BMC – 1– Elbert et al.
In: Lifespan Development and the Brain: The perspective
of Biocultural Co-
Constructivism, Eds : P. Baltes, P. Reuter-Lorenz &
F. Rösler.
Press, 2006, pp326-349.
The Influence of
Organized Violence and Terror on Brain and
Mind – a
Co-Constructive Perspective
Address of the authors:
D-78457 Konstanz
Germany
Thomas.Elbert@Uni-Konstanz.de
Brigitte.Rockstroh@Uni-Konstanz.de
Iris.Kolassa@Uni-Konstanz.de
Maggie.Schauer@vivo.org
Acknowledgement: The research was supported by the Deutsche Forschungsgemeinschaft and the European Refugee Fund
BMC – 3– Elbert et al.
„Genetic interventions make us better animals. Humans, we
become, however, because of
the ways that culture and our
individual constructions exploit the brain and make it our
servant.“ (Baltes & Singer, 2001).
ABSTRACT
The human brain is formed by two interactive systems, the
genetic-biological and the socio-cultural systems. The brain, in turn,
regulates behavior and thereby acts on the societal environment. This chapter
examines how experience shapes the brain and describes
the interaction of brain, behavior,
and culture under conditions of extreme and traumatic
stress as present in many war-torn
regions around the globe. Traumatic events massively
change the brain’s structure and
function. Within our model of biological-cultural interaction we analyze how
these experiences foster violent behavior and deal with the societal
consequences of the traumatization of large parts of
the population.
INTRODUCTION
In this day and age human beings are raised and live in a
complex socio-cultural environment with increased demands for the brain, the
body, and the social structures to
adapt. More information at increasingly
complex levels has to be processed than ever before at an ever increasing
velocity and over an extended life-span. This places a high
pressure on the individual and
society to continuously adjust to new environmental conditions, resulting in a
stream of continuous microstressors. At the same
time, modern societies are becoming increasingly aware of the effects of macrostressors including traumatic stress, which, although
seemingly transient, may be changing the brain’s processing
machinery, resulting in
characteristic behavioral, physiological, and psychological
(mal)adaptations to environmental
conditions and – when a whole community is affected
– in a change in the local culture.
This in turn will impinge on all individuals in the community, even those not
affected by the traumatic experience in the first place, as human
behavior represents the
co-constructive expression of biological-genetic and sociocultural
conditions. While recent neuroscientific advances
have substantially improved
our understanding of neuroplasticity, i.e., the brain’s extraordinary ability to
change its
BMC – 4– Elbert et al.
structure and function in response to experience, less
effort has been devoted to understanding mechanisms in relation to affect and
distress and little is known on how changes
on the level of the individual
interact with those on a community level. Social stress and
organized violence serve as good
models for studying this interaction of adaptive alterations in individual and
societal minds. We currently witness a qualitative change in the
way wars are waged and organized
violence is exerted; in other words, a transformation
in the “culture of violence” cannot
be overlooked. Moreover, scientific methods are
available to study how traumatic
stressors change individuals and communities, so that
we can expect increasing knowledge
about how social stressors and related learning conditions shape the structure
and function of both, the brain and the “societal mind” including individual
behavior and interactions on the community level.
The human brain constitutes the joint product or
co-construction of two interactive
systems of impact; the internal
genetic-biological and the external socio-cultural systems
(Baltes, 1999).
The social environment into which malleable individuals are born, together with
their response to this environment – the way in which individuals live their
lives – lead to the cultural
determination of gene expression. In turn, individuals shape
their socio-cultural environment by
imposing structure and function resulting from a history of genetic expression.
Stressors exert a powerful influence on the brain, at the same
time modifying brain structure,
brain function, neuropsychological performance, and peripheral physiological
responses. Extreme or continuous stress may drive the individual
into an increasingly maladaptive
state with the potential for mental disorders. Cultural
settings can support only a limited
number of such individuals before these become a
driving force in cultural
mal-adaptations.
This chapter extends the co-constructive perspective to
effects of extreme social
and traumatic stress (as, for
instance, in organized violence) on the brain with its behavioral consequences.
We will first describe evidence on neuroplasticity in
the brain and
outline a theoretical model on how
traumatic experiences change the brain on a structural
and functional level. Then, we will
discuss characteristics of organized violence and “new
wars” as conditions of traumatic
stress to which large parts of the population are exposed
in many war-torn regions around the
globe, especially in sub-Saharan
BMC – 5– Elbert et al.
EXPERIENCE SHAPES THE BRAIN: NEURAL ADAPTATION AND
PLASTICITY
The brain is continuously modified by experience. The study
of sensory representations
in the cortex has provided an
excellent model for studying how the brains’ representations of the periphery
are dynamically modified (Elbert & Rockstroh,
2004). Cortical representations mirror the spatial arrangement of the
corresponding peripheral receptors in
the form of cortical maps. Although
genetically encoded programs control the connections of these maps from the
periphery to the cortical destination, their organization ultimately depends on
the efficacy of the synapses connecting the nerve cells within the network,
which is affected by external input. For instance, two receptors of the same
fingertip are more frequently activated in synch than two receptors in
different digits. According to Hebb’s learning model,
synchronous stimulation should lead to connections between the representations
of the same fingertip but to a separation from those of the other
digits: representational zones are
shaped by the temporal pattern of such coincident experience. An alteration in
behaviorally relevant afferent input will trigger a
reorganization
of the map: The representation of a
fingertip can be enlarged, representations of adjacent
fingers can invade its territory,
or the representation of two fingers can get fused. Using
magnetic source imaging, we have demonstrated
that skilled string instrument players – a
category for which both cultural
and psychological preconditions are necessary – have
larger representational zones of
their left hand in their cerebral cortex compared to the
brains of people who do not engage
in such extensive practice (Elbert, Pantev, Wienbruch, Rockstroh, & Taub, 1995). Using the same culturally determined quasi-
experimental set-up, structural MRI
reveals that the change in function is intertwined
with structural alterations (the
depth of the left-hemispheric central sulcus) that
extend
into the macroscopic range (e.g., Schlaug, Jäncke, Huang, Staiger, & Steinmetz, 1995).
