Sickle cell disease (SCD) is a red blood cell disorder that causes many complications including life-long pain. Treatment of pain remains challenging due to a poor understanding of the mechanisms and limitations to characterize and quantify pain. In the present study, we examined simultaneously recording functional MRI (fMRI) and electroencephalogram (EEG) to better understand neural connectivity as a consequence of chronic pain in SCD patients. We performed independent component analysis and seed-based connectivity on fMRI data. Spontaneous power and microstate analysis was performed on EEG-fMRI data. ICA analysis showed that patients lacked activity in the default mode network (DMN) and executive control network compared to controls. EEG-fMRI data revealed that the insula cortex's role in salience increases with age in patients. EEG microstate analysis showed patients had increased activity in pain processing regions. The cerebellum in patients showed a stronger connection to the periaqueductal gray matter (involved in pain inhibition), and negative connections to pain processing areas. These results suggest that patients have reduced activity of DMN and increased activity in pain processing regions during rest. The present findings suggest resting state connectivity differences between patients and controls can be used as novel biomarkers of SCD pain.
Unlike focal or partial epilepsy, which has a confined range of influence, idiopathic generalized epilepsy (IGE) often affects the whole or a larger portion of the brain without obvious, known cause. It is important to understand the underlying network which generates epileptic activity and through which epileptic activity propagates. The aim of the present study was to investigate the thalamocortical relationship using non-invasive imaging modalities in a group of IGE patients. We specifically investigated the roles of the mediodorsal nuclei in the thalami and the medial frontal cortex in generating and spreading IGE activities. We hypothesized that the connectivity between these two structures is key in understanding the generation and propagation of epileptic activity in brains affected by IGE. Using three imaging techniques of EEG, fMRI and EEG-informed fMRI, we identified important players in generation and propagation of generalized spike-and-wave discharges (GSWDs). EEG-informed fMRI suggested multiple regions including the medial frontal area near to the anterior cingulate cortex, mediodorsal nuclei of the thalamus, caudate nucleus among others that related to the GSWDs. The subsequent seed-based fMRI analysis revealed a reciprocal cortical and bi-thalamic functional connection. Through EEG-based Granger Causality analysis using (DTF) and adaptive DTF, within the reciprocal thalamocortical circuitry, thalamus seems to serve as a stronger source in driving cortical activity from initiation to the propagation of a GSWD. Such connectivity change starts before the GSWDs and continues till the end of the slow wave discharge. Thalamus, especially the mediodorsal nuclei, may serve as potential targets for deep brain stimulation to provide more effective treatment options for patients with drug-resistant generalized epilepsy.
Motor imagery-based (MI based) brain-computer interface (BCI) using electroencephalography (EEG) allows users to directly control a computer or external device by modulating and decoding the brain waves. A variety of factors could potentially affect the performance of BCI such as the health status of subjects or the environment. In this study, we investigated the effects of soft drinks and regular coffee on EEG signals under resting state and on the performance of MI based BCI. Twenty-six healthy human subjects participated in three or four BCI sessions with a resting period in each session. During each session, the subjects drank an unlabeled soft drink with either sugar (Caffeine Free Coca-Cola), caffeine (Diet Coke), neither ingredient (Caffeine Free Diet Coke), or a regular coffee if there was a fourth session. The resting state spectral power in each condition was compared; the analysis showed that power in alpha and beta band after caffeine consumption were decreased substantially compared to control and sugar condition. Although the attenuation of powers in the frequency range used for the online BCI control signal was shown, group averaged BCI online performance after consuming caffeine was similar to those of other conditions. This work, for the first time, shows the effect of caffeine, sugar intake on the online BCI performance and resting state brain signal.
Brain-computer interface (BCI) systems allow users to directly control computers and other machines by modulating their brain waves. In the present study, we investigated the effect of soft drinks on resting state (RS) EEG signals and BCI control. Eight healthy human volunteers each participated in three sessions of BCI cursor tasks and resting state EEG. During each session, the subjects drank an unlabeled soft drink with either sugar, caffeine, or neither ingredient. A comparison of resting state spectral power shows a substantial decrease in alpha and beta power after caffeine consumption relative to control. Despite attenuation of the frequency range used for the control signal, caffeine average BCI performance was the same as control. Our work provides a useful characterization of caffeine, the world's most popular stimulant, on brain signal frequencies and their effect on BCI performance.
Introduction One major challenge in the treatment of pain from sickle cell disease (SCD) is the current lack of an objective measure of pain. Therefore, we used functional magnetic imaging (fMRI) to compare a specific brain network in SCD patients with healthy subjects to develop objective methods to assess pain. We hypothesize that in SCD patients, the default-mode-network (DMN) is less active in comparison to healthy subjects. DMN is a prevalent network dynamic that appears in the absence of overt behavior and is thought to be responsible for a host of visceral mental activities. This DMN difference may be due to prolonged SCD-related pain. Methods Ten healthy subjects (6 males and 4 females; age: mean=23.3, SD= 3.3 years) and ten SCD patients (5 males, 5 females; age: mean= 28.5, SD=7.1 years) participated in the study following informed consent to the procedures approved by the IRB of the University of Minnesota. Patients were recruited by hematologists at the University of Minnesota Medical Center. None of the patients were experiencing acute crisis during the experiments. FMRI data was acquired with a 3T Siemens Trio whole-body scanner with echo-planar imaging (EPI) sequence. Each fMRI recording lasted about 6minutes. The experiment procedures were well tolerated by all subjects. Both independent component analysis (ICA) and seed-based region of interest (ROI) analysis were applied to the fMRI data, and the analysis was performed using the BrainVoyager QX software. Results Experimental and analyticalprocedures were applied to both groups under similar conditions and the recorded data in the two groups have comparable quality. Using the data driven ICA-based analysis, each fMRI data set was decomposed into thirty independent components. The DMN component waseasilyidentified in all of the ten healthy subjects. In contrast, none of the ten SCD patients had any identifiable DMN component in the ICA-based analysis. Seed-based ROI analysis was also performed to find correlational networks. The ROIs were predetermined to be in medial prefrontal cortex (mPFC), posterior cingulate cortex (PCC), left and right lateral parietal cortex (LP). Using the time course extracted from the ROIs, DMN was revealed in all ten healthy subjects. However, DMN can only be found in three SCD patients.The identified DMN in patients showed incomplete clusters and had smaller cluster size comparing with the DMNin healthy subjects. By examining different possible ROI locations, DMN identified in patients consistently showed smaller number of voxels compared to controls. Conclusions Our findings suggest that the neurological signature of SCD patients may be altered by the chronic painful condition caused by the disease. Diminished activity in the DMN during rest has been previously reported by studies on both cognitive impairments and other types of chronic pain. It is currently unclear whether synchrony among the nodes in the default mode network can be reestablished once the pain condition is alleviated. Knowledge of the neurological characteristics of SCD patients may shed light in understanding in disease and the role of pain in SCD. Changes in DMN activity may also serve as a potential biomarker to quantify pain severity in the future.(This work was supported in part by NIH U01 HL117664 and NSF DGE-1069104.) References Baliki, M.N. (2008), ‘Beyond feeling: chronic pain hurts the brain, disrupting the default-mode network dynamics’, The Journal of Neuroscience, vol. 28, no. 6, pp. 1398-1403. Fox, M.D. (2005), ‘The human brain is intrinsically organized into dynamic, anticorrelated functional networks’,ProcNatlAcadSci USA, vol. 102, pp. 9673–9678. Disclosures No relevant conflicts of interest to declare.
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