High-resolution versus conventional manometry for the diagnosis of small bowel motor dysfunction.

BACKGROUND: The diagnosis of small bowel motility disorders is performed by manometric evaluation of the contractile patterns of the small intestine. Conventional intestinal manometry systems include few pressure sensors at relatively long intervals. We have recently shown that high-resolution jejunal manometry, with multiple closely spaced recording sites, allows the analysis of propagation patterns of intestinal motility in healthy subjects that cannot be detected with conventional manometry. The objective of this pilot study was to explore the feasibility and diagnostic value of high-resolution intestinal manometry in patients with suspected small bowel dysmotility. METHODS: Prospective pilot study evaluating intestinal motility patterns in 16 consecutive patients (16-61 years; 11 women) with severe, chronic digestive symptoms referred for the evaluation of intestinal motility and in 18 healthy controls (21-38 years; 8 women). A 36-channel high-resolution manometry catheter was orally placed under radiological guidance in the jejunum. Intestinal motility was continuously recorded for 3 h fasting and 2 h after a 450 kcal meal. The manometric recordings were analyzed in two formats: (a) with the high-resolution data from 34 channels and (b) showing only the recordings from 5 channels separated by 7 cm intervals, mimicking a conventional manometry recording. KEY RESULTS: In the analysis mimicking conventional manometry, abnormal motility criteria were detected in six patients and in no healthy subject [bursts (n = 3), postprandial minute rhythm (n = 1) and myopathic pattern (n = 2)]. These classical dysmotility criteria were also detected by high-resolution manometry. High-resolution analysis detected one or more abnormal findings in seven additional patients that were not observed in any healthy subject, specifically: (a) abnormal propagation of Phase III (n = 3); (b) reduced propagated activity during Fasting Phase II (n = 4); (c) increased propagated activity during Fasting Phase II and postprandial phase (n = 1). CONCLUSIONS AND INFERENCES: This pilot study suggests that high-resolution intestinal manometry may improve the sensitivity of conventional manometry in the detection of intestinal motor dysfunction.

Meal composition influences postprandial sensations independently of valence and gustation.

BACKGROUND: Palatability of meals with identical composition has been shown to influence postprandial sensations. Our aim was to determine to what extent meal composition influences postprandial sensations independently of palatability. METHODS: Randomized, crossover, double-blind trial comparing the postprandial responses to a low-fat vs a high-fat test meal, with the same physical and organoleptic characteristics (taste, smell, texture, color, and temperature). The test meal consisted in 150 g hummus containing either 17.7 g fat (low-fat) or 22.3 g fat (high-fat), 19.8 g toasts, 120 mL water and 50 g apple puree. In 12 non-obese healthy men, palatability, homeostatic sensations (hunger/satiety, fullness) and hedonic sensations (digestive well-being, mood) were measured on 10 cm scales before and during the 60-min postprandial period. Comparisons between meals were performed with a two-way repeated measures ANCOVA with premeal data as co-variate. KEY RESULTS: Both test meals were rated equally palatable (palatability scores 3.8 ± 0.3 low-fat, 3.3 ± 0.2 high-fat; P = .156). As compared to the high-fat meal, the low-fat meal induced more satisfaction (meal effect on well-being F(1,21) = 4.92; P = .038) and tended to improve mood (meal effect F(1,21) = 3.02; P = .064), and this was associated with a non-significant decrease in satiety (meal effect F(1,21) = 2.29; P = .145) and fullness (meal effect F(1,21) = 1.57; P = .224). CONCLUSIONS AND INFERENCES: The composition of meals with equal palatability influences postprandial satisfaction, even without significant impact on homeostatic sensations, although an effect on homeostatic sensations has not been excluded. These conditioning factors may have clinical implications in patients with impaired meal tolerance or meal-related symptoms.

Effects of meal palatability on postprandial sensations.

