Low-frequency stimulation of the pedunculopontine nucleus affects gait and the neurotransmitter level in the ventrolateral thalamic nucleus in 6-OHDA Parkinsonian rats

Wen, Peng; Li, Min; Xiao, Haijun; Ding, Rui; Chen, Huan; Chang, Jing‐Yu; Zhou, Ming; Yang, Yong; Wang, Jun; Zheng, Weiran; Zhang, Wangming

doi:10.1016/j.neulet.2015.06.006

Cited by 20 publications

(16 citation statements)

References 26 publications

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“…This is not surprising given that both dopamine replacement and STN deep brain stimulation generally fail to ameliorate these symptoms sufficiently [66,67]. While the underlying pathophysiology specific to PIGD is unknown, several mechanisms have been proposed including cholinergic projections from the pedunculopontine nucleus and cortical pathology [68,69]. Our findings are in line with autopsy studies which show that PIGD patients have similar midbrain pathology as non-PIGD [70].…”

Section: Substantia Nigra Volume Is Not Associated With Tremor or Pigdsupporting

confidence: 86%

Substantia Nigra Volume Dissociates Bradykinesia and Rigidity from Tremor in Parkinson’s Disease: A 7 Tesla Imaging Study

Poston

Cruadhlaoich

Santoso

et al. 2020

JPD

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Background: In postmortem analysis of late stage Parkinson's disease (PD) neuronal loss in the substantial nigra (SN) correlates with the antemortem severity of bradykinesia and rigidity, but not tremor. Objective: To investigate the relationship between midbrain nuclei volume as an in vivo biomarker for surviving neurons in mild-to-moderate patients using 7.0 Tesla MRI. Methods: We performed ultra-high resolution quantitative susceptibility mapping (QSM) on the midbrain in 32 PD participants with less than 10 years duration and 8 healthy controls. Following blinded manual segmentation, the individual volumes of the SN, subthalamic nucleus, and red nucleus were measured. We then determined the associations between the midbrain nuclei and clinical metrics (age, disease duration, MDS-UPDRS motor score, and subscores for bradykinesia/rigidity, tremor, and postural instability/gait difficulty). Results: We found that smaller SN correlated with longer disease duration (r =-0.49, p = 0.004), more severe MDS-UPDRS motor score (r =-0.42, p = 0.016), and more severe bradykinesia-rigidity subscore (r =-0.47, p = 0.007), but not tremor or postural instability/gait difficulty subscores. In a hemi-body analysis, bradykinesia-rigidity severity only correlated with SN contralateral to the less-affected hemi-body, and not contralateral to the more-affected hemi-body, possibly reflecting the greatest change in dopamine neuron loss early in disease. Multivariate generalized estimating equation model confirmed that bradykinesia-rigidity severity, age, and disease duration, but not tremor severity, predicted SN volume. Conclusions: In mild-to-moderate PD, SN volume relates to motor manifestations in a motor domain-specific and lateralitydependent manner. Non-invasive in vivo 7.0 Tesla QSM may serve as a biomarker in longitudinal studies of SN atrophy and in studies of people at risk for developing PD.

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Section: Substantia Nigra Volume Is Not Associated With Tremor or Pigdsupporting

confidence: 86%

Substantia Nigra Volume Dissociates Bradykinesia and Rigidity from Tremor in Parkinson’s Disease: A 7 Tesla Imaging Study

Poston

Cruadhlaoich

Santoso

et al. 2020

JPD

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“…Therefore, it has gained wide attention whether the PPN-DBS could improve the axial symptoms of PD patients [58]. Results in the PD animal model showed that low-frequency PPN-DBS can improve the gait disorders and postural abnormalities [59][60][61].…”

Section: Inspiration To Surgical Workmentioning

confidence: 99%

The prevalence of freezing of gait in Parkinson’s disease and in patients with different disease durations and severities

