Intramuscular Injection Of Hypertonic Saline Research Articles

Intra- and interindividual reliability of muscle pain induced by an intramuscular injection of hypertonic saline injection into the quadriceps.

Intramuscular injections of hypertonic saline are commonly used to induce experimental muscle pain, but reliability data on this technique are lacking. This study investigated the intra- and interindividual reliability of pain measures from a hypertonic saline injection into the vastus lateralis. Fourteen healthy participants (6 female) attended three laboratory visits where they received an intramuscular injection of 1 mL hypertonic saline into the vastus lateralis. Changes in pain intensity were recorded on an electronic visual analogue scale, and pain quality was assessed after pain had resolved. Reliability was assessed with the coefficient of variation (CV), minimum detectable change (MDC) and intraclass correlation coefficient (ICC) with 95% CIs. Mean pain intensity displayed high levels of intraindividual variability (CV = 16.3 [10.5-22.0]%) and 'poor' to 'very good' relative reliability (ICC = 0.71 [0.45-0.88]) but had a MDC of 11 [8-16] au (out of 100). Peak pain intensity exhibited high levels of intraindividual variability (CV = 14.8 [8.8-20.8]%) with 'moderate' to 'excellent' levels of relative reliability (ICC = 0.81 [0.62-0.92]), whereas the MDC was 18 [14-26] au. Measures of pain quality exhibited good reliability. Interindividual variability in pain measures was high (CV > 37%). Intramuscular injections of 1 mL of hypertonic saline into the vastus lateralis display substantial levels of interindividual variability, but MDC is below the clinically important changes in pain. This model of experimental pain is suitable for studies involving repeated exposures. Many pain research studies have performed intramuscular injections of hypertonic saline to investigate responses to muscle pain. However, the reliability of this technique is not well established. We examined the pain response over three repeated sessions of a hypertonic saline injection. The pain induced by hypertonic saline has considerable interindividual variability but has largely acceptable intraindividual reliability. Therefore, the injections of hypertonic saline to induce muscle pain are a reliable model of experimental muscle pain.

Muscle pain from an intramuscular injection of hypertonic saline increases variability in knee extensor torque reproduction.

The intensity of exercise-induced pain (EIP) reflects the metabolic environment in the exercising muscle, so during endurance exercise, this may inform the intelligent regulation of work rate. Conversely, the acute debilitating effects of EIP on motor unit recruitment could impair the estimation of force produced by the muscle and impair judgement of current exercise intensity. This study investigated whether muscle pain that feels like EIP, administered via intramuscular injection of hypertonic saline, interferes with the ability to accurately reproduce torque in a muscle group relevant to locomotive exercise. On separate days, 14 participants completed an isometric torque reproduction task of the knee extensors. Participants were required to produce torque at 15% and 20% maximal voluntary isometric torque (MVIT), without visual feedback before (baseline), during (pain/no pain), and after (recovery) an injection of 0.9% isotonic saline (Control) or 5.8% hypertonic saline (Experimental) into the vastus lateralis of the right leg. An elevated reported intensity of pain, and a significantly increased variance in mean contraction torque at both 15% (P = 0.049) and 20% (P = 0.002) MVIT was observed in the Experimental compared to the Control condition. Both 15 and 20% target torques were performed at a similar pain intensity in the Experimental condition (15% MVIT: 4.2 ± 1.9; 20% MVIT: 4.5 ± 2.2; P > 0.05). These findings demonstrate that the increased muscle pain from the injection of hypertonic saline impeded accurate reproduction of knee extensor torque. These findings have implications for the detrimental impact of EIP on exercise regulation and endurance performance.NEW & NOTEWORTHY We provide novel data demonstrating that the presence of muscle pain interferes with estimations of torque produced by the knee extensors, which could impair judgment of work rate during endurance exercise. The novelty of our study is in the application of the hypertonic saline experimental model into a quadriceps muscle during short, submaximal isometric contractions at an intensity that provides a more translatable assessment of the impact of exercise-induced pain on work-rate regulation during whole body exercise.

