Perceptual amplification following sustained attention: implications for hypervigilance.

It is known that attending to a cutaneous stimulus briefly increases its subjective intensity. The purpose of the present study was to determine whether an extended period of attention would produce a longer-lasting perceptual amplification. Eighty subjects were assigned alternately to experimental and control groups. Members of the two groups received identical series of tactile stimuli (near-threshold von Frey filaments applied to the forearm), but those in the experimental group carried out a two-interval forced-choice detection task that required attention to the filaments, while subjects in the control group attended instead to a video game. After this initial phase, all subjects gave magnitude estimates of the intensity of a wide range of von Frey filaments. The experimental group gave estimates 42% greater than those of the control group, both for filaments used in the initial phase, and others not presented previously; the perceptual amplification did not, however, transfer to a different type of pressure stimulus, a 5 mm-diameter rod applied to the skin. The aftereffect of sustained attention lasted for at least 15 min. This phenomenon, demonstrated in normal subjects, may have implications for the hypervigilance of some chronic pain patients, which is characterized by both heightened attention to pain and long-lasting perceptual amplification of noxious stimuli.

Effects of chronic pain history on perceptual and cognitive inhibition.

Measures of sensory and cognitive inhibition were obtained from university students with and without a history of chronic pain. The form of sensory inhibition measured was diffuse noxious inhibitory controls (DNIC), the capacity of a painful stimulus to reduce the subjective intensity of a second stimulus delivered to a remote body site. To measure cognitive inhibition, the Stroop effect was used. Participants with a history of chronic pain showed less DNIC (i.e., less sensory inhibition) than the healthy controls, but had a smaller Stroop effect (indicating greater cognitive inhibition). The fact that chronic pain history is associated with opposite changes in these two measures casts doubt on the view that the two inhibitory processes are related. Scores on each experimental measure were equivalent in pain-history subjects with ongoing chronic pain and those whose chronic pain had resolved. This equivalence suggests that chronic pain in childhood or adolescence may have lingering effects on sensory and cognitive inhibition.

Attention and pain: are auditory distractors special?

It is well established that manipulations of attention and emotional state can modulate pain. Some researchers have used olfactory or visual distractors to manipulate these factors in combination, and have found that attention and emotion have different effects on pain intensity and unpleasantness. Specifically, distraction from pain was found to markedly reduce its intensity while having little effect on its unpleasantness. Other evidence indicates, however, that the strength of intermodal attentional shifts depends on the specific modalities involved, with auditory-somesthetic shifts being relatively weak. The present study was, therefore, undertaken to determine how pain intensity and unpleasantness are affected when auditory, rather than olfactory or visual, distractors are used. Attention was directed either to the pain from noxious thermal stimuli, or to simultaneously presented environmental sounds that had either positive (e.g., bird chirping) or negative (e.g., alarm clock) associations. To manipulate attention, subjects were instructed to make two-alternative forced-choice discrimination judgments concerning the temperature of the thermal stimuli (in heat blocks) or the loudness of the sound clips (in sound blocks). Unpleasant sound clips were used during half of the heat blocks and half of the sound blocks, with pleasant sounds in the other half. Participants rated two components of pain: intensity and unpleasantness, after each block of trials. Although pain unpleasantness was influenced both by attentional direction and by the valence of the sound clips, pain intensity was not affected by either of these experimental manipulations. The failure of auditory distractors to modulate pain intensity differs from the previously documented ability of olfactory distractors to do so. Our findings are, however, consistent with evidence that one can attend simultaneously to auditory and cutaneous stimuli. Thus, environmental sounds are not effective at reducing pain intensity, but are capable of modulating pain unpleasantness, perhaps because it is constructed at a later stage.

Pacinian Signals Determine the Direction and Magnitude of the Effect of Vibration on Pain.

Although the ability of vibration to reduce pain has been extensively documented, an occasional participant reports that vibration increases pain. For pain patients, such reports may reflect pathophysiology, but this is unlikely in studies of experimental pain in healthy participants. In the present series of experiments on 27 pain-free individuals, we manipulated both the frequency (12, 50, and 80 Hz) and amplitude of vibration to more fully characterize vibratory pain modulation. The noxious stimulus was pressure applied to a finger, and vibration was delivered to the fleshy palmar pad at the base of the same finger. Subjects continuously reported pain on a Visual Analog Scale. Intermittent vibration was used to minimize peripheral vibratory adaptation. Pain records at 12 and 50 Hz were similar; pooling them revealed significant hypoalgesia at the highest amplitude. At 80 Hz, in contrast, the middle amplitude produced hypoalgesia, but a significant shift toward hyperalgesia occurred at the highest amplitude. The strong correlation ( r = .81) between the Pacinian-weighted power of a vibration and the absolute value of the pain modulation it produces indicates that the Pacinian system plays a key role in vibratory hypoalgesia or hyperalgesia.

