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1.
Clin Neurophysiol ; 126(8): 1617-23, 2015 Aug.
Article in English | MEDLINE | ID: mdl-25481337

ABSTRACT

OBJECTIVE: To evaluate multifocal visual evoked potentials (mfVEP) changes in optic neuritis (ON) and fellow eyes during first year after the attack. METHODS: Eighty-seven patients and twenty-five controls were examined. Patients were classified as multiple sclerosis (MS) group, high risk (HR) or low risk (LR) groups for conversion to MS. mfVEP recordings and retinal nerve fiber layer (RNFL) thickness were analyzed. RESULTS: Recovery of amplitude and shortening of latency was fastest within the first 3months. The largest amplitude reduction and longest latency delay of the ON eye were recorded in the MS group. This was accompanied by deterioration of both parameters in fellow eyes (p<0.03). mfVEP remained stable in fellow eyes of the LR group. Inter-eye asymmetry showed similar amount of amplitude reduction and latency delay in all three groups. RNFL thickness strongly correlated with mfVEP amplitude as early as 3 months after ON (R(2)=0.6, p=0.001). CONCLUSION: mfVEP amplitude is an early predictor of post-ON axonal loss. The apparent more severe involvement of ON eyes in the MS subgroup may be due to subclinical inflammation along the visual pathway. SIGNIFICANCE: Severity of amplitude reduction and latency delay after episode of ON is not MS-related. Retro-chiasmal demyelination is a possible factor contributing to amplitude and latency differences between MS and non-MS patients.


Subject(s)
Evoked Potentials, Visual/physiology , Optic Neuritis/diagnosis , Visual Pathways/physiopathology , Visual Perception/physiology , Adult , Axons/physiology , Demyelinating Diseases/physiopathology , Disease Progression , Female , Humans , Male , Middle Aged , Optic Neuritis/physiopathology , Young Adult
2.
Mult Scler ; 18(4): 425-32, 2012 Apr.
Article in English | MEDLINE | ID: mdl-21965421

ABSTRACT

BACKGROUND: Gray matter atrophy has been implicated in the development of secondary progressive multiple sclerosis (SPMS). Cortical function may be assessed by transcranial magnetic stimulation (TMS). Determining whether cortical dysfunction was a feature of SPMS could be of pathophysiological significance. OBJECTIVES: Consequently, novel paired-pulse threshold tracking TMS techniques were used to assess whether cortical dysfunction was a feature of SPMS. METHODS: Cortical excitability studies were undertaken in 15 SPMS, 25 relapsing-remitting MS patients (RRMS) and 66 controls. RESULTS: Short interval intracortical inhibition (SPMS 3.0 ± 2.1%; RRMS 12.8 ± 1.7%, p < 0.01; controls 10.5 ± 0.7%, p < 0.01) and motor evoked potential (MEP) amplitude (SPMS 11.5 ± 2.2%; RRMS 26.3 ± 3.6%, p <0.05; controls 24.7 ± 1.8%, p < 0.01) were reduced in SPMS, while intracortical facilitation (SPMS -5.2 ± 1.9%; RRMS -2.0 ± 1.4, p < 0.05; controls -0.9 ± 0.7, p < 0.01) and resting motor threshold were increased (SPMS 67.5 ± 4.5%; RRMS 56.0 ± 1.5%, p < 0.01; controls 59.0 ± 1.1%, p < 0.001). Further, central motor conduction time was prolonged in SPMS (9.1 ± 1.2 ms, p < 0.001) and RRMS (7.0 ± 0.9 ms, p < 0.05) patients compared with controls (5.5 ± 0.2 ms). The observed changes in cortical function correlated with the Expanded Disability Status Scale. CONCLUSION: Together, these findings suggest that cortical dysfunction is associated with disability in MS, and documentation of such cortical dysfunction may serve to quantify disease severity in MS.


Subject(s)
Evoked Potentials, Motor , Motor Cortex/pathology , Multiple Sclerosis, Chronic Progressive/pathology , Multiple Sclerosis, Relapsing-Remitting/pathology , Adult , Aged , Atrophy/physiopathology , Female , Humans , Male , Middle Aged , Motor Cortex/physiopathology , Multiple Sclerosis, Chronic Progressive/physiopathology , Multiple Sclerosis, Relapsing-Remitting/physiopathology , Neural Conduction , Neural Inhibition/physiology , Transcranial Magnetic Stimulation
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