Contributions
Abstract: EP1393
Type: ePoster
Abstract Category: Clinical aspects of MS - 8 Clinical assessment tools
Background: Critical flicker frequency (CFF) has been suggested as a marker for neuro-axonal damage resulting from demyelinating optic neuritis (ON). Neuro-axonal damage of the retina is frequently observed in patients with multiple sclerosis.
Objective: To examine CFF in eyes with and without ON (NON) of MS patients and eyes of healthy controls (HC) and to further investigate possible associations with visual function as well as with the Expanded Disability Status Scale (EDSS).
Methods: A total of 140 eyes from 39 MS patients (28 ON-eyes; 50 NON-eyes) and 31 HC were evaluated. All patients and HC underwent monocular and binocular CFF measurements with the HEPAtonorm™-Analyzer, monocular high contrast visual acuity (HCVA) testing with ETDRS charts (logMAR units), binocular low contrast letter acuity (LCLA) testing with 2.5% contrast Sloan charts, visual evoked potentials (VEP) and spectral domain optical coherence tomography (OCT) with analysis of the peripapillary retinal nerve fibre layer (pRNFL) thickness. Trained neurologists assessed the EDSS for all patients. Monocular measurements were analyzed with generalized estimating equations (GEE), binocular measurements with t-test and Spearman correlation analysis.
Results: Mean monocular CFF for eyes of MS patients amounted to 40.9 ± 4.4 Hz and was significantly lower than in HC (44.8 ± 4.4 Hz, p < 0.001). Worse EDSS was a moderate predictor for reduced CFF
(r2 = 0.261, B = -2.060, p < 0.001). In contrast, there was no significant difference in CFF between ON-eyes (39.7 ± 5.2 Hz) and NON-eyes (41.5 ± 4.3 Hz, p = 0.127). Likewise, there was no association between CFF and pRNFL thickness (B = 0.009, p = 0.750). CFF was mildly associated with VEP P100 latency (r2 = 0.069, B = -0.056, p = 0.043), HCVA (r2 = 0.074, B = -6.021, p = 0.002) and LCLA
(r2 = 0.120, ρ = 0.41, p = 0.010).
Conclusion: CFF reduction in MS occurs independently of ON, and is not dependent on retinal axonal damage. Its moderate correlation with EDSS suggests that CFF potentially reflects global disease processes or higher cortical processing and neurodegeneration rather than focal optic nerve damage.
Disclosure: This study was supported by a research grant from Novartis
Ayadi: nothing to disclose
Zimmermann: received speaking fees from TEVA, unrelated to this work.
Mikolajczak: received personal fees from TEVA, Biogen and Bayer Healthcare, unrelated to this work.
Dörr: received grants, personal fees and non-financial support from Bayer Healthcare and Novartis, personal fees and non-financial support from Biogen, personal fees from Genzyme, Allergan, and Merck-Serono, unrelated to this work.
Brandt: received consulting fees for research from Novartis, Biogen, Motognosis, Teva and Bayer, unrelated to this work.
Paul: received research support from the Deutsche Forschungsgemeinschaft (DFG) (grant Exc. 257) and from the Guthy Jackson Charitable Foundation and National Multiple Sclerosis Society, research grants and speaker honoraria from Bayer, Teva, Genzyme, Merck, Novartis, MedImmune and is member of the steering committee of the OCTIMS study (Novartis), unrelated to this work.
Abstract: EP1393
Type: ePoster
Abstract Category: Clinical aspects of MS - 8 Clinical assessment tools
Background: Critical flicker frequency (CFF) has been suggested as a marker for neuro-axonal damage resulting from demyelinating optic neuritis (ON). Neuro-axonal damage of the retina is frequently observed in patients with multiple sclerosis.
Objective: To examine CFF in eyes with and without ON (NON) of MS patients and eyes of healthy controls (HC) and to further investigate possible associations with visual function as well as with the Expanded Disability Status Scale (EDSS).
Methods: A total of 140 eyes from 39 MS patients (28 ON-eyes; 50 NON-eyes) and 31 HC were evaluated. All patients and HC underwent monocular and binocular CFF measurements with the HEPAtonorm™-Analyzer, monocular high contrast visual acuity (HCVA) testing with ETDRS charts (logMAR units), binocular low contrast letter acuity (LCLA) testing with 2.5% contrast Sloan charts, visual evoked potentials (VEP) and spectral domain optical coherence tomography (OCT) with analysis of the peripapillary retinal nerve fibre layer (pRNFL) thickness. Trained neurologists assessed the EDSS for all patients. Monocular measurements were analyzed with generalized estimating equations (GEE), binocular measurements with t-test and Spearman correlation analysis.
Results: Mean monocular CFF for eyes of MS patients amounted to 40.9 ± 4.4 Hz and was significantly lower than in HC (44.8 ± 4.4 Hz, p < 0.001). Worse EDSS was a moderate predictor for reduced CFF
(r2 = 0.261, B = -2.060, p < 0.001). In contrast, there was no significant difference in CFF between ON-eyes (39.7 ± 5.2 Hz) and NON-eyes (41.5 ± 4.3 Hz, p = 0.127). Likewise, there was no association between CFF and pRNFL thickness (B = 0.009, p = 0.750). CFF was mildly associated with VEP P100 latency (r2 = 0.069, B = -0.056, p = 0.043), HCVA (r2 = 0.074, B = -6.021, p = 0.002) and LCLA
(r2 = 0.120, ρ = 0.41, p = 0.010).
Conclusion: CFF reduction in MS occurs independently of ON, and is not dependent on retinal axonal damage. Its moderate correlation with EDSS suggests that CFF potentially reflects global disease processes or higher cortical processing and neurodegeneration rather than focal optic nerve damage.
Disclosure: This study was supported by a research grant from Novartis
Ayadi: nothing to disclose
Zimmermann: received speaking fees from TEVA, unrelated to this work.
Mikolajczak: received personal fees from TEVA, Biogen and Bayer Healthcare, unrelated to this work.
Dörr: received grants, personal fees and non-financial support from Bayer Healthcare and Novartis, personal fees and non-financial support from Biogen, personal fees from Genzyme, Allergan, and Merck-Serono, unrelated to this work.
Brandt: received consulting fees for research from Novartis, Biogen, Motognosis, Teva and Bayer, unrelated to this work.
Paul: received research support from the Deutsche Forschungsgemeinschaft (DFG) (grant Exc. 257) and from the Guthy Jackson Charitable Foundation and National Multiple Sclerosis Society, research grants and speaker honoraria from Bayer, Teva, Genzyme, Merck, Novartis, MedImmune and is member of the steering committee of the OCTIMS study (Novartis), unrelated to this work.