BACKGROUND: Food palatability has been shown to influence satiation and meal consumption; our aim was to determine its effects on postprandial satisfaction, ie digestive well-being (primary outcome), and homeostatic sensations (satiety, fullness). METHODS: Randomized, cross-over trial comparing the postprandial responses to conventional (potato-cheese cream followed by vanilla cream) vs unconventional test meals (mixture of both creams) with identical composition and physical characteristics (color, texture, consistency, temperature) but distinctively different palatability. In 22 non-obese healthy men sensations were measured on 10 cm scales before and during the 60-min postprandial period (-5 to +5 score scales for palatability, satiety, well-being, and mood, and 0-10 score scales for fullness and discomfort). Comparisons between meals were performed with a 2-way repeated measures ANCOVA with premeal data as co-variate. KEY RESULTS: As compared to the palatable conventional meal, the unconventional meal was rated unpalatable (-1.8 ± 0.4 score vs 2.8 ± 0.1 score potato cream and 2.9 ± 0.2 vanilla cream; P < .001 for both), induced significantly more fullness sensation [meal effect F (1, 19) = 7.389; P = .014] but had less effect on digestive well-being [meal effect F (1, 19) = 47.016; P < .001] and mood [meal-effect F (1, 19) = 6.609; P = .019]. The difference in satiety was not significantly different. CONCLUSION & INFERENCES: Meal palatability influences the postprandial experience: it bears a direct relation to the hedonic response (well-being/mood) but an inverse relation to homeostatic sensations (fullness). These relations could be applicable to influence eating behavior, because at equal conditions, more palatable meals induce less fullness but more satisfaction, and vice-versa.

Education of the postprandial experience by a sensory-cognitive intervention.

BACKGROUND: Ingestion of a meal induces homeostasis-related sensations (satiety/fullness) that have a hedonic dimension (satisfaction/mood). We have previously shown that a previous physiological intervention, a meal preload, influences the responses to a subsequent meal, specifically: it increases satiety/fullness and decreases satisfaction. We now wished to determine the differential effects of education on the homeostatic and hedonic postprandial experience. METHODS: Randomized, parallel study comparing the effect of real vs sham education on the responses to a probe meal. In two groups of healthy subjects (n = 14 each), homeostatic (satiety, fullness) and hedonic sensations (digestive well-being, mood) in response to a probe meal (250 mL soup, 25 g bread) were measured on 2 separate days before and after a single sensory-cognitive educational intervention (taste recognition test of supra- and sub-threshold tastands for real and sham education, respectively). KEY RESULTS: Before education, in both groups the probe meal induced homeostatic sensations (satiety, fullness) with a positive hedonic dimension (increased digestive well-being and mood). In contrast to sham education, real education enhanced both homeostatic and hedonic responses to the probe meal (P < .05 vs sham education for all). CONCLUSIONS AND INFERENCES: Education modifies the subjects' receptiveness and influences the responses to a meal, not only the hedonic postprandial experience, but also homeostatic sensations. Since homeostatic and hedonic responses are dissociable, education might be tailored to target different conditions.

Comparison between small bowel manometric patterns and full-thickness biopsy histopathology in severe intestinal dysmotility.

BACKGROUND: Intestinal manometry is the current standard for direct evaluation of small bowel dysmotility. Patients with abnormal motility can either be diagnosed of pseudo-obstruction when there are radiological findings mimicking mechanical intestinal obstruction or of enteric dysmotility when these findings are absent. The aim of the present study was to prospectively compare small bowel manometric abnormalities with histopathological findings in intestinal full-thickness biopsies in patients with severe dysmotility disorders. METHODS: We investigated 38 patients with intestinal manometry and a subsequent full-thickness intestinal biopsy. Manometric recordings were read by 4 investigators and a diagnostic consensus was obtained in 35 patients. Histopathological analysis, including specific immunohistochemical techniques of small bowel biopsies was performed and compared to manometric readings. KEY RESULTS: Patients with abnormal intestinal manometry had abnormal histopathological findings in 73% of cases. However, manometric patterns did not match with the specific neuromuscular abnormalities. Among patients with a neuropathic manometry pattern and abnormal histopathology, only 23% had an enteric neuropathy, whereas 62% had neuromuscular inflammation, and 15% an enteric myopathy. On the other hand, patients with a myopathic manometry pattern all had abnormal histopathology, however, none of them with signs of enteric myopathy. CONCLUSION & INFERENCES: Small bowel dysmotility detected by intestinal manometry is often associated with abnormal neuromuscular findings in full-thickness biopsies. However, there is no correlation between the specific manometric patterns and the histopathological findings.

Appetite influences the responses to meal ingestion.

