Penetrating these developmental trends, and expressed through them, are genetic factors.
Moreover, penetrance or expression of genes may vary. Particular clinical outcomes driven by genetic unfolding may be iso- 46 Toward a New Diagnostic System for Child Psychopathology morphic with those arising from experience. For example, social withdrawal may be determined by a biological factor with measurable markers e. Malleability in the developing child is not unlimited. From the time of their birth, individuals show individuality in the intensity or the sensitivity of their responses. The concept of temperament seeks to describe or dimensionalize this. Some groups have also included hypersensitivity and hyposensitivity to sensory stimuli within the concept of temperament e.
These concepts, although descriptively derived, are robust and are found in most cultures. They may approximate neuroregulatory factors predictive of behavioral expression and emotional regulation that might serve as the foundation of a future diagnostic system. Current examples of such research include links to later brainstem auditory evoked response Woodward et al.
Social Communication As noted, survival of a social animal requires sensitivity to signals from others and the capacity to send comprehensible signals. The beginnings of cognitive and social development occur before birth Karmiloff-Smith, ; Locke, Mehler and his colleagues Bertoncini et al. Between 1 and 4 months of age infants learn to distinguish each of the speech sounds that make up all human languages Kuhl, By 6 months of age, infants are able to distinguish subtle variants in phonetic characteristics between their native language and other languages Kuhl et al.
They can also imitate the repeated presentation of certain adult facial movements, including tongue protrusion Field et al. By 3 months of age infants frequently display full-face and partial expression of interest, joy, sadness, and anger, and the patterns of muscle movements involved in these expressions remain stable through the first 9 months Izard, Infants actively engage in behaviors that lead directly to better social engagement e. An infant may selectively signal his caretaker that he is ready to interact by looking at her and smiling.
These caregiver—baby sequences, designed to highlight and encourage the types of social signaling that will be important in later social communication, are universal experiences in well-adapted dyads, surpassing those in experimental learning laboratories in persistence and ingenuity. The older infant actively sustains and perpetuates these sequences. If, in an experimental paradigm, a mother is instructed to suddenly stop interacting, a young child will characteristically perceive that something is different and may become upset or look puzzled.
The infant may use additional behaviors to control his distress in this situation: looking away, self-comforting, or even self-stimulation. By 12—14 months of age children will respond to others in distress, 48 Toward a New Diagnostic System for Child Psychopathology using empathic patting and facial expressions of concern ZahnWexler et al.
Similar behavioral propensities are observed in other primates, suggesting evolutionary selection for social behavior. Darwin commented on this in e. Some human gestures and expressions are quite similar to those of other closely related primates, some are not. Chimpanzees show elaborate emotional signaling systems employing facial expression, gesture, and cries e.
Like human infants, chimp babies come into the world with the innate capacity to display facial expression of emotions. The innate nature of this phenomenon is shown by the observation that rhesus monkeys reared from birth in complete isolation showed appropriate responses to motion-picture- and slide-presented faces of monkeys displaying fear and threat Sackett, Evolutionary survival has apparently selected for human infants to be born prepared to recognize their parents and discern social signals from background noise, and to quickly learn to emit and respond to nonverbal social signals with increasing sophistication and effectiveness.
This concept encompasses reciprocal babbling, spontaneously sharing food and toys, and attunement of expression and emotional responses. Scaife and Bruner provided an early report on the development of joint attention. Understanding Early Development and Temperament 49 The infant sat in the lap of the investigator, who, after ascertaining that the child was settled and alert, made eye contact with the child, then silently turned her head away to fixate a signal light 1.
Older infants may also look back to the investigator after looking toward the light. Other investigators have reported similar findings e. In the past 20 years there have been many studies of theory of mind in children e. The child is placed on one side of the Plexiglas, and his mother is placed on the far side of the second box. If she displays a fearful or angry face, the child usually will not cross, but when his mother shows a joyful face, he most often will readily cross. Social Knowledge: Folk Psychology and Folk Physics Understanding that other people have minds that differ from ours is certainly important, but what must we know socially in order to interact with others and socially survive?
In its simplest form folk psychology implies the human tendency to view human actions in terms of beliefs, attitudes, and knowledge, whereas objects are 50 Toward a New Diagnostic System for Child Psychopathology viewed in mechanistic and nonmental terms—for example, people have minds and objects do not e. Though folk psychology may sometimes attribute causality to human actions that is simplistic in comparison with psychological concepts, and ignore the complex biopsychosocial underpinnings of why we feel and act as we do, it appears to be a fair description of how we tend to view the world.
The question is, how do we come to have these beliefs? It has been argued, mostly on anecdotal grounds, that even 2month-old infants appear to respond differently to people than to objects Brazelton et al. Presented with an object, infants look at it intently, sit up straight, remain relatively still, and alternate between gazing fixedly at the object and glancing away. In addition, infants may give a full greeting response to people, but they rarely do so to objects. In the past decade many more studies have established that by 4 years of age, perhaps even by 3 years, children differ in their understanding of people and objects.
