Referred symptom from myofascial pain syndrome: One of the most important causes of sensory disturbance in breast cancer patients using taxanes.

The aim of this retrospective study was to evaluate common causes of upper extremity sensory disturbance in breast cancer patients. Breast cancer patients who received surgery and taxane chemotherapy (CTx) with upper extremity sensory disturbance that began after CTx were included. With comprehensive clinical history, physical examination and electrodiagnostic results, diagnosis for each patient was made. Fifty-two patients were included: 23 (44.2%) were diagnosed with chemotherapy-induced peripheral neuropathy (CIPN), 7 (13.5%) with myofascial pain syndrome (MPS), six (11.5%) with carpal tunnel syndrome (CTS), four (7.7%) with CIPN and MPS, and three (5.8%) with CIPN and CTS. CIPN was more correlated with sensory symptoms at upper and lower extremities, a shorter time from CTx start, and adriamycin and cytoxan (AC) plus paclitaxel, than with AC plus docetaxel and fluorouracil, epirubicin and cyclophosphamide plus taxanes. MPS was correlated with longer duration of CTx and use of hormone therapy. CTS was correlated with wrist trauma history. Patients with CIPN showed similar degrees of pain even after 3 months of treatment, in comparison to the patients with MPS and CTS. When breast cancer patients complain of upper extremity sensory disturbance, various causes, especially referred symptom from MPS, should be considered for effective treatment.

Spatial pain propagation over time following painful glutamate activation of latent myofascial trigger points in humans.

UNLABELLED: The aim of this present study was to test the hypothesis that tonic nociceptive stimulation of latent myofascial trigger points (MTPs) may induce a spatially enlarged area of pressure pain hyperalgesia. Painful glutamate (.2 mL, 1M) stimulation of latent MTPs and non-MTPs in the forearm was achieved by an electromyography-guided procedure. Pain intensity (as rated on the visual analog scale [VAS]) and referred pain area following glutamate injections were recorded. Pressure pain threshold (PPT) was measured over 12 points in the forearm muscles and at the mid-point of tibialis anterior muscle before and at .5 hour, 1 hour, and 24 hours after glutamate injections. The results showed that maximal pain intensity, the area under the VAS curve, and referred pain area were significantly higher and larger following glutamate injection into latent MTPs than non-MTPs (all, P < .05). A significantly lower PPT level was detected over time after glutamate injection into latent MTPs at .5 hour (at 4 points), 1 hour (at 7 points), and 24 hours (at 6 points) in the forearm muscles. However, a significantly lower PPT was observed only at 24 hours after glutamate injection into non-MTPs in the forearm muscles (at 4 points, P < .05) when compared to the pre-injection PPT. PPT at the mid-point of the tibialis anterior was significantly decreased at 1 hour only as compared to the pre-injection PPT in both groups (< .05). The results of the present study indicate that nociceptive stimulation of latent MTPs is associated with an early onset of locally enlarged area of mechanical hyperalgesia. PERSPECTIVE: This study shows that MTPs are associated with an early occurrence of a locally enlarged area of pressure hyperalgesia associated with spreading central sensitization. Inactivation of MTPs may prevent spatial pain propagation.

Comparación entre anestesia general con o sin bloqueo paravertebral preincisional con dosis única y dolor crónico postquirúrgico, en cirugía radical de cáncer de mama / Chronic postoperative pain after general anesthesia with or without a singledose preincisional paravertebral nerve block in radical breast cancer surgery

