Anxiety Disorders: Emory University

Heim C, Nemeroff CB. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA. · CNS Spectr. · Pubmed #19169190 links to  free full text

Abstract: Exposure to a traumatic event is required for the diagnosis of posttraumatic stress disorder (PTSD). The symptoms of PTSD are believed to reflect stress-induced changes in neurobiological systems and/or an inadequate adaptation of neurobiological systems to exposure to severe stressors. More recently, there have been attempts to link the identified neurobiological changes to the specific features that constitute PTSD, such as altered mechanisms of learning and extinction, sensitization to stress, and arousal. Furthermore, there have been efforts to understand whether certain neurobiological changes in PTSD reflect preexisting vulnerability factors rather than consequences of trauma exposure or correlates of PTSD. Genetic variability, sex differences, and developmental exposures to stress influence neurobiological systems and moderate PTSD risk. On the basis of these findings, important hypotheses for developing novel strategies to identify subjects at risk, promote resilience, and devise targets for the prevention or treatment of PTSD can be derived.

Heim C, Newport DJ, Mletzko T, Miller AH, Nemeroff CB. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 101 Woodruff Circle, WMRB, Suite 4311, Atlanta, GA 30322, USA. · Psychoneuroendocrinology. · Pubmed #18602762 No free full text.

Abstract: Childhood trauma is a potent risk factor for developing depression in adulthood, particularly in response to additional stress. We here summarize results from a series of clinical studies suggesting that childhood trauma in humans is associated with sensitization of the neuroendocrine stress response, glucocorticoid resistance, increased central corticotropin-releasing factor (CRF) activity, immune activation, and reduced hippocampal volume, closely paralleling several of the neuroendocrine features of depression. Neuroendocrine changes secondary to early-life stress likely reflect risk to develop depression in response to stress, potentially due to failure of a connected neural circuitry implicated in emotional, neuroendocrine and autonomic control to compensate in response to challenge. However, not all of depression is related to childhood trauma and our results suggest the existence of biologically distinguishable subtypes of depression as a function of childhood trauma that are also responsive to differential treatment. Other risk factors, such as female gender and genetic dispositions, interfere with components of the stress response and further increase vulnerability for depression. Similar associations apply to a spectrum of other psychiatric and medical disorders that frequently coincide with depression and are aggravated by stress. Taken together, this line of evidence demonstrates that psychoneuroendocrine research may ultimately promote optimized clinical care and help prevent the adverse outcomes of childhood trauma.

Bremner JD, Elzinga B, Schmahl C, Vermetten E. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA. · Prog Brain Res. · Pubmed #18037014 No free full text.

Abstract: Posttraumatic stress disorder (PTSD) is associated with long-term changes in neurobiology. Brain areas involved in the stress response include the medial prefrontal cortex, hippocampus, and amygdala. Neurohormonal systems that act on the brain areas to modulate PTSD symptoms and memory include glucocorticoids and norepinephrine. Dysfunction of these brain areas is responsible for the symptoms of PTSD. Brain imaging studies show that PTSD patients have increased amygdala reactivity during fear acquisition. Other studies show smaller hippocampal volume. A failure of medial prefrontal/anterior cingulate activation with re-experiencing of the trauma is hypothesized to represent a neural correlate of the failure of extinction seen in PTSD. The brain has the capacity for plasticity in the aftermath of traumatic stress. Antidepressant treatments and changes in environment can reverse the effects of stress on hippocampal neurogenesis, and humans with PTSD showed increased hippocampal volume with both paroxetine and phenytoin.

Bremner JD. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1256 Briarcliff Road, Room 308e, Mailstop 1256/001/AT, Atlanta GA 30306, USA. · Neuroimaging Clin N Am. · Pubmed #17983968 No free full text.

Abstract: Traumatic stress has a broad range of effects on the brain. Brain areas implicated in the stress response include the amygdala, the hippocampus, and the prefrontal cortex. Studies in patients who have posttraumatic stress disorder (PTSD) and other psychiatric disorders related to stress have replicated findings in animal studies by finding alterations in these brain areas. Brain regions implicated in PTSD also play an important role in memory function, highlighting the important interplay between memory and the traumatic stress response. Abnormalities in these brain areas are hypothesized to underlie symptoms of PTSD and other stress-related psychiatric disorders.

