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Biomedical subjects

Lin Chang

Publications and source records attributed to Lin Chang.

At least 19 recordsLinked to original sources
PubMed2006

Effect of sex on perception of rectosigmoid stimuli in irritable bowel syndrome.

In irritable bowel syndrome (IBS) patients, the relationship between sex and sensitivity to visceral stimuli is incompletely understood. Our aim was to evaluate the effect of sex on perceptual responses to visceral stimulation in IBS. Fifty-eight IBS patients (mean age 42+/-1 yr; 34 men, 24 women) and 26 healthy controls (mean age 38+/-3 yr; 9 men, 17 women) underwent barostat-assisted distensions of the rectum and sigmoid colon. Rectal discomfort thresholds were measured using a randomized, phasic distension paradigm before and after repeated noxious sigmoid stimulation (SIG, 60-mmHg pulses). Sex had a significant effect on rectal discomfort thresholds. Women with IBS were the most sensitive (lower thresholds [27+/-2.7 mmHg] and higher ratings), with significantly lower rectal discomfort thresholds compared with men with IBS (38+/-2.3 mmHg) and healthy women who were the least sensitive (41.9+/-3.2 mmHg; both P<0.01). There were no significant differences in rectal discomfort thresholds between healthy men (34+/-4.3 mmHg) and men with IBS. Across both IBS and control groups, women demonstrated a significant lowering of discomfort thresholds after noxious sigmoid stimulation (P<0.01), while men did not. Sex significantly influences perceptual sensitivity to rectosigmoid distension. Women show greater perceptual responses to this paradigm.

Adult↗
PubMed2006

Efficacy and safety of hypertonic saline solutions in the treatment of severe head injury.

BACKGROUND: The present study was undertaken to evaluate the efficacy and safety of hypertonic saline (HS) in the treatment of intracranial hypertension after severe head injury. METHODS: This prospective, observational study was performed in an 11-bed neurosurgery intensive care unit of a teaching hospital. From February 2002 to September 2004, 18 severely head-injured patients with elevated intracranial pressure (ICP) and Glasgow Coma Scale scores of 5 to 8 (mean, 5.9 +/- 1.2) were admitted to the unit and treated according to a standard protocol. One dose per day of 3% saline was administered by rapid infusion (300 mL/20 min) when ICP values exceeded 20 mm Hg. After infusion, cerebral blood flow, ICP, blood pressure, end-tidal carbon dioxide, and heart rate were monitored continuously for 60 minutes and recorded. Serum osmolarity, sodium, potassium, chloride, arterial carbon dioxide pressure, arterial oxygen pressure, hemoglobin, lactic acid, and pH were measured immediately before infusion (zero time) and 20 and 60 minutes after infusion. Mean arterial pressure, cerebral perfusion pressure (CPP), mean flow velocity (MFV), and pulsatility index (PI) were also recorded and analyzed. RESULTS: Intracranial pressure fell immediately after initiation of infusion with further significant decreases observed at 20 and 60 minutes (30.4 +/- 8.5, 24.3 +/- 7.4, and 23.8 +/- 8.3 mm Hg, respectively; P < .01). At these respective times CPP increased significantly (78.7 +/- 8.7, 83.2 +/- 7.8, and 87.2 +/- 12.8 mm Hg), PI dropped rapidly (1.51 +/- 0.42, 1.38 +/- 0.32, and 1.34 +/- 0.33) and MFV increased (66.26 +/- 25.91, 71.92 +/- 28.13, and 68.74 +/- 28.44). Serum sodium increased from 141.3 +/- 7.2 to 146.3 +/- 7.2 mmol/L after 20 minutes and returned to 144.3 +/- 7.36 mmol/L at 60 minutes. Potassium concentrations decreased significantly from 3.9 +/- 0.39 to 3.55 +/- 0.35 mmol/L after 20 minutes (P < .01). Lactic acid values at 0, 20, and 60 minutes were 1.6 +/- 0.5, 1.47 +/- 0.48, and 1.38 +/- 0.53 mmol/L, respectively (P < .01). CONCLUSION: Rapid infusion of single dose daily of HS is a safe alternative for the treatment of elevated ICP in severe head injury. Further evaluations of long-term consequences and complications and of maximal tolerance to this treatment are required.

