Anxiety Disorders: Massachusetts General Hospital

Pollack MH. · Center for Anxiety and Traumatic Stress Disorders, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. · J Clin Psychiatry. · Pubmed #19371505 No free full text.

Abstract: Generalized anxiety disorder (GAD) has a lifetime prevalence in the US population of about 5.7%. Typically, GAD begins in early adulthood and tends to have a chronic and persistent course. The disorder frequently presents comorbidly with other conditions, and about 90% of patients with GAD have at least 1 comorbid lifetime psychiatric disorder. Patients with GAD tend to be high users of medical services; the disorder is associated with significant physical as well as psychological symptomatology and impacts health, family relationships, and employment. Pharmacologic and psychosocial treatments are available for GAD. Different side effect profiles, speed of onset of action, and discontinuation requirements of individual drugs need to be taken into account when selecting treatment. Treatment selection should include consideration of comorbidity, psychological function, social impairment, and refractoriness, as well as the need for ongoing intervention for many individuals. Innovative treatments, including anticonvulsants, atypical antipsychotics, and others, as well as treatment targeting concomitant insomnia, may help improve outcomes for affected individuals.

Simon NM. · Massachusetts General Hospital, Center for Anxiety and Traumatic Stress Disorders, Department of Psychiatry, Simches 2200, 185 Cambridge St, Boston, MA 02114, USA. · J Clin Psychiatry. · Pubmed #19371501 No free full text.

Abstract: Generalized anxiety disorder (GAD) has a high rate of comorbidity with other psychiatric disorders, including major depressive disorder (MDD), bipolar disorder, other anxiety disorders, and substance use disorders. The similarities between GAD and MDD have led some to suggest that GAD should be reclassified as a mood disorder. The concurrence of GAD with another disorder heightens a patient's risk for impairment, disability, and suicidality. Clinical trials for GAD and disorders that are most likely to occur with GAD have generally not taken comorbidity into account, and there is a paucity of data guiding how comorbidity should inform treatment selection. Research into the biology and psychopathology underlying the high rate of comorbidity of GAD and into efficacious interventions for GAD with comorbidity is needed.

Joshi G, Wilens T. · Pervasive Developmental Disorders Program, Clinical and Research Programs in Pediatric Psychopharmacology, Massachusetts General Hospital, Harvard Medical School, 32 Fruit Street, Boston, MA 02114, USA. · Child Adolesc Psychiatr Clin N Am. · Pubmed #19264265 No free full text.

Abstract: The growing literature shows the pervasiveness and importance of comorbidity in youth with bipolar disorder (BPD). For instance, up to 90% of youth with BPD have been described to manifest comorbidity with attention-deficit hyperactivity disorder. Multiple anxiety, substance use, and disruptive behavior disorders are the other most commonly reported comorbidities with BPD. Moreover, important recent data highlight the importance of obsessive-compulsive and pervasive developmental illness in the context of BPD. Data suggest that not only special developmental relationships are operant in the context of comorbidity but also that the presence of comorbid disorders with BPD results in a more severe clinical condition. Moreover, the presence of comorbidity has therapeutic implications for the treatment response for both BPD and the associated comorbid disorder. Future longitudinal studies to address the relationship and the impact of comorbid disorders on course and therapeutic response over time are required in youth with BPD.

Chosak A, Marques L, Greenberg JL, Jenike E, Dougherty DD, Wilhelm S. · OCD & Related Disorders Program, Simches Research Building, Massachusetts General Hospital, 185 Cambridge Street, Boston MA 02114, USA. · Expert Rev Neurother. · Pubmed #18671665 No free full text.

Abstract: Obsessive-compulsive disorder and body dysmorphic disorder have many similarities in clinical presentation. Obsessive-compulsive disorder has historically been considered an anxiety disorder, whereas body dysmorphic disorder has been grouped among the somatoform disorders. Researchers in these areas are currently debating whether the similarities warrant the inclusion of body dysmorphic disorder within a proposed category of obsessive-compulsive spectrum disorders. This article describes the association between obsessive-compulsive disorder and body dysmorphic disorder as evidenced by the emerging literature, and presents theoretical and clinical implications of this association.

