Cause of Guillain–Barre Syndrome
Answer:
Introduction:
1. The cause of Guillain–Barré syndrome (GBS) is the nerve dysfunction produced by the attack of immune system on the nerve cells of peripheral nervous system and its associated structures. Two major variants of GBS have been implicated in the different forms of immune attack. In one variant the white blood cells damage the myelin sheath due to the activation of the complement
group of blood proteins. This is the demyelinating variant. Another variant is the axonal variant in which the cell membrane of the axon is damaged by IgG antibodies and complement without the direct involvement of lymphocytes (Hughes, 2012).
As GBS is a post infectious syndrome, the infection and the specificity of the antibodies produced in response to the infection, partly determines the variant of GBS and its severity. There is production of cross reactive antibodies produced by molecular mimicry of antigens borne by the pathogens that bind to gangliosides. In molecular mimicry, the immune system is countering microbial substances causing infection but the antibodies produced also counter the natural substances present in the body. GM1, GD1a, GT1a, and GQ1b are some of the gangliosides against which antibodies have been produced. A variety of anti-ganglioside antibodies have been related with different features and not all of them cause the disease. Heterodimeric binding (simultaneous binding to more than one type of epitope) of the antibodies or the occurrence of other strains of bacteria in the bowel has been implicated recently in determining the response (Winer, 2011).
2. The diagnosis of GBS can be ascertained from findings such as fast progress of muscle paralysis and lack of reflexes. Cerebrospinal fluid (to check protein and white blood cells levels), nerve conduction, antiganglioside antibodies, blood tests (to check sodium and potassium levels), magnetic resonance imaging of the spinal cord, needle electromyography (EMG) and nerve conduction studies are helpful examinations commonly done in the diagnosis of GBS. The direct assessment of nerve conduction of electrical impulses may be used to eliminate other reasons of acute muscle weakness and differentiate the various types of GBS (Yuki & Hartung, 2012).
The treatment options include immunotherapy, palliative treatment for pain and respiratory failure, and rehabilitation. Immunotherapy includes plasmapheresis and the administration of intravenous immunoglobulins (IVIg). Plasmapheresis sifts antibodies out of the bloodstream thereby decreasing their attack on the nervous system and IVIg neutralizes the harmful antibodies and inflammation. Palliative treatment for pain may be needed in some cases. However, more studies are needed to ascertain which medication should be used. Breathing support and intubation of the windpipe may be needed in cases with respiratory failure. Intensive rehabilitation is needed in most of the cases after the acute phase in order to improve the activities of daily living and long-term symptoms. This may be done by multidisciplinary teams including neurologists, rehabilitation physicians, physiotherapists, psychologists, occupational therapists, dieticians, social workers, other allied health professionals, and nurses. Certain modifications at home, gait aids, orthotics and splints may be helpful. Counseling, support and psychological therapy may also be needed for anxiety, fear and depression (van den Berg et al., 2014).
References
Hughes, R. A. C. (2012). Guillain-Barré Syndrome. Springer Science & Business Media.
van den Berg, B., Walgaard, C., Drenthen, J., Fokke, C., Jacobs, B. C., & van Doorn, P. A. (2014). Guillain–Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nature Reviews Neurology, 10(8), 469–482. https://doi.org/10.1038/nrneurol.2014.121
Winer, J. B. (2011). Guillain–Barré syndrome: Clinical variants and their pathogenesis. Journal of Neuroimmunology, 231(1–2), 70–72. https://doi.org/10.1016/j.jneuroim.2010.09.017
Yuki, N., & Hartung, H.-P. (2012). Guillain–Barré Syndrome. New England Journal of Medicine, 366(24), 2294–2304. https://doi.org/10.1056/NEJMra1114525
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