These beliefs apparently arise through interactions with people and objects, although adults may also provide cognitive and linguistic knowledge to help them articulate these beliefs. It might be questioned whether there may be a biological propensity to learn this type of information much of which is nonverbal , similar to our propensity, in childhood, to learn language. Cognitive knowledge, of the sort represented by the aptitudes and skills measured on standard IQ tests, is equally important.
In addition, we need language skills: vocabulary and grammar. The body of general social knowledge that we begin to acquire in early childhood, and that we expand greatly in our first 10 years of life, is crucial to our being able to engage in social interactions. He likens the situation to a game of chess. It is said that chess masters can glance at the pieces on the board and accurately intuit the next best moves.
Amateur chess players must try to cognitively work out an approach using a cumbersome and often unsuccessful move-by-move strategy. Humans have the capacity to learn to play social chess with others well beyond an amateur level, even if some do it better than others. What happens if they fail to acquire such a body of social knowledge is discussed in Chapter 8. Clinical Relevance Rapid early neurological development is experience-expectant and experience-dependent.
The implications for allocations of social resources and for prevention and early intervention are obvious. Current diagnostic systems describe behaviors and emotional responses that have gone awry. DSM-IV describes it for adults better than for children, and minimally describes the difficulties of very young children and infants. DC 0—3 categorizes disorders of stress modulation, affective regulation, self-regulation, communication, and relationships, but only up to the age of 36 months.
What is missing is a diagnostic system that describes what optimal or normal development would look like, describes it from birth to maturity, and, going beyond Axis IV in DSM-IV or Axes II and IV in DC 0—3, describes the fashion in which interpersonal relationships foster mental health or lead to symptomatology.
What early interventions might work? The link between prevention programs, or early stimulation programs, or programs to support parents, and the later well-being of children is tenuous. However, a diagnostic system that is firmly founded in early development, that encompasses the concepts of temperament and social communi- 52 Toward a New Diagnostic System for Child Psychopathology cation, and that characterizes reciprocal behaviors with significant others, appears to be vital to decide if any intervention has been effective in changing the developmental trajectory. Such a diagnostic system would be consistent with a model of human development that postulates that human infants are endowed with a behavioral capacity to emit social signals involving facial expression and sounds, and that they have a propensity to look to complex social stimuli such as faces, and to monitor sounds within the range of human speech.
These propensities, called affective reciprocity, are modified through experience to lead to the development of joint attention. The subsequent development of a theory of mind in the young child may facilitate the development of a body of social knowledge that will be necessary for all later human interactions. Dev Psychopathology, 9 4 — Allmann JM Evolving brains.
New York: Freeman. Stress impairs prefrontal cortical function. Baron-Cohen S Mindblindness. Dev Psychopathology, 13 2 — In A Goldberg Ed. Bennett SL Ed. New York: Guilford Press. J Neurophysiol, — Brain Lang, — New York: Wiley-Interscience. Brothers L A biological perspective on empathy. Bryan RM Jr. Am J Physiol, H—H Child Dev, 67 2 — Cherniak C Neural component placement. Trends Neurosci, — Proc Nat Acad Sci U. Dawson G Frontal electroencephalographic correlates of individual differences in emotion expression in infants: A brain systems perspective on emotion.
In NA Fox Ed. Eibl-Eibesfeldt I Human ethology. New York: Aldine de Gruyter. Infant Behav Dev, — Annu Rev Neurosci, — Goerner S Chaos, evolution and deep ecology. Mahwah, NJ: Erlbaum. Sexual differentiation of the central nervous system. Psychopharamcol, — Sci Am, — Behav Neurosci, 4 — Physiol Behav, 57 4 — Izard C Innate and universal facial expressions: Evidence from developmental and cross-cultural research.
Psychol Bull, — Endochrinology Rev, — Kagan J Biology, context, and developmental inquiry. Annu Rev Psychol, — Karmiloff-Smith A Annotation: The extraordinary cognitive journey from fetus through infancy. Neuroscientist, 5 3 — J Cell Biol, — Patterns of myelination in autopsied infants. J Neuropathol Exp Neurol, — Neurosci Biobehav Rev, 22 2 — Krubitizer L The organization of neocortex in mammals: Are species differences really so different? Trends Neuroscience, — Kuhl PK Perception, cognition, and the ontogenetic and phylogenetic Understanding Early Development and Temperament 55 emergence of human speech.
Science, — LeDoux JE Emotion and the amygdala. P Aggleton Ed. New York: Wiley-Liss. LeDoux JE Emotion, memory and the brain. The ontogenesis of human social signals: From biological imperative to symbolic utilization. Hillsdale, NJ: Erlbaum. Imitation of facial and manual gestures by human neonates.