Moreover, the musician’s cerebral cortex not only
exemplifies adaptation (or in some
cases maladaptation;
Elbert et al., 1998) to somatosensory requirements
but also differs
from “normal” cortex in many
regions (e.g., Pantev et al., 1998; Christian & Schlaug,
2003) and probably also in other respects which are not
(yet) accessible to our observations.
Reorganization varies with perceptual correlates of superior
performance – an
adaptive advantage of cortical
plasticity. Adaptive cortical plasticity can also be observed
BMC – 6– Elbert et al.
in disabled persons – as in blind
individuals who are forced by their disability to rely on
non-visual modalities, including
hearing, for information about their external environment. Sensory input via
non-visual avenues thus gains greater behavioral relevance and
becomes a focus of greater
attention to enable effective interaction with the world. For
instance, when attention is
directed to peripheral auditory space, localization of sounds is
better in blind than in sighted
people (e.g., Lessard, Pare, Lepore,
& Lassonde, 1998). Individuals who lost their
sight at an early age may outperform sighted persons in nonvisual
tasks, including speech perception (e.g., Muchnik, Efrati, Nemeth, Malin, & Hildesheimer, 1991), verbal memory (e.g., Röder, Rösler, & Neville, 2001),
and musical abilities (e.g., Gougoux, Lepore, Lassonde, Voss, & Zatorre, 2004). Behaviorally relevant
stimulation over extended periods
has been found to produce a substantial enlargement in
the representational zones of the
involved portions of the tonotopic system in animals
(Recanzone, Merzenich,
Jenkins, Grajski, & Dinse,
1992) and humans (Elbert et al.,
2002). In addition, there is cross-modal plasticity in the
blind, such that auditory (e.g.,
Gougoux, Zatorre,
Lassonde, Voss, & Lepore,
2005) and tactile (e.g., Kujala et al., 1997)
stimuli come to be processed in
visual cortex. Obviously, environmental demands and
the individual experiences can
dramatically remodel the brain’s functional organization.
During “critical periods” of development, sensory
stimulation without explicit behavioral significance is sufficient to alter the
organization of the sensory cortex (e.g.,
Bao, Chang, Davis, Gobeske, Merzenich et al., 2003). In contrast, functional reorganization in the
adult cortex seems to be driven mainly by stimuli related to reinforcement,
i.e., it requires a behaviorally relevant context (e.g., review Elbert & Rockstroh, 2004). The effects of reinforcement are mediated
by cholinergic (Kilgard &
Merzenich, 1998) and dopaminergic pathways (Bao, Chan,
& Merzenich, 2001) which by
themselves are subject to plastic
alterations, as seen in psychosis. While the model of the
blind demonstrates that similar
mechanisms also act beyond the representational cortex,
additional mechanisms may come into
play in associative or polymodal areas. Already at
the level of the primary sensory
cortex, context and top-down modulation driven by attention and motivation
affect reorganization (e.g., Braun et al., 2002).
Plastic alterations are not necessarily adaptive. Stressful
life experiences during
“critical periods” may affect brain
organization in harmful ways. Childhood and adolescence are determined as
critical periods of cognitive and emotional development (e.g.,
BMC – 7– Elbert et al.
Steinberg, 2005), as well as vulnerable phases for the
development of the stress system
(Charmandari,
Kino, Souvatzoglou, & Chrousos,
2003). Since it is known that even a
single traumatic experience can
initiate a cascade of dynamic brain processes which may
result in enhanced vulnerability to
subsequent stressors (Schauer et al., 2003; Neuner et
al., 2004a) or even in a break-down of normal functioning as
seen in the pathologies of
the trauma spectrum, children
growing up in a culture of violence may be particularly affected. Here we
propose that violent and traumatic experiences by altering the individual
brain and mind, i.e., by modifying
behavior, can induce a spiral of violence in which an
increasing number of individuals
influenced by traumatic experiences themselves commit
crimes in the community. Thus,
wartime strategies are increasingly characterized by mutual hate of
ethnicities. Forcible displacement of civilians is used by both guerrilla and
anti-guerrilla forces, in an
attempt to unite one's own group through crimes against humanity. Wars are
accompanied by systematic killings and ethnic cleansings, whole regions are
left uninhabitable for the local people since towns are devastated,
infrastructure
ruined, and landmines make much of
the land inaccessible
POSTTRAUMATIC STRESS DISORDER AS A MODEL OF TRAUMATIC
STRESS EFFECTS ON THE BRAIN
In an attempt to understand the consequences of these
atrocities on brain and mind (Elbert
& Schauer, 2002, Neuner, 2003), we have studied refugees in
in crises regions such as the
Balkans (Neuner, Schauer,
Roth, & Elbert, 2002), the West
Nile (Neuner et al., 2004a, Neuner, Schauer, Klaschik, Karunakara, & Elbert,
2004b; Karunakara et al.,
2004), Rwanda (Schaal & Elbert, 2005; Onyut
et al., 2004), and Somalia
(Odenwald et
al., 2005). In all these regions, we conducted diagnostic interviews and
found high prevalence rates of
posttraumatic stress disorder ranging from 15% to 50%.
An amazing finding was the ability of displaced persons from
remote areas in
were illiterate, to describe the
classic symptoms of severely traumatized individuals as if
taken from a psychiatric textbook.
The core symptoms of Posttraumatic Stress Disorder
(PTSD) are: (1) re-experiencing symptoms that manifest at
night in the form of nightmares and in the waking state as flashbacks and
intrusive recollections which are so intense that the victim actually believes
to be back amidst the atrocities, (2) an exaggerated
BMC – 8– Elbert et al.
startle response and a persistent hyperarousal, difficulties in calming down or falling
asleep; all these symptoms describe
a readiness for fight or flight rather than a permanently enhanced autonomic
activation, and (3) an active avoidance of places or thoughts
associated with traumatic
experiences and/or passive avoidance symptoms, i.e., numbing
emotional responsiveness as a way
to cope with unbearable feelings. In severe cases this
may include dissociative
symptoms, e.g., feelings of detachment or estrangement from
the external world (derealization) and of oneself (depersonalization), or even
persecutory
delusions.
