Mental disorder is a cause of crime: "crime" vs. psychiatric phenotypes

The term “crime” is in no less need of a precise definition than “mental”, “disorder”, or “cause”. Leaving aside the legal definition, let us consider how crimes, generally in the form of violent, sexual or aggressive behaviours against others, are approached from the perspective of being caused by mental disorders. 

The focus on mental disorder also directs the searchlight of forensic psychiatry towards individual criminal acts or towards patterns of criminal behaviors occurring in individuals rather than to crime as a societal or group phenomenon. For a number of questions, this is too narrow a perspective.

A crime takes place in a situation, between people, and the vast majority of crimes are clearly influenced by the situations in which they arise. Only rarely is a crime planned and determined by a single mind. A major shortcoming of the psychiatric approach is the emphasis on the individual and the relative down-tuning of the role of the interaction between people, including co-perpetrators and victims. 

The capacity to empathize and act compassionately shows not only a constitutional inter-individual variation but also an intra-individual variation in partially state-dependent actual functioning (cf. Constantino & Todd, 2003; Gabbard, 2004). Each and every one of us may stop forming meta-representations of the other’s mind, the ordinary household quarrel being just as good an example as more dramatic scenes of conflict. 

A person who commits a heinous crime on his own is more likely to differ from the normal variation on at least some mental features than someone taking part in a similar crime as part of a group of offenders. Even small groups may release dynamics that deprive their members of inhibitory forces. A mathematical hypothesis to predict an individual’s actual capacity for empathy (E) would assume that his or her natural capacity for empathy (e) should be divided by the square root of the number of people (n) involved and interacting in the actual act.

Another situational factor that plays a major role in the background to many violent crimes is the influence of drugs. These effects are not easily defined in relation to other mental factors or to situations. Alcohol, for example, may trigger aggression and reduce inhibitory faculties but can also diminish reactivity and reduce anxiety, thus acting as a susceptibility factor or as a protective factor depending on the situation, the degree of influence, and the subject’s other psychological and psychiatric problems. When faced with the task of explaining the background to a particular criminal act, aspects of reduced or changed mental abilities have to be considered in the context of situational, social factors, each of which may constitute an INUS condition.

Perhaps due to this empirical dilemma, psychiatric research has instead attempted a shortcut to explain crimes by diagnosing patterns of crimes as mental disorders. Here, the lack of definitional clarity has become abysmal. Diagnoses such as kleptomania, intermittent explosive disorder, paedophilia, or psychopathy, have been defined on the basis of criminal behaviour patterns and mainly researched among convicted offenders. In order to have them constitute mental disorders, heterogeneous aspects of inner phenomena or cognitions have been assembled into diagnostic designations. By their circular reasoning and limited empirical support from general population studies, these diagnoses have continued to fuel heated controversies about which aspects should be counted as “belonging” to the respective syndromes. It came as no surprise when a recent large-scale meta-analysis of the predictive value of the different “facets” of psychopathy for crimes showed that the strongest predictor was – criminal behaviours (Walters, 2008).

This blog post is largely excerpted from the paper "Mental disorder is a cause of crime" I co-authored with Susanna Radovic, Christer Svennerlind, Pontus Höglund and Filip Radovic in 2009. 

Mental disorder is a cause of crime: what is meant by "cause"?

In psychiatric terminology, behaviour is considered an aspect of the mental. The easiest way to deal with the relationship between mental disorder and crime would therefore be just to consider criminal acts to be a form of mental disorder. This stance has never been met with much enthusiasm, however, neither in clinical psychiatry, nor in science or jurisprudence.

Thought of as two distinct phenomena, the connection has been postulated as leading from mental disorder to crime and to be, at least in some respect, causal. At the same time, it is evident that causation in this context cannot mean that mental disorder is a necessary or sufficient cause of crimes.

Modern medicine has increasingly come to work with probabilistic models. Probabilistic theory defines the relation between “risk” factors and effects as an increased probability of the effect in the presence of the risk factor (cf. Reichenbach, 1956; Cartwright, 1979). In our context, probabilism would mean that particular forms of mental disorders are likely to be associated with particular forms of criminal acts. The risk factor may then be assumed to be a (full or partial, see below) cause of the event (meaning that causation is “attributed” to the factor) if there is a temporal relation so that the risk factor can be shown to generally precede the effect, if covariation with other factors (referred to as “confounders”) can be accounted for by logistic or other multivariate statistical models, and if reasonable models are at hand for understanding how the causation operates. 

