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Traumatology
DOI: 10.1177/153476560501100301
2005; 11; 145 Traumatology
Ronald A. Ruden
A Neurological Basis for the Observed Peripheral Sensory Modulation of Emotional Responses
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Traumatology, Vol. 11, No. 3 (September 2005)
A Neurological Basis for the Observed Peripheral Sensory Modulation of Emotional
Responses
Ronald A. Ruden
1
A new therapy for phobias, PTSD, addictive behaviors and other psychological issues was first
described by Dr. Roger Callahan and involves thought activation of the problem followed by
tapping on certain acupoints in a specific sequence. In addition, a gamut procedure involving
further tapping, eye movements and following simple commands is used. He calls his method
Thought Field Therapy. In most cases, the problems were reportedly cured in a matter of minutes.
We theorize about the neuroanatomical and neurophysiological mechanisms underlying the
success of this technique.
We propose that tapping and other sensory stimulation procedures globally increase serotonin.
The important structures specifically involved in this therapy are the prefrontal cortex and the
amygdala. The success of this technique requires that glutamate first be increased in the circuit
that involves the conditioning stimulus and the unconditioned stimulus. This analysis does not
define sequences for tapping. We suggest the name Psychosensory Therapy to encompass this
specific treatment as well as to define a broader new paradigm for the treatment of these
problems.
Key Words: Thought Field Therapy, serotonin, glutamate, tapping, amygdala, prefrontal cortex,
phobia, Post Traumatic Stress Disorder, craving, addictive behavior
INTRODUCTION
More than a decade ago, Callahan found that tapping under the eye of an individual with a
water phobia immediately and permanently cured this problem (Callahan, 1997). Callahan
believes that activating a distressful thought produces a perturbation in the energy field that
surrounds the body. His model is based on traditional Chinese medicine; that is, when energy flow
is disturbed a person becomes ill. By tapping on specific traditional Chinese medicine acupoints in
a specific sequence these perturbations in the energy ‘Thought Fields’ resume normal functioning
and healing occurs. He calls his method CallahanTechniques-Thought Field Therapy (CT-TFT)
(Callahan 1995, 2001). Variations on this therapy have been developed and are available as web
based documents. These therapies constitute a field called Energy Psychology
(www.energypysch.org).
From an observational point of view, when TFT is applied, it literally appears that a
dimmer switch has been thrown. After a successful treatment, as measured by a decreasing SUD
that ultimately reaches 1or 0, (Subjective Units of Distress, a 0-10 scale where 0 is none and 10
extreme distress as reported by the patient) (modified from Wolpe 1958) thoughts that had been
clear were less so. Not only does the ability to generate a clear image diminish, the response to
1
Ronald A. Ruden, M.D., Ph.D. may be reached at edrrr@yafferuden.com
145
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146 Neurological Basis of Emotional Responses
that thought is often gone, and for good! Sometimes the individual feels euphoric, sometimes
confused as to what happened, but always calmer.
A large study that involved over 29,000 patients was conducted using these procedures.
The results (Andrade & Feinstein,
2003) are remarkable. For a wide range of problems, such as
specific phobias, panic disorders, post-traumatic stress disorders, acute stress disorders, and
anxiety-depressive disorders this method was deemed successful by independent evaluation in
76% of the subjects. Also, in this category were a variety of painful emotional states including
grief, guilt, anger shame, jealousy, rejection, and other painful memories. These techniques also
seemed to help impulse control disorders and cravings. These researchers noted that most of the
treatments did not require the special protocols developed by Callahan (1995), rather they found
that for most disorders one sequence sufficed.
Fear, anger, grief, depression, anxiety, aggression, cravings and other emotions represent a
complex neurophysiological response that involves both cortical and subcortical systems. There
are many ways to alter these systems. These methods include the psychotherapies,
phamacotherapies, yoga, meditation, electro-convulsive shock, acupuncture, hypnosis,
psychosurgery, EMDR, stem cell implantation, biofeedback, systematic desensitization,
neuroloinguistic programming and others. We make the assumption that the mind is what the brain
produces and therefore these methods must variously affect the brain’s electrical activity, the
concentration of neurochemicals, the threshold to neuronal activation and the neural connections
that are available. By its effects we judge that TFT calls forth similar responses.
