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Biofeedback for anal incontinence: Does it work?
A772 AGA ABSTRACTS • G3180
SOCIAL DESIRABILITY INFLUENCES SELF-REPORTED GASTROENTEROLOGY AND PSYCHOLOGICAL SYMPTOMS IN WOMEN WITH IRRITABLE BOWEL SYNDROME. ME Jarrett, M. Heitkemper, RL Burr, RL Levy, MK Lustyk, V Hertig. University of Washington, Seattle WA. The purpose of this preliminary report is describe how an orientation towards social desirability responses affects the reporting of gastrointestinal (GI) and psychological symptoms in women with Irritable Bowel Syndrome (IBS) compared to nonsymptomatic controls. Methods: Women with medically diagnosed IBS (n = 40) and healthy controls (n = 19) ages 21-45 were interviewed and completed questionnaires including the Marlowe-Crowne Social Desirability scale (M-C SDS, 20 items) and Symptom Checklist-90 (SCL-90). They were then followed for one menstrual cycle with a symptom diary. Summary measures included: the mean M-C SDS score, the mean score over the menstrual cycle for G! (abdominal pain, bloating, constipation, and diarrhea) and psychological distress (SCL-90 subscale; daily anxiety, depression, and anger). Results: The mean level for the M-C SDS did not differ significantly between groups (IBS, M = 8.7 -+4.3; Control 9.6 + 4.2). However the higher the M-C SDS the higher mean daily GI symptom (abdominal pain, rs = 297, p = .13; bloating, rs = .470 p = .01; and constipation, rs = 463 p = .02; but not diarrhea, rs = -.067, p = .74) in the IBS group (n = 27). The M-C SDS was negatively correlated with SCL-90 subscales scores (IBS (n = 40) anxiety, rs = -.305 p = .05; depression, rs = -.377 p --- .02, hostility, q = -.304 p = .05; interpersonal sensitivity, rs = -.364 p = .02) although less so in the daily measures (1BS (n =27), anxiety, rs = -.278 p = .16; depression, rs = -.049 p = .81, anger, rs = -.149 p = .46). Conclusions: Even though the women with IBS in this sample did not differ from controls in their mean score on a social desirability scale, their reports of GI symptoms and psychological distress were influenced by their need to respond in a socially appropriate manner. These results are consistent with the findings in patients being evaluated for intractable pain. This type of self reporting bias may reflect either a personality style that is influenced by social context, e.g., the legitimacy of physical but not psychological symptoms or an awareness that health care systems are more responsive to somatic symptoms or both. Funded by National Institute of Nursing Research, NR04101. • G3181 CHOLESTEROL MODULATES GUINEA-PIG GALLBLADDER SMOOTH MUSCLE ACTION POTENTIAL CHARACTERISTICS. L. J. Jennings*, Qi-Wei Xu*, M.T. Nelson" and G.M. Mawe*. Departments of Anatomy and Neurobiology* and Pharmacology °, College of Medicine, University of Vermont, Burlington, VT, USA, 05405. Increased cholesterol in bile has been related to impaired gallbladder motility, a causative factor in cholesterol gallstone formation. The natural hydrophobicity of cholesterol has hindered the investigation of its effects in in-vitro systems. The development of cyclodextrins with hydrophobic pores that can help solubilize compounds such as cholesterol has led to an increased interest in the effects of cholesterol in-vitro. The aims of this study were to initially verify whether cholesterol could be delivered to gallbladder muscle via cyclodextrins and to subsequently test the effect of cholesterol on the electrical properties of intact gallbladder muscle. METHODS: We incubated dissociated cells and whole mount preparations (n = 3) with 13-methylcyclodextrins that were complexed with a cholesterol ester conjugated to a BODIPY fluorophore (cholesteryl 4, 4-difluoro-5, 7-dimethyl-4-bora-3a, 4a-diaza-s-indacene-3-dodecanoate; Molecular Probes) and subsequently fixed the tissue with 4% paraformaldehyde. The tissue was then examined unde~ confocal microscopy (Noran; Z series configuration, excitation 488 emission 51-550 nm) for evidence of fluorescent incorporation. Intracellular voltage recordings were obtained from smooth muscle in whole mount preparations prior to (control) and during (up to 120 