Therapists and their clients benefit from understanding how anxiety is generated in the brain, how it can become panic or unbounded worry, and ultimately how the brain re-establishes the neurochemical balance that is basic to a state of well-being.

Drawing on her experience diagnosing and treating anxiety in people with ASD at the treatment center she founded in Sydney, Australia, Dr. Chalfant provides clear, understandable explanations of the different types of anxiety disorders, how they affect people across the autism spectrum, and what interventions can help. The book teaches parents:
-to know how and why their child is prone to anxiety
-to understand their role in their child's anxious behavior
-to recognize and respond to anxious behavior appropriately

Case studies and research findings help to illustrate the author's points and clarify the causes and symptoms of anxious behavior.

Managing Anxiety explains a range of different types of strategies that can help manage and treat anxiety in school, home, and clinical settings and takes into consideration the different roles people play in a child's or adult's life: parent, sibling, teacher, etc. Readers learn about ways to modify behavior and/or the environment to indirectly reduce anxiety, as well as interventions, such as medication or psychotherapy, which deal with symptoms directly. The discussion of more formal interventions--psychotherapy, Cognitive Behavior Therapy (CBT), and medication--show how these methods can target specific anxieties. Because anxiety is generally more common in parents and siblings of a child with ASD, the author also offers ways they too can reduce their symptoms.

Author: Anne M. Chalfant, Psy.D.
Paperback: 275 pages
Company: Woodbine House (2011-08-05)
ISBN: 1606130048
List Price: $19.95
Amazon Price: $10.75
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Childhood Anxiety Disorders represent one of the most common psychological disorders found among the general population. They can be serious, distressful, and functionally impairing, so much so that there has been an explosion of interest in their treatment, primarily from pharmacological and cognitive-behavioral perspectives.
Addressing these perspectives is the Second Edition of Child Anxiety Disorders. Beidel and Alfano pay close attention to new pharmacological and psychological interventions as well as multi-center trials that compare single and combined treatment modalities. Additionally, they include new case studies, sections on stability of childhood fears and the longitudinal course of anxiety disorders, and a new chapter on sleep and anxiety disorders. Written on the cusp of newly published information and studies, Child Anxiety Disorders is relevant, informative, and indispensible.

Treatment Resistant Anxiety Disorders: Resolving Impasses to Symptom Remission brings together leading cognitive behavioral therapists from major theoretical orientations to provide clinicians with a greatly needed source of information, skills, and strategies from a wide range of CBT approaches.

It describes how to combine empirically-based findings, broad based and disorder specific theoretical models, and individualized case conceptualization to formulate and apply specific strategies for varied aspects of resistance during treatment of anxiety disorders.

A comprehensive and accessible book on anxiety for clients and therapists alike.

Anxiety disorders are the most common and frequently misdiagnosed and undertreated of all mental health conditions. Dealing with Anxiety and Related Disorders: Understanding, Coping, and Prevention explains in accessible language the myths, misunderstandings, and realities of anxiety disorders, including often misdiagnosed somatoform and dissociative disorders.

Psychologist Rudy Nydegger approaches anxiety and related disorders, including panic disorder, social phobia, obsessive-compulsive disorder, and PTSD, with the most up-to-date and professionally sound information available. The history of and theories about anxiety disorders are thoroughly discussed, as are the most recent ideas and findings. Readers are provided with comprehensive information on each disorder—its description, clinical symptoms, dynamics, and available treatments, including alternative and experimental approaches. Ways in which patients can get help and help themselves are discussed, as are steps family members and friends can take when they know a loved one is struggling with an anxiety disorder. Detailed case studies illustrate both the disorders and the options for treatment.

This landmark work is indispensable for anyone studying anxiety or seeking to deliver effective psychological and pharmacological treatments. David H. Barlow comprehensively examines the phenomena of anxiety and panic, their origins, and the roles that each plays in normal and pathological functioning. Chapters coauthored by Barlow with other leading experts then outline what is known about the classification, presentation, etiology, assessment, and treatment of each of the DSM-IV anxiety disorders. A definitive resource for researchers and clinicians, this is also an ideal text for graduate-level courses.

This book synthesizes the best of the new research related to anxiety disorders and how they are classified and diagnosed. Dr. Dean McKay and his co-editors have brought together leading authorities from multiple theoretical traditions to present the new directions and perspectives in the field of anxiety research.

The contributors also discuss why current classification systems are inadequate, and what revisions should be made. The book presents in-depth discussions of how anxiety disorders are understood and assessed, as well as potential new implications for DSM-V.

Key features: Covers the existing descriptive approach to the study of anxiety disorders, its adequacy in diagnosis, and its limitations Discusses the major theoretical and methodological approaches used to assess anxiety, such as fear circuitry, taxometric methods, actigraphy, neuroscience, and behavioral genetics Reviews diagnostic and classification controversies that center on specific anxiety disorders, such as obsessive-compulsive disorder, social anxiety, posttraumatic stress disorder, and worry

This book covers the full spectrum of theoretical and empirical approaches used in the study, diagnosis, and classification of anxiety problems. In short, this volume serves as the authoritative reference book on the conceptualization and diagnosis of anxiety disorders.

Hardcover: 552 pages
Company: Springer Publishing Company (2009-06-22)
ISBN: 0826132472
List Price: $80.00
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This new edition has been thoroughly updated with the latest anxiety research and medications, and also includes new therapeutic techniques that have been proven effective for the treatment of anxiety and anxiety-related conditions. Each worksheet in this book will help you learn the skills you need to manage your anxiety and start living more freely than you ever thought possible.

With this workbook, you'll learn a range of proven methods for overcoming anxiety:

A strategy-filled handbook to understand, manage, and conquer your own stress.

Anxiety disorders are the most common mental illness in the United States.

Afflicting 19.1 million American adults between the ages of 15 and 54 (or 13% of the population), anxiety disorders are so common today it is impossible to remain untouched by them, directly or indirectly.

