2008年1月27日 星期日

On Inhibition/Disinhibition in Developmental Psychopathology: Views From Cognitive and Personality Psychology and a Working Inhibition Taxonomy

On Inhibition Disinhibition in Developmental Psychopathology: Views From Cognitive and Personality Psychology and a Working Inhibition Taxonomy
[Articles]
Nigg, Joel T.1,2
1Department of Psychology, Michigan State University
2Correspondence concerning this article should be addressed to Joel T. Nigg, Department of Psychology, 135 Snyder Hall, Michigan State University, East Lansing, Michigan 48824-1117. Electronic mail may be sent to nigg@pilot.msu.edu.
Preparation of this article was supported by National Institute of Mental Health Grant RO3-MH57244.
I acknowledge helpful discussions and/or comments on all or part of earlier drafts by Tom Carr, B.J. Casey, John Henderson, Stephen Hinshaw, Oliver John, Jerome Kagan, and Rose Zacks.
Received Date: February 17, 1999; Revised Date: September 24, 1999; Accepted Date: October 6, 1999
Abstract
Disinhibition is a common focus in psychopathology research. However, use of inhibition models often is piecemeal, lacking an overarching taxonomy of inhibitory processes. The author organizes key concepts and models pertaining to different kinds of inhibitory control from the cognitive and temperament/personality literatures. Within the rubrics of executive inhibitory processes, motivational inhibitory processes, and automatic attentional inhibition processes, 8 kinds of inhibition are distinguished. Three basic temperament traits may address key executive and motivational inhibitory processes. Future developmental psychopathology research should be based on a systematic conceptual taxonomy of the kinds of inhibitory function relevant to a given disorder. Such an approach can clarify which inhibition distinctions are correct and which inhibition deficits go with which disorders.
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Arguably, few constructs play so central a role in conceptions of developmental psychopathology as disinhibition. Failure of one type of inhibition or another plays a role in investigations of child and adult conditions as diverse as attention deficit hyperactivity disorder (ADHD; Barkley, 1997a), shyness, anxiety (for a review, see Albano, Chorpita, & Barlow, 1996) and mood disorders generally (Segal, 1996), alcoholism and substance abuse (Sher & Trull, 1994), antisocial behavior (Newman & Wallace, 1993), schizophrenia (Nestor & O'Donnell, 1998), obsessive–compulsive disorder (OCD; Rosenberg et al., 1997), Tourette's syndrome (Ozonoff, Strayer, McMahon, & Fillouz, 1998), learning delays (Dempster & Corkill, 1999), and posttraumatic stress disorder (PTSD; Cloitre, 1998). The widespread interest in inhibition reflects not only the ubiquity of impulse control problems in psychopathology but also developments in the basic sciences from which psychopathologists borrow, especially the cognitive and personality/temperament fields (Dempster, 1992; Gray, 1991).
Clinical researchers often adopt cognitive, personality, or temperament models but not always with a clear rationale for selecting one paradigm over another. At other times, a disorder is studied with multiple paradigms, with a conclusion of a global inhibitory deficit. However, although journal articles regularly target inhibition (see, e.g., Chen et al., 1998; Ozonoff et al., 1998), the relations among the various authors' different meanings of inhibition are not clearly articulated in the literature (Harnishfeger, 1995). How can the various inhibition constructs currently in use be related to one another? What would be a workable taxonomy of types of inhibition to guide clinical research? Adopting a framework to answer these questions enables systematic mapping of inhibitory deficits in relation to specific psychopathological disorders. This article therefore reappraises the construct of inhibition for developmental psychopathology.
Background: Basic Issues in Developmental Psychopathology Research
Severe and impairing psychological disorders afflict up to 10% of children (Costello, 1989) and at least 15% of adults (Kessler et al., 1994), with moderate problems affecting many more. These impairing conditions are costly in every sense. The current nosology (American Psychiatric Association, 1994) is primarily descriptive and has well-known limitations (Achenbach, Conners, Quay, Verhulst, & Howell, 1989; Clark, Watson, & Reynolds, 1995). Finding causal mechanisms to form a superior basis for taxonomy is a priority. A goal of clinical research is therefore to understand which basic psychological processes, such as inhibitory functions, may develop abnormally in particular disorders (Wakefield, 1992). A developmental psychopathology perspective (Cicchetti, 1984) assumes that such dysfunctions, if present, influence psychopathology in reciprocal, dynamic fashion with other contextual factors in development. As part of such models, clear linking of specific inhibitory processes to different disorders thus can contribute to a more sophisticated, process-based account of psychopathology.
I therefore examine various kinds of inhibition in two key areas of basic psychological science often drawn on in clinical research: cognitive psychology/cognitive neuroscience and personality/temperament. The aim is to provide a framework by which research on inhibitory dysfunction in psychopathology can be initially evaluated and eventually integrated. In turn, such a framework can help to lay the groundwork for mechanism-based taxonomic efforts.
Assumptions in This Article
The Neuropsychological Viewpoint and the Conceptual Nervous System
One assumption of this article is that it is useful to note neural systems within which particular inhibitory processes may be implemented. However, neural systems are not viewed as a reductionist substitute for psychological processes (see G. A. Miller, 1996). Cognitive and personality models often propose neural correlates in what is sometimes referred to as the conceptual nervous system (Klein & Taylor, 1994). It is important to remember that the systems noted herein are presumed to interact with other, distributed neural systems in implementing the functions under discussion.
The clinical neuropsychological literature documents release of inhibition of various kinds secondary to brain lesion or drug response, resulting in extremes of impulsive and disorganized behavior (Fuster, 1997; Wilens, Wyatt, & Spencer, 1998). Neuropsychological theories of inhibition emphasize executive functioning (a term for regulatory control) and the multiple brain circuits connecting parallel regions of brain prefrontal cortex and thalamic and subcortical (basal ganglia) structures (Alexander, Crutcher, & DeLong, 1991; Cummings, 1993). These parallel circuits can be understood in relation to different kinds of inhibition (Alexander et al., 1991; Casey, in press; Fuster, 1997). For example, the system linked to lateral orbito-prefrontal cortex may relate to social and behavioral inhibition and hyperactivity (Fuster, 1997), as dramatically evidenced in the disinhibition to immediate cues observed in patients with orbitofrontal lesions. The anterior cingulate gyrus may be especially critical to the kind of interference control used to focus attention (Cabeza & Nyberg, 1997; S. E. Peterson, Fox, Snyder, & Raichle, 1990; Posner & Raichle, 1994). Because this literature informs cognitive and personality theories, the different literatures may be approaching similar systems from different levels of analysis. I therefore refer schematically to neuropsychological models when relevant and use the neuropsychological lens as one way to link the different ideas about inhibition.
Central Versus Peripheral Processes
A second emphasis herein is on central rather than peripheral processes. Inhibition in early stages of sensation and perception, for example, is not emphasized. Similarly, inhibition of motor response can occur centrally or peripherally. It is assumed that, for most disorders, central inhibitory systems are of greater import. Accordingly, the focus is on inhibitory processes in relation to higher order cognition and complex behavior, especially in relation to attention, executive processes, and motivated behavior.
Developmental Considerations
Organizing types of inhibition would be simplified if they were static across development. Yet different kinds of inhibitory control develop at different rates throughout childhood (Dempster, 1993; Rothbart & Bates, 1998). Thus, one organization of inhibitions may not hold for all points in development (see also Kopp, 1982). Development is also pertinent to the neural correlates discussed in the conceptual nervous system. For example, regions of anterior cortex important for inhibitory control continue to develop throughout childhood (Krasnegor, Lyon, & Goldman-Rakic, 1997). The structure of inhibitory control also may mature with brain development (Harnishfeger, 1995; Passler, Isaac, & Hynd, 1985). I thus note illustrative developmental data for the inhibition constructs.
Inhibition as a General Construct: Introductory Comments
This is not the first attempt to survey the relevance of inhibitory concepts to developmental psychopathology. For example, Milich and Kramer (1984) critiqued the handful of measurement-based constructs in the clinical literature at that time. Yet the field lacks a full overview of a wide range of contemporary constructs and methods. Although many areas of psychology examine inhibition and related constructs, the central thesis of the present article is that a lack of integration of personality and cognitive models in particular limits clinical research. These models concern themselves with distributed psychological and neural systems of behavioral control. They are in that sense distinct from models of local-level neural dysfunction, such as those that posit widespread inhibitory failures in local cell assemblies and that have been put forward with regard to schizophrenia (Cohen & Servan-Schreiber, 1992; Nestor & O'Donnell, 1998). Once one moves to the level of dedicated neural or psychological systems, it appears that multiple if related inhibitory functions must be considered for many disorders. These functions are accessed by the cognitive and personality models that follow.
Inhibition in Cognitive Psychology and Cognitive Neuroscience
Multiple approaches to inhibition can be discerned in a burgeoning cognitive literature on the widespread implications of the inhibition metaphor. These entail revised understandings of perception and selective attention (Houghton & Tipper, 1994), memory and learning (Bjork, 1989; Hasher & Zacks, 1988), and behavioral control (Logan & Cowan, 1984). Although thinking about inhibitory functions has a century-long history in cognitive psychology, it has, according to some observers, gained particular prominence in the past decade as the information-processing or computer metaphor has been replaced by connectionist and computational models (Bjork, 1989; Dempster, 1992). A further reason for the return of inhibition to center stage may be its ability as a construct to answer objections and problems with the “limited capacity” metaphor of attention and interference (Dempster, 1992; May, Kane, & Hasher, 1995). In any event, recent work in this area is voluminous (see, e.g., Dagenbach & Carr, 1994; Dempster & Brainerd, 1995; Golding & MacLeod, 1998; Sarason, Pierce, & Sarason, 1996). Thus, my review is necessarily selective, with the aim of synthesizing major themes in the cognitive literature that may enrich thinking about inhibition in developmental psychopathology.
This section proceeds from relatively general to relatively specific inhibition processes. I begin with a broad type of inhibition, interference control, that is relevant to both motor control and working memory function (cognitive inhibition). I next move to consideration of primary motor inhibition and then to inhibition as measured in particular contexts, including visual and selective attention and oculomotor control. Throughout, distinctions between relatively automatic and relatively controlled inhibitory processes are noted (Schneider & Shiffrin, 1977). Discussion of each approach to inhibition is anchored by a paradigmatic task or measurement paradigm, reference to a possible neural implementation, comments on developmental progression, and illustrative clinical findings. An overarching issue is to what extent these various measurement paradigms tap either the same process in different contexts or different processes.
Interference Control
Interference control can refer to suppressing a stimulus that pulls for a competing response so as to carry out a primary response, to suppressing distractors that might slow the primary response, or to suppressing internal stimuli that may interfere with the current operations of working memory. Experimental tasks that implicate interference control include some priming tasks as well as “flanker” tasks (Gratton, Coles, & Donchin, 1992) in the selective attention literature.
Motor interference: Stroop effect.
Perhaps the most widely cited measure of interference control in the psychopathology literature is the Stroop effect. This effect is widely studied in both neuropsychology (Diamond, Prevor, Callender, & Druin, 1997) and cognitive psychology (MacLeod, 1991). The essential phenomenon is that it takes respondents longer to name the ink color of a color word printed in a contrasting color (e.g., naming the color red when the word “green” is printed in red ink) than of a neutral stimulus (e.g., “xxxx”) printed in the same ink color. Apparently, the printed word is automatically processed in a manner faster than and competing with the effort to name the ink color. This presumed competing process must be suppressed to most rapidly name the ink colors, although theoretical debate continues regarding the underlying mechanism (MacLeod, 1991).
The Stroop effect, then, can serve as a paradigmatic task for interference control. However, a range of stimulus-incompatibility tasks have been used to examine this basic process. These all rely on training a “well-learned” response that then competes with a less well-learned response. For example, developmentally similar tasks that require controlling an interfering prepotent response to carry out an effortful primary response have been examined with very young preschool children. These studies demonstrate dramatic failures of inhibitory control in early development. The “A-not-B” error made by 9-month-old infants is a classic example. Diamond and colleagues (Diamond, 1997; Diamond et al., 1997) noted that toddlers at about this age reach for an object where it was last found even though they have seen it moved (A-not-B error) but, while doing so, look at the place where the object is now. This behavior suggested to Diamond (1997) a failure to control the prepotent motor response. Three-year-olds, likewise, continue to sort cards by color even when they know (based on their verbal report) that the rule has been changed to sort by shape (Diamond et al., 1997; Zelazo, Frye, & Rapus, 1996). Whether these preschool tasks are analogues for failed interference control (Diamond et al., 1997) or instead reflect limits in metacognitive processes (Zelazo et al., 1996) remains unclear. The Stroop effect per se requires automatized reading and so cannot be demonstrated until the early school years. Yet, by the third grade, the effect is sufficiently developed that it predicts behavioral adjustment (Nigg, Quamma, Greenberg, & Kusche, 1999). Preliminary age norms and the Stroop effect's longstanding use in neuropsychological clinical evaluation augment its interest for clinical research.
The Stroop effect has been extensively investigated in psychopathology. For example, it is used to examine inhibitory deficit in schizophrenia (Perlstein, Carter, Barch, & Baird, 1998). It also is believed to differentiate groups of school-age and adolescent children with ADHD from controls (Pennington & Ozonoff, 1996). As a result, the Stroop effect is featured as a marker of interference control in major theories of child psychopathology (see, e.g., Barkley, 1997b).
Thus, theoretical developments regarding underlying mechanisms and developmental changes in this effect are likely to remain of keen interest. With regard to neural correlates, in very young children, failure on this task has been related to damage to dorsolateral prefrontal cortex (Diamond et al., 1997). In adulthood, imaging data indicate that Stroop responding activates dorsolateral prefrontal cortex but appears to depend even more heavily on the anterior cingulate gyrus (Cabeza & Nyberg, 1997). These regions are usually associated with the deliberate control of attention and behavior. These findings thus support the notion that the Stroop and related tasks exemplify executive or goal-directed inhibitory process.
