Visual evoked potentials in early Alzheimer's dementia: an exploratory study.

Topographical maps of visual evoked potentials (VEPs) were recorded from 10 possible Alzheimer's disease (AD) patients and 10 control subjects. The purpose of the study was to determine if the two types of VEPs could function as a diagnostic screening for AD. Results of the statistical analysis did not reveal any latency differences between VEPs for the components elicited by either the pattern shift visual evoked potential (PSVEP)--or flash visual evoked potential (FVEP)--elicited components for AD patients compared with the control subjects; however, the information provided insight into results that are frequently lost with conventional evoked potential data. Statistically significant differences in amplitude were found between the P1 and the N2 of the PSVEP at 124, 126, and 130 ms, and at 116 ms for the FVEP.

Differences in superficial and deep source contributions to middle latency auditory evoked potential Pa component in normal subjects and patients with neurologic disease.

Multichannel brain-mapped middle latency auditory evoked potential (MLAEP) data obtained from 15 normal subjects and three neurologically impaired subjects using the common average reference (CAR) were converted off-line to source current density (SCD). This technique is sensitive to activity generated in the superficial cerebral cortex. The SCD maps were subtracted from the CAR maps (CAR-SD). The derived CAR-SD maps are believed to represent the proportion of scalp-recorded activity that is generated deep to the cerebral cortex. Topographic analysis of this data manipulation technique supports the hypothesis that Pa originated from within the temporal lobes bilaterally as well as from a deeper subcortical system.

The effects of anterior temporal lobectomy (ATL) on the middle-latency auditory evoked potential (MLAEP).

The anatomical and physiological origins of the middle-latency auditory evoked potential (MLAEP) are not well understood. The present investigation was conducted to determine whether the MLAEP derives its origins in part from the anterior temporal lobe. Twelve subjects with intractable seizures were evaluated with the MLAEP pre and post excision of the anterior-mesial temporal lobe (ATL) unilaterally. In our study, component Pa latency was unaffected by the ATL. The Na latency and the Na/Pa amplitude showed significant increases after ATL. The results we interpreted as being consistent with currently held beliefs regarding the origins of Pa. The changes in Na latency and Na/Pa amplitude are hypothesized to reflect a loss of the modulating influence of the cortex on the subcortical generators of Na.

The normal scalp topography of the middle latency auditory evoked potential Pa component following monaural click stimulation.

The scalp topography of the middle latency auditory evoked potential (MLAEP) Pa component following left and right ear click stimulation was investigated in 15 normal hearing and neurologically intact right-handed subjects. An unbiased reference was employed. The Pa component showed a broad voltage field that was recorded maximally at the Cz and Fz leads regardless of which ear was stimulated. A broad negative voltage field that occurred coincident in time with the Pa component was recorded posterior to the T3, P3, Pz, P4 and T4 electrode leads. This negative voltage field peaked in amplitude at the T5, O1, Oz, O2, and T6 electrode leads. An unexpected finding was that the peak latency of the Pa component occurred significantly earlier following stimulation of the right ear.