Light Touch Contact Improves Pain-Evoked Postural Instability During Quiet Standing

To investigate if attention to additional sensory information from the fingertip can improve postural stability during pain, which is known to impair balance. In 16 healthy volunteers, experimental pain was induced by intramuscular injection of hypertonic saline in the right vastus medialis muscle (isotonic saline used as nonpainful control, intramuscular injection in the same location). Pain intensity was assessed on an 11-point numeric rating scale (NRS; 0 representing "no pain" and 10 "maximum pain"). Subjects were asked to stand as still as possible on a force plate for 40 seconds with their eyes closed. Their postural stability was quantified by the area and velocity of center of pressure (CoP) displacement. The CoP was recorded with and without pain during two different conditions: 1) no touch and 2) the subjects were asked to lightly touch a curtain with their right index finger and focus their attention on keeping it as still as possible. Hypertonic injections induced higher NRS scores compared with control injections (P < 0.05). During the hypertonic injection condition, the CoP area and velocity in both directions increased during no touch compared with the light touch condition (P < 0.05). No differences were found during light touch between the hypertonic and isotonic injection conditions. Although experimental knee-related pain impaired postural stability, lightly touching a curtain with the fingertip decreased postural sway during painful conditions. Providing additional sensory information while pain patients are performing balance exercises may improve postural stability and increase the quality of exercise, consequent rehabilitation protocols, and clinical outcomes.

Minocycline Prevents Muscular Pain Hypersensitivity and Cutaneous Allodynia Produced by Repeated Intramuscular Injections of Hypertonic Saline in Healthy Human Participants.

Four repeated injections of HS at 48-hour intervals induce a state of persistent hypersensitivity in healthy human participants. This hypersensitivity was characterized by bilateral muscular hyperalgesia and cutaneous cold allodynia, symptoms commonly reported in many chronic pain conditions. Minocycline pretreatment abolished the development of this state.

Abnormal Spontaneous Brain Activity in Acute Low-Back Pain Revealed by Resting-State Functional MRI.

Neuroimaging studies have revealed that low-back pain (LBP) alters spatiotemporal dynamics of the blood oxygen level-dependent signal in response to persistent noxious stimulus. This study aimed to investigate changes in spontaneous neural activity of various brain regions in acute LBP using resting-state functional magnetic resonance imaging and amplitude of low-frequency fluctuation (ALFF). Twelve healthy subjects underwent two separate resting-state functional magnetic resonance imaging scans at health status as baseline and after intramuscular injection of hypertonic saline (0.5 mL, 5%) into the back muscles to induce acute LBP. Compared with baseline, acute LBP showed decreased ALFF in the right posterior cingulate cortex/precuneus and left primary somatosensory cortex (S1) but increased ALFF in the right medial prefrontal cortex, right middle temporal gyrus, bilateral inferior temporal gyrus, bilateral insula, right anterior cingulate cortex, and left cerebellum. In addition, significant negative correlations were observed between visual analog scale scores and ALFF of the bilateral medial prefrontal cortex, left inferior frontal gyrus, left S1, right anterior cingulate cortex, and left middle temporal gyrus. These findings suggest that abnormally spontaneous neural activity involving some brain regions are responsible for sensory, affective, and cognitive functions, which may be implicated in the underlying pathophysiology of acute LBP.

Pain inhibits pain; human brainstem mechanisms

Conditioned pain modulation is a powerful analgesic mechanism, occurring when a painful stimulus is inhibited by a second painful stimulus delivered at a different body location. Reduced conditioned pain modulation capacity is associated with the development of some chronic pain conditions and the effectiveness of some analgesic medications. Human lesion studies show that the circuitry responsible for conditioned pain modulation lies within the caudal brainstem, although the precise nuclei in humans remain unknown. We employed brain imaging to determine brainstem sites responsible for conditioned pain modulation in 54 healthy individuals. In all subjects, 8 noxious heat stimuli (test stimuli) were applied to the right side of the mouth and brain activity measured using functional magnetic resonance imaging. This paradigm was then repeated. However, following the fourth noxious stimulus, a separate noxious stimulus, consisting of an intramuscular injection of hypertonic saline into the leg, was delivered (conditioning stimulus). During this test and conditioning stimulus period, 23 subjects displayed conditioned pain modulation analgesia whereas 31 subjects did not. An individual's analgesic ability was not influenced by gender, pain intensity levels of the test or conditioning stimuli or by psychological variables such as pain catastrophizing or fear of pain. Brain images were processed using SPM8 and the brainstem isolated using the SUIT toolbox. Significant increases in signal intensity were determined during each test stimulus and compared between subjects that did and did not display CPM analgesia (p<0.05, small volume correction). The expression of analgesia was associated with reduction in signal intensity increases during each test stimulus in the presence of the conditioning stimulus in three brainstem regions: the caudalis subdivision of the spinal trigeminal nucleus, i.e., the primary synapse, the region of the subnucleus reticularis dorsalis and in the dorsolateral pons in the region of the parabrachial nucleus. Furthermore, the magnitudes of these signal reductions in all three brainstem regions were significantly correlated to analgesia magnitude. Defining conditioned pain modulation circuitry provides a framework for the future investigations into the neural mechanisms responsible for the maintenance of persistent pain conditions thought to involve altered analgesic circuitry.

