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BACKGROUND: To prospectively analyze factors associated with detecting epileptogenic lesions on MRI within the work-sharing process of neurologists, epileptologists, radiologists and neuroradiologists. METHODS: We assembled four sets of six MRI scans, each set representing five typical epileptogenic lesions (hippocampal sclerosis or limbic encephalitis; focal cortical dysplasias; periventricular nodular or other heterotopias; long-term epilepsy associated tumors; gliotic scar, hemosiderin or cavernoma), and non - lesional epilepsy. At professional conferences, we invited neurologists, epileptologists, radiologists, and neuroradiologists to read two out of four MRI sets, one of which was presented with a clinical focus hypothesis. Participants were randomly assigned to MRI sets. Effects of examiners' specialty, duration of training and professional experience on detection rate of epileptogenic lesions were investigated. RESULTS: Fourty-eight neurologists, 22 epileptologists, 20 radiologists and 21 neuroradiologists read 1323 MRI scans. Overall, 613 of 1101 (55.7%) epileptogenic lesions were detected. Long-term epilepsy associated tumors (182/221, 82.4%) were found more frequently than gliotic scar, hemosiderin or cavernoma (157/220, 71.4%), hippocampal sclerosis or limbic encephalitis (141/220, 64.1%), nodular heterotopia (68/220, 30.9%) and focal cortical dysplasias (65/220, 29.5%, p < 0.001). Provision of a focus hypothesis improved the detection of hippocampal sclerosis or limbic encephalitis (86/110, 78.2% vs 55/110, 50%, p < 0.001) and focal cortical dysplasias (40/110, 36.4% vs 25/110, 22.7%, p = 0.037). Neuroradiologists and epileptologists were more likely than radiologists and neurologists to be amongst the most successful readers. In multivariable analysis, type of epileptogenic lesion, specialty of MRI reader, and provision of focus hypothesis predicted correct identification of epileptogenic lesions. CONCLUSIONS: Epileptogenic lesions are often not recognized on MRI even by expert readers. Their detection can be improved by providing a focus hypothesis. These results stress the need for training in the MRI characteristics of epilepsy - specific pathology, and, most importantly, interdisciplinary communication between neurologists/epileptologists and (neuro)radiologists to improve detection of epileptogenic lesions.
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A large-group one session treatment (LG-OST) combining exposure and diaphragmatic breathing as a bodily coping element was carried out to investigate its feasibility and effectiveness in a sample of 43 highly dental fearful individuals treated simultaneously. We assessed subjective dental fear, dysfunctional dental-related beliefs, and perceived control pre- and post-intervention and at four-month follow-up. Participants additionally performed a behavioural approach test (BAT) pre- and post-intervention. During the applied exposure exercises, four participants (9.3%) discontinued the program all reporting too high levels of distress. Regarding subjective dental fear and dysfunctional dental related beliefs post treatment effects, LG-OST showed medium to large effect sizes, ranging from Cohen's d = 0.51 to d = 0.84 in the Intention-to-Treat analysis. Subjective dental fear improved clinically significantly in about one fourth (25.6%) of therapy completers. All post-treatment effects remained stable over time. Concerning the behavioral fear dimension, we observed a strong ceiling effect. Already at pre-assessment, participants accomplished more than six out of seven BAT-steps. Thus, behavioral approach did not increase significantly following treatment. Overall, the LG-OST protocol proved feasible and efficient. Compared to other one-session individual and multi-session group treatments the observed LG-OST effects were smaller. However, if LG-OST could match the efficacy of highly intensive short treatments delivered in an individual setting in the future, for example, by applying a wider array of exposure exercises, it could be a very useful treatment option as an intermediate step within a stepped care approach.
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PURPOSE: Carbonic anhydrases play a central buffering role in current models of fluid transport in corneal endothelium, but in humans, clinical use of carbonic anhydrase inhibitors (CAIs) for the management of glaucoma does not cause corneal swelling. This study compares species differences in response to CAIs in human versus bovine corneal endothelial transport. METHODS: Short-circuit current (Isc) measurements were performed on bovine and human corneal endothelium under identical conditions. The effects of four CAIs (acetazolamide, brinzolamide, dorzolamide, and ethoxzolamide) were measured. Endothelial expression of carbonic anhydrase II and IV was evaluated by immunofluorescence microscopy. Functional presence of carbonic anhydrase activity was determined using the Hansson's cobalt sulfide histochemical method. RESULTS: All four CAIs decreased bovine Isc (% change in Isc: acetazolamide, -21.0 ± 9.5, n = 8; brinzolamide, -35.5 ± 13.5, n = 9; dorzolamide, -33.6 ± 7.2, n = 8; ethoxzolamide, -35.3 ± 12.9, n = 8). That decrease was not present in humans (% change in Isc: acetazolamide, 16.2 ± 20.1, n = 3; brinzolamide, 6.7 ± 13.9, n = 3; dorzolamide, 8.0 ± 20.4, n = 3; ethoxzolamide, -4.8 ± 10.3, n = 2). Despite no functional effect of CAIs on Isc, both carbonic anhydrase II and IV were present in human corneal endothelium by immunofluorescence microscopy. Histochemical analysis of human corneal endothelium revealed functionally active carbonic anhydrase activity inhibited by brinzolamide. CONCLUSIONS: Carbonic anhydrase facilitates ion transport impacting the corneal endothelial Isc in bovine but not human corneal endothelium, despite its presence and functional activity in human tissue. This finding supports the clinical observation of no corneal swelling in humans administered CAIs and suggests that alternative ion transport mechanisms may be operational in corneal endothelium of different species.
