Useless Hand Syndrome and Astereognosis in Multiple Sclerosis

B. Okuda
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Abstract

Useless hand syndrome (UHS) by Oppenheim, comprising clumsiness of complex finger movements and loss of manual dexterity, arises from cervical cord lesions in multiple sclerosis (MS) [1]. From Oppenheim’s report, UHS has been attributed to impaired proprioception, resembling the nature of sensory ataxia [1,2]. In fact, T2 MRI showed high cervical lesions (C2-C4), consistently involving the posterior cord at the C3 to C4 level, in all of our patients with MS and UHS. However, I do not necessarily support the above-mentioned mechanism underlying UHS, because UHS was not associated with disturbance of deep sensations in some cases. As reported previously, UHS might be attributable to astereognosis rather than sensory ataxia, suggesting a disorder of sensorimotor integration [3]. While posterior cord lesions cause both of UHS and sensory ataxia, the underlying mechanism appears to differ, at least in part. In this regard, concurrent sensory disturbances may be helpful in elucidating the underlying mechanism of UHS. In all of our patients, stereognosis was most severely disturbed, whereas disturbance of other combined sensations such as two-point discrimination and graphesthesia ranged from severe to moderate. Combined sense was not necessarily impaired in parallel with deep sense.
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多发性硬化症的残手综合征与立体诊断
Oppenheim定义的无用手综合征(UHS)是由多发性硬化症(MS)的颈脊髓病变引起的,包括复杂手指运动的笨拙和手部灵巧性的丧失[1]。根据Oppenheim的报告,UHS被归因于本体感觉受损,类似于感觉性共济失调的性质[1,2]。事实上,在我们所有的MS和UHS患者中,T2 MRI显示高颈椎病变(C2-C4),一贯累及C3至C4水平的后脊髓。然而,我并不一定支持上述UHS的机制,因为UHS在某些情况下与深层感觉的干扰无关。如先前报道,UHS可能是由立体认知而非感觉共济失调引起的,提示感觉运动整合障碍[3]。虽然后脊髓损伤可引起UHS和感觉性共济失调,但其潜在机制似乎有所不同,至少部分不同。在这方面,并发感觉障碍可能有助于阐明UHS的潜在机制。在我们所有的患者中,立体知觉受到最严重的干扰,而其他组合感觉如两点辨别和图形感觉的干扰从严重到中度不等。综合感觉并不一定与深层感觉同时受损。
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