Neuronal activity in the basal ganglia and thalamus in patients with dystonia

Zhuang, Ping; Li, Yongjie; Hallett, Mark

doi:10.1016/j.clinph.2004.06.006

Cited by 137 publications

(115 citation statements)

References 43 publications

Supporting

Mentioning

102

Contrasting

Unclassified

Order By: Relevance

“…The presence of lowfrequency discharge in the GPi in patients with dystonia is similar to that in other hyperkinetic disorders, including chorea/ ballismus and motor tics [197,203,204]. Other studies have shown the emergence of low-frequency oscillations in single-cell and LFP activities in the basal ganglia or thalamus [200,201,[205][206][207], comparable with those found in PD. Electrocorticographic recordings over the MC in patients with isolated dystonia showed less coupling between the phase of beta-band oscillations and the amplitude of gamma-band oscillations than found in patients with PD [208].…”

Section: Dystoniasupporting

confidence: 72%

“…Based on pharmacologic studies, there seems to be a relative increase in the activity of striatal neurons of the direct pathway over those that give rise to the indirect pathway in dystonia [195,196], and single-cell recording studies in patients undergoing functional neurosurgical treatments have demonstrated low discharge rates in both GPe and GPi [197][198][199][200][201][202], in distinction to the aforementioned changes in PD where GPi discharge rates are generally increased. The presence of lowfrequency discharge in the GPi in patients with dystonia is similar to that in other hyperkinetic disorders, including chorea/ ballismus and motor tics [197,203,204].…”

Section: Dystoniamentioning

confidence: 99%

See 1 more Smart Citation

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

2016

View full text Add to dashboard Cite

Deep brain stimulation (DBS) is highly effective for both hypo-and hyperkinetic movement disorders of basal ganglia origin. The clinical use of DBS is, in part, empiric, based on the experience with prior surgical ablative therapies for these disorders, and, in part, driven by scientific discoveries made decades ago. In this review, we consider anatomical and functional concepts of the basal ganglia relevant to our understanding of DBS mechanisms, as well as our current understanding of the pathophysiology of two of the most commonly DBS-treated conditions, Parkinson's disease and dystonia. Finally, we discuss the proposed mechanism(s) of action of DBS in restoring function in patients with movement disorders. The signs and symptoms of the various disorders appear to result from signature disordered activity in the basal ganglia output, which disrupts the activity in thalamocortical and brainstem networks. The available evidence suggests that the effects of DBS are strongly dependent on targeting sensorimotor portions of specific nodes of the basal gangliathalamocortical motor circuit, that is, the subthalamic nucleus and the internal segment of the globus pallidus. There is little evidence to suggest that DBS in patients with movement disorders restores normal basal ganglia functions (e.g., their role in movement or reinforcement learning). Instead, it appears that high-frequency DBS replaces the abnormal basal ganglia output with a more tolerable pattern, which helps to restore the functionality of downstream networks.

show abstract

Section: Dystoniasupporting

confidence: 72%

Section: Dystoniamentioning

confidence: 99%

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

2016

View full text Add to dashboard Cite

show abstract

“…Similarly irregular firing patterns have also been recorded in the GPi of humans either with severe dystonia or severe TS (41). § § Although it is possible that these firing patterns may be a downstream effect of striatal abnormalities in these conditions, they highlight the possible significance of an intrinsic GPi defect.…”

Section: Discussionmentioning

confidence: 86%

Altered parvalbumin-positive neuron distribution in basal ganglia of individuals with Tourette syndrome

Kalanithi

Zheng

Kataoka

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

486

384

View full text Add to dashboard Cite

Tourette syndrome (TS) is a childhood neuropsychiatric disorder characterized by motor and vocal tics. Imaging studies found alterations in caudate (Cd) and putamen volumes. To investigate possible alterations in cell populations, postmortem basal ganglia tissue from individuals with TS and normal controls was analyzed by using unbiased stereological techniques. A markedly higher total neuron number was found in the globus pallidus pars interna (GPi) of TS. In contrast, a lower neuron number and density was observed in the globus pallidus pars externa and in the Cd. An increased number and proportion of the GPi neurons were positive for the calcium-binding protein parvalbumin in tissue from TS subjects, whereas lower densities of parvalbumin-positive interneurons were observed in both the Cd and putamen of TS subjects. This change is consistent with a developmental defect in tangential migration of some GABAergic neurons. The imbalance in striatal and GPi inhibitory neuron distribution suggests that the functional dynamics of cortico-striato-thalamic circuitry are fundamentally altered in severe, persistent TS.T ourette syndrome (TS) is a childhood neuropsychiatric disorder characterized by persistent motor and vocal tics, which may or may not abate upon entering adulthood. Tics are sudden stereotyped motor sequences of varying intensity and complexity, often preceded by compulsions or sensory phenomena. Neither the etiology nor the pathophysiology of TS is well understood. Both genetic and environmental factors are thought to be important, but the exact role of each has not yet been identified (1). Epigenetic events that increase the risk of developing tic disorder or TS include perinatal hypoxic-ischemic events that damage the periventricular germinal matrix and adjacent deep regions of the brain (2). A considerable amount of data implicates the cortico-striato-thalamo-cortical circuit in TS pathophysiology, particularly basal ganglia (BG) abnormalities. The BG, a richly interconnected set of nuclei, is essential for the initiation and correct implementation of learned sequences of motor and cognitive segments that characterize purposive behavior. The two major inputs into the BG, from the cerebral cortex and the intralaminar nuclei of the thalamus, enter into the striatum, which consists of the caudate (Cd) and putamen (Pt). The firing of cortical inputs drives activity in both medium spiny neurons (MSNs) (3) and several types of interneurons, including parvalbumin (PV)-positive (PVϩ) GABAergic interneurons (4). Striatal PVϩ interneurons are connected by electrical junctions and form a web of inhibitory synapses throughout the striatum, coordinating the activities of MSNs, and likely increasing their threshold of firing in response to cortical inputs (5, 6). MSNs, which are the large majority of neurons in the striatum, project to the globus pallidus pars interna (GPi), either directly or indirectly via the subthalamic nucleus and the globus pallidus pars externa (GPe). These two pathways can be differentiate...

show abstract

“…The current pathophysiological model of dystonia was also questioned by data showing that pallidal DBS was able to inihibit a subpopulation of motor thalamic neurons (120) and the abscence of difference between GPe and GPi firing rate (119). However, clear correlation between abnormal neuronal activitiy and EMG activity was reported in the basal ganglia and thalamus of patients with dystonia (116,(121)(122)(123). Moreover, single unit recording performed in cerebellar relays of the thalamus revealed abnormal firing pattern and increased response to peripheral inputs in dystonic patients (123)(124)(125).…”

Section: Or Cerebellum (93)mentioning

confidence: 99%

Dystonia Pathophysiology: A Critical Review

Burbaud¹

2012

Dystonia - The Many Facets

View full text Add to dashboard Cite

Neuronal activity in the basal ganglia and thalamus in patients with dystonia

Cited by 137 publications

References 43 publications

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

Altered parvalbumin-positive neuron distribution in basal ganglia of individuals with Tourette syndrome

Dystonia Pathophysiology: A Critical Review

Contact Info

Product

Resources

About