Tremor-frequency (3–6 Hz) activity in the sensorimotor arm representation of the internal segment of the globus pallidus in patients with Parkinson's disease

Lemstra, Afina W.; Metman, Leo Verhagen; Lee, J. I.; Dougherty, Patrick M.; Lenz, Frederick A.

doi:10.1016/s0304-3940(99)00343-2

Cited by 55 publications

(48 citation statements)

References 12 publications

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“…This may account at least in some of the cases for the lack of correlation between the STN tremor-frequency neuronal activity and the tremor recorded in the sampled muscles. Our observation is consistent with previous reports showing that neuronal oscillations in the globus pallidus are not always coherent with the tremulous limb (Hurtado et al 1999;Lemstra et al 1999;Raz et al 2000), although their oscillation frequency is similar to the frequency of the limb tremor (Hutchison et al 1997). Several studies of multilimb EMG recordings in PD patients also indicated that tremor in different limbs is largely uncorrelated (Ben-Pazi et al 2001;Hurtado et al 2000;Raethjen et al 2000).…”

Section: Tremor-frequency Neuronal Activity: Relation To Tremorsupporting

confidence: 92%

“…Instead there is growing evidence suggesting that beta oscillations play an anti-kinetic role and contribute to bradykinesia and rigidity in PD (Brown 2003;Chen et al 2007;Kuhn et al 2006Kuhn et al , 2008Ray et al 2008). On the other hand, oscillatory firing in the tremor frequency range is frequently coherent with the tremor of a particular limb although uncorrelated oscillations are commonplace as well (Hurtado et al 1999(Hurtado et al , 2005Lemstra et al 1999;Raz et al 2000). It was originally suggested by Alberts et al (1969) that PD tremor is generated by segregated parallel networks, each involving a different limb.…”

Section: Introductionmentioning

confidence: 99%

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Increased Gamma Oscillatory Activity in the Subthalamic Nucleus During Tremor in Parkinson's Disease Patients

Weinberger¹,

Hutchison²,

Lozano³

et al. 2009

Journal of Neurophysiology

127

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. Rest tremor is one of the main symptoms in Parkinson's disease (PD), although in contrast to rigidity and akinesia, the severity of the tremor does not correlate well with the degree of dopamine deficiency or the progression of the disease. Studies suggest that akinesia in PD patients is related to abnormal increased beta (15-30 Hz) and decreased gamma (35-80 Hz) synchronous oscillatory activity in the basal ganglia. Here we investigated the dynamics of oscillatory activity in the subthalamic nucleus (STN) during tremor. We used two adjacent microelectrodes to simultaneously record neuronal firing and local field potential (LFP) activity in nine PD patients who exhibited resting tremor during functional neurosurgery. We found that neurons exhibiting oscillatory activity at tremor frequency are located in the dorsal region of STN, where neurons with beta oscillatory activity are observed, and that their activity is coherent with LFP oscillations in the beta frequency range. Interestingly, in 85% of the 58 sites examined, the LFP exhibited increased oscillatory activity in the low gamma frequency range (35-55 Hz) during periods with stronger tremor. Furthermore, in 17 of 26 cases where two LFPs were recorded simultaneously, their coherence in the gamma range increased with increased tremor. When averaged across subjects, the ratio of the beta to gamma coherence was significantly lower in periods with stronger tremor compared with periods of no or weak tremor. These results suggest that resting tremor in PD is associated with an altered balance between beta and gamma oscillations in the motor circuits of STN.

