[Postural sway in patients with hereditary ataxia].

[Postural sway in patients with hereditary ataxia].
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[遗传性共济失调患者的姿势摇摆]。

DOI:
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发表时间:
1994
期刊:
Rinsho shinkeigaku = Clinical neurology
影响因子:
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通讯作者:
K. Hirayama
K. Hirayama
中科院分区:
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文献类型:
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作者:
Masato Asahina;M. Nakajima;S. Kojima;K. Hirayama

文献摘要

被引文献

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本文应用姿势描记法对常染色体显性遗传性共济失调患者直立姿势不稳定进行了研究。在测力平台上对姿态摇摆进行了定量测量,分析了摇摆频率。来自27个家庭的30例患者(15名男性和15名女性,平均年龄53.1岁(SD 11.1))被分为两个临床组。12例患者(A组)有“纯”小脑体征,无躯体感觉传入症状。B组有18例患者出现下肢感觉障碍或反射减弱,胫神经刺激后体感诱发电位中头皮P37潜伏期延迟。两组患者的姿势摆动均大于正常人。A组患者的前后/侧向摆动比率较高。B组患者闭眼时摇摆增加。在摇摆频率方面,A组患者的功率谱峰值约为3 Hz。B组患者的功率谱峰值在1 Hz附近,其中12例患者还有另一个3 Hz分量。MRI显示小脑前叶的萎缩在具有3 Hz功率谱峰的患者中比在缺乏3 Hz功率谱峰的患者中更突出。定量姿势描记术可用于检测常染色体显性遗传性共济失调患者小脑前叶和脊髓上行系统的紊乱。
Instability of erect stance in patients with autosomal dominant hereditary ataxia was investigated by posturography. Postural sway on a force-measuring platform was measured quantitatively and sway frequencies were analyzed. Thirty patients from 27 families (15 men and 15 women, mean age of 53.1 years (SD 11.1)) were divided into two clinical groups. Twelve patients (group A) had "pure" cerebellar signs with no somatosensory afferent symptoms. Eighteen patients (group B) had sensory disturbances or diminished reflexes of the lower limbs, and a delayed latency of scalp P37 in somatosensory evoked potentials subsequent to tibial nerve stimulation. Postural sway of the patients of both groups was larger than that of normal subjects. Group A patients had a high antero-posterior/lateral sway ratio. Group B patients had increased sway with eyes closed. With respect to sway frequencies, group A patients had a power spectrum peak around 3 Hz. Group B patients had a power spectrum peak around 1 Hz, and twelve of them had another 3 Hz component. Atrophy of the anterior lobe of the cerebellum shown by MRI was more prominent in patients who had the 3 Hz power spectrum peak than in patients lacking the 3 Hz peak. Quantitative posturography was useful to detect disturbances of the anterior lobe of the cerebellum and the spinal ascending system in patients with autosomal dominant hereditary ataxia.