Summary of GBS
Guillain-Barré syndrome (GBS) is an acute-onset, immune-mediated disorder that affects the peripheral nervous system through demyelination of certain types of neuronal and glial cells (Burns, 2008). GBS can also be simply defined as a disorder in which the immune system attacks part of the peripheral nervous system (National Institute of Neurological Disorders and Strokes, 2010). This disorder is typically seen in patients whom have recently been sick various infections. Some of the viral and bacterial infections that are known to predate the onset of GBS are Campylobacter jejuni, Cytomegalovirus, Mycoplasma pneumonia, Epstein-Barr virus, and the influenza virus. Other factors that have been associated with this disorder are surgery, immunization, and parturition (Burns, 2008).
Symptoms that usually accompany GBS are symmetrical paresthesias, sensory processing disturbances, weakness of the limb muscles, areflexia or hyporeflexia, cranial nerve weakness, a high protein concentration in the cerebrospinal fluid, and diaphragmatic weakness. The progression of this disorder is rapid. Most clients reach the lowest point of this disorder within two to four weeks from onset. GBS is a serious disorder, because in many cases the patients experience loss of total muscle control, which results in them being put on a ventilator to assist with their breathing (Burns, 2008).
There is still a lot to be researched and learned about this disorder, because the exact cause of GBS is still unknown. Cerebrospinal fluid analysis and electrodiagnostic testing are used to detect GBS. There are several other diseases and disorders that should be considered and eliminated as possibilities before a diagnosis of GBS is given, but the quick onset, symmetrical paresthesias, and high levels of protein concentration in cerebrospinal fluid are common indicators of this disorder. There is no known cure for GBS, but plasmapheresis and high-dose immunoglobulin therapy are used to treat the complications of it. Both plasmapheresis and high-dose immunoglobulin therapy reduce the severity and duration of GBS (Burns, 2008).
GBS is a fairly rare disorder, but it is the most common cause of acute flaccid paralysis in developed countries (Moffat, Bohmert, & Hulme, 2008). The incidence of GBS is one or two per 100,000 people, and the lifetime likelihood of someone acquiring this disorder is one in 1000 (Burns, 2008). The most common form of GBS is acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and the least common form of GBS is Miller Fisher syndrome (MFS). There is typically a full recovery by GBS patients that take advantage of multidimensional therapeutic opportunities along with fast and effective medical care. Residual muscle weakness is the most common complaint after recovery from GBS (National Institute of Neurological Disorders and Strokes, 2010). The recovery period for GBS ranges from a few months to a few years, but the residual muscle weakness may last for up to three years. A relapse of GBS is somewhat rare for this disease if a full recovery is made (Burns, 2008). Usually GBS occurs in sporadic cases, but two of the most common outbreaks occurred in El Sult, Jordan and in the U.S. in the 1970’s. The speculated causes for these outbreaks were water pollution in Jordan and the administering of a swine flu vaccine in the U.S. (Sliman, 1978; Pollack, 2009).
It is imperative for the human body to interact with its environment. Stimuli from the environment are sensed by receptors peripherally in our bodies. This information travels through afferent pathways to the central nervous system where a response is determined. The initiation of the body’s response to the environmental stimulus, whether it be inhibitory or excitatory, travels from the central nervous system down efferent pathways to the target tissue. The medium that information is passed along these afferent or efferent pathways occurs in neurons or glial cells. Action potentials, or rapid reversal of electrical charges on either side of the cell membrane, coupled with chemical transmission of neurotransmitters are how the human body communicates the environmental stimulus (sensory input) and bodily response (motor output) throughout the body. Myelination allows and promotes this whole process (Bear, Connors, & Paradiso, 2007).
Neurons and glial cells have axons between the soma and terminal bouton. Axons have myelinated and unmyelinated regions, which allow information to travel through electrical impulses from the soma to the terminal bouton. At the terminal bouton of a neuron, neurotransmitters are released into the synaptic cleft after the action potential reaches the bouton, which allows the soma of the post-synaptic neuron or glial cell to receive information from the pre-synaptic neuron or glial cell. The process may then starts over until the information reaches either the central nervous system or target tissue. The alternating myelinated and unmyelinated portions of an axon are how these action potentials travel down the axon. The unmyelinated portion, Nodes of Ranvier, propagates an action potential, while the myelinated portion insulates, for lack of a better word, the electrical impulses or action potentials (Bear, Connors, Paradiso, 2007).
In GBS, Schwann cells or other nerve or glial cells in the periphery are affected, which decreases the efficacy partially or entirely of action potential transmission, which results in the widespread GBS symptoms. In other words, GBS patients’ bodies cannot communicate within itself or with its surrounding environment. This disorder is debilitating, because it’s not a single neuron or glia that’s being affected. Bundles of nerves are affected, which causes the widespread and devastating symptoms. Two-thirds of GBS have had a viral or bacterial infection that caused this process to happen within the body. Researchers have narrowed it down even more to say that most GBS patients had an upper respiratory infection or gastrointestinal infection prior to the GBS symptoms. This is important to recognize, because the antibodies that were originally fighting off these infections begin attacking nerve cells in the periphery, which brings us full circle to the decreased efficiency in nerve cells and body structures (Moffat, Bohmert, & Hulme, 2008).
