Abstract
Rapid eye movement sleep behavior disorder (RBD) contributes to injury due to the alteration of the expected atonia during rapid eye movement (REM) sleep. It occurs before the overt signs of Parkinson's disease (PD). The co-expression of PD and RBD is characterized by non-tremor predominant subtype and higher incidence of freezing. Freezing of gait (FOG) is a debilitating symptom seen in PD patients that lead to falls. While this phenomenon is understood poorly, the involvement of the pedunculopontine nucleus (PPN) and the neural circuits that control locomotion and gait have been examined. This network has also the same control for REM sleep and arousal. The close relationship between PD and RBD and FOG's consequences has led us to explore the relationship between RBD and PD with FOG. This review provides an overview of the neural connections that control gait, locomotion, and REM sleep. The neural changes were seen in PD with FOG and RBD, and sensory and motor changes observed in these two diseases. The functional neuroanatomy that controls REM sleep, arousal, and locomotion overlap significantly with multiple neural circuits affected in RBD and PD with FOG. Visual perception dysfunction and motor symptoms that primarily affect gait initiation are common to both patients with RBD and FOG in PD, leading to freezing episodes. Prospective studies should be conducted to elucidate the relationship of RBD and PD with FOG subtype and find innovative treatment approaches and diagnostic tools for PD with FOG.
Highlights
BackgroundRapid eye movement behavior sleep disorder (RBD) is characterized by a loss of normal muscle atonia and subsequent dream enactment [1]
Visual perception dysfunction and motor symptoms that primarily affect gait initiation are common to both patients with Rapid eye movement sleep behavior disorder (RBD) and Freezing of gait (FOG) in Parkinson's disease (PD), leading to freezing episodes
RBD likely happens before the overt motor, cognitive and autonomic impairments in PD proposed by Braak's staging system, which postulates that medullary structures are affected first in synucleinopathies and eventually ascend to more rostral structures; a prominent degeneration in the sublaterodorsal nucleus (SLD) will cause rapid eye movement (REM) sleep without atonia and RBD [3, 4]
Summary
Rapid eye movement behavior sleep disorder (RBD) is characterized by a loss of normal muscle atonia and subsequent dream enactment [1]. Fasano et al state that 90% of the lesions in their study were functionally connected to the bilateral dorsal medial cerebellum in FOG patients and a separate anatomic structure that lead to asterixis or hemichorea [29] These findings show a heterogeneous involvement of the neural networks that control REM sleep, locomotion, and posture. SMA - supplementary motor cortex; STN - subthalamic nucleus, Gpi/Snr - globus pallidus internus/substancia nigra pars reticulata; PPN - pedunculopontine nucleus; RSN - reticulospinal nucleus; SLD - sublaterodorsal nucleus; vMRF - ventromedial reticular formation; CPG - central pattern generators; CLR - cerebellar locomotor region; Spinal MN - spinal motor neuron; Spinal IN - spinal interneurons; MLR - mesencephalic locomotor region; RBD - rapid eye movement sleep behavior disorder; PD - Parkinson's disease; FOG - freezing of gait.
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