Despite its popularity as a measure of interference control, the Stroop itself has well-known limitations pertaining to its unique task properties. For instance, it has the unusual feature of obliging participants to extract specific features of a single target, rather than specific targets, from the stimulus. It therefore may reflect different features of interference control than are exemplified in everyday activities (Treisman, 1969). Demonstrations of a psychopathological deficit based on this task therefore need additional experimental tasks to supplement the traditional Stroop. One such task might be the flanker task (Gratton, Coles, & Donchin, 1992), in which the competing stimulus is spatially adjacent to the target; modifications of the Stroop also target this issue.
The role of motivation: Emotional Stroop.
An important extension of the Stroop phenomenon in psychopathology research is the emotional Stroop. In this phenomenon, reaction times are longer for naming the ink color of threat-related words (in the case of anxious patients) or other psychopathologically relevant content (J. M. G. Williams, Mathews, & MacLeod, 1996). This task is interesting because the putative competing processing pathway, to use a connectionist metaphor, that must be contained now involves emotionally valenced stimuli. Do these activate different neural pathways than those activated by the traditional Stroop task, thanks to the need to suppress motivationally significant information? Or is the interference still simply part of a semantic network and thus controlled by the same interference control mechanism as in the regular Stroop task? Recent imaging data provide some support for the second possibility, although activation regions did vary across tasks (George et al., 1994). However, psychopathology data indicate that anxious patients show deficits on this but not the traditional Stroop (Matthews & MacLeod, 1985; J. M. G. Williams et al., 1996). The task may exemplify the role of limbic-based motivational systems moderating interference control for emotionally significant stimuli (Derryberry & Tucker, 1994). In either case, the emotional Stroop adds an interesting dimension to the analysis of interference control, in which it is possible that a different challenge to inhibitory systems may pertain. The emotional Stroop has contributed to establishing attentional biases that are associated with anxiety conditions and to differentiating these from response in depression (for which evidence has not consistently supported an attentional bias; Mineka, Watson, & Clark, 1998; J. M. G. Williams et al., 1996). The relevance to anxiety reflects the idea that anxiety brings a greater preoccupation with threatening stimuli. Depression, in contrast, brings a greater selection for negative self-referential memories (Mineka et al., 1998).
Cognitive interference: Directed forgetting.
Interference control can also be cited when one considers keeping unwanted thoughts out of mind even when not blocking a competing motor response. An extensive literature concerns the control or suppression of unwanted thoughts (interference in the contents of working memory), particularly in relation to anxiety and obsessive conditions (Dempster & Brainerd, 1995). This inhibition of unwanted mental contents may arguably be distinguishable from that of the Stroop-like interference control. One extensively investigated measurement paradigm that illustrates this function is the directed forgetting paradigm. Much of the directed forgetting literature examines retrieval inhibition in relation to memory processes (Bjork, 1989; MacLeod, 1998). For example, participants first listen to a word list. Some participants are told to forget the list so far (“it was just practice”), whereas others are instructed to remember it. A second (interference) list is presented. Participants are then asked to recall words from the first list. Recall accuracy is lower for the “forget” words than the “remember” words, whereas recognition memory is similar for the two lists. This pattern is usually interpreted as indicating that a cognitive inhibition mechanism suppressed the information from working memory but not from recognition memory (S. P. Wilson & Kipp, 1998). The role of selective rehearsal is a confound in some versions of this task, as explained by S. P. Wilson and Kipp (1998). Those authors distinguished the process in directed forgetting, which they called cognitive inhibition, from interference control, which they argued occurs prior to storage in recognition memory, as when irrelevant meanings of polysemous words are suppressed while reading. Herein, I refer primarily to effortful interference control of motor response (e.g., the Stroop effect) but, following S. P. Wilson and Kipp (1998), use the term cognitive inhibition for the process that suppresses information from working memory.
Developmental effects on this process are notable. Most of the few extant studies of children are reviewed by S. P. Wilson & Kipp (1998) and by Harnishfeger (1995). For instance, Bray and colleagues (Bray, Hersh, & Turner, 1985; Bray, Justice, & Zahm, 1983) showed that second-grade children have difficulty suppressing the to-be-forgotten items and experience interference from these items in their recall. By fifth grade, successful inhibition of these items is apparent. A series of experiments suggested that these effects are not due to selective rehearsal effects. Harnishfeger and Pope (1996) examined first, third, and fifth graders and college students. Their data indicated that first graders were unable to deploy the inhibition necessary to prevent intrusion from the to-be-forgotten items. Third graders showed partial ability to do so, with fifth graders doing quite well. However, the adults showed better interference control than did the fifth graders. Using a different paradigm to examine suppression of irrelevant information from working memory, Lorsbach and Reimer (1997) obtained similar results. However, it is again open to question whether these effects were due to lack of an effective interference control mechanism or to limits on metacognitive strategies (see Zelazo & Frye, 1999).
On the other end of the life span, this form of cognitive inhibition appears to decline again with old age. Compared with younger adults, older adults recalled fewer of the to-be-remembered items and, in so doing, experienced more intrusions of to-be-forgotten items during recall (Zacks & Hasher, 1994). On the basis of several experiments using different methodologies, Zacks and Hasher (1994) suggested that older adults had more, not fewer, contents in working memory. Although these contents were extraneous, it is difficult to explain this result solely on the basis of limitations in working memory capacity. Instead, the problem seems to include inefficient inhibition of to-be-forgotten material (Hasher & Zacks, 1988).
This account of working memory has direct implications for interpretations of deficient working memory in various disorders. Child ADHD is one prime example. Working memory in ADHD typically has been examined in terms of short-term recall accuracy (e.g., digit span recall), but such experiments do not resolve whether memory capacity or interference control is impaired. The directed forgetting paradigm might be useful to clarify that issue (see Pennington, Bennetto, McAleer, & Roberts, 1996, for further discussion). Directed forgetting has not been used in studies of childhood psychopathology. It has been used to study adult PTSD and OCD (Cloitre, 1998). A problem in controlling working memory contents seems integral to both disorders. PTSD is associated with difficulty suppressing thoughts of the traumatic event, OCD with difficulty suppressing repetitive thoughts about cleaning, checking, counting, and so on.
A key issue is whether inhibition of a competing motor response (the Stroop effect) and protecting working memory (directed forgetting) activate different processes. Although imaging data on Stroop tasks are extensive, similar data are not so plentiful with regard to directed forgetting. Pending more data on the latter, psychopathology research could benefit from a distinction between (a) intentionally inhibiting competing automatic motor/vocal responses (motor interference control) and (b) intentional interference control in relation to the contents of working memory (cognitive inhibition). For example, individuals with ADHD might have problems controlling task-irrelevant information that pertains to motor response, whereas those with attention deficit disorder (without hyperactivity) may have a specific deficit in controlling the contents of working memory or internal distraction (Shaw & Giambra, 1993).
Intentional Motor Inhibition
A fundamental kind of inhibition of interest to psychopathologists entails the deliberate control of a primary motor response in compliance with changing context cues. For instance, a long tradition of neuropsychological research has looked at the go/no-go task. This task requires a child to “go” (e.g., press a key) when a frequent stimulus (e.g., the letter “A”) appears but to make no response (“no-go”) when an infrequent stimulus (e.g., the letter “B”) appears. The task thus requires inhibiting a dominant or prepotent response. Imaging data suggest that lateral orbital prefrontal cortex and its associated subcortical structures play a role in go/no-go response deficits in child ADHD (Casey et al., 1997). The go/no-go task has also been modified to assess motivational response in the laboratory. Newman and colleagues (e.g., Newman, Patterson, & Kosson, 1987) measured the rate at which participants learned to inhibit when monetary incentives and costs were linked to successful go/no-go inhibition. More is said about this approach in the section entitled Inhibition in Models of Personality and Temperament below.
A related paradigm that I suggest captures the same underlying process and is more developed theoretically is the stop signal paradigm. The stop signal paradigm is usually associated with the work of Logan and colleagues (Logan & Cowan, 1984). The presentation of the paradigm here largely follows Logan (1994). This forced choice paradigm typically entails viewing a computer display and pressing one of two keys as rapidly as possible depending on whether an X or an O appears. This rapid keypress response becomes the dominant or prepotent response, termed the go response. On a minority (e.g., 25%) of trials, a tone sounds. The participant tries to withhold the keypress when he or she hears the tone. The timing of the tone is varied, making it sometimes easy and sometimes harder to stop (e.g., if the tone sounded right before the target appeared, it would be relatively easy to stop compared with a tone that sounded later). Like a check swing in baseball, the task requires inhibition of an about-to-be-executed (prepared) motor response. On the basis of response times, stopping success, and stop signal timing, the speed of the stop process can be calculated. Failure to inhibit can be due to a fast go process or a slow stop process.
Logan (1994) conceptualized the paradigm as pertaining to the cessation of thought and action (thus, in theory, it includes a cognitive component, despite the usual association to motor inhibition) in response to either a change in the environmental signal or a change in goal. Thus, to pursue the goal successfully, one needs to change course in response to new information—the first step is to stop the current thought or action. Logan explicitly linked this process to executive control. Stopping is therefore like the Stroop and negative priming (discussed in the section entitled Inhibition as an Unintentional Side Effect of Focused Attention? The Case of Negative Priming below) tasks in that the inhibition process is activated in response to demands from executive control systems. However, in contrast to the active suppression of a competing (but never intended) response required by the Stroop task, the primary, intended response to a relevant stimulus in the stop signal paradigm must be suppressed when an infrequent cue occurs. This response is prepotent in that it has been prepared for repeat execution. The stopping that the task requires is considered by Logan to be an analogue to the subtle stopping and changing necessary during dynamic regulation of behavior in everyday life. One could suggest that stopping may relate to orbito-prefrontal cortex, an area associated with overt behavioral control (cf. Casey et al., 1997; Fuster, 1997).
The underlying theoretical model is the “race” model (Logan & Cowan, 1984). The essence of this model is that the go process and the stop process are independent. Once the go process is launched, the stop process must be launched proximally enough in time to have a chance of stopping task execution. However, the race model is not a process model. It is simply a model that accounts statistically for the observed stopping distributions (Logan, 1994). Its assumptions are few, chiefly that the go and stop processes are independent. Logan and Cowan (1984) argued that stopping inhibition is a general “amodal, central process” in adults. That is, although stopping a response may require multiple component processes, these are thought to be unified in a general higher order process across different contexts. As evidence for a general process, stopping requires a similar time course across different task modalities (motor, language, oculomotor). Evidence is scarce as to the component processes themselves, but Logan (1994) reviewed a handful of initial electroencephalographic and psychophysiological studies and concluded that there may be a central (cortical) and peripheral (midbrain) process in stopping. This idea needs further elucidation.
Developmentally, the task reveals measurable and interesting age-related changes. The inhibition process can be measured from age 7, although it is less variable in older children and adults (Schachar & Logan, 1990, Experiment 1). Speed of the inhibition process improves by about 50 ms from about age 7 to about age 9, peaking in young adulthood, and declining only slightly thereafter (B. R. Williams, Ponesse, Schachar, Logan, & Tannock, 1999). However, prior to age 6, reliable measurement of the speed of the stop process is in doubt. Speed of the go process appears to be more strongly related to age than does speed of the stop process during childhood (Nigg, 1999a; B. R. Williams et al., 1999).
Applications of the task to the study of child psychopathology are of interest, especially with regard to both ADHD and conduct disorder (CD; marked by aggression and by violation of the rights of others, often in an opportunistic or impulsive fashion). These two disorders often co-occur (Hinshaw, 1987). Schachar and Logan (1990, Experiment 2) introduced the stop task to the child clinical literature. They found task deficits unique to ADHD children that pertained to a slow stop process rather than a fast go process and less frequent stopping (but not to deficient detection of the stop cue). Oosterlaan, Logan, and Sergeant (1998) meta-analyzed the several stop task studies of child psychopathology reported in the subsequent near-decade. ADHD children had slower go reaction times and slower stop reaction times than controls, but the effect size was larger for stop reaction times. Highlighting the problem of specificity to one disorder, however, children with CD also had a slower stop reaction time than did controls (although the effect was not as large as for ADHD). The CD and ADHD groups did not differ significantly. Children with anxiety did not differ from controls.
An issue in the literature reviewed by Oosterlaan et al. (1998) was that most studies looking at ADHD did not covary CD symptoms and studies looking at CD did not generally covary ADHD symptoms. This is important because each group of children, even though not meeting criteria for the other diagnosis, are usually expected to have elevated rates of these associated behaviors (Hinshaw, 1987). Recent data suggest that stopping deficits in child ADHD are independent of associated oppositional and conduct problems (Nigg, 1999a). It is still unclear whether the somewhat weaker but still significant findings associated with CD could be related to subclinical ADHD symptoms in that group.
One problem with the stop task as typically used (though not a problem in principle) is that it pits a visual-motor go task against an auditory-motor stop signal. For at least some disorders, this could introduce a confound. For instance, children with ADHD may have particular difficulty processing information in the auditory modality (Pearson, Lane, & Swanson, 1991; Prior, Sanson, Freethy, & Geffen, 1985; for a review, see Riccio, Hynd, Cohen, & Hall, 1994). It is important to verify stop signal inhibition with a visual-versus-visual task in ADHD (see Rubia, Oosterlaan, Sergeant, Brandeis, & Leeuwen, 1998) and perhaps in other disorders as well. Despite these issues, the task is promising as a measure of motor inhibition for psychopathology research.
