Sleep Disordered Breathing after Stroke: Clinical Profile of Patients with Obstructive- as Opposed to Central-Sleep Apnea

Abstract Aim: In order to define the clinical and instrumental profile of patients with Obstructive Sleep Apnea/Hypopnea (OSAH) and to compare them with that of cases with Central Sleep Apnea/Hypopnea (CSAH), a series of stable strokes were studied. Methods: Thirty four patients were submitted to both clinical and polisomnographyc study (PSG) after 4 months of stroke. A Sleep Disordered Breathing (SDB) was diagnosed in all cases with an AHI>5. Patients were classified as affected by predominantly OSAH (pOSAH), predominantly CSAH (pCSAH), or normal patients. Comparisons were made among the groups and correlation analyses were done in each group. Significance was set at p<0.005. Results: Thirty-four ischemic strokes were enrolled (55% embolic, 6% large artery, 32% lacunar, 9% with undetermined cause). The 76% of them had a SDB ( pOSAH=61%; pCSAH=39%). Nearly the 47% of cases had an obstruction of the upper airways alone or combined with an increase in pharyngeal tissue. No significant differences were found between pOSAH and pCSAH. In pOSAH cases, 8 cases (50%) had an obstruction of the upper airways; in 4 of them it was combined with an increase in pharyngeal tissue; the time interval from stroke to PSG (Δ t), was inversely related to both TST (p 0.017) and TSP (p 0.039); the NIH-SS at entry was directly related to the number of arousals /h of sleep (p 0.044); the more severe AHI the higher is ODI (p 0.000). In the pCSAH group, 4 cases (40%) had an obstruction of the upper airways combined with an increase in pharyngeal tissue; two of these 4 cases had also a BMI>30. In CSAH, Δt was inversely related to SE Index (p 0.021), and directly related to both the number of arrhythmias/h sleep (p 0.016) and ODI (p 0.033). No correlations were found between the number of arrhythmias/h sleep and causes of stroke both in pOSAH and in pCSAH groups. Conclusions: Our data suggest a direct effect of stroke on the peripheral breathing system with subsequent alteration of loop gain and CSAH phenotype, at least in a subgroup of cases. To confirm this hypothesis multicenter clinical sleep studied are needed.