Minuchin P Families and individual development: Provocations from the field of family therapy. Morell V Ecology returns to speciation studies. Science, — Brain Res, — Early Hum Dev, 18 1 — Infant Ment Health J, — Plutchik R Emotion—A psychoevolutionary synthesis. Psychophysiology, — Monog Soc Res Child Dev, — Neuron, — Cell, — Sackett G Monkeys reared in isolation with pictures as visual input: Evidence for an innate releasing mechanism.
Sapolsky R Stress, the aging brain and the mechanisms of neuron death. Sapolsky R Glucocorticoids and hippocampal atrophy in neuropsychiatric disorders. Sapolsky RM Is impaired neurogenesis relevant to the affective symptoms of depression? Biol Psychiatry, — Endocrinology Rev, Nature, — Child Dev, 70 2 — Schore AN Early organization of the nonlinear right brain and development of a predisposition to psychiatric disorders.
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Snyder EY Neural stem-like cells: Developmental lessons with therapeutic potential. Neuroscientist, 4 6 — Dev Psychol, — Spinelli DN Plasticity triggering experiences, nature, and the dual genesis of brain structure and function. In N Guzenhauser Ed. Spitz R Hospitalism: An inquiry into the genesis of psychiatric conditions in early childhood. Psychoanal Study Child, Stern D The first relationship. New Scientist, — Tronick EZ Emotions and emotional communications in infants. Tuszynski MH Gene therapy: Applications to the neurosciences and to neurological disease.
Vis Cogn, — Waddington VCH Principles of development and differentiation. Dev Brain Res, — Weinstock M Does prenatal stress impair coping and regulation of hypothalamic—pituitary—adrenal axis? Neurosci Biobehav Rev, 21 1 :1— Winnicott DW The maturational process and the facilitating environment. London: Karnac Books and the Institute of Psychoanalysis. Dev Psychol, 37 4 — Nowhere is the need for a melding of basic and clinical science more salient than in the study of anxiety. Conceptualizations of anxiety have taxed psychiatric wisdom because of difficulties in clearly distinguishing normal from pathological anxiety and in understanding interactions between psychosocial and biological factors.
Historically, thinkers from Freud on have taken an evolutionary view of anxiety as an emergency emotion that aids adaptation. Anxiety neuroses were themselves viewed as the evolutionary remnants of prehistoric human experiences. The phenomenological properties of an anxiety attack were thought to represent replays of a prior conflicted reminiscence. This theory emphasized the dual nature of human anxiety, noting a physiological, possibly subcortical component, intrinsic to the organism, and a psychological component, arising during development with cortical maturation.
Although some current theoreticians emphasize subcortical contributions to anxiety Graeff, ; Graeff et al. As a corollary to emphasizing dual roles for higher and more primitive brain regions, Freud stressed the developmental aspects of anxiety, refusing to equate the early physiologic anlage of anxiety with mature anxiety Freud, Instead, he suggested that although anxiety can always be seen as a response to perceived danger, the response is elicited by threats of different salience at each developmental stage.
This ontogenetic array of perceived threats was summarized in the epigraph that early fear of the threat of the loss of the mother, as necessary caretaker, is in maturity represented as the threat of the psychological loss of the love of the mother.
This theory produced advances in the understanding of stress physiology and generated hypotheses about pre vention of depression Sapolsky, We propose a similar evolutionary theory for anxiety disorders. We first review general principles that inform the current evolutionary theory in light of recent research on the biology and developmental plasticity of fear responses. We then apply evolutionary theory to two conditions, social phobia and panic disorder, for which there is a wealth of relevant research.
In fear conditioning experiments, an explicit neutral cue stimulus, such as a tone or a light, is paired with an aversive unconditioned stimulus, such as a shock LeDoux, Circuits based in the cortex, hippocampus, or other limbic structures are also activated by visualization of the context, allowing higher-order processes to impact on amygdalabased processes LeDoux, ; McNish et al. Hence, a subcortical substrate facilitates arousal in the face of potential adversity. The conditioned fear response to an explicit cue can be contrasted with the reaction to other danger-related stimuli, such as dangerous contexts or overtly threatening scenarios.
Unconditioned, contextually conditioned, and cue-specific conditioned fear responses can each be differentiated on neuroanatomical and pharmacological grounds Davis ; Graeff, ; Graeff et al. As such, each response may poten- A Perspective on Two Anxiety Disorders 61 tially model unique aspects of human anxiety. For example, as outlined in the following paragraph, systems related to cue-specific conditioned fear may play a role in phobias, and systems related to unconditioned fear may play a role in disorders related to spontaneous panic attacks.
Clinical studies also implicate a network of distinct fear-relevant circuits in various forms of anxiety. Although neuroimaging and lesion studies suggest involvement of the human amygdala in cuespecific fear conditioning Bechara et al. Pharmacological studies also emphasize a role for different circuits in various aspects of anxiety.