Autonomic responses to exercise: cortical and subcortical responses during post-exercise ischaemia and muscle pain.

Sustained isometric contraction of skeletal muscle causes an increase in blood pressure, due to an increase in cardiac output and an increase in total peripheral resistance-brought about by an increase in sympathetically-mediated vasoconstriction. Both central command and reflex inputs from metaboreceptors in the contracting muscles have been shown to contribute to this sympathetically mediated increase in blood pressure. Occluding the blood supply and trapping the metabolites in the contracted muscle (post-exercise ischaemia) has shown that, while heart rate returns to baseline following exercise, the increase in MSNA and blood pressure persists in the absence of central command-sustained by peripheral inputs. Post-exercise ischaemia activates group III and IV muscle afferents, which are also activated during noxious stimulation. Indeed, post-exercise ischaemia is painful, so what is the role of pain in the increase in blood pressure? Intramuscular injection of hypertonic saline causes a deep dull ache, not unlike that produced by post-exercise ischaemia, and we have shown that this can cause a sustained increase in MSNA and blood pressure. We have used functional Magnetic Resonance Imaging (fMRI) of the brain to identify the cortical and subcortical sites involved in the sensory processing of muscle pain, and in the generation of the autonomic responses to muscle pain, produced either by post-exercise ischaemia or intramuscular injection of hypertonic saline. During static hand-grip exercise there were parallel increases in signal intensity in the contralateral primary motor cortex, deep cerebellar nuclei and cerebellar cortex that ceased at the end of the exercise, reflecting the start and end of central command. Progressive increases during the contraction phase occurred in the contralateral insula, as well as the contralateral primary somatosensory cortex, and continued during the period of post-exercise ischaemia. Decreases in signal intensity occurred in the perigenual anterior cingulate cortex during the contraction phase; these too were sustained during post-exercise ischaemia. That similar changes occurred with intramuscular injection of hypertonic saline suggests that much of the cortical and subcortical changes seen during post-exercise ischaemia reflect the sensory and affective attributes of the muscle pain, rather than in furnishing the cardiovascular responses per se.

Resting-state connectivity in the default mode network and insula during experimental low back pain.

Functional magnetic resonance imaging studies have shown that the insular cortex has a significant role in pain identification and information integration, while the default mode network is associated with cognitive and memory-related aspects of pain perception. However, changes in the functional connectivity between the default mode network and insula during pain remain unclear. This study used 3.0 T functional magnetic resonance imaging scans in 12 healthy subjects aged 24.8 ± 3.3 years to compare the differences in the functional activity and connectivity of the insula and default mode network between the baseline and pain condition induced by intramuscular injection of hypertonic saline. Compared with the baseline, the insula was more functionally connected with the medial prefrontal and lateral temporal cortices, whereas there was lower connectivity with the posterior cingulate cortex, precuneus and inferior parietal lobule in the pain condition. In addition, compared with baseline, the anterior cingulate cortex exhibited greater connectivity with the posterior insula, but lower connectivity with the anterior insula, during the pain condition. These data indicate that experimental low back pain led to dysfunction in the connectivity between the insula and default mode network resulting from an impairment of the regions of the brain related to cognition and emotion, suggesting the importance of the interaction between these regions in pain processing.

