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Aims Our main objective was to determine the neuropathological correlates of dementia in patients with Lewy body disease (LBD). Furthermore, we used data derived from clinical, neuropathological and genetic studies to investigate boundary issues between Dementia with Lewy bodies (DLB) and Parkinson's disease with (PDD) and without (PDND) dementia. Methods One hundred and twenty-one cases with a neuropathological diagnosis of LBD and clinical information on dementia status were included in the analysis (55 PDD, 17 DLB and 49 PDND). We carried out topographical and semi-quantitative assessment of Lewy bodies (LB), Aβ plaques and tau-positive neuropil threads (NT). The APOE genotype and MAPT haplotype status were also determined. Results The cortical LB (CLB) burden was the only independent predictor of dementia (OR: 4.12, P < 0.001). The total cortical Aβ plaque burden was an independent predictor of a shorter latency to dementia from onset of motor signs ( P = 0.001). DLB cases had a higher LB burden in the parietal and temporal cortex, compared to PDD. Carrying at least one APOE ϵ4 allele was associated with a higher cortical LB burden ( P = 0.02), particularly in the neocortical frontal, parietal and temporal regions. Conclusions High CLB burden is a key neuropathological substrate of dementia in LBD. Elevated cortical LB pathology and Aβ plaque deposition are both correlated with a faster progression to dementia. The higher CLB load in the temporal and parietal regions, which seems to be a distinguishing feature of DLB, may account for the shorter latency to dementia and could be mediated by the APOE ϵ4 allele. [ABSTRACT FROM AUTHOR]

Introduction Many patients attending GI physiology units for assessment of dysphagia and GORD also complain of postprandial bloating and/or belching. Excessive fasting aerophagia has been recently described in patients with severe continuous bloating and belching. Exaggerated air swallowing might be more relevant for postprandial symptoms but, thus far, objective assessment of prandial aerophagia and normal values are lacking. Oesophageal impedance can detect air swallowing. We aimed to quantify aerophagia during meals in asymptomatic subjects and patients with postprandial bloating and belching. Methods We assessed aerophagia during meals using ambulatory impedance-pH monitoring in 39 healthy, asymptomatic controls (from the US-Belgian MII-pH Normal value study, Shay . 2004; mean age in original study 39, range 22–62) to establish normal 95% confidence intervals. We identified 38 patients (mean age 43, range 17–74) with postprandial bloating and/or belching who attended the GI physiology unit for assessment of dysphagia or GORD as primary symptoms. Mealtime air swallows were visually identified when swallows were associated with antegrade flow and fast impedance increase (at least 3000 Ω from baseline) in the most distal recording segment. A score of air swallows/10 min mealtime was calculated for each subject. In patients with mealtime exaggerated air swallowing (above 95th percentile of normal values) we examined for evidence of concomitant fasting aerophagia. Results The 95% percentile range of mealtime aerophagia in normal subjects was 6.8 to 9.4 episodes/10 min, mean 8.1. Patients had significantly higher mealtime air swallowing rates than controls (mean 11.8 episodes/10 min, SEM 1.0, p = ). There was no significant difference between predominant bloating and belching subgroups. Only 4 of 23 patients with exaggerated mealtime air swallowing had concomitant fasting aerophagia. OC-054 Prandial aerophagia in normal controls and patients with belching and bloating Conclusion We established normal values of mealtime air swallowing using oesophageal impedance. Patients with postprandial bloating and/or belching exhibit increased aerophagia during meals. Most of these patients do not have fasting aerophagia. Exaggerated air swallowing during meals can now be objectively detected and biofeedback techniques can be attempted to modify such behaviour as a potential therapeutic strategy for these patients with functional GI symptoms. [ABSTRACT FROM PUBLISHER]

Introduction Persistent reflux symptoms occur in a subgroup of patients following antireflux surgery. These symptoms can be due failure of the antireflux barrier. GI physiology studies are performed to evaluate the OGJ function and anatomy in these patients. Recent studies with high resolution manometry (HRM) have shown the presence of a dual high pressure zone (HPZ) at the OGJ as an expression of persistent hiatus hernia. However, the relation between dual high pressure zone, oesophageal hypomotility and persistent symptoms is unclear. The aim of this study was to evaluate reflux parameters and oesophageal motility patterns with HRM in a group of symptomatic patients after fundoplication. Methods Ten patients (5 male, 5 female; mean age 55 years) were selected based on the presence of persistent typical reflux symptoms post-Nissen fundoplication. The patients underwent HRM and impedance-pH monitoring ‘off’ PPI. The existence of dual HPZ, oesophageal hypomotility and amplitude of the after-contraction post multiple rapid swallowing (MRS) were evaluated together with acid and non-acid reflux parameters. Increased number of reflux events (post Nissen) was considered if >30/24 h. Results Six out of ten patients had a dual HPZ on HRM. Acid exposure time and number of acid reflux events in these patients was significantly higher than those with a single HPZ (12.7% vs 0.5%, p=0.01). The patients with a dual HPZ more commonly exhibited oesophageal hypomotility and poor response to MRS compared to the patients with a single HPZ (4/6 vs 1/4). In addition more of the patients with a dual HPZ showed impaired acid reflux clearance compared to patients with single HPZ (5/5 vs 1/3). Conclusion HRM and impedance-pH measurement allows a precise assessment of patients with symptoms postfundoplication. Our study suggests that the presence of a dual HPZ on oesophageal HRM is associated with impairment of oesophageal motility and impaired oesophageal acid clearance, and hence may be important in the persistence of GORD symptoms postoperatively. [ABSTRACT FROM PUBLISHER]