UNIVERSITY OF AMSTERDAM
The Role of Environmental Influences in the Relationship
between Underlying Mechanisms of Aggression and
Recurrent Violent Offending
Insights for Reducing Recidivism
Bachelor Thesis
Specialization: Clinical Neuro-Psychology
Name: Supervisor: Department: Main research area: Specialization:
Anna van der Schoot, 10172815 Olympia Colizoli
Brain and Cognition
Brain Function and Structure Relationships Clinical Neuro-psychology
Amount of words abstract: 165 Amount of words total: 7676
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Table of Contents
Abstract 2.
Introduction 3.
Hypothetical Substantiation from Theoretical and Scientific Considerations 4.
The Relation between Underlying Mechanisms of Impulsiveness and Aggression 9.
The Role of the Underlying Mechanisms of Aggression in Offending 14.
Environmental Influences on the Underlying Mechanisms of Aggression in Offenders 18.
Conclusions and Discussion 24.
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Abstract
High criminality rates still remain a prevalent issue in society. One of the main
concerns is that violent reoffenders are still contributing to the high criminality rates. The
current methods to reduce reoffending risk during imprisonment do not prove to be effective.
Therefore, the aim of this thesis was to determine the precise underlying neural mechanisms
of aggression in violent offenders through biological and environmental approaches.
Subsequently, with prospects on reducing recidivism, methods for influencing the
contributing neural mechanisms to violent offending were examined. It was found that
different structures in the prefrontal cortex, which are attributed to impulsiveness and
inhibition deficits, are related to violent offending. Furthermore, it was shown that the neural
mechanisms underlying inhibition deficits were not influenced by prison environment.
Nevertheless, methods for improving inhibition abilities through affecting related brain
mechanisms proved to be effective. Some caution with the interpretation is required since
these methods were not studied in relation to direct observable behavior in the target group of
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Introduction
The government aims to provide safety for its citizens to go about their daily life in
society. However, high criminality rates still remain a prevalent issue and a threat to the government’s objectives. Different factors have been found to contribute to high criminality rates in society - one of the factors being, convicted offenders who reoffend after being
released from prison, known as recidivists. A large bulk of the population of offenders
consists of recidivists. In a report by the Dutch Ministry of Safety and Justice, a staggering
47.7% of ex-offenders were found to re-offend within two years of their release. The biggest
and most concerning issue is that 14.6% of these crimes being committed by re-offenders are
violent crimes (Ministerie van Veiligheid en Justitie, WODC, 2012).
To prevent or reduce recidivism, the Dutch prison system provides mandatory conduct
training. This conduct training, also called behavioral intervention, should prevent or reduce
recidivism. During conduct training, prisoners learn, for example, to deal with aggressive and
impulsive tendencies. There is only one intervention focusing solely on aggression: “Grip op Agressie” (Erkenningscommissie Gedragsinterventie justitie, 2014). The Accreditation Panel for Behavioral Intervention Programs of the Ministry of Security and Justice, which
determines whether these programs are effective for reducing and/or preventing recidivism, found that this intervention “Grip op Agressie”, met the quality standards for effectiveness (Erkenningscommissie Gedragsinterventies Justitie, 2013). However, the effectiveness of this
intervention is not entirely convincing as recidivism still occurs in half of the released
offenders population, according to government reports (Ministerie van Veiligheid en Justitie,
WODC, 2012).
The current intervention programs for reducing and preventing recidivism prove to be
ineffective in practice.Therefore, it is important to study the factors that increase the tendency
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some offenders reoffend when others do not. From a psychological point of view, it is not to
fight the symptoms but to work with the underlying mechanisms of problematic functioning.
According to the traditional paradigm in psychology, problematic functioning can be caused
in two ways – nature or nurture. Nature is an innate cause defined through biological
predetermined mechanisms within an individual. Nurture is an environmental cause that has
an effect on underlying biological mechanisms and changes these with subsequent effects for
behavior.
However, in this thesis, the concepts of nature and nurture are approached as factors
that can underlie certain behavior but are not necessarily the cause of the behavior. Nature and
nurture are discussed as the equivalents of biological and environmental mechanisms that
underlie aggression in recurrent violent offenders. This distinction should be considered when
interpreting the results with respect to the nature and nurture paradigm. In other words, to
tackle recidivism, it is necessary to look at the underlying biological and environmental
mechanisms of aggression. Subsequently, it is important to see whether the prison
environment contributes to the preservation of aggressive behavior and also how this affects
the tendency of recidivism to occur after release.
Hypothetical Substantiation from Theoretical and Scientific Considerations
Based on previous research and theoretical views it can be hypothesized that both
nature and nurture independently and interdependently contribute to recidivism. In this
section three arguments with a focus on nature, nurture as well as an interaction between
nature and nurture are presented. According to the nurture point of view, enriched
environments are essential for the maturation of the brain, specifically for the maturation of
the prefrontal cortex. Thus, an impoverished environment, like a prison, will hamper the
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focusing on nature, it can be hypothesized that offenders who have the tendency to reoffend,
already have an underlying mechanism that makes them more prone to aggressive tendencies
than non-reoffenders. Lastly, from a view where both nature and nurture interact to contribute
to recidivism, it can be argued that an impoverished environment, like a prison, will have a
negative effect on the underlying mechanisms of the brains of high recidivism risk offenders.
A negative effect could mean that underlying mechanisms that are deviant in offenders get
further impaired, which contributes to more problematic behavior and a subsequent higher
likelihood for recidivism. The nature-nurture interaction hypothesis gives rise to the
possibility that the environment can influence brain structures.