While fear and anxiety can serve as tools for survival, uncontrolled they lead to serious health concerns. Despite these facts and the known risks, few feel the need to educate themselves about the various dangers caused by anxiety until a medical crisis forces them to take action.

Anxiety Disorders explains the medical conditions and jargon used by medical professionals to describe and treat the problems caused by anxiety. The book identifies the origins of, symptoms and treatments for: Panic attacks Obsessive-compulsive behavior Post-traumatic stress Phobias

Anxiety disorders are by definition terrifying and crippling, but they are treatable. Dr. J. Paul Caldwell provides comprehensive, accurate, reassuring and up-to-date information for patients, caregivers and families.

Vetted by an esteemed roundtable of medical experts, Anxiety Disorders offers practical and consumer-oriented health advice.

This landmark work is indispensable for anyone studying anxiety or seeking to deliver effective psychological and pharmacological treatments. David H. Barlow comprehensively examines the phenomena of anxiety and panic, their origins, and the roles that each plays in normal and pathological functioning. Chapters coauthored by Barlow with other leading experts then outline what is known about the classification, presentation, etiology, assessment, and treatment of each of the DSM-IV anxiety disorders. A definitive resource for researchers and clinicians, this is also an ideal text for graduate-level courses.

Anxiety disorders are the most common mental illness in the United States.

Afflicting 19.1 million American adults between the ages of 15 and 54 (or 13% of the population), anxiety disorders are so common today it is impossible to remain untouched by them, directly or indirectly.

While fear and anxiety can serve as tools for survival, uncontrolled they lead to serious health concerns. Despite these facts and the known risks, few feel the need to educate themselves about the various dangers caused by anxiety until a medical crisis forces them to take action.

Anxiety Disorders explains the medical conditions and jargon used by medical professionals to describe and treat the problems caused by anxiety. The book identifies the origins of, symptoms and treatments for: Panic attacks Obsessive-compulsive behavior Post-traumatic stress Phobias

Anxiety disorders are by definition terrifying and crippling, but they are treatable. Dr. J. Paul Caldwell provides comprehensive, accurate, reassuring and up-to-date information for patients, caregivers and families.

Vetted by an esteemed roundtable of medical experts, Anxiety Disorders offers practical and consumer-oriented health advice.

This new edition has been thoroughly updated with the latest anxiety research and medications, and also includes new therapeutic techniques that have been proven effective for the treatment of anxiety and anxiety-related conditions. Each worksheet in this book will help you learn the skills you need to manage your anxiety and start living more freely than you ever thought possible.

With this workbook, you'll learn a range of proven methods for overcoming anxiety:

Written by international experts, Worry and its Psychological Disorders offers an up-to-date and complete overview of worry in a single volume. Divided into four sections, the book explores the nature of worry, the assessment of worry, contemporary theories of chronic and pathological worry, and the most recently developed treatment methods. It includes in-depth reviews of new assessment instruments and covers treatment methods such as Cognitive Behavioural Therapy and Metacognitive Therapy. Useful case studies are also included.

This important volume provides an invaluable resource for clinical practitioners and researchers. It will also be of relevance to those studying clinical or abnormal psychology at advanced level.

Paperback: 428 pages
Company: Wiley (2006-04-24)
ISBN: 047001279X
List Price: $67.95
Amazon Price: $40.00
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Nearly a third of all people will suffer from severe or debilitating fears—phobias, panic attacks, obsessions, worries, and more—over the course of a lifetime. Now Dr. David Tolin—a renowned psychologist and scientist at the Institute of Living and Yale featured on such programs as The OCD Project, Hoarders, The Dr. Oz Show, and Oprah—offers help for nearly every type of anxiety disorder. Dr. Tolin explains what fear really is, why you should face—not avoid—your fear, and how to beat your fear using gradual exposure techniques. Practical action steps and exercises help you learn this unique approach to facing fear without crutches or other unhelpful things found in many other programs in order to achieve a life that is free of debilitating anxieties.Self-help guide that gives you the tools to take charge and overcome your fears Written by a leading authority on anxiety and based on the latest researchProvides a practical, step-by-step plan for beating many different kinds of fears—including social anxiety, posttraumatic stress disorder (PTSD), obsessive-compulsive disorder, panic disorder, and phobias

Face Your Fears will change the way you think about fear and what to do about it. This up-to-date, evidence-based, and user-friendly self-help guide to beating phobias and overcoming anxieties walks you step by step through the process of choosing courage and freedom over fear.

Author: David F. Tolin
Hardcover: 304 pages
Company: Wiley (2012-01-18)
ISBN: 1118016734
List Price: $25.95
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The time is ripe to integrate and evaluate the research on anxiety disorders that occur at this stage of life. This book describes the various ways in which perinatal anxiety is expressed in women, as well as approaches for assessment and treatment.

The first half of the book describes the five main types of perinatal anxiety

-- worry and generalized anxiety
-- obsessions and compulsions
-- panic attacks
-- social anxiety
-- childbirth-related fear and trauma

and presents a biopsychosocial model.

Chapters in this half discuss

-- the nature, prevalence, and effects of each anxiety disorder
-- comorbidity between perinatal anxiety and perinatal depression
-- risk factors for perinatal anxiety

The second half of the book covers the assessment and treatment of perinatal anxiety, including pharmacotherapy, cognitive behavioral therapy, interpersonal therapy, psychoeducation, and self-help resources.

All of the chapters draw extensively from the research literature, and engaging case studies bring the material to life throughout the book.

This volume will be a tremendous resource for clinical psychologists, counselors, obstetricians, nurses, social workers, psychiatrists, and others who work with pregnant and postpartum women, as well as researchers and graduate students in any of these fields.

Author: Amy Wenzel, Scott Stuart
Hardcover: 275 pages
Company: American Psychological Association (APA) (2010-11)
ISBN: 1433809001
List Price: $69.95
Amazon Price: $44.96
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In recent years, researchers and psychiatrists have come to know more about anxiety disorders, their causes and possible methods of treatment. In fact, the medical literature fairly overflows with data on these conditions. In this text, the author distills that knowledge into an easy to use reference. A variety of different diagnoses, classifications and treatments are explored, with a particular focus on generalized anxiety disorder (GAD). The text not only profiles GAD completely, but it also discusses GAD in relationship to other anxiety disorders, such as panic disorder and obsessive-compulsive disorder. Psychiatrists and pharmacologists can benefit from this resource, as can trainees.

