Anales de psicologia (1999 in press).

With permission of editor, this paper is an updated reprint of an article that appeared in

Contemporary Hypnosis, 1998, 15, 22-33.

La naturaleza de la analgesia hipnótica: bases y evidencias neurofisiológicas

Helen J. Crawford, Ph.D.

Department of Psychology

Virginia Polytechnic Institute and State University

Blacksburg, Virginia 24061-0436

e-mail: hjc @ vt.edu phone: 504 231-6520

Timothy Knebel, Ph.D.

Department of Psychology

Virginia Polytechnic Institute and State University

Blacksburg, Virginia 24061-0436

Jennifer M. C. Vendemia

Department of Psychology

Virginia Polytechnic Institute and State University

Blacksburg, Virginia 24061-0436

James E. Horton

Department of Psychology

University of Virginia’s College at Wise

Wise, Virginia 24293-0016

Virginia Polytechnic Institute and State University

Blacksburg, Virginia 24061-0436

Key Words: Hypnosis, Hypnotic Analgesia, Pain, Somatosensory Evoked Potentials,

Electroencephalogram, Cerebral Blood Flow

Abstract

This paper reviews neurophysiological research (EEG, event-related potential,

cerebral blood flow, functional Magnetic Resonance Imaging, and neurochemical) that

supports the proposal that hypnotic analgesia is an active inhibitory process involving

several brain systems mediating attentional and nociceptive processes. Even though the

processes of hypnotic analgesia may be dissociated from conscious awareness and appear

to be beyond volitional control, it is proposed that hypnotic analgesia depends on the

activation of a supervisory, attention control system -- involving the anterior frontal

cortex -- which then participates with other cortical and subcortical systems in the

allocation of thalamocortical activities. Hypnotic analgesia affects the active allocation

of attention and disattention associated with the anterior frontal region, as well as spatio-

temporal aspects pain perception associated with the posterior cortical systems.

The Nature of Hypnotic Analgesia:

Neurophysiological Foundation and Evidence

Hypnosis is one of the best documented behavioral interventions for controlling

acute and chronic pain in adults and children (for reviews, see Barber, 1996; Barber &

Adrian, 1982; Chaves, 1989, 1994; Crawford, 1994a,b; 1995, in press; Evans, 1988;

Gibson, 1994; E. R. Hilgard & J. R. Hilgard, 1994; J. R. Hilgard & LeBaron, 1984;

Holroyd, 1996; Olness & Gardner, 1988). Hypnotically suggested analgesia involves

techniques of distraction, redefinition and dissociation to reduce or eliminate the

perception of pain. The positive correlation between standardized hypnotic susceptibility

test scores and degree of reduced pain obtained following hypnotically suggested

analgesia is significant, usually around 0.5. Low hypnotizable persons (“lows”) can

reduce the distress of accompanying pain due probably to the relaxation component of

hypnosis. Whereas, moderately to highly (“highs”) hypnotizable persons are more likely

to reduce -- and even eliminate -- both the distress and the sensory dimensions of pain

due to relaxation and attentional/disattentional (inhibitory) processes (Crawford, 1994a,b;

Hilgard & Hilgard, 1994). Further acceptance of hypnotic analgesia as an early

intervention, in conjunction with other medical interventions, for the treatment of acute

as well as chronic pain may occur by an understanding of its neurophysiological

underpinnings.

The purpose of the present paper is to review what we now know about the

neurophysiological bases of hypnotic analgesia as moderated by hypnotic susceptibility

level. It is placed within an evolving model that proposes (a) hypnotic analgesia depends

upon the activation of a supervisory, attention control system that suppresses incoming

painful stimuli at cortical and subcortical levels and thereby prevents them from reaching

conscious awareness, and (b) highly hypnotizable persons can better control pain because

of their more effective frontal attentional system that permits them to either attend to or

disattend incoming stimuli (for reviews, see Crawford, 1994a,b; in press; Crawford &

Gruzelier, 1992, Gruzelier, 1998). This paper may be considered a midstream report,

much like Crawford and Gruzelier’s (1992) general review on the

neuropsychophysiology of hypnosis.

