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In the following text we will examine the potential mechanisms underlying the well- documented, complex relationships between maltreatment in childhood and the subsequent development of psychopathology. Thousands of studies over the last fifty years have described various aspects of these relationships. Maltreatment in childhood increases risk for virtually every DSM-IV disorder, from autistic-spectrum disorders to schizophrenia to ADHD to major depression to substance abuse disorders. The mechanisms underlying this maltreatment related increase in risk of neuropsychiatric problems are undetermined. The key question addressed in this chapter is “How can abuse lead to psychopathology?” The perspective of the present chapter is neurodevelopmental. This “lens” provides significant insight about the sometimes confusing interrelationships between psychopathology, DSM-IV “diagnoses” and developmental trauma or neglect. A neurodevelopmental perspective is meant to compliment other theoretical and experimental views and can provide useful clues to the mechanisms underlying the origins of neuropsychiatric problems.
The primary premise of a neurodevelopmental perspective is that the human brain is the organ mediating all emotional, social, cognitive and behavioral functioning. Neuropsychiatric disorders and psychopathology, therefore, must involve altered functioning of systems in the brain. The specific nature of dysfunction (e.g., anxiety vs inattention vs affect regulation vs thought disorder) will be determined by which neural networks and brain areas are altered. The present chapter provides an overview of key neurodevelopmental processes and important neural networks which are impacted by abuse and suggests mechanisms which may underlie neuropsychiatric problems related to developmental maltreatment. The major conclusion of this chapter is that we can make plausible conclusions regarding the effects of abuse if we understand how these experiences impact the developing brain. Simply stated childhood trauma will result in alterations in the systems in the brain which mediate the stress response and neglect will result in dysfunctions in the neural systems which do not receive appropriately timed, patterned repetitive stimulation.
Two major forms of maltreatment will reviewed in the present chapter: neglect and trauma. Though often co-occurring, these two types of maltreatment are distinctly different in the impact they have on the developing brain, and, therefore, will have differing impact on the development of psychopathology. Neglect, defined from a neurobiological perspective, is the absence of an experience or pattern of experiences required to express an underlying genetic potential in a key developing neural system. Trauma, from a neurobiological perspective, is an experience or pattern of experiences which activate the stress response systems in such an extreme or prolonged fashion as to cause alterations in the regulation and functioning of these systems. Both neglect- and trauma-related abnormalities in neurodevelopment would be predicted to cause significant psychopathology.
Abuse can have a negative impact on development in several ways. Maltreatment may be the primary mediator of psychopathology when these abnormal experiences directly alter developing neural systems; for example, trauma may cause post-traumatic stress disorder or neglect an attachment disorder. In addition, trauma or neglect may play an exacerbating or expressing role for neuropsychiatric syndromes in individuals with genetic vulnerabilities (e.g., major depression and schizophrenia). And finally, symptoms and problems caused by maltreatment can be disrupting factors for subsequent developmental opportunities (e.g., the disrupting impact of hypervigilance on academic experiences or of neglect-related attachment problems on social development). Often these secondary and tertiary effects are as devastating as the primary abuse-related pathology. By Bruce Perry
 