By focusing on the cognitive-behavioral model and treatment options, Dugas and Robichaud present a detailed analysis of the etiology, assessment, and treatment of Generalized Anxiety Disorder (GAD).

Cognitive-Behavioral Treatment for Generalized Anxiety Disorder: From Science to Practice provides a review of the empirical support for the different models of GAD. It includes a detailed description of the assessment and step-by-step treatment of GAD (including many examples of therapist-client dialogue), data on treatment efficacy in individual and group therapy, and concludes with a description of maintenance and follow-up strategies.

The Companion Workbook includes:

This landmark work is indispensable for anyone studying anxiety or seeking to deliver effective psychological and pharmacological treatments. David H. Barlow comprehensively examines the phenomena of anxiety and panic, their origins, and the roles that each plays in normal and pathological functioning. Chapters coauthored by Barlow with other leading experts then outline what is known about the classification, presentation, etiology, assessment, and treatment of each of the DSM-IV anxiety disorders. A definitive resource for researchers and clinicians, this is also an ideal text for graduate-level courses.

With over 10% of all children meeting the criteria for an anxiety disorder, these disorders are among the most common psychiatric problems experienced by schoolage kids, and can significantly interfere with their family and peer relationships and their performance at school.

Therapists and their clients benefit from understanding how anxiety is generated in the brain, how it can become panic or unbounded worry, and ultimately how the brain re-establishes the neurochemical balance that is basic to a state of well-being.

Current estimates indicate that 20% of school-aged children, K-12, have one or more neurological conditions, and of these, most have multiple diagnoses. 

Challenging Kids, Challenged Teachers is an educator's go-to source for creating a supportive environment to successfully teach children with multiple neurological disorders including Tourette's Syndrome, OCD, ADHD, LD, Nonverbal Learning Disability, Pervasive Developmental Disorders, Asperger's Syndrome, Anxiety Disorders, Depression, Executive Dysfunction, Sensory Processing Disorder, Pediatric Autoimmune Neuropsychiatric Disorder Associated with Strep (PANDAS), Bipolar Disorder, "Storms" or "Rages", Oppositional Defiant Disorder, and Sleep Problems.  Parents, school psychologists, and social workers will also find this book essential reading.

The wealth of practical tools and strategies discussed in this book are founded on the authors' considerable experience treating children with neurological disorders in their private practices and conducting training workshops for teachers, as well as parenting their own children with multiple diagnoses.  Full of charts, graphs, lists, quotes, and vignettes, this well-organized resource makes it easy for busy teachers to find the information they need, including:

-Understanding neurological disorders and why they may overlap, the behaviors they cause, and sanity-saving premises about understanding these students

-Each disorder's characteristics, impacts on academics, behavior & social relationships, teacher/student-friendly strategies, other conditions to be on the lookout for

-Conditions commonly observed in students with neurological disorders such as handwriting & visual-motor integration issues, language deficits, and difficulties with written expression, math calculation, reading, and more

-Assistive technology, testing accommodations, homework issues, interventions to address challenging behaviors, school-based related services, positive school-home collaboration, and helping children with peer relationships

Challenging Kids, Challenged Teachers also includes a glossary and resources, and its appendix of screening tools, forms, and checklists are on the accompanying CD-ROM for easy reproduction.

J Mol Endocrinol. 2012 Feb 6;
Riester A, Spyroglou A, Neufeld-Cohen A, Chen A, Beuschlein F

Urocortin (Ucn) 1, 2, and 3 are members of the Corticotropin-Releasing Factor (CRF)-family that display varying affinities to the CRF receptor 1 (CRFR1) and 2 (CRFR2). Ucns represent important modulators of stress responses and are involved in the control of anxiety and related disorders. In addition to the central nervous system, Ucns and CRFRs are highly expressed in several tissues including the adrenal gland indicating the presence of Ucn-dependent regulatory mechanisms in these peripheral organ systems. Using knockout (KO) mouse models lacking single or multiple Ucn genes we examined the potential role of the three different Ucns on morphology and function of the adrenal gland. Adrenal morphology was investigated, organ size as well as cell size and number was quantified and growth kinetics were studied by PCNA staining and Ccnd1 expression analysis. Furthermore, mRNA-expression of enzymes involved in steroidogenesis and catecholamine synthesis was quantified by Real-Time PCR. Following this approach, Ucn2, Ucn1/Ucn2 dKO and Ucn1/Ucn2/Ucn3 tKO animals showed a significant cellular hypotrophy of the adrenal cortex and increase in Ccnd1 expression, whereas in all other genotypes, no changes were observable in comparison to age matched controls. For steroidogenesis, Ucn2/Ucn3 dKO animals displayed the most pronounced changes with significant increase of all investigated enzymes, providing indirect evidence for increased stress behavior. Taken together, these data suggest that mainly Ucn2 and Ucn3 could be involved in adrenal stress response regulation while Ucn2 additionally appears to play a role in morphology and growth of the adrenal gland.

Neurosci Lett. 2012 Jan 31;
Siopi E, Llufriu-Dabén G, Fanucchi F, Plotkine M, Marchand-Leroux C, Jafarian-Tehrani M

Comorbidity of cognitive and stress disorders is a common clinical sequel of traumatic brain injury (TBI) that is essentially determined by the site and severity of the insult, but also by the extent of the ensuing neuroinflammatory response. The present study sought to examine the late effects of closed-head TBI on memory function and anxiety in mice, in order to further examine the potential efficacy of an acute anti-inflammatory treatment with minocycline. The mouse model of closed-head injury by mechanical percussion was applied on anesthetized Swiss mice. The treatment protocol included three injections of minocycline (i.p.) at 5min (90mg/kg), 3h and 9h (45mg/kg) post-TBI. The Novel Object Recognition Test as well as the Elevated Plus Maze (EPM) and Elevated Zero Maze (EZM) tasks were employed to assess post-TBI memory and anxiety respectively. Our results revealed a recognition memory deficit that was significant up to at least 13 weeks post-TBI. However, neither EPM nor EZM revealed any alteration in post-TBI anxiety levels albeit some mild disinhibition. Most importantly, minocycline was able to attenuate the memory impairment in an effective and lasting manner, highlighting its therapeutic potential in TBI.

