13. Antel zyxwvutsrqpon JP, Noronha ABC, Oger JJF, Arnason BGW. Immunology of amyotrophic lateral sclerosis. In: Rowland L, ed. Human motor neuron diseases. New York: Raven Press, zyxwvuts 1982:395-402. 14. Brown RJ Jr, Hauser SL, Harrington H, Weiner HL. Pilot trial of rosis. Arch Neurol 198643383-4. 15. Henderson CE, Taguchi T , Changeux JP, et al. Neurite-promot- ing factors for spinal neurons: inhibitory substances in muscle of patients with spinal muscular atrophy. Abstract. zy SOC Neurosci 1985;11:661. high dose cyclophosphamide-ACTH in amyotrophic lateral scle- Nitrous oxide: Clinical and electrophysiologic investigation of neurologic complications Eric J. Heyer, David Article abstract-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 devel- oped signs of a sensorimotor polyneuropathy and of myelopathy. Routine blood studies, CSF examination, and myelogram were normal. Clinical elec- trophysiologic studies were performed serially. Nerve conduction studies demon- strated 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 elec- trophysiologic studies demonstrated improvement. Nitrous oxide produces multi- focal reversible dysfunction within the nervous system similar to that described in patients with vitamin B,, deficiency. zyxw I I NEUROLOGY 1986;361618-1622 M. Simpson, Ivan Bodis-Wollner, and Sidney P. Diamond Exposure to nitrous oxide produces a well-described syndrome of neurologic symptoms and In gen- eral, neurologic complications arise with prolonged ex- posure, on the order of several months to years.* This contrasts with the limited exposure (on the -order of hours) required to produce bone marrow or hematologic change^.^^^ This difference may be based on the dif- ferent enzyme reactions blocked by nitrous oxide.7 We present the case of a patient who developed a toxic polyneuropathy and myelopathy from excessive inhalation of nitrous oxide. He was studied using clini- cal electrophysiologic tests at several stages of his dis- ease. Case report. Three months before admission, this 25-year- old student noticed intermittent paresthesias in his feet. Ten weeks before admission these sensations became more pro- nounced and persistent, and 7 weeks later he noticed similar sensations in his hands. At that time, he complained of a feeling of heaviness while walking, awkwardness in writing, and a sensation of “throbbing” radiating from his neck into both arms, precipitated with neck flexion. One week before admission, the abnormal sensation progressed rostrally up his trunk. He had increasing difficulty walking due to problems maintaining balance, and trouble standing with his eyes closed. There was no impairment of bowel or bladder function, although he complained of being unable to sense the end of a urinary stream. He could attain erections, although he was unable to ejaculate. The patient had had extensive exposure to nitrous oxide. For the previous 2’/2 years, he had inhaled nitrous oxide for recreational purposes, although he claimed that heavy use ended about 6 to 7 months before admission. During this period, he consumed about one to two boxes of nitrous oxide, each box containing 24 cartridges, two to three times a week. For the previous 6 to 7 months, he had only occasional expo- sure to nitrous oxide-twice for dental procedures and a few 1618 NEUROLOGY 36 December 1986 times for recreational use. At these latter times, he used about one box of nitrous oxide cartridges. His medications consist of methyldopa and Dyazide (a combination of triamterene and hydrochlorothiazide) for control of hypertension. He denied use of any vitamins. Neurologic examination was performed 1 week before ad- mission, at which time he had signs of sensorimotor poly- neuropathy with mildly decreased sensation to touch, pin, vibration, and position in his feet, and slightly decreased sensation to touch and pin in his fingers. There was weakness of extensor hallucis longus bilaterally (4 + /5), and ankle jerks were absent. At the time of admission there was, in addition, slight weakness of finger extensors (4 + /5), marked decrease ofposi- tion and vibration sensation in both legs, and a level to touch, pin, and vibration over the thorax at T-5. Touch and pinprick sensibility were decreased in his fingers, but cutaneous tem- perature sensation was intact throughout his body. Abdomi- nal reflexes and ankle jerks were absent but the other deep tendon reflexes were normal bilaterally. Plantar responses were flexor. He was unable to ambulate due to impaired coor- dination. Routine laboratory studies were performed and found to be normal. In addition, serum folate level (15 pg/l), thyroid func- tion tests, serum lead level, latex fixation, antinuclear anti- body, monospot test, and VDRL were normal. Skin sensitivity for mumps and zyxwv Candida antigens were reactive, and nonreac- tive for intermediate-strength tuberculin-purified protein. Bone marrow biopsy was nondiagnostic, Schilling test was normal, and deoxyuridine suppression test was normal. A gallium scan and abdominal sonogram showed no abnormal areas of uptake or organomegaly. Complete myelogram dem- onstrated no abnormalities, and CSF analysis was normal (cell count, 6 RBC/mm3, 3 WBC/mm3, all monocytes; protein 29 mg/dl; glucose 67 mg/dl; VDRL negative; cytology negative; oligoclonal bands not present; IgC synthetic rate was normal [lo%]). Repeat CSF examination results 2 weeks later were also normal.