Effect of thoracoscopic splanchnic denervation on pain processing in chronic pancreatitis patients.

BACKGROUND: Central sensitisation due to visceral pancreatic nociceptive input may play an important role in chronic pancreatitis pain. Using quantitative sensory testing (QST), this first study investigates whether thoracoscopic splanchnic denervation (TSD), performed to reduce nociceptive visceral input, affects central sensitisation in chronic pancreatitis patients. PATIENTS AND METHODS: We studied 19 chronic pancreatitis patients (11 men, 8 women on stable opioid medication) and 18 healthy volunteers as preoperative controls. Preoperatively and 6 weeks after TSD, pain numeric rating scores, opioid medication, and thresholds to electric skin stimulation and pressure pain (measured in dermatomes T10 (pancreas), C5, T4, L1, L4) were documented. Treatment success was defined as cessation of opioids 6 weeks after TSD. RESULTS: Six weeks after TSD, there was a trend towards lower pain scores, only 10 patients were still on opioids (P<0.05 vs. preoperatively) and thresholds overall were significantly higher than preoperatively (pressure pain: +25%, P<0.001; electric: sensation +55%, pain detection +34%, pain tolerance +21%, P<0.05). Gender-specific differences in hypoalgesia patterns were seen. Preoperatively, TSD treatment successes consumed significantly less opioids than failures, without significant differences in preoperative patterns of neuroplasticity. CONCLUSIONS: TSD for chronic pancreatitis pain resulted in fewer patients on opioids and overall increases in pain thresholds. Our results suggest that TSD for reducing visceral nociceptive input may be effective in reducing resulting central sensitisation. Although patients benefiting from TSD consume less opioids preoperatively, we were unable to clearly link treatment success with specific perioperative patterns of neuroplasticity such as the presence or absence of hyperalgesia.     

Increased Sympathetic Activity in Chronic Pancreatitis Patients Is Associated With Hyperalgesia

ABSTRACT

Pain treatment in chronic pancreatitis patients is difficult, with pain frequently relapsing or persisting. Recent studies suggest that altered central nervous system pain processing underlies the chronic pain state in these patients. There is evidence that increased sympathetic activity may also play a role in some chronic pain syndromes. This study assessed sympathetic nervous system activity and its relation to pain processing in patients with severe painful chronic pancreatitis. The authors postulated that chronic pancreatitis patients with more sympathetic activity exhibit more generalized hyperalgesia. In 16 chronic pancreatitis patients, sympathetic activity was measured via venous plasma norepinephrine (NE) levels (supine, standing). Pain processing was quantified via pressure pain tolerance thresholds (PPTs) in dermatomes T10 (pancreatic area), C5, T4, L1. Five patients showed increased supine plasma NE levels (NE ≥ 3.0 nmol/L). PPTs were lower in patients with increased NE levels (INE) compared with patients with normal NE (NNE) (means [95% confidence interval]: INE 402 kPa [286–517] versus NNE 522 kPa [444–600]; P = .042). In severe chronic pancreatitis patients, increased sympathetic activity and hyperalgesia appear associated, suggesting that sympathetic activity may also play a role in these patients’ pain.     

Attentional modulation fails to attenuate the subjective pain experience in chronic,unexplained pain

Background: Chronic, unexplained pain is a common, ill‐understood clinical problem. Increased sensitivity for pain and other stimuli is often implied as an underlying mechanism. Attentional processes influence central pain processing and might mediate hypersensitivity at a cerebral level. Aims: To study patients with chronic, unexplained pain with respect to (a) subjective pain experience; (b) effects of attentional manipulation; (c) level at which alterations in pain processing occur: locally (symptomatic body region), or generalised. Methods: We compared 16 patients with chronic, unexplained limb pain with 16 matched healthy controls. Pain thresholds to electrical stimuli were recorded. Subjects then received individually thresholded painful and non‐painful stimuli, with manipulation of attention towards or away from pain. The intensity of pain perception was recorded by means of visual analogue scales (VAS). Pain thresholds and effects of Attention and Laterality on VAS scores were compared between groups by means of general linear modelling (restricted to 12 patients with unilateral pain and 12 controls). Results: Distraction increased thresholds for pain in healthy volunteers, but this effect was significantly attenuated in patients. Significant interactions between attention‐effects, stimulus laterality and stimulus intensity indicated that VAS scores for painful stimuli were attenuated during distraction in healthy controls, but not in pain patients. Conclusions: Results support the notion that pain processing is enhanced in chronic, unexplained pain, and that the influence of attentional modulation on pain processing is attenuated. Potential cerebral mechanisms are changes in either attentional allocation or attention‐mediated descending pain modulation. The changes seem to occur at a generalised level.     

