Answer 4 for NRS 455 Identify a common perceptual, neurological, or cognitive issue and discuss contributing factors Guillain-Barré syndrome

 GBS is thought to be triggered by an immune response to preceding infection that results in cross reaction with the peripheral nerves, in a process likely secondary to molecule mimicry. All myelinated nerves (motor, sensory, cranial, sympathetic) can be affected. GBS has different variants, which have different type and degree of pathological changes (Ogbebor et al, 2023). The variants of GBS include the following:

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• Acute inflammatory demyelinating polyneuropathy (AIDP)
• Acute motor axonal neuropathy (AMAN)
• Acute motor and sensory axonal neuropathy (AMSAN)
• Miller Fisher syndrome (MFS)
• Bickerstaff brainstem encephalitis (BBE)
• Pharyngeal-cervical-brachial (PCB) variants

AIDP displays prominent demyelination on electrodiagnostic studies and lymphocytic infiltrate on nerve biopsy. Similarly, demyelination is thought to be the underlying pathology in MFS and BBE variant. AMAN and AMSAN have prominent axonal loss without lymphocytic infiltrate or complement activation. In recovery, remyelination occurs over several weeks to months. Depending upon the extent and severity of the inflammatory response, axonal degeneration can also occur; in such patients, there is delayed and incomplete recovery. Antibody- and complement-mediated humeral response against axons leads to axonal variant of GBS (AMAN, AMSAN). In axonal variant, there is a paucity of inflammatory infiltrate and the primary immune response is directed at nodes of Ranvier. This leads to nerve conduction block, which presents as motor or sensory symptoms. This process can reverse rapidly or may progress to involve axonal degeneration. Two-thirds of patients provide a history of an antecedent respiratory tract or gastrointestinal tract infection that occurred usually within 4 weeks before presenting with symptoms of GBS. Infection with Campylobacter jejuni is the most common antecedent in GBS. Infection by C jejuni can lead to generation of antibodies to specific gangliosides, including GM1, GD1a, and GD1b, which are present in the peripheral nerve axons. These antibodies are strongly associated with AMAN and AMSAN. Antibodies against GQ1b ganglioside, a component of oculomotor nerve myelin, are frequently found in GBS variants MFS and BBE. Antibodies to GT1a, which cross-react with GQ1b, have also been associated with bulbar forms of GBS. Patients present within a few days to a week after the onset of symptoms. Symptoms typically progress over a period of 2 weeks and reach their nadir by 4 weeks. Some instances of GBS have followed vaccination, but the associated risks appear small or negligible, while other studies have failed to find an association between vaccination and subsequent GBS risk. The risk of GBS after vaccination appears substantially lower than the risk of GBS triggered by an acute infection (Shahrizaila , 2021). In Western countries, the incidence of GBS is approximately 1 to 2 cases per 100 000 person-years. After the first decade of life, the incidence of GBS increases by 20% for every 10-year increase in age, with a higher prevalence observed in males than in females. The incidence of different GBS variants is different across different geographical regions. In the United States, AIDP is the most common variant accounting up to 90% of the cases while AMAN, AMSAN, MFS, and BBE account for approximately 5% to 10% of the cases in the United States. Overall, patients with the axonal variants of GBS are younger than patients with demyelination variants.

 Clinical Features

The typical clinical features of GBS include a progressive and symmetric muscle weakness, usually ascending in nature, and absent or depressed deep tendon reflexes. Different variants of GBS can have different presentations and symptoms including sensory symptoms of pain, paresthesia, ophthalmoplegia, ataxia, encephalopathy, bulbar signs, and dysautonomia. Autonomic dysfunction occurs in 38% to 70% of patients with GBS. This includes ileus, hypertension, hypotension, fever, tachycardia, bradycardia, and urinary retention. Patients with dysautonomia tend to have more frequent cardiogenic complications, hyponatremia, and a higher morbidity and mortality with the possibility of sudden death. GBS with isolated sensory abnormalities is rare. In such cases, the reflexes are absent and there may be minor motor involvement. An association with antibodies to GD1b has been noted. Patients with suspected sensory GBS should be evaluated for acute paraneoplastic sensory neuropathy, which presents with asymmetric sensory loss and severe ataxia.

Health Education and Promotion

Health education is critical throughout the course of GBS. In the initial acute phase of GBS, the nurse should educate both the patient and family members about GBS including th