Symptoms of the trauma-spectrum and of PTSD in particular,
can be understood as a
consequence of plastic changes in
memory through stressful, traumatic experiences. Life
experiences are stored in
autobiographical memory. The autobiographical context memory has been called
“cold memory” (Metcalve & Jacobs, 1996). It
contains knowledge
about life-time periods and
specific events. The sensory-perceptual representations of a
traumatic event have been called
“hot” or non-declarative (implicit) memory. It comprises emotional and sensory
memories of all modalities. Cold memories (e.g., on March
24 at
smell) as well as with cognitive
(e.g., I can’t do anything), emotional (e.g., fear, sadness),
and physiological elements (e.g.,
heart racing, fast breathing, sweating).
Insert Figure 1 about here (fear network)
In individuals who are not affected by trauma or fear, hot
memories are linked with
autobiographic, declarative
memories. However, in traumatized persons, sensory and
emotional memories are activated by
environmental stimuli without being related to
autobiographic, declarative items
(i.e., dates and places of autobiographical occurrences)
– these autonomous hot memories
form a fear network (Lang, 1979). An example of such
a network is outlined in Figure 1.
The activation of a single memory item (e.g., seeing a
man in a uniform or feeling one’s
heartbeat) will cause the whole network to be activated.
According to Hebbian learning,
this will not only strengthen the interconnections between
existing network units, but will
also lead to an inclusion of additional network elements,
namely of those that are
synchronously activated. Such an inclusion of additional nodes
BMC – 9– Elbert et al.
will be strongest during subsequent
traumatic experiences or experiences with a strong
emotional component that
co-activate motivational and reward systems which enhance
the brain’s plasticity. As a
consequence, the number of non-declarative (hot) elements in
the fear network and their
interconnectivity will increase. At the same time, co-activation
of declarative autobiographical
memories becomes less likely since with an increasing
number of experiences, the network
contains more and more conflicting information:
typically a person can only
retrieve one context in which the fear network was previously
activated (as we know that we
cannot have been simultaneously at two places or create
one imagery for two different time
periods). As a result, hot and cold memory will separate, and only few
connections of hot memory contents with declarative autobiographic
memory will survive. This leads to
a fragmentation of the autobiographic memory, i.e.,
traumatized persons have
difficulties in reconstructing dates and sequences of events associated with
traumatic experiences. The described model assumes the fear network to be
an example of plastic changes in
the human brain in response to traumatic life events.
Studies on fear conditioning demonstrate that a single
stressful or traumatic event
can be sufficient to set-up a fear
network, but it will be connected to context. Repetitive
traumatic experience will
strengthen the fear – but the survivor begins to loose the context when the
fear happened, rendering the victim vulnerable for mental disorders. Whenever
the atrocities are multiple and repetitive, we find a linear relationship
between the
number of experienced traumata and
the proportion of survivors with PTSD, with a hundred percent traumatization in those who report some 25 or more fearful
events (e.g.,
Neuner et al., 2004a).
Memory is the ability to recall events from the past.
However, it is a common mistake to restrict the function of memory to
recollections of the past. What seems more
likely is that the ability to
envisage future scenarios was a driving force in the evolution
of memory, and of episodic memory
in particular. Hebbian types of memory fit this
explanation of memory well: every time a cell assembly is activated for
"read-out", the
content of the respective memory
will not only be read but also modified, i.e., neurons of
an activated cell assembly are not
only activated, but will also modify their connections
with each other. This
activation-modification takes place through both imagination and
present experiences. Since each
time a memory is activated, it is modified, a fear network, although originally
formed by traumatic experience, may become connected to pre
BMC – 10– Elbert et al.
sent conditions, e.g. when the
survivor is forced to live under unsafe condition. The resulting daily stress
affects the neuro-humoral axes which in turn exert
their effects back
on brain and mind. Thus, traumatic
stress drives the organism to its limits.
THE STRESS-INDUCED TILT OF NEURO-HUMORAL AXES
Allostasis1, the adaptation of the internal milieu to meet
perceived or anticipated threats
in the environment, has evolved as
a survival securing response to escape acute danger.
However, it may be an inappropriate response in the modern
human. The same physiological responses (like the supply of additional blood
and oxygen to muscles, etc.) are still
activated in the face of modern
stressors, which can, however, neither be attacked nor escaped from by running
away. Thus, prolonged stress turns adaptive allostasis
into allostatic load. Permanently warding off stress
turns the adaptive physiological responses
into maladaptive diseases in the
form of aches and pains, loss of appetite or overeating. A
chronically high allostatic load damages organs, including the brain
(McEwen, 2004).
Central-peripheral circuits triggered by specific
environmental cues that activate the
fight-flight-freeze defense cascade
strongly affect the dynamic storage of various elements of memory. The body’s
stress response is regulated by three systems (e.g., McEwen, 2002, 2004; Elbert
& Rockstroh, 2003): First, the hippocampus and
the hypothalamic-pituitary-adrenal (HPA) axis play a major role in the defense
cascade and are involved in the feedback regulation of cortisol
excretion. Second, the amygdala, the locus
coeruleus,
the adrenal gland, and the sympathetic nervous system are crucial in the
stress-
induced mobilization for fight or
flight; they are involved in sharpening awareness in
alarm situations and directing
blood flow toward the brain and major muscles and away
from the surface of the skin in
hands and feet as well as away from digestive and reproductive organs. A third,
less well explored axis involves the vasopressin-oxytocin
peptides (Heinrichs, Baumgartner, Kirschbaum,
& Ehlert, 2003). When functioning properly,
The body, including the brain, is able to deal with dangers
in a flexible and adaptive way. In contrast
to homeostasis, i.e., the
organism’s ability to maintain a steady internal state, allostasis
refers to the flexibility in the adjustment to stressors that range from Hans Selye’s types of physical deprivation (cold, noise,
deprivation of food, sleep, etc.) to the real or imagined fear-provoking situations that
trigger an alarm response. The Greek word ‘allo’,
meaning ‘variable’, is used by McEwen (2004) to emphasize the ability to
choose various attack and defence mechanisms to counter negative impact.
