Visual evoked potentials in multiple sclerosis: P100 latency and visual pathway damage including the lateral...

Area of Science:

• Neuroscience
• Ophthalmology
• Neurology

Background:

• Multiple Sclerosis (MS) is a demyelinating disease affecting the central nervous system.
• Visual pathway damage is common in MS, impacting visual evoked potentials (VEP).
• The P100 component of VEP reflects visual pathway integrity.

Purpose of the Study:

• To investigate the relationship between P100 latency in VEP and both pre- and postchiasmatic damage in MS patients.
• To identify specific anatomical structures associated with P100 latency delays.

Main Methods:

• VEP, optical coherence tomography (OCT), and MRI were performed on 31 MS patients and 31 controls.
• Associations were tested between P100 latency and peripapillary retinal nerve fiber layer (pRNFL), ganglion cell/inner plexiform layers (GCIPL), lateral geniculate nucleus (LGN) volume, optic radiation white matter lesions (OR-WML), non-lesional optic radiation fractional anisotropy (NAOR-FA), and primary visual cortex (V1) thickness.
• Effect sizes were quantified using marginal R-squared (mR²).

Main Results:

• MS patients showed significant differences in P100 latency, pRNFL, GCIPL, and LGN compared to controls.
• P100 latency was strongly associated with GCIPL (mR²=0.26) and moderately with OR-WML (mR²=0.17), NAOR-FA (mR²=0.13), and pRNFL (mR²=0.08).
• Multivariate analysis revealed GCIPL and NAOR-FA as significant predictors of P100 latency (mR²=0.41). In ON patients, LGN volume was significantly associated with P100 latency (mR²=-0.56).

Conclusions:

• P100 latency is influenced by damage in both anterior and posterior parts of the visual pathway in MS.
• In MS patients with prior optic neuritis, damage at the synaptic level in the LGN may contribute to delayed P100 latency.
• These findings support the role of post-chiasmatic structures in VEP signal generation and highlight distinct pathophysiological mechanisms in MS.