Ressler KJ, Mayberg HS. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 954 Gatewood Drive, Atlanta, Georgia 30329, USA. · Nat Neurosci. · Pubmed #17726478 links to  free full text

Abstract: Recent decades have witnessed tremendous advances in the neuroscience of emotion, learning and memory, and in animal models for understanding depression and anxiety. This review focuses on new rationally designed psychiatric treatments derived from preclinical human and animal studies. Nonpharmacological treatments that affect disrupted emotion circuits include vagal nerve stimulation, rapid transcranial magnetic stimulation and deep brain stimulation, all borrowed from neurological interventions that attempt to target known pathological foci. Other approaches include drugs that are given in relation to specific learning events to enhance or disrupt endogenous emotional learning processes. Imaging data suggest that common regions of brain activation are targeted with pharmacological and somatic treatments as well as with the emotional learning in psychotherapy. Although many of these approaches are experimental, the rapidly developing understanding of emotional circuit regulation is likely to provide exciting and powerful future treatments for debilitating mood and anxiety disorders.

Bremner JD. · Emory University, Atlanta, GA 30306, USA. · Expert Rev Neurother. · Pubmed #17425494 No free full text.

Abstract: Traumatic stress has a broad range of effects on brain function. Brain areas implicated in the stress response include the amygdala, hippocampus, and prefrontal cortex. Brain studies in patients with post-traumatic stress disorder replicated findings in animal studies by finding alterations in these brain areas. Brain areas implicated in post-traumatic stress disorder play an important role in the stress response as well as memory, highlighting the important interplay between memory and the traumatic stress response. Future studies are required to assess the relationship between recovery from traumatic stress and changes in brain function.

Chhatwal JP, Ressler KJ. · Department of Psychiatry, Emory University School of Medicine, Atlanta, GA, USA. · CNS Spectr. · Pubmed #17329982 links to  free full text

Abstract: The last decade has witnessed remarkable progress in the understanding of the mammalian cannabinoid system, from the cloning of the endogenous cannabinoid receptor to the discovery of new pharmacologic compounds acting on this receptor. Current and planned studies in humans include compounds with effects ranging from direct antagonists to inhibitors of reuptake and breakdown. This progress has been accompanied by a much greater understanding of the role of the cannabinoid system in modulating the neural circuitry that mediates anxiety and fear responses. This review focuses on the neural circuitry and pharmacology of the cannabinoid system as it relates to the acquisition, expression, and extinction of conditioned fear as a model of human anxiety. Preclinical studies suggest that these may provide important emerging targets for new treatments of anxiety disorders.

Bremner JD. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Ga 30306, USA. · Dialogues Clin Neurosci. · Pubmed #17290802 No free full text.

Abstract: Brain areas implicated in the stress response include the amygdala, hippocampus, and prefrontal cortex. Traumatic stress can be associated with lasting changes in these brain areas. Traumatic stress is associated with increased cortisol and norepinephrine responses to subsequent stressors. Antidepressants have effects on the hippocampus that counteract the effects of stress. Findings from animal studies have been extended to patients with post-traumatic stress disorder (PTSD) showing smaller hippocampal and anterior cingulate volumes, increased amygdala function, and decreased medial prefrontal/anterior cingulate function. In addition, patients with PTSD show increased cortisol and norepinephrine responses to stress. Treatments that are efficacious for PTSD show a promotion of neurogenesis in animal studies, as well as promotion of memory and increased hippocampal volume in PTSD.

Myers KM, Davis M. · Center for Behavioral Neuroscience, Emory University, Atlanta, GA, USA. · Mol Psychiatry. · Pubmed #17160066 No free full text.

Abstract: Excessive fear and anxiety are hallmarks of a variety of disabling anxiety disorders that affect millions of people throughout the world. Hence, a greater understanding of the brain mechanisms involved in the inhibition of fear and anxiety is attracting increasing interest in the research community. In the laboratory, fear inhibition most often is studied through a procedure in which a previously fear conditioned organism is exposed to a fear-eliciting cue in the absence of any aversive event. This procedure results in a decline in conditioned fear responses that is attributed to a process called fear extinction. Extensive empirical work by behavioral psychologists has revealed basic behavioral characteristics of extinction, and theoretical accounts have emphasized extinction as a form of inhibitory learning as opposed to an erasure of acquired fear. Guided by this work, neuroscientists have begun to dissect the neural mechanisms involved, including the regions in which extinction-related plasticity occurs and the cellular and molecular processes that are engaged. The present paper will cover behavioral, theoretical and neurobiological work, and will conclude with a discussion of clinical implications.