BMC – 11– Elbert et al.
these systems secure survival in
alarm situations. They also play a role in the stress-
protective effects of positive
social interactions. Dysregulations in these systems
may be
associated with clinical disorders.
This happens, for instance, when neural representations
of fearful past experiences
activate the HPA axis permanently. The excreted stress hormones ultimately make
their way back to the brain, affecting both behavior and health.
Two prime targets for stress hormones in the brain are the
hippocampus and the
amygdala.
It is well established that acute elevations of adrenal stress hormones
(catecholamines
and glucocorticoids) enhance memory consolidation of
emotionally
arousing, contextual
(hippocampus-dependent) information in a dose-dependent manner
in animals (Roozendaal,
De Quervain, Ferry, Setlow,
& McGaugh, 2001) and humans
(e.g., Buchanan & Lovallo,
2001). These enhancing effects of stress hormones are mediated by the basolateral nucleus of the amygdala
(e.g., Cahill, Babinsky, Markowitsch,
&
McGaugh, 1995). As the BLA projects to the hippocampal
dentate gyrus it may modulate
hippocampus-dependent memory
storage (e.g., Packard, Cahill, & McGaugh, 1994).
Lesions of the BLA and the basomedial amygdala (BMA), but not the central or medial nuclei,
attenuate hippocampal LTP in the dentate gyrus (Ikegaya, Saito, & Abe,
1996b),
while stimulation of the BLA and
BMA facilitate LTP in the dentate gyrus of rats (Ikegaya, Saito, & Abe, 1996a). Thus, the amygdala seems to play an important role in mediating hippocampal neuroplasticity.
While the memory-supporting effects of stress hormones are
certainly adaptive
when lasting memories of vital
information (e.g., dangerous situations) have to be established, this mechanism
may become maladaptive under conditions of extreme stress: persistent and
intrusive memories of the traumatic event might be formed which promote the
development of PTSD. Elevated glucocorticoid levels do not only enhance memory
consolidation, but also impair memory retrieval (e.g., de Quervain,
Roozendaal, Nitsch,
McGaugh, & Hock, 2000). In addition, chronic glucocorticoid excess can lead to
disturbances of synaptic
plasticity, atrophy of dendritic branching, and a an
enhanced
susceptibility to other neurotoxic insults (Sapolsky,
1999). Moreover, stress-related enhanced corticotrophin releasing hormone (CRH)
secretion during “critical periods” of
brain plasticity in childhood and
adolescence enforces hippocampal volume loss,
sensitization of hippocampal glucocorticoids
receptors, and altered feedback properties of the
HPA axis, which in turn promote endocrine hyperresponsivity to subsequent social stress.
BMC – 12– Elbert et al.
The seminal studies by Meaney and
his group provide clear evidence that perinatal
stress
already changes the HPA axis,
delays cognitive and emotional development, and may
impair avoidance learning for the
rest of the life (e.g., Meaney, Aitken,
van Berkel, Bhatnagar,
& Sapolsky, 1988). In addition, the medial
prefrontal cortex (mPFC), and here in
particular the anterior cingulate cortex (ACC), are affected by stress. For these
regions
high concentrations of mineralocorticoid (MR) and glucocorticoid
(GR) receptors have
been described, highlighting the
pivotal role of these regions in mediating stress-induced
changes in attention and
(emotional) memory (Erickson, Drevets, & Schulkin, 2003).
Thus, stressful experiences differentially activate a
variety of responses designed by
evolution to counter danger. The
different chemical messengers may cause deficits in
hippocampus-based learning and
memory, and their effects on the amygdalae and the
medial prefrontal and cingulated
cortex may lead to an impaired inhibition of fear responses. A fragmentation of
autobiographical memory due to a separation of emotional
and declarative autobiographic
memory contents is further promoted by these mechanisms. Repeated exposure to
traumatic or chronic stress may lead to long-term dysregulations
and impaired functioning of these systems and may cause symptoms of stress-
related disorders such as hyperarousal, dissociation, flashbacks, avoidance, and
depression. These symptoms in turn may promote maladaptive behaviors like
social withdrawal,
inappropriate aggression, and
self-sedation with drugs.
FUNCTIONAL CHANGES OF THE BRAIN IN PTSD
How can we detect signs of a fear network in the brain? One
would expect that stimuli
specifically related to the
individual traumatic experience are necessary to activate the
fear network. However, contrary to
expectations, it seems that emotionally arousing stimuli, not necessarily
related to the traumatic event, suffice to activate the whole fear network. Junghöfer, Bradley, Elbert, and Lang (2001) introduced
affective material into the
rapid serial visual presentation
(RSVP) paradigm: When presenting stimuli from the International Affective
Picture System (IAPS) in fast succession (3 or 5 Hz) each emotional
stimulus, presented for some 300ms,
should activate only one or more elements in a large
fear network. Using this technique,
Junghöfer et al. (2003) demonstrated that indeed,
many elements or nodes of the
network will be activated and the whole network will ignite. This stimulation
proved capable of evoking affective processing and even provoked
BMC – 13– Elbert et al.
flash-backs in severely traumatized
survivors of organized violence including torture. (It
should be noted that this was the
case in individuals for whom flash-backs were so common that the one contingent
on the RSVP didn’t add to their suffering, as they reported).
In both controls and traumatized individuals, the affective
material activated the visual
cortex and associated areas.
However, only in traumatized survivors suffering from
PTSD, the pre- and orbitofrontal
areas and the cingulate gyrus
were also activated
(Junghöfer et al., 2003; the group
difference is displayed in Figure 2). These data suggest
that torture, like any other
massive experience, dramatically alters the functional organization of the
brain: an enlarged fear network is activated by any aversive material.