Smoller JW, Gardner-Schuster E, Covino J. · Harvard Medical School, Psychiatric Genetics Program in Mood and Anxiety Disorders, Massachusetts General Hospital, Boston, MA, USA. · Am J Med Genet C Semin Med Genet. · Pubmed #18412108 No free full text.

Abstract: Panic disorder and phobic anxiety disorders are common disorders that are often chronic and disabling. Genetic epidemiologic studies have documented that these disorders are familial and moderately heritable. Linkage studies have implicated several chromosomal regions that may harbor susceptibility genes; however, candidate gene association studies have not established a role for any specific loci to date. Increasing evidence from family and genetic studies suggests that genes underlying these disorders overlap and transcend diagnostic boundaries. Heritable forms of anxious temperament, anxiety-related personality traits and neuroimaging assays of fear circuitry may represent intermediate phenotypes that predispose to panic and phobic disorders. The identification of specific susceptibility variants will likely require much larger sample sizes and the integration of insights from genetic analyses of animal models and intermediate phenotypes.

Pauls DL. · Harvard Medical School, Psychiatric and Neurodevelopmental Genetics Unit in Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA 02114, USA. · Am J Med Genet C Semin Med Genet. · Pubmed #18412099 No free full text.

Abstract: Obsessive compulsive disorder (OCD) is a common psychiatric disorder that can have disabling effects on both adults and children. Twin, family, segregation, and linkage studies have demonstrated that OCD is familial, that the familiality is due in part to genetic factors and there are regions of the genome which very likely harbor susceptibility loci for OCD. Over 60 candidate gene studies have been conducted. Most studies have focused on genes in the serotonergic and dopaminergic pathways. Unfortunately, none have achieved genome-wide significance and with the exception of the glutamate transporter gene, none have been reliably replicated. Future research will requite much larger samples and the collaboration of researchers to be able to identify susceptibility loci for OCD.

Schmahmann JD, Weilburg JB, Sherman JC. · Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA. · Cerebellum. · Pubmed #17786822 No free full text.

Abstract: A central aspect of the cerebellar cognitive affective syndrome is the dysregulation of affect that occurs when lesions involve the 'limbic cerebellum' (vermis and fastigial nucleus). In this case series we describe neuropsychiatric disturbances in adults and children with congenital lesions including cerebellar agenesis, dysplasia, and hypoplasia, and acquired conditions including cerebellar stroke, tumor, cerebellitis, trauma, and neurodegenerative disorders. The behaviors that we witnessed and that were described by patients and families included distractibility and hyperactivity, impulsiveness, disinhibition, anxiety, ritualistic and stereotypical behaviors, illogical thought and lack of empathy, as well as aggression and irritability. Ruminative and obsessive behaviors, dysphoria and depression, tactile defensiveness and sensory overload, apathy, childlike behavior, and inability to appreciate social boundaries and assign ulterior motives were also evident. We grouped these disparate neurobehavioral profiles into five major domains, characterized broadly as disorders of attentional control, emotional control, and social skill set as well as autism spectrum disorders, and psychosis spectrum disorders. Drawing on our dysmetria of thought hypothesis, we conceptualized the symptom complexes within each putative domain as reflecting either exaggeration (overshoot, hypermetria) or diminution (hypotonia, or hypometria) of responses to the internal or external environment. Some patients fluctuated between these two states. We consider the implications of these neurobehavioral observations for the care of patients with ataxia, discuss the broader role of the cerebellum in the pathogenesis of these neuropsychiatric symptoms, and revisit the possibility of using cerebellar stimulation to treat psychiatric disorders by enhancing cerebellar modulation of cognition and emotion.

Milad MR, Rauch SL. · Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA. · Ann N Y Acad Sci. · Pubmed #17698998 No free full text.

