Arch Neuropsychiatry 2019;56302−310httpsdoi.org10.29399.docx

Arch Neuropsychiatry 2019;56:302−310
https://doi.org/10.29399/npa.23369
302
REVIEW
Effect of Exercise on Major Depressive Disorder and
Schizophrenia: A BDNF
Focused Approach
Evrim GÖKÇE , Emel GÜNEŞ , Erhan NALÇACI
Department of Physiology, Ankara University, Faculty of
Medicine, Ankara, Turkey
Psychiatric disorders are remarkable health problems that cause
a
massive social and economic burden, and the issue of their
long-term
and effective treatment is subjected to discussion. The effect of
physical
activity and exercise is under investigation in the treatment of
the major
depressive disorder (MDD) and schizophrenia which are
accompanied by
cognitive dysfunctions. Scientists focus on the positive effects
of exercise
on learning, memory and attention parameters while
investigating the
regulatory role of brain-derived neurotrophic factor (BDNF). In
this

review, the effect of aerobic exercise on peripheral BDNF
levels in MDD
and schizophrenia is examined by including human studies in
which
acute and chronic aerobic exercise are applied. The results
showed that
aerobic exercise caused different responses on BDNF levels,
and some
of the studies were accompanied by the improvement in
cognitive
functions in BDNF changes. In order to comprehend the effect
of aerobic
exercise in MDD and schizophrenia, it is understood that
applying
studies on larger and paired participant groups with different
exercise
frequencies and tensions in necessary.
Keywords: Brain derived neurotrophic factor, aerobic exercise,
schizophrenia, major depressive disorder, cognitive functions
ABSTRACT
Cite this article as: Gökçe E, Güneş E, Nalçacı E. Effect of
Exercise on Major Depressive Disorder and Schizophrenia: A
BDNF Focused Approach. Arch Neuropsychiatry
2019;56:302-310.
302
Correspondence Address: Emel GÜNEŞ, Ankara Üniversitesi
Tıp Fakültesi, Fizyoloji Anabilim Dalı, Ankara, Turkey • E-
mail: [email protected]
Received: 04.09.2018, Accepted: 27.03.2019, Available Online
Date: 15.10.2019

©Copyright 2019 by Turkish Association of Neuropsychiatry -
Available online at www.noropskiyatriarsivi.com
Epidemiological studies indicate that physical activity and
exercise can
prevent and delay the initiation and development of psychiatric
disorders
and have therapeutic effects when used as supportive therapy.
Numerous
animal models and human studies have shown that exercise
promotes
psychological health and well-being, increases cognitive
performance
and functional recovery, and provides a series of structural
changes in the
brain (1, 2). Due to its roles in learning and memory, this
research focuses
on the hippocampus and also emphasizes the mechanisms of
plasticity
triggered by exercise in the prefrontal cortex where executive
functions
are embedded (3). It is considered that the mediators in the
relationship
between exercise and the brain may be myokines secreted by
muscles
that act as a secretory organ in the periphery, as well as a series
of growth
factors. Brain-derived neurotrophic factor (BDNF), a member of
the family
of neurotrophic factors involved in neuronal transport,
modulation, and
plasticity, has become the focus of research seeking an
understanding of
the relationship between exercise and the brain.

BDNF
BDNF, secreted from both the central nervous system and
peripheral
tissues, is a protein of the neurotrophin family, including the
nerve growth
factor, neurotrophin-3 and neurotrophin-4/5. This structure,
which is
synthesized in the form of pre-pro-BDNF in the endoplasmic
reticulum
and which moves to the trans-golgi network through the Golgi
body, is
secreted as mature BDNF or pro-BDNF and is stored in platelets
at a high
level (4). BDNF, with the sources of neurons, microglia and
astrocytes in
the brain, are also secreted from vascular endothelium,
lymphocytes and
smooth/striated muscles. Tropomyosin receptor kinase B
(TrkB), one of
the BDNF receptors, binds to the mature BDNF while p75 (low-
affinity
nerve growth factor receptor) binds to pro-BDNF.
BDNF was first isolated from the tissue of pig brains in 1982
and detected
in human blood in 1995. It has been reported to cross the blood-
brain
barrier and the serum and plasma levels of BDNF have been
associated
with age, gender, and body mass index (5). BDNF is a protein
that affects
neuronal survival, neurogenesis and neuroplasticity in the
central nervous
system and play a role in cell differentiation, axon and dendrite
growth,

synapse formation and synaptic plasticity, and its expression
and release
are related to neuronal activity. BDNF is critical for synaptic
formation
in dopaminergic, glutamatergic and serotonergic neuronal
conduction
and cognitive processes. The main effect of BDNF is on
synaptic
function and neuronal morphology in a region-specific manner
(6). It is
responsible for short-term memory and long-term memory
potentiation
and performs tasks related to remembering, cognition,
emotional state,
spatial direction, and learning (7). BDNF messenger RNA
(mRNA) has
been widely observed in the hippocampus and cerebral cortex.
BDNF-
containing vesicles are found in both the axonal terminals and
dendrites,
and BDNF is also secreted from astrocytes (8). BDNF secretion
may be
via Ca2+ influx from the postsynaptic or presynaptic area Ca2+
influx or
Ca2+ release from intracellular stores (9). Studies reporting the
cognitive
benefits of exercise suggest that BDNF is involved in this
mechanism (10,
11). Animal studies showed that BDNF and tropomyosin
receptor kinase
B (TrkB) receptor activation was increased in various brain
regions during
and after exercise, while human studies detected peripheral
BDNF in the
serum and plasma and found a relationship between the cerebral
and

INTRODUCTION
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Gökçe et al. Exercise, BDNF and CognitionArch
Neuropsychiatry 2019;56:302−310
303
peripheral BDNF levels, which varied according to the type,
duration and
frequency of exercise in different studies (12–14).
Exercise, BDNF and Cognition
Meta-analytical reviews indicate that acute and chronic aerobic
exercise
has a developmental effect on cognition with the most dramatic
effect seen
on its executive functions (15). In this area, where the
mechanism of action
is not fully elucidated, BDNF is suggested to have a potential
mechanism.
The BDNF response to aerobic exercise has been investigated in
the
literature in relation to different acute and chronic exercise
programs at
different doses. In addition to aerobic exercise-induced BDNF
responses,
these studies have also examined cognitive performance
findings. The
method generally used in the studies examining the effects of
aerobic

exercise on BDNF and cognition is the measurement of the
BDNF level
before and after exercise and the application of cognitive tests.
The effect
of BDNF on cognition has been explored mainly through
memory tasks.
The definition of the hippocampus as the main site for BDNF
expression
in the brain (16) its effect on memory tasks makes this choice
meaningful.
Although human studies offer limited opportunities to monitor
BDNF
levels in the brain, it has been found that the peripheral BDNF
levels,
hippocampal volume, and spatial memory results are correlated
(17).
Effect of Exercise on BDNF and Cognitive Function in Healthy
Individuals
Meta-analytical reviews examining the effect of acute exercise
on
peripheral BDNF (18) reported contradictory results, but
predominantly
indicated an increase in BDNF and agreed that this increase was
transient. On the other hand, due to the different methods used
in these
studies, it is established that the responses detected were not
completely
consistent. After 30 minutes of acute exercise, an increase was
observed
in the cognitive functions and BDNF levels of healthy subjects
evaluated
by the Face Recognition Test and the Stroop Test, but the
relationship
between the two parameters was not evaluated (19).

In a review suggesting a positive relationship between exercise
severity
and peripheral BDNF levels, it was reported that high-intensity
acute
exercise provided the greatest increase in BDNF in healthy
subjects. On
the other hand, the BDNF level returned to baseline between 10
and 60
minutes (18). After 20 minutes of intense exercise, healthy
individuals
showed improvement in cognitive findings and BDNF levels
assessed by
the visual spatial perception test, and a significant relationship
was found
between motor memory and BDNF data (20).
In a study evaluating cognitive performance by the reaction
time in the
Visual Spatial Attention Test and EEG after 30 minutes of
moderate acute
exercise in non-trained individuals, the BDNF levels increased
and the
reaction time decreased in exercise groups. The neuroelectric
signals,
which were interpreted as increased attention in EEG (P3
amplitude) and
readiness to respond to stimulus (CNV amplitude), were only
increased
in trained individuals. A significant relationship between BDNF
and
cognitive performance levels was not found. The researchers
interpreted
their results as cardiovascular fitness being involved in the
mechanism of
action of exercise on cognition (21).

A study conducted with healthy subjects that performed severe
acute
aerobic exercise evaluated the BDNF level, inhibitory control
using the
Stroop Test, and cognitive flexibility using Part B of the Trail-
Making Test,
and reported increased cognitive success findings and BDNF
levels. A
significant relationship was found between the increased BDNF
level
and cognitive flexibility success findings. The authors
suggested that
improvement in cognitive performance related to the prefrontal
area in
response to acute exercise could be attributed to an increase in
the BDNF
level (10).
In another study conducted in healthy individuals, the BDNF
level and
executive functions were evaluated using the Wisconsin Card
Sorting
Test before and after high-intensity intermittent exercise, and
while the
plasma BDNF level did not change, the serum BDNF level
increased.
According to the results of the Wisconsin Card Sorting Test, the
number
of categories completed and the number of correct responses
increased,
and the number of total and recurrent errors decreased. The
authors
did not find a significant relationship between BDNF
concentration
and the results of executive functions related to the prefrontal
cortex;

however, they commented that cognitive performance responded
more
to the increased intensity of exercise (22). It was also reported
that
the increase in BDNF after acute aerobic exercise was
associated with
exercise duration. The increase in BDNF was significantly
higher than in
exercise lasting longer than 30 minutes compared to exercise for
less than
30 minutes. This can be interpreted as different exercise times
affecting
brain functions differently. In a study on acute exercise and its
effect on
cognitive functions, it was shown that cognitive benefit
emerged only
through exercise lasting longer than 20 minutes (23). Other
studies
suggested that the duration and intensity of exercise produced
the best
result related to moderate exercise, and therefore the effect of
regular
exercise on BDNF and cognition was more dramatic (18, 24).
Regular
exercise increases the BDNF level in the hippocampus and
improves
learning and memory processes.
Chronic exercise in children and young adults improved
working
memory, selective attention, and inhibitory control findings
(25). In a
six-month aerobic exercise study conducted with elderly men,
the gray
matter volume increased and the peripheral BDNF increased in
the

