A 20-year-old woman presented with progressive paresthesia in her legs and hands, and unsteady gait for 15 days. She had inhaled N2O about 100–200 whipped cream chargers many times daily, for recreational purposes for at least one year. Neuropsychological test showed mild impairment of the cognition, and the Mini mental state examination (MMSE) score was 23. The deficit domains of the MMSE included orientation (minus 3 scores), attention and calculation (minus 4 scores). Neurological examination revealed distal slight weakness, decreased vibration and proprioception, bilateral hyporeflexia, sensory ataxia, positive Babinski sign and Romberg sign.
Laboratory tests revealed decreased level of folic acid (4.40 ng/ml, reference range > 5.4 ng/ml), but the others were normal, including red blood cell, hemoglobin, mean corpuscular volume, serum vitamin B12 (800 pg/ml, reference range 211–911 pg/ml) and homocysteine (8μmmol/L, reference range 0-15 μmol/L). The antibodies of human immunodeficiency virus and neurosyphilis were negative. The results of cerebrospinal fluid test (CSF) were normal for leucocyte count (5/L, reference range 0–8/L), glucose (3.1 mmol/L, reference range 2.5–4.5 mmol/L), and protein concentration (33 mg/dl, reference range 15–45 mg/dl). The inflammatory, immune and infectious biomarkers of both CSF and serum were also unremarkable.
The cranial MRI yielded normal findings. The spinal cord MRI showed abnormal longitudinally extensive T2 weighted hyperintensities involving the posterior columns from C1 through T12, with inverted V or “rabbit ears” sign on cervical spinal MRI, but without contrast enhancement (Figs. 1 and 2). Electromyography showed multiple peripheral neurogenic damage, also with decreased nerve conduction velocity and abnormal somatosensory evoked potential. However, visual evoked potential showed normal response.
Three months later, with a high dose of supplementation of intramuscular vitamin B12 injections (1 mg per day) and the cessation of N2O exposure, the symptoms of sensation and gait resolved markedly, and the cognitive function fully recovered (MMSE 30). The abnormal hyperintensities of spinal MRI also dissolved with three months’ follow up (Figs. 3 and 4). The diagnosis of N2O induced SCD was supported by clinical history, clinical manifestations, MRI findings, the distinct relationship between N2O exposure, also with the favorable prognosis by the vitamin B12 supplementation.