Abstract: Advances in neuroimaging techniques over the past two decades have allowed scientists to investigate the neurocircuitry of anxiety disorders. Such research has implicated the orbitofrontal cortex (OFC). Characterizing the role of OFC in anxiety disorders, however, is principally complicated by two factors-differences in underlying pathophysiology across the anxiety disorders and heterogeneity in function across different OFC sub-territories. Contemporary neurocircuitry models of anxiety disorders have primarily focused on amygdalo-cortical interactions. The amygdala is implicated in generating fear responses, whereas cortical regions, specifically the medial OFC (mOFC) and the ventromedial prefrontal cortex (vmPFC), are implicated in fear extinction. In contrast to mOFC, anterolateral OFC (lOFC) has been associated with negative affects and obsessions and thus dysfunctional lOFC may underlie different aspects of certain anxiety disorders. Herein, we aim to review the above-mentioned theories and provide a heuristic model for conceptualizing the respective roles of mOFC and lOFC in the pathophysiology and treatment of anxiety disorders. We will also review the role of the OFC in fear extinction and the implications of this role to the pathophysiology of anxiety disorders.

Huffman JC, Stern TA. · Department of Psychiatry, Massachusetts General Hospital, Boston, MA 02114, USA. · Dialogues Clin Neurosci. · Pubmed #17506224 No free full text.

Abstract: The use of cardiovascular medications can have a variety of neuropsychiatric consequences. Many cardiovascular agents cause higher rates of fatigue and sedation than placebo, and case reports of medication-induced mood syndromes, psychosis, and cognitive disturbances exist for many cardiovascular drugs. Depression has been associated with P3-blockers, methyldopa, and reserpine, but more recent syntheses of the data have suggested that these associations are much weaker than originally believed. Though low cholesterol levels have been associated with depression and suicide, lipid-lowering agents have not been associated with these adverse effects. Finally, cardiovascular medications may have beneficial neuropsychiatric consequences; for example, the use of clonidine in patients with attention deficit-hyperactivity disorder, the use of prazosin for patients with post-traumatic stress disorder; and the use of propranolol for performance anxiety and akathisia.

Huffman JC, Smith FA, Quinn DK, Fricchione GL. · Harvard Medical School and Department of Psychiatry, Massachusetts General Hospital, Boston, MA 02114, USA. · Harv Rev Psychiatry. · Pubmed #17162654 No free full text.

Abstract: Depression, anxiety, and other psychological variables following acute myocardial infarction (MI) have been the subject of intense study over the last two decades. Through selective literature review and editorial commentary, we address six vital, unanswered questions concerning these psychological variables and their impact on coronary outcome. The picture that emerges is complex. Despite all that has been learned about the nature, consequences, and management of post-MI depression and related disorders, there remain many open issues. First, the prevalence, phenomenology, medical impact, and method of diagnosis of post-MI depression and other psychiatric syndromes remain unclear. In addition, at least four pathophysiologic mechanisms have been proposed to explain the link between depression and cardiac disease, but evidence of causation remains elusive. There have been increasingly well-designed treatment studies of post-MI depression, but the optimal agents and timing of treatment have yet to be defined. Finally, few recent studies of post-MI anxiety have been conducted. To make further progress, large, multicenter trials that use optimized screening tools, obtain data at several time points, consider multiple psychosocial variables, and correct carefully for medical/cardiac severity are required.

Spencer TJ. · Pediatric Psychopharmacology Unit, Psychiatry Service, Massachusetts General Hospital, and the Department of Psychiatry, Harvard Medical School, Boston, Mass. 02114, USA. · J Clin Psychiatry. · Pubmed #16961427 No free full text.

Abstract: In recent years, evidence has been accumulating regarding high levels of comorbidity between attention-deficit/hyperactivity disorder (ADHD) and a number of disorders, including mood and anxiety disorders and conduct disorder. Thus, ADHD is most likely a group of conditions, rather than a single homogeneous clinical entity, with potentially different etiologic and modifying risk factors and different outcomes. Follow-up studies of children with ADHD indicate that subgroups of subjects with ADHD and comorbid disorders have a poorer outcome as evidenced by significantly greater social, emotional, and psychological difficulties. Investigation of these issues should help to clarify the etiology, course, and outcome of ADHD.

