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Updated: Feb 8, 2026

06:49
Visual Evoked Potential Recording in a Rat Model of Experimental Optic Nerve Demyelination
Published on: July 29, 2015
12.8K
Evaluation of optic nerve functions in subacute combined degeneration using visual evoked potential and diffusion
Jayantee Kalita1, Neetu Soni2, Deepanshu Dubey1
11 Department of Neurology, Sanjay Gandhi Post Graduate medical Sciences , Lucknow , India.
The British Journal of Radiology
|July 11, 2018
Summary
Subacute combined degeneration (SACD) can cause subclinical optic nerve dysfunction, indicated by abnormal diffusion tensor imaging (DTI) and visual evoked potential (VEP) findings. Cobalamin treatment improves these DTI and VEP markers, suggesting myelin repair.
Area of Science:
- Neuroscience
- Ophthalmology
- Radiology
Background:
- Subacute combined degeneration (SACD) is a neurological disorder often associated with vitamin B12 deficiency.
- Optic nerve involvement in SACD can be subtle and may not be detected by conventional imaging.
- Diffusion tensor imaging (DTI) and visual evoked potentials (VEP) offer sensitive methods to assess white matter integrity and function.
Purpose of the Study:
- To evaluate optic nerve involvement in SACD using DTI and VEP.
- To assess the impact of cobalamine treatment on DTI and VEP parameters in SACD patients.
- To correlate DTI findings with VEP abnormalities in the optic nerve.
Main Methods:
- Six SACD patients and six controls underwent visual acuity, visual field, color vision, and pattern shift VEP testing.
- Optic nerve MRI and DTI were performed, calculating fractional anisotropy ratio (FAR), axial diffusivity ratio (ADR), radial diffusivity ratio (RDR), and mean diffusivity ratio (MDR).
- Patients received hydroxyl cobalamine treatment, with repeat VEP and DTI studies at 3 months.
Main Results:
- While visual functions were normal, five SACD patients showed prolonged P100 latency on VEP.
- SACD patients exhibited reduced optic nerve FAR and increased MDR and RDR compared to controls.
- Reduced FAR correlated significantly with prolonged P100 latency (r = -0.88).
Conclusions:
- Optic nerve DTI reveals reduced fractional anisotropy (FA) values in SACD patients, correlating with prolonged P100 latency.
- Cobalamine treatment led to an increase in FAR and improvement in P100 latency, indicating myelin repair.
- DTI and VEP abnormalities suggest subclinical optic nerve myelin dysfunction in SACD, responsive to treatment.
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