prefrontal and cingulate cortex areas associated with increased
physical
activity (26).
Effect of Exercise on BDNF and Cognitive Function in Major
Depressive Disorder (MDD) and Schizophrenia
MDD, which is one of the leading causes of global disease
burden,
manifests with cognitive and somatic symptoms. In recent years,
BDNF
has been used as a biomarker in psychiatric disorders, such as
MDD,
schizophrenia and bipolar disorder, and the BDNF level has
been shown
to be lower in patient groups than in healthy individuals (27–
29). It
was suggested that the BDNF level is lower in MDD cases, and
a higher
level BDNF is associated with less depressive symptoms and
improved
cognitive functions compared to the healthy population (30, 31).
In
case studies, granular neuron loss, reduced hippocampal
volume, and
regressed peripheral level of BDNF and BDNF mRNA
expression in
lymphocytes were reported (32), and suicidal behavior was
associated
with a low peripheral/cerebral BDNF level (in the hippocampus
and
prefrontal cortex) (33). It was found that the peripheral level of
BDNF
could be used to predict the response to antidepressant
treatment in
MDD, and there was an increase in this level in response to
drug therapy;

however, the results regarding the relationship between
improvement in
mood and BDNF increase were contradictory (34).
It is not yet clear whether the clinical manifestation of the
BDNF variant
Val66Met is a risk factor for MDD. However, in a review, it
was proposed that
this variant reduced the response to drug treatment (35).
Schizophrenia,
on the other hand, is a severe mental disorder characterized by
psychosis
and generally presents with cognitive dysfunctions related to
problem
solving, memory, and executive functions (36). Animal models
have
drawn attention to the role of BDNF in the development and
activation
of psychosis-related neurotransmitters. It is stated that the
changes in
the BDNF level may contribute to neuroplasticity disorder
during brain
development and synaptic connection disorders, and the
morphological,
neurochemical and cell architecture anomalies observed in the
brain in
schizophrenia (37). It is well known that in schizophrenia,
neurocognitive
losses are observed in memory, attention, processing speed, and
executive
Gökçe et al. Exercise, BDNF and Cognition Arch

304
functions. A meta-analytical review of 16 studies reported that
patients
with schizophrenia had significantly lower peripheral BDNF
(27), with
memory disturbances and smaller hippocampal volume findings
being
associated with a reduced BDNF level (38). In untreated
psychosis, the
serum BDNF level was shown to be low and correlated with the
duration
of psychosis, and drug-induced psychosis models indicated a
relationship
between a reduced BDNF mRNA concentration and psychotic
symptoms
(39). The visual spatial memory performance and attention were
found to
be poor in schizophrenia patients with the BDNF Val66Met
variant, and
a low BDNF level was observed to be correlated with reduced
cognitive
functions (40).
MATERIAL AND METHODS
For this review, human studies published in English were cross-
searched
on the PubMed and Web of Science search engines using the
keywords
BDNF-exercise-cognition-major depressive
disorder/schizophrenia and
BDNF-exercise-major depressive disorder/schizophrenia and
those that
only included aerobic exercise were selected. Two studies
examined the
effect of aerobic exercise on cognition and BDNF in

schizophrenia, three
examined the effect of aerobic exercise on cognition and BDNF
in MDD,
and seven studies examined the effect of aerobic exercise on
BDNF in
MDD. Three of the studies used acute and nine used chronic
aerobic
exercise as a method. The total number of participants in 12
studies was
385. In MDD and schizophrenia, the responses of peripheral
BDNF to
exercise, the relationship between exercise and cognitive
performance
findings, and the underlying mechanism of these responses were
discussed, and how BDNF and cognitive functions changed with
aerobic
exercise was examined.
RESULTS
The findings suggest that aerobic exercise increases the
peripheral
BDNF level. No significant increase in BDNF was observed in
three of
the MDD studies, whereas a significant increase in BDNF was
noted
in all the remaining studies. While four studies examining
BDNF and
cognitive performance findings together showed a significant
increase
in both parameters, the improvement in cognitive performance
was not
accompanied by an increase in BDNF in one of the studies.
DISCUSSION
Effects of Exercise in MDD
It is reported that 5% of the global population has been

diagnosed with
MDD and 1% with schizophrenia, and 20-30% of all of these
patients are
resistant to treatment (41– 43). It is known that in MDD, the
workload
capacity of individuals is reduced by 80 to 90% compared to
their healthy
counterparts, and physical activity is decreased in schizophrenia
and is
accompanied by cognitive disorders (44, 45).
Studies have shown that neuronal activity affects the synthesis,
secretion
and signaling of neurotrophin, which has an impact on the
postsynaptic
response, synaptic morphology, presynaptic transmitter
secretion, and
membrane excitability.
In nine of the 12 studies we reviewed, an increase in BDNF was
reported
in the period following aerobic exercise (46–54). These data
seem to
agree with the premise that exercise contributes to the
promotion and
maintenance of neuron functions through a mechanism mediated
by neurotrophins. It has been suggested that one of the
mechanisms
Table 1. Summary of studies investigating the effect of aerobic
exercise on BDNF and cognitive functions in schizophrenia and
major depressive disorder.
Researcher
Participants

(Exercise/Control)
Exercise modelity Cognitive effect BDNF response
Kimhy et al., 2015* 13/13
12 weeks, 3 times per week,
60 minutes
In exercise group global cognitive
performance↑
In exercise group
%11, in standard
treatment group %1,9 ↑
Nuechterlein et al., 2016* 7/9
30-45 minutes
In exercise group social cognition, working
memory, processing speed, attention-
vigilance performance ↑
In exercise group ↑
Gourgouvellis et al., 2018 ** 8/8
60 minutes
In exercise group global cognition,
recognition memory, visual learning and
memory performance ↑

Vedovelli, 2017** 22/10
60 minutes
In exercise group processing speed,
executive function, attention, working
memory, işlemleme hızı, recall, response
inhibiton ↑
Krogh et al., 2014** 41/38
45 minutes/streching
In aerobic exercise group verbal memory
performance ↑
No significant change
Kallies et al., 2018** 30/-
Acute aerobic exercise, not
specified frequency/duration
- ↑
Kerling et al., 2017 ** 22/-
45 minutes
- No significant change

Salehi et al., 2016** 20/-
40-45 minutes
- ↑
Schuch et al., 2014** 15/11
3 weeks, 3 times per week, not
specified duration
- In exercise group ↑
Toups et al., 2011**
70/- 12 weeks, not specified
frequency
- No significant change
Meyer et al., 2016** 24/-
Acute aerobic exercise,
30 minutes
- ↑
Meyer et al., 2016** 24/-
Acute aerobic exercise,
30 minutes
- ↑
*Schizophrenia studies
**MDD studies
Gökçe et al. Exercise, BDNF and CognitionArch

305
responsible for increased BDNF may be the increase in the
cerebral
blood flow. Another proposition is that exercise-related increase
in the
insulin-like growth factor (IGF)-1 and norepinephrine levels
may increase
the expression of BDNF mRNA. It has also been argued that
decreased
blood volume due to water loss may increase the BDNF
concentration.
BDNF plays several important roles in synaptic plasticity and
affects
different aspects of synaptic transmission. In the central
nervous
system, BDNF can increase the number of excitatory and
inhibitory
synapses by regulating axonal morphology or directly
improving
synapse formation (6). Furthermore, it enhances the maturation
and
stabilization of neurotransmitter secretion at the cellular and
molecular
level, which increases the number of functional synapses. It
regulates
the increase in proteins involved in neurogenesis, learning and
memory,
and neuronal survival, including those regulating the protein
quality
control, mitochondrial biogenesis, and the resistance of cells to
oxidative,
metabolic and proteotoxic stress. In the literature, it has been

reported
that BDNF secreted from the cerebral endothelium following
acute
aerobic exercise was responsible for the effect of exercise on
cognition
(55). This function of BDNF appears to be consistent with the
memory
responses obtained from studies that included the findings of
cognitive
function in this review.
The mechanism of action of BDNF on neuroplasticity is claimed
to be
through increasing the calcium mRNA, cAMP response binding
protein
(CREB), and synapse I level (56). Exercise can produce
persistent increases
in phosphorylated CREB and BDNF levels that continue
throughout the
exercise period. An exercise-induced increase in BDNF levels
increases
the expression of key presynaptic molecules associated with
synaptic
transmission, such as synapse I and synaptophysin with a
vesicular
function at the presynaptic nerve terminals. Especially in
glutamatergic
synapses, BDNF plays a key role in initiating signal
transduction with
the TrkB and p75 receptors in regulating activity-dependent
synaptic
structure and function. Mature BDNF primarily stimulates the
TrkB
receptor, while proBDNF targets the p75 receptor. Mature
BDNF binds to
the extracellular domain of receptor TrkB and activates

phosphorylated
TrkB, phosphotidylinositol-3 kinase (PI3K), mitogen-activated
protein
kinase (MAPK), phospholipase-Cγ (PLCγ) and guanosine
triphosphate
(GTPase) pathways. The PI3K pathway showing an
antiapoptotic effect
modulates the synaptic plasticity of N-methyl-D-aspartate
(NMDA)
receptors and increases dendritic growth and branching (Figure
1) (57).
The PLCγ pathway is responsible for increased CaMKII and
CREB activation
through the secretion of intracellular Ca2+. The MAPK signal is
required
for the activation of the extracellular signal-regulated kinase 1
and CREB.
This pathway is important for the synthesis of the cytoskeleton
protein,
as well as dendritic growth and branching in hippocampal
neurons. The
activation of the GTPase pathway stimulates the synthesis of
actin and
microtubules, resulting in the growth of neuronal fibers (58).
The BDNF
responses seen in the reviewed studies on chronic aerobic
exercise may
be related to increased CREB phosphorylation of the repetitive
stimulus,
leading to prolonged structural and functional changes in
synapses. It is
reported that the CREB function in activity-dependent long-
term neuronal
plasticity is a necessary molecule for long-term memory
formation. It has

