Table of Contents
Guillain-Barre Syndrome is composed of four types of mild secondary neuropathy. The first subtype is the acute inflammatory demyelinating polyradiculoneuropathy. It is characterized by symptoms associated with autoimmune neuritis that is mainly caused by advancements made in T-cells against impeding peptides. Second, there are the acute motor axonal neuropathy and motor sensory axonal neuropathy which are caused by immediate alterations of the antibodies present in the axolemma section of the macrophages (Hughes and Cornblath, 2005). Third, there is the Fisher’s syndrome which is caused by immediate alterations to the antibodies associated with GQ1b present within the C. jejuni walls of the ganglioside structures. Thus, the purpose of this paper is to examine Guillain-Barre Syndrome in its clinical context in order to include report associated with diagnosis, treatment and prognosis in that matter.
Guillain-Barre Syndrome was first described by Jean Baptiste Octave Landry de Thezillat in 1859. He described it as acute ascending paralysis. In due course, the acute paralysis was depicted as having dust-bin characteristics so that it was associated with such conditions as myelitis and marginal neuritis. Despite his attention towards the disease, he died from it at 39 years of age. In 1916, Guillan, Barre and Strohl provided a presentation to the Paris hospitals postulating that there were soldiers who recovered from the mild form of paralysis (Hughes and Cornblath, 2005). They later conducted extensive research in order to ascertain the root causes of the cure for the disease. They specifically put much emphasis on lumbar puncture technique of curing the condition with positive results. Nowadays, the presentation of albumin-cytological dissociation has been used extensively to identify Guillain-Barre Syndrome from other poliomyelitis conditions.
Global occurrence of Guillain-Barre Syndrome has been determined at 0.6 to 4 cases per 100,000 in any given year (Hughes & Cornblath, 2005). In Europe, the statistics is placed at 1.2-1.9 per 100,000 people within any given year. There are fewer cases of Fisher’s syndrome given that Italian researchers have placed the figure at 0.1 per 100,000 people within any given year. In respect to gender, it is ascertained that males are 1.5 times likely to suffer from the condition in comparison to their female counterparts. In Asia, the disease is commonly associated with children, as opposed to adults. The annual incidence for adults within any given year is placed at 0.66 per 100,000 people (Hughes & Cornblath, 2005).
In both the Caribbean island and Curacao, the research conducted indicates that there has been a sharp increase in the occurrence of the condition from 1.62 in the period between 1987 and 1991 to about 3.2 per 100,000 people in the period between 1992 and 1999(Hughes & Cornblath, 2005). Notably, it is ascertained that cases of the disease have continued to be sporadic given that populations, throughout the globe, are exposed to bacterium enteritis, which is caused by immediate contamination of water, and other C. jejuni related illnesses (Hughes & Cornblath, 2005).
Accordingly, the disease has been associated with certain vaccines as influenza immunizations. This association was formulated in the course of swine flu immunization period in the USA in 1976. However, recent studies have shown that the disease is not in any way associated with the influenza vaccines administered in the period between 1990 and 2003(Hughes & Cornblath, 2005). Consequently, rabies vaccine that is attributed with significant brain material causes mild Guillain-Barre Syndrome in a case of 1 per 1000 cases reported globally (Hughes and Cornblath, 2005).
For experienced neurologists, the process of identifying the disease amongst patients is fairly-conducted. However, for a new doctor who has recently graduated from medical school the process of identifying the disease is challenging. Notwithstanding, the disease has a complete set of test criteria that have stood positive over a substantial time. Doctors evaluate patients with the following symptoms in order to ascertain the presence of Guillain-Barre Syndrome; the first symptom is attributed with mild neuropathy, which should reach its peak, in a period of between 4 and 5 weeks. Second, the patient should suffer from weakened form of hyporeflexia or areflexia. Third, the patients should exhibit high-levels of protein concentrations especially in the CSF (Hughes & Cornblath, 2005).
