![]() ![]() It is essential that contrast is administered if the diagnosis is suspected as non-contrast sequences are essentially normal 2. Radiological studies are requested to exclude other causes and in cases where nerve conduction studies and CSF examination are equivocal. MRI of the spine is most useful, helping to exclude other etiologies, such as transverse myelitis and compressive causes of polyradiculopathy. Nerve conduction abnormalities include slow or blocked nerve conduction, prolongation of distal latency, and f-waves.Ĭhronic inflammatory demyelinating polyneuropathy (CIDP) is considered the chronic counterpart to Guillain-Barré syndrome. ![]() ![]() Guillain-Barré syndrome is diagnosed by the combination of clinical presentation, CSF study, and electrophysiological criteria.ĬSF abnormalities are characterized by increased protein without pleocytosis, which is a non-specific finding, seen in many of the conditions which mimic GBS on imaging and clinically 1,2. anti-GQ1b antibodies are present in most cases.characterized by ataxia, ophthalmoplegia, and areflexia without weakness.both axonal subtypes are thought to be due to antibodies to gangliosides which result in macrophages invading the axons at the nodes of Ranvier 3.acute motor-sensory axonal neuropathy (AMSAN).acute motor axonal neuropathy (AMAN) (historically Chinese paralytic syndrome).acute inflammatory demyelinating polyradiculoneuropathy (AIDP).Several subtypes have been described including: The classical presentation of Guillain-Barré syndrome includes symmetrical ascending muscle paresis/paralysis, areflexia/hyporeflexia, and variable sensory or autonomic involvement. ![]()
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