Evaluation of optic nerve functions in subacute combined degeneration using visual evoked potential and diffusion tensor imaging-a pilot study.

OBJECTIVE

: To evaluate optic nerve involvement in subacute combined degeneration (SACD) using diffusion tensor imaging (DTI) and visual evoked potential (VEP) studies, and their changes following cobalamine treatment.

METHODS

: Six patients with SACD and six healthy matched controls were included. Visual acuity, field of vision, and color vision were tested. Pattern shift VEP was done, and P100 latency and amplitude were measured. Optic nerve MRI, and DTI of optic nerve to muscle ratio were measured, and fractional anisotropy ratio (FAR), axial diffusivity ratio (ADR), radial diffusivity ratio (RDR), and mean diffusivity ratio (MDR) were calculated. The patients received hydroxyl cobalamine 1000 µg intramuscularly and their clinical examination, VEP and DTI studies were repeated at 3 months.

RESULTS

: The age of the patients ranged between 16 and 60 years and two were females. Their visual acuity, field of vision, and color vision were normal. P100 latency was prolonged in five patients (10 eyes) and amplitude was reduced in one (1 eye). The SACD patients had reduced FAR (1.94 ± 0.55 vs 2.81 ± 0.42; p = 0.01) and increased MDR (1.00 ± 0.04 vs 0.95 ± 0.01; p = 0.01) and RDR (0.96 ± 0.03 vs 0.89 ± 0.01; p = 0.002) compared to the controls. The FAR value correlated with P100 latency (r = -0.88). At 3 months, FAR value increased which was associated with improvement in P100 latency.

CONCLUSION

: In SACD patients, optic nerve FAR is reduced and correlates with P100 latency. Both these parameters improve on cobalamine treatment.

ADVANCES IN KNOWLEDGE

: Subclinical VEP abnormalities are common in SACD but conventional MRI sequence of optic nerve is normal. DTI of optic nerve reveals reduced fractional anisotropy (FA) values which improve after cobalamine treatment. FA values correlate with prolongation of P100 latency. DTI and VEP abnormalities suggest subclinical optic nerve myelin dysfunction.