Romanoff MR. · Massachusetts General Hospital, Boston, USA. · J Am Acad Nurse Pract. · Pubmed #16958771 No free full text.

Abstract: PURPOSE: To educate primary care providers on the physical effects of posttraumatic stress disorder (PTSD), explain why military veterans are at great risk, and describe how to identify PTSD in primary care clients. DATA SOURCES: Current scientific and psychiatric literature on PTSD. CONCLUSIONS: PTSD is prevalent in the military community because of the frequency and type of trauma seen in the combat zone. With the ongoing military deployments, assessment for the presence of PTSD is increasingly important for comprehensive and high-quality primary care. Clients with trauma histories, such as veterans, are at increased risk for physical disorders such as heart disease and psychological disorders such as anxiety, depression, and PTSD. IMPLICATIONS FOR PRACTICE: Primary care clinicians, including those outside the military health system, are essential in identifying trauma histories and directing clients to appropriate care.

Ceranoglu TA, Stern TA. · Massachusetts General Hospital, Child and Adolescent Psychiatry Service, Charlestown, MA 02129, USA. · J Intensive Care Med. · Pubmed #16946447 No free full text.

Abstract: Adults with a myriad of medical and surgical conditions are at risk for pain, delirium, and disfigurement. Needless to say, these critical illnesses are profoundly stressful for patients and their caregivers. However, physicians rarely consider the reactions of children to their parents' illnesses. The article presents the case of a 15-year-old girl who developed posttraumatic stress disorder following her mother's severe burn and complicated course in a critical care unit; the case is used to discuss strategies for the detection of psychological vulnerability and for the implementation of care. By learning more about the children of adult patients, by screening for interpersonal dysfunction, and by maximizing support systems, clinicians can improve function and minimize distress.

Rauch SL, Shin LM, Phelps EA. · Psychiatric Neuroscience Division, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, USA. · Biol Psychiatry. · Pubmed #16919525 No free full text.

Abstract: The prevailing neurocircuitry models of anxiety disorders have been amygdalocentric in form. The bases for such models have progressed from theoretical considerations, extrapolated from research in animals, to in vivo human imaging data. For example, one current model of posttraumatic stress disorder (PTSD) has been highly influenced by knowledge from rodent fear conditioning research. Given the phenomenological parallels between fear conditioning and the pathogenesis of PTSD, we have proposed that PTSD is characterized by exaggerated amygdala responses (subserving exaggerated acquisition of fear associations and expression of fear responses) and deficient frontal cortical function (mediating deficits in extinction and the capacity to suppress attention/response to trauma-related stimuli), as well as deficient hippocampal function (mediating deficits in appreciation of safe contexts and explicit learning/memory). Neuroimaging studies have yielded convergent findings in support of this model. However, to date, neuroimaging investigations of PTSD have not principally employed conditioning and extinction paradigms per se. The recent development of such imaging probes now sets the stage for directly testing hypotheses regarding the neural substrates of fear conditioning and extinction abnormalities in PTSD.

Hoge EA, Austin ED, Pollack MH. · Department of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. · Depress Anxiety. · Pubmed #16892420 No free full text.

Abstract: The growing recognition and occurrence of traumatic exposure in the general population has given increased salience to the need to understand the concept of resilience. More than just the "flip side" of a risk factor, the notion of resilience encompasses psychological and biological characteristics, intrinsic to an individual, that might be modifiable and that confer protection against the development of psychopathology in the face of stress. In this review, we provide some perspective on the concept of "resilience" by examining early use of the term in research on "children at risk" and discuss the relationship between risk and resilience factors. We then review psychological and biological factors that may confer resilience to the development of posttraumatic stress disorder (PTSD) following trauma, examine how resilience has been assessed and measured, and discuss issues to be addressed in furthering our understanding of this critical concept going forward.

