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Brain, Vol. 110, No. 1, 107-120, 1987
© 1987 Oxford University Press

research-article

PATHOLOGY OF THE OPTIC NERVE AND VISUAL ASSOCIATION AREAS

INFORMATION GIVEN BY THE FLASH AND PATTERN VISUAL EVOKED POTENTIAL, AND THE TEMPORAL AND SPATIAL CONTRAST SENSITIVITY FUNCTION

CHRISTINE E. WRIGHT, NEVILLE DRASDO and GRAHAM F. A. HARDING

From the Clinical Neurophysiology Unit, Department of Vision Sciences, Aston University Birmingham, UK

Correspondence to: Correspondence to: Dr C. E. Wright, Clinical Neurophysiology Unit, Department of Vision Sciences, Aston University, Aston Triangle, Birmingham B4 7ET, UK.

Spatial and temporal contrast sensitivity functions (CSF) were compared with visual evoked potentials (VEP) in two groups of patients with pathology selectively affecting different parts of the visual pathway. These consisted of 10 patients with a selective delay of the pattern VEP due to demyelination of one optic nerve (unilateral optic neuritis) and 11 patients with a selective delay of the flash VEP due to pathology of the visual association areas (primary presenile dementia, or Alzheimer's disease). The results led to the following conclusions.

1. Comparison of the VEP and CSF results indicated that VEP latency was more closely associated with the temporal CSF than the spatial CSF. Pathology of the visual association areas which selectively increased the latency of the flash P2 component also reduced sensitivity at low and medium temporal frequencies. In demyelination of the optic nerve, a highly significant correlation was found between the delay of the pattern reversal VEP and sensitivity at high temporal frequencies.

2. Comparison of the results in these two types of pathology suggests that the pattern VEP and flash P1 component, the spatial CSF, and temporal CSF at high temporal frequencies are all processed in the geniculostriate pathway.

3. The flash P2 component and temporal CSF at low and medium frequencies were affected differently from the other measures. The possibility that these processes are transmitted by nongeniculate pathways is discussed.

Received October 18, 1985. Revised February 28, 1986. Accepted April 8, 1986.


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