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Peter Svensson

Publications and source records attributed to Peter Svensson.

63 records · Page 4Linked to original sources

Analysis of stimulus-evoked pain in patients with myofascial temporomandibular pain disorders.

The pathophysiological mechanisms of myofascial temporomandibular disorders (TMD) are still under investigation. The hypothesis that TMD pain is caused by a generalized sensitization of higher order neurons in the nociceptive pathways combined with a decreased efficacy of endogenous inhibitory systems has recently gained support in the literature. This study was designed to further investigate the somatosensory sensibility within and outside the craniofacial region. Twenty-two patients fulfilled the research diagnostic criteria for TMD for myofascial pain (Dworkin and LeResche, J Craniomandib Disord Facial Oral Pain 6 (1992) 301) and 21 age- and sex-matched subjects served as a control group. The somatosensory sensibility to a deep tonic input was tested by standardized infusions of hypertonic saline into the masseter and anterior tibialis muscle. Furthermore, pressure pain thresholds (PPTs) and heat pain thresholds (HPTs) were assessed with phasic stimuli at the same sites before and following the infusions. Myofascial TMD patients reported infusion of hypertonic saline to be more painful on 10 cm visual analogue scales (peak pain 8.8 +/- 0.4 cm) than control subjects (6.8 +/- 0.5 cm, t-test: P = 0.003) in the masseter but not in the anterior tibialis (7.4 +/- 0.5 vs. 6.6 +/- 0.5 cm, P=0.181). The perceived area of experimental masseter pain measured on drawings was marginally larger in TMD patients (2.6+/-0.5 arbitrary units (a.u.)) than in control subjects (1.4 +/- 0.2 a.u., Mann-Whitney: P = 0.048) but no differences were observed for the anterior tibialis (P = 0.771). The PPTs were lower in the myofascial TMD patients compared to the control group, both in the masseter (analysis of variance (ANOVA): P = 0.002) and in the anterior tibialis (P = 0.005), whereas there were no significant differences in HPT (ANOVAs: P = 0.357, P = 0.101). There were no significant correlations between measures of somatosensory sensibility and measures of clinical pain intensity, pain duration, graded chronic pain scores or somatization or depression scores (Pearson: R < 0.304, P > 0.172). The present study in a well-defined group of myofascial TMD patients found that the responsiveness to both tonic and phasic deep stimuli, but not to phasic superficial inputs at the pain threshold level, in the craniofacial region was higher compared with a control group. These findings suggest that myofascial TMD pain is associated with a facilitation of stimulus-evoked pain primarily, but not exclusively related to the painful region.

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Effect of tonic muscle pain on short-latency jaw-stretch reflexes in humans.

The modulation of human jaw-stretch reflexes by experimental muscle pain was studied in three experiments. Short-latency reflex responses were evoked in the masseter and temporalis muscles by fast stretches (1 mm displacement, 10 ms ramp time) before, during and 15 min after a period with tonic pain. In Expt. I, a dose of 5.8% hypertonic or 0.9% isotonic (control) saline was infused in random order into the left masseter for up to 15 min (n=12). The level of excitation of the left masseter was kept constant at 15% of maximal effort by visual feedback and on-line calculation of the root-mean-square value of the surface electromyogram (sEMG). In Expt. II, a dose of 5.8% saline was infused into the left masseter but with feedback from the right masseter sEMG (n=12). In Expt. III, both sEMG and intramuscular (im) EMG was recorded from the left and right masseter muscles. The feedback was from either the sEMG or imEMG of the left masseter in which 5.8% saline was infused (n=12). In all experiments, subjects continuously rated their perceived pain intensity on a 10-cm visual analogue scale (VAS). Infusion of 5.8% saline caused moderate levels of pain (mean VAS 4.9-5.0 cm) whereas infusion of 0.9% saline was almost pain-free (mean VAS 0.3 cm). The pre-stimulus EMG activity in the masseter, which served as the feedback muscle during the recording, was constant across the different conditions. During painful infusion of 5.8% saline in Expts. I and III, the pre-stimulus sEMG activity in the non-painful masseter was significantly higher than baseline when the sEMG on the painful side was used as feedback signal, and in Expt. II significantly lower on the painful side when the non-painful side served as feedback signal (Student-Newman-Keuls: P<0.05). Isotonic saline did not affect the pre-stimulus sEMG activity or the jaw-stretch reflex parameters. The peak-to-peak amplitude of the stretch reflex in the painful masseter normalized to the pre-stimulus EMG activity was significantly higher during the pain conditions compared with the pre- and post-infusion conditions in all experiments. These results indicate that experimental jaw-muscle pain facilitates the short-latency (8-9 ms), probably monosynaptic, jaw-stretch reflex as revealed by both sEMG and imEMG. This effect could not be accounted for by variability in pre-stimulus EMG activity. An increased sensitivity of the fusimotor system at this level of static muscle excitation is suggested as a possible mechanism, which could contribute to an increased stiffness of the jaw-muscles during pain.

