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The Ideodynamic Action Hypothesis of Therapeutic Suggestion

The Ideodynamic Action Hypothesis ofTherapeutic Suggestion: Creative Replay in thePsychosocial Genomics of Therapeutic HypnosisErnest Lawrence Rossi

Abstract:Current research in neuroscience and the psychosocial genomics of memory, learning, and behaviorhave important implications for the theory and practice of therapeutic hypnosis and psychotherapy.It is proposed that many phenomena associated with therapeutic suggestion and hypnosis - typi-cally explained by the ideodynamic action hypothesis - actually describe the phenotypic or observ-able cognitive-behavioral manifestations of activity-dependent gene expression, brain plasticity, andmind-body healing. This conceptual review outlines how the neuroscience trace reactivation theoryof the construction and reconstruction of consciousness, memory, and behavior is consistent with anupdate of the classical Ideodynamic action hypothesis of therapeutic suggestion: therapeutic hyp-nosis can facilitate brain plasticity and mind-body healing by replaying the activity-dependent geneexpression/protein synthesis cycle in the recons truction of fear, stress, and post-traum atic mem oriesand symptoms. A new psychosocial genomic paradigm of m ind-body research is proposed for assess-ing the possible role of therapeutic hypnosis and related p sychotherapeu tic processes.Keywords: Ideodynamic action hypothesis, psychosocial genomics, stress, therap eutic hypnosis,activity-dependent gene expression, memory, learning.


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Ernest Lawrence Rossi

The Classical Ideodynamic Action Hy-pothesis of HypnosisSince its inception by Mesmer over 200 yearsago, no general agreement has been achievedabout the essential nature of hypnosis and ther-apeutic suggestion (Bongartz, 1992). Recently,for example, an eminent, international author-ity on the history of research in hypnosis, thelate And re Weitzenhoffer, cog ently sum med upthe current theoretical picture (Weitzenhoffer,2001).

"My position today (Weitzenhoffer, 2000) isthat any theorizing regarding hypnosis hasbeen and continues to be prem ature. Thereis still much groundwork to be done beforeanyth ing fruitful of the sort can be acco m-plishe d. Today I have little in the line of atheory - just a few hypotheses which are in-sufficient to accoun t for all the facts that h avebeen satisfactorily established." (p. 157).

In his historical and critical effort to assem-ble, describe, and clarify "the facts that havebeen satisfactorily established," regardingsuggestibility, however, Weitzenhoffer (2000)describes the ideodynamic action hypothesisas coming closest to a theory of "hypnotic ef-fects" as follows.

"Few formulations regarding what the sug-gestion process is, exist that can be calleda theory. The most widely accepted andinfluential so-called theory, still really ahypothesis, is known as the ideodynamic ac-tion theory, often being improperly referredto as the "ideomotor theory" and as a theoryof hypn osis. Strictly speaking, it pertainsdirectly only to suggested behavior. It hasnothing to do with hypnosis, but of course,indirectly it does. Of all the hypo theses thathave been proposed regarding the productionof hypnotic effects (understood as suggestedeffects), it is the one that comes closest tobeing a theory and more workers in the fieldhave ascribed to it than any other hypothe sis,(p . 123).If the responses Involved here [e.g. automa-tisms, postural sway suggestion, Chevreulexplorer pendulum etc.] are to be viewed asbeing ideodyna mic in their entirety, they callfor a more complex picture of the neuromo-

processes in which feedback plays an im-portant part. This last is important becausethis, combined with the capacity for self-termination, probably makes some complexautomatisms appear like intentional behavior(p . 12 8) . . . Las t , / a r more complex responsesthan the one originally suggested might beexpected to take place through ideodynam icaction because one idea often leads to an-other idea, indeed to a whole chain of ideas,with loops and side branches. Not only is itreasonable to posit that a number of associ-ated and interlinked ideodynam ic responsescan thus take place, but also that the morecomplex composite "idea" thus formed mayhave the capacity to produce its own specificideodynamic effect. Indeed, the overall re-sponse to a suggestion has the potential forbeing something quite different than whatwas originally propo sed." (p. 129, italicsadded).

