Dr. Joseph Newman is Professor Emeritus in the Department of Psychology at the University of Wisconsin-Madison, where he served as Director of Clinical Training and Chair before retiring in 2014. He was the inaugural President of the Society for the Scientific Study of Psychopathy and a recipient of the R. D. Hare Lifetime Achievement Award. His research highlighted the crucial role of attention in moderating the behavioral, emotional, and brain abnormalities associated with psychopathy. For access to his publications, visit https://www.researchgate.net/profile/Joseph-Newman-2
Question 1. How did you get involved in psychopathy research?
I did not start out with an interest in psychopathy. As a graduate student at Indiana University, I took a wonderful course in psychopathology taught by Dr. Richard Rose. He included a brief section on psychopathy and assigned Robert Hare’s (1970) short but masterful book (Psychopathy: Theory and Research) on the topic.
At the time, my primary interest was in the Learned Helplessness Model of Depression. Though I would have preferred to study learned helplessness depression in humans, Dr. John Kelsey, was investigating learned helpless in laboratory rats. Ethan Gorenstein (a fellow graduate student) and I volunteered to assist him run his experiments in order to learn more about the topic. Dr. Kelsey was a knowledgeable and enthusiastic teacher. He met with us regularly to discuss research on learned helplessness and related topics. One of those topics concerned the effects of creating lesions in the septal-hippocampal region of rats. I was especially interested in this topic because I had learned that rats with septal lesions were resistant to learned helplessness while taking an undergraduate course from Dr. Earl Thomas at Haverford / Bryn Mawr College). As luck would have it, John Kelsey was an expert on the effects of limbic system lesions, including the septum. When I asked about the consequences of lesioning the septum in rats, he immediately described a list of characteristics and laboratory anomalies that corresponded to what I had just learned about psychopathy in Dr. Rose’s course and Dr. Hare’s book. I promptly began reading everything that I could on the topic. Because the year was 1976, articles were not available on the Internet, but Dr. Kelsey gave me access to his small room full of reprints and books on the topic.
In 1980, Gorenstein and I co-authorized an article that summarized the implications of our thoughts and readings for psychopathy and other syndromes of disinhibition, which we regarded as a new perspective and model for research.
Question 2. Can you describe what are “syndromes of disinhibition”?
As already described, my interest in psychopathy was shaped by our animal model. Theory and evidence regarding the consequences of septal lesions provided a road map for understanding the less developed literature on performance anomalies in psychopathy. Animals with septal lesions and psychopathic people display overlapping problems in a variety of domains (for example, both show failures to inhibit punished responses, failure to delay gratification, and lashing out with violent behavior in certain situations). However, it was generally accepted that the common core underlying their abnormal laboratory behaviors was a failure to inhibit dominant (i.e., pre-potent) responses, which we chose to label “disinhibition” (see Gorenstein & Newman, 1980 or Patterson & Newman, 1993 for details.)
Though Gorenstein and I emphasized the implications of our model for psychopathy, we noted that disinhibited behavior was also prominent in other clinical syndromes, including early-onset alcoholism and other substance abuse, antisocial personality disorder, attention deficit hyperactivity disorder, histrionic personality / somatization disorder, and impulsivity as manifested by neurotic extraverts. Moreover, there was evidence that all of these problems ran in families and, thus, might be genetically related as well as behaviorally overlapping. In other words, our initial assumption was that the various syndromes of disinhibition shared a common predisposition and that the ultimate expression of the predisposition was dependent on other genetic and environmental factors. After a decade of research on this topic, however, we proposed that the essential problem in psychopathy was different than the one underlying the other syndromes of disinhibition (see Patterson & Newman, 1994 for details). While it seems true that all of the syndromes of disinhibition are characterized by a failure to inhibit dominant responses, the underlying psychobiological mechanism in psychopathy appears to differ from the one underlying other syndromes of disinhibition. For this reason, our more recent publications distinguish between psychopathy and externalizing psychopathology and highlight the distinct problems that contribute to the dysregulatory psychopathology characterizing these syndromes.
Question 3. What role does cognition play in understanding psychopathy?
In our view, psychopathy is associated with a fundamental cognitive deficit that parallels, and helps explain, their behavioral style. In contrast to non-psychopathic individuals, psychopathic individuals do not stop and reflect when they receive negative feedback. For example, when their behavior results in punishment or fails to achieve an expected goal–suggesting that something important has changed or is poorly understood and needs correcting–they remain focused on their original goal-directed strategy rather than altering their focus to reflect on the negative consequences. Consequently, they do not benefit from the negative feedback or learn to identify circumstantial cues that might help them predict punishment and avoid negative feedback in the future. Furthermore, because psychopathic individuals often fail to develop the kinds of associations that usually enable others to evaluate the potential consequences of their behavior, they are prone to poorly considered impulsive action. This view of the cognitive deficit in psychopathy is primarily attention-based: The information guiding behavior in psychopathy is impoverished because psychopathic individuals fail to attend to cues that would otherwise provide a meaningful context for evaluating and regulating their behavior.
Question 4. What is the response modulation hypothesis? Can you describe one implication this theory has for intervention?