J Nucl Med. 2012 Feb 6;
Lohith TG, Zoghbi SS, Morse CL, Araneta MF, Barth VN, Goebl NA, Tauscher JT, Pike VW, Innis RB, Fujita M

Nociceptin/orphanin FQ peptide (NOP) receptor is a new class of opioid receptor that may play a pathophysiologic role in anxiety and drug abuse and is a potential therapeutic target in these disorders. We previously developed a high-affinity PET ligand, (11)C-NOP-1A, which yielded promising results in monkey brain. Here, we assessed the ability of (11)C-NOP-1A to quantify NOP receptors in human brain and estimated its radiation safety profile. METHODS: After intravenous injection of (11)C-NOP-1A, 7 healthy subjects underwent brain PET for 2 h and serial sampling of radial arterial blood to measure parent radioligand concentrations. Distribution volume (V(T); a measure of receptor density) was determined by compartmental (1- and 2-tissue) and noncompartmental (Logan analysis and Ichise's bilinear analysis [MA1]) methods. A separate group of 9 healthy subjects underwent whole-body PET to estimate whole-body radiation exposure (effective dose). RESULTS: After (11)C-NOP-1A injection, the peak concentration of radioactivity in brain was high (∼5-7 standardized uptake values), occurred early (∼10 min), and then washed out quickly. The unconstrained 2-tissue-compartment model gave excellent V(T) identifiability (∼1.1% SE) and fitted the data better than a 1-tissue-compartment model. Regional V(T) values (mL·cm(-3)) ranged from 10.1 in temporal cortex to 5.6 in cerebellum. V(T) was well identified in the initial 70 min of imaging and remained stable for the remaining 50 min, suggesting that brain radioactivity was most likely parent radioligand, as supported by the fact that all plasma radiometabolites of (11)C-NOP-1A were less lipophilic than the parent radioligand. Voxel-based MA1 V(T) values correlated well with results from the 2-tissue-compartment model, showing that parametric methods can be used to compare populations. Whole-body scans showed radioactivity in brain and in peripheral organs expressing NOP receptors, such as heart, pancreas, and spleen. (11)C-NOP-1A was significantly metabolized and excreted via the hepatobiliary route. Gallbladder had the highest radiation exposure (21 μSv/MBq), and the effective dose was 4.3 μSv/MBq. CONCLUSION: (11)C-NOP-1A is a promising radioligand that reliably quantifies NOP receptors in human brain. The effective dose in humans is low and similar to that of other (11)C-labeled radioligands, allowing multiple scans in 1 subject.

Pediatr Cardiol. 2012 Feb 8;
Koopman HM, Vrijmoet-Wiersma CM, Langius JN, van den Heuvel F, Clur SA, Blank CA, Blom NA, Ten Harkel AD

The objective of this multicenter study was to evaluate psychological functioning and disease-related quality of life (DRQoL) in pediatric patients with an implantable cardioverter defibrillator (ICD) in The Netherlands. Thirty patients were investigated; the mean age was 16.3 years, and the mean duration of implantation was 3.6 years. To assess psychological problems, three domains of the Symptom Checklist (SCL-90-R) were administered to the 25 patients >13 years old. DRQoL was assessed with a disease-specific pediatric questionnaire, the short-form 11-item Worries About (WA)ICDs Scale. Patients ≥13 years old scored significantly higher than the reference group on the domains of anxiety, depression, and sleeping problems of the SCL-90-R (T = 7.5, p 

J Affect Disord. 2012 Feb 4;
Polak AR, Witteveen AB, Reitsma JB, Olff M

BACKGROUND: Although posttraumatic stress disorder (PTSD) has been associated with disturbances in verbal memory, studies examining executive functioning in PTSD show mixed results. METHODS: A systematic review and meta-analysis were performed to compare executive functioning in patients with current PTSD and controls without any psychiatric disorder. Standard mean differences (SMD) in executive functioning scores were calculated using random-effects models. Covariates were added to examine whether differences exist between subgroups. RESULTS: Across 18 studies, 1080 subjects were included. In comparison with 431 exposed controls and 227 healthy controls, 422 people with PTSD showed significantly impaired executive functioning. Subgroup analyses revealed more pronounced differences between PTSD patients and exposed controls than healthy controls. Male gender, higher age, war trauma, and higher severity of co-morbid depressive symptoms were related to poorer executive functioning in PTSD patients compared to exposed controls. LIMITATIONS: Due to insufficient data and heterogeneity, not all subgroup differences or characteristics could be taken into account. CONCLUSIONS: Overall, PTSD patients were found to show impaired executive functioning. Future research should further elucidate the subgroup effects and focus on clinical implications with regard to daily functioning and treatment outcome.

