18(2) 61 –74
© The Author(s) 2012
Reprints and permission:
This article is a follow-up to a 2009 report by Harper, Raso lkhan i-
Kalhorn, and Drozd (2009) on a qEEG study of the reaction
of the brain to EMDR therapy, based on a theory proposed
by Rasolkhani-Kalhorn and Harper (2006). During the EEG
study of EMDR, bilateral sensory input was provided by
vibrating pads held in the palms of the hands of the partici-
pants. This clinical EEG study was supplemented by labo-
ratory studies, which allowed for more control of input
parameters. Following are the main findings:
Similarity of results of animal studies by others of
depotentiation of glutamate receptors on fear
memory synapses through direct tetanic (electri-
cal) stimulation led us to the conclude that EMDR
and similar therapies cause a similar depotentiation
through the creation of powerful waves of neuronal
Sensory inputs (vibrating pads in palms of hands)
greatly magnify the power of the low-frequency por-
tion of the neuronal firing spectrum (delta waves).
Frequency of the powerful waves created in the mem-
ory areas of the brain, between 1 and 2 Hz (1 to 2 rep-
etitions per second), remained unchanged through
all brain states investigated in the study.
A delta wave power increase of 50% to 100% occur-
ring during exposure to the fear memory without
sensory input suggested a reason for the success of
exposure therapies such as flooding in which no
sensory input is included.
The frequency and power of waves created during these
therapies are much like those generated during the
natural memory editing system of slow-wave sleep.
The results of this study of EMDR therapy can be gener-
alized to include all exposure therapies, which are those in
which the client is exposed to a fear memory as part of the
therapy. These therapies have this in common: They work
by utilizing a natural mechanism of the brain to remove the
material basis for the fear memory. This mechanism is depo-
tentiation of glutamate receptors on synapses mediating the
memory in the lateral nucleus of the amygdala as discovered
by animal studies such as those by Lin, Lee, and Gean (2003)
and Rubin, Gerkin, Bi, and Chow (2005).
Dr. Edna Foa and others developed exposure therapy itself
in 1999, and use of this term as a general name may be mis-
leading. For this reason, the term depotentiation therapy is
suggested for this group of therapies. To save five syllables in
each use of this term, dep. therapy is used instead in this report.
1A center for Psychotherapy, Colorado Springs, Co., and Guadalajara,
Melvin Harper, Provincia 1072, Guadalajara, 44620, Mexico
Taming the Amygdala: An EEG Analysis
of Exposure Therapy for the Traumatized
Animal and human studies have shown that the emotional aspects of fear memories mediated in the lateral nucleus of
the amygdala can be extinguished by application of low-frequency tetanic stimulation or by repetitive sensory stimulation,
such as tapping the cheek. Sensory input creates a remarkable increase in the power of the low-frequency portion of the
electroencephalogram (EEG) spectrum. Glutamate receptors on synapses that mediate a fear memory in attention during
exposure therapy are depotentiated by these powerful waves of neuronal firings, resulting in disruption of the memory
network. In this study, the role of sensory input used in the principal exposure therapies is examined through analysis of
the raw EEG data obtained in clinical and lab tests. Nearly all sensory inputs applied to the upper body result in wave power
sufficiently large to quench fear–memory networks regardless of input location and type and whether the sensory input
is applied unilaterally or bilaterally. No power advantage is found for application of sensory input at energy meridians or
gamut points. The potential for new or extended applications of synaptic depotentiation in amygdalar memory networks
EEG, PTSD, exposure therapy, brain stimulation, amygdalar evolution, cross-species therapy.
62 Traumatology 18(2)
Included in the dep. therapy group are the following:
• Those in which specific sensory input is not given
• Behavioral therapy (Wolpe, 1958)
• Flooding therapy (Keane, Fairbank, Caddell, &
• Exposure therapy (Foa et al., 1999)
• Those in which sensory input is given during ther-
apy (fast dep. therapy)
• Eye movement desensitization and reprocessing
therapy (EMDR; Shapiro, 1989)
• Thought field therapy (TFT; Callahan, 1996)
• Emotional freedom technique (EFT; Craig, 2008)
• Others being developed, such as havening ther-
apy (Ruden, 2010)
Experiments carried out by Dr. Francine Shapiro in 1989
proved that mild brain stimulation created by sensory input
is a necessary component of fast depotentiation therapies, in
this case EMDR. Her PTSD (posttraumatic stress disorder)
patients were instructed to keep a fear memory in mind
while she performed EMDR therapy without using sensory
input. They were then given a test for evidence of PTSD; no
posttherapy change was found. Subsequently, she performed
EMDR using sensory input to relieve the PTSD symptoms.
