Clinical-radiological dissociation in a patient with nitrous oxide-induced subacute combined degeneration: a case report

Abstract

Background: Several recent studies have reported subacute combined degeneration (SCD) induced by nitrous oxide (N 2 O) abuse. However, the association between the evolution of dynamic neuroimaging and clinical manifestations has not been reported in patients with N 2 O-induced SCD. Case presentation: We described the case of a 24-year-old man who developed SCD with inverted V-sign hyperintensities over the posterior aspect of the spinal cord caused by frequent, excessive N 2 O inhalation. One month after treatment, his weakness and paresthesia resolved and serum vitamin B 12 levels exceeded the normal levels. However, the hyperintensities had extended horizontally and longitudinally on T2-weighted magnetic resonance imaging (MRI), compared to those on the initial scan. Two months after treatment, the patient experienced some residual numbness in the distal limbs, and his serum homocysteine levels were normal, but the abnormal signals seen on cervical T2-weighted MRI had decreased only slightly compared to those seen on the one-month follow-up MRI. The evolution of conventional MRI findings lagged compared to the clinical manifestation, which was suggestive of a clinical-radiological dissociation. Conclusions: Clinical-radiological dissociation might have occurred in this case because T2-weighted imaging was not sensitive enough to reveal cytotoxic edema. Moreover, the serum vitamin B 12 level is not a good indicator of cellular vitamin B 12. Thus, clinicians should recognize this phenomenon, comprehensively assess the condition of patients with N 2 O-induced SCD, and avoid terminating treatment based on the resolution of clinical symptoms and serological results.

Clinical epidemiological characteristics of nitrous oxide abusers: A single‐center experience in a hospital in China

“…In our study, 53% of the patients showed abnormal signals in the cervical spinal cord, mostly associated with only the posterior funiculus, which is in agreement with previous findings about SCD (Cao et al, 2018). A previous study had shown that the evolution of conventional MRI findings lagged compared to the clinical manifestation because T2-weighted imaging is not sensitive enough to show cytotoxic edema, suggesting clinical-radiological dissociation (Jiang & Shang, 2020); moreover, we also found that the incidence of MRI lesions is higher in patients with an N 2 O exposure time of ≤6 months. Peripheral nerve damage is common in N 2 O abusers.…”

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

“…In recent years, N 2 O has gained increasing popularity worldwide especially among young people due to its euphoric effects [ 10 , 11 ]. According to previous studies, it is not unusual that N 2 O can cause cobalamin deficiency and SCD [ 5 , 7 , 11 – 13 ]. Although 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 B 12 [ 14 – 17 ].…”

“…We speculated the possible reasons are as follows: Copper is a cofactor for a variety of biological reactions and thought to be necessary for methionine synthase and S-adenosylhomocysteine hydrolase, which play vital roles within the methylation cycle [ 10 ]. N 2 O can oxidize the cobalt ion which attenuates the function of methylcobalamin, inhibits methionine synthase, and elevates the concentration of homocysteine [ 5 ]. This might be followed by a decrease in the activity of S-adenosylhomocysteine hydrolase and a consequent decline in copper concentration by feedback regulations.…”

“…Subacute combined degeneration (SCD) is a neurological disease usually induced by vitamin B 12 deficiency [ 1 – 4 ]. Previous studies demonstrate that SCD can result from recreational nitrous oxide (N 2 O) abuse and cause various neuropsychiatric disorders [ 5 – 9 ]. However, no literature has been concerned about the serum copper and cerebellar changes through the diagnostic process.…”

A Case Report of Subacute Combined Degeneration Due to Nitrous Oxide-Induced Vitamin B12 Deficiency

“…Vitamin B12 supplementation should be started immediately upon suspected diagnosis since the response to treatment is associated with the severity and duration of symptoms. The recovery time will depend on the severity of symptoms and the degree of lesions in the spinal cord [ 7 ]. Patients should be educated on the importance of the cessation of the recreational use of nitrous oxide.…”