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Rapid Elimination Of A Phobia
By Sensory Overload
Ronald A. Ruden M.D., Ph.D. "When ever I feel afraid I hold my head erect and whistle a
happy tune so no one will suspect I'm afraid. The result of this deception is very strange to tell, for when I fool the people I fear, I fool myself as well!" From " I Whistle A Happy Tune" by
Richard Rodgers and Oscar Hammerstein II. Copyright 1951 Richard Rogers and Oscar Hammerstein II
Fear makes us remember. Yet recent research into conditioned fear responses(1), suggest that exposure to a fear stimulus
causes the response to become labile, susceptible to disruption. This is a paradoxical result. Why should exposure to a conditioned fear stimulus make the response labile? Should not
our inherent survival mechanisms prevent this? Finally, what are the implications for the treatment of fear driven responses such as phobias and PTSD? Introduction
The amygdala is a biological centurion. When danger is present it sends a command to our body to fight or flee. The amygdala's role in producing a fear response is well documented in the literature(2)
. Both lesion studies, which show fear reduction, and stimulation studies which are associated with autonomic and behavioral changes characteristic of fear argue
for a critical role of the amygdala in the regulation of fear. The amygdala subserves several functions. It is a parallel
processor receiving inputs from the cortex, hippocampus and the thalamus. It also is the site for the formation and storage of Pavlovian (US-CS) fear conditioning. There are two major
subsystems of the amygdala. The basolateral (BLA) nucleus, site of input from other parts of the brain and believed to be storage site for conditioned fear stimuli, and the central(CE)
nucleus, which sends the signal to other areas involved the fear response. The surprising result arising from research is that reactivation of a fear memory appears to make the memory labile which, under
experimental conditions, can then be extinguished. For example, infusion of anisomycin, a protein synthesis inhibitor, into the amygdala at the time of reactivation produces an amnestic response(1)
. Thus, mice, fear conditioned by receiving a foot shock in a chamber, did not respond to subsequent placement in the chamber if they received anisomycin in the chamber. On
the other hand, fear conditioned mice receiving anisomycin outside the chamber responded with fear on subsequent placement in the chamber. These authors postulate a
disruption of memory storage. The observation that disruption is possible has important implications for the treatment of fear. If the response is labile, is there another way we can delink the
thought from the response? Case
Thirty one year old physician with a multi-decade fear of cats. Patient grew up with mother who was also cat phobic and
would pull her away from any cat. Her initial phobic memory occurred at the age of 10 when, while visiting a friend saw a cat perched on the top of a stair case looking down. Since that
time, her adult life consisted of avoiding cats, not visiting friends who owned cats, making them lock the cat in a room if she had to be in the same house, being escorted to the
bathroom just in case the cat got out. She ran out of stores, such as a corner grocery if she saw a cat. Her typical response was clearly flight or fight, experiencing palpitations, diaphoresis,
shortness of breath, and severe anxiety. This history was corroborated by both friends and family.
After one session (see methods) she was able to walk into a house with a cat. Though she was nervous and anxious, she states she failed to develop a flight or fight response. Two
further sessions took away the anxiety. Though she states she does not desire to own a cat she is now comfortable. She can actually pet the cat and cats no longer generate anxiety. Method
Protocol is modified from Callahan(3).
The protocol is simple, but important. Get a detailed history of the phobia, make sure that you understand what causes the physiological response. For example, an elevator phobia can
come from claustrophobia, or loss of control or fear of moving chambers, etc. Then have individual focus on that which produces the greatest fear response. Let the individual
generate a number from 0-10 based on the amount of distress experienced. Have the individual maximize the discomfort.
Then tap (gently but firmly) using both forefinger and middle finger under the right eye 5x then over the end of the eyebrow, 5x then under the axilla about 4 inches below the deepest part
of the axilla (the subject needs to be in just a shirt, have them remove sweaters or sweatshirts) 5x, then with both hands tap 5x 2-3" below suprasternal notch.
