Brain, Vol. 122, No. 10, 1989-1997,
October 1999
© 1999 Oxford University Press
Brain structures related to active and passive finger movements in man
1 Department of Brain Pathophysiology, Kyoto University Graduate School of Medicine, Kyoto and 2 Department of Radiology and Biomedical Imaging Research Center, Fukui Medical School, Fukui, Japan
Correspondence to:
Hiroshi Shibasaki, MD, Department of Brain Pathophysiology, Kyoto University School of Medicine, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan
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Abstract |
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A PET study was performed in six normal volunteers to elucidate the functional localization of the sensory afferent component during finger movement. Brain activation during the passive movement driven by a servo-motor was compared with that during an auditory-cued active movement which was controlled kinematically in the same way as the passive one. A newly developed device was used for selectively activating proprioception with a minimal contribution from tactile senses. Active movement was associated with activation of multiple areas, including the contralateral primary sensorimotor cortex, premotor cortex, supplementary motor area (SMA), bilateral secondary somatosensory areas and basal ganglia and ipsilateral cerebellum. In contrast, only the contralateral primary and secondary somatosensory areas were activated by the passive movement. It is likely that the contribution of proprioceptive input to the activation of the premotor cortex, SMA, cerebellum and basal ganglia, if any, is small. However, the present results do not rule out the possibility that the cutaneous afferent input or the combination of cutaneous and proprioceptive input participates in the activation of those areas during the active movement.
passive movement; active movement; PET; primary sensorimotor cortex
fMRI = functional MRI; rCBF = regional cerebral blood flow; SI = primary somatosensory cortex; SII = secondary somatosensory cortex; SI-MI = primary sensorimotor complex; SMA = supplementary motor area; SPM = statistical parametric map
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Introduction |
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TopAbstractIntroductionSubjects and methodsResultsDiscussionReferences |
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The cortical representation of voluntary movement revealed by activation studies in humans includes both input and output functions of motor control. Previous PET and functional MRI (fMRI) studies of active movements showed the participation of the primary sensorimotor cortex (SI-MI), lateral premotor cortex, supplementary motor area (SMA), superior and inferior parietal cortex, basal ganglia and cerebellum (Roland et al., 1980
; Colebatch et al., 1991; Deiber et al., 1991, 1996; Grafton et al., 1993; Matelli et al., 1993; Sabatini et al., 1993; Shibasaki et al., 1993; Dettmers et al., 1995, 1996; Sadato et al., 1996). However, the motor tasks employed in those studies were inevitably accompanied by somatosensory feedback (input) components. Attempts to segregate the motor output function from the contribution of the afferent component have rarely been reported. Weiller and colleagues reported that the brain activation associated with the active motor task at the elbow was essentially the same as that associated with passive movement (Weiller et al., 1996).
In the present study, we investigated the brain structures involved in active and passive finger movements, by comparing the same joint displacement caused either by a servo-motor or by volitional muscle contraction. Since the execution of finger movement is the most common task that has been used in various experimental designs, it is important to separate the planning/execution of the volitional finger movement from the afferent input. The servo-motor system used here was specially designed to selectively activate the human proprioceptors, and this enabled us to detect the cortical representation of proprioception (Mima et al., 1996, 1997b). The kinematics of the active and passive movement were controlled by video and EMG monitoring.
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Subjects and methods |
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Subjects
We studied six normal right-handed men, aged 20–27 years (mean 22.5 years). All subjects gave written informed consent before the experiments, which were approved by the Committee of Medical Ethics, Graduate School of Medicine and Faculty of Medicine, Kyoto University, and Fukui Medical University. A small catheter was placed in the cubital vein of each subject's left arm for injection of the radiotracer. The subjects lay in a supine position with their eyes closed and covered by a patch. The subject's head was immobilized with an elastic band and sponge cushions. During PET scans, surface EMG from bilateral finger extensors (extensor digiti communi muscle), bilateral wrist flexors (flexor carpi radialis muscle) and the right biceps and triceps muscles, and the bipolar electrooculogram were recorded using an EEG machine (Synafit, San-ei Co., Tokyo, Japan). The movement was also monitored by video recording.