Objetivo: En la cirugía del cáncer de mama, en más del 50% de las pacientes con mastectomía y/o linfadenectomía persiste el dolor en el primer año. Nuestro objetivo fue determinar la asociación entre la técnica anestésica, la intensidad del dolor agudo postquirúrgico y el desarrollo del dolor crónico postquirúrgico. Pacientes y métodos: Cuarenta pacientes fueron asignadas aleatoriamente a recibir anestesia general o anestesia general con bloqueo paravertebral para mastectomía radical modificada. Se midió el dolor mediante escala visual analógica a los 60 minutos, a las 24 horas y a los 4-5 meses se realizó encuesta de dolor crónico postquirúrgico. Resultados: No hubo diferencias significativas respecto al dolor agudo. Veintinueve pacientes contestaron a la encuesta telefónica. En el grupo del bloqueo paravertebral sólo hubo un caso de dolor neuropático y ninguno de miembro fantasma mientras que en el grupo de anestesia general hubo 7 casos de dolor neuropático asociados a 3 casos de miembro fantasma [6,7% frente a 50%; test exacto de Fischer, p = 0,01, con un RR de 7,5 (IC95% 1,0-53,5)]. Hubo dolor miofascial (contracturas en cuello) en ambos grupos sin diferencias significativas. Conclusiones: A los 4-5 meses de la cirugía la anestesia general con bloqueo paravertebral preincisional presenta menos casos de dolor crónico que sí se utiliza anestesia general y analgesia con cloruro mórfico(AU)

Background and objective: Over 50% of patients still experience pain a year after mastectomy with or without lymphadenectomy. We aimed to determine the association between anesthetic technique, acute postoperative pain intensity, and the development of chronic postoperative pain. Patients and methods: Forty patients were randomly assigned to receive general anesthesia with or without a paravertebral nerve block for modified radical mastectomy. Postoperative pain was assessed on a visual analog scale at 60 minutes and 24 hours; the patients were also asked to respond to a telephone questionnaire on chronic pain 4 to 5 months later. Results: No significant differences in acute pain were observed. Twenty-nine responded to the telephone questionnaire. Only 1 patient in the paravertebral block group reported chronic neuropathic pain and none had phantom breast pain. Only 1 patient (6.7%) in the paravertebral block group reported chronic neuropathic pain and none had phantom breast pain. In the group that received general anesthesia alone, 1 patient reported phantom breast pain and 6 patients had neuropathic pain, associated with phantom breast pain in 2 cases (incidence of chronic pain 50%; P = .01, Fischer exact test; relative risk, 7.5, 95% confidence interval, 1.0-53.5). The incidences of myofascial pain (neck muscle tightness) were similar in the 2 groups. Conclusions: Four to 5 months after mastectomy, fewer cases of chronic pain developed in the group operated under general anesthesia with a preincisional paravertebral block than in the group that received only general anesthesia, with postoperative morphine chloride for analgesia(AU)

Increased spontaneous electrical activity at a latent myofascial trigger point after nociceptive stimulation of another latent trigger point.

OBJECTIVE: To investigate the changes in surface and intramuscular electromyographic (EMG) activity at latent trigger points (TrPs) in the extensor carpi radialis brevis muscle after injection of either glutamate or isotonic saline into latent TrPs in the infraspinatus muscle. METHOD: Nociceptive muscle stimulation was obtained by a bolus injection of glutamate (0.2 mL, 0.5 M) into a latent TrP located in the right infraspinatus muscle in 12 healthy volunteers. A bolus of isotonic saline (0.9%, 0.2 mL) injection served as control. Injections were guided by intramuscular EMG showing resting spontaneous electrical activity at the latent myofascial TrP in the infraspinatus muscle. Intramuscular (at the TrP) and surface EMG activities of both infraspinatus and extensor carpi radialis brevis muscles were recorded before, during, and after injection for a period of 6 minutes to monitor changes produced in EMG activity. RESULTS: Glutamate injection into latent TrPs induced higher pain intensity than isotonic saline injection (P<0.001). The analysis of variance showed a significant increase in root mean square score of intramuscular EMG activity at TrP in the extensor carpi radialis brevis after glutamate (mean+/-SD: 212.0+/-215.6 microV) but not isotonic saline (mean+/-SD: 74.2+/-72.2 microV) injections (P<0.001). No changes in surface EMG activity were found. No significant changes in root mean square of intramuscular and surface EMG activity in the infraspinatus muscle were found. CONCLUSIONS: Our results show that an increased nociceptive activity at latent TrPs in the infraspinatus muscle may increase motor activity and sensitivity of a TrP in distant muscles at a same segmental level.