Hence, medications that treat panic disorder are seen as acting via brain systems intimately tied to innate or immediately present danger, whereas medications that treat generalized anxiety disorder may act via other brain systems that show stronger associations with less direct or immediate danger Bowlby, ; Graeff, ; Graeff et al. Finally, ethology also implicates multiple fear circuits in anxiety. Human alarm systems are thought to develop from the systems of lower mammals.
The basic operations of these systems are evolutionarily conserved, in that the systems involve primitive portions of the brain, produce similar effects on peripheral physiology across species, and are similarly moderated by chemical perturbations Graeff, ; Graeff et al. The systems possess obvious survival value, in that organisms without such systems would face risk from separation and predators.
Given that distinct brain circuits are implicated in distinct aspects of anxiety, different evolutionary pressures are thought to have shaped a distinct set of circuits, possibly producing variability in the regulation of each circuit. There is relatively little genetic variability in traits carrying a strong selective advantage, for if a trait is highly adaptive, the forces of natural selection create population homogeneity. Because genes from individuals with frank defects in alarm systems are unlikely to propagate, individual differences in anxiety are 62 Toward a New Diagnostic System for Child Psychopathology more likely to result from relatively subtle perturbations of alarm circuits.
For example, such perturbations could involve abnormalities in input systems to circuits underlying conditioned, contextual, or unconditioned fears; hypersensitivity in limbic structures essential to the process of conditioned fear; or abnormalities in higher brain centers that modulate subcortical fear circuits. These perturbations may relate to plasticity in anxiety-related circuitry, as conceptualized from developmental, neural, and psychological perspectives.
Plasticity: Behavioral and Brain Systems Current theories of chronic psychiatric disorders emphasize developmental psychopathological perspectives. Evolutionary theories of anxiety benefit from such perspectives, if one accepts the developmental principle that there is a changing ontogenetic field in which the context of the signal function of anxiety changes over the lifespan.
Evidence from developmental research on behavioral, psychological, and neural systems supports this view. Behavioral Plasticity: Pathology as Failure of Adaptive Processes From the behavioral perspective, plasticity can be viewed as the ability to adjust behavior to changing life circumstances.
As such changes are a vital part of childhood, many forms of childhood psychopathology can be viewed as failures of behavioral plasticity or as distortions of the adaptive developmental process. Thus, separation anxiety disorder represents an anachronistic developmental failure in adaptation where new demands are met with the apprehension appropriate to situations in which a caretaker is needed for survival. Although this developmental perspective is most clearly illustrated for separation anxiety disorder, it can be similarly applied to other anxiety disorders. If relatively liberal impairment thresholds are used, the majority of adult anxiety, as well as affective disorders, are presaged by childhood anxiety, though most childhood anxiety disorders studied prospectively prove to be transient Pine et al.
These findings lead to a view of anxiety disorders as pathologies in developmental processes.
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There are relatively high rates of anxiety and fear during childhood which typically recede with age. Anxiety disorders may result from failures in development, producing maladaptive regulation of fear responses. Short- and Long-Term Plasticity in Fear-Relevant Circuitry Given the view of anxiety disorders as failures in adaptive processes, variations in anxiety, both between individuals and in the same individual over time, may be attributed to developmental variation.
Systems mediating fear conditioning to explicit cues exhibit both short- and long-term plasticity. Fear conditioning results from shortterm changes in amygdala neurons, mediated by glutamate Davis, ; LeDoux, ; McNish et al. Long-term plasticity in the amygdala can be facilitated by neurons relying on corticotropin-releasing factor CRF as a neurotransmitter.
Similarly, neural circuits mediating anxiety associated with attachment and separation behaviors exhibit both short- and long-term plasticity. Ultrasonic distress vocalization and related protest behaviors in mammals serve to maintain the attachment of mother—infant pair-bonds, which, in turn, form the basis for later separation, independent adult action, and procreative aims of a species Panksepp, The survival value of attachment-oriented behaviors are com- 64 Toward a New Diagnostic System for Child Psychopathology plemented by the distress signal and associated anxiety that mark attempts to recapture the bond between mother and infant.
These compounds control acute changes in adult pair-bonding, monogamy, and paternal behavior. Close cousins, the montane voles, differing in only one amino acid in their nonapeptides, show none of the affiliative, monogamous, or caretaking roles of the prairie cousins. Parallel work examines long-term plasticity in circuits effected by attachment behaviors.
Variations in maternal behavior produce hippocampally mediated changes in the stress response of rodent pups that persist throughout the life of an organism Francis et al. Although studies in lower mammals emphasize the role of hippocampal or amygdala-based plasticity, a more prominent role for cortical plasticity may be expected in fear among primates.