The Neurodevelopmental Impact of Neglect
Deprivation during the sensitive period of a given neural system will result in insufficient patterned, repetitive activity to stimulate adequate organization. The deprived developing neural network will have altered neural microarchitecture which may include cell migration, synaptogenesis, dendritic sprouting. The result is a neural system less functionally capable. This deprivation – neglect – can take multiple forms. In some rare cases, a single domain of functioning is primarily impacted. Our clinical group has worked with several children raised with cognitive stimulation, physical and emotional warmth but physically restrained for multiple years and, therefore, unable to sit, stand or walk. Most neglect takes the form of chaotic, mis-timed, inconsistent experience related to the isolation, personal chaos, incompetence, ignorance, domestic violence, substance abuse or psychopathology of the primary caregiver. This can manifest as delays in motor, self- regulatory, affective and cognitive functioning. A common manifestation of this form of neglect is in speech and language acquisition; if the infant or toddler hears few words, the developing speech and language systems will be impacted (Huttenlocher et al., 2002); the result is impaired speech and language.
The earlier and more pervasive the neglect is, the more devastating the developmental problems for the child. Indeed, a chaotic, inattentive and ignorant caregiver can produce pervasive developmental delay (PDD; DSM IV-R) in a young child (Rutter, Andersen-Wood, Beckett, et al. 1999). Yet the very same inattention for the same duration if the child is ten will have very different and less severe impact than inattention during the first years of life. Studies of the neurodevelopmental impact of neglect are not as common as those on the effects of trauma. Both animal studies, descriptive reports with severely neglected children and some recent studies with adopted children following neglect which document some aspects of the neurodevelopmental impact of neglect.
Animal Studies: Hubel and Weisel’s landmark studies on development of the visual system using sensory deprivation techniques helped define the concepts of critical and sensitive period (Hubel & Wiesel. 1963). In hundreds of other studies, extremes of sensory deprivation (Hubel & Wiesel. 1970; Greenough, Volkmar, & Juraska. 1973) or sensory enrichment (Greenough & Volkmar. 1973; Diamond, Krech, & Rosenzweig. 1964; Diamond, Law, Rhodes, et al. 1966) have been studied. These include disruptions of visual stimuli (Coleman & Riesen. 1968), environmental enrichment (Altman & Das. 1964; Cummins & Livesey. 1979), touch (Ebinger. 1974; Rutledge, Wright, & Duncan. 1974), and other factors that alter the typical experiences of development (Uno, Tarara, Else, & et.al. 1989; Plotsky & Meaney. 1993; Meaney, Aitken, van Berkal, Bhatnagar, & Sapolsky. 1988).
These findings generally demonstrate that the brains of animals reared in enriched environments are larger, more complex and functional more flexible than those raised under deprivation conditions. Relationships between experience and brain cytoarchitecture have demonstrated a relationship between density of dendritic branching and the complexity of an environment (Diamond & Hopson. 1998). Rats raised in environmentally enriched environments have higher density of various neuronal and glial microstructures, including a 30% higher synaptic density in cortex compared to rats raised in an environmentally deprived setting (Bennett, Diamond, Krech, & Rosenzweig. 1964; Altman & Das. 1964). Animals raised in the wild have from 15 to 30% larger brain mass than their offspring who are domestically reared (Darwin. 1868; Rohrs. 1955; Rohrs & Ebinger. 1978; Rehkamper, Haase, & Frahm. 1988).
Animal studies suggest that critical periods exist during which specific sensory experience was required for optimal organization and development of the part of the brain mediating a specific function (e.g., visual input during the development of the visual cortex). While these phenomena have been examined in great detail for the primary sensory modalities in animals, few studies have examined the issues of critical or sensitive periods in humans. What evidence there is would suggest that humans tend to have longer periods of sensitivity and that the concept of critical period may not be useful in humans (Perry, 2006). Yet altered emotional, behavioral, cognitive, social and physical functioning has been demonstrated in humans following specific types of neglect. For obvious ethical reasons, most of these findings come from descriptive clinical rather than experimental studies.
Neglect in Early Childhood: The majority of clinical reports on neglect have focused on institutionalized children or feral children. As early as 1833, with the famous Kaspar Hauser, feral children had been described (Heidenreich. 1834). Hauser was abandoned as a young child and raised from early childhood (likely around age two) until seventeen in a dungeon, experiencing relative sensory, emotional and cognitive neglect. His emotional, behavioral and cognitive functioning was, as one might expect, very primitive and delayed.
In the early forties, Spitz described the impact of neglectful caregiving on children in foundling homes (orphanages). Most significant, he was able to demonstrate that children raised in fostered placements with more attentive and nurturing caregiving had superior physical, emotional and cognitive outcomes (Spitz. 1945; Spitz. 1946). Dennis (1973) described a series of findings from children raised in a Lebanese orphanage. These children were raised in an institutional environment devoid of individual attention, cognitive stimulation, emotional affection or other enrichment. Prior to 1956 all of these children remained at the orphanage until age six, at which time they were transferred to another institution. Evaluation of these children at age 16 demonstrated a mean IQ of approximately 50. When adoption became common, children adopted prior to age 2 had a mean IQ of 100 by adolescence while children adopted between ages 2 and 6 had IQ values of approximately 80 (Dennis. 1973). This graded recovery is consistent with the known principles of neurodevelopment described above; the older a child was at time of adoption, (i.e., the longer the child spent in the neglectful environment) the more pervasive and resistant to recovery were the deficits.
Money and Annecillo (1976) reported the impact of change in placement on children with psychosocial dwarfism (failure to thrive). In this preliminary study, 12 of 16 children removed from neglectful homes recorded remarkable increases in IQ and other aspects of emotional and behavioral functioning. Furthermore, they reported that the longer the child was out of the abusive home the higher the increase in IQ. In some cases IQ increased by 55 points. A more recent report on a group of 111 Romanian orphans (Rutter & English and Romanian Adoptees study team. 1998; Rutter, Andersen-Wood, Beckett, et al. 1999) adopted prior to age two from very emotionally and physically depriving institutional settings demonstrate similar findings. Approximately one half of the children were adopted prior to age six months and the other half between six months and 2 years old. At the time of adoption, these children had significant delays. Four years after being placed in stable and enriching environments, these children were re-evaluated. While both groups improved, the group adopted at a younger age had a significantly greater improvement in all domains. As a group, these children were at much greater risk for meeting diagnostic criterion for autism- spectrum disorder, a finding that sheds light on the evolving relationships between early life trauma, neglect and subsequent development of severe neuropsychiatric problems including psychotic disorders and schizophrenia (Read et al., 2001).
These observations are consistent with the clinical experiences of the ChildTrauma Academy working with maltreated children for the last fifteen years. During this time we have worked with more than 1000 seriously children. We have recorded increases in IQ of over 40 points in more than 60 children following removal from neglectful environments and placed in consistent, predictable, nurturing, safe and enriching placements (Perry, 2005). In a group of 200 children under the age of 6 at time of removal, significant developmental delays were seen in more than 85% of the children. The severity of these developmental problems increased with age, suggesting, again, that the longer the child was in the neglectful environment – the earlier and more pervasive the neglect – the more indelible and pervasive the deficits.
 