Increased sympathetic activity in chronic pancreatitis patients is associated with hyperalgesia

Pain treatment in chronic pancreatitis patients is difficult, with pain frequently relapsing or persisting. Recent studies suggest that altered central nervous system pain processing underlies the chronic pain state in these patients. There is evidence that increased sympathetic activity may also play a role in some chronic pain syndromes. This study assessed sympathetic nervous system activity and its relation to pain processing in patients with severe painful chronic pancreatitis. The authors postulated that chronic pancreatitis patients with more sympathetic activity exhibit more generalized hyperalgesia. In 16 chronic pancreatitis patients, sympathetic activity was measured via venous plasma norepinephrine (NE) levels (supine, standing). Pain processing was quantified via pressure pain tolerance thresholds (PPTs) in dermatomes T10 (pancreatic area), C5, T4, L1. Five patients showed increased supine plasma NE levels (NE ≥ 3.0 nmol/L). PPTs were lower in patients with increased NE levels (INE) compared with patients with normal NE (NNE) (means [95% confidence interval]: INE 402 kPa [286-517] versus NNE 522 kPa [444-600]; P = .042). In severe chronic pancreatitis patients, increased sympathetic activity and hyperalgesia appear associated, suggesting that sympathetic activity may also play a role in these patients' pain.     

Pain and somatosensory findings in patients 3 years after total hip arthroplasty

Background: Chronic hip pain after total hip arthroplasty (THA) is a significant problem, but the aetiology remains unclear. Aims: To determine sensory function in patients with chronic hip pain 3 years after THA. Patients without hip pain after THA served as controls. Methods: Eighteen patients with chronic hip pain and 18 controls without chronic hip pain were recruited from a previous questionnaire study about hip pain after total hip arthroplasty. All participants answered questions about pain and mental vulnerability and underwent clinical examination followed by quantitative sensory testing (brush‐evoked allodynia, pinprick hyperalgesia, mechanical and thermal thresholds). Results: Brush‐evoked allodynia was present in 4 patients with hip pain (P=0.1) and pinprick hyperalgesia (P=0.02) was more frequent in patients with chronic hip pain. Mechanical and thermal thresholds were similar in patients and controls. Patients with chronic hip pain had higher scores on the mental vulnerability scale (P<0.001). Chronic hip pain was significantly associated with low back pain (P=0.002). Conclusions: We found signs of hypersensitivity on the operated side, which was more prominent in patients with pain. Pain referred from the back or deeper structures in the hip seems to play a role for the pain in subgroups of patients. In addition, chronic hip pain was associated with mental vulnerability.     

Gender differences in pain and secondary hyperalgesia after heat/capsaicin sensitization in healthy volunteers.

In most published studies women are more sensitive to experimental pain than men. Enhanced central pain processing in women has been suggested, but psychosocial factors might also have affected the findings. Data from five completed healthy volunteer studies were analyzed to investigate gender differences in development of secondary hyperalgesia. Cutaneous hyperalgesia was induced with the heat/capsaicin sensitization model. Outcome measures were areas of secondary hyperalgesia to brush and von Frey hair stimulation after heat and capsaicin sensitization, rating of pain during heat/capsaicin sensitization, and heat pain detection thresholds. There was a trend toward smaller areas of secondary hyperalgesia in women. After adjusting for estimated gender differences in forearm surface area, areas to brush but not von Frey hair stimulation after capsaicin sensitization were larger in women. Peak pain, but not total pain, during prolonged noxious thermal stimulation was higher in women. There was no gender difference in pain ratings during capsaicin sensitization or in heat pain detection thresholds. The results provided only limited support to the hypothesis that gender differences in clinical pain syndromes can be explained by enhanced central sensitization in women. PERSPECTIVE: Our findings suggest that gender differences in nociceptive transmission and neuronal sensitization are small and provide only limited support to the hypothesis that gender differences in acute and chronic pain syndromes can be explained by enhanced central sensitization in women.     

