Neurophysiologie clinique = Clinical neurophysiology · 2025
Evaluation of cortical excitability with transcranial magnetic stimulation in patients with obstructive sleep apnea syndrome.
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Çaman Tuğçe Akçadağ, Özdemir İnan, Çaman Mahmut Bilal, Aksu Serkan, Bek Semai, Kutlu Gülnihal
Аннотация
OBJECTIVES: Cognitive impairment constitutes one of the most prevalent sequelae associated with obstructive sleep apnea (OSA). Given the established correlation between chronic hypoxia in patients with OSA and the deterioration of cortical functions, this study hypothesize that levels of cortical excitability diminish in direct relation to the severity of hypoxic episodes.
METHODS: A cohort of 102 individuals diagnosed with OSA participated. Patients exhibiting a T90 value of ≥30 % were categorized into the desaturated cohort, whereas those with a T90 value of <30 % were designated as the non-desaturated cohort. To evaluate alterations in cortical excitability, Transcranial Magnetic Stimulation (TMS) was employed to quantify various parameters including resting muscle motor evoked potential (MEP) latency and amplitude, resting motor threshold, active muscle MEP latency andamplitude, and active motor threshold in both the dominant and non-dominant abductor pollicis brevis (APB) muscles.
RESULTS: The findings indicated that resting dominant APB muscle MEP latency (t=-2.659; p = 0.009), active dominant APB muscle MEP latency (Z=-2.322; p = 0.020), resting non-dominant APB muscle MEP latency (Z=-2.666; p = 0.008), and active motor threshold for dominant APB (Z=-2.410; p = 0.016) were significantly elevated in the desaturated cohort compared to the non-desaturated cohort.
CONCLUSION: This study showed that chronic hypoxia in patients with OSA is associated with modifications in cortical excitability as assessed through TMS. A marked decrease in cortical excitability was identified in the desaturated cohort. It is hypothesized that a disturbance in gamma-aminobutyric acid (GABA) and glutamate transmission could be crucial to understanding OSA and cortical excitability.
METHODS: A cohort of 102 individuals diagnosed with OSA participated. Patients exhibiting a T90 value of ≥30 % were categorized into the desaturated cohort, whereas those with a T90 value of <30 % were designated as the non-desaturated cohort. To evaluate alterations in cortical excitability, Transcranial Magnetic Stimulation (TMS) was employed to quantify various parameters including resting muscle motor evoked potential (MEP) latency and amplitude, resting motor threshold, active muscle MEP latency andamplitude, and active motor threshold in both the dominant and non-dominant abductor pollicis brevis (APB) muscles.
RESULTS: The findings indicated that resting dominant APB muscle MEP latency (t=-2.659; p = 0.009), active dominant APB muscle MEP latency (Z=-2.322; p = 0.020), resting non-dominant APB muscle MEP latency (Z=-2.666; p = 0.008), and active motor threshold for dominant APB (Z=-2.410; p = 0.016) were significantly elevated in the desaturated cohort compared to the non-desaturated cohort.
CONCLUSION: This study showed that chronic hypoxia in patients with OSA is associated with modifications in cortical excitability as assessed through TMS. A marked decrease in cortical excitability was identified in the desaturated cohort. It is hypothesized that a disturbance in gamma-aminobutyric acid (GABA) and glutamate transmission could be crucial to understanding OSA and cortical excitability.