BACKGROUND: We have previously shown that the postprandial experience includes cognitive sensations, such as satiety and fullness, with a hedonic dimension involving digestive well-being and mood. Preload conditioning has been shown to modulate appetite and food consumption under certain conditions, but its effects on the responses to meal ingestion are not clear. We hypothesized that appetite modulation by preload conditioning has differential effects on the cognitive and the emotive responses to meal ingestion. METHODS: The effects of preload conditioning (ingestion of a low- vs a high-calorie breakfast) on appetite and on the cognitive and emotive responses to a comfort probe meal ingested 2 hours later (ham and cheese sandwich with orange juice; 300 mL, 425 Kcal) was tested in healthy subjects (n=12) in a cross-over design. Sensations were measured at regular intervals 15 minutes before and 60 minutes after the probe meal. KEY RESULTS: As compared to the low-calorie breakfast, the high-calorie breakfast reduced basal hunger sensation and influenced the responses to the subsequent probe meal: it increased satiety (4.3±0.2 score vs 2.7±0.2 score; P<.001) and fullness (5.4±0.5 score vs 3.1±0.5; P<.001), but reduced the expected postprandial experience of digestive well-being after a palatable meal (1.3±0.7 score vs 3.0±0.3; P=.045). CONCLUSION AND INFERENCES: Appetite modulation by preload conditioning has differential effects on the cognitive and emotive responses to a meal. Preload conditioning of the postprandial experience may be applicable to dietary planning and prevention of postprandial symptoms.

Brain networks associated with cognitive and hedonic responses to a meal.

BACKGROUND: We recently reported interrelated digestive, cognitive, and hedonic responses to a meal. The aim of this study was to identify brain networks related to the hedonic response to eating. METHODS: Thirty-eight healthy subjects (20-38 age range) were evaluated after a 5-hour fast and after ingestion of a test meal (juice and warm ham and cheese sandwich, 300 mL, 425 kcal). Perceptual and affective responses (satiety, abdominal fullness, digestive well-being, and positive mood), and resting scans of the brain using functional MRI (3T Trio, Siemens, Germany) were evaluated immediately before and after the test meal. A high-order group independent component analysis was performed to investigate ingestion-related changes in the intrinsic connectivity of brain networks, with a focus on thalamic and insular networks. KEY RESULTS: Ingestion induced satiation (3.3±0.4 score increase; P<.001) and abdominal fullness (2.4±0.3 score increase; P<.001). These sensations included an affective dimension involving digestive well-being (2.8±0.3 score increase; P<.001) and positive mood (1.8±0.2 score increase; P<.001). In general, thalamo-cortical connectivity increased with meal ingestion while insular-cortical connectivity mainly decreased. Furthermore, larger meal-induced changes (increase/decrease) in specific thalamic connections were associated with smaller changes in satiety/fullness. In contrast, a larger meal-induced decrease in insular-anterior cingulate cortex connectivity was associated with increased satiety, fullness, and digestive well-being. CONCLUSIONS AND INFERENCES: Perceptual and emotional responses to food intake are related to brain connectivity in defined functional networks. Brain imaging may provide objective biomarkers of subjective effects of meal ingestion.

Relation between cognitive and hedonic responses to a meal.

BACKGROUND: Ingestion of a meal induces cognitive and hedonic sensations and our aim was to determine the relation between both dimensions. METHODS: In three groups of healthy non-obese men (n=10 per group) three types of meals with equivalent levels of palatability were tested: a liquid meal, a solid-liquid low-calorie meal, and a solid-liquid high-calorie meal. The cognitive and hedonic responses were measured on 10-cm scales before and during the 30-minute postprandial period. KEY RESULTS: The liquid meal induced a relatively strong cognitive response with satiation (4.7±0.7 score increment), fullness (3.3±0.7 score increment), and inhibition of desire of eating a food of choice; in contrast, its impact on sensation of digestive well-being and satisfaction was not significant (0.7±0.7 score increment). The high-calorie solid-liquid meal, with larger volume load and caloric content, induced much lower satiation (2.4±0.8 score increment; P=.041 vs liquid meal) and fullness sensation (1.3±0.6 score increment; P=.031 vs liquid meal), but a markedly higher level of satisfaction (2.7±0.4 score increment; P=.021 vs liquid meal); the low-calorie mixed meal had less prominent effects with significantly lower satisfaction (1.0±0.4 score increment; P=.039 vs high-calorie meal). CONCLUSIONS AND INFERENCES: The cognitive (satiation, fullness) and hedonic responses (satisfaction) to meals with equivalent levels of palatability, that is, equally likable, are dissociable. The characteristics of meals in terms of satiation and rewarding power could be adapted to specific clinical targets, whether nutritional supplementation or restriction.

