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多巴反应性肌张力障碍——临床和遗传异质性。

Dopa-responsive dystonia--clinical and genetic heterogeneity.

机构信息

Parkinson's Disease Centre and Movement Disorders Clinic, Baylor College of Medicine, McNair Campus, 7200 Cambridge Street, Suite 9A, Houston, TX 77030, USA.

出版信息

Nat Rev Neurol. 2015 Jul;11(7):414-24. doi: 10.1038/nrneurol.2015.86. Epub 2015 Jun 23.

Abstract

Dopa-responsive dystonia (DRD) encompasses a group of clinically and genetically heterogeneous disorders that typically manifest as limb-onset, diurnally fluctuating dystonia and exhibit a robust and sustained response to levodopa treatment. Autosomal dominant GTP cyclohydrolase 1 deficiency, also known as Segawa disease, is the most common and best-characterized condition that manifests as DRD, but a similar presentation can be seen with genetic abnormalities that lead to deficiencies in tyrosine hydroxylase, sepiapterin reductase or other enzymes that are involved in the biosynthesis of dopamine. In rare cases, DRD can result from conditions that do not affect the biosynthesis of dopamine; single case reports have shown that DRD can be a manifestation of hereditary spastic paraplegia type 11, spinocerebellar ataxia type 3 and ataxia telangiectasia. This heterogeneity of conditions that underlie DRD frequently leads to misdiagnosis, which delays the appropriate treatment with levodopa. Correct diagnosis at an early stage requires use of the appropriate diagnostic tests, which include a levodopa trial, genetic testing (including whole-exome sequencing), cerebrospinal fluid neurotransmitter analysis, the phenylalanine loading test, and enzyme activity measurements. The selection of tests for use depends on the clinical presentation and level of complexity. This Review presents the common and rarer causes of DRD and their clinical features, and considers the most appropriate approaches to ensure early diagnosis and treatment.

摘要

多巴反应性肌张力障碍(DRD)包括一组具有临床和遗传异质性的疾病,这些疾病通常表现为肢体起始、日间波动的肌张力障碍,并对左旋多巴治疗有明显而持久的反应。常染色体显性 GTP 环水解酶 1 缺乏症,又称 Segawa 病,是最常见和特征最明显的 DRD 表现形式,但也可见于导致酪氨酸羟化酶、蝶呤还原酶或其他参与多巴胺生物合成的酶缺乏的遗传异常。在极少数情况下,DRD 可能由不影响多巴胺生物合成的疾病引起;个别病例报告表明,DRD 可能是遗传性痉挛性截瘫 11 型、脊髓小脑性共济失调 3 型和毛细血管扩张性共济失调的表现。导致 DRD 的这种情况的异质性常常导致误诊,从而延迟了使用左旋多巴进行适当的治疗。早期正确诊断需要使用适当的诊断测试,包括左旋多巴试验、基因测试(包括外显子组测序)、脑脊液神经递质分析、苯丙氨酸负荷试验和酶活性测量。测试的选择取决于临床表现和复杂程度。本综述介绍了 DRD 的常见和罕见病因及其临床特征,并考虑了最适当的方法,以确保早期诊断和治疗。

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