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Experimental human muscle pain and muscular hyperalgesia induced by combinations of serotonin and bradykinin.

In the present study, we assessed the muscle pain and possible development of muscular hyperalgesia to mechanical stimuli after two subsequent intramuscular infusions of serotonin (5-HT) and bradykinin (BKN). The pain intensity after the infusions was continuously scored on a visual analogue scale (VAS). The subjects drew the distribution of the pain areas on a map. Pressure pain thresholds (PPTs) and suprapressure pain thresholds (SPPTs) stimulations as 150% of the pre-infusion PPTs were assessed with a pressure algometer at the injection site (10 cm below the patella), at the ankle, and at the contralateral leg and ankle. Skin sensibility was assessed with a Von Frey hair at the same sites. This was done before and after an infusion into the tibialis anterior (TA) muscle on the right leg in ten volunteers. The first infusion in each combination was either serotonin (20 nmol) or isotonic saline (NaCl 0.9%). The second infusion was bradykinin (5 or 10 nmol) or isotonic saline. The two infusions were given over 20 s and separated by 3 min. The isotonic saline followed by BKN did not induce muscle pain or muscular hyperalgesia. However, the combination of 5-HT and BKN (10 nmol) produced: (1) significantly higher VAS scores (P < 0.05) compared with all other combinations; (2) significantly longer pain offset (P < 0.05) compared with the combinations of isotonic saline and BKN; (3) significantly lower PPTs at 5, 20, and 40 min post-infusion (P < 0.05) compared with baseline PPT and PPTs after all other combinations. Cutaneous sensibility to mechanical stimuli and SPPTs were not affected by any of the combinations. The combinations of serotonin and bradykinin produce experimental muscle pain and muscular hyperalgesia to mechanical stimuli. Pre-treatment with serotonin may enhance the effect of bradykinin in the generation of muscle pain and muscular hyperalgesia in humans.

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Modulation of exteroceptive suppression periods in human jaw-closing muscles by local and remote experimental muscle pain.

The exteroceptive suppression periods (ES) in human jaw-closing muscles can be conditioned by a wide range of somatosensory stimuli and cognitive states. The aim of this study was to examine the effects of tonic experimental jaw-muscle pain versus remote muscle pain on the short-latency (ES1) and long-latency (ES2) reflex in the jaw-closing muscles. Twelve healthy subjects participated in the first experiment with jaw-muscle pain. In random order 5% hypertonic or 0.9% isotonic saline was infused into the left masseter muscle for 15 min. The pain intensity was scored continuously by the subjects on a 10-cm visual analogue scale (VAS). Electromyographic (EMG) activity was recorded bilaterally from the masseter and temporalis muscles during the pre-infusion, early phase of infusion (from 120 to 480 s), late phase of infusion (from 540 to 900 s) and post-infusion. An electrical stimulus was delivered to the skin above the left mental nerve (ipsilateral to the painful muscle) to evoke the ES in the contracting jaw-closing muscles. Ten healthy subjects participated in experiment 2 which was as identical to experiment 1 except that the electrical stimulus was delivered to the right mental nerve (contralateral to the painful muscle). Nine healthy subjects participated experiment 3 where remote muscle pain was induced in the left tibialis anterior muscle. In experiment 1 painful infusion of hypertonic saline caused a significantly later onset latency of ES2 in the left masseter muscle during the late phase of infusion compared to pre-infusion values (P < 0.05). The duration of ES2 in the same muscle was significantly shorter during the late infusion phase compared to pre- and post-infusion values (P < 0.05) and the degree of suppression was significantly reduced during the early infusion compared to the pre-infusion values (P < 0.05). Isotonic saline did not influence the ES1 or ES2. In experiment 2, similar significant inhibitory changes were found in the ES2 on the painful side. In experiment 3, no significant effects on ES1 and ES2 were observed during painful infusion of hypertonic saline into the leg muscle. These results indicate that the effects of tonic jaw-muscle pain on ES2 can be distinguished from a generalized effect of muscle pain. Furthermore, there seems to be a differential and lateralized effect of jaw-muscle pain on the brain stem reflex circuits involved in the generation of ES1 and ES2 probably through a presynaptic mechanism.