Davis M, Barad M, Otto M, Southwick S. · Department of Psychiatry, Emory University, Atlanta, GA, USA. · J Trauma Stress. · Pubmed #17075906 No free full text.

Abstract: Given the ever-increasing sources of trauma both nationally and globally, it is imperative to develop new and better treatments for anxiety disorders such as posttraumatic stress disorder (PTSD). This review is a collection of presentations that seek to do just that, either by using pharmacotherapy to try to prevent or erase the formation of traumatic fear memories, or to enhance exposure-based cognitive-behavioral therapy using pharmacological agents that have been effective in enhanced extinction of fear in rodents.

Bremner JD. · Departments of Psychiatry and Radiology, Emory University School of Medicine, Atlanta VAMC, Decatur GA 30306, USA. · CNS Neurol Disord Drug Targets. · Pubmed #17073653 No free full text.

Abstract: Studies in animals showed that stress is associated with changes in hippocampal function and structure, an effect mediated through decreased neurogenesis, increased glucocorticoids, and/or decreased brain derived neurotrophic factor. Antidepressants and some anticonvulsants block the effects of stress and/or promote neurogenesis in animal studies. Patients with posttraumatic stress disorder (PTSD) have been shown to have smaller hippocampal volume on magnetic resonance imaging and deficits in hippocampal-based memory. Symptom activation is associated with decreased anterior cingulate and medial prefrontal function, which is proposed as the neural correlate of a failure of extinction seen in these patients. Treatment with antidepressants and phenytoin reverse hippocampal volume reduction and memory deficits in PTSD patients, suggesting that these agents may promote neurogenesis in humans.

Francati V, Vermetten E, Bremner JD. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, USA. · Depress Anxiety. · Pubmed #16960853 No free full text.

Abstract: Posttraumatic stress disorder (PTSD) is an anxiety disorder associated with changes in neural circuitry involving frontal and limbic systems. Altered metabolism in these brain structures after a traumatic event is correlated to PTSD. Developments in the field of neuroimaging have allowed researchers to look at the structural and functional properties of the brain in PTSD. Despite the relative novelty of functional imaging and its application to the field of PTSD, numerous publications have brought to light several of the circuits implied in this disorder. This article summarizes the findings with regard to PTSD in the functional imaging techniques of single-photon emission computed tomography (SPECT), positron emission tomography (PET), and functional magnetic resonance imaging (fMRI). Furthermore, we discuss strengths and weaknesses of the various techniques and studies. Finally, we explore the future potential of functional neuroimaging studies in PTSD.

Davis M, Ressler K, Rothbaum BO, Richardson R. · Emory University School of Medicine, Department of Psychiatry, Atlanta, Georgia 30329, USA. · Biol Psychiatry. · Pubmed #16919524 No free full text.

Abstract: Administration of benzodiazepines or serotonin reuptake inhibitors in combination with behavior therapy for the treatment of many anxiety disorders has generally lead to only modest gains. In this article we suggest that pharmacotherapy aimed not at treating the symptoms of anxiety but instead aimed at improving the learning that takes place in exposure therapy might actually improve the effectiveness of exposure therapy. This idea was based on animal work showing that the partial N-methyl-D-aspartate (NMDA) agonist D-cycloserine (DCS) facilitated extinction of fear when given either before or shortly after exposure to fearful cues, reduced return of fear that is normally seen when extinction training is followed by stress, and led to generalized extinction, where DCS given in combination with exposure to one fearful cue led to extinction to another cue previously paired with the same aversive event. These finding suggested that DCS might facilitate exposure-based psychotherapy, which was verified in a small clinical study showing that DCS facilitated exposure therapy for fear of heights in a well-controlled virtual reality environment.