All hypotheses are derived from different theoretical views and relevant research. To
understand the underlying causes of being an offender it is important to look at the different
contributing behavioral components and the related underlying brain mechanisms. The group
that represents the biggest portion of recidivists are violent offenders. (Ministerie van Veiligheid en Justitie, WODC, 2012). A violent offense is defined as an offense that is accompanied with a high level of aggression (Tapscott, Hancock, & Hoaken, 2012).
Aggression can thus be seen as an evident behavioral component of violent offending.
A theoretical explanation for the neural substrate as underlying mechanism of
aggression, stems from the Cognitive Depletion (CD) theory. According to the CD theory, a
state of self-regulation, refers to the capacity for altering one's own responses, especially to
bring them into line with standards in society and to support the pursuit of long-term goals. A
major tenet of the CD theory is that engaging in acts of self-regulation draws from a limited
"reservoir". When this reservoir gets depleted, it results in a reduced capacity for further
self-regulation. From the CD’s theoretical view, aggressive behavior can therefore be seen as the
consequence of a lack of self-regulation, and a depleted reservoir (Baumeister, Vohs, & Tice,
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However, innate self-regulation is lower in some people, which leads to a higher
tendency to act with aggression (as with offenders). The CD theory does state anything about
differences between people in behalf of the limit of their reservoirs. One behavioral
component that is related to aggression and can be seen as the equivalent of this reservoir is
impulsiveness. Impulsiveness involves a tendency to act on a whim, displaying behavior
characterized by little or no forethought, reflection, or consideration of the consequences.
When losing so-called “impulsive control”, it is very likely that expression of whimsy
behavior will occur (van den Bos, 2007).
It can be argued that impulsiveness and self-regulation are a key factor in one form of
aggression: reactive aggression. Reactive aggression is the reaction to a perceived threat, it is
impulsive, hostile, an act of self-protection and accompanied with a lack of self-regulation. It
mostly derives from a state of anger. Reactive aggression can be seen as the most prominent
form of aggression among violent offenders (Tapscott at al., 2012). Proactive aggression on
the other hand, is a planned instrumental reaction to a perceived opportunity of positive
outcome; it is deliberate and implied for reaching personal goals. It is not accompanied with
anger and is often seen in premeditated crimes (Tapscott at al., 2012).
Reactive aggression is the form of aggression that is prominent in violent offenses,
but, what contributes to the inclination towards aggressiveness being higher in some people
that leads them to offending, while in others it does not? It is important to see whether there
are specific brain mechanisms that can be related to impulsiveness and self- regulation.
Studying differences in brain mechanisms underlying differences in between people in
impulsiveness and self- regulation, can give insight in the inter-individual differences in the
expression of aggression.
Accordingly, it can be argued from the Cognitive Energetic Model (CEM) that the
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CEM argues that the prefrontal cortex plays an important role for impulsiveness, a trait that is
not only prominent in children with Attention Deficit Hyperactive Disorder (ADHD) but is
also a key concept in reactive aggression (Tapscott at al., 2012). The CEM states that there is
an arousal deficiency in brains of ADHD children. This arousal deficiency derives from lower
resting state activation in frontal areas in ADHD brains in comparison to normal brains. Due
to low frontal resting state, the brain activity levels need more time to arrive at a desired state
of arousal to perform a task. Subsequently, to arrive at a desired state of activation, the brain
needs to give more effort. This extra boost of arousal can cause the brain to over activate
(Sergeant, 2000). Over-activation of the brains of ADHD children was in the study of
Sergeant (2000) reflected through more errors on a specific task compared to normal children.
It can be argued that the main argument of the CEM for low frontal resting state
activity in ADHD brains can be applied similarly for high-risk recidivism offenders.
Impulsiveness plays a factor in both ADHD and aggressive behavior. Subsequently,
aggression in offenders is not in line with the perceived threat. Since the reaction is not in
proportion with the stressor, it can be seen as over-activity. Aggressive behavior itself can
therefore be explained from a similar “over-activation” view as stated in the CEM. Therefore,
frontal resting state could also be low in the brain of offenders. Accordingly, the research
by Giancola and Zeichner (1994) gave insight in the fact that prefrontal functioning is
different in higher aggressive men. From the results it was found that men who were more
aggressive performed less on a tasks of frontal lobe functioning than men who were lower in
aggression.
The theoretical views from both CD and CEM theory give insights in the underlying
mechanisms of offending. From the hypothesis where nature and nurture interact, it was stated
that a stressful environment, like a prison, will have a negative effect on deviant underlying
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brain structure stems from research on the plasticity of adult brains. In a study done by
Maguire et al. (2000), which studied the brains of taxi drivers. It was found that taxi drivers
had larger posterior hippocampi than non-taxi driving control subjects. Thus, brain structure
seems to adapt with more exposure to the same environmental influences, even in adults.
Studies have also shown that the environment can have negative effects on the brain.
Research from Krech, Rosenzweig and Bennett (1962) shows that depletion of resources from
the environment has its effects on underlying brain mechanisms and subsequent behavior.
Rats were placed in different environments. Rats in enriched environments showed better
discriminating skills after being placed in an environment with ability to exercise and play.
Both morphology and biochemistry of the animal's correlated with better problem-solving
ability. Reversed effects were found with deprived rats in blunt cages.
Based on the represented arguments from theoretical backgrounds and subsequent
research, more specific representations of the nature-nurture hypothesis can be made. For
nature, it can be hypothesized that processes of impulsiveness and lack of self-regulation
underlie aggressiveness in offenders. Subsequently, it is possible that the prefrontal cortex is
the neural equivalent of these processes. For nurture, it can be hypothesized that a deviation in
the prefrontal cortex is formed through environmental influences and that a non-stimulation
environment, like a prison, will further impair these mechanisms. Impairment has in this way
subsequent effects for aggression and recidivism risk. The main objective of this thesis is
therefore: What is the role of environmental quality in the relationship between the prefrontal
cortex and impulsivity and its subsequent effects on aggressive behavior?
