Influence of dopamine deficiency in early Parkinson's disease on the slow stimulation multifocal-ERG.
OBJECTIVE
In animal studies intravitreal injection of tetrodotoxin (TTX) results in mfERG waveform changes similar to those observed in glaucoma. As TTX blocks amacrine as well as ganglion cells, there is still a question regarding the underlying cell population responsible for these changes in waveform. In an attempt to assess the contribution of the amacrine cells to these changes, a mfERG was obtained from patients with Parkinson's disease as some amacrine cells are mediated by dopamine, a substance lacking in Parkinson's.


METHODS
Eight patients with early Parkinson's disease underwent ophthalmologic examination, testing of contrast sensitivity and electrophysiological examination according to ISCEV standard at least 12 h following their last medication with Dopamine. A slow stimulation mfERG was obtained with a stimulus base interval of 53.3 ms and with a stimulus base interval of 106.6 ms. During MF-ERG recordings 103 hexagons stimulated the central 50 deg of the retina simultaneously and independently (m-sequence 2(13), L(max): 200 cd/m(2), approximately 100% contrast).


RESULTS
Contrast sensitivity and ISCEV standard electrophysiological testing was unremarkable. When the mfERG was analyzed, only four patients had an adequate signal-to-noise ratio to allow further data analysis - one of whom was diagnosed with a multi system atrophy in retrospect. The first order response component was analyzed at a filter setting of 10-300 Hz and at 100-300 Hz (OPs) and compared to mfERGs of a control group. On average, in patients, the amplitude of N1P1 was slightly lower in the central and nasal response averages. When the three OPs at a latency of 72-89 ms were analyzed in the 53.3 ms base interval recording, the most marked difference in amplitude was observed in the superior nasal response average of the first OP. Here a mean amplitude of 1.3 nV/deg(2) in patients compared to a mean amplitude of 1.9 nV/deg(2) in the control group (P: 0.08).


CONCLUSIONS
In contrast to our previous findings in NTG, there was a consistent presence of three OPs. Under the stimulus conditions applied, we did not find an influence of dopaminergic amacrine cells on the mfERG in our patients with moderate stages of Parkinsion's. The difficulties in obtaining an adequate signal-to noise ratio due to e.g. muscle artifacts even in Parkinson patients of moderate disease stages render a success of mfERG recording in patients with more advanced stages unlikely. The question of the influence of dopaminergic amacrine cells on the mfERG could possibly be addressed using MPDT in animal research.
Palmowski-Wolfe
Anja M
AM
Department of Ophthalmology, University of Saarland, D 66421, Homburg, Germany.
Perez
Maria Timoner
MT
Behnke
Stefanie
S
Fuss
Gerhard
G
Martziniak
Martin
M
Ruprecht
Klaus W
KW
D015350:Contrast Sensitivity / Q000502:physiology*; D018450:Disease Progression; D004298:Dopamine / Q000097:blood / Q000172:deficiency*; D004596:Electroretinography; D006801:Humans; D008875:Middle Aged; D010300:Parkinson Disease / Q000097:blood* / Q000503:physiopathology*; D010775:Photic Stimulation / Q000379:methods; D010865:Pilot Projects; D012160:Retina / Q000503:physiopathology*
D004298:Dopamine