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Chapter 7 Widespread Brainstem Neurodegeneration in Huntington's Disease (HD)

机译：第7章亨廷顿舞蹈病（HD）中广泛的脑干神经变性

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The involvement of the brainstem is still not among the established degenerative features of HD (Bruyn et al. 1979; Koeppen 1989; Lange and Aulich 1986; Oyanagi et al. 1989; Rub et al. 2014a; Vonsattel and DiFiglia 1998; Vonsattel et al. 1985). Although some of the unexplained HD disease symptoms (e.g., oculomotor dysfunctions) also suggested degeneration of select brainstem nuclei, damage to the brainstem and its possible clinical relevance in HD has been controversially discussed for many decades (see Sects. 6.2, 6.5, and 6.6). Previous assumptions that select nuclei of the brainstem may also undergo neurodegeneration during HD (i.e., dopaminergic and GABAergic substantia nigra, auditory superior olive, lateral ves-tibular nucleus, precerebellar inferior olive) (Figs. 1.4, 7.1, 7.2, and 7.3) have not been revisited or taken into account by current researchers (see Chap. 1) (Bruyn et al. 1979; Bollen et al. 1986; Koeppen 1989; Kremer et al. 1992; Lange and Aulich 1986; Lange et al. 1976; Lasker and Zee 1997; Leigh et al. 1983, 1985; Oyanagi et al. 1989; Rub et al. 2009, 2014a; Vonsattel 2008; Vonsattel and DiFiglia 1998; Vonsattel et al. 1985; Walker 2007a, b). These assumptions, however, were confirmed by recent systematic patho'anatomical investigations of serial brainstem sections stained for neuronal Nissl material (with Darrow red) and lipofuscin pigment (with aldehyde-fuchsin) of clinically diagnosed and genetically confirmed HD patients that suffered from chorea, cognitive decline, and personality changes and also showed disease signs possibly related to brainstem damage (i.e., broad-based gait, gait imbalance, dysphagia, slowed horizontal saccades, inability to start horizontal saccades without initial head thrust, slowed and saccadic smooth pursuits, falls) (Rub et al. 2014a).
机译：脑干受累仍不属于HD退化的既定特征（Bruyn等人1979; Koeppen 1989; Lange和Aulich 1986; Oyanagi等人1989; Rub等人2014a; Vonsattel和DiFiglia 1998; Vonsattel等人（1985年）。尽管某些无法解释的HD疾病症状（例如动眼功能障碍）也提示某些脑干核变性，但数十年来对脑干的损害及其在HD中可能的临床意义的讨论一直存在争议（见6.2、6.5和6.6节）。 ）。先前选择脑干核的假设也可能在HD期间发生神经退行性变（即多巴胺能和GABA能黑质，听觉上橄榄，小叶外侧核，小脑前下橄榄）（图1.4、7.1、7.2和7.3）。目前的研究人员未对其进行重新研究或考虑（见第1章）（Bruyn等人1979; Bollen等人1986; Koeppen 1989; Kremer等人1992; Lange和Aulich 1986; Lange等人1976; Lasker ;和Zee 1997; Leigh等人，1983，1985; Oyanagi等人，1989; Rub等人，2009，2014a; Vonsattel 2008; Vonsattel和DiFiglia 1998; Vonsattel等人1985; Walker 2007a，b）。然而，这些假设已通过最近对一系列经临床诊断和遗传学证实患有HD的舞蹈病患者的神经干Nissl物质（带有Darrow红）和脂褐素色素（带有醛-品红）染色的连续脑干切片进行的系统病理解剖学研究证实，认知能力下降和人格改变，还显示出可能与脑干损伤相关的疾病征象（即，广泛的步态，步态失衡，吞咽困难，水平扫视减慢，无法在没有最初的头部推力的情况下开始水平扫视，缓慢而连续的眼跳，跌倒）（Rub等，2014a）。

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