Objective: To determine whether sleepiness and its evolution over sustained wakefulness could be reversed by nasal continuous positive airway pressure (CPAP) therapy in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS).Methods: Twelve OSAHS patients underwent three 32-h sessions of study: one before CPAP therapy (T0), the second (T3) and the third (T6), respectively, after 3 and 6 months of therapy. Each session included one night of sleep followed by 24 h of sustained wakefulness, during which EEG recordings and subjective ratings were performed every hour.Results: The waking EEG in treated OSAHS patients was partially improved after 3 months of CPAP and their subjective complaint of sleepiness was normalized after 6 months. Theta power (3.9-7.8 Hz) was decreased as well as its time course during the diurnal period but beta power (12.7-29.2 Hz) remained higher.Conclusions: CPAP partially reverses waking EEG abnormalities in OSAHS patients with reduced theta activity after 3 months and removes the subjective complaint of sleepiness after 6 months. Nevertheless, the persistence of increased beta activity in treated patients suggests that efforts to stay awake remain strong after CPAP treatment. Significance: CPAP influences the EEG's time course over sustained wakefulness in a frequency-specific manner in OSAHS patients. (C) 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

It is well known that most patients with obstructive sleep apnoea/hypopnoea syndrome (OSAHS) suffer sleepiness, although the underlying mechanisms of this relationship remain unclear. The present study examined the relationship between nocturnal variables and the subsequent waking electroencephalogram (EEG), in order to determine if sleepiness was related to OSAHS severity and due to sleep fragmentation or to nocturnal hypoxaemia.In total, 12 moderate-to-severe OSAHS patients underwent a total sleep night followed by a 24-h period of sustained wakefulness where the waking EEG was measured every hour.The results showed that alpha (7.9-12.6 Hz) and beta (12.7-29.2 Hz) activities were strongly related to OSAHS severity, mainly reflected by the apnoea index. Moreover, spectral power in most of the waking EEG components was significantly correlated with nocturnal hypoxaemia indices, namely alpha and beta activity when hypoxaemia becomes severe. However, no correlation was found between the waking EEG and sleep fragmentation parameters.In conclusion, the present results suggest that the difficulty in maintaining an optimal level of alertness, reflected by a higher activity in awake alpha and beta bands (7.9-29.2 Hz) in obstructive sleep apnoea/hypopnoea syndrome, was better explained by: 1) the apnoea as opposed to the hypopnoea index; and 2) nocturnal hypoxaemia as opposed to sleep fragmentation.

Objective: This study investigated if obstructive sleep apnea syndrome (OSAS) may be associated with higher activity in different frequency bands of the EEG during a sustained wakefulness paradigm.Methods: Twelve OSA patients and 8 healthy controls were studied with the Karolinska Drowsiness Test (KDT) and subjective ratings of sleepiness (VAS and KSS) conducted every hour during 24 h of sustained wakefulness.Results: The waking EEG activity, mainly in the low (0.5-7.8 Hz) and fast (12.7-29.2 Hz) frequency band, increased as time awake progressed in both groups but more obviously in OSA patients. A similar pattern was observed for rated sleepiness in both groups. Moreover, VAS ratings of alertness were closely related to the awake theta, fast alpha and beta bands in controls but not in OSA patients.Conclusions: OSAS was associated with a wake-dependent increase in low (0.5-7.8 Hz) and fast (12.7-29.2 Hz) frequency range activity. Variations in behavioural sleepiness measured by VAS ratings closely reflect most of the waking EEG parameters in controls but not in OSA patients.Significance: In a sustained wakefulness paradigm, higher activity in delta, theta and beta bands associated with OSAS indicates that OSA patients show marked signs of higher sleepiness and stronger efforts than controls to stay awake, even though they tend to underestimate their sleepiness. (c) 2007 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

The respiratory disorders expressed by obstructive hypopneas and apneas during sleep, as well as the sequences of crescendo in respiratory effort without hypopneas or apneas which define the upper airway resistance syndrome, terminate with (thanks to) an arousal, defined by EEG changes. In some cases, the activation of the central nervous system is restricted to a sympathetic activation, which has been mainly studied in the cardiovascular area, and is not always accompanied by a cortical arousal. Various approaches (heart rate, blood pressure, pulse transit time, peripheral arterial tonometry) make the identification of sympathetic activation possible. Sympathetic activation seems to be more sensitive than cortical arousal to the stimulations generated by the respiratory system via an activation of mechanoreceptors stimulated by the increased respiratory effort in response to total or partial occlusion of the upper airway. The mechanisms of the cortical or autonomic arousal are not fully understood, but their detection could be a diagnostic tool for the identification of such disorders. Such tools are currently under validation.

