Developmental theory of crime
| Criminology and penology |
|---|
 |
| People |
|---|
| Topics |
In 1993, American psychologist
Antisocial Personality Disorder
| Personality disorders |
|---|
| Cluster A (odd) |
| Cluster B (dramatic) |
| Cluster C (anxious) |
| Not otherwise specified |
| Depressive |
| Others |
Antisocial personality disorder (ASPD) is recognized by the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). It is a disorder characterized by a severe disregard for the rights of others. In most of the studies described below, individuals who exhibit antisocial behavior, but have not been diagnosed with ASPD, are used as subjects.
Age and antisocial personality disorder
The number of arrests spikes in adolescence, but subsequently declines. This spike leads people to wonder whether more offenders are appearing or more offenses are committed by the same few offenders. Evidence shows that there is an increase in both. The most persistent 5% of offenders are responsible for more than 50% of known crimes committed.[5]
Several experiments have been conducted to investigate the relationship between extremity and stability of offenses. In one such experiment a group of third grade boys was studied. Out of the most aggressive 5%, 39% of them scored above the 95th percentile on aggression ten years later, and 100% of them were above the median.[5]
Aggression and antisocial behavior in a child is a predictor of adult antisocial behavior.
Continuity and stability of antisocial behavior
The continuity and stability of antisocial behavior lies at the root of Moffitt's theory. The adolescent limited offenders exhibit antisocial behavior without stability over their lifetime, while life-course-persistent offenders typically display antisocial behavior from very early ages. Biting and hitting as early as age 4 followed by crimes such as
Donker et al. presents a test concerning the prediction on the stability of
The original sample of children (ages 6–11) in 1983 consisted of 1,125 subjects. Three main areas were studied in the subjects: status violations, overt behavior, and covert behavior. Children exhibiting overt behavior were found to have two times greater risk for covert behavior as an adolescent and three times greater risk for it in adulthood. This violates the longitudinal law and proves Moffitt's expectations correct. Further results also supported this violation, but only with respect to overt behavior, not covert behavior.[7] There is a difference in the continuity of antisocial behavior between men and women as well. In one longitudinal study an entire county's population was followed from age 8 to 48. Only 18% of the women who ranked high in antisocial behavior at age 8 rank high at age 48, while 47% of men stay in the high category. About 37% of both men and women, however, retained low antisocial behavior through age 48.[6]
Life-course-persistent offenders
Biological risk factors
The following
Brain Injury
- According to multiple studies, a correlation was found between brain insult suffered during pre-frontal cortex. Damage to this part of the brain early in childhood correlates to an antisocial behavior that extends through the life-course.[10]
Brain activity
- The Continuous Performance Task test (CPT) was used to test frontal lobe function. Larger neurocognitive impairments were found in the life-course persistent group (LCP) than in the control group. Additionally, positron emission tomography (PET), near-infrared spectroscopy, and magnetoencephalography imaging studies have shown more right hemisphere activation during the CPT, so these results are consistent with right hemisphere dysfunction in subjects displaying antisocial behavior.[11]
- Reduced anterior cingulate.[10]
- Spatial capabilities
- In the previous Pennsylvania study, the life-course persistent (LCP) group showed significant impairments on spatial tests compared with the control group. No significant differences were shown between the adolescent limited (AL) group and the control group with respect to spatial IQ.[11]
- Verbal capabilities
- Children exhibiting antisocial behavior early in life, many of whom are the same individuals who continue their trajectory into adulthood, often have difficulties with oral communication.verbal IQ (and regular IQ) scores than the adolescent limited group, and no significant differences were shown between the adolescent limited (AL) group and the control group with respect to verbal IQ.[11]
Minor physical anomalies
- Moffitt writes, "toxic agents.[5] Minor physical anomalies (MPAs) are features such as low-seated ears, furrowed tongue, and adherent ear lobes. Evidence supporting the link between minor physical anomalies and antisocial behavior shows that the link only exists when adverse environmental factors are present.[8]
Social risk factors
In many studies, the individuals displaying antisocial behavior developed in a family exhibiting "deviant behavior", in an "adverse home environment", or in something similar.[5] However most studies do not specify the exact traits that characterize the tested 'deviant' or 'adverse' environment. Many that are cited include abuse, neglect, socioeconomic status, parental antisocial behavior, etc. There is no evidence that social factors, such as these, can induce antisocial behavior without accompanying biological factors.
