Conversely it may be argued that as undesirable behaviours are suppressed while the individual is imprisoned, there may be opportunity for the offender to participate in rehabilitative projects such as social skills and educational programs to learn acceptable alternative behaviours as an alternative to crime (Sanson, 1995). It has been suggested that rehabilitation is more effective at reducing reoffending than punishment (Birgden, 2008) and that the most effective way to produce behavioural change is not to simply suppress the inappropriate behaviours, but promote socially acceptable ones (Blackman, 1996). Rehabilitation attempts to bring about individual changes in offenders, and is sometimes expressed as offender treatment (Hollin & Palmer, 2009), and rehabilitative projects can be used both for offenders while imprisoned, and as sentences for offenders who have committed crimes not worthy of imprisonment.
Rehabilitation of offenders as a means of treatment and addressing recidivistic behaviours can be implemented using a number a methods which attempt to address core issues within the offender (McGuire, 2002). There are many proposed reasons why individuals become criminals, and Joseph (2001) found that both genetic and environmental factors play significant roles in the individual differences associated with criminal and antisocial behaviour. For example, it has been highlighted that a stable family environment may minimise predisposition to crime, and that development of criminal behaviour was correlated with poor family communication and weak bonds (Garnefski & Okma, 1996; Schmitz, 2003). It has also been suggested that childhood victimization leads to development of personality disorders later in life (Widom, 1994). These factors may contribute to the fact that offenders have failed to learn socially appropriate behaviours, and therefore may benefit from rehabilitation projects using techniques such as cognitive-behavioural modification to attempt to help offenders face the consequences of their actions and develop new ways to control their behaviour (Husband & Platt, 1993; McGuire, 2000).
Meta analyses led to formulations of principles of effective practices when working with offenders, and three key principles were established: risk principle, needs principle and responsivity principle (Hollin & Palmer, 2009). Adherence to the risk principle was seen as a critical factor in relation to outcome (Andrews & Dowden, 2006) and it has been suggested that effective treatment would be cognitive behavioural in orientation, and a structured programme delivered by highly trained staff (Hollin & Palmer, 2009). Many cognitive skills programmes have been developed to help the offender implement personal changes, and programmes such as Reasoning and Rehabilitation (R & R) and Think Fast aim to promote alternative ways of thinking for the offender through cognitive behavioural techniques such as role-play and reinforcement, hopefully leading to prosocial behaviour (Hollin & Palmer, 2009). Blud, Travers, Nugent and Thornton (2003) examined the effects of R&R on cognitive functioning, and found that the majority of measures showed change in the anticipated direction, indicating a positive effect on prisoner’s cognitive skills. Wilson, Attrill, and Nugent (2003) had similar findings in their large scale prison study. Studies examining the effectiveness of R&R on reconviction rates reported a significantly lower reconviction rate for offenders who completed treatment (Friendship, Blud, Erikson, Travers, & Thornton, 2002; Robinson, 1995). However, there have been criticisms of the methods of measurement of cognitive behavioural techniques due to the majority of studies not employed randomised control trials, which are seen to be the ‘gold standard’ for research.
However, it has been duly noted that even successfully reported interventions have major limitations in that they have a relatively narrow focus, and do not fully account for the multidetermined nature of antisocial and criminal behaviour (Borduin, 1994; Zigler, Taussig, & Black, 1992). Causal modelling studies have consistently demonstrated the multiple roots of delinquent behaviour with links to family, peer groups, schools and neighbourhood systems (e.g. Patterson & Dishion, 1985; Simcha-Fagan & Schwartz, 1986) supporting social-ecological beliefs about the origins of criminal behaviour (Bronfenbrenner, 1979). Multisystemic therapy (MST) was designed to tackle these multiple causes of antisocial and criminal behaviour, and it has been proven that it has a significant effect on criminal activity of serious juvenile offenders in several trials (e.g. Borduin & Henggeler, 1990; Henggeler, Schoenwald, Borduin, Rowland, & Cunningham, 1998). MST interventions are individualised for every offender, and extremely flexible, but almost always use some form of home and community-based service delivery including sessions in the family home and parent empowerment sessions, and sessions in schools and recreation centres (Schaeffer & Borduin, 2005). A long-term follow up study comparing MST to individual therapies including cognitive practices found that participants who received MST had significantly lower recidivism and arrest rates than other individuals who received individual therapies (Schaeffer & Borduin, 2005).