Bowlby argued that protest signals become increasingly important for the maintenance of mother—brood mutuality as phylogenetic complexity increases. Darwin similarly noted that small primate broods necessitate longer periods of caretaking. Although the neurochemical regulation of separation anxiety appears similar in primates and rodents Kalin, ; Panksepp, ; Panksepp et al. These internalized patterns shape later social behavior, facilitating survival. Thus, among primates, cortical perception of dangerous social situations may play a unique role in mediating emotional states associated with subcortically based change.
Such a unique role might be expected in light of the species-typical complex web of social relationships that encourages the manipulation of mental scenarios to anticipate the reactions of conspecifics. Manipulations of the rearing environment may alter inborn response systems, which in turn may disrupt plasticity in cortical circuits essential for social adjustment and the control of A Perspective on Two Anxiety Disorders 65 fear-relevant behaviors.
Poorly mothered primates show both abnormalities in fear-relevant behaviors as well as an inability to assume the necessary social behaviors for coitus and species survival Coplan et al. In summary, anxiety disorders can be seen as failures in adaptive processes. Such adaptive processes are thought to involve changes in cortical and subcortical systems. Studies with lower mammals show that life experiences impinge on evolutionarily adaptive subcortical systems to create differences in the predilection to experience fear and anxiety. Studies with primates suggest that life experiences might also change adaptive cortical systems, further contributing to differences in later anxiety-related behavior.
As a result, the current theories emphasize the role of developmental plasticity in evolutionarily adaptive biological systems. Although each anxiety disorder is presumably the by-product of vulnerabilities in some core alarm system, there is relatively firm evidence to support the view of anxiety disorders as a family of distinct conditions. These data include the unique phenomenology, family history, treatment, course, and biology of each disorder.
Panic disorder shows a unique association with respiratory dysfunction Klein, ; Papp et al. With social phobia, there is evidence of a unique developmental course, treatment response pattern, family profile, and biological correlates Pine et al. We discuss evolutionary theories for two anxiety disorders, social phobia and separation anxiety 66 Toward a New Diagnostic System for Child Psychopathology disorder, for which there is a wealth of relevant developmental, neuroscientific research.
As demonstrated by Sapolsky , useful evolutionary theories must go beyond post hoc rationalizations and generate hypotheses that change the conceptualization of a syndrome. Accordingly, we offer evolutionary theories for social phobia and panic disorder that generate explicit testable hypotheses. Given the view of these anxiety disorders as developmental conditions, hypotheses involve predictions concerning the relationship between child and adult disorders. Each disorder is first discussed within the context of existing developmental, clinical psychobiological data and within the context of evolutionary theory.
Developmental hypotheses are then put forth, with respect to behavioral and biological aspects of each condition. Social Phobia Social phobia is thought to involve the circuitry of fear conditioning. An amygdala-based circuit may be oversensitive to signals that arise in social interchanges, such as facial expressions LeDoux, Recent functional imaging data confirm the involvement of the fear-conditioning circuit in social perception: the amygdala responds selectively to fearful faces, even when presented below the level of conscious perception Breiter et al.
Moreover, preliminary evidence suggests that adults with social phobia show enhanced sensitivity in their amygdala for facial displays of emotion Birbaumer et al. Social phobia also is unique from the developmental perspective. Many adults report preteen onset of social phobia, whereas panic and generalized anxiety disorders typically arise after puberty Pine, ; Schneier et al.
Prospective studies confirm these findings in all three anxiety disorders, while also revealing marked specificity in the course of social phobia as distinct from the other anxiety disorders Pine et al. Kagan and colleagues note a biological predisposition for shyness as a temperamental trait in a sizable minority of preschool children. Such children exhibit signs of behavioral inhibition, the tendency to withdraw from novelty, particularly social novelty.
Like social pho- A Perspective on Two Anxiety Disorders 67 bia, this behavioral pattern is thought to result from activity in the amygdala-based fear circuit. Although the precise relationship between behavioral inhibition and individual childhood anxiety disorders remains a matter of dispute, there is evidence of a specific tie with social phobia Kagan, Neuroscientific and developmental data suggest that social phobia may result from a perturbation in the sensitivity of the fear circuit, as it responds to cues of potentially hostile social scenarios Birbaumer et al.
Based on developmental data, such hypersensitivity is expected to arise early in life, preceding overt manifestation of the disorder Kagan, ; Kagan et al. From the evolutionary standpoint, the propensity for our species to develop social phobia may derive from the selective advantage conveyed to ancestors who were particularly sensitive to cues of social hostility Ohman, Although currently observable remnants of this selective advantage may not be obvious, they may be observable where predators abound.
Even now, humans develop amid the dangers of war zones and ghettos. Recently emerging literature on conduct disorder reveals the potential survival value of an amygdala-based brain circuit responsive to social displeasure in some contexts. The pattern of repeated aggressive and rule-violating behavior of conduct disorder is particularly common among children living under social duress. Conduct disorder often persists and sometimes develops into antisocial personality disorder Moffitt, Anxiety and conduct disorders frequently co-occur Bird et al.
