Headache from clinically confirmed hemicrania continua arising from the sternocleidomastoid muscle: a case report.

BACKGROUND: A patient with a history of cluster headaches, now in remission, presented with confirmed hemicrania continua that resolved with a local anaesthetic injection into the Sternocleidomastoid (SCM) muscle. To the best of our knowledge, this is the first reported case of a trigeminal autonomic cephalalgia arising from a soft tissue source in the neck. CASE PRESENTATION: A 66-year-old man with a history of cluster headaches presented with a six-month history of a new constant right-sided headache. The new headaches were associated with tearing and redness of the right eye and responded to indomethacin, thus meeting the International Classification of Headache Disorders (ICHD-3) diagnostic criteria for hemicrania continua. The history and physical examination suggested a cervical source of the headache arising from the ipsilateral SCM muscle. Injection of the muscle with 1% lidocaine resulted in the elimination of the pain for 1 month without indomethacin. CONCLUSIONS: Due to the convergence of trigeminal, cervical and autonomic nerve fibres, various combinations of headache syndromes can result. This case report demonstrates how a meticulous examination is a crucial component of headache evaluation. Treatment directed to this muscle spared this patient further daily indomethacin and associated side effects.

Abdominal skeletal muscle activity precedes spontaneous menstrual cramping pain in primary dysmenorrhea.

BACKGROUND: Dysmenorrhea is a pervasive pain condition that affects 20-50% of reproductive-aged women. Distension of a visceral organ, such as the uterus, could elicit a visceromotor reflex, resulting in involuntary skeletal muscle activity and referred pain. Although referred abdominal pain mechanisms can contribute to visceral pain, the role of abdominal muscle activity has not yet been investigated within the context of menstrual pain. OBJECTIVE: The goal of this study was to determine whether involuntary abdominal muscle activity precedes spontaneous episodes of menstrual cramping pain in dysmenorrheic women and whether naproxen administration affects abdominal muscle activity. STUDY DESIGN: Abdominal electromyography activity was recorded from women with severe dysmenorrhea (n = 38) and healthy controls (n = 10) during menses. Simultaneously, pain was measured in real time using a squeeze bulb or visual analog rheostat. Ninety minutes after naproxen administration, abdominal electromyography activity and menstrual pain were reassessed. As an additional control, women were also recorded off menses, and data were analyzed in relation to random bulb squeezes. Because it is unknown whether mechanisms of menstrual cramps are different in primary or secondary dysmenorrhea/chronic pelvic pain, the relationship between medical history and abdominal muscle activity was examined. To further examine differences in nociceptive mechanisms, pressure pain thresholds were also measured to evaluate changes in widespread pain sensitivity. RESULTS: Abdominal muscle activity related to random-bulb squeezing was rarely observed in healthy controls on menses (0.9 ± 0.6 episodes/hour) and in dysmenorrhea participants off menses (2.3 ± 0.6 episodes/hour). In dysmenorrheic participants during menses, abdominal muscle activity frequently preceded bulb squeezing indicative of menstrual cramping pain (10.8 ± 3.0 episodes/hour; P < .004). Whereas 45% of the women with dysmenorrhea (17 of 38) had episodes of abdominal muscle activity associated pain, only 13% (5 of 38) had episodes after naproxen (P = .011). Women with the abdominal muscle activity-associated pain were less likely to have a diagnosis for secondary dysmenorrhea or chronic pelvic pain (2 of 17) than women without this pain phenotype (10 of 21; P = .034). Similarly, women with the abdominal muscle activity-associated pain phenotype had less nonmenstrual pain days per month (0.6 ± 0.5) than women without the phenotype (12.4 ± 0.3; P = .002). Women with abdominal muscle activity-associated pain had pressure pain thresholds (22.4 ± 3.0 N) comparable with healthy controls (22.2 ± 3.0 N; P = .967). In contrast, women without abdominal muscle activity-associated pain had lower pressure pain thresholds (16.1 ± 1.9 N; P = .039). CONCLUSION: Abdominal muscle activity may contribute to cramping pain in primary dysmenorrhea but is resolvable with naproxen. Dysmenorrheic patients without cramp-associated abdominal muscle activity exhibit widespread pain sensitivity (lower pressure pain thresholds) and are more likely to also have a chronic pain diagnosis, suggesting their cramps are linked to changes in central pain processes. This preliminary study suggests new tools to phenotype menstrual pain and supports the hypothesis that multiple distinct mechanisms may contribute to dysmenorrhea.