Predicting the spatiotemporal expression of local and referred acute muscle pain in individual subjects

While current data suggest that all referred pain derives from common mechanisms of central sensitisation, there is a paucity of data directly comparing referral in different limbs. Does a common mechanism result in similar precepts of referral from similar stimuli in different limbs? We tested the hypothesis that, in a given subject, the incidence, intensity and spatiotemporal expression of referred pain are similar during the muscle pain induced by bolus intramuscular injection of hypertonic saline into flexor carpi radialis (FCR) and tibialis anterior (TA). We also tested the hypothesis that an increase in stimulus intensity causes a parallel increase in the incidence and intensity of local and referred pain, by comparing the responses to 5 and 10% hypertonic saline in two groups of subjects. 29 subjects mapped areas of local and referred pain, rating intensities on a visual analogue scale every 30s until the cessation of pain. Following an injection of 5% hypertonic saline into TA, 86% of subjects who had previously reported referred pain (or its absence) in the hand during FCR pain reported referred pain (or its absence) in the foot. Following an injection of the 10% solution, 67% of subjects reported a pattern in the lower limb that was the same as that seen in the upper limb. We conclude that the expression of referred pain is largely consistent in widely separated limb segments in individual subjects and is largely dependent on inter-subject differences. This may have implications for the development of chronic pain following an acute episode of pain.

Individual differences in the cardiovascular responses to tonic muscle pain: parallel increases or decreases in muscle sympathetic nerve activity, blood pressure and heart rate

We recently showed that acute muscle pain, induced by bolus intramuscular injection of hypertonic saline, causes a sustained increase in muscle sympathetic nerve activity (MSNA) and a modest increase in blood pressure and heart rate. However, it is not known whether long-lasting (tonic) pain, which more closely resembles chronic pain, causes a sustained increase in MSNA and blood pressure. We tested this hypothesis by recording MSNA in 12 healthy subjects. Tonic pain was induced for ~60 min by slow intramuscular infusion of hypertonic saline (7%) into the ipsilateral tibialis anterior muscle. Pain was sustained at a tolerable level (5/10 to 6/10 on a visual analog scale). Seven subjects showed progressive increases in mean MSNA amplitude during tonic pain, increasing to 154 ± 17% (SEM) at 45 min and remaining essentially constant for the duration of the infusion. In these subjects, blood pressure and heart rate also increased. Conversely, for the other five subjects MSNA showed a progressive decline, with a peak fall of 67 ± 11% at 40 min; blood pressure and heart rate also fell in these subjects. We conclude that tonic muscle pain has long-lasting effects on the sympathetic control of blood pressure, causing a sustained increase in some subjects yet a sustained decrease in others. This may have implications for individual differences in the cardiovascular consequences of chronic pain.

Adaptations in the gait pattern with experimental hamstring pain

Pain changes movement but most studies have focused on basic physiological adaptations during non-functional movement tasks. The existing studies on how pain affects lower extremity gross movement biomechanics have primarily involved movements in which the quadriceps is the primary muscle and little attention has been given to how pain in other muscles affects functional movement. The purpose of this study was to investigate the changes in the gait patterns of healthy subjects that occur during experimental muscle pain in the biceps femoris. In a cross-over study design, 14 healthy volunteers underwent EMG assisted 3D gait analyses before, during and after experimental biceps femoris pain induced by intramuscular injections of hypertonic saline. Isotonic saline injections were administered as a non-painful control. The experimental biceps femoris pain led to reductions in hip extensor moments, knee flexor and lateral rotator moments. No changes in lower extremity kinematics and EMG activity in any of the recorded muscles were observed. It is concluded that experimental muscle pain in the biceps femoris leads to changes in the gait pattern in agreement with unloading of the painful muscle. The changes are specific to the painful muscle. The present study provides support to the theory that musculoskeletal pain is a protective signal leading to changes in movement patterns that serve to unload the painful tissue.

Pain-induced Changes in the Activity of the Cervical Extensor Muscles Evaluated by Muscle Functional Magnetic Resonance Imaging

To investigate the effect of experimental neck muscle pain on the activation of the cervical extensor muscles during the performance of a cervical extension exercise by the use of muscle functional magnetic resonance imaging. The activity of the multifidus, semispinalis cervicis, semispinalis capitis, and splenius capitis muscles was investigated bilaterally at 2 cervical levels (C2 to C3 and C7 to T1) in 15 healthy individuals. Measurements were taken at rest and after the performance of a cervical extension exercise without and with induced pain of the right upper trapezius (intramuscular injection of hypertonic saline). In the pain condition, the activity of the multifidus/semispinalis cervicis was reduced bilaterally at the C7 to T1 level (P=0.045). For the semispinalis capitis, there were no significant differences between both conditions. The splenius capitis showed a significantly higher T2 shift at the left side at the C2 to C3 level (P=0.008) and a lower T2 shift at the right side at the C7 to T1 level (P=0.023). This is the first study that has shown pain to immediately affect the activity of both deep and superficial cervical extensor muscle layers during a cervical extension exercise. The findings support recommendations for evaluation of cervical extensor muscle function early in the management of painful cervical spine injuries.