been reported that by increasing the presence and activity of
CaMKII
and BDNF levels and reducing calcineurin phosphatase levels,
exercise
boosts the synthesis of important signaling molecules that are
critical for
learning and memory (59).
In their study with MDD cases, Gourgouvellis et al. observed an
increase in the BDNF level and visual learning, memory and
recognition
memory performance following cognitive behavioral therapy
and
aerobic exercise (48). In accordance with these results, in the
literature,
increased BDNF and CREB mRNA levels were associated with
exercise
in mice, and the highest BDNF expression was associated with
the
highest CREB expression and spatial memory ability (60). In
another
study, it was found that exercise increased the active CREB
form,
and the learning ability of mice was also significantly increased
after
exercise, and the highest elevation in the BDNF level belonged
to those
that learned fastest (61).
The acute aerobic exercise studies included in this review (53,
54) also
reported elevated BDNF levels. Considering the studies that did
not
report an increase in BDNF in response to chronic aerobic
exercise, it

can be regarded that transient BDNF elevations are responsible
for the
chronic benefits of exercise in MDD. It could be the case that
exercise has
a curative effect through transient elevations in BDNF without
long-term
changes in basal BDNF, which leads to long-term
neurophysiological
changes. The clinical effectiveness of exercise in curing MDD
may also
result from its favorable effects on monoaminergic function,
neurogenesis,
and immunity. Exercise causes changes in markers associated
with the
monoamine metabolism, including monoamine, monoamine
receptors,
and carriers, and among these changes are the activation of
serotonergic
neurons in the dorsal raphe nucleus (DRN) by low-intensity
exercise. It
has been suggested that the effect of exercise on serotonergic
activity
can explain its curative effect on depressive symptoms. The
central
serotonergic system is built into the DRN and has projections
over
large areas of the brain. It is considered that exercise
demonstrates
its antidepressant effect through the serotonergic neurons in
DRN.
Accordingly, increased serotonin synthesis, metabolism, and
secretion
are observed during and after exercise. It has been shown that
exercise
has the effects of inducing hippocampal BDNF expression by
increasing

the NE/5-HT levels of antidepressants. This has led to the
hypothesis
that increased BDNF mRNA expression associated with exercise
may be initiated by monoaminergic activation. Studies indicate
that
noradrenaline-mediated signaling may be particularly important
in the
modulation of the BDNF gene expression through exercise.
These results
confirm that noradrenaline stimulation is an important initial
event in
cellular mechanisms, leading to improved BDNF transcription
following
physical exercise. Together with antidepressants, exercise is
thought to
have a similar effect on the induction of noradrenaline
activation and
increase in BDNF via β-adrenergic receptors (Figure 2) (62).
Evidence from human and animal studies has shown that
monoaminergic
hypofunction is a curable component of depression (63).
Therefore,
antidepressant drugs have been developed to increase
serotonergic (5-
Figure 1. Binding of mature BDNF to receptor TrkB activates
PI3K, MAPK, PLCγ and GTP-
less pathways.
Gökçe et al. Exercise, BDNF and Cognition Arch
306

However, three of the reviewed studies showed that aerobic
exercise did
not cause an increase in BDNF in cases with MDD (69–71).
Consistent
with these results, a meta-analysis in the literature reported that
chronic
aerobic exercise did not affect the BDNF level in MDD and
suggested that
the predominance of female patients in the sample included in
the study
might have led to this finding (72). The authors reported that
the cerebral
blood flow, blood volume, and other circulating
neurotransmitters
might be the cause of the exercise-triggered changes in neuronal
life, synaptogenesis, and neural circuitry. In another chronic
aerobic
exercise study conducted with healthy individuals by the same
group of
researchers, the findings indicated a rapid increase in the BDNF
level in
men following exercise, but no changes were observed in
women (73).
Effects of Exercise in Schizophrenia
BDNF, which increases the expression of dopamine receptors in
the
brain by mimicking the effect of antipsychotic drugs, is
reported to
regress manic mood (74, 75). Similarly, schizophrenia studies
have
shown that exercise improves cognitive abilities and physical
health (2,
76) and that low-level BDNF is associated with negative
symptoms and

may contribute to the psychopathology of the disease (77).
Since BDNF is widely distributed throughout the central
nervous system
and plays a role in various psychiatric disorders, impairment in
BDNF
signaling is not specific to schizophrenia. However, considering
the
effect of BDNF on the plasticity and neuronal viability of
dopaminergic,
serotonergic, and cholinergic neurons, and the importance of all
these
pathways in the pathophysiology of schizophrenia, it can be
concluded
that BDNF can be a useful biological marker for the clinical
status and/
or prognosis of people with this disease.
In the schizophrenia studies included in this review (46, 47), the
increase
in the peripheral BDNF level and the improved cognitive
performance
findings in response to exercise support the idea that exercise
can
enhance neurotrophic and neuroprotective mechanisms, and thus
leading to an improvement in the symptoms of schizophrenia.
One of
the possible ways in which aerobic exercise improves the
symptoms
of schizophrenia is that it enhances drug efficacy by affecting
the
pharmacokinetics of antipsychotics, for example, by changing
drug
distribution and reducing drug excretion (78).
BDNF is a neurotrophin that is not only related to neuronal

protection
and development but also effective in synaptic regulation,
learning, and
memory. Since BDNF plays an important role in regulating
synaptic
plasticity, schizophrenia deficits can be understood in the
context of
learning and the molecular and cellular mechanisms of memory.
Concerning the pathogenesis of schizophrenia, particularly
neurodevelopmental and neurotoxicity-related factors,
neurotrophins,
such as BDNF can provide an explanatory framework at
molecular
and cellular …
HEALTH AND WELL-BEING IN SOCIAL SCIENCES
Experiences of housing support in everyday life for persons
with schizophrenia and the role of the media from a societal
perspective
HENRIKA JORMFELDT, Associate Professor in Nursing &
MALIN HALLÉN, Senior Lecturer
in Media and Communication Studies
School of Health and Welfare, University of Halmstad,
Halmstad, Sweden
Abstract
Background: The mental health-care system in Sweden, as in
many other counties, has its main focus on the reduction of
psychiatric symptoms and the prevention of relapses. People

diagnosed with schizophrenia often have significant health
issues and experience reduced well-being in everyday life. The
social imaginary of mental illness as an imbalance of the brain
has implications concerning general attitudes in society. The
news media are an important source of information on
psychiatric disorders and have an important role in cultivating
public perceptions and stigma. News media can contribute
to the mental illness stigma and place individuals with mental
illnesses at risk of not receiving adequate care and support.
The aim of this preliminary study was to describe users’
experiences of housing support in everyday life.
Results: The results revealed three themes of housing support,
which were needed, but frequently insufficiently fulfilled
in the municipality. The three themes were: ‘‘Support to
Practice Healthy Routines in Daily Life,’’ ‘‘Support to Shape
Meaningful Contents in Everyday Life,’’ and ‘‘Support to Meet
Needs of Integrity and Respect.’’
Conclusions: The findings support previous studies arguing that
current health care and housing support fails to meet
basic needs and may lead to significant and unnecessary health
risks. Further investigation is needed regarding the links
between attitudes to mental illness in society and political and
financial principles for health care and housing support for
persons with schizophrenia. Further research is needed
regarding the role of the media in policymaking concerning
health
promotion interventions for people diagnosed with
schizophrenia.
Key words: Housing support, media, narratives, persons
diagnosed with schizophrenia, social sciences
(Accepted: 22 March 2016; Published: 9 May 2016)
The mental health-care system in Sweden, as in

many other counties, has a strong focus on the reduc-
tion of psychiatric symptoms and prevention of
relapses (Van Wel & Landsheer, 2011) in which posi-
tive dimensions of health have not been viewed as
suitable for evidence-based practice in health care
(Jormfeldt, 2011). Barriers regarding health promo-
tion among persons with severe mental illness have
been associated with stigma, as well as professional
and organizational obstacles in the health-care ser-
vices provided (Ehrlich et al., 2014). It has been
argued that the contemporary paradigm, which focuses
on neurological explanations regarding mental ill-
ness in society, fails to take psychological and rela-
tional explanations of mental illness into account
(Rose & Abi-Rached, 2013; Williams, Katz, &
Martin, 2011). The news media are an important
source of information on psychiatric disorders and
have an important role to play in cultivating public

perceptions and stigma (Klin & Lemish, 2008).
Previous research on news media content has estab-
lished that journalistic coverage of mental illness is
largely characterized by inaccuracies, exaggerations,
and misinformation and might even contribute to
mental illness stigma through negative news content.
For example, inaccurate stories on recovery may
promote the belief that mental illness cannot be
rehabilitated effectively (Wahl, 2003). News media
can contribute to the mental illness stigma by nega-
tive portrayals of individuals with these illnesses;
therefore, making them vulnerable to social rejection
and discrimination and at risk of not receiving
adequate care and support (Klin & Lemish, 2008).
People diagnosed with schizophrenia belong to a risk
Correspondence: H. Jormfeldt, School of Health and Welfare,
University of Halmstad, SE-301 18 Halmstad, Sweden. E-mail:
[email protected]
International Journal of
Qualitative Studies

on Health and Well-being
�
# 2016 H. Jormfeldt & M. Hallén. This is an Open Access
article distributed under the terms of the Creative Commons
Attribution 4.0 International
License (http://creativecommons.org/licenses/by/4.0/), allowing
third parties to copy and redistribute the material in any
medium or format and to remix,
transform, and build upon the material for any purpose, even
commercially, provided the original work is properly cited and
states its license.
1
Citation: Int J Qualitative Stud Health Well-being 2016, 11:
30571 - http://dx.doi.org/10.3402/qhw.v11.30571
(page number not for citation purpose)
http://creativecommons.org/licenses/by/4.0/
http://www.ijqhw.net/index.php/qhw/article/view/30571
http://dx.doi.org/10.3402/qhw.v11.30571
group for developing metabolic syndrome, cardio-
vascular disease, type 2 diabetes and reduced life
expectancy, as well as reduced well-being in every-
day life (Heald et al., 2010; Lassenius, Åkerlind,
Wiklund-Gustin, Arman, & Söderlund, 2013). The
causes of this risk are avoidable as it is related to

lifestyle in terms of inactivity, overweight, smoking,
and poor diet as well as the side effects of anti-
psychotic medication (Comptom, Daumit, & Druss,
2006). The general public, as well as policymakers,
frequently do not have sufficient knowledge of cur-
rent daily living conditions and the prerequisites for
health among people with severe mental illness.
People with mental disorders and their families are
acutely aware of the negative images of mental illness
in the news (and entertainment) media. However,
their perspectives about the prerequisites for health as
successful stories of recovery have rarely been in-
cluded as sources of news items (Stuart, 2006). The
aim of this preliminary study was to describe users’
experiences of housing support in everyday life.
Materials and methods
The sample in the present preliminary study con-
sisted of the members of the local service user

