Thomas Noh1, Gamaleldin Osman2, Mokbel Chedid3, Hebah Hefzy4. 1. Department of Neurosurgery, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115, USA. Electronic address: Tnoh@bwh.harvard.edu. 2. Department of Neurology, Henry Ford West Bloomfield Hospital, 6777 West Maple Road, West Bloomfield, MI 48322, USA. Electronic address: gosman1@hfhs.org. 3. Department of Neurosurgery, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI 48202, USA. Electronic address: mchedid1@hfhs.org. 4. Department of Neurology, Henry Ford West Bloomfield Hospital, 6777 West Maple Road, West Bloomfield, MI 48322, USA. Electronic address: hhefzy1@hfhs.org.
Abstract
BACKGROUND: Recreational use of nitrous oxide (NO) in the general public has led to increasing reports of NO-induced demyelination (NOID). We describe the varying clinical presentations and pathophysiology, and offer a treatment paradigm. METHODS: A literature search of MEDLINE and EMBASE resulted in 42 publications with 37 studies meeting the inclusion criteria, for a total of 51 patients. Our case series included 5 patients seen from 2014 to 2018 followed over 3-60 months. RESULTS: Those with sensory symptoms and subjective weakness were categorized as having "mild" symptoms (25%). Symptoms indicating involvement outside the dorsal columns such as observer-graded weakness were categorized as "moderate" (61%). Patients with the aforementioned plus cognitive effects were categorized as "severe" (12%). There was no dose-dependent relationship between the amount of NO used and clinical impairment. There was a trend between the severity of neurologic impairment and serum levels of B12. Two patients were noncompliant. One initiated only oral therapy and did not improve. One received injections a month apart and worsened. CONCLUSIONS: Patients with NOID tend to have worse symptoms when presenting with lower serum vitamin B12 levels and have good recovery rates when treated with intramuscular B12 and oral supplementation.
BACKGROUND: Recreational use of nitrous oxide (NO) in the general public has led to increasing reports of NO-induced demyelination (NOID). We describe the varying clinical presentations and pathophysiology, and offer a treatment paradigm. METHODS: A literature search of MEDLINE and EMBASE resulted in 42 publications with 37 studies meeting the inclusion criteria, for a total of 51 patients. Our case series included 5 patients seen from 2014 to 2018 followed over 3-60 months. RESULTS: Those with sensory symptoms and subjective weakness were categorized as having "mild" symptoms (25%). Symptoms indicating involvement outside the dorsal columns such as observer-graded weakness were categorized as "moderate" (61%). Patients with the aforementioned plus cognitive effects were categorized as "severe" (12%). There was no dose-dependent relationship between the amount of NO used and clinical impairment. There was a trend between the severity of neurologic impairment and serum levels of B12. Two patients were noncompliant. One initiated only oral therapy and did not improve. One received injections a month apart and worsened. CONCLUSIONS:Patients with NOID tend to have worse symptoms when presenting with lower serum vitamin B12 levels and have good recovery rates when treated with intramuscular B12 and oral supplementation.
Authors: Maximilian Einsiedler; Paul Voulleminot; Stanislas Demuth; Pauline Kalaaji; Thomas Bogdan; Lucas Gauer; Cécile Reschwein; Aleksandra Nadaj-Pakleza; Jérôme de Sèze; Laurent Kremer; Ivana Schroder; Kévin Bigaut Journal: J Neurol Date: 2021-07-10 Impact factor: 6.682