Neurophysiology of Pain

Pain is a dynamic, multifaceted experience involving sensory-discriminative,

motivational-affective, cognitive and motoric dimensions (e.g., Melzack,, 1992; Melzack

& Casey, 1968; Melzack & Wall, 1965; Price, 1988). Neuroimaging studies support the

view that any sensory event engages an extensive network of brain systems working both

sequentially and in parallel (Posner & Raichle, 1994). Pain is no exception. The

physical significance, intensity, duration, somatic involvement, location, and overall

unpleasantness of pain is profoundly influenced by a complex array of environmental,

social, emotional and situational variables synthesized through neural activation of

cortical and subcortical systems (Chandler & Dong, 1995).

During the administration of experimental pain, activation of various regions of the

brain reflect processing of different aspects of pain (for review, see Treede, Kenshalo,

Gracely, & Jones, 1999). These may include primary (S1) and secondary (S2)

somatosensory cortex (e.g., Downs, et al., 1998; Howland, Wakai, Mjaanes, Balog, &

Cleeland, 1995), thalamus (e.g., Craig, 1998; Craig, Bushnell, Shang, & Blomqvist,

1994), insula (e.g., Downs et al., 1998), anterior cingulate cortex (e.g., Davis, Wood,

Crawley, & Mikulis, 1995; Devinsky, Morrell, & Vogt, 1995; Downs, et al., 1998;

Hutchison, Davis, Lozano, Tasker, & Dostrovsky, 1999; Jones, Brown, Friston, Qi, &

Frackowiak, 1991; Sweet, 1995; Talbot, Marrett, Evans, Meyer, Bushnell, & Duncan,

1991), basal ganglia (Chundler & Dong, 1995), and anterior frontal cortex (e.g., Bromm

& Chen, 1995; Derbyshire, Chen, & Jones, 1996; Derbyshire et al., 1994; Downs, et al.,

1998). These many discrete brain regions have been identified as subserving four main

functions: “sensation-perception (primary somatosensory cortex, thalamus and insula);

attention (anterior cingulate cortex); descending pain control (periaqueductal grey); and

an extensive network related to sensory-motor integration (supplementary motor cortex,

bilateral putamen and insula, anterior lobe and vermis of the cerebellum and superior

colliculus)” (Iadarola et al., 1998, p. 931 ). Recently, Ploghaus et al. (1999) showed that

the expectation of pain activates sites that are “distinct from, but close to, locations

mediating pain experience itself” (p. 1979).

There are several descending inhibitory systems that modulate sensory input,

including higher centers (e.g., anterior frontal cortex), the midbrain (e.g., hypothalamus),

the periaqueductal gray area (Depaulis & Bandler, 1991; Franzén & Ahlquist, 1996), and

the spinal cord (for review, see Markenson, 1996). Phylogenetically speaking, regions of

the anterior frontal cortex are relatively recent, and in humans these regions have been

widely associated with programming and regulating behavior including attention and

inhibitory processes (e.g., Luria, 1966; Norman & Shallice, 1986; Pribram, 1991; Stuss,

Shallice, T., Alexander, M. P., & Picton, 1995). Since hypnotic analgesia is attention-

based, we would anticipate the interactive involvement of attentional systems, inhibitory

processes, and multiple pain systems of the brain

Neurophysiology of Hypnotic Analgesia

The search for neurophysiological markers or changes during hypnotic analgesia has

occurred for the past 30-40 years. The 1990’s “Decade of the Brain” has brought new,

sophisticated techniques and theories that are now being applied to the study of pain

processing and the manipulation of attentional and pain processes through hypnotic

analgesia. New technologies available to researchers include electroencephalographic

(EEG) frequency analysis, EEG topographic brain mapping, somatosensory event-related

potential (SERP) topographic brain mapping, positron emission tomography (PET),

regional cerebral blood flow (rCBF), single photon emission computed tomography

(SPECT), and functional Magnetic Resonance Imaging (fMRI).

