How Can Children's Drawings Help With Psychological And Somatic Disorders?
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Article Contents
Abstract
Objective To provide a new approach for conceptualizing and studying functional somatic symptoms (FSS) in children and adolescence.Methods A developmental model is proposed based on the synthesis of the extant literature and previous theoretical perspectives of FSS in children and adolescents.Results Multiple run a risk and protective factors from child, familial, social, and environmental domains, the interactions across risk domains, and potential developmental pathways of FSS are identified.Conclusions This commodity underscores the necessity of taking a broader, developmental view of FSS. The tenets of developmental psychopathology emphasize the utility of viewing FSS on a continuum of severity rather than every bit a discrete entity or diagnosis. This article concludes with directions for future enquiry and handling implications.
Functional somatic symptoms (FSS), divers as physical symptoms of unknown pathology (Dhossche, Ferdinand, van der Ende, & Verhulst, 2001; Steinhausen, 2006), affect 10–30% of children and adolescents in the United States (Campo & Fritsch, 1994) and may include headaches, intestinal hurting, musculoskeletal pain, vomiting, chest pain, fatigue, and dizziness. FSS take been studied as private symptoms (eastward.g., recurrent abdominal pain; Walker et al., 2006b) and every bit symptom constellations (e.grand., the Somatic Complaints subscale on the Child Beliefs Checklist; Achenbach, Conners, Quay, Verhulst, & Howell, 1989). In addition to their high prevalence, FSS are associated with loftier levels of functional damage and comorbid psychiatric symptoms, particularly anxiety and depression (Garber, Zeman, & Walker, 1990; Walker & Greene, 1989). Children with FSS are ofttimes seen in pediatric settings. Indeed, two–4% of all pediatric visits are reportedly due to FSS (Campo & Reich, 1999). This high level of medical attention is not only costly to families and club, only may lead to unnecessary and unsafe medical procedures (Campo & Fritsch, 1994; Campo & Reich, 1999).
The traditional Western medical approach to affliction is to find a pathological origin for symptoms. Nevertheless, this approach has limitations when practical to children with FSS. First, this arroyo emphasizes the presence or absenteeism of a diagnosis. No empirical evidence yet has been institute to support FSS as a discrete diagnostic entity. Rather, empirical research shows considerable heterogeneity in the clinical presentation, class, and outcome of FSS in children and adolescents, which leads to the 2nd limitation. The traditional medical arroyo does not recognize differences in trajectories and outcomes.
Developmental psychopathology (Cicchetti & Sroufe, 2000; Cummings, Davies, & Campbell, 2000) offers an alternative perspective for studying FSS in childhood and adolescence. Get-go, through the developmental lens, childhood behaviors are viewed on a continuum from normal to aberrant (or matted). 2nd, developmental psychopathology seeks to identify risk factors that influence the severity, trajectories, and outcomes of maladaptive kid behavior. The extant literature does non provide extensive evidence for the contribution of i particular gene to FSS, rather the studies to date offer clues to the multiple factors that may underlie the evolution and progression of FSS. By applying a developmental psychopathology perspective, issues concerning the antecedents, course, and result of FSS can be addressed, cartoon upon the extant literature across multiple disciplines (e.g., psychology, psychiatry, nursing, and pediatrics). The purpose of this article is to review the literature regarding private differences in clinical presentation and pathways of FSS in children and adolescents. Second, this review aims to identify clues in the literature regarding the take chances factors from child, social, and environmental domains that directly influence or moderate outcomes of FSS. 3rd, this article identifies theories that suggest mechanisms for the maintenance and progression of FSS. Finally, future inquiry directions and clinical implications are discussed.
Pathways and Progression of FSS
A prototypical question posed by developmental psychopathologists is whether different risk factors and pathways can distinguish cases of disordered behavior and increase the power of predicting adult consequence. The timing of symptom manifestation and the identification of combinations of hazard and protective factors have helped guide developmental psychopathologists in delineating trajectories of childhood disorders (Cicchetti & Sroufe, 2000). Subsequently, the research pertaining to the variability in clinical presentation and continuity of FSS over fourth dimension is reviewed to illuminate potential pathways of FSS in childhood.
Variability in Clinical Presentation
Cooccurring Maladjustment May Occur for Some
The prognosis can be worse for kid-onset problems when they are persistent and/or comorbid, every bit is the example for antisocial behavior with attention-deficit/hyperactivity disorder (Moffitt, 1990, 1993). Due to the nascent country of the literature in this expanse, in that location has been no evidence to demonstrate a similar pattern for FSS in childhood. However, it is documented across disciplines that children with FSS often brandish elevated levels of psychiatric symptoms, and the frequency of FSS tend to increase with the severity of anxiety and low symptoms (Bernstein et al., 1997; Dhossche et al., 2001; Garber et al., 1990; Last, 1991; Livingston, Taylor, & Crawford, 1988; McCauley, Carlson, & Calderon, 1991; Walker & Greene, 1989). This is particularly salient given that symptoms such equally generalized anxiety, thoughts of death, and those typical of externalizing behaviors, including hyperactivity, oppositionality, and conduct problems, accept been found to cooccur with FSS in children betwixt the ages of 3 and 6 (Aromaa, Sillanpaa, Rautava, & Helenius, 2000; Domenech-Llaberia et al., 2004; Stevenson, Simpson, & Bailey, 1988; Zuckerman, Stevenson, & Bailey, 1987). For example, a significantly higher occurrence of conduct problems has been found in boys with headaches and in children with FSS age 6 and younger compared to healthy children (Egger, Angold, & Costello, 1998; Zuckerman et al., 1987).