Glenohumeral Joint Pain Referral Patterns: A Descriptive Study.

BACKGROUND: Pain diagrams are a useful tool to help physicians understand the varying presentation patterns of specific pain generators. This study is the first to describe the potential pain patterns of the glenohumeral joint (GHJ) based on responses to diagnostic image-guided GHJ injections. PURPOSE: To determine potential GHJ pain referral patterns. METHODS: 162 consecutive patients undergoing 168 GHJ injections recorded their preprocedure pain scores and drew accurate pain diagrams prior to undergoing fluoroscopically guided GHJ injections with local anesthetic. Postprocedure pain scores were recorded and those with complete relief were considered responders. Pain diagrams were overlaid via computer software to facilitate analysis and a composite pain map. A responder composite was also compared with a nonresponder composite. RESULTS: The GHJ was shown to cause pain in traditionally localized areas of the anterior and/or posterior shoulder and upper arm regions in 100% of patients who experienced complete pain relief after injection. Among 100% responders, 18% had neck pain and 6% had scapular pain. Pain was shown to radiate distally, with anterior forearm pain in 9%, posterior forearm pain in 8%, and hand pain in 9%. No patients with pain both in the medial neck and below the elbow were found to be 100% responders. Similarly, no patients were 100% responders if they had pain in the medial scapula and below the elbow, or medial scapula and medial neck. CONCLUSIONS: Anterior or posterior shoulder and upper arm pain, or a combination of the two, is the most common pain referral area from a symptomatic shoulder joint. Referral to the lateral neck, in combination with shoulder pain, was occasionally seen. Pain referral to the forearm and hand was less common. Rarely did a symptomatic shoulder joint refer pain to the scapula or to the medial neck.

Referred pain location depends on the affected section of the sacroiliac joint.

PURPOSE: Pain referred from the sacroiliac joint (SIJ) may originate in the joint's posterior ligamentous region. The site of referred pain may depend on which SIJ section is affected. This study aimed to determine the exact origin of pain referred from four SIJ sections. METHODS: The study included 50 patients with SIJ dysfunction, confirmed by more than 70 % pain relief after periarticular injection of local anesthetic into the SIJ. The posterior SIJ was divided into four sections-upper, middle, lower, and other (cranial portion of the ilium outside the SIJ)-designated sections 1, 2, 3, and 0, respectively. We then inserted a needle into the periarticular SIJ under fluoroscopy. After the patient identified the area(s) in which the needle insertion produced referred pain, we injected a mixture of 2 % lidocaine and contrast medium into the corresponding SIJ section. RESULTS: Referred pain from SIJ section 0 was mainly located in the upper buttock along the iliac crest; pain from section 1, around the posterosuperior iliac spine; pain from section 2, in the middle buttock area; pain from section 3, in the lower buttock. In all, 22 (44.0 %) patients complained of groin pain, which was slightly relieved by lidocaine injection into SIJ sections 1 and 0. CONCLUSIONS: Dysfunctional upper sections of the SIJ are associated with pain in the upper buttock and lower sections with pain in the lower buttock. Groin pain might be referred from the upper SIJ sections.

Botulinum toxin for myofascial pain syndromes in adults.

