathy CIDP and multifocal motor neuropathy.
CIDP features weakness that can recur, repeatedly, over the course of years. Multifocal motor neuropathy typically affects many different muscles in a small part of a limb or limbs.
Usually the symptoms are more severe on one side of the body. The initial signs and symptoms of GBS are varied and there are several disorders with similar symptoms. Therefore, doctors may find it difficult to diagnose GBS in its earliest stages. In GBS, deep tendon reflexes in the legs, such as knee jerks, are usually lost.
Reflexes may also be absent in the arms. There is a change in the cerebrospinal fluid that bathes the spinal cord and brain in people with GBS. Researchers have found the fluid contains more protein than usual but very few immune cells measured by white blood cells. Therefore, a physician may decide to perform a spinal tap or lumbar puncture to obtain a sample of spinal fluid to analyze. This procedure is usually safe, with rare complications. However, some therapies can lessen the severity of the illness and shorten recovery time.
There are also several ways to treat the complications of the disease. There are currently two treatments commonly used to interrupt immune-related nerve damage.
One is plasma exchange PE, also called plasmapheresis ; the other is high-dose immunoglobulin therapy IVIg. Both treatments are equally effective if started within two weeks of onset of GBS symptoms, but immunoglobulin is easier to administer.
Using both treatments in the same person has no proven benefit. The blood cells from the liquid part of the blood plasma are extracted and returned to the person. Plasma contains antibodies and PE removes some plasma; PE may work by removing the bad antibodies that have been damaging the nerves.
Immunoglobulins are proteins that the immune system naturally makes to attack infecting organisms. IVIg therapy involves intravenous injections of these immunoglobulins. The immunoglobulins are developed from a pool of thousands of normal donors. The IVIg can also shorten recovery time. However, controlled clinical trials have demonstrated that this treatment is not effective. Supportive care is very important to address the many complications of paralysis as the body recovers and damaged nerves begin to heal.
Sometimes a mechanical ventilator is used to help support or control breathing. The autonomic nervous system that regulates the functions of internal organs and some of the muscles in the body can also be disturbed, causing changes in heart rate, blood pressure, toileting, or sweating.
Therefore, the person should be put on a heart monitor or equipment that measures and tracks body function. Occasionally GBS-related nerve damage can lead to difficulty handling secretions in the mouth and throat. As individuals begin to improve, they are usually transferred from the acute care hospital to a rehabilitation setting.
Here, they can regain strength, receive physical rehabilitation and other therapy to resume activities of daily living, and prepare to return to their pre-illness life.
Complications in GBS can affect several parts of the body. Often, even before recovery begins, caregivers may use several methods to prevent or treat complications.
Injections of blood thinners can help prevent dangerous blood clots from forming in leg veins. Inflatable cuffs may also be placed around the legs to provide intermittent compression.
All or any of these methods helps prevent blood stagnation and sludging the buildup of red blood cells in veins, which could lead to reduced blood flow in the leg veins. Muscle strength may not return uniformly; some muscles that get stronger faster may tend to take over a function that weaker muscles normally perform—called substitution.
Guillain-Barré Syndrome Fact Sheet
Professional Reference articles are designed for health professionals to use. A large number of infections have been linked, including Campylobacter jejuni , Epstein Barr virus, cytomegalovirus, mycoplasma and human immunodeficiency virus [ 1 , 2 ]. This association with preceding infection suggests that antibodies to the infectious organism also attack antigens in peripheral nerve tissue. Miller Fisher syndrome is thought to be an inflammatory neuropathy affecting the cranial nerves especially the eye muscles, causing ophthalmoplegia , accompanied by areflexia and ataxia but not weakness. Bickerstaff's brainstem encephalitis is considered part of Miller Fisher syndrome with additional features of drowsiness and extensor plantar responses.
Although the cause is unknown, the underlying mechanism involves an autoimmune disorder in which the body's immune system mistakenly attacks the peripheral nerves and damages their myelin insulation. In those with severe weakness, prompt treatment with intravenous immunoglobulins or plasmapheresis , together with supportive care, will lead to good recovery in the majority of people. This is followed by weakness of the legs and arms that affects both sides equally and worsens over time. The plateau phase can take between two days and six months, but the most common duration is a week. This may consist of upper respiratory tract infection rhinitis, sore throat or diarrhea. In children, particularly those younger than six years old, the diagnosis can be difficult and the condition is often initially mistaken sometimes for up to two weeks for other causes of pains and difficulty walking, such as viral infections,  or bone and joint problems.