Nitrous oxide: clinical and electrophysiologic investigation of neurologic complications.
Prolonged exposure to nitrous oxide produces a recognized neurologic syndrome. We report clinical and electrophysiologic studies of nervous system involvement in a 25-year-old student who abused nitrous oxide. He developed signs of a sensorimotor polyneuropathy and of myelopathy. Routine blood studies, CSF examination, and myelogram were normal. Clinical electrophysiologic studies were performed serially. Nerve conduction studies demonstrated reduced amplitude and slowed sensory potentials, and mildly prolonged late responses. Sensory evoked potentials revealed prolonged latency of scalp-evoked potentials from tibial nerve stimulation with normal median nerve values. The foveal visual evoked potential was delayed in the right eye, with normal visual acuity, funduscopic examination, and spatial contrast sensitivity. Repeat electrophysiologic studies demonstrated improvement. Nitrous oxide produces multifocal reversible dysfunction within the nervous system similar to that described in patients with vitamin B12 deficiency.
D000328:Adult; D005073:Evoked Potentials, Somatosensory; D005074:Evoked Potentials, Visual; D006801:Humans; D008297:Male; D008475:Median Nerve / Q000503:physiopathology; D009422:Nervous System Diseases / Q000139:chemically induced / Q000209:etiology* / Q000503:physiopathology; D009431:Neural Conduction; D009609:Nitrous Oxide / Q000009:adverse effects; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced / Q000209:etiology / Q000503:physiopathology; D013118:Spinal Cord Diseases / Q000139:chemically induced / Q000209:etiology / Q000503:physiopathology; D019966:Substance-Related Disorders / Q000150:complications*; D013979:Tibial Nerve / Q000503:physiopathology; D014806:Vitamin B 12 Deficiency / Q000503:physiopathology
D009609:Nitrous Oxide