Functional reorganization of cervical flexor activity because of induced muscle pain evaluated by muscle functional magnetic resonance imaging

There is mounting evidence of an association between chronic neck pain and impaired cervical flexor muscle performance. It is likely that the deep cervical flexors demonstrate changes very early after the onset of pain, but evidence is currently lacking. This study investigated the effect of experimental neck muscle pain on the activation of the cervical flexor muscles during the performance of craniocervical flexion (CCF) by use of muscle functional magnetic resonance imaging. Activity of the longus colli (Lco), longus capitis (Lca) and sternocleidomastoid (SCM) muscles were investigated bilaterally and at three cervical levels (C0–C1, C2–C3 and C6–C7) in 14 healthy subjects. Measurements were performed at rest and after the performance of CCF without and with induced pain of the upper trapezius (intramuscular injection of hypertonic saline). In the non-pain condition, the Lca (p = 0.005) and Lco (p = 0.029) were significantly more active during CCF compared to SCM. In the pain condition, the activity of the Lco and Lca was reduced bilaterally and at multiple levels (p ≤ 0.009), whereas the left SCM showed increased activity at only the C6–C7 level (p ≤ 0.001). The results suggest that local excitation of nociceptive afferents causes an immediate reorganization of the cervical flexor muscle activity similar to that identified in clinical populations.

Experimental calf muscle pain attenuates the postural stability during quiet stance and perturbation

Background The purpose of this study was to evaluate how acute pain changes the postural control and stability during quiet standing and after unexpected perturbations. Methods Nine subjects stood as quiet as possible on a movable force platform that recorded the centre of pressure position and provided unexpected floor perturbations, before, during and after experimental calf muscle pain. Bilateral surface electromyography from the tibialis anterior and medial gastrocnemius muscles was recorded. The foot pressure distributions were measured using pressure insoles. Intramuscular injections of hypertonic saline were administrated (right leg) to induce acute pain in the tibialis anterior and/or medial gastrocnemius muscles, and an isotonic injection was used as control. Findings Simultaneous pain in tibialis anterior and medial gastrocnemius altered the postural control. During quiet standing: higher medial-lateral centre of pressure speed and increased total sway displacement ( P < 0.05), weight moved to the non-painful side, ( P < 0.05) and plantar centre of pressure of the left foot was shifted towards the heel’s direction ( P < 0.05). During forward perturbation: higher mean displacement in the medial-lateral direction ( P < 0.05). After the perturbation: larger sway area ( P < 0.05). Pain only in the medial gastrocnemius muscle increased medial-lateral centre of pressure speed ( P < 0.05) during the quiet standing. Pain only in the tibialis anterior muscle increased peak pressure on the contralateral foot ( P < 0.05). Interpretation These findings suggest that large acute painful areas on the calf muscles impair the postural control and potentially increase the risk factors for falls. Further strategies aiming to reduce pain in patients may lead to improvement in balance.

Changes in the Spatiotemporal Expression of Local and Referred Pain Following Repeated Intramuscular Injections of Hypertonic Saline: A Longitudinal Study

Intramuscular injection of hypertonic saline produces a dull ache that is felt in the muscle belly but also often refers into distal structures. We have previously observed in 2 subjects that the pattern of pain referral alters during painful stimuli separated by a week. In this investigation, we tested the hypothesis that the intensity and area of pain in the local and referred regions exhibits plasticity when an identical noxious stimulus is delivered to the same site over sequential trials. Bolus 1 mL intramuscular injections of 5% hypertonic saline were made into the same site of the tibialis anterior (TA) muscle on the same day each week for 4 consecutive weeks. Twenty-one subjects mapped the areas of local and referred pain and rated the intensities on a visual analog scale every 30 seconds until the cessation of pain. Over 4 weeks there was a progressive reduction in the area and intensity of local pain and a reciprocal increase in the expression of referred pain. We conclude that the decrease in perceived local pain and increase in perceived referred pain reflects plastic processes occurring centrally. What happens to the intensity of pain induced by repeated noxious stimuli over time? Does it stay the same, increase or decrease? Here we show that weekly injections of hypertonic saline into the tibialis anterior cause decreases in local but increases in referred pain, suggesting central changes in processing noxious inputs.

