Misconceptions about speech impairment in Parkinson's disease
Misconceptions about speech impairment in Parkinson's disease
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关于帕金森病言语障碍的误解
作者：
C. Moreau;S. Pinto
言语障碍在帕金森氏病(PD)中非常常见和令人不安。它们通常被归类为构音障碍，这是一组言语障碍的统称，是由于中枢或外周神经系统受损而导致的对言语机制的肌肉控制障碍。它指明了由于语言肌肉的瘫痪、虚弱或不协调而导致的口头交流问题“(第246页)。在帕金森病患者中，已经报道了以下不同的言语维度：音调单调、重音减少、音量单调、辅音不精确、不适当的沉默、短促的说话、刺耳和喘息的声音、低音和变速。此外，响度降低，也被称为低音症，已经被早期描述。帕金森的开创性描述中报告了帕金森的言语障碍，但没有系统和准确地提到其出现的时间，而是报告了这种障碍发生的时间和疾病的进展(第5页)。Gowers报告说“颌骨通常在四肢后方受累”(第38页)，构音障碍在首发症状中暂时未被发现为主要体征(183例原发帕金森综合征患者中有7例；第432页)。“随着疾病的发展，由失衡和构音障碍引起的症状可能逐渐出现”(第243页)；这种症状进行性恶化的概念化可能有助于将构音障碍定义为晚期症状。直到最近，帕金森病患者的构音障碍还被认为是“其他运动异常”的一部分(第73页)，与交流脱节。未经治疗的患者最初的缺陷是无法控制呼吸以达到说话的目的，随后发音症状向前发展，累及喉、咽、舌头，最后是嘴唇(第751页)。Selby(1968)提出的从呼吸系统到喉和喉上发音症状的尾侧进展的这种理解，代表了不同病理过程的贡献，这些病理过程是关节功能障碍不同方面的基础，可能导致限制构音障碍作为唯一的运动表达，并低估呼吸和发声迹象(例如，呼吸控制障碍、发声障碍和发声困难)，这是导致言语清晰度下降的主要因素。左旋多巴的出现改变了帕金森病患者言语障碍的全球图景，导致他们被“相对忽视”，人们一致认为，多巴胺能药物可能改善某些言语维度，相反，有助于加剧其他维度的缺陷。在L-多巴的这个括号之后，DBS的出现带来了类似于毁损皮质下核团治疗PD的情况：DBS后构音障碍的处理往往受到限制，以避免言语障碍的恶化，并希望对呼吸控制和/或响度等言语维度产生潜在的积极影响。超过90%的帕金森氏症患者抱怨自己的嗓音强度低，沟通质量差，导致生活质量显著下降和社会孤立。上述陈述可能是基于随着时间的推移而转变为对帕金森病言语障碍的误解的概念而产生的。
Speech disorders are very common and disturbing in Parkinson’s disease (PD). They are often gathered under the generic term dysarthria, “a collective name for a group of speech disorders resulting from disturbances in muscular control over the speech mechanism due to damage of the central or peripheral nervous system. It designates problems in oral communication due to paralysis, weakness, or incoordination of the speech musculature” (p. 246). In PD, the following deviant speech dimensions have been reported: monotony of pitch, reduced stress, monotony of loudness, imprecise consonants, inappropriate silences, short rushes of speech, harsh and breathy voice, low pitch, and variable rate. Additionally, reduced loudness, also called hypophonia, has been early described. Speech impairments in PD were reported in the seminal descriptions of James Parkinson, without systematic and precise reference to its timing of appearance, but rather reporting that such impairment occurs “as time and the disease proceed” (p. 5). Gowers reported that “the jaw is usually affected late after the limbs” (p. 38), and dysarthria was not spotted for a while as a main sign among initial symptoms (7 cases among 183 patients with primary parkinsonism; p. 432). “As the disorder progresses, symptoms due to imbalance and dysarthria may gradually appear” (p. 243); this conceptualization of progressive worsening of the symptom probably contributed to define dysarthria as a late symptom. Until recently, dysarthria in PD was presented as part of “other motor abnormalities” (p. 73), disconnected from communication. “The initial defect in the untreated patient is a failure to control respiration for the purpose of speech and there follows a forward progression of articulatory symptoms involving larynx, pharynx, tongue and finally lips” (p. 751). This understanding of a caudorostral progression of the symptom proposed by Selby (1968), from the respiratory system to the larynx and the supralaryngeal articulation, represents contributions of different pathological processes that underlie different aspects of dysarthrophonia, which might have contributed to both restrict dysarthria as a sole motor expression and underestimate respiratory and phonatory signs (e.g., respiratory control deficit, hypophonia, and dysphonia) for the benefit of articulation deficits, major contributors to speech intelligibility decline. The advent of levodopa modified the global picture of speech disorders in PD, leading them to be “relatively neglected,“ with the consensual point of view that dopaminergic medication may improve some speech dimensions and, on the contrary, contribute to the exacerbation of other dimension deficits. Following this L-dopa parenthesis, the advent of DBS brought back a situation similar to that of the era of lesioning subcortical nuclei for the treatment of PD: Managing dysarthria following DBS is often restricted to avoid a worsening of speech disorders and to hope for potential positive effects on speech dimensions such as respiratory control and/or loudness. More than 90% of the patients with PD complain about their low voice intensity and poor quality of communication, leading to a dramatic impairment in quality of life and social isolation. The above-mentioned statements might have been generated upon conceptions that have turned, with time, into misconceptions about speech impairment in PD.
影响因子：
4.1
作者：
Kelly VE;Johnson CO;McGough EL;Shumway-Cook A;Horak FB;Chung KA;Espay AJ;Revilla FJ;Devoto J;Wood-Siverio C;Factor SA;Cholerton B;Edwards KL;Peterson AL;Quinn JF;Montine TJ;Zabetian CP;Leverenz JB
通讯作者：
Leverenz JB