Anatomy, physiology, and pathophysiology of the pedunculopontine nucleus

Abstract

The pedunculopontine nucleus is composed of cholinergic and non-cholinergic neurones and is located in the caudal pontomesencephalic tegmentum. Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post-mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man.

Imagined gait modulates neuronal network dynamics in the human pedunculopontine nucleus

“…A high filter order (1000) was used to isolate narrow sub-bands of the LFP in order to distinguish, for example, high alpha oscillations (10-12 Hz) from low beta oscillations (12)(13)(14)(15)(16)(17)(18)(19)(20). The filtered signal was Hilbert transformed to extract the signal phase, and then the spike phase distribution (i.e.…”

“…Within the MLR, the pedunculopontine nucleus (PPN), that is extensively connected with the basal ganglia 11 , has a central role in the initiation and maintenance of gait [12][13][14] and lesions of the PPN induce gait deficits 14 . Gait and postural disturbances in PD are accompanied by cell loss within the PPN [14][15][16] , but are partially relieved by deep brain stimulation (DBS) in the PPN [17][18][19] , supporting the central role of the PPN in locomotion.Much is understood about the development and function of spinal cord CPGs 20 . However, while CPG function is controlled by afferent projections from the MLR 9, 10 , little is understood about activity within the MLR, and its response to movement.…”

The pathology roadmap in Parkinson disease

“…34,42 The pedunculopontine nucleus is rostral to the locus coeruleus and includes a mixture of cholinergic, glutamatergic and GABAergic neurons with an array of targets in the mesencephalon and diencephalon. 43 The pedunculopontine nucleus was reported to exhibit Lewy pathology by Braak's group. 4,28 Lewy pathology and neuronal loss also were reported.…”

Effects of subthalamic and nigral stimulation on gait kinematics in Parkinson's disease

“…This decreased vertical acceleration, as well as an increased gait asymmetry, is characteristic for axial motor impairment (33). The consistence of these kinematic findings with results from PPN stimulation may support the view that nigral stimulation might entrain pedunculopontine locomotor integration (30,31,34).…”