Cognitive and hedonic responses to meal ingestion correlate with changes in circulating metabolites.

BACKGROUND: We have previously shown that meal ingestion induces cognitive perception (sensations) with a hedonic dimension (well-being) that depends on the characteristics of the meal and the appropriateness of the digestive response. The aim of the present study is to identify metabolomic biomarkers of the cognitive response to meal ingestion. METHODS: In 18 healthy subjects, the response to a test meal (Edanec, 1 kcal/mL) ingested until maximum satiation (50 mL/min) was assessed. Perception measurements and blood samples were taken before, at the end of the meal, and 20 min after ingestion. The cognitive response and the hedonic dimension were measured on 10 cm scales. Metabolomic analysis was performed using nuclear magnetic resonance (NMR) spectroscopy and values of triglycerides, insulin, peptide YY (PYY), and glucagon-like peptide-1 (GLP-1) were determined using conventional laboratory techniques. KEY RESULTS: Ingestion up to maximum satiation induced sensation of fullness and decreased digestive well-being. The total amount ingested by each subject correlated with the basal sensation of hunger, but not with other sensations or blood metabolite levels. Immediately after ingestion, satiation correlated with an increase in glucose (R = 0.49; p = 0.038) and valine levels (R = 0.48; p = 0.043). Twenty-minutes after finalizing ingestion, triglyceride levels had significantly increased which correlated with the recovery in well-being (R = 0.48; p = 0.046) and the decrease in desire to eat a food of choice (R = -0.56; p = 0.016). The increase in lipids inversely correlated with abdominal discomfort (R = -0.51; p = 0.032). CONCLUSIONS & INFERENCES: Cognitive and hedonic responses to meal ingestion correlate with changes in circulating metabolites, which may serve as objective biomarkers of perception.

Intestinal gas content and distribution in health and in patients with functional gut symptoms.

BACKGROUND: The precise relation of intestinal gas to symptoms, particularly abdominal bloating and distension remains incompletely elucidated. Our aim was to define the normal values of intestinal gas volume and distribution and to identify abnormalities in relation to functional-type symptoms. METHODS: Abdominal computed tomography scans were evaluated in healthy subjects (n = 37) and in patients in three conditions: basal (when they were feeling well; n = 88), during an episode of abdominal distension (n = 82) and after a challenge diet (n = 24). Intestinal gas content and distribution were measured by an original analysis program. Identification of patients outside the normal range was performed by machine learning techniques (one-class classifier). Results are expressed as median (IQR) or mean ± SE, as appropriate. KEY RESULTS: In healthy subjects the gut contained 95 (71, 141) mL gas distributed along the entire lumen. No differences were detected between patients studied under asymptomatic basal conditions and healthy subjects. However, either during a spontaneous bloating episode or once challenged with a flatulogenic diet, luminal gas was found to be increased and/or abnormally distributed in about one-fourth of the patients. These patients detected outside the normal range by the classifier exhibited a significantly greater number of abnormal features than those within the normal range (3.7 ± 0.4 vs 0.4 ± 0.1; p < 0.001). CONCLUSIONS & INFERENCES: The analysis of a large cohort of subjects using original techniques provides unique and heretofore unavailable information on the volume and distribution of intestinal gas in normal conditions and in relation to functional gastrointestinal symptoms.

Digestive, cognitive and hedonic responses to a meal.

BACKGROUND: Gut dysfunctions may be associated to digestive symptoms. We hypothesized that the gut can also originate pleasant sensations, and wished to demonstrate the hedonic component of the digestive response to a meal. METHODS: Healthy subjects (n = 42) were evaluated during basal fasting conditions and during experimentally induced fullness sensation (either by gastric distension or duodenal nutrient infusion). In each set of studies, a 240 mL test meal (12 kcal broth) and water, as inert control meal, were administered on separate days in a randomized, cross-over design. Gastric accommodation, the cognitive response and the hedonic dimension (both by 10 score scales) were measured 9 min before and 60 min after the meal. KEY RESULTS: In basal conditions, the test meal induced a significantly greater gastric relaxation than the control meal (166 ± 28 mL isotonic volume increase 67 ± 14 mL; p = 0.002). Both meals induced epigastric fullness (3.8 ± 0.7 score and 3.2 ± 0.8 score, respectively; p = 0.740), but contrary to the inert meal, with the active meal this conscious sensation had a pleasant dimension (digestive comfort increase by 1.3 ± 0.6 score with active meal vs -1.1 ± 0.6 decrease with inert meal; p = 0.015). Experimentally induced fullness was associated to a decrease in digestive well-being or abdominal discomfort, which improved only after the active meal but not the inert meal. CONCLUSIONS & INFERENCES: When appropriate conditions are met, the response to a meal includes a hedonic dimension involving pleasant sensation of digestive well-being.