Inhibition in the Context of Attentional Orienting
Like executive functions, attentional systems have not yet achieved a consensus paradigm across the cognitive and neuropsychological literatures. Thus, several approaches are in use (reviewed by Mirsky, 1996; Taylor, 1995). The point for present purposes is that inhibitory processes are accessible from within some of these models. For example, a model for allocation of visual attention suggested by Posner and Peterson (1990) and Posner and Raichle (1994) has been used in studies of ADHD as well as of schizophrenia. The present overview of Posner's paradigm closely follows Rafal and Henik (1994). The measurement paradigm is described first and then the theory.
The measurement paradigm is as follows. A display is presented with a central visual fixation point and two peripheral points, usually boxes displayed on the computer screen. The task is to press a response key as rapidly as possible on detection of a target (e.g., an asterisk) in either of the peripheral boxes. This three-step set-up is illustrated in Figure 1.

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Figure 1. Basic setup of visual orienting experiment (not to scale). Double lines indicate peripheral brightening, a warning cue.
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Prior to the appearance of the target, a warning cue appears either peripherally (e.g., a brightening of one of the peripheral boxes, symbolized in Figure 1 by double lines around one of the boxes) or centrally (e.g., appearance of an arrow at the central fixation point). If the peripheral cue is not predictive of target appearance, it is believed to activate exogenous attentional response mechanisms. A predictive central cue is referred to as an endogenous cue. Warning cues thus may be either correct (“valid”), enhancing reaction time to the target, or incorrect (“invalid”), interfering with reaction time to the target under most circumstances. The outcome variable that measures attentional allocation is reaction time. By varying the type of cue, the probability that the cue is correct, and the timing of the cue–target interval (stimulus onset asynchrony, or SOA), distinct attentional (and corresponding inhibitory) systems can be activated. However, these time delays are very rapid compared with some other attentional paradigms used in psychopathology; typical stimulus onset asynchronies range from 200 ms to 800 ms. Thus, the meaning of sustained attention in this paradigm is different than in paradigms that measure attentional focus over several minutes.
The underlying model posits three visual attention systems. A posterior attentional system (subserved by posterior parietal cortex, the pulvinar region of the thalamus, and the superior colliculus in the midbrain; Posner & Raichle, 1994) is responsible for automatic orientation (disengaging, moving, engaging) of visual attention in response to motion, change, or other visual cues. Such orienting can be “covert” (prior to or in the absence of eye movements) or “overt” (with eye movement). The anterior system (anchored in the anterior cingulate cortex) controls effortful or intentional (“top-down”) attentional focusing in response both to visual cues and to goal-directed strategy considerations (Posner & Raichle, 1994). It thus overlaps conceptually and anatomically with the construct of executive control. Finally, a vigilance network (subserved by right prefrontal and parietal as well as subcortical pathways that mediate arousal) is responsible for maintaining alertness and attention over time on a target (Posner & Raichle, 1994).
The cue–response paradigm described above can shed light on inhibitory functions because facilitory and inhibitory components are required in the process of attentional orienting (Posner & Peterson, 1990; Rafal & Henik, 1994). Thus, exogenous cues activate the automatic (posterior) orienting system. From an inhibitory vantage point, the posterior system is not vulnerable to expectancy effects, is difficult to voluntarily suppress, and is not interfered with by memory load (Jonides, 1981). In contrast, endogenous (central, probabilistic) cues activate the intentional (anterior) orienting system and are associated with expectancy and goals. This orienting is relatively easy to suppress intentionally. When the two systems compete, the anterior system may be able sometimes to inhibit the posterior orienting response to a partial degree (Dankert, Maruff, Crowe, & Currie, 1998).
Within the posterior attention system, parietal cortex lesions result in “neglect” or extinction. That is, when shown an object in both visual fields, patients with these lesions see only the object in the visual field ipsilateral to the lesion. Within the cue paradigm, this leads to excessive cost to orient to unattended locations (very long reaction times). Most evidence to date indicates that in these patients and in unaffected adults, an inhibitory process suppresses awareness of information at the unattended location (Rafal & Henik, 1994). In the patients, this inhibition process is not overridden, and so it is difficult for attention to access those locations.
Furthermore, when SOAs (cue–target delay) are on the order of 800 ms, orienting to the location of nonpredictive exogenous cues is delayed if a target appears in that location, a phenomenon known as inhibition of return (Posner, Rafal, Choate, & Vaughn, 1985). This inhibition persists for some time and has been extensively investigated in its own right (for reviews, see Houghton & Tipper, 1994; Rafal & Henik, 1994). Thus, the paradigm also offers a look at an automatic inhibitory process that occurs in response to reflexive orienting. Although there is debate about whether attention or the oculomotor system itself is inhibited, inhibition of return appears to illustrate an automatic side-effect inhibition in response to attentional processes.
To organize these attention-relevant inhibitory processes, Rafal and Henik (1994) suggested that three distinct inhibitory processes with differing neural correlates can be identified in orienting of visual attention: (a) inhibition of orienting to unattended locations, probably mediated by posterior cortical networks at the temporal-parietal juncture; (b) inhibition of reflexive orienting in the service of a goal, likely mediated by anterior attentional systems in prefrontal cortex; and (c) inhibition of return, apparently mediated by midbrain structures, especially the superior colliculus.
Developmentally, a sensitive period in the development of inhibition of return seems to occur with maturation of the colliculus around 3 to 6 months of age (Rothbart, Posner, & Rosicky, 1994). Evidence also indicates that the posterior orienting system develops between 3 and 6 months of age. Then, beginning in the latter half of the first year and continuing into the second year of life, orienting begins to come into the service of self-regulation (Posner, Rothbart, & Thomas-Thrapp, 1997). Executive override of automatic orienting is observable by 18 months of age (Rothbart, Posner, & Rosicky, 1994). Automatic and covert orienting develops during early to middle childhood sufficiently that individual differences can be reliably measured, although children's reaction times are slower than adults' (Pearson & Lane, 1990).
Application of the paradigm to psychopathology began with studies of adult schizophrenia. Posner, Early, Reiman, Pardo, and Dhawan (1988) suggested a left-brain attentional dysfunction, although these results have proven difficult to replicate. Subsequently, the paradigm has attracted interest extensively in relation to child ADHD (see, e.g., Aman, Roberts, & Pennington, 1998; Carter, Krener, Chaderjian, Northcutt, & Wolfe, 1995; Nigg, Swanson, & Hinshaw, 1997; Novak, Solanto, & Abikoff, 1995; Swanson et al., 1991). Most studies found abnormalities of attention in ADHD, but the pattern of results varied across studies. These studies tended to emphasize attention functioning and not inhibitory processes in their data analyses. The studies varied widely in their methodologies and sampling, and most did not control comorbidity, so perhaps it is not surprising that results and conclusions varied as well. Developmental effects may also contribute to inconsistent findings. Children's reaction times are far more variable than those of adults, making it more difficult to find reliable group differences at the modest cue-effect magnitudes usually observed. Overall, the paradigm's potential for illuminating disinhibition has yet to be realized in studies of psychopathology.
However, closer consideration of inhibitory models in use of this paradigm (cuing cost effects, inhibition of return) should prove of interest. For example, no study has pitted exogenous versus endogenous cuing processes to examine inhibitory effects in child disorders such as ADHD. One way to do so would be to set low-probability invalid exogenous cues (e.g., 20% of trials get a cue, cue is always opposite to where the target will appear) to evaluate whether endogenous (anterior) system processes can successfully inhibit the automatic orienting system when these cues appear. Dankert et al. (1998) used the latter design to show that the ability of the anterior system to suppress the response of the posterior system was weakened in Alzheimer's patients.
Inhibition as an Unintentional Side Effect of Focused Attention? The Case of Negative Priming
A robust and theoretically rich cognitive paradigm surrounds the phenomenon of negative priming (Tipper, 1985). This paradigm was developed specifically to study inhibitory processes in attention. The basic phenomenon can be described as follows. First, a person must respond to one stimulus or stimulus property (e.g., name the red object and ignore the green object). In the subsequent “probe” trial, the stimulus to be named is the same as the one that was ignored in the ignored repetition trial. So, if the person suppressed a (green) chair to name a (red) car, they now are asked to name a (red) chair. In the control sequence, there is no association between the stimuli on the two trials. It takes longer for normal participants to name the object after it has been ignored in the prior trial than when it was not present in the prior trial. This time discrepancy between the control and ignored repetition trials is the measure of inhibitory effect. Normal adults, and possibly children by middle childhood, exhibit longer latencies on the test trials, due to the presumed operation of inhibitory processes on the stimuli that had been actively ignored on Trial n - 1. As documented in recent reviews, this phenomenon is robust across a wide range of task properties, including Stroop color words, pictures, letters, words, digits, novel shapes, and three-dimensional objects, and across multiple response tasks, including naming, manual keypress, same–different matching, lexical decision, counting, and reaching (Fox, 1995; May et al., 1995). Furthermore, the inhibitory function bridges stimulus properties (e.g., from pictures to words naming those pictures), indicating that a cognitive and not simply a perceptual phenomenon is occurring. Extensions of this approach continue to appear (Carlson-Radvansky & Jiang, 1998).
This effect occurs during effortful attention, and researchers are in debate as to whether the inhibitory process per se is effortful or automatic. However, in contrast to the effortful suppression of interfering stimuli and associated motor response exemplified on Stroop-type tasks, it can be argued that the theoretical model here presumes that a relatively automatic side-effect mechanism suppresses activated but irrelevant mental representations in the service of goals. Negative priming may represent “the most direct index” of this mechanism (May et al., 1995, p. 35). However, controversy also remains as to whether inhibition is the underlying process (Milliken, Joordens, Merikle, & Seiffert, 1998).
With this caution in mind, it remains intriguing to consider the implications of this task for psychopathology because if an inhibitory model of the task can be supported, it potentially contrasts with other paradigms measuring behavioral inhibition. In studies of adults, failure of negative priming (indicating presumed weakening of this inhibitory system) has been reported in schizophrenia, OCD, and anxiety (Fox, 1994; for a review, see Fox, 1995). However, negative priming is normal in adults with ADHD (Butler, Huang, Nigg, & Henderson, 2000), indicating that an automatic cognitive inhibitory function may differentiate these disorders.
Developmentally, however, negative priming studies of children are rare; studies of child clinical samples are even rarer. Ozonoff et al. (1998) found normal inhibition effects in older children (mean age 12 years) with mild Tourette's syndrome but impaired inhibition in children with Tourette's syndrome plus either ADHD or OCD. Tipper, Bourque, Anderson, and Brehaut (1989) examined children compared with adults using a modified Stroop experiment with Stroop (color-conflict interference), negative priming (ignored repetition), habituation (repeat ignored), and control (neutral) conditions. They found mixed evidence for the emergence of inhibitory abilities by second grade as detected by the negative priming paradigm. It appeared that the negative priming effect was smaller in children than adults and that effects in children were more difficult to detect becaue of larger distractor intrusion effects. Still, a majority of children showed a negative priming effect (Tipper et al., 1989, Experiment 3). Harnishfeger, Nicholson, and Digby (1993) also found that the inhibition effect was unreliable in young children (first graders) and variable thereafter, although a subset of children showed the inhibition effect consistently. Thus, it appears that the negative priming effect develops inconsistently in early childhood up to first grade, with widely varying rates of development during middle childhood. The effect becomes more robust from middle childhood to adulthood. Maturational delays in inhibitory abilities might be detected with this task in child disorders, but the wide individual differences in rate of development are a complication.
Oculomotor Inhibition Paradigms: Antisaccade and Visual-Delayed Response
Oculomotor recordings constitute a field of their own with regard to the study of inhibitory control, albeit with as much of a measurement as a theoretical basis. The antisaccade task exemplifies this approach. In the usual version of the task, participants must resist the reflexive eye movement toward a newly appearing peripheral target and instead execute a visual saccade (eye movement) in the opposite direction. The participant begins by viewing a central fixation point on a computer screen. A target then appears in either the left or right periphery. Participants are instructed not to look at the target but to move their eyes in the opposite direction. Percentage of saccades in the wrong direction indexes inability to inhibit the reflex, and an increase in correct antisaccade latency (relative to correct prosaccade latency) indexes regulatory demands of successful inhibition. In the delay-saccade task, participants wait a period of time after the cue for a signal and then move their eyes to the remembered location. Percentage of premature saccades indexes the degree of inhibitory problem.
Oculomotor measures such as the antisaccade task and its variants provide an intriguing tool for direct evaluation of inhibitory functions, for several reasons. First, the visual cue effects, the visual guidance systems, and their neural underpinnings are relatively well understood. Further, the overt oculomotor response may escape the ancillary problems in motor and language development that often accompany childhood disorders, such as ADHD, and that can influence performance on many laboratory tasks. Finally, an oculomotor approach allows evaluation of inhibition of a reflexive response as well as of oculomotor inhibition of return. On the other hand, it is unclear that the same brain system inhibits eye movements and other behaviors. In particular, the frontal eyefields, which also participate in spatial attention generally (Gitelman et al., 1999), may be uniquely important in the inhibition of midbrain (collicular) mediated reflexive eye movements (Rafal, Henik, & Rhodes, cited in Rafal & Henik, 1994).
Nevertheless, performance on this task is also disrupted by orbitofrontal lesions in human adults (Guitton, Buchtel, & Douglas, 1985). Moreover, task performance is decremented by increasing memory load, supporting the notion that suppression of the saccade demands executive, prefrontal-type processes (Roberts, Hager, & Heron, 1994). Thus, performance on oculomotor tasks may provide converging evidence of deficits in executive-based inhibitory mechanisms.