The first process of diagnosing the disease is for the presiding doctor to identify the existence of mild marginal neuropathy and not conus lesions as the causes of Guillain-Barre Syndrome. For patients who lack sensory features, doctors are advised to look-out for such disorders as poliomyelitis, botulism and mild myopathy. In other cases, it has been noted that Hypokalemia has been often missed as a form of diagnosis alternative. In case of mild marginal neuropathy identification, doctors are encouraged to establish the likelihood of Guillain-Barre Syndrome together with other alternative diagnosis as vasculitis and tick paralysis. For Fisher’s syndrome, the disease is diagnosed by the presence of mild brainstem lesions (Hughes & Cornblath, 2005).
In case of Guillain-Barre Syndrome, the onset period has been defined to last for up-to 4 weeks. However, its diagnosis overlaps with that of CIDP so that about 8 % to 16 % of the patients are presented as having episodes of unfair initial improvements (Hughes & Cornblath, 2005). In a recent study conducted, it was established that patients who depicted deterioration symptoms after 9 weeks of the disease onset period were likely to develop CIDP (Hughes & Cornblath, 2005).
There are two basic ways of investigating the disease. These are both the neurophysiological testing and lumbar puncture. Accordingly, higher-levels of protein concentrations are identified in about 80 % of the patients (Hughes & Cornblath, 2005). However, the CSF protein is considered to be lower in the course of onset period of illness. It is stated that CSF should be evaluated by the doctor before the initiation of the treatment process using immunoglobulin which is likely to cause aseptic meningitis. Further research is encouraged in order to provide a basis for excluding similar causes of the disease (Hughes & Cornblath, 2005).
The typical pathological representation of Guillain-Barre Syndrome is multifocal mononuclear cell permeation within the marginal nervous system. It should be noted that, at this point, the distribution of cell inflammation is similar to the resultant clinical deficit. Notably, the macrophages are depicted as having invaded the healthy myelin sheaths and the immediate denuded axons. This medical happening occurs within the experimental autoimmune neuritis (Hughes & Cornblath, 2005). It is stated that the invasion of Schwann cells original membrane is caused by processes involved with matrix metalloproteinase, or activated toxic nitric oxide components released by damaged macrophages. Therefore, the pathological process occurs whenever antibodies are bound on the exterior of Schwann cells, binding of relevant complement, and possible intense damage to the Schwann cell (Hughes & Cornblath, 2005).
The basic symptoms of the disease are intense pain, paraesthesia or in some cases immense levels of weakness within the patients’ limbs. The resultant weakness is either proximal or distal in nature. In extreme Guillain-Barre Syndrome cases, both of the aforementioned natures are possible (Kuwabara et al., 2004). Pain is a profound visible symptom amongst children. Additionally, children depict distorted facial nerves in comparison to either motor or ocular nerves. In cases of automatic involvement, there is urine retention as well as postural hypotension. Severe cases are presented with mass muscle wastage after two weeks of illness. Recovery takes about four weeks as patients regain strength. Statistically, about 4 % to 15 % of the affected patients die, and another 20 % are disabled completely despite the administration of modern treatment (Hughes & Cornblath, 2005).
Recent evidence-based research indicates that the elderly patients are the most-affected. In children, recovery is likely to take place quick and is entirely complete while death is considered to be exceptional. In both children and adults, Guillain-Barre Syndrome is considered to be bedbound and requires artificial forms of ventilation (Hughes & Cornblath, 2005). It is also ascertained that patients with quick onset period are more likely to react negatively in comparison to their slower counterparts. Patients who show improvement within a 14-day period are likely to cure without treatment but may undergo mild disability malfunctions. Patients who have either suffered diarrheal illnesses or C. jejuni experience severe effects of the disease and are likely to respond poorly to treatment hence slower recovery (Hughes & Cornblath, 2005).
Recent research conducted postulates that multidisciplinary levels of care are needed in the process of both prevention and management of Guillain-Barre Syndrome from getting complicated. Patients who exhibit severe cases of the disease should be subjected to intensive therapy session in order to catapult prophylactic intubation. These patients should also be evaluated and monitored for possible cardiac arrhythmia (Hughes & Cornblath, 2005). In adults, comprehension stockings and subcutaneous heparin should be administered in order to prevent deep vein thrombosis amongst the patients. Immunizations are also possible treatment ways for the disease. In this case, tetanus toxoid is administered to suppress the possibility of the syndrome altogether.