Then pick up the subjects right hand and begin tapping about 1" behind the fourth and fifth knuckle on the back of the hand. Tap firmly and rapidly while you ask the individual to close then
open their eyes and while keeping their head forward have them look down to the left look down to the right, rotate their eyes clockwise then counter clockwise, hum a tune and count to five
slowly out loud. When this is done tap 5x on the side of the right hand about halfway between the wrist and base of little finger. Then repeat the cycle. The treatment should take about
2 minutes to complete. Then ask them to give you their distress level again. If it is still high, repeat the process after tapping 15x on the side of the right hand. If the individual is down to a
0 or 1 have them try to generate the phobic response and treat as above. Provide instructions on how the subject can do this for themselves. Have the person return within the next several
days to assess progress. Repeat treatment but try to uncover any hidden fears or previous trauma impeding resolution.
Discussion
Roger Callahan and colleagues(3)
have treated thousands of patients. He calls his technique "tapping". According to his model, energy, qi, is blocked by a perturbation produced by a
traumatic event. This results in a phobia. By tapping on select acupuncture meridian points the energy can once again flow causing the block to be removed and the phobia cured. He
reports dramatic success for a wide variety of conditions from post-traumatic stress disorder to depression and addictive behaviors.
His model, clearly based in Eastern medicine, is difficult for the allopathic physician to understand. Thus, his techniques are dismissed because the mechanism makes no physiological sense
and the rapidity by which he achieves results appears magical. The dramatic effects seen in this case study as well as other patients I have treated here confirm the lability of a reactivated
fear response. There is a strong similarity to other techniques such as exposure therapy and EMDR(3a). The neurobiological mechanisms are of course open to speculation but an
alternative explanation to energy flow can be offered. Maren(2) describes the basal/lateral (BLA) nucleus in the amygdala as the site for unconditioned/conditioned fear
associations. As mentioned above, this nucleus has input from a variety of sources which include the thalamus, neocortex, and monosynaptic projections from the dorsal hippocampus. It
appears that once the associative connections are made and stored in the BLA a fear stimulus can produce a response by projections to the central nucleus of the amygdala. It is from
here that efferents flow to brain stem nuclei such as the hypothalamus and the locus coeruleus to produce the visceral component of fear. Work in LeDoux's lab(4) and elsewhere(5,6)
have shown that once an amygdala driven response is activated, it is subject to disruption. Experiments with muscimol, a GABAA agonist delivered to the amygdala in animals after training and in there
training environment showed inhibition of the fear response. These experiments, which involved step down avoidance, novel environments and classical conditioning, are probably not
similarly encoded neurobiologically, but the final common response pathway may in fact be the amygdala . This strongly suggests that the amygdala via GABA receptors is involved with
mediating the posttraining response. Additional evidence for this comes from microdialysis studies of fear conditioned mice where, during fear stimulus GABAergic transmission and levels of
GABA dropped dramatically and stayed low for several hours(7). Based on research mentioned above, elevated GABA levels appear to modulate a fear response. Can this information be
used to understand the results obtained with the Callahan protocol? Both the cortex and the thalamus send sensory information to the amygdala. Between the BLA nucleus and the central nucleus
lie a group of interconnected GABAergic neurons. The anatomy is such that the potential for a feedforward mechanism to the effector cells of the central nucleus is present. It is possible, by
mechanisms which we can not yet understand, that activation of a specific pathway, coupled with non- threatening sensory overload causes the development of this feedforward loop
(possibly by deinihibition of these GABA neurons). This allows us to explain the requirement of the specific thought that generates the fear response since a feedforward mechanism
requires those neurons to be activated. Given the highly divergent neuroanatomy of the BLA nucleus, a feedback mechanism seems less likely.
It is possible then to postulate that the Callahan protocol raises GABA in the central nucleus of the amygdala during a time when the content/context specific stimulus produces a
fear response. This may be the result of a restored feed-forward inhibition to the central nucleus(9). If one delinks this specific content response, it may not be possible to
reproduce the exact setting which allowed for the primary induction of the fear response and it will be extinguished. However, this response disruption may require several sessions
to activate and strengthen the feed-forward mechanism. Finally, it has not escaped notice that the central nucleus has projections to many other stress related nuclei in the brain
including the hypothalamus and the nucleus accumbens which are involved in trauma related and mood disorders as well as addictive behaviors. The use of the Callahan protocol or some
modified form appears effective in the treatment of phobias. __________________
References
1. Nader, K., Schafe, G.E., and Le Doux, J.E. Fear memories require protein Synthesis in the amygdala for reconsolidation after retrieval. Nature, 406 :722-26 (2000). 2. Maren, S. Neurobiology of Pavlovian fear conditioning. Annu. Rev. Neurosci., 240:897-931 (2001).3. Callahan, R.J.,Tapping the Healer Within. Contemporary Books Chicago,
Illinois (2001). Andrade, J., Feinstein, D. Preliminary report of the first large-scale study of energy psychology.