Experimental hypervigilance changes the intensity/unpleasantness ratio of pressure sensations: evidence for the generalized hypervigilance hypothesis.

Patients with chronic pain conditions such as fibromyalgia often demonstrate hypervigilance-undue alertness for unpleasant or threatening bodily sensations-as well as enhancement of these sensations. The generalized hypervigilance hypothesis (GHH) of Rollman and colleagues asserts that hypervigilance leads to this perceptual amplification. However, cause-and-effect relationships are difficult to establish in studies using a quasi-experimental design. In the present study, we sought to address this issue by attempting to induce hypervigilance experimentally, in one of two groups to which young, healthy adults had been randomly assigned. Those in the experimental group wrote about the flu and practiced counting their own blinks, breaths, and heartbeats; those in the control group wrote about a neutral topic and counted innocuous lights and sounds. Next, both groups rated the intensity and unpleasantness of pressure sensations (ranging from mild to painful) caused by a series of applications of a weighted rod to the forearm. The intensity/unpleasantness ratio of these ratings was significantly greater in the experimental group, suggesting that induced hypervigilance had caused perceptual amplification that generalized to pressure sensations, which had not been part of the experimental manipulation. Psychometric measures of anxiety and catastrophizing were equivalent in the two groups, indicating that the experimental manipulation operated via attentional rather than emotional changes. The results support the GHH.

Somesthetic senses.

This is a review of recent advances in our understanding of the sensory modalities of touch, temperature sensitivity, and pain. Most of the research described is psychophysical or perceptual in nature, but physiological and imaging studies are included when they sharpen issues or reveal underlying mechanisms. Coverage of touch research comprises the subjects of acuity, vibrotaction and texture perception, perception of location and movement, tactile attention, and cross-modal phenomena. For pain, the covered topics are central sensitization, pain-touch and pain-pain interactions, placebo effects, the role of attention and emotion in pain, and the genetics of pain. For touch, the topics are arranged roughly in order of increasing cognitive involvement, but such an ordering is not feasible for pain, where attitudes and expectations can substantially affect even the most "sensory" of judgments.

Somatosensory coding of roughness: the effect of texture adaptation in direct and indirect touch.

To examine somatosensory mechanisms contributing to the perception of roughness, subjects examined surfaces with rigorously specified spatial textures under conditions of direct moving contact between the fingertip and the surface (direct touch) and contact through a rigid probe (indirect touch). Subjects were trained to scan the surfaces along a consistent path and with a speed of 2.7 cm/s. With each mode of touch, periods of prolonged inspection of a single adapting surface were followed by shorter periods in which the roughness of multiple test surfaces was reported. Adaptation caused a drop in perceived roughness under conditions of indirect touch, reflecting the reduced sensitivity of vibrotactile mechanisms that are the main recipients of textural information transmitted through the probe. During direct touch, adaptation had no significant effect on the perception of textures with spatial period >200 mum, which are spatially encoded. The results have an important implication for the physiological basis of the spatial code, which is believed to involve somatosensory cortical neurons with highly structured receptive fields: these cortical populations appear to be less susceptible to adaptation than otherwise similar neuronal populations in the visual system.

The coding of roughness.

This review examines the way information about textures is captured, encoded, and processed by the somatosensory system to produce sensations of roughness/smoothness. Textures with spatial periods exceeding about 200 microm are encoded spatially, so roughness is nearly independent of the speed and direction of their movement across the skin. The information consists of spatial variations in activity among slowly adapting (SA1) mechanoreceptors, and appears to be extracted by specialized cortical neurons. Perception of the roughness of finer surfaces is mediated by detection, primarily by Pacinian afferents, of cutaneous vibrations generated when textures move across the skin. Movement is necessary to the perception of these textures, and vibrotactile adaptation interferes with it. The code is an intensitive one (i.e., the amount of activity in Pacinian afferents).

Vibrotactile amplitude and frequency discrimination in temporomandibular disorders.

