Tonic Heat Stimuli Research Articles

Indifference or hypersensitivity? Solving the riddle of the pain profile in individuals with autism.

Excitatory-inhibitory (E/I) imbalance is a mechanism that underlies autism spectrum disorder, but it is not systematically tested for pain processing. We hypothesized that the pain modulation profile (PMP) in autistic individuals is characterized by less efficient inhibitory processes together with a facilitative state, indicative of a pronociceptive PMP. Fifty-two adults diagnosed with autism and 52 healthy subjects, age matched and sex matched, underwent quantitative sensory testing to assess the function of the (1) pain facilitatory responses to phasic, repetitive, and tonic heat pain stimuli and (2) pain inhibitory processes of habituation and conditioned pain modulation. Anxiety, pain catastrophizing, sensory, and pain sensitivity were self-reported. The autistic group reported significantly higher pain ratings of suprathreshold single ( P = 0.001), repetitive (46°C- P = 0.018; 49°C- P = 0.003; 52°C- P < 0.001), and tonic ( P = 0.013) heat stimuli that were cross correlated ( r = 0.48-0.83; P < 0.001) and associated with sensitivity to daily life pain situations ( r = 0.39-0.45; P < 0.005) but not with psychological distress levels. Hypersensitivity to experimental pain was attributed to greater autism severity and sensory hypersensitivity to daily stimuli. Subjects with autism efficiently inhibited phasic but not tonic heat stimuli during conditioned pain modulation. In conclusion, in line with the E/I imbalance mechanism, autism is associated with a pronociceptive PMP expressed by hypersensitivity to daily stimuli and experimental pain and less-efficient inhibition of tonic pain. The latter is an experimental pain model resembling clinical pain. These results challenge the widely held belief that individuals with autism are indifferent to pain and should raise caregivers' awareness of pain sensitivity in autism.

No temporal contrast enhancement of simple decreases in noxious heat.

Offset analgesia (OA) studies have found that small decreases in the intensity of a tonic noxious heat stimulus yield a disproportionately large amount of pain relief. In the classic OA paradigm, the decrease in stimulus intensity is preceded by an increase of equal size from an initial noxious level. Although the majority of researchers believe this temporal sequence of two changes is important for eliciting OA, it has also been suggested that the temporal contrast mechanism underlying OA may enhance detection of simple, isolated decreases in noxious heat. To test whether decreases in noxious heat intensity, by themselves, are perceived better than increases of comparable sizes, we used an adaptive two-interval alternative forced choice task to find perceptual thresholds for increases and decreases in radiant and contact heat. Decreases in noxious heat were more difficult to perceive than increases of comparable sizes from the same initial temperature of 45°C. In contrast, decreases and increases were perceived equally well within a common range of noxious temperatures (i.e., when increases started from 45°C and decreases started from 47°C). In another task, participants rated the pain intensity of heat stimuli that randomly and unpredictably increased, decreased, or remained constant. Ratings of unpredictable stimulus decreases also showed no evidence of perceptual enhancement. Our results demonstrate that there is no temporal contrast enhancement of simple, isolated decreases in noxious heat intensity. Combined with previous OA findings, they suggest that long-lasting noxious stimuli that follow an increase-decrease pattern may be important for eliciting the OA effect.NEW & NOTEWORTHY Previous research suggested that a small decrease in noxious heat intensity feels surprisingly large because of sensory enhancement of noxious stimulus offsets (a simplified form of “offset analgesia”). Using a two-alternative forced choice task where participants detected simple increases or decreases in noxious heat, we showed that decreases in noxious heat, by themselves, are no better perceived than increases of comparable sizes. This suggests that a decrease alone is not sufficient to elicit offset analgesia.

A tonic heat test stimulus yields a larger and more reliable conditioned pain modulation effect compared to a phasic heat test stimulus.