Toufexis DJ, Myers KM, Davis M. · Emory University, Department of Psychiatry, Yerkes National Primate Center, 954 Gatewood Drive NE, Atlanta, GA 30329, USA. · Horm Behav. · Pubmed #16904674 No free full text.

Abstract: Disorders of anxiety and fear dysregulation are highly prevalent. These disorders affect women approximately 2 times more than they affect men, occur predominately during a woman's reproductive years, and are especially prevalent at times of hormonal flux. This implies that gender differences and sex steroids play a key role in the regulation of anxiety and fear. However, the underlying mechanism by which these factors regulate emotional states in either sex is still largely unknown. This review discusses animal studies describing sex-differences in and gonadal steroid effects on affect and emotional learning. The effects of gonadal hormones on the modulation of anxiety, with particular emphasis on progesterone's ability to reduce the responsiveness of female rats to corticotropin releasing factor and the sex-specific effect of testosterone in the reduction of anxiety in male rats, is discussed. In addition, gonadal hormone and gender modulation of emotional learning is considered and preliminary data are presented showing that estrogen (E2) disrupts fear learning in female rats, probably through the antagonistic effect of ERalpha and ERbeta activation.

Bremner JD. · Department of Psychiatry and Behavioral Sciences, Emory Center for Positron Emission Tomography, Emory University School of Medicine, SS No. 539-64-8946, Suite 306E, 1256 Briarcliff Rd, Atlanta, GA 30307, USA. · Ann N Y Acad Sci. · Pubmed #16891564 No free full text.

Abstract: Preclinical studies show that stress is associated with changes in structure of the hippocampus, a brain area that plays a critical role in memory, inhibition of neurogenesis, and memory deficits. Studies in animals showed that both serotonin reuptake inhibitors (SSRIs) and the epilepsy medication phenytoin (dilantin) block the effects of stress on the hippocampus. Imaging studies in posttraumatic stress disorder (PTSD) have found smaller volume of the hippocampus as measured with magnetic resonance imaging (MRI) in patients with PTSD related to both combat and childhood abuse. These patients were also found to have deficits in memory on neuropsychological testing. Functional imaging studies using positron emission tomography (PET) found decreased hippocampal activation with memory tasks. In an initial study, we found that a year of treatment with paroxetine led to a 5% increase in hippocampal volume and a 35% increase in memory function. A second study showed that phenytoin was efficacious for symptoms of PTSD and led to a significant 6% increase in both right hippocampal and right whole brain volume, with no significant change in memory. These studies suggest that medications may counteract the effects of stress on the brain in patients with PTSD.

Davis M, Myers KM, Chhatwal J, Ressler KJ. · Emory University School of Medicine, Center for Behavioral Neuroscience, and the Yerkes National Primate Center, Atlanta, Georgia 30329, USA. · NeuroRx. · Pubmed #16490415 No free full text.

Abstract: SUMMARY: A great deal is now known about the mechanisms of conditioned fear acquisition and expression. More recently, the mechanisms of inhibition of conditioned fear have become the subject of intensive study. The major model system for the study of fear inhibition in the laboratory is extinction, in which a previously fear conditioned organism is exposed repeatedly to the fear-eliciting cue in the absence of any aversive event and the fear conditioned response declines. It is well established that extinction is a form of new learning as opposed to forgetting or "unlearning" of conditioned fear, and it is hypothesized that extinction develops when sensory pathways conveying sensory information to the amygdala come to engage GABAergic interneurons through forms of experience-dependent plasticity such as long-term potentiation. Several laboratories currently are investigating methods of facilitating fear extinction in animals with the hope that such treatments might ultimately prove to be useful in facilitating exposure-based therapy for anxiety disorders in clinical populations. This review discusses the advances that have been made in this field and presents the findings of the first major clinical study to examine the therapeutic utility of a drug that facilitates extinction in animals. It is concluded that extinction is an excellent model system for the study of fear inhibition and an indispensable tool for the screening of putative pharmacotherapies for clinical use.