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Section: Tremor-frequency Neuronal Activity: Relation To Tremorsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Increased Gamma Oscillatory Activity in the Subthalamic Nucleus During Tremor in Parkinson's Disease Patients

Weinberger¹,

Hutchison²,

Lozano³

et al. 2009

Journal of Neurophysiology

127

View full text Add to dashboard Cite

show abstract

“…3C), there is only a partial overlap in the times of oscillatory neuronal activity and tremor. In line with previous reports (Lemstra et al, 1999;Raz et al, 2000;Hurtado et al, 2005), these results support the hypothesis of dynamical functional connection between the basal ganglia networks involved in tremor generation and the skeleton-motor periphery. We therefore limited this paper to population level analysis of the tremor and the pallidal oscillations (see below).…”

Section: Neuronal Firing Ratessupporting

confidence: 92%

“…Human studies have reported a high fraction of GPi cells oscillating at the tremor frequency (Hutchinson et al, 1997b); however, recent primate (Raz et al, 2000) and human (Hurtado et al, 1999(Hurtado et al, , 2005Lemstra et al, 1999) studies show that these oscillations are not fully coherent with the simultaneous recorded tremor. Our results also reveal several discrepancies between the pallidal oscillations and the tremor.…”

Section: Single-cell Oscillationsmentioning

confidence: 94%

Dopamine Replacement Therapy Does Not Restore the Full Spectrum of Normal Pallidal Activity in the 1-Methyl-4-Phenyl-1,2,3,6-Tetra-Hydropyridine Primate Model of Parkinsonism

et al. 2006

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Current physiological studies emphasize the role of neuronal oscillations and synchronization in the pathophysiology of Parkinson's disease; however, little is known about their specific roles in the neuronal substrate of dopamine replacement therapy (DRT). We investigated oscillatory activity and correlations throughout the different states of levodopa-naive parkinsonism as well as "Off-On" and dyskinetic states of DRT in the external globus pallidum (GPe) of tremulous (vervet) and rigid-akinetic (macaque) monkeys and in the internal globus pallidum (GPi) of the vervet monkey. We found that, although oscillatory activity of cells and interneuronal correlation in both pallidal segments increases after induction of parkinsonism with 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP) and decreases in response to DRT, important differences exist between the two pallidal segments. In the GPi, the fraction of oscillatory cells and relative power of oscillations were significantly higher than in the GPe, and the dominant frequency was within the range of 7.5-13.5 Hz compared with a range of 4.5-7.5 Hz within the GPe. The interneuronal correlations were mostly oscillatory in the GPi, whereas at least half are non-oscillatory in the GPe. We demonstrate that the tremor characteristics after exposure to DRT do not resemble those of the normal or the levodopa-naive state. Moreover, although DRT reverses the MPTP-induced neuronal changes (rate, pattern, and pairwise correlations), the balance between GPe and GPi fails to restore. We therefore suggest that this imbalance reflects additional abnormal organization of the basal ganglia networks in response to dopamine replacement and may constitute the physiological substrate of the limitations and side effects of chronic DRT.

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“…Double tremor oscillations in range are not coherent with simultaneously recorded tremors (Raz et al, 2000;Lemstra et al, 1999;Hurtado et al, 2005). However, a strong coherence at range is observed in the primary motor cortex, supplementary motor cortex, premotor cortex, diencephalon (possibly thalamus), and contralateral cerebellum (Timmermann et al, 2003).…”

Section: Magnetoencephalography (Meg)mentioning

confidence: 86%

Thalamic Deep Brain Stimulation for Parkinson’s Disease

Morigaki¹,

Saijo²,

Kaji³

et al. 2011

Diagnosis and Treatment of Parkinson's Disease

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Tremor-frequency (3–6 Hz) activity in the sensorimotor arm representation of the internal segment of the globus pallidus in patients with Parkinson's disease

Cited by 55 publications

References 12 publications

Increased Gamma Oscillatory Activity in the Subthalamic Nucleus During Tremor in Parkinson's Disease Patients

Increased Gamma Oscillatory Activity in the Subthalamic Nucleus During Tremor in Parkinson's Disease Patients

Dopamine Replacement Therapy Does Not Restore the Full Spectrum of Normal Pallidal Activity in the 1-Methyl-4-Phenyl-1,2,3,6-Tetra-Hydropyridine Primate Model of Parkinsonism

Thalamic Deep Brain Stimulation for Parkinson’s Disease

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