Schizophrenia/Psychosis

Recent headlines point to research that suggests atypical antipsychotics are no more effective than their older counterparts in the treatment of children and adolescents with schizophrenia and psychosis.

Although several studies indicate that psychotherapy (alone or in combination with medications) can help psychiatric patients reach recovery faster and stay well longer, a declining number of office-based psychiatrists are providing psychotherapy to their patients.

DSM-IV-TR, our current diagnostic classification system of psychiatric disorders, follows the diagnostic paradigm first established by DSM-III in 1980.

Commercially available telephone sex with women has been available at all hours of the day or night for over 25 years to anyone who pays the fee.

Diagnostic assessment of psychiatric disorders and their comorbidities is a challenge for many clinicians. In emergency settings, there is no time to conduct lengthy interviews, and collateralinformation is often unavailable.

In the new century, the dementias will probably become 1 of the 2 or 3 dominant behavioral health problems in the United States. This article provides an overview of the major clinical features of these cognitive loss syndromes and emphasizes the perspective of the practicing psychiatrist.

Neuroimaging is often used in clinical psychiatry to rule out medical and neurological conditions that can mimic psychiatric disease rather than for the diagnosis of specific psychiatric disorders.

William Bruce, a young man with symptoms of paranoid schizophrenia, was released from Maine’s state-run Riverview Psychiatric Center in April, 2006. Two months later, he killed his mother with a hatchet. Bruce subsequently was found not criminally responsible by reason of insanity and was recommitted to Riverview.

Adolescents who present with symptoms that suggest a psychotic disorder pose a number of diagnostic and treatment challenges. This article attempts to provide a practical guide to the assessment and management of adolescents with severe psychotic illness, including schizophrenia, schizophrenia-like disorders, and bipolar disorder.

A 52-year-old female college professor was referred to a psychiatrist by a nurse practitioner at the college health clinic. The referring diagnosis was “adjustment disorder with depressed mood versus atypical depression with somatization; rule out fibromyalgia.”

In his review of my book, Doing Psychiatry Wrong: A Critical and Prescriptive Look at a Faltering Profession (Psychiatric Times, June 2008, page 57), S.N. Ghaemi, MD, MPH, citing George Orwell, writes that I “seek to justify an opinion” rather than “seek the truth.” He claims that my “errors are numerous and fundamental.”

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

Universal prevention has been a focus of psychiatric research for the past 4 decades. Using a public health approach, research has shown that mitigating major risk factors, such as poverty and early life stress, and promoting protective factors can improve behavioral outcomes.

Debates over conflicts of interest (COIs) in medical research and practice are intensifying with recent proposals to ban industry funding of medical education, to better “manage” industry-physician relationships, and to mandate public disclosure of industry payments to physicians and medical institutions. Caught in the cross fire are prominent psychiatrists accused of underreporting payments received from pharmaceutical companies.

Polypharmacy is used increasingly in the treatment of depression.1 Although it can be beneficial-and at times may even be unavoidable-it can also be overused, resulting in drug-drug interactions, accumulation of adverse effects, reduced treatment adherence, and unnecessary increases in the cost of health care.2 This article describes current trends in psychiatric polypharmacy in the treatment of depression along with ways to use polypharmacy to optimize treatment outcomes.

The Supreme Court has staked out new legal ground by ruling that a judge has the right to deny a patient with schizophrenia (or anyone with a mental illness) the right to represent himself or herself in a trial-even though the court deemed him mentally qualified to stand trial.

This month I will examine the relationship between alcohol use disorder, stress, and a neuropeptide called substance P (SP). The data that led directly to research with human subjects came from the mouse-based genetic manipulation of a gene called neurokinin-1 receptor (NK1R), the receptor for SP. To understand this research thread, I will need to review some basic biology behind a class of biochemicals called tachykinins, of which SP is its most famous member. I begin, however, with an attempt to understand the relationship between the experience of stress, relapse rates in alcohol-dependent populations, and how mouse research ended up helping a cohort of stressed-out patients.

The rising prevalence and dispersion of obesity in North America in the past decade is analogous to a communicable disease epidemic. Longitudinal and cross-sectional associations between major depressive disorder, schizophrenia, and obesity have been established. Existing evidence also indicates that there is an association between bipolar disorder and obesity.

Despite its wretched history, psychosurgery is back with a new name-neurosurgery for mental disorders-and with renewed confidence in its benefits.1 Two technologies are now available that produce small lesions in the brain: stereotactic microablation and gamma knife radiation (no burr holes necessary). Concomitant functional imaging allows for precision targeting that makes these procedures state of the art, but it is possible that deep brain stimulation (DBS), which has shown early promise in clinical trials and is an exciting research tool, may replace ablative procedures that destroy brain cells. Both new stereotactic neurosurgery and old psychosurgery were the focus of recent mass media reports.

In clinical medicine, the term recovery connotes the act of regaining or returning to a normal or usual state of health. However, there is lack of consensus about the use of this term (which may indicate both a process and a state), as well as of the related word remission, which indicates a temporary abatement of symptoms. Such ambiguities also affect the concepts of relapse (the return of a disease after its apparent cessation) and recurrence (the return of symptoms after a remission).

The brutal murder of New York psychologist Kathryn Faughey and attempted murder of psychiatrist Kent Shinbach this past February has provoked warnings to psychiatrists about personal safety and overreliance on clinical judgment. David Tarloff, a person with schizophrenia, was indicted for the attacks. According to press reports, Tarloff blamed Shinbach for having him institutionalized in 1991. While he was wait-ing to see Shinbach, Tarloff allegedly entered Faughey's nearby office and slashed her to death with a meat cleaver and knives. Shinbach heard her screams, tried to rescue her, and was assaulted and robbed.

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.

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.

Psychiatry has seen a transition from art to science in the past century and, largely because of 2 developments in the past several decades, this has also been the case for the field of eating disorders.

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