Pharmacogenetic predictor of extrapyramidal symptoms induced by antipsychotics: multilocus interaction in the mTOR pathway.

Antipsychotic (AP) treatment-emergent extrapyramidal symptoms (EPS) are acute adverse reactions of APs. The aim of the present study is to analyze gene-gene interactions in nine genes related to the mTOR pathway, in order to develop genetic predictors of the appearance of EPS. 243 subjects (78 presenting EPS: 165 not) from three cohorts participated in the present study: Cohort 1, patients treated with risperidone, (n=114); Cohort 2, patients treated with APs other than risperidone (n=102); Cohort 3, AP-naïve patients with first-episode psychosis treated with risperidone, paliperidone or amisulpride, n=27. We analyzed gene-gene interactions by multifactor dimensionality reduction assay (MDR). In Cohort 1, we identified a four-way interaction, including the rs1130214 (AKT1), rs456998 (FCHSD1), rs7211818 (Raptor) and rs1053639 (DDIT4), that correctly predicted 97 of the 114 patients (85% accuracy). We validated the predictive power of the four-way interaction in Cohort 2 and in Cohort 3 with 86% and 88% accuracy respectively. We develop and validate a powerful pharmacogenetic predictor of AP-induced EPS. For the first time, the mTOR pathway has been related to EPS susceptibility and AP response. However, validation in larger and independent populations will be necessary for optimal generalization.

Parkin loss of function contributes to RTP801 elevation and neurodegeneration in Parkinson's disease.

Mutations in the PARK2 gene are associated with an autosomal recessive form of juvenile parkinsonism (AR-JP). These mutations affect parkin solubility and impair its E3 ligase activity, leading to a toxic accumulation of proteins within susceptible neurons that results in a slow but progressive neuronal degeneration and cell death. Here, we report that RTP801/REDD1, a pro-apoptotic negative regulator of survival kinases mTOR and Akt, is one of such parkin substrates. We observed that parkin knockdown elevated RTP801 in sympathetic neurons and neuronal PC12 cells, whereas ectopic parkin enhanced RTP801 poly-ubiquitination and proteasomal degradation. In parkin knockout mouse brains and in human fibroblasts from AR-JP patients with parkin mutations, RTP801 levels were elevated. Moreover, in human postmortem PD brains with mutated parkin, nigral neurons were highly positive for RTP801. Further consistent with the idea that RTP801 is a substrate for parkin, the two endogenous proteins interacted in reciprocal co-immunoprecipitates of cell lysates. A potential physiological role for parkin-mediated RTP801 degradation is indicated by observations that parkin protects neuronal cells from death caused by RTP801 overexpression by mediating its degradation, whereas parkin knockdown exacerbates such death. Similarly, parkin knockdown enhanced RTP801 induction in neuronal cells exposed to the Parkinson's disease mimetic 6-hydroxydopamine and increased sensitivity to this toxin. This response to parkin loss of function appeared to be mediated by RTP801 as it was abolished by RTP801 knockdown. Taken together these results indicate that RTP801 is a novel parkin substrate that may contribute to neurodegeneration caused by loss of parkin expression or activity.

Nitrergic and purinergic mechanisms evoke inhibitory neuromuscular transmission in the human small intestine.

