Mood Disorders

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Research emerging from the field of emotion science suggests that individuals who have anxiety and mood disorders tend to experience negative affect more frequently and more intensely than do healthy individuals, and they tend to view these experiences as more aversive, representing a common diathesis across anxiety and mood disorders.1-5 Deficits in the ability to regulate emotional experiences, resulting from unsuccessful efforts to avoid or dampen the intensity of uncomfortable emotions, have also been found across the emotional disorders and are a key target for therapeutic change.

Lecturing around the country has left us with the powerful impression that both psychiatrists and primary care physicians are hungry for new ways to think about and treat depression and the myriad symptoms and syndromes with which it is associated-including attention deficit disorder, insomnia, chronic pain conditions, substance abuse, and various states of disabling anxiety. Primary care physicians also seem especially excited to learn that depression is not just a psychiatric illness but a behavioral manifestation of underlying pathophysiological processes that promote most of the other conditions they struggle to treat-including cardiovascular disease, diabetes, cancer, and dementia.1,2

The words attributed to Socrates resonate with the perspectives of many contemporary parents and clinicians.1 The endurance of the concern suggests something fundamental about the psychopathology of deviant, disruptive behavior of youth. Yet clinicians struggle to understand its origins, to help parents control their children, and to help the children control themselves. Clinically, this manifests in failed pharmacological treatments, incompleted courses of individual therapy, problems in engaging families in treatment, and controversies over which therapy is most effective.

Recent research has raised concerns about the adequacy of psychiatric diagnostic evaluations conducted in routine clinical practice, particularly the detection of disorders that are comorbid to the principal diagnosis.

In this column, I will discuss new progress on this Internet-boosted line of inquiry. I will begin with a few basics about differential gene expression and microarrays and will then move on to something that researchers are calling “convergent functional genomics.” As you shall see, the clever use of online databases both confirmed and extended the work done at the bench.

The editors of Diagnostic Manual-Intellectual Disability (DM-ID) have set out to complete the difficult task of compiling the evidence base on mental disorders in the field of intellectual disability (ID) into one reference book while modifying DSM-IV diagnostic criteria for use in persons with the disorder who present with mental and behavioral disorders.

The fact that treatment with interferon (IFN)-α has become the world’s foremost human model for studying how the innate immune system promotes depression points to a disturbing clinical truth: patients who elect to receive (IFN)-α therapy for any of the several disease states to which it is applied face a high likelihood of experiencing a multitude of psychiatric symptoms severe enough to affect their social and occupational functioning and overall well-being.1

Depression complicates medical illnesses and their management, and it increases health care use, disability, and mortality. This article focuses on the recent research data on diagnosis, etiopathogenesis, treatment, and prevention in unipolar, bipolar, psychotic, and subsyndromal depression.

The loss of a loved one is one of the most traumatic events in a person’s life. In spite of this, most people cope with the loss with minimal morbidity. Approximately 2.5 million people die in the United States every year, and each leaves behind about 5 bereaved people.

There is substantial comorbidity with oppositional defiant disorder (ODD) and conduct disorder (CD) in children with attention-deficit/hyperactivity disorder (ADHD). It is important to determine the effect of comorbid ODD and CD on the clinical course in youth with ADHD. Biederman and associates1 recently published clinical findings from a 10-year prospective, longitudinal study of boys with ADHD, following them into early adulthood.

Traumatic brain injury (TBI) is the major cause of death and disability among young adults. In spite of preventive measures, the incidence of a TBI associated with motor vehicle accidents, falls, assault, and high-contact sports continues to be alarmingly high and constitutes a major public health concern. In addition, the recent military operations in Iraq and Afghanistan have resulted in a large number of persons with blast injuries and brain trauma. Taking into account that cognitive and behavioral changes have a decisive influence in the recovery and community reintegration of patients with a TBI, there is a renewed interest in developing systematic studies of the frequency, mechanism, and treatment of the psychopathological alterations observed among these patients.

Although several antimanic agents are available to treat individuals with bipolar disorder (BD), many patients have a less than satisfactory response or experience adverse effects.1 With the exception of lithium, all of the current antimanic agents are either anticonvulsant or antipsychotic drugs. It is remarkable that no drug has been developed specifically for BD, especially because this illness was conceptualized more than a century ago.

An international team of experts recently proposed expanding the diagnostic criteria for several subtypes of bipolar disorder, adding a pediatric bipolar disorder category and eliminating the schizoaffective disorder category.

For many years, research on mood disorders has focused on neurotransmitters, particularly on the monoamines (serotonin, norepinephrine, and dopamine) and their action at the neuronal junction, or synapse. Although the monoamine theory helps explain the action of tricyclics, monoamine oxidase inhibitors, and SSRIs, it fails to account for many other things.

In May 2007, the novelist Ann Bauer went public with the tribulations of her autistic son. When catatonia developed, a diagnosis of schizophrenia was made, and antipsychotic medications were prescribed, but with little benefit. When the catatonia syndrome was recognized as independent of schizophrenia and successfully treated, her son returned to a more normal life.1,2