The interest in conditioned pain modulation (CPM) as a clinical tool for measuring endogenously induced analgesia is increasing. There is, however, large variation in the CPM methodology, hindering comparison of results across studies. Research comparing different CPM protocols is needed in order to obtain a standardized test paradigm. The aim of the study was to assess whether a protocol with phasic heat stimuli as test-stimulus is preferable to a protocol with tonic heat stimulus as test-stimulus. In this experimental crossover study, we compared 2 CPM protocols with different test-stimulus; one with tonic test-stimulus (constant heat stimulus of 120-second duration) and one with phasic test-stimuli (3 heat stimulations of 5 seconds duration separated by 10 seconds). Conditioning stimulus was a 7°C water bath in parallel with the test-stimulus. Twenty-four healthy volunteers were assessed on 2 occasions with minimum 1 week apart. Differences in the magnitude and test-retest reliability of the CPM effect in the 2 protocols were investigated with repeated-measures analysis of variance and by relative and absolute reliability indices. The protocol with tonic test-stimulus induced a significantly larger CPM effect compared to the protocol with phasic test-stimuli (P < 0.001). Fair and good relative reliability was found with the phasic and tonic test-stimuli, respectively. Absolute reliability indices showed large intraindividual variability from session to session in both protocols. The present study shows that a CPM protocol with a tonic test-stimulus is preferable to a protocol with phasic test-stimuli. However, we emphasize that one should be cautious to use the CPM effect as biomarker or in clinical decision making on an individual level due to large intraindividual variability.

Empathy Predicts an Experimental Pain Reduction During Touch.

Previous studies have provided evidence for pain-alleviating effects of segmental tactile stimulation, yet the effect of social touch and its underlying mechanism is still unexplored. Considering that the soma affects the way we think, feel, and interact with others, it has been proposed that touch may communicate emotions, including empathy, interacting with the identity of the toucher. Thus, the goal of the current study was to examine the analgesic effects of social touch, and to test the moderating role of the toucher's empathy in analgesia using an ecological paradigm. Tonic heat stimuli were administered to women. Concurrently, their partners either watched or touched their hands, a stranger touched their hands, or no one interacted with them. The results revealed diminished levels of pain during partners' touch compared with all other control conditions. Furthermore, taking into account the dyadic interaction, only during the touch condition we found 1) a significant relationship between the partners' pain ratings, and 2) a significant negative relationship between the male touchers' empathy and the pain experience of their female partners. The findings highlight the powerful analgesic effect of social touch and suggest that empathy between romantic partners may explain the pain-alleviating effects of social touch. Pain research mostly concentrates on different factors around a single pain target, without taking into account various social interactions with the observers. Our findings support the idea that pain perception models should be extended, taking into account some psychological characteristics of observers. Our conclusions are on the basis of advanced statistical methods.

(365) Pain modulation and autonomic function: the effect of clonidine

The α2-agonist clonidine is an analgesic agent, whose yet uncertain action may involve either increase in pain modulation efficiency, change in autonomic function and/or decrease in anxiety level. We aimed to examine the effect of oral clonidine on pain perception in healthy subjects, in order to reveal its mode of action. This randomized, double blind, placebo controlled study included 40 healthy subjects. Subjects received either 0.15 mg oral clonidine or placebo. We measured: 1. measured pain parameters of heat pain thresholds, tonic heat stimulus, mechanical temporal summation, offset analgesia (OA) and conditioned pain modulation (CPM); 2. autonomic parameters of deep breathing ratio and heart rate variability indices obtained before, during and after tonic heat stimulus; and 3. psychological parameters of anxiety and pain catastrophizing. Clonidine decreased systolic blood pressure (p=0.022) and heart rate (p=0.004) and increased rMSSD (p=0.020), though no effect was observed on pain perception, pain modulation and psychological parameters. Autonomic changes were correlated with pain modulation capacity; for OA, the separate slope model was significant (p=0.008) such that in the clonidine group more efficient OA was associated with lower heart rate (r=0.633, p=0.005) unlike the placebo group. A similar trend was found for CPM. The change in autonomic function which was related to the increase in pain modulation capacity, and the lack of change in anxiety suggest a combined modulatory-autonomic mode of analgesic action for clonidine.

