Bipolar Disorder

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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.

Everyone is unique at the level of social, cultural, psychological, biological, and possibly "energetic" functioning. By extension, in every person, the complex causes or meanings of symptoms are uniquely determined. The diversity and complexity of factors that contribute to mental illness often make it difficult to accurately assess the underlying causes of symptoms and to identify treatments that most effectively address them.

The mind-brain dichotomy has been on a roller-coaster ride over the past few hundred years. Clinically astute European neuropsychiatrists in the 18th and 19th centuries described various neuropsychiatric disorders based on observations of their patients.

Psychiatry has gone wrong by being too symptom-focused, too brain-oriented, and riddled with misdiagnoses. It should go back to seeking the "meaning" of things in patients' subjective experiences. This is the main theme of this short polemic based on case studies. The author selectively cites studies or opinions to make his point rather than trying to get at the truth by offering other perspectives. As George Orwell pointed out, books are of 2 types: those that seek to justify an opinion and those that seek the truth.

Psychiatry is changing so rapidly that it seems impossible to predict 1 year ahead, let alone 10 years. In 1967, when my psychiatry training ended, the community psychiatry movement had just begun, DSM-II was in the works, and the biological revolution was still around the corner.

Prognostication is a major part of what physicians do in many fields of medicine, and it is particularly relevant when a treatment or procedure is controversial or anxiety-provoking. Being able to accurately tell a prospective ECT patient how likely he or she is to respond would be helpful.

The March 27 announcement from the FDA that it is looking into a possible connection between Merck's biggest seller, Singulair (montelukast sodium) and suicidality once again raises questions about whether the agency is requiring close enough scrutiny during clinical trials of possible connections between new drugs and psychiatric effects.

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.

Since the discovery of dopamine as a neurotransmitter in the late 1950s, schizophrenia has been associated with changes in the dopaminergic system. However, the dopamine hypothesis of schizophrenia cannot explain all the symptoms associated with this disorder. Therefore, research has also focused on the role of other neurotransmitter systems, including glutamate, g-aminobutyric acid, serotonin, and acetylcholine (ACh) in schizophrenia.

The vesicular monoamine transporter (VMAT) is a membrane-embedded protein that transports monoamine neurotransmitter molecules into intraneuronal storage vesicles to allow subsequent release into the synapse.1,2 By accumulating both newly synthesized neurotransmitter molecules and freshly returned neurotransmitter molecules from the synapse, VMAT function plays a critical role in the signaling process between monoamine neurons. The VMAT exists in 2 distinct forms: VMAT1 and VMAT2.3

The modern era of psychopharmacology is only 60 years old, having begun with the discovery of the psychotherapeutic benefits of reserpine, lithium, monoamine oxidase inhibitors, and chlorpromazine in the late 1940s and early 1950s, which was followed a few years later by the synthesis and testing of the tricyclic antidepressants and benzodiazepines.

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.

Concern about the rising number of preschool-age children receiving atypical antipsychotics, α-agonists, or other psychotherapeutic medications recently motivated pediatric mental health professionals to develop best-practice algorithms for psycho-pharmacological treatment of young children. It also prompted some states and mental health providers to initiate medication monitoring and consultation programs.

The number of prescriptions for antipsychotic treatment of teenagers has increased sharply in office-based medical practice. Adolescents with psychotic symptoms frequently present for clinical evaluation, and early-onset schizophrenia spectrum disorders (onset of psychotic symptoms before the age of 18 years) represent an important consideration in the differential diagnosis in these youths

Congress substituted a 0.5% increase in Medicare fees for the first 6 months of 2008 for the 10% reduction that would otherwise have been enacted. That reduction in what is called the Medicare fee "update" was predetermined by a formula Congress itself put in place.

Reading crystal balls has always been difficult. Nevertheless, it may be a worthwhile exercise to stop and make some educated guesses about where the field of psychopharmacology will stand 10 years from now--knowing full well that insights and discoveries we cannot predict or anticipate now may pop up to dramatically change the course and direction of clinical psychopharmacology.

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.