association, The Interest Alliance for Schizophrenia
and Allied Disorders. The local association embraces
approximately 50 members; involving people diag-
nosed with schizophrenia, their relatives, and others
with an interest regarding the particular diagnosis.
Forty-two letters with information about the purpose
of the study and an invitation to write down short
narratives concerning experiences of municipality sup-
port in everyday life were sent to all of the members
of the local service user association. The members
of the association were asked to recall situations
concerning municipality support in topics, such as
housekeeping, diet, physical activity, equality and
integrity, inclusion in society, participation in care
planning, health promotion and illness prevention,
and participation in meaningful activities or employ-
ment, as these topics where frequently highlighted
as problem areas during members? meetings in the

local association and thus appeared to be crucial to
health promotion from their perspective. Twenty-
four letters with narratives regarding experiences of
support in everyday life from the municipality came
in return during July and August, 2011. Five of the
letters with narratives were written by individuals
with personal experiences of housing support due to
mental disability, 14 letters were written by relatives
of persons receiving community support, and five
letters were written by members with experiences
of housing support among people diagnosed with
schizophrenia from a professional perspective.
The data were analyzed using a qualitative con-
tent analysis method, inspired by Graneheim and
Lundman (2004), and carried out by the first
author. The narratives were read several times to
become acquainted with the content. Meaning units
were identified, condensed, abstracted, and labeled

with a code. The codes were compared with each
other in order to identify similarities and differences
regarding the content of the narratives in relation to
the aim of the study. The findings were evaluated
by means of discussions among both authors with
regard to each step of the analysis.
Ethics
According to the Swedish Health Care Act (2003:
460), concerning the Ethical Review of Research
Involving Humans, an ethical review was not neces-
sary as participants were recruited among members
of the local organization and no sensitive personal
information was requested. Instead, only informa-
tion without links to a specific person regarding ex-
periences of the housing support provided by the
municipality was asked for. All of the participants
gave their informed consent verbally and by writing
down and sending their narratives to the authors.

Confidentiality was assured in accordance with World
Medical Association Declaration of Helsinki (2013).
Results
The narratives collected from the members of the
local service user association revealed three themes
regarding experiences of housing support in every-
day life support which were needed, but frequently
insufficiently fulfilled through municipality provi-
sion. The three themes were as follows: ‘‘Support
to Practice Healthy Routines in Daily Life,’’ ‘‘Sup-
port to Shape Meaningful Contents in Everyday
Life’’ and ‘‘Support to Meet Needs of Integrity and
Respect.’’
Support to Practice Healthy Routines in Daily Life
Relatives’ narratives indicated a lack of support on
the subject of routines concerning housekeeping,
diet, and physical activity. Narratives showed an
absence of support among service users in getting up

in the morning and not staying in bed all day as well
as a lack of support to maintain hygiene routines,
uphold physical activity, prepare regular meals, and
purchase nutritive food.
Several descriptions affirmed lack of support regard-
ing dietary interventions despite the evidence of the
lifesaving nature of these interventions. Narratives
H. Jormfeldt & M. Hallén
2
showed concerns because service users often eat
large portions and have an insufficient fiber intake in
combination with too much fat and sugar due to the
side effects of medical treatment.
Several descriptions revealed that obesity, which is

a well-known common issue related to antipsychotic
medication among people diagnosed with schizo-
phrenia, was seldom viewed as a serious matter
among municipality staff, even though these issues
require regular health checks by a physician. One
member of the user association*a relative of a
person diagnosed with schizophrenia*stated that:
The staff from the municipal social services
do not sufficiently recognize the needs of the
service users who, as a result, receive too little
encouragement to engage in activities and
recover.
Support to Shape Meaningful Contents in
Everyday Life
Narratives from both the relatives and from a pro-
fessional perspective revealed that service users seldom
received sufficient support in their daily tasks, which
was perceived as a drawback in their efforts to
become involved in the society. The housing support

provided by the municipality in the service users’
accommodations was described as ‘‘storage’’ instead
of care by the service users’ relatives. The realities
described by the narratives showed that the service
users often became too dependent upon their rela-
tives to be able to participate in society?s basic
activities, because support, company, and reassur-
ance from staff were absent. Another issue frequently
reported was the nonexistence of support or solu-
tions to service users’ difficulties to use public
transport. One relative expressed the following:
The service user does not have the same
opportunities to develop their capabilities . . .
they don’t get recognized and encouraged
enough to carry out things properly. They
simply don’t get help . . ..
Support to Meet Needs of Integrity and Respect
Some narratives spoke of the experiences of under-
standing and respectful behavior among staff, even

though an ‘‘us and them’’ perspective was evident in
most staff�user relationships, as well as experiences
of inequalities regarding power and decision-making.
Narratives of relatives expressed their experiences of
violations of both service users’ and their relatives’
dignity when staff were intruding their individual
integrity by claiming transparency regarding the ser-
vice user’s health status and personal relationships.
Narratives frequently described insufficient knowl-
edge among staff concerning the special difficulties
related to the diagnosis such as lack of motivation
and side effects of medical treatment. Moreover,
they easily accepted service users’ wishes to draw
back and isolate themselves without considering
the hostile effects of isolation, and the fact that the
diagnosis of schizophrenia often involves a tendency
to immure oneself. One service user described his
experiences as this:

The first years when I became ill I was just
assigned to an apartment and left all by myself
with prescribed medication. It took me several
years of misery before staff paid any attention
to my situation and gave me a hand to get
me back on track. Now I have got sufficient
support from staff but I should have got it from
the beginning.
Discussion
The lack of support regarding positive dimensions
of health among people with severe mental illness
has been revealed previously (Ehrlich et al., 2014;
Jormfeldt, 2011) and, according to the findings of
this preliminary study, this topic still needs attention.
The results of this preliminary study show that
current available housing support for people diag-
nosed with schizophrenia fails to meet basic needs
and may lead to significant and unnecessary health

risks and reduced well-being in line with previous
studies conducted by Comptom et al. (2006), Heald
et al. (2010), and Lassenius et al. (2013). There is a
reason to believe that stigma and barriers regarding
health promotion among people with severe mental
illness (Ehrlich et al., 2014) are related to the
negative media portrayals of mental illness (Wahl,
2003). Furthermore, the current focus on the reduc-
tion of psychiatric symptoms and prevention of
relapses in mental health care could be transformed
by media information concerning the fact that
mental illness can be rehabilitated effectively (Van
Wel & Landsheer, 2011). Further studies are needed
regarding the public discourse of mental illness in
public debate and within the scientific community to
increase awareness of how the current discourse
shapes the existing delivery of education, research,
and clinical praxis in mental health services. An

important topic in future research should be the role
of media portrayals of mental illness as it directly
affects people with mental illnesses by impeding
their social participation and interferes with their
recovery (Klin & Lemish, 2008). In addition, further
research is required regarding the perspective of
Experiences of housing support in everyday life
30571 - http://dx.doi.org/10.3402/qhw.v11.30571 3
professionals in mental health services and journal-
ists focusing on mental health and illness.
Acknowledgments
We thank the members of the local user association
of The World Fellowship for Schizophrenia and
Allied Disorders, who generously shared their ex-
periences of housing support with us.

Conflict of interest and funding
The authors have not received any funding or
benefits from industry or elsewhere to conduct this
study.
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http://www.wma.net
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PRAXIS Mini-Review Praxis 2014; 103(1): 2 7 - 3 2 27
Klinik für Forensische Psychiatrie, Psychiatrische

Universitätsklinik Zürich
Friederike Boudriot, Angela Guldimann, Elmar Habermeyer
Schizophrenie und Gewalt
Schizophrenia and Violence
Zusammenfassung
Schizophrene Menschen haben ein
gegenüber der Ällgemeinbevölkerung
erhöhtes Risiko, straffällig zu werden.
Der weitaus überwiegende Teil schi-
zophrener Patienten begeht jedoch
keine Straftaten und das Risiko, von
einer Gewalttat eines Schizophrenen
betroffen zu sein, ist für die Ällgemein-
bevölkerung gering. Die Ursachen von
Dehnquenz bei Schizophrenen sind
komplex, jedoch können bestimmte
Risikomerkmale (z.B. eine begleitende
Substanzabhängigkeit) benannt wer-
den. Die Behandelbarkeit und Legal-
prognose schizophrener Straftäter sind
gut, was dafür spricht, dass bei Risiko-
patienten durch Etablierung eines ge-
eigneten Helfernetzes auch präventiv
gearbeitet werden kann.
Schlüsselwörter: Schizophrenie - De-
linquenz - Gewalt - Risiko
Einleitung
Der Krankheitsbegriff der Schizophre-
nie geht auf den Schweizer Psychiater
Eugen Bleuler (1857-1939) zurück.

