Biomedical Engineering Reference
In-Depth Information
taken, using a related EEG measure, the antidepressant treatment response (ATR)
index [86]. The ATR can be computed using a simplified electrode array with five
electrodes placed over prefrontal and frontal brain regions (FPz, AT1, AT2, A1,
A2), instead of ~35 to 40 electrodes placed over all scalp locations for measuring
cordance (“full-head montage”), making this a technology well suited for use in
outpatient physicians' offices and avoiding the need to send patients to a dedicated
EEG facility.
The EEG features comprising ATR were derived from the power spectra; ATR
(revision 4.1) is a nonlinear combination of three features measured at two time
points (in this trial, at baseline and week 1): (1) absolute power in an alpha subband
(8.5 to 12 Hz), (2) absolute power in a second alpha subband (9 to 11.5 Hz), and (3)
relative power in a combined theta and alpha band (3 to 12 Hz), calculated as the
ratio of absolute combined theta and alpha power divided by total power (2 to 20
Hz). ATR is a weighted combination of the relative theta and alpha power at week 1
and the difference of alpha power between baseline (alpha: 8.5 to 12 Hz) and week
1 (alpha: 9 to 11.5 Hz), and is scaled to range from 0 (low probability of response to
treatment) to 100 (high probability of response).
In the BRITE-MD study, subjects began with a 1-week test period of
escitalopram, and then were randomized to receive either continued escitalopram
treatment, a switch to bupropion, or a combination of the two medications. EEG
data were recorded before and after the 1-week test period. In outpatients with
major depression, individuals who received treatment consistent with their
biomarker prediction were significantly more likely to experience response and
remission than individuals who were randomized to a treatment not predicted to be
useful [86-89]. Further development and replication projects are under way, and
must be completed before this paradigm of early physiological change can be
considered for clinical application.
11.2.2.2 Loudness-Dependent Auditory Evoked Potential
The second approach utilizes an EEG measure that is proposed to reflect central
serotonergic activity, the loudness-dependent auditory evoked potential (LDAEP)
[90-92]. In the measurement of LDAEP indices, subjects listen to a set of sine wave
tones at a series of loudness levels, while evoked potentials are being recorded [93].
The variation in the ratio of N1 to P2 amplitude values in the primary auditory cor-
tex is measured with dipole source analysis, and the tangential dipole is reported to
have a strong signal in the presence of low serotonergic activity; conversely,
low-amplitude dipole signals are associated with high central serotonergic activity
[94]. This phenomenon has been attributed to the serotonergic innervation of the
primary auditory cortex [95]. For use as a biomarker in depression, qEEG data
recorded prior to treatment would be interpreted to indicate whether a depressed
patient has a low or high level of central serotonergic activity; those with low activ-
ity would be predicted to have a favorable response to a serotonergic medication
(whereas high activity would be linked to better outcomes with a noradrenergic
agent).
This method been examined using treatment with SRIs [96-98] or a
noradrenergic agent [99, 100], and the relationship between level of serotonergic
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