Developmental investigation of antisaccade measures is somewhat limited. Preliminary evidence suggests that the task is quite difficult for children (with high error rates even in normal grade-school-age children). Knowledge about the development of oculomotor inhibitory control is likely to increase as the paradigm draws more interest in developmental psychopathology. Oculomotor paradigms, either antisaccade or delay-saccade task, have suggested inhibitory problems in child ADHD (Aman et al., 1998; Ross, Hommer, Brieger, Varley, & Radant, 1994; Rothlind, Posner, & Schaughency, 1991), child OCD (Rosenberg et al., 1997), and schizophrenia (Fukishima, Fukishima, Miyasaka, & Yamashita, 1994). Each of these disorders is associated with apparent deficits in certain kinds of behavioral inhibition. In ADHD, gross motor response to immediate stimuli appears to be excessive; in OCD, the need to repeat grooming behaviors (e.g., washing) cannot be suppressed; in schizophrenia, multiple inhibition deficits occur (e.g., tangential speech is not inhibited during psychosis).
Cognitive Models: Summary and Consolidation
The cognitive approaches are extensive; the preceding review samples several of the available measurement approaches. For example, one could link field dependence (Wapner & Demick, 1991) to inhibitory control, and the kinds of inhibition discussed herein might also be accessed by means of text comprehension (Gernsbacher & Faust, 1995), event-related potential, and connectionist (Dell & O'Seaghdha, 1994) paradigms. Additional theoretical material is also covered by Dempster and Corkill (1999). However, the approaches reviewed here provide a reasonable coverage of major kinds of inhibition studied in cognitive psychology.
An important consideration in applying these approaches to psychopathology is that individual differences and cross-context variation in response to most of these tasks by children with psychopathology are not well studied. It seems likely that effects of these various inhibitory processes would be modulated by factors such as temperamental traits (discussed below in the section entitled Child Temperament), contextual incentives, and arousal or motivation (Sergeant, Oosterlaan, & van der Meere, 1999). For example, performance by schizophrenic patients on the Wisconsin Card Sorting Test (a neuropsychological executive function measure) seems to be influenced by immediate incentives (Vollema, Geurtsen, & van Voorst, 1995). Emotional Stroop phenomena illustrate further that under certain conditions, motivationally salient stimuli can play a role in performance (Derryberry & Tucker, 1994). Further exploration of these effects in conjunction with inhibitory paradigms is important.
Overall, the foregoing illustrates that multiple kinds of inhibitory processes are under examination in cognitive psychology. At the neural level of analysis, these could include systems based in orbitofrontal cortex, anterior cingulate cortex, frontal eye fields, posterior cortex, and the midbrain/superior colliculus (see Table 1). Empirical studies of relations among these measures are few. However, preliminary data suggest that measures such as the Stroop and stopping are not highly intercorrelated (Pennington, 1997) and may tap different processes and that measures such as negative priming and antisaccade inhibition are differentially impaired in different disorders.

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Table 1 Inhibition Systems in Cognitive Psychology and Cognitive Neuroscience
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Several other ways of approaching the task of organizing inhibition constructs in cognition and neuroscience could be considered. For instance, one could look at levels of analysis, such as (a) directly observable neural inhibition, (b) reciprocal inhibition of lower order processing units (e.g., competing cells in visual perception), and (c) higher order reciprocal inhibition (such as that posited between the cerebral hemispheres; Tucker & Williamson, 1984), as well as (d) top-down gating mechanisms (Klein & Taylor, 1994). One could also consider the level of processing (e.g., perceptual, attentional, or output control) or regions of gross brain anatomy (e.g., midbrain, limbic system, cortex). A further consideration is by what criteria to split or lump different kinds of inhibition. If one requires clear double dissociations in neural activation between two tasks, for example, fewer distinctions can be asserted (Casey, in press), whereas if functional differences are the focus, many more can be suggested (Dempster, 1993). For examining developmental psychopathology, a relatively fine-grained set of distinctions deserves consideration. Table 1 therefore gives a relatively detailed breakdown of inhibitory systems, along with plausible neural correlates and differential contextual functions.
The table follows in many respects the suggestions of Harnishfeger (1995) and Rafal and Henik (1994). Harnishfeger defined behavioral inhibition as the automatic or intentional delay of overt motor response (such as a keypress). Cognitive inhibition requires the active suppression of mental contents. Whereas cognitive inhibition entails active suppression of information to exclude it from working memory, interference control pertains to the ability to maintain response performance in the presence of competing, distracting, or interfering stimuli that evoke a competing motor response (Dempster, 1993). In the psychopathology literature, a similar trichotomy was outlined by Barkley (1997a, 1997b) in his theory of child ADHD. A caveat regarding Table 1 is the apparent similarity of oculomotor tasks to motor inhibition. They are assigned a separate cell due to the role of the frontal eye fields in inhibition of reflexive eye movement. However, this latter differentiation is tentative; other frameworks might integrate oculomotor and other motor control systems (Gitelman et al., 1999). Whether multiple processes or a single process expressed in different task contexts is represented could be debated in some other instances also. In particular, motivational processes may deserve more emphasis, as discussed below. Overall, these processes have been examined unsystematically for candidate disinhibitory disorders such as ADHD, OCD, CD, and anxiety.
A complication for Table 1 is that development of these capacities may not be uniform. Failures of interference control are measurable in preschool and beyond, possibly approaching adult levels by fifth grade for some tasks. Behavioral inhibition appears to mature all the way up to early adulthood. At the same time, behavioral inhibition (e.g., stop task) develops earlier than cognitive inhibition (e.g., directed forgetting, negative priming). These developmental effects raise theoretical complications. For one thing, wide variation in the rates of development of some types of inhibition raises the possibility that the structure of types of inhibition may alter with individual differences in development. Therefore, the distinctions shown here may not be empirically demonstrable to an equal degree in early development. At the same time, developmental variation might aid in measuring maturational delays in psychopathology. With this initial taxonomy in mind, I now consider personality and temperament models pertinent to inhibition and psychopathology.
Inhibition in Models of Personality and Temperament
Preliminary Remarks
The relation of personality to temperament (Halverson, Kohnstamm, & Martin, 1994) and the relation of personality to psychopathology (DiLalla, Gottesman, & Carey, 1993; Nigg & Goldsmith, 1994; Watson & Clark, 1994) are areas of active inquiry. Temperament and personality models are related in the following discussion, but important distinctions exist between these. Temperament is usually seen as a more biologically based set of predispositions that contribute to later personality. Personality is usually thought to include more influences of learning history (Rothbart & Bates, 1998). Personality and temperament usually represent a more general level of analysis than is found in cognitive theories, and work in this area has emphasized individual differences rather than normative response. Thus, personality or temperament is another vantage point from which to understand inhibitory processes in psychopathology. However, cognitive and personality approaches are not unrelated. In theory, individual differences in cognitive response and information processing are related to variation in personality (Wallace & Newman, 1997) and temperament (Rothbart, Derryberry, & Posner, 1994). At times, personality or temperament approaches may simply represent a different level of analysis of a system studied in cognitive psychology.
Theories of temperament and personality are too numerous and complex to catalogue fully here (Goldsmith et al., 1987; Halverson et al., 1994; Bates & Wachs, 1994). Emphasis is therefore placed on trait models that have been particularly influential in psychopathology research and that have placed an explicit focus on inhibitory processes. All theorists assume that traits are not fully deterministic. Rather, they are expressed under particular incentive contexts. Given the availability of prior, related reviews of this domain (see, e.g., McBurnett, 1992; Zuckerman, 1991), my summaries are at times brief, with an eye toward comparison in the same article of constructs from cognitive and personality/temperament theories. As with the cognitive models, links to development and to psychopathology are noted whenever possible for each model. I begin with factor-based personality models then move to psychobiological models of personality and to key temperament models.
Factor Analytic Based Personality Models: Two, Three, and Five Factors
H. J. Eysenck and three-factor models.
Three-factor psychometric models (see, e.g., H. J. Eysenck & Eysenck, 1985; Tellegen, 1985) assume that a few “super traits” contain several more context-specific lower order traits. The higher order factors are emphasized here. H. J. Eysenck's (1947) initial model posited three factors: Extraversion, Neuroticism, and Psychoticism. However, for many years, the measurement instrument for this model (the Eysenck Personality Inventory [EPI]) included only Extraversion and Neuroticism. Extraversion referred to being outgoing and sociable, as well as active and impulsive. Neuroticism referred to emotional stability versus a tendency to feel negative emotions such as anxiety and hostility/anger. The traits derived from a top-down factor analytic approach. H. J. Eysenck built on Pavlovian learning principles, and posited that these personality factors were biologically based, temperamental traits. H. J. Eysenck hypothesized that trait standing depends on variation in the activation thresholds by which cortical systems inhibit “arousal” signals from the ascending reticular activating system (Extraversion) and “activation” signals from the limbic system (Neuroticism). Although the hypothesis of cortical arousal differences underlying the dimensions has garnered mixed empirical support at best (Gale & Edwards, 1986), H. J. Eysenck set the stage for contemporary psychobiological models that appeal to inhibitory brain systems (see, e.g., Gray, 1982).
Items for inhibition or impulsivity were originally contained in the Extraversion factor of the EPI. Subsequent criticisms (e.g., Guilford, 1975; for historical review, see Zuckerman, 1991) suggested that in fact the sociability and impulsivity subfactors did not belong together. After some debate, in 1975, H. J. Eysenck (H. J. Eysenck & Eysenck, 1975) published a revised instrument, the Eysenck Personality Questionnaire (EPQ), which added Psychoticism. Most of the impulsivity items from the Extraversion factor were either dropped or moved to the Psychoticism scale. As a result, data from the EPQ and the older EPI were not comparable. Psychometric problems with the Psychoticisim scale (J. Block, 1977) led to a further revision in 1985. Psychoticism was described (H. J. Eysenck & Eysenck, 1985; Zuckerman, 1991) as reflecting aggressive, antisocial, and impulsive characteristics. It is often viewed as an index of behavioral disinhibition versus constraint (Watson & Clark, 1993) or of psychopathy or “impulsive unsocialized sensation seeking” (Zuckerman, Kuhlman, Joireman, Teta, & Kraft, 1993). In contrast, Extraversion primarily reflects sociability, yet it also includes sensation-seeking items, a point targeted in subsequent criticism by Zuckerman (1991).
This basic structure has been replicated in newer three-factor models developed in the United States with more current factor analytic data, using somewhat different theoretical approaches. Tellegen's (1985) instrument measures Negative Emotionality (Neuroticism), Positive Emotionality (Extraversion), and Constraint (low Psychoticism). Watson and Clark (1993) proposed that the three factors be labeled Negative Temperament, Positive Temperament, and Disinhibition (versus Constraint). Correlational studies indicate high convergence across the measures of these theories, suggesting they are probably tapping closely related constructs (Watson, Clark, & Harkness, 1994). Behavioral inhibition seemed to reside most heavily in the third factor (Constraint). However, that factor also contains elements of hostility in some models. Neuroticism, which implicates emotional regulation (Rothbart & Ahadi, 1994), is also relevant to inhibition.
These basic three factors have received extensive application in studies of the relation of psychopathology to personality in adults (Carey & DiLalla, 1994) and limited study in children (Dykman & Ackerman, 1991). Overall, the three-factor models underscore a type of inhibition of complex behavior that refers to inhibiting socially inappropriate responses, as well as impulsive behavior triggered by proximal cues.
The Big Five.
Closely related to the three-factor models is the five-factor approach, which arose from top-down empirical factor analyses of trait adjectives (Digman, 1990). The Big Five factors are Neuroticism, Extraversion/Sociability, Conscientiousness, Agreeableness, and Openness/Intellect. Neuroticism and Extraversion are essentially the same as in the three-factor models, whereas Conscientiousness and Agreeableness combine to form the Psychoticism/Constraint dimension found in the three-factor models (Zuckerman et al., 1993).
From a developmental point of view, data suggest that something like the Big Five can be retrieved from ratings of children at least by early adolescence (Digman, 1994). In a recent study, John, Caspi, Robins, Moffitt, and Stouthamer-Loeber (1994) obtained maternal California Child Q-Sort ratings of 350 children 12–13 years of age from the Pittsburgh Youth Study and retrieved the Big Five factors. Externalizing behavior problems were associated with high Extraversion, low Agreeableness, and low Conscientiousness. Internalizing behavior problems were associated with low Conscientiousness and high Neuroticism. However, John et al. also identified two additional factors: Irritability (correlated with anxious distress as part of Neuroticism) and Positive Activity (correlated with sociability as part of Extraversion). The data were interpreted as suggesting that as of age 12–13, personality has not yet cohered into the Big Five traits seen in adults and that vestiges of early temperament distinctions are still needed to describe personality structure at this age (a point discussed below). A key issue for this literature concerns heterotypic continuity—whether the traits labeled in childhood reflect the same basic processes as in adults.
Further linkage of the Big Five to developmental psychopathology is limited. Huey and Weisz (1997) reported that high Extraversion and low Agreeableness were related to child externalizing problems and Neuroticism to child internalizing, partially replicating John et al. (1994). Also partially replicating the child data, Nigg and Hinshaw (1998) found that paternal high Neuroticism and low Agreeableness were associated with comorbid conduct or oppositional disorders in child ADHD. Maternal Conscientiousness was nonsignificantly lower in mothers of boys with ADHD without CD or oppositional defiant disorder.
Overall, the five-factor approach enjoys strong psychometric support, with growing applicability to child samples. It remains weak in theoretical justification and neurobiological specification. The Conscientiousness factor connotes higher level inhibition of immediate impulses and ability to delay gratification in response to social prohibitions and goals. This has the advantage that, unlike in the three-factor models, Conscientiousness is distinct from hostility; it thus represents a somewhat narrower trait than in the three-factor models.
The J. H. Block and Block two-factor psychodynamic trait model.