1911 veröffenthchte er seine richtungs-
weisende Monographie «Dementia
praecox oder Gruppe der Schizophre-
nien» mit der er diesen Begriff in der
medizinisch-psychiatrischen Fachwelt
verankerte [1]. Etymologisch setzt sich
der Begriff Schizophrenie aus den grie-
chischen Wörtern «schizo» (ich spalte)
und «phren» (Seele, Geist) zusammen.
Er beschreibt die «Spaltung» bzw. das
Äuseinanderfallen zentraler und übh-
cherweise integrierter geistig-seelischer
Funktionen wie Denken, Fühlen und
Wahrnehmung. Dementsprechend be-
schreiben auch die modernen diagnos-
tischen BGassifikationssysteme ICD-10
[2] und DSM-V [3] die Schizophrenie
als schwere psychische Erkrankung, die
durch Wahrnehmungsveränderungen
(z.B. Halluzinationen, Verkennungen,
Wahnwahrnehmungen) und Störungen
des Denkens (z.B. formale Denkstörun-
gen wie Gedankenabreissen, Gedan-
keneinschiebungen und Zerfahrenheit,
inhaltliche Denkstörungen mit Wahn-
bildungen, Ich-Störungen), des Fühlens
(z.B. verflachte oder unangemessene
Affekte) und des Handelns (z.B. Des-
organisation) imponieren. Hinsichtlich
der vorherrschenden Symptomatik, des
Verlaufes und der Prognose besteht eine
zum Teil erhebliche Heterogenität. Dies
findet Niederschlag in der Beschreibung
verschiedener Prägnanztypen, die je-
doch keine klar abgegrenzten Entitäten

darstellen und innerhalb des Langzeit-
verlaufes wechseln können [4].
Die Lebenszeitprävalenz schizophrener
Erkrankungen liegt kulturübergreifend
bei 0,6-1,0%. Beide Geschlechter sind
gleich häufig betroffen, Männer er-
kranken im Allgemeinen früher (15-25
Jahre) [5] als Frauen (25-35 Jahre). Die
Häufigkeit der Erkrankung und die auf-
grund des frühen Erkrankungsahers
langen Verläufe machen deutlich, dass
die Problematik nicht nur das psychia-
trische Fachgebiet betrifft, sondern für
viele medizinische Bereiche Relevanz
hat.
Die Ätiopathogenese der Schizophrenie
ist multifaktoriell [5]: Änlagebeding-
te genetische bzw. prä- und perinatal
erworbene Faktoren (Infektionen im
Mutterleib und/oder Geburtskomplika-
tionen) führen über neuronale Entwick-
lungsstörungen und damit verbundene
Veränderungen der Konnektivität zu
einer erhöhten Vulnerabilität. Lebens-
geschichtliche Belastungen und/oder
Substanzkonsum werden nachfolgend
als Auslöser der klinisch erkennbaren
Krankheitsentwicklung gesehen und
beeinflussen deren Verlauf Weitere
Ursachen der sehr unterschiedlichen
Krankheitsverläufe, die zwischen einer
weitgehenden Erholung (1/3 der Fälle)
und schweren Defizitsyndromen in ei-
nem weiteren Drittel schwanken kön-

nen, werden u.a. neurotoxische und
immunmodulatorische Prozesse disku-
tiert. Darüber hinaus ist wie bei vielen
potenziell chronischen Erkrankungen
die Compliance bezüglich der Medika-
menteneinnahme, aber auch der Grad
der Anpassung der individuellen Le-
bensbedingungen an die Gegebenheiten
der Erkrankung relevant.
Delinquenz
Das Krankheitsbild der Schizophrenie
ist mit vielen Vorurteilen belastet: In der
Ällgemeinbevölkerung aber auch bei
Psychologie- und Medizinstudenten zei-
Im Artikel verwendete Abkürzungen:
CI Konfidenzintervall
DSM-5 Diagnostisches und Statistisches
Manual Psychischer Störungen,
Fifth Edition
FU Fürsorgeriscbe Unterbringung
ICD-10 internationale Kiassifikation
psychischer Störungen
OR Odds Ratio
© 2014 Verlag Hans iHuber, Hogrefe AG, Bern DOi
10.1024/1661-8157/a001527

PRAXIS Mini-Review Praxis 2014; 103(1): 27-32 28
gen sich negative Einsteüungen gegen-
über Menschen mit Schizophrenie, wo-
bei die Vorstellung, dass diese Personen
rasch die Kontrolle über sich verlieren
weit verbreitet ist und Stereotypien hin-
sichtlich ihrer Gefährlichkeit bestehen
[6,7]. Diese Haltung wird auf den ersten
Blick durch unterschiedliche empirische
Befunde gestützt: Schizophrene Men-
schen sind in JustizvoUzugsanstalten
überrepräsentiert [8], was für eine er-
höhte Gefährdung, straffällig zu werden,
spricht. In einer Metaanalyse [9], in der
20 Studien aus elf Ländern eingeschlos-
sen waren, fand sich für Männer mit
Erkrankungen aus dem schizophrenen
Formenkreis ein ca. vierfach erhöh-
tes Risiko für Gewalthandlungen (OR
4,0; 95%-CI 3,0-5,3) im Vergleich zur
Allgemeinbevölkerung, für Frauen ein
ca. achtfach erhöhtes Risiko (OR 7,9;
95%-GI 4,0-15,4). Das Risiko für Ge-
walttaten ist bei komorbidem Substanz-
missbrauch noch einmal stärker erhöht
(OR für Schizophrene ohne Substanzab-
hängigkeit 2,1; 95%-CI 1,7-2,7; OR für
Schizophrene mit Substanzmissbraucb
8,9; 95%-CI 5,4-14,7).
Betrachtet man nicht nur die relativen
Risiken, sondern absolute Zahlen, dann
relativieren sich die vorgenannten Ergeb-
nisse: Trotz des erböhten Risikos, straf-
fällig zu werden, begeht nämlich nur ein

sehr kleiner Teü der Betroffenen, nämlich
ca. ein Patient pro 2000 Krankheitsfälle,
tatsächlich Gewaltdelikte. Das entspricht
bei einer für die Allgemeinbevölkerung
formulierten Basisrate von Gewaltstraf-
taten von 1:10000 zwar einem deutlich
erhöhten Risiko, die konkrete Gefähr-
dung für die Allgemeinbevölkerung
bleibt jedoch ausserordentlich gering: Bei
einer Prävalenz schizophrener Erkran-
kungen von 1% muss man 100 Personen
treffen, um einem Erkrankten zu begeg-
nen. Diese Zahl muss dann mit 2000
multipliziert werden, um die statistische
Wahrscheinlichkeit eines Kontaktes mit
einem gewaltbereiten Schizophrenen zu
erfassen. Das Risiko, einen gewaltberei-
ten schizophrenen Menschen zu treffen,
liegt somit bei 1:200000. Die Gefahr,
Opfer eines Gewaltdeliktes zu werden,
ist für die Allgemeinbevölkerung somit
niedrig [10].
Dennoch ist das Thema für den Leser-
kreis der PRAXIS nicht irrelevant, denn
die vorab dargestellten Berechnungen
haben wenig Relevanz für Angehörige
und für Mitarbeiter des medizinischen
Betreuungssystems. Da diese Personen
engere bzw. häufigere Kontakte zu Be-
troffenen haben, ist ihre Gefährdungsla-
ge eine andere: Studien konnten zeigen,
dass Opfer von Gewaltdelikten mehr-
heitlich Personen aus dem näheren Um-
feld waren, die Delikte wurden zumeist
in der eigenen Wohnung bzw. Wohnum-

gebung begangen (exemplarisch [11]).
Die Gefährdungen betreffen somit we-
niger die Allgemeinbevölkerung als viel-
mehr das persönliche Umfeld und pro-
fessionelle Helfer.
Mögliche Ursachen und
Erklärungsmodelle
Psychopathologie und Delinquenz
Das vorherrschende psychopathologische
Bild beeinfiusst die Ausgestaltung delin-
quenten Verhaltens bei Schizophrenen.
Entsprechend sind einige Prägnanztypen
schizophrener Erkrankungen und ver-
wandter Krankheitsbilder für die foren-
sische Psychiatrie besonders bedeutsam
(Tab. 1). In Anlehnung an diese Zusam-
menhänge wurden 1) impulsive Taten
mit starker Affektbeteiligung im Rabmen
akuter Positivsymptomatik, 2) geplante
(oft chronisch) wahnhaft motivierte Ta-
ten und 3) «dissozial» anmutende Taten
im Rahmen chronischer Verläufe mit so-
zialer Verwahrlosung, Kritikminderung
und Empathiemangel beschrieben [12].
Insbesondere für das Verständnis von
Gewalthandlungen im Rahmen akuter
Krankheitsstadien ist das Konzept der
sogenannten «threat/control-override»
Symptome relevant [13]. Hierbei han-
delt es sich um einen charakteristischen
Symptomenkomplex mit 1) bedrohlich
erlebten Icb-Störungen (Betroffene ha-

ben das Gefühl, in ihrem Denken und
Handeln von anderen kontrolliert, be-
einfiusst bzw. beherrscht zu werden) und
2) der wahnhaften und massiv ängsti-
genden Überzeugung, dass andere Men-
schen einem Schaden zufügen woüen. In
diesem Kontext spiegelt die Kriminah-
tät betroftener Personen Defizite in der
Realitätswahrnehmung bzw. -kontroUe
wider, die direkt auf sogenannte Positiv-
symptome zurückgehen.
Unabhängig davon können aber auch
sogenannte Negativsymptome in Form
von kognitiven Leistungseinbussen und
affektiven Veränderungen, die zu sozia-
lem Rückzug und defizitären Problem-
lösungsstrategien führen, Patienten in
Belastungssituationen, z. T. aber auch in
Alltagssituationen, massiv überfordern
und insbesondere zu Schwierigkeiten
bei der Einschätzung der Motive ihres
Gegenübers führen. Ausserdem kommt
es bei vielen chronischen Patienten im
Zuge der krankheitsbedingten Persön-
lichkeitsveränderung zu einem reduzier-
ten Empathievermögen, wie es schon Bl-
euler [1] als autistisches Grundsymptom
der Erkrankung beschrieben hat.
Es leuchtet unmittelbar ein, dass die
Auswirkungen der vorgenannten krank-
heitsbedingten Faktoren durch vorab
bestebende Persönlicbkeitsstörungen,
komorbiden Substanzkonsum, aber
auch durch krankheitsbedingten sozia-
len Abstieg mit nachfolgend akzentuier-
ten psychosozialen Schwierigkeiten und

einem fehlenden Hilfesystem verstärkt
werden können. Letztlich resultiert ein
Konglomerat unterschiedlicher Fakto-
ren, die im individuellen Zusammen-
spiel und mit unterschiedlicher Ausprä-
gung zur Delinquenz eines Betroftenen
beitragen.
Neurobiologische Aspekte
Es gibt inzwischen zahlreiche Befunde
zu genetischen, neurophysiologischen
und morphologischen Veränderungen,
die mit schizophrenen Erkrankungen
einerseits und/oder mit aggressivem Ver-
halten andererseits in Verbindung stehen
PRAXIS Mini-Review Praxis 2014; 103(1): 27-32 29
Tab. 1: Forensisch-relevante Subtypen
ïUDtypen
Paranoide
Schizophrenie
(F20.0)
Hebephrene
Schizophrenie
(F20.1)
Katatone
Schizophrenie
(F2O.2)