Neurobiological Findings
All of these reported developmental problems – language, fine and large motor delays, impulsivity, disorganized attachment, dysphoria, attention and hyperactivity, and a host of others described in these neglected children – are caused by abnormalities in the brain. Despite this obvious statement, very few studies have examined directly any aspect of neurobiology in neglected children. One early clue in humans On autopsy, the brain of Kasper Hauser (see above) was notable for small cortical size and few, non-distinct cortical gyri – all consistent with cortical atrophy (Simon, 1978).
Our group has examined various aspects of neurodevelopment in neglected children ((Perry & Pollard. 1997; Perry, 2005). Globally neglected children had smaller the frontal- occipital circumference, a measure of head size and in young children a reasonable measure of brain size. Neuroimaging demonstrated that 64.7 % of the brain scans were abnormal in the children with global neglect and 12 % in children following chaotic neglect. The majority of the findings were “enlarged ventricles” or “cortical atrophy” (Figure 2). Once removed from the neglectful settings, recovery of function and relative brain-size were observed. The degree of recovery over a year period however was inversely proportional to age in which the child was removed from the neglecting caregivers. The earlier in life and the less time in the sensory-depriving environment, the more robust the recovery (Perry, 2005).
In the study of Romanian orphans described above, the 38 % had FOC values below the third percentile (greater than 2 SD from the norm) at the time of adoption. In the group adopted after six months, fewer than 3 % and the group adopted after six months 13 % had persistently low FOCs four years later (Rutter & English and Romanian Adoptees study team. 1998; O’Connor, Rutter, & English and Romanian Adoptees study team. 2000). Strathearn (2001) has followed extremely low birth weight infants and shown that when these infants end up in neglectful homes they have a significantly smaller head circumference at 2 and 4 years, but not at birth. This is despite having no significant difference in other growth parameters.
Studies from other groups report similar altered neurodevelopment in neglected children. Teicher has reported altered corpus callosum development in neglected children (Teicher et al., 2004). Altered brain-related measures (e.g., salivary cortisol) have been demonstrated in children adopted following neglect (Gunnar et al., 2001). Chugani and colleagues have demonstrated decreased metabolic activity in the orbital frontal gyrus, the infralimbic prefrontal cortex, the amygdale and head of the hippocampus, the lateral temporal cortex and in the brainstem in a group of Romanian orphans (Chugani, et al., 2001).
 
Neurodevelopmental Impact of Trauma
The brain’s stress mediating systems are widely distributed; involve brain and the autonomic nervous system as well as neuroendocrine and neuroimmune responses. Clearly stress-related neural networks permeate the entire brain. The capacity, then, of a use- dependent alteration in the organization and functioning of neural systems involved in dozens of functions could easily take place with prolonged activation. The specific nature of which of these myriad systems becomes altered depends upon the specific nature of the threat response in any given circumstance.
The human brain is continually sensing, processing, storing, perceiving and acting in response to information from the external and internal environments. This continuous monitoring is process is especially sensitive to input that may indicate threat. These “worlds” – external as ‘sensed’ by our five senses and internal as ‘sensed’ by a set of specialized neurons throughout the body (e.g., glucose or sodium sensitive neurons) – are always changing. Our physiology and neurophysiology are characterized by a continuous process of modulation, regulation, compensation, activation – all designed to keep our body’s systems in some state of equilibrium or homeostasis. Whenever the incoming information from either inside or outside the body alter this homeostasis (Perry and Pollard, ) or indicate similarity to a pattern of activity previously associated with a threat (Perry, ), the brain initiates compensatory, adaptive responses to re-establish homeostasis or to take the necessary actions to survive.
 

Sequential Processing of Threat Related Neural Activity
This process begins when our senses transform forms of energy (e.g., light, sound, pressure) into patterned activity of sensory neurons. The first ‘stops’ for sensory input from the outside environment (e.g., light, sound, taste, touch, smell) and from inside the body (e.g., glucose levels, temperature) are the lower, ‘regulatory’ areas of the brain (see later). These neural patterns of activity created by sensory input first come into the brain separately – visual input comes into one nuclei, auditory another, olfactory another and so on. The “first stops” for primary sensory input are in lower parts of the brain that are incapable of conscious perception.
 
