
Contributions
Abstract: P565
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Neurophysiology
Background and objectives: Central nervous system (CNS) demyelinating diseases are common secondary causes of central origin of autonomic dysfunction. Autonomic dysfunction (AD) in MS is explained by lesions in regions responsible for autonomic regulation such as nuclei in the periventricular region of fourth ventricle in the brainstem as well as medullar lesions. However, there is little known for autonomic dysfunctions in patients with neuromyelitis optica (NMO). In this study, we report the profile of autonomic dysfunction in patients with NMO spectrum disorder (NMOSD).
Methods: We prospectively performed autonomic function test (AFT) in NMOSD patients; sympathetic skin response (SSR), quantitative sudomotor axon reflex test (QSART) and cardiovascular tests which include heart rate response to deep breathing (HRdb), blood pressure and heart rate responses to Valsalva maneuver and head-up tilt. Demographic and radiological findings were reviewed.
Results: A total of 14 patients (mean age, 47.5 ±16.3 years; F:M=11:3) were enrolled in this study and mean EDSS score was 3.3 ± 2.3. The duration from onset to AFT was 51±43.4 months and the number of attacks was 3.43 ± 2.5. Among them, 78.6% of enrolled patients-11 patients-had abnormal AFT results. The cardiovagal dysfunction was most commonly observed (7/11 patients, 63.6%), and
4 patients had abnormal results in SSR, 3 in QSART, 4 in adrenergic function. The patients with autonomic dysfunction showed severe neurologic deficit (EDSS score of 3.6 ± 2.5 vs. 2.0 ± 1.0,
p = 0.296), and there was a significant negative correlation between number of attacks and Valsalva ratio (r = -0.586, p = 0.028). The patients with myelitis attacks had frequent autonomic dysfunction (8/9 patients, 88.9%), and the cardiovagal abnormalities were associated with myelitis attacks (p = 0.021). There was a tendency of an association between the length of spinal cord lesions and the presence of cardiovagal dysfunction (5.7 vs 2.5 vertebral segments, p = 0.333). Brainstem attacks were associated with cardiovagal abnormalities (p = 0.029).
Conclusion: Our study suggests that autonomic dysfunction is common in patients with NMOSD. The preferential locations of brain and spinal cord lesions could affect the profile of autonomic dysfunction in NMOSD. Further large cohort studies are needed to evaluate the pathophysiological mechanism of autonomic dysfunction in patients with NMOSD.
Disclosure:
Ye Sel Kim : nothing to disclosure
Jin Myoung Seok: nothing to disclosure
Misong Choi: nothing to disclosure
Eun Bin Cho: nothing to disclosure
Hye Lim Lee: nothing to disclosure
Sa-Yoon Kang: nothing to disclosure
Kwang Ho Lee: nothing to disclosure
Byoung Joon Kim: nothing to disclosure
Ju-Hong Min: nothing to disclosure
Abstract: P565
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Neurophysiology
Background and objectives: Central nervous system (CNS) demyelinating diseases are common secondary causes of central origin of autonomic dysfunction. Autonomic dysfunction (AD) in MS is explained by lesions in regions responsible for autonomic regulation such as nuclei in the periventricular region of fourth ventricle in the brainstem as well as medullar lesions. However, there is little known for autonomic dysfunctions in patients with neuromyelitis optica (NMO). In this study, we report the profile of autonomic dysfunction in patients with NMO spectrum disorder (NMOSD).
Methods: We prospectively performed autonomic function test (AFT) in NMOSD patients; sympathetic skin response (SSR), quantitative sudomotor axon reflex test (QSART) and cardiovascular tests which include heart rate response to deep breathing (HRdb), blood pressure and heart rate responses to Valsalva maneuver and head-up tilt. Demographic and radiological findings were reviewed.
Results: A total of 14 patients (mean age, 47.5 ±16.3 years; F:M=11:3) were enrolled in this study and mean EDSS score was 3.3 ± 2.3. The duration from onset to AFT was 51±43.4 months and the number of attacks was 3.43 ± 2.5. Among them, 78.6% of enrolled patients-11 patients-had abnormal AFT results. The cardiovagal dysfunction was most commonly observed (7/11 patients, 63.6%), and
4 patients had abnormal results in SSR, 3 in QSART, 4 in adrenergic function. The patients with autonomic dysfunction showed severe neurologic deficit (EDSS score of 3.6 ± 2.5 vs. 2.0 ± 1.0,
p = 0.296), and there was a significant negative correlation between number of attacks and Valsalva ratio (r = -0.586, p = 0.028). The patients with myelitis attacks had frequent autonomic dysfunction (8/9 patients, 88.9%), and the cardiovagal abnormalities were associated with myelitis attacks (p = 0.021). There was a tendency of an association between the length of spinal cord lesions and the presence of cardiovagal dysfunction (5.7 vs 2.5 vertebral segments, p = 0.333). Brainstem attacks were associated with cardiovagal abnormalities (p = 0.029).
Conclusion: Our study suggests that autonomic dysfunction is common in patients with NMOSD. The preferential locations of brain and spinal cord lesions could affect the profile of autonomic dysfunction in NMOSD. Further large cohort studies are needed to evaluate the pathophysiological mechanism of autonomic dysfunction in patients with NMOSD.
Disclosure:
Ye Sel Kim : nothing to disclosure
Jin Myoung Seok: nothing to disclosure
Misong Choi: nothing to disclosure
Eun Bin Cho: nothing to disclosure
Hye Lim Lee: nothing to disclosure
Sa-Yoon Kang: nothing to disclosure
Kwang Ho Lee: nothing to disclosure
Byoung Joon Kim: nothing to disclosure
Ju-Hong Min: nothing to disclosure