A neurobiological model should be able to explain several characteristics of this therapy.
Firstly, why is it necessary to activate the distress before it can be treated? Secondly, why is the
treatment specific, that is, if an individual has a snake phobia and an elevator phobia these
problems need to treated separately? Thirdly, why does the same protocol work for many different
problems? Fourthly, why does the distress appear to diminish during tapping as measured by a
decreasing SUD? Fifthly, what is the transduction event that converts tapping into a biological
event in the brain? Lastly, how does this treatment produce a rapid and sometimes permanent
change in an individual’s response to the distressful thought?
THE AMYGDALA AND EMOTION
Neuroimaging (Phan, Wager, Taylor, & Liberzon, 2004),
lesional (Cousens & Otto, 1998;
LeDoux, Cicchetti, Xagoraris, & Romanski, 1990; Blanchard & Blanchard, 1972) and
neuroanatomic (Sah, Faber, Lopez De Armentia, & Power, 2003) studies point to the amygdala as
the final common pathway for expression of emotions. The amygdala is well suited for this job. It
receives input from the hippocampus, the prefrontal cortex, the thalamus, midbrain nuclei, and
other cortical and subcortical areas (Maren, 2001). For our purposes, we can consider the
amygdala to be divided into several nuclei: the basolateral (BL), the lateral (LA) and the
basomedial (BM) that together make up the basolateral complex, the BLA (Maren, 2001). It is the
lateral nucleus where the information from other areas is received. The associations between a
conditioned stimulus and response are believed to be stored in the BLA and when appropriate, a
signal is sent to the Central (Ce) nucleus of the amygdala. (Fig. 1)
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Fig. 1
Activation of the Ce is necessary to produce the behavioral, autonomic and endocrine
components of an emotional response by activating other areas of the brain. The Ce projects
neurons to the nucleus accumbens, the prefrontal cortex and other structures. (Fig. 2)
Fig. 2
Of all the emotional states we experience, none is more primitive or powerful than fear. If
we understand how a fear response is disrupted, we may be able to understand how tapping works.
For a model of fear we chose phobias.
ENCODING FEAR
Fear produces responses that are characteristic, easily recognized and involuntary.
Evolution has crafted these responses to promote survival in the face of present and future threats.
However, an inappropriate fear response, such as a phobia that provides no evolutionary
advantage, causes physiological changes that can produce distress and dysfunction. Phobias are
characterized by a persistent, irrational and excessive fear of objects or situations. Since there is no
real imminent danger associated with these objects or situations, they can be considered
conditioning stimuli (CS). Phobias can be associated with anything: bugs, colors, numbers, light,
dark, bridges, tunnels, elevators and planes. Not everyone develops a phobia. It has been
suggested that a special genetic and environmentally modulated neurobiological landscape is
necessary to encode a phobia. (Gapenstrand, Annas, Ekbolm, Oreland, & Fredrikson, 2001). This
unique moment during phobia encoding would be almost impossible to reproduce. Treatment that
disrupts the encoded phobic response may therefore extinguish it forever.
Phobias are learned and as such are fundamentally different from responses to an innate
(unconditioned) fear stimulus. A fear response (FR) occurs by exposure to an innate fear stimulus.
Such stimuli, which are reflective of the fear of being killed, are hard wired in the brain and
include: fear of the unknown (novel situations), heights (falling), closed spaces (being trapped),
open spaces (no place to hide), creepy crawly things (land based predators) and something coming
out of our visual fields (air based predators).
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148 Neurological Basis of Emotional Responses
These survival stimuli do not reach consciousness because details are unimportant, only
the emotion of fear is experienced and responded to. Avoidance is mandated. Accordingly, the
thalamus, which is the first sensory connection in the brain, has direct projections to the amygdala
(Doron & LeDoux, 1999).