Dahlin C. · Palliative Care Service, Massachusetts General Hospital, Boston, MA 02115, USA. · Home Healthc Nurse. · Pubmed #16680051 No free full text.

This publication has no abstract.

Geller DA. · Pediatric Obsessive Compulsive Disorder Program, Division of Pediatric Psychopharmacology, Massachusetts General Hospital, YAW 6A, Fruit Street, Boston, MA 02114, USA. · Psychiatr Clin North Am. · Pubmed #16650713 No free full text.

Abstract: The available literature indicates that OCD affecting children and adolescents is highly prevalent. Pediatric-onset OCD seems to share important similarities with the adult disorder but also shows important differences.For example, the clinical phenotype of OCD is remarkably consistent at all ages with some allowances for developmental expression. Pediatric patients frequently demonstrate poor insight into the nature of their obsessions, which in association with their limited verbal expression may make the diagnosis more difficult. Obsessions involving fear of harm and separation, compulsions without obsessions, and rituals involving family members are more common in younger patients. Treatment response,including serotonergic specificity and the need for robust dosing, is another feature shared by early- and adult-onset OCD. Imporfant differences across the life span can also be identified. Perhaps the clearest difference pertains to age of onset. Age-at-onset data have shown a bimodal distribution of age of onset of OCD, with one peak in preadolescent childhood and another peak in adulthood. Another distinction between child and adult OCD is gender representation. Whereas adult studies report equal gender representation or a slight female preponderance, pediatric clinical samples are clearly male predominant. Patterns of psychiatric comorbidity in pediatric OCD show high rates of tic and mood and anxiety disorders, similar to the patterns in adults, but also show a distinct association with disruptive behavior disorders (ADHD and oppositional defiant disorder) and other specific and pervasive developmental disorders. Family studies indicate that the disorder is highly familial and that a childhood onset of the disorder seems to be associated with a markedly increased risk for familial transmission of OCD, tic disorders, and ADHD.Both scientifically and clinically, the recognition of developmentally specific OCD phenotypes may be valuable. For example, research efforts aimed at identifying OCD-associated genes are likely to be more successful if developmentally homogeneous samples are studied instead of combining data from children, adolescents, and adults, as has been common in OCD studies.Clinical management is also informed by an appreciation of the unique cor-relates of OCD affecting youth, especially comorbidity with chronic tic dis-orders and ADHD and their impact on treatment.The so-called "spectrum disorders" related to OCD are less prominent in children and adolescents than in adults. Although sharing some features with typical OCD, these symptoms are less clearly ego-dystonic and less anxiety producing, frequently provide a measure of gratification, and are less responsive in general to SSRIs. Often cognitive antecedents to these behaviors are less well developed than in more typical OCD, and behavioral interventions are the mainstay of treatment but with more variable success.

Fava M. · Depression Clinical and Research Program, Massachusetts General Hospital, Boston, MA 02114, USA. · J Psychopharmacol. · Pubmed #16644769 No free full text.

Abstract: Despite the efficacy of currently available antidepressant treatment, residual symptoms are common among individuals treated for major depressive disorder and are associated with an increased risk of relapse and poor psychosocial functioning. However, distinguishing treatment-emergent side effects from residual symptoms can be challenging for clinicians. Anxiety, sleep disturbance, somnolence/fatigue, apathy and cognitive dysfunction are among the more frequent residual symptoms. Approaches to the management of residual symptoms include addressing treatment-emergent side effects and co-morbid conditions, optimizing antidepressant dosing and using augmentation therapy. Clinicians are often guided in their decisions by anecdotal impressions. Studies assessing the evaluation and treatment of residual symptoms and side effects will contribute importantly to the optimal acute and long-term management of depression.

Finn CT, Smoller JW. · Harvard Medical School, Department of Psychiatry and Psychiatric Genetics Program in Mood and Anxiety Disorders, Massachusetts General Hospital, Boston, MA, USA. · Harv Rev Psychiatry. · Pubmed #16603476 No free full text.

