Connectivity of the human pedunculopontine nucleus region and diffusion tensor imaging in surgical targeting

Muthusamy, Karthikeyan; Aravamuthan, Bhooma R.; Kringelbach, Morten L.; Jenkinson, Ned; Voets, Natalie L.; Johansen‐Berg, Heidi; Stein, John; Aziz, Tipu Z.

doi:10.3171/jns-07/10/0814

Cited by 114 publications

(72 citation statements)

References 58 publications

(67 reference statements)

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“…In addition, electrophysiological recording during deep brain stimulation (DBS) in PD patients have shown that individual dorsal PPN neurons increase their firing rates with increased stepping frequency (Piallat et al, 2009). A direct monosynaptic pathway linking CN/PPN and motor cortices has been demonstrated in monkeys using tract tracing and diffusion tensor imaging (Aravamuthan et al, , 2009Muthusamy et al, 2007). Our finding supports the idea that this part of the MLR controls motor aspects of gait in humans and could help to target the lateral mesencephalus for DBS in PD patients with gait disorders.…”

Section: Discussionmentioning

confidence: 99%

Functional Parcellation of the Lateral Mesencephalus

Karachi¹,

André²,

Bertasi³

et al. 2012

Journal of Neuroscience

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The mesencephalic locomotor region (MLR), which includes the pedunculopontine nucleus (PPN) and the cuneiform nucleus (CN), has been recently identified as a key structure for locomotion and gait control in mammals. However, the function and the precise anatomy of the MLR remain unclear in humans. To study the lateral mesencephalus, we used fMRI in 15 right-handed healthy volunteers performing two tasks: imagine walking in a hallway and imagine an object moving along the same hallway. Both tasks were performed at two different speeds: normal and 30% faster. We identified two distinct networks of cortical activation: one involving motor/premotor cortices and the cerebellum for the walking task and the other involving posterior parietal and dorsolateral prefrontal cortices for the object moving task. In the lateral mesencephalus, we found that two different but anatomically connected parts of the MLR were activated during the fast condition of each task. The CN and the dorsal part of the PPN were activated during the fast imaginary walking task, whereas the ventral part of the PPN and the ventral part of the reticular formation were activated while subjects were imagining the object moving fast. Our data suggest that the lateral mesencephalus participates in different aspects of gait in humans, with the CN and dorsal PPN controlling motor aspects of locomotion and the ventral PPN being involved in integrating sensory information.

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Section: Discussionmentioning

confidence: 99%

Functional Parcellation of the Lateral Mesencephalus

Karachi¹,

André²,

Bertasi³

et al. 2012

Journal of Neuroscience

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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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“…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%

“…Evidence of a connection between the PPN and the motor cortex (MCx) in non-human primates (Matsumura et al, 2000) and the recent evidence of this connection in humans Muthusamy et al, 2007) suggest that this direct transmission of cortical oscillations is possible. Cortical oscillatory activity could also be transmitted to the PPN indirectly via the basal ganglia.…”

Section: Introductionmentioning

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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Connectivity of the human pedunculopontine nucleus region and diffusion tensor imaging in surgical targeting

Cited by 114 publications

References 58 publications

Functional Parcellation of the Lateral Mesencephalus

Functional Parcellation of the Lateral Mesencephalus

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

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

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