Brainstem and Diencephalon
Neural input from our senses directly connects to the lower areas of the CNS in the brainstem, diencephalon and hypothalamus. For example, our internal organs directly relay information to the amygdala and locus coeruleus directly or through the nucleus paragigantocellularis and nucleus tractus solitaries (Elam et al., 1986; Nauta and Whitlock, 1956; Saper, 1982). Other primary sensory input from visual, auditory, tactile and olfactory systems directly connect into these lower brain nuclei where the process of sorting, integrating, interpreting, storing (if appropriate) and responding to these incoming signals begins. These brainstem and diencehpalic nuclei project to the thalamus which begins the process of integrating this information, relaying sensory information to the primary sensory receptive areas of the cortex. These primary sensory regions project to adjacent cortical association areas. A feedback process involves projections from key cortical areas back to the lower parts of the brain; visual, auditory and somatosensory cortical association areas send projections to the hippocampus, amygadala, orbitofronatal cotex, entorhinal cortex, and cingulate gyrus and other brain structures. This reciprocal processing allows the brain to sort, process and “act” on the threat related signals from the body and the external world.
The Reticular Activating System: Key to this entire process is the role of an array of important neurotransmitter networks; the monoamine systems; epinephrine, norepinephrine, dopamine and serotonin – have key nuclei (clusters of cell bodies) which send direct axonal projections to virtually all other areas of the brain and lower to influence the autonomic neurons which leave the brain and directly influence heart, lung, gut, skin and the rest of the organs of the body. Collectively this network has been referred to as the reticular activating system. The reticular activating system (RAS) is a network of ascending, arousal-related neural systems in the brain that consists of locus ceruleus noradrenergic neurons, dorsal raphe serotonergic neurons, cholinergic neurons from the lateral dorsal tegmentum, and mesolimbic and mesocortical dopaminergic neurons, among others. Much of the original research on arousal, fear, and response to stress and threat was conducted using various lesion models of the reticular activating system (Moore and Bloom, 1979). The reticular activating system appears to be an integrated neurophysiological system involved in arousal, anxiety, and modulation of limbic and cortical processing (Munk et al., 1996). Working together, the brain-stem monoamine systems in the reticular activating system provide the flexible and diverse functions necessary to modulate stress, distress and trauma. A key component of the RAS is the locus coeruleus.
The Locus Coeruleus: The locus coeruleus is involved in initiating, maintaining, and mobilizing the total body response to threat (Aston-Jones et al., 1986). A bilateral grouping of norepinephrine-containing neurons originating in the pons, the locus coeruleus sends diverse axonal projections to virtually all major brain regions and thus functions as a general regulator of noradrenergic tone and activity(Foote et al., 1983). The locus coeruleus plays a major role in determining the “valence,” or value, of incoming sensory information; in response to novel or potentially threatening information, it increases its activity (Abercrombie and Jacobs, 1987a; Abercrombie and Jacobs, 1987b). The ventral tegmental nucleus also plays a part in regulating the sympathetic nuclei in the pons/medulla(Moore and Bloom, 1979). Acute stress results in an increase in locus coeruleus and ventral tegmental nucleus activity and the release of catecholamines throughout the brain and the rest of the body. These brain-stem catecholamine systems (locus coeruleus and ventral tegmental nucleus) play a critical role in regulating arousal, vigilance, affect, behavioral irritability, locomotion, attention, and sleep, as well as the startle response and the response to stress (Levine et al., 1990; Morilak et al., 1987a; Morilak et al., 1987b; Morilak et al., 1987c).
Hypothalamus and Thalamus: Sensory thalamic areas receive input from various afferent sensory systems, and at this level, “feeling” begins. Although thalamic nuclei are important in the stress response, these regions have been studied primarily as “waystations” that transmit important arousal information from the reticular activating system neurons (e.g., locus coeruleus noradrenergic neurons) to key limbic, subcortical, and cortical areas involved in sensory integration and perception of threat-related information (Castro-Alamancos and Connors, 1996). The neuroendocrinological—and likely neuroimmunological—afferent and efferent wings of the threat response are mediated by hypothalamic and other anatomically related nuclei. Studies have demonstrated important roles for various hypothalamic nuclei and hypothalamic neuropeptides in the stress response in animals (Bartanusz et al., 1993; Miaskowski et al., 1988) (Rosenbaum et al., 1988), and humans (Young and Lightman, 1992).
The Limbic System: The central role of the subcortical network of brain structures in emotion was hypothesized by Papez (Papez, 1937)and elaborated by MacLean who coined the term limbic system. This sub-cortical network is responsible for a range of emotion- and relational-related functions. Among the key subcomponents of the limbic system are two brain areas known to be intimately involved in the stress response: the amygdala and hippocampus.
Amygdala: The amygdala has emerged as the key brain region responsible for the processing, interpretation, and integration of emotional functioning(Clugnet and LeDoux, 1990). Just as the locus coeruleus plays the central role in orchestrating arousal, the amygdala plays the central role in the brain in processing afferent and efferent connections related to emotional functioning (LeDoux et al., 1988; Pavlides et al., 1993b; Phillips and LeDoux, 1992b). The amygdala receives input directly from the sensory thalamus, the hippocampus (via multiple projections), the entorhinal cortex, and the sensory association and polymodal sensory association areas of the cortex as well as from various brain-stem arousal systems via the reticular activating system(Selden et al., 1991). The amygdala processes and determines the emotional valence of simple sensory input, complex multisensory perceptions, and complex cognitive abstractions, even responding specifically to complex socially relevant stimuli. In turn, the amygdala orchestrates the organism’s response to this emotional information by sending projections to brain areas involved in motor (behavioral), autonomic nervous system, and neuroendocrine areas of the CNS (Davis, 1992a; Davis, 1992b; LeDoux et al., 1988). In a series of landmark studies, LeDoux and colleagues demonstrated the key role of the amygdala in “emotional” memory (LeDoux et al., 1990). Animals, including humans, store emotional as well as cognitive information, and the storage of emotional information is critically important in both normal and abnormal regulation of anxiety. The “site” at which anxiety is perceived is the amygdala (Davis, 1992a). It is in these limbic areas that the patterns of neuronal activity associated with threat-and mediated by the monoamine neurotransmitter systems of the reticular activating system—become an “fear.”
Hippocampus: This brain area is involved in the storage of various kinds of sensory information and is very sensitive to “stress” activation (Pavlides et al., 1993a; Phillips and LeDoux, 1992a; Sapolsky et al., 1984). The hippocampus appears to be critical in the storage and recall of cognitive and emotional memory(Selden et al., 1991).Any emotional state related to arousal or threat may alter hippocampal functioning, changing the efficiency and nature of hippocampal storage and retrieval. Threat alters the ability of the hippocampus and connected cortical areas to “store” certain types of cognitive information (e.g., verbal) but does not affect the storage of other types (e.g., nonverbal).
Hormonal signals affect heterogeneous corticosteroid nuclear receptors, i.e. type 1 (mineralocorticoid) or type 2 (glucocorticoid) in the hypothalamic-pituitary-adrenal (HPA) axis. Stressful life events such as isolation increase HPA axis activity(McEwen, 2001). The hippocampus, amygdala, and mPFC are limbic structures that are targets for and also modulate adrenal steroids. Glucocorticoids can result in neurotoxic damage to the hippocampus with suppression of neurogenesis (McEwen, 2001; Sapolsky, 2000). Exposure to stress results in release of corticotrophin releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol via activation of the HPA axis. During periods of stress there is partial resistance to feedback inhibition of cortisol release and increase in plasma cortisol levels, in addition to a decrease in glucocorticoid receptors(Sapolsky and Plotsky, 1990). Glucocorticoid receptors are present in the brain in high density in areas relevant to stress and anxiety such as the hypothalamus, hippocampus, serotonergic and noradrenergic cell bodies on both neurons and glia. Based on animal studies, mineralocorticoid expression is high in limbic regions such as hippocampus, septum and amygdala(Reul and de Kloet, 1985; Veldhuis and De Kloet, 1982). Animal studies suggest that stress experienced during critical years of development can have long lasting effects on HPA axis. For instance, rats that experience in utero stress or early maternal deprivation have increased corticosterone concentrations when exposed to stress. Early postnatal stress is associated with changes in basal concentrations of hypothalamic CRH, mRNA, hippocampal glucocorticoid receptor mRNA, and median eminence CRH, in addition to the stress-induced CRH, cortocosterone, and ACTH release(Levine et al., 1993a; Levine et al., 1993b; Stanton et al., 1988). Adults with PTSD and non-human primates with early adverse experiences have elevated CRH concentrations and decreased cortisol levels in the cerebrospinal fluid (Coplan et al., 1996). Finally a number of studies are indicating the crucial role of corticotrophin-releasing factor (CRF) and the sensitivity of CRF receptors in mediating stress reactivity in humans (Kehne, 2007).
Cortex: The quality and intensity of any emotional response, including anxiety, are dependent on subjective interpretation or cognitive appraisal of the specific situation eliciting the response (Maunsell, 1995; Singer, 1995). Most theories addressing the etiology of anxiety disorders focus on the process by which stimuli are “mislabeled” as being “threat” related, thereby inducing a fear response and anxiety in situations where no true threat exists. How individuals “cortically interpret” the limbic-mediated activity (i.e., their internal state) associated with arousal plays a major role in their subjective sense of anxiety (Gorman et al., 1989). Klüver-Bucy syndrome, which results from damage to or surgical ablation of the temporal lobes, is characterized by absence of fear in response to current and previously threatening cues (Kluver and Bucy, 1937). The general disinhibition characteristic of this syndrome suggests loss of the capacity to interpret incoming threat-related cues from lower brain areas.
 