Nociceptive and non-nociceptive hypersensitivity at latent myofascial trigger points.

OBJECTIVE: The aim of the study was to evaluate whether or not there exists nociceptive and non-nociceptive hypersensitivity at latent myofascial trigger points (MTrPs). METHODS: Eleven healthy volunteers participated in this study, which consisted of 3 sessions of electromyography-guided intramuscular injection with a minimum of a week interval in between. In each session, a bolus of either hypertonic saline (6%, 0.1 mL, each), glutamate (0.1 mL, 0.5 M, each), or isotonic saline (0.9%, 0.1 mL, each) was randomly injected into a latent MTrP and a non-MTrP located in the right or left gastrocnemius medialis muscles. After each injection, participants were asked to rate the perceived pain intensity on an electronic visual analog scale (VAS) and to mark the pain areas on pain drawings. Maximal pain intensity (VAS(peak)), the area under the curve (VAS(auc)), and local and referred pain areas were extracted. RESULTS: Injections of either hypertonic saline, glutamate, or isotonic saline into the latent MTrPs induced a higher VAS(peak) and larger VAS(auc) than the non-MTrPs (all, P<0.05). Furthermore, the MTrPs with referred pain after painful injections were found to show higher VAS(peak) and larger VAS(auc) than those without referred pain (both, P<0.001). CONCLUSIONS: These results confirm the existence of nociceptive hypersensitivity at latent MTrPs and provide the first evidence that there exists non-nociceptive hypersensitivity (allodynia) at latent MTrPs. Finally, the occurrence of referred muscle pain is associated with higher pain sensitivity at latent MTrPs.

Evaluation of sympathetic vasoconstrictor response following nociceptive stimulation of latent myofascial trigger points in humans.

AIM: Myofascial trigger points (MTrPs) are a major cause of musculoskeletal pain. It has been reported that stimulation of a latent MTrP increases motor activity and facilitates muscle pain via activation of the sympathetic nervous system. However, the magnitude of the sympathetic vasoconstrictor response following stimulation of MTrP has not been studied in healthy volunteers. The aims of this study were to (1) evaluate the magnitude of the vasoconstrictor response following a nociceptive stimulation (intramuscular glutamate) of MTrPs and a breath-hold manoeuvre (activation of sympathetic outflow) and (2) assess whether the vasoconstrictor response can be further modulated by combining a nociceptive stimulation of MTrPs and breath-hold. METHODS: Fourteen healthy subjects were recruited in this study. This study consisted of four sessions (normal breath group as control, breath-hold group, glutamate MTrP injection group and glutamate MTrP injection + breath-hold group). Skin blood flow and skin temperature in both forearms were measured with laser Doppler flowmetry and infrared thermography, respectively, in each session (before the treatment, during the treatment and after the treatment). RESULTS: Glutamate injection into MTrPs decreased skin temperature and blood flow in the peripheral area. The magnitudes of the reduction were comparable to those induced by the breath-hold manoeuvre, which has been used to induce sympathetic vasoconstrictor response. CONCLUSION: The combination of glutamate injection into latent MTrPs together with the breath-hold manoeuvre did not result in further decrease in skin temperature and blood flow, indicating that sympathetic vasoconstrictor activity is fully activated by nociceptive stimulation of MTrPs.

Acidic buffer induced muscle pain evokes referred pain and mechanical hyperalgesia in humans.

