FV 16 Brain arousal regulation as response predictor for antidepressant therapy in major depression
A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a hig...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Schmidt, F. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Umfang: |
2 |
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| Übergeordnetes Werk: |
Enthalten in: Medical students' biomedical and clinical knowledge: Combining longitudinal design, eye tracking and comparison with residents' performance - Södervik, Ilona ELSEVIER, 2017, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:128 ; year:2017 ; number:10 ; pages:313-314 ; extent:2 |
| Links: |
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| DOI / URN: |
10.1016/j.clinph.2017.06.058 |
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ELV025048368 |
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| 520 | |a A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. | ||
| 520 | |a A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. | ||
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10.1016/j.clinph.2017.06.058 doi GBV00000000000269A.pica (DE-627)ELV025048368 (ELSEVIER)S1388-2457(17)30274-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn 80.00 bkl Schmidt, F. verfasserin aut FV 16 Brain arousal regulation as response predictor for antidepressant therapy in major depression 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. Sander, C. oth Hegerl, U. oth Enthalten in Elsevier Science Södervik, Ilona ELSEVIER Medical students' biomedical and clinical knowledge: Combining longitudinal design, eye tracking and comparison with residents' performance 2017 Amsterdam [u.a.] (DE-627)ELV000764582 volume:128 year:2017 number:10 pages:313-314 extent:2 https://doi.org/10.1016/j.clinph.2017.06.058 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 80.00 Pädagogik: Allgemeines VZ AR 128 2017 10 313-314 2 128.2017, 10, e313-, (2 S.) 045F 610 |
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10.1016/j.clinph.2017.06.058 doi GBV00000000000269A.pica (DE-627)ELV025048368 (ELSEVIER)S1388-2457(17)30274-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn 80.00 bkl Schmidt, F. verfasserin aut FV 16 Brain arousal regulation as response predictor for antidepressant therapy in major depression 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. Sander, C. oth Hegerl, U. oth Enthalten in Elsevier Science Södervik, Ilona ELSEVIER Medical students' biomedical and clinical knowledge: Combining longitudinal design, eye tracking and comparison with residents' performance 2017 Amsterdam [u.a.] (DE-627)ELV000764582 volume:128 year:2017 number:10 pages:313-314 extent:2 https://doi.org/10.1016/j.clinph.2017.06.058 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 80.00 Pädagogik: Allgemeines VZ AR 128 2017 10 313-314 2 128.2017, 10, e313-, (2 S.) 045F 610 |
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10.1016/j.clinph.2017.06.058 doi GBV00000000000269A.pica (DE-627)ELV025048368 (ELSEVIER)S1388-2457(17)30274-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn 80.00 bkl Schmidt, F. verfasserin aut FV 16 Brain arousal regulation as response predictor for antidepressant therapy in major depression 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. Sander, C. oth Hegerl, U. oth Enthalten in Elsevier Science Södervik, Ilona ELSEVIER Medical students' biomedical and clinical knowledge: Combining longitudinal design, eye tracking and comparison with residents' performance 2017 Amsterdam [u.a.] (DE-627)ELV000764582 volume:128 year:2017 number:10 pages:313-314 extent:2 https://doi.org/10.1016/j.clinph.2017.06.058 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 80.00 Pädagogik: Allgemeines VZ AR 128 2017 10 313-314 2 128.2017, 10, e313-, (2 S.) 045F 610 |
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10.1016/j.clinph.2017.06.058 doi GBV00000000000269A.pica (DE-627)ELV025048368 (ELSEVIER)S1388-2457(17)30274-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn 80.00 bkl Schmidt, F. verfasserin aut FV 16 Brain arousal regulation as response predictor for antidepressant therapy in major depression 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. Sander, C. oth Hegerl, U. oth Enthalten in Elsevier Science Södervik, Ilona ELSEVIER Medical students' biomedical and clinical knowledge: Combining longitudinal design, eye tracking and comparison with residents' performance 2017 Amsterdam [u.a.] (DE-627)ELV000764582 volume:128 year:2017 number:10 pages:313-314 extent:2 https://doi.org/10.1016/j.clinph.2017.06.058 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 80.00 Pädagogik: Allgemeines VZ AR 128 2017 10 313-314 2 128.2017, 10, e313-, (2 S.) 045F 610 |
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10.1016/j.clinph.2017.06.058 doi GBV00000000000269A.pica (DE-627)ELV025048368 (ELSEVIER)S1388-2457(17)30274-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn 80.00 bkl Schmidt, F. verfasserin aut FV 16 Brain arousal regulation as response predictor for antidepressant therapy in major depression 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. Sander, C. oth Hegerl, U. oth Enthalten in Elsevier Science Södervik, Ilona ELSEVIER Medical students' biomedical and clinical knowledge: Combining longitudinal design, eye tracking and comparison with residents' performance 2017 Amsterdam [u.a.] (DE-627)ELV000764582 volume:128 year:2017 number:10 pages:313-314 extent:2 https://doi.org/10.1016/j.clinph.2017.06.058 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 80.00 Pädagogik: Allgemeines VZ AR 128 2017 10 313-314 2 128.2017, 10, e313-, (2 S.) 045F 610 |
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A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. |
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A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. |
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A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show (a) a high level of EEG-vigilance (an indicator of brain arousal) and (b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14±1days following onset of antidepressant treatment (T1). Response was defined as a ⩾ 50% HAMD-17-improvement after 28±1days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1 0). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133=4.780, p =0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130=4.978, p =0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders. |
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