Heterogeneity of Adaptive Responses to Threat: Hyperarousal and Dissociation
Individual responses to threat can vary tremendously. This is not surprising considering the vast distribution of neural functions which are available to the stress- response network. This network involves the entire brain, and, indirectly, the whole body. This allows the response to potential threat to be appropriate and proportional to the need. The specific adapative changes taken by the brain to respond to the incoming threat-related signals will vary depending upon many factors; different elements of the widely distributed neural system will be recruited and others will be shut down to conserve energy and focus the body’s response to threat. Under normal circumstances (i.e., a normal stress-response capability), the responses are graded, proportional to the level of percieved threat; when the threat is mild, a moderate activation of key systems takes place; when extreme, intense and prolonged activation will occur. Further, adaptive responses to threat are specific to the nature of the threat; either preparing to flee or fight or preparing to be overwhelmed and injured. In cases of abnormal development or sensitivity of the stress-response systems (see later sections) the responses to potential threat are inappropriate and out of proportion; trauma can make the system over-active and overly reactive.
Two major, inter-related response patterns – hyperarousal and dissociative – have been described (Perry et al., 1995). The hyperarousal response has been well characterized; it was originally described as the fight or flight response (Cannon, 1914). As described above, incoming signals activate the locus coeruleus and through a cascade of neural activation recruiting key limbic and cortical areas to focus on, and respond to, the threat. These neural and neuroendocrine activations prepare the body to fight or flee. Cortisol and adrenaline course through the body; heart rate increases, glycogen is mobilized from muscles; all distracting information is tuned out. However, when fighting or fleeing is not possible, the brain will recruit a different set of neural systems and utilize avoidant, dissociative adaptations. Dissociation is basically a mental mechanism by which one withdraws attention from the outside world and focuses on the inner world. Dissociation may involve a distorted sense of time, a detached feeling that you are “observing” something happen to you as if it is unreal, the sense that you may be watching a movie of your life. In extreme cases, especially if the trauma is repetitive and painful (e.g., sexual abuse), the child may withdraw into an elaborate fantasy world where she may assume special powers or strengths. Like the alarm response, this “defeat” or dissociative response is graded. The intensity of the dissociation varies with the intensity and duration of the traumatic event.
The neurobiology of dissociation is related but somewhat different from that of the hyperarousal response. Both utilize the monoamine systems in the brainstem and diencephalon; but somewhat different elements of these complex networks. In animals, the ‘defeat’ response has a distinct neurobiology which is similar to dissociation response in humans. Indeed, the neurobiology and phenomenology of dissociation appears to most approximate the ‘defeat’ reaction described in animals (Henry, Stephens, and Ely, 1986; Heinsbroek, van Haaren, Feenstra, and Boon, 1991; Miczek et al., 1990). As with the hyperarousal/fight or flight response, dissociation involves brainstem-mediated CNS activation which results in increases in circulating epinephrine and associated stress steroids (Glavin, 1985; Henry, Liu, Nadra, Qian, Mormede, Lemaire, Ely, and Hendley, 1993; Herman, Guillonneau, Dantzer, Scatton, Semerdjian-Rouquier, and Le Moal., 1982). A major CNS difference, however, is that, in dissociation, vagal tone increases dramatically, decreasing blood pressure and heart rate (occasionally resulting in fainting) despite increases in circulating epinephrine. In addition, there appears to be an increased relative importance of dopaminergic systems, primarily mesolimbic and mesocortical (Kalivas, 1985; Kalivas, Richardson-Carlson, and Van Orden, 1986; Kalivas, Duffy, Dilts and Abhold, 1988; Abercrombie, Keefe, DiFrischia, and Zigmond 1989). These dopaminergic systems are intimately involved in the reward systems, affect modulation (e.g., cocaine-induced euphoria) and, in some cases, are co-localized with endogenous opioids mediating pain and other sensory processing. These opioid systems are clearly involved in altering perception of: painful stimuli, sense of time, place and reality. Indeed, most opiate agonists can induce dissociative responses. Of primary importance in mediating the freeze or surrender dissociative response are endogenous opioid systems (Abercrombie and Jacobs, 1988).
For most children and adults, however, the adaptive response to an acute trauma involves a mixture of hyperarousal and dissociation. During the actual trauma, a child will feel threatened and the arousal systems will activate. With increased threat, the child moves along the arousal continuum. At some point along this continuum, the dissociative response is activated. This results in the host of protective mental (e.g., decreases in the perception of anxiety and pain) and physiological responses (decreased heart rate) that characterize the dissociative response. Whatever the adaptive response during a trauma, the key issue for subsequent psychopathology is how long these systems are activated. The longer and more intense the activation during the actual traumatic event (s), the more likely there will be molecular changes in the stress-response systems that lead to long-term functional changes. Trauma can cause alterations that lead to sensitized, dysfunctional neural networks; essentially the state of fear can become the persisting trait of anxiety. What were once adaptive neurobiological states can become, over time, maladaptive traits (Perry et al., 1995)
 