Fig. 3
An innate (unconditioned) fear stimulus (UFS) leading to a FR in the presence of another object or
situation sets the stage for the generation of the phobia. For example, traveling over a bridge (CS),
one might look down and see the height (UFS). It is the height that causes you to become fearful.
This occurs at the subconscious level: one is not immediately aware why you are frightened;
however, since you are consciously aware that you are on a bridge, if the neural landscape is
primed, the bridge then becomes associated with the fear response. Thus, when you bring an
image of a bridge to consciousness, you become fearful. (Fig. 4) It is important to note that not all
CS that are involved with fear responses reach conscious awareness. Thus, in Panic Disorder and
PTSD much of the conditioning stimuli remain in the subconscious. These subconscious CS can
still produce a fear response through the final common pathway, the amygdala. It is the biological
consequences of this response that make us remember.
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Fig. 4
NEUROPHYSIOLOGY
One laboratory model for the study of phobias and its treatment is Pavlovian fear
conditioning and extinction (Maren, 2001). Fear conditioning occurs when a conditioning stimulus
(CS), generally a tone, is followed by an unconditioned fear stimulus (UFS), generally a mild foot
shock. Conditioned fear requires learning and produces a stereotypical freezing behavior that can
be measured and used for research purposes. After several pairings of the tone with shock, the
animal comes to react with fear to the tone (CS), just as the bridge (CS) was able to produce fear.
It is the anticipation of the shock (the tone) that produces the fear, not the shock itself. However,
unlike phobias, conditioned fear is an appropriate response designed to increase survival. This
association is felt to be stored in the BLA. Research data suggests that glutamate agonists enhance
learning and glutamate antagonists inhibit the learning of the fear response in mice (Myers &
Davis, 2002). Glutamate, an excitatory amino acid, is involved in activating genes that are
necessary for memory storage and retrieval (Reidel, Platt, & Micheau, 2003). These genes alter the
wiring and firing of neurons. This implies that glutamate is released locally (Tsvetkov, Shin, &
Bolsakov, 2004) where learning takes place. GABA, an inhibitory amino acid, inhibits glutamate
and, as such, GABA agonists inhibit fear conditioning and GABA antagonists accelerate it (Myers
& Davis 2002).
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150 Neurological Basis of Emotional Responses
Another model for phobias is called Passive Step Down Avoidance. Here an animal is
placed on a platform that begins to vibrate. The animal becomes fearful and attempts to escape by
stepping down onto a grid. The grid is electrified and gives a shock to the animal and the animal
returns to the platform. When the animal remains on the platform for a preset time, for example, 5
minutes, the animal is considered trained in step down avoidance. Here, too, glutamate agonists
enhance (Liang, Hu, & Chang, 1996) and GABA agonists inhibit (Castellano & Pavone, 1988)
learning.
While a phobia and the various conditioned fear paradigms are encoded differently, the
association between the CS and the UFS in the amygdala leads to activation of the Ce and a fear
response. Experiments that extinguish this response may therefore be of help in understanding
tapping.
EXTINCTION TRAINING
Removal of a fear response to a conditioned stimulus can be accomplished by several
methods. One laboratory model uses a technique called extinction training. Here, exposure to the
CS is not paired with the UFS. During this training, learning takes place. These new pathways lead
to a decrement in the fear responses. Extinction does not appear to be simple forgetting (where no,
non-reinforced CSs are presented) because if extinction training is carried out so that the CS no
longer produces the FR, spontaneous recovery (recovery of response over time), renewal (recovery
of response when CS is presented in a novel environment), or reinstatement (recovery of response
after presentation of UFS under the situation where the UFS/CS link was forged) can occur over
time. Thus, the link between the CS and UFS remains intact. For humans, extinguishing of a
phobia has been studied with a technique called Systematic Desensitization (Wolpe, 1958). This
approach is similar to extinction training. (Davis &, Myers, 2002). The medial prefrontal cortex
appears to modulate responsiveness during extinction training. Recent research has shown that
stimulation of the medial prefrontal cortex reduces the outflow of the Ce of the amygdala by
gating BLA to Ce pathway. (Quirk, Likhtik, Pelletier, & Pare, 2003) (Fig 5). This has been
ascribed to a connection between the prefrontal cortex and a group of inhibitory neurons
intercalated between the BLA and the Ce. (Pare, Royer, Smith, & Lang, 2003).
