Mental disorder is a cause of crime

The next couple of entries in the Forensic Friday series will continue the series on causation by addressing the notion that “mental disorder is a cause of crime”. This statement is really the foundation of forensic psychiatry. 

If mental disorders do not cause crimes, why should we have forensic psychiatry at all? After all, we don't have forensic internal medicine for diabetics who commit crimes, even if they may have done so during hypoglycaemia and need treatment while serving prison.

In coming posts, we will look at the historical roots of forensic psychiatry and adress each of the definitions “mental”, “disorder”, "cause" and “crime” conceptually, epistemologically, and empirically. The blog posts will be based on the paper "Mental disorder is a cause of crime" I co-authored with Susanna Radovic, Christer Svennerlind, Pontus Höglund and Filip Radovic in 2009. Without the collaborative work behind that paper, I wouldn't have been able to write any of the following texts. Many of them will be expanded and up-dated versions of paragraphs from the paper.  Of course, my version of philosphical analysis is over-simplified and not up to the level of my colleagues from philosophy, but I write this from the perspective of a clinician. On the other hand, I will go deeper into empirical data and try to sum up the considerable developments we have seen since 2009. 

Neither “mental”, “disorder” or “crime”, nor the “causation” implied, are clear-cut concepts. “Mental” denotes heterogeneous aspects of a person, such as inner experiences, cognitive abilities, and behaviour patterns, described in a non-physical vocabulary. In psychology and psychiatry, “mental” describes law-bound, caused aspects of human functioning that in some respect are predictable and generalizable. A corner-stone in these sciences is behaviour, as it is the easiest aspect to observe and quantify, and in itself contains a better-than-chance prediction of future behaviour. Indeed, even interviews and other more clearly “mental” assessments focus on reporting behaviours rather than “inner” mental processes.

Problems defined as “disorders” seem to be end-points of dimensional inter-individual differences rather than natural categories.

Deficits in cognitive faculties, such as attention, verbal understanding, and reality assessment, may be susceptibility factors that relate to behaviours, such as crimes, as risk factors in the sense of increasing the probability for a specific negative behaviour, and/or as causes in the sense of INUS conditions (insufficient but non-redundant parts of unnecessary but sufficient conditions).

Neurobiological measures (e.g. regional brain activity, neurotransmitters, genetics) may be related to crimes in a similar way as assessments of mental health problems or cognitive faculties.

Attributing causation to behaviours is not unbiased, and factors we feel estranged from, such as mental disorders, tend to attract disproportionate attention in explaining abject behaviours, such as crimes. 

When a forensic psychiatrist testifies in court, (s)he may describe mental health assessments, effects on accountability and ability, but the court and laypersons will understand what is said in terms of “causation”. Sometimes we are either lead to or volunteering to proffer an opinion on causation per se. I hope that this blog series will clarify what we can know and what we can’t know about whether mental disorders cause crimes based on psychiatry and psychology. To be continued.

Risk assessments in forensic psychiatry

Risk assessments form a core task for forensic psychiatrists. This is not the place to review the scientific literature on the various methods and instruments used for this purpose, an excellent meta-analysis is provided by Seena Fazel and colleagues here. Instead, I will raise some simple points that sometimes disappear in the scientific litterature and expert evaluations.

Generally, risk assessments in forensic psychiatry are based on a rating scale or a check-list, in which items reflecting risk (and sometimes also protective) factors are systematically weighted and added. The results of one or several such scales are subsequently evaluted by a clinician, who can override or modify the results from the instruments in a final evaluation documented for the court, hospital record or similar. In Sweden, the global risk is assessed as Low, Medium or High (for unspecified crimes during an unspecified time-frame).

Scientific support for the methods are derived from longitudinal studies (prospective or retrospective), comparing assessments to actual outcomes. Assessments of risk for relapse in violence or criminality typically have Areas Under Receiver Operating Characteristics (ROC) Curves (AUC) between 0.70 and 0.80, considered modest or moderate predictive validity. To AUCs, other statistics, such as Diagnostic Odds Ratios (DOR) and Number Needed to Detain (NND), are added for further detail. The overall consensus seems to be that a. these instruments perform better than chance alone and b. that there is no clear evidence that one method is better than the other.

Some aspects are clearly missing in this picture. First, the strongest predictor of future human behaviour is the previous behaviour of the individual. Who among us will be slim and fit a month from New Year's Eve? Probably those who were last year. This is the backbone of every psychiatric risk assessment instrument. The relevant question for science would be "does this instrument/method add predictive value to that derived from the individual's history of previous behaviours?". Why keep repeating that methods are better than random when this can be achieved by common sense alone?

In the whole Swedish population, the risk of being convicted for a violent crime is <4%. After one conviction, the risk for another conviction is still less than 50%, but after two convictions, a majority will go on to reoffend (59%), climbing to 68% after three convictions, >80% after seven and >90% after 11 (Örjan Falk and coworkers, here). These figures may solve the old ethical dilemma whether preventive efforts can be directed at individuals who have not yet offended. It may suffice to do something about those who have.

Second, the time-frame is neglected. Often, the studied time-frame is determined by convenience: researchers take what they can get from data-sets. But clearly, the risk for reoffending varies according to situational factors, such as relapse in substance abuse or unstable social relations. And preventive efforts are best motivated when relapse comes in a reasonable brief time-frame, in some way corresponding to the “normal” prison sentence the offender would have received. It hardly seems justified to allocate large ressources to prevent a threat five years down in time, while 20 years of efforts are clearly appropriate to prevent a murder.