Shapiro made the obvious deduction from these experiments
that sensory input is an essential element of EMDR therapy.
Nevertheless, many have since questioned the relevance of
such input during therapy, including Davidson and Parker
(2001) and Renfrey and Spates (1994). Others, such as
Devilly (2005), Gaudiano and Herbert (2000), and Ost and
Easton (2006), debate the effectiveness of exposure therapies
Still other therapists believe that sensory input must be
applied specifically to energy meridians and the gamut point
on the back of the hand. (Thought field therapy developer
Callahan in 1996 suggested the name gamut point for a spe-
cific location on the back of the hand because of the large
number of treatments using this location.)
To examine these and other issues, analysis of EEG
records from the EMDR clinical sessions and lab experiments
was undertaken in the current study. Since clinical studies do
not lend themselves to sufficiently controllable input condi-
tions, over 50 experiments were carried out in an EEG lab to
record waves created by the more common sensory stimula-
tion methods used in dep. therapy. This allowed a more accu-
rate analysis of the range of power and frequency of waves
generated during baseline periods and during sensory stimu-
lation of various kinds. The results and conclusions of these
studies are reported here.
EEG Relevance in
The EEG waves on records studied in this project are thought
to originate primarily through the firing of principal neurons
in the memory areas of the brain, particularly the hippocampus,
amygdala, and the ventromedial prefrontal cortex (VMPFC,
Figure 1). In general, memory is recorded by neurons in these
areas firing at about 8 to 10 times per second (8 to 10 Hz,
alpha waves), and memory erasure (extinction) by neurons
firing at 1 to 4 times per second (1 to 4 Hz, delta waves).
These two frequency ranges are ordinarily found to occur
during the waking state and slow-wave sleep, respectively.
Information on locations within the brain most active in
contributing to the EEG was obtained through two-dimen-
sional mapping of the distribution of wave power intensity
(Figure 2, from Participant 3). A LORETA mapping of the
Figure 1. Photo of the ventral (lower) surface of the brain
displaying ventromedial prefrontal cortex (VMPFC) and
amygdalae; the hippocampi are located immediately below and in
the same plane as the amygdalae
Source: Original image from Dubuc (2003) reprinted with permission.
Figure 2 .Topographic maps of areas of maximum intensity of
electrical activity, Participant 3. Left: activity before brain stimulation
while the participant was in a relaxed attentional state; right: activity
during the final 5 min of EMDR Phase 4, with sensory input (BBS
[bilateral brain stimulation], pads in hands). Fp1 and Fp2: locations of
EEG electrodes principally used in this study
EEG obtained during the EMDR session of Participant 2
confirmed and extended the interpretation of location data.
The raw EEG data contain detailed information about the
activity of memory neurons during dep. therapy and the EEG
protocols leading up to the therapy sessions. The recorded
waves are sufficiently powerful to be manipulated mathemat-
ically for extraction of frequency and power, using advanced
forms of wavelet analysis such as Fourier transforms (first
extensively used in seismology). Although not as precise in
location as fMRI, the EEG has the great advantage of being a
continuous record over several minutes or hours. A large
database builds as data are received and analyzed in the pro-
cessing programs. The EEG tracks this process precisely in
real time for subsequent quantitative analyses. Power is
expressed in microvolts squared (uV2, millionths of a volt
squared). Frequency of the waves of neuronal depolarizations
is expressed in Hertz (one repetition per second is 1 Hz).
The quantitative analysis of the EEG in this study should
not be confused with conventional qEEG (quantitative elec-
troencephalogram) analysis. We used only the actual power
and LORETA analyses from the qEEG processed data on the
first three participants, and instead, carried out full analysis of
the frequency and power information in the raw data to deter-
mine the following parameters for all participants: the firing
frequencies and power of the principal neurons; the shape and
amplitude of the peaks and troughs of the waves of depolar-
ization, and thus, the likelihood of memory erasure or mem-
ory enhancement; and the presence of electrical activity from
bioelectrical sources such as eye movements (artifacts).
Standard qEEG is more likely to be used to determine
deviation of an individual EEG from large database norms
rather than to investigate behavior of the brain during specific
conditions such as those in this study, particularly the reac-
tion to repetitive low-frequency sensory input. QEEG analy-
sis is extended to precise timing of EEG event arrivals and the
variations in response time and phase between various possi-
ble sources within each hemisphere or between the two hemi-
spheres. Many, such as Schiff (2005), believe the qEEG
interpretation is overextended and may lead to false conclu-
sions. It is for this reason that we used raw data processing
only in this study. However, we recognize that even this sim-
pler approach to EEG interpretation can give ambivalent
results because of the complexity of the brain itself and the
variable emotional and cognitive responses to day-to-day life.