Widespread sensory hypersensitivity is a feature of chronic whiplash-associated disorder but not chronic idiopathic neck pain

OBJECTIVES: To investigate sensory changes present in patients with chronic whiplash-associated disorders and chronic idiopathic neck pain using a variety of quantitative sensory tests to better understand the pain processing mechanisms underlying persistent symptoms. METHODS: A case control study was used with 29 subjects with chronic whiplash-associated disorders, 20 subjects with chronic idiopathic neck pain, and 20 pain-free volunteers. Pressure pain thresholds were measured over the articular pillars of C2-C3, C5-C6, the median, radial, and ulnar nerve trunks in the arm and over a remote site, the muscle belly of tibialis anterior. Heat pain thresholds, cold pain thresholds, and von Frey hair sensibility were measured over the cervical spine, tibialis anterior, and deltoid insertion. Anxiety was measured with the Short-Form of the Spielberger State Anxiety Inventory. RESULTS: Pressure pain thresholds were decreased over cervical spine sites in both subject groups when compared with controls (P < 0.05). In the chronic whiplash-associated disorders group, pressure pain thresholds were also decreased over the tibialis anterior, median, and radial nerve trunks (P < 0.001). Heat pain thresholds were decreased and cold pain thresholds increased at all sites (P < 0.03). No differences in heat pain thresholds or cold pain thresholds were evident in the idiopathic neck pain group at any site compared with the control group (P > 0.27). No abnormalities in von Frey hair sensibility were evident in either neck pain group (P > 0.28). DISCUSSION: Both chronic whiplash-associated disorders and idiopathic neck pain groups were characterized by mechanical hyperalgesia over the cervical spine. Whiplash subjects showed additional widespread hypersensitivity to mechanical pressure and thermal stimuli, which was independent of state anxiety and may represent changes in central pain processing mechanisms. This may have implications for future treatment approaches.     

Quantitative somatosensory testing of subjects with chronic post-traumatic headache: Implications on its mechanisms

BackgroundChronic headache is one of the most prominent symptoms among subjects with traumatic head injury (THI). Despite the relatively high prevalence of chronic post-traumatic headache (CPTHA) and its enormous effect on the already poor quality of life of subjects with THI, its mechanisms has not been studied in depth.ObjectiveTo conducted quantitative somatosensory testing in THI subjects with and without chronic post-traumatic headache (CPTHA) in order to shed light on the yet, unknown pathophysiology of CPTHA.MethodsTHI subjects with and without CPTHA and healthy controls underwent thermal and mechanical threshold measurements in painful and pain-free regions in the head and in their hands (a remote pain-free region) and filled out and the post-traumatic stress disorder (PTSD) inventory. In addition, the THI and CPTHA filled out the Mc’Gill pain questionnaire (MPQ).ResultsTHI subjects with CPTHA had significantly higher thermal thresholds in both the head and hand indicating central damage to the pain and temperature system and in addition, a significantly lower pressure-pain threshold in the head as well as more severe PTSD symptomatology than the pain-free THI subjects and healthy controls.ConclusionsThe sensory profile of subjects with CPTHA suggests that CPTHA may be a form of central pain. The cranial mechanical hyperalgesia may originate from peripheral tissue damage accompanying the THI. Psychological factors may contribute to the development, and maintenance of CPTHA in susceptible individuals.     

Generalized deep-tissue hyperalgesia in patients with chronic low-back pain.

