L Buratti1, C Petrelli1, E Potente1, A Plutino1, G Viticchi1, L Falsetti2, L Provinciali1, M Silvestrini3. 1. Neurological Clinic, Marche Polytechnic University, Ancona, Italy. 2. Internal and Subintensive Medicine, Ospedali Riuniti Ancona, Italy. 3. Neurological Clinic, Marche Polytechnic University, Ancona, Italy. Electronic address: m.silvestrini@univpm.it.
Abstract
OBJECTIVE: The etiology of transient global amnesia (TGA) is largely undetermined. The aim of this study was to investigate whether the prevalence of obstructive sleep apnea syndrome (OSAS), a condition associated with subtle changes in brain structures involved in memory processes, increases in subjects who have previously experienced a TGA episode. METHODS: Twenty-nine patients who had had a TGA episode were included. A case-control model was used, matching cases with controls by sex, age, and body mass index category. Diagnosis of OSAS was based on the results of the Berlin Questionnaire, which was later confirmed by means of an all-night polysomnography recording. RESULTS: The prevalence of OSAS among TGA patients was significantly higher with respect to that in controls (44.8% vs 13.8%, p = 0.020, χ2 test). At logistic regression model, subjects with TGA had an odds ratio of 8.409 (95% confidence interval = 1.674-42.243; p = 0.010) of having OSAS when compared with controls. CONCLUSIONS: According to our findings, an accurate investigation of sleep disturbances could be considered for a complete assessment of patients with TGA. The subtle cerebral anatomo-functional damage induced by the repeated nocturnal apneic episodes may be a pathophysiologic link between OSAS and TGA.
OBJECTIVE: The etiology of transient global amnesia (TGA) is largely undetermined. The aim of this study was to investigate whether the prevalence of obstructive sleep apnea syndrome (OSAS), a condition associated with subtle changes in brain structures involved in memory processes, increases in subjects who have previously experienced a TGA episode. METHODS: Twenty-nine patients who had had a TGA episode were included. A case-control model was used, matching cases with controls by sex, age, and body mass index category. Diagnosis of OSAS was based on the results of the Berlin Questionnaire, which was later confirmed by means of an all-night polysomnography recording. RESULTS: The prevalence of OSAS among TGA patients was significantly higher with respect to that in controls (44.8% vs 13.8%, p = 0.020, χ2 test). At logistic regression model, subjects with TGA had an odds ratio of 8.409 (95% confidence interval = 1.674-42.243; p = 0.010) of having OSAS when compared with controls. CONCLUSIONS: According to our findings, an accurate investigation of sleep disturbances could be considered for a complete assessment of patients with TGA. The subtle cerebral anatomo-functional damage induced by the repeated nocturnal apneic episodes may be a pathophysiologic link between OSAS and TGA.