Enhanced lateral premotor activity during paradoxical gait in Parkinson's disease

Hanakawa, Takashi; Fukuyama, Hidenao; Katsumi, Yukinori; Honda, Manabu; Shibasaki, Hiroshi

doi:10.1002/1531-8249(199903)45:3<329::aid-ana8>3.0.co;2-s

Cited by 212 publications

(126 citation statements)

References 34 publications

(39 reference statements)

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“…The authors suggested that utilization of nonaffected brain areas is a compensatory mechanism for basal ganglia dysfunction in movement activation. 33 In our study, we also observed a compensation for the impairment of stride-length regulation under external stimulation via treadmill walking in all patient groups. As in PD, external stimuli could enable the PMC and SMA to better compensate for deficiencies in thalamo-cortical output either caused by antidopaminergic effects of antipsychotic treatment or by a primary pathophysiological condition of schizophrenia.…”

Section: Discussionsupporting

confidence: 72%

Gait disturbances in patients with schizophrenia and adaptation to treadmill walking

Putzhammer

Perfahl

Pfeiff

et al. 2005

Psychiatry Clin Neurosci

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This study evaluated the gait patterns of schizophrenic patients at free gait and at three fixed velocities on a treadmill. The effects of illness and antipsychotic treatment on gait parameters and on adaptation to treadmill walking were compared. Gait parameters of 14 drug-naïve schizophrenic patients, 14 patients treated with conventional antipsychotics, 14 patients treated with olanzapine, as well as 14 matched controls were assessed on a walkway and on a treadmill at three different velocities (very slow, intermediately slow, and comfortable) using an ultrasonic movement analysis system. At free gait, all patients showed a significantly decreased gait velocity, predominantly due to a shorter stride length, when compared to the controls, with the most striking difference observed between the patients treated with conventional neuroleptics and the controls ( anova , P £ 0.001). Cadence (steps per second) did not differ between the investigated groups. When gait was evaluated on the treadmill, differences in stride length and cadence were significant only at the very slow treadmill velocity ( anova , P £ 0.05). In all patient groups, mean stride length was decreased and cadence compensationally increased. Significant differences between the patient groups were no longer detectable. With increasing treadmill velocities, gait parameters of all patient groups normalized. The results show that, like in patients with Parkinson's Disease, impaired gait parameters can also be normalized in schizophrenic patients by external stimulation via treadmill walking.

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Section: Discussionsupporting

confidence: 72%

Gait disturbances in patients with schizophrenia and adaptation to treadmill walking

Putzhammer

Perfahl

Pfeiff

et al. 2005

Psychiatry Clin Neurosci

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“…PMC activation increases in akinetic PD patients relative to controls have been reported earlier (Catalan et al, 1999;Hanakawa et al, 1999;Haslinger et al, 2001;Rascol et al, 1997;Sabatini et al, 2000;Samuel et al, 1997). These studies suggested a compensatory role of the PMC for SMA activation deficits: a feature that we could not detect in this cohort.…”

Section: Correlates Of the Changes In Movement Characteristics Over Timesupporting

confidence: 55%

“…activation paradigms and sequenced unimanual finger movements have also reported increased SMA activation in PD (Jahanshahi et al, 1995), particularly with increasing sequence length and complexity (Catalan et al, 1999). It has subsequently been suggested that lateral premotor (PMC), parietal and cerebellar regions compensate for SMA hypoactivity during parkinsonian movements (Catalan et al, 1999;Hanakawa et al, 1999;Haslinger et al, 2001;Rascol et al, 1997;Sabatini et al, 2000;Samuel et al, 1997). In keeping with the improvement in volitional movements by external cueing in PD, these areas were mainly found to be hyperactive during externally triggered motor tasks.…”

