Guillain-Barre Syndrome affects 1 to 2 out of every 100,000 people worldwide. It can affect people of all ages, but it is most common in adults, with those over 50 most at risk. Males are approximately 1.5 times more likely to be affected than females. 

While Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) is the most common form of GBS in North America, other regions have different subtypes which are more prevalent. In Asia, Miller Fisher Syndrome is most common, while in South America, Acute Motor Axonal Neuropathy (AMAN) is more common. All are forms of Guillain-Barre Syndrome, but vary in which nerves they attack and how symptoms manifest. Why specific variants are more common in different regions is not entirely known, but likely is the product of both environmental factors and genetic predispositions.

Guillain-Barre Syndrome is caused by the immune system attacking the nervous system because of molecular mimicry. Molecular mimicry is a mechanism where infectious agents like bacteria or viruses possess molecules that are very similar structurally to molecules found normally in the human body. When the immune system mounts antibodies against these foreign pathogens, the antibodies attack both the infectious molecules and similar native ones. In the case of GBS with AIDP, the antibodies attack the myelin sheath of motor and sensory nerves.

In other subtypes of GBS, the same mechanism applies with small variations. In Miller Fisher Syndrome, antibodies attack both the myelin sheath as well as a part of the nerve cell called the axon, which protrudes out and is responsible for transmitting signals to other cells. Antibodies in Miller Fisher Syndrome specifically attack the cranial nerves extending from the brain to the head and neck, causing a paralysis of the muscles that move the eyes and issues with balance and coordination. In AMAN, the antibodies specifically target the axons of motor nerves, causing a rapid loss of muscle strength and mobility.

Over 70% of individuals with GBS report experiencing some form of infection within 6 weeks of onset. While the infection is most often gastrointestinal or respiratory, a number of different pathogens can trigger GBS. A few which are well documented include:

• Campylobacter jejuni (the most common trigger, often from undercooked poultry)

• Influenza viruses 

• Cytomegalovirus (CMV) 

• Epstein-Barr virus

• Zika virus

• COVID-19

It is important to note that only a small number of people who have an infection go on to develop GBS, and it’s not known why the autoimmune reaction is triggered in some people and not others.

Rarer drivers of GBS can include flu vaccinations (1-2 cases per million doses given), as well as pregnancy, lymphoma, and autoimmune conditions such as lupus.

Guillain-Barre Syndrome is an ascending paralysis, and symptoms usually begin in the feet and legs before spreading to the upper extremities. The symptoms progress through stages:

• Early stage: 

  • A feeling of pins and needles in the feet and hands

  • Unsteady gait

  • In Miller Fisher Syndrome, eye muscle weakness

• Mid-stage: Motor symptoms worsen

  • Loss of sensation in the fingers and toes

  • Progressive weakness of the muscles

  • Difficulty walking

  • Difficulty speaking or chewing

• Severe/late-stage: Autonomic nervous system symptoms appear

  • Rapid heart rate

  • Difficulty maintaining healthy blood pressure

  • Difficulty breathing

  • Urinary incontinence

  • Complete paralysis of the limbs and respiratory muscles can occur, requiring a ventilator

Early diagnosis can be difficult, as early stage Guillain-Barre Syndrome can resemble a number of other neurological disorders. While recent diagnosis of an infection combined with paralysis symptoms can prompt a physician to suspect GBS, there are three main tests done to aid diagnosis:

• The first and easiest test is a physical exam to check for areflexia, or a loss of reflexes such as the knee jerk when the knee is tapped. A loss of reflexes is consistent with GBS.

• The gold standard tests are electrodiagnostic studies, such as electromyography (EMG) and nerve conduction studies (NCS). In these tests, electrodes are placed on the skin and electrical shocks are applied to measure how well the signal travels. NCS measures speed of conduction, and a slower time is consistent with damage to the myelin sheath. EMG can detect denervation, showing that the nerves cannot properly stimulate the surrounding muscle.

• If results remain inconclusive, analysis of the cerebrospinal fluid can be done by a lumbar puncture, also known as a spinal tap. A result of a high level of protein and a low level of white blood cells is consistent with GBS.

While tests can also be done to check for antibodies consistent with auto-immunity against nerves, it can take days to yield results, and a negative result does not necessarily rule out GBS. This is in part because different subtypes of GBS may produce different antibodies, and because tests to detect them only have moderate sensitivity.  

While there is no known cure for Guillain-Barre Syndrome, there are two main treatments used to speed recovery and reduce symptoms:

• Intravenous Immunoglobulin (IVIG): Large amounts of healthy antibodies from donors are injected, and this helps block and dampen the activity of the person’s own damaging antibodies. One dose is given every day for around five consecutive days. This is generally the first line treatment due to safety and efficacy. It is most effective when given within 7-14 days of symptom onset.

• Plasmapheresis or Plasma Exchange: The plasma, or liquid part of the blood which contains the antibodies, is separated from the blood cells, and the blood cells are returned to the body. This helps wash out the damaging antibodies. Often this procedure will be repeated multiple times over a period of two weeks. 

There are other supportive procedures implemented depending on an individual’s symptoms:

• Around 25% of patients may progress to requiring intubation with a ventilator due to respiratory muscle weakness and trouble breathing. 

• Due to prolonged paralysis and limited movement, people prone to blood clots are put on anticoagulants.

• Bedbound individuals should also be repositioned often to prevent bedsores.

• Physical and occupational therapy during recovery can improve outcomes and help individuals regain strength and mobility more quickly. 

The outlook for Guillain-Barre syndrome is generally positive, although recovery can be slow and vary greatly. While symptoms peak around 2-4 weeks after onset, complete recovery can take anywhere from a few weeks to years. However, around 80% of patients are able to walk independently six months after diagnosis. While most people make a full recovery within one year, 15-20% may have lingering neurological issues, such as hand or foot weakness.

After an initial episode of GBS, relapse is uncommon, but can occur in 2-5% of patients. The mortality rate for GBS is around 3-7%, most often due to respiratory failure or secondary infections.

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