Meaning correlations between children's FSS and self-reported anxiety and depression (with somatic symptoms removed from questionnaires) take been constitute to be.43 and.37, respectively (Garber, Walker, & Zeman, 1991). In a longitudinal study of adolescents, FSS were significantly correlated with self-reports of feet in boys (rs =.30–.42) and girls (rdue south =.31–.36) at ages 13, 15, and xviii (Rauste-von Wright & von Wright, 1981). Longitudinal data also demonstrate some support for high levels of FSS in children predicting a later psychiatric disorder (Egger, Costello, Erkanli, & Angold, 1999; Zwaigenbaum, Szatmari, Boyle, & Offord, 1999). For example, Zwaigenbaum and colleagues found that high FSS at baseline was associated with major depressive disorder (MDD) 4 years subsequently, independent of gender, baseline emotional disorder, and sociodemographic factors. In addition, the authors found that having an emotional disorder at baseline moderated the human relationship betwixt FSS and afterwards MDD. Specifically, the authors constitute that the adolescents at the greatest risk for MDD were those with high levels of FSS but without an emotional disorder at baseline compared to peers with low FSS and no emotional disorder. The authors interpret their findings as evidence indicating FSS equally an early expression of depressive feelings. In their longitudinal report, Dhossche and colleagues (2001) did non discover that youth with high FSS were at a greater risk for a psychiatric disorder at a half dozen- to 8-year follow-up, despite using like measurements of FSS and psychiatric disorders to those used in the Zwaigenbaum study. However, Dhossche and colleagues did not investigate the moderating effects of emotional disorders in their study. At this point, the data are mixed apropos whether or not a chronic grade of FSS is a risk gene for later psychopathology, specifically clinical low.
Likewise having early psychological issues, some other potential moderator of the association between FSS and psychological issues may be gender. In Egger and colleagues' (1998, 1999) longitudinal studies, data advise that the type of FSS may predict a particular psychiatric diagnosis (as divers by DSM-III-R criteria, American Psychiatric Association, 1987), depending on the kid'due south sex. For instance, musculoskeletal pains predicted low in boys and both depression and anxiety disorders in girls. The combination of headaches and abdominal hurting also predicted anxiety disorders in girls, whereas abdominal pain predicted oppositional defiant disorder and attention-deficit/hyperactivity disorder in boys (Egger et al., 1999). Moreover, thirty.6% girls with one or more psychiatric diagnosis reported concurrent chronic headaches compared to 9.3% of girls without a psychiatric diagnosis, simply this difference was not found in boys.
Functional Impairment
In addition to psychological bug, children with FSS have issues in social and school realms. Research shows that children with headache and other FSS accept more than problems in daycare, fewer hobbies, and report a greater impact of their symptoms on daily life and leisure activities (Aromaa et al., 2000; Bandell-Hoekstra et al., 2002). FSS are often associated with frequent and prolonged daycare and school absences in pediatric, psychiatric, and community samples (Bernstein et al., 1997; Domenech-Llaberia et al., 2004; Rothner, 1993; Walker, Garber, Van Slyke, & Greene, 2001). The relationship among school attendance, FSS, and psychiatric problems (i.due east., feet and depressive symptoms) is of import to delineate because missing school may accept adverse consequences for youth, including strain on or loss of peer relationships, social isolation, and academic difficulties (Bernstein et al., 1997; Vannatta, Gartstein, Brusque, & Noll, 1998). Moreover, children with frequent school absenteeism (i.due east., school refusers) are often referred to a social worker rather than to a psychiatrist, perhaps due to perceived malversation (Stickney & Miltenberger, 1998). Empirical piece of work from the pediatric and schoolhouse refusal literature suggests that many children with FSS are non receiving the advisable treatment for their problems due to the complexity of their presentation (for further reading meet Bernstein et al., 1997; Honjo et al., 2001; King & Bernstein, 2001; Last, 1991).
Pain Severity
Pain severity has been noted as an important gene in determining a kid's quality of life and may alter the presentation and course of FSS. Research has shown that children with higher levels of hurting are more depressed, have a harder time changing their moods or feelings when in pain, and feel more functional impairment, such every bit lower social competence and more than school absences, when compared to children with lower levels of pain or no hurting (Cunningham et al., 1987; Gladstein & Holden, 1996; Kashikar-Zuck, Goldschneider, Powers, Vaught, & Hershey, 2001). In a customs sample of children, Egger et al. (1998) found that the significant damage associated with headache pain was specific to depression, but not anxiety, in girls. It follows that having both a psychiatric disorder, particularly depression, and severe FSS may indicate more functional impairment and consequently a worse prognosis, at least in the curt-term (Mulvaney, Lambert, Garber, & Walker, 2006). These findings accept direct clinical implications. For example, Gladstein and Holden (1996) suggest using the level of damage or disability associated with symptoms, rather than the classification and diagnosis the presenting problem, for planning treatment.
