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      Subacute combined degeneration induced by nitrous oxide inhalation : Two case reports

      case-report
      , M.MED a , , M.MED a , , MD b , , MD a ,
      Medicine
      Wolters Kluwer Health
      proton Nitrous Oxide Subacute Combined Degeneration

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          Abstract

          Rationale:

          Nitrous oxide (N 2O), commonly known as “laughing gas,” is being increasingly abused by young people as a recreational drug; this can subsequently result in myelopathy and peripheral neuropathy, however, in China, few cases of neurologic deterioration by N 2O abuse have been reported.

          Patient concerns:

          Herein, we present 2 patients who developed progressive limb weakness, numbness, and ataxia. Both of them had recreationally inhaled N 2O intermittently for a long time.

          Diagnosis:

          Subacute combined degeneration (SCD) based on myelopathy and polyneuropathy after N 2O abuse.

          Interventions:

          The 2 patients were treated with cessation of N 2O inhalation, methylcobalamin capsule 500 μg tid (ter in die, which means 3 times a day), and compound vitamin B 1 tablet tid p.o.(per os, which means taken orally) for 1 month.

          Outcomes:

          The symptoms of altered sensation and the patients’ gait improved significantly.

          Lessons:

          The 2 cases raise awareness of the important mechanisms of N 2O neurotoxicity, and clinicians should be made fully aware of such substance-related diseases. The incidence of N 2O -induced neurotoxicity is insufficiently recognized and should be considered as an important cause of SCD, especially in adolescents with undifferentiated weakness and abnormal sensation; this is essential because serious complications such as irreversible paralysis can result from the absence of early diagnosis and treatment.

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          Most cited references16

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          Sensitivity of serum methylmalonic acid and total homocysteine determinations for diagnosing cobalamin and folate deficiencies.

          Patients with cobalamin (vitamin B12) deficiency usually lack many of the classic features of severe megaloblastic anemia; because of the low diagnostic specificity of decreased serum cobalamin levels, demonstrating the deficiency unequivocally is often difficult. We examined the sensitivity of measuring serum concentrations of methylmalonic acid and total homocysteine for diagnosing patients with clear-cut cobalamin deficiency and compared the results with those of patients with clear-cut folate deficiency. Serum metabolites were measured for all patients seen from 1982 to 1989 at two university hospitals who met the criteria for cobalamin and folate deficiency states and for such patients seen from 1968 to 1981 from whom stored sera were available. In all, 406 patients had 434 episodes of cobalamin deficiency and 119 patients had 123 episodes of folate deficiency. Criteria for deficiency states included serum vitamin levels, hematologic and neurologic findings, and responses to therapy. Responses were documented in 97% of cobalamin-deficient patients and 76% of folate-deficient patients. Metabolite levels were measured by modified techniques using capillary-gas chromatography and mass spectrometry. Most of the cobalamin-deficient patients had underlying pernicious anemia; two thirds were blacks or Latinos. Hematocrits were normal in 28% and mean cell volumes in 17%. Of the 434 episodes of cobalamin deficiency, 98.4% of serum methylmalonic acid levels and 95.9% of serum homocysteine levels were elevated (greater than 3 standard deviations above the mean in normal subjects). Only one patient had normal levels of both metabolites. Serum homocysteine levels were increased in 91% of the 123 episodes of folate deficiency. Methylmalonic acid was elevated in 12.2% of the folate-deficient patients; in all but one, the elevation was attributable to renal insufficiency or hypovolemia. For the cobalamin-deficient patients, measuring serum metabolite concentrations proved to be a highly sensitive test of deficiency. We conclude that normal levels of both methylmalonic acid and total homocysteine rule out clinically significant cobalamin deficiency with virtual certainty.
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            Neurologic, psychiatric, and other medical manifestations of nitrous oxide abuse: A systematic review of the case literature.

            Nitrous oxide (N2 O) is known to have abuse potential, although debate regarding the toxic effects of such abuse continues. Our objective was to review the case literature and present the neurologic, psychiatric and medical consequences of N2 O abuse.
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              • Record: found
              • Abstract: found
              • Article: not found

              Biologic effects of nitrous oxide: a mechanistic and toxicologic review.

              Nitrous oxide is the longest serving member of the anesthesiologist's pharmacologic armamentarium but remains a source of controversy because of fears over its adverse effects. Recently, the Evaluation of Nitrous oxide In a Gas Mixture for Anaesthesia (ENIGMA) trial reported that nitrous oxide use increases postoperative complications; further preclinical reports have suggested that nitrous oxide may contribute to neurocognitive dysfunction in the young and elderly. Therefore, nitrous oxide's longevity in anesthetic practice is under threat. In this article, the authors discuss the evidence for the putative toxicity of nitrous oxide, from either patient or occupational exposure, within the context of the mechanism of nitrous oxide's action. Although it would seem prudent to avoid nitrous oxide in certain vulnerable populations, current evidence in support of a more widespread prescription from clinical practice is unconvincing.
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                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Wolters Kluwer Health
                0025-7974
                1536-5964
                May 2020
                01 May 2020
                : 99
                : 18
                : e19926
                Affiliations
                [a ]Department of Neurology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, Shandong Province
                [b ]Shanghai Mental Health Center, Shanghai Jiaotong University School of Medicine, Shanghai Key Laboratory of Psychotic Disorders, Shanghai, China.
                Author notes
                []Correspondence: Renliang Zhao, Doctor of Medicine, Chief Physician, Professor, Department of Neurology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao 266003, Shandong Province, China (e-mail: zhrenliang@ 123456163.com ).
                Article
                MD-D-19-04577 19926
                10.1097/MD.0000000000019926
                7440322
                32358361
                4ca62d83-63de-4a74-98c6-c30bcd7ce5ce
                Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

                History
                : 2 July 2019
                : 5 February 2020
                : 17 March 2020
                Categories
                5300
                Research Article
                Clinical Case Report
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                proton nitrous oxide subacute combined degeneration

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