160
S.-H. Lee and Y. Park
with schizophrenia, respectively [54]. On the other hand, Kim and colleagues were
unable to identify any differences between patients with bipolar disorder and healthy
controls [60]. Despite these inconsistencies, the bipolar disorder seems to be associated with a disorganized connectivity pattern in the delta band, characterized by
higher density of connections and lower path length and modular organization.
When compared to patients with schizophrenia, the patients with bipolar disorder
exhibited lower inter-hemispheric theta coherence in the parietal region and higher
intra-hemispheric beta1 (12–20 Hz) coherence [54]. With regard to the alpha band
(8–12/13 Hz), the results are more consistent and abnormal neuronal connectivity
is found in patients with bipolar disorder when compared with healthy controls [9,
54, 60]. Specifically, enhanced intra-hemispheric parieto-temporal and centroparietal
coherence were observed in patients with bipolar disorder [54]. Kim and colleagues
showed that patients with bipolar disorder had lower SL values and nodal strength,
especially in a fronto-central-parietal network [60]. In addition, patients with bipolar
disorder had lower clustering coefficient and global efficiency, but higher values of
characteristic path length than healthy controls. Similarly, Bhattacharya observed
the strongest reduction in the degree of long-range phase synchrony in the alpha
band [9]. Furthermore, alpha EEG coherence abnormalities seem to persist even in
patients with bipolar disorder who are in an active phase (manic and/or depressive)
[101].
¨
Ozerdem and colleagues used a visual oddball paradigm to investigate the eventrelated gamma coherence in patients with manic [104] and euthymic [103] bipolar
disorder. The authors showed that patients with manic bipolar disorder exhibited
reduced fronto-temporal coherence in the right hemisphere. Interestingly, this difference was also confirmed in patients with euthymic bipolar disorder. In Valesques
et al. [138], gamma EEG coherence was explored in patients with depression and
manic bipolar disorder and manic bipolar disorder alone compared with healthy controls during a prosaccadic paradigm [138]. Interestingly, patients with manic bipolar
disorder exhibited higher gamma coherence in the bilateral frontal region, whereas
patients with depression and bipolar disorder showed increased coherence in the
right frontal region in comparison with healthy controls. These results suggest that
abnormal information processing in bipolar disorder may rely either on increased
or decreased gamma coherence, depending on the functionality of each brain region
during the examined task.
In a recent review, Özerdem et al. reported that (a) the decrease of higher frequency
theta (6–8 Hz) response might reflect impaired cognition in bipolar disorder, (b)
breaks of spontaneous alpha oscillation might indicate a deficit of the central nerve
system in bipolar disorder, and (c) beta oscillations might reflect treatment response
in bipolar disorder [102] (see Fig. 7.5).
S.-H. Lee and Y. Park
with schizophrenia, respectively [54]. On the other hand, Kim and colleagues were
unable to identify any differences between patients with bipolar disorder and healthy
controls [60]. Despite these inconsistencies, the bipolar disorder seems to be associated with a disorganized connectivity pattern in the delta band, characterized by
higher density of connections and lower path length and modular organization.
When compared to patients with schizophrenia, the patients with bipolar disorder
exhibited lower inter-hemispheric theta coherence in the parietal region and higher
intra-hemispheric beta1 (12–20 Hz) coherence [54]. With regard to the alpha band
(8–12/13 Hz), the results are more consistent and abnormal neuronal connectivity
is found in patients with bipolar disorder when compared with healthy controls [9,
54, 60]. Specifically, enhanced intra-hemispheric parieto-temporal and centroparietal
coherence were observed in patients with bipolar disorder [54]. Kim and colleagues
showed that patients with bipolar disorder had lower SL values and nodal strength,
especially in a fronto-central-parietal network [60]. In addition, patients with bipolar
disorder had lower clustering coefficient and global efficiency, but higher values of
characteristic path length than healthy controls. Similarly, Bhattacharya observed
the strongest reduction in the degree of long-range phase synchrony in the alpha
band [9]. Furthermore, alpha EEG coherence abnormalities seem to persist even in
patients with bipolar disorder who are in an active phase (manic and/or depressive)
[101].
¨
Ozerdem and colleagues used a visual oddball paradigm to investigate the eventrelated gamma coherence in patients with manic [104] and euthymic [103] bipolar
disorder. The authors showed that patients with manic bipolar disorder exhibited
reduced fronto-temporal coherence in the right hemisphere. Interestingly, this difference was also confirmed in patients with euthymic bipolar disorder. In Valesques
et al. [138], gamma EEG coherence was explored in patients with depression and
manic bipolar disorder and manic bipolar disorder alone compared with healthy controls during a prosaccadic paradigm [138]. Interestingly, patients with manic bipolar
disorder exhibited higher gamma coherence in the bilateral frontal region, whereas
patients with depression and bipolar disorder showed increased coherence in the
right frontal region in comparison with healthy controls. These results suggest that
abnormal information processing in bipolar disorder may rely either on increased
or decreased gamma coherence, depending on the functionality of each brain region
during the examined task.
In a recent review, Özerdem et al. reported that (a) the decrease of higher frequency
theta (6–8 Hz) response might reflect impaired cognition in bipolar disorder, (b)
breaks of spontaneous alpha oscillation might indicate a deficit of the central nerve
system in bipolar disorder, and (c) beta oscillations might reflect treatment response
in bipolar disorder [102] (see Fig. 7.5).