Subacute Combined Degeneration of the Spinal Cord Secondary to Nitrous Oxide Abuse

Abstract

Here, we report a case of subacute combined degeneration (SCD) of the spinal cord in the setting of nitrous oxide poisoning seen at the Medical Ward, Queen Elizabeth Hospital Birmingham Our patient was a 28-yearold lady who presented with impaired sensations in the lower limbs and difficulty walking for approximately one and a half months. Her clinical symptoms did not match common neurological conditions. Upon detailed history, she revealed that she had been frequently using nitrous oxide recreationally for several years. Although her baseline investigations were normal, her magnetic resonance imaging (MRI) of the spine showed bilateral symmetrical T2 hyperintense signal changes in the dorsal columns extending from C2 to C6 spinal segment. Based on history, clinical findings, and MRI of the cervical spine, the diagnosis of SCD of the spinal cord was made, and her symptoms fully resolved with treatment.

Nitrous Oxide as an Emerging Cause of Subacute Combined Degeneration and Polyneuropathy: A Two-Case Report

“…The clinical presentation of our cases is similar to that of cases previously described by other authors [ 3 , 10 , 11 , 13 , 14 , 18 , 19 ]. They exhibit certain characteristics that need to be highlighted.…”

“…N 2 O induces irreversible inhibition of vitamin B 12 . This is due to the oxidation of cobalt, which is part of vitamin B 12 , converting it from its monovalent active form (Co + ) to its inactive divalent (Co 2+ ) or trivalent (Co 3+ ) forms [ 11 - 13 ]. Under normal conditions, vitamin B 12 acts as a coenzyme for two important enzymes.…”

“…Under normal conditions, vitamin B 12 acts as a coenzyme for two important enzymes. In its methyl-cobalamin form, it acts as a coenzyme of methionine synthase, and in its adenosyl-cobalamin form, it participates as a coenzyme of methylmalonyl-CoA mutase [ 11 , 13 ].…”

“…The failure of this pathway leads to the accumulation of methylmalonyl-CoA and propionyl-CoA, which retrogradely induces an increase in odd-chain and branched-chain fatty acids that accumulate in the lipids of the membranes of the nervous system. Changes in the fatty acid composition of myelin can alter its integrity and cause demyelination [ 5 , 11 , 13 , 14 ]. This metabolic pathway can be seen in detail in Figure 4 .…”

“…The functional alteration of the aforementioned metabolic pathways leads to the accumulation and elevation of homocysteine (due to failure of methionine synthase) and methylmalonic acid (due to failure of methylmalonyl-CoA mutase) [ 13 , 14 ]. Furthermore, it has consequences for the function of the nervous system by generating alterations in the formation and maintenance of myelin sheaths and a deficit in energy production in the axons [ 1 , 11 , 13 , 14 ]. Neurological complications such as subacute combined degeneration (SCD) and polyneuropathy, previously mentioned, could result from this [ 6 , 7 , 11 , 12 ].…”