What, precisely, is the action of the ideody-namic action hypothesis of suggestion thatWeitzenhoffer describes here? Historically theideodynamic, a word that does not appear inmost English dictionaries, referred to an idea- a "mental" process - that generates a dynam-ic - "an energy, relating to or tending towarda change or productive activity" (New WorldDictionary, 2ed College Edition, 1986). Mo rethan a century ago Bernheim (1886/1957) of-fered a charming description of ideodynamicaction (with ideomotor, ideo-sensory, ideo-re-flexive components) that gave rise to hypnoticautomatisms (involuntary action) such as theChevreul pendulum and "table turning" inseances.

"A well-known experiment shows the influ-ence of an idea upon the act. I hold the endof my watch chain between two fingers atthe height of my forehead; the watch hangsvertically suspended and moves to the rightor left, backwards or forwards, or in a cir-cle, according as I conceive the idea of thesesuccessive m ovem ents. I try in vain not tointerfere voluntarily, but am unconscious ofthe motion, which my hand imparts to thechain. Simply the idea of motion is enoughto occasion it. Is this not the secret of tableturning, which has turned so many heads for


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movements, results in the tipping of the ta-ble." (p. 133, italics adde d).

While the Ideodynamic action hypothesis ofsuggestion has played an important role tow ardthe development of a theory of hypnosis forover 100 years, current neuroscience does notrecognize this historical priority. Neuro scien-tists are now rediscovering many phenomenapreviously subsumed under the ideodynamicaction hypothesis and, without any regard forthe history of hypnosis, give these phenomenadifferent name s derived from recent experim en-tal research on activity-dependent gene expres-sion, behavior state-related gene expression,and brain plasticity in the molecular dynamicsof memory, learning, behavioral adaptation,sensation, perception, emotions, dreaming,stress, trauma, and healing (Hua et al., 2005;Kan del, 2000 ). There has been little or nocommunication between the three disciplinesof therapeutic hypnosis, neuroscience, andpsychosocial genomics (Rossi, 1972-2005).This paper is a conceptual review integratingthe current neuroscience "trace reactivationtheory" of memory and learning with themolecular-genomic mechanisms of the ideo-dynamic action hypothesis of therapeutic sug-gestion, hypnosis, and psychotherapy (Rossi,2000 a, 2002 b, 2004a,b, 2005a,b).The Neuroscience Trace ReactivationTheory of Memory Consolidat ionThe central issue of the current neurosciencetrace reactivation theory of memory consoli-dation is to determine how new experiencesare converted into stable, long-term memory,while still being available for change andupdating with later experien ce. Exp erimen-tal evidence documents that after a salient,new, surprising, unusual, or unexpected lifeexperience many brain circuits replay thememorable event during the "offline " periodsof rest, recovery, quiet time, sleep, and dream-ing. This reactivation and replay of the novelexperience integrates and consolidates thememory (Sutherland & McNaughton, 2000;Wittenberg et al., 2002).New memories initially consist of separateparts, which are stored in different regions ofthe cortex of the brain where they were first

with the hippocampus. The hippocampus isthe focal area of the brain that converts shortmem ories to long term. Later, when the newmemory is "replayed offline during rest," di-rect links form a mon g the individual parts in thecortex that initially encoded the memory. Thenew short term memory becomes consolidatedinto a long term memory that is now independ-ent of its initial links with the hippocampus.The hippocampus is then free to operate onfurther new experiences that need to be linkedand converted into long term memory. Hoff-man and McNaughton (2002) describe howthe concurrent reactivation or replay betweenbrain cells encoding different parts of memoryis essential for linking the correct pieces ofmemory together into a coherent whole as fol-lows.

"Neural ensembles in the rat hippocampus &neocortex show memory trace reactivationduring "offline periods" of quiet wakeful-ness, slow-wave sleep, and in some casesREM sleep. Reactivation of recent memorytraces is also observed during sleep in motorareas ofthe zebra finch brain...neuro-imag-ing in humans reveals that brain areas withincreased signal during a task have contin-ued or reappearing activity after the task iscompleted." (p. 2070, italics added)

