Clinical, Electrophysiological and Radiological Features of Nitrous Oxide-Induced Neurological Disorders

Abstract

Purpose: We summarized the clinical manifestations, laboratory and electrodiagnostic characteristics and magnetic resonance imaging (MRI) findings of nitrous oxide (N₂O) abuse-induced neurological disorders.

Patients and methods: We retrospectively reviewed 33 patients with N₂O abuse-induced neurological disorders and reported their demographic data, clinical manifestations, laboratory examinations, nerve conduction studies, together with spinal and brain MRI.

Results: The most frequent clinical manifestations included numbness and weakness in the extremities and unspecified gait disturbance. Low serum vitamin B₁₂ levels were found in 9 patients, and high homocysteine levels were noted in 27 patients. Nerve conduction studies showed a sensory-motor neuropathy. Sixteen patients showed bilateral high-intensity T2 signal within the posterior column on spinal MRI, and four patients showed cerebral white matter lesions on brain MRI.

Conclusion: N₂O abuse has become a significant public health problem because of the severe neurological disorders related to chronic abuse. Clinical physicians should be aware of the toxic effects of N₂O.

Keywords: neurological disorders; neuropathy; nitrous oxide; subacute combined degeneration; vitamin B12.

Figure 1

Motor nerve conduction study results in the health control (HC) and N₂O abuse groups. (A) The compound muscle action potential amplitude, (B) motor conduction velocity, (C) distal latency, and (D) F-wave latency of each motor nerve for the HC (grey bar) and N₂O-abuse (black bar) groups. Notes: Data are presented as mean ± standard error of the mean. Significant difference is indicated by **p < 0.01; ***p < 0.001. Abbreviations: M, median nerve; U, ulnar nerve; P, peroneal nerve; T, tibial nerve.

Figure 2

Sensory nerve conduction study results in the health control (HC) and N₂O-abuse groups. (A) The sensory nerve action potential amplitude and (B) sensory conduction velocity of each sensory nerve for the HC (gray bar) and N₂O-abuse (black bar) groups. Notes: Data are presented as mean ± standard error of the mean. Significant differences are indicated by **p < 0.01; ***p < 0.001. Abbreviations: M, median nerve; U, ulnar nerve; S, sural nerve.

Figure 3

Spinal cord MRI of a N₂O-abuse patient who complained of unsteadiness while walking and limb numbness for 2 weeks. (A) Sagittal T2 MRI of the cervical spine demonstrating a high-signal lesion representing demyelination C2-C6. (B) Axial T2 MRI of the cervical spine shows hyperintense, symmetric and inverted V-shaped signals involving the dorsal columns of C2-C6. (C) Gadolinium-enhanced T1 MRI reveals the enhancement of the dorsal columns. (D) Gadolinium-enhanced axial T1 MRI shows a V-shaped enhancement of the dorsal columns.

Figure 4

The distribution of lesions detected in the spinal cord of N₂O-abuse patients. The cervical spinal cord was more frequently impaired than other areas of the spinal cord. C3, C4 and C5 were the most common affected vertebral level.

Figure 5

Axial fluid-attenuated inversion recovery (FLAIR) scan of a N₂O-abused patient who complained of memory decline for 1 month. (A and B) showed mild white matter lesions in periventricular regions.