BeyinMer / Beyin Dinamiği Araştırma Merkezi
Permanent URI for this collectionhttps://hdl.handle.net/11413/6773
BeyinMer / Beyin Dinamiği Araştırma Merkezi / Brain Dynamics Research Center
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Publication Open Access Brain's alpha activity is highly reduced in euthymic bipolar disorder patients(Springer, Van Godewijckstraat 30, 3311 Gz Dordrecht, Netherlands, 2012-02) Güntekin, Bahar; Turp Gölbaşı, Bilge; Atagün, Murat İlhan; Özerdem, Ayşegül; Tülay, Elif; BAŞAR, EROL; TR142226; TR204666; TR25145; TR140995; TR142311Brain's alpha activity and alpha responses belong to major electrical signals that are related to sensory/cognitive signal processing. The present study aims to analyze the spontaneous alpha activity and visual evoked alpha response in drug free euthymic bipolar patients. Eighteen DSM-IV euthymic bipolar patients (bipolar I n = 15, bipolar II n = 3) and 18 healthy controls were enrolled in the study. Patients needed to be euthymic at least for 4 weeks and psychotrop free for at least 2 weeks. Spontaneous EEG (4 min eyes closed, 4 min eyes open) and evoked alpha response upon application of simple visual stimuli were analyzed. EEG was recorded at 30 positions. The digital FFT-based power spectrum analysis was performed for spontaneous eyes closed and eyes open conditions and the response power spectrum was also analyzed for simple visual stimuli. In the analysis of spontaneous EEG, the ANOVA on alpha responses revealed significant results for groups (F(1,34) = 8.703; P < 0.007). Post-hoc comparisons showed that spontaneous EEG alpha power of healthy subjects was significantly higher than the spontaneous EEG alpha power of euthymic patients. Furthermore, visual evoked alpha power of healthy subjects was significantly higher than visual evoked alpha power of euthymic patients (F(1,34) = 4.981; P < 0.04). Decreased alpha activity in spontaneous EEG is an important pathological EEG finding in euthymic bipolar patients. Together with an evident decrease in evoked alpha responses, the findings may lead to a new pathway in search of biological correlates of cognitive impairment in bipolar disorder.Publication Metadata only Lithium excessively enhances event related beta oscillations in patients with bipolar disorder(Elsevier Science Bv, Po Box 211, 1000 AE Amsterdam, Netherlands, 2015-01-01) Atagün, Murat İlhan; Güntekin, Bahar; Tan, Devran; Tülay, Emine Elif; BAŞAR, EROL; 25145; 204666; 103606; 142226Background: Previous resting-state electroencephalography studies have consistently shown that lithium enhances delta and theta oscillations in default mode networks. Cognitive task based networks differ horn resting-state networks and this is the first study to investigate effects or lithium on evoked and event-related beta oscillatory responses of patients with bipolar disorder. Methods: The study included 16 euthymic patients with bipolar disorder on lithium monotherapy, 22 euthymic medication-free patients with bipolar disorder and 21 healthy participants. The maximum peak-to-peak amplitudes were measured for each subject's averaged beta responses (14-28 Hz) in the 0-300 ms time window. Auditory simple and oddball paradigm were presented to obtain evoked and event-related beta oscillatory responses. Results: There were significant differences in beta oscillatory responses between groups (p=0.010). Repeated measures ANOVA revealed location (p=0.007), laterality X group (p=0.043) and stimulus X location (p=0.013) type effects. Serum lithium levels were correlated with beta responses. Limitations: The lithium group had higher number of previous episodes, suggesting that patients of the lithium were more severe cases than patients of the medication-free group. Discussion: Lithium stimulates neuroplastic cascades and beta oscillations become prominent during neuroplastic changes. Excessively enhanced beta oscillatory responses in the lithium-treated patients may be indicative of excessive activation of the neuron groups of the certain cognitive networks and dysfunctional GABAergic modulation during cognitive activity. (C) 2014 Elsevier B.V. All rights reserved.