J. H. Block & Block (1980) used a Q-Sort rating methodology in a longitudinal developmental investigation of their model. The model, based on ego psychology and Lewin's (1935) ideas of interrelated need systems in the human personality, is relevant to inhibition because of an overarching emphasis on regulatory functions. The fundamental premise of the model is that ego-functions comprise a “boundary system” mediating the relation between the inner needs and the sensorimotor system (behavioral response).
Two core properties of this boundary system characterize Lewin and thus the J. H. Block and Block model. The first is permeability, which J. H. Block and Block (1980) fashioned into the construct of ego control. Ego control functions to contain or fail to contain (inhibit?) psychological needs, tensions, or forces as they would otherwise be expressed in behavior. J. H. Block and Block pointed out that ego control can be maladaptive at both extremes. Extreme undercontrol (an impulsive person), as well as overcontrol (an overly inhibited person), can lead to psychopathology. A problem with this formulation, however, is that an overcontrolled person (such as someone who is anxious or obsessive) might be expected to exhibit poor inhibition in some areas, for example, in controlling anxious or obsessive thoughts. Thus, the explanatory scope of the ego-control factor is a strength, but its generality limits the model's ability to account for distinct types of inhibitory control (a similar point might apply to the preceding models).
The second core feature of the boundary system for Lewin was elasticity, which J. H. Block and Block (1980) fashioned into ego resilience. This pertains to the dynamic capacity of the person to moderate his or her modal level of ego control in either direction as suitable to the context. Better adaptation results as ego resilience increases and poorer adaptation as ego resilience decreases. Low ego resilience (ego brittleness) is associated with inability to respond to changing demands.
Although J. H. Block and Block (1980) theorized that ego control and ego resilience are orthogonal, Eisenberg and colleagues (Eisenberg & Fabes, 1992; Eisenberg, Fabes, Guthrie, & Reiser, in press) argued that medium levels of ego control should be associated with higher levels of ego resilience.
Developmental outcomes have been a feature of research with this model, aided by the California Child Q-Sort (Caspi et al., 1992), which provides a psychometrically robust language by which parents or observers can describe child characteristics. The two major traits have substantial predictive power for long-term adjustment (J. H. Block & Block, 1980). Explaining inhibition in psychopathology would seem to require consideration of both dimensions. The hyperactive child, for example, should have low modal levels of both ego control and ego resilience—he or she being unable to adapt a high level of impulsivity to changes in context.
Because internalizing and externalizing problems are positively correlated in childhood, showing divergence in particular control systems between externalizing and internalizing problems helps to shed light on their etiology. Huey and Weisz (1997) reported that low ego control was related to higher externalizing behavior problems, whereas high ego control was related to higher internalizing behavior problems. That finding supported the contention that failure of a general inhibitory control system (ego control) is maladaptive at both extremes in children. Consistent with the prediction of Eisenberg and colleagues (Eisenberg & Fabes, 1992; Eisenberg, Fabes, et al., in press), Robins, John, Caspi, Moffitt, and Stouthamer-Loeber (1996), using the Pittsburgh Youth Study data set at age 12–13, reported that children high in ego resilience and with moderate levels of ego control were least likely to evidence psychopathology. Children with low ego resilience and low ego control were more likely to have externalizing psychopathology (e.g., aggression, hyperactivity). Children with low ego resilience and high levels of ego control tended to exhibit internalizing psychopathology (e.g., anxiety, depression). These studies bolstered earlier literature suggesting that low ego control (tendency to poorly contain needs and impulses) may contribute to a range of externalizing behavior problems. Overall, the J. H. Block and Block (1980) model has the advantage of conceptual sophistication and psychometric strength. It lacks an articulated psychobiological model to support linkage with developments in neuroscience.
Psychobiological Models of Personality
Gray's psychobiological model.
An active recent line of psychopathology investigation has arisen from the theoretical modifications to Eysenck's model proposed by Jeffrey Gray, a student of Eysenck, on the basis of his research program over the past three decades. At the same time, Gray's animal-based model has been somewhat difficult to access due to its technical complexity and lack of a clear measurement methodology for human research. I make my own attempt to render the theory accessible here (see also Gray, 1991; McBurnett, 1992; Newman & Wallace, 1993).
Working from the principles of classical conditioning and a motivational model developed by N. E. Miller (1959), Gray (1971, 1982, 1991) used existing and new animal research to develop a psychobiological model. Gray has presented the model somewhat differently over time; I follow Gray (1991) for the most part. The first two systems are mutually competitive. The behavioral activation or approach system (BAS) activates motor response to signals for reward (“conditioned appetitive stimuli”) and active avoidance behavior in response to nonreward or punishment. It is mediated neurally by ascending dopaminergic fibers in the reward or appetitive system of the brain; these fibers project from subcortical structures to prefrontal cortex.
The behavioral inhibition or anxiety system (BIS) is of central interest. In a circumplex factor space with Extraversion and Neuroticism on the two axes, this dimension lies between Extraversion and Neuroticism but closer to Neuroticism (Gray, 1991). It thus represents neurotic introversion at the anxious pole. This system in Gray's theory is mediated by the subcortical septal-hippocampal structure and multiple associated structures. It has two modes of operation. In the first mode, “checking,” the hippocampal formation mediates a comparative function of determining whether current stimuli correspond to what was expected and, in turn, estimating what is to be expected next. This checking mode is ongoing (or, more precisely, very frequent). The second BIS mode is the “control” function. This mode is engaged when a triggering cue is detected. The BIS then responds to learned signals for punishment or nonreward, unconditioned fear stimuli, and (controversially) novelty. Then, three behavioral outputs occur: (a) stopping ongoing motor activity (passive avoidance); (b) heightened arousal, giving the next action greater vigor and speed; and (c) enhanced inspection of and attentional orienting to the environment and the triggering stimuli.
Whereas the anatomical centerpiece is the subcortical septal-hippocampal formation, Gray (1971, 1982) worked out the anatomy of this conceptual nervous system in extensive detail. These limbic structures have linkages to orbital prefrontal cortex. Prefrontal cortex is presumed to prepare and/or control motor plans and to feed this information back to the septal-hippocampal circuit (Gray, 1982). The frontal cortex thus may sometimes inhibit the fear response. However, most significant for present purposes is that the BIS entails a bottom-up mechanism for inhibition of ongoing behavior. Activation is equated psychologically with anxiety (Gray, 1982). Connections of the septal-hippocampal system to the thalamus and midbrain enable theorists to begin to integrate cognitive functions of attentional orienting, for instance, with personality attributes using this model (see, e.g., Rothbart, Derryberry, & Posner, 1994; Wallace & Newman, 1997).
The third behavioral system is a fight/flight (F/F) system (Gray, 1991). The F/F system responds to pain (unconditioned punishment) and nonreward (rather than the cues to these, which trigger the BIS). The F/F system generates behavior directed either to escape (active avoidance) or to defensive aggression, depending on the stimulus context. The hypothesized substrate includes the ventromedial hypothalamus and the amygdala. Psychologically, activation is likened to panic. Notably, F/F response is inhibited by the BIS.
A fourth, modulating, system is also important. Gray (1982) posited a nonspecific arousal system (NAS), linked with the ascending reticular activation system, which is positively responsive to activation of either the BAS or the BIS. That is, presence of cues for reward or punishment lead to heightened arousal and alertness. This in turn strengthens the intensity of any behavioral response that follows introduction of motivationally relevant cues. The importance of this system to mechanisms of disinhibition in psychopathology is highlighted in modifications of the model proposed by Newman and Wallace (1993; Wallace & Newman, 1997).
Additional model components should be noted. A “decision mechanism,” which Gray (1982) attributed to activity in the medial hypothalamus, must determine the relative weighting of stimuli for the BAS and BIS. The hippocampal formation (or more specifically, the subiculum; see Gray, 1982) is believed by Gray to maintain a critical “comparator” function. The decision and comparator components create a further opportunity to bridge the model with cognitive psychology. One could speculate that high anxiety would lead to continued cognitive intrusions into consciousness (working memory, conscious attention) from the checking process. These intrusions might reflect poor cognitive inhibition of the automatic checking procedure, such that it interferes with ongoing goal-directed activity. Such an inhibitory process could be related to the anterior (attention-based) interference control processes described earlier.
With regard to psychopathology, Gray (e.g., 1991) suggested that mania (characterized by extreme impulsivity, recklessness, pressured speech, and loose associations) might reflect low BIS activity combined with a very active approach system or that aggressive psychopathy reflects low BIS activity plus high F/F response. Gray (1982) suggested that overactivity of the checking mode of the BIS would lead to symptoms of OCD. Gorenstein and Newman (1980) suggested that dysfunction in the septal-hippocampal behavioral inhibition system might serve as an analogue for psychological mechanisms underlying an array of disinhibitory psychopathology, including substance abuse, alcoholism, psychopathy, and hyperactivity (also see Fowles, 1980). Newman et al. (1987), using a go/no-go task with reward and punishment conditions, have shown that adult psychopaths appear to have dysfunctions under this model, in that when both rewards and punishments are present, they overrespond to the rewards and underrespond to the punishments.
In relation to child disorders, Newman and Wallace (1993) conjectured that child ADHD might be due to a failure in response modulation similar to that found in adult psychopathy. In contrast, Quay (1988, 1997) proposed that impulsive behavior in the ADHD combined type is due to an underactive BIS (reviving the “weak-BIS” model of Fowles, 1980, but applying it to ADHD). Quay proposed that childhood undersocialized aggressive conduct disorder is due to the response-modulation problem (“BAS dominance” when faced with both reward and punishment cues) that Newman and colleagues identified in psychopathy. Although recent data cast doubt on these formulations of ADHD (Iaboni, Douglas, & Baker, 1995; see Nigg, 1999b), several studies have supported the importance of motivational inhibition for child and adult antisocial disorders (see, e.g., Dougherty, Quay, & Ramos, 1993; Newman & Kosson, 1986; Newman, et al., 1987).
Overall, the concept of behavioral inhibition developed by Gray has been generative in psychopathology research because of its detailed psychobiological outline. It suffers from a limited account of the human behavioral phenotype in comparison with other personality models. Lack of a well-established personality trait measure has slowed applications to human behavior (G. D. Wilson, Gray, & Barrett, 1990; but see Carver & White, 1994; Torrubia, Avila, Molto, & Grande, 1995).
Other psychobiological models.
Models similar to Gray's have been proposed subsequently in the psychiatry literature. For example, Cloninger (1987) proposed three genotypic (rather than phenotypic) systems: (a) Novelty Seeking, correlated phenotypically with Tellegen's Constraint factor (negatively; Waller, Lilienfeld, Tellegen, & Lykken, 1991); (b) Harm Avoidance, related to a BIS similar in some respects to Gray's; and (c) Reward Dependence, related to Extraversion (Waller et al., 1991). This model has been used to examine inhibitory problems related to such disorders as alcoholism (Cloninger, Sigvardsson, Przybeck, & Svrakic, 1995) and eating disorders (G. T. Wilson, Heffernan, & Black, 1996). However, empirical studies indicated some problems with the initial trait constructs (Waller et al., 1991).
Siever and Davis (1991) proposed a similar model geared to the study of personality disorders. It includes (a) Anxiety/Inhibition, parallel to Gray's BIS; (b) Impulsivity/Aggression, parallel to Gray's BAS; (c) Affective Instability, reminiscent of Neuroticism; and (d) Cognitive/Perceptual Organization. Empirical linkage of this model to existing personality and temperament models is needed.
Zuckerman (1991) developed his own five-factor, psychobiological model of personality. In its current form (Zuckerman, Joireman, Kraft, & Kuhlman, 1999; Zuckerman et al., 1993), it has the following factors: (a) Sociability is correlated with Extraversion in other major models and is similar in hypothesized neurology to Gray's BAS; (b) Impulsive Unsocialized Sensation Seeking (correlated with Eysenck's Psychoticism, Zuckerman's Sensation-Seeking Scales, and the Big Five's low Conscientiousness) is central to inhibited and disinhibited behavior; disinhibited behavior is accompanied by sensation seeking and poor socialization (perhaps due to failure of avoidance learning); (c) Neuroticism–Anxiety is closely aligned with the Neuroticism dimension in the other major models. It entails frequent experience of negative emotions, especially anxiety; (d) Hostility/Aggression: Like the Big Five, Zuckerman provides a separate dimension for this factor; and (e) Activity Level is preserved as separate from Extraversion, reflecting Zuckerman's greater reliance on temperament models.
With regard to the handling of impulsivity and sensation or excitement seeking, Zuckerman's model has the advantage of combining these related traits into a single major factor. The model provides a theoretical framework for dividing behavioral inhibition problems into several domains: (a) disinhibited sensation seeking (poor behavioral inhibition in the presence of punishment cues), (b) poor control of negative affect, and (c) poor control of hostile-aggressive impulses. However, whereas expression of aggression/hostility may be mediated by a different system than other behaviors, inhibition of these behaviors may be under the control of an anxiety or behavioral inhibition system (Gray, 1982), enabling reduction to two key inhibitory systems.
Child Temperament
Kagan's psychobiological model of behavioral inhibition.
Readers conversant with child development may have noted little coverage of temperament models to this point. In fact, certain child temperament models emphasize inhibitory control. Particularly pertinent to the present discussion is the model of behavioral inhibition developed by Kagan and colleagues (Kagan, Resnick, & Snidman, 1987). After initial work with infants and toddlers, Kagan's group reported follow-ups into childhood and then adolescence, showing modest continuity from early uninhibited temperament to later psychopathology, including Child Behavior Checklist externalizing behaviors (Schwartz, Snidman, & Kagan, 1996). The presentation here relies heavily on a recent description of the model by Kagan (1997). The starting point for the model is the degree of inhibition of behavior in the presence of unfamiliar, novel, or “discrepant” events, measured by laboratory observation in most studies. Discrepant events generate vigilance, quieting of behavior, and orienting to the novel stimulus in young (preschool) children. Kagan, Resnick, and Snidman (1990) and Kagan, Snidman, and Arcus (1998) speculated that higher inhibition is due to low neural activation thresholds in the amygdala and its associated circuitry.