The important implication for therapeutichypnosis and psychotherapy is that the access,reactivation, and replaying of any part of amemory tends to reactivate a possible thera-peutic reconstruction of the whole originalexperience. Humans often are able to recalldistant past mem ories in vivid detail. Rece ntmemories are susceptible to disruption and/orchan ge, however, espec ially in the first minutesto days after a memorable event - before thehippocampus is able to convert the short termmemories to long term during an appropriaterest period. This may be one the source ofso-called "hypnotic amnesia," that is a stand-ard phenomenon that is used to assess "hyp-notic susceptibility" on standardized scalescommonly used in assessing the reality of the"trance state" in hypnosis research (Hilgard,1965, 1991) and clinical practice (Erickson,1980). Some forms of "hypnotic amnesia"may occur when the hippocampus has not had


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tex. Research is now required to assess thishypothesis.Repetition is a cardinal process in the historicalaccounts of hypnotic induction and therapeuticsuggestion as well as the modern standardizedhypnotic susceptibility scales. Wh y is repeti-tion needed ? W hat ideodynam ic action is fa-cilitated by repetition? The trace reactivationtheory of memory consolidation implies that"ideodynamic action" on the neuroanatomicallevel may be the replay between the cortex andhippocampus that is well described by Lisman& Morris (2001).

"Newly acquired sensory information is fun-neled through the cortex to the hippocampus.Surprisingly, only the hippocampus actuallylearns at this time it is said to be online.Later, when the hippocam pus is offline (prob-ably during sleep), it replays stored informa-tion, transmitting it to the cortex. The cortexis considered to be a slow learner, capableof lasting memory storage only as a resultof this repeated replaying of information bythe hippoc amp us. In some views, the hip-pocampus is only a temporary memory store once m emory traces bec ome stabilized inthe cortex, memories can be accessed even ifthe hippocampus is removed. There is nowdirect evidence that some form of hippocam-pal replay occurs . . . These results supportthe idea that the hippocampus is the fast on-line learner that "teaches" the slower cortexoffline." (p. 248 -249, italics added)

Research by Shimizu et al., (2000) providesmore detail about how repetition, recall, crea-tive replay required for the transformations ofconsciousness, memory, and behavior on thecellular level. They found that the NMDA (N-Methyl-D-Asparate) receptor on brain cells inthe CA l region ofthe hippocampus serves as a"gating switch" in the construction and recon-struction of memory.

"Our results indicate that memory consoli-dation may require multiple rounds of site-specific synaptic modifications, possibly toreinforce plastic changes initiated duringlearning, thereby making memory tracesstronger and more stable. Recent studiesreport that the learning-induced correlation

suggest the existence ofthe natural conditionwithin the hippocampus by which recurrentsynaptic strengthening can occur duringmem ory consolidation . We hypothes ize thatsuch synaptic re-entry reinforcement (SRR)process can also be applied to explain howthe hippocampus transfers newly createdmemories to the cortex for permanent stor-age. As the hippocampus undergoes reacti-vation during consolidation, it may also actas a coincidence regenerator for activatingneurons in the cortical area such as the as-sociation cortex. This would allow corticalneurons previously corresponding to the dif-ferent sensory modalities to be reactivatedtogether, leading to the strengthening of theconnections between them through SRR.Indeed, such a coordinated reactivation ofhippocampal-cortical neurons after learninghas been observed recently . . . Once thesecortical connections are fully consolidatedand stabilized, the hippocampus itself be-com es dispensable for the retrieval ofthe 'oldmemory'. . .Therefore, we postulate that thehippocampus, by serving as a coincidenceregenerator, may induce the reinforcementof synaptic connection within the cortexduring memory consolidation as the cellularmeans to convert short-term memories intolong-term memories." (Pp. 1172-1173, ital-ics added)

Ultradian Tinne Frame of Brain Plasticity,Healing and the Basic Rest Activity CycleA recent review of these psychobiological dy-namics of the "multiple rounds of site-specificsynaptic modifications, possibly to reinforceplastic changes initiated during learning"described above by Shimizu et al. (2000) wasillustrated by Cohen-Cory (2002) who alsoprovides more detail about the time parametersof activity-dependent synaptogenesis and brainplasticity in the central nervous system as wellas the body.

