Botulism Mimicking Miller Fisher Syndrome

PRACTICAL IMPLICATIONS

Consider botulism in the differential diagnosis of Miller Fisher syndrome, the pharyngeal-cervical variant of Guillain-Barré syndrome, and myasthenia gravis, as time-dependent treatment can dramatically improve patient outcomes.

We describe a case of food-borne botulism whose initial presentation evoked Miller Fisher syndrome.

A 53-year-old woman with a medical history of psoriatic arthritis presented to our emergency department with vomiting and progressive diplopia over the prior 4 days; she also experienced inability to swallow and constipation. Neurologic examination showed diplopia, bilateral ptosis, dysphonia, and bilateral facial palsy. Her pupils' size was normal. Her motor and sensory examinations were normal. Deep tendon reflexes were mildly decreased. We considered Miller Fisher syndrome most likely in the differential diagnosis, but a neuromuscular junction disorder, such as myasthenia gravis or Lyme disease, could not be excluded.^1–3 We performed brain MRI to exclude CNS involvement. Laboratory blood tests, including autoimmunity, acetylcholine receptor antibody, and Lyme test, were unremarkable.⁴ The lumbar puncture was performed with no findings of albumin cytologic dissociation; however, we started empirical treatment with IV immunoglobulin (0.4 g/kg for 5 days). Nerve conduction studies and EMG tests were performed. Motor and sensory conduction were normal (except for small M-wave amplitudes and the presence of short bursts of low-voltage compound motor units and excessive action potentials) as well as F-wave latencies.⁵ Repetitive nerve stimulation (RNS) resulted in an incremental response from baseline of the compound muscle action potential. Furthermore, the incremental response was greater at higher frequencies (30 and 50 Hz) documenting a neuromuscular presynaptic disorder of which botulism was the most likely cause. In contrast, RNS in myasthenia gravis demonstrates a progressive decline in compound muscle action potential amplitude.⁶ Reviewing her recent medical history, the patient said that she ate cooked vegetables stored in a tin can a week before hospitalization. Because botulinum toxin can be detected in the serum up to 12 days following ingestion, in addition to identified in stool, vomit, and/or suspected food sources, stool and blood samples were obtained to screen for Clostridium botulinum.⁷ Botulism antitoxin was administered to the patient 24 hours after her admission without clinical worsening or side effects. Blood and stool tests confirmed the diagnosis of botulism a week later; AChR, anti-Musk, and Gq1b antibodies were negative. After 9 days, the patient was discharged home in a good health condition. At follow-up, 6 months later, she was fully recovered.

Appendix. Authors

Study Funding

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