Review of the Self-Ordered Pointing Task

The prefrontal cortex is a major recipient of subcortical dopaminergic projections. Accordingly, almost all of the behavioral tasks that are known to critically depend on the prefrontal cortex are sensitive to dopamine levels. A curious exception is the Self Ordered Pointing task (SOPT), in which subjects must select each of 9 designs by pointing at each one once; after each selection, the locations of the designs are randomized. Therefore, in order to succeed at this task subjects must remember the designs themselves and not the locations to which they pointed.

The dorsolateral prefrontal cortex is necessary for performance on this task, as indicated both by human and nonhuman primate lesion studies as well as neuroimaging of healthy adults, which is no surprise given this region's role in actively maintaining information across time. But whereas reductions in prefrontal dopamine seem to impair performance on a variety of working memory tasks (such as delayed response, N-back or Wisconsin Card Sort), no such impairment is seen in SOPT, neither resulting from dopamine antagonists, dopamine disorders like phenylkeonturia, nor genetic polymorphisms like Met COMT.

This has led many to suggest that the SOPT differs fundamentally from a host of other "executive" or "prefrontal" tasks, with some even suggesting that SOPT may not require inhibition. This claim is particularly confusing, given that intuitively the task seems to require inhibition of previous actions - otherwise, subjects would point to the same design twice (as they sometimes do).

However, others have come to the opposite conclusion. For example, Collins et al demonstrated that when PFC lesioned monkeys were physically prevented from selecting the same design twice in a row (the just-selected designs were removed from the subsequent display), their performance was equivalent both to controls and to their own pre-lesion performance. However, in another version of the task where previously-selected designs changed colors, monkeys with prefrontal lesions were still impaired. If PFC-lesions decrease SOPT performance because of active memory impairments, the monkeys should have performed fine on this version of the task, since there is no need to actively maintain previously selected items (after all, they change color!). Therefore, Collins et al argued that inhibitory deficits are the reason that PFC lesioned monkeys, but not prefrontal dopamine-depleted monkeys, show impaired SOPT performance.

One possible reason for the discrepancy in conclusions is that "perseveration" may not be synonymous with "inhibitory failure. " For example, perseveration could also result from impaired "shifting" mechanisms, identified as distinct from inhibition in this latent factor analysis. Furthermore there are high correlations between SOPT performance and card sorting tasks, such as with WCST and with the Dimensional Change Card Sort. Alternatively, perseveration could result from impaired monitoring mechanisms, as suggested by this study.

Regardless of whether SOPT involves inhibition, shifting, and/or monitoring, it is clear that SOPT does not rely on dopamine levels. This alone makes it an interesting object for study. As it turns out, however, SOPT performance follows an interesting developmental trajectory as well.

Aging has profound effects on SOPT, moreso than the effect of aging on measures of simple span measures of memory capacity. Aging is associated both with decline in frontal structural integrity (cortical thickness, number of large neurons and weight) as well as with decreases in dopamine transport efficacy; it is therefore possible that age-related variation in SOPT indexes structural deterioration as dissociated from functional deterioration resulting from neurochemical change. Work by Bryan and Luszcz (2001) also points towards the utility of using SOPT as a marker of age-related change, since SOPT performance was related to processing speed and perseverative but not WM indices.

At the other end of the developmental continuum, versions of the SOPT have been used with children as young as 10 months, without problematic floor effects. In preschool children, the "stationary box" variant of the task has proven effective; in this paradigm, an array of 3, 6 or 9 differently-patterned boxes is presented to the child, each of which contains a small treat. The children are allowed to open one box at a time, after which a delay of 5 seconds or 10 seconds is imposed. During this delay, the locations of the boxes may be changed (this would be the "scrambled boxes" version). After all of the treats have been received, the process may be repeated.

One advantage of the SOPT is that a variety of measures can be derived from the results, although mean number of errors is the most frequently used. In addition to error rate, one can define "error distance" as the number of trials since a child had last reached to the same box. On less abstract or stationary versions of the task, one can derive indices of strategy by analyzing the spatial pointing sequences used (by proximity, by category, etc.) Other measures include the number of reaches before the first error, the slope of the increase in error rate as a function of set size, and the increase in errors on the second iteration of the task relative to the first (a putative measure of proactive interference).

In summary, the Self-Ordered Pointing Task is a unique and promising paradigm in many ways. It shows several dissociations from other tests of working memory and executive processes - in that it is not sensitive to cortical dopamine levels - and yet is nonetheless sensitive to prefrontal damage. It is also easily adapted for use with kids, and provides a variety of possible measures for analysis.

References:

Bryan J, Luszcz MA. (2001). Adult age differences in self-ordered pointing task performance: contributions from working memory, executive function and speed of information processing. J Clin Exp Neuropsychol. 2001 Oct;23(5):608-19.

Collins P, Roberts AC, Dias R, Everitt BJ, Robbins TW. (1998) Perseveration and strategy in a novel spatial self-ordered sequencing task for nonhuman primates: effects of excitotoxic lesions and dopamine depletions of the prefrontal cortex. J Cogn Neurosci. May;10(3):332-54

Diamond A, Briand L, Fossella J, Gehlbach L. (2004) Genetic and neurochemical modulation of prefrontal cognitive functions in children. Am J Psychiatry. 2004 Jan;161(1):125-32

Ewing-Cobbs L, Prasad MR, Landry SH, Kramer L, DeLeon R. (2004). Executive functions following traumatic brain injury in young children: a preliminary analysis. Dev Neuropsychol. 2004;26(1):487-512

Hongwanishkul D, Happaney KR, Lee WS, Zelazo PD. (2005). Assessment of hot and cool executive function in young children: age-related changes and individual differences. Dev Neuropsychol. 2005;28(2):617-44

Joseph RM, Steele SD, Meyer E, Tager-Flusberg H. Self-ordered pointing in children with autism: failure to use verbal mediation in the service of working memory? Neuropsychologia. 2005;43(10):1400-11

Petrides, E., and Milner, B. 1982. Deficits on subject-ordered tasks after frontal- and temporal-lobe lesions in man. Neuropsychologia 20: 249-262.

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