Trauma Alters Stress-Mediating Neural Networks
The clinical impact of traumatic stress on the developing child has been well documented. The simplest are the studies examining the development of obvious trauma- related psychopathology such as post-traumatic stress disorder (for review see; Perry, 1994; 2001b; Glaser, 2000; Teicher et al., 2002; DeBellis and Thomas, 2003; Bremner, 2003). The increased incidence of PTSD following trauma, the list of attenuating and exacerbating has been well documented. Table 1 summarizes the key factors which appear to be related to subsequent development of trauma-specific psychopathology.
Traumatic stress results in altered measures of brain function and in brain-mediated functioning in children. These include measures of hippocampal function, adrenergic receptor functioning, hippocampal and cortical structural development, cardiovascular functioning and emotional, social and behavioral functioning (Perry, 1998; Teicher et al., 1994; 1997; De Bellis et al., 1994; 1997; 1999a; 1999b, 1997; Scaer et al, 2001; Carrion et al., 2001; 2002a). Magnetic resonance imaging (MRI) has revealed reductions in hippocampus (Bremner et al., 1997; Stein et al., 1997; Bremner et al., 2003a), alterations in cerbellar vermis (Anderson, et al., 2002) and altered amygdala (Driessen et al., 2000; Schmahl et al., 2003) volumes as well as deficits in verbal declarative memory measured with neuropsychological testing among women who were sexually abused as children. Sexually abused girls demonstrate neuroendocrine abnormalities as adolescents (Putnam, 1998).
Functioning of monoamine systems in adults is influenced by developmental trauma (Perry, 1995; 2001a; 2001b). Further, developmental trauma appears to influence genetic expression of at least one potential genetic marker for depression. A study of a polymorphism for the promoter region of the serotonin transporter (5-HTT) gene found that childhood maltreatment increased the risk of depression in early adulthood for persons with the common “short” allele compared to persons with the long allele; the short allele is associated with lower transcriptional efficiency of the promoter (Caspi, 2003).
The most overwhelming evidence for the impact of developmental trauma on stress- related neural networks and their functioning comes from a retrospective epidemiological study of 17,000 adults. Over the last ten years the Adverse Childhood Experience (ACE) studies, have been reporting on increased risk of a host of emotional, social, behavioral and physical health problems following abuse and related traumatic experiences in childhood (Anda et al.1991; 2001; Dube et al., 2001a; 2001b; 2002a; 2002b; 2003a; 2003b; . These epidemiological findings converge with evidence from neurobiology about numerous effects of childhood stress on brain and physical systems (Glaser, 2000). These epidemiological studies examined the relationship between adverse childhood experiences including child abuse and a wide range of functioning in adult life. The findings are consistent with the view that developmental trauma impacts the stress-response systems, and, therefore, can have destructive impact on all of the neural systems and functions that are interconnected to this widely distributed network.
Among the ACE findings are a graded increase in risk (i.e., more abuse = more risk) for affective symptoms and panic attacks; for memory problems; for hallucinations; for poor anger control; for perpetrating partner violence; unhealthy sexual behavior (early intercourse, promiscuity, sexual dissatisfaction); suicide; substance abuse; alcohol use and abuse; smoking. In addition there is a significant increased risk for a range of physical health problems following child abuse. Risk for the major causes of death in adult life is increased following adverse childhood experiences (Felitti et al.,1998). Taken together there is little doubt that developmental trauma alters key neural systems involved in mediating the stress response, and, thereby, results in a host of neuropsychiatric and related functional problems.
 
