scholarly journals Advanced time-series analysis of MEG data as a method to explore olfactory function in healthy controls and Parkinson's disease patients

2009 ◽  
Vol 30 (9) ◽  
pp. 3020-3030 ◽  
Author(s):  
Sanne Boesveldt ◽  
Cornelis J. Stam ◽  
Dirk L. Knol ◽  
Jeroen P.A. Verbunt ◽  
Henk W. Berendse
2016 ◽  
Vol 89-90 ◽  
pp. 1-6 ◽  
Author(s):  
Cristina Linares ◽  
Pablo Martinez-Martin ◽  
Carmen Rodríguez-Blázquez ◽  
Maria João Forjaz ◽  
Rocío Carmona ◽  
...  

1988 ◽  
Vol 69 (1) ◽  
pp. 24-33 ◽  
Author(s):  
Aiman Abdel-Malek ◽  
Charles H. Markham ◽  
Panos Z. Marmarelis ◽  
Vasilis Z. Marmarelis

2019 ◽  
Author(s):  
Mikkel C. Vinding ◽  
Panagiota Tsitsi ◽  
Josefine Waldthaler ◽  
Robert Oostenveld ◽  
Martin Ingvar ◽  
...  

AbstractParkinson’s disease is characterized by a gradual loss of dopaminergic neurons, which are associated with altered neuronal activity in the beta band (13-30 Hz). Assessing beta band activity typically involves transforming the time-series to get the power of the signal in the frequency-domain. Such transformation assumes that the time-series can be reduced to a combination of steady-state sine-and cosine waves. However, recent studies have suggested that this approach masks relevant biophysical features in the beta band activity—for example, that the beta band exhibits transient bursts of high-amplitude activity.In an exploratory study we used magnetoencephalography (MEG) to record cortical beta band activity to characterize how spontaneous cortical beta bursts manifest in Parkinson’s patients ON and OFF dopaminergic medication, and compare this to matched healthy controls. From three minutes of MEG data, we extracted the time-course of beta band activity from the sensorimotor cortex and characterized high-amplitude epochs in the signal to test if they exhibited burst like properties. We then compared the rate, duration, inter-burst interval, and peak amplitude of the high-amplitude epochs between the Parkinson’s patients and healthy controls.Our results show that Parkinson’s patients OFF medication had a 6-17% lower beta bursts rate compared to healthy controls, while both the duration and the amplitude of the bursts were the same for Parkinson’s patients and healthy controls and medicated state of the Parkinson’s patients. These data thus support the view that beta bursts are fundamental underlying features of beta band activity, and show that changes in cortical beta band power in PD can be explained primarily by changes in the underlying burst rate. Importantly, our results also revealed a relationship between beta bursts rate and motor symptom severity in PD: a lower burst rate scaled with increased in severity of bradykinesia and postural/kinetic tremor. Beta burst rate might thus serve as neuromarker for Parkinson’s disease that can help in the assessment of symptom severity in Parkinson’s disease or evaluate treatment effectiveness.


2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Mikkel C Vinding ◽  
Panagiota Tsitsi ◽  
Josefine Waldthaler ◽  
Robert Oostenveld ◽  
Martin Ingvar ◽  
...  

Abstract Parkinson’s disease is characterized by a gradual loss of dopaminergic neurons, which is associated with altered neuronal activity in the beta-band (13–30 Hz). Assessing beta-band activity typically involves transforming the time-series to get the power of the signal in the frequency domain. Such transformation assumes that the time-series can be reduced to a combination of steady-state sine- and cosine waves. However, recent studies have suggested that this approach masks relevant biophysical features in the beta-band—for example, that the beta-band exhibits transient bursts of high-amplitude activity. In an exploratory study, we used magnetoencephalography to record beta-band activity from the sensorimotor cortex, to characterize how spontaneous cortical beta bursts manifest in Parkinson’s patients on and off dopaminergic medication, and compare this to matched healthy controls. We extracted the time-course of beta-band activity from the sensorimotor cortex and characterized bursts in the signal. We then compared the burst rate, duration, inter-burst interval and peak amplitude between the Parkinson’s patients and healthy controls. Our results show that Parkinson’s patients off medication had a 5–17% lower beta bursts rate compared to healthy controls, while both the duration and the amplitude of the bursts were the same for healthy controls and medicated state of the Parkinson’s patients. These data thus support the view that beta bursts are fundamental underlying features of beta-band activity, and show that changes in cortical beta-band power in Parkinson’s disease can be explained—primarily by changes in the underlying burst rate. Importantly, our results also revealed a relationship between beta burst rate and motor symptom severity in Parkinson’s disease: a lower burst rate scaled with increased severity of bradykinesia and postural/kinetic tremor. Beta burst rate might thus serve as a neuromarker for Parkinson’s disease that can help in the assessment of symptom severity in Parkinson’s disease or in the evaluation of treatment effectiveness.


