Category: Choreas (Non-Huntington's Disease)
Objective: To investigate the mechanisms of neuronal discharges of the globus pallidus which drive choreic movements.
Background: Synchronized bursts and the low discharge rates of neurons in the internal globus pallidus (GPi) have been hypothesized to underlie the development of choreic movements. There are, however, few physiological studies that have examined the activity of neurons in the GPi in patients with chorea.
Method: Five patients with choreic movements (striatal lacunar infarction, dentatorubral-pallidoluysian atrophy, diabetic hemichorea-hemiballism, Huntington’s disease, tardive dyskinesia) were treated with either pallidotomy or GPi DBS. During intra-operative mapping, we recorded spontaneous neuronal activity from single neurons in the GPi and the external globus pallidus (GPe). Neuronal discharge rates and patterns were analyzed and compared with those collected from patients with Parkinson’s disease (PD) in the off-state.
Results: Choreic movements were abolished after pallidal surgery in all patients. We analyzed 49 GPi and 44 GPe neurons from the chorea patients and 183 GPi and 176 GPe neurons from 28 patients with PD off-medication. The discharge rates of GPi and GPe neurons in choreic disorders were significantly lower than those from GPi and GPe in PD and GPi neurons in the choreic patients had more burst activity. Covariance analysis also revealed that the percentage of spikes in bursts and discharge rates in GPi were significantly correlated in patients with chorea, and the linear regressions between them in PD and chorea were on the continuous distribution, suggesting that discharge rate is a significant determinant for differentiating patients with choreic from those with PD.
Conclusion: A combination of lower discharge rates and more burst activity of neurons in GPi is a driving force for choreic movements, and a decrease in mean discharge rates may be determinant of burstiness in the GPi and responsible for the transition from a non-choreic to a choreic state. As striatal lesions were present in all our patients we hypothesize that disruption of striatal input to the GPi leads to the observed physiological changes in GPi neuronal activity and subsequent development of choreic movement.
To cite this abstract in AMA style:
T. Hashimoto, T. Goto, K. Yoshida, L. Johnson, C. Hendrix, J. Vitek. Pallidal activity as a driving force of choreic movements [abstract]. Mov Disord. 2023; 38 (suppl 1). https://www.mdsabstracts.org/abstract/pallidal-activity-as-a-driving-force-of-choreic-movements/. Accessed November 22, 2024.« Back to 2023 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/pallidal-activity-as-a-driving-force-of-choreic-movements/