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{
"name": "Височная боль"
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{
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{
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"code": "G12",
"name": "Спинальная мышечная атрофия и родственные синдромы",
"icd_name": "Спинальная мышечная атрофия и родственные синдромы",
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"slug": "g12_spinalnaya_myshechnaya_atrofiya_i_rodstvennye_sindromy",
"lead": "Нарушение здоровья, относящееся к группе системные атрофии, поражающие преимущественно центральную нервную систему",
"description": "Термин “спинальная мышечная атрофия” (СМА), или “спинальная амиотрофия”, является широким понятием, объединяющим группу заболеваний, сопровождающихся дегенерацией двигательных нейронов в спинном мозге и (или) стволе головного мозга и характеризующихся преимущественно аутосомно-рецессивным типом наследования. ",
"etiology": "<p>В большинство случаев СМА обусловлена дефицитом протеина мотонейронов, именуемым SMN (протеин выживаемости мотонейронов) </p>\r\n<p>Этот протеин, как следует из его названия, необходим для нормального функционирования мотонейронов. </p>\r\n<p>SMN – связанная СМА обычно подразделяется на 3 категории. Тип 1 — наиболее тяжелый, с самым ранним началом, а тип 3 — наименее тяжелый, с наиболее поздним возрастом начала. Некоторые специалисты выделяют еще тип 4 для обозначения умеренной или мягкой СМА с дебютом во взрослом возрасте </p>\r\n<p>Все эти типы связаны с генетическими поломками (мутациями) на хромосоме 5, что влияет на количество синтезируемого SMN – протеина. Более высокие уровни протеина снижают тяжесть СМА. </p>\r\n<p>Существуют также формы СМА, не связанные с протеином SMN и не являющиеся результатом мутаций на хромосоме 5. </p>",
"pathogenesis": "<p>СМА вызвана мутацией в гене SMN1, который в норме производит белок SMN.</p>\r\n<p>Из-за мутации гена, у людей с СМА производится меньшее количество белка SMN, что приводит к потере моторных нейронов.</p>",
"diagnostics": "<p>При подозрении — консультация невролога и генетика. </p>\r\n<p>Биохимия крови: креатинкиназа — в норме при СМА тип I, в норме или незначительно повышена при других типах. </p>\r\n<p>Генетическое обследование: пренатально или постнатально. Тест ДНК путем определения выпадения гена SMN1. </p>\r\n<p>Электронейромиография — показывает снижение нервных импульсов, помогает дифференцировать СМА от других нервно-мышечных болезней. Сенсорная нервная проводимость обычно нормальная. </p>\r\n<p>Биопсия мышц — гистологические признаки атрофии мышечных волокон, помогает дифференцировать СМА от других нервно-мышечных болезней. </p>",
"treatment": "<p>Специального лечения пока не разработано. </p>\r\n<p>Необходимы мультипрофессиональный подход и паллиативная помощь для улучшения качества жизни. </p>\r\n<ol>\r\n<li>Помощь в передвижении и самообслуживании. </li>\r\n<li>Фиксация корпуса и конечностей (корсеты, туторы и др.). </li>\r\n<li>Физиотерапия, эрготерапия (восстановлением утраченных двигательных навыков), физическая терапия и специальные сиденья могут уменьшить развитие контрактур суставов и сколиоза. </li>\r\n<li>Дыхательные упражнения. </li>\r\n<li>Респираторная поддержка, в том числе ИВЛ (неинвазивная через маску или инвазивная через трахеостому), может понадобиться на дому при прогрессировании болезни. </li>\r\n<li>Кормление через гастростому необходимо при прогрессировании проблем с глотанием. </li>\r\n</ol>",
"prevention": "<p>Возможна только пассивная профилактика — консультирование родителей с риском СМА о возможных последствиях и пренатальная ДНК-диагностика во время беременности через биопсию ворсин хориона для принятия решения о рождении или прерывании беременности. </p>",
"clinical_picture": "<p>Наиболее тяжёлой формой является I тип спинальной мышечной атрофии (синдром Верднига-Гоффмана), манифестирующий в раннем детстве (в первые 6 месяцев). Характерен синдром «вялого ребёнка» (слабый крик, сниженная двигательная активность, вялое сосание, потеря массы тела, сниженные глотательный, сосательный и кашлевой рефлексы). Такие дети неспособны удерживать головку, переворачиваться и сидеть, отстают в моторном развитии (грубая задержка). Могут развиваться деформации суставов и конечностей, контрактуры, дыхательные и бульбарные нарушения (расстройство глотания (дисфагия), нарушение артикуляции (дизартрия) и звучности речи (дисфония). Средняя продолжительность жизни таких детей – 2 года. Причиной смерти, как правило, становится тяжёлая дыхательная недостаточность или развитие пневмонии. </p>\r\n<p>Для II типа спинальной амиотрофии характерны более поздняя манифестация (6-18 месяцев) и хронически прогрессирующее течение. У таких детей наблюдается отставание в моторном развитии, тремор пальцев, прогрессирование слабости кашлевого рефлекса, поверхностного диафрагмального дыхания и межрёберных мышц. В начале дети с данной формой заболевания могут ползать, сидеть без поддержки, а некоторые и стоять при поддержке, но эти способности утрачиваются по мере роста и увеличения массы тела. Формируются скелетные и мышечные деформации (в том числе сколиоз, деформации грудной клетки и псевдогипертрофия икроножной мышцы), контрактуры, а также возникают нарушения дыхания (вплоть до развития дыхательной недостаточности). </p>\r\n<p>Наиболее лёгкое течение из детских форм характерно для III типа спинальной мышечной атрофии (синдрома Кугельберга-Веландера). Первые проявления, как правило, обнаруживаются у детей после 1,5 лет и характеризуются сложностями с комплексными двигательными навыками (бег, подъём по ступенькам и т.п.). Симптоматика прогрессирует медленно, нарушения глотания и жевания развиваются значительно позже. </p>\r\n<p>Взрослая форма (тип IV) имеет мягкое течение, при котором наиболее часто первыми поражаются мышцы плечевого пояса. </p>",
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