2020 ◽  
Vol 45 (5) ◽  
pp. 401-406 ◽  
Author(s):  
Emilie Aubry-Lafontaine ◽  
Cécilia Tremblay ◽  
Pascali Durand-Martel ◽  
Nicolas Dupré ◽  
Johannes Frasnelli

Abstract Olfactory dysfunction (OD) in Parkinson’s disease (PD) appears several years before the presence of motor disturbance. Olfactory testing has the potential to serve as a tool for early detection of PD, but OD is not specific to PD as it affects up to 20% of the general population. Olfaction includes an orthonasal and a retronasal components; in some forms of OD, retronasal olfactory function is preserved. We aimed to evaluate whether combined testing components allows for discriminating between PD-related OD and non-Parkinsonian OD (NPOD). The objective of this study is to orthonasal and retronasal olfactory function in PD patients and compare them to a NPOD group and to healthy controls. We hypothesized that this combined testing allows to distinguish PD patients from both other groups. We included 32 PD patients, 25 NPOD patients, and 15 healthy controls. Both olfactory components were impaired in PD and NPOD patients, compared with controls; however, NPOD patients had significantly better orthonasal scores than PD patients. Furthermore, the ratio of retronasal/orthonasal score was higher in PD than in both other groups. In the NPOD group, orthonasal and retronasal scores were significantly correlated; no such correlation could be observed in PD patients. In summary, PD patients seem to rely on compensatory mechanisms for flavor perception. Combined orthonasal and retronasal olfactory testing may contribute to differentiate PD patients from patients with NPOD.


2021 ◽  
Author(s):  
Mikkel C. Vinding ◽  
Allison Eriksson ◽  
Cassia Low Man Ting ◽  
Josefine Waldthaler ◽  
Daniel Ferreira ◽  
...  

Parkinson's disease (PD) is associated with functional changes in the neural activity within the brain's sensorimotor network, which in turn are related to the characteristic motor symptoms in PD. The functional changes in PD are particularly prominent in terms of oscillatory neuronal activity in the characteristic sensorimotor alpha and beta rhythms. However, summaries in terms of alpha or beta power do not capture the full range of the complex dynamic nature of the signals from the somatosensory cortex. This raises the question of how to quantify and summarise the functional changes in such oscillatory features in a manner that captures the relevant disease- and symptom-related neural activity. We investigated the role of spontaneous cortical somatosensory activity in the electrophysiological alpha and beta bands among a cohort of early- to mid-stage PD patients (N=78) and age- and gender-matched healthy controls (N=60) using source reconstructed resting-state magnetoencephalography (MEG) recordings. We quantified the oscillatory features of the neural time series by its oscillatory alpha power, beta power, and 1/f broadband characteristics using power spectral density, and additionally by characterising "burst" properties in the signals. We examined the relationship between the signal features and disease state, age, sex, and cortical thickness. Using multiple regression, we examined the relative contribution of the oscillatory features on the clinical manifestation of motor symptoms in the PD group. Our results show that PD patients differ from healthy controls on several of the oscillatory features, showing higher beta-band power, higher burst amplitude, and steeper 1/f broadband characteristics compared to healthy controls, as well as a steeper age-related decrease in the bursts rate. While there was a high degree of correlation between some of the oscillatory features, several features also appeared functionally separated, showing independent feature-to-symptom relationships. For instance, oscillatory beta power increased with the severity of midline function symptoms, while burst rate decreased with the severity of bradykinesia. Our study shows that quantification of distinct features within the oscillatory sensorimotor neural time series in PD captures different underlying mechanisms related to disease progression and symptom severity, which in turn has a potential for a more individualised and precision-based approach to assessing functional neural changes in PD.


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