Abstract
The P3 component of both auditory-event- and visual-event-related potentials of 13 patients with Huntington's disease was studied and compared with the P3 component of normal patients. The latencies of the patients' P3 components were compared with the latency-age regression lines generated by the normal population in both modalities. A P3 latency was considered abnormal if it fell above the 2-SE limit for the latency-age regression line. The incidence of normal or abnormal P3 latencies in the two modalities was compared with the results of computed tomography, electroencephalography, and neuropsychological testing. Nine patients had abnormal P3 latencies and ten patients had abnormal visual P3 latencies, with seven having abnormal latencies on both tests and 12 having abnormal latencies on one of the two tests. An abnormal P3 latency in one modality did not imply an abnormal P3 latency in the other. An abnormality of the P3 latency did not correlate with an abnormality in results from computed tomography, electroencephalography, or neuropsychological testing.
Highlights
In the auditory modality, a sequence of tonal signals was presented; the target tone had a fundamental frequency of 2,220
Hz. and the nontarget tone had a fundamental frequency of 440 Hz
The function and chorea.' Disturbances of fortable" yet still sufficient for the patient latencies of the patients' P3 components were compared with the latency-age regression lines generated by t he normal p op ulation in both modalities
Summary
The patients performed well on both the auditory and visual tasks. The mean auditory reaction time was 414 ms (SD, 129 ms), with a range of 207 to 644 ms. This study demonstrates a high incidence of abnormal P3 latencies of event-related potentials to auditory and visual stimuli in patients with Huntington's chorea. We examined the possibility that performing two separate tests (ie, visual and auditory) effectively lowered the confidence limits of the one-tailed comparison from 97.5% to 95%, increasing the number of patients, who were classified as abnormal. A prolongation of P3 latency in patients with dementias of various causes has been described.[5] the mean P3 latency of patients with Parkinson's disease has been shown to be longer than the mean latency of age matched control subjects.' There is evidence that the P3 latency can be "normal" in a significant proportion of patients with dementia.' In our study, the probability of detecting an abnormal P3 latency was enhanced by testing two different sensory modalities.
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