www. emofree.com/research/andradepaper.htm
3a. Rauch, S. A. M., Cahill, S.P., Treatment and prevention of posttraumatic stress disorder. Prim. Psych. 10(8):61-65 (2003).4.Muller, J., Corodimas, K.P., Fridel, Z. LeDoux, J.E. Functional inactivation
of the lateral and basal nuclei of the amygdala by muscimol infusion prevents fear conditioning to an explicit conditioned stimulus and contextual stimuli. Behav. Neurosci. 111(4):683-91. 1997.
5. Izquierdo, I. DaCunha, C. Rosat, R. Jerusalinsky, D. Ferreira, M.B. Neurotransmitter receptors involved in post-training memory processing by
the amygdala, medial septum, and hippocampus of the rat. Behav. Neural. Biol. 58(1):16-26(1992). 6. Brioni, J.D., Nagahara, A.H., McGaugh, J.L. Involvement of the
amygdala GABAergic system in the modulation of memory storage. Brain Res. 487(1):105-12 (1998). 7. Stork,O., Ji, F.Y., Obata, K. Reduction of extracellular GABA in the mouse
amygdala during and following confrontation with a conditioned fear stimulus. Neurosci Lett. 327(2):138-142(2002). 8. For a more technical look at the amygdala and its GABAergic connections
see Pare,D., Royer,S.,Smith,Y., and Lang,E.J.. Contextual inhibitory gating of impulse traffic in the intra-amygdaloid network. Ann. N.Y.Acad. Sci. 985:78-91 (2003). Focus Points
Fear makes us remember. Yet recent research into fear memory and retrieval suggests that activation of a conditioned fear response makes it subject to extinction. Experimental work has shown that a conditioned fear response can be extinguished by a protein synthesis inhibitor or a GABA agonist injected into
the dorsal hippocampus or amygdala during activation by a stimulus.This de-linking of a stimulus- response can be replicated by sensory overload using tactile, auditory, visual and cognitive stimuli in rapid
succession during activation. This technique provides an alternative approach to the treatment of conditioned fear responses, which in humans are called phobias. Questions
TYPE A QUESTIONS
Please select the best answer1. The response to a fear stimulus appears to be stored in the A. Pre-frontal cortex
B. The basal ganglia
C. The amygdala
D. The temporal lobe 2. Which of the following is true regarding extinction of a fear response?
A. It is permanent and can never be extinguished.
B. Requires activation of the fear response.
C. Animal models cannot be used to predict human
responsiveness.
D. It is a placebo effect because the anticipation of a result
causes the effect. 3. Which neurotransmitter is believed to be responsible for the observed effect? A. Norepinephrine
B. ACTH
C. Cortisol
D. GABA TYPE K QUESTIONS
Use the following key to answer questions 4-6:
A. if only choices 1,2 and 3 are correct
B. if only choices 1 and 3 are correct
C. if only choices 2 and 4 are correct
D. if only choice 4 is correct
E. if all choices are correct 4. The amydala has direct projections to: 1. Hypothalamus
2. Occipital cortex
3. Nucleus accumbens
4. Motor cortex 5. The Callahan protocol: 1. Uses an acupuncture model to explain the results
2. Requires the individual to tune into the distressful
thought
3. May require several treatments
4. Can be used for other problems when there is a content
specific problem which causes distress 6. This technique:
1. Surprises a patient
2. Can be done by the patient themselves.
3. Provides immediate relief
4. Is often permanent, even after one session ___________________________________________
Answers 1. C 2. B 3. D 4. B 5. E 6. E |
