血管性與原發性巴金森氏症病患度量姿勢反應大小之能力：能力缺失與前置提示之影響

Abstract

目的：本實驗的目的在探討原發性巴金森氏症患者、血管性巴金森氏症患者與年齡相符的健康成人在接受三種不同牽拉位移量的前向腰部牽拉干擾時，其姿勢反應策略與度量姿勢反應大小能力的差異。並檢測一外加的聽覺前置提示對於三組受試者度量姿勢反應大小能力的影響。方法：本研究共蒐集10位原發性巴金森氏症患者 (平均年齡= 68.6 ± 6.5歲；8男與2女)、9位單純基底核或合併基底核與大腦白質區損傷的血管性巴金森氏症患者 (平均年齡= 73.8 ± 7.8歲；9男)與10位年齡相符的健康成人 (平均年齡= 74.2 ± 6.6歲；8男與2女)。每位受試者需接受認知執行功能測試 (包括修正版威斯康辛卡片分類測驗 (MCST)與叫色測驗 (Stroop Test))與動作功能測驗 (含巴金森氏症分級量表-動作檢查 (UPDRS-ME)、三公尺計時起走測試 (TUG)與伯格式平衡量表 (BBS))。此外，在評估反應性姿勢控制方面，每位受試者分別在有與沒有關於牽拉位移量大小的前置提示的情境下，接受由一自製的多方向人體牽拉系統 (MDP) (多如有限公司，台灣)所產生的三種不同牽拉位移量 (2、4和6公分)但固定牽拉速度 (9公分/秒)的前向腰部牽拉干擾。每個提示情境下，每個牽拉位移量各進行6次連續牽拉測試，即共18次測試。在提示情境下，受試者在牽拉開始前會先聽到一個關於即將產生的牽拉干擾強度的前置提示，在無提示情境下受試者將無法預知干擾強度。本研究以內側腓腸肌 (MG)、脛前肌 (TA)與第一腰椎旁的脊旁肌 (PARA)的肌肉活化順序、肌肉起始潛伏期 (muscle onset latency)與肌肉活化和腓腸肌-脛前肌共同收縮 (MG-TA co-contraction)的發生率 (occurrence rate)分析受試者所使用的反應性姿勢策略。在度量姿勢反應能力方面，則進一步量測腓腸肌和脊旁肌的肌肉活化程度 (肌肉活化晚期的肌電圖平均積分，AIEMGlate)、最大前後向力矩 (peak moment)以及此三個參數和牽拉位移量間的相關性(CORRMG、CORRPARA和CORRMoment)。結果：臨床測試方面，原發性與血管性巴金森氏症患者在MCST、TUG以及BBS的表現皆較健康成人差 (p< .05)。血管性巴金森氏症患者則較原發性巴金森氏症患者呈現較明顯的執行功能 (executive function)、步行和平衡能力的損傷，但此結果未達統計上顯著差異 (p> .05)。當接受一前向腰部牽拉干擾時，三組受試者皆呈現類似的遠端肌肉比近端肌肉先收縮 (MG→PARA)的姿勢肌收縮次序與肌肉活化模式。然而，相較於血管性巴金森氏症患者與健康成人，原發性巴金森氏症患者傾向以不同的肌肉反應型態 (主為腓腸肌-脛前肌共同收縮與代償性的脊旁肌活化現象) 回復與維持平衡。肌肉起始潛伏期在三組間與不同牽拉位移量之間並沒有顯著差異 (p> .05)。隨著牽拉位移量增加，原發性與血管性巴金森氏症患者皆能顯著增大其最大前後向力矩以及腓腸肌和脊旁肌的肌肉活化程度 (p< .05)。而且其肌肉活化程度及最大前後向力矩與牽拉位移量之間的相關係數亦呈現顯著正相關性。至於前置提示的影響部份，本研究發現相較於無提示情境，在提示情境下健康成人較能適當地調節脊旁肌肌肉活化程度 (p< .05)。但是，原發性巴金森氏症患者在提示情境下的肌肉活化程度與牽拉位移量之間的相關性反而較無提示情境時為差。討論及結論：血管性與原發性巴金森氏症患者接受前向腰部牽拉干擾時雖然呈現不同的姿勢肌活化模式，但卻皆保有隨干擾大小度量姿勢反應大小的能力。顯示此兩組病患仍保有姿勢準備狀態 (postural set)的功能。這可能因為患者與動作準備相關的感覺動作皮質區與小腦迴路都仍完好所致。此外，一外加的聽覺前置提示並無法增進血管性與原發性巴金森氏症患者度量姿勢反應的能力。這可能因為使用外顯式 (explicit)資訊反而使對這些病患分心或增加其轉換任務 (switching task)的需求。最後，本研究顯示，認知執行功能的缺失並不會影響血管性與原發性巴金森氏症患者的度量姿勢反應大小的能力。