If social phobia results from specific enhanced sensitivity for social cues in an evolutionary adaptive, developmentally preserved circuit, such enhanced sensitivity might alert children with conduct disorder to social pressures, which effectively moderates behavior. Therefore, one might predict that childhood social phobia, but not other forms of anxiety, would signal a more benign course away from conduct disorder. There is evidence to support this view. Kerr and colleagues found that symptoms of behavioral inhibition predict a rela- 68 Toward a New Diagnostic System for Child Psychopathology tively transient course for aggressive symptoms in children.
Raine Raine, ; Raine et al. Recent data extend these findings to symptom ratings of both social phobia and conduct disorder Pine et al. Specifically, symptoms of social phobia, but not other anxiety disorders, were shown to predict a more transient course of conduct disorder symptoms. This evolutionary view of social phobia also generates more specific predictions in terms of neural physiology.
For example, one might predict that increased sensitivity of the amygdala-based fear circuit to social cues, as assessed using functional magnetic resonance imaging fMRI , also predicts a more benign course for conduct disorder. Similarly, increased sensitivity to social cues in young inhibited or even asymptomatic children might predict the onset of social phobia. Such a theory might suggest survival of this characteristic in the population through its ability to adaptively influence behavior in some situations, as hypothesized for conduct disorder.
Finally, such a theory generates a set of specific, testable hypotheses that may change conceptualizations of social phobia and enhance understandings of pathophysiology. The cause of this association remains an area of intense debate. Klein provides an essentially evolutionary perspective, viewing the panic attack as an alarm reaction that developed to alert organisms to cues of impending suffocation. Cognitive theories emphasize the role of mental distortions related to hypersensitivity to somatic respiratory cues, social stress, or loss of control Barlow, ; Marks, Psychodynamic views also focus on the misapprehension of body sensations and add the idea of fear of loss of protection shown by the expression of aggression and potential protest toward the perceived caretaker.
Despite debate on specifics, there is clear consensus across the various theories on two key points that inform the current theory. Namely, the spontaneous panic attack involves a prominent respiratory component and represents an adult phenomenon with childhood antecedents. The current theory places these points within the context of evolutionary psychobiology. Spontaneous panic attacks exhibit very low rates before puberty, with an initiation, steady rise, and eventual peak from puberty through early adulthood Pine, ; Pine et al.
Few adolescents who suffer spontaneous panic attacks develop full-blown panic disorder, which has a median age of onset in the 20s Pine et al. Nevertheless, most adults with panic disorder had suffered from a childhood anxiety disorder or an adolescent panic attack Klein, ; Pine et al. Hence, panic disorder, like social phobia, might result from failure in adaptive processes, as signaled by various forms of anxiety during childhood.
The association between separation anxiety and panic disorders has sparked particular interest. Despite some controversy, the weight of the evidence supports an association between the two conditions. From the neurobiological perspective, the pharmacology and neuroanatomy of separation reactions in animals bears similarity to the pharmacology of human spontaneous panic Panksepp, ; Panksepp et al. Both conditions can be differentiated on pharmacological and anatomical grounds from other forms of fear.
From the clinical perspective, separation anxiety disorder identifies a particularly familial form of panic disorder, with an early age of onset Battaglia 70 Toward a New Diagnostic System for Child Psychopathology et al. Such early-onset panic disorder is more familial and more closely tied to the spontaneous panic attack, which, in turn, is most closely tied to respiratory factors Briggs et al. Children of parents with panic disorder exhibit high rates of separation anxiety, also suggesting a familial and possibly genetic association Capps et al.
Adults with panic disorder retrospectively report high rates of separation anxiety disorder, and prospectively followed children with separation anxiety disorder exhibit high rates of panic as adults Klein, ; Pine et al. Difficulty with separation experiences among adults can presage the development of panic attacks, occurring either naturally Brown et al. Finally, children with separation anxiety disorder exhibit many of the classic respiratory manifestations seen in adults with panic disorder Pine et al.
The data on the developmental course of spontaneous panic attacks and on the relationships between panic attacks, respiration, and separation anxiety form the basis for the current evolutionary theory. This theory suggests that both the spontaneous panic attack and separation anxiety disorder involve perturbations in brain circuits centrally involved in respiratory control. This may account for the prominent role of vocalization in separation anxiety among both animals and humans.
From a developmental, evolutionary standpoint, the current theory posits a pubertal change in the common circuitry that mediates separation anxiety before puberty and panic reactions after puberty. Evolutionarily, a change in this circuit was ontogenetically adaptive for our ancestors in the face of changing environmental demands at puberty. These demands required different forms of respiratory control as the need for vocalizations to maintain physical attachment diminished.
Conversely, as humans spent decreasing amounts of time in proximity to caretakers, the respiratory system was refined to facilitate rapid physical exertion upon exposure to unexpectedly dangerous situations, including suffocation.