Trajectories and Outcome
Continuity
Enquiry suggests that adults' FSS have their roots in babyhood and may exist continuous over time (Campo & Garber, 1998; Fritz, Fritsch, & Hagino, 1997). Walker, Garber, Van Slyke and Greene (1995) plant that children with functional abdominal pain demonstrated college levels of intestinal discomfort, other FSS, and functional disability (such every bit schoolhouse or work absences) than healthy controls at a 5- to vi-year follow-up when they were adolescents and young adults. Similarly, in an epidemiological written report of adolescents, Dhossche et al. (2001) found that adolescents with a specific FSS tended to report the same symptom along with other FSS at a 6-year follow-upward. One longitudinal study of approximately 2,000 community youth found that from late adolescence to early machismo FSS were stable at a 4-fold higher rate than expected (Steinhausen, 2006). Moreover, Steinhausen plant that a high number of FSS in late boyhood predicted phobic disorders and posttraumatic stress disorders in young adult males and somatoform disorders and some anxiety disorders in immature adult females. These results provide some support for carve up pathways of FSS for males and females.
FSS tend to increase in community and clinical samples over time, but findings do not converge on the stability of symptoms (Aro, Paronen, & Aro, 1987; Dhossche et al., 2001; Walker, Garber, & Greene, 1994), where stability is divers as the number of symptoms and not the item constellation of symptoms. There is modest support for the stability of the number of FSS over time, peculiarly in girls (Aro et al., 1987; Dhossche et al., 2001; Rauste-von Wright & von Wright, 1981). Notwithstanding, the continuity of FSS is not universal. For instance, in a pediatric sample of children with recurrent abdominal pain, the correlation betwixt the number of FSS at baseline and i-year follow-upwards was.29 (p <.01), which, to the authors, indicated a rather unstable form of FSS (Walker et al., 1994). This lack of stability could be due to differential trajectories of FSS beyond babyhood.
In their 5-year prospective written report, Mulvaney and colleagues (2006) delineated three differential pathways of FSS in a sample of 132 pediatric patients with recurrent abdominal pain: A depression-chance group (70% of the sample), a curt-term adventure group (16%), and a long-term gamble grouping (14%). The get-go two groups showed relatively long-term improvement, whereas, the latter group (the long-term risk) showed elevated levels of FSS beyond time. In addition, the long-term hazard group demonstrated significantly more than anxiety and depression, lower perceived self-worth, and more negative life events than the other groups at baseline.
In conclusion, although many studies have investigated the cooccurrence of FSS and internalizing and/or externalizing behaviors, few explicate possible mechanisms for this clan. Moreover, not all children with FSS proceed to develop feet or depression symptoms, allow solitary a total-diddled psychiatric disorder. Indeed, information technology may be a smaller subset of children with a chronic course of FSS who are at the greatest risk for an emotional disorder, as seen in Mulvaney et al. (2006). At this betoken, it is not possible to determine whether the comorbidity of FSS, anxiety, and depression represents a unmarried underlying phenomenon or distinct disorders.
Hazard Factors of FSS
Since finding a definite and exclusive cause of abnormal kid behavior is rare, the purpose of the developmental psychopathology perspective is to define a number of adventure and protective factors that contribute to a child's development. Establishing a process or condition as a risk factor is complex by nature. For instance, sometimes one status may serve every bit a risk or a protective factor for dissimilar outcomes: Being male is a run a risk factor for conduct disorder merely is a protective factor for anorexia nervosa (Cicchetti & Sroufe, 2000). Moreover, a status normally conceived as an outcome may too serve as both a protective factor and a risk factor for other maladjusted behavior. For example, feet is a risk factor for low in girls just may exist a protective factor for bear disorder in boys. Subsequently, risk from child (i.e., age, gender, puberty, stress reactivity, and coping) and ecology (i.e., family unit, social, and sociodemographic) domains are reviewed, followed by a review of interactions amid adventure factors across domains.
Child Factors
The child characteristics historic period, gender, puberty, stress reactivity, and coping have been shown to affect the prevalence and course of FSS in children and adolescents and are briefly discussed below.
Age and Gender
Age and gender have both proven to be factors directly affecting the type and frequency of FSS. Some developmental trends for the type and frequency of FSS have emerged from the literature. Outset, the pattern of symptom presentation appears to change as a role of the child'southward developmental status (Achenbach et al., 1989; Offord et al., 1987). For example, intestinal hurting is the virtually common complaint effectually 9 years of age, and headache is the most frequent complaint around historic period 12. Earlier the age of vi, pseudoseizures are rare; however, they become most apparent during adolescence (Campo & Fritsch, 1994). Second, the incidence of FSS tends to exist low in early on childhood. Studies have demonstrated that in early childhood, eight–ix% of preschoolers have recurrent stomachaches, and 2–iii% have recurrent headache (Domenech-Llaberia et al., 2004; Zuckerman et al., 1987). Withal, the prevalence of FSS, especially polysymptomatic presentation, increases with age (Campo, Jansen-McWilliams, Comer, & Kelleher, 1999; Egger et al., 1998). Regarding gender, epidemiological research has shown that before puberty there is no difference in the prevalence of FSS for boys and girls (Berntsson & Kohler, 2001; Campo et al., 1999). In boyhood, though, girls tend to report more than twice equally many FSS equally boys (Achenbach et al., 1989; Guidetti & Galli, 2001; Offord et al, 1987; Rauste-von Wright & von-Wright, 1981).