Summary
All of the major molecular processes involved in brain development can be impacted by abuse. With either neglect or trauma, the timing (the earlier in life the more impact), intensity, pattern and duration of the maltreatment can alter virtually every brain system and brain area. The result is that in any given child, the individual history of maltreatment results in a unique pattern of altered neural systems and resulting psychopathology. The result is that development maltreatment is the Great Impostor. Depending up the age, nature and pattern of maltreatment a child may develop symptoms that mimic dozens of traditional DSM-IV diagnoses from autism or ADHD or “learning disorder.” Further, developmental stressors may “express” underlying genetic vulnerabilities; a genetically- vulnerable child may develop a pathological phenotype while a hardier child may not.
This complexity poses a fundamental challenge to any attempts to create simple over-inclusive descriptive categories of psychopathology. Future classification of human psychopathology will need to incorporate a more neurodevelopmentally-informed perspective in order to accurately understand the mechanisms which underlie neuropsychiatric symptoms in a given child or adult. This more mechanism-focused classification would approximate the current model of diagnostic classification in other areas of medicine where there is a more direct connection between the disease process and the pathophysiology. The hope and the promise is that understanding the mechanisms underlying the psychopathology will lead to more effective interventions, and, ultimately, more important, changes in practice, programs and policy that will help prevent the development of abuse-related psychopathology.

 
Treatmnet of Trauma and Neglect
Effective trauma treatment needs to involve (1) learning to tolerate feelings and sensations by increasing the capacity for interoception, (2) learning to modulate arousal, and (3) learning that after confrontation with physical helplessness it is essential to engage in taking effective action. Introception is the process of embodied mindfulness, and in neuroscientific terms it is becoming aware of visceral afferent information (bodily sensations)
Being traumatized is continuing to organize your life as if the trauma was still going on unchanged and every new encounter or event is contaminated by the past. After trauma the world is experienced with a different nervous system, a survivor’s energy now becomes about suppressing inner chaos at the expense of spontaneous involvement in life. These attempts to maintain control of these unbearable physiological reactions can result in a whole a range of physical symptoms such as autoimmune diseases, this is why it is important in trauma treatment to engage the entire organism, body, mind and brain. Deactivation of the left hemisphere of the brain has a direct impact on the capacity to organize experience into logical sequences and to translate our shifting feelings and perceptions into words. Without sequencing we cannot identify cause and effect, grasp the long-term effects of our actions or create coherent plans for the future.

When something reminds traumatized people of the past, their right brain reacts as if the trauma were happening in the present but because their left brain may not be working very well, they may not be aware that they are re-experiencing and reenacting the past, they are just furious, terrified, enraged, shamed or frozen. After the emotional storm passes, they may look for something or somebody to blame for it, for their behaviour, they may say,
“I acted this way because you looked at me like that or because you were late”. This is called being stuck in fight or flight.
In trauma recovery where the left hemisphere is activated through speaking of the traumatic past and making sense of what happened within a safe environment, the left brain can talk the right brain out of reacting by saying that was then and this is now. This can only happen when safety is establish through attunement with a therapist where the amygdala is down regulated, this can often take some time for traumatized people as the amygdala tends to stay in a heightened state of arousal ready for fight or flight even years after then traumatic event or experience. Even the slightest detection of a threat can cause extreme arousal of this system. Minor stimuli will illicit major responses.
This is why it is important to engage the left-brain in trauma recovery, whilst body based interventions are absolutely imperative for trauma recovery, these interventions may be undermined should they exclude left-brain based activities. Body based interventions such as dance; massage and yoga are a fantastic adjunct to psychodynamic psychotherapy. Lazar’s study lends support to the notion that treatment of traumatic stress may need to include becoming mindful: that is, learning to become a careful observer of the ebb and flow of internal experience, and noticing whatever thoughts, feelings, body sensations, and impulses emerge. In order to deal with the past, it is helpful for traumatized people to learn to activate their capacity for introspection and develop a deep curiosity about their internal experience. This is necessary in order to identify their physical sensations and to translate their emotions and sensations into communicable language—understandable, most of all, to themselves.
Traumatized individuals need to learn that it is safe to have feelings and sensations. If they learn to attend to inner experience they will become aware that bodily experience never remains static. Unlike at the moment of a trauma, when everything seems to freeze in time, physical sensations and emotions are in a constant state of flux. They need to learn to tell the difference between a sensation and an emotion (How do you know you are angry/afraid? Where do you feel that in your body? Do you notice any impulses in your body to move in some way right now?). Once they realize that their internal sensations continuously shift and change, particularly if they learn to develop a certain degree of control over their physiological states by breathing, and movement, they will viscerally discover that remembering the past does not inevitably result in overwhelming emotions.
After having been traumatized people often lose the effective use of fight or flight defenses and respond to perceived threat with immobilization. Attention to inner experience can help them to reorient themselves to the present by learning to attend to non-traumatic stimuli. This can open them up to attending to new, non-traumatic experiences and learning from them, rather than reliving the past over and over again, without modification by subsequent information. Once they learn to reorient themselves to the present they can experiment with reactivating their lost capacities to physically defend and protect themselves.
 