Wahnhafte Störung
(F22.O)
Betrottene Bereiche
Wahrnehmung,
Wahn, Halluzina-
tionen
Aftektive Verände-
rungen
Psychomotorik
Wahrnehmung,
Wahn
Symptomatik
Verfolgungswahn,
Ich-Störungen,
Stimmen hören
Inadäquater, flacher
Affekt,
zielloses Verhalten,
Denkstörungen
Stupor, Erregung,
Haltungsstereo-
typien,
Negativismus
Liebeswahn,
Eifersuchtswahn

Anmerkungen
Häufigster Subtyp
Verfolgungswahn:
sich in die Enge
getrieben fühlen.
keinen Ausweg
wissen, vermeintliche
Notwehrsituation
^ Gewalt
Sozialer Abstieg,
Kritikminderung
-^ Eigentumsdelikte
Selten: katatoner
Erregungssturm
mit ungerichteter
Gewaltanwendung
Häufig auf spezifi-
sche Person bezogen
—> Gewalt gegen
Partner und/oder
vermeintlichen
Nebenbuhler
(Übersicht bei Kalus [14]). Spezifische
Auslöser bzw. hirnorganische Läsionen,
die Gewalt begünstigen können, sind da-
bei jedoch (noch) nicht identifiziert wor-
den. Vielmehr ergibt sich eine den vorab
dargestellten komplexen ätiologischen
Bedingungen ähnliche Konstellation,
bei der es vorwiegend um neurobiolo-
gische Vulnerabilitäten geht, die je nach

Lebenssituation und Krankheitsverlauf
in unterschiedlicher Art und Intensität
verhaltenswirksam werden können. Da-
bei sind jene Hirnstrukturen, die gene-
rell mit Aggressivität im Zusammenhang
stehen, zu einem beträchtlichen Teil
identisch mit jenen, die bei scbizopbre-
nen Erkrankungen alteriert sind (orbi-
tofrontaler Cortex, anteriorer cingulärer
Cortex, Basalganglien und Amygdala).
Gleicbes gilt für die Neurotransmitter
Dopamin und Serotonin, wobei bei schi-
zophrenen Erkrankungen bzgl. Dopa-
min in limbischen Hirnarealen, die für
Flucht und Gegenwehr zuständig sind,
eine Uberaktivität und in den frontalen
Regionen, die für die Verhaltenshem-
mung bzw. -kontroUe relevant sind, ein
Serotoninmangel vorliegt.
Die biopsychosozialen Wechselwirkun-
gen zwischen Lebensereignissen, Ver-
baltensstilen bzw. neurobiologischen
Faktoren und die daraus resultierenden
Entstehungsmechanismen aggressiven
Verhaltens bei schizophrenen Menschen
lassen sich modellhaft darstellen (Abb. 1;
vergl. [15,16]): Genetische Faktoren,
prämorbide Persönlichkeit, Wertvorstel-
lungen und Sozialisationserfahrungen
bilden dabei die Grundlage, auf der sich
die schizophrenen Krankheitssymptome
aber auch eine unabhängig davon be-
stebende Gewaltbereitscbaft manifestie-
ren. Diese Vulnerabilitäten werden von

Faktoren wie Stress, Substanzabusus,
Krankheitseinsicht und Behandlungs-
möglichkeiten beeinflusst. Gewisse
Symptomausprägungen können dann
eine ängstlich gespannte Feindseligkeit
und wehrhafte Grundstimmung hervor-
rufen. Die infolge des Serotonindefizits
krankheitsbedingt verminderte frontale
Hemmung (top-down-Kontmle) aggres-
siven Verhaltens und die parallel dazu
durch den Dopaminüberschuss erhöhte
Reagibilität des limbischen Systems (bot-
tom-up-drive) begünstigen aggressives
Verhalten auf einer neurobiologischen
Ebene. Dieses Modell ist zwar plastisch,
hinsichtlich der Identifikation von Risi-
kopatienten jedoch wenig hilfreich, denn
es gilt für viele Patienten und sagt nichts
darüber aus, ob und mit welcher Wahr-
scheinlichkeit diese Patienten Gewalt ein-
setzen.
Risikomerkmale
Mangels biologisch fassbarer Risiko-
merkmale ist man darauf angewiesen,
klinisch-psychopathologische Warnzei-
chen für Gewaltdelikte deskriptiv zu er-
fassen. Diese können nicht als sicherer
Indikator für Gewalthandlungen gelten,
sondern legen vorwiegend einen erhöh-
Drogen
Stress

Gene
Störung der
Informations-
verarbeitung,
kognitive
Beurteilung
Top-down
Kontrolle
Frontale Ver-
haltensregulation
reduziert

Bottom-up drive
Amygdala,
limbisches
System erhöht
Krankheits-
symptome
Paranoia,
Halluzinationen
Reaktion
Flucht
Gegenwehr

Abb. 1: Entstehungsbedingungen von Aggressionen bei
Schizophrenie.
ten Betreuungsbedarf und ein sorgfäl-
tiges Monitoring nahe. Dass es daran
bislang fehlt, verdeutlichen Erhebungen
in unterschiedlichen Massnahmeein-
richtungen, nach denen bis zu 85% der
infolge von Delikten zwangsweise unter-
gebrachten Patienten, zuvor schon in der
Allgemeinpsychiatrie behandelt worden
waren [11]. Der Zeitraum zwischen Er-
krankung und Aufnahme in einer Foren-
sischen Klinik liegt bei ca. sieben Jahren
[17]. In dieser Zeit wäre also Raum für
präventive Bemühungen. Argumente für
einen möglichst verbindlichen Behand-
lungsrahmen, sei es ambulant oder stati-
onär, ergeben sich bei Patienten, die:
• wiederholt im Rahmen akuter Krank-
heitsphasen gewalttätig wurden,
• im Kontext dieser Gewalthandlungen
Waffen eingesetzt haben,
• ihre Gewalthandlungen durch Wahn-
symptome der Verfolgung und insbe-
sondere leiblichen Beeinträchtigungen
begründet haben,
• eine Tötungsabsicht oder massive Ver-

letzungsabsicht bzw. einen sexuellen
Übergriff vorhatten,
• eine Vorgeschichte mit Gewaltdelin-
quenz auch unabhängig von der Schi-
zophrenie aufweisen,
• einen massiven Drogenabusus aufwei-
sen und intoxikiert Gewalt eingesetzt
haben,
• einen erheblichen sozialen Abstieg
erlitten haben und vor ungeklärten
privaten, Wohn- und Arbeitsverhält-
nissen steben,
• Gewalt angedroht haben,
• im Vorfeld Suizidhandlungen began-
gen baben,
• eine Vorgeschichte, bizarrer, mögli-
cherweise auch nicht strafbarer Fehl-
handlungen aufweisen und/oder
• einen sozialen Rückzug bzw. eine mas-
sive Verschlossenheit aufweisen [18,19].
Beim Vorliegen einer Risikokonstellati-
on sollten die Betroftenen, insbesondere
wenn sie wiederholt ibre Behandlung ei-
genmächtig beendet bzw. die Medikation
eigenmächtig reduziert oder abgesetzt ha-
ben, einer fachärztlichen Versorgung zu-
geführt werden. Sofern man als Hausarzt

Key messages
• Schizophrene Menschen haben ein gegenüber der
Allgemeinbevölkerung
deutlich erhöhtes Risiko, gewalttätig zu werden; dennoch
begehen nur einer
unter 2000 Betroffenen ein Gewaltdelikt.
• Das von schizophrenen Patienten ausgehende Risiko für
Mitglieder der Allge-
meinbevölkerung ist gering.
• Von Gewalthandlungen gefährdet sind vorwiegend Angehörige
und Mitglie-
der des sozialen bzw. medizinischen Betreuungs- und
Versorgungssystems.
• Schizophrene Patienten sind effektiv behandelbar, die
Legalprognose ist in der
Regel gut.
• Risikopatienten sollten einer fachärztlichen Behandlung
zugeführt werden.
Mit einem engmaschigen Monitoring kann auch bei nicht-
complianten Pati-
enten auf akute Krisensituationen reagiert werden.
Lernfragen
1. Welche der folgenden Aussagen zu Gewalt bei schizophrenen
Patienten trifft
zu? (Einfachauswahl, eine richtige Antwort)
a) Gewalttaten schizophrener Patienten zeichnen sich
typischerweise durch
eine zufälHge Opferauswahl aus.

b) Komorbidität beeinflusst das Risiko gewalttätigen Verhaltens
bei schizo-
phrenen Patienten nicht.
c) Das Risiko, einen gewaltbereiten schizophrenen Menschen zu
treffen ist
weitaus geringer als das allgemeine Risiko, einen
gewaltbereiten Menschen
zu treffen.
d) Die Gewaltbereitschaft schizophrener Menschen ist
therapeutisch schwer
zu beeinflussen.
2. Welche der folgenden Situationen gilt als mögliches
Warnzeichen eines beson-
ders erhöhten Risikos für gewalttätiges Verhalten?
(Einfachauswahl, eine rich-
tige Antwort)
a) Vorliegen einer katatonen Schizophrenie
b) Wiederholte Drohungen mit Gewalt
c) Krankheitsanamnese mit raschem, akutem Krankheitsbeginn
und früher
stationärer Behandlung
d) Selbständige Wobnsituation, auch bei ansonsten
sozialpsychiatrisch gut
eingebundenen schizophrenen Patienten
3. Welche der folgenden Aussagen über die Behandlung von
schizophrenen Pa-
tienten mit einem individuell besonders erhöhten Gewaltrisiko
trifft zu? (Ein-
fachauswahl, eine richtige Antwort)

a) Selbst bei guter Behandlung der schizophrenen
Grunderkrankung bleibt
das Gewaltrisiko der betroffenen in der Regel hoch.
b) Eine Behandlung mit Depotneuroleptika ist wegen der
spezifischen anti-
aggressiven Wirkkomponente zu bevorzugen.
c) Durch eine geeignete antipsychotische Behandlung lässt sich
das Gewalt-
risiko effektiv senken.
d) Eine Behandlung in der Allgemeinpsychiatrie ist in der Regel
nicht
möglich.
zuweisende Funktion hat, sollten Beden-
ken hinsichtlich eines erhöhten Gewaltri-
sikos gegenüber dem Facharzt aktiv the-
matisiert werden. Gegebenenfalls können
in Zusammenarbeit mit der Kindes-und
Erwachsenenschutzbehörde Massnah-
men wie eine fürsorgerische Unterbrin-
gung (Fü) diskutiert und beschlossen
werden, um zur Risikominimierung not-
wendige Behandlungsmassnahmen - vor
allem in Krisensituationen - auch bei
malcomplianten oder behandlungsun-
willigen Patienten durchzusetzen. Medi-
kamentös ist langfristig der Einsatz von
Depotneuroleptika anzustreben, wobei

