Topography of cortical and subcortical connections of the human pedunculopontine and subthalamic nuclei

Aravamuthan, Bhooma R.; Muthusamy, Karthikeyan; Stein, John; Aziz, Tipu Z.; Johansen‐Berg, Heidi

doi:10.1016/j.neuroimage.2007.05.050

Cited by 174 publications

(142 citation statements)

References 55 publications

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“…Cholinergic cells predominate in PPNc, but PPNc and anteromedial pars dissipata also contain large populations of GABAergic or glutamatergic neurons [77][78][79]. The input and output relationships of the various neuron groups in the PPN have not been precisely determined, but it is known that the nucleus gives rise to projections to the basal ganglia, thalamus, basal forebrain, reticular formation, and spinal cord [69,74,[80][81][82][83][84][85][86][87][88][89][90][91][92][93], thus being, at the same time, part of the extended basal ganglia family of nuclei [74], and a conduit of descending basal ganglia outputs. The function(s) of this nucleus are poorly understood, although portions of the (primate) PPN are implicated in the control of gait and balance because of overlap with the physiologically identified mesencephalic locomotor region and possibly other motor functions (see below).…”

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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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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“…In some patients, PPN DBS reduces gait and freezing problems unresponsive to drug and conventional stimulation approaches directed at subthalamic and pallidal targets, reduces falls and occasionally improves patients' state of vigilance and quality of sleep (Pereira et al, 2008;Ferraye et al, 2010). The magnitude of the effects, the exact location of the stimulation electrode and best technique of implantation of DBS leads into this nucleus are still being debated (Aravamuthan et al, 2007(Aravamuthan et al, , 2008(Aravamuthan et al, , 2009Weinberger et al, 2008;Fu et al, 2009;Shimamoto et al, 2010). There have also been several small experimental trials of extradural motor cortex stimulation in human patients (Benvenuti et al, 2006;Strafella et al, 2007;Cilia et al, 2007Cilia et al, , 2008Arle et al, 2008;Lefaucheur, 2009;Pagni et al, 2008).…”

Section: New Targets For Dbs In Pdmentioning

confidence: 99%

Parkinson's Disease Therapeutics: New Developments and Challenges Since the Introduction of Levodopa

Smith

Wichmann

Factor

et al. 2011

Neuropsychopharmacol

194

137

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The demonstration that dopamine loss is the key pathological feature of Parkinson's disease (PD), and the subsequent introduction of levodopa have revolutionalized the field of PD therapeutics. This review will discuss the significant progress that has been made in the development of new pharmacological and surgical tools to treat PD motor symptoms since this major breakthrough in the 1960s. However, we will also highlight some of the challenges the field of PD therapeutics has been struggling with during the past decades. The lack of neuroprotective therapies and the limited treatment strategies for the nonmotor symptoms of the disease (ie, cognitive impairments, autonomic dysfunctions, psychiatric disorders, etc.) are among the most pressing issues to be addressed in the years to come. It appears that the combination of early PD nonmotor symptoms with imaging of the nigrostriatal dopaminergic system offers a promising path toward the identification of PD biomarkers, which, once characterized, will set the stage for efficient use of neuroprotective agents that could slow down and alter the course of the disease.

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“…This cortical oscillatory activity could also be transmitted to the PPN directly via a connection between the motor cortex and PPN (demonstrated in non-human primates and humans (Matsumura et al, 2000;Aravamuthan et al, 2007;Muthusamy et al, 2007) but not verified in rodents) or indirectly via the basal ganglia (Inglis and Winn, 1995;Lee et al, 2000;Pahapill and Lozano, 2000). To examine relationships between oscillatory activity in the PPN and MCx after dopamine cell lesion, PPN spike and PPN LFP activity were recorded simultaneously with MCx LFP activity in intact rats and in lesioned rats 7-10 days after injection of 6-OHDA into the medial forebrain bundle.…”

Section: Ppn and MCX Spike And Lfp Relationships In The Urethane-anesmentioning

confidence: 99%

Altered neuronal activity relationships between the pedunculopontine nucleus and motor cortex in a rodent model of Parkinson's disease

Aravamuthan

Bergstrom

French

et al. 2008

Experimental Neurology

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The pedunculopontine nucleus (PPN) is a new deep brain stimulation (DBS) target for Parkinson's disease (PD), but little is known about PPN firing pattern alterations in PD. The anesthetized rat is a useful model for investigating the effects of dopamine loss on the transmission of oscillatory cortical activity through basal ganglia structures. After dopamine loss, synchronous oscillatory activity emerges in the subthalamic nucleus and substantia nigra pars reticulata in phase with cortical slow oscillations. To investigate the impact of dopamine cell lesion-induced changes in basal ganglia output on activity in the PPN, this study examines PPN spike timing with reference to motor cortex (MCx) local field potential (LFP) activity in urethane-and ketamine-anesthetized rats. Seven -ten days after unilateral 6-hydroxydopamine lesion of the medial forebrain bundle, spectral power in PPN spike trains and coherence between PPN spiking and PPN LFP activity increased in the ∼1 Hz range in urethane-anesthetized rats. PPN spike timing also changed from firing predominantly in-phase with MCx slow oscillations in the intact urethane-anesthetized rat to firing predominantly antiphase to MCx oscillations in the hemi-parkinsonian rat. These changes were not observed in the ketamine-anesthetized preparation. These observations suggest that dopamine loss alters PPN spike timing by increasing inhibitory oscillatory input to the PPN from basal ganglia output nuclei, a phenomenon that may be relevant to motor dysfunction and PPN DBS efficacy in PD patients.

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Topography of cortical and subcortical connections of the human pedunculopontine and subthalamic nuclei

Cited by 174 publications

References 55 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?

Parkinson's Disease Therapeutics: New Developments and Challenges Since the Introduction of Levodopa

Altered neuronal activity relationships between the pedunculopontine nucleus and motor cortex in a rodent model of Parkinson's disease

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