Pathophysiological distortions in time perception and timed performance
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Distortions in time perception and timed performance are presented by a number of different neurological and psychiatric conditions (e.g. Parkinsonâs disease, schizophrenia, attention deficit hyperactivity disorder and autism). As a consequence, the primary focus of this review is on factors that define or produce systematic changes in the attention, clock, memory and decision stages of temporal processing as originally defined by Scalar Expectancy Theory. These findings are used to evaluate the Striatal Beat Frequency Theory, which is a neurobiological model of interval timing based upon the coincidence detection of oscillatory processes in corticostriatal circuits that can be mapped onto the stages of information processing proposed by Scalar Timing Theory.
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Table 1 Summary of individual differences and pathophysiological distortions in time perception and time performance Basic timing procedures Individual differences Neurological condition(s) Bisection function (point of subjective equality geometric mean) equal influence of both âshort and longâ anchors Some ânormalâ participantâs exhibit greater influence of the âshortâ anchor on the point of subjective equality Autism may lead to greater influence of the âshortâ anchor duration (Allman et al., 2011a). Left temporal lobe resection (in contrast to the right temporal lobe) produces over-estimation and depression produces underestimation of duration (Vidalaki et al., 1999; Melgire et al., 2005; Balci et al., 2009; Gil and Droit-Volet, 2009) Auditory/visual differences in point of subjective equality when trained in same sessionexplained by âmemory mixingâ Some ânormalâ participants do not exhibit the auditory/visual difference in point of subjective equality Participants at âhigh riskâ for schizophrenia as well as individuals with schizophrenia exhibit greater auditory/ visualâpoint of subjective equality differenceâperhaps due to a relative decrease in attention and/or clock speed for visual signals. This is in contrast to participants at risk for affective disorders and those with temporal lobe resection (Melgire et al., 2005; Penney et al., 2005; Carroll et al., 2008) Ordinal comparison procedure with multiple standards Individual differences in âmemory mixingâ, i.e. some ânormalâ participantâs display little or no âmixingâ of the different standards in memory âMemory mixingâ effect can be influenced by feedback with differential effects of valence (e.g. positive versus negative feedback effects)âsuggesting the involvement of dopamine (Gu and Meck, 2011b) Peak-interval timing procedures with associated measures of accuracy (peak time) and precision (peak spread) Individual differences in accuracy and precision (Rakitin et al., 1998; Meck, 2002a, b). Individual differences in âmigrationâ with multiple standard durations (Malapani et al., 1998) Individual differences in peak time in ADHD and normal adults as a function of drug treatment (nicotine or haloperidol) and the probability of intertrial interval feedback. Dopamine-controlled regulation of clock speed is used to explain the drug and feedback effects (Levin et al., 1996; Lustig and Meck, 2005; Meck, 2005). Patients with Parkinsonâs disease tested OFF their levodopa medication exhibit large âmigrationâ effectsâsuggesting a role for dopamine in this form of âmemory mixingâ (Malapani et al., 1998; Koch et al., 2005, 2008a) Ambiguous tempo judgement paradigms Large individual differences in the strength of beat based versus interval timing are observed (Grahn and McAuley, 2009) Quinpirole (dopamine D2 receptor agonist) sensitized rats more readily engage in rhythmical (beat-based) timing behaviour reminiscent of the ânon-functionalâ fixation to time observed in obsessiveâcompulsive disorder (Gu et al., 2008, 2011a) Time estimation up to 60 s Individual differences in time perception due to spatial asymmetries and ânormalâ levels of neglect in healthy individuals (Vicario et al., 2008; Grondin, 2010; Hurwitz and Danckert, 2011) Underestimation of time in patients with unilateral neglect (Danckert et al., 2007)
Time Perception other than interval timing
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Figure 1
Figure 1 The information processing model of interval timing as specified by scalar expectancy theory. Adapted from Gibbon et al. (1984). Page 658
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Figure 2 Striatal beat frequency model of interval timing. In this model, intervals are timed via striatal spiny neurons that monitor activation patterns of oscillatory neurons in the cortex. These cortical neurons have patterns of activity that fire with different frequencies and converge onto spiny neurons, as illustrated. At the beginning of an interval, these oscillating neurons are synchronized and the status level of the spiny neurons reset by phasic dopaminergic input from the ventral tegmental area and substantia nigra pars compacta, respectively. The delivery of reinforcement at the target duration produces a pulse of dopamine thereby strengthening the synapses in the striatum that are activated as a result of the beat frequency pattern of these cortical neurons at that specific point in time. In this manner, mechanisms of long-term potentiation (LTP) and long-term depression are used to strengthen and weaken synaptic weights in order to produce a record in memory of the target duration. Later, when the same signal duration is timed again, neostriatal GABAergic spiny neurons compare the current pattern of activation of these cortical neurons with the pattern stored in memory in order to determine when the target duration has been reached. When the clock and memory patterns match as determined by coincidence detection, the spiny neurons fire to indicate that the interval has elapsed. In this model, clock speed is determined by the levels of tonic dopamineâglutamate activity in ventral tegmental areaâcortical pathways, which modulates the frequency of cortical oscillations (Cheng et al., 2006, 2007a, b, c). Adapted from Matell and Meck (2004). Page 666
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Figure 3
Figure 3 A diagram of the corticostriatal and corticocerebellar circuits proposed to be involved in the interval-timing and motor-control components of procedural learning that are dysfunctional in Parkinsonâs disease and schizophrenia (Pascual-Leone et al., 1993; Andreasen et al., 1999; Kumari et al., 2002; Doyon et al., 2003). Full coloured lines represent excitatory input to various areas. Dashed lines and black lines represent inhibitory input to areas. Adapted from Meck (2005). AV = Anterior ventral; GPe = globus pallidus external capsule; GPi = globus pallidus internal capsule; IO = inferior olive; MTL = medial temporal lobe; PN = pontine nuclei; Red N = red nucleus; Ret N = reticular nucleus; SNc = substantia nigra pars compacta; VA = Ventral anterior; VLc/x = ventrolateral thalamic nucleusâcaudal and area divisions; VLm = ventrolateral medial thalamic nucleus; VLo = ventrolateral thalamic nucleusoral division; VN = vestibular nuclei. Page 671
Figure 3