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Modulation of an inhibitory reflex in single motor units in human masseter by tonic painful stimulation.

Perioral electrical stimuli cause inhibitory reflex responses in single motor-units (SMU) and surface electromyographic (EMG) recordings from voluntary contracted human jaw-closing muscles. Tonic experimental masseter pain has recently been shown to reduce the inhibitory reflex response in surface EMG recordings but the effect on SMU activity has not been described. In this study, motor-unit action potentials were recorded with wire electrodes inserted into the left masseter in eleven subjects. The subjects kept the SMU firing rate around 10 Hz by feedback. Ninety-nine electrical stimuli were applied sequentially to the left mental nerve with increasing stimulus delays in steps of 1 ms after the preceding motor unit action potential. The inhibitory reflex in SMU was recorded before, during and after infusion of hypertonic saline (5%) into the ipsilateral masseter muscle. Spike train data were used to calculate (1) the mean pre- and post-stimulus inter-spike-intervals (ISI) in all of the 99 trials, (2) cumulative changes in firing probability, and (3) estimation of the compound inhibitory post-synaptic potential (IPSP) in the masseter motoneuron. Tonic masseter pain did not change pre-stimulus SMU firing characteristics but the mean ISI for the first post-stimulus discharge (158.2+/-9.2 ms) was significantly decreased compared to the pre-pain (175.8+/-11.3 ms, P<0.05) and post-pain conditions (172. 6+/-11.6 ms, P<0.05). The post-stimulus firing probability was significantly increased and the relative amplitude of the estimated IPSP significantly decreased during tonic masseter pain compared to pre-pain and post-pain conditions. In conclusion, this study indicates that tonic masseter pain has a net excitatory effect on the inhibitory jaw-reflexes, which could be mediated by presynaptic mechanisms on the involved motoneurons.

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Mechanical hyperesthesia of human facial skin induced by tonic painful stimulation of jaw muscles.

The function of the somatosensory system in patients with painful temporomandibular disorders is still a matter of discussion. We wished to determine cutaneous sensitivity to innocuous mechanical stimuli in the orofacial region before, during (3 and 12 min) and after standardized experimental jaw-muscle pain. Twelve healthy subjects were exposed to tonic infusion of hypertonic (5%) and isotonic (0.9%) saline into the masseter muscle. All subjects experienced moderate pain with hypertonic saline, and the area of self-reported pain increased significantly from 3 min after infusion start to 12 min after infusion start (mean +/- SEM: 115+/-49%; P < 0.05). The psychophysical ratings of punctate von Frey hair stimulation were significantly increased 12 min after start of hypertonic saline infusion as compared to baseline and post-baseline ratings at the site of infusion (50+/-10%; P < 0.05) and at two adjacent facial sites (18+/-7%, 37+/-9%; P < 0.05). In contrast, isotonic saline infusion was associated with a significant decrease in ratings at post-baseline as compared to baseline ratings. The psychophysical ratings of a stroking cotton swab stimulation were not significantly affected by infusion of saline. These results in a human model of jaw-muscle pain are comparable to animal studies demonstrating increased size of cutaneous receptive fields and increased responsiveness of brain stem neurons to cutaneous mechanical stimuli. Similar hyperexcitability changes may be part of the pathophysiological mechanisms involved in painful temporomandibular disorders.

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The influence of low back pain on muscle activity and coordination during gait: a clinical and experimental study.