Puberty
The physiological and neurobiological changes associated with puberty may play a role in these sexual practice and historic period differences (Susman, Reiter, Ford, & Dorn, 2002). In fact, experts on adolescent development have long considered puberty as a precursor of mood and behavior changes (Susman, Dorn, & Schiefelbein, 2003). The timing of puberty is important, for early-onset puberty in girls indicates a longer lifetime of estrogen exposure, which may predispose adolescents to run a risk for autoimmune diseases, such every bit chronic fatigue syndrome (Susman et al., 2002). Studies take found that avant-garde pubertal status in girls is associated with the frequency of FSS (Aro & Taipale, 1987; Rhee, 2005). Other evidence suggests that cluster headaches start earlier in females than in males (peradventure due to girls' before pubertal onset) and take a bimodal historic period at onset-distribution, with a number of women having their offset attacks afterward menopause (Ekbom, Svensson, Traff, & Waldenlind, 2002).
Stress Reactivity: Contributions of Physiology
Children's limbic hypothalamic–pituitary–adrenocortical (L-HPA) and autonomic nervous systems (ANS) have demonstrated hyperresponsivity to physically aversive events and psychologically stressful situations (Gunnar, Bruce, & Hickman, 2001; Scharff, 1997). Heightened physiological reactivity is associated with internalizing behaviors in early and middle babyhood (Bauer, Quas, & Boyce, 2002; Boyce et al., 2001). In the clinical setting, children with FSS tend to exist described every bit conscientious or obsessive (perfectionistic), sensitive, insecure, and anxious (Garralda, 1996; Kowal & Pritchard, 1990). Children with these temperamental vulnerabilities are hypothesized to be at-take a chance for developing feet disorders and are more than likely to generate distress responses to potentially threatening or uncertain stimuli (Dorn et al., 2003).
Blood pressure, middle rate, adrenaline, nonadrenaline, oxytocin, and cortisol have been measured as physiological markers of stress reactivity in children with FSS (Alfven, de la Torre, & Uvnas-Moberg, 1994; Borres, Tanaka, & Thulesius, 1998; Dorn et al., 2003; Rauste-von Wright & von Wright, 1981); however, cortisol (a mark of 50-HPA) and claret pressure (a marker of ANS) are the merely common measures across studies. There have been inconsistent findings for cortisol (Alfven et al., 1994; Dorn et al., 2003; Rauste-von Wright & von Wright, 1981). It should be noted, withal, that the measurement of cortisol, the induction of stress, the construction of comparison groups, and sample sizes were all variable beyond studies. In the written report of Alfven and colleagues (1994), children with recurrent abdominal pain (RAP) showed a lower cortisol concentration than controls after a claret depict and demonstrated the same pattern 3 months afterward. A airplane pilot study of children with RAP found that cortisol levels increased following a combination of social and cognitive stressors, but the results did non reach significance, perhaps due to the small sample size (Dorn et al., 2003). In a customs sample of adolescents, Rauste-von Wright and von-Wright (1981), however, found that FSS were negatively correlated with the increased excretion of cortisol after a real-life stressor (a compulsory exam for Finnish students seeking admission to university) in 18-year-one-time girls only. No conclusions tin be drawn for blood pressure, since one of the studies did not notice differences (Dorn et al., 2003), and the other written report included many nonsomatic symptoms of anxiety and depression in their definition of "symptoms" relating to blood pressure, obscuring any meaningful relation to FSS (Borres et al., 1998).
Coping
FSS too may reflect an anxious child'south increased focus on bodily sensations and rumination on physical symptoms, as opposed to adaptively coping with the hurting or sensation. Empirical testify suggests that children and adolescents with FSS take fewer adaptive coping strategies and, to some extent, a heightened emotional response to stress compared to children with organic illness and community samples of children (Aromaa et al., 2000; Bandell-Hoekstra et al., 2002; Rauste-von Wright & von Wright, 1981; Rocha, Prkachin, Beaumont, Hardy, & Zumbo, 2003; Ruchkin, Eisemann, & Haeggloef, 2000; Thomsen et al., 2002; Walker, Smith, Garber, & Van Slyke, 1997). In studies of coping in children and adolescents, coping questionnaires defined the stressor every bit the pain itself (Bandell-Hoekstra et al., 2002; Thomsen et al., 2002; Walker et al., 1997), as general difficulties or bug (Rauste-von Wright & von Wright, 1981; Ruchkin et al., 2000), or as daily hassles (Walker, Smith, Garber, & Claar, 2007). Cumulatively, these studies offering support for the idea that children and adolescents with high levels of FSS use poor coping strategies characterized by detachment, rumination over pain, avoidance, anger, cerebral interference, or some combination of these processes.