Obviously, the (medial) prefrontal cortex (including the anterior cingulate) lost its ability to
regulate these hyper-responsive
fear structures, including the interplay between amygdala
and frontal cortex.
Insert Figure 2 about here
A BNORMAL BRAIN WAVES INDICATE PLASTIC CHANGES IN
ARCHITECTURE AND FUNCTION OF NEURAL NETWORKS
Slow brain waves, when focally generated and present during
the waking state do not appear in healthy individuals and thus signal altered
cortical function (Rockstroh, Ray,
Wienbruch, & Elbert, 2005). In psychiatric disorders, slow waves
may indicate dysfunctional neural networks even when macroscopic structural
lesions are not detectable. The
regional distribution is
disease-specific. Indeed, the distribution of focal slow wave generators
determined from the spontaneous magnetoencephalogram
(by fitting single
equivalent dipoles) differed in
patients with PTSD from patients with other psychiatric
diagnoses. When compared to the
norm group of healthy controls, PTSD patients displayed high concentrations of
abnormal brain waves in the pre- and orbitofrontal
cortex,
while depressed patients showed
hypoactive regions, particularly in frontal areas. The
“dysfunctional” significance of
this brain activity is supported by its variation with successful therapeutic
intervention in PTSD (Elbert et al., 2005). When mapping abnormal
slow wave activity in 23 survivors
of severe torture with a current diagnosis of PTSD,
BMC – 14– Elbert et al.
who had experienced multiple forms
of psychological traumata (Schauer et al., 2005b),
the number of dissociative
experiences was significantly and positively related to the density of abnormal
slow wave generators in the left ventral region of the anterior cortical
structures (correlations range from
.4 to .65). Statistically partialling out the level of
posttraumatic stress disorder did
not influence these relationships, suggesting that the
level of dissociation contributes a
separate component over and above PTSD symptoms
to abnormal brain activity. This is
theoretically consistent with DSM-IV not including
dissociation as a PTSD criterion.
Furthermore, the patient group showed significantly
more abnormal slow waves in the
left ventral region than a culturally matched control
group without torture experience.
Left frontal areas subserve
language and executive function. However, more recently
neuroimaging
studies showed the left ventral prefrontal cortex also to be involved in both
verbal memory encoding and
retrieval (Iidaka, Sadato,
Yamada, & Yonekura, 2000). This
might explain why dissociative individuals lack conscious, verbal access to
certain previous traumatic experiences. It is a common experience in clinical
practice that patients
with PTSD have difficulties in
verbalizing their traumatic experiences. The quality of
emotional memories during
re-experiencing symptoms is more emotional and sensory in
nature, while feelings cannot be
verbally expressed. A disruption of these frontal networks would explain why individuals
experiencing intrusions and dissociative episodes
are unable to actively retrieve and
verbalize previous traumatic experiences. We assume
that extreme traumatic stress such
as torture initially prompts active or passive avoidance
strategies in an attempt to reduce
overwhelming fear, which may result in a permanent
disruption of left frontal
networks. The neural mechanisms of this disconnection may in
part be explained by long-term
depression (LTD) as indicated above, i.e., by anti-Hebbian
learning but also by the
strengthening of inhibitory synapses. This hypothesis of a functional
disconnection of affective from language processing areas as a consequence of
trauma-induced plastic changes in
the brain’s emotion and memory systems remains to be
validated in future studies.
Insert Figure 3 and 4 about here
BMC – 15– Elbert et al.
STRUCTURAL CEREBRAL CHANGES ASSOCIATED WITH PTSD
Several studies on PTSD patients with traumata resulting
from combat, prolonged childhood abuse, rape, and traffic accidents have been
conducted to analyze structural changes
associated with PTSD. A
meta-analysis of 14 studies of adult patients that met DSM criteria for PTSD,
that had a minimum patience sample size of N=10, that included a well-
matched control group was performed
by Smith (2005). The studies were highly variable
with respect to participant age,
gender distribution, type and duration of trauma, severity
of symptoms, duration of disorder,
constitution of control groups, imaging parameters,
and volumetric measurement methods.
Nonetheless, tests of heterogeneity were only
marginally significant suggesting
that most of the differences between individual studies
in observed effect sizes were
within the range of what might be expected from noise. On
average (weighted by sample size),
patients with PTSD had 12% smaller hippocampal
volumes. These volume differences
are similar in magnitude to those that have been reported in meta-analyses of
patients suffering from depression. While the animal studies as
well as the building-block effect
in humans mentioned above (Neuner et al., 2004a)
suggest that the hippocampal atrophy might occur in
response to exposure to exceptionally
stressful events, Gilbertson et al.
(2002) argued that they rather reflect pre-existing differences that predispose
an individual to development of PTSD under traumatic circumstances. To this
end, Gilbertson et al. (2002) studied pairs of identical twins in which one
member of each pair experienced
combat in
PTSD. Furthermore, more severe PTSD
was associated with an even smaller hippocampus. However, the crucial finding
was that the stay-at-home siblings of PTSD combat-
veterans also had smaller hippocampi and the hippocampal
volume of the stay-at-home
siblings was even equally
predictive of the severity of the combat sibling’s PTSD. Given
that each stressful experience
increases the vulnerability to develop PTSD (Neuner
et al.,
2004a) and given that siblings share a history of traumatic
stressors it is likely that the
resulting vulnerability is somehow
reflected in the hippocampal size. Therefore, the
results of Gilbertson may not contradict the assumption that traumatic stress
affects the
morphology of the brain and that of
medial temporal lobe in particular. No knowledge
exists as to whether hippocampal damage in PTSD is reversible through therapy,
as studies conducted so were not controlled for temporal dynamics.
BMC – 16– Elbert et al.
Based on the findings in rodents, one might expect
structural changes in the
amygdala
of severely traumatized persons. However, no differences in amygdala
size or
volume between patients with PTSD
and subjects without PTSD have been found (e.g.,
de Bellis
et al., 2002).