In other cases, risk factors can be judged to be coincidental to or reflections of common causes. By using probabilism in this way, scientific exploration has been made possible beyond experimental models testing causation. The terms “risk” and “risk factors” are assigned to the cardiologist Dawber (Kannel, Dawber, Kagan, Revotskie & Stokes, 1961) as a model to identify background factors, such as elevated blood pressure, cholesterol, and smoking, behind coronary heart disease. They have become central to medical research and have even come to represent a paradigmatic feature of today's society (Beck, 1992). The concept of risk is therefore a means of avoiding statements of causation, and “explanatory value” in this context will mean “proportion of the variation statistically related to the variation in the risk factor”, which does not necessarily “explain” it in the common, causal meaning of the word.

In the vast majority of those afflicted, mental disorder does not lead to crime. A possible definition of causation in this context would therefore be that a mental factor is a cause of a crime if the mental factor is an insufficient but necessary part of a set of conditions that together are unnecessary but sufficient for the crime (a so-called INUS condition, Mackie, 1965, 1974). Suppose, for example, that a lit match causes a forest fire. The lighting of the match is not by itself sufficient; many matches are lit without bringing about forest fires. But the lit match is in this case a part of a constellation of conditions that together are sufficient for the fire. The match was dropped on a pile of dry leaves, and a gust of wind contributed to the lighting of the fire. Each of the components, the match, the pile of leaves, and the wind, is an INUS condition, each was insufficient, each was necessary, and all together were sufficient for the forest fire, even if other sets of conditions also could have led up to the same effect.

Counter-factuality is thus a prerequisite for a factor to be an INUS condition under the given set of conditions (it should be possible to conclude that “if the mental factor had not occurred or been present, then the crime would not have occurred”, cf. Lewis, 1973; Mackie, 1965, 1974). From this follows manipulability, that it is possible to change the effect or the probability of the effect by changing the cause.

Mackie’s model provides a useful framework to deal with causation behind complex human behaviours such as violent crime. The way we attribute causation even in the sense of INUS conditions in complex chains of events has to be considered. Singling out one of the INUS conditions as the cause of a certain event is often a matter of choice and not based on rigorous scientific investigations. Since each factor, by definition, forms a necessary part of the overall condition, we do not really have any grounds for pinpointing one of them as contributing to the effect to a higher degree than the others. 

Human minds, however, strive to attribute causes in order to be able to predict what will happen in the future. Only in very rare instances are such attributions of causation based on experiments or strict, logical deductions. As the factors that may be shown to cause human actions in the INUS sense are invariably numerous and interact in complex constellations, the way we identify causes and assign importance to them is in itself the object of psychological research (Cheng, 1997).

As for crime and punishment, there is every reason to believe that mental disorders attract undue attention among possible explanatory factors. Generally, we have a strong tendency to assign causation of undesired events to factors that are strange or exotic in relation to ourselves, classically to other ethnic groups or to people with features that in one way or the other make them different from us. This powerful force directs our attention towards mental disorders among all the possible INUS conditions that may be discerned in the background to a crime. 

In forensic psychiatric research and expert opinion, the attribution of causation has no doubt been influenced by ideas developed within the professional psychiatric paradigm. And for the causation that is to be judged by the lawyer, counter-faction will be non-informative. How could any mental condition (i.e. inner experiences, cognitions, and/or behaviour patterns) be ruled out as a contributing factor in the very complex sets of factors influencing human action?

This blog post is to a large extent excerpted from the paper "Mental disorder is a cause of crime" I co-authored with Susanna Radovic, Christer Svennerlind, Pontus Höglund and Filip Radovic in 2009. 

Mental disorder is a cause of crime: the jurisprudence perspective

From the legislators’ point of view, the assumption that there may be a causal connection between mental disorder and crime has major consequences. Almost all countries consider accountability a requisite for punishment, and mental disorders are virtually the only legally acceptable factor that can be used in a defence claiming reduced accountability or insanity. 

The role attributed to mental disorders ultimately depends on the guiding aims of penal law. Justice may be understood as the establishment of guilt or as some form of equalling out wrongs, whereas modern penal systems serve several, partly conflicting, goals. If retribution is the goal, reduced accountability due to mental disorder must be considered as humans have unequal chances of refraining from crime (Rhee & Waldman, 2002). If the goal instead is crime prevention (through treatment, incapacitation, deterrence, or combinations thereof), sanctions have to be devised in relation to the risk of criminal recidivism and their scientifically documented, preventive effect. 