Lin

et al. 2020

Chin Neurosurg Jl

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Background: The prevalence rates of freezing of gait (FOG) in Parkinson's disease (PD) vary widely, ranging from 14.0 to 55.1%. Our aim is to calculate the overall prevalence of FOG in all PD patients with different disease durations and severities. Methods: Using Medline/PubMed/Embase, we carried out a systematic literature search for studies reporting the PD and clinically relevant FOG. Results: After primary screening, a total of 35 studies were identified and further analyzed for inclusion into the analysis, and 29 studies fulfilled the quality criteria and included in this meta-analysis. The overall prevalence of FOG in PD was 39.9% (95% CI 35.3-44.5%). The FOG identified by the freezing of gait questionnaire item 3 may be more prevalent (43.8%, 95% CI 38.5-49.1%) than the FOG identified by the Unified Parkinson's Disease Rating Scale item 14 (36.0%, 95% CI 29.0-43.1%). Disease duration and severity are both the clinical features associated with the FOG. The highest FOG prevalence rate in PD patients was seen in patients with disease durations ≥ 10 years, at 70.8%, followed that of PD patients with disease durations ≥ 5 years (53.3%), and PD patients with disease durations < 5 years (22.4%). FOG presented in 28.4% of PD patients with Hoehn and Yahr staging (H&Y) score ≤ 2.5, and in 68.4% of PD patients with H&Y score ≥ 2.5. Conclusion: This meta-analysis confirms that the prevalence of FOG in PD is considerable, and highlights the need for accurate identification of FOG in PD.

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“…Effects of PPN stimulation were also explored in 6OHDA-lesioned rats. 53 Automated gait analysis was employed to assess stride length, base of support, and the maximum area of a paw that came into contact with the glass plate. The base of support and maximum area were larger in lesioned animals, and this was partially corrected by PPN stimulation.…”

Section: Cholinergic Disturbances In Pdmentioning

confidence: 99%

Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease

Pérez-Lloret

Barrantes

2016

npj Parkinson's Disease

179

122

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In view of its ability to explain the most frequent motor symptoms of Parkinson’s Disease (PD), degeneration of dopaminergic neurons has been considered one of the disease’s main pathophysiological features. Several studies have shown that neurodegeneration also affects noradrenergic, serotoninergic, cholinergic and other monoaminergic neuronal populations. In this work, the characteristics of cholinergic deficits in PD and their clinical correlates are reviewed. Important neurophysiological processes at the root of several motor and cognitive functions remit to cholinergic neurotransmission at the synaptic, pathway, and circuital levels. The bulk of evidence highlights the link between cholinergic alterations and PD motor symptoms, gait dysfunction, levodopa-induced dyskinesias, cognitive deterioration, psychosis, sleep abnormalities, autonomic dysfunction, and altered olfactory function. The pathophysiology of these symptoms is related to alteration of the cholinergic tone in the striatum and/or to degeneration of cholinergic nuclei, most importantly the nucleus basalis magnocellularis and the pedunculopontine nucleus. Several results suggest the clinical usefulness of antimuscarinic drugs for treating PD motor symptoms and of inhibitors of the enzyme acetylcholinesterase for the treatment of dementia. Data also suggest that these inhibitors and pedunculopontine nucleus deep-brain stimulation might also be effective in preventing falls. Finally, several drugs acting on nicotinic receptors have proved efficacious for treating levodopa-induced dyskinesias and cognitive impairment and as neuroprotective agents in PD animal models. Results in human patients are still lacking.

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Low-frequency stimulation of the pedunculopontine nucleus affects gait and the neurotransmitter level in the ventrolateral thalamic nucleus in 6-OHDA Parkinsonian rats

Cited by 20 publications

References 26 publications

Substantia Nigra Volume Dissociates Bradykinesia and Rigidity from Tremor in Parkinson’s Disease: A 7 Tesla Imaging Study

Substantia Nigra Volume Dissociates Bradykinesia and Rigidity from Tremor in Parkinson’s Disease: A 7 Tesla Imaging Study

The prevalence of freezing of gait in Parkinson’s disease and in patients with different disease durations and severities

Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease

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