Les anomalies respiratoires que constituent les hypopnees et les apnees obstructives au cours du sommeil, ainsi que les sequences d'augmentation de l'effort respiratoire sans hypopnee ni apnee qui definissent le syndrome de resistance des voies aeriennes superieures, se terminent par (grâce a) un eveil, caracterise par des modifications electroencephalographiques. Dans certains cas, l'activation du systeme nerveux se limite a une activation sympathique, surtout etudiee dans le domaine cardio-vasculaire, qui n'est pas toujours associee a une activation corticale. Differentes approches (frequence cardiaque, pression arterielle, temps de transit de pouls, tonometrie arterielle peripherique) permettent d'identifier cette activation sympathique, qui parait plus sensible que l'eveil cortical aux stimulations issues du systeme respiratoire. Cette activation sympathique est realisee par le biais de l'activation des mecanorecepteurs mis en jeu par l'augmentation de l'effort respiratoire en reponse a l'occlusion, totale ou partielle, des voies aeriennes superieures. Les mecanismes en jeu dans cette activation corticale ou autonomique restent a preciser, mais ces methodes de detection pourraient constituer des outils diagnostiques permettant d'identifier ces affections. Ces outils sont actuellement en cours de validation.

The respiratory disorders expressed by obstructive hypopneas and apneas during sleep, as well as the sequences of crescendo in respiratory effort without hypopneas or apneas which define the upper airway resistance syndrome, terminate with (thanks to) an arousal, defined by EEG changes. In some cases, the activation of the central nervous system is restricted to a sympathetic activation, which has been mainly studied in the cardiovascular area, and is not always accompanied by a cortical arousal. Various approaches (heart rate, blood pressure, pulse transit time, peripheral arterial tonometry) make the identification of sympathetic activation possible. Sympathetic activation seems to be more sensitive than cortical arousal to the stimulations generated by the respiratory system via an activation of mechanoreceptors stimulated by the increased respiratory effort in response to total or partial occlusion of the upper airway. The mechanisms of the cortical or autonomic arousal are not fully understood, but their detection could be a diagnostic tool for the identification of such disorders. Such tools are currently under validation.

BACKGROUND:Current disease management in rheumatoid arthritis (RA) has moved towards "inverting the therapeutic pyramid" by introducing disease-modifying anti-rheumatic drugs (DMARDs) early. Despite the logic of early DMARD therapy, there is a dearth of supportive evidence for this approach. We report a randomised controlled trial comparing sulphasalazine monotherapy with diclofenac monotherapy in early RA. The primary aim was to provide unequivocal evidence that early DMARDs prevent erosive damage. The secondary aim was to evaluate if sulphasalazine used alone has comparable symptomatic benefits to NSAIDs.METHODS:117 patients with RA for under 12 months of diagnosis (mean 2 months) were randomised (62 sulphasalazine; 55 diclofenac). Sulphasalazine patients comprised 76% women, and 58% were rheumatoidfactor positive. Diclofenac patients comprised 74% women, and 54% were seropositive. 36% completed 12 months of therapy (16 sulphasalazine; 26 diclofenac); sulphasalazine was given for a mean period of 21 weeks and diclofenac for a mean period of 33 weeks. Results were analysed on an intention to treat basis.RESULTS:After 12 months the mean number of new erosions in patients randomised to receive sulphasalazine was 2.0 (95%CI 0.9, 3.1) and in patients randomised to receive diclofenac was 7.5 (95%CI 4.1, 10.9; p = 0.002 by Student's unpaired t-test). An analysis of valid compliant completers showed the mean number of new erosions in patients who received 12 months therapy with sulphasalazine was 2.3 (95%CI 0.6, 4.0) and in patients who received 12 months diclofenac was 10.5 (95%CI 5.0, 15.9; p = 0.018 by Student's unpaired t-test). The Ritchie articular index, swollen joint counts and pain scores decreased with both sulphasalazine and diclofenac, with mean falls in both groups of 15-20% at 2 weeks and 30-40% at 4 and 8 weeks. There were no differences between treatments. Disease activity scores showed similar highly significant mean decreases within both treatment groups (P < 0.001 in all cases) of 0.5 at 2 weeks and 1.0 at 4 weeks; at 12 and 26 weeks they were significantly lower with sulphasalazine (p = 0.036 and 0.045). 75% of the patients given sulphasalazine and 65% of those given diclofenac had one or more adverse events with no major differences between treatments.CONCLUSIONS:These results show that an accelerated dosing schedule of sulphasalazine has identical effects to diclofenac in reducing symptoms, indicating it is a rapidly effective DMARD. They also provide unequivocal evidence, analysed on an intention to treat basis, that early treatment with sulphasalazine significantly reduces the extent of radiological progression in active RA.

The number and percentage of T cells bearing Fc gamma receptors (T gamma) was quantitated in peripheral blood of patients with the autoimmune disease chronic ITP. In over half the patients, low initial percentages were obtained, the great majority of which returned to within the normal range after incubation under capping conditions. The phenomenon could be reproduced by pretreating normal T cells with immune complex containing sera or aggregated HGG. Furthermore, a reversible reduction in T gamma cells was observed in control patients with nonimmune thrombocytopenia and in pregnancy. In each case an association was observed between the reduced T gamma cell levels and the presence of circulating immune complexes, which suggested that the results could be explained by masking of Fc gamma receptors with preformed IgG-containing complexes. By contrast, patients with other autoimmune diseases such as scleroderma and rheumatoid arthritis had high or normal numbers of T gamma cells, respectively. Taken together, the findings do not support the existence of a gross deficiency of suppressor cells in patients with autoimmune disease and emphasize the need for caution in selection of markers for identification of T cell subsets.