Tremor in the monkey with a cerebellar lesion

Gemba, Hisae; Sasaki, Kohsuke; Yoneda, Y.; Hashimoto, Shuji; Mizuno, Noboru

doi:10.1016/0014-4886(80)90152-1

Cited by 19 publications

(10 citation statements)

References 7 publications

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“…In chemically induced animal models of tremor 69 – 81 ( Table 2 ), we found that agents working on the cholinergic axis are able to induce tremor. For example, agents that promote the cholinergic nervous system, such as oxotremorine, 70 arecoline, 70 nicotine, 75 pilocarpine, 72 and physostigmine, 74 can produce tremor in rodents.…”

Section: Resultsmentioning

confidence: 92%

Animal Models of Tremor: Relevance to Human Tremor Disorders

Pan

et al. 2018

Tremor and Other Hyperkinetic Movements

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Section: Resultsmentioning

confidence: 92%

Animal Models of Tremor: Relevance to Human Tremor Disorders

Pan

et al. 2018

Tremor and Other Hyperkinetic Movements

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“…) and monkeys (Gemba et al. ; Sasaki and Gemba ). In humans, high‐resolution scalp EEG recordings suggest that brain activation during preparation for self‐paced movement in humans initiates 1 ~ 2 sec before the movement onset in the supplementary motor area (SMA), pre‐SMA, premotor cortex, primary motor cortex, and the anterior cingulate cortex (Cui et al.…”

Section: Discussionmentioning

confidence: 99%

Reappraisal of field dynamics of motor cortex during self‐paced finger movements

et al. 2013

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BackgroundThe exact origin of neuronal responses in the human sensorimotor cortex subserving the generation of voluntary movements remains unclear, despite the presence of characteristic but robust waveforms in the records of electroencephalography or magnetoencephalography (MEG).AimsTo clarify this fundamental and important problem, we analyzed MEG in more detail using a multidipole model during pulsatile extension of the index finger, and made some important new findings.ResultsMovement-related cerebral fields (MRCFs) were confirmed over the sensorimotor region contralateral to the movement, consisting of a temporal succession of the first premovement component termed motor field, followed by two or three postmovement components termed movement evoked fields. A source analysis was applied to separately model each of these field components. Equivalent current diploes of all components of MRCFs were estimated to be located in the same precentral motor region, and did not differ with respect to their locations and orientations. The somatosensory evoked fields following median nerve stimulation were used to validate these findings through comparisons of the location and orientation of composite sources with those specified in MRCFs. The sources for the earliest components were evoked in Brodmann's area 3b located lateral to the sources of MRCFs, and those for subsequent components in area 5 and the secondary somatosensory area were located posterior to and inferior to the sources of MRCFs, respectively. Another component peaking at a comparable latency with the area 3b source was identified in the precentral motor region where all sources of MRCFs were located.ConclusionThese results suggest that the MRCF waveform reflects a series of responses originating in the precentral motor area.

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“…Because the cerebellum modulates movement via this efferent pathway, the loss of Purkinje cells should be considered a functional deficit. Cerebellar damage is known to be associated with abnormalities in gait and posture, limb movement deficits (including ataxia and intention tremor), dysarthria, and oculomotor disturbances across species (Gemba et al, 1980;Trouillas et al, 1997;Fonnum and Lock, 2000;Sarna and Hawkes, 2003;). In the present study, no observations of this nature were noted in affected animals.…”

Section: Cerebellar Lesionsmentioning

confidence: 99%

Six-Month Continuous Intraputamenal Infusion Toxicity Study of Recombinant Methionyl Human Glial Cell Line-Derived Neurotrophic Factor (r-metHuGDNF) in Rhesus Monkeys

Hovland¹,

Boyd²,

Butt³

et al. 2007

Toxicologic Path.

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Recombinant human glial cell line-derived neurotrophic factor (r-metHuGDNF) is a potent neuronal growth and survival factor that has been considered for clinical use in the treatment of Parkinson's disease (PD). Here we present results of a 6-month toxicology study in rhesus monkeys conducted to support clinical evaluation of chronic intraputamenal infusion of r-metHuGDNF for PD. Monkeys (6-9/sex/group) were treated with 0 (vehicle), 15, 30, or 100 micro g/day r-metHuGDNF by continuous unilateral intraputamenal infusion (150 micro l/day flow rate) for 6 months; a subset of animals (2-3/sex/group) underwent a subsequent 3-month treatment-free recovery period. Notable observations included reduced food consumption and body weight at 100 micro g/day and meningeal thickening underlying the medulla oblongata and/or overlying various spinal cord segments at 30 and 100 micro g/day. In addition, multifocal cerebellar Purkinje cell loss (with associated atrophy of the molecular layer and, in some cases, granule cell loss) was observed in 4 monkeys in the 100-micro g/day group. This cerebellar finding has not been observed in previous nonclinical studies evaluating r-metHuGDNF. The small number of affected animals precludes definitive conclusions regarding the pathogenesis of the cerebellar lesion, but the data support an association with r-metHuGDNF treatment.

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Tremor in the monkey with a cerebellar lesion

Cited by 19 publications

References 7 publications

Animal Models of Tremor: Relevance to Human Tremor Disorders

Animal Models of Tremor: Relevance to Human Tremor Disorders

Reappraisal of field dynamics of motor cortex during self‐paced finger movements

Six-Month Continuous Intraputamenal Infusion Toxicity Study of Recombinant Methionyl Human Glial Cell Line-Derived Neurotrophic Factor (r-metHuGDNF) in Rhesus Monkeys

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