RESUMEN
Schizophrenia is often characterized by dysconnections in the brain, which can be estimated via functional connectivity analyses. Commonly measured using resting-state functional magnetic resonance imaging (fMRI) in order to characterize the intrinsic or baseline function of the brain, fMRI functional connectivity has significantly contributed to the understanding of schizophrenia. However, these measures may not capture the full extent of functional connectivity abnormalities in schizophrenia as fMRI is temporally limited by the hemodynamic response. In order to extend fMRI functional connectivity findings, the complementary modality of magnetoencephalography (MEG) can be utilized to capture electrophysiological functional connectivity abnormalities in schizophrenia that are not obtainable with fMRI. Therefore, we implemented a multimodal functional connectivity analysis using resting-state 7 Tesla fMRI and MEG data in a sample of first-episode patients with schizophrenia (nâ¯=â¯19) and healthy controls (nâ¯=â¯24). fMRI and MEG data were decomposed into components reflecting resting state networks using a group spatial independent component analysis. Functional connectivity between resting-state networks was computed and group differences were observed. In fMRI, patients demonstrated hyperconnectivity between subcortical and auditory networks, as well as hypoconnectivity between interhemispheric homotopic sensorimotor network components. In MEG, patients demonstrated hypoconnectivity between sensorimotor and task positive networks in the delta frequency band. Results not only support the dysconnectivity hypothesis of schizophrenia, but also suggest the importance of jointly examining multimodal neuroimaging data as critical disorder-related information may not be detectable in a single modality alone.
Asunto(s)
Mapeo Encefálico/métodos , Encéfalo/diagnóstico por imagen , Imagen por Resonancia Magnética/métodos , Magnetoencefalografía/métodos , Imagen Multimodal/métodos , Esquizofrenia/diagnóstico por imagen , Adulto , Encéfalo/fisiopatología , Femenino , Humanos , Masculino , Vías Nerviosas/diagnóstico por imagen , Vías Nerviosas/fisiopatología , Descanso , Esquizofrenia/fisiopatologíaRESUMEN
OBJECTIVE: We used a combination of simulation and recordings from human subjects to characterize how saccadic eye movements affect the magnetoencephalogram (MEG). METHODS: We used simulated saccadic eye movements to generate simulated MEG signals. We also recorded the MEG signals from three healthy adults to 5° magnitude saccades that were vertical up and down, and horizontal left and right. RESULTS: The signal elicited by the rotating eye dipoles is highly dependent on saccade direction, can cover a large area, can sometimes have a non-intuitive trajectory, but does not significantly extend above approximately 30Hz in the frequency domain. In contrast, the saccadic spikes (which are primarily monophasic pulses, but can be biphasic) are highly localized to the lateral frontal regions for all saccade directions, and in the frequency domain extend up past 60Hz. CONCLUSIONS: Gamma band saccadic artifact is spatially localized to small regions regardless of saccade direction, but beta band and lower frequency saccadic artifact have broader spatial extents that vary strongly as a function of saccade direction. SIGNIFICANCE: We have here characterized the MEG saccadic artifact in both the spatial and the frequency domains for saccades of different directions. This could be important in ruling in or ruling out artifact in MEG recordings.
Asunto(s)
Magnetoencefalografía/normas , Movimientos Sacádicos , Adulto , Artefactos , Encéfalo/fisiología , Ritmo Gamma , Humanos , Magnetoencefalografía/métodos , Persona de Mediana EdadRESUMEN
Deep brain stimulation (DBS) relieves disabling symptoms of neurologic and psychiatric diseases when medical treatments fail, yet its therapeutic mechanism is unknown. We hypothesized that ventral intermediate (VIM) nucleus stimulation for essential tremor activates the cortex at short latencies, and that this potential is related to the suppression of tremor in the contralateral arm. We measured cortical activity with electroencephalography in 5 subjects (seven brain hemispheres) across a range of stimulator settings, and reversal of the anode and cathode electrode contacts minimized the stimulus artifact, allowing visualization of brain activity. Regression quantified the relationship between stimulation parameters and both the peak of the short latency potential and tremor suppression. Stimulation generated a polyphasic event-related potential in the ipsilateral sensorimotor cortex, with peaks at discrete latencies beginning less than 1 ms after stimulus onset (mean latencies 0.9 ± 0.2, 5.6 ± 0.7, and 13.9 ± 1.4 ms, denoted R1, R2, and R3, respectively). R1 showed more fixed timing than the subsequent peaks in the response (P < 0.0001, Levene's test), and R1 amplitude and frequency were both closely associated with tremor suppression (P < 0.0001, respectively). These findings demonstrate that effective VIM thalamic stimulation for essential tremor activates the cerebral cortex at approximately 1 ms after the stimulus pulse. The association between this short latency potential and tremor suppression suggests that DBS may improve tremor by synchronizing the precise timing of discharges in nearby axons and, by extension, the distributed motor network to the stimulation frequency or one of its subharmonics.
Asunto(s)
Corteza Cerebral/fisiopatología , Estimulación Encefálica Profunda/métodos , Potenciales Evocados/fisiología , Tiempo de Reacción/fisiología , Tálamo/fisiología , Temblor/terapia , Anciano , Biofisica , Mapeo Encefálico , Electroencefalografía , Femenino , Humanos , Masculino , Persona de Mediana Edad , Factores de Tiempo , Temblor/patologíaRESUMEN
Subthalamic deep brain stimulation (DBS) is superior to medical therapy for the motor symptoms of advanced Parkinson's disease (PD), and additional evidence suggests that it improves refractory symptoms of essential tremor, primary generalized dystonia, and obsessive-compulsive disorder. Despite this, its therapeutic mechanism is unknown. We hypothesized that subthalamic stimulation activates the cerebral cortex at short latencies after stimulus onset during clinically effective stimulation for PD. In 5 subjects (six hemispheres), EEG measured the response of cortex to subthalamic stimulation across a range of stimulation voltages and frequencies. Novel analytical techniques reversed the anode and cathode electrode contacts and summed the resulting pair of event-related potentials to suppress the stimulation artifact. We found that subthalamic brain stimulation at 20 Hz activates the somatosensory cortex at discrete latencies (mean latencies: 1.0 ± 0.4, 5.7 ± 1.1, and 22.2 ± 1.8 ms, denoted as R1, R2, and R3, respectively). The amplitude of the short latency peak (R1) during clinically effective high-frequency stimulation is nonlinearly dependent on stimulation voltage (P < 0.001; repeated-measures analysis of variance), and its latency is less variable than that of R3 (1.02 versus 19.46 ms; P < 0.001, Levene's test). We conclude that clinically effective subthalamic brain stimulation in humans with PD activates the cerebral cortex at 1 ms after stimulus onset, most likely by antidromic activation. These findings suggest that alteration of the precise timing of action potentials in cortical neurons with axonal projections to the subthalamic region may be an important component of the therapeutic mechanism of subthalamic brain stimulation.