Chronic low back pain (CLBP) is a major clinical problem with a substantial socio-economical impact. Today, diagnosis and therapy are insufficient, and knowledge concerning interaction between musculoskeletal pain and motor performance is lacking. Most studies in this field have been performed under static conditions which may not represent CLBP patients' daily-life routines. A standardized way to study the sensory-motor interaction under controlled motor performances is to induce experimental muscle pain by i.m. injection of hypertonic saline. The aim of the present controlled study was to analyze and compare electromyographic (EMG) activity of and coordination between lumbar muscles (8 paraspinal recordings) during gait in 10 patients with CLBP and in 10 volunteers exposed to experimental back muscle pain induced by bolus injection of 5% hypertonic saline. When the results are compared to sex- and age-matched controls, the CLBP patients showed significantly increased EMG activity in the swing phase; a phase where the lumbar muscles are normally silent. These changes correlated significantly to the intensity of the back pain. Similar EMG patterns were found in the experimental study together with a reduced peak EMG activity in the period during double stance where the back muscles are normally active. Generally, these changes were localized ipsilaterally to the site of pain induction. The clinical and experimental findings indicate that musculoskeletal pain modulates motor performance during gait probably via reflex pathways. Initially, these EMG changes may be interpreted as a functional adaptation to muscle pain, but the consequences of chronic altered muscle performance are not known. New possibilities to monitor and investigate altered motor performance may help to develop more rational therapies for CLBP patients.

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Sensory-motor interactions of human experimental unilateral jaw muscle pain: a quantitative analysis.

Experimental muscle pain was elicited by bolus injection of 0.15 ml of 5% hypertonic saline into the human masseter muscle. The sensory experience was described using 10-cm visual analogue scales (VAS) and the McGill Pain Questionnaires (MPQ) on 10 subjects. Effects of pain on deliberately unilateral mastication were quantitatively assessed in 13 other male subjects using kinematic recordings of the mandible and jaw muscle electromyography (EMG). Jaw movement and EMG data were transformed into single masticatory cycles which were averaged within subjects to produce mean masticatory cycles. Injection of 5% saline through normal and anesthetized skin produced similar VAS profiles and MPQ features. Displacement of the mandible during painful mastication was significantly smaller in the vertical axis (10.0 +/- 11.5%, P < 0.05) and in the lateral axis (22.6 +/- 20.9%, P < 0.05) as compared to pre-pain values. The mean opening and closing velocities of the mandible were significantly reduced (10.5 +/- 16.3% and 15.3 +/- 21.2%, P < 0.05) and the cumulated distance of the jaw movement was also significantly smaller during pain (10.5 +/- 11.8%, P < 0.05). Moreover, agonist EMG activity during pain was significantly lower in the ipsilateral masseter muscle (20.3 +/- 25.4%, P < 0.05) as compared to pre-pain root-mean-square (RMS) values. The observed sensory-motor interactions can be explained by a facilitatory effect of activity in nociceptive muscle afferents on inhibitory brain-stem interneurons during agonist action. Thus, generated movements have smaller amplitudes and they are slower which most likely represents a functional adaptation to experimental jaw muscle pain.

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Quantitative determinations of sensory and pain thresholds on human oral mucosa by argon laser stimulation.

High-energy light from an argon laser was applied to human oral mucosa in order to investigate regional pain sensitivity. Significant regional differences in sensory and pain thresholds were observed between the test sites on the hard and soft palatal mucosa, the buccal mucosa, the tongue, the lower lip, and the skin on the hand. Pain thresholds were lowest on the tip of the tongue and highest on the hard palate. Sensory and pain thresholds were influenced by different stimulus parameters: pulse duration and laser beam diameter. Blackening of the mucosa in regions with high optical reflectance, such as the hard palate, increased light absorption and, hence, reduced both thresholds significantly. Reflectance spectrophotometric measurements indicated that the hard palatal mucosa reflected argon laser light about 1.5 times more than the tip of the tongue. The different threshold values could, in part, be ascribed to different reflectance and absorption properties of the mucosal areas but also indicated substantial regional variation in pain sensitivity of the human oral mucosa. Measurement of laser thresholds is an appropriate and standardized method for investigating sensory differences in human oral mucosa and may be used to study various pain conditions, e.g., burning mouth syndrome.

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