Guillain-Barré Syndrome (Continued)

The differential diagnosis for AIDP needs to be carefully considered because the classic electrophysiologic features are often not present early in the disease process. Acute spinal cord lesions may be confused with AIDP. Spinal cord lesions may cause rapidly progressive paralysis, but sensory examination usually demonstrates a spinal cord level. In a process involving only anterior horn cells, flaccid paralysis can occur, but with more extensive spinal cord injury, hyperreflexia and spasticity are seen. These upper motor neuron signs are often very helpful in distinguishing a spinal cord lesion from AIDP. However, in the acute state, these other features (e.g., hyperreflexia) may not be present. Spinal cord lesions also typically cause early bowel and bladder dysfunction. Back pain may be a feature of either disorder. If there is high clinical suspicion for a primary spinal cord injury, magnetic resonance imaging can be diagnostically helpful. Clinical findings in a number of toxic, metabolic, or infectious processes, including arsenic poisoning, may be very similar to those in the AIDP but should generally be able to be differentiated and should be considered very rare causes of polyneuropathy. A carefully documented history and appropriate laboratory studies usually point to the specific mechanism. Infectious diseases that should be considered include poliomyelitis, diphtheria, Lyme disease, West Nile infection, and human immunodeficiency virus (HIV). CSF pleocytosis should be a strong clue that the underlying process is infectious. The presence of a “bulls-eye” rash or presence in an endemic area should prompt evaluation for Lyme disease; Lyme serology and spinal fluid evaluation can be performed. West Nile exposure can be evaluated in blood or spinal fluid. As is the case with Lyme disease, markers for acute infection should be sought. An AIDP clinical picture can also be associated with acute HIV infection, which should be considered. Pupillary abnormality points to either diphtheria or botulism, both of which also have predominant bulbar symptoms. Acute intermittent porphyria (AIP) may mimic classic AIDP, and the patient should be questioned about use of any medication that could precipitate a porphyric crisis. Clues to an attack of AIP include a personal or family history of similar events, coexisting acute neuropsychiatric symptoms, and severe abdominal pain. Severe weakness can occur as part of a porphyric attack; the pathology is primarily axonal rather than demyelinating, although this distinction is difficult to establish in the acute setting; urine porphyrins can be tested if the clinical suspicion is high. The scalp and skin should be carefully examined to exclude the presence of a tick that could produce tick paralysis. Associated facial palsy may suggest sarcoidosis, whereas bulbar symptoms may also be seen with myasthenia gravis and rarely could mimic AIDP.

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