Invited Symposium: Neural Bases of Hypnosis
Pain is a dynamic, multifaceted experience comprised of sensory-discriminative, motivational-affective, cognitive and motoric components (e.g., Melzack, 1992; Melzack & Wall, 1965; Price, 1988). Psychological components such as attentional deployment, stress, and past experiences can have a major impact on the degree to which pain is experienced. It is well established that hypnotically suggested analgesia is highly effective in the reduction or elimination of acute and chronic pain, especially in moderately to highly hypnotizable individuals (Crawford, 1994a,b; in press; Hilgard, & Hilgard, 1994). Yet, only recently have we begun to unravel the underlying neurophysiological processes that are involved in hypnotic analgesia.
The aim of this paper is to review recent research, particularly from our laboratory, that supports our proposal that hypnotic analgesia is an active inhibitory process that depends upon a supervisory attentional control system that operates to reallocate thalamocortical activities so that incoming painful stimuli are suppressed at cortical and subcortical levels and do not enter conscious awareness. Furthermore, we provide evidence that highly hypnotizable persons can better control pain because of their more effective frontal attention system that permits them to either attend to or disattend incoming stimuli.
Hypnotic analgesia is attention-based in that persons inhibit incoming sensations from awareness while often simultaneously deploying their attention elsewhere. Somewhat paradoxically, some highs can also attend to and describe their hand being in normally painful ice cold water while continuing to have no awareness of distress or pain (unpublished data); this suggests a strong dissociative aspect of hypnotic analgesia (Hilgard, 1986; Hilgard & Hilgard, 1994). Most important in any consideration of hypnotic analgesia is the moderating effect of hypnotic susceptibility.
Hypnotic susceptibility is an enduring trait (Piccione, Hilgard, & Zimbard, 1989) that is, like the tip of an iceberg, reflective of underlying individual differences in information processing. In contrast to hypnotically nonresponsive persons ("lows"), highly hypnotizable persons ("highs") have a greater disposition for more focused and sustained attention, deeper absorptive involvement in experiences be they positive or negative in nature, and greater cognitive flexibility that is the ability to shift from one strategy to another or from one alternate state of consciousness to another (Crawford, 1989; Crawford & Allen, 1983; Crawford, Brown, & Moon, 1993; Crawford & Gruzelier, 1992; Tellegen & Atkinson, 1974). Highs show superior performance on certain attention tasks (for review, see Crawford 1994b) and faster reaction times to complex decision-making tasks (Crawford, Horton, & Lamas, 1998).
Furthermore, highs may have significantly shorter latencies for certain somatosensory and auditory event-related potentials (Crawford et al., under review; Crawford, Horton, & Lamas, 1998; Lamas, Crawford, & Vendemia, 1997; Lamas & Crawford, 1998). A rather robust finding is that highs generate significantly more theta EEG activity than lows. This theta activity may originate in the hippocampal region and be associated with focused attentional and inhibitory processes (e.g., Crawford, 1990; Crawford & Gruzelier, 1992; Sabourin et al., 1990). Furthermore, Crawford, Clarke, and Kitner-Triolo (1996) found highs had greater enhanced power in upper theta, upper alpha, and mid beta (around 20 Hz) bands -- all bands that are sometimes associated with attentional processing in the literature. In conjunction with behavioral data, these neurophysiological data provide support for the proposal that highs have more effective attention processing systems than lows in normal every-day experiences as well as during hyp nosis. Hypnosis often involves an amplification of focused attention and inhibition that draws upon these underlying abilities seen in highs.
How then does hypnotic analgesia affect the neurophysiological representation of pain? In its most elementary representation, pain is a nociceptive spinal reflex (Sherrington, 1947). Once within the brain complex neural networks are involved including: 1) a sensory-discriminative network that involves the primary (S1) and secondary (S2) somatosensory cortices, thalamus, and insula; 2) an attentional network that includes the anterior cingulate and anterior regions of the brain interacting with other brain regions; 3) a motor network that includes the premotor cortex, frontal oculomotor fields, putamen, globus pallidus, red nucleus and superior colliculus; and 4) a descending control network involving the periaqueductal grey and higher cortical areas (e.g., Iadarola et al., 1998). Of great important to hypnotic analgesia are the descending inhibitory systems that modulate sensory input such as higher cortical centers, the midbrain, the periaqueductal grey area, and the spinal cord (for reviews see Handwer ker & Kobal, 1993; Willis & Westlund, 1997).