Despite the success rates of cognitive behavioural and MST therapies for many different types of offender, there is some concern regarding the recidivism rates of dangerous sexual offenders (Proulx et al., 1999). Many sexual offenders upon prison release will be required to undergo community-based treatment programs; however, therapy alone cannot be relied upon to reduce reoffending risks (McConaghy, 1993). It has therefore been proposed that biological approaches aiming to reduce the danger of recidivism during a period of time when cognitive and behavioural treatments are taking effect may be appropriate for the limited population of sex offenders who may represent an imminent risk to the community (Maletzky & Field, 2003).
This limited population is identified using semiquantitative scales which predict sexual risk to be at large. A number of contributory factors such as deviant sexual arousal, central nervous system (CNS) dysfunction, and prior responses to sex offender treatment may be examined to enable a conclusion to be reached deciding whether biological treatments are appropriate for the particular individual (Maletzky & Field, 2003). Some sex offenders may be at a higher risk than others and more likely to need biological treatments as there may be underlying physiological causes, such as the aforementioned dysfunction of the CNS. For example, Burns and Swerdlow (2003) also report the ceasing of paedophilic behaviours after a patient with a history of sex offending had an orbitofrontal tumour removed. This would suggest that biological treatments would be a necessary and effective way of treating sex offenders.
There are a number of biological treatment options available for the treatment of sex offenders, and one of these is castration. Castration has been reported as having high success rates for reducing recidivism, and many studies examining recidivism rates post castration consistently report recidivism rates of less than 2% (e.g. Ortmann, 1980; Sturup, 1968). However, the reliability of these figures has been questioned as they were based on retrospective accounts, and also may not have considered the fact that some individuals may have committed sexual crimes which went undetected (Maletzky & Field, 2003). Castration has also been viewed as a barbaric punishment, and a form of physical assault (Maletzky, 1997) and is therefore not widely used unless specially requested by the offender as a substitution for other punishments (Maletzky & Field, 2003).
The most widely used biological treatment for sexual offenders across Europe and Canada is cyproterone acetate (CPA) (Maletzky & Field, 2003). Rosler & Witzum, 2000 report the clinical usefulness of CPA in their review in reducing recidivism rates, however very few follow up studies measuring actual recidivism rates of sex offenders after CPA treatment exist. There are however, reports that offenders receiving CPA showed a decrease in arousal as measured by the penile plethysmograph (Bradford & Pawlak, 1993), and a significantly reduced number of erections and sexual interest; however this study only included nine men (Cooper, 1981). Meyer and Cole (1997) also found that most patients reported reductions in sexual thoughts and fantasies, and a decrease in urges to commit sexual crimes.
There are many proposed theories as to why individuals become criminals, and these have implications to the type of sentencing which should be the most effective. It is widely believed that prison should be both a general and specific deterrent and should act as disincentive not to commit a crime when thinking about committing an offence in terms of risks and benefits. Much emphasis has been placed on the role of cognitive deficits play in offenders who commit criminal acts, resulting in many sentences for criminal activity incorporating cognitive behavioural therapies. Extended therapies in the form of MBT exist due to the belief that individuals perform criminal acts due to a number of factors, and MBT aims to address this. Biological methods are not generally used on criminals in general, however in specific offender groups for example sex offenders, there seems to be good use for biological therapies and these are widely used. In conclusion, there are many sentences for criminals which address the issue of either punishment or rehabilitation and some aspects of both, and can be seen to have both positive and negative aspects.
References
Bouchard, T (1994). Genes environment and personality. Science, 264, 1700-1701.
Bouchard, T.J., Lykken, D.T., McGue, M., Segal, N.L., & Tellegen, A. (1990). Sources of human psychological differences: the Minnesota study of twins reared apart. Science, 250, 223-228.
Brennan, P., Grekin, E. R., & Mednick, S. A. (1999). Maternal smoking during pregnancy and adult male criminal outcomes. Archives of General Psychiatry, 56, 215-219.
Brunner, H. G., Nelen, M., Breakefield, X. O., Ropers, H. H., & van Oost, B. A. (1993). Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A. Science, 262, 578-580.
Cadoret, R. J., Yates, W. R., Troughton, E., Woodworth, G., & Stewart, M. A. (1995). Genetic-environmental interaction in the genesis of aggressivity and conduct disorders. Archive General Psychiatry, 52, 916-924.
Carey, G. (1994). Genetics and violence. In A. J. Reiss, Jr., K. A. Miezek, & J.A. Roth (Eds.) Understanding and preventing violence (pp. 21-58). Washington, DC: National Academy Press.