As this research becomes more interdisciplinary in nature, researchers must continue

to be vigilant to ensure that they incorporate adequate research designs developed within

the field of hypnosis (Barabasz & Barabasz, 1992; Crawford & Gruzelier, 1992; Hilgard,

1965). It is imperative to use participants who have been well-screened and categorized

using standardized hypnotic susceptibility scales, and adequate comparisons of attention

to the pain (“attend”) and hypnotic analgesia conditions that are counterbalanced or

placed within an A-B-A design. The studying of Aptitude (trait) X Treatment

interactions, through a combination of experimental and correlational methods (Crawford

& Allen, 1983; Cronbach; 1975; Tellegen, 1981) is crucial in hypnosis research.

Hypnotic susceptibility level is important to evaluate since it appears that highly

hypnotizable persons can better control pain because of their more effective frontal

attentional system that permits them to either attend to or disattend incoming stimuli

(e.g., Crawford, Brown, & Moon, 1993; Crawford, Knebel et al., 1998; Spiegel, Bierre &

Rootenberg, 1989; Zachriae & Bjerring, 1994; for reviews, see Crawford, 1994a,b; in

press; Crawford & Gruzelier, 1992; Crawford, Horton, McClain-Furmanski, &

Vendemia, 1998). Comparisons between low and highly hypnotizable persons is crucial

to sort out the effects of hypnotic analgesia per se from more general relaxation and other

effects. The highly hypnotizable person should be screened for inclusion based upon

previously demonstrated abilities to greatly reduce or eliminate the perception of distress

and sensory pain.

Anterior frontal (prefrontal) cortex activation may occur during painful stimulation

(Crawford, Horton et al., 1998; Crawford, Horton, McClain-Furmanski et al., Downs et

al., 1998; Iadorola et al., 1998) and/or the anticipation of pain (Ploghaus et al., 1999).

Thus, we propose it is also involved, in cooperation with subcortical regions including

the thalamus, in the gating or inhibiting of somatosensory input when hypnotic analgesia

is employed. The anterior frontal cortex is activated during directed attention and

inhibition (e.g., Posner & Petersen, 1990). It also operates at early stages of sensory

processing on cortical and subcortical structures, from “the periphery through dorsal

column nuclei and thalamus to the sensory cortex” (Yamaguchi & Knight, 1990, p. 281).

Surprisingly, on-going chronic pain may actually disrupt anterior frontal activation

(Derbyshire et al., 1994, 1996). If that is the case, then hypnotic analgesia techniques

may activate inhibitory processing of the anterior frontal cortex and thereby result in the

downward inhibition of incoming pain and pain memories.

Recent studies of cerebral blood flow and brain wave electrical activity (EEG and

somatosensory event-related potentials at surface and subcortical region recording sites)

support the proposal that the anterior frontal attention system is, through interaction with

other cortical and subcortical regions, actively involved in suppressing incoming

information about noxious stimuli during hypnotic analgesia. These studies will now be

reviewed.

Neuroimaging Research

Changes in rCBF metabolism, as measured by the 133-xenon method, accompanying

rest, ischemic pain without suggested analgesia, and ischemic pain with suggested

analgesia conditions in sessions with and without hypnosis were investigated by

Crawford, Gur, Skolnick, Gur and Benson (1993). Participants were healthy young men:

six were very low in hypnotizability (as measured by three standardized scales of

hypnotic susceptibility) and five were very high in hypnotizability. Training in applying

techniques of hypnotic analgesia to both cold pressor pain and ischemic pain preceded

the rCBF study. Highs who participated consistently eliminated all pain perception in

these training sessions. No rCBF differences were observed during waking, but

following a hypnotic induction only the highs showed a dramatic increase in rCBF,

ranging from 13% to 28% during rest, that may reflect increased cognitive effort or

arousal during hypnosis. It should be noted that other rCBF, PET and SPECT studies

have reported increases and decreases in cerebral blood flow in various cortical and

subcortical regions during hypnotic rest or hallucinatory suggestions (De Benedittis &

Longostreui, 1988; De Benedittis & Carli, 1990; Grond, Pawlik, Walter, Lesch, & Heiss,

1995; Halama, 1989; Maquet et al., 1999; Meyer, Diehl, Ulrich, & Meinig, 1989;