Factors that would be considered mitigating in the context of retribution (such as youth, poor social integration, impulsivity, deficits in other mental faculties) may instead call for harsher preventive measures, such as long-term incarceration or intensive societal surveillance. 

Every attempt at implementing a purposeful societal approach to criminal offenders would thus require a clearly stated aim, or combination of aims, for the penal law. If the legislator wants the system to fulfil several aims, it has to be clearly stated what these aims are and what their relative priorities should be when conflicts ensue. No system could fully serve each and every aim. 

The lawyer’s perspective is focused on the procedures of the judicial process. In the individual case, the causal role of a mental disorder behind a crime has to be determined, and the normal requirements of justice, such as equality, predictability, and transparency, have to be upheld. Lawyers must know what expertise to ask for and exactly what type of knowledge the different experts can provide. They must also be familiar with the grounds for questioning expert opinions and seek a second view, or with how to challenge a testimony presented in the courtroom. 

At the end of the day, it is also lawyers who will have to evaluate the causal relation between the psychiatric problems diagnosed and the crime committed. “Beyond any reasonable doubt”, the normal standard of certainty in law, has to be accommodated to the lesser precision of the clinical judgment of psychiatrists.

This blog post is partly excerpted from the paper "Mental disorder is a cause of crime" I co-authored with Susanna Radovic, Christer Svennerlind, Pontus Höglund and Filip Radovic in 2009. 

What is a mental "disorder" (part 3): validity of diagnoses according to the Robins & Guze criteria (1970)

In psychiatry, validity has mostly been an issue when determining how “validly” a diagnostic instrument may identify a categorical diagnosis. Comparatively less attention has been focused on the validity of the diagnostic constructs. 

A few leading psychiatrists have developed criteria for the validity of disorders (Andreasen, 1995; Kendell & Jablensky, 2003; Kendler, 1980; Robins & Guze, 1970). Robins and Guze argued that psychiatric diagnoses should be based on systematic studies instead of “a priori principles” and defined five areas in which such studies should be carried out: 1) systematic clinical descriptions, 2) laboratory studies, 3) delineation from other disorders, 4) follow-up studies, and 5) family studies. 

Kendler (1980) added that diagnostic validity should require follow-up studies showing diagnostic consistency over time, similar rates of relapse and recovery, and homogeneous response to treatment, while family studies should show aggregation of similar symptom constellations among relatives. 

Andreasen (1995) declared that psychiatry had reached the stage where it was now “founded on diagnoses that are validated by clinical description and epidemiological criteria” and called for a “second structural program for the validation of psychiatric diagnoses” based on “methods that are being applied to track mental illnesses back to the organ system from which they emanate, the brain, and to the aberrations occurring at a molecular level in DNA”. 

Kendell and Jablensky (2003) attempted to emphasize the scientific basis for diagnostic classifications by separating validity from utility. They suggested that diagnostic categories “should be regarded as valid only if shown to be discrete entities with natural boundaries that separate them from other disorders” or from normality by a “zone of rarity”, or if defining characteristics, such as chromosome or biochemical abnormalities, delineate the diagnosis from other conditions with similar symptoms, and concluded that “most diagnostic concepts have not been shown to be valid in this sense”. 

When the DSM-5 was published in 2013, a wider public debate on the validity of psychiatric diagnoses ensued. The field trials had shown very poor test-retest reliability and prevelences for some disorders varied considerably by small changes in diagnostic criteria, such as the age when symptoms of ADHD should first have been apparent (as detailed in books by, among others, Greenberg and Frances). The NIMH then suggested an alternative model that allowed also subsets of functions and symptoms but required theoretical and/or empirical co-variates for each problem type (RDoC). In these debates, validity of diagnoses was often referred to as validity of assessment, and vice-versa. 

It may therefore be useful to go back to the original Robins and Guze criteria and re-assess them in view of recent empirical findings.

Clinical validity (Robins and Guze criteria 1 and 3)

Considering what we now know about the epidemiology of mental health problems, it is obvious that what Andreasen expected in 1995 has not come about. First, no mental disorder (besides mental symptoms induced by medical diseases, such as Huntington’s chorea) has yet been statistically distinguished from the normal variation by a “zone of rarity” or shown to constitute a “taxon” among other problem types in the population variance (Cloninger, 1999). Instead, the notions of “broader phenotypes” or “sub-threshold” disorders (initially described in relatives of probands in genetic research) and “spectra” of “overlapping” or “comorbid” disorders, have gained wider acceptance. 

