Multifocal ERG abnormalities in epileptic patients treated with vigabatrin
Besch D., Kurtenbach A., Jägle H., Zrenner E., Schiefer U.
Abteilung für Pathophysiologie des Sehens und Neuroophthalmologie,
Universitäts-Augenklinik, Schleichstr. 12-16, 72076 Tübingen
Objective: To define functional and electrophysiological abnormalities
in patients under anti-epileptic therapy with vigabatrin.
Methods: 23 patients treated with vigabatrin (age range 25-66 years)
were examined with the VERIS System using a resolution of 61 hexagonal
elements within a 30° visual field. Both multifocal ERG (m-ERG) and
multifocal OPs (m-OPs) were recorded. The results were related to findings
in psychophysical tests (color vision, dark adaptation threshold, visual
fields) and standard electrophysiology.
Results: Average peak amplitudes and implicit times of first order
kernels were determined showing a normal amplitude and implicit time of
the first wave (N1) in all patients. The positive deflection (P1) was
subnormal in all patients with an additional peripheral amplitude reduction
in patients with severe visual field constrictions (4/23) (< 30°).
Furthermore, in those patients there was a diffuse local P1 reduction
revealing a "negative configuration". Photopic multifocal P1/N1
ratio of these local signals showed reduced results (<1,8) compared
to normal responses (range:1,88- 2,32). For the second order kernel, responses
were delayed in patients with moderate to severe visual field defects
(16/23). M-OPs revealed prolonged latencies for both first and second
order kernels in 18/21 patients, all showing visual field loss. Multifocal
ERG findings were also compared to photopic Ganzfeld-ERG results (especially
the b/a ratio) which revealed to be at the lower normal range. In Ganzfeld-ERG
patients with visual field defects revealed altered OP waveforms and in
some patients a delayed cone single flash response (9/23) was found. Visual
acuity, anterior and posterior segments, color vision and dark adaptation
thresholds were normal.
Conclusion: Multifocal components are thought to be mainly generated
by bipolar cells and/or inner nuclear layer activity (Hood 2000). The
data of our vigabatrin patients therefore indicate functional changes
of the inner retinal cell transmission due to alterations of bipolar and/or
amacrine cell activity.
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