Aust N Z J Psychiatry. 2012 Feb; 46(2): 118-31
Swinbourne J, Hunt C, Abbott M, Russell J, St Clare T, Touyz S

Objective: To investigate the prevalence of comorbid eating and anxiety disorders in women presenting for inpatient and outpatient treatment of an eating disorder and women presenting for outpatient treatment of an anxiety disorder. Methods: The prevalence of comorbidity was investigated from a sample of 152 women, which included 100 women presenting for treatment of an eating disorder and 52 women presenting for treatment of an anxiety disorder. Results: Of women presenting for treatment of an eating disorder, 65% also met criteria for at least one comorbid anxiety disorder; 69% of these reported the onset of the anxiety disorder to precede the onset of the eating disorder. Of the anxiety disorders diagnosed, social phobia was most frequently diagnosed (42%) followed by post-traumatic stress disorder (26%), generalised anxiety disorder (23%), obsessive-compulsive disorder (5%), panic/agoraphobia (3%) and specific phobia (2%). We also found that 13.5% of women presenting for anxiety treatment also met criteria for a comorbid eating disorder. Furthermore, 71% (n = 5) reported the onset of the anxiety disorder to precede the onset of the eating disorder. Discussion: The results of this study suggest that the prevalence of eating and anxiety disorder comorbidity is high. The present research should improve the clinical understanding of the comorbidity between eating disorders and anxiety disorders. In particular, it is anticipated that this research will have significant aetiological and therapeutic implications especially with regard to improving the clinical effectiveness of psychological treatments for eating disorders and highlighting the importance of screening for eating pathology in the clinical assessment of anxiety disorders.

Postgrad Med. 2012 Jan; 124(1): 152-65
McGuire JF, Lewin AB, Horng B, Murphy TK, Storch EA

Obsessive-compulsive disorder (OCD) is an anxiety disorder that affects between 1% to 2% of individuals and causes considerable impairment and disability. Although > 50% of individuals experience symptom onset in childhood, symptoms can continue to develop throughout adulthood. Accurate and timely assessment of clinical presentation is critical to limit impairment and improve prognosis. Presently, there are 2 empirically supported treatments available for OCD in children and adults, namely cognitive-behavioral therapy and pharmacotherapy with serotonin reuptake inhibitors. This article provides an introduction to the phenomenology, etiology, and clinical course of OCD. Assessment practices used to evaluate symptom severity are described, and evidence-based treatment options are reviewed, with appropriate distinctions drawn between children and adults. Finally, recommendations for assessment and treatment practices for OCD are explicated.

J Consult Clin Psychol. 2012 Feb 6;
Jarrett MA, Ollendick TH

Objective: The present study evaluated a 10-week psychosocial treatment designed specifically for children with attention-deficit/hyperactivity disorder (ADHD) and a comorbid anxiety disorder. Method: Using a nonconcurrent multiple baseline design, the authors treated 8 children ages 8-12 with ADHD, combined type, and at least 1 of 3 major anxiety disorders (separation anxiety disorder, generalized anxiety disorder, social phobia). The integrated treatment protocol involved parent management training for ADHD and family-based cognitive-behavioral therapy for anxiety. Pretreatment assessments included semistructured diagnostic interviews and other standardized measures to determine study eligibility. Children were randomized to 1 of 3 baseline control conditions (i.e., 2, 3, or 4 weeks) and subsequently treated in a university-based psychosocial treatment clinic. Weekly assessments of ADHD and anxiety disorder symptoms occurred throughout treatment and comprehensive assessments were obtained at pretreatment, 1-week posttreatment, and 6-months posttreatment. Results: Single-case results supported greater success in the treatment phase relative to the baseline phase for both ADHD and anxiety symptoms, and ADHD and anxiety symptoms appeared to change concurrently. Pre-post group analyses revealed significant and clinically meaningful improvements in ADHD and anxiety symptoms at 1-week posttreatment, but only anxiety symptoms moved into the subclinical range. At 6-months follow-up, treatment effects were maintained with new movement into the subclinical range for ADHD. Conclusions: The present study provides initial data on an integrated treatment protocol for ADHD and anxiety. Further replication and evaluation are needed. Implications of the findings are discussed. (PsycINFO Database Record (c) 2012 APA, all rights reserved).

Hum Psychopharmacol. 2012 Feb 7;
Muscatello MR, Spina E, Bandelow B, Baldwin DS

OBJECTIVE: Certain drugs used in the treatment of patients with anxiety disorders can interact with other psychotropic drugs and with pharmacological treatments for physical illnesses. There is a need for an updated comparative review of clinically relevant drug interactions in this area. DESIGN: Relevant literature on drug interactions with medications used in the treatment of anxiety disorders was identified through a search in MEDLINE and EMBASE. RESULTS: Drug interactions involving medications used to treat anxiety disorders may be pharmacokinetic, such as enzyme inhibition or induction in the cytochrome P450 system and transporter-mediated drug interactions, or pharmacodynamic, such as additive effects in causing drowsiness or additive effects at neurotransmitter receptors. Certain selective serotonin reuptake inhibitors (fluoxetine, fluvoxamine, and paroxetine) are particularly liable to be potentially involved in untoward pharmacokinetic interactions. CONCLUSIONS: The potential for drug interactions with medications used in anxiety disorders should be the cause of clinical concern, particularly in elderly individuals. However, the liability for harmful drug interactions may be anticipated, and the risk reduced. Although not all interactions are clinically relevant, careful monitoring of clinical response and possible interactions is essential. Copyright © 2012 John Wiley & Sons, Ltd.

Altern Ther Health Med. 2011 Nov; 17(6): 30-34
Cuthbert S, Rosner A

Abstract not Available.

