A Review of Guillain-Barre Syndrome
Introduction
By Cassandra Lis
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Guillain-Barré syndrome (GBS) is a rare disorder characterized by neuropathy that has a mortality rate of 4% to 7%. The effects of Guillain-Barré syndrome are the most common cause of quadriparesis, muscle weakness in all four limbs, in the world (1-2 cases per 100,000 people). Before 1979, the most common cause of quadriparesis was polio, but the introduction of the vaccine eradicated polio in the US and the rest of the world besides Pakistan, Afghanistan, and Nigeria. (3) In this disorder, it is believed that the immune system attacks the nerves, so symptoms relating to nerve degeneration are normally the symptoms that are first noticed. Some of the symptoms of this disorder are weakness in legs, unsteady walking, feeling achy, shooting pain, high pulse, and labored breathing. The most common first symptom is weakness and tingling in the lower extremities which later spreads to the upper body.
There are four main types of Guillain-Barré syndrome: acute inflammatory demyelinating polyradiculoneuropathy, Miller Fisher syndrome, Acute motor axonal neuropathy, and acute motor-sensory axonal neuropathy. Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is the type of Guillain-Barré that is most common in Europe and North America and people in these regions use GBS and AIDP interchangeably (4). AIDP has three phases as it progresses, the first of which being rapidly worsening muscle weakness. After this stage, the muscle weakness becomes stable but other symptoms occur like cardiac disruptions or gastric dysmotility (4). The final stage is when the symptoms gradually fade away. However, many people have weakness or pain for years after the syndrome (4).
Miller Fisher syndrome (MFS) has a different characterization than AIDP. This syndrome is associated with unsteady ambulation, areflexia (loss of reflexes), and ophthalmoplegia (weakness of eye muscles)(5). MFS shares characteristics with Bickerstaff brainstem encephalitis, which impacts the central nervous system more than MFS does. People who have had MFS normally recover in a few months, but there are also numerous patients who display other forms of GBS in addition to the MFS. In these overlap cases, respiratory failure is also a common side effect. (5)
Acute motor axonal neuropathy (AMAN) is less common in western countries, but accounts for 30% to 50% of Guillain-Barré syndrome cases in both Asia and Latin America (6). This form of GBS is more severe in its onset of weakness and poor reflexes than AIDP. Many patients with this form of GBS need assistance with respiration, which is achieved through the use of a ventilator (6). AMAN onset is often associated with enteritis caused by Campylobacter jejuni. Recovery in AMAN differs from the other forms of GBS because it can occur much quicker. However, if the person has severe axonal degeneration, the recovery process is longer (6).
Acute motor-sensory axonal neuropathy (AMSAN) is similar to AMAN in both its proposed pathological mechanism and symptoms. However, this disease is very severe, so the recovery process is very poor (7). This is because the illness affects the sensory nerves and roots, which causes motor and sensory dysfunction (7).
Guillain-Barré syndrome has many different causes, and the majority of them are bacterial or viral in nature. Campylobacter jejuni, influenza virus, cytomegalovirus, Epstein-Barr virus, Zika virus, Hepatitis A/B/C/E, HIV, mycoplasma pneumonia, surgery, Hodgkin’s lymphoma, vaccinations (very rarely), and COVID-19 infections are all believed to trigger the syndrome. Although these can trigger Guillain-Barré syndrome, the actual underlying cause of this disorder is unknown. It does not spread between people and it is not a heritable illness. The specific mechanisms of the disease are currently being investigated and are of high interest in the medical community.
Current research is finding that several medicines are also associated with the onset of forms of GBS. For example, a 2019 case study finds that rivaroxaban, also known as xarelto, may be associated with GBS (3). Rivaroxaban is a commonly used anticoagulant, which prevents deep vein thrombosis, strokes, and heart attacks. The patient in the case study had a history of diabetes, and they developed quadriparesis after 5 days of treatment with rivaroxaban. Nerve conduction studies found that there was a reduction in amplitude for both the tibial and right peroneal nerves (3). There was also reduced sensory nerve action potential in the right ulnar nerve. These findings indicated that the patient was experiencing demyelinating neuropathy. The surprising finding about this patient was that there were no recent records of infection or vaccinations, which indicated that something new or unknown caused the onset of GBS (3). Rivaroxaban was stopped and the patient was treated with intravenous immunoglobulin and neurorehabilitation to combat the GBS. He was able to walk after 2 months of stopping the rivaroxaban. The reason why rivaroxaban causes GBS is unknown, but it is likely that there was an allergic reaction to the drug or a neurotoxin effect that caused demyelination (3).
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Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2021, Kenyon College.