min) application of cyclodextrin complexed cholesterol (Sigma); control responses were compared with responses obtained during cholesterol application (Students t-test). The recording conditions have been described previously (Zhang et al, 1993, Am. J. Physiol., 265, C1552-C1561). RESULTS: Examination of fixed cells and whole mount preparations revealed generalized cellular incorporation of the BODIPY conjugated cholesteryl ester. Fluorescence was not detected from control preparations in which the fluorophore alone was loaded into cyclodextrins. The presence of cyclodextrin complexed cholesterol (50 ~tg/ml) in the superfusion media significantly altered the conformation characteristics of the action potential. The frequency of spontaneous action potentials was significantly (P<0.0001) reduced in the presence of cholesterol (control 0.3 -+0.01 vs. cholesterol 0.13 _+0.01 Hz; n=6) as was the amplitude of the action potential spike (control 40.8 -+4.1 vs. cholesterol 30.8 -+4.5 mV; P<0.008) and the duration of the plateau phase of the action potential (control 418 -+ 36 vs. cholesterol 273 -+ 66 msec; P<0.04) whereas cyclodextrin alone had no effect CONCLUSIONS: These findings suggest that excess cholesterol may be incorporated into gallbladder smooth muscle and acts to decrease gallbladder motility, at least in part, through alterations in ionic conductances that contribute to the smooth muscle action
GASTROENTEROLOGY Vol. 114, No. 4
potential. These effects may contribute to the impaired gallbladder motility seen in patients with lithogenic bile. Supported by NIH Grants NS26995 and DK45410 and a Canadian Gastroenterological Association Fellowship awarded to Q-W. X. G3182
BIOFEEDBACK FOR ANAL INCONTINENCE: DOES I T WORK? LL Jensen, AC Lowry. Colon & Rectal Surgery Assoc. Ltd. St. Paul, MN. In recent years, biofeedback has emerged as a promising treatment option for patients with anal incontinence. The purpose of this study is to assess the efficacy in a large number of patients. METHOD: A retrospective chart review of patients with incontinence treated with biofeedback was performed. The biofeedback was done in an outpatient setting using the EMG biofeedback technique with intra anal sensor. The patients sit upright watching a computer screen display of their sphincter and gluteus maximus muscle activity. The mean number of visits was three. Patients did home exercises using an audio tape as a guide. No home trainers were used. All patients completed an incontinence score pre- and postbiofeedback as well as a subjective assessment of their results. RESULTS: Between January 1988 and December 1996, 370 patients with anal incontinence enrolled in our biofeedback program; 330 (89%) were female with an average age of 56 (range, 11-94) years. Etiologies included idiopathic incontinence in 162, sphincter injury in 90, rectal surgery in 49, and colon resection in 33. The remaining 36 had a variety of etiologies. The mean number of accidents per week decreased by 2.5 (1-5) following biofeedback. Using a previously published incontinence scoring system (maximum score 30), the mean incontinence score decreased from 21 (3-30) pre-treatment to 3 (0-30) post-treatment. Seventy-nine percent of the patients subjectively rated their improvement >_90%. Pre Rx Incontinence Solid Stool Liquid Stool or Mucus Flatus only
Post Rx
262
Normal 128
Gas Only 75
StoolOnly 59
Liquid Stool or Mucus 0
59 49
29 33
20 16
0 0
10 0
There were no complications. CONCLUSION: In this series of 370 patients, 81% of the patients were perfectly continent or were incontinent to flatus only after biofeedback therapy. Biofeedback for anal incontinence is an efficacious treatment option for patients with anal incontinence. • G3183