Effects of Intramuscular Anesthesia on the Expression of Primary and Referred Pain Induced by Intramuscular Injection of Hypertonic Saline

Intramuscular injection of hypertonic saline produces pain in the belly of the injected muscle (primary pain) and, often, pain that projects distally (referred pain). While it is known that referred pain can be induced during complete sensory block of the distal site, there is little evidence as to whether the perception of referred pain depends on ongoing input from the primary stimulus. We assessed whether blocking the noxious input following the induction of pain blocks the primary but not the referred pain. A cannula was inserted into the tibialis anterior muscle in 15 subjects (8 male, 7 female). In a quasi-random crossover design conducted over 2 experimental sessions, each subject received a bolus intramuscular injection of .5 mL of 5% hypertonic saline, followed 90 seconds later by either: A) A second bolus injection or; B) An injection of 2 mL lignocaine through the same cannula. Protocol A was followed 60 seconds later by either a sham injection or an injection of lignocaine, while protocol B was followed 60 seconds later by either a sham injection or an injection of hypertonic saline. Subjects mapped the areas of primary and referred pain, and rated the intensities at these sites every 30 seconds until the cessation of pain. In all subjects, the area and intensity of primary pain rapidly disappeared within 7.5 minutes of intramuscular lignocaine injection (P < .02 relative to the nonanesthesia condition). With the exception of 2 subjects, in whom the referred pain continued in the absence of primary pain, the referred pain declined in parallel with local pain: the mean total pain intensity declined by 74% in both regions. We conclude that the maintenance of referred muscle pain usually depends on ongoing noxious inputs from the site of primary muscle pain. Referred pain is a significant clinical problem, and commonly occurs with pain originating in muscle but not from skin. It is important to know the primary source of the pain so that treatment can be directed to this site rather to the site of referral.

Experimentally reduced hip abductor function during walking: Implications for knee joint loads

Hip and knee functions are intimately connected and reduced hip abductor function might play a role in development of knee osteoarthritis (OA) by increasing the external knee adduction moment during walking. The purpose of this study was to test the hypothesis that reduced function of the gluteus medius (GM) muscle would lead to increased external knee adduction moment during level walking in healthy subjects. Reduced GM muscle function was induced experimentally, by means of intramuscular injections of hypertonic saline that produced an intense short-term muscle pain and reduced muscle function. Isotonic saline injections were used as non-painful control. Fifteen healthy subjects performed walking trials at their self-selected walking speed before and immediately after injections, and again after 20 min of rest, to ensure pain recovery. Standard gait analyses were used to calculate three-dimensional trunk and lower extremity joint kinematics and kinetics. Surface electromyography (EMG) of the glutei, quadriceps, and hamstring muscles were also measured. The peak GM EMG activity had temporal concurrence with peaks in frontal plane moments at both hip and knee joints. The EMG activity in the GM muscle was significantly reduced by pain (−39.6%). All other muscles were unaffected. Peaks in the frontal plane hip and knee joint moments were significantly reduced during pain (−6.4% and −4.2%, respectively). Lateral trunk lean angles and midstance hip joint adduction and knee joint extension angles were reduced by ⩽1°. Thus, the gait changes were primarily caused by reduced GM function. Walking with impaired GM muscle function due to pain significantly reduced the external knee adduction moment. This study challenge the notion that reduced GM function due to pain would lead to increased loads at the knee joint during level walking.