Adolescent↗
PubMed2006

Clinical experience of hydroxyethyl starch (10% HES 200/0.5) in cerebral perfusion pressure protocol for severe head injury.

BACKGROUND: The present study was undertaken to evaluate 10% hydroxyethyl starch (HES 200/0.5) with regard to its clinical outcome and safety in the treatment of severe head injury. METHODS: Retrospective review of patient data from a prospectively designed standard treatment protocol for severe head injury. The standard protocol included (1) cerebral perfusion pressure higher than 60 mm Hg, (2) colloid solution (10% HES 200/0.5) 1000 mL/d in combination with crystalloid solution, (3) stepwise management of intracranial hypertension. Renal function, coagulation function, and electrolytes were evaluated every other day. The data of intracranial pressure, mean arterial pressure, cerebral perfusion pressure, intake, output, mannitol, complications, and outcome were recorded and analyzed. RESULTS: There were 78 patients, aged 45.61 +/- 21.80 years, in this study. The initial Glasgow Coma Scale score was 6.35 +/- 1.38. Seventy-three patients received operations with intracranial pressure monitoring. Blood transfusion was surgery related (days 1 and 2); otherwise, it was rarely used (P<.05). Prolonged prothrombin time was shown only 7 (2.65%) times of 234 of blood sampling. There was no anaphylactic reaction, pulmonary complications, or renal function deterioration in the course of our observation. The chart review of the patients at 6 months revealed the following: favorable outcome, 55.1%; unfavorable outcome, 33.3%; and mortality, 11.6%. CONCLUSIONS: The 10% HES (200/0.5) can be used in the treatment protocol of severe head injury. There is no definite bleeding complications documented by current dosage of HES. Besides, balanced fluid management can be achieved without causing serious pulmonary complications. However, a further randomized, prospective study is needed to define the actual benefit of HES in fluid management and clinical outcome.

Adult↗
PubMed2006

Gender, age, society, culture, and the patient's perspective in the functional gastrointestinal disorders.

Patients with functional gastrointestinal disorders (FGID) often experience emotional distress, a perceived lack of validation, and an unsatisfactory experience with health care providers. A health care provider can provide the patient with a framework in which to understand and legitimize their symptoms, remove self-doubt or blame, and identify factors that contribute to symptoms that the patient can influence or control. This framework can be strengthened with the consideration of various important factors that impact FGID but are often overlooked. These include gender, age, society, culture, and the patient's perspective. There is evidence for sex- and gender-related differences in FGID, particularly irritable bowel syndrome (IBS). Whereas the majority of FGID, including IBS, bloating, constipation, chronic functional abdominal pain, and pelvic floor dysfunction, are more prevalent in women than men, functional esophageal and gastroduodenal disorders do not appear to vary by gender. Limited studies suggest that sex differences in visceral perception, cardioautonomic responses, gastrointestinal motility, and brain activation patterns to visceral stimuli exist in IBS. Gender differences in social factors, psychological symptoms, and response to psychological treatments have not been adequately studied. However, there appears to be a greater clinical response to serotonergic agents developed for IBS in women compared to men. The impact of social and cultural factors on the meaning, expression, and course of FGID are important. The prevalence of IBS appears to be lower in non-Western than Western countries. Although further studies are needed, the existing literature suggests that they are important to consider from both research and clinical perspectives.

Age Factors↗
PubMed2006

Longitudinal change in perceptual and brain activation response to visceral stimuli in irritable bowel syndrome patients.