DIFFERENTIAL E~'~'ECTS OF NAPROXEN ON ISCHEMIA AND REPERFUSION-INDUCED EXCITATION OF JEJUNAL AFFERENTS IN THE ANAESTHETISED RAT. W. Jiang & D. Grundy. Dept. of Biomedical Science, University of Sheffield, UK. Introduction: Ischemia has been shown to trigger the release of a number of inflammatory mediators which can sensitize nociceptive afferents. Prostaglandins have been implicated in the activation of afferents during mesenteric ischemia (Longhurst et al., Am. J. Physiol. 262, H1482-1485. 1992). The aim of the present work was to investigate the effects of naproxen, a non-selective cyclo-oxygenase enzyme inhibitor, on the responses of jejunal mesenteric afferents to ischemia and reperfusion in a novel model of highly focal ischemia. Methods: Experiments were performed in the pentobarbitone anaesthetised (60 mg kg -I, i.p. then 0.5 mg kg -l min-l, i.v.) male adult Hooded Lister rats (300-400g). A jugular vein and carotid artery were cannulated for systemic administration of drugs and continuous monitoring of blood pressure. Extracellular afferent recordings were made from mesenteric nerve bundles innervating a 3-5 cm section of the jejunum which was cannulated for measuring intraluminal pressure (data not shown). Ischemia was produced by clamping the mesenteric artery supplying the entire blood flow to the isolated loop. In time control experiments (n=5) a series of 3 ischemia episodes (8 min duration) were performed separated by 15 min periods of reperfusion when the clip was removed and blood flow re-established.Naproxen (10 mg kg -l, i.v.) was administered 15 min before the 2nd ischemic episode in 5 further experiments. Data are presented as the mean _+SE. Significant difference was performed using Student's paired or un-paired t-test as appropriate with Bonferonni corrections for multiple comparisons. Results: Ischemia cause a marked increase in afferent discharge (AD) which started within 60 sec of onset and which showed two distinctive peaks in activity. One ocurring 196.1-+ 20.3 sec after ischemia and the other after 420.6-+36.2 sec. On reperfusion, discharge retumed rapidly to baseline before developing another transient peak. The mean increase in afferent discharge (AAD) at each peak during ischemia and during the reperfusion peak were increased significantly compared with the baseline discharge (table). Naproxen had no effect on baseline discharge or either of the peak increases in afferent discharge during ischemia. However, naproxen significantly attenuated the increased afferent firing during the early period of reperfusion (#: P < 0.05 vs. Ctrl).
SOCIAL DESIRABILITY INFLUENCES SELF-REPORTED GASTROENTEROLOGY AND PSYCHOLOGICAL SYMPTOMS IN WOMEN WITH IRRITABLE BOWEL SYNDROME. ME Jarrett, M. Heitkemper, RL Burr, RL Levy, MK Lustyk, V Hertig. University of Washington, Seattle WA. The purpose of this preliminary report is describe how an orientation towards social desirability responses affects the reporting of gastrointestinal (GI) and psychological symptoms in women with Irritable Bowel Syndrome (IBS) compared to nonsymptomatic controls. Methods: Women with medically diagnosed IBS (n = 40) and healthy controls (n = 19) ages 21-45 were interviewed and completed questionnaires including the Marlowe-Crowne Social Desirability scale (M-C SDS, 20 items) and Symptom Checklist-90 (SCL-90). They were then followed for one menstrual cycle with a symptom diary. Summary measures included: the mean M-C SDS score, the mean score over the menstrual cycle for G! (abdominal pain, bloating, constipation, and diarrhea) and psychological distress (SCL-90 subscale; daily anxiety, depression, and anger). Results: The mean level for the M-C SDS did not differ significantly between groups (IBS, M = 8.7 -+4.3; Control 9.6 + 4.2). However the higher the M-C SDS the higher mean daily GI symptom (abdominal pain, rs = 297, p = .13; bloating, rs = .470 p = .01; and constipation, rs = 463 p = .02; but not diarrhea, rs = -.067, p = .74) in the IBS group (n = 27). The M-C SDS was negatively correlated with SCL-90 subscales scores (IBS (n = 40) anxiety, rs = -.305 p = .05; depression, rs = -.377 p --- .02, hostility, q = -.304 p = .05; interpersonal sensitivity, rs = -.364 p = .02) although less so in the daily measures (1BS (n =27), anxiety, rs = -.278 p = .16; depression, rs = -.049 p = .81, anger, rs = -.149 p = .46). Conclusions: Even though the women with IBS in this sample did not differ from controls in their mean score on a social desirability scale, their reports of GI symptoms and psychological distress were influenced by their need to respond in a socially appropriate