Although in early childhood the eliciting context often used to identify inhibited youngsters is peer interactions, Kagan et al. (1998) argued that distinct systems may mediate social inhibition (response to unfamiliar people) as opposed to withdrawal or inhibited response to challenging or threatening tasks or places. Further, response to punishment is distinguished from response to novelty. Kagan thus differs from Gray in important ways. Kagan's theory of behavioral inhibition pertains to response to the unfamiliar (novelty) and only secondarily to punishment cues, and the hypothesized substrate is anchored in the amygdala rather than the septal-hippocampal structure (J. Kagan, personal communication, May 17, 1998). Because a feature in early childhood is social withdrawal, the construct may overlap at a phenotypic level with low Extraversion (Kagan, Snidman, & Reznick, 1989). However, a qualification is that only a minority of extraverts would be expected to have been uninhibited children as defined by Kagan (J. Kagan, personal communication, May 27, 1999). Thus, social novelty is a typical, but not a necessary, eliciting context for the reactivity Kagan describes. Kagan's reactivity/inhibition is also clearly related to Neuroticism (fearfulness and reactivity), particularly in its emphasis on distress proneness and limbic reactivity under particular contexts.
Thus, behaviorally inhibited youngsters are those who are most reactive to novelty. They show the greatest distress and the largest physiological response. For example, behaviorally inhibited children exhibit higher heart rates as well as greater sympathetic cardiac reactivity than do uninhibited children (Snidman, Kagan, Riordan, & Shannon, 1995). However, they also respond with the greatest behavioral restraint (inhibition). Often, inhibited children are treated as a category rather than treating inhibition as a dimension, as might be done in most temperament or personality models. This approach is supported by observations of apparent qualitative aspects of inhibitory behavior at the behavioral extremes (Kagan, 1998).
Developmentally, the physiological and behavioral measures of this trait do not stabilize until about 1 year of age (Snidman et al., 1995). Overall levels of inhibition decline through middle childhood at least for some children (Asendorpf, 1994), indicating that children who are fearful in early life often become less so with age. However, inhibition classifications remain somewhat stable over time for children who are extremely inhibited or uninhibited. As predicted (Kagan, 1997), early behavioral inhibition predicts anxiety disorders later in development (Albano et al., 1996), and early fearlessness predicts externalizing psychopathology 12 years later (Schwartz et al., 1996).
Kagan's model has the advantage of being based on child observational data. Further study using this model in relation to the development of ADHD, anxiety disorders, and other child disorders is underway in several laboratories. Although it is not a comprehensive model of personality, the specific operational definition of behavioral inhibition (behavioral restraint, increased heart rate) and the emphasis on specific eliciting contexts (e.g., novelty) are advantages that should enhance studies of cognitive processing and temperamental inhibition.
Integrative modeling: Rothbart and Eisenberg.
Rothbart and colleagues have articulated a view of temperament and personality that highlights inhibitory control and attempts to integrate several key personality and temperament conceptions. It thus is a natural final model to discuss. In factor analytic work on infants and toddlers, Rothbart and colleagues (e.g., Rothbart & Ahadi, 1994) identify (a) Positive Affect and (b) Activity Level as factors. Factor analysis of early school-age children (Ahadi, Rothbart, & Ye, 1993; Rothbart, Ahadi, & Hershey, 1994) linked these in a trait labeled approach and thought to have much in common with Surgency or Extraversion in personality models. Rothbart and colleagues equated it with Gray's BAS, suggesting that it is an appetitive system with dopaminergic substrates (see Derryberry & Rothbart, 1997). It is thought to be one of the earliest developing traits, with individual differences apparent by 6 months of age.
Their factor analytic research also identified temperamental (c) Irritability/Anger and (d) Fearfulness. Rothbart and Ahadi (1994), on the basis of prior factor analytic data, suggested that these temperament traits later consolidate into a dimension that they label reactivity or negative affectivity and that is related to later Neuroticism. They argued that this dimension is closely related to both Gray's BIS and Kagan's inhibition construct and thus is associated with hippocampal and amygdala neural subsystems. Behavioral inhibition, when governed by this system, is “motivational” because it is reactive to stimuli for fear and anxiety in the environment. This domain is thought to develop slightly later than the approach system, with individual differences apparent at 8–10 months of age. Both the approach and the reactivity dimensions include important self-regulatory features. They direct behavior and modify it on the basis of contingencies in the environment and emotional response and reactivity to those cues. However, retaining a distinction between fear and irritability may be important; the former predicts internalizing and the latter externalizing behaviors (Rothbart & Bates, 1998).
Finally, Rothbart's temperament work identified a factor for (e) Attentional Persistence, which was related to a trait called effortful control. This is posited to allow for development of the personality trait of Constraint (Tellegen, 1985; Watson & Clark, 1993). Linking this domain explicitly to Posner's attentional model (see discussion of this model in the section Inhibition in the Context of Attentional Orienting above), they argued that this type of effortful control is mediated by frontal, executive systems, in particular, the anterior attentional system (Posner & Raichle, 1994) anchored in anterior cingulate cortex. It thus serves to regulate the development and expression of the other dimensions. The effortful control dimension is late in developing, initially appearing at the end of the first year (Derryberry & Rothbart, 1997). It continues to mature and shape social development throughout early childhood (Kochanska, Murray, & Coy, 1997).
A related formulation has been advanced by Eisenberg and colleagues (Eisenberg & Fabes, 1992; Eisenberg, Fabes, et al., in press), who drew on Rothbart as well as J. H. Block and Block (1980). They emphasized factors for Negative Emotionality and Regulation (a somewhat broader construct than effortful control). Their longitudinal research program provided further empirical support for the basic model proposed by them and by Rothbart. Negative Emotionality and Regulation are empirically distinct factors (Eisenberg, Guthrie, et al., 1997), with differential prediction to psychopathology (Eisenberg, Guthrie, et al., in press) and adjustment (Eisenberg et al., 1998). Further, their data suggest that Negative Emotionality and Regulation may interact in predicting both social adjustment and psychopathology (Eisenberg, Fabes, et al., in press). Like five-factor models, they suggest distinguishing fearfulness/anxiety from irritability/hostility within the Neuroticism-like factor. Further cross-cultural support for this type of two-factor model of inhibitory control comes from work in Finland by Pulkkinen (1996, 1998).
Additional recent longitudinal developmental work has underscored the importance of effortful control or regulation to the development of psychological structures that govern behavioral inhibition in preschool children. In particular, Kochanska and colleagues have shown that early focused attention (age 8–10 months) predicts later behavioral compliance (age 13–15 months; Kochanska, Tjebkes, & Forman, 1998). Further, supporting the work of Eisenberg and colleagues, they have shown that effortful attention contributes to better affective modulation (Kochanska, Coy, Tjebkes, & Husarek, 1998). Finally, the mechanism of these effects may be through internalization of behavioral control in the development of conscience in early childhood (Kochanska, 1997; Kochanska et al., 1997), underscoring the importance of this domain of inhibitory control to social development and, by implication, behavioral disorders.
Overall, then, from the point of view of inhibitory control, Rothbart and Ahadi's (1994) formulation is heuristic and provides a promising way forward for developmental work. It suggests two major inhibition systems in early temperament, one reactive and limbic based and one intentional, goal based, and instantiated in frontal cortex.
Personality and Temperament Models: Summary and Consolidation
This sampling of temperament and personality has bypassed other approaches that place less emphasis on inhibitory control (see, e.g., Buss & Plomin, 1975; Depue & Iacono, 1989; Goldsmith, 1996; Panksepp, 1982; Strelau, 1983). Many of the temperament models are concerned with regulation of emotion (Bates & Wachs, 1994; Campos, Campos, & Barrett, 1989), a topic beyond the scope of the present review. However, this overview reveals the extensive consideration of behavioral inhibition in personality and temperament models.
Despite theoretical differences among the models reviewed, empirical considerations enable substantial consolidation at the phenotypic level. First, an extensive correlational and factor analytic literature shows that the “Big Two” of Extraversion and Neuroticism are essentially the same basic dimensions across the several models described above (see, e.g., Goldberg & Rosolack, 1994; Waller et al., 1991; Watson & Clark, 1992; Zuckerman, Kuhlman, & Camac, 1988; Zuckerman et al., 1993, 1999; also see reviews by Digman, 1990; Watson et al., 1994). Yet it should be noted that for Gray (1991) and Cloninger (1987), behavioral inhibition lies midway between the two main factors. It thus pertains to neurotic introversion (or anxiety, for Gray) versus stable extraversion; preliminary data support this supposition, at least for Gray's model (Newman & Wallace, 1993; Zuckerman et al., 1999). It is also likely that Kagan's inhibition construct is a blend, probably corresponding to introverted neuroticism but specifying a different set of eliciting contexts than does Gray's construct. Some caution is warranted in linking constructs, studied with very different methodologies, from adult ratings of personality, Gray's emphasis on animal research, and Kagan's observations of children (see Kagan, 1998). Nevertheless, Kagan and Gray identified crucial kinds of behavioral regulation that may be described at the facet level within neurotic introversion.
One caveat is that Neuroticism is likely more than anxiety; it also may reflect emotional intensity (Eisenberg, Fabes, et al., in press). Newman and Wallace (1993) thus linked Neuroticism with Gray's NAS, rather than his BIS, emphasizing, as have the temperament theorists, strength of emotional responding. However, factor analyses of questionnaire measures of Gray's BIS show that it also loads with Neuroticism (Zuckerman et al., 1999).
The same studies cited earlier (e.g., Waller et al., 1991; Watson & Clark, 1992; Zuckerman et al., 1988) show convergence in the broad trait of Constraint (although the intercorrelations across measures are not quite as strong as for Extraversion and Neuroticism). At least for the three-factor models, this third factor appears to be substantially the same trait across models, so that low Psychoticism (Eysenck), Constraint (Tellegen), and low Disinhibition (Watson) are the same essential trait. When linked to the Big Five, this third trait is shown to be some combination of Conscientiousness (planful control) and Agreeableness (friendliness, warmth, or hostility; see, e.g., Watson & Clark, 1992; Zuckerman et al., 1993). Conscientiousness corresponds to low Impulsive Sensation Seeking in Zuckerman's model (Zuckerman et al., 1993). The planful control aspect of this trait is of greatest interest to the current article.
Further differentiating Conscientiousness from hostility/agreeableness seems useful (Digman, 1994; Rothbart & Ahadi, 1994; Watson & Clark, 1994; Zuckerman et al., 1993). Rothbart and Ahadi (1994) argued on the basis of developmental evidence that effortful control (which they linked with attentional control) should be related to frontal brain processes. Indeed, as articulated in various theories, this dimension seems to refer, at least in part, to executive control. Yet, by adulthood, this trait is partially related to motivational inhibition as well (Zuckerman, 1991). It is therefore important to bear in mind the close interrelatedness of executive and motivational systems. These may be more readily distinguished in childhood (Rothbart & Ahadi, 1994) and may jointly contribute to adult personality. Table 2 summarizes the phenotypic parallels across models for major traits. Traits that are located in factor space “between” major personality dimensions are placed off center in the table, notably those of Gray, Kagan, and Siever and Davis (1991).

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Table 2 Simplified Structural (Phenotypic) Equivalence of Major Trait Models
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The J. H. Block and Block (1980) model is omitted from Table 2 only because it is not easily reduced to the other traits. In part this is because their traits have overarching regulatory significance (Eisenberg, Fabes, et al., in press). Eisenberg, Fabes, et al. (1996) found that Rothbart's attentional control was related to ego control primarily and to ego resiliency secondarily in parent and teacher reports of children in kindergarten through second grade. Zuckerman et al. (1993) looked at adult self-reports. Ego resilience was related to low Neuroticism and ego (under)control to Impulsive Sensation Seeking, although both traits were also associated with Extraversion. Further data are needed to clarify the relationship of ego control and ego resilience to the inhibitory functions described in Table 2. Portrayal of these relations would likely appear as an oversimplification. Therefore, the J. H. Block and Block model is omitted from Table 2, despite its generative importance.
Despite the overall consolidation offered above, there is reason not to stop at two inhibition-relevant systems (Constraint and Neuroticism). In particular, there is a theoretical distinction between Kagan's model (response to novelty, mediated by the amygdaloid complex) and Gray's (response to punishment cues, mediated by the septal-hippocampal formation; also see Derryberry & Rothbart, 1997). Anatomical differences between these two models may not hold (for instance, the amygdala may play a greater role in fear conditioning than Gray allowed; see Gallagher & Holland, 1994; Whalen, 1998), but the noted phenotypic differences nevertheless pertain. Despite these differences, both kinds of inhibition may be related, in slightly different ways, to Neuroticism and low Extraversion in the three-factor personality space. Gray's construct is related to anxiety (Zuckerman's Neuroticism–Anxiety comes to mind), and empirical data show it fits in the three-factor models as neurotic introversion (Zuckerman et al., 1999). Kagan's inhibited children seemed to exhibit later low Extraversion as well as high Harm Avoidance, a facet of Constraint (Caspi & Silva, 1995). They would be expected to be low on the irritable/aggressive elements of Neuroticism but high on the fearful/anxious elements of Neuroticism (Rothbart & Ahadi, 1994). Caspi and Silva (1995) found that inhibited children were later low on the aggression facet of Tellegen's Negative Emotionality, but further data are needed regarding later anxiety elements of Neuroticism. Both Kagan's and Gray's constructs may thus pertain to neurotic introversion, with the caveat that they pertain to the fearful aspects of Neuroticism. They may be best thought of as different facets, pertaining to different eliciting contexts and, of course, different data sources.