Pain Modulation and Autonomic Function: The Effect of Clonidine.

The α2-agonist clonidine is an analgesic agent, whose yet uncertain action may involve either increase in pain modulation efficiency, change in autonomic function, and/or decrease in anxiety level. The present study aimed to examine the effect of oral clonidine on pain perception in healthy subjects in order to reveal its mode of action. Randomized, double-blind, placebo-controlled study. Forty healthy subjects. Subjects received either 0.15 mg oral clonidine or placebo. We measured pain parameters of heat pain thresholds, tonic heat stimulus, mechanical temporal summation, offset analgesia (OA) and conditioned pain modulation (CPM); autonomic parameters of deep breathing ratio and heart rate variability indices obtained before, during, and after tonic heat stimulus; and psychological parameters of anxiety and pain catastrophizing. Clonidine decreased systolic blood pressure (P = 0.022) and heart rate (P = 0.004) and increased rMSSD (P = 0.020), though no effect was observed on pain perception, pain modulation, and psychological parameters. Autonomic changes were correlated with pain modulation capacity; for OA, the separate slope model was significant (P = 0.008); in the clonidine group, more efficient OA was associated with lower heart rate (r = 0.633, P = 0.005), unlike in the placebo group. The change in autonomic function that was related to the increase in pain modulation capacity, and the lack of change in anxiety, suggest a combined modulatory-autonomic mode of analgesic action for clonidine.

Alexithymic Trait, Painful Heat Stimulation, and Everyday Pain Experience.

Alexithymia was found to be associated with a variety of somatic complaints, including somatoform pain symptoms. This study addressed the question of whether the different facets of alexithymia are related to responses in heat pain stimulation and its interrelations with levels of everyday pain as assessed by self-report. In the study, sensitivity to heat pain was assessed in 50 healthy female participants. Alexithymia facets were assessed by the Toronto Alexithymia Scale. Pain threshold and tolerance were determined using a testing the limits procedure. Participants, furthermore, rated subjective intensities and unpleasantness of tonic heat stimuli (45.5-47.5°C) on visual analog scales and on a questionnaire. Possible confounding with temperature sensitivity and mood was controlled. Everyday pain was assessed by self-report addressing everyday pain frequency, intensity, and impairment experienced over the last 2 months. Main results were that the facets of alexithymia were differentially associated with pain perception. The affective scale "difficulties in describing feelings" was associated with hyposensitivity to pain as indicated by higher pain tolerance scores. Furthermore, everyday pain frequency was related to increased alexithymia values on the affective scale "difficulties in identifying feelings," whereas higher values on the cognitive alexithymia scale "externally oriented thinking" were related to lower pain impairment and intensity. We conclude that the different facets of alexithymia are related to alternations in pain processing. Further research on clinical samples is necessary to elucidate whether different aspects of alexithymia act as a vulnerability factor for the development of pain symptoms.

Endogenous pain inhibition during menstrual cycle in migraine

Migraine is a common headache disorder that can vary menstrually in women and has been linked to an impairment of endogenous pain inhibitory systems. One of these endogenous pain inhibitory systems, namely conditioned pain modulation (CPM; formerly diffuse noxious inhibitory controls-like), has been shown to be affected by the menstrual cycle. The aim of this study was to examine CPM over the menstrual cycle in migraineurs and healthy controls. Twenty healthy women and 32 female migraineurs were examined on days 1, 4, 14 and 22 of the menstrual cycle. Detection and pain thresholds for electrocutaneous stimuli were first assessed at baseline. Second, tonic heat stimuli were applied concurrently to the electrical stimuli, and the difference in electrical thresholds to baseline were analysed as indicating CPM inhibition. Migraineurs revealed higher detection thresholds than the control group but similar pain thresholds for the electrical current. Likewise, pain sensitivity for tonic heat stimulation also did not differ between groups. With regard to our main hypotheses, we found that CPM inhibition neither differed between migraineurs and healthy volunteers nor varied over the menstrual cycle. Our findings suggest that CPM inhibition is not altered in female migraineurs; thus, it is questionable whether CPM really plays a role in the development of migraine or whether migraine leads to a dysfunctional CPM inhibition.