Rainville et al., 1999; Szechtman, Woody, Bowers, & Nahmias, 1998; Walter et al.,

1990). Germaine to our prior research, Rainville et al. (1999) reported bilateral PET

activation in anterior frontal cortex with predominant activity in the left hemisphere and

corresponding right hemisphere activation of the anterior cingulate associated with the

hypnotic state in highs (no lows were assessed). These studies provide strong evidence

for neurophysiological changes during hypnosis

During hypnotic analgesia, our rCBF study (Crawford et al., 1993) found that only

highly hypnotizable persons showed increased bilateral rCBFactivation in the anterior

frontal cortex as well as the somatosensory cortex. Similar frontal cortex increases have

been observed during hypnotic suggestions for pain modulation in subsequent PET

(Rainville, 1998; Rainville et al., 1999; Wik, Fischer, Bragée, Finer & Fredrickson,

1999) and SPECT (Heinrichs, Klemm, Scholz, & Biersack, 1997) research. We

interpreted such increased anterior frontal rCBF to reflect greater inhibitory processing

and supervisory planning occurring in these regions during hypnotic analgesia. This

research supports the view that hypnotic analgesia involves the supervisory attentional

control system (Hilgard, 1986) of the anterior frontal cortex in a topographically specific

inhibitory feedback circuit that cooperates in the regulation of thalamocortical activities

(e.g., Birbaumer, Elbert, Canavan, and Rockstroh, 1990) (Crawford, in press).

The increased blood flow in the somatosensory region observed during hypnotic

analgesia (Crawford et al., 1993) is difficult to interpret in light of recent conflicting

findings. Our fMRI research (Crawford, Horton, et al., 1998) found inconsistent bilateral

and unilateral primary and secondary somatosensory activation reductions and/or

increases during successful hypnotic analgesia. Rainville et al. (1999) reported suggested

pain reduction was accompanied by PET changes in somatosensory cortex. While the

somatosensory cortex is assumed to be involved in pain processing, neuroimaging studies

have reported increased blood flow (e.g., Casey et al., 1994; Coghill et al., 1994;

Heinrichs et al., 1997), no changes (Derbyshire et al., 1994, Jones et al., 1991; Rainville,

Duncan, Price, Carrier, & Bushnell, 1997), or decreased activity (Apkarian et al., 1992).

Only when we better understand the complex interplay between thalamic nuclei (and

other brain regions) and the somatosensory cortex during attention or disattention to pain

will we be able to interpret these findings.

In a SPECT study using thermal stimulation during hyperanalgesia and

hypoanalgesia, Heinrichs et al. (1997) reported continuing activation of the frontal lobe

during hypnotic suggestions. Interestingly, suggestions of increased pain was associated

with a distinct activity in the postcentral gyrus of the somatosensory system. This latter

finding was also observed by Hofbauer, Rainville, Duncan and Bushnell (1998; see also

Rainville et al., 1999).

A PET study of hypnotically responsive women with fibromyalgia (Wik et al., 1999)

underpins and extends our prior findings. During hypnotic analgesia, in comparison to

rest, patients reported substantial decreases in their chronic pain. Reduced pain

perception was accompanied by increased activation in the bilateral orbitofrontal cortex

(BA 11) in accordance with Crawford et al. (1993). Increases were also observed in

bilateral subcollosal cingulate (BA 24), right thalamus, and left inferior parietal (BA

40/39) areas. Decreases were observed in bilateral anterior (BA 24/33) and posterior

(BA 23/31) cingulate. Wik et al. noted that all areas, but the inferior parietal, are related

to limbic system structures that are engaged during pain defense or emotional processing.

Reduced cingulate activation suggests less attention was given to the encoding of the

associative significance of pain. They suggest that “the left inferior parietal activation

may then reflect psychological mechanisms serving to prevent awareness of pain, once

signaling has reached higher centres” (p. 11).