To investigate this nature- nurture interactive view, it is first important to describe the
link between the prefrontal cortex and mechanisms that instigate aggression and how impulse
control plays its part. This is of relevance because it has to be clear how these mechanisms
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relevance to see how the underlying mechanisms of aggression work in the specific
population of offenders, it is important to see if there is already, as hypothesized by the nature
view, a decline in impulse control in offenders which is causing reactive aggressive acts.
Finally, to answer the research question, it is important to look at how and if the prison
environment has a negative effect on the underlying structures of aggressiveness in high
recidivism risk offenders.
The Relation between Underlying Mechanisms of Impulsiveness and Aggression
The first section of this thesis describes the first component of the nature-nurture
interaction hypothesis: nature. Impulsiveness contributes to the degree of aggressiveness a
person exerts (Baumeister et al., 2007; Tapscott at al., 2012; van den Bos, 2007). The CEM
states that for nature, the neural derivative of impulsiveness is a specific arousal deficiency in
the frontal lobe that can result in over activation when preparing for a task (Sergeant, 2000).
Therefore, it can be hypothesized that an arousal deficiency, or other kinds of deviation in the
frontal lobe, can also be present in the brains of higher aggressive people. In this section, this
thesis examines what can be stated as the neural base of impulsiveness and if this underlying
structure can also be related to aggression. This is of relevance because it has to be clear how
these mechanisms work before a search for the influence of environment can take place.
The well-known case of Phineas Gage describes the very first evidence for frontal lobe
damage related to impulsive behavior. As described by Harlow, the frontal region of Gages
brain was damaged by an accident in which an iron rod was pierced through his skull (Harlow 1868). A description of his behavior after severe frontal lobe damage states that “he is fitful,
irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint of advice when it conflicts with his desires, …. devising many plans of future operation, which are no sooner
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arranged than they are abandoned in turn for others appearing more feasible” (Harlow,
1868).
To link Gage’s impulsive behavioral change to an exact brain region, Ratiu et al.(2004) conducted a study to determine the exact location of Gage’s brain damage.
Computed tomography (CAT) scanning was used to create a three-dimensional reconstruction of Gage’s skull. CAT is a computer technique that scans predetermined parts of the brain. In Gage’s case, 1.5 mm-thick slices of the skull were scanned. To determine the precise location of impact and trajectory of the iron rod, the slices were combined to create a biochemical
model. The resulting three-dimensional picture showed that the injury was limited to the left
frontal lobe. In precise terms, only the medial and lateral orbito-frontal and dorsolateral
prefrontal regions of the left frontal lobe were injured. This shows that more impulsive
behavior can be a result of damage to these precise areas of the prefrontal lobe. However, this
cannot be seen as conclusive evidence for the direct neural substrate of impulsivity since no
harsh conclusions can be made based on one single case. Subsequently, in reality the
behavioral changes of Gage could be much more complex than can be derived from one
description by Harlow (1868). It is important to see if measurements of impulsiveness can be
related to the brain regions specified by Ratiu et al. (2004).
A task that can be used to measure inter-individual differences in impulsiveness, is the
Go/NoGo tasks. Go/NoGo tasks require a participant to perform an action when given a
certain stimuli (e.g., press a button - Go) and inhibit that action under a different set of stimuli
(e.g., not press that same button - No-Go) (Swick, Asley & Turken, 2011). In other words,
when the button is not pressed in the NoGo trial, inhibition is successful. When the button is
pressed, inhibition is unsuccessful and unintended behavior is exerted. Inhibition can be seen
as the equivalent for the degree in which a person exerts unintended behavior in other words,
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therefore, Go/NoGo tasks can be used to state something about a person’s impulsiveness and
self-regulation abilities.
To determine whether the orbitofrontal and dorsolateral regions, as found to be of
importance for impulsive behavior by Ratiu et al. (2004), can also be related to overall
impulse control, Swick, Ahsley and Turken (2008) conducted a study using Go/NoGo tasks.
The participants of this study consisted of a patient group with left inferior frontal gyrus (IFG)
lesions and a comparison patient group with orbitofrontal lesions. There were easy and hard
conditions, defined by the predictability of the Go versus NoGo situations. In the easy
condition, Go versus NoGo was predictable since NoGo stimuli were shown in 50% of the
trials. In the hard conditions, Go versus NoGo was random and, therefore, not predictable. It
was found that left IFG patients pressed the button for the NoGO trials more often than
controls in both easy and hard conditions, but were more impaired in the hard condition when
a greater degree of inhibitory control was required. However, the patient control group with
orbitofrontal cortex lesions showed intact performance. Results showed that impulse control
was implicated in the patients with left IFG lesions, in contrast to the patients control group,
where impulse control is not related to orbitofrontal cortex lesions. Therefore, impulsiveness
can be seen as related to the left IFG but not to the orbitofrontal cortex.
However, there are limitations referring the use of easy trials to define implication of
impulse control. In trials where inhibition is very predictable, it is unlikely that subjects have
to stop an initiated response; instead, they are probably making a decision about whether to
act or not because it is easy to predict if the following stimuli will be a NoGo stimuli. In this
way, it could be that subjects do not have to stop an initiated response because they already
know on beforehand that they do not have to act. Therefore, no response is initiated before the
NoGo stimuli is shown. This deciding whether to act or not, is a different process than
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IFC damage may thus have affected the decision by impairing representation of task rules
(Aron, Robbins and Poldrack, 2014). Subsequently, no hard conclusions can be made, since
there is never a one-on-one comparison of brain damage between one person and the other,
which links to the same behavioral consequences. The use of participants with lesions is
therefore susceptible to bias.
