Interval Timing Sensitivity in Persons at Risk for Schizophrenia

Given the findings of different sensitivities to modality effects in young and aged populations, it is worthwhile to consider whether the existence of modality effects may prove a useful tool for examining the cognitive and neurophysiological bases of timing via studies of patient populations. For example, a number of studies have reported temporal processing deficits in patients diagnosed with schizophrenia (Sz). Overestimation of duration in the seconds range has been reported for verbal estimation tasks (Clausen, 1950; Densen, 1977; Johnson and Petzel, 1971; Lhamon and Goldstone, 1956; Wahl and Sieg, 1980; Weinstein et al., 1958), and underestimation in the seconds range has been reported for reproduction and production tasks (Clausen, 1950; Johnson and Petzel, 1971; Tysk, 1983, 1990; Wahl and Sieg, 1980). Overestimation in verbal estimation tasks and underestimation in production tasks by patients diagnosed with Sz may be consistent with either an increased internal clock speed or an increased memory storage speed, depending on the training and test procedures used and the pattern of obtained results (e.g., Meck, 1983, 1996; Meck and Benson, 2002).

One difficulty with studying cognitive processing in a psychiatric population, however, is that performance deficits may be a consequence of a lack of motivation or task comprehension rather than a specific cognitive deficit. In addition, psychiatric patients are often medicated, and most psychoactive drugs have varied effects on cognitive processing. These difficulties may be circumvented through studying unmedicated individuals at genetic risk for the psychiatric disorder in question. The risk to offspring of one schizophrenic parent, the relatives most commonly studied in high-risk research, has been estimated to be 12% (Gottesman et al., 1987; Holzman and Matthysse, 1990). Moreover, the pattern of empiric risks for schizophrenia in relatives of schizophrenic probands is not Mendelian, but suggests instead the action of multiple genes (e.g., Gottesman et al., 1987). It appears that the clinical illness is not expressed in all individuals who carry the full genetic liability because the concordance rate for the disorder is only about 45% in monozygotic twins (e.g., Gottesman et al., 1982; Kendler, 1988). Some clinically unaffected individuals, however, may show cognitive or other neurobehavioral deficits associated with schizophrenia. Thus, the rate of such deficits in high-risk individuals may be greater than the expected rate of the illness itself (e.g., Erlenmeyer-Kimling, 1996). Importantly, participants at high risk for developing schizophrenia (i.e., first-degree relatives of diagnosed schizophrenic patients) sometimes exhibit structural and functional abnormalities of the brain that are similar to those exhibited by schizophrenia patients (for a review, see Cannon, 1996).

Recently, Penney et al. (submitted) examined differences in temporal processing between individuals at high risk for schizophrenia (HrSz) and normal controls (NC) using the duration bisection task. Both groups of participants showed a robust difference between auditory and visual signal classification. Interestingly, however, the HrSz group showed a statistically larger difference between the auditory and visual response functions than did the NC group. Within the framework outlined above, this result suggests a greater auditory-visual clock speed difference for the HrSz participants than for the NC participants. One possibility is that the HrSz participants had a slower visual temporal accumulation than normal because they were less able to maintain the mode switch in a closed state, indicating an attentional dysfunction.

As mentioned earlier, studies of seconds-to-minutes range timing in schizophrenic patients have usually found overestimation on estimation tasks and underestimation on production or reproduction tasks. These studies have been interpreted as indicative of an increased clock rate in schizophrenic patients, an interpretation that has been assumed consistent with animal studies of the effects of dopamine agonists on interval timing (Rammsayer, 1990). However, as described above, a clock rate difference by itself will not always result in a behavioral effect. To obtain underestimation, the information-processing model requires that the stored memory values be distorted short. As a consequence, accumulated time on the test trial reaches the stored subjective time target value before the objective time target duration has elapsed. Therefore, the timing dysfunction in diagnosed schizophrenic patients may be due to disruption of frontal lobe structures involved in memory storage. In the Penney et al. (2002) study, the HrSz auditory response functions were equal to those of the NC group, whereas the visual functions were shifted farther to the right. Our interpretation does not necessarily require a faster overall clock rate for the HrSz participants, although we do require a larger relative difference between auditory and visual clock rates for the HrSz participants. Given that a number of studies using a variety of tasks have found attentional deficits in both schizophrenic patients and individuals at high risk for schizophrenia (e.g., Erlenm-eyer-Kimling and Cornblatt, 1992; Erlenmeyer-Kimling et al., 1979; Mirsky et al., 1995; Nuechterlein, 1977), it is not unreasonable to interpret the auditory-visual difference for HrSz participants as the result of an attentional effect at the level of the mode switch.

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