Grundmann Kathrin, Laubis-Herrmann Ulrike, Bauer Ingrid, Dressler Dirk, Vollmer-Haase Juliane, Bauer Peter, Stuhrmann Manfred, Schulte Thorsten, Schöls Ludger, Topka Helge, Riess Olaf
Department of Neurology, University of Tübingen, Germany.
Arch Neurol. 2003 Sep;60(9):1266-70. doi: 10.1001/archneur.60.9.1266.
Dystonia is a clinically and genetically heterogeneous movement disorder characterized by sustained muscle contractions affecting one or more sites of the body, frequently causing twisting and repetitive movements or abnormal postures. A 3-base pair (GAG) deletion in the DYT1 gene is held responsible for most cases of early-onset primary generalized dystonia in the Ashkenazi Jewish population as well as in non-Jewish patients.
To investigate the prevalence of the GAG deletion in the DYT1 gene and the phenotypic variability in the general population by testing patients with different subtypes of dystonia from 4 different movement disorder outpatient clinics in Germany.
Two hundred fifty-six patients were tested for the GAG deletion mutation in the DYT1 gene by means of published primers and polymerase chain reaction amplification to determine GAG deletion status.
Six of the 256 patients did carry the GAG-deletion in the DYT1 gene. However, only 2 of the 6 mutation carriers presented with what is thought to represent classic features of early-onset primary generalized dystonia. The DYT1 mutation was also detected in 2 patients with multifocal dystonia, 1 of them presenting with involvement of cranial and cervical muscles, and in 2 patients with writer's cramp of both hands with only slight progression. Our findings demonstrate that the mutation may be associated with not only generalized but also segmental and multifocal forms of dystonia.
Our data underline the wide range of phenotypic variability of the DYT1 mutation. A priori prediction of the mutation carrier status in dystonic patients and genetic counseling of affected families with respect to the clinical manifestation may prove difficult.
肌张力障碍是一种临床和遗传异质性的运动障碍,其特征为持续的肌肉收缩,影响身体的一个或多个部位,常导致扭曲和重复性运动或异常姿势。DYT1基因中的一个3碱基对(GAG)缺失是导致阿什肯纳兹犹太人群以及非犹太患者中大多数早发性原发性全身性肌张力障碍病例的原因。
通过对德国4个不同运动障碍门诊诊所中不同亚型肌张力障碍患者进行检测,调查DYT1基因中GAG缺失的患病率以及普通人群中的表型变异性。
采用已发表的引物和聚合酶链反应扩增对256例患者进行DYT1基因中GAG缺失突变检测,以确定GAG缺失状态。
256例患者中有6例确实携带DYT1基因中的GAG缺失。然而,6例突变携带者中只有2例表现出被认为代表早发性原发性全身性肌张力障碍的典型特征。在2例多灶性肌张力障碍患者中也检测到DYT1突变,其中1例累及颅颈部肌肉,在2例双手书写痉挛且仅轻微进展的患者中也检测到该突变。我们的研究结果表明,该突变可能不仅与全身性肌张力障碍有关,还与节段性和多灶性肌张力障碍形式有关。
我们的数据强调了DYT1突变表型变异性的广泛范围。对肌张力障碍患者的突变携带者状态进行先验预测以及就临床表现对受影响家庭进行遗传咨询可能会很困难。