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Abstract Details

Case series on Nitrous Oxide Toxicity
Neuromuscular and Clinical Neurophysiology (EMG)
P3 - Poster Session 3 (5:30 PM-6:30 PM)
12-024

Describe N2O toxicity. 

Nitrous oxide (N2O) is widely available as a propellant in canisters of whipped cream, as an automobile power booster, or as a sedative agent for surgical procedures.  N2O abuse can result in pathology of the central and/or peripheral nervous system, with spinal cord involvement most commonly reported.

We performed a chart review of patients at our institution with (N2O) toxicity who developed peripheral neuropathy and had an electromyography (EMG)/nerve conduction study (NCS) done between 2013-2018.  We identified three patients and wanted to characterize their clinical and electrodiagnostic findings.

All patients were males in their early 20s. Two patients endorsed inhaling automotive grade N2O. All patients reported a symmetric ascending pattern of sensory loss with lower extremity weakness over a course of more than four weeks duration. On neurological examination, all patients had preferential ankle dorsi-flexor weakness, with profound weakness in two of the patients.  Two patients were areflexic in the lower extremities while the third had normal reflexes. All patients were noted to have elevated methyl malonic acid and homocysteine levels, but only 2 patients showed low B12 levels.   Cerebrospinal fluid studies were normal in the two patients checked.  Nerve conduction studies revealed low amplitude sensory responses in a length dependent pattern. All patients had normal upper extremity motor amplitudes, yet absent or nearly absent peroneal motor responses, and active denervation changes on electromyography. Upper extremity F-waves were normal in one patient, prolonged in another, and absent in the third.  

This case series highlights the fact that patients with N2O toxicity can present with predominately peripheral nervous system pathology, a lack of myelopathic signs, and in some instances with very severe lower extremity weakness yet intact upper extremity strength.   The electrodiagnostic pattern was found to be primarily an axonal, length, dependent sensorimotor polyneuropathy with variable demyelinating features.

Authors/Disclosures
Haoming Pang, MD (University of South Florida, Tampa General Hospital)
PRESENTER
Dr. Pang has nothing to disclose.
Bhavesh Trikamji, MD (University of California Los Angeles) Dr. Trikamji has nothing to disclose.
Luis A. Chui, MD No disclosure on file
Margaret Adler, MD (Harbor UCLA Department of Neurology) Dr. Adler has nothing to disclose.