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Fig. 5
(Modified from Quirk, 2003)
Here, if danger is present, as evaluated by the prefrontal cortex, then an inhibitory signal is
sent to the inhibitory GABA neurons in the amygdala. If danger is considered minimal or absent,
such as during extinction training or desensitization, then the prefrontal cortex becomes
unavailable to send a signal to these GABA neurons, allowing for activation of these inhibitory
neurons and blocking the CeÆbrainstem transmission (Sotres-Bayon, Bush, & LeDoux, 2004).
This process makes sense in that it allows for conscious evaluation of danger. Desensitization, like
extinction, does not affect the encoding, as it leaves the CS to US (stored in the BLA of the
amygdala) pathway intact, allowing for reinstatement, renewal and spontaneous recovery to occur.
Here as well, glutamate enhances and GABA diminishes the effectiveness of extinction training
(Davis & Myers, 2002). These results are critical in understanding the decrement in distress seen
during tapping and sensory stimulation.
Chemical approaches to extinguishing this response have also been carried out. In a
classical Pavlovian Fear Conditioning study, two animals were given a shock after a tone and this
process was repeated until they froze in response to the tone. They then received infusions of
anisomycin, a protein synthesis inhibitor (Nader, Schafe, & LeDoux, 2004). One animal received
the infusion after the tone (where the animal froze) the other without the tone (no freezing). The
animal that received the anisomycin after the tone no longer froze when exposed to the tone,
permanently. The animal that received the anisomycin without exposure to the tone still froze
when the animal heard the tone. This remarkable result is critical to understanding the temporal
relationship between activation and permanently de-linking a distressful thought and its emotional
response. A similar experiment was repeated with a GABA agonist muscimol (Muller, Corodimas,
Feidel, & Ledoux, 1997). Here, the muscimol was given before training and retesting. As long as
the muscimol was in the animal’s system, the animal that received the muscimol could not learn or
express the learning. The conclusions were that a fear response could only be disrupted shortly
after being activated by a protein synthesis inhibitor and that a GABA agonist could temporarily
disrupt learning and subsequent fear responses. Extinguishing a fear response has also been
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152 Neurological Basis of Emotional Responses
accomplished via serotonin pathways. Wistar rats had electrodes placed in the dorsal raphe
nucleus, the source of serotonergic projections to the brain. Serotonin modulates information
processing. It decreases pattern recognition and diminishes associative processing. (Spoont, 1992).
Using a passive step down avoidance paradigm, the animal was placed on the platform after
training and the dorsal raphe stimulated. It was found that fear memories could be permanently
disrupted by stimulation of the dorsal raphe (causing a global release of serotonin) when the
animal was on the platform. Thus, on subsequent testing, the animal that had been trained to avoid
stepping down, no longer retained that fear. In another experiment under similar conditions,
chemical depletion of serotonin from the raphe nucleus prior to electrical stimulation prevented
the loss of fear. These results imply that serotonin plays a role in extinction (Fiberger, Lepiane, &
Phillips, 1978).
WHY TAPPING WORKS
Using this information, we would like to speculate about a potential mechanism for
tapping of the fear response. The tapping protocol begins with imaginal re-activation (affect
activation) of the feared object (modified from Callahan, 2001) (Fig. 6).
Fig. 6
We believe that ‘affect activation’ is the critical aspect for success of this method. One
needs to elicit the actual target emotions, in vivo, in order to interrupt the pathway. During affect
activation, we propose that glutamate is locally released in areas corresponding to the neural
circuit that initially encoded the conditioned fear. Without local release of glutamate, no amount of
tapping or sensory stimulation will be effective. We hypothesize that multi-sensory stimulation
(tapping, massage, eye movement, etc.) causes a generalized release of serotonin via ascending
pathways. This release is non-specific and global, that is, it is not related to the content or context
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of the feared object. (Fig 7). This release is different than that seen by desensitization or
extinction training that alters serotonin levels in the prefrontal cortex. (Santini, Ge, Ren, Pena De
Ortiz, & Quirk, 2004) Multi-sensory stimulation affects the entire brain including the amygdala
and prefrontal cortex.