Inflammation meets sensitization—an explanation for spontaneous nociceptor activity?

Anti-nerve growth factor (anti-NGF) treatment is analgesic in chronic inflammatory pain conditions without reducing inflammation. Hypothesizing that ongoing pain induced by inflammatory mediators is increased by long term sensitization of nociceptors, we combined the non-inflammatory NGF-sensitization model with an inflammatory ultraviolet-B (UV-B) model in human volunteers. UV-B irradiation of the skin presensitized with NGF 3weeks before intensified the pre-existing NGF hyperalgesia during the inflammatory phase of UV-B and caused spontaneous pain in about 70% of the subjects. Pain levels paralleled the intensity of UVB inflammation. Hyperalgesia recorded on a VAS (0–100) was additive after combined NGF/UV-B treatment versus single NGF or UV-B treatment for mechanical impact and tonic heat stimuli, again paralleling the intensity of the UV-B inflammation. In contrast, ratings to tonic mechanical pressure (100kPa for 10seconds, peak VAS 58±7 vs VAS 21±5 [NGF] and VAS 12±3 [UV-B]) and pinprick (150mN for 5seconds, peak VAS 33±7 vs VAS 10±2 [NGF] and VAS 8±3 [UV-B]) increased in a supra-additive manner. This supra-additive effect faded 24hours after irradiation, although heat sensitization remained increased. Hyperalgesia and spontaneous pain coexisted in NGF/UV-B treated skin but did not significantly correlate (r<−0.1 at day 1 and r<0.2 at day 3). We conclude that NGF can sensitize nociceptive endings such that inflammatory mediators may cause sufficient excitation to provoke spontaneous pain. Our results suggest that neuronal sensitization and level of inflammation represent independent therapeutic targets in chronic inflammatory pain conditions.

Prediction of postoperative pain by preoperative pain response to heat stimulation in total knee arthroplasty

It has been estimated that up to 54% of the variance in postoperative pain experience may be predicted with preoperative pain responses to experimental stimuli, with suprathreshold heat pain as the most consistent test modality. This study aimed to explore whether 2 heat test paradigms could predict postoperative pain after total knee arthroplasty (TKA). Patients scheduled for elective, unilateral, primary TKA under spinal anesthesia were consecutively included in this prospective, observational study. Perioperative analgesia was standardized for all patients. Outcomes were postoperative pain during walk: from 6 to 24hours (primary), from postoperative day (POD) 1 to 7 (secondary), and from POD 14 to 30 (tertiary). Two preoperative tonic heat stimuli with 47°C were used; short (5seconds) and long (7minutes) stimulation upon which patients rated their pain response on an electronic visual analog scale. Multivariate stepwise linear and logistic regressions analyses were carried out, including 8 potential preoperative explanatory variables (among these anxiety, depression, preoperative pain, and pain catastrophizing) to assess pain response to preoperative heat pain stimulation as an independent predictor for postoperative pain. A total of 100 patients were included, and 3 were later excluded. A weak correlation [rho (95% confidence interval); P value] was observed between pain from POD 1 to 7 and pain response to short [rho=0.25(0.04 to 0.44); P=.02] and to long [rho=0.27 (0.07 to 0.46); P=.01] heat pain stimulation. However, these positive correlations were not supported by the linear and logistic regression analyses, in which only anxiety, preoperative pain, and pain catastrophizing were significant explanatory variables (but with low R-squares; 0.05 to 0.08). Pain responses to 2 types of preoperative heat stimuli were not independent clinically relevant predictors for postoperative pain after TKA.