While tissue acidosis causes local deep-tissue pain, its effect on referred pain and mechanical muscle hyperalgesia is unknown. The aim of this study was to investigate a human experimental acidic muscle pain model using a randomized, controlled, single-blinded study design. Seventy-two subjects (36 female) participated in three visits, each involving one 15 min intramuscular infusion into the anterior tibialis muscle: acidic phosphate buffer (pH 5.2) at 40 ml/h (N=69) or 20 ml/h (N=54), normal phosphate buffer (pH 7.3) at 40 ml/h (N=70), or isotonic saline at 40 ml/h (N=19). Pain ratings and pressure sensitivity of superficial and deep tissues were assessed before, during, and 20 min after infusion. Acidic buffer produced light to moderate, rate-dependent, muscle pain (not sex-dependent) compared to the control infusions, that referred pain to the ankle in 80% of women and 40% of men. Pain did not vary across self-reported menstrual phases. Pressure pain thresholds (PPTs) were reduced over the infused muscle with acidic infusion, defined as primary mechanical hyperalgesia. PPTs decreased at the ankle in those with referred pain in response to acidic buffer, i.e. referred mechanical hyperalgesia, but not at the foot. No pain or changes in PPTs occurred in the contralateral leg. These results demonstrate muscle acidosis can lead to local and referred pain and hyperalgesia, with significant sex differences in development of referred pain.

Induction of muscle cramps by nociceptive stimulation of latent myofascial trigger points.

The aim of this present study is to test the hypothesis that nociceptive stimulation of latent myofascial trigger points (MTrPs) increases the occurrence of local muscle cramps. Nociceptive muscle stimulation was obtained by a bolus injection of glutamate (0.1 ml, 0.5 M) into a latent MTrP and a control point (a non-MTrP) located in the right or left gastrocnemius medialis muscles in 14 healthy subjects. A bolus of isotonic saline (0.9%, 0.1 ml) injection served as a control. The injections were guided by intramuscular electromyography (EMG) showing resting spontaneous electrical activity at a latent MTrP and no such activity at a non-MTrP. Intramuscular and surface EMG activities in the gastrocnemius medialis muscle were recorded pre-, during-, and post-injection for a period of 8 min to monitor the occurrence of muscle cramps, which are characterized by a brief episodic burst of high levels of EMG activity. The results showed that glutamate and isotonic saline injections into the latent MTrPs induced higher peak pain intensity than into the non-MTrPs (both P < 0.05). Glutamate injection induced higher peak pain intensity than isotonic saline injection into either latent MTrPs or non-MTrPs (both P < 0.05). Muscle camps were observed in 92.86% of the subjects following glutamate injection into the latent MTrPs, but not into the non-MTrPs (P < 0.001). No muscle cramps were recorded following isotonic saline injection into either the latent MTrPs or the non-MTrPs. These results suggest that latent MTrPs could be involved in the genesis of muscle cramps. Focal increase in nociceptive sensitivity at MTrPs constitutes one of the mechanisms underlying muscle cramps.

AlOH3-adjuvanted vaccine-induced macrophagic myofasciitis in rats is influenced by the genetic background.

Macrophagic myofasciitis (MMF) is a specific histopathologic lesion involved in the persistence for years of aluminum hydroxide [Al(OH)(3)] at the site of previous intramuscular (i.m.) injection. In order to study mechanisms involved persistence of MMF lesions, we set up an experimental model of MMF-lesion in Sprague-Dawley and Lewis rat, by i.m. injections of 10 microL of an Al(OH)(3)-adjuvanted vaccine. An evaluation carried out over a 12-month period disclosed significant shrinkage of MMF lesions with time. A radioisotopic study did not show significant aluminium uptake by Al(OH)(3)-loaded macrophages. A morphometric approach showed that Lewis rats with Th1-biased immunity had significantly smaller lesions than Sprague-Dawley rats with balanced Th1/Th2 immunity. Concluding, our results indicate that genetic determinatives of cytotoxic T-cell responses could interfere with the clearance process and condition the persistence of vaccine-induced MMF-lesions.

Referred pain and hyperalgesia in human tendon and muscle belly tissue.