Cassel, E. & Bernstein, D. (2001). Criminal behaviour. Massachusetts: Allyn & Bacon.
Eysenck, H. J. (1996). Personality and crime: Where do we stand? Psychology, Crime, & Law, 2, 143-152.
Farrington. D. P. (1992). Explaining the beginning, progress and ending of antisocial behaviour from birth to adulthood. In J. McCord (Ed.) Facts, Frumeworks and Forecasts. Advances in Criminological Theory (pp. 253-286). London: Transaction Publishers.
Garnefski, N., & Okma, S. (1996). Addiction-risk and aggressive/criminal behavior in adolescence: Influence of family, school, and peers. Journal of Adolescence, 19, 503-512.
Gibson, C. L., & Tibbetts, S. G. (2000). A biosocial interaction in predicting early onset of offending. Psychological Reports, 86, 509-518.
Gottesman, I. I., & Goldsmith, H. H. (1994). Developmental psychopathology of antisocial behavior: Inserting genes into its ontogenesis and epigenesis. In C. A. Nelson (Ed.) Threats to optimal development: Integrating biological, psychological, and social risk factors (pp. 69–104). Hillsdale, NJ: Erlbaum.
Grove, W., Elke, D., Ecker, L., Heston, L., Bouchard, T.J., Segal, D., et al. (1990). Heritability of substance abuse and antisocial behavior: a study of monozygotic twins reared apart. Biological Psychiatry, 27, 1293-1304.
Holmes, S. E., Slaughter, J. R., & Kashani, J. (2001). Risk factors in childhood that lead to the development of conduct disorder and antisocial personality disorder. Child Psychiatry and Human Development, 31, 183-193.
Joseph, J. (2001). Is crime in the genes? A critical review of twin and adoption studies of criminality and antisocial behavior. The Journal of Mind and Behavior, 22, 179-218.
Miles, D. R., & Carey, G. (1997). Genetic and environmental architecture of human aggression. Journal of Personality and Social Psychology, 72, 207-217.
Oliver, L., Nagayama, L., Hall, G. C., & Neuhaus. S. M. (1993). A comparison of the
personality and background characteristics of adolescent sex offenders and other
adolescent offenders. Criminal Justice and Behavior. 20, 359-370.
Plomin, R., Chipuer, H. M., & Loehlin, J. C. (1990). Behavior genetics and personality. In L. A. Pervin (Ed.). Handbook of personality theory and research (pp. 119–133). New York: Guilford Press.
Raine, A. (2002). Annotation: The role of prefrontal deficits, low autonomic arousal, and early health factors in the development of antisocial and aggressive behavior in children. Journal of Child Psychology and Psychiatry, 43, 417–434.
Raine, A., Brennan, P., & Mednick, S. A. (1994). Birth complications combined with early maternal rejection at age 1 year predispose to violent crime at age 18 years. Archives of General Psychiatry, 51, 984-988.
Raine, A., Brennan, P., & Mednick, S. A. (1997). Interaction between birth complications and early maternal rejections in predisposing individuals to adult violence: Specificity to serious, early-onset violence. American Journal of Psychiatry, 154, 1265-1271.
Raine, A., Park, S., Lencz, T., Bihrle, S., LaCasse, L., Widom, C.S., et al. (2001). Reduced right hemisphere activation in severely abused violent offenders during a working memory task: An fMRI study. Aggressive Behavior, 27 111-129.
Rhee, S.H. & Waldman, I. (2002). Genetic and environmental influences on antisocial behavior: a meta-analysis of twin and adoption studies. Psychological Bulletin, 128, 490–529.
Rutter, M., Giller, H. & Hagell, A. (1998). Antisocial Behavior by Young People. Cambridge University Press: Cambridge.
Schmitz, M. F. (2003). Influences of race and family environment on child hyperactivity and antisocial behavior. Journal of Marriage & the Family, 65, 835-849.
Tehrani, J., & Mednick, S. (2000). Genetic factors and criminal behavior. Federal Probation, 64, 24-28.
Volkow, N. D., Tancredi, L. R., Grant, C., Gillespie, H., Valentine, A., Mullani, N ., et al. ( 1995). Brain glucose metabolism in violent psychiatric patients: A preliminary study. Psychiatry Research: Neuroimaging, 61, 243-253.
Widom, C.S (1994) childhood victimization and risk for adolescent problem behaviours. In M.E Lamb and R . Ketterlinus (Eds.) Adolescent Problem Behaviors (pp. 127-164). Hillsdale, NJ : Erblaum