Spinal Level. Hypnotic analgesia apparently has an inhibitory effect on peripheral spinal reflex activity (for review, see Price, 1996). Changes in both the latency and amplitude of spinal reflexes have been observed (Danzinger et al., 1998; Hagbarth & Finer, 1963; Santacangelo, Busse, & Carli, 1989; Kiernan, Dane, Phillips, & Price, 1995).
Neurochemical processes. Since some inhibitory processes operate via endogenous opioid peptides, the effect of hypnotic analgesia on the opiate descending control mechanism has been investigated. Hypnotic analgesia has generally not been reversed by the opiate antagonist naloxone (Barber & Mayer, 1977; Goldstein & Hilgard, 1975; 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, with no significant changes in plasma levels of epinephrine, dopamine or serotonin (Domangue et al., 1985).
EEG Activity. The background EEG during ongoing tonic pain is impacted by hypnotic analgesia. In a patient undergoing dental surgery with only hypnotic analgesia, Chen, Dworkin, and Bloomquist (1981) found that the left hemisphere alpha and theta EEG power decreased. Karlin, Morgan, and Goldstein (1980) reported greater right parieto-occipital involvement, as assessed by total EEG power, to cold pressor pain (immersion of hand into ice cold water 1 - 2 degrees C).
In another cold pressor pain study, Crawford (1990) reported an interaction between conditions (attend and hypnotic analgesia during hypnosis) and hypnotic level in the upper theta (5.5 - 7.5 Hz) frequency band. Overall, highs generated substantially more theta power than did lows at midfrontal, temporal, parietal, and occipital sites. In the temporal region (T3, T4), when attending to cold pressor pain to the left hand, highs had significantly more left hemisphere dominant high theta power. By contrast, during hypnotic analgesia highs showed a significant reduction in left hemisphere power and an increased in right hemisphere power in the upper theta band. Lows showed no hemispheric differences and remained similar in both conditions. De Pascalis and Perrone (1996) reported significant reductions of delta, and beta in the right hemisphere in stimulus-bound EEG following electric shocks to the left wrist in highs but not lows.
Event-Related Potentials. The amplitude of somatosensory ERPs can be affected by attentional manipulations. Thus it is not surprising there are significant decreases in the amplitudes of late SERP components in response to unpleasant cutaneous stimulation occurring during hypnotic analgesia (e.g., Arendt-Nielsen, Zachariae, & Bjerring, 1990; Crawford, 1994a; Crawford et al., 1998b; De Pascalis & Carboni, 1997; De Pascalis, Crawford, & Marucci, 1992; Mészáros, Bányai, & Greguss, 1980; Miltner, Johnson, Braun, & Larbig, 1989; Sharev & Tal, 1989; Spiegel, Bierre, & Rootenberg, 1989; Zachariae & Bjerring, 1990, 1994; Zachariae, Bjerring, Arendt-Nielsen, Nielsen, & Gotliebsen, 1991). However, there are exceptions (e.g., Meier, Klucken, Soyka, & Bromm, 1993). Inconsistent findings may be due in part to the choice of SERP components (P100, P250, P200, P300, N140, and/or N150-P250 complex), recordings often being limited to vertex and nearby regions, and varying intensities of painful stimulation among st udies.
Recently our laboratory has also been documenting the effect of hypnotic analgesia upon the anterior frontal (prefrontal) region since recent neuroimaging studies document this region to be important in pain processing (e.g., Crawford, Gur, Skolnick, Gur, & Benson, 1993; Davis, Taylor, Crawley, Wood, & Mikulis, 1997; Davis, Wood, Crawley, & Millulis, 1995; Derbyshire et al., 1996; Devinsky, O., Morrell, M. J., & Vogt, 1995; Iadarola et al., 1998; Jones, Brown, Friston, Qi & Frackowiak, 1991; Talbot, Marrett, Evans, Meyer, Bushnell, & Duncan, 1991). The anterior frontal cortex has been shown to control input to the more posterior systems of the cortex (e.g., Skinner & Yingling, 1977) and gate the early stages of somatosensory processing (e.g., Desmedt & Tomberg, 1989; Yamaguchi & Knight, 1990).
In a study of moderately to highly hypnotizable persons with chronic low back pain, Crawford et al. (1998b) documented not only reduced P200 and P300 amplitudes more posteriorly during hypnotic analgesia, but also anterior frontal changes. The anterior frontal changes included an enhanced N140 and a pre-stimulus positive-going contingent variation at the left anterior frontal (Fp1) region only. Unlike the classic contingent negative variation, a positive-moving contingent variation may result from inhibitory processing and "a disfacilitation in cortical neuronal networks" (Rockstroh et al., 1993, p. 236; for reviews, see Birbaumer et al., 1990; Tecce & Cattanach, 1982). More recently, in a study of healthy young adults (Crawford et al., under review) reductions of P70 amplitudes in the far anterior frontal region along with reduced P200 and P300 amplitudes more posteriorly in highs but not lows. Enhancements of N140 and N250, associated with inhibitory processing, were observed. Horton, McClain-Furmanski , Mészáros, and Crawford (1998) replicated these findings.