dies nicht in einer spezifisch antiaggres-
siven Wirkung dieser Präparate, sondern
aufgrund der verbesserten Kontrolle über
die Einnahme und wegen der stabileren
Plasmaspiegel begründet ist.
Legalprognose
Die Sinnhaftigkeit einer präventiven
Behandlung erschliesst sich aus den
Behandlungserfolgen im psychiatri-
schen Massnahmebereich: Untersu-
chungen zu Rückfaüraten von Straftä-
tern [20,21] haben gezeigt, dass Häftlinge
deutlich höhere Rückfallraten (48%) als
Absolventen einer stationären Massnah-
me (20%) haben. Noch geringer sind die
Rückfallraten bei Tätern, die - wie dies
bei schizophrenen Patienten oft der Fall
ist - bei Verurteilung als schuldunfähig
(4,5%) eingestuft wurden. Bei einer Op-
timierung der Versorgung schwer kranker
und gewaltbereiter schizophrener Patien-
ten in der medizinischen Regelversorgung
dürften ähnliche Behandlungs- und da-
mit auch Präventionseftekte möglich sein.
Dabei geht es keinesfalls darum. Betroffe-
ne präventiv wegzusperren, sondern dar-
um, über die Grenzen der medizinischen
Disziplinen und der mit Betroffenen be-
trauten Professionen bzw. Institutionen
hinweg, für besonders problematische
Fälle ein möglichst effektives interdiszip-
linäres und -professionelles Helfernetz zu
entwickeln. Lässt sich dabei eine adäquate
medikamentöse Behandlung nicht sicher-

stellen, muss es vorwiegend um eine eng-
maschige Verlaufskontrolle gehen. Wenn
durch das sorgfältige Monitoring gesund-
heitliche Krisen rechtzeitig erkannt und
gegebenenfalls auch entschärft werden,
kann auch diese Massnahme helfen, De-
likte zu verhindern.
Abstract
Äs compared to the general population
schizophrenic patients are at increased
risk of becoming delinquent. The ma-
jority of schizophrenic patients do not
commit any crime, and the risk of the
general population to be a target of a
violent act by a person with schizo-
phrenia is low. The causes of delin-
quency in schizophrenia are complex,
but certain risk characteristics (e.g. an
accompanying substance abuse) have
been identified. The treatability and
legal prognosis of schizophrenic of-
fenders are good, which suggests that
establishing a suitable helpers network
could also be used for violence preven-
tion in patients at risk.
Keywords: schizophrenia - delinquen-
cy - violence - risk
Résumé
Les personnes schizophrènes ont en
comparaison avec la population géné-
rale un risque elevé de tomber dans la

délinquance. La majorité des patients
schizophrènes n'ont commis aucun
crime, et Je risque de la population
générale d'être affectée par un acte de
violence par un schizophrène est faible.
Les causes de la délinquance des schizo-
phrènes sont complexes, mais certaines
caractéristiques de risque (par exemple,
un abus de substances d'accompagne-
ment) ont pu être identifiées. La trai-
tabilité et le prognostic ligal des délin-
quants schizophrènes sont bons, ce
qui suggère qu'un réseau d'aide adapté
pourrait être utilisé aussi préventive-
ment chez les patients à risque.
Mots-dés: schizophrénie - délinquance
- violence - risque
Korrespondenzadresse
PD Dr. med. Elmar Habermeyer
Direktor
Klinik für Forensische Psychiatrie
Psychiatrische Universitätsklinik Zürich
Lenggstrasse 31
8032 Zürich
[email protected]
lnteressensi<onflil<t: Die Autoren erklären, dass
l<ein interessensi<onfiii<t besteht.
Manusi<ript eingereicht: 18.7.2013, revidierte
Fassung angenommen: 4.9.2013.
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O R I G I N A L P A P E R
Violent Crime in Asperger Syndrome: The Role of Psychiatric
Comorbidity
Stewart S. Newman Æ Mohammad Ghaziuddin
Published online: 1 May 2008
� Springer Science+Business Media, LLC 2008
Abstract Although several studies have suggested an
association between violent crime and Asperger syndrome
(AS), few have examined the underlying reasons. The aim
of this review is to determine to what extent psychiatric
factors contribute to offending behavior in this population.
Online databases were used to identify relevant articles
which were then cross-referenced with keyword searches
for ‘‘violence,’’ ‘‘crime,’’ ‘‘murder,’’ ‘‘assault,’’ ‘‘rape,’’ and
‘‘sex offenses.’’ Most of the 17 publications which met the
inclusion criteria were single case reports. Of the 37 cases
described in these publications, 11 cases (29.7%) cases had
a definite psychiatric disorder and 20 cases (54%) had a
probable psychiatric disorder at the time of committing the

crime. These findings underscore the role of psychiatric
disorders in the occurrence of violent crime in persons with
Asperger syndrome and highlight the need for their early
diagnosis and treatment.
Keywords Crime � Violence � Asperger syndrome �
Autism � Comorbidity
Introduction
Asperger syndrome (AS) was first described under the title
‘‘autistic psychopathy’’ by Hans Asperger, an Austrian
physician interested in the habilitation of children with
behavioral problems (Asperger 1944). Fifty years after its
initial description, it was introduced as a distinct category
in the DSM-IV (APA 1994) and the ICD-10 (WHO 1993).
At present, it is conceptualized as a variant of autism,
marked by social deficits and intense focused interests in
the presence of normal intelligence and relatively well-
preserved communication skills. In addition, most affected
persons have an odd and pedantic manner of speaking

(Klin et al. 2005); and poor nonverbal communication
(Wing 1981). Although its exact prevalence is uncertain, it
is being increasingly recognized in children and adults.
Recent figures place its prevalence rate between one and
five per thousand (Chakrabarti and Fombonne 2005;
Mattila et al. 2007).
An interesting but controversial aspect of Asperger syn-
drome is its association with violent crime. Although
Asperger used the label ‘‘autistic psychopathy’’ as a stable
personality style and not as an index of criminality, reports
have continued to describe links between AS and violent
crime. It was probably Mawson et al. (1985) who first
reported an association between Asperger syndrome and
violent crime. They described a 44-year-old man who had a
long history of violent behavior that led to frequent admis-
sions to psychiatric hospitals (Mawson et al. 1985). A few
years later, Baron-Cohen (1988) described a 21-year-old
man with a history of recurrent violence towards his 71-year-

old girlfriend. The author speculated that while the primary
cause of the patient’s violent feelings could not be ascer-
tained, one factor that maintained them was his deficit in
social cognition (Baron-Cohen 1988). Ghaziuddin et al.
S. S. Newman
University of Oregon, Eugene, OR, USA
Present Address:
S. S. Newman
Private Practice, Portland, OR, USA
M. Ghaziuddin (&)
University of Michigan, Ann Arbor, MI, USA
e-mail: [email protected]
123
J Autism Dev Disord (2008) 38:1848–1852
DOI 10.1007/s10803-008-0580-8
(1991) reviewed the published literature on this topic from
1994 to 1990 and concluded that there was no clear associ-
ation between AS and violent crime and suggested that
people with AS were no more likely to commit violent crime

than the rest of the population (Ghaziuddin et al. 1991).
However, since the publication of that review, reports
have continued to appear suggesting a link between As-
perger syndrome and crime, especially violent crime,
including murder (Schwartz-Watts 2005). Several mecha-
nisms have been suggested to explain this association, such
as, lack of empathy; social naiveté, excessive interests
getting out of control etc. Some authors have focused on
the tendency of persons with AS to collect objects of
special interest as a prelude to criminal behavior. Thus,
Chen et al. (2003) described a 21-year-old male with As-
perger syndrome who had a history of repeatedly stealing
certain objects, such as, plastic bags, boxes and paper cups
(Chen et al. 2003). Others have suggested that persons with
AS sometimes indulge in criminal behavior because of
their sexual preoccupations. For instance, Chesterman and
Rutter (1993) described a 22-year-old male with Asperger
syndrome who had a history of stealing cotton lingerie and

masturbating while holding women’s nightdresses. Kohn
et al. (1998) described a 16-year-old male with Asperger
syndrome who had the habit of grabbing and fondling
women in an attempt to make them his ‘girlfriends.’ Milton
et al. (2002) described the case of a Caucasian male in his
early thirties with AS who had a history of recurrent sexual
offences, such as, touching the private parts of young
women; watching women in public toilets; and making
obscene phone calls at times pretending to be a gynecol-
ogist. Bankier et al. (1999) discussed the case of a 25-year-
old male with a history of selective mutism, severe social
withdrawal, and recurrent violence against his mother, who
met the profile of Asperger syndrome. In addition, at least
two reports have suggested that persons with AS may be
predisposed to committing arson. Everall and LeCouteur
(1990) described a 17-year-old boy with a history of fire-
setting. In a retrospective study examining the role of
neuropsychiatric disorders in a group of 126 juvenile

offenders referred to a forensic service in Sweden, Sip-
onmaa et al. (2001) found four persons with definite
Asperger syndrome. The diagnoses of Asperger syndrome
and PDDNOS were over-represented in the arson group
than it was in any other offending group (Siponmaa et al.,
2001).
Few studies, however, have examined the role of psy-
chiatric factors that might contribute to the occurrence of
violent crime in this population. In one of the few reports
on this topic, Palermo (2004) emphasized the importance
of psychiatric factors by describing two cases of AS and
one of PDDNOS, all of whom had a history of violence and
arson, and additional psychiatric disorders. Other reports
have alluded to the psychiatric status of the offenders but
not provided enough details. Surveys of special hospitals,
for example, have found an excess of persons with AS.
Scragg and Shah (1994) studied the entire male population
in a maximum security hospital in the U.K., and found nine