BACKGROUND & AIMS: Symptom-related fears and associated hypervigilance toward visceral stimuli may play a role in central pain amplification and irritable bowel syndrome (IBS) pathophysiology. Repeated stimulus exposure leads to decreased salience of threat and reduction of hypervigilance. We sought to evaluate hypervigilance in IBS visceral hypersensitivity and associated brain activity. METHODS: Twenty IBS patients (14 female; moderate to severe symptoms) and 14 healthy controls participated in symptom and rectal distention assessments 6 times over 12 months. In a subset of 12 IBS patients, H2 15O-positron emission tomography images were obtained during baseline, rectal distentions, and anticipation of an aversive distention during the first and last session. Statistical parametric mapping (SPM99) was used to identify areas and networks activated during each session as well as those with differential activation across the 2 sessions. RESULTS: Perceptual ratings of the rectal inflations normalized over 12 months, whereas IBS symptom severity did not. There were no sex-related differences in these response patterns. Stable activation of the central pain matrix was observed over 12 months, and activity in limbic, paralimbic, and pontine regions decreased. During the anticipation condition, there were significant decreases in amygdala, dorsal anterior cingulate cortex, and dorsal brainstem activation at 12 months. Covariance analysis supported the hypothesis of changes in an arousal network including limbic, pontine, and cortical areas underlying the decreased perception seen over the multiple stimulations. CONCLUSIONS: In IBS patients, repeated exposure to experimental aversive visceral stimuli results in the habituation of visceral perception and central arousal, despite stable activation of networks processing visceral pain and its anticipation.

Abdominal Pain↗
PubMed2006

Irritable bowel syndrome: new and emerging therapies.

PURPOSE OF REVIEW: Irritable bowel syndrome refers to abdominal discomfort associated with altered bowel habits. Recent evidence suggests that the primary pathophysiologic mechanism is brain-gut dysregulation. Many central and peripheral factors are involved. This article will review important pathophysiologic mechanisms with a focus on new and emerging therapies. RECENT FINDINGS: Prior gastroenteritis and small intestinal bacterial overgrowth may be important for treatment of irritable bowel syndrome. Understanding of serotonergic receptors in gastrointestinal function has led to the development of serotonergic agents such as alosetron and tegaserod. Novel agents targeting other receptor sites include neurokinin and neurohormonal modulators, chloride channels and opioid receptors. Other therapeutic approaches - behavioral treatments, probiotics, antibiotics and alternative therapies - have developing roles in the treatment of irritable bowel syndrome. SUMMARY: A better understanding of pathophysiologic mechanisms has resulted in therapeutic advances. Prokinetic therapies may have a role in nondiarrhea predominant irritable bowel syndrome. Antidepressants are used to modulate pain and treat comorbid psychological distress. Newer agents target various receptor sites. Advances in psychological/behavioral treatments and alternative modalities hold promise for the future.

Antidepressive Agents↗
PubMed2006

Incidence of ischemic colitis and serious complications of constipation among patients using alosetron: systematic review of clinical trials and post-marketing surveillance data.

BACKGROUND: Ischemic colitis and serious complications of constipation have been reported in association with the use of alosetron, which is approved for women with severe diarrhea-predominant IBS who have failed conventional therapies. This systematic review calculated the incidence of these adverse events in alosetron-using patients in clinical trials and post-marketing surveillance. METHODS: A panel of experts in epidemiology and functional bowel disorders reviewed clinical trial report forms and FDA MedWatch forms of each reported case of ischemic colitis or serious complications of constipation. Experts were blinded about whether patients used alosetron or placebo. Using pre-specified criteria, experts rated the likelihood of an accurate diagnosis and an association between medication use and adverse events. Cases that were not consistent with the reported diagnosis or not possibly associated with medication use were eliminated from calculation of incidence rates of adverse events. RESULTS: Pooled data from clinical trials indicate an increased rate of ischemic colitis among alosetron-using patients compared to placebo-using patients (0.15%vs 0.0%, respectively, p = 0.03), but there was no significant difference in the rate of serious complications of constipation. All (19/19) alosetron-using patients with ischemic colitis had reversible colitis without long-term sequelae. Based on post-marketing surveillance data, the post-adjudication rate of ischemic colitis is 1.1 per 1,000 patient-years of alosetron use and the rate of serious complications of constipation is 0.66 per 1,000 patient-years of alosetron use. CONCLUSION: The incidence of ischemic colitis and serious complications of constipation is very low and is rarely associated with long-term sequelae or serious morbidity.