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Hence, changes in the regulation of separation, respiration, and underlying panic circuitry facilitate successful navigation of individuation, self-care, and changing socioenvironmental pressures around puberty. The adaptive plasticity in this circuit, however, is hypothesized to leave our species vulnerable for separation anxiety disorder before puberty and spontaneous panic attacks after puberty. This theory generates a number of testable hypotheses, some of which have already received preliminary support.
First, children with A Perspective on Two Anxiety Disorders 71 separation anxiety disorder, like adults with panic disorder, are expected to exhibit enhanced sensitivity to respiratory stimulants, manifested both in terms of dyspnea complaints and physiology. Such enhanced sensitivity is a by-product of plasticity in systems mediating both separation anxiety and panic.
Preliminary data from our group are consistent with this hypothesis Pine et al. Second, respiratory sensitivity to cues of suffocation should become increasingly prominent as children with separation anxiety disorder approach puberty, reflecting the evolutionary advantage of adapting the respiratory system for prompt mobilization.
Such alterations in puberty facilitate biological responses to circumstances that require sudden mobilization of the respiratory system designed to escape predators, engage in combat for sexual primacy, or elude suffocating circumstances. However, overpriming may result in a propensity for panic attacks in our species. Third, such changes in respiration will be paralleled by changes in other biological systems related to a diminution in separation anxiety. For example, one might expect changes in the coupling between the hypothalamic—pituitary—adrenal HPA axis and the respiratory system, as the HPA axis and the respiratory system are coactivated during separation Panksepp et al.
Although respiratory mobilization is part of both separation anxiety and panic, HPA activation is adaptive for separation anxiety but maladaptive in suffocation Klein, Finally, respiratory and HPA axis change will be tied to social changes at puberty, given that the relevant circuitry is thought to facilitate adaptation to socioenvironmental challenges at puberty. Viewed from a psychological perspective, the acute body consciousness of pubertal adolescents possessing an underlying subcortical vulnerability may promote maladaptive overinterpretation of bodily sensations.
This, in turn, may be coupled with the generation of anxiety from psychological conflicts, as judged by a relatively socially immature organism. The introduction of adolescence as a psychosocial phase in development places the procreatively competent postpubertal human in a position where she is capable of reproduction but societally inhibited, leading to anxiety about misconstruals of social signals and intrapsychic desires.
In summary, there are intimate connections between respiration, spontaneous panic, and separation anxiety. From a developmental, neuroscientific, and family-genetic perspective, separation anxiety disorder presages an increased risk for spontaneous panic arising 72 Toward a New Diagnostic System for Child Psychopathology during puberty. From an evolutionary perspective, a common biological system is involved in the regulation of separation reactions, respiration, and panic. Developmental changes in this system facilitate the navigation of puberty but also expose our species to the risk for spontaneous panic.
An evolutionary view of anxiety is by no means new, as debate on the primary role of physiological versus psychological factors has characterized evolutionarily based theories arising throughout the century. The current essay adds developmental and neuroscientific perspectives to this debate. Earlier principles are placed within a developmental context, calling attention to the welldocumented plasticity in fear-related behaviors and associated neural circuits. Moreover, such developmental views are integrated with current knowledge on the distinctions among fear-relevant circuits that mediate responses to various forms of danger.
Most significant, this chapter applies evolutionary theory to two anxiety disorders, social phobia and panic disorder, demonstrating that such a view generates a new set of testable hypotheses that may advance our understanding of pathophysiology. In short, the evolutionary view provides a rational explanation of the segregation of two anxiety syndromes, linking the phenomenology to specific physiological evolutionarily determined precursors.
Barlow DH Anxiety and its disorders: The nature and treatment of anxiety and panic. NeuroReport, — Bowlby J Attachment and loss Vol. Br J Psychiatry, — Br J Psychiatry Suppl, — J Abnorm Psychol, — Longitudinal perspectives. Psychiatr Clin North Am, — In JS March Ed. New York, Guilford Press. Darwin C The expression of the emotions in man and animals 3rd ed. Davis M Neurobiology of fear responses: The role of the amygdala. J Neuropsychiatry Clin Neurosic, — Ann of NY Acad Sci, — Freud S Inhibitions, symptoms, and anxiety.
In J Strachey Ed. London: Hogarth Press. Freud S The neuro-psychoses of defense. Gilbert P Evolution and social anxiety: The role of attraction, social competition, and social hierarchies. Psychiatric Clin North Am, — J Clin Psychiatry, — Graeff FG Serotonergic systems. Psychiatr Clin North Am, — Neurosci Biobehav Rev, — Proc R So Med, — In DA Hope Ed.
Nebraska Symposium on Motivation. Omaha: University of Nebraska Press. J Autism Child Schizophr, — Insel TR A neurobiological basis of social attachment.