Differentiating between heat pain intensities: The combined effect of multiple autonomic parameters

Although it is well known that pain induces changes in autonomic parameters, the extent to which these changes correlate with the experience of pain is under debate. The aim of the present study was to compare a combination of multiple autonomic parameters and each parameter alone in their ability to differentiate among 4 categories of pain intensity. Tonic heat stimuli (1minute) were individually adjusted to induce no pain, low, medium, and high pain in 45 healthy volunteers. Electrocardiogram, photoplethysmogram, and galvanic skin response were recorded, and the following parameters were calculated: heart rate; heart rate variability—high frequency (0.15 to 0.4Hz) spectral power; skin conductance level; number of skin conduction fluctuations; and photoplethysmographic pulse wave amplitude. A combination of parameters was created by fitting an ordinal cumulative logit model to the data and using linear coefficients of the model. Friedman test with post-hoc Wilcoxon test were used to compare between pain intensity categories for every parameter alone and for their linear combination. All of the parameters successfully differentiated between no pain and all other pain categories. However, none of the parameters differentiated between all 3 pain categories (i.e., low and medium; medium and high; low and high). In contrast, the linear combination of parameters significantly differentiated not only between pain and no pain, but also between all pain categories (P<.001 to .02). These results suggest that multiparameter approaches should be further investigated to make progress toward reliable autonomic-based pain assessment.

Anesthesia Literature Review

Anesthesia Literature Review

Cerebral processing of pain in school-aged children with neonatal nociceptive input: An exploratory fMRI study

Due to maturation-related plasticity of the developing nociceptive system, neonatal nociceptive input, as induced by medical procedures in the neonatal intensive care unit (NICU), may cause long-term alterations in pain processing. Using functional magnetic resonance imaging, this study investigated the cerebral pain response in school-aged children and adolescents (11–16 yr) with experience in a NICU after preterm (⩽31 weeks gestational age, N = 9) or fullterm birth (⩾37 weeks gestational age, N = 9) as compared to fullterm control children without early hospitalization ( N = 9). NICU children had been recruited retrospectively among former patients of the Children’s University Hospital Mannheim. All children had participated in our previous studies [46,49] entailing psychophysical measurements. In response to tonic (30 s) heat stimuli of individually adjusted moderate pain intensity, which were of comparable temperature across groups, the preterm but not the fullterm NICU children exhibited significant activations in a number of brain regions (thalamus, anterior cingulate cortex, cerebellum, basal ganglia, and periaquaeductal gray) that were not significantly activated in controls. The preterms showed significantly higher activations than controls in primary somatosensory cortex, anterior cingulate cortex, and insula. This exaggerated brain response was pain-specific and was not observed during non-painful warmth stimulation. Preterms’ continuous pain ratings revealed a tendency for increased sensitization within and a lack of habituation across trials. In highly vulnerable children such as preterms, neonatal nociceptive input may, aside from other neurodevelopmental consequences, persistently increase the gain within pain pathways.

Catastrophizing delays the analgesic effect of distraction

Behavioral analgesic techniques such as distraction reduce pain in both clinical and experimental settings. Individuals differ in the magnitude of distraction-induced analgesia, and additional study is needed to identify the factors that influence the pain relieving effects of distraction. Catastrophizing, a set of negative emotional and cognitive processes, is widely recognized to be associated with increased reports of pain. We sought to evaluate the relationship between catastrophizing and distraction analgesia. Healthy participants completed three sessions in a randomized order. In one session (Pain Alone), pain was induced by topical application of a 10% capsaicin cream and simultaneous administration of a tonic heat stimulus. In another session (Pain+Distraction), identical capsaicin+heat application procedures were followed, but subjects played video games that required a high level of attention. During both sessions, verbal ratings of pain were obtained and participants rated their degree of catastrophizing. During the other session (Distraction Alone) subjects played the video games in the absence of any pain stimulus. Pain was rated significantly lower during the distraction session compared to the “Pain Alone” session. In addition, high catastrophizers rated pain significantly higher regardless of whether the subjects were distracted. Catastrophizing did not influence the overall degree of distraction analgesia; however, early in the session high catastrophizers had little distraction analgesia, though later in the session low and high catastrophizers rated pain similarly. These results suggest that both distraction and catastrophizing have substantial effects on experimental pain in normal subjects and these variables interact as a function of time.