Indeed, developmental data support the phenotypic distinction between inhibition to learned punishment cues (Gray) and inhibition to novelty (Kagan). For example, Asendorpf (1990) longitudinally evaluated 99 German children beginning in preschool over 4 years to Grade 1, using multiple measures across multiple settings. The focus was on social inhibition, based on Kagan's approach/avoidance model of temperament. Observational (videotape) and parent and teacher rating data were gathered at multiple time points for three settings: (a) social inhibition with stranger adult/peer, (b) dyadic play with a familiar peer, and (c) regular classroom free-play (which featured a group that became more familiar over time). Asendorpf found support for a two-factor model of social inhibition, in that inhibition with strangers was different than inhibition in the familiar classroom situation (the latter presumed to index evaluative concerns that develop over time in a familiar group). Inhibition toward strangers was quite stable over time. Yet, despite decreasing correlation between stranger and classroom inhibition scores over time, inhibition in the class setting did not decrease any more than did stranger inhibition, suggesting that new situation-specific processes influenced intraindividual differences in the classroom. This classroom socialization process was related to rates of failure in initiation attempts with peers. Asendorpf thus identified two kinds of social inhibition: (a) inhibition due to unfamiliarity (of person or setting), and (b) inhibition due to social-evaluative concerns (presumably learned from situation-specific rejection experiences). These data suggest that motivational inhibition includes two systems.
When considering psychopathothology more directly, a similar three-part consolidation again emerges in empirical studies of the personality disorders. For example, Livesley, Jang, and Vernon (1998) found that personality disorder symptoms cohered into major dimensions for (a) Emotional Dysregulation, much like Neuroticism but also including specific personality disorder features such as schizotypal cognition and suspiciousness; (b) Impulsiveness, linked with sensation seeking and recklessness in a factor most similar to Zuckerman's (1991) Impulsive Sensation Seeking; and (c) Inhibition, or Social Withdrawal, a trait they termed as consistent with Kagan's inhibition concept. These factors are also reminiscent of those of Siever and Davis (1991).
Taking all of the preceding together, a consolidation emerges consisting of three higher order inhibition-relevant domains, in which the motivational (or reactivity) domain is divided into two key traits. Table 3 summarizes the resultant phenotypic consolidation of the major conceptions of inhibition. The key traits are (a) anxiety/fear (Gray's BIS, or neurotic introversion), (b) novelty response (Kagan's BIS), and (c) effortful control/conscientiousness.

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Table 3 Proposed Consolidated Organization of Inhibitory Control in Childhood
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The last two of the three systems in Table 3 are based on Rothbart and colleagues (e.g., Rothbart & Ahadi, 1994). First listed is a motivational factor that inhibits behavior in bottom-up fashion in response to signals for punishment, associated with anxiety. Although this trait is related to Neuroticism, as well as to Psychoticism (negatively), in the personality literature, the system is best described by Gray's BIS or neurotic introversion. A second motivational system suppresses behavior in response to novelty and is best described by Kagan's BIS, although linkage of Kagan's construct to the others is more tentative. The executive factor pertains to top-down effortful control, attentional control, and planfulness and is supported by the development of prefrontal cortex. This trait is related to Constraint, low Impulsive Sensation Seeking, Conscientiousness, and low Psychoticism. It is best described in childhood by Rothbart's effortful control. Agreeableness or hostility is omitted as a separate inhibitory system following Gray (1982), who argued that inhibition of aggression is governed by the BIS.
Overall Taxonomy and Integration of Cognitive and Personality Approaches
The preceding sections noted empirical support for multiple inhibitory systems in the cognitive literature and for three inhibitory systems in the personality/temperament domain. What about linkage of cognitive and personality domains? A few empirical and conceptual efforts pertain.
Empirical and Conceptual Considerations
Early studies tried to link laboratory and ratings data of temperament constructs and did not directly assess the cognitive models of inhibition reviewed here (Bentler & McClain, 1976; Olson, 1989), although results supported multiple factors. White et al. (1994) studied 400 youngsters from the high-risk Pittsburgh Youth Study. Cognitive measures included the Stroop error score, trailmaking test, and a time perception task. Personality measures included Newman's cardplaying task to assess the Gray BIS, self-report ratings on Eysenck's junior personality scales, and parent ratings using the California Q-Sort. A factor analysis yielded two factors (explaining about 32% of the variance), labeled Behavioral Impulsivity and Cognitive Impulsivity. The behavioral factor included all of the rating scale data (personality measures), and the cognitive factor included all of the laboratory test results. A three-factor solution from these measures would be of interest.
These early studies could be criticized for failing to make distinctions among the types of inhibition reviewed here and/or for use of suboptimal cognitive or personality measures. Problems with method variance in these studies further limit their utility. That is, laboratory scores went on one factor and ratings data on another factor (see, e.g., White et al., 1994), making it difficult to determine whether the two factors were really method factors or construct factors. Greater success was obtained in more recent studies. For example, Kochanska and colleagues (e.g., 1997) showed that parent ratings of inhibitory control using Rothbart's Child Behavior Questionnaire were correlated with laboratory measures of Stroop-like interference control using an age-appropriate shape-matching task in 5-year-olds.
Equally promising were results attained by Kindlon, Mezzacappa, and Earls (1995), who looked only at cognitive-laboratory measures in a sample of 48 normal and 88 behaviorally disturbed children (nearly all boys). Although they did not report the variable intercorrelations, a factor analysis suggested two factors: (a) Executive Inhibitory Control (Stroop words and colors correct, Trailmaking B, stop task, and examiner redirection to task during testing) and (b) Motivational Inhibitory Control (Newman cardplaying task cards played, go/no-go avoidance learning). Follow-up study of 42 children (half with clinical problems, most boys; Mezzacappa, Kindlon, Saul, & Earls, 1998) provided apparent physiological support for these two factors. Because limbic structures, by way of the hypothalamus, influence the pituitary-adrenal axis and thus peripheral sympathetic nervous activity (Fowles, 1980; Kagan et al., 1990), measures of peripheral physiology can help to verify the idea of a limbic-based inhibitory system (Fowles, 1980). In Mezzacappa et al.'s (1998) data, executive control was associated with vagal modulation of high-frequency heart rate variability, and motivational control was associated with sympathetic modulation of low-frequency heart rate variability. Results support temperamental models (Gray, 1982; Kagan et al., 1987) in linking sympathetic cardiac modulation to motivational control.
These provocative data also support the possibility that executive and motivational inhibition systems are dissociable empirically. Although limbic arousal may inhibit motor behavior in response to immediate fear, novelty, or both, frontal systems would inhibit motor behavior and autonomic response in response to longer term goals (Rothbart, Derryberry, et al., 1994; for a somewhat different account of these systems, see Casey, in press). However, because the executive systems also probably play a role in inhibition and regulation of motivational response, these systems would be partially overlapping and reciprocal in influence.
Yee and Vaughan (1996) attempted to relate social/personality and cognitive constructs of inhibition to one another. They noted that Tipper and Baylis (1987) found a significant correlation between weak negative priming (suggesting ineffective suppression) and questionnaire self-report of cognitive intrusions on Broadbent's Cognitive Failures Questionnaire (CFQ). More recently, Kramer, Humphrey, Larish, Logan, and Strager (1994) replicated that correlation in a study of older adults, while simultaneously failing to find an association between stop task performance and either negative priming or the CFQ. Logan, Schachar, and Tannock (1997) reported that poor inhibition on the stop task was correlated with high scores on the Eysenck impulsivity scale. These single-instrument results for adults suggest that selected self-report personality measures and well-chosen cognitive measures of inhibition can be linked; they also provide empirical support for the earlier distinction between behavioral (motor, stop task) and cognitive (attention, negative priming) inhibition.
However, context effects may complicate these sorts of studies. Yee and Vaughan (1996) pointed out that a high degree of life stress is correlated with poorer performance on selective attention tasks in several studies. Perhaps because of the relation of distraction to stress, models that attempt to account for the effect of distraction (cognitive interference) on personality and task performance have pertained mainly to anxiety (M. W. Eysenck & Calvo, 1992; Revelle & Loftus, 1990). These models assume that anxiety and its accompanying poor control of mental interference take up limited resources needed for efficient processing in working memory of controlled (executive) tasks. It is unclear, however, that such difficulties are specific to worry or anxiety. For example, ADHD adults reported high rates of off-task thoughts during an experimental procedure (Shaw & Giambra, 1993).
Development dynamics must be considered as well. Despite marked continuities in trait standing (Caspi & Silva, 1995), personality and temperament also change with development, more so for some individuals. For example, Kagan's behavioral inhibition declines through childhood for more resilient children (Asendorpf, 1994). In adulthood, Neuroticism, Extraversion, and Openness decline, and Agreeableness and Conscientiousness increase (McCrae et al., 1999). Such changes could impact the structure of relations among traits. In the cognitive domain, developmental data were reviewed by Dempster (1993). He defined interference control as the suppression or inhibition of “stimuli or associations that are not relevant for the task at hand” (Dempster, 1992; p. 51). Dempster (1993) argued that the development of different types of interference control occurs at differing rates, varying with regard to temporal and formal task characteristics. For example, the ability to control motor interference (such as is observed on the A-not-B task in infants) increases rapidly from birth to age 5 then improves gradually to adulthood. In contrast, sensitivity to perceptual interference remains substantially unchanged until about age 5 and then begins to improve steadily.
Summary and Comment
Studies using well-selected cognitive measures and studies of adults have yielded the best results to date. From the point of view of a taxonomist who prefers to split rather than lump concepts, existing data suggest overall that (a) by elementary school age, it is reasonable to distinguish effortful behavioral (motor) inhibition, cognitive (working memory) inhibition, and automatic inhibitory processes in attention; (b) two higher order behavioral inhibitory systems that emerge in laboratory data are the executive (suppression of behavior or thought in the service of a later goal) and the motivational (suppression of behavior in response to immediate incentives, fear, and anxiety). Further, it appears that (c) two motivational inhibitory control systems are distinguishable, one based on social novelty and the other on learned social context demands (or punishment cues). It appears to be difficult but not impossible to integrate cognitive tasks with temperament ratings in children and even more feasible in adults, although a full range of measures and approaches has yet to be examined in the same study in children or adults. Further evidence about the structure of these inhibition measures is still needed, including quantitative genetic data and further imaging data. However, on the basis of data available at present, a suggested organization of these inhibitions can be advanced.
A Proposed Integrative Taxonomy of Inhibition
It is often suggested that development of frontal cortex corresponds to development of inhibitory control broadly defined (see, e.g., Bjorkland & Harnishfeger, 1990; Schore, 1996), and clinical reviews have catalogued a variety of measures but without much cross-domain integration (Milich & Kramer, 1984; Zaparniuk & Taylor, 1997). It therefore seems useful to suggest a more specific, integrated taxonomy of inhibitions for developmental psychopathology.
The taxonomy in Table 4 combines the organization of inhibition in cognitive and personality approaches, respectively. The distinctions in the table have at least preliminary empirical support. It would be possible to argue for fewer (Casey, in press, suggests a single system in basal ganglia) or more (Dempster, 1993, adds multiple domain-specific processes; Kagan, 1998, also suggests more distinctions) basic inhibition processes. However, the taxonomy in Table 4 preserves those distinctions that seem the most potentially important to psychopathology research, when doing so can be supported by at least some empirical evidence. The general conception outlined here is similar in some ways to that described by Derryberry and Tucker (1994), who pointed out that reciprocal influences of limbic and frontal cortical systems are a hallmark of many current models of self-regulation. The current proposition assumes that limbic and cortical inhibitory systems work in concert to regulate behavior but that each can have an inhibitory influence on the other under particular context conditions. The proposal in Table 4 posits eight inhibition processes, in three fundamental classes, relevant to psychopathology research. I comment on each of these in turn.

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Table 4 Heuristic Taxonomy of Inhibition Constructs and Measurement Paradigms
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Executive inhibitions.
Four types of inhibition fall under the rubric of executive inhibitory control. Definitions of executive control vary across neuropsychological (Lyon & Krasnegor, 1996) and computational (Meyer & Kieras, 1997) models and could be the focus of an entire review in their own right. They can be defined here as processes for intentional control or suppression of response in the service of higher order or longer term goals (as opposed to immediate stimulus incentives). Data and theory (Rothbart, Derryberry, et al., 1994) suggest that this system is anchored in part by anterior cingulate cortex and associated subcortical-thalamic connections. Close anatomical connections with motor, language, and memory systems (Rothbart, Derryberry, et al., 1994) may be differentially activated by different task demands (e.g., motor interference control vs. cognitive inhibition). However, I advocate a distinction between (a) the interference control and suppression functions in attention reflected in activation of the anterior cingulate (Cabeza & Nyberg, 1997) and (b) the disinhibition of social and motor control that seems related to impairment in lateral orbito-prefrontal cortex or its associated subcortical connections (Casey et al., 1997; Fuster, 1997; Guitton et al., 1985). Capturing this distinction in the personality domain may require attending to either specific lower order facets of the superfactors or combinations of them.
It is unclear whether controlled cognitive inhibition (protecting working memory) is subserved by systems the same as or different than those responsible for executive control of motor response. However, keeping this distinction seems important because, in psychopathology research, failures in cognitive inhibition are often linked with anxiety and internalizing problems (Yee & Vaughan, 1996), whereas problems in behavioral inhibition are usually linked with externalizing psychopathology such as ADHD (Barkley, 1997a; Oosterlaan et al., 1998).