"During development, more synapses areestablished than ultimately will be retained.Therefore, the elimination of excess syn-aptic inputs is a critical step in synapticcircuit maturation. Synapse elimination isa competitive process that involves interac-


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more rapid in the CNS than at the NMJ[Neuro Muscular Junction], where synapseelimination has been well characterized. Atthe vertebrate NMJ, a single muscle cell isinitially innervated by multiple motor axons.The transition from multiple innervations toinnervation by a single motor axon occursgradually as some terminal branches retractfrom each muscle fiber b efore others, a proc-ess requiring about 24 hours for withdrawalof the presynaptic terminal. . . In the CNS,as with the NMJ, a developmental, activity-dependent remodeling of synaptic circuitstakes place by a process that may involve theselective stabilization of coactive inputs andthe elimination of inputs with uncorrelatedactivity. The anatomical refinement of synap-tic circuits occurs at the level of individualaxons and dendrites by a dynamic processthat involves rapid elimination of synapses.As axons branch and remodel, synapsesform and dismantle with synapse eliminationoccurring rapidly, in less than two hours. .. hippocam pal neurons in which glutamatereceptor function was altered demon stratedthat synapse disassem bly in the CNS occursrapidly, within 1.5 hours afrer synapses areno longer functional (p. 771) . . . Studies in-vestigating the effects of long-term synapticplasticity have generally used experimentalparadigm s in which repetitive, high-fre-quency stimulation gives rise to synapticpotentiation [called long-term potentiation,LTP] that is accom panied by structural andmolecular changes at the level of single syn-apses. . . Recent imaging experiments revealthat both NMDA and AMPA receptor activa-tion are indeed involved in synapse forma-tion and maturation." (p. 773, italics added).

Notice how the time frame of 1.5 to 2 hours re-quired for brain plasticity via synaptogenesis,as reviewed above by Cohen-Cory (2002), ap-pears to be identical to Kleitm an's 1.5 to 2 hourBasic Rest-Activity Cycle (BRAC), which isthe fundamental time parameter of the REMdream cycle where it was originally discov-ered (Aserinsky & Kleitman, 1953; Kleitman& Rossi, 1992). Most of the basic chronobio-logical life processes of homeostasis, adapta-tion (Lloyd and Rossi, 1992, 1993; Rossi,1982, 1986,1986/1993, 1996, 2002a; Rossi &

(Kandel, 2000) as well as the dynamics of neu-roendocrinology and psychoimmunology aresimilar. The time param eters of this broad psy-chobiological perspective suggests that MiltonErickson's typical 90-120 sessions of thera-peutic hypnosis may have been efficacious, atleast in part, because of their association andutilization with the natural chronobiology ofKleitman's BRAC (Rossi , 1982, 1986, 1992,2002 a). From this neuroscienc e perspec tive,brain plasticity in general and synaptogenesis,in particular, is the most recent addition to thelist of complex adaptive systems of the BRACthat is evident on all levels from the molecu-lar-genomic to the cognitive-behavioral thatwe facilitate via the psychosocial genomics ofactivity-dependent therapeutic hypnosis andrelated psychotherapeutic processes (Rossi,1996, 2002a, 2004a).

The Shaky Memory Trace: The Evocationand Therapeutic Resynthesis of Fear,Stress, and Post-Traumatic MemoriesCurrent neuroscience research documentshow the classical process of Pavlovian fearconditioning requires the recall and re-activa-tion of a conditioned memory before it can beextinguished and/or reconstructed at the geneexpression and protein synthesis level as dem-onstrated experimentally by Nader et al. (2000a & b). Nad er et al. (2000a) sum marize theirresearch with these words, "Our data showthat consolidated fear memories, when reacti-vated, return to a liable state that requires denovo [gene expression] a nd protein synthesisfor reconsolidation. These findings are notpredicted by traditional theories of memoryconsolidation (p.723, italics added).Dudai comments on the potentially therapeuticimplications of this finding in a paper titled,"The Shaky Trace," (2000).