For anatomical reference, a high-resolution whole-brain MRI for each subject was obtained separately, using a standard 1.5 T MRI system (GE Signa, Milwaukee, Wis., USA). A regular head coil and a conventional T1-weighted, spoiled-Grass volume sequence with a flip angle of 30°, echo time of 5 ms, repetition time of 33 ms and field of view of 24 cm were used. Matrix size was 256 x 256, slice thickness 1.5 mm and pixel size 0.937 x 0.937 mm. Volume data of 124 sagittal slices were interpolated and resliced to transaxial images with voxel size 0.937 x 0.937 x 0.937 mm. Each high-resolution image was normalized to the template T1-weighted images by linear transformation.
Tasks
For the passive movement task, a specially equipped device for flexing the finger joint was used (MySystems Inc., Yamaguchi, Japan) (Mima et al., 1996). The task was a repetitive flexion–extension movement of the right middle finger at the metacarpophalangeal joint (Fig. 1). The distal part of the middle finger was immobilized by an individually moulded plastic cap (Exafine, GC Co., Tokyo, Japan) which could effectively abolish the pressure or tactile sense caused by the passive movement. This selective stimulation of the proprioceptors has been confirmed in previous electrophysiological studies (Mima et al., 1996, 1997b). Other fingers of the right hand were fixed to the device and held in a rubber pad. Brisk passive movement was elicited every 0.5 s by a servo-motor, which was driven so as to cause a 20° flexion movement of the finger in 0.1 s. The flexed finger then returned to the resting position in 0.1 s, followed by the next movement 0.3 s later. Each flexion–extension movement was accompanied by a beep produced by the equipment. The kinematic parameters of the passive movement were determined by the preliminary recordings of the active repetitive movement using a mechanogram.
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An active movement task was performed at the same joint. By using the same plastic cap as that used for the passive movement task, unwanted displacement of the other joints was avoided. The movement was auditory-cued by the beeps produced by the device described above. Before the scanning of each active movement task, subjects practised in order to be able to mimic the passive movement and to move their middle finger rapidly and constantly through an angle of 20°.
For the resting condition, the subjects lay quietly without any intentional movement. During the passive movement and the resting scans, subjects were instructed not to mentally simulate or practise the movement. To cancel the effects of auditory stimuli, beeps caused by the device were presented to the subjects during all scans, including those carried out in the resting condition.
PET scans
The PET scans were performed with a General Electric Advance tomograph (GE Medical Systems, Milwaukee, Wis., USA) with the interslice septa retracted. The physical characteristics of this scanner have been described in detail previously (DeGrado et al., 1994). This scanner acquires 35 slices with an interslice spacing of 4.25 mm. In 3D mode, the scanner acquires oblique sinograms with a maximum cross-coincidence of ±11 rings. A 10-min transmission scan using two rotating 68Ge sources was performed for attenuation correction. Images of regional cerebral blood flow (rCBF) were obtained by summing the activity during the 60 s period following the first detection of an increase in cerebral radioactivity after intravenous bolus injection of 10 mCi of 15O-labelled water (Sadato et al., 1997). The images were reconstructed with the Kinahan–Rogers reconstruction algorithm (Kinahan and Rogers, 1989). Hanning filters were used, giving transaxial and axial resolutions of 6 and 10 mm (full-width at half-maximum), respectively. The field of view and pixel size of the reconstructed images were 256 and 2 mm, respectively. No arterial blood sampling was performed, and thus the images collected were those of tissue activity. Tissue activity recorded by this method is nearly linearly related to rCBF (Fox et al., 1984; Fox and Mintun, 1989).
Both active and passive movement tasks started 30 s prior to the injection. The pixel size of the reconstructed images was 2 mm. Each subject had 12 consecutive scans (four scans for each condition) performed at 10 min intervals. The sequential order of tasks was pseudorandomized and counterbalanced among the subjects.
Data analysis
The data acquired were analysed with the Statistical Parametric Mapping (SPM95, Wellcome Department of Cognitive Neurology, London, UK) software implemented in Matlab (The Mathworks Inc., Mass., USA). The scans of each subject were realigned, and all images were transformed into a standard stereotaxic space (Talairach and Tournoux, 1988). Each image was smoothed by using a Gaussian filter of 15 mm in the x, y and z axes to improve the signal-to-noise ratio. ANCOVA (analysis of covariance), using the global activity as a confounding covariate, was performed on a pixel-to-pixel basis. The results of t statistics (SPM{t}) were then transformed to a normal standard distribution (SPM{Z}). The threshold for SPM{Z} was set to Z > 3.09 with correction for multiple comparisons at voxel level using the theory of Gaussian fields (Friston et al., 1995). The statistical threshold used was a corrected P value of <0.05.