Relating inhibition to brain activation and not lesions and to study the different
processes in right and left IFG, Swann et al. (2012) conducted a study where precise brain
activation during inhibition tasks was measured using electrocorticography (ECoG). ECoG
measures brain activity by using electrodes placed directly on the exposed surface of the brain
to record electrical activity from the cerebral cortex (Swann et al., 2012). In four patients,
brain activity was measured while they performed a stop-signal task. On each trial,
motor-response was initiated; pressing a button. A stop-signal, which was randomly implemented on
a minority of the trials, required the patient to stop the initiated motor response. For each patient, right IFG beta frequency band (∼16 Hz) response was greater in unsuccessful stop trial, compared to successful stop trials. In addition, the right IFG response occurred
100-250ms after the stop signal, a time range consistent with a putative inhibitory control process
rather than with stop-signal processing or feedback regarding success. In each patient, for stop
trials, alpha/beta activity got desynchronized in the primary motor cortex (M1). Together, the
results suggest that behavioral stopping is implemented via synchronized activity in the beta
frequency band in a right IFG network, with downstream effects on M1. Concluding, impulse
control, the equivalent of inappropriate response tendencies, may be displayed via a specific
right IFG/primary motor cortical network.
From the conclusions drawn from the study by Swann et al. (2012) it seems that the
right inferior frontal cortex, not the left IFG, is involved in inhibition of unintended responses.
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Swick et al. (2008), the left IFG can be seen as the substrate of deliberate deciding whether to
act or not. However, in the study of Swann et al. (2012) there was no measurement of activity
in the left IFG. Only the right IFG was assessed, therefore, there cannot be a conclusion that
determines the precise differences between left and right IFG functioning during inhibition
tasks.
Nevertheless, it can be argued that both impulse control and deliberate
decision-making can be affected by aggression. When impulse control is low, aggression can be
exerted. When rational decision making is impaired, the assessment of the situation can be
disturbed and, therefore, the inappropriate response of aggression can be exerted. However,
the previous studies used impulsiveness as a representation of aggression. Impulsiveness is
related to aggression. Neural mechanisms can be similar, but not the same.
To find closing evidence for which precise neural mechanisms of impulsiveness are
involved in acts of aggression, Pawliczeka et al. (2013) conducted a study that relates the
neural bases of inhibitory control to the expression of aggression. Aggression was measured
with the Aggression Questionnaire (AQ, Buss and Perry, 1992). Men scoring above the 85th
percentile of the total scores were indicated as high aggressive, while men scoring under the
15th percentile were indicated as low aggressive. Brain activity was measured using
functional magnetic resonance imaging (FMRI). In FMRI, activity is measured by the ratio
between the oxygen-rich and oxygen-poor hemoglobin, oxygen levels increase when activity
increases and is displayed with the use of coloring in a three-dimensional image of the brain
on a computer (Pawliczeka et al., 2013). Neural activation was compared during an emotional
version (including angry and neutral faces) of the stop-signal task. Angry faces were
implemented as stop condition. The high aggressive group made more mistakes by responding
to angry faces, compared to the low aggressive group. This higher motor impulsivity was
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primary motor cortex.
Thus, more aggressive behavior is related to lower response inhibition and, therefore,
impulsivity. The neural equivalent of this mechanisms is situated in the right pre-SMA,
included the right middle frontal and motor cortex. Notably, the study by Pawliczeka et al.
(2013) showed an extra result when checking for response inhibition in relation to activation
levels over several consecutive trials. Response inhibition improved during anger trials in
both groups, suggesting a facilitation effect through heightened activation in the related brain
regions. In both groups, inclusion of the anger stimuli enhanced the activation of the motor
and somatosensory areas, which modulates executive control, and of the limbic regions
including the amygdala. It seemed that these structures, and the subsequent effects on
behavior, can be altered with repetition training of response inhibition in reaction to triggering
stimuli.
In conclusion of this section, high aggressiveness can be related to less impulse
control/inhibition. The underlying neural mechanisms of impulse control are the inferior frontal gyrus’ of both hemispheres. More precisely, the left inferior frontal gyrus is related to the process of deliberately deciding on whether to act or not, whereas the right inferior frontal
gyrus is related to a process of undeliberate inhibition of unwanted behavior. Both left and
right inferior frontal structures can be seen as controlling the inhibition of an inappropriate
response tendency such as aggression. Subsequently, for not only the tendency but also the
direct inhibition of unintended behavioral responses, the primary motor cortex and
pre-supplementary motor area (SMA) seem to be related.
These conclusions, however, are made upon the distinction between degrees of
aggressiveness based on reports of aggression (Buss and Perry, 1992). When using
self-reports of aggression, no direct conclusions can be made regarding aggressive behavior,
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aggressive in reality. To see whether these underlying structures play a role in the
manifestation of aggressive behavior, it is important to look at the deviant underlying
structures in violent offenders. In violent offenders, there can be certainty that aggressiveness
is acted out since violent offences are accompanied with a high level of aggression.
The Role of the Underlying Mechanisms of Aggression in Offending
Previously, different structures in the prefrontal cortex were found to be of importance
for impulsiveness related to aggression. However, these results did not give concluding
evidence that these underlying mechanisms could be directly linked to the expression of
aggression. To see how the underlying mechanisms of the expression of aggression work, it is important to look at the specific offenders’ population. Therefore, this section further elaborates on the notion of the nature view in finding which precise underlying mechanisms
contribute to aggression in violent offenders. Knowing the exact neural substrate of
aggression in offenders sets the base for better insight in why some offenders reoffend, while
others do not and moreover, to reduce recidivism, if these factors can be influenced.
