Objective: To quantify the characteristics of oscillatory neurons in the GPi in patients with PD.

Background: Abnormal oscillatory activity has been predicted to play a role in the generation of parkinsonian motor symptoms. The internal globus pallidus (GPi) of the basal ganglia is in a unique and powerful position to influence motor processing by receiving both direct and indirect pathways in basal ganglia, and projecting the information to the pallidal receiving area of thalamus. According to the pathophysiology model of Parkinson’s disease (PD), excessive neuronal activity in the GPi promotes bradykinesia. Despite the clinical importance of the GPi in common movement disorders such as PD, we still have limited data to understand the mechanism of parkinsonian motor symptoms.

Method: Nine PD patients who underwent unilateral pallidotomy or bilateral electrode implantation for GPi deep brain stimulation treatment were studied.  Microelectrode recording was performed in the GPi and the electromyogram (EMG) was simultaneously recorded. The interspike intervals (ISI) and coefficient of variation of ISI were assessed. Spectral analysis was used to evaluate neuronal oscillatory activity. Mean spontaneous firing rates (MSFR) and proportions of patterns of GPi oscillatory neurons were calculated. Coherence analysis was used to study relationship between oscillatory activity and limb symptoms.

Results: Seventy-nine GPi neurons were identified. There were 25.3% (20/79) β frequency oscillatory neurons, 24.1% (19/79) non-oscillatory neurons, and 50.6% (40/79) tremor frequency (3-6 Hz) oscillatory neurons . Of the tremor frequency neurons, 40% (16/40) were significantly coherent with the electromyogram (EMG) activity during tremor. The median coherence magnitude was 0.7 (range of 0.44 to 0.92, mean value: 0.70 ± 0.21). ISI analysis showed the mean firing rate of neurons with all three patterns (n=79) was 81.5 ± 7.4 Hz (range of 65.2 to 104.8 Hz).

Conclusion: The hyperactivity of GPi neurons and the high proportion of tremor related oscillatory neurons in GPi in PD, support prediction that increased firing rate and altered neuronal oscillatory patterns in GPi not only promotes akinesia but also promotes tremorgenesis. The high coherence between GPi and the EMG of limb tremor suggests that the pallidum is able to trigger hyperactivity in the cerebellothalamic circuit, leading to parkinsonian resting tremor.

References: 1. Albin RL, Young AB, Penney JB. The functional anatomy of basal ganglia disorders. Trends Neurosci (1989) 12(10):366-75. d 2. DeLong MR. Primate models of movement disorders of basal ganglia origin. Trends Neurosci (1990) 13(7):281-5. 3. Helmich RC, Janssen MJ, Oyen WJ, Bloem BR, Toni I. Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor. Ann Neurol (2011) 69(2):269-81. 4. Helmich RC, Hallett M, Deuschl G, Toni I, Bloem BR. Cerebral causes and consequences of parkinsonian resting tremor: a tale of two circuits? Brain (2012) 135(Pt 11):3206-26. 5. Albin RL, Young AB, Penney JB. The functional anatomy of disorders of the basal ganglia. Trends Neurosci (1995) 18(2):63-4.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/oscillaotory-activity-in-the-globus-pallidus-internus-in-patients-with-parkinsons-disease/