• T Shimizu, Y Nishimura, Y Fujishima, H Miyajima, and N Honda.
• Rinsho Shinkeigaku. 1989 Sep 1; 29 (9): 1129-35.

AbstractWe have experienced a case of myeloneuropathy following habitual abuse of nitrous oxide. We report clinical and pathological findings of this case with review of literatures. A 36-year-old dentist was first admitted to our hospital on August 17, 1983 because of numbness of both lower legs and unsteady gait. He had recreationally inhaled nitrous oxide 30 to 60 minutes everyday since a year ago. Neurological examination showed ataxic broad-based gait, moderate loss of pain and touch sensation in the lower limbs up to patella. Position and vibratory senses were more severely impaired. Deep tendon reflexes increased in the upper extremities and at the knees, but diminished at ankle jerks. Muscle strength was normal. Prominent Lhermitte's sign was present. Except for reduced serum vitamin B12 level, laboratory results were normal. Needle electromyography showed high amplitude and long duration NMU in the right quadriceps and anterior tibial muscles. Motor nerve conduction velocity was 34 m/sec at the right posterior tibial nerve and could not be detected at the left. Sural nerve biopsy was performed. The density of the myelinated fibre measured on transverse section was in normal range but degenerated fibres were occasionally recognized. Single teased nerve fibre showed various degree of myelin ovoid along the fibre. Myelin loss was shown to occur in some parts of the fibre. Electron microscopy showed myelin splitting and formation of intramyelinic vacuoles containing myelin debris. Axon was almost normal at least in the early stage of degeneration. Later, axon disappeared with destruction of myelin sheath. These nerve changes largely demonstrated demyelination but it was occasionally accompanied with axonal degeneration.(ABSTRACT TRUNCATED AT 250 WORDS)

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