Mandibular Advancement Devices in Obstructive Sleep Apnea Patients Intolerant to Continuous Positive Airway Pressure Treatment.

Obstructive sleep apnea (OSA) is defined as episodes of upper airway obstruction occurring during sleep. Conservative treatment of OSA consists of continuous positive airway pressure (CPAP). An alternative treatment in mild-to-moderate OSA could be the use of intraoral mandibular advancement devices (MAD). The aim of this study was to evaluate therapeutic efficacy of MAD in OSA patients intolerant to CPAP. The study group included 8 patients, who fulfilled specific inclusion criteria during a dental examination, out of the 30 CPAP intolerant patients who were referred for the possible use of MAD. The selected patients used MAD for 30 days and then switched to CPAP for 10 days to compare the effectiveness of both treatment methods. They had 3 polysomnographic (PSG) examination: baseline before treatment, and at the end of MAD and CPAP. We found that either treatment method resulted in comparable symptomatic improvements in OSA patients. In detail, the apnea-hypopnea index decreased, along with the overall number of obstructive, central, and mixed apneic episodes during sleep time. The mean arterial oxygen saturation (SaO2) improved and the minimum SaO2 level noted during night time got enhanced. Differences in the sleep apnea indices after MAD and CPAP treatments were insignificant, but there was a consistent impression that CPAP was superior to MAD as it tended to improve symptoms to a somehow greater extent. We conclude that MAD is a sufficiently effective treatment alternative for OSA patients who are intolerant to CPAP or in whom CPAP therapy fails.

CDP-choline, but not cytidine, protects hippocampal CA1 neurones in the gerbil following transient forebrain ischaemia.

The effects of CDP-choline (citicoline), cytidine monophosphate or cytidine on the number of CA1 hippocampal neurones surviving five-minute forebrain ischaemia have been evaluated in gerbils. The substances tested were given in daily doses equivalent on a molar basis to 500 mg/kg CDP-choline, starting immediately after ischaemia. On day five the brains were perfused, postfixed, cut into 10 microm slices and stained with cresyl violet, and the number of neurones in the CA1 sectors was counted manually under a light microscope at magnification x 400. The results indicate a significant degree of protection provided by citicoline, but no protection by cytidine monophosphate or cytidine. The choline moiety of CDP-choline appears to be essential for the neuroprotective properties of the drug.

Blood-brain barrier disturbances and morphological changes in rat brain after photochemically induced focal ischaemia.

The disturbances in cerebral circulation lead to focal brain ischaemia and brain infarcts. The pathogenesis of brain ischaemia has been a subject of numerous experimental studies employing different models and focusing on the anatomy of collateral circulation. The aim of this study was the evaluation of our own model of focatcerebral damage caused by a photodynamic reaction, and determination of its utility as a model of brain necrosis and blood-brain barrier damage in the rat. Wistar rats were used for the experiments. The animals were anaesthetised with 3% chloral hydrate (325 mg/kg) and injected intravenously with 40 mg/kg of 3% solution of rose bengal. After removal of the periostium the brain was irradiated through the skull for 30 min with a 250 W halogen, air-cooled light source. The material for morphologic studies was sampled 24 h, 4 days and 7 days after irradiation. The brains were fixed by perfusion, embedded in paraffin, and stained with haematoxilin-eosin (HE), acid vanadium fuchsin, cresyl violet, and GFAP. The results document the usefulness of this method for studying focal brain ischaemia in rats. The observed morphological changes and disturbances in blood-brain barrier provided information about the dynamics of the formation of gliosis, the formation of necrotic foci, and the quality and extent of brain damage in the surrounding tissue.