Gillespie CF, Ressler KJ. · Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA 30329, USA. · CNS Spectr. · Pubmed #16400246 links to  free full text

Abstract: Anxiety disorders are a common focus of clinical concern and certain forms of anxiety may be conceptualized as disorders of emotional learning. Behavior therapies effective in the treatment of anxiety are modeled on extinction training as a means of reducing pathological anxiety. The present understanding of human anxiety has been informed by preclinical research using rodent models to study the acquisition and extinction of fear. Glutamate appears to have a central role in both of these processes. The authors review this literature and discuss novel applications of D-cycloserine, a partial N-methyl-D-aspartate agonist, for the treatment of anxiety.

Nemeroff CB. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA. · J Clin Psychiatry. · Pubmed #16336032 No free full text.

Abstract: Treatment options for bipolar depression and treatment-resistant unipolar depression include augmentation of antidepressant therapy with a nonantidepressant drug, including atypical antipsychotics. Risperidone is effective in combination with fluvoxamine, paroxetine, or citalopram in treatment-resistant unipolar depression, with reported remission rates of 61% to 76%. Olanzapine in combination with fluoxetine is safe and effective in patients with bipolar depression and those with fluoxetine-resistant unipolar depression. Ziprasidone and aripiprazole augmentation of various selective serotonin reuptake inhibitors has been reported to be effective in refractory unipolar depression in open-label studies. Data on use of quetiapine or clozapine as augmentation therapy for depression or anxiety are not yet available. Further double-blind, placebo-controlled studies of augmentation of antidepressants with atypical antipsychotics in refractory depression and anxiety are justified based on the available literature.

Nemeroff CB, Bremner JD, Foa EB, Mayberg HS, North CS, Stein MB. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, Atlanta, GA 30322-4990, USA. · J Psychiatr Res. · Pubmed #16242154 No free full text.

Abstract: This article reviews the state-of-the-art research in posttraumatic stress disorder (PTSD) from several perspectives: (1) Sex differences: PTSD is more frequent among women, who tend to have different types of precipitating traumas and higher rates of comorbid panic disorder and agoraphobia than do men. (2) Risk and resilience: The presence of Group C symptoms after exposure to a disaster or act of terrorism may predict the development of PTSD as well as comorbid diagnoses. (3) Impact of trauma in early life: Persistent increases in CRF concentration are associated with early life trauma and PTSD, and may be reversed with paroxetine treatment. (4) Imaging studies: Intriguing findings in treated and untreated depressed patients may serve as a paradigm of failed brain adaptation to chronic emotional stress and anxiety disorders. (5) Neural circuits and memory: Hippocampal volume appears to be selectively decreased and hippocampal function impaired among PTSD patients. (6) Cognitive behavioral approaches: Prolonged exposure therapy, a readily disseminated treatment modality, is effective in modifying the negative cognitions that are frequent among PTSD patients. In the future, it would be useful to assess the validity of the PTSD construct, elucidate genetic and experiential contributing factors (and their complex interrelationships), clarify the mechanisms of action for different treatments used in PTSD, discover ways to predict which treatments (or treatment combinations) will be successful for a given individual, develop an operational definition of remission in PTSD, and explore ways to disseminate effective evidence-based treatments for this condition.

Bremner JD. · Emory University School of Medicine, Atlanta, GA, USA. · J Trauma Dissociation. · Pubmed #16150669 No free full text.

Abstract: The events of 9/11 and the widening impact of psychological trauma today have raised a higher level of awareness about the potentially deleterious effects of psychological trauma on the individual. One area of interest after 9/11 was the early trauma response and the most effective way to deal with the window of time immediately after traumatization in order to prevent long term psychopathology. Understanding the neurobiology of the acute trauma response may be useful in designing prevention and treatment strategies. Studies in animals and humans have shown that biological stress response systems, including norepinephrine and cortisol, are affected in both the acute and chronic stages of the trauma response. Brain areas involved in memory, including the hippocampus, amygdala, and prefrontal cortex, may be areas of intervention to ameliorate the early trauma response. Due to the difficulty of performing research in this time period, most research to date has been in patients with chronic disorders such as chronic posttraumatic stress disorder (PTSD). Only a few treatment studies have been performed in the early trauma period, and more research in this area is needed.

Nemeroff CB, Vale WW. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA. · J Clin Psychiatry. · Pubmed #16124836 No free full text.