Homotopic and heterotopic variation in skin blood flow and temperature following experimental muscle pain in humans

The aim of the present study was to explore variation in skin blood flow and temperature following experimental muscle pain. In 14 male human subjects, 2 ml and 4.8 ml of hypertonic (5.8%) saline were injected into the left tibialis anterior (TA) muscle to induce muscle pain. The subjects rated the pain intensity on a 10 cm visual analogue scale (VAS). Using laser-Doppler flowmetry and thermography, the skin blood flow and temperature were assessed at four different skin areas: ipsilateral muscle pain area (5 × 5 cm), ipsilateral referred pain area (5 × 10 cm), and two corresponding mirror areas on the contralateral non-injected leg. Compared with 2 ml hypertonic saline injection, significantly longer pain duration (1599 ± 119 s) and stronger pain intensity (VAS peak: 6.9 ± 0. 6 cm) were found after the injection of 4.8 ml hypertonic saline ( P < 0.001, respectively). In addition, 4.8 ml hypertonic saline evoked a significant increase in skin blood flow and higher skin temperature around the injection site, the referred pain area, and the contralateral area to the injection site ( P < 0.05). By contrast, 2 ml hypertonic saline injection only elicited an increase in skin blood flow, but not temperature, at the injection area and the contralateral mirror area to the injection site ( P < 0.05). These results suggested that the vasodilation in different skin areas following intramuscular injection of hypertonic saline was dose-dependent. Injection of 4.8 ml hypertonic saline after local intramuscular anesthesia (2% lidocaine) did not evoke any significant changes in skin blood flow or skin temperature in any of the four observation areas. This suggested that both homotopic and heterotopic vascular reactions triggered by hypertonic saline stimulation of thin muscle afferent fibers were a neurogenically associated reaction.

Changes in the degree of motor variability associated with experimental and chronic neck–shoulder pain during a standardised repetitive arm movement

The aim of the present study was to investigate the effect of experimental and chronic neck-shoulder pain on the magnitude of cycle-to-cycle variability of task timing, kinematics and muscle activation during repetitive arm movement performed for 3 or 5 min. In an experimental part, acute muscle pain was induced in healthy subjects by intramuscular injection of hypertonic saline in trapezius (n = 10) and infraspinatus (n = 10) muscles. In a clinical part, workers with (n = 12) and without (n = 6) chronic neck-shoulder pain were compared. Cycle-to-cycle standard deviations of task duration, arm and trunk movement in 3D and surface electromyographic (EMG) root mean square activity were computed to assess the degree of variability. The variability in task timing increased in presence of both experimental and chronic pain (P < 0.05) compared with non-painful conditions. Experimental pain increased the variability of the starting position of the arm (P < 0.05), the arm range of motion (P < 0.01), the arm and trunk movement area (P < 0.01) and the acceleration of the arm (P < 0.01). In the chronic pain condition, the variability of arm and trunk acceleration (P < 0.01) and EMG activity (P < 0.05) was decreased compared with healthy controls. These results indicate that pain alters the magnitude of motor variability, and that the transition from acute to chronic pain is accompanied by changes in motor patterns. Experimental pain likely resulted in a quest for a motor solution reducing nociceptive influx, while chronic pain was characterised by a diminished motor flexibility.

Effects of Gabapentin on Experimental Somatic Pain and Temporal Summation

Gabapentin is used for treatment of neuropathic pain, but its effect on different somatic pain modalities and integrative mechanisms are not completely understood. The aim of this double-blind, placebo-controlled experimental pain study, conducted on 20 healthy volunteers, was to examine the effect of a single dose of 1200 mg gabapentin on multi-modal experimental cutaneous and muscle pain models. The following pain models were applied: (1) pain thresholds to single and repeated cutaneous and intramuscular electrical stimulation (temporal summation to 5 stimuli delivered at 2 Hz); (2) stimulus-response function relating pain intensity scores (visual analog scale, VAS) to increasing current intensities for electrical skin and muscle stimuli (single and repeated, determined at baseline); and (3) the pain intensity (VAS) and pain areas after intramuscular injection of hypertonic saline. Pain assessments were performed prior to, and at 4, 6, and 8 hours after medication. When responses were averaged across the post-dose times, gabapentin: (1) significantly increased the temporal summation pain threshold in skin compared with placebo (P = .03); (2) significantly reduced the area under the pain intensity curve to hypertonic saline injections in the muscle (P = .02); and (3) significantly reduced the area of pain evoked by hypertonic saline (P = .03). Gabapentin reduces temporal summation of skin stimuli at pain threshold intensities; this may have potential as a biomarker for drugs with efficacy on neurogenic pain. The data also suggest that tonic muscle pain is responsive to gabapentin treatment and suggest further clinical studies.