BACKGROUND: Inhibitory neuromuscular transmission in the human colon is due to nitrergic and purinergic (P2Y1 -mediated) inputs. The aim of this study was to determine the mechanisms of neuromuscular transmission in different regions of the human small intestine. METHODS: Ileal (n = 6) and jejunal (n = 6) samples underwent histological examination and were studied using sharp microelectrodes in smooth muscle cells and conventional muscle bath techniques. Electrical field stimulation (EFS) was used to stimulate inhibitory neurons. KEY RESULTS: No histological abnormalities were found. Resting membrane potential was -39.7 ± 1.5 and -45.5 ± 2.1 mV in the jejunum and ileum, respectively. Slow waves and spontaneous contractions were recorded at a frequency of about 8-9 and 6-7 cpm in the jejunum and ileum, respectively. In non-adrenergic, non-cholinergic conditions, EFS caused an inhibitory junction potential and mechanical relaxation. Both responses were blocked by tissue incubation with the nitric oxide synthase inhibitor (Nω-nitro-l-arginine 1 mM) and the P2Y1 receptor blocker 2'-deoxy-N(6) -methyladenosine 3',5'-bisphosphate tetrasodium salt (MRS2179; 10 µM). Both exogenous addition of sodium nitroprusside (1 µM) and the preferential P2Y1 receptor agonist ADPßS (1 µM) hyperpolarized and relaxed smooth muscle cells. MRS2179 (10 µM) blocked ADPßS-induced responses. CONCLUSIONS & INFERENCES: Similar to colon, inhibitory neurotransmission in the human small intestine is mainly mediated by purinergic (via P2Y1 receptors) and nitrergic inhibitory neurotransmission. Similar mechanisms of inhibitory neurotransmission are present in different regions of the human intestine.

Mechanisms of abdominal distension in severe intestinal dysmotility: abdomino-thoracic response to gut retention.

BACKGROUND: We previously showed that abdominal distension in patients with functional gut disorders is due to a paradoxical diaphragmatic contraction without major increment in intraabdominal volume. Our aim was to characterize the pattern of gas retention and the abdomino-thoracic mechanics associated with abdominal distension in patients with intestinal dysmotility. METHODS: In 15 patients with manometrically proven intestinal dysmotility, two abdominal CT scans were performed: one during basal conditions and other during an episode of severe abdominal distension. In 15 gender- and age-matched healthy controls, a basal scan was performed. KEY RESULTS: In basal conditions, patients exhibited more abdominal gas than healthy subjects, particularly in the small bowel, and the volume significantly increased during an episode of distension. During episodes of abdominal distension, the increase in abdominal content was associated with increased girth and antero-posterior abdominal diameter, as well as a cephalic displacement of the diaphragm, which reduced the height of the lung. The consequent reduction in the air volume of the lung was attenuated by an increase in the antero-posterior diameter of the chest. CONCLUSIONS & INFERENCES: Abdominal distension in patients with severe intestinal dysfunction is related to marked pooling of gut contents, particularly in the small bowel. This increase in content is accommodated within the abdominal cavity by a global and coordinated abdomino-phreno-thoracic response, involving an accommodative ascent of the diaphragm and a compensatory expansion of the chest wall.

Functional gut disorders or disordered gut function? Small bowel dysmotility evidenced by an original technique.

BACKGROUND: This study aimed to determine the proportion of cases with abnormal intestinal motility among patients with functional bowel disorders. To this end, we applied an original method, previously developed in our laboratory, for analysis of endoluminal images obtained by capsule endoscopy. This novel technology is based on computer vision and machine learning techniques. METHODS: The endoscopic capsule (Pillcam SB1; Given Imaging, Yokneam, Israel) was administered to 80 patients with functional bowel disorders and 70 healthy subjects. Endoluminal image analysis was performed with a computer vision program developed for the evaluation of contractile events (luminal occlusions and radial wrinkles), non-contractile patterns (open tunnel and smooth wall patterns), type of content (secretions, chyme) and motion of wall and contents. Normality range and discrimination of abnormal cases were established by a machine learning technique. Specifically, an iterative classifier (one-class support vector machine) was applied in a random population of 50 healthy subjects as a training set and the remaining subjects (20 healthy subjects and 80 patients) as a test set. KEY RESULTS: The classifier identified as abnormal 29% of patients with functional diseases of the bowel (23 of 80), and as normal 97% of healthy subjects (68 of 70) (P < 0.05 by chi-squared test). Patients identified as abnormal clustered in two groups, which exhibited either a hyper- or a hypodynamic motility pattern. The motor behavior was unrelated to clinical features. CONCLUSIONS & INFERENCES: With appropriate methodology, abnormal intestinal motility can be demonstrated in a significant proportion of patients with functional bowel disorders, implying a pathologic disturbance of gut physiology.

Intestinal motor activity, endoluminal motion and transit.