Section: Introductionmentioning

confidence: 90%

Correlates of movement initiation and velocity in Parkinson's disease: A longitudinal PET study

et al. 2007

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Limited data exist concerning the mechanisms that underlie the different motor features of Parkinson's disease (PD) and their course over time. Our aims were (1) to identify longitudinal changes in PD patients and (2) to determine the neural correlates of the changes in movement initiation and velocity that occur in the course the disease. Thirteen early stage PD patients were scanned twice off antiparkinsonian medication with PET. Imaging was performed at baseline and again after 2 years while the subjects performed a motor task that was kinematically controlled across time. Paced reaching movements were made towards targets that were presented in a predictable order. Measures of movement onset time (OT) and mean velocity (MV) were recorded during PET. OT and MV decreased significantly from baseline to follow-up. With advancing disease, increasing subcortical activation was detected in the pallidum bilaterally and in the left putamen. In the cortex, motor-related activation increased in the right pre-SMA, anterior cingulate cortex and the left postcentral gyrus. Progressive delays in movement initiation (OT) correlated with increases in the right dorsal premotor cortex (dPMC). Slowing of movement (MV) was associated with declining activation in the left dorsolateral prefrontal cortex and dPMC. Our data suggest that with advancing PD, motor performance is associated with the recruitment of brain regions normally involved in the execution of more complex tasks.

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“…It is the response to this information which seems to be exaggerated in PD participants. A PET study confirms that PMC mediates locmotor affordance processing, since PMC was more active when participants stepped over transverse lines than lines parallel with the direction of walking (Hanakawa et al, 1999). Importantly, this difference was more pronounced in PD participants than in control participants performing the same step.…”

Section: Implications For Models Of Visually Controlled Walkingmentioning

confidence: 57%

Insights into the neural control of locomotion from walking through doorways in Parkinson's disease

et al. 2010

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. (2010) 'Insights into the neural control of locomotion from walking through doorways in Parkinson's disease. ', Neuropsychologia., 48 (9). pp. 2750-2757. Further information on publisher's website:http://dx.doi.org/10. 1016/j.neuropsychologia.2010.05.022 Publisher's copyright statement: NOTICE: this is the author's version of a work that was accepted for publication in Neuropsychologia. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reected in this document. Changes may have been made to this work since it was submitted for publication. A denitive version was subsequently published in Neuropsychologia, 48, 9, July 2010, 10.1016/j.neuropsychologia.2010.05.022. Additional information:Use policyThe full-text may be used and/or reproduced, and given to third parties in any format or medium, without prior permission or charge, for personal research or study, educational, or not-for-prot purposes provided that:• a full bibliographic reference is made to the original source • a link is made to the metadata record in DRO • the full-text is not changed in any way The full-text must not be sold in any format or medium without the formal permission of the copyright holders.Please consult the full DRO policy for further details. behaviour to investigate the visual control of locomotion and the role of the basal ganglia in this system. We use a variable-width doorway to measure the scaling of motor output to visual input specifying door width. By measuring walking behaviour as participants passed through the doorway, we show that both PD and healthy control participants scaled their locomotor outputs to door width. Both groups reacted to narrower doors by walking more slowly with shorter strides. However, the changes were greater in the PD group, where walking speed dramatically decreased while approaching the doorway. Such a pattern could help explain why doorways cause freezing episodes in PD. Neither explicit perceptual judgements of door width, nor performance on motor tasks, predicted the door behaviour.On the basis of these findings, we propose that PD is associated with a visuomotor disturbance, such that responses to action-relevant visual information are exaggerated. In the PD group, dopaminergic medications improved many baseline gait variables but did not affect their sensitivity to door width, suggesting that this visuomotor effect is not mediated by the basal ganglia. This hypothesis provides a novel framework for interpreting a variety of results with PD patients.

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Enhanced lateral premotor activity during paradoxical gait in Parkinson's disease

Cited by 212 publications

References 34 publications

Gait disturbances in patients with schizophrenia and adaptation to treadmill walking

Gait disturbances in patients with schizophrenia and adaptation to treadmill walking

Correlates of movement initiation and velocity in Parkinson's disease: A longitudinal PET study

Insights into the neural control of locomotion from walking through doorways in Parkinson's disease

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