Acta Neurol Taiwan. 2011 Dec; 20(4): 229-131
Kwan SY

Sleep disorder is common in all societies, so are in the patients with epilepsy (PWE). In the International Classification of Sleep Disorders (ICSD) published 2001, it is categorized into four main subsidiaries, which are (1) dyssomnias, (2) parasomnias, (3) sleep disorders associated with mental, neurologic, or other medical disorders and (4) proposed sleep disorders (1). No matter what the final diagnosis is, the results usually are poor quality of sleep and excessive daytime sleepiness. There are complex pathophysiologic mechanisms that underlie the interaction of sleep and epilepsy. These include (1) epilepsy seizure per se, (2) psychotic and psychiatric impact from epilepsy and (3) side effects from antiepileptic drugs (AEDs). In PWE, poor sleep quality causes sleep deprivation, which in turn exaggerates the attacks of seizures and falls into vicious cycles. Thus, it is worth paying attention to this field. Sleep is an extremely valuable physiological activating technique in epilepsy and is used routinely in the electroencephalographic (EEG) recording. The importance in the activation of epileptiform discharges (EDs) during sleep was first demonstrated by Gibbs and Gibbs in 1947 (2). It is proposed that non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep have contrasting effects on ictal and interictal EDs. EDs are likely to propagate during NREM sleep, including its synchronized EEG transients, such as K-complexes and sleep spindles. In contrast, REM sleep, with its asynchronous cellular discharge patterns and skeletal motor paralysis, is resistant to propagation of EDs and to clinical motor accompaniment. In addition, the preserved skeletal muscle tone in NREM permits seizure-related movement, whereas the lower motor neuron inhibition in REM prevents seizure-related movement (3). These can explain why clinical seizures and interictal EDs tend to occur in NREM rather than REM sleep. Seizures markedly activated by sleep including the seizures of frontal lobe origin and the generalized tonic seizures of Lenox-Gastaut syndrome. The epilepsies that having interictal EDs markedly activated during NREM sleep include benign rolandic epilepsy, temporal lobe epilepsy and infantile spasm. While the Landau-Kleffner syndrome and the atypical benign rolandic epilepsy possess the most striking increase of EDs with continuous spike-and-wave complexes during slow wave sleep (CSWS) or electrical status epilepticus during sleep (ESES) in EEG (Figure 1) and absence of normal sleep activities. On days after nocturnal seizures, patients had more severe excessive daytime sleepiness as compared with days after seizure free nights. As compared with seizurefree nights, nights with seizures were characterized by a reduction of REM and stage 3 sleep, prolonged REM latency and reduced sleep efficiency(4). These findings held true even on seizure-free nights. Nocturnal generalized seizures would decrease sleep time and REM sleep percentage, prolong REM latency, and fragment sleep(5). Multiple focal seizures in a night also significantly reduced REM sleep. In addition, not only seizures occurring at night but also those occurring during the day can affect sleep architecture, with proved significant reduction of REM sleep and prolongation REM latency in the following nights(6). Psychological or psychiatric problems, having a high incidence in PWE, may also play a role in disturbing normal sleep. It was reported that 40% of respondents with insomnia and 46.5% of respondents with hypersomnia had a psychiatric disorder. Anxiety disorders were found to be the most common mental disorders (7). Another study found that 93% of depressed inpatients complained of insomnia (8). In PWE, depression is the most frequent comorbid psychiatric disorder, with a prevalence of 10% to 20% among patients with controlled seizures and 20% to 60% among those with refractory epilepsy(9,10). The prevalence of anxiety disorder, panic disorder, obsessive-compulsive disorder and phobias is also high in PWE, with estimates of 3% to 66% (10). Psychosis consisting of visual or auditory illusions and hallucinations, paranoia, depersonalization, derealization, autoscopy, or delusion is reported in 0.6% to 7% of PWE in the community, and in 19% to 27% of hospital-derived populations (11). The overall frequency of psychosis among PWE is approximately 7% to 14%. Reports suggest that up to 69% of patients with temporal lobe epilepsy and 72% of patients with generalized epilepsy suffer from personality disorders (12). Even as benign as juvenile myoclonic epilepsy, 14% was reported to have personality disorders (13). Sleep disturbance in PWE may be secondary to AEDs they are treated with. Most old AEDs were reported to result in a normalization of the sleep architecture and sleep efficiency (14). Studies suggest that phenytoin (PHT), phenobarbital (PB), carbmazepine (CBZ) and clonazepam (CZP) can decrease sleep latency. PB and ethosuximide (ESM) can decrease awakening and arousal. CBZ and CZP can decrease wake time after sleep onset. PHT, PB and ESM can increased stage 1 and stage 2 sleep. CZP can increase stage 2 sleep. PHT, CBZ and valproic acid (VPA) can increased slow wave sleep. PB, VPA and CZP can decrease REM sleep. In newer AEDs, gabapentin (GBP) can decrease awakening and arousal but increased slow wave sleep (14). However, AEDs can also have negative effect on sleep architecture. VPA and ESM can increase awakening and arousal. VPA can increase wake time after sleep onset. PHT, CZP and ESM can decrease slow wave sleep. ESM will increase REM sleep. In newer AEDs, GBP can increase REM sleep, lamotrigine produced somnolence in 14% and insomnia in 6% of patients. Topiramate produced somnolence in approximately 30% of patients treated. Somnolence and insomnia occurred in 18 and 6%, respectively of patients receiving tiagabine(15). The mechanisms of sleep disorders related to AEDs are complex, some related to their direct sedative effect on central nervous system, and can be ameliorated by gradual escalating the dosages when initiation of treatment. Some are more complicated, for example, the slow wave sleep-enhancing effects were thought to reflect the effect of CBZ on 5-hydroxytryptamine (5-HT) levels or its effect on adenosine receptors that modulate the release of 5-HT and catecholamines (16). Therefore, it is not difficult to expect that sleep disorders are more prevalent in patients with polytherapy than in those with monotherapy and improved after reducing the number of AEDs. Under the invention of modern diagnostic tools especially video monitoring with polysomnography, the types and causes of sleep disorders are much easier to be clarified than before. In the paper "Sleep Quality and Daytime Sleepiness in Patients with Epilepsy" by Chen NC et al (Acta Neurologica Taiwanica Vol 21 No 2 June 2011), they adopted self-rated questionales of Epworth Sleepiness Scale (ESS) and the Pittsburg Sleep Quality Index (PSQI) as tools to estimate excessive daytime sleepiness and sleep quality. They had three main findings: (1) Twenty percent of PWE (23/117) in contrast to 7% of healthy controls (2/30) had excessive daytime sleepiness. (2) There is a significantly higher prevalence of poor sleep quality in the partial seizure, non-seizurefree, and polytherapy groups. (3) The poor seizure control was the strongest independent risk factor for poor sleep quality. Their findings are consistent with the studies in the past decades and worth paying appreciation for it has been the first large scale study in Taiwanese PWE (117 cases) ever since. Indeed, the complex relationship between epilepsy and sleep disorder must be addressed in order to provide the best management of sleep disturbance in PWE.