Some chronic painful conditions including e.g. fibromyalgia, whiplash associated disorders, endometriosis, and irritable bowel syndrome are associated with generalized musculoskeletal hyperalgesia. The aim of the present study was to determine whether generalized deep-tissue hyperalgesia could be demonstrated in a group of patients with chronic low-back pain with intervertebral disc herniation. Twelve patients with MRI confirmed lumbar intervertebral disc herniation and 12 age and sex matched controls were included. Subjects were exposed to quantitative nociceptive stimuli to the infraspinatus and anterior tibialis muscles. Mechanical pressure (thresholds and supra-threshold) and injection of hypertonic saline (pain intensity, duration, distribution) were used. Pain intensity to experimental stimuli was assessed on a visual analogue scale (VAS). Patients demonstrated significantly higher pain intensity (VAS), duration, and larger areas of pain referral following saline injection in both infraspinatus and tibialis anterior. The patients rated significantly higher pain intensity to supra-threshold mechanical pressure stimulation in both muscles. In patients, the pressure pain-threshold was lower in the anterior tibialis muscle compared to controls. In conclusion, generalized deep-tissue hyperalgesia was demonstrated in chronic low-back pain patients with radiating pain and MRI confirmed intervertebral disc herniation, suggesting that this central sensitization should also be addressed in the pain management regimes.     

Neurophysiological characterization of postherniotomy pain

Inguinal herniotomy is one of the most frequent surgical procedures and chronic pain affecting everyday activities is reported in approximately 10% of patients. However, the neurophysiological changes and underlying pathophysiological mechanisms of postherniotomy pain are not known in detail, thereby precluding advances in treatment strategies and prophylaxis. Therefore, we examined forty-six patients reporting moderate to severe postherniotomy pain affecting daily activities for more than a year postoperatively, and compared them with a control group of patients without pain 1 yr postoperatively. A quantitative sensory testing protocol was used, assessing sensory dysfunction type, location and severity. We assessed the protocol test-retest variability using data from healthy control subjects. All patients (pain and pain-free) had signs of nerve damage, seen as sensory dysfunction. Detection thresholds for tactile and warmth stimulation were significantly increased while cold detection and pressure pain detection thresholds were significantly decreased in pain patients compared to controls. Repetitive punctuate and brush stimulation resulted in significantly more frequent and intense pain on the painful side than on the unaffected side in pain patients, and was not observed in controls. Our findings showed large and small fiber dysfunction in both pain and pain-free patients but more profound in pain patients and with signs of central sensitization (abnormal temporal summation). The specific finding of reduced pain detection threshold over the external inguinal annulus is consistent with damage to the cutaneous innervation territory of nervous structures in the inguinal region. The correspondence between pain location and sensory disturbance suggests that the pain is neuropathic in nature. Whether the underlying pathophysiological mechanisms are related to direct intraoperative nerve injury or nerve injury due to an inflammatory mesh response remains to be determined.     

Bilateral widespread mechanical pain hypersensitivity as sign of central sensitization in patients with cluster headache

Objective.— To investigate bilateral widespread pressure pain hyperalgesia in deep tissues over symptomatic (trigemino‐cervical) and nonsymptomatic (distant pain‐free) regions in patients with cluster headache (CH). Background.— Central sensitization is claimed to play a relevant role in CH. No study has previously searched for widespread pressure hyperalgesia in deep tissues over both symptomatic (trigemino‐cervical) and nonsymptomatic (distant pain‐free) regions in patients with CH. Methods.— Sixteen men (mean age: 43 ± 11 years) with CH in a remission phase and 16 matched controls were recruited. Pressure pain thresholds (PPTs) were bilaterally measured over the supra‐orbital (V1), infra‐orbital (V2), mental (V3), median (C5), radial (C6), and ulnar (C7) nerves, C5‐C6 zygapophyseal joint, mastoid process, and tibialis anterior muscle by an assessor blinded to the subjects' condition. Results.— The results showed that PPT levels were significantly decreased bilaterally in patients with CH as compared with healthy controls (all sites, P < .001). A greater degree of sensitization over the mastoid process (P < .001) and a lower degree of sensitization over the tibialis anterior muscle (P < .01) was found. Conclusions.— Our findings revealed bilateral widespread pressure pain hypersensitivity in patients with CH confirming the presence of central sensitization mechanisms in this headache condition.     