subjects who met the characteristics of Asperger syndrome.
The authors concluded that the rate of AS was higher in
that hospital than that in the general population. There have
also been reports in the media, especially in the United
States, speculating on an association between AS and
random acts of campus violence in the United States. Thus,
despite the public health importance of the topic, relatively
little is known about the psychiatric status of violent
offenders with Asperger syndrome. The purpose of this
review is to examine this issue.
Method
We performed an extensive computer-assisted search of
professional databases including MEDLINE, CINAHL,
Cochrane database of systematic reviews, and pertinent
textbooks and related resources, to identify all published
papers describing the association of Asperger syndrome
with crime and violence. Reference lists of articles were
also examined for additional sources. Searches were per-

formed using the keywords ‘Asperger syndrome,’
‘pervasive developmental disorders;’ and ‘autistic psy-
chopathy.’ These categories were cross referenced with the
keywords ‘‘violence,’’ ‘‘crime,’’ ‘‘murder,’’ ‘‘assault,’’
‘‘rape,’’ and ‘‘sex offenses.’’ The articles were reviewed to
determine if they included sufficient information of the
criminal behavior.
For the purpose of this review, violent crime was defined
as any act for which the person could be charged with a crime
(including but not limited to murder, attempted murder,
assault and/or battery, sexual assault, arson, stalking, rob-
bery) or which resulted in a significant injury to another
person. Since the study was based on the information already
contained in the published reports, it was not possible to
examine the motives or the reasons for the violent act.
Therefore, the definition of violent crime was based on the
observed behavior and its consequences rather than the
intent. Temper tantrums, nonspecific behavioral problems,

and self-injurious behaviors were excluded. Articles were
also excluded if they did not include sufficient information to
determine the diagnosis of the subjects or a detailed
description of the criminal behavior. Only articles published
in English were reviewed.
Subjects were divided into three categories; those with
definite psychiatric disorder; those with probable psychi-
atric disorder; and those with no clear evidence of a
psychiatric disorder. To be classified as suffering from a
J Autism Dev Disord (2008) 38:1848–1852 1849
123
‘‘definite’’ psychiatric disorder, the subject had to have a
psychiatric diagnosis given by a psychiatrist and/or to have
symptoms and behavior described in sufficient detail to
allow for a diagnosis to be made. Cases that probably had a
psychiatric illness but did not have enough details descri-
bed of their behavior were classified as having had a

‘‘probable’’ psychiatric disorder. Finally, cases who had no
evidence of a psychiatric disorder based on the description
given in the report were classified as not having any such
disorder. The first author examined the case histories and
then both the authors, after discussion, jointly categorized
whether or not the act described in the publication met the
inclusion criteria.
Results
Computerized database searches yielded 59 candidate
articles for review. An additional 13 articles were found
through reference lists, resulting in a total of 72 publica-
tions. Of these, 54 were excluded for not meeting the
inclusion criteria, leading to a total of 18 publications.
Another article (Anckarsater 2005) was excluded because,
on further examination, it had the same cases that had been
included in a previous publication (Soderstrom et al.
2005). This led to a total of 17 publications and 37 cases.
Of these, 11 (29.7%) cases had evidence of a definite

psychiatric disorder and 20 (54%) cases of probable psy-
chiatric disorder. In only six cases (16.2%), was there no
clear evidence of a comorbid psychiatric disorder
(Table 1).
Discussion
The main finding of the study is that an overwhelming
number of cases had co-existing psychiatric disorders at the
time of committing the offence. Eleven cases (29.7%)
cases had a definite psychiatric disorder and 20 cases
(54%) had a probable psychiatric disorder. Examples of
cases with a definite psychiatric disorder included the three
cases described by Palermo (2004) had comorbid psychi-
atric disorders (ADHD and Mood Disorders). Four of the
34 cases in Wing’s study were categorized as having a
definite psychiatric disorder (Wing 1981). In Baron-
Cohen’s (1988) study, the patient, a 21-year-old man,
believed that he looked like a werewolf and was obsessed
with his jaw. He too was classified as having a definite

psychiatric disorder. All the nine cases described by Scragg
and Shah (1994) were in a maximum security hospital for
mentally ill offenders. Because sufficient details of their
behavior were not given, these nine cases were classified as
having a probable psychiatric disorder. Thus, on the whole,
the findings suggest that impairment of mental health may
be an important reason why some persons with Asperger
syndrome commit violent criminal acts.
The association between violent crime and mental
health is well established (Swanson et al. 1990). Psychi-
atric problems are over-represented among violent
offenders although the nature of the association between
psychiatric disorder and criminality is not clearly under-
stood. Factors such as substance abuse; family history of
criminality and other psychosocial stressors are also
important. Therefore, when violent crime occurs in the
Table 1 Psychiatric comorbidity of AS subjects with violent
criminal behavior

Study N Psychiatric disorder Comments
Wing (1981) 4 Definite ‘‘Bizarre and antisocial acts’’
Mawson et al. (1985) 1 Probable History of psychiatric
admissions
Baron-Cohen (1988) 1 Definite Obsessed with his jaw. Probable
dysmorphophobia
Everall and Lecouteur (1990) 1 Not clear No clear comorbid
diagnosis. Compulsive fire-setter
Chesterman and Rutter (1993) 1 Probable Probable Obsessive
Comp Disorder. ‘‘Personality Disorder’’
Scragg and Shah (1994) 9 Probable All patients probably had a
comorbid psychiatric diagnosis
Kohn et al. (1998) 1 Probable Diagnosed with ‘conduct disorder
Bankier et al. (1999) 1 Probable Diagnosed with ‘‘obsessional
neurosis’’
Siponmaa et al. (2001) 4 Probable History of fire-setting
Milton et al. (2002) 1 Nil No comorbid diagnosis. Paraphilia
and serial sexual offenses
Silva et al. (2002) 1 Nil Case report on Jeffery Dahmer.
Diagnosis doubtful
Silva et al. (2003) 1 Not clear Case report on Theodore
Kaczynski, History not clear
Palermo (2004) 3 Definite Pt 1: ADHD; Pt 2: Depression; Pt 3:

Mood disorder
Silva et al. (2005) 1 Nil Case report on Joel Rifkin, Diagnosis
doubtful
Schwartz-Watts (2005) 3 Cases 1 & 3, Definite Pt 1: Overdose,
3: Nil; 3: Schizoaffective disorder
Soderstrom et al. (2005) 3 Probable From 100 admissions to
forensic hospital
Haskins and Silva (2005) 1 Definite Major Depression
1850 J Autism Dev Disord (2008) 38:1848–1852
123
setting of Asperger syndrome, the cause may lie as much in
the diagnosis of AS as in the other factors that contribute to
its occurrence in the general population, including
comorbid mental disorders.
Persons with Asperger syndrome have sometimes been
described as lacking in empathy and in their ability to
experience the feelings and emotion states of others. In
fact, diagnostic measures of autism often incorporate
questions dealing with the child’s ability to share feelings

with and offer comfort to others. As an extension of this
belief, persons with Asperger syndrome have been descri-
bed as lacking in conscience, which increases their risk for
committing crime. However, although some persons with
Asperger syndrome may be described as defiant and
oppositional, aggressive behavior is not one of its defining
or discriminating features (DSM, APA 1994).
It is important to emphasize that six cases (15%) did not
have any comorbid psychiatric disorder which suggests that
some persons with AS indulge in violent crime for no
apparent reason. These persons may meet the criteria for
antisocial personality disorder although the two conditions
are regarded as distinct entities (Wing 1981). In a cohort of
violent offenders, Anckarsater (2005) found that 18 of the
89 offenders subjects had a history of an ASD (five cases
had autism; three had Asperger syndrome and 10 had
atypical autism). Although Asperger sydnrome symptoms/
autistic traits were positively correlated with the Psy-

chopathy Checklist-Revised scores (PCL-R; Hare 1991),
the superficiality that characterized psychopathy was dif-
ferent from the social disability of autism (Anckarsater
2005). Studies comparing differences in the social
impairment of AS with those of conduct disorder (which is
often regarded as a forerunner of antisocial personality
disorder) have also reached similar conclusions (Green
et al. 2000).
Since the study consisted of 37 subjects, it may be
criticized as being too restrictive and hence not being
representative. The most common reason why subjects
were excluded was a lack of clarity about the diagnosis.
For instance, two reports were excluded because the sub-
jects had mental retardation (Simblett and Wilson 1993;
Cooper et al. 1993), which is not consistent with a diag-
nosis of Asperger syndrome based on the DSM-IV (APA
1994) criteria. In other cases, the diagnosis was made for
the first time in adulthood without a reliable early devel-

opmental history (for example, Murrie et al. 2002).
Another reason why subjects were excluded was a lack of
clarity about the reason for referral and insufficient
description of the offending behavior. Thus, the study by
Mandell and colleagues (2005) was excluded because the
nature of the behavioral problems was not specified.
Another study was excluded because the offender had a
history of stealing (Chen et al. 2003) but not of any violent
crime. Finally, one study (Anckasarter 2005) was excluded
because its sample was common to another study that was
included (Soderstrom et al. 2005). Thus, on the whole, the
findings of our study seem to be representative of persons
with Asperger syndrome referred to specialist services.
Our review did not attempt to find out if, based on recent
literature, persons with AS can be described as being at
greater risk of committing violent crime than the general
population. For this purpose, systematic population-based
studies are required. In perhaps the only study of its kind,

Woodbury-Smith and colleagues (2006) compared the rates
of offending behavior in a community sample of persons
with high-functioning forms of ASD with a matched gen-
eral population control group. Although the study was
based on a small sample of 24 cases, and did not examine
the psychiatric comorbidity of the offenders in a systematic
manner, its findings provide further support that persons
with ASD do not seem to be at an increased risk of criminal
behavior. More studies of this nature are urgently needed.
In conclusion, this review found that most of the cases
of Asperger syndrome who commit violent crime suffer
from additional psychiatric disorders. While this finding in
itself does not fully explain why some persons with AS
commit violent crimes, it suggests that co-existing mental
disorders raise the risk of offending behavior in this group,
as it does in the general population. Thus, persons with AS
charged with violent crimes should be examined for the
presence of additional psychiatric disorders. Clinicians

should look beyond the diagnosis of AS and attempt to
explore the factors that might contribute to criminal
behavior in this population. In addition, professionals
working in forensic settings should be trained in the rec-
ognition and treatment of persons with autistic spectrum
disorders and special services should be designed for
mentally ill offenders with Asperger syndrome.
Acknowledgments The authors acknowledge their gratitude to
Cheryl King, Ph.D. and to the NARSAD Foundation.
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