The purpose of this study was to determine whether the elevation in vibrotactile detection threshold, found in many individuals with temporomandibular disorders (TMD), is paralleled by suprathreshold impairments. Participants with TMD were compared with pain-free control subjects in their ability to discriminate on the basis of differences in amplitude and frequency between vibratory stimuli delivered to the face. The TMD group was significantly impaired with respect to frequency discrimination, but not amplitude discrimination. This dissociation suggests that the cortical processing of vibrotactile signals may be affected in TMD patients. TMD participants' estimates of the intensity of their spontaneous and palpation-evoked pain did not significantly correlate with performance on either discrimination task; this finding makes it unlikely that impaired vibrotaction in TMD is primarily the result of a pain-dependent gating of tactile signals.

Reduction of TMD pain by high-frequency vibration: a spatial and temporal analysis.

Under some conditions, vibration delivered to the skin can reduce pain (vibratory analgesia). Previous studies of this phenomenon in a clinical context have been somewhat variable in terms of stimulus control, and have not examined the way in which the spatial distribution of pain is affected. In the present study, we used rigorously controlled conditions to examine vibratory analgesia in participants (N=17) with painful temporomandibular disorders (TMD). Results of 20- and 100-Hz vibration were compared with data from a no-vibration control condition. The results document for the first time that vibratory analgesia occurs in TMD chronic pain conditions. We measured its time course using continuous visual analog scale (VAS) recording, and its spatial aspects by asking subjects to indicate painful regions on standardized drawings. VAS ratings and drawings both showed that pain is reduced by 100-Hz, but not by 20-Hz, vibration. The effectiveness of the high-frequency vibration cannot be attributed to a mechanism involving Pacinian corpuscles, since these receptors are lacking in the skin of the orofacial region. Spatial analyses revealed that ipsilateral and contralateral effects of vibration were statistically equivalent, suggesting that vibratory analgesia relies at least in part on central nervous system processes rather than local mechanisms.

Vibrotactile threshold is elevated in temporomandibular disorders.

Experimental pain can elevate vibrotactile threshold, a phenomenon attributed in the literature to the operation of a 'touch gate.' It is not known, however, whether clinical pain produces similar effects. To explore this possibility, we measured vibrotactile threshold in patients with temporomandibular disorders (TMD) whose pain had a prominent myalgic component. Two-interval forced-choice tracking was used to determine threshold for a 25-Hz vibratory stimulus presented on the cheek. Threshold was found to be significantly elevated in the TMD group, compared to an age- and gender-matched control group of pain-free individuals. Within the TMD group, those with a supra-median level of muscle tenderness (corrected for background levels of spontaneous pain) had significantly higher threshold than those with lower levels of palpation pain. These findings are consistent with the idea of a touch gate, and suggest the usefulness of further research in this area with clinical pain populations. The effects of an adapting stimulus (25 Hz, 20 dB SL) were also studied, and found to produce parallel elevations in vibrotactile threshold in the TMD and pain-free groups. This result indicates that at least some adaptation occurs at a higher (subsequent) level of somatosensory information processing than does the touch gating implied by the unadapted thresholds.

Generalized vibrotactile allodynia in a patient with temporomandibular disorder.

This report presents the findings from a psychophysical study of vibrotactile responses in a patient diagnosed with temporomandibular disorder (TMD). This patient unexpectedly reported pain due to innocuous vibrotactile stimulation, and this allodynia appeared to have a component of temporal summation. The pain response occurred not only in the region of the clinical pain (the face), but also on the volar forearm, where the patient reported no clinical pain. Administration of the N-methyl-D-aspartate (NMDA) receptor antagonist dextromethorphan (DM), but not vehicle, attenuated the vibration-induced pain at both sites.

Vibratory antinociception: effects of vibration amplitude and frequency.

The ability of cutaneous vibration to compromise detection of a nociceptive stimulus was examined in 2 sets of psychophysical experiments. The noxious stimulus was a 10-millisecond burst of radiant heat from a CO(2) laser; at the near-threshold levels used it generally yielded a mild pricking sensation. In both experiments, the detectability (d(e)') of the laser was measured in the presence of different vibratory stimuli and in the absence of vibration. Periods of vibration lasted 10 seconds, bracketing the time of occurrence of the laser. Vibratory and laser stimuli were presented 2.3 cm apart on the dorsal surface of the forearm. Confidence rating procedures yielded receiver operating characteristic curves from which detectability of the laser was calculated. In an amplitude study, vibrations ranging from 10 to 45 dB above threshold were used; results indicated that nociceptive sensitivity gradually declined as vibration amplitude increased. In a frequency study, vibrations ranging from 20 to 230 Hz were used; all interfered with nociception. Combining the results of the 2 studies permitted the conclusion that signals in multiple vibrotactile channels are able to modulate nociception. No one mechanoreceptive channel appears to have a privileged role.

