Abstract

We report the first case of acute autonomic, motor and sensory neuropathy (AASMN) associated with meningoencephalitis. A 62-year-old man presented with fever, neck stiffness, and coma. Respiratory failure developed. Magnetic resonance images showed an abnormality in the medial temporal lobe. Cerebrospinal fluid analysis revealed pleocytosis with a high protein level. Intensive care gradually improved the consciousness level, but paralysis of the four extremities persisted. Nerve conduction studies revealed demyelinating sensory and motor polyneuropathy. Severe orthostatic hypotension, urinary retention, and constipation were also present. Clinical autonomic tests suggested both sympathetic and parasympathetic dysfunction. After intravenous immunoglobulin therapy, motor and sensory symptoms resolved rapidly; dysautonomia resolved gradually over the next 2 months. The response to immunological therapy and the presence of antecedent infection suggest that AASMN is a postinfectious, immune-mediated, autonomic, sensory and motor nervous system dysfunction.

Highlights

  • Acute autonomic, motor and sensory neuropathy (AASMN) is a relatively new clinical entity and a rare neuromuscular disorder, characterized by prominent dysautonomia with somatic motor and sensory involvement.[1]

  • AASMN has been categorized as a variant form of acute autonomic and sensory neuropathy or as Guillain-Barré syndrome (GBS) with dysautonomia.[1]

  • We report here the first case of AASMN associated with antecedent meningoencephalitis

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Summary

Introduction

Motor and sensory neuropathy (AASMN) is a relatively new clinical entity and a rare neuromuscular disorder, characterized by prominent dysautonomia with somatic motor and sensory involvement.[1]. He received intravenous immunoglobulin (IVIg) therapy, and the motor and sensory disturbances resolved rapidly, followed by a gradual improvement in dysautonomia. Neurologic examinations revealed nuchal stiffness, but muscle strength and deep tendon reflexes were normal. One month after symptom onset, he became alert, and repeated CSF examinations revealed no leukocytes, with a normal protein level (56 mg/dl).

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Conclusion
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