The sensitivity of tendon and tendon-bone junction is not fully described although these tissues have high clinical impacts. This study assessed (1) pain intensity and referred pain caused by hypertonic saline injection to the proximal tendon-bone junction (PTBJ), tendon and muscle belly sites of tibialis anterior muscle and (2) pressure pain sensitivity, pre, during and post hypertonic saline injections. Eighteen subjects (14 males and 4 females) participated. Subjects also had constant mechanical stimulation for 120s at 130% of baseline pressure pain threshold (PPT) during which VAS parameters were recorded. VAS parameters after hypertonic saline for PTBJ (VAS area, VAS peak), and tendon sites (VAS area, duration and time to maximum VAS) were significantly (P < 0.05) higher than muscle belly. During hypertonic saline pain all three sites displayed local and frequently enlarged and referred pain areas. Hypertonic saline pain at the PTBJ and tendon transiently increased pressure sensitivity at these sites (P < 0.05). When referred pain was caused by mechanical stimulation it occurred predominantly at the PTBJ and tendon sites (86% cases). Constant mechanical stimulation caused steadily increasing pain (summation of pain) at all sites. Hypertonic saline pain at the tendon and PTBJ caused significantly higher (P < 0.001) final VAS scores compared to the muscle belly site. The results indicate the PTBJ and tendon sites are more sensitive and susceptible to sensitisation by hypertonic saline than muscle belly. Furthermore, there may be site specific central changes reflected by the differences in the results regarding sensitivity and summation over time.

Excitatory amino acid concentrations increase in the spinal cord dorsal horn after repeated intramuscular injection of acidic saline.

Chronic muscle pain is common and often difficult to treat. In this study, we further characterize a model of chronic muscle pain induced by repeated intramuscular injection of acidic saline. Two injections of acid into muscle separated by 5 days result in secondary mechanical hyperalgesia that lasts for up to 4 weeks. Blockade of spinal NMDA receptors prior to the second injection intramuscular acid injection delays the onset of hyperalgesia, where as the maintenance phase of hyperalgesia, evaluated 1 week after the second intramuscular injection, is dependent on activation of spinal AMPA/kainate and NMDA receptors. In order to determine if behavioral hyperalgesia and glutamate receptor involvement are associated with increased concentrations of excitatory amino acids (EAA), we utilized microdialysis to evaluate extracellular glutamate and aspartate concentrations in the spinal dorsal horn during the first and second intramuscular acid injections, and 1 week after the development of mechanical hyperalgesia. The second intramuscular injection evoked a calcium-dependent increase in both spinal glutamate and aspartate concentrations. Glutamate concentrations within the dorsal horn were also increased 1 week after the second acid injection. Our data suggest increased release of spinal EAAs in the dorsal horn contributes to the development and maintenance of hyperalgesia.

Low frequency therapeutic EMF differently influences experimental muscle pain in female and male subjects.

Effects of a pulsating, half sine wave magnetic field (MF) with a frequency of 100 pps and 15 mT rms flux density, generated by the MD TEMF device (EMF Therapeutics, Inc., Chattanooga), on subjective pain rating, heart rate, and arterial blood pressure were tested in a double blind, crossover design study employing experimental muscle pain. Each of 24 healthy volunteers (12 females and 12 males, 24.7 +/- 3.2 years of age) received painful stimulation induced by the infusion of 5% hypertonic saline (HS) into the erector spinae muscle during real and sham MF exposure, in counterbalanced order. Exposure to MF differently affects subjective pain estimates in females and males. MF exposure increased averaged pain level and time integral of pain ratings in females, whereas no statistically significant difference for these characteristics was found in males. Pain related elevation of systolic and diastolic blood pressure was observed during both real and sham EMF exposure in female and male subjects.

Experimental muscle pain reduces initial motor unit discharge rates during sustained submaximal contractions.