The Relationship Between Pain Perception and Interoception

The question of whether the perception of externally applied pain stimuli and the perception of interoceptive stimuli are based upon similar neuronal or behavioral processes is still open to debate. If such a similarity exists, one would expect that persons who are highly sensitive to visceral stimuli would also exhibit a higher sensitivity to pain stimuli. The present study investigated the sensitivity to heat pain of individuals with high vs. low cardiac interoceptive sensitivity. Pain threshold and pain tolerance were assessed using a testing-the-limits procedure. Furthermore, participants rated the subjective intensity and unpleasantness of tonic heat stimuli on visual analog scales and in a questionnaire. The results show that pain experience did not differ between participants with high and low interoceptive sensitivity, nor did correlation analyses reveal significant relationships between pain experience and cardiac interoceptive sensitivity. These findings suggest that the pathway of peripheral pain processing is at least partially independent of the pathway of interoceptive sensations.

Do burn injuries during infancy affect pain and sensory sensitivity in later childhood?

Studies in animals and humans suggest that neonatal and early infant pain or stress experiences can induce long-term alterations in somatosensory and pain processing. We studied pain and sensory sensitivity in school-aged children (9–16 years) who had suffered moderate (N=24) or severe (N=24) burn injuries in infancy (6–24 months of age) and 24 controls. Quantitative sensory testing entailing detection and pain thresholds for thermal and mechanical stimuli and perceptual sensitization to tonic heat and repetitive mechanical stimuli was performed. Two testing sites (thenar, trigeminal region), both not affected by the burn injury, were used to determine whether there are global changes in pain sensitivity. The result pattern suggests a differential impact of burn severity. Compared to controls, moderately burned children showed significantly higher mechanical detection thresholds (thenar) and significantly lower mechanical pain thresholds and significantly greater perceptual sensitization to repetitive mechanical stimuli (both testing sites). No significant alterations were observed for thermal stimuli. In contrast, severely burned children showed, compared to controls, primarily alterations in thermal pain sensitivity (elevated pain thresholds at both testing sites, significantly greater perceptual sensitization at the thenar). In these children, mechanical pain sensitivity and detection thresholds were not consistently altered. This differential pattern of altered sensory and pain sensitivity may reflect differences in experienced stress, pain and analgesic treatment between moderately and severely burned children. Most importantly, our findings suggest that early traumatic and painful injuries, such as burns, can induce global, long-term alterations in sensory and pain processing.

The effects of DNIC-type inhibition on temporal summation compared to single pulse processing: Does sex matter?

A few experimental observations have suggested that diffuse noxious inhibitory control (DNIC)-type inhibition acts preferentially on the pain system if this is in a sensitised state, e.g. after slow temporal summation (wind-up). However, firm evidence is still missing. Furthermore, sex-related factors, which seem to affect temporal summation as well as DNIC effects, might thus also modulate the interaction of these two processes. To answer these questions, we investigated 40 young and pain-free subjects (20 female and 20 male). The conditioning stimulus in our DNIC paradigm was realized by immersion of the hand into a water tub containing either 42 °C (non-painful heat) or 46 °C (painful heat) hot water. The test stimuli were either single pulses or series of five pulses (0.5 Hz repetition frequency) produced by a pressure algometer. The VAS ratings for the last stimulus in the series were significantly higher than for the single pulse (temporal summation). The ratings were significantly reduced by the 42 °C conditioning stimulus and even more by the 46 °C conditioning stimulus, suggesting DNIC-like inhibition. This was equally true both for the single pulse and for the series of pulses. Sex differences were not observed for temporal summation, DNIC inhibition or for the interaction of the two processes, although women exhibited significantly lower pressure pain thresholds and higher ratings for the tonic heat stimuli. In conclusion, DNIC-type inhibition apparently does not preferentially act on a sensitised pain system after slow temporal summation. Considering the sex of the subjects does not change this insight.