A programme for evaluation of intestinal motility has been recently developed based on endoluminal image analysis using computer vision methodology and machine learning techniques. Our aim was to determine the effect of intestinal muscle inhibition on wall motion, dynamics of luminal content and transit in the small bowel. Fourteen healthy subjects ingested the endoscopic capsule (Pillcam, Given Imaging) in fasting conditions. Seven of them received glucagon (4.8 microg kg(-1) bolus followed by a 9.6 microg kg(-1) h(-1) infusion during 1 h) and in the other seven, fasting activity was recorded, as controls. This dose of glucagon has previously shown to inhibit both tonic and phasic intestinal motor activity. Endoluminal image and displacement was analyzed by means of a computer vision programme specifically developed for the evaluation of muscular activity (contractile and non-contractile patterns), intestinal contents, endoluminal motion and transit. Thirty-minute periods before, during and after glucagon infusion were analyzed and compared with equivalent periods in controls. No differences were found in the parameters measured during the baseline (pretest) periods when comparing glucagon and control experiments. During glucagon infusion, there was a significant reduction in contractile activity (0.2 +/- 0.1 vs 4.2 +/- 0.9 luminal closures per min, P < 0.05; 0.4 +/- 0.1 vs 3.4 +/- 1.2% of images with radial wrinkles, P < 0.05) and a significant reduction of endoluminal motion (82 +/- 9 vs 21 +/- 10% of static images, P < 0.05). Endoluminal image analysis, by means of computer vision and machine learning techniques, can reliably detect reduced intestinal muscle activity and motion.

Non-anatomical intestinal transplantation.

INTRODUCTION: Intestinal transplantation is the only long-range treatment option for patients with intestinal failure. We report an exceptional case of isolated intestinal transplantation with the implant in a non-anatomical position. CLINICAL CASE: The patient was a thirty-eight-year-old man (60 kg weight, 180 cm height, 18.3 body mass index) with intestinal failure and home parenteral nutrition due to a short-bowel syndrome for which intestinal transplantation was indicated. The patient had a vascular malformation with the cava vein located left to the aorta, and the intestine was implanted with a 180 masculine rotation around the mesenteric axis, so that the implant s superior mesenteric artery and vein matched the recipient s cava and aorta. Postoperative follow-up was excellent and the patient was discharged after six weeks with a 10-kg gain in body weight. DISCUSSION: This non-anatomical intestinal implantation of the small bowel, previously unreported, offers technical advantages over other options. Adequate intestinal function represents a unique model to prove the viability of intestinal implants in a non-anatomical position.

Trasplante intestinal en posición no anatómica / Non-anatomical intestinal transplantation

Introducción: el trasplante intestinal es el único tratamiento eficaz a largo plazo de los pacientes con fallo intestinal. Se presenta un caso clínico excepcional de trasplante intestinal aislado en posición no anatómica. Caso clínico: se trata de un varón de 38 años de edad con fallo intestinal y nutrición parenteral domiciliaria por un síndrome de intestino corto al que se le indicó un trasplante intestinal. Fue incluido en lista de espera con un peso de 60 kg, 180 cm de altura y 18,3 de índice de masa corporal. El receptor presentaba una trasposición de los grandes vasos con la vena cava situada a la izquierda de la arteria aorta por lo que el intestino se implantó con una rotación del injerto de 180º sobre su eje mesentérico, con el objetivo de que la vena y la arteria mesentérica superior del injerto coincidieran con la vena cava y la arteria aorta del receptor. El paciente presentó excelente postoperatorio y fue dado de alta a las 6 semanas con un aumento de peso de 10 kg. Discusión: esta implantación no anatómica del intestino, previamente no referida en la literatura, ofrece ventajas técnicas sobre otras alternativas. La adecuada función intestinal constituye un modelo único que prueba la viabilidad del intestino implantado en posición no anatómica(AU)

Introduction: intestinal transplantation is the only long-range treatment option for patients with intestinal failure. We report an exceptional case of isolated intestinal transplantation with the implant in a non-anatomical position. Clinical case: the patient was a thirty-eight-year-old man (60 kg weight, 180 cm height, 18.3 body mass index) with intestinal failure and home parenteral nutrition due to a short-bowel syndrome for which intestinal transplantation was indicated. The patient had a vascular malformation with the cava vein located left to the aorta, and the intestine was implanted with a 180º rotation around the mesenteric axis, so that the implant's superior mesenteric artery and vein matched the recipient's cava and aorta. Postoperative follow-up was excellent and the patient was discharged after six weeks with a 10-kg gain in body weight. Discussion: this non-anatomical intestinal implantation of the small bowel, previously unreported, offers technical advantages over other options. Adequate intestinal function represents a unique model to prove the viability of intestinal implants in a non-anatomical position(AU)