167例老年胰腺癌特点及与糖尿病、慢性胰腺炎的关系分析

目的 :分析 16 7例老年胰腺癌的临床特征 ,探讨胰腺癌与糖尿病、慢性胰腺炎之间的关系。方法 :对 16 7例胰腺癌和16 7例对照组进行回顾性对比分析 ,计算其相对危险度 (RR) ,评价胰腺癌与糖尿病、慢性胰腺炎的关系。结果 :(1)胰腺癌的临床表现以腹痛、黄疸、消瘦、腹胀和上腹不适为主 ,男性多见。无一例是早期胰腺癌。 (2 )在胰腺癌组中 2年内确诊糖尿病有4 5例 (2 6 .95 % ) ,对照组中有 4例 (2 .4 0 % ) ,两组有显著差异 (P <0 .0 1)。胰腺癌组中糖尿病病史两年以上有 12例 (7.19% ) ,对照组中有 14例 (8.38% ) ,两组无显著差异 (P >0 .0 5 )。 (3)胰腺癌组和对照组分别检出慢性胰腺炎 6例和 1例 ,两组无显著差异 (P >0 .0 5 )。结论 :老年人胰腺癌确诊相对较晚 ,常伴有糖尿病的发生 ,但糖尿病不是胰腺癌的危险因素 ,糖尿病是胰腺癌的继发性结果。慢性胰腺炎与胰腺癌发生无相关性。老年人出现血糖异常须警惕胰腺癌的发生。     

Gender-related effects of chronic non-malignant pain and opioid therapy on plasma levels of macrophage migration inhibitory factor (MIF)

Macrophage migration inhibitory factor (MIF) is a cytokine produced by neuroendocrine and immune tissues that possesses several characteristics of a neuroendocrine mediator. Chronic pain is known to affect and to be affected by neuroendocrine and immune mechanisms. In the present study, the plasma levels of MIF and several hormones (cortisol, estradiol, testosterone) were determined to evaluate their mutual behaviour in controls and in chronic pain patients. Blood samples were collected from males and females divided into groups depending on their age (younger or older than 55) and health condition: (1) pain-free control subjects; (2) chronic non-malignant pain subjects. Moreover, two additional groups were added to evaluate the effects of short- and long-term opioid administration: (3) short-term opioid-treated chronic pain patients and (4) long-term opioid-treated chronic pain patients (longer than 6 months). MIF in control/younger men was higher than in all the other control and chronic pain groups. MIF was lower in pain patients than in controls of both sexes. MIF was not changed by morphine administration; its levels remained lower in opioid-treated subjects than in controls after both short- and long-lasting administration. Chronic pain changed hormone plasma levels differently in male and female patients. MIF was positively correlated with testosterone and negatively with estradiol. These results demonstrate sex differences in the younger men and women and a strong pain-induced decrease of MIF availability. These findings suggest the involvement of this cytokine in the sex differences observed in chronic pain conditions.     

Mechanisms of opioid-induced tolerance and hyperalgesia.

Opioid tolerance and opioid-induced hyperalgesia are conditions that negatively affect pain management. Tolerance is defined as a state of adaptation in which exposure to a drug induces changes that result in a decrease of the drug's effects over time. Opioid-induced hyperalgesia occurs when prolonged administration of opioids results in a paradoxic increase in atypical pain that appears to be unrelated to the original nociceptive stimulus. Complex intracellular neural mechanisms, including opioid receptor desensitization and down-regulation, are believed to be major mechanisms underlying opioid tolerance. Pain facilitatory mechanisms in the central nervous system are known to contribute to opioid-induced hyperalgesia. Recent research indicates that there may be overlap in the two conditions. This article reviews known and hypothesized pathophysiologic mechanisms surrounding these phenomena and the clinical implications for pain management nurses.     