"The current textbook version, in a nutshell,goes like this. Training modifies proteinsat synapses in the neuronal circuit that ac-quires the new memory. This alters synapticefficacy and thus the encoding of informa-tion in that circuit. But protein moleculessurvive only for periods of minutes to weeks,whereas many memories are destined to livelonger It seems that at least part of the im-


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of gene expression in the modified neurons.The new gene products promo te long-lastingre-modeling of the activated sy napses, in aprocess that involves cross talk between the.synapses and neurona l cell bodies. It takes afew hours for the new pattern of gene expres-sion and the synaptic change to be consoli-dated. During this time, the process can behalted by inhibitors of protein synthesis. . .""So it seems \hdX fear-associated memoriesbecome temporarily labile on retrieval. W hyshould the brain invest so much energy inthe original consolidation and then risk los-ing the trace by interference each time it isused? One can come up with teleologicalexplana tions for exam ple, that the brainprefers plasticity at the expense of stability or mechan istic ones, suggesting in-builtconstraints on the synaptic m achinery. . .More generally, might these results apply todifferent types of memory? Previous studieshinted that Pavlovian fear conditioning maynot be unique in being shaky on retrieval.But even if just a few types of memo ry mustreconsolidate after use, the implications ofthe results of Nader et al. (2000a) are re-markable. Consider, for example, the pros-pect of intentionally recalling the memory ofa traumatic experience and then selectivelyerasing it. What such a possibility wouldmean for psychoana lysts on the one hand,and poets on the other, is quite a differentmatter." (p, 686, italics ad ded).

These experimental findings may have impor-tant implications for understanding the longand controversial tradition of using hypnosisto facilitate memory recall and emotional re-experiencing in the so-called "cathartic cure."The implication is that "intentionally recall-ing the memory of a traumatic experience andthen selectively erasing it" is precisely whattook place during many historical approachesto reactivating traumatic memory recall andtheir "Mental Liquidation" (Pierre Janet'soriginal words, 1925/1976, pp. 589) via thera-peutic hypnosis. Extending the implications ofDudai 's remarks, / hypothesize that this activ-ity-dependent process of reactivating a fearmem ory in order to extinguish a nd re-constructit on the level of gene expression, protein syn-

cal essence of creative replay in the practiceof therapeutic hypno sis and psychotherapy.We can generalize this mind-body essence oftherapeutic suggestion to the many alternativeand complementary approaches to medicine aswell as the creative process in cultural rituals(Greenfield, 1994, 2000) and the humanisticarts in general. They all typically engage theideodynamic recall and replay of memory inthe therapeutic reconstruction of human learn-ing and behavior (Rossi, 2000a, b; 2002a,2004 b). This appears to be the neurobiologi-cal substance of the popular psychotherapeuticmetaphor, "Every Replay is a Reframe."The concept of positive, creative, therapeuticreplay during offline psychological states aspotentially important periods for the trans-formation of psychological experience andmind-body healing finds further support in theresearch of Lisman & Morris (2001).

". . , newly acquired sensory information isfunneled through the cortex to the hippoc-am pus. Surprisingly, only the hippoc amp usactually learns at this time it is said tobe online. Later, when the hippocamp us isoffline (probably during sleep), it replaysstored information, transmitting it to thecortex. The cortex is considered to be a slowlearner, capable of lasting memory storageonly as a result of this repeated replaying ofinformation by the hippocampus. In someviews, the hippocampus is only a tempo-rary memory store once memory tracesbecome stabilized in the cortex, memoriescan be accessed even if the hippocampus isremoved. There is now direct evidence thatsome form of hippocampal replay occurs. . . These results support the idea that thehippocam pus is the fast online learner that"teaches" the slower cortex offline." (p .248-249, italics added)

The creative replay of problems and traumaticmemories was a typical hypnotherapeuticapproach practiced frequently by Milton H;Erickson when I studied with him during thelast 8 years of his life (1973a & b). Erick son's(1970/1980) described his use of trauma reac-tivation for therapeutic replay in dreams in aseries of hypnotherapeutic sessions with sug-gestions such as these,


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but with a different cast of cha racte rs. Th istime maybe it wo n't be so dark. M aybe youcan see a bit more clearly. It wo n't be pleas-ant, but maybe it wo n't hurt so much . Sogo ahead as soon as you can and have yourdrea m.' Within four minutes the dream de-veloped; 20 minutes later, streaming withperspiration, Edw ard said, 'It was bad. Itwas awful bad. But it didn 't hurt so much, ,," (pp, 62-63)

