Modeling the Effects of PD

The curvilinear psychophysics of the pacemaker-accumulator model gives rise to the finding relevant to the duration-dependent timing effects stemming from PD. As can be seen in Figure 20.3, the high-gain-high-decay function crosses the low-gain-low-decay function. Consider a timing task where there are two target intervals, the durations of which fall on either side of the crossover point between the two functions. Now consider the case where the low-gain-low-decay function represents the psychophysical function associated with encoding time intervals in the OFF-medication state by PD patients, and the high-gain-high-decay function is associated with PD patients' decoding temporal memories in the OFF state. Such a mismatch between encoding and decoding will yield migration of mean production times because the memory of the shorter interval is now compared to a relatively slower clock, while the longer interval is compared to a relatively faster clock. The association of different psychophysical functions is of course motivated by the findings that encoding and decoding are associated with different behavioral effects in the experiments with PD patients employing the encode-decode design and the ON-OFF L-Dopa manipulation.

The fact that timing by PD patients in the ON conditions is accurate implies in the context of this model a similarity in the model's psychophysical functions associated with encoding and decoding temporal memories. However, the form of the slowed encode effect found in the OFF-ON group restricts the possible forms of the model's psychophysical functions. More specifically, if timing in the ON-drug condition is associated with a third set of model parameters (the first two being those that define the model's function for encoding and decoding temporal memories in the OFF-drug conditions), then we need only choose changes in parameters that give rise to a model decode-ON psychophysical function that accumulates more slowly than the putative encode-OFF function described above. This can be accomplished by assuming that encoding and decoding ON-drug are associated with the same very low gain-very low decay state of the pacemaker-accumulator. Such a system could give rise to accumulation that is slower for both target intervals, but is relatively faster over some range of longer time intervals.

To summarize, migration and slowed encode can be accommodated by Miall's pacemaker-accumulation model by assuming that the absence of DA increases the two parameters of the model, but does so more for encoding than for decoding. Although nothing in the model informs us of the potential origin of such a different effect of DA on encoding and decoding, we may surmise several potential factors contributing to this difference. Because encoding and decoding are dissociable cognitive functions, it is reasonable to assume that somewhat different brain circuitry underlies the two processes, allowing for somewhat different DA action. It could also be that the additional effort involved in the processing of feedback modulates the effect of DA on encoding relative to decoding.

0 0

Post a comment