Laboratory “markers” (Robins and Guze criterion 2)

Findings from the laboratory have provided no further support for the categorical system. Andreasen (1995) noted that the “markers” required by Robins and Guze “had not emerged” and that they had rather “risen and fallen” (e.g. the dexamethasone suppression test for depression), but her confidence in the development of new methods, such as brain imaging and molecular genetics, remained unbroken. Findings from studies using these increasingly sophisticated technical methods, however, have been at least as difficult to replicate, and/or as unspecific in relation to diagnostic categories, as those produced by the older models. Reports on new technologies to differentiate between a (small) group of patients and controls abound in the scientific literature, but no method with diagnostic specificity in relation to other problem types has yet been established.

Longitudinal follow-up (Robins and Guze criterion 4)

Research on longitudinal diagnostic stability is impeded by the artefactual hiatuses caused by the division in child- and adolescent psychiatry vs. adult psychiatry at about age 18, or in adult general psychiatry vs. “neuropsychiatry”. Child psychiatric conditions are often interpreted in terms of cognitive disabilities rather than disease, even in conditions for which medication is the standard treatment. With increasing age, definitions subsequently become more influenced by adult designations of symptoms, introducing concepts such as “paediatric” mania or “prodrome” schizophrenia. To what extent these clinical conditions really correspond to similar conditions in adulthood has not been established, but differences in symptom presentation and treatment responses seem to differ (e.g. SSRI treatment of depression in adolescents, Weller, Tucker, & Weller, 2005), and heterotypical progressions of problems from childhood into adulthood are the rule rather than the exceptions (Hofvander, Ossowski, Lundström, & Anckarsater, 2010).

Nor do longitudinal treatment effects seem to respect diagnostic categories. Pharmacological remedies alleviate symptoms across diagnostic divisions, no matter if their target is specific or wide. Lithium stabilizes mood in borderline personality disorder just as in bipolar disorder, atypical neuroleptics tranquilize, and serotonin reuptake inhibitors influence mood and anxiety regardless of diagnostics (Kramer, 1997). Psychotherapies and psychosocial interventions also have effects across diagnostic categories.

Familial aggregation (Robins and Guze criterion 5)

Familial aggregations of disorders have been studied by epidemiological methods to assess the overall importance of heritable factors for the variance in psychiatric phenomena. Family and adoption studies, not least twin studies, have provided ample support for the notion that hereditary factors play important causative roles in the variation of all mental health problems and associated features (Rutter & Silberg, 2002). This strand of research has used categorical as well as dimensional definitions (Levy, Hay, McStephen, Wood, & Waldman, 1997). More recent twin studies also collect data on co-existing and interacting problem constellations (Lichtenstein, et al., 2009) and follow developmental trajectories from adolescence (Silberg, Rutter, Neale, & Eaves, 2001) into the adulthood disorders (Cardno, Rijsdijk, Sham, Murray, & McGuffin, 2002; Kendler, Gardner, Annas, & Lichtenstein, 2008; Kendler, Gardner, & Prescott, 2003). Separate aetiologies have been reported for features previously linked into syndromes (Ronald, Happe, Price, Baron-Cohen, & Plomin, 2006), and conceptually different facets of clinical problem constellations have been found to have aetiological factors in common (Larsson, Andershed, & Lichtenstein, 2006).

Conclusion

None of diagnostic labels in use today meet the Robins & Guze criteria for validity. Psychiatrists are reluctant to recognize this, and often intertwine "valid assessments" with "valid diagnoses". A possible way forward would be to define "mental disorder" on the level of functioning and/or subjective suffering only, and then pursue research on symptom complexes, their aetiology and how they respond to treatment. Treatment efforts aimed at improving global functioning may also be evaluated on more relevant measures than reductions of some specific symptom cluster. But recognizing the lack of scientific validity for today's diagnoses may have far-reaching consequences for their use in legal contexts. 

This post is partly excerpted from Anckarsäter H. Beyond categorical diagnostics in psychiatry: scientific and medicolegal implications (2010). Should someone need a full-length manuscript or a reference list, don't hesitate to contact through the blog or e-mail henrik.anckarsater@neuro.gu.se.