In relation to personality, the executive processes may be unified under a higher order personality dimension related to the Constraint/Conscientiousness constructs described earlier and perhaps best specified in childhood by Rothbart and Ahadi's (1994) effortful control. Although effortful control is usually associated primarily with attentional control, it is also seen as relating to executive motor control as defined here (M. K. Rothbart, personal communication, September 27, 1999). However, empirical linkages between these levels of analysis need further examination. For example, it remains to be seen whether combinations of personality traits would better identify individuals showing impaired function on some of the cognitive tasks. A further issue is whether lower order components of personality models, such as the deliberation or discipline facets of Big Five Conscientiousness, the control facet of the Tellegen (1985) Constraint factor, or the various kinds of reciprocal inhibition built into Gray's model, could be linked better with the relatively molecular level of analysis represented by the executive cognitive measures (Livesley et al., 1998).
With regard to psychopathology, the executive inhibitions seem to be relevant to ADHD, OCD (perhaps an automatic inhibitory process as tapped by negative priming), and schizophrenia. However, cognitive inhibition is also relevant to anxiety conditions and may form a bridge to both automatic and motivational inhibitions as discussed below.
Motivational inhibitions.
The second class of processes proposed arise from the motivational-based models of temperament and personality, which can be linked with selected cognitive models that emphasize emotionally salient stimuli such as the Newman go/no-go task. Whereas the domain of motivated behavior is large (see Derryberry & Tucker, 1994), the focus here is motivated inhibition of behavior or thought. As defined here, motivational refers specifically to bottom-up (limbic->cortical) interruption of ongoing behavior or suppression of behavioral response due to fear or anxiety in the presence of immediate novel social situation or cues for punishment. Of course, one could put too fine a point on the distinction between the executive and motivational systems as well. For one thing, broader conceptions of motivation are possible (Derryberry & Rothbart, 1997). The anatomical systems listed are interconnected (Casey, in press), and goals in an executive sense seem reminiscent of rewards in a motivational sense.
A further issue is whether these motivational inhibitions represent effortful or automatic processes. Experientially, they might sometimes seem effortful or automatic. I suggest that executive systems can sometimes override (effortfully) the fear/anxiety-based inhibition systems. Overall, the data reviewed earlier (Mezzacappa et al., 1998), along with recent theoretical proposals and developmental data (Rothbart, Derryberry, et al., 1994), support the executive–motivational distinction as defined here. Data (see, e.g., Asendorpf, 1990) also support the proposal that at least two kinds of motivational inhibitory function exist and respond to different incentive contexts. Cognitively, they might be accessed by executive tasks with motivational conditions attached to them (Newman's go/no-go task, the emotional Stroop) or possibly by other automatic attentional processes as noted below. In relation to higher order personality traits, Gray's behavioral inhibition is usually seen as a combination of high Neuroticism and low Extraversion. Although evidence for linking Kagan's inhibition to higher order personality traits is less clear, I suggest here that Kagan's behavioral inhibition also reflects elements of low Extraversion and high Neuroticism. The two traits differ at a lower order level of analysis, with regard to eliciting contexts and neural systems. With regard to psychopathology, Gray's BIS seems important for anxiety on one end of the spectrum and psychopathy (remorseless antisocial behavior) on the other. Kagan's BIS may have added importance for social withdrawal.
Automatic inhibition.
Table 4 also notes the existence of exemplar automatic inhibitory processes that pertain to the operation of attention and may be relevant for psychopathology. From a measurement point of view, one could distinguish attentional and oculomotor inhibition of return, providing automatic counterparts to effortful cognitive and motor inhibition, respectively. However, both inhibitions of return are mediated by midbrain and thalamic structures, so, for the sake of parsimony, they are lumped together in Table 4.
The role of the posterior attention system in inhibiting unattended locations is of interest for some disorders (e.g., the inattentive subtype of ADHD [Aman et al., 1998] and anxiety conditions). The relation of personality to the automatic inhibition domain remains unclear, but higher order personality traits might be pertinent. For instance, Wallace and Newman (1997) argue that Neuroticism is related to the automatic orienting of attention through subcortical and midbrain effects on both motivation and attention (the relevant attentional system is assigned to posterior cortex in Table 4, but the posterior attention system is also known to involve subcortical structures; see Gray, 1982; Posner & Peterson, 1990; and the earlier discussion of attention systems). Derryberry and colleagues (Derryberry & Reed, 1994; Derryberry & Tucker, 1994) provided a rich discussion of ways in which anxiety and fear alter both the breadth and the direction of attentional orienting, implicating the posterior orienting system. The role of anxiety systems in automatically filtering attention (e.g., on the emotional Stroop) provides further evidence that Neuroticism, or Rothbart's reactivity dimension, may play a role in automatic attentional allocation.
Thus, motivational and automatic inhibitory processes often work in concert. However, at other times, they operate separately (e.g., in cases of neglect following stroke). Therefore, despite their association in some contexts, they remain distinguished in Table 4.
Comment and critique.
Consideration together of cognitive (relatively molecular) and personality (relatively molar) approaches to inhibitory control invites efforts to integrate levels of data analysis and measurement domains. Both levels of analysis are in fact included in several recent theoretical proposals that have attempted to apply an individual differences approach to cognitive or psychobiological models (see, e.g., Logan et al., 1997; Rothbart & Ahadi, 1994; Wallace & Newman, 1997). Furthermore, others have suggested reciprocal interaction of cognitive and emotional regulatory systems (Derryberry & Tucker, 1994; G. A. Miller, 1996). Yet surprisingly little recent research on inhibition in developmental psychopathology has considered more than one of these levels of analysis together across multiple disorders. Although such efforts face the challenges of finding cross-method convergence of measures (White et al., 1994), of isolating inhibitory processes in multifactorial cognitive and personality measures, and of providing further evidence as to the validity of some of the distinctions proposed (e.g., motivational vs. executive systems), it is to be hoped that more such efforts will ensue.
Developmental considerations could influence the taxonomy as presented here. Different components of emotional regulation may become important with development, such as the distinction between anxiety and hostility (Rothbart & Ahadi, 1994; Zuckerman et al., 1993). A further issue is that because these inhibition systems likely develop at somewhat different rates, developmental alterations in one system may influence development of another. Thus, motivational inhibition systems may develop earlier than executive systems. As a result, disruption in development of the motivational system might be expected to lead to correlated problems in development of executive control (see Derryberry & Rothbart, 1997, for more discussion of this idea). Likewise, weak development of attentional control could subsequently interfere with consolidation of emotion regulation processes.
Developmental issues also complicate measurement because not all paradigms are equally accessible at all stages in development. The translation from early precursor to later emerging processes is still a work in progress in the field. This is particularly an issue for cognitive models in the transition from preschool to elementary school age. For example, behavioral inhibition as measured by the stop task appears to be reliable beginning at around age 7. The situation is similar with interference control as measured by the Stroop, although recent efforts suggest it is possible to trace the heterotypic continuity of these constructs. For instance, similar regions of dorsolateral prefrontal cortex appear to be related to the A-not-B error in infancy (Bell, 1998), to stimulus-incompatibility errors in preschool and early childhood (Diamond et al., 1997), and to Stroop performance in adulthood (Cabeza & Nyberg, 1997). The situation is a bit clearer in the temperament domain, where continuities between measures of inhibition to novelty as defined by Kagan appear to be measurable beginning by about 1 year of age. However, continuity between effortful control measures in childhood and in adulthood is still under evaluation.
Looking Ahead: Disinhibition in Developmental Psychopathology
General Implications of the Inhibition Taxonomy
What are the implications of a relatively broad taxonomy of inhibitory processes for research in developmental psychopathology? The outlines of a few implications are briefly noted by way of conclusion. One implication is that it is not sufficient for theories of a particular disorder to address only one type of inhibition, without explaining theoretically why that particular understanding of inhibition is most pertinent for a given disorder. A second implication is that more precision is called for in defining the system thought to be impaired in a given disorder. For instance, the theories of child ADHD refer to behavioral inhibition (Barkley, 1997a, 1997b; Quay, 1988, 1997). However, distinctions between motivational and executive systems, between cognitive and behavioral, or between motoric and other types of inhibitory control are imprecisely drawn. A similar issue arises for child anxiety disorder: Current theories emphasize behavioral inhibition in the temperamental sense intended by Kagan and colleagues (see Albano et al., 1996, for a review), yet one might also find dissociable but additional deficits in an executive system or systems for cognitive interference control (M. W. Eysenck & Calvo, 1992).
A third implication is that theories of inhibition in different disorders need to be brought into greater empirical and conceptual contact. To pursue the prior example, theories of a deficit in the motivational inhibition system in ADHD (Quay, 1988) imply that anxiety and ADHD would be unlikely to co-occur. Likewise, theories of excess behavioral inhibition in child anxiety imply that externalizing problems should be unlikely in that group. Yet internalizing (e.g., anxiety) and externalizing problems are positively correlated (Achenbach, Howell, Quay, & Conners, 1991). How can integrated theories of inhibitory deficit account for such comorbidity?
In answering such questions, a refined nosology might link breakdowns in particular inhibitory systems with more homogeneously defined psychiatric phenotypes than are currently recognized. For example, perhaps a homogeneous subgroup of anxiety patients suffer cognitive inhibition problems, certain children diagnosed with ADHD have deficits in executive motor inhibition, and antisocial children and adults have deficits in the motivational inhibitory system. Before such a nosology would be satisfactory, empirical research making use of a taxonomy such as this one would need to look at multiple types of inhibition constructs and multiple disorders and to address two fundamental issues in the taxonomic enterprise: specificity and differential deficit.
Specificity
Specificity pertains to the question of which, if any, inhibitory deficits are unique to a particular disorder (e.g., ADHD, overanxious disorder, CD). The issue is that if an inhibitory deficit is not specific to ADHD, for example, it cannot be a necessary and sufficient cause of the disorder, and its consequent importance in etiological theories declines. Theories of inhibition in ADHD, anxiety, CD, and other disorders do not at present fully meet this challenge.
For instance, this article has noted data suggesting that stop inhibition is impaired in ADHD and CD but remains intact in anxiety disorder (Oosterlaan et al., 1998). Negative priming is impaired in schizophrenia, OCD, and anxiety but spared in Tourette's syndrome (a tic disorder; Ozonoff et al., 1998). Motivational inhibition may be particularly impaired in psychopathy and severe antisocial conditions (Newman & Wallace, 1993) but needs more study in other disorders to show specificity. Most crucially, several kinds of inhibition may be impaired in multiple disorders, including Stroop-type interference control (ADHD, schizophrenia) and the oculomotor antisaccade task (ADHD, OCD; Rosenberg et al., 1997; Rothlind et al., 1991). Other deficits may be more disorder specific (e.g., cognitive interference control and anxiety-spectrum conditions). To clarify matters, control of comorbid symptoms should become more routine (see, e.g., Nigg, Hinshaw, Carte, & Treuting, 1998; Ozonoff et al., 1998), and comparison of several disorders on several kinds of inhibition is needed (see, e.g., Casey, in press; Pennington, 1997).
Differential Deficit
The related issue of differential deficit is equally critical. It pertains to whether a deficit in inhibition can be discriminated from a generalized performance deficit or, alternatively, whether a deficit in one type of inhibition can be distinguished from a deficit in another type of inhibition. Chapman and Chapman (1978, 1989) best described the problem, which they discussed in relation to schizophrenia. The problem has two parts. First, deficits in specific theorized functions must be demonstrably independent of the general poor performance often observed in clinical groups on most laboratory tests. Second, and more crucial, differences in task performance do not guarantee differences in true scores unless tasks are psychometrically adequate to this inference. Artifactual findings can appear because of differences in the psychometric characteristics of the two tasks, such as differences in reliability, true score variances, or average item difficulty (the last, of course, influences the former two). Researchers in child psychopathology also have noted these issues (Sergeant & van der Meere, 1990). Several remedies are possible. At the performance level, more attention to Task × Group interactions rather than to group main effects is called for in psychopathology studies. Equivalent reliability and variance are not so easy to achieve, though. Thus, the Chapmans suggested additional, more sophisticated remedies (Chapman & Chapman, 1978). Although the issue of task difficulty per se might be applied more readily to cognitive tests than to personality measures, the issue of equal scale reliability and variance generalizes to personality ratings scales as well. An argument that one but not another type of inhibitory dysfunction characterizes ADHD versus CD, or the inattentive versus the combined type of ADHD, or ADHD versus anxiety disorder needs to address these issues.
Conclusion
This article aimed to bring into the same discussion cognitive and personality approaches to inhibition that might best pertain to developmental psychopathology. A “splitter” viewpoint was adopted to outline eight kinds of inhibition across different tasks and measurement paradigms that psychopathologists should consider. These can be grouped under the broad rubrics of executive, motivational, and automatic inhibitory processes. A taxonomy was suggested for organizing the most salient of these various kinds of inhibition for purposes of research in developmental psychopathology. Personality and cognitive models themselves have an unclear degree of overlap. They represent two different levels of analysis in most applications and thus, two vantage points from which to approach the problem of inhibitory psychopathology. However, most progress is likely to ensue when these approaches are studied together, so that the extent one inhibitory construct is distinct from another in reflecting a particular psychopathological deficit can be clarified. In addition to studying more than one measure of inhibition, investigators are encouraged to study more than one disorder (or at least, comorbid and noncomorbid forms of a disorder) to enable examination of the specificity of a hypothesized deficit to a given syndrome. Existing theories of disinhibition in psychopathology address only a subset of the inhibitions that may exist. Thus, systematic empirical study of these multiple inhibitions is needed to clarify (a) to what extent these different inhibition functions are in fact different processes and (b) the extent of inhibitory deficit in particular disorders. Clinical and basic science research thus have a potentially useful complementarity in answering these questions. Once inhibitory deficits in a given disorder are mapped, the real work of determining the causal role of inhibitory deficits in the disorder can begin. Such work must address the two fundamental issues of specificity and differential deficit. At that point, the field will discover to what extent the inhibition construct can indeed account for the development of specific kinds of psychopathology.
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