Equipment and Procedures
For the clinical studies, two different sets of equipment were
used, as detailed in an earlier paper (Harper et al., 2009). A
Lexicor Neurosearch 24 EEG unit was used to provide
EEGs of study Participants 1 through 3; the two electrode
BrainMaster Atlantis II was used for the remainder of the
participants and for the lab experiments. For the Lexicor
unit, a 19-channel full-head electrocap was used; electrodes
were placed according to a standard location technique. The
two electrodes of the BrainMaster unit were placed at stan-
dard locations in the temporal and frontal areas, most com-
monly at the Fp1 and Fp2 locations as shown in Figure 2. A
Tac/Audioscan unit provided vibratory sensory input to the
palm of the hand during Phase 4 of the EMDR protocol
used in all the clinical trials. A digital metronome was used
to help guide input frequency during some of the lab exper-
Clinical and Lab Procedures
Three- and 5-min EEG recordings were made of each phase
of the EMDR sessions. The EEG of relaxed states, with eyes
open and then closed, were recorded to provide a baseline
against which other attentional states could be compared.
The next step was to record waveforms created while the
participant was thinking of the fear memory with eyes closed,
with no sensory input. This procedure was followed by 2 to
8 brief eyes-closed recordings of the EEGs of participants
receiving Phase 4 of EMDR therapy. Sensory input during
this part of the study was supplied by vibrating pads in the
palms of the hands while the participant kept the memory in
attention. The EEG protocol concluded with a brief recording
of the relaxed state after the EMDR session. Thirty to 40 min
of EEG records were obtained from each participant.
For the lab experiments, the participant was instructed to
relax and think of neutral, nonemotional subjects. An EEG
baseline value was obtained for each separate experiment,
followed by recordings of the EEG resulting from sensory
input such as tapping or eye movements.
Volunteer participants for this study were chosen through
a clinical interview and a battery of tests designed to assess
their suitability for the procedure. A fear memory target was
agreed beforehand with each participant. The actual EEG
recording session followed 2.5 to 4 hr of participant contact.
Follow-up sessions were held with participants to determine
their ongoing experience after the therapy. Finally, each par-
ticipant was contacted 9 to 18 months following the EEG-
EMDR sessions. All clinical results were positive. The lab
experiments provided most of the data used in this study.
EEG records from the first three participants were processed
conventionally, including subjecting the data to a z-score
analysis (comparisons of power, timing, and frequency
records with average base levels for these parameters). As
noted previously, we found that this kind of data processing
is not relevant to the questions we wished to answer, and so
we were unable to use most of these processed data. Instead,
we performed wavelet analysis of the raw data from the
EEG records. Programs developed by the NeuroGuide and
64 Traumatology 18(2)
BrainMaster companies were used in the analysis. Average
power and frequency were calculated at intervals to ade-
quately characterize the various groups of EEG responses
after filtering to eliminate extraneous artifacts such as muscle
(EMG) or cable noise. Simple mathematical programs were
used to obtain frequency statistics. Artifacts, primarily from
muscle contractions (EMG) or cable noise, were removed
from the records prior to power and frequency analysis.
Sensory input during the therapy and during the lab experi-
ments often resulted in development of high-amplitude wave
trains similar to artifacts. However, this input was generally
given at a lower frequency than the natural firing frequency
of the neurons (about 1.78 Hz) and so can be reliably distin-
guished from extraneous artifacts. Electrode pop (bounce) as
illustrated in Rowan and Tolunsky (2003, p. 138) was found
only when tapping within about 4 cm of the electrode (see
also supplementary backup data). Records used are available
for inspection, downloading, or further analysis at the website
http://www.mindspaces.org, or by contacting the author.
Synaptic potentiation and depotentiation. A fear memory is
formed through a process called synaptic potentiation, which
is thought to result in strengthening of a specific circuit
through the lateral amygdala (LeDoux, 2003). Reversal of
potentiation occurs through synaptic depotentiation, which
causes closure of AMPA (alpha-amino-3-hydroxy-5-methyl-
4-isoxazole) glutamate receptor channels on the synapses
involved. Research by Lin et al. (2003) indicates that this
closure is caused by the action of calcineurin released when
calcium ions enter the synapse (mainly through NMDA,
N-methyl-D-aspartate receptors) during the minimum phase
of the depolarizing wave (Figure 3); the depotentiated
receptors are subsequently internalized within the synapse
(Earnshaw & Bressloff, 2006), and the material basis of the
fear memory has been removed.
