Functional significance of the cortico–subthalamo–pallidal ‘hyperdirect’ pathway

Nambu, Atsushi; Tokuno, Hironobu; Takada, Masahiko

doi:10.1016/s0168-0102(02)00027-5

Cited by 1,149 publications

(1,037 citation statements)

References 54 publications

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“…The BG may be involved in emotion processing in the same way they are in motor and cognitive functions. Cortico‐BG‐thalamocortical loops may inhibit nonrelevant information (nontarget emotions/related facial features) and activate relevant ones (target emotions/related facial features) just as they select a specific movement by inhibiting competing programs and disinhibiting the selected one 121. Moreover, BG‐based circuits are involved in automated chunked representations of action/cognitive sequences and contribute to the suppression of goal‐directed behavioral control when it becomes habitual 122.…”

Section: Discussionmentioning

confidence: 99%

Facial emotion recognition in Parkinson's disease: A review and new hypotheses

et al. 2018

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Parkinson's disease is a neurodegenerative disorder classically characterized by motor symptoms. Among them, hypomimia affects facial expressiveness and social communication and has a highly negative impact on patients' and relatives' quality of life. Patients also frequently experience nonmotor symptoms, including emotional‐processing impairments, leading to difficulty in recognizing emotions from faces. Aside from its theoretical importance, understanding the disruption of facial emotion recognition in PD is crucial for improving quality of life for both patients and caregivers, as this impairment is associated with heightened interpersonal difficulties. However, studies assessing abilities in recognizing facial emotions in PD still report contradictory outcomes. The origins of this inconsistency are unclear, and several questions (regarding the role of dopamine replacement therapy or the possible consequences of hypomimia) remain unanswered. We therefore undertook a fresh review of relevant articles focusing on facial emotion recognition in PD to deepen current understanding of this nonmotor feature, exploring multiple significant potential confounding factors, both clinical and methodological, and discussing probable pathophysiological mechanisms. This led us to examine recent proposals about the role of basal ganglia‐based circuits in emotion and to consider the involvement of facial mimicry in this deficit from the perspective of embodied simulation theory. We believe our findings will inform clinical practice and increase fundamental knowledge, particularly in relation to potential embodied emotion impairment in PD. © 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

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Section: Discussionmentioning

confidence: 99%

Facial emotion recognition in Parkinson's disease: A review and new hypotheses

et al. 2018

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“…The arrangement of the intrinsic basal ganglia pathways into direct/indirect and hyperdirect pathways is incorporated into several interpretations of basal ganglia function, including the hypothesis that these pathways may play a role in action selection [e.g., 15,[17][18][19], the scaling of movement parameters [20], and, in a more general sense, "motor motivation", or action Bvigor^ [21], and cost/benefit aspects of actions [21,22].…”

Section: Functional/anatomic Considerations Of the Basal Ganglia Circmentioning

confidence: 99%

“…While much sparser than the indirect pathway, the hyperdirect projection has received increasing attention. By circumventing the striatum, it may provide a mechanism for cortical inputs to influence GPi and SNr output with shorter latencies and thereby assist in situations that require rapid Bstop^responses to external and internal triggers [17,19,[28][29][30][31][32][33][34][35][36][37][38][39][40][41].…”

Section: Functional/anatomic Considerations Of the Basal Ganglia Circmentioning

confidence: 99%

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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“…The direct pathway, arising from inhibitory striatal efferents containing GABA, substance P and dynorphin, projects directly to the internal part of the globus pallidus (GPi), whereas the indirect pathway, arising from striatal efferents containing both GABA and enkephalin, projects to the GPi via the external part of the globus pallidus (GPe) and subthalamic nucleus (STN). The centresurround model, described by Nambu et al (2002), includes an additional pathway called the 'hyperdirect' pathway from the cerebral cortex to the GPi via the STN, bypassing the striatum. The hyperdirect pathway, which provides a widespread excitation of the GPi (Mink 1996), is thought to suppress large areas of the thalamus and cerebral cortex related to both the selected motor program and competing programs before movement begins.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, single cell studies have shown that neurons in the BG are direction-specific (Nambu et al 2002) and fire in relation to movement about a particular joint in a particular limb (Teulings et al 1997). In neurodegenerative diseases, a certain degree of distortion of the body maps occurs, which is thought to lead to a loss of functional segregation between neurons in neighbouring modules.…”

Section: Introductionmentioning

confidence: 99%

Increased bradykinesia in Parkinson’s disease with increased movement complexity: elbow flexion–extension movements

2008

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The present research investigates factors contributing to bradykinesia in the control of simple and complex voluntary limb movement in Parkinson's disease (PD) patients. The functional scheme of the basal ganglia (BG)-thalamocortical circuit was described by a mathematical model based on the mean firing rates of BG nuclei. PD was simulated as a reduction in dopamine levels, and a loss of functional segregation between two competing motor modules. In order to compare model simulations with performed movements, flexion and extension at the elbow joint is taken as a test case. Results indicated that loss of segregation contributed to bradykinesia due to interference between competing modules and a reduced ability to suppress unwanted movements. Additionally, excessive neurotransmitter depletion is predicted as a possible mechanism for the increased difficulty in performing complex movements. The simulation results showed that the model is in qualitative agreement with the results from movement experiments on PD patients and healthy subjects. Furthermore, based on changes in the firing rate of BG nuclei, the model demonstrated that the effective mechanism of Deep Brain Stimulation (DBS) in STN may result from stimulation induced inhibition of STN, partial synaptic failure of efferent projections, or excitation of inhibitory afferent axons even though the underlying methods of action may be quite different for the different mechanisms.

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Functional significance of the cortico–subthalamo–pallidal ‘hyperdirect’ pathway

Cited by 1,149 publications

References 54 publications

Facial emotion recognition in Parkinson's disease: A review and new hypotheses

Facial emotion recognition in Parkinson's disease: A review and new hypotheses

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

Increased bradykinesia in Parkinson’s disease with increased movement complexity: elbow flexion–extension movements

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