Warning: array_key_exists(): The first argument should be either a string or an integer in D:\Inetpub\webs\924517_web\www\lang_set.inc.php on line 7 Prof. MUDr. Cyril Höschl DrSc. FRCPsych.

Brunovsky M, Horacek J, Viktorinova M, Novak T, Bravermanova M, Goetz M, Höschl C. QEEG signatures of remitted bipolar patients and offspring of bipolar parents. Abstracts of the 5th Biennial Cambridge & Bedford International Conference on Mental Health. Clare College, Cambridge University 11-14 Sept 2015

11. 9. 2015 - 14. 9. 2015

National Institute of Mental Health, Klecany, Czech Republic

Charles University, 3rd Faculty of Medicine, Prague, Czech Republic

Charles University, 2nd Faculty of Medicine, Motol University Hospital, Prague, Czech Republic

E mail: Martin.Brunovsky@nudz.cz

Background: The bipolar affective disorder is a devastating illness that is often diagnosed for the first time in adulthood. Neuroimaging and electrophysiological studies of neural impairments of bipolar affective disorder (BD) have revealed various state- and trait-dependent patterns (and their changes induced by different therapeutic approaches), reflecting complex network of different neurons that are topographically distributed over the heterogeneous brain areas. While several investigators have described functional abnormalities of various cortico-limbic networks including the default mode network in adults with bipolar disorder, we still do not know whether similar abnormalities are detectable even at younger age.

The main objectives of the present study were: (1) to elucidate vulnerability QEEG markers related to emotional processing (neutral and negative state) induced by autobiographic script in remitted patients with BD compared to healthy controls (HC) and (2) to identify early electrophysiological markers in a sample of offspring of parents with BD (high-risk population).

Methods: EEG data were obtained during transient sadness and neutral mood state induced by a written, autobiographical script in 30 remitted patients with BD (MADRS< 10, YMRS< 7) and 30 matched HC. In the second study, event-related potentials (P300) and resting state EEG were recorded in 30 children (8-17 years) of parents with BD (BDO group) and their age- and gender-ratio-matched control group consisting of 30 healthy children participants (HCP). The localization of the within-group (sad vs. neutral mood state) and between-group (BP vs. HC; BDO vs. HCP) differences in resting electrical activity (cortical 3D distribution of current source density) was assessed by standardized low-resolution brain electromagnetic tomography (sLORETA). The P300 latency and the N2/P3 peak-to-peak amplitude in BDO and HCP groups were computed and evaluated at the Cz electrode.

Results: Compared to neutral state, the induction of sadness in HC led to the significant increase of gamma sources in subgenual and anterior cingulate (Brodmann's areas /BA/ 25, 32). The changes in patients with BD were observed in the same frequency band but in the more pronounced areas involving large part of anterior cingulate and mediofrontal cortex (BA 10, 11, 24, 25, 32). The comparison of emotionally-related differences between both groups revealed the significant increase of gamma sources in posterior cingulate (BA 23,31) and significant decrease of alpha-2 sources in inferior frontal gyrus (BA 10,47) as a potential trait marker in remitted patients with BD.

The offspring study revealed significant differences in the beta-3 and gamma sources between BDO and HCP groups. sLORETA analysis showed that the beta-3 and gamma current source densities in frontal lobe regions such as the inferior frontal gyrus (BA 45, 47), medial frontal gyrus (BA 6, 9, 32) and cingulate (BA 23, 24, 32) were significantly lower in the BDO group than in HCP (p<0.05).

Conclusion: The mood challenge paradigm used in adult groups can unmask the trait-marker in remitted patients with BD. Our finding of abnormal neuronal activity is in accordance with previous studies of bipolar disorder and could be interpreted within the framework of aberrant fronto-cingular connectivity revealed during induced sadness in euthymia patients with BD. In addition to cingulate hyperactivity during sad mood induction in adult BD, the observed diminution of corticolimbic activity in BDO compared to HCP group could be interpreted within the context of the default mode network where the deficit of the beta-3 and gamma (i.e. excitatory) current sources in mediofrontal and anterior cingulate areas might reflect the early electrophysiological trait marker of BD in this high-risk population.

This study was supported by grants from the Ministry of Health of the Czech Republic (IGA NT/12024-5 and NT/13337–4) and by project PRVOUK P34.