Two sensory channels mediate perception of fingertip force.

In two experiments we examined the ability of humans to exert forces accurately with the fingertips, and to perceive those forces. In experiment 1 participants used visual feedback to apply a range of fingertip forces with the distal pad of the thumb. Participants made magnitude discriminations regarding these forces, and their just noticeable differences were calculated at a series of standards by means of a two-interval, forced-choice tracking paradigm. As the standard increased, participants demonstrated a relative improvement in force discrimination; and the presence of a possible inflection point, at approximately 400 g, suggested that two sensory channels may contribute to performance. If this is the case, the operative channel at low forces is almost certainly the slowly adapting type I (SA-I) channel, while another mechanoreceptor class, the SA-II nail unit, is a plausible mediator of the more accurate performance seen at high force levels. To test this two-channel hypothesis in experiment 2, we hydrated participants' thumbnails in order to reduce nail rigidity and thus prevent stimulation of underlying SA-II mechanoreceptors. This technique was found to reduce sensory accuracy in a force-matching task at high forces (1000 g) while leaving low force matching (100 g) unimpaired. Taken together, these results suggest that two sensory channels mediate the perception of fingertip forces in humans: one channel predominating at low forces (below approximately 400 g) and another responsible for perceiving high forces which is likely mediated by the SA-II nail unit.

Coolness both underlies and protects against the painfulness of the thermal grill illusion.

We investigated the contributions of warm and cool signals in generating the thermal grill illusion (TGI), a phenomenon in which interlaced warm and cool bars generate an experience of burning, and under some conditions painful, heat. Each subject underwent 3 runs, 2 of which tested the effects of preadapting subjects to the grill's warm or cool bars (while the interlaced bars were thermally neutral) on the subsequent intensity of the illusion. In a control run, all bars were neutral during the adaptation phase. Thermal visual analogue scale ratings during the warm and cool adaptation periods revealed significant and equivalent adaptation to the 2 temperatures. Adaptation to the grill's cool bars significantly reduced pain and perceived thermal intensity of the TGI, compared to the control condition, while adaptation to the grill's warm bars had little effect. These results suggest that the cool stimulus triggers the pain signals that produce the illusion. The inability of warm adaptation to attenuate the TGI is at odds with theories suggesting that the illusion depends upon a simple addition of warm and cool signals. While the grill's cool bars are necessary for the TGI's painfulness, we also observed that the more often a participant reported feeling coolness or coldness, the less pain he or she experienced from the TGI. These results are consistent with research showing that cool temperatures generate activity in both thermoreceptive-specific, pain-inhibitory neurons and nociceptive dorsal horn neurons.

How does vibration reduce pain?

Cutaneous vibration is able to reduce both clinical and experimental pain, an effect called vibratory analgesia. The traditional explanation for this phenomenon is that it is mediated by lateral inhibition at the segmental (spinal cord) level, in pain-coding cells with center-surround receptive fields. We evaluated this hypothesis by testing for two signs of lateral inhibition-namely (1) an effect of the distance between the noxious and vibratory stimuli and (2) an inhibition-induced shift in the perceived location of the noxious stimulus. The experiment involved continuous ratings of the pain from pressure applied to the back of a finger, alone and in the presence of vibration delivered to sites on the palm of the hand both near to and far from the site of painful stimulation. Neither prediction of the segmental hypothesis was supported. There was also little evidence to support the view (widely held by subjects) that distraction is the primary mechanism of vibratory analgesia. The results are more consistent with a recently proposed theory of interactions between two cortical areas that are primarily involved in coding pain and touch, respectively.

Is touch gating due to sensory or cognitive interference?

Touch gating, the attenuation of tactile sensitivity in the presence of pain, is a well-documented phenomenon, but its mechanism is unknown. The ability of pain to capture attention suggests that touch gating may be an example of distraction, but the fact that pain raises tactile but not auditory thresholds argues that touch gating is a form of somatosensory interaction. Therefore, the present study was carried out to determine whether touch gating is the result of sensory or cognitive interference. Touch gating was repeatedly produced by delivering a colocalized painful heat stimulus (45°C) during forced-choice measurements of vibration threshold on the palm. Noxious heat significantly increased thresholds compared with those measured at normal skin temperature, and this interference did not decline over the course of an extended series of experiments during which pain intensity significantly habituated. Touch gating was thus related to the constant physical intensity, rather than to the changing subjective intensity, of the noxious stimulus. For comparison, a form of unambiguously cognitive interference, the Stroop effect, was also measured repeatedly; it declined significantly across sessions, unlike touch gating interference. Finally, touch gating was not correlated with measures of participants' distractibility, fear of pain, hypervigilance, or anxiety, variables previously found to influence pain on a cognitive level. Taken together, the results suggest that touch gating is a robust, stimulus-locked form of sensory interaction, rather than a transitory result of distraction or other cognitive processes.