Reduced anterior cingulate involvement during hypnotic analgesia has previously

been observed in somatosensory event-related potentials (Kropotov, Crawford, &

Polyakov, 1997; see discussion in next section) and fMRI (Crawford, Horton et al., 1998)

research using noxious electrical stimulation, and PET research using painfully hot water

(Rainville, 1998; Rainville et al., 1997, 1999). In fMRI research, Crawford, Horton et al.

(1998) observed hemispheric shifts in activation and deactivation in various cingulate

regions in highs who eliminated all conscious awareness of sensory and distress pain. In

PET research, Rainville et al. (1997) observed decreased anterior cingulate activation

(BA 24) correlated with reduced distress perception. Furthermore, Crawford, Horton et

al. (1998) reported continued frontal activation with shifts in activation in the insula,

thalamus, sensorimotor cortex, and parietal regions during hypnotic analgesia.

These neuroimaging studies provide strong evidence that hypnotic analgesia impacts

neural pathways that modulate sensory-discriminative, emotional processing, attention,

and sensory-motor integration networks associated with pain (e.g., Iadarola et al., 1998).

Somatosensory Event-Related Potentials

Scalp-recorded somatosensory event-related potentials (SERPs) show significant

changes in mid to late components in response to unpleasant cutaneous stimulation

during hypnotic analgesia (e.g., Arendt-Nielsen, Zachariae, & Bjerring, 1990; Crawford,

1994a; Crawford, Knebel, et al., 1998; Danziger et al., 1998; De Pascalis, Crawford, &

Marucci, 1992; Horton, McClain-Furmanski, Mészáros, & Crawford, 1998; Mészáros &

Bányai, 1978; Mészáros, Bányai, & Greguss, 1978; McClain-Furmanski, Horton, &

Crawford, 1999; Sharev & Tal, 1989; Spiegel, Bierre, & Rootenberg, 1989; Zachariae &

Bjerring, 1994; for reviews, see Crawford, 1994a,b, in press; Crawford & Gruzelier,

1992, De Pascalis, 1998; Spiegel, 1996) in mid frontal, central, parietal, and/or occipital

regions. Few of these studies evaluated SERP changes in the anterior frontal region

during hypnotic analgesia, yet recent neurophysiological models of attention and pain

point to the importance of evaluating anterior frontal activity during hypnotic analgesia

processes.

Our research has been expanded to include anterior frontal cerebral dynamics as well

as more posterior regions by evaluating SERP activity in (1) scalp-recorded temporal

anterior frontal, mid-frontal, central and parietal regions in participants drawn from two

populations: healthy young adults (Crawford et al, 1997, 1999; Horton et al., 1998,

McClain-Furmanski, 1998) and adults with chronic low back pain (Crawford, Knebel et

al., 1998); and (2) temporarily implanted intracranial electrodes in the anterior cingulate

and anterior temporal cortex, as well as other areas (Kropotov et al., 1997).

In this review, an emphasis is placed upon findings from our recent study (Crawford,

Knebel et al., 1998) of 17 men and women, aged 19 to 43 years, with chronic low back

pain. On the Stanford Hypnotic Susceptibility Scale Form C (SHSS:C; Weitzenhoffer &

Hilgard, 1962) the participants were found to be all moderately to highly hypnotizable

except for one low hypnotizable man.

Three experimental sessions occurred approximately one week apart. The first

session involved the assessment of hypnotic susceptibility and pain control training, the

second involved SERP assessment to noxious electrical stimuli during attention and

hypnotic analgesia conditions, and the third involved EEG assessment to cold pressor

pain during attention and hypnotic analgesia conditions. At the first session, following

the SHSS:C, participants were taught hypnotic analgesia techniques to control pain

experimentally produced pain. Participants dipped their left hand into water and ice for

60 second immersions (‘cold pressor test”). By the third hypnotic analgesia dip, 60%

had completely eliminated all pain perception and 80% had completely eliminated all

distress perception. In comparison to unselected college students, these results are of a

surprising magnitude and raise important research questions whether adults with chronic

pain are more hypnotizable than the general population. If they are hypnotizable, then

hypnotic analgesia techniques should be quite suitable for assisting in the control of their

own pain (Crawford, Knebel et al., 1998).