BACKGROUND: This is an updated version of the original Cochrane review published in Issue 4, 2012. Myofascial pain syndrome (MPS) is a regional muscular pain syndrome characterised by the presence of trigger points, which are painful points in one or more muscles. The pain can be felt at the site where the trigger point is located or it can be felt away from that place when the muscle is pressed (referred pain). Botulinum toxin is a protein produced by the bacterium Clostridium botulinum and is a potent neurotoxin that eventually inhibits muscle contractions. It is capable of selectively weakening painful muscles and interrupting the pain cycle. OBJECTIVES: To assess the effectiveness and safety of botulinum toxin A (BTXA) in the treatment of myofascial pain syndrome (MPS), excluding MPS in neck and head muscles. SEARCH METHODS: This is an updated version of the original Cochrane review published in Issue 4, 2012. The search strategy for the update was the same as in the original review and we searched CENTRAL in The Cochrane Library (2013, Issue 11 of 12), MEDLINE (Ovid) (2012 to 29 November 2013) and EMBASE (Ovid) (2012 to 27 November 2013). The search strategy was composed of terms for myofascial pain and botulinum toxin. For the original review, we also searched the Cochrane Pain, Palliative and Supportive Care (PaPaS) Review Group Specialised Register until December 2011, PubMed (from 1966 to 2011) and LILACS (from 1982 to 2011). There was no language restriction. SELECTION CRITERIA: We included randomised controlled trials (RCTs) involving botulinum toxin for treating participants with MPS. We excluded studies with MPS of the neck and head from this review as they have already been assessed in existing systematic reviews. We considered a diagnosis of MPS to be based on the identification of trigger points in the taut band through palpation of sensitive nodules, local twitch response and specific patterns of referred pain associated with each trigger point. DATA COLLECTION AND ANALYSIS: Two review authors independently screened identified studies, extracted data, assessed trial quality and analysed results using the Cochrane PaPaS Review Group criteria. MAIN RESULTS: Four studies with a total of 233 participants, comparing BTXA with placebo, met the inclusion criteria. In one study with 145 participants, significant improvement rates of pain intensity scores and duration of daily pain were demonstrated when comparing BTXA with placebo. The three other studies showed that there was no statistically significant difference between BTXA and placebo in pain intensity. AUTHORS' CONCLUSIONS: Since the first publication of this review, no new studies were found. There is inconclusive evidence to support the use of botulinum toxin in the treatment of MPS based on data from four studies with a total of 233 participants, which we considered were of sufficient quality to be included in this review. Meta-analyses were not possible due to the heterogeneity between studies. We suggest that in future studies the same methodology to assess pain, a standardised dose of treatment, follow-up of at least four months (to observe the maximum and minimum curve of the drug effect) and appropriate data presentation should be used. More high-quality RCTs of botulinum toxin for treating MPS need to be conducted before firm conclusions on its effectiveness and safety can be drawn.

Nummular headache after trans-sphenoidal surgery: a referred pain-based headache syndrome.

Nummular headache (NH) is a newly categorized primary headache characterized by a consistent location, shape and size of painful area in each attack. The etiopathogenesis is entirely unknown. Currently, the peripheral theory of epicranial neuralgia is accepted more widely than the central theory but it cannot fully explain the clinical picture. We report a patient who suffered from a relapsing and remitting course of NH at the high parietal area and vertex shortly after resection for pituitary prolactinoma via a trans-sphenoidal approach. There was no focal trophic change or paresthesia but a mild allodynia in the painful area. The patient did not exhibit trigeminal sensory disorder or cranial trauma thoroughly. The pain responded well to gabapentin. Therefore, physicians should be aware of postoperative NH, which is amenable to treatment. The findings in our patient support a dual mechanism of NH and suggest that central NH is a form of referred pain.

Effect of combination of trigger point injection and stellate ganglion block on non-odontogenic mandibular molar pain referred from masseter muscle: a case report.

We report a case of myofascial pain syndrome (MPS), manifested as nonodontogenic mandibular molar pain referred from the masseter muscle, relieved by a combination of trigger point injection (TPI) and stellate ganglion block (SGB). The patient was a 32-year-old woman who had experienced cold hypersensitivity in the right third mandibular molar 2 months prior to visiting our department. Subsequently, she had visited a family dentist and undergone pulpectomy under local anesthesia. She eventually visited our clinic because there was no marked change in her symptoms. On the first visit, no tooth abnormality was found and the patient was neither anxious nor depressive. Tender points were found in the right masseter and temporal muscles during muscle palpation. Referred pain radiating to the right mandibular molars was observed when pressure was applied to the central portion of the right masseter muscle. As a result, we diagnosed MPS based on evidence of nonodontogenic tooth pain caused by referred pain from the masseter muscle. We performed TPI with 2% lidocaine hydrochloride to the tender point in the masseter muscle. Although the visual analog scale (VAS) pain score dropped from 97 to 36, complete pain relief was not achieved. The TPI was effective for approximately 7 hrs, after which severe throbbing pain returned. The sustained nature of the tooth pain suggested that it was sympathetic nerve-dependent. Subsequently, we performed SGB, resulting in a reduction in the VAS pain score from 90 to 32. Therefore, we performed another TPI and the VAS pain score dropped to 0. We continued SGB and TPI for the next 3 days and the symptoms disappeared. Thus, a combination of TPI and SGB controlled MPS manifested as masseter muscle-mediated nonodontogenic tooth pain.

