Left Prefrontal Beta Research Articles

Cortical correlates of susceptibility to upper limb freezing in Parkinson's disease.

Freezing behavior is an unmet symptom in Parkinson's disease (PD), which reflects its complex pathophysiology. Freezing behavior can emerge when attentional capacity is reduced, i.e. under dual task interference. In this study, we characterized the cortical network signatures underlying the susceptibility to freezing during continuous finger tapping. Fourteen PD patients with STN-DBS and thirteen age- and gender-matched healthy controls performed continuous tapping with the index finger as single motor task and during dual tasking. Synchronized EEG and mechanogram of the finger tapping were recorded. Subsequently, we analyzed cortical activity and cortico-cortical phase synchronization. We correlated these spectral measures with the biomechanically confirmed numbers of freezing episodes during finger tapping. During dual tasking compared to the single motor task, PD patients showed an increase of cortico-cortical phase synchronization over the left prefrontal area from 13 to 30Hz. This correlated with increased occurrence of freezing episodes. Interestingly, PD patients lacked the increase of prefrontal cortico-cortical synchronization from 4 to 7Hz during dual tasking as observed in healthy controls. Dual task interference led to an increase of left prefrontal beta band synchronization (13-30Hz) in PD and this increment predicted the number of freezing episodes. This increment may underscore the relevance of prefrontal executive dysfunction in freezing susceptibility. These findings enhance our understanding of the pathological network mechanisms behind increased susceptibility to freezing behavior.

Aberrant prefrontal beta oscillations predict episodic memory encoding deficits in schizophrenia.

Verbal episodic memory is one of the core cognitive functions affected in patients with schizophrenia (SZ). Although this verbal memory impairment in SZ is a well-known finding, our understanding about its underlying neurophysiological mechanisms is rather scarce. Here we address this issue by recording brain oscillations during a memory task in a sample of healthy controls and patients with SZ. Brain oscillations represent spectral fingerprints of specific neurocognitive operations and are therefore a promising tool to identify neurocognitive mechanisms that are affected by SZ. Healthy controls showed a prominent suppression of left prefrontal beta oscillatory activity during successful memory formation, which replicates several previous oscillatory memory studies. In contrast, patients failed to exhibit such a left prefrontal beta power suppression. Utilizing a new topographical pattern similarity approach, we further demonstrate that the degree of similarity between a patient's beta power decrease to that of the controls reliably predicted memory performance. This relationship between beta power decreases and memory was such that the patients' memory performance improved as they showed a more similar topographical beta desynchronization pattern compared to that of healthy controls. Together, these findings support left prefrontal beta desynchronization as the spectral fingerprint of verbal episodic memory formation, likely indicating deep semantic processing of verbal material. These findings also demonstrate that left prefrontal beta power suppression (or lack thereof) during memory encoding are a reliable biomarker for the observed encoding impairments in SZ in verbal memory.

The Efficacy of Neurofeedback in Patients with Major Depressive Disorder: An Open Labeled Prospective Study.

The purpose of this study was to evaluate the effect of neurofeedback on depressive symptoms and electrophysiological disturbances in patients with major depressive disorder. We recruited participants suffering from depression to evaluate efficacy of left prefrontal beta with alpha/theta training. An 8-week, prospective, open-label study was undertaken. Twenty participants were recruited. The treatment protocol was twice or three times a week training of beta at F3 with alpha/theta at Pz for 8 weeks. When every visit, patients were received beta training for 30 min, and then alpha/theta training for 30 min. Baseline, 4 and 8 week scores of; the Hamilton rating scale for Depression (HAM-D), the Hamilton rating scale for Anxiety (HAM-A), the Beck Depression Inventory (BDI)-II, the Beck Anxiety Inventory (BAI), Clinical global impression-severity (CGI-S), and pre- and post-treatment resting state EEGs were compared. Interhemispheric alpha power asymmetry (A score) was computed for homologous sites F3-F4. Pre- and post-training clinical assessments revealed significant improvements in HAM-D, HAM-A, BDI, and CGI-S scores. Cumulative response rates by HAM-D were 35.0 and 75.0 % at 4 and 8 weeks, respectively, corresponding cumulative remission rates by HAM-D were 15.0 and 55.0 %, respectively. No significant differences were found between pre- and post-treatment A score. Neurofeedback treatment could improve depressive symptoms significantly. In addition, anxiety symptoms and clinical illness severity decreased significantly after neurofeedback treatment. Despite its several limitations, such as, small sample size and lack of a control group, this study suggested neurofeedback has significant effects in patients with major depressive disorder.