Obstructive sleep apnea in multiple sclerosis: the relationship of lesion location, apnea hypopnea index, and brain atrophy
ECTRIMS Online Library. Levit E. 09/11/19; 278780; P419
Elle Levit
Elle Levit
Contributions
Abstract

Abstract: P419

Type: Poster Sessions

Abstract Category: Clinical aspects of MS - MS symptoms

E. Levit1, J. Sloane2

1Neurology, Beth Israel Deaconess Medical Center, Brookline, 2Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, United States

Background: The objectives of this cross-sectional study were to assess the prevalence and severity of obstructive sleep apnea (OSA) in patients with multiple sclerosis (MS) who reported subjective symptoms of fatigue, and to explore physical risk factors and radiographic localization of MS lesions that might herald risk for OSA.
Introduction: Fatigue affects approximately 90% of MS patients during the disease course, and OSA may contribute to fatigue. OSA is an under-recognized complication of MS, with rates as high as 58% in MS patients. Patients with brainstem involvement have higher apnea hypopnea indices (AHI) compared to patients without brainstem involvement, suggesting regional brainstem dysfunction from MS lesions may contribute to OSA severity by undermining airway patency during sleep.
Methods: We performed a cross-sectional study involving MS patients with OSA and without OSA. Lesions were counted in each brainstem region by two reviewers and averaged. Standardized third ventricular width (sTVW) was measured as a surrogate for total brain atrophy. Correlation analyses were applied to variables after controlling for confounding MS-independent OSA risk factors age, BMI, and male gender.
Results: There were significant relationships between AHI and number of lesions in the pons (p=0.003), medulla (p=0.048) and all intratentorial lesions (p=0.013) after controlling for MS-independent OSA risk factors. The relationship between midbrain lesions and AHI did not reach significance (p=0.064). Positive correlation found with sTVW and AHI after controlling for age, BMI, and male gender (p=0.003). There was also an association with increased brain atrophy and increasing expanded disability status scale (EDSS) (p=0.01).
Discussion: We hypothesized that given the importance of brainstem control over upper airway patency, damage to various brainstem regions could result in increased AHI, as we saw in our study after controlling for MS-independent OSA risk factors. Our work suggests that lesion location in MS patients could contribute to development of increased AHI and therefore presumably OSA severity. It is possible that early MS treatment may help prevent or moderate MS comorbidities such as OSA and decrease fatigue. We present additional data to support that that OSA may contribute to brain atrophy seen in MS, which raises the possibility that treatment of OSA could potentially decrease brain atrophy over time.
Disclosure:
Elle Levit: nothing to disclose.
Jacob Sloane: ​Served of advisory boards for Biogen, Genentech, Celgene, EMD Serono, Genzyme. Grant funding from Biogen, Genentech​, EMD Serono, National MS Society.

Abstract: P419

Type: Poster Sessions

Abstract Category: Clinical aspects of MS - MS symptoms

E. Levit1, J. Sloane2

1Neurology, Beth Israel Deaconess Medical Center, Brookline, 2Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, United States

Background: The objectives of this cross-sectional study were to assess the prevalence and severity of obstructive sleep apnea (OSA) in patients with multiple sclerosis (MS) who reported subjective symptoms of fatigue, and to explore physical risk factors and radiographic localization of MS lesions that might herald risk for OSA.
Introduction: Fatigue affects approximately 90% of MS patients during the disease course, and OSA may contribute to fatigue. OSA is an under-recognized complication of MS, with rates as high as 58% in MS patients. Patients with brainstem involvement have higher apnea hypopnea indices (AHI) compared to patients without brainstem involvement, suggesting regional brainstem dysfunction from MS lesions may contribute to OSA severity by undermining airway patency during sleep.
Methods: We performed a cross-sectional study involving MS patients with OSA and without OSA. Lesions were counted in each brainstem region by two reviewers and averaged. Standardized third ventricular width (sTVW) was measured as a surrogate for total brain atrophy. Correlation analyses were applied to variables after controlling for confounding MS-independent OSA risk factors age, BMI, and male gender.
Results: There were significant relationships between AHI and number of lesions in the pons (p=0.003), medulla (p=0.048) and all intratentorial lesions (p=0.013) after controlling for MS-independent OSA risk factors. The relationship between midbrain lesions and AHI did not reach significance (p=0.064). Positive correlation found with sTVW and AHI after controlling for age, BMI, and male gender (p=0.003). There was also an association with increased brain atrophy and increasing expanded disability status scale (EDSS) (p=0.01).
Discussion: We hypothesized that given the importance of brainstem control over upper airway patency, damage to various brainstem regions could result in increased AHI, as we saw in our study after controlling for MS-independent OSA risk factors. Our work suggests that lesion location in MS patients could contribute to development of increased AHI and therefore presumably OSA severity. It is possible that early MS treatment may help prevent or moderate MS comorbidities such as OSA and decrease fatigue. We present additional data to support that that OSA may contribute to brain atrophy seen in MS, which raises the possibility that treatment of OSA could potentially decrease brain atrophy over time.
Disclosure:
Elle Levit: nothing to disclose.
Jacob Sloane: ​Served of advisory boards for Biogen, Genentech, Celgene, EMD Serono, Genzyme. Grant funding from Biogen, Genentech​, EMD Serono, National MS Society.

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