Endothelins implicated in referred mechanical hyperalgesia associated with colitis induced by TNBS in mice.

This study evaluated the contribution of endothelins to changes in sensitivity to mechanical stimulation of the lower abdomen and hind paw associated with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. The frequency of withdrawal responses to 10 consecutive applications of von Frey probes to the lower abdomen (0.07 g) or hind paw (0.4 g) was assessed in male BALB/c mice before and after intracolonic TNBS injection (0.5 mg in 100 microL of 35% ethanol). TNBS (0.5 mg) induced referred mechanical hyperalgesia in the abdomen (response frequencies at 24 h: saline 11.0% +/- 3.1%, TNBS 48.0% +/- 6.9%) and hind paw (frequencies at 24 h: saline 12.5% +/- 4.7%, TNBS 47.1% +/- 7.1%) lasting up to 72 and 48 h, respectively. Mice receiving 1.0 or 1.5 mg TNBS assumed hunch-backed postures and became immobile during abdominal mechanical stimulation, suggestive of excessive ongoing pain. Atrasentan (ETA receptor antagonist; 10 and 30 mg/kg, i.v.) given 24 h after TNBS abolished hind paw and abdominal mechanical hyperalgesia for 2-3 h. A-192621 (ETB receptor antagonist; 20 mg/kg, i.v.) attenuated abdominal mechanical hyperalgesia at the 3 h time point only. Thus, endothelins contribute importantly to abdominal and hind paw referred mechanical hyperalgesia during TNBS-induced colitis mainly through ETA receptor-signaled mechanisms.

Spinal NKCC1 blockade inhibits TRPV1-dependent referred allodynia.

BACKGROUND: The Na+, K+, 2Cl- type I cotransporter (NKCC1) and TRPV1 receptors, at the level of the dorsal horn, have been implicated in mediating allodynia in response to an inflammatory insult. The NKCC1 cotransporter regulates intracellular [Cl-] and thus the magnitude and polarity of GABAA receptor responses in neurons. TRPV1 receptors transduce diverse chemical and natural stimuli in nociceptors and are critical for inflammatory hyperalgesia. RESULTS: Here we have tested the role of spinal NKCC1 cotransporters and TRPV1 receptors in referred allodynia in a model of visceral hyperalgesia in mice. Intrathecal (IT) injection of the NKCC1 inhibitor bumetanide (BUM, 1 nmol) inhibited referred, abdominal allodynia evoked by an intracolonic capsaicin injection. BUM was effective when injected IT either before or up to 4 hrs after the establishment of referred allodynia. The TRPV1 antagonist AMG 9810 (1 nmol) also inhibited referred allodynia in this model suggesting the involvement of an endogenous TRPV1 agonist in the dorsal horn in referred allodynia. In support of this suggestion, the endovanilloid TRPV1 agonist, narachidonoyl- dopamine (NADA, 1 or 10 nmol, IT) evoked stroking allodynia in the hindpaw that was blocked by co-treatment with AMG 9810 (1 nmol). The TRPV1-dependent stroking allodynia caused by NADA appeared to be functionally linked to NKCC1 because BUM (1 nmol) also inhibited NADA-evoked stroking allodynia. CONCLUSION: Our findings indicate that spinal NKCC1 and TRPV1 are critical for referred allodynia mediated by a painful visceral stimulus. Moreover, they suggest that endogenous TRPV1 agonists, released in the CNS in painful conditions, might stimulate TRPV1 receptors on primary afferents that, in turn, play a role in increasing NKCC1 activity leading to allodynia.

The proteinase inhibitor camostat mesilate suppresses pancreatic pain in rodents.