Detecting the emergence of chronic pain in sickle cell disease.

CONTEXT: Sickle cell disease (SCD) is an inherited hematological disease marked by intense pain. Early in life the pain is episodic, but it becomes increasingly chronic in many cases. Little is known about this emergence of a chronic pain state. OBJECTIVES: The goal of this study was to determine whether adult SCD patients whose pain is still largely episodic show early signs of the disturbed pain processing (hyperalgesia and increased temporal summation) and cognition (hypervigilance and catastrophizing) that are characteristic of a chronic pain state. METHODS: SCD patients (n=22) and healthy controls (n=52) received noxious pressure stimulation for up to three minutes and periodically reported pain intensity and unpleasantness on 0-10 scales, allowing the rate of pain increase (temporal summation) to be determined. Pain intensity discrimination also was measured, and attitudes toward pain were assessed. RESULTS: There were no overall differences in pain ratings or temporal summation between patient and control groups. However, patients' experimental pain ratings tended to increase with age and those reporting a history of very painful episodes showed particularly rapid temporal summation of pain unpleasantness. Patients were significantly impaired at discriminating intensities of noxious stimulation. Patients were more hypervigilant than controls, but catastrophizing was elevated only during pain episodes. CONCLUSION: Most SCD patients whose pain remits entirely between episodes are not in a chronic pain state, but some--those who are older and have a history of highly painful episodes--appear to be transitioning into it. These early signs of disturbed processing may aid clinicians seeking to forestall disease progression.

Changes in pain from a repetitive thermal stimulus: the roles of adaptation and sensitization.

This study examined processes that contribute to the changing painfulness of a repeatedly presented thermal (heat) stimulus. The 3-second pulses were presented to the side of the hand at a rate of 4/min, too slow to engage wind-up. Over the course of 32 trials, pain intensity (measured by verbal report on a 0-100 scale) first declined and then (in most cases) rose again, indicating adaptation and sensitization, respectively. The magnitude of adaptation grew across a series of 3 runs, indicating that adaptation has a slow as well as a fast component. The rate of sensitization depended on stimulus temperature, but not on subjective pain intensity; this result implies that sensitization takes place at an early processing stage. Adaptation and sensitization were comparable in participants with fibromyalgia, temporomandibular disorders, and in healthy controls, indicating that these processes occur before the perceptual amplification that characterizes fibromyalgia and temporomandibular disorders. The ability of vibration to reduce pain has previously been shown to involve segmental inhibition; the finding in the present study that vibratory gating of pain is significantly (inversely) related to the rate of sensitization suggests that the latter also reflects segmental processes. Several lines of evidence thus point to the conclusion that adaptation and sensitization occur at early stages of sensory information processing.

Temporomandibular disorder modifies cortical response to tactile stimulation.

UNLABELLED: Individuals with temporomandibular disorder (TMD) suffer from persistent facial pain and exhibit abnormal sensitivity to tactile stimulation. To better understand the pathophysiological mechanisms underlying TMD, we investigated cortical correlates of this abnormal sensitivity to touch. Using functional magnetic resonance imaging (fMRI), we recorded cortical responses evoked by low-frequency vibration of the index finger in subjects with TMD and in healthy controls (HC). Distinct subregions of contralateral primary somatosensory cortex (SI), secondary somatosensory cortex (SII), and insular cortex responded maximally for each group. Although the stimulus was inaudible, primary auditory cortex was activated in TMDs. TMDs also showed greater activation bilaterally in anterior cingulate cortex and contralaterally in the amygdala. Differences between TMDs and HCs in responses evoked by innocuous vibrotactile stimulation within SI, SII, and the insula paralleled previously reported differences in responses evoked by noxious and innocuous stimulation, respectively, in healthy individuals. This unexpected result may reflect a disruption of the normal balance between central resources dedicated to processing innocuous and noxious input, manifesting itself as increased readiness of the pain matrix for activation by even innocuous input. Activation of the amygdala in our TMD group could reflect the establishment of aversive associations with tactile stimulation due to the persistence of pain. PERSPECTIVE: This article presents evidence that central processing of innocuous tactile stimulation is abnormal in TMD. Understanding the complexity of sensory disruption in chronic pain could lead to improved methods for assessing cerebral cortical function in these patients.