The human ACC is implicated in evaluating the emotional
significance of stimuli,
in attentional
function, and in detecting errors of performance (Cardinal, Parkinson, Hall,
& Everitt,
2002). More recently it has been suggested that the ACC “disambiguates”
similar conditioned stimuli
depending on their association with reinforcement to prevent
generalization between conditioned
stimuli, i.e. the ACC appears to discriminate similar
stimuli (stimuli that share common
elements) on the basis of their differential association
with reinforcement. Some evidence
for structural alterations in the ACC of traumatized
patients exists. Rauch et al. (2003)
found decreased volumes of the pregenual portion of
the ACC (>25%) in combat nurses
from the Vietnam War with PTSD compared to combat nurses without PTSD. The pregenual ACC, to which the results were specific, is
thought to subserve
affective function while the dorsal ACC is thought to subserve
cognitive motor functions. However, more research on structural (and
functional) alterations
of the ACC in traumatized
individuals with PTSD is necessary.
In sum, structural, functional, and neuroendocrine
changes can be observed in the
brains of survivors of organized
violence that can be linked to the (re)organization of
memory. In threat situations when
flight is impossible, fight futile, and only freezing and
fainting are left as response
options in our evolutionary repertoire, the functioning of
frontal and medial temporal lobe
structures, which form the gateway to autobiographical
memory, is altered: “hot” and
“cold” memories lose their connection. We suggested that
this disconnection of hot and cold
memories, accompanied by an expanding fear network,
explains flashbacks and the
individual’s entrapment in speechless terror and fear. Since
the hot emotional memory is
disconnected from autobiographical cold memory, the victim is unable to relate
the proper autobiographical dates and places of occurrence to the
flashback episodes. If one could
restore this connection, the horror of the memories might
be alleviated. However, the psychic
scar inflicted to the mind cannot be undone, but there
are narrative approaches that can
help to alleviate PTSD symptoms. Reweaving hot
memory contents back into cold
memory networks can bring relief to the injured mind. In
BMC – 17– Elbert et al.
addition, documenting and
acknowledging human rights
of terror and organized violence,
and enables them to tell their stories.
VIOLENCE BREEDS VIOLENCE: CONSEQUENCES OF STRESSEFFECTS ON
BEHAVIOR AND CULTURE
The previous sections summarized evidence, how brain and
mind are affected by experiences of organized violence. A resulting question is
how these changes, induced by
stressful experiences preset the
individual behavior with corresponding consequences for
the society, including the way of
dealing with violence. Therefore, in the second part of
this chapter we will discuss the
relationship between stress-induced changes and behavior
on a societal level, with the
theoretical model of stress effects on brain and mind serving
as background to understand the
cycle of violence.
The saying “violence breeds violence” was coined 40 years
ago by Curtis (1963),
who expressed the concern that
“abused and neglected children would become tomorrow’s murderers and
perpetrators of other crimes of violence”. The validity of this finding
obviously cannot be assessed by
direct experimental manipulations. However, converging
evidence exists that experiencing
violence – which, as we have seen modifies brain and
mind - is related to expressing
violence: For instance, parents who were abused as children are more likely to
abuse their own children. Rates of abuse double for parents who
themselves grew up in violent
environments compared to parents who did not. Prospective and retrospective
studies on children who were abused or neglected disclose a high
incidence of later delinquency.
Children clinically referred to residential treatment with a
history of abuse scored
significantly higher on measures of reactive and verbal aggression
than non-abused control children
(Conner, Doerfler, Volungis,
Steingard, & Melloni,
2003). Finally, a large proportion
of homicide offenders come from unfavorable home
environments and up to 80% of
subjects within delinquent samples report witnessing of
violence in their childhood or
adolescence.
It is important to note that effects are exerted from early
on, i.e., when plasticity for
the brain and mind is greatest.
Developmental studies indicate that abuse and neglect are
related to aggression and later
antisocial behavior in children as young as infants and toddlers. Thus, violent
childhood experiences may leave their mark on brain and mind of the
affected individuals, a
vulnerability that interacts with future stressful experiences. In
BMC – 18– Elbert et al.
deed, childhood experience seem to
be an important factor in this dynamical interaction,
as Van der
Kolk & Fisler (1994)
emphasize: “Abused children often fail to develop the
capacity to express specific and differentiated
emotions: Their difficulty putting feelings
into words interferes with flexible
response strategies and promotes acting out”.
Traumatic stress, whether experienced in adulthood or
earlier, furthers violent behavior. Although the “critical period” of stress
system development suggests that childhood trauma should have more effects on
the brain and behavior than adult trauma, evidence seems insufficient and
studies are scarce until now. Our own studies with children
in Ugandan refugee camps and
survivors of the Rwandan genocide (Schaal &
Elbert,
2005) are designed to provide further evidence.
Many studies addressing consequences of traumatic
experiences in war veterans
found increased impulsive
aggression towards intimate partners (Byrne & Riggs, 1996)
and unknown persons (e.g., Begic & Jokic-Begic, 2001).
Similarly, high rates of traumatic experiences were found in a sample of
juvenile delinquents (Abram et al., 1994).
Over 90% of the sample (N = 898) had experienced one or more
traumatic events; the
most prominent event was witnessing
violence. Approximately 11% of the sample even
met criteria for PTSD in the past
year. Thus, traumatic events seem to play an important
role in individuals with violent or
antisocial behavior. Similar results come from two
studies of our group on forensic
psychiatric patients (Saleptsi et al., 2004; Garieballa et
al., submitted), which found higher than normal rates of
PTSD among those patients.
Similarly, Timmerman & Emmelkamp
(2001) found sexual and emotional abuse to be
significantly more prevalent among
forensic patients than among prisoners. Using structural equation modelling, Orcutt, King, and King
(2003) examined the impact of early-
life stressors, war-zone stressors,
and PTSD symptom severity on partner's reports of recent male-perpetrated
intimate partner violence among 376
symptom severity with intimate
partner violence. In addition, indirect effects (i.e., via
PTSD) of stressful early life experiences, childhood
antisocial behavior, and traumatic
war-zone experiences were found on
intimate partner violence. Thus, experiencing PTSD
symptoms as a result of previous
trauma appears to increase an individual’s risk for perpetrating intimate
partner violence.