The firing frequency of the neurons contributing to the EEGs
recorded during clinical and laboratory studies in this project
fall in the range of 1.5 to 2 Hz (they fire 1.5 to 2 times per
second); average frequency calculated from 69 measurements
of EEG samples from EEGs of the 6 participants is 1.78 Hz
with a standard deviation of 0.13. This delta frequency pattern
was substantially the same in all records examined, regardless
of participant, the mental state of the participant during the
recordings, or of sensory input (Figure 4).
A power variation with a frequency of 0.2 to 0.33 Hz can
be seen on many of the records; that is, a wave-like change
in power occurs over intervals of about 3 to 5 s.
Maximum spectral power occurring in the delta range (from
near 0 to 4 Hz) was determined for each type of sensory
input in numerous separate computations. Each was found
to have a characteristic magnitude that usually varied only
with changes in recording conditions, including sensitivity
of the electrodes used during the experiment. In general,
power of sensory inputs such as tapping decreases as the
distance from the sensory cortex increases (e.g., neck taps
were usually more powerful than shoulder taps). This
decrease is possibly the result of two factors: decay of sen-
sory input signals with distance, and a general decrease in
sensitivity of the skin away from the head. The former is
unlikely since conduction loss is minimal (Ehrenstein &
Lecar, 1972), and the variation of power is thought to result
from variation in receptor density and type. Mann (1981),
partially on the basis of data from Woodworth and
Schlosberg (1965), lists the number of sensitive points per
square centimeter on certain areas of the upper body: 100 at
the tip of the nose, 50 on the forehead, 29 on the chest, 15
on the inside (volar area) of the forearm, and 14 on the back
of the hand. The skin area with the greatest density of touch
receptors is on the palm of the hand, with 120 per square
centimeter, an increase relative to the back of the hand by a
factor of 8.6 fold. This difference in sensitivity to touch is
directly reflected in the power of the EEG recorded at these
two sites: 2.2 uV2 on the back of the hand compared to
20uV2 on the palm of the hand, a 9-fold power increase
Delta wave power expressed as a multiple of that of the
relaxed state for the more frequently used sensory input sites
used during dep. therapy was found to be: cheek, up to X90;
neck, X19; shoulder, X5 to X38; palms of hands, X5; back of
hands, X1.1; knee, X1.0 (no increase). These are only exam-
ples of a wide range of values determined. A larger set of
power values noted in this study is shown in supplementary
data at the website http://www.mindspaces.org.
Figure 3 .Theoretical waveform required for depotentiation, left
curve (from data derived by Hölscher, Anwyl, & Rowan, 1997).
Actual waves recorded during sensory input from tapping the
shoulder are displayed on the right. One wavelength is shown.
AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole) and NMDA
(N-methyl-D-aspartate) are synaptic receptors
Note: All EEG identifiers for this and subsequent figures are available at
the website http://www.mindspaces.org. All figures are from eyes-closed
data, except Figure 10.
Figure 4. Junction at 40 s between relaxed state and tapping cheeks. No change in wave frequency (about 1.4 Hz) occurs at the junction.
Graphs on right show that power at the Fp1 electrode, recording mainly from the left hemisphere, changes within 2 s from 4.3 to 150 uV2, a
35-fold increase (from lab experiment, eyes closed)
Vibrating pads in the palms of the hands were found to
create waves of neuronal firing with power usually 3 to 4
times greater than that of the relaxed state (using a Tac/
Audioscan unit set at 1 Hz and maximum intensity). Lateral
eye movements cause an increase of 12 to 20 times the
relaxed state, and eye blinks, up to 350 times (see below
for more on eye movements). Also of interest, clapping the
hands increases delta wave power by a factor of about 5 fold
over that of the relaxed state.
Bringing the fear memory into attention without sensory
input caused an increase in EEG delta wave power and z
scores of 1.5 to 2 times or more that of the relaxed state
(see supplementary material for an example). Diepold and
Goldstein (2009) have earlier reported changes in the qEEG
response when their patient focused on the fear memory
state. Specifically, they report 25 statistically abnormal val-
ues of coherence and phase during the neutral baseline but
only 8 during the fear memory state for this patient.
Examples of the average absolute power (as opposed to
power as a multiple of that of the relaxed state reported
above) during the clinical phase of the study are shown in
Figure 5: relaxed state, 30 uV2; fear memory only, 45 uV2;
and with sensory input from vibrating pads in the palms of
the hands, 90 uV2. Examples of absolute power values obtained
during the laboratory study are given in supplementary mate-
rials at the website http://www.mindspaces.org.
As illustrated in Figures 6 to 8, wave power is not signifi-
cantly changed when the sensory input procedure is changed
from bilateral (e.g., tap right temple, then left temple alter-
nately), to simultaneous (tap both temples simultaneously),
or to unilateral tapping of the cheeks and temporal bones.
