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.

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“…Flash VEP is now well established in the diagnosis of multiple sclerosis 76 and epilepsy 29 . VEPs measure the electrophysiological responses of the anterior visual pathway to flash and checkerboard visual stimuli.…”

Visual acuity evaluated by pattern-reversal visual-evoked potential is affected by check size/visual angle

“…Since the first use of the white-black chessboard reversal pattern and the grating pattern to study vision and the revealing of tight correlations between components of the VEP and visual acuity [1,2] , researchers have attempted to apply the technique to clinical evaluation and ophthalmological assessment [3][4][5] . Because of the method-ological advantages of VEPs (simple waveform, repeatability, and small inter-individual variation), increasing attention has been paid to the study of diseases involving visual problems, such as in the field of oculopathy (amblyopia [6,7] , refractive errors, field defects, diseases of the optic nerve, glaucoma [8] and color blindness), in diseases with latent impairment of vision (multiple sclerosis [9] , diabetes [10] ), and in psychological dysfunctions (schizophrenia, dementia, epilepsy) [11][12][13][14] . So far only some changes in the early components (especially the P100) have been associated with certain diseases.…”

Altered visual contrast gain control is sensitive for idiopathic generalized epilepsies

“…Using the same paradigm, Sundqvist et al (1999) also found no effect on the VEP in 16 juvenile myoclonic epilepsy patients treated with VPA monotherapy at 1000mg and 2000mg/day for 6 months each. Using an on-off SSVEP paradigm, Geller et al (2005) found no effect of VPA on the second harmonic amplitude in generalized epilepsy compared to healthy controls. In contrast to the above, amplitude of the flash VEP in photosensitive epilepsy patients decreased following treatment with VPA (Herrick and Harding, 1980).…”

“…In a group of patients with unspecified epilepsies on monotherapy with carbamazepine, levetiracetam, or VPA, no significant change was observed in P100 amplitude compared to healthy controls not taking medications (Tumay et al, 2013). Carbamazepine had no effect on SSVEP amplitude compared to healthy controls not taking any medication (Geller et al, 2005). In a group of 30 focal and generalized epilepsy patients, monotherapy using phenytoin, carbamazepine, or phenobarbital did not change the latency or amplitude of P100, but polypharmacy decreased the amplitude and increased latency (Drake et al, 1989).…”