BMC – 19– Elbert et al.
Another example of the relation between stressful life
experiences and subsequent
violent behavior becomes obvious in
the results of a study by Freeman,
comparison groups of patients with
schizophrenia or substance abuse, and they reported
significantly higher levels of
potentially dangerous firearm-related behaviors. Thus, experiencing violence
that leads to trauma and PTSD lowers the threshold to exert violence.
PTSD may increase the vulnerability for violence and
impulsive aggression, in particular
when confronted with stress.
However, it seems important to note that violent outbursts
increase, but not organized
violence.
THE CULTURE OF ORGANIZED VIOLENCE – A BREEDING GROUND
FOR TRAUMA-SPECTRUM DISORDERS
Beyond trauma-related factors, cultural factors, i.e.
society’s attitude to violence, plays a
role in the prevalence and spread
of violence. DeFronzo & Prochnow
(2004) analyzed the
rate of serial homicide across 50
States within the
local culture, with higher rates of
violence being found in states supporting game hunting,
military training, and a local
culture supporting punitive violence.
Organized violence comprises war, torture, and other severe
human rights
can be distinguished (see Neuner, 2003). The first type is the permanent
state-sponsored
persecution that is present in all
dictatorships, and even in some countries that are considered democracies. This
harassment includes different forms of violence like torture, extralegal
executions, disappearances etc. The second type is the massive violence
committed against people in an interstate or civil war. The third type of
organized violence is
characterized by violence committed
by terror organizations. All three types aim to systematically augment anxiety
and depression in the population and to mentally destroy at
least some part of the population
by inducing trauma-spectrum disorders.
“New wars” (Kaldor, 1999) involve
conditions of particular traumatization of large
groups of people. The public view
of wars is dominated by knowledge about the 20th
century’s World Wars. However,
currently wars fought between two or more fighting
countries are the exception rather
than the rule. In 2001, more than nine out of ten wars
BMC – 20– Elbert et al.
(91%) were intra-state conflicts or civil wars (Schreiber,
2002). Although foreign armies
may participate in the fighting,
these wars do not originate from conflicts between nations
but arise within a country. There
are two different reasons for civil wars: Currently, in
about half of the intra-state conflicts,
a rebel army fights for the autonomy or secession of
a region. In the other half of the
wars, rebels aim to overthrow the ruling regime. Kaldor
(1999) introduced the term “New War” to describe these
currently dominant ways of warfare, with prominent characteristics such as (Neuner, 2003):
• Irregular forces: fighting is dominated by irregular
forces, including paramilitary
units, rebel forces, mercenary
troops, and foreign armies that intervene in civil wars
on one side. The majority of
fighters on all sides of the conflicts have limited military training. Since
many characteristics of regular armies, like uniforms and regular salaries, are
not applicable to the majority of fighters, the clear separation between
civilians and soldiers disappears. Forcibly recruited child soldiers belong to
the usual repertoire of most forces
in the new wars (Schreiber, 2002). Parties to the
conflict are frequently led by
powerful warlords who do not depend on governments. Since war offers them the
opportunity to maintain power without oversight
by regulating institutions, they
have no immediate interest in a termination of war.
Consequently, many wars are extended by deliberately
delaying peace negotiations
and an unwillingness of both war
parties to fight decisive battles against each other.
• Justification by identities: conflicts are justified based
on the parties’ affiliation to
different ethnic groups, cultures,
or religions. Myths about ancient rivalries and
wars between the ethnic groups are
used to motivate the public for the war.
• Civilian targets: Since the best way to gain power in new
wars is by controlling and
frightening the civilian population
and by displacing civilians, new warfare strategies include systematic
atrocities like massacres and mass rapes to frighten civilians
and to make regions uninhabitable
for the group to be expelled. Another reason for
the prevalence of atrocities in
current wars is the assumption that they help to unite
the group committing the
atrocities. Once a person has participated in committing
war crimes, it is almost impossible
to leave the group since the perpetrator will always be rejected by others.
Easily available small weapons are sufficient for this
type of warfare.
BMC – 21– Elbert et al.
• Economic factors: In a global economy, the war parties are
usually not self-
sufficient but get resources from
supporting foreign countries and exile communities. Very often, the conflicts
are fought to win or keep control over local resources
like diamonds, minerals, oil, and
drugs.
In the New Wars, more than 80% of casualties are civilians.
The consequences of violence and the resulting traumatic stress severely impact
the daily lives of millions of war-
affected people and of millions of
people that are on the run because of fear and anxiety
induced. As outlined in the next
section, the result is a high rate of trauma-spectrum disorders in these
populations (e.g. Neuner et al., 2004a; Karunakara et al., 2004; Schaal
&
Elbert, 2005) and many people are affected by trauma in a
sub-clinical fashion. Will these
victims fight back?
THE CYCLE OF ORGANISED VIOLENCE
The prevalence of PTSD in populations living in war regions
varies with the type and
number of traumatic events
experienced. In some cases, prevalence rates of more than
50% can be found, i.e., more than half of the community
suffers from this disabling condition, which impairs normal family life and
renders the person unable to earn a living.
This assumption is supported by one of our large scale
projects (Karunakara et al., 2004)
which screened 3231 refugees in
northern
earlier, this demographic survey
revealed a surprisingly high prevalence of chronic mental illness. In one
settlement with a count of approximately 12,000 refugees, 70% had experienced
war, 78% had been threatened with a weapon, 61% had been assaulted, and
49% had been abused or tortured. The prevalence of disabling
chronic mental illness in
six camps ranged from 20% up to
56%. In one camp, more than half of the population
was unable to function due to
persistent mental health problems. These and other epidemiological findings
demonstrate that communities at large are affected and not just a few
individuals.