The development of self-efficacy was documented across the sessions through the

successful transfer of newly learned skills from the reduction of experimental pain to the

reduction of their own chronic pain. Overall the participants reported significant chronic

pain reduction (McGill Pain Questionnaire), increased psychological well-being (Beck

Depression Inventory; SCL-90-R) and increased sleep quality (fewer minutes to fall

asleep).

In the second experimental session, the participants had their SERPs recorded at the

scalp while 30 noxious electrical stimuli were administered to the left middle finger

during conditions of waking and hypnosis. Reported below are the results of the within-

subjects, A-B-A design following a hypnotic induction in which blocks of stimuli were

presented in conditions of attend, hypnotic analgesia, and attend. The two attend

conditions were averaged and compared to the hypnotic analgesia condition.

For the adults with chronic low back pain, during hypnotic analgesia, hypothesized

inhibitory processing was implicated by an enhanced N140 in the anterior frontal (Fp1,

Fp2) region. This component is thought to reflect the “complex reciprocal interactions

between posterior and prefrontal [anterior frontal] cortex and subcortical structures” that

play “a key role in governing sequential attention processes” (Desmedt & Tomberg,

1989, p. 343). Additionally, during hypnotic analgesia, a greater N250 negativity was

observed in the fronto-central region. These findings suggest an “active disattention

during hypnotic analgesia, rather than the normally increasing spotlighted attention

towards relevant incoming sensory signals” (Crawford, Knebel et al., 1998, p 111).

Reductions of perceived intensity of pain during hypnotic analgesia were

accompanied by reduced P200 amplitudes in the mid-frontal, central and left parietal

regions, and reduced P300 amplitudes in the right midfrontal and central regions. These

findings may be interpreted as suggesting the reduced involvement of the parietal cortex.

One of the functions of the parietal cortex is to determine positions of body parts by

organizing sensory inputs received from the somatosensory and anterior frontal cortex

(Desmedt & Tomberg, 1989).

Our laboratory is the first to examine hypnotically related changes in the contingent

variations, which are related to arousal and attention (Tecce, 1972; Tecce & Cattanach,

1982) in the pre-stimulus SERP period prior to the regularly occurring electrical stimulus

that occurred every three seconds for 30 trials. Much work has centered around the CNV

(contingent negative variation), hypothesized to reveal enhanced cortical excitability

enabling a preparatory state. Additionally, there is a positive-moving contingent

variation (CPV) that may result from inhibitory processing and “a ‘disfacilitation’ in

cortical neuronal networks” (Rockstroh, Müller, Wagner, Cohen, & Elbert, 1993, p. 236;

for review, see Birbaumer et al., 1990). If hypnotic analgesia involves inhibitory

processing, then such a positive-moving contingent variation may be present.

Among the adults with chronic low back pain, we observed additional evidence for

the occurrence of inhibitory processing during hypnotic analgesia: a positive-going slope

of the prestimulus contingent cortical potential only in the left anterior frontal region.

This may reflect a lowering of cortical activity (Birbaumer et al., 1990; Rockstroh et al.,

1993) and increased inhibitory processing (Tecce, 1972; Tecce & Cattanach, 1972). The

asymmetry is strong evidence against eye movement artifact. Gruzelier (Gruzelier, 1988;

Crawford & Gruzelier, 1992) suggests a decreased involvement of the left anterior region

during hypnotic induction and certain hypnotic phenomena. In a recent study of healthy

young adults (Crawford et al., 1999) we found the CPV to be present at all evaluated

scalp sites.

Kropotov et al. (1997) was the first to demonstrate the potential involvement of the

anterior cingulate and the anterior temporal cortex in hypnotically suggested analgesia.

They recorded intracranial SERPs to 30 painful cutaneous stimuli in conditions of attend,

hypnotic analgesia, and attend in two female patients with obsessive-compulsive disorder

bearing multiple temporarily implanted intracranial electrodes. These electrodes were

located in the anterior cingulate cortex, amygdala, temporal cortex, and parietal cortex.

