Background. Nitrous oxide abuse (“laughing gas”, N2O) is common among young people attending nightclubs. Contrary to popular belief about the safety of N2O, in some cases neurological complications develop due to a deficiency of vitamin B12, the activity of which is blocked by N2O. Purpose of the study – to determine the typology and course of neurological disorders in a group of patients who regularly use “laughing gas”. To note the key diagnostic markers that allow verification of vitamin B12 deficiency induced by nitrous oxide consumption. To describe pathogenetic therapy features and follow-up. Materials and methods. The study included 12 patients (10 men and 2 women) aged 18 to 45 years (average age 29 years) with a diagnosis of B12-deficient myelopolyneuropathy induced by regular use of nitrous oxide. Results. The most common neurological complication of nitrous oxide abuse for more than 1 month was a generalized lesion of the peripheral nerves with acute or subacute distal symmetric sensory or sensorimotor axonal polyneuropathy. In the clinical picture, sensory complaints and disorders prevailed. Paresis developed in half of the cases. A typical neuroimaging symptom characteristic of funicular myelosis was rarely detected (16.7 %). A decrease in B12 vitamin level could most reliably be diagnosed only indirectly, by the presence of hyperhomocysteinemia (91.7 % of cases). In all cases that were followed-up, prolonged therapy with cyanocobalamin led to partial (n = 5; 62.5 %) or complete (n = 3; 37.5 %) regression of neurological symptoms. Conclusion. Caution regarding the use of nitrous oxide should be in all cases of predominantly sensory polyneuropathy with acute or subacute development in young and middle-aged people. A thorough history taking (targeted survey on the fact of nitrous oxide consumption) and diagnostics (testing the level of homocysteine, if possible methylmalonic acid) allow you to not miss a deficiency of vitamin B12, the treatment of the consequences of which with timely verification and adequate correction is quite effective. It is recommended that the level of homocysteine in the blood to be regularly monitored during the treatment (in order to achieve its normalization).
16Лекции и обзоры 4'2015 ТОМ 5 VOL. 5Нервно-мышечные Б О Л Е З Н И Neuromuscular DISEASES Дизиммунные заболевания периферического ней-ромоторного аппарата (острые и хронические дизим-мунные полиневропатии, миастения гравис и миасте-ноподобные заболевания, миозиты и полимиозиты и др.) поражают зачастую лиц трудоспособного возра-ста и в большинстве своем достаточно инвалидизиру-ющие. Проблема терапии данной группы заболеваний нервной системы занимает особое место и требует отдельного рассмотрения.К основным видам лечения дизиммунных заболе-ваний в неврологии, доказавшим свою эффективность в контролируемых исследованиях, относят корти-костероидные препараты (КСП), программный плаз-маферез (ПП), а также высокодозную внутривенную иммунотерапию (ВВИ). Выбор того или иного метода определяется множеством факторов, основными из которых являются диагноз, наличие противопока-заний и высоких рисков развития побочных эффектов, доступность и безопасность того или иного вида лече-ния. При этом следует отметить, что КСП неэффек-тивны и не показаны при синдроме Гийена-Барре (СГБ) [1] и мультифокальной моторной нейропатии (ММН) [2], а также в лечении отдельных форм хрони-ческой воспалительной демиелинизирующей поли-невропатии (ХВДП); кроме того, длительная терапия КСП чревата развитием множества побочных эффек-тов. Проведение ПП, в свою очередь, требует соответ-ствующего оснащения клиники, наличия подготов-ленных медицинских кадров, а также отсутствия таких состояний, как эрозивно-язвенное поражение желу-дочно-кишечного тракта, менструации, тромбоцито-пении и анемии, обострения геморроя и др., способ-ных привести к кровотечению на фоне необходимого при проведении ПП введения высоких доз гепари-
Background. Today, the issues of differential diagnosis of chronic hereditary and acquired demyelinating neuropathies are still relevant. The variety of phenotypic variants of chronic inflammatory demyelinating polyradiculoneuropathy and hereditary neuropathy with liability to pressure palsies, their remitting course and the non-specificity of neurophysiological changes necessitate the identification of clear markers that can help in the differential diagnosis of the neuropathies under discussion already at the stage of the analysis of the electroneuromyographic study data.Aim. To determine neurophysiological differential diagnostic markers in the manifestation of chronic inflammatory demyelinating polyradiculoneuropathy and hereditary neuropathy with liability to pressure palsies.Materials and methods. A retrospective analysis of the data of neurophysiological examination of 25 patients with hereditary neuropathy with liability to pressure palsies and 25 patients with chronic inflammatory demyelinating polyradiculoneuropathy.Results. A combination of such indicators as the age of the onset of the disease <33 years, the latency of the dM-wave with m.ADM ><3.7 ms and with m.AH ><4.8 ms (AUROC >0.7), the value of the conduction velocity along of the motor fibers of the ulnar nerve at the level of the elbow joint <37.5 m/s (AUROC >0.8), the conduction velocity along of the sensory fibers of the median nerve at the level of the wrist <48 m/s (AUROC >0.8), absence of conduction block along the median nerve in any area, and also the presence along the ulnar nerve at the level of the elbow joint is characteristic of hereditary neuropathy with liability to pressure palsies and allows to exclude chronic inflammatory demyelinating polyradiculoneuropathy.Conclusion. Neurophysiological markers have been identified that can help in the differential diagnosis of two chronic remitting demyelinating neuropathies: chronic inflammatory demyelinating polyradiculoneuropathy and hereditary neuropathy with liability to pressure palsies. However, only a combined analysis of clinical, anamnestic and paraclinical data makes it possible to establish a final diagnosis.
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