ABSTRACT
OBJECTIVE: It is well recognized that nitrous oxide abuse can lead to vitamin B12 deficiency presenting with neurological complications. Nevertheless, establishing this diagnosis can be challenging, and treatment guidelines are lacking. METHODS: In this paper, we present a case series of eight patients and discuss the diagnostic challenges and treatment options for vitamin B12 deficiency due to nitrous oxide abuse presenting with neurologic complications. RESULTS: Biochemical findings are not always straightforward and complementary testing is often necessary. Magnetic Resonance Imaging (MRI) revealed a longitudinally myelopathy extending over a long segment typically involving the dorsal columns of the cervical cord. To increase the lesion conspicuity, dedicated MRI sequences are needed. In our practice, we recommend the use of T2-weighted images (WI) with fat suppression (FS). Treatment consists of cessation of nitrous oxide abuse and supplementation with intramuscular injections of cobalamin. Due to a lack of treatment guidelines, we also describe the treatment schedule used in our neurology clinic and give a brief overview of treatment options suggested in the literature. CONCLUSION: We described diagnostic steps en treatment plans in patients presenting with subacute neurological complications due to nitrous oxide abuse. ABBREVIATIONS: crea: creatinine; HCy: homocysteine; MCA: 2-methylcitric acid; MMA: methylmalonic acid; MRI: magnetic resonance imaging; SEP: somatosensory evoked potentials.
Subject(s)
Vitamin B 12 Deficiency , Vitamin B 12 , Humans , Vitamin B 12/therapeutic use , Nitrous Oxide/adverse effects , Vitamin B 12 Deficiency/complications , Vitamin B 12 Deficiency/diagnosis , Vitamin B 12 Deficiency/therapy , Methylmalonic Acid , Creatinine , Homocysteine , VitaminsABSTRACT
IgLON5-associated encephalitis is a syndrome with different clinical presentations consisting of sleep dysfunction, bulbar dysfunction, chorea, and progressive supranuclear palsy-like symptoms whereas dysautonomy and cognitive decline usually appear in later stages of the disease. We report a case of a patient with IgLON5-associated encephalitis presenting with rapidly progressive cognitive decline and atypical inflammatory lesions on brain magnetic resonance imaging, oligoclonal bands on cerebrospinal fluid, anti-IgLON5 antibodies exclusively of the IgG1 class, and a fierce inflammatory reaction on brain biopsy, who responded favorably to immunotherapy.