Such intense states of psycho biological arousalwere characteristic of many of Erickson's casehistories (Rossi, 1973a). Erickson (1948/1980)maintained that ''therapy results from an innerresynthesis of the patient's behavior achievedby the patient himself. . . this experience ofre-associating and reorganizing his own expe-riential life that eventuates in a cure, not themanifestation of responsive behavior, whichcan, at best, satisfy only the observ er., ,Not un-til sometime later did the therapist [Erickson]learn by what train of thought he had initiatedthe neuro-psycho-physiological process. . ."(pp. 38-39, italics added).One of the mo st interesting lines of research onthe natural dynamics of replay during dream-ing indicates a possible psychosocial genomicmechanism for mind-body healing by replay-ing traumatic memories with a more creativeand therapeutic script as illustrated above byErickson. It has been found that when exp eri-mental animals experience novelty, environ-mental enrichment and physical exercise, thezif-268 gene is expressed during their REMsleep (Ribeiro, 2003; Ribeiro et al., 1999,2002, 2003 ). Zif-268 is an immed iate-earlygene and behavioral-state related gene that isassociated with the generation of proteins andgrowth factors that facilitate brain plasticity,Ribeiro et al (2004) recently summarized thecomplementary role of "neural replay" duringthe stage of REM dreaming versus deep slowwave sleep in the consolidation of new memo-ries as follows,

"The discovery of experience-dependentbrain reactivation during both slow-wave(SW) and rapid eye-movement (REM) sleepled to the notion that the consolidation ofrecently acquired memory traces requiresneural replay during sleep. . . Based on our

complementary roles in memory consolida-tion: pretranscriptional recall during SWsleep and transcriptional storage during RE Msleep, , .In conclusion, sustained neuronalreverberation during SW sleep, immed iatelyfollowed by plasticity-related gene expres-sion during REM sleep, may be sufficientto explain the beneficial role of sleep on theconsolidation of new me mo ries," (p. !26-135, italics added.)

Two recent papers provide new details of howthe reactivation of fear, stress, and traumatical-ly encoded memories in a therapeutic contextcan be the first step in initiating a molecular-genom ic of reconstructing them at the levels ofgene expression, brain plasticity, and behavior.Lee et al. (2004) summarize their research asfollows.

"The idea that new memories undergo atime-dependent consolidation process af-ter acquisition has received considerableexperimental support. More controversialhas been the demonstration that establishedmemories, once recalled, become labile andsensitive to disruption, requiring "reconsoli-dation" to become permanent. . . .We showthat consolidation and reconsolidation aredoubly dissociable component processes ofmemory. Consolidation involves fgene tran-scription and expression of] brain-derivedneurotrophic factor (BDN F) but not thefgene] transcription factor Zif-268, wherea sreconsolidation recruits Zif268 but notBDNF . These findings confirm a requirementfor BDN F specifically in mem ory consolida-tion and also resolve the role of Zif-268 inbrain plasticity, learning, and memory. " (pp.839, italics added).

Are lated pa per by Eranklin et al , (2004) extendsthese findings by imaging activity-depend-ent gene expression in the anterior cingulatedcortex during the activation of fear memories.These finding have particular significance fortherapeutic hypnosis because the anterior cin-gulated cortex has been implicated in hypnoticsusceptibility (Rainville et al. 1997, 1999)

"Although the molecular, cellular, andsystems mechanisms required for initialmemory processing have been intensively


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genetic results demon strating that the an-terior cingulate cortex plays a critical rolein remote memo ry for contextual fear condi-tioning. Imaging of activity-dependent genesshows that the anterior cingulate is activatedby remote memory and that this activation isimpaired by a null -CaM KII mutation thatblocks remote memory. Accordingly, revers-ible inactivation of this structure in normalmice disrupts remote memory without affect-ing recent memory." (pp. 881, italics added).

From the neuroscience perspective, the (I)apparently simple process of recalling and (2)creatively replaying fear, stress, and traumaticmem ories w ithin a new positive therapeuticperspective can (3) initiate the molecular-ge-nomic dynam ics of Erickson's neuro-psycho-physiological pro cess of healing. I proposethat the psychosocial genom ics o f gene expres-sion and brain plasticity is operative within thenatural 4-stage ultradian creative process ofdeconstructing the old neural networks that aencoded posttraumatic stress disorder (PTSD)and re-synthesizing new neural networks capa-ble of elective problem solving and symptomresolution (Rossi, 2002a, 2004b).This creative cycle engages potentially thera-peutic feedback loops whereby ideodynamicaction generates "far more complex responsesthan the one originally called for" as describedby Weitzenhoffer (2000, p. 128).A Psychosocial Genom ic Research P aradigmfor Therapeutic H ypnosisIn a pioneering paper Whitney et al. (2003)have documented how individuality and vari-

ation in gene expression patterns in the bloodcan be assessed with DNA microarray technol-ogy to investigate questions about states ofbehavior, consciousness, stress, and humancondition in general.