In violent offenders, there can be certainty that aggressiveness is expressed since
violent offences are accompanied with a high level of aggression (Tapscott et al., 2012). To
see whether impulsiveness can be related to the direct expression of aggression, Babinski,
Hartsough and Lambert (1999) conducted a study in which participants were followed
prospectively from childhood to early adolescence to relate early impulsiveness to offending
later in life. Early childhood behavior ratings by parents and teachers showed that
hyperactivity-impulsivity symptoms predict a greater likelihood of having an arrest record for
males but not for females. For male subjects who were identified as recidivists (convicted 10
times or more), hyperactivity-impulsivity were significant predictors. Therefore, it appears
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offending and even stronger, to recidivism risk.
However, Babinski et al. (1999) emphasize on the relationship between early
symptoms of attention deficit hyperactivity disorder (ADHD) and offending. Even though this
impulsive population has a higher chance of conviction in adulthood, the ADHD population
does not necessarily generalize to the whole aggressive offenders’ population. There cannot
be assumed that impulsiveness in both groups has the same underlying mechanisms because
there is little insight in whether impulsiveness would be present independently without
ADHD, or the other way around, there is no evidence that there is no ADHD among
aggressive offenders. Without this generalization, there cannot be concluding evidence that
impulsiveness predicts offending since this concept can be underlying different behavioral
symptoms and, therefore, also has different underlying neural mechanisms. Subsequently,
there cannot be concluding evidence that the difference between offenders at higher risk for
recidivism (violent offenders) and offenders that do not recidivate (normal offenders) can be
linked to differences in the neural substrate of impulsiveness.
To see whether the kind of offense can be traced back to neural differences, Aigner et
al. (2000) conducted a study to see if the brains of violent offenders were different from
non-violent offenders. In the high violence group, it was demonstrated that 65.5% of the subjects
had abnormalities in the brain structures, as compared to 16.6% of the low violence group.
Overall, abnormalities were situated in prefrontal regions and consisted of enlarged or
reduced lobes or lesions in this area. The authors concluded that not only impulsiveness is
related to deviations in the prefrontal cortex (Swann et al., 2012; Pawliczeka et al., 2013), but
also the aggression in violent offenders can be linked back to impairments in the prefrontal
regions.
However, the focus in the study of Aigner et al. (2000) study lies on abnormalities and
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brain abnormalities in prefrontal regions. Therefore, abnormalities in prefrontal regions
cannot be used as a general equivalent of aggression for the whole violent offenders’
population.
To specify the precise underlying mechanisms of aggression in violent offenders,
Philipp-Wiegmann et al. (2011) focused on a process that was previously shown to be
impaired in general aggressive individuals: inhibition (Swann et al., 2012). To study the
impairment of inhibition in aggressive offenders, prisoners who had committed severe violent
crimes were compared to controls with no history of violence in their ability to inhibit an
induced response. The ability to inhibit a response was measured with the use of transcranial
magnetic stimulation (TMS) on both hemispheres. TMS is a technique that uses
electromagnetic induction to stimulate brain areas. To simulate inhibition, the premotor cortex
was stimulated. Stimulation of the premotor cortex activated the tendency to move which had
to be deliberately inhibited by the participants. A reduced cortical inhibition (ISI: 3 ms) was
found in the left premotor cortex of violent offenders compared to control subjects. The
authors concluded that inhibition problems are related to the premotor cortex in violent
offenders. These findings corroborate with the hypothesis of inhibition deficits and frontal
cortex dysfunction in violent offenders.
However, cortical inhibition was merely 3 ms slower in offenders than it was in the
control goup. Even though on brain functioning level this is a relevant difference, it does not
prove that this relates to the expression of aggression directly. The offenders in the study of
Philipp-Wiegmann et al. (2011) only showed the inhibition deficit on a neural level and not
on a behavioral level. In case that the measurement also applied at the behavioral level, the 3
ms delay of inhibition should have resulted in a motor response. However, no motor response
was shown.
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not prepared for action. It needs to overcompensate and can, therefore, be the brain
mechanism underlying inhibition problems and the expression of aggression in violent
offenders (Sergeant, 2000). This hypothesis can be supported by measurements of brain
activity with the use of electroencephalogram (EEG). EEG is a method that measures brain
activity by registration of brain waves. Different kinds of brain waves relate to different kinds
of processes. For example, alpha waves are one type of brain waves that are related
to inhibition of areas of the cortex not in use and beta waves are associated with motor
control. When an action has to be conducted, alpha activity is decreased and beta activity is
increased. The suppression of an action is the equivalent of inhibition (Keune et al., 2012).
Therefore, it can be hypothesized that in the brains of violent offenders there is a deficit in the
decreasing of alpha and increasing of beta waves.
Keune et al. (2012), examined if this assumption applied for violent offenders by
studying brain activation in a state of rest. Activity was assessed by measuring anterior brain
asymmetry through the alpha and beta band in resting-state with the use of EEG. Brains of
imprisoned violent offenders were characterized by stronger alpha activity in the right
hemisphere than the left-hemispheric, which was putatively extreme in anterior regions in one
third of the cases. Too much alpha activity, as in this case, indicates that the brain is resting
too much and not prepared for action. Therefore, in support of the notion made by the CEM, it
can be stated that a higher degree of aggression is associated with overcompensating of the
brain, caused by stronger right-frontal alpha activity.