Camostat mesilate, an orally available proteinase inhibitor, is clinically used for treatment of pancreatitis. Given recent evidence that pancreatic proteinases including trypsin and/or proteinase-activated receptor-2 (PAR2) might be involved in pancreatic pain, we examined if camostat mesilate could suppress spinal Fos expression, a marker for neuronal activation, following specific application of trypsin to the pancreas, and pancreatitis-related referred allodynia. Trypsin, administered into the pancreatic duct, caused delayed expression of Fos proteins in the superficial layer of the bilateral T8 and T9 spinal dorsal horns in rats. The trypsin-induced spinal Fos expression was completely abolished by oral pre-administration of camostat mesilate at 300 mg/kg. After hourly repeated (6 times in total) administration of caerulein, mice showed typical symptoms of pancreatitis, accompanied by mechanical allodynia in the upper abdomen (i.e., referred hyperalgesia/allodynia), as assessed by use of von Frey filaments. Camostat mesilate at 100-300 mg/kg, given orally twice before the 1st and 4th doses of caerulein, abolished the pancreatitis-related abdominal allodynia, while it partially prevented the inflammatory signs. The same doses of camostat mesilate, when administered once after the final dose of caerulein, also revealed significant anti-allodynic effect. These data suggest that camostat mesilate prevents and/or depresses pancreatitis-induced pain and/or referred hyperalgesia/allodynia, in which proteinases including trypsin would play a critical role.

Localized myofascial pain responds better than referring myofascial pain to botulinum toxin injections.

Myofascial pain of the muscles of mastication is a common temporomandibular disorder. Patients unresponsive to conservative treatment modalities pose a therapeutic challenge to the treating clinician. The efficacy of intramuscular botulinum toxin injections for recalcitrant cases is still not well established due to mixed results from clinical trials. The Diagnostic Criteria of Temporomandibular Disorders (DC/TMD) classified chronic muscle pain broadly into a localized pattern (when pain is localized to the site of palpation or the muscle palpated) and a referring pattern (when the pain spreads beyond the boundary of the muscle being palpated). The medical records of 25 consecutive patients treated with botulinum were analysed retrospectively. Significant pain reduction was achieved in 69.2% of the patients with localized myofascial pain and 16.7% of the patients with referring myofascial pain (P=0.015). Seventy-seven per cent of the patients with localized myofascial pain reported using less analgesic throughout the follow-up period, whereas only 25% of the patients with referring myofascial pain (P=0.017). The effects of botulinum toxin in responsive patients subsided after a mean of 3.21 months. Patients with localized myofascial pain benefited from botulinum toxin injections, but patients with referring myofascial pain responded poorly to this treatment.

Antinociceptive effect of botulinum toxin type A on experimental abdominal pain.

Visceral pain, especially in the abdominal region, represents one of the most common types of pain. Its chronic form is usually very hard to treat by conventional analgesic agents and adjuvants. We investigated the antinociceptive effect of botulinum toxin type A (BTX-A) in male Wistar rats in two models of visceral pain: peritonitis induced by intraperitoneal injection of 1% acetic acid and colitis induced by intracolonic instillation of 0.1% capsaicin. Pain was measured as the number of abdominal writhes. Additionally, referred mechanical sensitivity in the ventral abdominal area was evaluated by von Frey test and the extent of spinal c-Fos expression was immunohistochemically examined. BTX-A significantly reduced the number of abdominal writhes in both models of visceral pain after intrathecal application in a dose of 2 U/kg. In the experimental colitis model, BTX-A (2 U/kg) reduced both referred mechanical allodynia and c-Fos expression in the dorsal horn of the spinal cord (S2/S3 segments). In contrast to intrathecal administration, BTX-A (2 U/kg) administered into the cisterna magna had no effect on pain suggesting that the primary site of its action is a spinal cord.

Bladder pain relief by HMGB1 neutralization and soluble thrombomodulin in mice with cyclophosphamide-induced cystitis.

