Visual Evoked Potentials in Pre-Senile Dementia

Pattern Visual Evoked Potential Mapping in Alzheimers Disease Correlations with Visuospatial Impairment

“…Psychometric tests revealed alterations of visuospatial abilities in 40% of our cases, although none of them pre sented abnormalities of primary visual functions or signif icant reduction of visual acuity. A similar frequency was reported by Mendez et al [1], An open question is whether or not there is an involve ment of optic pathways and/or primary visual cortex in the pathophysiology of visual dysfunction in AD patients [7,[12][13][14]22].…”

“…The increase of mean latencies of later pattern VEP components observed in our AD patients suggests that visual function impairment could be mainly ascribed to selective dysfunction o f specific cortico-cortical con nections between the striate cortex and the numerous interrelated visual associative structures. Previous neuro physiological studies have already demonstrated a se lective delay of P2 Hash VEP [13][14][15][16][17] or of later pattern VEP components [24,26], while PI flash VF.P [25] and P I 00 pattern VEP [15, 16, 25. 26] remained relatively unchanged.…”

“…26] remained relatively unchanged. Some authors considered these findings as typical of the dementia process and proposed using the P2-P100 latency difference as a specific indicator of dementia [14][15][16], since both N70 and P I 00 PVEP and flash PI components are believed to be generated within the primary visual cortex [15. 27] while the later VEP components reflect the integrity of visual cortical-subcor tical networks [25].…”

“…An involvement of the anterior optic pathway has also been suggested by the reduction of the amplitude of the pattern ERG [11,12], On the other hand, a pathology of the visual associative areas is indicated by the significant delay of the latency of the P2 flash visual evoked potential (VEP) component [13][14][15][16][17], Topographic mapping can be used to study the distri bution on the scalp of evoked activities. Since modifica tions of the generators of evoked activity will result in changes of the distribution of VEP components on the whole scalp, the VEP mapping technique should be more sensitive and therefore more suitable than conventional VEP recording from only posterior scalp derivations for detecting abnormalities of visual processing.…”

Parkinson’s Dementia and Alzheimer’s Dementia: An Evoked Potential Comparison

“…A differential ERP N1 component delay in PD dementia is a conten tious finding, however. In follow-up studies attempting to replicate this finding, an N1 delay in demented PD patient groups com pared with AD groups has not been emergent [11][12][13], A differential flash visual evoked potential (VEP) P2 component latency delay may be a feature of AD, not present in patients with depression or non-demented individuals with cortical atrophy [14], This effect, coupled with an intact pattern-reversal VEP P I00 component latency has been noted in studies comparing elderly AD patients with controls [15,16]. The latency difference between the flash-VEP P2 and the pattern-reversal VEP P I00 is thus consistently increased in AD in these studies, this effect being considered to reflect pathological involvement of the parastriate visual association cortex, with relative sparing of the primary visual (striate) cortex in AD; positron emission tomographic studies [17] and autopsy [18] pathological analysis in AD support this view.…”