Hypnotically suggested analgesia led to a successful reduction of self-reported pain

perception and accompanying SERP intracranial changes in the hypnotically responsive

patient, but not in the non-hypnotically responsive patient. As shown in Figure 1,

reduced pain perception to noxious electrical stimuli to the right middle finger was

accompanied by (a) a significant reduction of the positive SERP component within the

range of 140-160 msec poststimulus recorded in the left anterior cingulate cortex, and (b)

a significant enhancement of the negative SERP component 200-260 msec poststimulus

recorded in the left anterior temporal cortex. No significant changes were observed in

other cortical regions or at the scalp-recorded mid-frontal Fz.

____________________

Insert Figure 1 about here

____________________

These findings are consistent with recent research (e.g., Bromm & Chen, 1995;

Derbyshire et al., 1996; Talbot et al., 1991) which implicates the anterior cingulate

cortex’s involvement in pain processing and the organization of responses to emotional

and noxious stimuli (Devinsky et al., 1995). We also interpret these findings to be

“indicative of increased active and controlled inhibitory processing of the incoming

painful stimuli . . . [and] further evidence that hypnotic analgesia is analogous to a No-

Go condition of response inhibition” (Kropotov et al., 1997, p. 6).

In summary, somatosensory event-related research strongly demonstrates that active

inhibitory processes in the brain are involved in hypnotic analgesia. Future work will

include evaluating earlier SERP components as well as localizing their sources in cortical

and subcortical structures.

EEG Activity

Further evidence of inhibitory processes occurring during hypnotic analgesia may be

gleaned from studies of EEG activity. Most hypnosis studies have evaluated EEG

activity during the administration of ongoing tonic pain, usually cold pressor pain.

Stimulus-bound EEG activity following phasic painful stimuli has yet to be addressed.

In a patient undergoing dental surgery with hypnosis as the sole anesthetic, total

EEG power decreased with a greater diminution in the left hemisphere in alpha and theta

EEG bands (Chen, Dworkin, & Bloomquist, 1981). Karlin, Morgan, and Goldstein

(1980) reported hemispheric shifts in total EEG power during hypnotic analgesia to cold

pressor pain that were interpreted as greater overall right-hemisphere involvement at the

bipolar parieto-occipital derivation.

Crawford (1990) evaluated the accompanying EEG during 60-sec immersions of the

left hand into ice cold water during conditions of attend and hypnotic analgesia. Of

particular interest were interactions between condition and hypnotic level in the high

theta (5.5 - 7.5 Hz frequency band). First, as has been shown often in the literature (e.g.,

Sabourin, Cutcomb, Crawford, & Pribram, 1990; for a review, see Crawford &

Gruzelier, 1992), highs generated significantly more high theta than did lows at mid

frontal (F3, F4), temporal (T3, T4), parietal (P3, P4) and occipital (O1, O2) sites. This

theta activity is thought to possibly originate in the hippocampal region and be associated

with focused attention, and thus reflective of the more effective attention system

observed in highly hypnotizable persons (for review, see Crawford & Gruzelier, 1992).

The low hypnotizables showed no significant hemispheric asymmetries, while the high

hypnotizables did. In the temporal region (T3, T4), when concentrating on the pain the

highs were significantly more left hemisphere dominant in high theta. By contrast,

during hypnotic analgesia the highs showed a significant shift to less left hemispheric

theta power and greater right hemisphere theta power.

Using phasic pain consisting of electric shocks to the left wrist, De Pascalis and

Perrone (1996) assessed ongoing bilateral EEG activity recorded from mid frontal,

central and posterior regions during waking, hypnosis with no analgesia, and hypnosis

with analgesia in low and high hypnotizables. They did not evaluate the stimulus-bound

EEG following each painful stimuli, although the SERPs were evaluated in a separate

publication (De Pascalis et al., 1992). During hypnotic analgesia, highs showed

reductions of total power, delta (0.5 - 3.75 Hz) and beta 1 (13-15.75 Hz) in the right

hemisphere, which was accompanied by a decrease in sympathetic activity level as

evidenced by heart period variability. De Pascalis and Perrone found no differences in

high theta (6-7.5 Hz) at recorded sites, but it should be noted that they did not record

from the temporal region where Crawford (1990) observed high theta hemispheric shifts.