To further clarify the location of the activated areas with respect to the central sulcus, PET images of each subject were realigned to the MRI scan without stereotaxic normalization and analysed. Additionally, the change in rCBF at the peak activation area of interest was compared among the three conditions using ANOVA (analysis of variance).
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Results |
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Task performance
The EMG of the right hand was silent during the passive movement and the resting conditions. During the active movement condition, all subjects followed the auditory cue correctly and performed the controlled finger movement at 2 Hz. The kinematics of the active movement (duration and magnitude) showed no significant difference among four similar sessions for each subject and did not differ from those of the passive movement. The mean duration of the active flexion–extension movement was 22.9 ± 4.0 ms (mean ± standard deviation), while that for the passive movement was 22 ms. The mean magnitude was 22.4 ± 6.4°, whereas it was 20° for the passive movement. No significant eye or left hand movement was detected during any PET scan.
Change in rCBF
The rCBF changes were assessed using a categorical design (active movement versus resting, passive movement versus resting and active versus passive movement) (Fig. 2). When the passive movement was compared with the active one, no significant focal activation was revealed. The stereotaxic coordinates of the activated foci and the Z value at the maxima for each comparison are shown in Table 1.
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Passive movement activated the left primary somatosensory area (SI), posterior to the posterior commissure line, and the inferior parietal lobule, probably corresponding to the second somatosensory area (SII). However, both sites failed to reach statistical significance. In contrast, activation caused by active movement at the same joint included the left SI-MI, the SMA, the left lateral premotor cortex, the left inferior parietal lobe, the right superior temporal lobule extending to the inferior parietal lobe, the right cerebellum and the bilateral basal ganglia. When active movement was compared with passive movement, a similar activation was revealed in the same areas as those where active movement showed activation compared with the resting condition. However, the activated area around SI-MI was more localized to the anteromedial part when active movement was compared with passive movement than with the resting condition. Individual analysis coregistered with individual MRI clearly disclosed the anatomical relationship between these activated foci around the central sulcus (Fig. 3
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To strengthen the power of the statistical analysis, we examined the adjusted response at some of the pixels which showed the peak activation [Table 1
: left MI (–36, –24, 52), left SI (–42, –30, 48), left SII (–48, 30, 16), right cerebellum (10, –70, –20) and SMA (–8, –2, 48) in Talairach space]. Post hoc comparisons among the three conditions were tested using Scheffe's method (Fig. 4). At the left SI and SII, the adjusted response during both active and passive movements was significantly larger than that during the rest condition, and that during the active movement was larger than that during the passive movement. At the left MI, right cerebellum and SMA, the response during the active movement was significantly larger than that during both the passive movement and the resting condition. However, the difference between the responses during the passive movement and the resting condition did not reach statistical significance.
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Discussion |
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Brain structures activated in association with passive and active movements of the finger were clearly different. Passive movement elicited a weak and spatially limited brain activation compared with active movement, which was controlled kinematically in the same way as passive movement. These findings contrast strongly with a previous PET study on passive movement (Weiller et al., 1996
) and a sensory activation study using fMRI (Puce et al., 1995; Yetkin et al., 1995), both of which demonstrated similar sensorimotor cortical activation during the sensory and the motor task. However, these results are not directly comparable with the present results because of the difference in the sensory tasks employed. The previous PET study by Weiller and colleagues adopted a larger movement (90°) at the proximal joint (elbow) without controlling the tactile input (Weiller et al., 1996). For the fMRI study, tactile stimulation such as the use of an air-puff or brushing was used for activation (Puce et al., 1995; Yetkin et al., 1995). A recent fMRI study using a `passive movement' (Alary et al., 1998) did not monitor muscle activity during the task and did not report the kinematic parameters of the stimuli in a quantitative way.
