Proton magnetic resonance spectroscopy study of brain metabolism in obstructive sleep apnoea syndrome before and after continuous positive airway pressure treatment.

STUDY

OBJECTIVES

Obstructive sleep apnoea syndrome (OSAS) causes sleep related oxygen desaturation, excessive daytime sleepiness (EDS), and cognitive impairment. The role of hypoxic brain damage, sleep fragmentation, and the associated comorbidities (hypertension, vascular disorders) in the pathogenesis of cognitive deficits remains controversial. The aim of this study was to evaluate the cerebral metabolism of OSAS patients in vivo before and after CPAP treatment.

DESIGN AND PATIENTS: Fourteen OSAS patients without cardiovascular or cerebrovascular impairment underwent the same protocol before and after 6 months of CPAP including: overnight videopolysomnography (VPSG), Multiple Sleep Latency Test (MSLT), and within the next 2 days neuropsychological and 1H-MRS evaluations. Single voxel 1H-MRS was performed in the parietal-occipital cortex, and absolute concentrations of N-acetyl-aspartate (NAA), creatine, and choline were measured, acquiring spectra at multiple echo-times and using water as internal standard. Ten matched controls were also studied.

RESULTS

OSAS patients had a mean RDI of 58/hr, a mean arousal index of 57/hr, and a mean nadir SpO2 of 71%. Before CPAP, all patients showed a normal global cognitive functioning, with only a small number of pathological tasks in working memory and attention tests in a minority of patients. CPAP therapy was effective in resolving sleep apnoea and normalizing sleep structure, and improving EDS and neuropsychological alterations. Before CPAP treatment cortical [NAA] in OSAS (11.86 mM +/- 0.80, mean +/- SD) was significantly lower than in controls (12.85 +/- 0.93; P = 0.01) and positively correlated with minimum SpO2 during sleep (r = 0.69; P = 0.006) and MSLT scores (r = 0.62; P = 0.01). Cortical [NAA] reduction persisted after therapy (11.94 +/- 1.33; P = 0.87 versus pre-CPAP).

CONCLUSIONS

OSAS patients have cortical metabolic changes consistent with neuronal loss even in the absence of vascular comorbidities. Metabolic changes persisted after CPAP in the absence of EDS, nocturnal arousals, and major cognitive deficits, likely related to hypoxic damage prior to CPAP treatment.