The aim of this human study was to investigate the effect of experimentally induced muscle pain on the modifications of motor unit discharge rate during sustained, constant-force contractions. Intramuscular and multichannel surface electromyographic (EMG) signals were collected from the right and left tibialis anterior muscle of 11 volunteers. The subjects performed two 4-min-long isometric contractions at 25% of the maximal dorsiflexion torque, separated by a 20-min rest. Before the beginning of the second contraction, hypertonic (painful; right leg) or isotonic (nonpainful; left leg) saline was injected into the tibialis anterior. Pain intensity scores did not change significantly in the first 150 s of the painful contraction. Exerted torque and its coefficient of variation were the same for the painful and nonpainful contractions. Motor unit discharge rate was higher in the beginning of the nonpainful contraction than the painful contraction on the right side [means +/- SE, 11.3 +/- 0.2 vs. 10.6 +/- 0.2 pulses/s (pps); P < 0.01] whereas it was the same for the two contractions on the left side (11.6 +/- 0.2 vs. 11.5 +/- 0.2 pps). The decrease in discharge rate in 4 min was smaller for the painful (0.4 +/- 0.1 pps) than for the control contractions (1.3 +/- 0.1 pps). Initial value and decrease in motor unit conduction velocity were not different in the four contractions (right leg, 4.0 +/- 0.1 m/s with decrease of 0.6 +/- 0.1 m/s in 4 min; left leg, 4.1 +/- 0.1 m/s with 0.7 +/- 0.1 m/s decrease). In conclusion, stimulation of nociceptive afferents by injection of hypertonic saline did not alter motor unit conduction velocity but reduced the initial motor unit discharge rates and the difference between initial and final discharge rates during sustained contraction.

Experimental muscle pain and tenderness following infusion of endogenous substances in humans.

Several human models of myofascial pain exist, but none are similar to clinical pain. The aim of the present study was to develop a clinically relevant model of prolonged human myofascial pain using infusion of the naturally occurring endogenous substances. Initially, bradykinin (Bk), serotonin (5-hydroxytryptamine (5-HT)), histamine (His), prostaglandin E(2) (PGE(2)), adenosine-tri-phosphate (ATP), and their combinations were infused into the trapezius muscle of 36 healthy subjects in a total of 67 sessions to identify substances, which could induce a moderate muscle pain. PGE(2), ATP, and a combination of Bk, 5-HT, His, and PGE(2) produced the intended moderate pain. These substances were further examined in a randomised, blinded, placebo-controlled dose-finding design in 15 healthy subjects in 68 sessions. PGE(2) (3, 6, and 12 nmol/ml) induced mild pain and tenderness not different from placebo. ATP (9000, 18,000, and 36,000 nmol/ml) induced pain of moderate to strong intensity (P=0.04) and the dose of 18,000 nmol/ml furthermore produced moderate local tenderness (P=0.04). Because of unacceptable side effects in subsequent examinations, further studies of ATP in humans were suspended. Infusion of the combination of Bk (92 nmol), 5-HT (156 nmol), His (140 nmol), and PGE(2) (1.95 nmol) produced a moderate pain intensity (P=0.04) and mild tenderness (P=0.04) without inducing unacceptable side effects. Intramuscular infusion of a combination of Bk, 5-HT, His, and PGE(2) induced a prolonged moderate pain and tenderness in healthy humans, and this model may be a valuable tool in future studies of the pathophysiological mechanisms of myofascial pain.

Lesions of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation.

In skeletal muscle, a local increase of acetylcholine (ACh) in a few end plates has been hypothesized to cause the formation of contraction knots that can be found in myofascial trigger points. To test this hypothesis in rats, small amounts of an acetylcholinesterase inhibitor [diisopropylfluorophosphate (DFP)] were injected into the proximal half of the gastrocnemius muscle, and the muscle nerve was electrically stimulated for 30-60 min for induction of muscle twitches. The distal half of the muscle, which performed the same contractions, served as a control to assess the effects of the twitches without DFP. Sections of the muscle were evaluated for morphological changes in relation to the location of blocked end plates. Compared with the distal half of the muscle, the DFP-injected proximal half exhibited significantly higher numbers of abnormally contracted fibers (local contractures), torn fibers, and longitudinal stripes. DFP-injected animals in which the muscle nerve was not stimulated and that were allowed to survive for 24 h exhibited the same lesions but in smaller numbers. The data indicate that an increased concentration of ACh in a few end plates causes damage to muscle fibers. The results support the assumption that a dysfunctional end plate exhibiting increased release of ACh may be the starting point for regional abnormal contractions, which are thought to be essential for the formation of myofascial trigger points.