In conclusion of this section, the underlying brain mechanisms of aggression in
offenders are strongly related to those of impulsiveness and general aggression. Moreover,
brains of violent offenders are different from those of other offenders based on deviations in
the prefrontal regions. More precisely, inhibition problems are also present in this population
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conclusions support the notion derived from the CEM, that there is a deficiency in the arousal
in the prefrontal cortex of violent offenders which leads to over activation and, therefore, the
expression of aggression. Inhibitory deficits which are reflected through problems with
activation in the prefrontal cortex and deviations in the premotor cortex can, therefore,
contribute to the fact that especially violent offenders are at high risk of recidivism. It is
now clear that there are different regions of the brain that are deviant in violent offenders.
What remains is the last component of the nature-nurture hypothesis: nurture. The question
remains if the prison environment contributes to the problem of recidivism by influencing the
deviant mechanisms of the brain underlying violent offending and moreover if this can be
changed with prospects on reducing recidivism.
Environmental Influences on the Underlying Mechanisms of Aggression in Offenders
In this last section there will be discussed whether nurture, that is to say –environment,
has an influence on the previously stated regions in the brain which are linked to
aggressiveness in offenders. To be more specific, this section offers a close examination if the
different parts of the inhibitory circuits and to impulsiveness related regions (inferior frontal
gyrus, primary motor cortex the over-activity of alpha brain waves; Swann et al., 2011;
Philipp-Wiegmann et al., 2012; Pawliczeka et al., 2013; Keune et al., 2012) that are found to
be linked to the expression of aggression in violent offenders can be influenced by
environment. In order to reduce recidivism, one should not fight the symptoms but work with
underlying mechanisms of problematic functioning. The question remains if the prison
environment contributes to the problem of recidivism by influencing the deviant mechanisms
of the brain underlying violent offending and moreover if this can be changed with prospects
on reducing recidivism.
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negative effects on underlying brain mechanisms and subsequent behavior in rats. It can be
hypothesized that nurture contributes to higher recidivism. Specifically, negative
environmental influences like a non-stimulating prison environment, can further degrade
inhibitory connections or heighten alpha activity. Hochstetler and Delisi (2005) studied if
different environmental characteristics in prison had a similar effect on the exerted aggressive
behavior by inmates. Surveys were used to examine how inmate individual characteristics,
inmate attitudes, self-control, affective experiences of prison including perception of the
environment, participation in the inmate economy and witnessing victimization predicted
serious prison misconduct. Results showed that participation in the inmate economy and
witnessing victimization were particularly significant correlates of misconduct. In conclusion,
this provides support that specific prison environmental characteristics affect aggressive
behavior in prison.
However, only direct effects of the prison environment characteristics on behavior
were noted. How the underlying brain mechanisms of these offenders were affected was not
studied. It merely states that a prison environment does have some influence on prison
behavior, it does not show that this has an influence on outside prison behavior and could lead
to reoffending. In line with previous findings (Swann et al., 2011; Philipp-Wiegmann et al.,
2012; Pawliczeka et al., 2013; Keune et al., 2012) the study of Barbosa and Monteiro, (2008)
shows that offenders are often found to have inhibitory dysfunctions which relate to prefrontal
functioning. In addition to the previous studies, however, this study includes recurrent
offenders. The hypothesis questioned whether people who repeatedly participate in forms of
recurrent crime exhibit an executive deficit. A battery to assess executive dysfunction was
administered – the Behavioural Assessment of the Dysexecutive Syndrome (BADS) –to an
experimental group of 30 inmates convicted of crimes against property, and a control group of
21
group in their global scores on the battery, as well as on the majority of subscales. So, it
seems that criminal recurrence and the resistance to penal measures is related to scarcity of
inhibitory control that these individuals have over their behavior (Barbosa and Monteiro,
2008). Not only are inhibition problems found in offenders in general, they also have a
connection with especially recurrent criminal behavior. This study however, does not prove
that the prison environment itself induced executive dysfunction. Subsequently, direct brain
measurements of these dysfunctions having a neural substrate are not shown.
Anckarsäter et al. (2007) studied whether the prison environment itself has an
significant effect on deviant regions of the brain in prisoners. The study included a take on the
influence of the prison environment by following a group of high risk offenders who had, in
line with the previous findings (Keune et al., 2012), predetermined activity problems. This
study included nine offenders convicted of lethal or near-lethal violence in whom single
photon emission tomography (SPECT) previously had demonstrated frontotemporal
hypofusion (FTHF). SPECT is diagnostic technique by which a 3-dimensional image is
obtained of the distribution of the radioactive isotope in the body. Areas that show higher
activation, mean higher rates of isotope and deeper colors will be shown (Anckarsäter et al.,
2007). In this case, FTHF means a remarkably low disposition of isotopes equivalent to
activity problems in fronto-temporal regions. Anckarsäter et al. (2007) studied the influence
of environment on FTHF by conducting a follow-up study consisting of prisoners with
predetermined FTHF. The mean interval was 4 years in which they all were imprisoned. The
results showed that the initially observed hypoactivity was found to have remained unchanged
at follow-up.
Again, this proves that there are indeed violent offenders that have brain activity
problems, but these deviations seem to be constant over time spend in prison. This leads to the
22
of this highly aggressive group. Reoffending can be related to a stable dysfunction in
prefrontal regions and there is no influence of prison characteristics that further aggravates the
underlying brain mechanisms, heightening the chance for recidivism. It could be that
recidivism in some violent prisoners is a product of just the pre-imprisoned deviations in
underlying mechanisms, so nurture has no effect. However, the study by Anckarsäter et al.
(2007) had very low number of participant, therefore, harsh conclusions cannot be made.