Effect of biological and social risk factors together
| Biological | Social |
|---|---|
| Genetic | Abuse |
| Brain Injury | Neglect |
| Brain Activity | Socioeconomic Status |
| Minor Physical Anomalies (MPAs) | Parental deviant behavior |
Moffitt projects that initial biological predispositions combined with an adverse rearing environment will initiate the risk of life-course persistent antisocial behavior. She conducted a longitudinal study in New Zealand of boys exhibiting a range of antisocial tendencies. Of the 536 boys, 75 of them had adverse home environments and neuropsychological problems. Those 75 boys scored more than 4 times higher on aggression than the boys with adverse home environments or neuropsychological problems (one of the two).
Genetic and environmental interactions
- The first biological allelesresponsible for antisocial behavior, no such discovery has been made thus far.
Minor physical anomalies and environmental interactions
- In one study testing 129 boys from age 12 to 21 years with genes.
Brain activity and environmental interactions
- A link between prefrontal cortex dysfunction and antisocial behavior has been found in many studies. Some frontal lobe lesions have been responsible for impulsivity and disinhibition, which are key characteristics of Antisocial Personality Disorder.Functional MRI scans were used in another study with violent offenders and abusive environments. Four groups were composed of non-violent controls with no history of abuse, violent offenders with a history of abuse, violent offenders with no history of abuse, and non-violent controls with a history of abuse. The violent offenders who had been abused showed reduced function in the right hemisphere, particularly the right temporal cortex. According to the authors of this article, this experiment's results imply that good right hemispheric functioning may protect against violence in abused children.[8]
Adolescence-limited offenders
Although the biological risk factor do not apply to this group, one point worth noting is that the myelination of the frontal cortex continues into our 20's.[8] This continuing development may help to explain why antisocial behavior ceases after adolescence and why such a spike in crime exists there in the first place.
Cause
According to Terrie Moffitt, there are 3 etiological hypotheses for adolescent-limited offenders:
1. Adolescence-limited antisocial behavior is motivated by the gap between biological maturity and social maturity
2. It is learned from antisocial models who are easily
3. It is sustained according to the reinforcement principles of learning theory[5]
Neuroethical implications
This type of theory leads to several different
See also
References
- ^ Psychological Review. 100(4):674-701, October 1993
- ISBN 978-0-8133-4886-5. Retrieved 28 January 2021.
- ^ a b c d Martens, W. H. J. (2000). Antisocial and psychopathic personality disorders: Causes, course, and remission-a review article. International Journal of Offender Therapy and Comparative Criminology, 44(4), 406-430.
- ^ Moffitt, T. E., & Caspi, A. (2001). Childhood predictors differentiate life-course-persistent and adolescence-limited antisocial pathways among males and females. Development and Psychopathology, 13, 355-375.
- ^ a b c d e f g h i j k l Moffitt, Terrie E., 1993, Adolescence-Limited and Life-Course Persistent Antisocial Behavior: A Developmental Taxonomy. Psychological Review 100:674-701.
- ^ a b c Huesmann, L. R., Dubow, E. F., & Boxer, P. (2009). Continuity of aggression from childhood to early adulthood as a predictor of life outcomes: Implications for the adolescent-limited and life-course-persistent models. Aggressive Behavior, 35, 136-149.
- ^ Donker, A. G., Smeenk, W. H., van der Laan, P. H., & Verhulst, F. C. (2003). Individual stability of antisocial behavior from childhood to adulthood: Testing the stability postulate of Moffitt's developmental theory. Criminology, 41(3), 593-609.
- ^ a b c d e f g Raine, A. (2002). Biosocial studies of antisocial and violent behavior in children and adults: A review. Journal of abnormal child psychology, 30(4), 311-326.
- ^ Andrews, T. K., Rose, F. D., & Johnson, D. A. (1998). Social and behavioural effects of traumatic brain injury in children. Brain Injury, 12(2), 133-138.
- ^ a b c d Raine, A., & Yang, Y. (2006). Neural foundations to moral reasoning and antisocial behavior. Social, Cognitive and Affective Neuroscience, 1, 203-213.
- ^ a b c d e Raine, A. (2005). Neurocognitive impairments in boys on the life-course persistent antisocial path. Journal of Abnormal Psychology, 114(1), 38-49.
- ^ a b Silberg, J., Moore, A. A., & Rutter, M. (2014). Age of onset and the subclassification of conduct/dissocial disorder. Journal of Child Psychology and Psychiatry. Epub ahead of print.
- ^ Skardhamar, T. (2009). Reconsidering the theory on adolescent-limited and life-course-persistent antisocial behaviour. British Journal of Criminology, 49, 863-878.