The essential features of the response modulation hypothesis are: (1) that an attention deficit interferes with the ability of psychopathic individuals to process potentially important contextual cues and (2) that this difficulty processing diverse aspects of a situation is the primary cause of their fearless, callous, and impulsive behavior. As noted above, the failure of psychopathic individuals to process contextual information typically occurs when they are engaged in goal-directed behavior (as when they fail to inhibit reward seeking behavior that results in punishment). However, our research indicates that the deficit is much more general and likely to occur whenever the contextual information is inconsistent with their primary focus of attention.
A notable aspect of the response modulation hypothesis is that psychopathic individuals do process inhibitory, emotion, and other contextual cues when they are consistent with their primary focus of attention. Indeed, considerable research shows that their significant laboratory deficits involving response inhibition, emotion processing, and even amygdala activation may be eliminated by redirecting their attention to the crucial stimuli. That fact that their deficits may be ameliorated by manipulating their focus of attention suggests that the capacity for inhibiting inappropriate responses and reacting to emotion cues is largely intact, though underutilized. Moreover, to the extent that psychopathic individuals habitually fail to attend to such cues, their internalized representations of such information are likely to be less developed (that is, weaker and less elaborated) and, thus, less likely to influence their reactions, decisions and ultimate behavior.
Treatment Implications: Because the response modulation hypothesis identifies a specific deficiency as the key variable moderating clinical symptoms (for example, impulsive / irresponsible behavior, fearlessness, lack of empathy, lack of insight), it also provides a target for clinical interventions. In light of the fact that laboratory manipulations that redirect attention to crucial environmental cues ameliorate behavioral and affective deficits in psychopathy, it is plausible that clinical interventions that use attention training and associated cognitive remediation might bring about meaningful changes in their processing of affective/inhibitory cues and reduce their impulsive / antisocial behavior (see Baskin-Sommers, Curtin, & Newman, 2015).
Question 5. Considering research is generally ahead of application in the field, what is one improvement in the field of psychopathy that you hope to see take place over the next five to ten years?
If we assume that successful treatment and prevention depends upon specifying the underlying problem/s in psychopathy, then it is essential to identify psychopathic individuals who share an underlying problem and distinguish them from other individuals displaying similar symptoms. This idea is not new and was prominent in Cleckley’s (1976) book on psychopathy. It was also prominent in early models that distinguished primary psychopathy from secondary psychopathy (that is, psychopathy which was considered to be secondary to exaggerated emotional reactivity) and from subcultural delinquents (i.e., psychopathic behavior reflecting social contexts that impede normal socialization).
Before I retired, my lab published a number of papers that emphasized a distinction between psychopathy and other externalizing problems. In our view, most externalizers are characterized by high emotional reactivity and situation-specific deficits in cognitive control that stem from this reactivity (for example, in situations with salient cues indicating opportunities for reward or desired drugs). Psychopathy, conversely, is associated with a primary deficit in attention that undermines their ability to process important inhibitory and emotion cues that automatically influence the behavior of non-psychopathic individuals.
Based on the distinction between psychopathy and externalizing, we (Baskin-Sommers, Curtin, & Newman, 2015) conducted a preliminary investigation that provided prisoners with several sessions of training in affective cognitive control (directed at the underlying externalizing problem) or attention to contextual cues (directed at the underlying problem in psychopathy). As predicted, psychopathic offenders who received attention to context training improved on the relevant training tasks as well as on other tests of attention to contextual information, though they did not benefit from the affective control training. Conversely, externalizers showed significantly greater improvement on the training and other relevant tasks following affective cognitive control training than following attention to context training. Clearly, more work is needed to clarify the value of such deficit-matched treatments in the clinical domain. Nevertheless, it is worth noting that some investigators have highlighted the importance of distinguishing between conduct disordered children and adolescents with and without callous-unemotional traits for similar reasons. And, here too, there is growing evidence that parent training and other interventions, which accommodate the cognitive-emotional styles of the respective groups, yield better outcomes than interventions that cater to the cognitive-emotional needs of the other diagnostic subtype (Hawes, Price, & Dadds, 2014). I would love to see more work that focuses on and attempts to ameliorate the specific information processing limitations of distinct diagnostic subtypes.
Literature Cited
Baskin-Sommers, A. R., Curtin, J. J., & Newman, J. P. (2015). Altering the cognitive-affective dysfunctions of psychopathic and externalizing offender subtypes with cognitive remediation. Clinical Psychological Science, 3(1), 45-57.
Cleckley, H. (1976). The mask of sanity (5th ed.). Mosby.
Gorenstein, E. E., & Newman, J. P. (1980). Disinhibitory psychopathology: A new perspective and a model for research. Psychological Review, 87(3), 301–315. https://doi.org/10.1037/0033-295X.87.3.301
Hare, R. D. (1970). Psychopathy: Theory and research. John Wiley.
Hawes, D.J., Price, M.J. & Dadds, M.R. (2014). Callous-unemotional traits and the treatment of conduct problems in childhood and adolescence: A comprehensive review. Clinical Child Family Psychology Review, 17, 248–267. https://doi.org/10.1007/s10567-014-0167-1
Patterson, C. M. & Newman, J. P. (1993). Reflectivity and learning from aversive events: Toward a psychological mechanism for the syndromes of disinhibition. Psychological Review, 100, 716-736.
