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Neurology with dementia with Lewy bodies
Published in John O'Brien, Ian McKeith, David Ames, Edmond Chiu, Dementia with Lewy Bodies and Parkinson's Disease Dementia, 2005
The EPS in PD, PDD and DLB are therefore likely to be a spectrum, with a shift towards greater nondopaminergic motor system involvement through PD to DLB. This is consistent with previous studies reporting motor features mediated by nondopaminergic pathways (speech, posture and balance) to correlate more closely with incident dementia in PD than tremor, rigidity and bradykinesia (Foltynie et al, 2002). Degeneration within cholinergic brainstem nuclei, such as the pedunculopontine nucleus, may contribute significantly to the nondopaminergic clinical features.
Sleep dysfunction in Parkinson’s disease
Published in Jeremy Playfer, John Hindle, Andrew Lees, Parkinson's Disease in the Older Patient, 2018
Sleep disorders related to PD are multifactorial and for this reason, attributing causation is complex. The pathophysiology of much of sleep disturbance in PD is complex and largely unknown. Degeneration of central sleep regulatory neurones, either directly due to dopaminergic cell loss, or due to an indirect effect of dopaminergic cell loss in the brainstem and related thalamocortical pathways, is implicated.17,19,20 A preclinical pathological staging of PD has been proposed by Braak.21 It has been believed traditionally that the pathological process of degeneration of dopaminergic neurones starts in the substantia nigra. Braak proposes an alternative and has introduced the concept of a six-stage pathological process, beginning at clearly designated ‘induction sites’.21 In Braak stage-1 of PD, there is degeneration of the olfactory bulb and the anterior olfactory nucleus and this may clinically manifest as olfactory dysfunction. Progression of the pathological process to the lower brainstem occurs in Braak stage-2 and these are key areas mediating NMS – such as olfaction, sleep homeostasis and other autonomic features. The brainstem areas, particularly the raphe nucleus (serotonin), locus caeruleus (norepinephrine) and pedunculopontine nucleus play a major role in the sleep–wake cycle and mediate the so-called flip-flop switch (seeFigure 9.2) that mediates thalamocortical arousal.22 The clinico-pathological correlates are becoming increasingly evident. There is strong evidence that symptoms such as olfactory dysfunction and sleep disturbances like RBD or excessive day-time sleepiness may indeed precede the development of motor symptoms of PD, thus correlating with Braak stages 1 and 2.2,23,24,25
Spinal cord stimulation for gait disturbances in Parkinson’s disease
Published in Expert Review of Neurotherapeutics, 2023
Nora Vanegas-Arroyave, Joseph Jankovic
Deep brain stimulation (DBS) has been an effective treatment for the motor symptoms of PD. However, gait disturbances are not consistently alleviated by DBS, and, in some cases, they may even appear de novo or worsen postoperatively [20–24]. Transient improvement of axial symptoms including gait in PD has been demonstrated using low-frequency (80 Hz) stimulation [25] and there is evidence of superior effects of closed loop DBS, to suppress beta band activity within the STN and reduce FOG during a stepping in place task [26]. In addition to conventional, DBS targets (STN and Globus pallidus – GPi), studies in nonhuman primates have suggested that dysfunction of the pedunculopontine nucleus (PPN) is at least partly responsible for the axial motor symptoms and particularly gait issues associated with PD [8]. Interestingly, the PPN is highly connected to the GPi, the cerebellum, and the spinal cord [27]. Cholinergic neurons of the PPN and their projections are known to be particularly important for locomotion and it has been postulated that the PPN may function as an integrative interface between various brainstem and subcortical structures involved in locomotion. However, human studies of PPN DBS have reported marked outcome variability [28–32] and the use of PPN DBS for FOG continues to be an investigational procedure. Additional targets, including the zona incerta, the cuneiform nucleus, and the substantia nigra, have been investigated in small series of patients. To date, information on the efficacy of these new targets is limited.
Current perspectives on galvanic vestibular stimulation in the treatment of Parkinson’s disease
Published in Expert Review of Neurotherapeutics, 2021
Soojin Lee, Aiping Liu, Martin J. McKeown
The pedunculopontine nucleus (PPN) has afferent and efferent connections with the cerebellum, BG, thalamus, cerebral cortex, and spinal cord [74], and the cerebellar control of movement and postural balance may be related to its pathway with the PPN [75]. The PPN may also act as an interface between the signals relayed from the cerebellum and BG systems to the cerebral cortex, playing important functional roles in the motor control system and executive function [76]. The PPN is implicated in the freezing of gait (FOG) in PD in many studies and has been suggested as a potential target area for DBS to treat FOG and other gait disturbances [74]. The vestibular nuclei have direct projections to the PPN [73], and RN-GVS modulates the PPN connectivity with pallidum and cerebellar cortex in PD patients [77], suggesting GVS might be useful in ameliorating gait disturbances.
Neuro-ophthalmology of movement disorders
Published in Expert Review of Ophthalmology, 2018
High frequency of ocular motor signs in PD suggests impaired interaction between basal ganglia and ocular motility pathways [16]. Ocular motor symptoms in PD are likely the result of the imbalance between direct and indirect basal ganglia pathways causing increased output from the substantia nigra that leads to the excessive inhibition of superior colliculus. While voluntary saccade pathways connecting cortex with superior colliculus include basal ganglia, reflexive saccades generation pathways bypass basal ganglia that can explain preservation of reflexive saccades in early stages of PD when voluntary saccades are impaired [17]. Impaired anti-saccades in PD patients can be the result of a dysfunction of the pedunculopontine nucleus due to correlation between degree of the anti-saccades latency and impaired postural control in PD patients [18]. Square wave jerks observed in some PD patients, but much more frequently noted in patients with PSP, are thought to be the result of compensatory increased activity in frontal eye field in response to the excessive inhibition of superior colliculus [17].