Carbolines↗
PubMed2005

A comparison of visceral and somatic pain processing in the human brainstem using functional magnetic resonance imaging.

Evidence from both human and animal studies has demonstrated a key role for brainstem centers in the control of ascending nociceptive input. Nuclei such as the rostral ventromedial medulla and periaqueductal gray (PAG) are able to both inhibit and facilitate the nociceptive response. It has been proposed that altered descending modulation may underlie many of the chronic pain syndromes (both somatic and visceral). We used functional magnetic resonance imaging to image the neural correlates of visceral and somatic pain within the brainstem. Ten healthy subjects were scanned twice at 3 tesla, during which they received matched, moderately painful, electrical stimuli to either the midline lower abdomen or rectum. Significant activation was observed in regions consistent with the PAG, nucleus cuneiformis (NCF), ventral tegmental area/substantia nigra, parabrachial nuclei/nucleus ceruleus, and red nucleus bilaterally to both stimuli. Marked spatial similarities in activation were observed for visceral and somatic pain, although significantly greater activation of the NCF (left NCF, p = 0.02; right NCF, p = 0.01; Student's paired t test, two-tailed) was observed in the visceral pain group compared with the somatic group. Right PAG activity correlated with anxiety during visceral stimulation (r = 0.74; p < 0.05, Pearson's r, two-tailed) but not somatic stimulation. We propose that the differences in NCF and right PAG activation observed may represent a greater nocifensive response and greater emotive salience of visceral over somatic pain.

Abdomen↗
PubMed2005

Ghrelin blunted vascular calcification in vivo and in vitro in rats.

Ghrelin is a new peptide with regulatory actions in growth hormone secretion in the anterior pituitary gland and in energy metabolism. Currently, ghrelin has potently protective effects in cardiovascular diseases. We used an in vivo model of rat vascular calcification induced by vitamin D3 and nicotine and one of cultured rat vascular smooth muscular cells (VSMCs) calcification induced by beta-glycerophosphate to study the possible mechanism in the regulatory action of ghrelin in vascular calcification. Calcification increased total Ca2+ content and 45Ca2+ deposition in aortas and VSMCs and alkaline phosphatase (ALP) activation in plasma, aortas and VSMCs. However, calcified aortas and VSMCs showed a significant decrease in osteopontin (OPN) mRNA expression and a marked reduction of ghrelin levels in plasma and its mRNA expression in aortas. The aortic calcification was significantly attenuated by subcutaneous administration of ghrelin 30 and 300 nmol kg(-1) day(-1) for 4 weeks, and the latter dosage was more potent than the former. Ghrelin treatment at the two dosages reduced the total aorta Ca2+ content by 24.4% and 28.1%, aortic 45Ca2+ deposition by 18.4% and 24.9%, plasma ALP activity by 36.6% and 76.7%, and aortic ALP activity by 10.3% and 47.6% (all P < 0.01 or 0.05), respectively. Ghrelin at 10(-8)-10(-6) mol/L attenuated the calcification in cultured VSMCs, with decreased total Ca2+ content, 45Ca2+ deposition and ALP activity and increased OPN mRNA expression, in a concentration-dependent manner. In addition, endothelin levels in plasma and aortas and its mRNA expression in aortas significantly increased with calcification, but ghrelin treatment significantly decreased endothelin levels and mRNA expression, with the high dosage being more potent than the lower dosage. These results indicate that local ghrelin in vascular was down-regulated during vascular calcification, whereas administration of ghrelin effectively attenuated vascular and VSMCs calcification.

Animals↗
PubMed2005

Adrenomedullin(27-52) inhibits vascular calcification in rats.