Third, the type of outcome should be specified. A high risk for threats is not easily compared to a medium or low risk for murder.  

Therefore, my advice is:

• for legislators and courts: base risk management decisions on what is known about previous violent behaviours.
• for health care staff: assess risk in a here-and-now perspective based on both actuarial and clinical factors with your patient's best interest as goal (which includes not to commit violent crimes!), do your utmost to help and prevent misfortunes of every kind, but desist from speculating about future behaviour.
• for scientists in the field: develop evidence-based treatments that prevent violence and study risk in fine-grained, clinically meaningful models.

Persistent aggressive antisocial behaviour: a promising phenotype

The main ambition for this blog is to provide a decent, science-related and thought-provoking text on forensic psychiatry once a week ("Forensic Friday"). Let's start by the quite basic question: what is the object of forensic psychiatry? What are we working with? During my first decade or so in this peculiar speciality, I often wondered where the focus of my research and clinical work lay. In psychoses, disorders of empathy, psychopathy, personality disorders, autism spectrum disorders, ADHD or even learning disorders? I have always been fascinated by psychiatry as science and loved working with patients. Frankly, I came to forensic psychiatry because there were good research opportunities and plenty of time to spend with each patient, not because I was more interested in criminology than any other occasional reader of Agatha Christie. But somehow, I had to integrate criminal behaviours in the models I worked with. And some years ago, it dawned on me that the real object of our work lies there, hidden in plain sight. Persistent aggressive antisocial behaviour per se is the core phenotype that forensic psychiatry should put center stage, diagnose, understand from the perspectives of etiology, comorbidity and longitudinal development, and learn to prevent and treat.

Persistent aggressive antisocial behaviour indeed seems a highly promising phenotype for research. In its prototypical form, it has an early onset (it may be recognized sometimes between 3 and 5 years of age according to the life-course persistent overt type described by Moffitt), clear genetic liability (about 65% of variance, Burt et al, 2009), high stability into adulthood (a majority still have aggressive antisocial behaviours as adults) and is observable and thus relatively easy to measure. There are interesting etiological hypotheses, such as associations with sex steroids and monoaminergic neurotransmission (e.g. the cerebrospinal fluid ratio between dopamine and serotonin metabolites), hypofunctioning in prefrontal cortex or limbic dysregulation, impulsivity and reactions to drugs. An adolescent-onset subtype is more related to psychosocial factors and has better prognosis.

Its epidemiology is actually well studied. The small subgroup of the population who have the early-onset form of persistent aggressive antisocial behaviour is responsible for the majority of violent crimes (the prevalence will vary across societies, but in modern Sweden, it is as low as 1%, Falk et al 2013). The male:female sex ratio is at least 9:1, maybe even 98:2 for the most aggressive types, and other known co-variates are substance abuse (type-2 alcoholism with early-onset, polysubstance abuse), ADHD and personality disorder. The group of aggressive children also grow up to account for considerable proportions of all psychiatric patients, being over-represented in every diagnostic category in adult psychiatry (Kim-Cohen et al., 2003, one of the most important papers ever published in psychiatry!). Märta Wallinius defended her PhD thesis on aggressive antisocial behaviour in 2012, and it is accessible here.

The Life History of Aggression (LHA) scale was developed by Brown and Goodwin (1982) for research in veterans displaying pathological aggression and self-harm, and has been further validated by Coccaro and co-workers (1997). It contains 11 items describing aggressive, antisocial and self-harming behaviours, each measured by frequency and yielding 0-5 points, thus giving a maximum score of 55, with three subscales for the different types of behaviours included. Scores have a left-skewed (thankfully!) but overall normal distribution, with clear pathology at about +2 standard deviations. The LHA may be used as an expert assessment or as a self-rating. We are currently investigating whether it can also be rated for a specific time-frame, thus measuring also changes in aggressive behaviour.

There are also numerous scales measuring traits related to aggression, such as aggressiveness, anger, impulsivity and so on, but I think that it is important to keep the phenotype definition behavioural, as this will be much more reliable and clinically relevant. In forensic psychiatry, we really cannot be too preoccupied with people's feelings of anger, it is the behaviours that have to change.

Some individuals with persistent aggressive antisocial behaviour may be happy with their behaviour style as it is. In these cases, psychiatry will have little to contribute and it seems best that the penal system is left to do its job undisturbed by medical opinion. But in my experience as a doctor in correctional facilities of different kinds, the vast majority of antisocially aggressive persons are profoundly unhappy about how they constantly screw up their relationships, life plans and dreams. They would be more than happy to test various forms of treatments, be they pharmacological, physical, psychological or educational. And if an intervention would help some tens of percents of affected persons to refrain from half of their future violent crimes, a very significant reduction in societal violence at large might be achieved. With enormous positive health effects at large. 

Why  did it take so long for me too relaize this stunningly simplicit model? And why is this promising phenotype obscured in ratings of controversial diagnoses like psychopathy, conduct disorder or antisocial personality disorder? I think that the answer is simple and a bit humiliating for forensic psychiatry. Persistent aggressive antisocial behaviour is too simple, too obvious, not enough psy-whatever and is difficult to make a big fuss about. There is little money or prestige involved for the expert assigning this diagnosis or from creating diagnostic instruments and specialist training to recognize it. So therefore we have chased illusional diagnoses instead of finding a way to help people stop being aggressive with each other outside of those situations when physical aggression can be pro-social: in sports with clear rules and in tasks contributing to societety's legally regulated monopoly of violence. There is an urgent need for controlled treatment studies with reduced aggressive behaviour as primary end-point, and this should be the primary goal for forensic psychiatric research.