Client Factors and Theory
There are a number of client factors affected by GBS. The anatomical structures affected in patients with GBS are the previously stated nerve structures, the nervous system, and all systems that are affected by the nervous system. In other words, almost every anatomical system in the entire body is affected by this disorder. Some specific examples of these would be loss of motility in the digestive system, diaphragmatic weakness with the respiratory and musculoskeletal system, and general weakness in the musculoskeletal system affecting muscle movement.
Bodily functions that are affected are again endless. Due to the loss of function in various anatomical structures the body cannot possibly function in a normal pattern. GBS makes performance in areas of occupation difficult if not impossible. Specifically, dressing, eating, grooming, work, play, leisure, education, and social participation are affected areas of occupation under the Occupational Therapy Practice Framework. Respiration and efficiency in the cardiovascular system are major anatomical systems and body functions that are also affected with GBS.
The Ecology of Human Performance theory would be one option for therapeutic intervention. This theory states that an individual’s performance range should be maximized. The Biomechanical frame of reference could be used in the therapeutic intervention. This frame of reference applies principles of physics to human movement and posture with respect to the forces of gravity. For the residual weakness, an occupational therapist could use the biomechanical frame of reference in combination with the rehabilitative frame of reference, which aims to make clients as independent as possible in spite of any residual impairment.
When working with patients with GBS muscle strengthening and relearning how to move and use the body should be focused upon. Through strengthening of the weakened muscles, dressing, grooming, eating, and many other areas of occupations will be improved. Range of motion should also be focused upon in the therapeutic setting with GBS clients, especially if the client has been bedridden for a long period of time. Various stretches, weight lifting, resistance bands, and activities that incorporate each of these would be great options for therapeutic interventions (Ryan & Sladyk, 2005).
Two adaptive equipment suggestions for clients with GBS are the bath chair and adaptive eating utensils. The bath chair will help the client with bathing. Until muscle strength is increased after a GBS episode, activities requiring endurance of muscle activity may be difficult for the client. The bath chair will allow the client to sit, which may be easier on the lower extremities, while bathing. This chair should only be used after postural strength, specifically epaxial and hypaxial muscle strength, it regained. Complete postural strength doesn’t have to be regained, but the client should be able to sit steadily upright for at least half an hour. The time frame for this improvement with different GBS patients will vary greatly, but the occupational therapist should be able to assess when their client is ready for independent bathing.
The adaptive eating utensils will help the client with GBS be able to eat quicker and easier after their GBS episode. These utensils have a larger handle that doesn’t require as many precise movements from the hands. The client will need to regain some strength in the hand muscles, but this would be a great step towards eventually eating with regular utensils again. Occupational therapists should be aware that some of these adaptive eating utensils may be heavier due to their larger size, which would be beneficial in muscle strengthening, but the client with GBS may have to work their way up to these heavier utensils. Occupational therapist should start their client out with lightweight adaptive eating utensils. This piece of equipment may take longer to find and may cost a little bit more, but this step is important if you’re client is trying to regain the ability to independently eat as quickly as possible. Hand strengthening should occur throughout the therapeutic interaction though, so once the occupational therapist sees improvement with the task of eating they could add in the heavier adaptive eating utensils to further strengthen the muscles needed for regular eating utensils.
Bear, M., Connors, B., & Paradiso, M. (2007). The action potential. Neuroscience: Exploring the Brain, 75-100. Baltimore, MD: Lippincott Williams & Wilkins.
Burns, T. (2008). Guillain-Barré syndrome. Semin Neurol, 28(2), 152-167. New York, NY: Thieme Medical Publishers.
Moffat, M., Bohmert, J., & Hulme, J. (2008). Impaired motor function and sensory integrity associated with acute or chronic polyneuropathies. Neuromuscular Essentials, 223-236. Thorofare, NJ: SLACK Inc.
National Institute of Neurological Disorders and Strokes. (2010). NINDS Guillain-Barré syndrome information page. National Institutes of Health. Retrieved from http://www.ninds.nih.gov/disorders/gbs/gbs.htm.
Pollack, A. (2009). Fear of a swine flu epidemic in 1976 offers some lessons, and concerns, today. New York Times. Retrieved from http://www.nytimes.com/2009/05/09/health/09vaccine.html.
Ryan, S. & Sladyk, K. (2005). Activities of daily living. Ryan’s occupational therapy assistant: principles, practice issues, and techniques, 443-453. Thorofare, NJ: SLACK Inc.
Sliman, N. (1978). Outbreak of Guillain-Barré syndrome associated with water pollution. British Medical Journal, 1(6115), 751-752. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1603330/.