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The GuillainBarre Syndrome

Among the group of acute diseases, the Guillain-Barre syndrome (GBS) is one of them. The disease is also known as acute polyneuropathy. The illness starts in most cases by a prior infection caused by different micro-organisms. The ailment can be because of a lot of symmetrical motor deficiencies as also sensory problems. The Guillian-Barre disease can be considered as a illness caused by post infection illness as a more than 60% of the patients suffering from the Guillian-Barre ailment have complained about some infectious diseases prior to the manifestation of Guillian-Barre disease. The immune system of individuals is considered to have been impacted through these infections rendering it to react and work against the peripheral nerve antigens. It is assumed that the time from the initial infection and the manifestation of the first symptom to appear ranges from one to four weeks. Kirsten et al. (2003) stated that Guillian-Barre syndrome (GBS) is a serious illness, also known as "demyelinating polyneuropathy"

Normal anatomy of an organ: since Guillian-Barre syndrome impairs peripheral nerves, we shall go through the normal anatomy of peripheral nerves. 31 pairs of spinal nerves are present in humans (8 cervical, 5 lumbar, 5 sacral and 1 coccygeal spincal nerve, and 3 major neural plexuses are found: the cervical (C-1 to C-4), brachial (C5 to T-1), and lumbosacral (T-12 to S-4) and cranial nerves (12 pairs). The second classification can be categorized on the direction the electric impulse is conducted: afferent nerves (from sensory neurons right up to the central nervous system), efferent (from central nervous system to the motor neurons- muscle and glands), and mixed (containing both afferent and efferent nerves) (Kimura, 2006). Anatomically, nerves consists of three parts: endoneurium (matrix present between axons), perineurium (cells connecting axons of each fascicle together) and epineurium (connective tissue). Two types of axons are found : myelinated (myelin is present, a spiral pane of membrane which envelopes the axon, they are more thick than one micron and is able to regenerate) and unmyelinated (not having myelin, but have Schwann cell cytoplasm, without spiraling Schwann cell cytoplasm enveloping the axon).

The composition of Myelin is 70% lipids and 30% protein. However deviations in its structure can be found, depending on its position in the nervous system either being a part of central nervous system or peripheral nervous system. The myelin sheath which is on the axons carries the function of an electrical insulator, also carries the function to avoid short-circuits between variable atoms, and to allow conduction of electric impulses through axons. Nodes are found on axons known as Ranvier nodes which are the sole points where the axon is uncovered by myelin sheath, hence in those locations the exchange of ions between axon and the extracellular fluid happens. At the node of the Ranvier, the axonal membrane depolarizes that magnifies the action capability which is conducted through the axon, and this action gives the foundation of salutatory (jumping) conduction.

Etiology and risk factors that contribute to the disease process: It is considered as an autoimmune response of the body, the underlying cause might be some gastro-intestinal or respiratory infection. People across every age can be affected, however it is observed that is more prevalent among young adults and the aged. Males stand at a higher risk of infection by Guillian-Barre syndrome, however children getting affected is least. The commonest cause of these infections is Campylobacter jejuni, but other organisms might be responsible for such infections: Epstein Barr virus, Mycoplasma pneumoniae and cytomegalovirus. Some findings also point out that HIV infection can lead to Guillian-Barre syndrome. Besides, certain vaccines, anesthesia and organ transplantations are also said to be among the reasons leading to the causes of Guillian-Barre syndrome. Vivid medical images of Guillian-Barre syndrome are available which are described as: acute inflammatory demyelinating polyradiculopathy (AIDP), acute motor axonal neuropathy (AMAN); acute motor sensory axonal neuropathy (AMSAN); Miller Fisher syndrome with ataxia, areflexia and ophthalmoplegia, that might manifest along with limb weakness, ptosis and facial and bulbar paralysis. (Kirsten et al, 2003).

Guillain-Barre syndrome could be linked with the risk factors stated hereunder in the opinion of Parrillo & Dellinger (2001): non-definite respiratory infections, non-definite gastrointestinal disease, and immunization with rabies vaccine (Simple rabbies brain rabies vaccine), a vaccine with a live vaccine virus, and the swine influence vaccine during 1976. Lynn et al (2003) confirmed that some of the dangerous factors could be Coxsackie virus, herpes simplex, hepatitis A, hyperthyroidism, hematologic malignancies and consumption of certain medications. In Guillain-Barre syndrome some pathological processes might be primary (a serious axonal loss) or secondary (inflammatory-demyelinative processes).

Pathological process initiate in the root of the nerve (generally motor nerve). The process comprises lymphocytes which infiltrate in the roots of the spine and peripheral nerves, and this procedure is normally accompanied with myelin loss. This myelin loss leads to various deficiencies and troubles associated with transmission of electric impulses of nerves (transmission interruption and maybe paralysis). In case the medical presence is acute, the patients might experience inflammation, interruption of axonal operation and loss of function. In certain instances, there is a possibility that the immune system to attach axons leading them to be devoid of their function. The antecedent illness might outcome in the body's immune system to trigger a response, and make the antibodies to react with the particular antigens that are at the moment in axon capsules, which implies that the antibodies might react with myelin leading to demyelization.

According to Kirsten and Richards (2003) a lot of symptoms are noticeable in Gullain-Barre syndrome which can differ in their veracity. The disease is characterized with weakness in the limbs along with areflexia that starts with lack of sensation in the fingers and toes, staying from seven to ten days. Additional symptoms that might happen are symmetric weakness in the motor nerves that might be increasing gradually and ascending (the weakness emanates from lower extremities), with some sensory deficiencies, paralysis in the face and weakness, opthalmoplegia, complains of burning ache, and visibility of several sensory symptoms.