The line of research on this topic is rather scarce, however, influence on the
underlying brain mechanisms of aggressive offenders can be approached from a different
point of view. As mentioned before, the research of Pawliczeka et al. (2013) showed that
using the emotional stop task, response inhibition improved during anger trials, suggesting a
facilitation effect through heightened activation in the related brain regions. Most importantly
it shows that these areas can be influenced by some sort of environmental stimuli. That brain
mechanisms of aggression can be influenced by recurrent exposure gives rise to the possible
idea that some sort of “training” can target the deviant mechanisms underlying aggression in
offenders that are at high risk of recidivism. Therefore, methods that focus on changing
interconnectivity of inhibitory circuits or lowering alpha activity/heightening beta activity in
the prefrontal cortex need to be explored in their use for changing aggression in violent
offenders.
A method for altering brain activity is EEG neurofeedback. EEG neurofeedback uses
feedback to inform the person involved if desired or not desired brain activity is apparent. With the aid of this "feedback" one could affect one’s own brain activity via operant conditioning (Allen, Harmon-Jones & Cavander, 2001). The aim of neurofeedback is to
suppress the waves that are related to a specific complaint and to reinforce the waves that
reduce the complaint. As studied by Keune et al. (2012), brains of imprisoned violent
23
neurofeedback would be used to imply conditioned changes in the brain waves of offenders,
the excessive presence of alpha waves should be suppressed and opposing beta waves should
be reinforced.
Accordingly, Allen et al. (2001) conducted a study in which the effectiveness of EGG
neurofeedback for changing alpha/betha ratios in the brain were examined. In this study, alpha
activity of the left prefrontal cortex was trained. If desired alpha waves showed in the EEG
measurement, a sound was played. In this way participants knew when the desired activity
was present. After the five-day training, a significant difference was found in the level of
alpha activity in the left prefrontal cortex. Subsequently, assessment of pre -and post training
measurements of perceived intensity of emotions, showed that participants felt that their
reactions to emotionally charged video fragments were less intense after training. This was in
line with EMG facial registration of implicit emotion expression.
Facilitation of both alpha activity and perceived emotions shows that there could be an
influence on the underlying functional dysfunctions that are related to aggressiveness in
offenders with EEG neurofeedback. It was proven that alpha activity can indeed be influenced
by conditioned feedback. Moreover this also had effects on the experienced emotions. In
broader context this can mean that asymmetrical alpha activity in the left prefrontal cortex of
offenders can be changed with EEG neurofeedback, subsequently, this can even have effects
for the experienced emotions and lowering of aggressive tendencies. Changing of alpha
activity particularly in aggressive offenders was, however, not studied. Therefore, these
conclusions can only apply to a normal population. Subsequently, EEG neurofeedback is a
costly and extensive method, it is in reality not the most convenient method to use on an
inmate population. It is not applicable for large populations with challenging behavior.
A more usable method that can be implemented in prison is physical exercise. Most
24
but do not have a special set of structured activities. Prisoners are free to spend their time at
the gym as they please, therefore, there is sometimes no exercise at all, just attendance
(Muller & Vegter, 2009).
In the study of Eggermont et al. (2009) it was examined whether physical exercise can
benefit cognitive abilities. A study was conducted within an elderly population to determine
the relationship between physical activity and cognition, specifically executive function.
Participants aged 70 or more, were assessed on activity with use of the Physical Activity
Scale for the Elderly (PASE) and cognitive function, using a battery of neuropsychological
tests. Results showed that older adults who engaged in more physical activity performed
significantly better on all cognitive tests compared to not physical active elderly.
The link between cognitive functioning in elderly and offenders can be made through
the fact that in offenders inhibition processes strongly overlap with executive functioning
processes. For example, use of executive functions is necessary in situations where
adjustment of behavior required and situations where automatic behavior and habits must be
restrained are also underlying inhibition (Eggermont et al., 2009). Therefore, it can be argued
that physical exercise can possibly contribute by influencing the inhibition deficiencies in
violent offenders. However, there can merely be speculations about these effects for
aggressive offenders, since populations are not comparable.
In conclusion of this section, it seems that the prison environment elicits more
aggressive behavior in recurrent offenders who have predetermined inhibitory problems.
However, the prison environment did not show to have a worsening effect on the neural
correlate of inhibition deficiencies. Prison time itself does not worsen vulnerable underlying
mechanisms in offenders and can , therefore, not be seen as contributing to recidivism. It can
be stated that mechanisms in offenders who are at risk for recidivism already have underlying
25
prison environment itself had no further influence on the relationship between the underlying
mechanisms of aggression and recidivism. Nevertheless, positive changes in the underlying
mechanisms that contribute to aggression in violent offenders may be implemented with EEG
neurofeedback and physical exercise.
Conclusions and Discussion
The current intervention programs for reducing and preventing recidivism proves to be
ineffective in practice. Therefore, the aim of this thesis was to provide more insight in the
cause of this problem but more important: if there can be a way to reduce recidivism. This
problem was approached from the traditional two way paradigm in psychology: is it caused
by nature or by nurture. For nature, it was hypothesized that processes of impulsiveness and
lack of self-regulation underlie aggressiveness in offenders. Subsequently, the prefrontal
cortex could be seen the neural equivalent of these processes. For nurture, it was
hypothesized that a deviation in the prefrontal cortex is formed through environmental
influences and that a non-stimulation environment, like a prison, will further impair these
mechanisms. Impairment has in this way subsequent effects for aggression and recidivism
risk. The main objective of this thesis was therefore: what is the role of environmental quality
in the relationship between the prefrontal cortex and impulsivity and its subsequent effects on
aggressive behavior.
