Neuronal Activity in GP and Vim of Parkinsonian Patients and Clinical Changes of Tremor through Surgical Interventions

Hayase, Nobuaki; Miyashita, Nobuo; Endo, Katsuyuki; Narabayashi, H.

doi:10.1159/000029643

Cited by 15 publications

(7 citation statements)

References 27 publications

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“…3). 14, 67–70, 76 Oscillations in single‐cell discharge have also been observed with extracellular recording techniques in parkinsonian patients undergoing functional neurosurgery 77–82. LFP recordings from implanted DBS electrodes in GPi and STN of such patients have shown similar oscillatory activity.…”

Section: Pathological Oscillatory Activity In Basal Ganglia–thalamocomentioning

confidence: 91%

Oscillations in the basal ganglia under normal conditions and in movement disorders

2006

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A substantial body of work within the last decade has demonstrated that there is a variety of oscillatory phenomena that occur in the basal ganglia and in associated regions of the thalamus and cortex. Most of the earlier studies focused on recordings in rodents and primates. More recently, significant advances have been made in this field of research through the analysis of basal ganglia field potentials recorded from implanted deep brain stimulation electrodes in the basal ganglia of human patients with Parkinson's disease and other disorders. It now appears that oscillatory activity may play a significant role in the pathogenesis of these diseases. The most significant finding is that in Parkinson's disease synchronized oscillatory activity in the 10- to 35-Hz band (often termed "beta-band") is prevalent in the basal ganglia-thalamocortical circuits, and that such activity can be reduced by dopaminergic treatments. The entrainment of large portions of these circuits may disrupt information processing in them and may lead to parkinsonian akinesia (and perhaps tremor). Although less firmly established than the role of oscillations in movement disorders, oscillatory activities at higher frequencies may also be a component of normal basal ganglia physiology.

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Section: Pathological Oscillatory Activity In Basal Ganglia–thalamocomentioning

confidence: 91%

Oscillations in the basal ganglia under normal conditions and in movement disorders

2006

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“…The nucleus lateralis oralis (LO/VOL) has received much attention in stereotactic treatment of Parkinson's disease and other involuntary motor disorders [135,184], and thalamotomy of the motor thalamus is effective for dystonia treatment even if the concrete target is not well defined [113]. Thalamotomy of the nucleus lateralis oralis ameliorates rigidity but not tremor [137], but the thalamotomy of the subregio intermedia (LIM/Vim), the cerebellar thalamus, results in a permanent abolition of the tremor without affecting the general somatic sensation [68,138]. Multiple sclerosis patients with disabling tremor have also benefited from thalamotomy [111].…”

