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Impaired visual function in glaucoma.

V Parisi1

  • 1Cattedra di Clinica Oculistica, Universita' di Roma 'Tor Vergata', Via Santa Maria Goretti 66, 00199, Rome, Italy. vparisi@tin.it

Clinical Neurophysiology : Official Journal of the International Federation of Clinical Neurophysiology
|February 13, 2001
PubMed
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Glaucoma visual field defects stem from both retinal impairment and delayed neural conduction in postretinal pathways. This study reveals both pattern electroretinogram (PERG) and visual evoked potential (VEP) abnormalities in open-angle glaucoma patients.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Visual Electrophysiology

Background:

  • Glaucomatous visual field defects are a primary cause of irreversible blindness.
  • The underlying mechanisms, whether retinal or postretinal, require further elucidation.

Purpose of the Study:

  • To investigate the origins of glaucomatous visual field defects.
  • To differentiate between retinal dysfunction and delayed neural conduction in the postretinal visual pathways.

Main Methods:

  • Assessed visual field using Humphrey perimeter (central 24-2 threshold test).
  • Simultaneously recorded visual evoked potential (VEP) and pattern electroretinogram (PERG).
  • Evaluated 21 patients with open-angle glaucoma (POAG) and 15 age-matched controls.

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Main Results:

  • POAG eyes showed significantly delayed P100 latency and reduced amplitudes in VEP, correlating with global visual field damage (MD).
  • POAG eyes exhibited significantly delayed P50 latency and reduced amplitudes in PERG, also correlating with MD.
  • Retinocortical time (RCT) and latency window (LW) were significantly prolonged in POAG eyes, indicating postretinal pathway delays.

Conclusions:

  • Open-angle glaucoma's global visual field damage results from both retinal impairment (PERG abnormalities) and postretinal pathway delays (RCT and LW).
  • Postsynaptic degeneration in the lateral geniculate nucleus is a potential contributor to the postretinal impairment.