High mobility group box 1 (HMGB1), one of damage-associated molecular patterns (DAMPs), plays roles in not only inflammation but also processing of somatic pain. Given that no evidence for roles of HMGB1 in visceral pain signaling is available, we asked if HMGB1 participates in bladder pain accompanying cystitis caused by cyclophosphamide in mice, using the anti-HMGB1 neutralizing antibody and recombinant human soluble thrombomodulin (rhsTM) that sequesters HMGB1 and promotes its degradation by thrombin. Cyclophosphamide, administered i.p., caused bladder pain-like nociceptive behavior and referred hyperalgesia accompanying cystitis symptoms including increased bladder weight, an indicator of edema, in mice. The cyclophosphamide-induced bladder pain and referred hyperalgesia, but not increased bladder weight, were prevented by i.p. preadministration of the anti-HMGB1 neutralizing antibody or rhsTM. HMGB1, given i.p., facilitated the bladder pain and referred hyperalgesia caused by a subeffective dose of cyclophosphamide, an effect blocked by rhsTM. In the cyclophosphamide-treated mice, HMGB1 levels greatly decreased in the bladder tissue, particularly in the urothelial cells, but did not change in the plasma. Low molecular weight heparin, known to inhibit the receptor for advanced glycation end products (RAGE), but not lipopolysaccharide from Rhodobacter sphaeroides, an inhibitor of toll-like receptor 4 (TLR4), blocked the cyclophosphamide-induced bladder pain and referred hyperalgesia. Thus, our data indicate involvement of HMGB1 in the cyclophosphamide-induced bladder pain signaling, but not cystitis itself, and suggest that targeting HMGB1 with rhsTM or blocking RAGE might serve as a novel therapeutic strategy for the management of bladder pain.

[Reduction of omalgia in laparoscopic cholecystectomy: clinical randomized trial ketorolac vs ketorolac and acetazolamide]. / Reducción de omalgia en colecistectomía laparoscópica: ensayo clínico aleatorizado con ketorolaco vs ketorolaco y acetazolamida.

BACKGROUND: Laparoscopy cholecystectomy for the surgical treatment of cholelithiasis has been considered the gold standard. The referred pain to the shoulder (omalgia) may be present to 63% of the patients and limits outpatient management. OBJECTIVE: The study was to evaluate the usefulness of acetazolamide associated with ketorolac for reduction of the omalgia to minimally invasive treatment. METHODS: We performed a clinical trial, randomized, double blind in patients undergoing laparoscopic cholecystectomy to assess the reduction of post-operative omalgia comparing ketorolac and ketorolaco+acetazolamida. 31 patients in each group were studied. The study group: 250 mg of acetazolamide before anesthetic induction and 30 mg of ketorolac in the immediate postoperative period. CONTROL GROUP: one tablet of placebo prior to the anesthetic induction and 30 mg of ketorolac in the immediate postoperative. The presence of omalgia was assessed using the analog visual scale. The variables recorded included: age, sex, flow of carbon dioxide intra-abdominal pressure, surgical time, urgent or elective surgery, omalgia, severity of pain evaluated by analog visual scale, addition analgesia. RESULTS: Both groups were homogeneous and statistical analysis showed no differences in the variables studied. The omalgia in the study group was presented at 9.67% and in the group control was the 58.06% (p < 0.001). CONCLUSION: 250 mg oral acetazolamide associated 30 mg of ketorolac reduces significantly the development of omalgia in patients undergoing laparoscopic cholecystectomy.

Antecedentes: la colecistectomía laparoscópica es el patrón de referencia del tratamiento de la colelitiasis sintomática. El 63% de los pacientes operados sufre dolor postquirúrgico referido al hombro (omalgia), circunstancia que limita el tratamiento ambulatorio. Objetivo: evaluar la utilidad de la acetazolamida asociada con ketorolaco para disminuir la omalgia consecutiva al tratamiento de mínima invasión. Material y métodos: ensayo clínico, aleatorizado, doble ciego realizado en pacientes a quienes se efectuó colecistectomía laparoscópica para evaluar la reducción de la omalgia postoperatoria y comparar el efecto de ketorolaco y ketorolaco más acetazolamida. En cada grupo se estudiaron 31 pacientes. El grupo de estudio recibió 250 mg de acetazolamida antes de la inducción anestésica, y 30 mg de ketorolaco en el postoperatorio inmediato. El grupo control recibió una tableta de placebo antes de la inducción anestésica, y 30 mg de ketorolaco en el postoperatorio inmediato. La omalgia se evaluó con la escala visual análoga. Las variables estudiadas incluyeron: edad, sexo, flujo de dióxido de carbono, presión intrabdominal, tiempo quirúrgico, cirugía electiva o urgente, omalgia, intensidad del dolor evaluada con la escala visual análoga y analgesia de rescate. Resultados: los grupos estudiados fueron homogéneos, el análisis estadístico no mostró diferencias en las variables estudiadas. En el grupo de estudio la omalgia coexistió en 9.67% de los pacientes y en el grupo control en 58.06% (p < 0.001). Conclusión: la administración por vía oral de 250 mg de acetazolamida y 30 mg de ketorolaco redujo significativamente la omalgia en los pacientes a quienes se realizó colecistectomía laparoscópica.

