title: Epilepsy and medication effects on the pattern visual evoked potential.
abstract: Visual disruption in patients diagnosed with epilepsy may be attributable to either the disease itself or to the anti-epileptic drugs prescribed to control the seizures. Effects on visual function may be due to perturbations of the GABAergic neurotransmitter system, since deficits in GABAergic cortical interneurons have been hypothesized to underlie some forms of epilepsy, some anti-epileptic medications increase cortical GABA levels, and GABAergic neural circuitry plays an important role in mediating the responses of cells in the visual cortex and retina. This paper characterizes the effects of epilepsy and epilepsy medications on the visual evoked response to patterned stimuli. Steady-state visual evoked potentials (VEP) evoked by onset-offset modulation of high-contrast sine-wave stimuli were measured in 24 control and 54 epileptic patients. Comparisons of VEP spectral amplitude as a function of spatial frequency were made between controls, complex partial, and generalized epilepsy groups. The effects of the GABA-active medication valproate were compared to those of carbamezepine. The amplitude of the fundamental (F1) component of the VEP was found to be sensitive to epilepsy type. Test subjects with generalized epilepsy had F1 spatial frequency-amplitude functions with peaks shifted to lower spatial frequencies relative to controls and test subjects with complex partial epilepsy. This shift may be due to reduced intracortical inhibition in the subjects with generalized epilepsy. The second harmonic component (F2) response was sensitive to medication effects. Complex partial epilepsy patients on VPA therapies showed reduced F2 response amplitude across spatial frequencies, consistent with previous findings that showed the F2 response is sensitive to GABA-ergic effects on transient components of the VEP.
authors.affiliation: Neurotoxicology Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA. geller.andrew@epa.gov
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Geller
authors.forename: H Ken
authors.initials: HK
authors.lastname: Hudnell
authors.forename: Bradley V
authors.initials: BV
authors.lastname: Vaughn
authors.forename: John A
authors.initials: JA
authors.lastname: Messenheimer
authors.forename: William K
authors.initials: WK
authors.lastname: Boyes
mesh_terms: D000328:Adult; D000927:Anticonvulsants / Q000627:therapeutic use*; D002220:Carbamazepine / Q000627:therapeutic use*; D004827:Epilepsy / Q000188:drug therapy* / Q000503:physiopathology; D005074:Evoked Potentials, Visual / Q000187:drug effects / Q000502:physiology*; D005260:Female; D005500:Follow-Up Studies; D018682:GABA Agents / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D010775:Photic Stimulation; D012160:Retina / Q000187:drug effects / Q000503:physiopathology; D014635:Valproic Acid / Q000627:therapeutic use*; D014792:Visual Acuity; D014793:Visual Cortex / Q000187:drug effects / Q000503:physiopathology
chemical_list: D000927:Anticonvulsants; D018682:GABA Agents; D002220:Carbamazepine; D014635:Valproic Acid