The Specificity and Mechanisms of Hemilateral Sensory Disturbances in Complex Regional Pain Syndrome

Hyperalgesia often extends from the affected limb to the ipsilateral forehead in patients with complex regional pain syndrome (CRPS). To investigate whether this is more common in CRPS than other chronic pain conditions, pressure-pain thresholds and sharpness to a firm bristle were assessed on each side of the forehead, at the pain site, and at an equivalent site on the contralateral side in 32 patients with chronic pain other than CRPS (neuropathic or nociceptive limb pain, radicular pain with referral to a lower limb or postherpetic neuralgia), and in 34 patients with CRPS. Ipsilateral forehead hyperalgesia to pressure pain was detected in 59% of CRPS patients compared with only 13% of patients with other forms of chronic pain. Immersion of the CRPS-affected limb in painfully cold water increased forehead sensitivity to pressure, especially ipsilaterally, whereas painful stimulation of the healthy limb reduced forehead sensitivity to pressure pain (albeit less efficiently than in healthy controls). In addition, auditory discomfort and increases in pain in the CRPS-affected limb were greater after acoustic startle to the ear on the affected than unaffected side. These findings indicate that generalized and hemilateral pain control mechanisms are disrupted in CRPS, and that multisensory integrative processes may be compromised.

Perspective

The findings suggest that hemilateral hyperalgesia is specific to CRPS, which could be diagnostically important. Disruptions in pain-control mechanisms were associated with the development of hyperalgesia at sites remote from the CRPS limb. Addressing these mechanisms could potentially deter widespread hyperalgesia in CRPS.     

Enhanced central pain processing of fibromyalgia patients is maintained by muscle afferent input: A randomized, double-blind, placebo-controlled study

Fibromyalgia (FM) syndrome is characterized by pain and widespread hyperalgesia to mechanical, thermal, and electrical stimuli. Despite convincing evidence for central sensitization of nociceptive pain pathways, the role of peripheral tissue impulse input in the initiation and maintenance of FM is unclear. Therefore this randomized, double-blind, placebo-controlled trial of 22 female normal controls (NCs) and 28 female FM subjects tested the effects of trapezius muscle (TrapM) tender point injections with 1% lidocaine on local pain thresholds as well as on remote heat hyperalgesia at the forearm. Prior to muscle injections shoulder pain was standardized by tonic mechanical muscle stimulation, resulting in local pain ratings of 4.0 ± 0.5 VAS units. Tonic muscle stimulation was interrupted for the TrapM injections but was continued afterwards at the same level. NC as well as FM subjects experienced significant increases of TrapM pressure pain thresholds from lidocaine injections but not from placebo injections (p < 0.001). Additionally, heat hyperalgesia of FM participants was significantly reduced at areas remote from the injection site (forearm) by lidocaine but not by placebo (p = 0.02). Neither lidocaine nor saline injections significantly affected clinical FM pain ratings, a result most likely due to the very low dose of lidocaine (50 mg) used in this trial. Conclusion: Lidocaine injections increased local pain thresholds and decreased remote secondary heat hyperalgesia in FM patients, emphasizing the important role of peripheral impulse input in maintaining central sensitization in this chronic pain syndrome; similar to other persistent pain conditions such as irritable bowel syndrome and complex regional pain syndrome.     

Depression and changed pain perception: hints for a central disinhibition mechanism