How can we model this co-constructivism of individual and
societal cycle of stress
and violence? Beyond the fact that
traumata and resulting trauma spectrum disorders are
a consequence of violence,
traumatic experiences can also cause domestic violence as
well as violent wars and conflicts,
a circumstance that receives more and more considera
BMC – 22– Elbert et al.
tion at a
political level. Organizations providing psychosocial interventions in war-
affected societies justify their
interventions not only as a means of improving mental
health care for individuals, but
also by referring to sociopolitical factors. A common
statement is that the treatment of
“traumatized societies” is necessary to break the “cycle
of trauma” (UNICEF, 2001). This
reasoning is based on the assumption that traumatized
individuals are more likely to
become perpetrators themselves. Through treatment one
aims not only to reduce PTSD
symptoms but also to foster reconciliation and forgiveness.
It remains to be empirically proven, whether this is the
case. While some investigations
indicate that traumatized
individuals are more likely to become perpetrators themselves
(e.g., intimate partner violence, delinquent behavior) there
is not enough evidence that
confirms a “cycle of violence”. The
model of stress effects on the brain’s structure and
function with concomitant
alterations of the mind, i.e., in memory, affect regulation, fear
network and PTSD symptoms offers a
platform to create and investigate hypotheses of
the cycle of violence.
OUTLOOK
Societal conflicts and civil war-affected communities
provide a background for the study
of the interaction of brain, mind,
and culture. This interaction should be of utmost interest
to scientific investigation, public
health, and politics. Knowledge of the brain’s ability to
adapt and reorganize also helps to
understand the enduring effects of social stress and
trauma on brain systems involved in
the regulation of affect and memory. Another challenge for future research is
to apply this knowledge of stress/trauma-induced brain plasticity to the level
of the society. Developing countries provide the most dramatic examples of
“societal trauma”. While globalization contains a great deal of developmental
chances for developing countries,
sub-Saharan
political infrastructure and has
thus been unable to participate in the opportunities offered
by globalization, in spite of its
wealth of natural resources.
Solely in Sub-Saharan Africa more than 10 countries are
currently affected by civil
wars. Many of these conflicts have
lasted for decades. With few exceptions, most African
countries have a recent history of
armed conflicts and currently suffer from the consequences, in particular from
the appalling degree of violence. The effects of these conflicts
BMC – 23– Elbert et al.
on politics, society, economy, and
(mental) health last for decades and have been termed
“development in reverse”.
Currently, psychosocial services in conflict and
post-conflict settings offer no feasible guidelines on how to treat mental
disturbances caused by traumatic experiences. Very
little is known about the
usefulness of psychiatric concepts and therapeutic approaches
for survivors of severe violence who above all still live in
stressful and potentially dangerous conditions such as refugee settlements.
Furthermore, it is unpredictable how long-
term development will be influenced
by the common mental health problems in the aftermath of trauma, particularly
if one considers the lack of access to high-quality treatment.
It has been argued that violence, conflict, and
demoralization in these communities
feed further violence, reinforcing
a downward spiral. As pointed out there is some evidence that in particular
early traumatic experiences may foster interfamilial and intimate
partner violence. However, there is
no sufficient evidence to suggest that traumatic experiences promote organized
violence on an individual or societal level. We are only beginning to
understand the consequences of violence on the individual’s brain, mind, and
behavior and how this impacts society. Perhaps some day we will also comprehend
the
roots of violence and how they can
be counteracted – a great endeavor. As long as the
underlying mechanisms of organized
violence are not properly understood, we will have
to focus on improving the
therapeutic approaches for helping the victims.
BMC – 24– Elbert et al.
Figure Captions
Figure 1. Example of a traumatic
memory structure: the hot (non-declarative) memory builds a fear network (upper
part). With each additional traumatic experience this fear network gets more
and more extended, while the connections to the specific cold autobiographic
events (lower part) weaken
further or even get lost
(“fragmentation” of declarative and non-declarative
memory).
Figure 2. Event-related magnetic
fields were recorded from 13 torture victims with a
current diagnosis of PTSD and a
group of 13 controls, matched for age,
gender as well as ethnic
background. Aversive and neutral IAPS pictures
(2x100 per affective condition) were presented for 333ms
each in an alternating fashion without ISI (upper row). The global activation
in the time
interval from 0 to 300ms post
stimulus onset is presented in the inset in the
lower right. Grey lines represent
PTSD patients, black lines controls. Responses to aversive stimuli are marked
by solid lines (upper curve of the
black and grey lines respectively),
responses to neutral ones by dashed
lines (lower curve of the black and
grey line respectively). Inverse source
analyses (L2-Minimum-Norm) were
performed, and group differences
were tested for an early 60-110ms
interval based on Statistical Parametric
Mapping (SPM). Sources were
localized bilaterally in occipital and occipito-parietal
areas with a right hemispheric dominance. Frontal difference activations were
distinctly stronger in PTSD patients in both hemispheres (with right hemisphere
dominance) as illustrated in the bottom row
(data from Junghöfer
et al., 2003).
Figure 3. An example of abnormal
neural generators in a PTSD patient scoring high
in dissociative
symptoms: white voxels depict deviations of more than
2
standard deviations (SD) from the
norm (healthy controls). Dark grey indicates activity below normal. The patient
displays a high density of focally
generated slow waves in the left
frontal region and the region of the ante
BMC – 25– Elbert et al.
rior cingulate. During the recording session, the patient was
fully awake
and had less than average global
power in the delta band (Schauer et al,
2005b).
Figure 4. Mean regional
distribution of abnormal slow waves for a group of 22
PTSD patients (left) and 15 depressive patients (right)
relative to 25 normal controls. The top row offers a front view, the bottom row
the perspective from above. Voxels with significant
differences to control groups are
marked with white to indicate higher
abnormal activity relative to controls,
dark shades indicate hypoactive
areas. Displayed are mean z-values (data
from Rockstroh
et al., 2005).
BMC – 26– Elbert et al.
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