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S.-H. Lee and Y. Park
left frontal region [19]. Empirical research has been in support of such hypothesis as increased relative alpha activity in the left hemisphere has been associated
with decreased scores on self-reported questionnaires of BAS in depressive patients
[21, 25].
Although theoretically supported, there are several confounding factors that ought
to be regarded in further studies on alpha asymmetry. Foremost, frontal alpha asymmetry is assumed to reflect the activity of the frontal lobe and any biological conditions that could influence its functioning should be controlled in order to properly
examine the effects of alpha asymmetry. Several conditions have been suggested to
influence frontal lobe functioning in major depressive disorder. First the subtypes of
depression (for example, melancholic vs. atypical depression) should be controlled
due to its different pathophysiology in relation to frontal lobe function. Second, the
various symptom manifestations (e.g., suicide ideation) that might influence frontal
lobe function ought to be considered. Frontal lobe function could be significantly
influenced by suicidal ideation. The disturbed functioning as well as reduced volumes of the orbitofrontal cortex have been reported to be associated with increased
impulsivity and aggression, which are vulnerabilities of suicidal behavior [87, 92].
Third, comorbid disorders ought to be regarded as different psychiatric disorders
are thought to have distinct alpha asymmetry patterns. For example, patients with
anxiety disorders often reveal an opposite pattern of alpha asymmetry in that greater
relative alpha power in the right hemisphere than the left [25].
7.3.3.2 Loudness Dependence of Auditory Evoked Potential (LDAEP)
The LDAEP has been related to depression, anxiety, and mood lability in clinical
samples as well as healthy participants. Several studies have suggested that sensory
processing sensitivity is associated with depression and anxiety. More specifically,
patients with anxiety or depression reported higher pain sensitivity, skin conductance,
or somatic sensations. Considering that LDAEP might reflect sensitivity (i.e., emotional and sensory) through its relations to central serotonin systems [62], LDAEP
might also reflect vulnerabilities toward depression.
The LDAEP has not only been associated with sensitivity but also with impulsivity. Previous studies reported that impulsive persons demonstrated faster reaction
time and more false alarm rates in a Go/No-go task. The LDAEP appears to reflect
impulsivity as the changes of No-go P3 amplitude correlated with LDAEP [62].
Additionally, LDAEP has been postulated to reflect impulsivity as represented by
motor and cognitive inhibition. An increasing number of researches have been supporting the relationship among LDAEP, impulsivity, and sensitivity, suggesting the
possibility of LDAEP as a valid biomarker of psychopathology.
In addition, LDAEP could be a trait-like state marker of mood disorder. While
LDAEP showed a similar pattern between patients and healthy controls, it was
known to predict treatment response of mood and anxiety symptom that were considered serotonin disturbances in their background pathology. There is a significant
correlation between a strong LDAEP—indicating low serotonergic function—and
S.-H. Lee and Y. Park
left frontal region [19]. Empirical research has been in support of such hypothesis as increased relative alpha activity in the left hemisphere has been associated
with decreased scores on self-reported questionnaires of BAS in depressive patients
[21, 25].
Although theoretically supported, there are several confounding factors that ought
to be regarded in further studies on alpha asymmetry. Foremost, frontal alpha asymmetry is assumed to reflect the activity of the frontal lobe and any biological conditions that could influence its functioning should be controlled in order to properly
examine the effects of alpha asymmetry. Several conditions have been suggested to
influence frontal lobe functioning in major depressive disorder. First the subtypes of
depression (for example, melancholic vs. atypical depression) should be controlled
due to its different pathophysiology in relation to frontal lobe function. Second, the
various symptom manifestations (e.g., suicide ideation) that might influence frontal
lobe function ought to be considered. Frontal lobe function could be significantly
influenced by suicidal ideation. The disturbed functioning as well as reduced volumes of the orbitofrontal cortex have been reported to be associated with increased
impulsivity and aggression, which are vulnerabilities of suicidal behavior [87, 92].
Third, comorbid disorders ought to be regarded as different psychiatric disorders
are thought to have distinct alpha asymmetry patterns. For example, patients with
anxiety disorders often reveal an opposite pattern of alpha asymmetry in that greater
relative alpha power in the right hemisphere than the left [25].
7.3.3.2 Loudness Dependence of Auditory Evoked Potential (LDAEP)
The LDAEP has been related to depression, anxiety, and mood lability in clinical
samples as well as healthy participants. Several studies have suggested that sensory
processing sensitivity is associated with depression and anxiety. More specifically,
patients with anxiety or depression reported higher pain sensitivity, skin conductance,
or somatic sensations. Considering that LDAEP might reflect sensitivity (i.e., emotional and sensory) through its relations to central serotonin systems [62], LDAEP
might also reflect vulnerabilities toward depression.
The LDAEP has not only been associated with sensitivity but also with impulsivity. Previous studies reported that impulsive persons demonstrated faster reaction
time and more false alarm rates in a Go/No-go task. The LDAEP appears to reflect
impulsivity as the changes of No-go P3 amplitude correlated with LDAEP [62].
Additionally, LDAEP has been postulated to reflect impulsivity as represented by
motor and cognitive inhibition. An increasing number of researches have been supporting the relationship among LDAEP, impulsivity, and sensitivity, suggesting the
possibility of LDAEP as a valid biomarker of psychopathology.
In addition, LDAEP could be a trait-like state marker of mood disorder. While
LDAEP showed a similar pattern between patients and healthy controls, it was
known to predict treatment response of mood and anxiety symptom that were considered serotonin disturbances in their background pathology. There is a significant
correlation between a strong LDAEP—indicating low serotonergic function—and