Motor learning in monkeys (Macaca fascicularis) with lesions in motor thalamus

Canavan, A. G. M.; Nixon, Philip D.; Passingham, Richard E.

doi:10.1007/bf00250573

Cited by 98 publications

(65 citation statements)

References 29 publications

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“…Studies of lesioning in the primate have found that pharmacologic (transient) inactivation of the basal ganglia receiving territory of the ventral motor thalamus resulted in a reduced number of internally or externally triggered movements and an increased reaction time (depending on the injection site), with no obvious effect on spontaneous movements outside the task [53]. Large bilateral permanent lesions interrupting the basal ganglia receiving areas and sparing the cerebellar receiving areas resulted in impaired motor learning without a significant effect on spontaneous movements, providing evidence for a role of the basal ganglia-thalamocortical components of the motor circuit in motor learning [54]. In contrast, interventions at the PPN level in primates seem to have more overt effects on spontaneous behavior, resulting in akinesia/bradykinesia [55].…”

Section: Functional/anatomic Considerations Of the Basal Ganglia Circmentioning

confidence: 93%

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

2016

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Deep brain stimulation (DBS) is highly effective for both hypo-and hyperkinetic movement disorders of basal ganglia origin. The clinical use of DBS is, in part, empiric, based on the experience with prior surgical ablative therapies for these disorders, and, in part, driven by scientific discoveries made decades ago. In this review, we consider anatomical and functional concepts of the basal ganglia relevant to our understanding of DBS mechanisms, as well as our current understanding of the pathophysiology of two of the most commonly DBS-treated conditions, Parkinson's disease and dystonia. Finally, we discuss the proposed mechanism(s) of action of DBS in restoring function in patients with movement disorders. The signs and symptoms of the various disorders appear to result from signature disordered activity in the basal ganglia output, which disrupts the activity in thalamocortical and brainstem networks. The available evidence suggests that the effects of DBS are strongly dependent on targeting sensorimotor portions of specific nodes of the basal gangliathalamocortical motor circuit, that is, the subthalamic nucleus and the internal segment of the globus pallidus. There is little evidence to suggest that DBS in patients with movement disorders restores normal basal ganglia functions (e.g., their role in movement or reinforcement learning). Instead, it appears that high-frequency DBS replaces the abnormal basal ganglia output with a more tolerable pattern, which helps to restore the functionality of downstream networks.

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Section: Functional/anatomic Considerations Of the Basal Ganglia Circmentioning

confidence: 93%

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

2016

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“…However, this view fails to explain several clinical and experimental observations, such as the fact that lesions of the motor thalamus do not result in akinesia [15] or that globus pallidus lesions do not improve it [16]. Consequently, the dysfunction of the motor circuit cannot alone account for akinesia.…”

Section: From the Motor To The Executive Hypothesismentioning

confidence: 97%

Deep Brain Stimulation of the Subthalamic Nucleus, but not Dopaminergic Medication, Improves Proactive Inhibitory Control of Movement Initiation in Parkinson's Disease

et al. 2013

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Slowness in movement initiation is a cardinal feature of Parkinson's disease (PD) that is still poorly understood and unsuccessfully alleviated by standard therapies. Here, we raise this major clinical issue within the framework of a novel theoretical model that allows a better understanding of the basic mechanisms involved in movement initiation. This model assumes that movement triggering is inhibited by default to prevent automatic responses to unpredictable events. We investigated to which extent the top-down control necessary to release this locking state before initiating actions is impaired in PD and restored by standard therapies. We used a cue-target reaction time task to test both the ability to initiate fast responses to targets and the ability to refrain from reacting to cues. Fourteen patients with dopaminergic (DA) medication and 11 with subthalamic nucleus (STN) stimulation were tested on and off treatment, and compared with 14 healthy controls. We found evidence that patients withdrawn from treatment have trouble voluntarily releasing proactive inhibitory control; while DA medication broadly reduces movement initiation latency, it does not reinstate a normal pattern of movement initiation; and stimulation of the STN specifically re-establishes the efficiency of the top-down control of proactive inhibition. These results suggest that movement initiation disorders that resist DA medication are due to executive, not motor, dysfunctions. This conclusion is discussed with regard to the role the STN may play as an interface between non-DA executive and DA motor systems in cortico-basal ganglia loops.

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“…Regarding the motor thalamus, the PMdc receives inputs from the oral and caudal parts of ventral lateral nucleus (VLo and VLc), whereas the main source of thalamic input to the PMv is area X and the ventral posterior lateral nucleus (Kurata 1994(Kurata , 2005Matelli et al 1989;Schell and Strick 1984). However, it has been demonstrated that monkeys with large anterior thalamic lesions, including in the ventral anterior nucleus and the anterior part of the VLo, were severely impaired at relearning a conditional motor task (Canavan et al 1989). Accordingly, inputs from the rostral motor thalamic nuclei to the PMdc may play a prominent role in conditional motor behavior.…”

Section: Specificity Of the Pmdc In Controlling Conditional Motor Behmentioning

confidence: 99%

Conditional Selection of Contra- and Ipsilateral Forelimb Movements by the Dorsal Premotor Cortex in Monkeys

Kurata

2010

Journal of Neurophysiology

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Kurata K. Conditional selection of contra-and ipsilateral forelimb movements by the dorsal premotor cortex in monkeys. J Neurophysiol 103: 262-277, 2010. First published November 4, 2009 doi:10.1152/jn.91241.2008. It has been suggested that the dorsal premotor cortex (PMd) may contribute to conditional motor behavior. Thus when a selection is instructed by arbitrary conditional cues, it is possible that the unilateral PMd affects behavior, regardless of which arm, contra-or ipsilateral, is to be used. We examined this possibility by recording neuronal activity and injecting muscimol into the caudal PMd (PMdc) of monkeys while they were performing a reaching task toward visuospatial targets with either the right or left arm, as instructed by low-frequency or high-frequency tone signals. Following the injection of a small amount of muscimol (1 L; 5 g/L) into the unilateral PMdc, monkeys exhibited two major deficits in behavioral performance: 1) erroneous selection of the arm not indicated by the instruction (selection errors) and 2) no movement initiation in response to a visuospatial target cue serving as a trigger signal for reaching within the reaction time limit (movement initiation errors). Errors were observed following unilateral muscimol injection into both right and left PMdc, although selection errors occurred with significantly greater frequency in the arm contralateral to the injection site. By contrast, movement initiation errors were more commonly observed in left-arm trials, regardless of whether the right or left PMdc was inactivated. Notably, errors rarely occurred following a ventral PM muscimol injection. These results suggest that the left and right PMdc cooperate to transform conditional sensory cues into appropriate motor output and can affect both contra-and ipsilateral body movement.

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Motor learning in monkeys (Macaca fascicularis) with lesions in motor thalamus

Cited by 98 publications

References 29 publications

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

Deep Brain Stimulation of the Subthalamic Nucleus, but not Dopaminergic Medication, Improves Proactive Inhibitory Control of Movement Initiation in Parkinson's Disease

Conditional Selection of Contra- and Ipsilateral Forelimb Movements by the Dorsal Premotor Cortex in Monkeys

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