Eur Eat Disord Rev. 2012 Feb 7;
Mansour S, Bruce KR, Steiger H, Zuroff DC, Horowitz S, Anestin AS, Sycz L

Individuals with eating disorders are said to be highly ambivalent towards change and thus have difficulty maintaining a commitment to, and motivation for, treatment. Self-Determination Theory postulates that autonomous motivation for therapy exists when individuals view their participation as freely chosen. OBJECTIVE: The present study was designed to ascertain whether or not autonomous motivation was associated with treatment response in individuals with bulimia-spectrum eating disorders (BSED). METHOD: One hundred and fifty-five women with DSM-IV-TR BSED participated in multimodal group therapy and completed measures to assess motivation, eating and comorbid symptoms. RESULTS: Hierarchical multiple regression analyses demonstrated that higher levels of autonomous motivation at pretreatment predicted lower post-treatment scores on measures of eating preoccupations (shape, weight and eating concerns), binge eating, anxiety/depression, relationship to self and others and impulsivity. DISCUSSION: These results indicate that autonomous motivation may be an important predictor of outcome following treatment for BSED. Copyright © 2011 John Wiley & Sons, Ltd and Eating Disorders Association.

Dev Cogn Neurosci. 2012 Jan; 2(1): 152-161
Meyer A, Weinberg A, Klein DN, Hajcak G

Because anxiety disorders appear to follow developmental trajectories that begin early in development, it may be useful to examine the neurodevelopmental correlates of specific cognitive processes that have been linked to anxiety. For instance, the error-related negativity (ERN) is a negative deflection in the event-related potential that is maximal approximately 50 ms following the commission of errors at fronto-central electrode sites, and has consistently been found to be more negative among anxious adults. Much less, however, is known about anxiety and the ERN in children-especially when this relationship develops. We recorded event-related potentials (ERPs) while 55 children aged 8 to 13 performed an arrow version of the flankers task. Parents and children both reported on children's anxiety. Results suggest that the relationship between the ERN and anxiety changes as a function of age. Among older children, a larger (i.e., more negative) ERN was significantly related to increased anxiety based on parent report. Although the relationship was less robust, the relationship between ERN and anxiety was opposite among younger children. These results are discussed in terms of existing work on anxiety and the ERN, and the need for longitudinal and developmental studies on the relationship between ERN and anxiety.

Vertex. 2011 Jul-Aug; 22(98): 262-7
Donnoli VF, Moroni MV, Cohen D, Chisari Rocha L, Marleta M, Sepich Dalmeida T, Bonani M, D'Alessio L

Introduction: The presence of negative symptoms (NS) in different clinical entities other than schizophrenia, with a dimensional approach of negative symptoms, was considered in this work. Objectives: Determine the presence and distribution of NS, in a population of patients with non schizophrenic psychiatric disorders attending ambulatory treatment at public hospitals. Methods: Patients with define DSM IV diagnosis criteria for different disorders; affective, alimentary, substance abuse, anxiety, personality disorders and patients with ILAE diagnoses criteria for temporal lobe epilepsy were included. All patients underwent the subscale PANNS for negative symptoms of schizophrenia. Student T test was calculated to determine the differences of frequency for NS among psychiatric disorders. Results: 106 patients were included; 60 women, 46 men, 38 years +/- 12.1. The 90% of patients have a low score of NS. Media 11.6, Max/min 9.38 -14.29. Emotional withdrawal and passive social withdrawal were more frequent in alimentary disorders than in affective disorder and than in epilepsy. Emotional withdrawal was more frequent in substance disorders than epilepsy. Conclusions: According this study, negative symptoms are present in a low to moderate intensity in non schizophrenic psychiatry entities and in the temporal lobe epilepsy.

J Occup Health Psychol. 2012 Feb 6;
Lagerveld SE, Blonk RW, Brenninkmeijer V, Meij LW, Schaufeli WB

The aim of this study was to compare the effectiveness of two individual-level psychotherapy interventions: (a) treatment as usual consisting of cognitive-behavioral therapy (CBT) and (b) work-focused CBT (W-CBT) that integrated work aspects early into the treatment. Both interventions were carried out by psychotherapists with employees on sick leave because of common mental disorders (depression, anxiety, or adjustment disorder). In a quasi-experimental design, 12-month follow-up data of 168 employees were collected. The CBT group consisted of 79 clients, the W-CBT group of 89. Outcome measures were duration until return to work (RTW), mental health problems, and costs to the employer. We found significant effects on duration until RTW in favor of the W-CBT group: full RTW occurred 65 days earlier. Partial RTW occurred 12 days earlier. A significant decrease in mental health problems was equally present in both conditions. The average financial advantage for the employer of an employee in the W-CBT group was estimated at $5,275 U.S. dollars compared with the CBT group. These results show that through focusing more and earlier on work-related aspects and RTW, functional recovery in work can be substantially speeded up within a regular psychotherapeutic setting. This result was achieved without negative side effects on psychological complaints over the course of 1 year. Integrating work-related aspects into CBT is, therefore, a fruitful approach with benefits for employees and employers alike. (PsycINFO Database Record (c) 2012 APA, all rights reserved).