Optimal Development
A child is most likely to reach her full potential if she experiences consistent, predictable, enriched, and stimulating interactions in a context of attentive and nurturing relationships. Aided by many relational interactions – perhaps with mother, father, sibling, grandparent, neighbour and more – young children learn to walk, talk, self-regulate, share, and solve problems. Every child will face new and challenging situations. These stress- inducing experiences per se need not be problematic. Moderate, predictable stress, triggering moderate activation of the stress response, helps create a capable and strong stress-response capacity, in other words, resilience. The first day of kindergarten, for example, is stressful for children. Those embedded in a safe and stable home base overcome the stress of this new situation, able to embrace the challenges of learning.
 


Further Reading:
Maltreatment and the Developing child 
Memories of Fear 
Trauma, Neglect and psychopathology 
 
Working with complex trauma, sexual trauma, personality disorders and relational trauma at Trauma Recovery Institute
Trauma Recovery Institute offers unparalleled services and treatment approach through unique individual and group psychotherapy. We specialise in long-term relational trauma recovery, sexual trauma recovery and early childhood trauma recovery. We also offer specialized group psychotherapy for psychotherapists and psychotherapy students, People struggling with addictions and substance abuse, sexual abuse survivors and people looking to function in life at a higher level. Trauma recovery Institute offers a very safe supportive space for deep relational work with highly skilled and experienced psychotherapists accredited with Irish Group Psychotherapy Society (IGPS), which holds the highest accreditation standard in Europe. Trauma Recovery Institute uses a highly structured psychotherapeutic approach called Dynamic Psychosocialsomatic Psychotherapy (DPP).
At Trauma Recovery Institute we address three of the core Attachment Styles, their origin’s the way they reveal themselves in relationships, and methods for transforming attachment hurt into healing. We use the latest discoveries in Neuroscience which enhances our capacity for deepening intimacy. The foundation for establishing healthy relationships relies on developing secure attachment skills, thus increasing your sensitivity for contingency and relational attunement. According to Allan Schore, the regulatory function of the brain is experience-dependent and he says that, as an infant, our Mother is our whole environment. In our relational trauma recovery approach you will learn to understand how the early patterns of implicit memory – which is pre-verbal, sub-psychological, and non-conceptual – build pathways in our brain that affect our attachment styles. Clinically, we can shift such ingrained associative patterns in our established neural network by bringing in new and different “lived” experiences in the Here and Now.
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The Role of the Therapist in transforming attachment trauma: Healing into wholeness takes the active participation of at least one other brain, mind, and body to repair past injuries – and that can be accomplished through a one-to-one therapeutic relationship, a therapeutic group relationship or one that is intimate and loving. In exploring the “age and stage” development of the right hemisphere and prefrontal cortex in childhood, we discover how the presence of a loving caregiver can stimulate certain hormones, which will help support our growing capacity for social engagement and pleasure in all of our relationships. Brain integration leads to connection and love throughout our entire life span. At trauma recovery institute we bring a deep focus to the role of Neuroscience in restoring the brain’s natural attunement to Secure Attachment. Our brain is a social brain – it is primed for connection, not isolation, and its innate quality of plasticity gives it the ability to re-establish, reveal and expand one’s intrinsic healthy attachment system.
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Dynamic Psychosocialsomatic Psychotherapy (DPP) at Trauma Recovery Institute Dublin

Dynamic Psychosocialsomatic Psychotherapy (DPP) is a highly structured, once to twice weekly-modified psychodynamic treatment based on the psychoanalytic model of object relations. This approach is also informed by the latest in neuroscience, interpersonal neurobiology and attachment theory. As with traditional psychodynamic psychotherapy relationship takes a central role within the treatment and the exploration of internal relational dyads. Our approach differs in that also central to the treatment is the focus on the transference and countertransference, an awareness of shifting bodily states in the present moment and a focus on the client’s external relationships, emotional life and lifestyle.
Dynamic Psychosocialsomatic Psychotherapy (DPP) is an integrative treatment approach for working with complex trauma, borderline personality organization and dissociation. This treatment approach attempts to address the root causes of trauma-based presentations and fragmentation, seeking to help the client heal early experiences of abandonment, neglect, trauma, and attachment loss, that otherwise tend to play out repetitively and cyclically throughout the lifespan in relationship struggles, illness and addictions. Clients enter a highly structured treatment plan, which is created by client and therapist in the contract setting stage. The Treatment plan is contracted for a fixed period of time and at least one individual or group session weekly.
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“Talk therapy alone is not enough to address deep rooted trauma that may be stuck in the body, we need also to engage the body in the therapeutic process and engage ourselves as clients and therapists to a complex interrelational therapeutic dyad, right brain to right brain, limbic system to limbic system in order to address and explore trauma that persists in our bodies as adults and influences our adult relationships, thinking and behaviour.”

 

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