Environmental Factors
Developmental psychopathology promotes an integrative model. It non only observes the contribution of the active individual, but also examines the dynamic processes and complex interplay between the individual and multiple contextual influences in the kid's e'er-changing environment (Cummings et al., 2000). Developmental psychopathologists describe this dynamic environmental exchange in terms of "contextualism." Each level of the child's ecological context is considered and synthesized as a part of the kid'south experience. For instance, the child's most proximal context (e.g., parenting), almost distal sphere of influence (e.k., cultural environment), and every context in between (due east.thousand., schoolhouse and neighborhood) are expected to influence the child, her experiences, and her evolution. After, contextual factors from family unit, social, and other environmental domains are discussed in relation to the development and maintenance of FSS in children and adolescents.
Family unit Factors
Empirical piece of work has shown that FSS are highly familial, such that children and other family members ofttimes share similar symptoms, be these general physical complaints, abdominal hurting, or headaches (Aromaa, Rautava, Helenius, & Sillanpaeae, 1998; Campo & Fritsch, 1994; Locke, Zinsmeister, Talley, Fett, & Melton, 2000; Walker, Garber, & Greene, 1991; Walker & Greene, 1989). Family factors also include loftier rates of wellness bug and long-term illnesses (e.g., diabetes) and psychological distress (Campo & Fritsch, 1994; Craig, Boardman, Mills, Daly-Jones, & Drake, 1993; Garralda, 1996; Zuckerman et al., 1987). A potential mechanism explaining the familial aggregation of learned affliction behaviors is exposure to family adversity during childhood. Craig, Cox, and Klien (2002) found that a mother's exposure to childhood adversity predicted FSS in her child. It is plausible that aspects of family unit adversity are transmitted across generations. Another written report found a moderating effect on familial transmission, such that in families with high levels of negative life events, mothers with high levels of FSS had boys with higher levels of FSS at follow-up than control families (Walker et al., 1994).
Social and Environmental Factors
A number of studies take investigated the association between social and ecology factors and FSS in children and adolescents. The factors that accept been studied include: negative or stressful life events (Boey & Goh, 2001; Walker, Garber, & Greene, 1993, 1994), family unit characteristics, such every bit marital discord or family cohesion (Terre & Ghiselli, 1997; Zuckerman et al., 1987), daily stressors in children'southward lives (Torsheim & Wold, 2001; Walker, Garber, Smith, Van Slyke, & Claar, 2001; Walker et al., 2007), social back up and social rewards for FSS (Torsheim & Wold, 2001; Walker, Claar, & Garber, 2002), and proxies of social disadvantage, such every bit neighborhood quality and socioeconomic condition (Alfven, 1993; Aromaa et al., 1998; Berntsson & Kohler, 2001; Chapman, 2005; Fearon & Hotopf, 2001; Zuckerman et al., 1987). Overall, empirical testify supports the notion that negative, adverse events or stressors in the abode or at school increase FSS in community and clinic samples of children.
Interactions Among Social, Ecology, and Child Risk Factors
Studies conducted by Walker and her colleagues (1994, 2001, 2002) provide some of the but inquiry investigating interactive effects on FSS in children and adolescents. Walker'south research group has found that the human relationship of stressors and social rewards to FSS is moderated past poor social and academic skills, high negative affectivity, and low self-worth. Walker'south studies draw children who are unhappy and lack competence in at least one area of operation as being at-run a risk for FSS in the face of stressful situations. Walker'due south studies (1994, 2001, 2002) have investigated the complex associations between child and contextual factors, with results supporting a social learning hypothesis. That is, children who may fear failure in social or academic realms are less apt to cope finer with negative life stressors and consequently experience uncomfortable somatic symptoms. Conveying these symptoms to others may benefit children by assuasive them to avoid the feared situation or considering they receive attention, thereby reinforcing the expression, and likely the experience, of the somatic distress (Walker et al., 2006a).
Taken together, the literature reviewed above suggests that numerous environmental stressors, ranging from the expiry of a parent to everyday stressors, are associated with increased FSS in children and adolescents. Longitudinal information suggest that daily stressors in school and family unit contexts produce greater somatic distress in children with low social competence, and that social rewards maintain FSS, especially when children accept depression self-esteem. Social disadvantage may compound these effects, peculiarly in children older than 7 years of historic period (Alfven, 1993; Berntsson & Kohler, 2001; Fearon & Hotopf, 2001). To clarify the complex relationship amidst social stressors, social rewards, ecology arduousness, historic period, and gender, the study of additive and interactive effects of these factors must continue.
Summary
This review has illuminated gamble and protective factors that contribute to the etiology and maintenance of FSS. Based on the literature reviewed earlier, child, family, social, and environmental factors, and comorbidity with internalizing disorders were associated with FSS. High cocky-esteem, social competence, and male person gender were identified as possible protective factors. Moreover, female gender, early-onset mood disorder, poor coping skills, and greater pain severity may increase the risk for FSS over time.
Psychological Theories and Possible Mechanisms of FSS
Child researchers from multiple disciplines accept investigated many theories in their search to explain the mechanisms influencing the origin and progression of FSS in children and adolescents. Every bit opposed to existence limited to one mechanism delineated by a particular theoretical orientation, developmental psychopathology allows researchers to draw from and incorporate multiple theories. Subsequently, some of the more prevalent theories and their corresponding mechanisms are described.
