| Abstract: |
Background: Guillain-Barré Syndrome (GBS) is an Acute Inflammatory Demyelinating Polyneuropathy (AIDP), an autoimmune disorder affecting the peripheral nervous system, usually triggered by an acute infectious process. It is included in the wider group of peripheral neuropathies. There are several types of GBS, but unless otherwise stated, GBS refers to the most common form, AIDP. It is frequently severe and usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. With prompt treatment by plasmapheresis or intravenous immunoglobulins and supportive care, the majority of patients will regain full functional capacity. However, death may occur if severe pulmonary complications and dysautonomia are present. The disorder is characterized by weakness which affects the lower limbs first, and rapidly progresses in an ascending fashion. Patients generally notice weakness in their legs, manifesting as ”rubbery legs” or legs that tend to buckle, with or without dysesthesias. As the weakness progresses upward, usually over periods of hours to days, the arms and facial muscles also become affected. Frequently, the lower cranial nerves may be affected, leading to bulbar weakness and respiratory difficulties. Most patients require hospitalization and about 30% require ventilatory assistance. Facial weakness is also commonly a feature, but eye movement abnormalities are not commonly seen in ascending GBS, but are a prominent feature in the Miller-Fisher variant. Sensory loss, if present, usually takes the form of loss of proprioception and areflexia, an important feature of GBS. Loss of pain and temperature sensation is usually mild. In fact, pain is a common symptom in GBS, presenting as deep aching pain, usually in the weakened muscles, which patients compare to the pain from overexercising. These pains are self-limited and should be treated with standard analgesics. Bladder dysfunction may occur in severe cases but should be transient. If severe, spinal cord disorder should be suspected. The diagnosis of GBS usually depends on findings such as rapid development of muscle paralysis, areflexia, absence of fever, and a likely inciting event. CSF and ECD is used almost every time to verify symptoms, but because of the acute nature of the disorder, they may not become abnormal until after the first week of onset of signs and symptoms.There currently is no cure for Guillain-Barre syndrome. However, treatments have been proven effective against this syndrome. Typical CSF findings include albumino-cytological dissociation. As opposed to infectious causes, this is an elevated protein level, without an accompanying pleocytosis. A sustained pleocytosis may indicate an alternative diagnosis such as infection. Electromyography (EMG) and Nerve Conduction Study (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing. Supportive care with monitoring of all vital functions is the cornerstone of successful management in the acute patient. Of greatest concern is respiratory failure due to paralysis of the diaphragm. Early intubation should be considered in any patient with a Vital Capacity (VC) <20 ml/kg, a Negative Inspiratory Force (NIF) < -25 cmH2O, more than 30% decrease in either VC or NIF within 24 hours, rapid progression of disorder, or autonomic instability.Objectives: The aim of this study is to discuss Guillian –Barre syndrome: definition, aetiology, manifestations, differential diagnosis, investigations and possible lines of treatment.
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