Serum copper decrease and cerebellar atrophy in patients with nitrous oxide-induced subacute combined degeneration: two cases report

Jie Cao,Zhijun Li,Lusen Ran,Chenchen Liu

doi:10.1186/s12883-021-02496-y

Jie Cao, Zhijun Li + Show 2 more

Open Access

https://doi.org/10.1186/s12883-021-02496-y

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Abstract

BackgroundSubacute combined degeneration (SCD) is a neurological complication commonly associated with vitamin B12 deficiency. It can result from nitrous oxide (N2O) abuse and cause neuropsychiatric symptoms. However, there has been no literature regarding alterations of serum copper and cerebellum in SCD patients.Case presentationWe reported two cases of young SCD patients with histories of N2O abuse. In these cases, elevated homocysteine, macrocytic anemia, spinal cord abnormalities, and peripheral nerve injuries were detected. In addition, decreased serum copper level and cerebellar atrophy were reported for the first time. The patients’ symptoms improved after withdrawal of N2O exposure and vitamin B12 supplements.ConclusionWe reported two SCD cases with serum copper alteration and cerebellar atrophy after N2O abuse for the first time. These might be crucial complements to the diagnosis of SCD.

Highlights

Subacute combined degeneration (SCD) is a neurological complication commonly associated with vitamin B12 deficiency
For the first time, we report two cases of SCD patients induced by nitrous oxide (N2O) abuse with decreased cupric ion and cerebellar atrophy, intending to explore new clinical features of the disease
Serum vitamin B 12 is a most convenient and accessible laboratory approach to evaluate cobalamin deficiency, it is to note that quite a few SCD patients are detected with normal or elevated serum vitamin B12 [14,15,16,17]

Summary

Introduction

Subacute combined degeneration (SCD) is a neurological complication commonly associated with vitamin B12 deficiency. For the first time, we report two cases of SCD patients induced by N2O abuse with decreased cupric ion and cerebellar atrophy, intending to explore new clinical features of the disease. Laboratory examinations showed increased serum vitamin B12 (>1525 pg/mL, normal range 180–914 pg/ mL) and decreased folic acid (3.54 ng/mL, normal range > 4.00 ng/mL) levels.

Results

Conclusion