Although patients with a depressive disorder report often of pain, their sensitivity to experimental pain is controversial, probably due to differences in sensory testing methods and to the lack of normal values. Therefore, we used a standardized and validated comprehensive sensory testing paradigm to assess the peripheral and central nervous system performance in depressive patients compared to healthy controls and chronic pain patients with fibromyalgia syndrome (FMS), in which depression is a common comorbidity. Twenty-five depressive psychiatric inpatients (pain-free: n=20), 35 FMS outpatients and 25 healthy controls underwent quantitative sensory testing (QST), including thermal and mechanical detection and pain thresholds, pain sensitivity and responsiveness to repetitive noxious mechanical stimuli (wind-up). In depressive disorder (to a lesser extent also in FMS), significantly decreased cold pain thresholds and an increased wind-up were found, although the mechanical pain thresholds and pain sensitivity were comparable to those of the healthy controls. All the detection thresholds were within the normal range in all the groups. In depressive disorder, there were no significant side differences in the detection and pain thresholds. The results contradict the former assumption of a general insensitivity to experimental pain in depressive disorder. In the mostly pain-free patients signs of an enhanced central hyperexcitability are even more pronounced than usually found in chronic pain patients (e.g. FMS), indicating common mechanisms in depressive disorder and chronic pain in accordance with the assumption of non-pain associated mechanisms in depressive disorder for central hyperexcitability, e.g. by inhibited serotonergic function. Furthermore, this trial demonstrates the feasibility of QST in depressive patients.     

Prevention of pancreatitis in patients with idiopathic recurrent pancreatitis: a prospective nonblinded randomized study using endoscopic stents

BACKGROUND AND STUDY AIMS: Currently there is no available therapy to prevent attacks of acute pancreatitis in patients with idiopathic recurrent pancreatitis (IRP). This randomized, nonblinded prospective, controlled trial was undertaken to evaluate the effectiveness of pancreatic duct stents in preventing attacks of pancreatitis in IRP. PATIENTS AND METHODS: During a 5-year period 34 patients met the diagnostic criteria for IRP. Patients were randomly assigned to one of two groups; 19 patients (14 women, 5 men, mean age 44) to the pancreatic stent group; and 15 patients (10 women, five men, mean age 47) to the control group. The stent group received three stents over a period of 1 year and the control group had selective pancreatograms but no stent. Mean follow-up was 33 months (range 13-77) and 35 months (range 10-78) in the stent and control groups, respectively. Episodes of pancreatitis, frequency and intensity of pain requiring emergency room visits, and hospitalizations were recorded. RESULTS: Recurrence of pancreatitis occurred in eight out of 15 patients (53%) in the control group, but in only two our of 19 patients (11%) in the stent group (P<0.02). Two patients in the control group who had recurrences of pancreatitis crossed over to stent therapy and had no further pancreatitis thereafter. Six patients each, 32% and 40% in the stent and control groups respectively, continued to have pancreatic type pain. In the study period 17 stents were occluded and 14 migrated out. CONCLUSION: The results of this study suggest that pancreatic duct stenting may prevent recurrent attacks of pancreatitis in IRP patients. Intermittent pancreatic duct sphincter dysfunction or relative outlet obstruction may be the underlying cause for the recurrent attacks of pancreatitis.     

Differences in somatic perception in female patients with irritable bowel syndrome with and without fibromyalgia

BACKGROUND: Irritable bowel syndrome (IBS) and fibromyalgia (FM) are considered chronic syndromes of altered visceral and somatic perception, respectively. Because there is a significant overlap of IBS and FM, shared pathophysiological mechanisms have been suggested. Although visceral perception has been well studied in IBS, somatic perception has not. AIMS: To compare hypervigilance and altered sensory perception in response to somatic stimuli in patients with IBS, IBS+FM, and healthy controls. METHODS: Eleven IBS females (mean age 40), 11 IBS+FM females (mean age 46), and ten healthy female controls (mean age 39) rated pain perception in response to pressure stimuli administered to active somatic tender points, non-tender control points and the T-12 dermatome, delivered in a predictable ascending series, and delivered in an unpredictable randomized fashion (fixed stimulus). RESULTS: Although IBS patients had similar pain thresholds during the ascending series compared with controls, they were found to have somatic hypoalgesia with higher pain thresholds and lower pain frequency and severity during fixed stimulus series compared with IBS+FM patients and controls (P<0.05). Patients with IBS+FM were more bothered by the somatic stimuli and had somatic hyperalgesia with lower pain thresholds and higher pain frequency and severity. CONCLUSIONS: Both hypervigilance and somatic hypoalgesia contribute to the altered somatic perception in IBS patients. Co-morbidity with FM results in somatic hyperalgesia in IBS patients.