Literature DB >> 12208006

Ipsilesional deficits during fast diadochokinetic hand movements following unilateral brain damage.

J Hermsdörfer1, G Goldenberg.   

Abstract

Impaired sensorimotor function of the hand ipsilateral to a unilateral brain lesion has been reported in a variety of motor tasks; however, elementary diadochokinetic movements, such as tapping with the index finger, seem to be preserved in chronic-lesion patients. Three different diadochokinetic movements (forearm diadochokinesis, hand tapping (HT) and finger tapping (FT)) were tested in patients with left brain damage (LBD) and right brain damage (RBD) and control subjects. Movements were measured three-dimensionally and the kinematics of joint angles were analyzed. While the patients' measures of movement speed and symmetry appeared normal, detailed kinematic analysis revealed clear deficits in several measures of movement variability, which reflected decreased regularity of the alternating movement cycles. This impairment was greater in LBD patients and tended to be greater during forearm diadochokinesis. The necessity of ipsilateral control in addition to dominant, contralateral control, especially during left hand and more complex or more proximal manual tasks may account for these findings. In addition, the role of apraxia (defined by impairments during the imitation of gestures) in the performance deficits of LBD patients was also assessed. Although, some performance decrements were associated with the presence of apraxia, these were different from the group findings and restricted to the two tapping tasks. Thus, although apraxia may have caused deficits in establishing dynamic representations of the elementary postures in conditions of high speed and low complexity, the disturbances during diadochokinetic movements must for the most part be attributed to more motor-related deficits of ipsilateral sensorimotor control, which are particularly apparent when the motor dominant left hemisphere is affected. The absence of clear correlations between performance deficits and lesion characteristics suggests that a distributed network is involved in this ipsilateral control.

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Year:  2002        PMID: 12208006     DOI: 10.1016/s0028-3932(02)00048-9

Source DB:  PubMed          Journal:  Neuropsychologia        ISSN: 0028-3932            Impact factor:   3.139


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