Brain regions related to the active movement included most parts of the classical motor system and were consistent with previous reports (Roland et al., 1980; Colebatch et al., 1991; Deiber et al., 1991, 1996; Grafton et al., 1993; Matelli et al., 1993; Sabatini et al., 1993; Shibasaki et al., 1993; Dettmers et al., 1995, 1996; Sadato et al., 1996). Cortical representation of the proprioception elicited by the passive finger movement included the contralateral SI and SII. Although the rCBF increase did not reach statistical significance in the multiple comparison using the whole brain volume, the present result is physiologically reliable (Kaas, 1983; Burton, 1986; Johnson and Hsiao, 1992) and similar to previous activation studies using vibrotactile or electrical nerve stimulation (Fox et al., 1987; Seitz and Roland, 1992; Tempel and Perlmutter, 1992; Burton et al., 1993; Ibanez et al., 1995; Casey et al., 1996). Peak activation at SI was also statistically larger in the passive movement condition than in the resting condition. Previous electrophysiological studies have suggested modality-specific organization within SI (deep versus cutaneous receptors for areas 3a + 2 versus areas 3b + 1, respectively) (Mima et al., 1997b; for reviews, see Mountcastle, 1984; Kaas and Pons, 1988). However, it is impossible to identify which part of SI was primarily activated by the proprioceptive stimulation because of the limited spatial resolution of the PET technique. For the same reason, it is difficult to differentiate between the activations at SI and MI. In proprioceptive stimulation, it is most likely that the activated area is confined to the postcentral area in Talairach's coordinates (posterior to the posterior commissure line at the level of the hand sensorimotor area). This notion was supported by the coregistration to the individual MRI using a single-subject analysis and also by the comparison of peak activation at SI and MI between tasks. The absence of MI activation in somatosensory stimulation generally agrees with previous reports (Fox et al., 1987; Seitz and Roland, 1992; Tempel and Perlmutter, 1992; Burton et al., 1993; Ibanez et al., 1995; Casey et al., 1996), although the somatosensory afferent input to MI has been shown in primates and humans (Goldring and Ratcheson, 1972; Lucier et al., 1975; Hore et al., 1976; Asanuma et al., 1980). The most likely reason for the absence of MI activation in the present study is that the sensory afferents were too small and transient to be detected by rCBF measurement. The present study demonstrates for the first time the different cortical representation of active and passive movements of the finger.
The active movement showed a greater rCBF increase at SI than the passive movement, suggesting that SI was more activated during the active movement. Because of the limited resolution of PET, we cannot exclude the possibility that the large MI activation caused an apparent expansion of the significant area in SPM analysis. Additional SI activation during active movement can be explained either by a corollary discharge from MI to SI (Pandya and Kuypers, 1969; for review, see Hepp-Raymond, 1988) or by the change in excitability of SI caused by the motor task (Rushton et al., 1981; Cohen and Starr, 1987; Prud'homme and Kalaska, 1994). Ipsilateral SI-MI was not activated by the active movement, probably because the motor task employed was a simple and easy, repetitive movement. The activation of the ipsilateral SI-MI has been reported in the various motor tasks (Colebatch et al., 1991; Grafton et al., 1992; Shibasaki et al., 1993; Kawashima et al., 1994), only when the complex and/or proximal limb movements were required.
The other area which showed a significant rCBF increase during passive movement was the contralateral inferior parietal cortex, corresponding to SII (Hari et al., 1983; Burton et al., 1995; Krubitzer et al., 1995; Mima et al., 1997a). Involvement of the insular or frontal cortex (Burton et al., 1997) was unclear due to spatial smoothing and normalization. Previous PET studies applying somatosensory stimulation revealed bilateral or contralateral SII activation depending on the stimulation method (Fox et al., 1987; Meyer et al., 1991; Seitz and Roland, 1992; Burton et al., 1993, 1997; Ibanez et al., 1995; Bonda et al., 1996; Xu et al., 1997). This divergence is probably associated with the fact that SII has bilateral but contralaterally dominant receptive fields (for review, see Burton, 1986). Interestingly, the ipsilateral SII was activated during the active movement but not during the passive one. Moreover, the contralateral SII was even more activated in the active movement condition compared with the passive one. Lesion studies in patients and primates suggest that the function of SII is that of a higher order somatosensory centre (Ridley and Ettlinger, 1976, 1978; Mishkin, 1979; Friedman et al., 1986; Murray et al., 1992; Caselli, 1993). In the active movement task in the present study, the 20° movement without visual feedback is likely to need tight coupling between the sensory and motor systems. Thus, it is highly probable that the activation of SII during active movement is associated with the sensorimotor integration using an auditory cue and proprioceptive afferent feedback (Huttunen et al., 1996). In a recent patient study, a sensorimotor integrative role of the human inferior parietal lobe was proposed (Mattingley et al., 1998). The other possible explanation is an effect of implicit attention to the moving hand, as active attention has been reported to increase SII activity (Mima et al., 1998).
