Schizophrenia/Psychosis

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The term “paranoia,” derived from the Greek &lduo;para” (beside) and “nous” (mind), was coined as a descriptor of psychopathology by Heinroth in 1818.1 By the end of the 19th century, 50% to 80% of patients in asylums in German-speaking coun­tries had received a diagnosis of paranoia.1 Beginning in 1899, Kraepelin’s efforts to define paranoia more precisely resulted in a decrease in diagnoses of paranoia in favor of dementia praecox and, later, schizophrenia.1,2 This narrowing of the definition of paranoia is reflected in current nosology and practice. In DSM-IV-TR, the prevalence of delusional disorder is estimated at 0.03% of the general population and accounts for 1% to 2% of psychiatric admissions. The prevalence of paranoid personality disorder is 0.5% to 2.5%; this condition accounts for 10% to 30% of psychiatric admissions.3

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.

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.

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.”

Here I will discuss several examples of recent, reasonable depictions of ECT in the media, and I will suggest how they could represent a shift in the way that this “controversial” therapy is regarded. I use the word “controversial” advisedly, because even on the day I write this, a newspaper article on deep-brain stimulation, in which ECT is described, reads: “New reports this month show that some worst-case patients-whose depression wasn’t relieved by medication, psychotherapy, or even controversial shock treatment-are finding lasting relief.

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

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.

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.

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.