Contributions
Abstract: EP1455
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Background: Global cerebral hypoperfusion is increasingly reported as a vascular aspect in patients with multiple sclerosis (MS). This hemodynamic impairment seems not to be secondary to axonal degeneration, as it can be documented at early stages of the disease. Typically, it is detected in the normal-appearing white matter (NAWM), and it might be caused by a widespread astrocyte dysfunction. Recently, an impaired cerebrovascular reactivity (CVR) could be documented in MS-patients by means of hypercapnic perfusion magnetic resonance imaging (MRI).
The aim of our study was to further investigate supposed hemodynamic impairment in MS-patients using functional sonographic methods.
Methods: Cerebrovascular reactivity was assessed by bilateral transcranial Doppler monitoring of the middle cerebral arteries (MCA). Mean flow velocities of both MCA were recorded before and after 30 seconds of breath holding. Breath-Holding-Index (BHI) was calculated according established formula, so that vasomotor response could be quantified for further comparative analysis.
Results: A total of 46 MS-patients from University Hospitals in Germany and Greece were included in this study (age = 41.0 ± 13.6 yrs; female = 67%; EDSS-score = 2.9 ± 2.3; disease duration = 10.3±9.3yrs). Initial mean flow velocities were 57 ± 17 cm/sec and increased after 30 sec of breathholding to 69 ± 21 cm/sec. In the group of the 31 healthy controls (age = 34.5 ± 11.2 yrs; female = 71%), initial mean flow velocities were 64 ± 17 cm/sec with an increase to 79 ± 17 cm/sec.
Thus, MS patients showed a significantly lower BHI compared to healthy controls (MS-patients= 0.69 ± 0.43; healthy controls = 0.93 ± 0.55; p=0.03) documenting a lower cerebrovascular response to hypercapnia.
There was no difference between the 27 RRMS-patients (BHI= 0.70 ± 0.43) and the 19 patients with progressive forms of the disease (BHI= 0.68 ± 0.44).
Conclusions: These preliminary sonographic results seem to confirm the previously provided evidence of an impaired CVR in patients with multiple sclerosis by MRI. However, further studies including analysis of MS-subgroups and comparison with age-matched controls are needed, in order to clarify a possible hemodynamic impairment in MS-patients. Moreover, the underlying pathophysiological mechanisms as well as the clinical impact of this observation remain speculative.
Disclosure: CK received Honora for oral presentations or travel grants for scientific meetings from Bayer Vital, Bristol-Meyer Squidd, and Boehringer Ingelheim, none related to this manuscript.
RG has received consultation fees and speaker"s honoraria from BayerSchering, BiogenIdec, MerckSerono, Novartis, Sanofi-Aventis and TEVA. He also acknowledges grant support from BayerSchering, BiogenIdec, MerckSerono, Sanofi-Aventis and TEVA, none related to this manuscript.
KV, IC, IK, CS, CL, JB, TK, and GT: nothing to disclose
Abstract: EP1455
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Background: Global cerebral hypoperfusion is increasingly reported as a vascular aspect in patients with multiple sclerosis (MS). This hemodynamic impairment seems not to be secondary to axonal degeneration, as it can be documented at early stages of the disease. Typically, it is detected in the normal-appearing white matter (NAWM), and it might be caused by a widespread astrocyte dysfunction. Recently, an impaired cerebrovascular reactivity (CVR) could be documented in MS-patients by means of hypercapnic perfusion magnetic resonance imaging (MRI).
The aim of our study was to further investigate supposed hemodynamic impairment in MS-patients using functional sonographic methods.
Methods: Cerebrovascular reactivity was assessed by bilateral transcranial Doppler monitoring of the middle cerebral arteries (MCA). Mean flow velocities of both MCA were recorded before and after 30 seconds of breath holding. Breath-Holding-Index (BHI) was calculated according established formula, so that vasomotor response could be quantified for further comparative analysis.
Results: A total of 46 MS-patients from University Hospitals in Germany and Greece were included in this study (age = 41.0 ± 13.6 yrs; female = 67%; EDSS-score = 2.9 ± 2.3; disease duration = 10.3±9.3yrs). Initial mean flow velocities were 57 ± 17 cm/sec and increased after 30 sec of breathholding to 69 ± 21 cm/sec. In the group of the 31 healthy controls (age = 34.5 ± 11.2 yrs; female = 71%), initial mean flow velocities were 64 ± 17 cm/sec with an increase to 79 ± 17 cm/sec.
Thus, MS patients showed a significantly lower BHI compared to healthy controls (MS-patients= 0.69 ± 0.43; healthy controls = 0.93 ± 0.55; p=0.03) documenting a lower cerebrovascular response to hypercapnia.
There was no difference between the 27 RRMS-patients (BHI= 0.70 ± 0.43) and the 19 patients with progressive forms of the disease (BHI= 0.68 ± 0.44).
Conclusions: These preliminary sonographic results seem to confirm the previously provided evidence of an impaired CVR in patients with multiple sclerosis by MRI. However, further studies including analysis of MS-subgroups and comparison with age-matched controls are needed, in order to clarify a possible hemodynamic impairment in MS-patients. Moreover, the underlying pathophysiological mechanisms as well as the clinical impact of this observation remain speculative.
Disclosure: CK received Honora for oral presentations or travel grants for scientific meetings from Bayer Vital, Bristol-Meyer Squidd, and Boehringer Ingelheim, none related to this manuscript.
RG has received consultation fees and speaker"s honoraria from BayerSchering, BiogenIdec, MerckSerono, Novartis, Sanofi-Aventis and TEVA. He also acknowledges grant support from BayerSchering, BiogenIdec, MerckSerono, Sanofi-Aventis and TEVA, none related to this manuscript.
KV, IC, IK, CS, CL, JB, TK, and GT: nothing to disclose