The most influential and long-standing theory pertaining to FSS, somatization disorder (or hysteria), and conversion disorder is Freud'due south psychodynamic theory (Freud, 1962). This theory highlights the kid's repressed needs and emotions as a causal function in the development of FSS. Psychodynamic thinkers view FSS as a psychological defense against repressed or unconscious emotions, thoughts, and impulses, while still allowing the individual to express distress through physical symptoms (Campo, 1995; Lask & Fosson, 1989). A second school of thought, attachment theory, frames FSS as a mode for the child to maintain close proximity to the attachment effigy (Bowlby, 1973). The child'south expression of concrete discomfort and distress acts as a care-eliciting part from the attachment figure (Campo & Fritsch, 1994). Neither psychodynamic nor zipper theory, still, has received much empirical attention with respect to FSS in children and adolescents.
Third, the family systems approach posits that children'south FSS serve a chatty function for family members to maintain their daily routine functioning as well every bit a way to avoid conflict and has been supported by empirical studies (Aro, 1987, 1989; Terre & Ghiselli, 1997; Zuckerman et al., 1987). According to Minuchin's family unit systems theory, children's FSS are conceptualized every bit a homeostatic mechanism for avoiding conflict in enmeshed, over-protective, and rigid families (Minuchin et al., 1975). FSS as well have been viewed equally having a communicative role, or being a "plea for help," for children (Campo & Fritsch, 1994), peculiarly in families characterized past poor parent–child relationships (Aro, 1989; Aro et al., 1987; Raust-von Wright & von-Wright, 1981).
Quaternary, social learning theorists frame FSS as a learned prepare of interpersonal or social behaviors that are often reinforced by family unit members and guild (Craig et al., 2002; Walker & Greene, 1989). Co-ordinate to this perspective, the expression of FSS may be reinforced by special attention from parents or by existence excused from disagreeable tasks, such as completing chores at home or taking a test at school (Walker et al., 2002). This perspective also asserts that children may larn the importance of health behavior and brandish rules from family members. For case, enquiry supports a high positive correlation between parents' and children's FSS in families of children with recurrent intestinal pain but not in families of children with an identified organic disease or in families with healthy children (Walker et al., 1993).
A fifth perspective, the cognitive psychobiological theory, delineates FSS as a event of physiological reaction to emotional arousal. Cognitive factors have been hypothesized to play a major office in the reporting of FSS. For example, children with FSS may have a heightened preoccupation with or sensitivity to physical sensations (eastward.g., attentional bias; Boyer et al., 2006). With distorted data processing and negative cognitions, children with FSS may frame symptoms equally a reason for serious concern, and this negatively biased internal monitoring leads to "amplification" or misinterpretation of common body sensations and/or normative levels of somatosensory inputs associated with illness or emotional distress (Campo & Reich, 1999). The distension and misinterpretation of physiological signals may, in turn, exist one of the primary processes in the development of FSS (Rief, Shaw, & Fichter, 1998).
Sixth, coping and stress response theories delineate that children's cognitive and behavioral responses to chronic pain influences their level of pain and psychological adjustment (Thomsen et al., 2002; Walker et al., 2007). Coping has been defined equally a kid's voluntary efforts to regulate their emotions, thoughts, behavior, physiology, and environment in response to stressful events (Compas, Conner-Smith, Saltzman, Thomsen, & Wadsworth, 2001). The fashion in which children cope with such stressors has a nifty touch on FSS, hurting intensity, and internalizing symptomatology. For example, in studies of children with recurrent abdominal hurting, those children who used more accommodating coping strategies (e.g., acceptance or distraction) in response to hurting demonstrated fewer FSS and symptoms of anxiety and depression. In contrast, passive coping responses, such as disengagement, were found to be strongly associated with increased levels of hurting, FSS, and depressive symptoms (Thomsen et al., 2002; Walker et al., 1997).
Lastly, due to the high comorbidity of symptoms and diagnoses, FSS take been hypothesized as a consequence of a psychiatric disorder, such as anxiety or depressive disorders (Campo & Reich, 1999). In the 1970s, FSS were viewed as "masked depression," a condition where children expressed their emotions through physical symptoms (Bschor, 2002; Carlson & Cantwell, 1980). Many studies have investigated the positive relation between internalizing and/or externalizing behaviors and FSS, simply few explicate possible mechanisms for this association.
A Developmental Perspective on FSS
The developmental psychopathology approach allows us to integrate the theoretical perspectives described earlier to empathize the etiology, pathways, and effect of FSS. The case below illustrates the combination of multiple theories (in parentheses) and developmental psychopathology constructs (noted in italics) with the extant literature reviewed in this commodity to lend a developmental perspective on FSS throughout babyhood and adolescence (Fig. 1). That is, the following integrative summary describes how most of the psychological theories described above can inform our agreement of mechanisms that influence the course of FSS at detail stages in childhood and adolescence. Some theories may be more important in earlier childhood (e.g., attachment theory), while others may exist more salient during adolescence (e.g., family unit systems theory).
Figure ane.
A working model for the report of functional somatic symptoms beyond childhood and boyhood.
Figure ane.
A working model for the study of functional somatic symptoms across babyhood and boyhood.