The conclusions on behalf of the nature hypothesis are that indeed different
mechanisms situated in the prefrontal cortex underlie aggressiveness. Based on the results
found in this thesis, higher aggressiveness can be related to a lack of impulse control and
inhibition problems. To be more specific, a lack of impulse control and inhibition problems are related to deviations in the inferior frontal gyrus’, primary motor cortex and right pre-supplementary motor area. Subsequently, for violent offenders in particular, inhibition
26
problems are also present and are related to deviations in brain activity in the prefrontal
cortex. Specifically a higher degree of aggression in violent offenders is associated with
stronger right-frontal alpha activity. These conclusions support the notion derived from the
Cognitive Energetic Model, that there is a deficiency in the arousal in the prefrontal cortex of
violent offenders which leads to over activation and, therefore, the expression of aggression.
It can be argued that underlying deviant mechanisms prune offenders to be more aggressive
with subsequent effects for the chance at recidivism.
For the conclusions on behalf of nurture, the prison environment influences the
expression of aggressiveness. However, this environment does not seem to act on the
underlying arousal deficiency in aggressive offender groups. Nevertheless, there are
environmental influences that are beneficial for changing the underlying structures linked to
the inhibitory deficits in offenders. Promising results are shown from brain activity training
with EEG neurofeedback and the relation between physical exercise and inhibition abilities.
Although aggressiveness in offenders was approached from a biological and an
environmental approach, nothing can be stated about the origin of the found deviations. For
this line of research it is important to make a clear distinction between cause and effect. On
one hand, aggressiveness can be innate and therefore causing offending. On the other hand
environmental influences during development could have formed these structures to be
different and therefore causing offending. Specifically, if underlying mechanisms are prune to
change by the prison environment, it can be stated that brains of offenders are wired
differently because of the environment they developed in created the deviant mechanisms
underlying violent offending. However, there are strong indications that aggressiveness is
mostly innate, as it was stated that impulsive processes are present from childhood (Babinski,
1999), biological (Eggermont et al., 2009) and not influenced by endured imprisonment
27
and non-aggressive groups could be innate or formed by environment is possible since the
direct origins of the deviating mechanisms in violent offenders were not studied. For further
research it can be interesting to focus on the origin of this aggressive behavior to find early
specifies in the development of the brain that can be used to predict offending. Naturally, it is
better to give insight in the origin of offending so that offending itself can be predicted so that
understanding recidivism is not even necessary.
Subsequently, for answering the research question evidence is limited. At this point no
significant conclusions can be made about direct prison environmental influences on
underlying structures. There was only one research that studied the underlying mechanisms in
relation to the change over time during imprisonment (Anckarsäter et al., 2007).
Subsequently, sample size was small and only brain hypoactivity was studied, while
aggressiveness in violent offenders is related to several deviant mechanisms (Swann et al.,
2011; Philipp-Wiegmann et al., 2012; Pawliczeka et al., 2013; Keune et al., 2012). It is
interesting to have future research focus on the prolonged effects of imprisonment on all the
different underlying mechanisms that are important for impulsiveness, inhibition and the
expression of aggression.
Moreover, caution is required with the interpretation of the relevance of every studied
structure in relation to aggression in offenders. This overview maintains different approaches
for studying the same relation between underlying brain mechanisms and aggressive
offending. In practice however, the processes related to the structures of executive
functioning, impulsive behaviour and inhibition are overlapping but not similar concepts.
Distinctive research on every process on its own and its importance for aggressive offending
is needed. Now there can only be speculated that the underlying structures are of importance,
since the mechanisms behind this could possibly be distinct in their degree of contribution to
28
Accordingly to the point of different processes, it is argued that the different tasks
used for measuring response inhibition are not measuring the same underlying construct. It
can be stated that using Go/noGo tasks as well as stop tasks measures different constructs,
since task instruction is different. Not-going cannot directly be the same as stopping an
initiated action (Swick, Asley & Turken, 2011). This can have his implications for
conclusions. Future research has to be distinctive in these tasks so that different underlying
mechanisms for both tasks are differentiated.
Critical notes can also be made in reference to studying the population of offenders. It
is important to look at the foundations of reactive aggression since this is the most prominent
form of aggression in offending. Subsequently, the focus of the intervention programs for
recidivism, lies on a non-clinical group since most clinical groups are placed separately for
specialized care and are, therefore, not part of the general prison population. However
throughout this line of research, there has been made no distinction between normal and
pathological participants in aggression and offenders research. It can be stated that a lot of
disorders are associated with expressing aggression, such as: ADHD, conduct disorders,
ODD, bi-polar disorders, antisocial personality disorders, depression, borderline, drug use etc.
Prevalence of this disorders are more common among standard prison facilities. A research of
Bulten and Nijman (2009) of the prevalence of disorders in Dutch prisons (excluding special
care units) stated that 81.7% of the prisoners had ever had a psychiatric disorder, addiction
included. 56.5% had still a psychiatric disorders. These disorders could have contributed to
offending in the first place and thereby could have biased results in the studies with
aggressive offender participant groups. This is due to the fact that brain functioning is deviant
is clinical populations so this could have biased conclusions about brain function in relation to
aggression. Further research has to be aware of this phenomenon and has to exclude these
29
offenders.
Further insight into the (negative) influence of prison on the underlying structures of
aggressive offenders is clinically relevant as a further decline in impulse control will enhance
the risk for aggressive recurrent criminal offenses. Subsequently, better ways to influence
these structures has to be studied to look at possibilities to lower the recurrent criminal rates.
This thesis provides the basis for approaching problematic functioning in terms of underlying
mechanisms and not just in terms of targeting the symptoms. Methods for studying underlying
mechanisms of problematic functioning as were shown in this thesis, can be implemented in a
larger context of social problems to provide better understanding and solutions for prevalent
30
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