scholarly journals Phase-dependent suppression of beta oscillations in Parkinson’s disease patients

2018 ◽  
Author(s):  
Abbey B. Holt ◽  
Eszter Kormann ◽  
Alessandro Gulberti ◽  
Monika Pötter-Nerger ◽  
Colin G. McNamara ◽  
...  

AbstractSynchronized oscillations within and between brain areas facilitate normal processing, but are often amplified in disease. A prominent example is the abnormally sustained beta-frequency (~20Hz) oscillations recorded from the cortex and subthalamic nucleus of Parkinson’s Disease patients. Computational modelling suggests that the amplitude of such oscillations could be modulated by applying stimulation at a specific phase. Such a strategy would allow selective targeting of the oscillation, with relatively little effect on other activity parameters. Here we demonstrate in awake, parkinsonian patients undergoing functional neurosurgery, that electrical stimulation arriving on consecutive cycles of a specific phase of the subthalamic oscillation can suppress its amplitude and coupling to cortex. Stimulus-evoked changes in spiking did not have a consistent time course, suggesting that the oscillation was modulated independently of net output. Phase-dependent stimulation could thus be a valuable strategy for treating brain diseases and probing the function of oscillations in the healthy brain.

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ashwini Oswal ◽  
Chunyan Cao ◽  
Chien-Hung Yeh ◽  
Wolf-Julian Neumann ◽  
James Gratwicke ◽  
...  

AbstractParkinson’s disease (PD) is characterised by the emergence of beta frequency oscillatory synchronisation across the cortico-basal-ganglia circuit. The relationship between the anatomy of this circuit and oscillatory synchronisation within it remains unclear. We address this by combining recordings from human subthalamic nucleus (STN) and internal globus pallidus (GPi) with magnetoencephalography, tractography and computational modelling. Coherence between supplementary motor area and STN within the high (21–30 Hz) but not low (13-21 Hz) beta frequency range correlated with ‘hyperdirect pathway’ fibre densities between these structures. Furthermore, supplementary motor area activity drove STN activity selectively at high beta frequencies suggesting that high beta frequencies propagate from the cortex to the basal ganglia via the hyperdirect pathway. Computational modelling revealed that exaggerated high beta hyperdirect pathway activity can provoke the generation of widespread pathological synchrony at lower beta frequencies. These findings suggest a spectral signature and a pathophysiological role for the hyperdirect pathway in PD.


2001 ◽  
Vol 8 (1-2) ◽  
pp. 99-110 ◽  
Author(s):  
K. L. Leenders ◽  
W. H. Oertel

Parkinson's disease is one of the most frequent neurodegenerative brain diseases. Its time course is slow and is characterized by progressive loss of dopaminergic and other brainstem neurons resulting in malfunctioning of the cerebral neuronal systems responsible for motor functions. The clinical signs are slowness of movement, muscle rigidity and rest-tremor amongst other features. The cause of the disease is unknown, but recently involvement of genetic factors is being researched. Positron emission tomography (PET) allows in vivo determination of striatai dopaminergic activity. This has increased our insight in the pathophysiology of the disease and permits direct study of disease progression at a biochemical level and equally to monitor whether potential neuroprotective interventions are indeed effective. Thus far no drug has emerged but promising substances are currently being studied.


2020 ◽  
Author(s):  
Ashwini Oswal ◽  
Chien-Hung Yeh ◽  
Wolf-Julian Neumann ◽  
James Gratwicke ◽  
Harith Akram ◽  
...  

AbstractParkinson’s disease (PD) is characterised by the emergence of pathological patterns of oscillatory synchronisation across the cortico-basal-ganglia circuit. The relationship between anatomical connectivity and oscillatory synchronisation within this system remains poorly understood. We address this by integrating evidence from invasive electrophysiology, magnetoencephalography, tractography and computational modelling in patients. Coupling between supplementary motor area (SMA) and subthalamic nucleus (STN) within the high beta frequency (21-30 Hz) range correlated with fibre tract densities between these two structures. Additionally within the STN, non-linear waveform features suggestive of cortical synchronisation correlated with cortico-STN fibre densities. Finally, computational modelling revealed that exaggerated hyperdirect cortical inputs to the STN in the upper beta frequency range can provoke the generation of widespread pathological synchrony at lower beta (13-20 Hz) frequencies. These observations reveal a spectral signature of the hyperdirect pathway at high beta frequencies and provide evidence for its pathophysiological role in oscillatory network dysfunction in PD.One sentence summarySignatures of the hyperdirect pathway and its likely role in pathological network disruption in Parkinson’s disease are identified.


Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 137
Author(s):  
Tina Levstek ◽  
Sara Redenšek ◽  
Maja Trošt ◽  
Vita Dolžan ◽  
Katarina Trebušak Podkrajšek

Telomeres, which are repetitive sequences that cap the end of the chromosomes, shorten with each cell division. Besides cellular aging, there are several other factors that influence telomere length (TL), in particular, oxidative stress and inflammation, which play an important role in the pathogenesis of neurodegenerative brain diseases including Parkinson’s disease (PD). So far, the majority of studies have not demonstrated a significant difference in TL between PD patients and healthy individuals. However, studies investigating the effect of TL on the symptomatology and disease progression of PD are scarce, and thus, warranted. We analyzed TL of peripheral blood cells in a sample of 204 PD patients without concomitant autoimmune diseases and analyzed its association with several PD related phenotypes. Monochrome multiplex quantitative PCR (mmqPCR) was used to determine relative TL given as a ratio of the amount of DNA between the telomere and albumin as the housekeeping gene. We found a significant difference in the relative TL between PD patients with and without dementia, where shorter TL presented higher risk for dementia (p = 0.024). However, the correlation was not significant after adjustment for clinical factors (p = 0.509). We found no correlations between TLs and the dose of dopaminergic therapy when the analysis was adjusted for genetic variability in inflammatory or oxidative factors. In addition, TL influenced time to onset of motor complications after levodopa treatment initiation (p = 0.0134), but the association did not remain significant after adjustment for age at inclusion and disease duration (p = 0.0781). Based on the results of our study we conclude that TL contributes to certain PD-related phenotypes, although it may not have a major role in directing the course of the disease. Nevertheless, this expends currently limited knowledge regarding the association of the telomere attrition and the disease severity or motor complications in Parkinson’s disease.


Synapse ◽  
1999 ◽  
Vol 31 (2) ◽  
pp. 134-139 ◽  
Author(s):  
Sylvie Chalon ◽  
Patrick Emond ◽  
Sylvie Bodard ◽  
Marie-Paule Vilar ◽  
Cynthia Thiercelin ◽  
...  

Author(s):  
Peter Falkai ◽  
Bernhard Bogerts

The traditional domains of neuropathology are well-defined organic brain diseases with an obvious pathology, such as tumours, infections, vascular diseases, trauma, or toxic and hypoxemic changes, as well as degenerative brain diseases (e.g. Alzheimer's disease, Parkinson's disease, and Huntington's chorea). Neuropathological investigations of these brain disorders have been rewarding, because patients with any of these conditions can be expected to have gross morphological or more or less specific neurohistological anomalies related to the clinical symptoms of the disorders. Moreover, the type of brain pathology of these well-defined disease entities is quite homogenous. For example, it is highly unlikely that a patient with Parkinson's disease would not exhibit morphological changes and Lewy bodies in the nigrostriatal system, just as much a person with Huntington's chorea would have a normal striatum, or a patient with Pick'sor Alzheimer's disease would have no changes in the cerebralcortex. In contrast, the history of the neuropathology of psychiatric disorders outside primary degenerative diseases is much more controversial, because no such obvious and homogenous types of brain pathology (as seen in neurological disorders) have yet been detected for the major psychiatric illnesses such as schizophrenia, affective disorders, substance-related disorders, or personality disorders. The scope of this chapter is to summarize the neuropathological findings in schizophrenia, affective disorders, and alcoholism. Tables 2.3.5.1, 2.3.5.2, 2.3.5.3, and 2.3.5.4 highlight the significant findings. It goes beyond the scope of this chapter to review thelarge body of literature on the dementias, including specifically Alzheimer's disease. Concerning this matter, the reader is referred to several comprehensive reviews (e.g. Jellinger and Bancher 1998).


2015 ◽  
Vol 27 (03) ◽  
pp. 1550025
Author(s):  
Whi-Young Kim ◽  
Jun-Hyoung Kim

The incidence of brain diseases, such as dementia, Parkinson's disease and motor nerve disorder, has increased since 1980s. According to a survey conducted on the incidence in England, US, Japan, Germany and Spain, the dementia death rate, including Alzheimer's disease, had increased by three times for men. The death rate from brain disease, such as Parkinson's disease and motor nerve disorder, has increased by 50% for both men and women. Although this increase can be assumed to be caused by changes in DNA when observing from a genetic perspective, it would take hundreds of years to confirm this. Therefore, environmental factors are regarded as the actual cause. In this situation of a rapidly increasing aging population, the prevention of senile and brain diseases is considered the most important measure because treatment is difficult and the after-effects are severe. A cerebrovascular ultrasonogram, which can frequently allow a self-inspection of the blood vessels for the early detection of the risk factors for disease, is actualized to model with a characteristic test and has shown performance. Supplementation of the system can facilitate an application in the measurement of brain disorder patients with other diseases in the future. This study examined the atypical characteristics through the production of a prototype.


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