Figure 9 shows the decrease of power sometimes associated
with accommodation (adaptation) to repetitive sensory input.
The Special Case of Eye Movements
Most of the signal created by movement of the eyes laterally
is the result of movement of an electrical dipole in the eyes,
which generates a powerful electrical signal. This signal has
a magnitude of about 150uV2 for a lateral eye movement of
30 degrees (Malmivuo, 1995, Figure 28.3) and constitutes
noise (artifacts) in EEG records of eye movements. It largely
obscures the electrical signal generated by the neurons them-
selves, which is the objective of most EEG analyses. The
residual power found after taking into account this purely
electrical component of eye movements suggests an approxi-
mate wave power from the neurons themselves of 30 to 40 uV2
or about the same as that of tapping the neck or shoulders
(Figure 10, see website http://www.mindspaces.org for
Based on results from all other upper-body somatosensory
inputs, it seems likely that the effect at the neuronal level of
66 Traumatology 18(2)
Figure 5. Examples of spectral power of EEG during three brain states recorded from Participant 2. Sensory input (BBS [bilateral brain
stimulation]) was vibrating pads in palms of hands. Red and green lines are from the Fp1 and Fp2 electrodes, respectively. Note changes in
scale between graphs
Figure 6. Power/frequency graphs, lab experiments (Participant 1). (1) relaxed state, (2) tap right temporal bone, (3) tap right and left
temporal bone simultaneously, (4) tap temporal bone right and left in sequence (bilaterally). Maximum power occurs at about 1.5 Hz on all
graphs and ranges from 2 to 17 uV2 (note changes of scale between the graphs)
Figure 7. Power/frequency graphs from lab experiments recorded when tapping the cheeks bilaterally (left) and while tapping right
cheek only (right)
Figure 8. Lab experiment to illustrate similarity of waveforms created by bilaterally tapping shoulders (top), and simultaneously tapping
shoulders (bottom). Power/frequency graphs on right of each panel show no significant differences
lateral eye movements is simply to cause bilaterally compa-
rable and nearly simultaneous waves of neuronal depolariza-
tions in both hemispheres.
Power at Energy Meridians and Gamut Points
As illustrated in Figure 11, tapping the “gamut point” (as
defined by Callahan, 1996) on the back of the left hand, or
any other point on the back of the hands, provides little more
power than that of the relaxed state and much less than tap-
ping the palm. Also, no significant differences in power
were found when tapping meridian points such as the upper-
inside corner of the eye as compared to tapping of nonmerid-
ian points on the cheek. Other illustrations of power
resulting from sensory input at meridians and gamut points
are available at http://www.mindspaces.org
Number of Depotentiating Waves Required
Lin et al. (2003) found that depotentiation of most synapses
mediating fear memories in animals subjected to tetanic
stimulation occurred during the first few minutes of stimula-
tion. They found that about 900 pulses were required for
complete depotentiation (as also determined by Earnshaw &
Bressloff, 2006). The principal neurons of memory areas of
participants in the current study have a natural firing fre-
quency averaging 1.78 Hz. If 900 pulses are required to
depotentiate fear memory synapses in humans, these could
be generated within about 500 s, or 8 min (900/1.78 = 506 s).
The least time required to eliminate a traumatic memory
during Phase 4 of EMDR therapy in the Harper et al. (2009)
study was 14 min for Participant 2. A count of delta waves
on the EEG records of this participant suggests that about
68 Traumatology 18(2)
Figure 9. EEG showing adaptation of neurons over a 20-s interval when tapping the cheeks during the lab experiment 1.5Hz. There was
no change in input over this interval. Eyes closed, delta filter applied
650 delta waves with power great enough to depotentiate
AMPA receptors were produced during Phase 4 of the
EMDR protocol by this participant, along with about 115
during exposure to the fear memory without brain stimula-
tion. The participant reported being unable to feel the fear or
even to remember the reason for fearing this memory after
these approximately 765 pulses. A cutoff power value of 75
uV2 was used in this calculation (detailed in backup data
available at http://www.mindspaces.org).
Summary of Results
1. The average firing frequency of principal neu-
rons in the memory areas of the brain for all
participants in this study, taken over 20- to 30-s
records, is 1.78 Hz, with a usual range of 1.5 to
2. Bilaterally or unilaterally applied brain stimulation
such as tapping produces essentially equal power
and frequency in both hemispheres simultaneously.
Figure 10. EEG produced by right lateral eye movements during lab experiment; difference of power between the two hemispheres
(left, top curve; right, bottom curve) is principally due to the purely electrical component of eye movement in right hemisphere
(Fp1 = 46 uV2, Fp2 = 191 uV2)
3. Stimulation at energy meridians and gamut points
showed no power or frequency advantage over
stimulation of any other points on the upper body.
