Schizophrenia/Psychosis

Many people assume that it is the emotional and psychotic symptoms that make it difficult for a person with schizophrenia to function in everyday life. In fact, research indicates that cognitive impairment is a major reason why functional outcome is so poor.1

The FDA Pediatric Advisory Committee met in November to review drug trials and safety data for several medications under consideration for pediatric-specific labeling. Drugs included the antipsychotics olanzapine (Zyprexa) and risperidone (Risperdal). Although not yet finding sufficient evidence of safety and efficacy in this population, the committee specified additional information that could be submitted for the applications to be reconsidered.

Eli Lilly and Company pleaded guilty on January 30 to one misdemeanor violation of misbranding Zyprexa (olanzapine) by promoting it for dementia. However, a question raised by bloggers and others remains: did the drug benefit the elderly despite the fact it was not approved by the FDA for such purposes?

My first job after residency involved working at a large Veterans Affairs hospital in an outpatient dual diagnosis treatment program that focused on the comorbidity of schizophrenia and cocaine dependence. Having recently completed a chief resident position at the same hospital’s inpatient unit that focused on schizophrenia without substance abuse, I was struck by how “unschizophrenic” my new patients were. They were organized and social. Their psychotic symptoms were usually limited to claims of “hearing voices,” for which insight was intact and pharmacotherapy was readily requested.

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.

In a resolution that has been expected since October 2008, pharmaceutical company Eli Lilly pled guilty to a criminal charge and has agreed to pay $1.42 billion in a settlement for what federal prosecutors called the illegal promotion of the antipsychotic drug Zyprexa (olanzapine). The drug was found to increase the risk of severe adverse effects, including sudden cardiac death, heart failure, and life-threatening infections, in certain populations.

Suicide risk assessment is a core competency that all psychiatrists must have.1 A competent suicide assessment identifies modifiable and treatable protective factors that inform patient treatment and safety management.2 Psychiatrists, unlike other medical specialists, do not often experience patient deaths, except by suicide. Patient suicide is an occupational hazard. A clinical axiom holds that there are 2 kinds of psychiatrists: those who have had patients commit suicide-and those who will.

Although most studies have focused on the risk of metabolic syndrome for patients with schizophrenia exposed to atypical antipsychotics, other psychiatric patients appear to be at risk for metabolic disturbances as well.7-9 Major depressive disorder (MDD) may be of particular interest because it is much more common than schizophrenia and is treated with a broad range of psychotropics.

The insanity defense represents a prominent symbol of the relationship between law and psychiatry. Despite the fact that it is infrequently raised and seldom successful, the insanity defense is the subject of intense legal and public scrutiny.

The development of new, more effective antipsychotics with fewer adverse effects (eg, extrapyramidal symptoms, tardive dyskin­esia, metabolic syndrome) is paramount.

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

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.