Section: Regio Superiormentioning

confidence: 99%

Functional anatomy of thalamus and basal ganglia

Herrero

Barcia

Navarro

2002

Child's Nervous System

573

415

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THALAMUS: The human thalamus is a nuclear complex located in the diencephalon and comprising of four parts (the hypothalamus, the epythalamus, the ventral thalamus, and the dorsal thalamus). The thalamus is a relay centre subserving both sensory and motor mechanisms. Thalamic nuclei (50-60 nuclei) project to one or a few well-defined cortical areas. Multiple cortical areas receive afferents from a single thalamic nucleus and send back information to different thalamic nuclei. The corticofugal projection provides positive feedback to the "correct" input, while at the same time suppressing irrelevant information. Topographical organisation of the thalamic afferents and efferents is contralateral, and the lateralisation of the thalamic functions affects both sensory and motoric aspects. Symptoms of lesions located in the thalamus are closely related to the function of the areas involved. An infarction or haemorrhage thalamic lesion can develop somatosensory disturbances and/or central pain in the opposite hemibody, analgesic or purely algesic thalamic syndrome characterised by contralateral anaesthesia (or hypaesthesia), contralateral weakness, ataxia and, often, persistent spontaneous pain. BASAL GANGLIA: Basal ganglia form a major centre in the complex extrapyramidal motor system, as opposed to the pyramidal motor system (corticobulbar and corticospinal pathways). Basal ganglia are involved in many neuronal pathways having emotional, motivational, associative and cognitive functions as well. The striatum (caudate nucleus, putamen and nucleus accumbens) receive inputs from all cortical areas and, throughout the thalamus, project principally to frontal lobe areas (prefrontal, premotor and supplementary motor areas) which are concerned with motor planning. These circuits: (i) have an important regulatory influence on cortex, providing information for both automatic and voluntary motor responses to the pyramidal system; (ii) play a role in predicting future events, reinforcing wanted behaviour and suppressing unwanted behaviour, and (iii) are involved in shifting attentional sets and in both high-order processes of movement initiation and spatial working memory. Basal ganglia-thalamo-cortical circuits maintain somatotopic organisation of movement-related neurons throughout the circuit. These circuits reveal functional subdivisions of the oculomotor, prefrontal and cingulate circuits, which play an important role in attention, learning and potentiating behaviour-guiding rules. Involvement of the basal ganglia is related to involuntary and stereotyped movements or paucity of movements without involvement of voluntary motor functions, as in Parkinson's disease, Wilson's disease, progressive supranuclear palsy or Huntington's disease. The symptoms differ with the location of the lesion. The commonest disturbances in basal ganglia lesions are abulia (apathy with loss of initiative and of spontaneous thought and emotional responses) and dystonia, which become manifest as behavioural and motor disturbances, respectively.

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“…81 Lesions that can effectively suppress rigidity or tremor of various origins are located in the ventrolateral thalamus, in the area that receives mainly cerebellar output. [82][83][84][85][86] Lenz and colleagues 87 could demonstrate that some thalamic neurons advance the tremor, suggesting an efferent role for this firing. The percentage of tremor cells among the different groups seems to be higher than for the subthalamic nucleus (STN) and globus pallidus pars interna (GPi).…”

Section: Cerebellothalamic Pathophysiological Models Ofmentioning

confidence: 99%

Pathophysiology of Parkinson's disease: From clinical neurology to basic neuroscience and back

Bergman¹,

Deuschl²

2002

Mov Disord.

270

190

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Parkinson's disease (PD) is characterized by motor and nonmotor (cognitive and limbic) deficits. The motor signs of PD include hypokinetic signs such as akinesia/bradykinesia, rigidity and loss of normal postural reflexes, and hyperkinetic signs such as tremor. Dopamine depletion in the striatum is the hallmark of PD and of its animal models, still the pathophysiology of the parkinsonian symptoms and especially of parkinsonian tremor are under debate. The most extreme hypotheses argue about peripheral versus central nervous system origin, intrinsic cellular oscillator versus network oscillators, and basal ganglia-based pathophysiology versus cerebellar-thalamic based pathophysiology. Recent studies support the view that parkinsonian symptoms are most likely due to abnormal synchronous oscillating neuronal activity within the basal ganglia. Peripheral factors do only play a minor role for the generation, maintenance, and modulation of PD tremor and other signs. The most likely candidates producing these neuronal oscillations are the weakly coupled neural networks of the basal ganglia-thalamo-cortical loops. However, the present evidence supports the view that the basal ganglia loops are influenced by other neuronal structures and systems and that the tuning of these loops by cerebello-thalamic mechanisms and by other modulator neurotransmitter systems entrain the abnormal synchronized oscillations. Neurosurgical procedures, such as lesions or high-frequency stimulation of different parts of the loop, might resume the normal unsynchronized activity of the basal ganglia circuitry, and, therefore, ameliorate the clinical symptoms of Parkinson's disease.

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Neuronal Activity in GP and Vim of Parkinsonian Patients and Clinical Changes of Tremor through Surgical Interventions

Cited by 15 publications

References 27 publications

Oscillations in the basal ganglia under normal conditions and in movement disorders

Oscillations in the basal ganglia under normal conditions and in movement disorders

Functional anatomy of thalamus and basal ganglia

Pathophysiology of Parkinson's disease: From clinical neurology to basic neuroscience and back

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