The development of FSS begins with a sensitive, broken-hearted, or emotionally reactive child who oftentimes perceives more threat and danger, exist it existent or imagined, in the environs compared to his or her same-age peers. In response to this perceived threat, the kid may showroom more signs of physiological reactivity than other children, due in function to a heightened awareness of bodily sensations (cerebral psychobiological and modeling theories). A sensitive or reactive kid may be more likely to use FSS in signaling caregivers to assistance cope with distress (attachment theory). The quality of the parent–child human relationship may shape the way a sensitive, broken-hearted, or emotionally reactive child copes with stress, which in turn, may affect the class of FSS (pathway/progression). For example, having a harmonious and open parent–kid relationship may minimize impairment associated with FSS, insofar as the responsive parent may be helpful in alleviating the child's fears or in providing alternative and more adaptive coping strategies (risk/protective factor), which could so lower the kid's physiological reactivity and somatic distress. On the other hand, a sensitive and/or anxious child may feel rejected by the parent or may be more than decumbent to go upset and emotionally overaroused in a parent–child relationship ridden past hostility and conflict. In such an acrimonious climate, or where emotional repression as opposed to emotional expression is accustomed, the child may begin to internalize feelings and express FSS more oft, equally it is the just outlet for an broken-hearted kid'due south feelings (psychodynamic theory). A child's expression of FSS might be exacerbated by vicarious learning through ascertainment of parental illness behaviors (modeling theory), reinforced by special attending or other rewards (social learning theory), or maintained past family conflict (family systems theory). This effect might be stronger in socially disadvantaged homes with few fiscal and social resources, which could potentially increase stress and conflict in the abode (contextualism).
A child's coping manner may depend on his or her temperament, developmental level, or severity of pain, which in plough, may bear upon the course of FSS. For example, younger children who plough to their caregiver for help in coping with stressful situations and adolescents who apply cognitive restructuring or distraction to cope with their emotional arousal may minimize impairment associated with FSS. However, a child who has learned and practiced poor coping strategies in the domicile is likely to acquit these strategies into school and other social environments. The repeated experience of declining to relate to peers or to cope with academic stress may perpetuate an already anxious kid's self-isolation and internalizing, further exacerbating FSS and the intensity of the pain.
If a child lacks social competence (hazard/protective cistron), and has a high level of anxiety (gamble factor), the child may eventually feel helpless and hopeless, which increases the risk for a later mood disorder and connected FSS (pathway/progression). With the onset of puberty, girls may be at greater run a risk for comorbid internalizing and continued FSS than boys, perhaps due to hormones, interpersonal relationship stressors, or socialization practices. Boys with FSS may follow a much different trajectory than girls, where early on concentration difficulties and beliefs bug prevent boys from learning appropriate coping styles. Social and academic failure and low cocky-esteem may lead to acrimony and acting out. If taken to an extreme, these boys may evidence an externalizing disorder, and to a lesser extent, FSS in later childhood and boyhood.
Directions for Future Research and Clinical Implications
The aim of this review was to demonstrate the utility of a developmental perspective in the study of FSS. Contrary to dualism grounded in the traditional medical model, this review has not established that FSS is a psychological disorder in children and adolescents. Rather, this commodity has demonstrated that comorbid psychiatric outcomes such as feet and low, while common, do not occur in all children presenting with FSS. The findings of this article underscore the demand to take a broader arroyo to the conceptualization of FSS in children and adolescents.
This broader arroyo, based on the tenets of developmental psychopathology, necessitates viewing FSS as a beliefs or set of behaviors occurring on a continuum, as opposed to equally a discrete entity or diagnosis. In order to further our understanding of the etiology, class, and effect of FSS in babyhood and adolescence, longitudinal studies must supercede cross-sectional designs that use large and varied age ranges. More epidemiological studies are needed to understand the extent to which FSS are normative at certain developmental periods, which would help identify when FSS are "clinically significant" and warrant treatment.
The developmental perspective on FSS presented in this article has delineated various ways FSS can emerge and develop through the interaction of child and contextual factors. Both adolescence and female person gender accept been shown to be risk factors for the development of FSS. In order to constitute that puberty directly contributes to an increase of FSS in girls (and mayhap a decrease in boys), prospective designs following prepubescent children through the stages of puberty are needed. Including hormone sampling also would strengthen findings pertaining to the function of puberty and hormones, aid analyze the developmental progression of FSS, and illuminate similarities/differences between child and developed forms of FSS. Moreover, investigations involving age, gender, and pubertal status are needed in lite of the fact that puberty is a biological marker for depressive disorders. That is, there are dramatic increases in the rates of depression, bipolar disorder, and completed suicide around puberty (Ryan & Dahl, 1993), particularly in girls (Zahn-Waxler, Klimes-Dougan, & Slattery, 2000). Thus, it is important to continue researching the effects of puberty on FSS, especially in girls.
A priority of future research should be to establish baseline levels of physiological functioning of children with FSS and to compare these levels to those of good for you children and children with other disorders. By doing so, enquiry could confirm a hyperresponsive reaction to stress in children and adolescents with FSS. Further, it is recommended that inquiry continue to investigate patterns of physiological reactivity of multiple concurrent systems (e.g., 50-HPA and ANS) in relation to FSS, in order to identify specific measures of physiological reactivity that discriminate children with FSS, internalizing issues, organic affliction, and comorbid problems (Bauer et al., 2002; Boyce et al., 2001). While this review briefly covered puberty and physiological reactivity to stressors, work investigating other biological substrates of FSS is offset to appear in the literature. For example, at that place is an emerging literature on genetic markers of risk for irritable bowel syndrome and functional dyspepsia (Yeo et al., 2004; Camilleri et al., 2002).
