158
S.-H. Lee and Y. Park
7.3.1.3 Mismatch Negativity (MMN)
Multiple studies have identified MMN deficits in patients with schizophrenia [79,
80, 117, 141]. A primary advantage of MMN is that it has been known to be relatively uninfluenced by the effects of antipsychotic medication [14, 135, 136]. In
addition, its deficits are thought to reflect the progression of a disease and premorbid neurocognitive impairment [134]. According to a study by ¸
Sevik et al. [120],
patients with schizophrenia demonstrated nearly identical MMN amplitudes to an
age- and education-matched sibling group. However, their MMN amplitudes were
significantly lower than those of healthy controls [120]. Similar findings were also
reported by Lee et al. [72, 74], who showed that patients with schizophrenia exhibited
comparable MMN amplitudes compared to that of first degree relatives, but significantly lower than education-matched healthy controls. In addition, the MMN amplitude of frontal electrodes and functional outcomes measurements showed the most
powerful correlations compared to other psychological measurements in patients
with schizophrenia.
The major pathology of MMN deficit appears to originate from dysfunctions
of the NMDA receptor system [48, 137]. NMDA-receptor-mediated glutamatergic
dysfunction may well explain the pathology of both schizophrenia and other neuropsychiatric diseases, which explicitly reflect MMN deficits [137].
Several studies have reported correlations between MMN and global social functioning in patients with chronic schizophrenia [57, 59, 72, 74, 79, 80], and one study
found a stable association over a 1-year period [79, 80]. A significant association
between MMN and Global Assessment of Functioning (GAF) scores have also been
noted in healthy participants [81], indicating that deficits in MMN can impact social
functioning not only in patients but in community samples as well.
Studies measuring MMN reduction in patients with first-episode schizophreniaspectrum showed a negligible effect size of 0.04 SD for MMN to a pitch-deviant
and a small to medium effect size of 0.47 SD for MMN to a duration-deviant. Effect
sizes for MMN reductions in patients with chronic schizophrenia were around 1
SD compared with controls, suggesting that the MMN deficit increases with the
progression of the disease. Despite the marked MMN reductions in patients with
chronic schizophrenia, the deficit does not seem to be severe during the first episode.
There is no consistent evidence for a marked deficit in pitch MMN in patients with
first-episode schizophrenia spectrum, while MMN may show a small to medium
effect size along with the progression of the disorder (Fig. 7.4).
7.3.2 Bipolar Disorder
Bipolar disorder is a major psychiatric illness characterized by recurrent manic,
depressive, mixed, and euthymic phases. Emotional dysregulation and cognitive
impairments, which possibly reflect structural and functional brain connectivity disturbances [11, 15], seem to be involved in the disorder [68]. Alterations in white mat-
S.-H. Lee and Y. Park
7.3.1.3 Mismatch Negativity (MMN)
Multiple studies have identified MMN deficits in patients with schizophrenia [79,
80, 117, 141]. A primary advantage of MMN is that it has been known to be relatively uninfluenced by the effects of antipsychotic medication [14, 135, 136]. In
addition, its deficits are thought to reflect the progression of a disease and premorbid neurocognitive impairment [134]. According to a study by ¸
Sevik et al. [120],
patients with schizophrenia demonstrated nearly identical MMN amplitudes to an
age- and education-matched sibling group. However, their MMN amplitudes were
significantly lower than those of healthy controls [120]. Similar findings were also
reported by Lee et al. [72, 74], who showed that patients with schizophrenia exhibited
comparable MMN amplitudes compared to that of first degree relatives, but significantly lower than education-matched healthy controls. In addition, the MMN amplitude of frontal electrodes and functional outcomes measurements showed the most
powerful correlations compared to other psychological measurements in patients
with schizophrenia.
The major pathology of MMN deficit appears to originate from dysfunctions
of the NMDA receptor system [48, 137]. NMDA-receptor-mediated glutamatergic
dysfunction may well explain the pathology of both schizophrenia and other neuropsychiatric diseases, which explicitly reflect MMN deficits [137].
Several studies have reported correlations between MMN and global social functioning in patients with chronic schizophrenia [57, 59, 72, 74, 79, 80], and one study
found a stable association over a 1-year period [79, 80]. A significant association
between MMN and Global Assessment of Functioning (GAF) scores have also been
noted in healthy participants [81], indicating that deficits in MMN can impact social
functioning not only in patients but in community samples as well.
Studies measuring MMN reduction in patients with first-episode schizophreniaspectrum showed a negligible effect size of 0.04 SD for MMN to a pitch-deviant
and a small to medium effect size of 0.47 SD for MMN to a duration-deviant. Effect
sizes for MMN reductions in patients with chronic schizophrenia were around 1
SD compared with controls, suggesting that the MMN deficit increases with the
progression of the disease. Despite the marked MMN reductions in patients with
chronic schizophrenia, the deficit does not seem to be severe during the first episode.
There is no consistent evidence for a marked deficit in pitch MMN in patients with
first-episode schizophrenia spectrum, while MMN may show a small to medium
effect size along with the progression of the disorder (Fig. 7.4).
7.3.2 Bipolar Disorder
Bipolar disorder is a major psychiatric illness characterized by recurrent manic,
depressive, mixed, and euthymic phases. Emotional dysregulation and cognitive
impairments, which possibly reflect structural and functional brain connectivity disturbances [11, 15], seem to be involved in the disorder [68]. Alterations in white mat-