Perpose: This study was aimed to investigate: (1) the differences in the reactive postural strategies and scaling functions in response to forward waist-pulling perturbation of three levels of pulling amplitude among healthy adults (HE), patients with idiopathic Parkinson’s disease (PD) and patients with vascular parkinsonism (VP) and (2) the effects of an auditory precue about upcoming perturbation magnitude on scaling reactive postural responses. Methods: Ten PD subjects (mean age= 68.6 ± 6.5 years, 8 males and 2 females), nine VP subjects with vascular lesions at the basal ganglia (BG) or with vascular BG lesions plus white matter changes (mean age= 73.8 ± 7.8 years, 9 males) and ten age-matched HE (mean age= 74.2 ± 6.6 years, 8 males and 2 females) participated in this study. In the clinical examination, each subject received the cognitive executive tests, including the Modified Card Sorting Test (MCST) and the Stroop Test, and the motor assessment, including the motor subscale of the Unified Parkinson’s Disease Rating Scale (UPDRS-ME), the Timed “Up & Go” test (TUG), and the Berg Balance Scale (BBS). To test the reactive postural control, each participant was randomly exposed to forward pulls of three consecutive 6-trial blocks of different perturbation amplitude (2, 4, and 6 cm) at a constant perturbation velocity of 9 cm/s, delivered by a custom-built Multidirectional Human Pulling (MDP) System (Advance Instrument Inc., Taipei, Taiwan), in both the Cue and No-cue conditions. To test the precuing effects, an auditory cue regarding the forthcoming perturbation amplitude was given prior to the perturbation onset in the Cue condition. The reactive postural strategies were investigated by examining the muscle activation sequence, muscle onset latency and occurrence rate of the tibialis anterior (TA), medial gastrocnemius (MG), paraspinal muscles at the L1 level of the spine (PARA) and MG-TA co-contraction. The ability to scale reactive postural responses was inferred by measuring the magnitude of the late muscle response (AIEMGlate of MG and PARA), peak anteroposterior moment, and the correlation between these variables and the pulling amplitude (CORRMG, CORRPARA and CORRMoment). Results: Both PD and VP subjects performed poorer on the MCST, the TUG and the BBS than the HE group (p< .05). The VP subjects revealed more evident, but non-significant (p> .05), deficits in mental shifting, gait and balance functions than PD. After exposure to forward waist-pulling perturbations, all subjects primarily activated muscles in the similar distal-to-proximal sequence (MG→PARA), and there were no significant differences in the muscle onset latency among groups and among the three levels of perturbation amplitude (p> .05). However, PD subjects tended to present altered muscle responses, such as MG-TA co-contraction and compensatory greater trunk muscle activation, compared to the HE and VP subjects. Both PD and VP groups significantly enlarged the peak moement and AIEMGlate of MG and PARA with the increased pulling amplitude (p< .05), as shown by significant positive correlation coefficients (rs) of CORRMG, CORRPARA and CORRMoment. The precuing did help the HE group scale AIEMGlate of PARA to the specific perturbation amplitude (p< .05). However, PD subjects, whose CORRMG and CORRPARA showed significant correlations in the No-cue condition, presented nonsignificant CORRMG and CORRPARA in the Cue condition. Discussion and Conclusions: The results indicated that VP and PD were distict entities and presented different patterns in response to waist-pulling perturbation. However, both VP and PD groups preserved the set-dependent scaling functions of reactive postural responses as the HE group. The preserved postual set in VP and PD might be attributed to the spared sensorimotor cortical area and cerebellar circuits responsible for movement preparation. Moreover, the absence of auditory precuing effects on improving the ability of scaling reactive responses in VP and PD subjects might be due to the increased distraction or switching load introduced by the provision of prior explicit information to these patients. Finally, our results suggest that the deficits of executive function might not affect the ability of scaling reactive postural responses in PD and VP.