Adrenomedullin (ADM) has the vasodilatory properties and involves in the pathogenesis of vascular calcification. ADM could be degraded into more than six fragments in the body, including ADM(27-52), and we suppose the degrading fragments from ADM do the same bioactivities as derived peptides from pro-adrenomedullin. The present study carries forward by assessing the effects on vascular calcification of the systemic administration of ADM(27-52). The rat vascular calcific model was replicated with vitamin D3 and nicotine. ADM or/and ADM(27-52) were systemically administrated with mini-osmotic pump beginning at seventh day after the model replication for 25 days. Vascular calcific nodules histomorphometry, vascular calcium content, vascular calcium uptake, alkaline phosphatase activity, and osteopontin-mRNA quantification in aorta were assessed. ADM limited 40.2% vascular calcific nodules (P<0.01), did not effect on calcium content (P>0.05), reduced 44.4% calcium uptake (P<0.01), lowered 21.1% alkaline phosphatase activity (P<0.01), and regulated 40.9% downwards osteopontin-mRNA expression (P<0.01) in the aorta of rats with vascular calcification. ADM(27-52) receded 32.0% vascular calcific nodules (P<0.01), taken from 55.5% calcium content (P<0.01), did not affect calcium uptake (P>0.05), inhibited 22.5% alkaline phosphatase activity (P<0.01), and restrained 21.9% osteopontin-mRNA expression (P<0.01) in the aorta of rats with vascular calcification. Both of ADM and ADM(27-52) did interact on vascular calcification each other. ADM could partially antagonize the effects of ADM(27-52) in taking from calcium content (17.5%, P<0.01) and in receding vascular calcific nodules (18.6%, P<0.01). ADM could obviously enhance the action of ADM(27-52) in inhibiting alkaline phosphatase activity (14.4%, P<0.01) and in reducing calcium uptake (11.4%, P<0.01). ADM(27-52) could partially antagonize the effects of ADM on regulating downwards osteopontin-mRNA expression (17.0%, P<0.01). It is concluded that ADM(27-52) derived from ADM acts as an inhibitory agent on vascular calcification, with special mechanisms different from ADM derived from ADM progenitor molecule.

Adrenomedullin↗
PubMed2005

Protective role of metallothionein in stress-induced gastric ulcer in rats.

AIM: To illustrate the pathophysiological role of metallothionein (MT) in gastric ulcer induced by stress. METHODS: Wistar rats underwent water-immersion-restraint (WIR) stress, ZnSO(4) (an MT inducer) treatment, WIR+ZnSO(4) or WIR+MT, and the ulcer index (UI) was estimated in excised stomach and liver tissues. The mRNA level of gastric MT was determined by semi-quantitative RT-PCR. The MT content in gastric and hepatic tissues was determined by Cd/hemoglobin affinity assay. The lipid peroxidation products malondialdehyde (MDA) and conjugated dienes (CD) were estimated by use of thiobarbituric acid reactive species and ultraviolet spectrophotometry. RESULTS: WIR stress induced severe gastric mucosal lesions in rats. Compared with control rats, stressed rats had increased lipid peroxide content in serum and stomach and liver tissues. MDA content was increased by 34%, 21% and 29% and CD level by 270%, 83% and 28%, respectively. MT content in the stomach and liver was increased by 0.74- and 1.8-fold, and the MT-mRNA level in the stomach was increased by 26%. Pretreatment with ZnSO(4) prevented gastric lesion development (the UI was 87% lower than that without pretreatment), and the MDA and CD content in serum and tissues was lower. The MT content in the liver was double in rats that were not pretreated, and the MT mRNA level in the stomach was 35% higher. MT administration 1 h before the WIR stress prevented gastric lesion development (the UI decreased by 47% compared with that in rats not pretreated), and the MDA and CD content in serum and tissues was significantly lower. CONCLUSION: In WIR-stressed rats, the MT level was increased in serum and in stomach and liver tissues. Pre-administration of exogenous MT or pre-induction of endogenous MT can protect the gastric mucosa against stress-induced ulcers and inhibits the formation of stress-induced lipid peroxide. MT could have a gastroprotective effect and might be a new interventive and therapeutic target in stress-induced gastric ulcers.

Animals↗
PubMed2005

[A new strategy to treat hyperhomocysteinemia].

Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. At present, the main therapeutic provision is to supply vitamin B(6), B(12) and folic acids, and the toxic and ill effect have been reported. Homocysteine, taurine, hydrogen sulfide and metallothionein are metabolic products from methionine. Homocysteine induces necrosis of endothelium, proliferation of vascular smooth muscle cells, proliferation and activation of vascular fibroblast cells and mitochondrial structural destruction and dysfunction of myocardium cells. Taurine, an end metabolic product of homocysteine, obviously reduces cardiovascular injury induced by homocysteine. The possible mechanism of antagonism by reducing oxidative stress and endoplasmic reticulum stress has been proved. Hydrogen sulfide, another end metabolic product of homocysteine, obviously reducing cardiovascular injury of homocysteine by scavenging oxidative radicals has been found. Metallothionein a derivant production of homocysteine metabolism, antagonism to homocysteine injury to cardiovascular system been discussed. Homocysteine, taurine, hydrogen sulfide and metallothionein, as a metabolic product of methionine, interactive antagonism and interactive biological influence have been reviewed. Induced endogenous or exogenous supply of taurine, hydrogen sulfide and metallothionein might resist cardiovascular injury induced by hyperhomocysteinemia. According to the methionine metabolic cycle, using endogenous antagonistic substances might be a new clinical preventive and treatment target of homocystinemia.

Animals↗
PubMed2005

Diagnosis and treatment of irritable bowel syndrome: state of the art.

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder with a wide variety of presentations that may include abdominal pain, bloating, diarrhea, constipation, or alternating bowel habits. Symptom-based criteria and a limited medical evaluation are used for diagnosis. The heterogeneity of IBS presenting symptoms, together with the pathophysiology of the disorder, is unclear, making treatment challenging. Treatment strategies are focused on specific symptoms, potential underlying disorders in stress responsiveness, and predisposing psychological features. Although only two medications, tegaserod for constipation-predominant IBS and alosetron for diarrhea-predominant IBS, are specifically indicated, a wide variety of treatment options are available and are discussed in this review.

Anti-Bacterial Agents↗
PubMed2005

New insights into the pathophysiology of irritable bowel syndrome: implications for future treatments.

Irritable bowel syndrome (IBS) is a multifactorial disorder characterized by abdominal pain and altered bowel habits. Chronic symptoms may occur due to changes in gastrointestinal motor function, enhanced perception of gut stimuli, and psychosocial factors. Recent data suggest that abnormal processing of afferent signals occurs in IBS patients. A newly recognized causative factor in a subset of IBS patients is post-infectious IBS. Altered transport of intestinal gas and bowel distention may contribute to abdominal discomfort, pain, and bloating. Changes in gut microflora have also been reported, but data remain scant. Advances have been made in our understanding of serotonin signaling and metabolism in IBS patients, in part due to the introduction of specific receptor agonists and antagonists. Finally, exciting data are emerging on genetic alterations that may contribute to the pathophysiology and treatment of IBS. Increasingly novel mechanisms are being identified that should aid in better understanding of the complex pathophysiology of IBS and developing new therapies.

Brain↗
PubMed2005

Is a negative colonoscopy associated with reassurance or improved health-related quality of life in irritable bowel syndrome?

BACKGROUND: Although colonoscopy is rarely of clinical use in irritable bowel syndrome (IBS), it is, nonetheless, frequently performed in IBS. Proponents contend that a normal colonoscopy provides reassurance and improves health-related quality of life (HRQOL). However, no previous data have measured these effects. We sought to measure the association of a normal colonoscopy with reassurance and HRQOL in patients with IBS aged <50 years. METHODS: We retrospectively evaluated 458 patients with IBS, aged 18 to 49 years. Subjects completed a symptom questionnaire, the Symptom Checklist 90 (SCL-90) psychometric checklist, and the Short Form 36 (SF-36) Health Survey. The main outcomes were HRQOL as measured by the mental component score (MCS) and the physical component score (PCS) of the SF-36 and reassurance as operationalized by a negative response to the question: "Do you think there is something seriously wrong with your body?" The independent variable was presence or absence of a previous normal colonoscopy. We performed regression analysis to control for potential confounders, including timing of colonoscopy. RESULTS: The unadjusted mean SF-36 PCS was 42 +/- 10 (0-100 scale: 0, worst) in patients with recent colonoscopy (<12 months), 45 +/- 11 in patients with distant colonoscopy (>12 months), and 45 +/- 10 in patients without colonoscopy (p = 0.78). The mean SF-36 MCS in the 3 groups were 42 +/- 13, 44 +/- 11, and 43 +/- 11 (p = 0.57). Colonoscopy did not impact the proportion reassured (69.3%, 67.2%, 66.6%; p = 0.85). There were no significant differences between groups for any outcomes when adjusting for potential confounders. CONCLUSIONS: We found no independent association between a negative colonoscopy and reassurance or improved HRQOL in IBS patients aged <50 years. These results suggest that the role of colonoscopy in IBS may be limited but require confirmation in prospective trials.