Abstract: The underlying causes of most mood and anxiety disorders remain unknown. There is a strong heritable component to psychiatric illnesses that, when coupled with environmental influences, results in increased vulnerability. Intensive research efforts have been expended to better characterize the genetic underpinnings of mental illness. However, most psychiatric disorders, including mood and anxiety disorders, are polygenetic in nature rather than determined by traditional autosomal-dominant Mendelian genetics. Recent technological advances, including the completion of the human genome inventory, chromosome mapping, high throughput DNA sequencing, and others, offer the promise of someday identifying the genetic basis of mental illnesses. In parallel, tremendous inroads have been made into understanding the neurobiological basis of mood and anxiety disorders and the influence of life events on risk and resilience. Evidence from preclinical, epidemiologic, and clinical studies has converged to convincingly demonstrate that stressful or traumatic events occurring in early life significantly increase the risk for depression and other psychiatric illnesses in adulthood. Neural circuits containing corticotropin-releasing factor (CRF) have been identified as an important mediator of the stress response. Early-life adversity, such as physical or sexual abuse during childhood, results in long-lasting changes in the CRF-mediated stress response and a greatly increased risk of depression in genetically predisposed persons. Identification and cloning of CRF receptors and characterization of their role in the stress response have enabled a better understanding of maladaptive responses to early-life adversity. In addition, studies of the CRF system have suggested molecular targets for new drug development, biological risk factors, and predictors of treatment response.

Hamann S. · Department of Psychology, Emory University, Atlanta, Georgia 30322, USA. · Neuroscientist. · Pubmed #16061516 No free full text.

Abstract: The amygdala is a structure in the temporal lobe that has long been known to play a key role in emotional responses and emotional memory in both humans and nonhuman animals. Growing evidence from recent neuroimaging studies points to a new, expanded role for the amygdala as a critical structure that mediates sex differences in emotional memory and sexual responses. This review highlights current findings from studies of sex differences in human amygdala response during emotion-related activities, such as formation of emotional memories and sexual behavior, and considers how these findings contribute to the understanding of behavioral differences between men and women. Clinical implications for the understanding of sex differences in the prevalence of affective and anxiety disorders are discussed, and future directions in the study of the amygdala's role in human sex differences are outlined.

Bremner JD. · Department of Psychiatry and Behavioral Sciences and Radiology, Emory Center for Positron Emission Tomography, Emory University, 1256 Briarcliff Rd, Atlanta, GA 30306, USA. · Expert Rev Neurother. · Pubmed #15853569 No free full text.

Abstract: Animal studies of the effects of stress on the brain have been used as a model for anxiety disorders. There is increasing evidence that brain areas involved in the stress response, including prefrontal cortex, hippocampus and amygdala, play a role in the symptoms of anxiety. In the past few years, brain imaging studies have been critical to advancing the understanding of the neural circuitry of anxiety disorders. Although some anxiety disorders may fit in with animal models of stress, both conceptually and in terms of imaging findings (e.g., post-traumatic stress and panic disorder), other anxiety disorders (e.g., obsessive-compulsive disorder) may require a more specific model to understand the neurobiology completely. This article reviews animal models for anxiety disorders, current brain imaging findings and outlines future directions for research in this area.

Ninan PT, Dunlop BW. · Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA. · J Clin Psychiatry. · Pubmed #15842181 No free full text.

Abstract: Panic disorder entered the psychiatric nomenclature a quarter-century ago, and an explosion of studies followed. Defining the core phenomenology of panic disorder can be advanced by an understanding of its pathophysiology and exploration of its etiology. The lessons learned can guide the delivery of treatments to enhance the likelihood of achieving remission and the discovery of novel treatments for panic disorder.

Lilienfeld SO. · Department of Psychology, Emory University, Room 206, 532 Kilgo Circle, Atlanta, Georgia 30322, USA. · Pediatrics. · Pubmed #15741383 links to  free full text

Abstract: Although numerous scientifically supported treatments are available for childhood psychiatric disorders, many of the most popular interventions for these conditions are based on weak or nonexistent data. This article offers basic guidelines for distinguishing scientifically supported from unsupported treatments for 3 important childhood psychiatric disorders: autistic disorder, attention-deficit/hyperactivity disorder, and conduct disorder. A key challenge for the future will be to place the treatment of childhood psychiatric disorders on firmer scientific footing.