Troubles associated with respiratory musculature have been seen as one of the symptoms of this ailment, and this weakness might lead to breakdown of respiratory function. Among the extremely acute symptoms of Gullain-Barre syndrome is malfunctioning of the autonomic nervous system. This malfunction can be the cause of heart problems (arrhythmia, fluctuations in blood pressure reading and pulse intensity), difficulties with sphincter (urine retention), papillary changes, and it might result in greater functioning of sweat glands (profuse sweating).

Medical procedures that are required to be performed on patients of Gullain-Barre syndrome are: lab analysis of cerebrospinal fluid, MRI (taking images of the anatomic changes in the nerves) and electrophysiologic tests (electromyographic tests and nerve conduction tests). Examination of cerebrospinal fluid is done through lumbar puncture which is a clinical method of drawing cerebrospinal fluid from the spinal cord through a needle insertion into the lower back of spinal cord. Following the lumbar puncture, the cerebrospinal fluid undergoes examination in the lab, to detect for irregular values of proteins and lymphocytes (a small amount is regarded as normal). Separate lab tests cover detecting the presence of antibodies due to C.Jejuni, cytomegalovirus, Epstain-Barr virus, M. Pneumoniae, alterations in the balance of several electrolytes and enzymes. Experiments that are directed on the nerve conditions are performed by electrical shocks which are applied in a lot of separate areas, through the skin, normally on the limbs, and the response of the nerve is noted down.

Electromyography (EMG) is an additional diagnostic method, and this is a clinical method wherein the electrical response of the muscle is being noted. (Parry, Steinberg, 2007). Electromyography results in Gullain-Barre syndrome might show an absent H reflex, low amplitude or lack of potential in sensory nerve, and erratic values of F wave. In lab tests higher values of protein are reported in cerebrospinal fluids. The proteins are more when the reading exceed 100mg/dL, and sometimes more than 1000mg/L. Due to this, the cerebrospinal fluid is not transparent any longer and changes to pale yellow. Possibility of presence of white blood cells (lymphocytes) is there, however a little rise of these cells in seen (in case of individuals having HIV infection this figure surges to 50 cells/ml of cerebrospinal fluid). In case of inflammation of meninges happens, presence of some inflammatory cells might be observed in the cerebrospinal fluid. However no other inflammatory cells are normally seen in the cerebrospinal fluid. But in case these are found, this must be the reason for apprehension and the preciseness of diagnosis will be doubted. The level of glucose is normal (49-80 mg/dL of cerebrospinal fluid), and it is never changed.

Additional lab tests which are performed are normal tests which can vouch the type of antecedent infection which resulted in the occurrence of Guillain-Barre syndrome. This is an attempt to locate which antibodies are being made by the immune system of the body, and which micro-organism is responsible for the generation of antibodies. At times, the biopsy of the nerve might be done; hence the portion of a nerve is picked and examined analytically. Clinical treatment of the Gullain-Barre syndrome and the treatment cover overall procedures, surgical procedures, symptomatic treatment and administration of medication. Normal procedures cover hospitalization (in case the patient is down with problems of respiratory system, unsteadiness of autonomic nervous system or additional health complexities).

It is important to check the ventilation and help in the breathing if needed, to closely look at the functioning of cardiovascular system and treatment of difficulties with arrhythmia or hypertension, and to assist patents to tide over the burning pain with several drugs (analgesic and higher dosage to control pain). In situations where the pain is recurrent and deep, it has been advocated by Wyckoff et al (2009) gabapentin (neurontin) and carbamazepine (tegretol) to be applied, alongwith some narcotics. Surgery might be done exclusively in situations where patient requires to be intubated by tracheotomy.

Symptomatic disease management is associated with treating additional symptoms which might happen as following symptoms of the ailment, and the therapies are being applied: supportive treatment, special nutrition plan, pulmonary treatment and support from the psychologist. Where the patient is affected with tracheotomy or lung weakness, feeding through a tube is needed, since it is the treatment of potential manifestation of depression or additional psychological malady.

The treatment which is administered are plasma exchange (200-250 cc/kg,) and intravenous administration of immunoglobulin (0.4 g/kg/day, for roughly five days), and the plasma exchange has been regarded to be the treatment of choice in case of Gullain-Barre syndrome. The plasma exchange implies that the blood of the patient having Gullain-Barre syndrome is drawn out from his body, and transmitted through several filters which are used to split the types of blood cells. The blood cells of a patient are suspended in artificial plasma or plasma extracted from a donor, and that plasma is returned to the body of the patient, with the anticipation that substances which cause harm to the myelin are taken out, while the plasma of the patient is being abandoned, since it possesses matter which may injure myelin.


Kimura, J. (2006). Peripheral nerve diseases. Elsevier Health Sciences.

Kirsten, J.C., Richards, M.R.C.P., Andrew, T., Cohen, F.R.C.A. (2003). Guillain-Barre syndrome. British Journal of Anaesthesia. Volume 3 Number 2, pp. 46-49.

Lynn , J.D., Newton, H.B., Rae-Grant , A.D. (2003). The 5-minute neurology consult. Lippincott Williams & Wilkins.

Parrillo, J. E., Dellinger, R. (2001). Critical care medicine: principles of diagnosis and management in the adult. Elsevier Health Sciences.

Parry, G.J., Steinberg, J.S. (2007). Guillain-Barre Syndrome: From Diagnosis to Recovery. Demos Medical Publishing.

Wyckoff, M., Wyckoff, M.M., Houghton, D., LePage, C.T. (2009). Critical care: concepts, role, and practice for the acute care nurse practitioner. Springer Publishing Company.

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