Neuropharmacology. 2012 Jan 31;
Wright RA, Johnson BG, Zhang C, Salhoff C, Kingston AE, Calligaro DO, Monn JA, Schoepp DD, Marek GJ

Group II metabotropic glutamate (mGlu) receptor agonists were efficacious in randomized clinical research trials for schizophrenia and generalized anxiety disorder. The regional quantification of mGlu(2) and mGlu(3) receptors remains unknown. A selective and structurally novel mGlu(2/3) receptor agonist, 2-amino-4-fluorobicyclo[3.1.0]hexane-2,6-dicarboxylic acid (LY459477) was tritiated and the distribution of mGlu(2) and mGlu(3) receptors was studied in transgenic mice lacking either mGlu(2), mGlu(3) or both receptors. LY459477 is an agonist with 1-2 nM potency for rodent and human mGlu(2) and mGlu(3) receptors. The functional selectivity of LY459477 was demonstrated by over 640-fold selectivity and the displacement binding selectivity was greater than 320-fold for all glutamate receptors except mGlu(6) (∼230-fold). More than 1000-fold selectivity was demonstrated for all non-glutamate receptors known to be targeted by antipsychotic drugs. Like atypical antipsychotic drugs, LY459477 reversed in vitro electrophysiological effects of a serotonergic hallucinogen and behavioral effects of phencyclidine or amphetamine. There was virtually no binding of [(3)H]LY459477 to any brain region in mice with a deletion of both mGlu(2) and mGlu(3) receptors. Regions enriched in mGlu(2) receptors included the medial prefrontal cortex, select hippocampal regions, the medial mammillary nucleus, the medial habenula, and the cerebellar granular cell layer. Regions enriched in mGlu(3) receptors were the dorsolateral entorhinal cortex, the hippocampal CA1 field, the piriform cortex, the substantia nigra, the thalamic reticular nucleus, and primary sensory thalamic nuclei. These findings suggest [(3)H]LY459477 should be a useful tool to further define the role of mGlu(2) and mGlu(3) receptors throughout the brain with respect to major neuropsychiatric syndromes. This article is part of a Special Issue entitled 'mGluR'

Early Interv Psychiatry. 2012 Feb 6;
Lim SW, Ha J, Shin YC, Shin DW, Bae SM, Oh KS

Aim: The aim of this study was to elucidate the clinical differences between early- and late-onset social anxiety disorder (SAD) in the Korean population. Methods: Three hundred and eighty-seven outpatients diagnosed with SAD participated in this study. Confirmation of SAD diagnosis was based on the Mini International Neuropsychiatric Interview. All subjects completed the Liebowitz Social Anxiety Scale and anxiety-trait-related scales such as the Anxiety Sensitivity Index, Retrospective Self-Report of Inhibition, Trait Form of the State-Trait Anxiety Inventory, and Beck Depression Inventory. Results: The early-onset group (n = 209) consisted of subjects aged up to 18 years at the time of onset, whereas the late-onset group (n = 178) consisted of subjects older than 18 years at the time of onset. Early-onset SAD patients were more likely to have the generalized subtype and to visit clinics with chief complaints other than social anxiety symptoms. They exhibited more severe symptoms and higher behavioural inhibitions. After adjusting for age and symptom severity, behavioural inhibition was the only significant difference between the two groups. The degree of behavioural inhibitions was associated with earlier onset age. Conclusion: Symptom severity and behavioural inhibitions, especially in social/school situations, were clinical characteristics that differentiated between early- and late-onset SAD.

J Health Psychol. 2012 Feb 7;
Rosenbaum DL, White KS, Gervino EV

Chest pain without detectable heart disease, noncardiac chest pain (NCCP), is linked with anxiety and depression. Theory posits stress and perceived control may relate to NCCP. We hypothesized stress would have direct and mediated effects via perceived control on anxiety and mood disorders in NCCP. Patients (N = 113) completed questionnaires and a structured diagnostic interview. Stress and perceived control were associated with anxiety and mood disorder severity. Perceived control fully mediated the relation between stress and mood disorder severity but not anxiety disorder severity. Results are partially supportive of anxiety-based theories of NCCP.

Prog Neuropsychopharmacol Biol Psychiatry. 2012 Jan 28;
Melo TG, Izídio GS, Ferreira LS, Silveira DS, Macedo PT, Cabral A, Ribeiro AM, Silva RH

Treatment of major depression, posttraumatic stress disorder and other psychopathologies with antidepressants can be associated with improvement of the cognitive deficits related to these disorders. Although the mechanisms of these effects are not completely elucidated, alterations in the extinction of aversive memories are believed to play a role in these psychopathologies. We have recently verified that female rats present low levels of extinction when submitted to the plus-maze discriminative avoidance task. In the present study, female rats were treated long term with clinically used antidepressants (fluoxetine, nortriptyline or mirtazapine) and subjected to the plus-maze discriminative avoidance task to evaluate learning, memory, extinction and anxiety-related behaviors as well as behavioral despair in the forced swimming test. All groups learned the task and exhibited retrieval. Chronic treatment with fluoxetine (but not with the other antidepressants tested) increased extinction of the discriminative task. In the forced swimming test, the animals treated with fluoxetine and mirtazapine showed decreased immobility duration. In conclusion, fluoxetine potentiated extinction, while both fluoxetine and mirtazapine were effective in ameliorating depressive-like behavior in the forced swimming test, suggesting a possible dissociation between the effects on mood and the extinction of aversive memories in female rats.

Brain Nerve. 2012 Feb; 64(2): 131-8
Inoue T, Koyama T

Abstract We reviewed recent advances in biological studies of anxiety disorders. The most important achievement was the discovery of the neural circuits of fear in the 1990s by using an animal model in which conditioned fear was induced. In the 2000s, this discovery led to further elucidation of neurotransmitters involved in fear and the precise neuronal mechanism of fear conditioning, thereby improving the understanding of neuroimaging findings of patients with anxiety disorders. The amygdala is a central region that is associated with the generation of fear, and its inactivation diminishes fear. In humans, amygdala activation has been consistently reported in anxiety disorders, indicating that hyperactivation of the amygdala is involved in the pathogenesis of anxiety disorders. Serotonin plays a key role in the treatment of anxiety disorders, and selective serotonin reuptake inhibitors (SSRIs) are currently regarded the first-line drugs used as anxiolytics. From animal studies, the mechanism underlying the anxiolytic effect of SSRIs is hypothesized as follows: SSRIs inhibit the neuronal activities of the amygdala, and this inhibition decreases the level of fear and anxiety. Animal studies of fear conditioning have proposed new treatment strategies for anxiety disorders: D-cycloserine, propranolol, and reactivation-extinction procedure. Among them, D-cycloserine, which is used as an adjunct to psychotherapy to facilitate extinction of fear, has been investigated in several randomized controlled trials, and its efficacies for several anxiety disorders have been established.