Kropotov, Crawford, and Polyakov (1997) recorded SERPs from temporarily implanted intracranial electrodes to noxious electrical stimuli presented to the right middle finger during attention and hypnotically induced analgesia. SERPs were recorded in the left anterior cingulate cortex, amygdala, temporal and parietal cortices of two patients. In the hypnotically responsive patient a significant reduction of the positive SERP component within the range of 140-160 ms poststimulus was recorded in the left anterior cingulate cortex during reduced pain perception. Additionally, there was a significant enhancement of the negative SERP component within the range of 200-260 ms recorded in the left anterior temporal cortex. These data further support our proposal that active inhibitory processing occurs during hypnotic analgesia.
Neuroimaging Studies. With the advent of various neuroimaging techniques including regional cerebral blood flow (rCBF) metabolism, positron emission tomography (PET), and functional Magnetic Resonance Imaging (fMRI), a new window on brain processes has been opened. The identification of multiple neural networks associated with pain processing is actively being explored by a number of laboratories, yet only a few studies have examined the effect of hypnotic analgesia using these new techniques.
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). Training in applying techniques of hypnotic analgesia to both cold pressor pain and ischemic pain preceded the rCBF study. As is the practice in our research protocol, to be included in the research highs had to consistently eliminate all pain perception in these training sessions. Following a hypnotic induction, highs (but not lows) showed a dramatic increase in rCBF that may reflect increased cognitive effort or arousal during hypnosis. During hypnotic analgesia highs showed increased bilateral rCBF activation in the anterior frontal cortex as well as the somatosensory cortex. Although one cannot discriminate between excitatory and inhibitory processes with this technique, Crawford et al. (1993) interpreted the increas ed anterior frontal rCBF to support our proposal that greater inhibitory processing occurs in these regions during hypnotic analgesia.
In the first fMRI study of hypnotic analgesia, we (Crawford, Horton, Harrington, Vendemia, Plantec, Yung, Shamro, & Downs, 1998; Crawford, Horton, Hirsch, Harrington, McClain-Furmanski, Shamro, & Downs, 1998) reported dynamic shifts in anterior and posterior regional activation between attention to and hypnotic analgesia of electrical stimulation, at touch vs strong pain levels, that were administered to the left middle finger among highly hypnotizable persons. Most importantly, during hypnotic analgesia we observed dynamic shifts (including reduced right hemisphere activation) in anterior cingulate activation. In a PET study using hypnotic suggestions to reduce distress but not sensory components of pain, Rainville et al. (1997) reported reductions in anterior cigulate activation correlated significantly with reduced perceptions of distress. Prior research has shown that the anterior cingulate has reciprocal connections with the thalamus and anterior frontal region, as well as other brain regions. It is involved in the attention pain system that is more closely associated with the affective pain component (Davis et al., 1995, 1997; Iadarola et al., 1998; Rainville et al., 1997), attentional deployment (Posner & Petersen, 1990), and the execution and suppression of motoric responses (for a review, see Devinksy, Morrell, & Vogt, 1995). Reductions in fMRI activity were observed in insula and thalamic regions, as well as frontal regions of the brain.
The growing body of literature supports our evolving neurophysiological model of attentional processes (Crawford, 1994a, b; Crawford et al., 1997; 1998a,b; Crawford & Gruzelier, 1992; Kropotov et al., 1997) that proposes that hypnotic analgesia is an active inhibitory process that operates to reallocate thalamocortical activities. Furthermore, the research supports the more general proposal that highly hypnotizable persons have more effective attentional and inhibitory systems than low hypnotizable persons. The application of hypnotic analgesia to neuropathic pain has recently shown accompanying neurophysiological changes in chronic low back pain (Crawford et al., 1998b) and fibromyalgia (Wik, Fischer, Gragee, Finer, & Fredrikson, 1998) populations, with exciting implications for its use in the early treatment of chronic pain and its possible intervention so that chronic pain does not develop.
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|Crawford, H.J.; Horton, J.E.; McClain-Furmanski, D.; Vendemia, J.; (1998). Brain Dynamic Shifts During The Elimination Of Perceived Pain And Distress: Neuroimaging Studies of Hypnotic Analgesia. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/woody/crawford0611/index.html|
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