"The extent, nature, and sources of vari-ation in gene expression among healthyindividuals are a fundamental, yet largelyunexplored, aspect of human biology. Fti-ture investigations of human gene expressionprograms associated with disease, and theirpotential application to the detection anddiagnosis, will depend upon an understand-ing of normal variation within and betweenindividuals, over time, and with age, gender,and other aspects of the human condition(p.l8 96 , i talics added)

This suggests that DNA microarrays (oftencalled "gene chips") could be used as a safeand relatively non-invasive approach for theassessment of the states of therapeutic hypno-sis (Ross i, 1999 ,200 0a,b). Table one is a briefsampling of gene candidates for assessing thepossible role of hypnotic susceptibility, thera-peutic hypnosis and related psychotherapeuticprocesses in modulating gene expression andbrain plasticity associated with memory, learn-ing, dreaming, performance, psychoimmunol-ogy, stress and mind-body healing.DNA microarrays could provide a more sensi-tive, comprehensive, and reliable measure ofthe varying psychological states, brain plastic-ity and mind-body healing as a bioinformat-ics approach to the psychosocial genomics oftherapeutic hypnosis (Rossi, 2004).

Call for papersThe Editor of the journal would like to invite medical doctors,psychotherapists, hypnotherapists and other mental health practitioners tosubm it papers for inclusion in the EJCH.A range of papers are acceptable such as case studies,

men tal health reviews, research studies,useful hypnotherapeutic protocols (scripts included) or other


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Table 1:A brief sam pling of gene candidates for assessing the possible role of hypnotic susceptibility,therapeutic hypnosis and related psychotherapeutic processes in modulating gene expression,brain plasticity and mind-body healing via DNA microarray technology (From Rossi, 2002a,2004).Hypnosis, Absorption, Personality and Gene ExpressionCOM T Lichtenberg et al,, 2000 , 2004THR A Rossi, 2004a,bP e r lBrain Plasticity in Consciousness, Memory, Learning and Behavior Changec-fos, c-Jun, krox, NGFI-A & B Bentivoglio & Grassi-Zucconi, 1999CRE B Kandel et al,, 2000BND F Spedding et al,, 2003CYP-17 Ridley, 1999~ 100 Imm ediate Early Genes Rossi, 2002aHeightened Gene Expression in the Human CortexSYN47 DC TN l Caceres et al. 2003M AP IB CAM K2A Preuss et al., 2005IMPAl RAB3GAPCDS2 ATP2B1KIF3A USP14Replay in the Reconstruction of Fear, Stress and Traumatic MemoriesZif-268 Ribeiro et al,, 200 2, 2004Chronic Psychosocial StressNerve Growth Factor (NGF) Alfonso et al., 2004Membrane Glycoprotein 6a (M6a)CDC -like Kinase 1 (CLK-1)G-protein alpha q (GNAQ)CR E- dependent reporter gene Alejel et al., 2002Acetylcholinesterase (AChE-S & AChE -R) Soreq & Seidman, 2001PsychoneuroimmunologyInterleuk in 1, 2, 16, Cox-2 Caste s et al,, 1999; Glase r et al,, 1990Clock Genes & Behavior State-Related Genes-10 0 sleep related genes Cirelli et al., 2004Clock, Period 1, BM AL Rossi, 2004Period 2 Rosbash & Takak shi, 2003Maternal hehavior and therapeutic touch


