Increased Timing Variability in Schizophrenia and Bipolar Disorder

Amanda R. Bolbecker, Daniel R. Westfall, Josselyn M. Howell, Ryan J. Lackner, Christine A. Carroll, Brian F. O'Donnell, William P. Hetrick

Theoretical and empirical evidence suggests that impaired time perception and the neural circuitry underlying internal timing mechanisms may contribute to severe psychiatric disorders, including psychotic and mood disorders. The degree to which alterations in temporal perceptions reflect deficits that exist across psychosis-related phenotypes and the extent to which mood symptoms contribute to these deficits is currently unknown. In addition, compared to schizophrenia, where timing deficits have been more extensively investigated, sub-second timing has been studied relatively infrequently in bipolar disorder. The present study compared sub-second duration estimates of schizophrenia (SZ), schizoaffective disorder (SA), non-psychotic bipolar disorder (BDNP), bipolar disorder with psychotic features (BDP), and healthy non-psychiatric controls (HC) on a well-established time perception task using sub-second durations. Participants included 66 SZ, 37 BDNP, 34 BDP, 31 SA, and 73 HC who participated in a temporal bisection task that required temporal judgements about auditory durations ranging from 300 to 600 milliseconds. Timing variability was significantly higher in SZ, BDP, and BDNP groups compared to healthy controls. The bisection point did not differ across groups. These findings suggest that both psychotic and mood symptoms may be associated with disruptions in internal timing mechanisms. Yet unexpected findings emerged. Specifically, the BDNP group had significantly increased variability compared to controls, but the SA group did not. In addition, these deficits appeared to exist independent of current symptom status. The absence of between group differences in bisection point suggests that increased variability in the SZ and bipolar disorder groups are due to alterations in perceptual timing in the sub-second range, possibly mediated by the cerebellum, rather than cognitive deficits.