Adolescent↗
PubMed2005

Brain responses to visceral and somatic stimuli in irritable bowel syndrome: a central nervous system disorder?

In healthy subjects, the brain regions most consistently activated in visceral and somatic pain are the key regions in the central pain matrix,including the mid/anterior insula, subregions of the ACC, PFC, thalamus,and in some cases, pontine regions such as the dorsal pons and PAG. Functional neuroimaging studies have demonstrated evidence of altered regional brain activation responses during visceral and somatic stimuli in IBS that have been associated with perceptual differences. Although perceptual studies have shown increased sensitivity to rectosigmoid distension in IBS, most somatic pain studies have demonstrated normal or decreased sensitivity compared with controls; however, a recent study showed increased sensitivity to thermal heat. Altered brain responses in IBS,particularly to visceral stimuli, include activation of regions concerned with attentional processes and response selection, corticolimbic regions concerned with emotional and autonomic responses to stimuli, and subcortical regions receiving cortical projections from the latter and afferent input from the soma and viscera. Altered activations of these regions also may be present in the absence of a noxious visceral stimulus. Changes in rCBF of some of these regions have been associated with treatment response in IBS. With regard to differences in cortical processing of visceral versus somatic stimuli in IBS, there have been only two studies. Greater activations of the dorsal ACC, thalamus, and PFC have been shown with visceral stimuli compared with somatic stimuli in IBS. A plausible hypothesis for the observations from brain imaging studies is that IBS patients demonstrate a compromised activation of pain inhibition circuits including those of the cortico-pontine circuit but increased activation of limbic and paralimbic circuits that may be related to pain facilitation.

Brain↗
PubMed2005

Differences in brain responses to visceral pain between patients with irritable bowel syndrome and ulcerative colitis.

Patients with mild chronic inflammation of the rectum or ileum have reduced perceptual responses to rectosigmoid distension compared to patients with irritable bowel syndrome (IBS). The current study sought to identify differences in regional cerebral blood flow (rCBF) during rectal distension, which might correspond to these perceptual differences. In 8 male ulcerative colitis (UC) patients with quiescent disease, 7 male IBS patients and 7 healthy male controls, rCBF was assessed using 15O-water positron emission tomography at baseline and during actual and anticipated but undelivered rectal distensions. No group differences were seen in anterior insula and dorsal anterior cingulate cortex (dACC), two regions consistently activated by painful intestinal stimuli. However, IBS patients showed greater activation of the amygdala, rostroventral ACC, and dorsomedial frontal cortical regions. In contrast, no significant differences were observed between UC and controls. When these two non-IBS groups were combined, functional connectivity analyses showed that right lateral frontal cortex (RLFC) activation positively correlated with activation of the dorsal pons/periaqueductal gray, a key region involved in endogenous pain inhibition. According to the connectivity analysis, this effect was mediated by inhibition of medial frontal cortex by the RLFC. Chronic colonic inflammation is not necessarily associated with increased visceral afferent input to the brain during rectal distension. In the sample studied, the primary difference between functional and quiescent inflammatory disease of the colon was in terms of greater activation of limbic/paralimbic circuits in IBS, and inhibition of these circuits in UC and controls by the RLFC.

Adult↗