Kagan J Temperament and the reactions to unfamiliarity. Kalin NH The neurobiology of fear. Klein DF False suffication alarms, spontaneous panics, and related conditions: An integrative hypothesis. Klein RG Anxiety disorders. London: Blackwell Scientific. LeDoux J The emotional brain: The mysterious underpinnings of emotional life. Marks IM Fears, phobias, and rituals: Panic, anxiety, and their disorders.
J Neurosci, — Cell Mol Neurobiol, — Moffitt TE Adolescence-limited and life-course-persistent antisocial behavior: A developmental taxonomy. Psychol Rev, — Nesse RM Proximate and evolutionary studies of anxiety, stress and depression: Synergy at the interface. New York: Random House. Ohman A Face the beast and fear the face: Animal and social fears as prototypes for evolutionary analyses of emotion. Panksepp J Affective neuroscience: The foundations of human and animal emotions.
In KT Strongman Ed. New York: Wiley. Pine DS Childhood anxiety disorders. Curr Opin Ped, — J Child Psychol Psychiatry, 41 5 — New York: McGraw-Hill. Raine A The psychopathology of crime: Criminal behavior as a clinical disorder. Sapolsky RM Stress, the aging brain, and the mechanisms of neuron death. Sapolsky R Glucocorticoids and hippocampal atrophy in neuropsychiatric disorders.
Arch Gen Psychiatry — Comorbidity and morbidity in an epidemiologic sample. Am J Ortho, — PFEFFER mpirically tested observations of children and adolescents suggest that depression is a heterogeneous phenomenon that can exist with varying intensity and other characteristics Compas et al. Specifically, depression occurs as a symptom of sadness for an unspecified time. It occurs as a syndrome or constellation of emotions and behaviors that occur together in an identifiable pattern at a rate that exceeds chance. It occurs as a disorder that includes a cluster of symptoms that characteristically co-occur and are associated with significant levels of discomfort and impairment.
Sadness, the most common of these phenomena, is experienced in everyday life and is associated with life events, especially losses, but a depressive disorder is less prevalent.
This chapter expands a discussion of this concept and proposes that an understanding of childhood depression as an evolutionary phenomenon can promote the development of E 78 A Perspective on Childhood Depression 79 new diagnostic and treatment options and of research to improve the lives of children afflicted with or at risk for depression.
We are now convinced, largely through the initial empirical research of Puig-Antich , that children of various ages do fit adult criteria for major depression and that prepubertal depressions have a chronic course and appear to be continuous with adolescent and adult depression Kovacs et al. Historical review of clinical observations and results of empirical psychosocial research highlight insights relating psychological etiological phenomena to depressive responses.
Freud proposed that melancholia is a state of intrapsychic dysfunction in which severe guilt is responsible for a protracted, intense mourning condition, which is evident as self-criticism, self-rejection, and internally directed anger. The resultant manifestations are sensitivity to repeated disappointment, aggression toward the self, intense need for narcissistic gratification, loss of self-esteem, and feelings of helplessness. Spitz , utilizing psychoanalytic principles and direct observations, reported on the entity of anaclitic depression, a preobjectal depressive state of infants who lack consistent caretaking and have not been able to build a stable representation of a caretaker.
Learned helplessness, 80 Toward a New Diagnostic System for Child Psychopathology another feature of depression, is manifest by social impairment, passivity, and change in psychomotor activity Seligman, Lewinsohn proposed depression to be a result of loss or reduction of reinforcement provided by the environment for acquisition of skills and understanding of consequences to environmental events.
A child, therefore, may become passive and withdrawn and exhibit other symptoms of depression. This is illustrated by observing the consequences for young children who are raised by depressed mothers who are less rewarding to their children, promote more conflict in the family, and may be more detached from their children. This maternal behavior promotes in children feelings of resentment, anger, depression, and other features of dysfunction. This historical review suggests new considerations about sadness and depressive affects.
Such affects may serve adaptive functions that can carry children and adolescents through the developmental cycle into adulthood Nettle, However, it is also evident that extremes of affect can be lethal and that if the homeostatic balance is overextended into a depressive disorder, the developmental process is impeded and the expression of chronic depression leads to poor socialization manifested as alienation or maladaptive roles.
They highlight varied presentations of the adaptive and psychopathological features of depression. Child 1 A year-old boy with a history of physical abuse in infancy was hospitalized in a psychiatric facility after running away from a residential treatment center. He wanted to kill himself by jumping off a nearby bridge. He was found wandering on a country road by the police, who brought him to a hospital emergency room. Three months before this episode of suicidal threat, the child en- A Perspective on Childhood Depression 81 tered the residential treatment center because he was unmanageable, irritable, and angry at home.
His father, a harsh disciplinarian, believed that his son was possessed by the devil and deserved to be punished for his unwillingness to cooperate with family life. She was unable to help them resolve their intense animosity. Different states have different policies. Francine Russo is a veteran journalist, specializing in psychology and behavior. She is also a speaker and author of They're Your Parents, Too!
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