4. An estimated 765 depotentiating neuronal pulses
were necessary to remove the fear memory for Par-
The intensity of human emotions is governed largely by the
amygdala, which has a design flaw: Unlike the hippocampus
and neocortex, it has no adequate gain control mechanism
(for comparison with the neocortex, see Hendler et al., 2003,
and for discussion of comparative evolution, see LeDoux,
2003, p. 212). Gain control, as in the recording of a song, is
used to control the volume of the recording. Similarly, gain
control during memory recording can establish the relative
intensity of the recorded emotions. Overdriving of the amyg-
dalar mechanism during such recordings can result in patho-
logical processing of sensory input during traumatic incidents.
This often results in overlearning of some emotional memo-
ries, and in more extreme cases, it results in symptoms of
It is thought that pathologically recorded emotional con-
tent mediated in the amygdala cannot be readily linked with
the cognitive content of the memory from the hippocampus
(Corrigan, 2002). For this reason, the brain cannot edit such
memories during slow-wave sleep, as normal memories are,
to return them to a more nearly homeostatic (base) level.
However, during dep. therapy, we can force the memory into
attention and thus into a labile state where it can then be
changed to a more reasonable response by the brain’s natural
It is to deal with psychological problems, particularly
traumatic memories, arising from this flaw in the brain’s
design that dep. therapies were developed. Through use of
our intellect, we have been able to compensate for poor evo-
lutionary strategies by overriding the brain’s usual programs
and mechanisms; this is a clear case of a victory of mind over
matter. Further possibilities for overcoming our evolution-
arily derived amygdalar disadvantages are suggested below.
Implications of Results of Frequency Analysis
Relevance of powerful low-frequency waves to depotentiation
therapies is that slow pulsation of neurons allows the calcium
ion content within fear memory synapses in the amygdala to
drop below the level at which AMPA receptors previously
potentiated at higher frequencies are stable. The average fre-
quency of the delta waves determined here, 1.78 Hz, is near the
midpoint of the frequency range most conducive to synaptic
depotentiation as determined primarily by animal studies of
depotentiation by researchers such as Clem and Huganir
(2010); Huang, Liang, and Hsu (2001); and Lin et al. (2003).
70 Traumatology 18(2)
It is thought that the principal neurons of the memory areas
of the brain (mainly the hippocampus, amygdala, and areas of
the prefrontal cortex) have this basic preferred frequency
established by pacemaker neurons in corticothalamic regions
and transmitted to the memory areas of the brain (as suggested
by Steriade, Curró Dossi, & Nuñez, 1991). The average fre-
quency of delta waves determined in the present study is
close to the 1.7 Hz found in thalamic pacemaker neurons of
the cat by Steriade et al. A similar value, about 1.86 Hz, was
found in the auditory cortex of Rhesus monkeys by Lakatos
et al. (2005, Figure 3). Both of these research groups calcu-
lated the frequencies by direct measurement of depolariza-
tion rates rather than by analysis of the EEG as done here.
It should be noted that there is a vast difference in reaction
to sensory inputs in the memory areas of the brain as com-
pared to that of the auditory cortex. Lakatos, Chen, O’Connell,
Mills, and Schroeder (2007) found that the firing frequency
of auditory cortex neurons changes to match the frequency
of incoming sensory signals and that these signals also reset
the phase of ongoing neuronal oscillations. This frequency
and phase change enable greater accuracy of interpretation of
incoming auditory signals. As noted by Harper et al. (2009),
the neurons contributing to the EEG of the memory areas of
the brain do not change from their basic firing mode when
sensory input frequency changes. In the current study, evi-
dence is also found that sensory input does not reset the phase
of ongoing neuronal oscillations; the inputs, even when
matching the preferred neuronal frequency, are often out of
phase with the ongoing neuronal oscillations of the neurons
creating the EEG.
The average firing rate of the neurons studied here, 1.78
times each second, is not clock like. The entire range from 1.5
to 2.0 Hz is seen in most recordings of more than a few sec-
onds. The rapid variation in frequencies is likely the result of
rapidly changing intensity of attention or emotions. In addi-
tion to these short-term frequency changes, there often appear
3- to 5-s wave-like changes in power of the EEG (illustrated in
supplementary information). Further analysis of these phe-
nomena is beyond the scope of this study.
Activity in the memory areas of the brain during slow-
wave sleep is time locked and synchronized by the high-
amplitude slow waves (Luo, Honda, & Inoué, 2001;
Wolansky, Clement, Peters, Palczak, & Dickson, 2006).
