Beta Oscillatory Activity in the Subthalamic Nucleus and Its Relation to Dopaminergic Response in Parkinson's Disease

2006 ◽  
Vol 96 (6) ◽  
pp. 3248-3256 ◽  
Author(s):  
Moran Weinberger ◽  
Neil Mahant ◽  
William D. Hutchison ◽  
Andres M. Lozano ◽  
Elena Moro ◽  
...  

Recent studies suggest that beta (15–30 Hz) oscillatory activity in the subthalamic nucleus (STN) is dramatically increased in Parkinson's disease (PD) and may interfere with movement execution. Dopaminergic medications decrease beta activity and deep brain stimulation (DBS) in the STN may alleviate PD symptoms by disrupting this oscillatory activity. Depth recordings from PD patients have demonstrated beta oscillatory neuronal and local field potential (LFP) activity in STN, although its prevalence and relationship to neuronal activity are unclear. In this study, we recorded both LFP and neuronal spike activity from the STN in 14 PD patients during functional neurosurgery. Of 200 single- and multiunit recordings 56 showed significant oscillatory activity at about 26 Hz and 89% of these were coherent with the simultaneously recorded LFP. The incidence of neuronal beta oscillatory activity was significantly higher in the dorsal STN ( P = 0.01) and corresponds to the significantly increased LFP beta power recorded in the same region. Of particular interest was a significant positive correlation between the incidence of oscillatory neurons and the patient's benefit from dopaminergic medications, but not with baseline motor deficits off medication. These findings suggest that the degree of neuronal beta oscillatory activity is related to the magnitude of the response of the basal ganglia to dopaminergic agents rather than directly to the motor symptoms of PD. The study also suggests that LFP beta oscillatory activity is generated largely within the dorsal portion of the STN and can produce synchronous oscillatory activity of the local neuronal population.

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Hayley J MacDonald ◽  
John-Stuart Brittain ◽  
Bernhard Spitzer ◽  
Simon Hanslmayr ◽  
Ned Jenkinson

Abstract There is an increasing recognition of the significant non-motor symptoms that burden people with Parkinson’s disease. As such, there is a pressing need to better understand and investigate the mechanisms underpinning these non-motor deficits. The electrical activity within the brains of people with Parkinson’s disease is known to exhibit excessive power within the beta range (12–30 Hz), compared with healthy controls. The weight of evidence suggests that this abnormally high level of beta power is the cause of bradykinesia and rigidity in Parkinson’s disease. However, less is known about how the abnormal beta rhythms seen in Parkinson’s disease impact on non-motor symptoms. In healthy adults, beta power decreases are necessary for successful episodic memory formation, with greater power decreases during the encoding phase predicting which words will subsequently be remembered. Given the raised levels of beta activity in people with Parkinson’s disease, we hypothesized that the necessary decrease in power during memory encoding would be diminished and that this would interfere with episodic memory formation. Accordingly, we conducted a cross-sectional, laboratory-based experimental study to investigate whether there was a direct relationship between decreased beta modulation and memory formation in Parkinson’s disease. Electroencephalography recordings were made during an established memory-encoding paradigm to examine brain activity in a cohort of adults with Parkinson’s disease (N = 28, 20 males) and age-matched controls (N = 31, 18 males). The participants with Parkinson’s disease were aged 65 ± 6 years, with an average disease duration of 6 ± 4 years, and tested on their normal medications to avoid the confound of exacerbated motor symptoms. Parkinson’s disease participants showed impaired memory strength (P = 0.023) and reduced beta power decreases (P = 0.014) relative to controls. Longer disease duration was correlated with a larger reduction in beta modulation during encoding, and a concomitant reduction in memory performance. The inability to sufficiently decrease beta activity during semantic processing makes it a likely candidate to be the central neural mechanism underlying this type of memory deficit in Parkinson’s disease. These novel results extend the notion that pathological beta activity is causally implicated in the motor and (lesser appreciated) non-motor deficits inherent to Parkinson’s disease. These findings provide important empirical evidence that should be considered in the development of intelligent next-generation therapies.


2009 ◽  
Vol 101 (2) ◽  
pp. 789-802 ◽  
Author(s):  
M. Weinberger ◽  
W. D. Hutchison ◽  
A. M. Lozano ◽  
M. Hodaie ◽  
J. O. Dostrovsky

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.


2017 ◽  
Vol 89 (1) ◽  
pp. 95-104 ◽  
Author(s):  
John A Thompson ◽  
Anand Tekriwal ◽  
Gidon Felsen ◽  
Musa Ozturk ◽  
Ilknur Telkes ◽  
...  