manner. These results are consistent with the findings in patients being evaluated for intractable pain. This type of self reporting bias may reflect either a personality style that is influenced by social context, e.g., the legitimacy of physical but not psychological symptoms or an awareness that health care systems are more responsive to somatic symptoms or both. Funded by National Institute of Nursing Research, NR04101. • G3181 CHOLESTEROL MODULATES GUINEA-PIG GALLBLADDER SMOOTH MUSCLE ACTION POTENTIAL CHARACTERISTICS. L. J. Jennings*, Qi-Wei Xu*, M.T. Nelson" and G.M. Mawe*. Departments of Anatomy and Neurobiology* and Pharmacology °, College of Medicine, University of Vermont, Burlington, VT, USA, 05405. Increased cholesterol in bile has been related to impaired gallbladder motility, a causative factor in cholesterol gallstone formation. The natural hydrophobicity of cholesterol has hindered the investigation of its effects in in-vitro systems. The development of cyclodextrins with hydrophobic pores that can help solubilize compounds such as cholesterol has led to an increased interest in the effects of cholesterol in-vitro. The aims of this study were to initially verify whether cholesterol could be delivered to gallbladder muscle via cyclodextrins and to subsequently test the effect of cholesterol on the electrical properties of intact gallbladder muscle. METHODS: We incubated dissociated cells and whole mount preparations (n = 3) with 13-methylcyclodextrins that were complexed with a cholesterol ester conjugated to a BODIPY fluorophore (cholesteryl 4, 4-difluoro-5, 7-dimethyl-4-bora-3a, 4a-diaza-s-indacene-3-dodecanoate; Molecular Probes) and subsequently fixed the tissue with 4% paraformaldehyde. The tissue was then examined unde~ confocal microscopy (Noran; Z series configuration, excitation 488 emission 51-550 nm) for evidence of fluorescent incorporation. Intracellular voltage recordings were obtained from smooth muscle in whole mount preparations prior to (control) and during (up to 120 min) application of cyclodextrin complexed cholesterol (Sigma); control responses were compared with responses obtained during cholesterol application (Students t-test). The recording conditions have been described previously (Zhang et al, 1993, Am. J. Physiol., 265, C1552-C1561). RESULTS: Examination of fixed cells and whole mount preparations revealed generalized cellular incorporation of the BODIPY conjugated cholesteryl ester. Fluorescence was not detected from control preparations in which the fluorophore alone was loaded into cyclodextrins. The presence of cyclodextrin complexed cholesterol (50 ~tg/ml) in the superfusion media significantly altered the conformation characteristics of the action potential. The frequency of spontaneous action potentials was significantly (P<0.0001) reduced in the presence of cholesterol (control 0.3 -+0.01 vs. cholesterol 0.13 _+0.01 Hz; n=6) as was the amplitude of the action potential spike (control 40.8 -+4.1 vs. cholesterol 30.8 -+4.5 mV; P<0.008) and the duration of the plateau phase of the action potential (control 418 -+ 36 vs. cholesterol 273 -+ 66 msec; P<0.04) whereas cyclodextrin alone had no effect CONCLUSIONS: These findings suggest that excess cholesterol may be incorporated into gallbladder smooth muscle and acts to decrease gallbladder motility, at least in part, through alterations in ionic conductances that contribute to the smooth muscle action
GASTROENTEROLOGY Vol. 114, No. 4
potential. These effects may contribute to the impaired gallbladder motility seen in patients with lithogenic bile. Supported by NIH Grants NS26995 and DK45410 and a Canadian Gastroenterological Association Fellowship awarded to Q-W. X. G3182