Fig. 7
During sensory stimulation, two events can occur. We postulate that serotonin decreases
the inhibitory signal from the prefrontal cortex to the intercalated neurons and allows for GABA
release. Ce outflow to the brainstem is inhbited and the patient experiences a decrease in distress
(decreased SUD during treatment) (Figs. 5 & 8). It is again important to note that both the
memory, as stored in the cortex and the connection between the CS and the UFS remain intact.
This allows for renewal, reinstatement and spontaneous recovery.
SerotoninÆPrefrontal CortexÆIntercalated GABA Neurons=>Ce ÆX (Brainstem)
Fig. 8
Simultaneously, serotonin causes GABA release via serotonergic receptors in the BLA. This
combination, GABA and serotonin, inhibits glutamate from activating protein synthesis,
preventing the re-storing and thus de-linking the CS to UFS pathway in the amygdala. This
blockade prevents the ultimate re-activation of the Ce and the fear response (Fig. 9).
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154 Neurological Basis of Emotional Responses
GABA
Serotonin
CS Æ Glutamate Æ X (UFS)
Fig. 9
To better understand this de-linking, imagine your amygdala is like a beach filled with holes
(CSs). Just before a specific thought activates an affective (fear) response, a certain hole in the
BLA fills with glutamate. This then links with a UFS and sends a signal to the Ce. During sensory
stimulation (tapping protocol), when a serotonin wave flows in, GABA is released and the
glutamate filled hole and only the glutamate filled hole interacts with the serotonin and solidifies
(protein synthesis is inhibited and the link to the UFS is disrupted,). Since the hole is now gone,
the ability to re-activate that CS to UFS link is lost. It suggests that phobias are stored not in the
cortex (memory), but in the CSÆ UFS connection in the BLA. This also explains the broad-based
effectiveness of this therapeutic approach. All holes on the beach can interact with serotonin when
activated. However, since only one hole can be activated at a time only one thought leading to
activation of a CS can be de-linked.
Thus, bringing a phobia to consciousness activates a specific glutamate driven circuit that
produces a fear response. Sensory stimulation (tapping protocol) raises serotonin and GABA is
released in the areas where the CS/UFS association is encoded, and the prefrontal cortex. This
decreases the distress by directly blocking Ce outflow and can de-link the CS/UFS connection.
After successful treatment, the ability to generate a sharp picture of the CS is diminished because
the efferent transmission from the Ce, that increases salience, does not occur.
The relationship between central neuromodulation and activation of peripheral sensory
receptors is of critical importance and has been studied by the use of electro acupuncture (EAc).
Significant improvements were observed in psychological functioning and pain modulation from
patients treated with EAc (Chen, 1992). Furthermore, the effect of EAc was attenuated after
biosynthesis of serotonin was reduced or by specific central serotonin receptor blockade (Chang,
Tsai, Yu, Yi, & Lin, 2004). Thus, a connection between peripheral receptors, serotonin and
behavior has been demonstrated. How sensory stimulation (tapping protocol) is transduced to a
rise in serotonin and GABA remains uncertain, but a simple mechanical process involving sensory
receptors has been proposed (Andrade & Feinstein, 2003).