Abstract: While psychiatrists may commonly discuss family history in clinical practice, there has been little systematic research documenting the role and effectiveness of genetic counseling for psychiatric disorders. In the coming years, the expected identification of susceptibility genes for psychiatric disorders may bring new opportunities and expectations from patients and families for the clinical translation of research findings in psychiatric genetics. We review evidence for possible increasing demand for genetic counseling, particularly if specific genes related to psychiatric disorders are identified. We then explore both the potential role of genetic counseling for psychiatric disorders and the issues involved in conveying genetic information in the clinical setting. Further research regarding the effectiveness of counseling interventions, as well as additional efforts directed at genetics education for clinicians, will be needed if emerging advances in genetic research are to be incorporated into clinical practice.

Evans KC, Dougherty DD, Pollack MH, Rauch SL. · Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. · Ann Clin Psychiatry. · Pubmed #16517451 No free full text.

Abstract: BACKGROUND: Functional neuroimaging has begun to show promise as a clinical tool in the prediction of treatment response in mood and anxiety disorders. Given the variance in patient responses to psychiatric treatments, the use of such predictive tools could be tremendously valuable, especially in situations where treatments carry substantial risks or costs. METHODS: A literature search was conducted in December 2004 to identify published neuroimaging treatment prediction papers. "Neuroimaging," "treatment," and "depression or anxiety" were used as keywords. Studies of treatment prediction were complemented by studies of treatment effects to provide context. RESULTS: Fifteen original published papers were identified as investigations of treatment prediction in mood and anxiety disorders. These studies have predominantly been conducted in patients with major depression (MDD) and obsessive-compulsive disorder (OCD). We review this literature and provide a discussion of design considerations in psychiatric neuroimaging studies of treatment response prediction. CONCLUSIONS: The neuroimaging literature pertaining to treatment response prediction is largely limited to studies of MDD and OCD. While these initial reports are preliminary, the findings reviewed suggest that treatment outcome may be predicted by patterns of pre-treatment brain activity in psychiatric patients. However, the actual clinical utility of such tests remains to be shown.

Deckersbach T, Dougherty DD, Rauch SL. · Department of Psychiatry, Massachusetts General Hospital/Harvard Medical School, Charlestown, Massachusetts 02129, USA. · J Neuroimaging. · Pubmed #16483270 No free full text.

Abstract: Neuroimaging research has emerged as a valuable tool in shaping our understanding of the pathophysiology of psychiatric disorders. We review functional neuroimaging findings pertaining to mood disorders (major depression, bipolar disorders) as well as selected anxiety disorders (posttraumatic stress disorder [PTSD] and obsessive-compulsive disorder [OCD]).

Milad MR, Rauch SL, Pitman RK, Quirk GJ. · Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Bldg 149 13th St., Charlestown, 02129, USA. · Biol Psychol. · Pubmed #16476517 No free full text.

Abstract: Fear extinction is the decrease in conditioned fear responses that normally occurs when a conditioned stimulus (CS) is repeatedly presented in the absence of the aversive unconditioned stimulus (US). Extinction does not erase the initial CS-US association, but is thought to form a new memory. After extinction training, extinction memory competes with conditioning memory for control of fear expression. Deficits in fear extinction are thought to contribute to post-traumatic stress disorder (PTSD). Herein, we review studies performed in rats showing that the medial prefrontal cortex plays a critical role in the retention and expression of extinction memory. We also review human studies indicating that prefrontal areas homologous to those critical for extinction in rats are structurally and functionally deficient in patients with PTSD. We then discuss how findings from rat studies may allow us to: (1) develop new fear extinction paradigms in humans, (2) make specific predictions as to the location of extinction-related areas in humans, and (3) improve current extinction-based behavioral therapies for anxiety disorders.

Pollack MH. · Center for Anxiety and Traumatic Stress Related Disorders, Massachusetts General Hospital, Harvard Medical School, Boston, Mass 02114, USA. · J Clin Psychiatry. · Pubmed #16336033 No free full text.