BIOFEEDBACK FOR ANAL INCONTINENCE: DOES I T WORK? LL Jensen, AC Lowry. Colon & Rectal Surgery Assoc. Ltd. St. Paul, MN. In recent years, biofeedback has emerged as a promising treatment option for patients with anal incontinence. The purpose of this study is to assess the efficacy in a large number of patients. METHOD: A retrospective chart review of patients with incontinence treated with biofeedback was performed. The biofeedback was done in an outpatient setting using the EMG biofeedback technique with intra anal sensor. The patients sit upright watching a computer screen display of their sphincter and gluteus maximus muscle activity. The mean number of visits was three. Patients did home exercises using an audio tape as a guide. No home trainers were used. All patients completed an incontinence score pre- and postbiofeedback as well as a subjective assessment of their results. RESULTS: Between January 1988 and December 1996, 370 patients with anal incontinence enrolled in our biofeedback program; 330 (89%) were female with an average age of 56 (range, 11-94) years. Etiologies included idiopathic incontinence in 162, sphincter injury in 90, rectal surgery in 49, and colon resection in 33. The remaining 36 had a variety of etiologies. The mean number of accidents per week decreased by 2.5 (1-5) following biofeedback. Using a previously published incontinence scoring system (maximum score 30), the mean incontinence score decreased from 21 (3-30) pre-treatment to 3 (0-30) post-treatment. Seventy-nine percent of the patients subjectively rated their improvement >_90%. Pre Rx Incontinence Solid Stool Liquid Stool or Mucus Flatus only
Post Rx
262
Normal 128
Gas Only 75
StoolOnly 59
Liquid Stool or Mucus 0
59 49
29 33
20 16
0 0
10 0
There were no complications. CONCLUSION: In this series of 370 patients, 81% of the patients were perfectly continent or were incontinent to flatus only after biofeedback therapy. Biofeedback for anal incontinence is an efficacious treatment option for patients with anal incontinence. • G3183
DIFFERENTIAL E~'~'ECTS OF NAPROXEN ON ISCHEMIA AND REPERFUSION-INDUCED EXCITATION OF JEJUNAL AFFERENTS IN THE ANAESTHETISED RAT. W. Jiang & D. Grundy. Dept. of Biomedical Science, University of Sheffield, UK. Introduction: Ischemia has been shown to trigger the release of a number of inflammatory mediators which can sensitize nociceptive afferents. Prostaglandins have been implicated in the activation of afferents during mesenteric ischemia (Longhurst et al., Am. J. Physiol. 262, H1482-1485. 1992). The aim of the present work was to investigate the effects of naproxen, a non-selective cyclo-oxygenase enzyme inhibitor, on the responses of jejunal mesenteric afferents to ischemia and reperfusion in a novel model of highly focal ischemia. Methods: Experiments were performed in the pentobarbitone anaesthetised (60 mg kg -I, i.p. then 0.5 mg kg -l min-l, i.v.) male adult Hooded Lister rats (300-400g). A jugular vein and carotid artery were cannulated for systemic administration of drugs and continuous monitoring of blood pressure. Extracellular afferent recordings were made from mesenteric nerve bundles innervating a 3-5 cm section of the jejunum which was cannulated for measuring intraluminal pressure (data not shown). Ischemia was produced by clamping the mesenteric artery supplying the entire blood flow to the isolated loop. In time control experiments (n=5) a series of 3 ischemia episodes (8 min duration) were performed separated by 15 min periods of reperfusion when the clip was removed and blood flow re-established.Naproxen (10 mg kg -l, i.v.) was administered 15 min before the 2nd ischemic episode in 5 further experiments. Data are presented as the mean _+SE. Significant difference was performed using Student's paired or un-paired t-test as appropriate with Bonferonni corrections for multiple comparisons. Results: Ischemia cause a marked increase in afferent discharge (AD) which started within 60 sec of onset and which showed two distinctive peaks in activity. One ocurring 196.1-+ 20.3 sec after ischemia and the other after 420.6-+36.2 sec. On reperfusion, discharge retumed rapidly to baseline before developing another transient peak. The mean increase in afferent discharge (AAD) at each peak during ischemia and during the reperfusion peak were increased significantly compared with the baseline discharge (table). Naproxen had no effect on baseline discharge or either of the peak increases in afferent discharge during ischemia. However, naproxen significantly attenuated the increased afferent firing during the early period of reperfusion (#: P < 0.05 vs. Ctrl).