Despite the limited data, zipper theory and physiological studies indicate the importance of parent–child human relationship and the caregiving environs on the development of FSS (Bowlby, 1973; Gunnar & Donzella, 2002). Unresponsive and/or rejecting parenting has been a gamble factor for a number of kid outcomes, especially in the presence of other adventure factors (Campbell, Pierce, Moore, & Marakovitz, 1996; Shaw et al., 1998), and hereafter studies of FSS should comprise observational measures of parenting styles, particularly in young children. In addition, time to come research could test the cumulative family arduousness hypothesis, which asserts that the number rather than type of run a risk factors increase the risk for maladaptive outcomes in children, to farther our understanding of how family adversity, such as marital conflict and socioeconomic condition (SES), influence the development of FSS. High family adversity, poor parenting, and low SES may collaborate in such a way to exponentially increase stress and feet in children's lives, for which they lack the skills to cope effectively.
The intent of the present developmental perspective is to encourage new directions of research to inform treatment interventions for children and adolescents with FSS. A limitation with the electric current review is that information technology assumes there is more than commonality than dissimilarities amongst children who nowadays with FSS across unlike pediatric specialty clinics, such as gastroenterology, neurology, and rheumatology (Wessely, Nimnuan, & Sharpe, 1999). However, as more is learned almost FSS, the model may need to be modified to fit sure pediatric specialties. The benefit of studying FSS together is that information technology can brand treatments more generalized and diagnostic schemes may exist more descriptive and more valuable to clinicians (Wessely et al., 1999).
A number of issues were not discussed in this review but are important to consider when exploring mechanisms of FSS. Beginning, the potential differences in risk associated with dissimilar types of FSS (e.g., pain vs. nonpain symptoms) were not investigated due to the paucity of literature in this expanse. In that location are instances where the literature is much more adult for one particular symptom, such as abdominal pain, and it is unclear whether this literature can, in fact, be generalized to other FSS or multiple FSS. Second, functional impairment or disability may vary past symptom type or may differ co-ordinate to the number of FSS present. For instance, within the pediatric chronic pain literature, the prevalence of restrictions in daily activities, health intendance utilization, and medication utilise accept been institute to vary by pain location in children and adolescents (Roth-Isigkeit, Thyen, Stöven, Schwarzenberger, & Schmucker, 2005). Perquin et al. (2000) constitute that half of children who report having chronic hurting have multiple pain (e.g., headache and back pain). This is of importance as multiple pain complaints, compared to single complaints, have been associated with higher levels of pain intensity and pain-related inability (Perquin et al., 2000).
3rd, the electric current article integrated findings from studies that used customs and tertiary intendance populations. It is of import to note that tertiary care populations, compared to community populations, are likely to have severer symptoms of longer duration and to accept developed secondary consequences of FSS. That is, the association between FSS and emotional symptomatology may be more pronounced in a 3rd intendance sample compared to a community sample, though, further research is needed to understand this causal link. Withal, this article has demonstrated that the trends for risk and protective factors can exist seen in both customs and tertiary care samples. Finally, potential differences between parent and child report of FSS must as well exist considered. Garber, VanSlyke, and Walker (1998) institute that mothers of children with recurrent abdominal pain reported more somatic symptoms than their children. In addition, mothers with higher levels of distress reported more child symptoms than did their children.
An obstacle that faces many medical providers is that they must provide an explanation for FSS to children and their families. Utilizing a developmental perspective of FSS tin can lessen the burden on pediatricians and medical specialists, particularly when psychological and psychiatric treatments are integrated into medical intendance as opposed to regarding them every bit dissever (Sharpe & Carson, 2001). Medical providers are encouraged to openly discuss psychosocial and environmental factors with families every bit this may provide multiple avenues for finding effective treatment interventions for children's FSS. The goal of conceptualizing FSS through a developmental lens is to decrease children's and adolescents' medical health care utilization and provide a quicker resolution of symptoms, distress, and disability with the utilize of an interdisciplinary treatment (see Bursch, Walco, & Zeltzer, 1998, for a treatment approach to pediatric chronic pain).
As a final note, developmental psychopathologists articulate that, even though the underlying liability to psychopathology may be dimensional, categorical distinctions are often necessary in the existent world (Rutter & Sroufe, 2000). For instance, clinicians have to determine whether or not to prescribe a psychotropic medication or to admit their patient to the hospital. Across that, insurance may not embrace rendered services for patients if they practice not come across diagnostic criteria. This being said, it is imperative that the diagnostic criteria for somatoform disorders outlined in the DSM-IV, particularly somatization disorder and pain disorder with psychological origin, exist revised to be appropriate for children and adolescents. Nosotros must keep to await at FSS as both a continuous and discrete miracle, in order to determine whether the severity of the complaints designates a particular pathway, which could help prescribe treatment to these children and adolescents.
Acknowledgments
The author would similar to gratefully acknowledge Dr Lynn Southward. Walker for her helpful comments on an earlier draft of this article. This piece of work was supported in office by an NIMH training grant (T32-MH18921) and NICHD Grant P30HD15052.
Conflicts of interest: None declared.
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