Abstract: Anxiety and depressive disorders often occur as comorbid illnesses and share many common symptoms. Risk factors for these disorders most likely include interactions of environmental and genetic factors. The presence of comorbid anxiety and depression adversely affects clinical and treatment outcomes. Selective serotonin reuptake inhibitors are usually considered first-line treatment for patients with these disorders, although alternative antidepressants or additional therapies are often necessary. Studies suggest that benzodiazepines, anticonvulsants, and atypical antipsychotics may be effective as augmentation therapy to optimize outcome, with buspirone and beta-blockers useful in some patients as well. Cognitive-behavioral therapy is also an effective therapeutic alternative for affected patients.

Roffman JL, Marci CD, Glick DM, Dougherty DD, Rauch SL. · Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. · Psychol Med. · Pubmed #16164763 No free full text.

Abstract: BACKGROUND: Studies measuring the effects of psychotherapy on brain function are under-represented relative to analogous studies of medications, possibly reflecting historical biases. However, psychological constructs relevant to several modalities of psychotherapy have demonstrable neurobiological correlates, as indicated by functional neuroimaging studies in healthy subjects. This review examines initial attempts to measure directly the effects of psychotherapy on brain function in patients with depression or anxiety disorders. METHOD: Fourteen published, peer-reviewed functional neuroimaging investigations of psychotherapy were identified through a MEDLINE search and critically reviewed. Studies were compared for consistency of findings both within specific diagnostic categories, and between specific modalities of psychotherapy. Results were also compared to predicted neural models of psychotherapeutic interventions. RESULTS: Behavioral therapy for anxiety disorders was consistently associated with attenuation of brain-imaging abnormalities in regions linked to the pathophysiology of anxiety, and with activation in regions related to positive reappraisal of anxiogenic stimuli. In studies of major depressive disorder, cognitive behavioral therapy and interpersonal therapy were associated with markedly similar changes in cortical-subcortical circuitry, but in unexpected directions. For any given psychiatric disorder, there was only partial overlap between the brain-imaging changes associated with pharmacotherapy and those associated with psychotherapy. CONCLUSIONS: Despite methodological limitations, initial neuroimaging studies have revealed convergent and mechanistically sensible effects of psychotherapy on brain function across a range of psychiatric disorders. Further research in this area may take advantage of emerging neuroimaging techniques to explore a broader range of psychotherapies, with the ultimate goal of improving clinical decision-making and treatment.

Biederman J. · Department of Pediatric Psychopharmacology Research, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. · Biol Psychiatry. · Pubmed #15949990 No free full text.

Abstract: Attention-deficit/hyperactivity disorder (ADHD) is a multifactorial and clinically heterogeneous disorder that is associated with tremendous financial burden, stress to families, and adverse academic and vocational outcomes. Attention-deficit/hyperactivity disorder is highly prevalent in children worldwide, and the prevalence of this disorder in adults is increasingly recognized. Studies of adults with a diagnosis of childhood-onset ADHD indicate that clinical correlates--demographic, psychosocial, psychiatric, and cognitive features--mirror findings among children with ADHD. Predictors of persistence of ADHD include family history of the disorder, psychiatric comorbidity, and psychosocial adversity. Family studies of ADHD have consistently supported its strong familial nature. Psychiatric disorders comorbid with childhood ADHD include oppositional defiant and conduct disorders, whereas mood and anxiety disorders are comorbid with ADHD in both children and adults. Pregnancy and delivery complications, maternal smoking during pregnancy, and adverse family environment variables are considered important risk factors for ADHD. The etiology of ADHD has not been clearly identified, although evidence supports neurobiologic and genetic origins. Structural and functional imaging studies suggest that dysfunction in the fronto-subcortical pathways, as well as imbalances in the dopaminergic and noradrenergic systems, contribute to the pathophysiology of ADHD. Medication with dopaminergic and noradrenergic activity seems to reduce ADHD symptoms by blocking dopamine and norepinephrine reuptake. Such alterations in dopaminergic and noradrenergic function are apparently necessary for the clinical efficacy of pharmacologic treatments of ADHD.