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SummaryThe classical ideodynamic action hypothesis of therapeutic suggestion has been updated with thecurrent neuroscien ce theory of memory consolidation via trace reactivation and replay. It is pro-posed that the ideodynamic action hypothesis of therapeutic suggestion describes the phenotypicor observable cognitive-behavioral manifestations of activity-dependent gene expression, brainplasticity, and mind-body healing. The activity-depen dent proc ess of reactivating an old traumaticmemory in order to re-construct it on the level of gene expression, protein synthesis, and brainplasticity is proposed as a new psychosocial genomic perspective on the role of creative replayin the humanistic and cultural arts as well as therapeutic hypnosis and related psychotherapeuticprocess es. Research on the psycho social genom ics of creative replay with DNA microarray w ouldbe an important step toward a general neurosc ience theory of the efficacy of therapeutic hypno sison all levels from the cognitive-behavioral to the genomic.ReferencesAlejel, T., Beimesche, S., Cierny, I,, Krause, D. & Knepel, W.(2002). Effect of antidepressant drugs and psychosocial stress onCRE-dependent reporter gene expression in the brain of transgenicmice. Experimental and Clinical Endocrinology & Diabetes: PosterNeuro/Psychoendocrinology.Alfonso, J., Pollevick, G., van der Hart. G., Flugge, G., Fuchs, E, &Frasch, A. Identification of genes regulated by chronic psychosocialstress and antidepressant treatment in the hippoc ampu s. EuropeanJournal of Neuroscience, 19, 3, 659-666,Aserinsky, E. & Kleitman, N, (1953). Regularly occurring periodsof eye motility and concomitant phenom ena during sleep. Science,118,273-274.Bentivoglio, M., & Grassi-Zucconi, G. (1999) Im mediate early geneexpression in sleep and wakefulness. In Lydic, R. & Baghdoyan, H.(Eds.) 1999. Handbook of Behavioral State Control: Cellular andMolecular Mechanisms. New York, CRC Press.Berman, D. and Dudai, Y. (2001). Memoty extinction, learninganew, and learning the new: Dissociations in the moleeular machin-ery of learning in the cortex. Science, 291, 2417-2419.Bemheim, H. (1886/1957), Suggestive Therapeutics: A Treatise onthe Nature and Uses of Hypnotism. Westport: Associated Booksell-Bongartz, E. (Ed.), (1992) Hypnosis: 175 Years after Mesmer: RecentDevelopments in Theory and Application. K onstanz: Universitats-vergag.Cdceres, M., Lachuer, J., Zapala, M., Redmond, J., Kudo. L.,Geschwind, D., Lockhart, D., Preuss, T., and Barlow, C, (2003).Elevated gene expression levels distinguish human from non-humanprimate brains. Proceedings of the National Academy of Scientists,100, 13030-13035,Castes, M .. Hagel, I., Palenque, M ,, Canelones, P., Corano, A., &Lynch, N. (1999). Immunological changes associated with clinicalimprovement of asthmatic children subjected to psychosocialintervention. Brain & Behavioral Immunology, 13(1), 1-13.Cirelli, C , Gutierrez, C, & Tononi, G. (2004), Extensive anddivergent effects of sleep and wakefulness on brain gene expression.Neuron, 41,35-4 3.Cohen-Cory, S. (2002). The D eveloping Synapse: Constructionand Modulation of Synaptic Structures and Circuits. Science 298:770-776.Dudai, Y, (2000). The shaky trace. Nature, 406, 686-687.Eriekson, M., (1948/1980). Hypnotic Psychotherapy, In E. Rossi(Ed.), The Collected Papers of Milton H. Erickson on Hypnosis. Vol.4, Innovative Hypnotherap y (pp. 35-48), New York: Irvington.Erickson, M. (1970/198 0), In E. Rossi (Ed.), The Collected P apers ofMilton H. Erickson on Hypnosis, Vol. 4, Innovative Hypnotherapy.Hypn osis: Its Renasce nce as a treatmen t modality. New York:Irvington. Pp. 52-75.Erickson, M, (1980 ). In E. Rossi (Ed.), The Collected Papers ofMilton H. Erickson on Hypnosis. Vol. 3 , The Hypnotic Investiga-tion of Psychodynamic proc esses. Section 1: Am nesia. New York:Irvington, Pp. 35-90.Frankland, P., Bontempi. B,, Talton, L. Kaczmarek, L., Silva, A.(2004). The Involvement of the Anterior Cingulate Cortex in RemoteContextual Fear Memory, Science, 304, 881-883.

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