Activation of the alpha-7 nicotinic acetylcholine receptor (α7 nAchR) reverses referred mechanical hyperalgesia induced by colonic inflammation in mice.

In the current study, we investigated the effect of the activation of the alpha-7 nicotinic acetylcholine receptor (α7 nAchR) on dextran sulphate sodium (DSS)-induced colitis and referred mechanical hyperalgesia in mice. Colitis was induced in CD1 male mice through the intake of 4% DSS in tap water for 7 days. Control mice received unadulterated water. Referred mechanical hyperalgesia was evaluated for 7 days after the beginning of 4% DSS intake. Referred mechanical hyperalgesia started within 1 day after beginning DSS drinking, peaked at 3 days and persisted for 7 days. This time course profile perfectly matched with the appearance of signs of colitis. Both acute and chronic oral treatments with nicotine (0.1-1.0 mg/kg, p.o.) were effective in inhibiting the established referred mechanical hyperalgesia. The antinociceptive effect of nicotine was completely abrogated by cotreatment with the selective α7 nAchR antagonist methyllycaconitine (MLA) (1.0 mg/kg). Consistent with these results, i.p. treatment with the selective α7 nAchR agonist PNU 282987 (0.1-1.0 mg/kg) reduced referred mechanical hyperalgesia at all periods of evaluation. Despite their antinociceptive effects, nicotinic agonists did not affect DSS-induced colonic damage or inflammation. Taken together, the data generated in the present study show the potential relevance of using α7 nAchR agonists to treat referred pain and discomfort associated with inflammatory bowel diseases.

Effects of intramuscular anesthesia on the expression of primary and referred pain induced by intramuscular injection of hypertonic saline.

UNLABELLED: 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. PERSPECTIVE: 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.

Hip joint pain referral patterns: a descriptive study.

OBJECTIVE: To determine hip joint pain referral patterns. DESIGN: Retrospective analysis. Setting. Multicenter. Patients. Fifty-one consecutive patients meeting clinical criteria of a symptomatic hip joint. Interventions. Fluoroscopically guided intra-articular hip joint injection. Outcome Measures. Anatomic pain map before hip injection and visual analog scale both before and after hip injection. RESULTS: The hip joint was shown to cause pain in traditionally accepted referral areas to the groin and thigh in 55% and 57% of patients, respectfully. However, pain referral was also seen in the buttock and lower extremity distal to the knee in 71% and 22%, respectively. Foot and knee pain were seen in only 6% and 2% of patients, respectively, while lower lumbar spine referral did not occur. Fourteen pain referral patterns were observed. CONCLUSIONS: Buttock pain is the most common pain referral area from a symptomatic hip joint. Traditionally accepted groin and thigh referral areas were less common. Hip joint pain can occasionally refer distally to the foot. Lower lumbar spine referral did not occur.

Laparoscopic cholecystectomy under spinal anesthesia.

BACKGROUND: Advantages of laparoscopic cholecystectomy (LC) such as less pain and short hospital stay make it the treatment of choice for cholelithiasis. There are limited data about LC under spinal anesthesia. This study was designed to evaluate LC under spinal anesthesia. METHODS: Twenty-nine patients underwent surgery for LC under spinal anesthesia at the 4th Department of Surgery of the Ankara Numune Education and Research Hospital between April 2005 and January 2006. All patients were informed about spinal anesthesia in detail. The patients also were informed about the risk of conversion to general anesthesia, and all patients provided informed consent. The election criteria for spinal anesthesia were as follows: American Society of Anesthesiologists (ASA) risk group 1 or 2; risk score for conversion from LC to open cholecystectomy (RSCO) less than negative 3; and presence of gallstone disease. Standard laparoscopic technique was applied to all patients. Simple questionnaire forms were developed for both patients and surgeons to provide comments about the operation. RESULTS: The operation was completed laparoscopically on 26 patients, while 3 patients needed general anesthesia due to severe right shoulder pain. None of the patients had cardiopulmonary problems other than transient hypotension during surgery. Intravenous fentanyl (25 microg) was needed in 13 patients due to severe right shoulder pain. Five patients still had severe shoulder pain after fentanyl injection. Local washing of the right diaphragm with 2% lidocaine solution was successful in the remaining 5 patients in whom fentanyl injection failed to stop the pain. All of the patients' answers to the questions regarding the comfort of operation were "very well" at the 1-month postoperative evaluation. All surgeons stated that there was no difference from LC under general anesthesia. CONCLUSIONS: All of the patients and surgeons were satisfied with LC under spinal anesthesia. Therefore, LC under spinal anesthesia may be an appropriate treatment choice to increase the number of patients eligible for outpatient surgery.