In both attend and analgesia conditions during hypnosis, highs evidenced a reduction of

low theta (4-5.75 Hz) with similar levels of activity in both hemispheres, whereas in

waking there was greater low theta present in the left hemisphere. The reduction of low

theta during hypnosis suggests greater cortical arousal or attention during hypnosis. This

provides further support to Crawford et al.’s (1993) previously discussed proposal that

hypnosis requires cognitive effort.

Other Neurophysiological Changes during Hypnotic Analgesia

Hypnotic analgesia can have an inhibitory effect on peripheral spinal reflex activity

that suggests it has an impact upon descending thalamo-spinal pathways for pain control

(for review, see Price, 1996). The Hoffman reflex amplitude decreased significantly

during hypnosis in high but not low hypnotizables, yet suggested analgesia had no effect

(Santarcangelo, Busse, & Carli, 1989). Reductions in brief latency (Hagbarth & Finer,

1963) and R-III amplitude (Danziger et al., 1998; Kiernan, Dane, Phillips, & Price,

1995) of spinal reflexes were observed during hypnotic analgesia. Danziger et al. (1998)

evaluated both the RIII reflex and SERPs to noxious stimuli during attend and hypnotic

analgesia conditions in highly hypnotizable participants (no lows). While all participants

displayed reduced late SERPs and increased pain tolerance during hypnotic analgesia,

there were two subgroups with distinct patters of RIII reflex modulation. One subgroup

showed a strong inhibition of the reflex, whereas the other subgroup showed a strong

facilitation of the reflex. While all shifted their attention away from the pain, some were

more reactive and others less reactive motorically. These are intriguing findings that

need further exploration.

Since some inhibitory processes operate via endogenous opioid peptides, several

studies assessed the potential effect of hypnotic analgesia on the opiate descending

control mechanism. Unlike opiate analgesia, hypnotic analgesia has generally not been

reversed by the opiate antagonist naloxone hydrochloride (Barber & Mayer, 1977;

Goldstein & Hilgard, 1988; Spiegel & Albert, 1983; but see Stevenson, 1978) except

under circumstances of stress (Frid & Singer, 1978). Preliminary studies (e.g.,

Domangue, Margolis, Lieberman, & Kaji, 1985; Sternbach, 1982) suggest other

neurochemical processes may be involved in hypnotic analgesia. The mean plasma level

of beta-endorphin-immunoreactivity was enhanced after hypnotic analgesia in arthritic

patients, while no changes in plasma levels of epinephrine, dopamine or serotonin

occurred (Domangue et al., 1985). The surprising paucity of research in this area leaves

it open to exciting explorations.

General Summary

The research reviewed here supports the view that hypnotic analgesia is an active

inhibitory process that involves attentional, inhibitory and multiple pain systems in the

brain. Even though the processes may be dissociated from conscious awareness and

appear to be beyond volitional control, we propose that hypnotic analgesia depends upon

the activation of a supervisory, attention control system -- involving the anterior frontal

cortex -- which then participates with other cortical and subcortical processes in the

allocation of thalamocortical activities. Hypnotic analgesia is the result of changes that

affect the active allocation of attention and disattention associated with the anterior

frontal region, as well as spatio-temporal aspects of the perception of pain associated

with the posterior cortical systems.

Footnotes

With the kind permission of the editor of Contemporary Hypnosis, this paper is an

updated and expanded reprint of an article by Crawford, Knebel, and Vendemia that

appeared in Contemporary Hypnosis, 1998, 15, 22-33.

Acknowledgments

Portions of the research from our laboratory were supported by grants to Crawford

from the National Institutes of Health (R21 RR09598), The Spencer Foundation, a

National Institutes of Health Biomedical Research Support Grant, and a Virginia Tech

Aspires Grant. We gratefully acknowledge our collaborators (J. H. Downs, III, L.

Kaplan, J. Kropotov, Y Polyakov, K.H. Pribram, M. Xie) who participated in some of

the studies discussed herein.

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Figure 1. In a hypnotizable patient, somatosensory event-related potentials at two

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