Sleep is a fundamental homeostatic process, and disorders of sleep can greatly affect quality of life. Parkinson’s disease (PD) is highly comorbid for a spectrum of sleep disorders and deep brain stimulation (DBS) of the subthalamic nucleus (STN) has been reported to improve sleep architecture in PD. We studied local field potential (LFP) recordings in PD subjects undergoing STN-DBS over the course of a full-night’s sleep. We examined the changes in oscillatory activity recorded from STN between ultradian sleep states to determine whether sleep-stage dependent spectral patterns might reflect underlying dysfunction. For this study, PD (n=10) subjects were assessed with concurrent polysomnography and LFP recordings from the DBS electrodes, for an average of 7.5 hours in ‘off’ dopaminergic medication state. Across subjects, we found conserved spectral patterns among the canonical frequency bands (delta 0–3 Hz, theta 3–7 Hz, alpha 7–13 Hz, beta 13–30 Hz, gamma 30–90 Hz and high frequency 90–350 Hz) that were associated with specific sleep cycles: delta (0–3 Hz) activity during non-rapid eye movement (NREM) associated stages was greater than during Awake, whereas beta (13–30 Hz) activity during NREM states was lower than Awake and rapid eye movement (REM). In addition, all frequency bands were significantly different between NREM states and REM. However, each individual subject exhibited a unique mosaic of spectral interrelationships between frequency bands. Our work suggests that LFP recordings from human STN differentiate between sleep cycle states, and sleep-state specific spectral mosaics may provide insight into mechanisms underlying sleep pathophysiology.


2017 ◽  
Vol 98 ◽  
pp. 100-107 ◽  
Author(s):  
Xinyi Geng ◽  
Jianguo Zhang ◽  
Yin Jiang ◽  
Keyoumars Ashkan ◽  
Thomas Foltynie ◽  
...  

2005 ◽  
Vol 194 (1) ◽  
pp. 212-220 ◽  
Author(s):  
Andrea A. Kühn ◽  
Thomas Trottenberg ◽  
Anatol Kivi ◽  
Andreas Kupsch ◽  
Gerd-Helge Schneider ◽  
...  

2011 ◽  
Vol 33 (7) ◽  
pp. 1275-1280 ◽  
Author(s):  
Maria Fiorella Contarino ◽  
Lo J. Bour ◽  
Maarten Bot ◽  
Pepijn Van Den Munckhof ◽  
Johannes D. Speelman ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Taylor J. Bosch ◽  
Stefan Kammermeier ◽  
Christopher Groth ◽  
Matt Leedom ◽  
Elizabeth K. Hanson ◽  
...  

Introduction: Posture and balance dysfunctions critically impair activities of daily living of patients with progressing Parkinson's disease (PD). However, the neural mechanisms underlying postural instability in PD are poorly understood, and specific therapies are lacking. Previous electrophysiological studies have shown distinct cortical oscillations with a significant contribution of the cerebellum during postural control tasks in healthy individuals.Methods: We investigated cortical and mid-cerebellar oscillatory activity via electroencephalography (EEG) during a postural control task in 10 PD patients with postural instability (PDPI+), 11 PD patients without postural instability (PDPI–), and 15 age-matched healthy control participants. Relative spectral power was analyzed in the theta (4–7 Hz) and beta (13–30 Hz) frequency bands.Results: Time-dependent postural measurements computed by accelerometer signals showed poor performance in PDPI+ participants. EEG results revealed that theta power was profoundly lower in mid-frontal and mid-cerebellar regions during the postural control task in PDPI+, compared to PDPI– and control participants. In addition, theta power was correlated with postural control performance in PD subjects. No significant changes in beta power were observed. Additionally, oscillatory changes during the postural control task differed from the resting state.Conclusion: This study underlines the involvement of mid-frontal and mid-cerebellar regions in postural stability during a balance task and emphasizes the important role of theta oscillations therein for postural control in PD.


2019 ◽  
Author(s):  
Shenghong He ◽  
Abteen Mostofi ◽  
Emilie Syed ◽  
Flavie Torrecillos ◽  
Gerd Tinkhauser ◽  
...  

AbstractEnhanced beta oscillations (13-30 Hz) in the subthalamic nucleus (STN) have been associated with clinical impairment in Parkinson’s disease (PD), such as rigidity and slowing of movement, with the suppression of STN beta activity through medication or deep brain stimulation correlating with improvement in these symptoms. Recent studies have also emphasized the importance of the time dynamics of the STN beta oscillations in the pathology of PD. An increased probability of prolonged beta bursts, defined as periods when beta band power exceeds a certain threshold, was more closely related to motor symptoms than average power; and the occurrence of beta bursts just before a go cue slows cued movements. Here we adopted a sequential neurofeedback-behaviour task paradigm to investigate whether patients with PD can learn to suppress pathological beta oscillations recorded from STN with neurofeedback training and whether the training improves the motor performance. Results from twelve patients showed that, compared with the control condition, the neurofeedback training led to reduced incidence and duration of beta bursts in the STN local field potential (LFP) and also reduced the synchrony between the STN LFP and cortical activities measured through EEG in the beta frequency band. The changes were accompanied by a reduced reaction time in cued movements. These results suggest that volitional suppression of beta bursts facilitated by neurofeedback training could help improve movement initialisation in Parkinson’s disease.Significance StatementOur study suggests that a neurofeedback paradigm which focuses on the time dynamics of the target neural signal can facilitate volitional suppression of pathological beta oscillations in the STN in Parkinson’s disease. Neurofeedback training was accompanied by reduced reaction time in cued movements, but associated with increased tremor in tremulous patients. The results strengthen the link between subthalamic beta oscillations and motor impairment, and also suggest that different symptom-specific neural signals could be targeted to improve neuromodulation strategies, either through brain stimulation or neurofeedback training, for patients with tremor and bradykinesia-rigidity.


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