Guillain-Barré Syndrome (GBS) is a rare neurological disorder where the body’s immune system mistakenly attacks the peripheral nervous system. This network of nerves connects the brain and spinal cord to the rest of the body. When these nerves are attacked, the protective covering, called the myelin sheath, or sometimes the nerve core itself, becomes damaged. This nerve injury leads to the primary symptoms of GBS, which include sudden onset of muscle weakness and tingling sensations, usually starting in the limbs.
Is Guillain-Barré Syndrome Passed Down?
Guillain-Barré Syndrome is not considered a hereditary condition that is directly passed down through a family in a clear inheritance pattern. The vast majority of cases are sporadic, meaning they occur randomly in individuals with no prior family history. It is not contagious, nor is it inherited like conditions such as cystic fibrosis or Huntington’s disease.
While GBS itself is not inherited, research suggests that certain genetic variations might increase an individual’s susceptibility to developing it. These variations often involve genes related to the immune system and inflammation, potentially making a person more prone to an autoimmune reaction following a trigger. However, possessing such a genetic profile does not guarantee development, as environmental factors play a significant role. The condition requires both a genetic predisposition and an immune-system trigger to manifest.
Understanding the Immune Trigger
Since GBS is not inherited, it is most often caused by an immune response mistakenly directed at the peripheral nerves following an antecedent event. Approximately two-thirds of people who develop GBS report having had a respiratory or gastrointestinal infection in the weeks prior to the onset of neurological symptoms. The most common identified trigger is infection with the bacteria Campylobacter jejuni, which causes gastroenteritis.
This mistaken attack is explained by a process called “molecular mimicry.” During an infection, the immune system produces antibodies to fight the foreign pathogen. In molecular mimicry, certain surface components of the infectious agent, such as the lipo-oligosaccharides of C. jejuni, closely resemble structures found on human nerve cells, specifically the gangliosides. The antibodies created to destroy the infection then cross-react and begin attacking the host’s own nerve components, resulting in the inflammation and damage characteristic of GBS.
Clinical Signs and Diagnosis
GBS typically begins with sensory changes, such as tingling, numbness, or pain, often in the feet and hands. This is rapidly followed by symmetrical muscle weakness that usually starts in the lower limbs and progresses upward, a pattern known as ascending paralysis. Weakness progresses over hours or days, with most patients reaching their point of maximum weakness (nadir) within about two weeks. In severe cases, the weakness can affect the muscles controlling breathing, requiring mechanical ventilation.
Diagnosis is based on clinical presentation and supported by specific diagnostic tests. A lumbar puncture (spinal tap) is often performed to analyze the cerebrospinal fluid (CSF). A classic finding is an elevated protein level in the CSF without a corresponding increase in white blood cells, a phenomenon called albuminocytologic dissociation. Nerve conduction studies (NCS) and electromyography (EMG) are also used to measure electrical signals, confirming the extent and type of nerve damage.
Treatment and Recovery Outlook
Treatment for acute GBS focuses on modulating the immune system to limit nerve damage and providing supportive care, particularly for breathing difficulties. The two primary therapies are Intravenous Immunoglobulin (IVIg) and Plasma Exchange (Plasmapheresis), both considered equally effective if started early in the disease course. IVIg involves infusing a concentrated dose of healthy antibodies collected from donors, which helps lessen the immune system’s attack on the nerves.
Plasma Exchange involves removing the patient’s blood, separating the liquid plasma containing the harmful antibodies, and returning the blood cells with a replacement fluid. Both treatments work to reduce the levels of autoantibodies attacking the peripheral nerves, which can shorten the duration of the illness. While there is no cure, the majority of people with GBS have a good recovery, though the process can be slow, lasting anywhere from a few weeks to several years. Some individuals may experience residual effects, such as lingering weakness, numbness, or fatigue.