The SMA receives inputs from the somatosensory system, especially proprioceptors (Cadoret and Smith, 1997; Mima et al., 1999). However, in spite of the fact that we compared the rCBF change at the peak pixel, there was no SMA activation associated with the passive movement. It is possible that the response of the SMA in the present passive movement task was too small or was temporally transient, so that the sensitivity of the PET was insufficient to delineate the activation. These results clearly suggest that the SMA represents kinematically similar active and passive movements in a very different way. The present study, indicating an absence of SMA activation associated with the sensory stimuli, disagrees with the previous studies using vibrotactile stimulation (Fox et al., 1987; Tempel and Perlmutter, 1992) but agrees with a study using electrical nerve stimulation (Ibanez et al., 1995). A possible contribution of motor response (tonic vibration reflex) elicited by the vibration stimuli was suggested as the generating mechanism of SMA activation (Ibanez et al., 1995). It is also probable that the sensory discrimination task may induce the subject to perform some exploratory movement or active touch, unconsciously. However, the present study does not rule out the possibility that the specific combination of cutaneous and proprioceptive inputs during the active movement may contribute to the activation of the SMA during the active movement task. It is possible that the SMA is sensitive to afferent information during the active motor task rather than that during the passive movement. The location of the activated foci within the SMA that are associated with the active movement is consistent with previous reports (for review, see Picard and Strick, 1996). Activation predominantly involved the posterior SMA (SMA proper) caudal to the anterior commissure line rather than the pre-SMA, probably because we made use of the simple externally triggered finger movement. However, our active movement task required the subject to control the timing, direction and amplitude of the movement so as to fit the preset joint angle. These specific requirements might also explain the activation at the left dorsal premotor cortex during the active movement (set-related neurons) (Mushiake et al., 1991; Kurata, 1993).
The absence of activation in the primary and secondary motor areas during the passive movement task can be partly explained by the lack of somatosensory attention during the passive movement which is present during the active movement. Even during the passive movement task, large and infrequent passive movements, such as the task used by Weiller and colleagues (Weiller et al., 1996), might implicitly capture the subject's attention and induce the brain activation associated with the somatosensory attentional shift. It has been reported that MI or SMA neurons are involved in the discrimination or categorization of the somatosensory stimuli (Mountcastle et al., 1992; Romo et al., 1993).
Subcortical structures including the bilateral basal ganglia and the ipsilateral (right) cerebellum were activated during the active movement but not during the passive one. This result is not surprising because these areas have been regarded as part of the motor system in the classical sense (for review, see Brooks, 1995). Although the absence of cerebellar activation during the sensory task generally agrees with previous reports (Fox et al., 1987; Seitz and Roland, 1992; Tempel and Perlmutter, 1992; Burton et al., 1993; Ibanez et al., 1995; Casey et al., 1996), a role for the cerebellum in sensory perception has been suggested recently (Gao et al., 1996; Jueptner et al., 1997). The absence of the cerebellar activation in the present study is in accord with an animal experiment in which the passive sensory stimulus itself failed to activate the dentate nuclei (Strick et al., 1983). Unlike previous studies in which cerebellar activation was observed (Weiller et al., 1996), the passive movement task in the present study strictly controlled the contribution of tactile sense and required neither conscious discrimination of the stimuli nor an active response to the stimuli.
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Acknowledgments |
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We wish to thank Dr Mark Hallett and Dr Kenji Ishii for useful comments and discussions. This study was partly supported by Grants-in-Aid for Scientific Research (A)09308031, (A)08558083 and (C)09670655, Priority Areas Grant 08279106 and International Scientific Research 10044269 from the Japan Ministry of Education, Science, Sports and Culture, Research for the Future Program Grant JSPS-RFTF97L00201 and JSPS-RFTF97L00203 from the Japan Society for the Promotion of Science and General Research Grant for Aging and Health from the Japan Ministry of Health and Welfare.
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Received March 7, 1999. Accepted May 4, 1999.
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