Midlatency auditory evoked responses: P1 abnormalities in adult autistic subjects
| Autor: | R. Erwin, Donald Guthrie, J. Schwafel, Peter E. Tanguay, Jennifer S. Buchwald, D. Van Lancker |
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| Rok vydání: | 1992 |
| Předmět: |
Adult
Male Adolescent medicine.diagnostic_test General Neuroscience Repeated measures design Electroencephalography Stimulation Stimulus (physiology) medicine.disease Electrophysiology Acoustic Stimulation Evoked Potentials Auditory Reaction Time medicine Humans Autism Neurology (clinical) Autistic Disorder Abnormality Psychology Neuroscience Reticular activating system |
| Zdroj: | Electroencephalography and Clinical Neurophysiology/Evoked Potentials Section. 84:164-171 |
| ISSN: | 0168-5597 |
| DOI: | 10.1016/0168-5597(92)90021-3 |
| Popis: | MLR recordings from a group of 11 high-functioning adult autistic subjects were compared with those from a control group of 11 normal subjects. Components selected for analysis were "Pa", the maximum positivity in the 25-40 msec latency range following stimulus onset, "P1", the maximum positivity within the 50-65 msec latency range, and "Nb," the maximum negative deflection in the 40-50 msec latency range. Statistical analyses of amplitude and latency data were conducted using repeated measures analysis of variance and t test group comparisons. The Pa component showed no significant difference between autistic and control groups. However, 2 types of abnormality were noted in the P1 component: (1) the P1 component was significantly smaller in the autistic subjects at slow rates of stimulation, and (2) the autistic P1 did not change as rates of click stimulation increased from 0.5 to 10/sec, in contrast to the normally produced P1 decrement. Data from the P1 model in the cat, and complementary data from the human, closely link the generator substrate of the P1 potential to cholinergic components of the ascending reticular activating system (RAS) and their thalamic target cells. This is the first report of abnormal P1 responses in autism and strongly suggests that the RAS and/or its post-synaptic thalamic targets may be dysfunctional in this syndrome. |
| Databáze: | OpenAIRE |
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