Internal brain clock timing mechanisms have been repeatedly identified as central to understanding Parkinson's disease. Yet another article, this time in Neuropsycholgia, by Guehl et al. (2008), implicates auditory temporal processing as a fundamental cognitive deficit.
Of significance is the hypothesis (which is contrary to the most popular hypothesis of a slowing of the internal clock or pacemaker) that deficient auditory temporal processing may be a function of memory or attention. The focus on attention is consistent with research that has speculated that controlled executive attention, which is primarily regulated by the prefrontal cortex, may play a key role in mental time-keeping.
Abstract
Of significance is the hypothesis (which is contrary to the most popular hypothesis of a slowing of the internal clock or pacemaker) that deficient auditory temporal processing may be a function of memory or attention. The focus on attention is consistent with research that has speculated that controlled executive attention, which is primarily regulated by the prefrontal cortex, may play a key role in mental time-keeping.
Abstract
- Previous research has suggested that Parkinson’s disease (PD) impairs perceptual acuity in the temporal domain. In the present study, psychophysical tests assessing several aspects of auditory temporal processing were administered to a group of PD patients treated with bilateral subthalamic nucleus (STN) stimulation and to a normal control group. Each patient was tested in three clinical conditions: without treatment, with levodopa therapy, and during STN stimulation. In all three conditions, the patients showed a significant deficit in the detection of very short temporal gaps within noise bursts and in the discrimination between the durations of two well-detectable time intervals (circa 50 ms) bounded by two temporally non-contiguous pairs of clicks. However, the patients showed no deficit in the detection of a temporal break produced by a local interval change in an otherwise isochronous sequence of 10 clicks spaced by 50-ms intervals. The latter result contradicts previous suggestions that PD slows down an internal clock or pacemaker involved in the perception of short durations. In this regard, we reinterpret previous evidence. Remarkably, the patients’ deficits were not diminished by levodopa therapy; in contrast, STN stimulation slightly improved performance, overall. We tentatively ascribe the deficit observed in the gap-detection test to a dysfunctioning of the auditory cortex, impairing its ability to track rapid fluctuations in sound intensity. We argue that the deficit in the duration-discrimination test is the consequence of an impairment in memory and/or attention rather than in the perception of time per se.
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