CONCLUSIONS AND OTHER THOUGHTS
This model suggests that activation of the affect followed by sensory stimulation provides
a neurobiological basis for this approach. This model provides an outline that addresses the
permanence, specificity, ability to generalize to other types of affective problems (via amygdala
de-linking) and the temporal relationship between activation of the affect and a successful
treatment. In addition, decreased prefrontal activity secondary to increased serotonin accounts for
the observed decrease in distress during treatment. Animal studies have confirmed experimentally
the relationship between activation and the ability to permanently disrupt a fear response. If we
consider UFSÆCe the final common pathway then de-linking the CSÆUFS allows us to
understand the ready treatment of different phobias, PTSD, and other primary amygdala based
emotional states. This model does not address other remarkable claims made by practitioners,
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namely surrogate tapping, where the therapists tap themselves and the patients is healed, and
distance healing. Current knowledge of biology and physics cannot explain these observations and
we await a more comprehensive theory. Nonetheless, the majority of what we observe can be
understood in this simple model.
For phobias, PTSD, panic disorder and other emotional states the amygdala is the final
common pathway. For disorders such as OCD, addictive cravings, depression, generalized
anxiety, the amygdala is one of many inputs to other part of the brain that affect these behaviors.
Thus, OCD has an abnormally functioning caudate nucleus and addictive cravings have an
abnormally functioning nucleus accumbens. For example, affect activation followed by sensory
stimulation of an individual for an addictive craving produces only a short-lived (hours to days)
benefit. This procedure does not change the underlying dysfunctional system that produced the
behavior, only that specific connection that produces a Ce efferent signal. The underlying
dysfunctional systems are permissive stressors that continually activate the amygdala for re-
learning and relapse. Treatments that seek to correct the dysfunction either by medications,
psychosocial intervention, or removing amygdala-based (such as PTSD) problems therefore
become important.
Among the major controversies present in the field of Energy Psychology, of which TFT is
representative, is the location and sequence of tapping. While the neurobiological model does not
require a specific sequence of tapping, sensory receptor density (location where you tap) may
affect the rate and intensity of serotonin release. It is possible that any stimulation that affects the
serotonin system can be used. Thus, tapping, acupuncture, humming, mind-full meditation,
cognitive tasks, eye movements and other sensory modalities that require focus (hence decreased
activity from other parts of the brain) may be useful to raise serotonin after affect activation.
It is interesting to speculate why serotonin reuptake inhibitors are useful in the treatment of
primary amygdala-based disorders (PTSD, phobias, panic disorder and other emotional states). It
is possible that the SSRI’s, by increasing serotonin, alter the brain’s ability to process information.
(Spoont 1992). This may prevent glutamate release in the amygdala or allow for the prefrontal
cortex to send a no-danger signal to the intercalated neurons. Return of these psychological
problems after removal of the drug (unless the problem is dealt with in another way) is usual.
Current treatment for emotional disorders can be classified into two major categories or
pillars, psychological (mind to brain) and pharmacological (drug). The psychological treatments
encompass hundreds of approaches that involve talking, exploring and thinking that are content
specific. Pharmacotherapy alters brain functioning by the introduction of chemicals based on a
particular diagnosis. The approach outlined above, involving appropriately timed non-specific
sensory input to the brain, changes both neurotransmission and neuromodulation that alters
connectivity. By doing so it affects memory retrieval and response. This specific therapy can be
considered part of a broad new third pillar. We suggest this pillar be called psychosensory
therapy, the application of sensory input to alter behavior, mood and thought. Other therapies that
can be included are yoga, exercise, EMDR, music therapy and many others. Future research will
better define this field.
This paper outlines a mechanism by which a potent, content specific and a non-specific
intervention are combined to produce a powerful treatment modality. We would suggest that these
specific treatments be called Affect Activation/Sensory Stimulation (AA/SS) based on the
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156 Neurological Basis of Emotional Responses
process. We can now argue that certain disorders, especially those rooted in feelings of anxiety or
a traumatic event, can be treated by this new therapy. Animal and human research, strongly
suggests that real or imaginal activation of an emotional response to a thought appears to make the
response labile, subject to disruption. When activation is followed by a simple procedure the
emotional response to the event appears to have vanished, often for good. If one uses this model
for therapy, uncovering that primal event from which the emotion arises becomes the goal. For all
three pillars, however, it is the skill of the therapist that remains critical for success. There is no
easy road to treat complex psychological disorders but a new approach can now be offered to aid
in reducing distress for our patients.
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