As indicated by the behavior of the neurons monitored on
the EEG in this study, the same is true during the waking
state when sensory input radically increases delta wave
Significance of Results of Power Analyses
Repetitive sensory input applied to most locations on the
upper body are shown in this study to cause remarkable
increases in delta wave EEG power compared to the relaxed
state, and it is concluded that all except tapping the back of
the hand are sufficient to erase fear memories. This conclu-
sion is based on the comparison of the spectral power of the
relaxed state with that of fear memory only. The average
power generated by fear memory alone is taken as the mini-
mum for synaptic depotentiation because it is known from
numerous case studies of exposure therapy without sensory
input that several therapy sessions are required to erase a
Evidence from this study indicates that the critical level
for rapid depotentiation of fear memory synapses is about 2
times the power generated when thinking of the fear memory
or about 3 times the power of the relaxed state. The great
surge of power caused by almost any repetitive sensory input
results in rapid depotentiation of fear memories. This accounts
Figure 11. Power/frequency graphs of data from Fp1 electrode recorded during lab experiments: comparisons of relaxed state,
tapping gamut point on left hand, and tapping of right palm. Note major scale change between palm taps and the other two states
for the great difference in contact time required for dep. ther-
apy with and without sensory input (Harper et al., 2009).
The right amygdala is thought to be more reactive to
negative emotional input than the left and may have a more
powerful input to certain negative emotional states than the
left (Iidaka et al., 2001, 2003). However, the therapist does
not have to take this hemispheric dichotomy into account
because the wave power produced by sensory input is
sufficient to depotentiate all fear memory synapses in both
From this study and our clinical experience, we find that
the client usually exhibits a delayed cognitive response to the
change in the memory trace at the molecular level. Therefore,
self-reports of fear memory status may lag the change at the
molecular level in the fear memory circuits. Full realization
of this vast change in the memory may come as a metacogni-
tion gradually over several days or even weeks. The memory
seems to have to be “refitted” into the normal memory sys-
tem since it has significantly decreased in relative subjective
importance. This longer-term editing procedure set in motion
by dep. therapy is likely to take place mostly during slow-
Low-frequency brain stimulation applied during dep. ther-
apy quickly shifts the memory areas of the brain into a neuro-
nal mode similar in power and frequency to that of slow-wave
sleep (Harper et al., 2009). In both brain stimulation studies
on animals and sleep studies in humans referenced above, this
brain rhythm has been found to be ideal for the homeostatic
adjustment of the power of synapses mediating memory.
Homeostatic processes return synaptic potentiation toward
baseline levels, and in the presence of normal waking levels
of the neurotransmitter acetylcholine (ACh), they are conjec-
tured to result in rapid and complete depotentiation of fear
memory synapses (for review, see Harper et al., 2009). ACh
levels are very low during slow-wave sleep (Gais & Born,
2004; Hasselmo, 1999; Power, 2004; Rasch, Born, & Gais,
2006), perhaps protecting the fear memory circuits in the
lateral amygdala from complete depotentiation as seems to
occur during dep. therapy. Details of naturally occurring
homeostatic processes can be found in publications by
Gilestro, Tononi, and Cirelli (2009); Liu, Faraguna, Cirelli,
Tononi, and Gao (2010); Tononi and Cirelli (2003); and
Yeung, Shouval, Blais, and Cooper (2004). Results of the
EEG study reported here suggest that depotentiation thera-
pies such as EMDR impose homeostasis on memory net-
works in the lateral tract of the amygdala by reproducing the
wave pattern of slow-wave sleep during the waking state.
Gamut Points and Energy Meridians
During energy meridian therapy such as TFT (thought field
therapy) and EFT (emotional freedom technique), the client
is typically instructed to perform various activities such as
moving the eyes in various directions while the gamut point
on the left wrist is being tapped. The eye movements create
powerful delta waves and are likely to be the sensory inputs
that result in depotentiation of fear memory synapses during
TFT and EFT therapy, rather than the much less powerful
waves created by tapping the gamut point. Also, evidence
from this study of wave power suggests that tapping of spe-
cific points on energy meridians is no more effective than
tapping other points on the upper body. At any rate, thera-
pists decide for themselves what method is best for them and
their clients on the basis of their own experience.
Information From Other Wave Frequencies
Although this study was primarily directed toward analysis
of delta waves, which are necessary for synaptic depotentia-
tion, important information can also be derived from analysis
of other frequencies of the EEG wave spectrum. An example
is the second most powerful waves observed in this study,
10-Hz alpha waves (10 neuronal firings per second). One
of the significant aspects of alpha waves is that depressed
patients may have higher alpha power than those with no
depression (Lorensen, Clarke, & Barry, 2006). Gregory et al.