Somatic Pain Sensitivity in Children With Recurrent Abdominal Pain

Evidence is accumulating that recurrent abdominal pain (RAP) in children is associated with visceral hyperalgesia. However, it is not known whether somatic sensitivity is altered as well. Therefore, the aim of our study was to assess somatic pain sensitivity in children with RAP and healthy controls at the abdomen and a distal site (thenar). We examined 20 children with RAP (age 8-14) and 23 healthy control children (age 9-14). Heat and mechanical pain thresholds as well as measures of perceptual sensitization in response to repetitive mechanical or tonic thermal noxious stimulation were assessed. At the abdominal site, pain sensitivity in children with RAP did not differ significantly when compared to controls. At the thenar, pain thresholds of children in the RAP group were not significantly different from control children. However, children with RAP showed less perceptual sensitization in response to tonic heat and repetitive mechanical stimuli (ps <or= 0.05) than controls. We found no evidence for somatic hyperalgesia in RAP arguing against generalized hyperalgesia in these children. Somatic hypoalgesia at the thenar might either be related to a dysregulation of sensory processing and/or attentional avoidance of pain-related stimuli.

Increased sensitivity to heat pain in chronic low blood pressure

While in elevated blood pressure reduced sensitivity to acute pain has been well established, little is known about possible alterations in pain perception within the lower range of blood pressure. In this study, sensitivity to heat pain was assessed in 40 subjects with chronic hypotension (mean blood pressure 96.5/57.7 mmHg) and 40 normotensive control persons (mean blood pressure 121.8/77.2 mmHg). Employing a contact thermode, heat stimuli were applied to the forearm. Pain threshold and tolerance were determined. Participants furthermore rated subjective intensities and unpleasantness of tonic heat stimuli (45.5–47.5 °C) on visual analogue scales and in a questionnaire. Possible confounding of sensitivity to heat pain with skin temperature, temperature sensitivity and mood was controlled for. In addition to blood pressure, functional features of the arterial baroreceptor system were related to pain experience. Therefore, estimates for the input on the baroreceptors, as well as baroreflex sensitivity were obtained. Hypotensive individuals exhibited markedly reduced pain threshold and pain tolerance, as well as increased sensory and affective pain experience. The measures related to the baroreceptor system were not associated with pain experience, suggesting that no significant modulation of heat pain occurs through this system. The results of this study complete the findings on hypertension-related hypoalgesia and suggest an inverse relationship between blood pressure and pain sensitivity across the whole blood pressure spectrum. Furthermore, increased proneness of hypotensive individuals to clinical pain may be discussed.

Subjective pain perception, spinal nociception and descending inhibition of experimentally induced pain in Parkinson's disease

Patients suffering from Parkinson's disease (PD) complain more often about acute and chronic pain, which can be subdivided into musculoskeletal pain, radicular-neuropathic pain, dystonic pain, central pain and akathisia. Previous studies of experimentally induced pain in PD revealed heterogeneous results. One recent study detected an increased perception of heat-induced pain, which was reversible after dopaminergic treatment. Possibly a reduced dopaminergic descending inhibitory control (DNIC) system contributes to this finding. Therefore, we investigated the DNIC system by using a tonic heat stimulus and a phasic electrical stimulus. In addition to thermal and electrical pain thresholds, we assessed spinal nociception by using the nociceptive flexion reflex (NFR).