Mechanisms of pain referral in patients with whiplash-associated disorder.

The aim was to investigate the mechanisms of pain referral in patients with whiplash associated disorder. Pain was induced in 12 controls and 12 patients with whiplash associated disorder by intramuscular electrical stimulation in the infraspinatus muscle and the ipsilateral upper arm, i.e., the area where all subjects perceived referred pain during conditioning stimulation in the infraspinatus muscle. Conditioning stimulation amounted to a pain intensity rated as 2/10 and 4/10. During conditioning stimulation in the infraspinatus muscle, sensitivity to test stimuli was assessed in the referred pain area (i.e., upper arm) and vice versa. Test stimuli consisted of intramuscular electrical stimulation corresponding to innocuous perception threshold, electrical pain threshold, and pain intensities rated as 2/10, 4/10 and 6/10, respectively. Compared to controls, patients with whiplash associated disorder had increased pain sensitivity (p< or =0.01) and indicated larger areas of referred pain ((p< or =0.003) during stimulation at the infraspinatus muscle; p< or =0.03 during stimulation at the upper arm), including proximal referral of pain which was never reported by controls (p< or =0.05). During conditioning stimulation in the infraspinatus muscle (4/10) all subjects reported referred pain in the upper arm (corresponding to the test site) and innocuous perception thresholds (p<0.05)(patients) and electrical pain thresholds (p<0.001) (controls) decreased. Conditioning stimulation in the upper arm did not affect sensitivity to test stimuli in the infraspinatus muscle. In conclusion, patients with whiplash associated disorder had increased sensitivity to painful stimulation, reported larger areas of referred pain during the same subjectively painful conditioning stimulation (i.e., lower absolute stimulus intensities), including proximal pain referral which was never seen in controls, indicating aberrant processing of nociceptive input. The perceptual integration of nociceptive stimuli during simultaneous stimulation did not differ between groups suggesting that divergence of nociceptive input from the focal pain area leading to excitation of neurones with projected fields in the referred pain area most likely explains referred pain in both groups alike.

Effectiveness of ropivacaine trigger points inactivation in the prophylactic management of patients with severe migraine.

OBJECTIVE: Tenderness and referred pain have been described in migraine and involved in its pathogenesis. The present study was performed to evaluate the prophylactic effectiveness of ropivacaine injections during a 12-week period. INTERVENTIONS: A total of 52 patients agreed to participate in the study. Trigger points were explored by manual palpation and injected weekly with 10 mg ropivacaine. The frequencies of migraine attacks were recorded from 4 weeks before the beginning of injections until 4 weeks after the last one, and a Clinical Global Impression improvement scale was completed in the final visit. RESULTS: All of the subjects had one or more trigger points, located in temporal and/or suboccipital areas in most of the cases. In nine (17.3%) patients the frequency of attacks was reduced >or=50%, and in 19 (36.5%) cases the reduction was comprised between 11% and 49%. A total of 31 (59.6%) patients reported to be much or very much improved after finishing the injection period. In 11 cases rescue medication intake was reduced >or=50% in comparison with baseline period, and the attacks of severe intensity decreased significantly. Eight (26.6%) out of 30 patients suffering chronic migraine reverted to episodic migraine. Local pain in injection sites was reported by 14 patients, and 13 subjects (25.5%) experienced postinjection soreness. CONCLUSIONS: Trigger points inactivation can be an effective palliative measure in the prophylactic management of severe refractory migraine.