(2009) suggested that higher alpha power is required to decrease
anxiety, a common goal for persons suffering from depres-
sion. This alpha wave behavior is in accordance with our
findings: The participant suffering from major depression, in
addition to PTSD, in our study had unusually high gamma
wave power (shown in the supplementary information under
alpha wave study at the http://www.mindspaces.org).
Prospective Applications of
Depotentiation of Amygdalar Synapses
The amygdala seems to have a more or less standard, built-in
emotional repertoire, ready for elaboration whenever a rele-
vant life event occurs. Depotentiation therapies deal with these
activated emotions retroactively, for the most part, although
Dr. Francine Shapiro (2001) has provided for prospective,
future reactions in her EMDR protocol. Many people have
reported that negative emotions in general seem to be less
extreme after EMDR or other exposure therapies.
One simple way of incorporating this mechanism of tam-
ing the amygdala is to include sensory input while thinking
or worrying about emotionally trying events we expect to
happen during the following day. Mere consideration of
expected emotional events while tapping the shoulder or
cheek is beneficial; life encounters become less emotionally
trying through use of this depotentiating procedure. Ultimate ly,
through neurofeedback training, we might be able to power
up the neurons that produce powerful delta waves at will.
This could enable personal amygdalar control on a real-time
The amygdala is under higher, cortical control by the
VMPFC (Figure 1) in many situations, but this control may
be overridden during traumatic events (Ruden, 2010, p. 27).
A shorter route to the amygdala from sensory receptors is
available for faster reactions to unexpected events through
the sensory thalamus. Other methods of increasing control
72 Traumatology 18(2)
of the amygdala can be learned, such as those taught during
training of Special Forces military personnel. Undergoing
“mock trauma shock,” perhaps through computer-generated
virtual reality, can give us much greater resilience when
exposed to real trauma. Including group dep. therapy for all
military personnel as a part of basic training would also
enhance resilience; targeting emotions likely to be experi-
enced in battle would increase resilience on the battlefield.
The author was an army medic and believes medics can be
taught dep. therapy as an adjunct to their basic training.
Other military personnel consider medics more approachable
than mental health professionals, who are usually officers.
Obviously, all these suggested extensions of dep. therapy
must be used with great caution to avoid possible negative
Cross-Species Use of Depotentiation Therapy
As LeDoux notes (2003, p. 212), the basis for emotional
reactions is highly conserved across species. Other animals
have the same evolutionarily challenged amygdala as ours.
We can extend the benefits of depotentiation therapy to
traumatized animals by finding ways to expose animals to
emotions aroused by a past traumatic event while provid-
ing repetitive sensory input such as tapping the cheek or
All depotentiation therapies have a high success ratio in
eliminating the emotional aspect of fearful stress memories
mediated in the amygdala. This study suggests that a wide
variety of mild brain stimulation through sensory inputs is
effective in erasing the physical basis for a fear memory in
the lateral amygdala, including unilateral as well as bilater-
ally applied stimulation. Almost all inputs examined here
produce powerful delta waves concurrently in both brain
hemispheres regardless of the mode of input. The brain itself
is bilaterally organized, and different reactions to such input
occur within each hemisphere. In addition, this study suggests
that tapping of energy meridians and gamut points creates
no power advantage over tapping other points on the upper
body. Nevertheless, sensory input in general dramatically
speeds the process of fear memory erasure.
This laboratory and clinical study supports findings of many
others such as Barrowcliff, Gray, Freeman, and MacCulloch
(2004) concerning EMDR therapy, and the empirical results
reported from the broad field of Energy Psychology by
researchers such as Hartung and Galvin (2003).
Choose a method of sensory input that produces sufficiently
powerful waves in the memory areas of the brain to quickly
depotentiate fear memory synapses; do not rely solely on
tapping the knee or the back of the hand to provide sensory
input. In refractory clients, repeating the therapy with higher
power input such as tapping the shoulder or cheek may be
necessary; if doubt exists for such clients, an EEG analysis
will reveal the degree to which the fear memory is held in
attention and whether the sensory input being applied is
powerful enough to depotentiate fear memory synapses in
both brain hemispheres.
Fast dep. therapy can be employed in mass emergen-
cies following disasters such as earthquakes, floods, and
wars; this might be best accomplished by developing and
proving in relief camps a protocol for group therapy such
as that proposed by Jarero and Artigas (2009) and used
successfully in the field, for example, with children after
the large earthquake near Istanbul in 1999 in which about
17,000 people were killed (Konuk et al., 2006). We can
vastly extend the ways of targeting the amygdala to attain
more direct and personal control of this ancient brain
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect
to the research, authorship, and/or publication of this article.
The author(s) received no financial support for the research,
authorship, and/or publication of this article.
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