Experimental muscle pain produces central modulation of proprioceptive signals arising from jaw muscle spindles.

The aim of the present study was to investigate the effects of intramuscular injection with hypertonic saline, a well-established experimental model for muscle pain, on central processing of proprioceptive input from jaw muscle spindle afferents. Fifty-seven cells were recorded from the medial edge of the subnucleus interpolaris (Vi) and the adjacent parvicellular reticular formation from 11 adult cats. These cells were characterized as central units receiving jaw muscle spindle input based on their responses to electrical stimulation of the masseter nerve, muscle palpation and jaw stretch. Forty-five cells, which were successfully tested with 5% hypertonic saline, were categorized as either dynamic-static (DS) (n=25) or static (S) (n=20) neurons based on their responses to different speeds and amplitudes of jaw movement. Seventy-six percent of the cells tested with an ipsilateral injection of hypertonic saline showed a significant modulation of mean firing rates (MFRs) during opening and/or holding phases. The most remarkable saline-induced change was a significant reduction of MFR during the hold phase in S units (100%, 18/18 modulated). Sixty-nine percent of the DS units (11/16 modulated) also showed significant changes in MFRs limited to the hold phase. However, in the DS neurons, the MFRs increased in seven units and decreased in four units. Finally, five DS neurons showed significant changes of MFRs during both opening and holding phases. Injections of isotonic saline into the ipsilateral masseter muscle had little effect, but hypertonic saline injections made into the contralateral masseter muscle produced similar results to ipsilateral injections with hypertonic saline. These results unequivocally demonstrate that intramuscular injection with an algesic substance, sufficient to produce muscle pain, produces significant changes in the proprioceptive properties of the jaw movement-related neurons. Potential mechanisms involved in saline-induced changes in the proprioceptive signals and functional implications of the changes are discussed.

Evidence for subnucleus interpolaris in craniofacial muscle pain mechanisms demonstrated by intramuscular injections with hypertonic saline.

The subnucleus interpolaris (Vi) has been identified as a major recipient for trigeminal ganglionic input from jaw muscles, and contains neurons with nociceptive properties similar to those in the subnucleus caudalis (Vc). Therefore, Vi may be another important site for processing craniofacial muscle nociception. The aims of present study were to define functional properties of Vi neurons that receive input from masseter muscle afferents by characterizing their responses to electrical, mechanical, and to chemical stimulation of the muscle. Ninety cells were identified as masseter muscle units in 11 adult cats. Most of these units (79%) received additional inputs from orofacial skin. Following the intramuscular injection of 5% hypertonic saline, 49% of the cells showed a significant modulation of either the resting discharge and/or responses to innocuous mechanical stimulation on their cutaneous receptive fields (RFs). The most common response to saline injection was an induction or facilitation of resting discharge which declined as an exponential decay function, returning to pre-injection level within 3-4 min. Forty-five percent of the muscle units that were tested with mechanical stimulation (13/29) showed a prolonged inhibition of mechanically-evoked responses. In most cases (8/13), the inhibitory response was accompanied by initial facilitation. The observations that Vi contained a population of neurons that receive small diameter muscle afferent inputs, responded to noxious mechanical stimulation on the muscle and to a chemical irritant that is known to produce pain in humans provide compelling evidence for the involvement of Vi in craniofacial muscle pain mechanisms.

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.

Exacerbation of soft tissue rheumatism by excess vitamin A: case reviews with clinical vignette.

In certain situations, health problems can arise if physicians are not aware of over-the-counter medications and vitamins a patient may be taking in addition to their regular prescriptions. Since many people do not consider OTC drugs to be medications, they often do not relay this information while discussing their medical histories. This article describes how the symptoms of soft tissue rheumatism can become worse if patients ingest an excess amount of vitamin A.