In 1990, The American College of Rheumatology laid out several sets of criteria for the diagnosis of fibromyalgia syndrome (FM). The first criterion required patients to report at least 3 months of widespread pain. Pain was considered widespread if it was present in four quadrants of the body—the right and left side as well as above and below the waist. Axial skeleton pain is also very commonly present in FM and is often considered a fifth “quadrant.” The second diagnostic criterion was widespread pain in response to a tender point examination. In this assessment the clinician presses on 18 specific areas with enough pressure to blanche his fingertip (∼4 kg). The patient's report of pain and not pressure on such testing in at least 11 of the tender points completes the requirements for the diagnosis of FM (Slide 1). Although these criteria were established to standardize patients for research studies, many physicians follow them for diagnostic purposes as well. However, these criteria must be viewed in the same context as the definition of hypertension (ie, blood pressures ≥140/90). Patients who do not quite attain these criteria should still be considered to have probable hypertension; and the same applies to FM. A patient who has three-quadrant pain and 9 tender points does not meet the criteria for FM, but the therapeutic approach to this patient is the same as it is for the patient with definitive FM.

Posttraumatic stress disorder (PTSD) was associated in the past mainly with combatrelated events. This was reflected in the names given to the disorder, ie, “shell shock,” “soldier's heart,” “combat neurosis,” and “operational fatigue.” Only following the realization that PTSD can be related to all types of traumatic events, including noncombat associated events, were the terms “traumatic neurosis” and, later, “PTSD” coined. These new terms reflect the understanding that the condition need not necessarily be associated with war, but may also be related to events such as a severe automobile accident, violent personal assault (eg, rape, physical attack, robbery, or mugging), terrorist attack, natural or human-made disaster (such as a fire), witnessing serious injury or death due to any of the above, as well as to other situations, such as being kidnapped or being held hostage.

The tendency to interpret the symptoms of what we would consider now as PTSD, as a “normal response” to traumatic events was another factor that held up progress in the field. It is important to note that PTSD is a pathological response: The vast majority of individuals who are exposed to a traumatic event will later adapt and continue on with their lives. Only a small percent, which partially depends on the type of trauma and is partially associated with several risk factors, will develop a pathological fixation on the traumatic event, namely, PTSD.

It has been estimated that approximately one-third of the population will be exposed to a severe trauma (according to the definition of PTSD) during their lifetime.

Various neuroimaging modalities are available for evaluating patients with temporal lobe epilepsy (TLE). All patients considering surgery should undergo magnetic resonance imaging, which is valuable in the detection and characterization of lesions, particularly mesial temporal sclerosis, the most common abnormality in TLE. A localized seizure focus is predictive of successful surgical outcome. Complimentary neuroimaging studies include positron emission tomography, single-photon emission tomography, and proton magnetic resonance spectroscopy.

New cognitive models of social phobia have been developed based, in part, on a growing number of studies suggesting that people with social phobia process information related to social threat differently than people who are not socially anxious and, in some cases, differently than individuals with other anxiety disorders. In addition to providing an overview of recent models of social phobia, this paper reviews the research literature to date on the following aspects of cognition in social phobia: attention, memory, attributions and appraisals, imagery and perspective, and perfectionism.

Clinical pathways generally recommend potential steps in the diagnosis and treatment of a condition or procedure for individual patients. Their usefulness in guiding clinicians through the steps of nonresponse or partial response to interventions has been documented. They are predominantly management tools based on clinical information developed from evidence-based psychiatry, practice guidelines, or expert consensus statements. Pathways may not be appropriate for use in all circumstances, nor are they a substitute for the practitioner's experience and judgment. Their applicability must be assessed by the responsible practitioner in light of relevant circumstances presented by individual patients in order to optimize treatment.

The transition from reproductive age to menopause is a major milestone in the female lifecycle. It is a hormonal process with a very clear end result: a menopausal state—though its commencement is gradual and vague. It is unavoidable and perfectly normal. The age of the transition varies widely, a fact that hints at the possibility that the reproductive clock is individualized, ticking at a diversified pace. Therefore, the study of the menopausal transition may actually be a derivative of the study of reproduction because it marks the closing of that chapter in a woman's life.

In a sequential approach, the period of transition is defined as perimenopause, or the menopausal transition, the beginning of the second phase in the life of the adult woman, characterized by a stable, low level of gonadal steroids, as opposed to the cyclic fluctuations during the reproductive phase. This imposed, though anticipated, closing of the reproductive chapter of life is often associated with mixed feelings.

As reviewed by Andrea Riccardo Genazzani, MD, PhD, and colleagues, gonadal steroids exercise a profound effect on many body systems, including the brain, in which they have specific receptors, influencing neurotransmitters and other central nervous system (CNS) mechanisms that are considered to be involved in the regulation of mood, cognition, and behavior. Therefore, it would be anticipated that the menopausal decrease in activity levels of female gonadal hormones, ie, estrogen and progesterone, resulting in substantial changes in mood, cognition, and behavior of menopausal women—but this is not the case. This fact illuminates two issues of social and clinical significance: Menopause, per sé, is a normal healthy situation, and even though it is normal it is characterized by age-related processes that may be slowed down or delayed by gonadal steroids.

Several lines of evidence suggest that the neuropeptide oxytocin (OT) may be involved in the pathophysiology of obsessive-compulsive behavior in humans and repetitive grooming behavior in animals. Trichotillomania (TTM), which is characterized by chronic hair pulling, may be conceptualized as a disorder of pathologic grooming. To investigate the role of OT in TTM, the cerebrospinal fluid (CSF) levels of OT in nine women with TTM and nine healthy female controls were measured. Early findings from this ongoing study fail to demonstrate a significant difference in CSF OT levels between women with TTM and healthy female controls.

This article presents a rationale for the hypothesis that an autoimmune mechanism might be involved in the pathogenesis of some forms of obsessive-compulsive aborder (OCO). Existing clinical studies suggesting that some individuals with OCD may have an autoimmune-mediated disorder are briefly summarized. A case example where intravenous immunoglobulin G has been successfully used to treat an adult with OCD spectrum disorder is presented. Preclinical data demonstrating that fragments from the group Αβ hemolytic streptococcus cell wall M proteins can generate antibodies that bind to rat and human tissue are also presented.

There is evidence supporting the presence of abnormalities in certain neurotransmitters, such as dopamine and noradrenaline, and in neuropeptides and other mechanisms, such as the immune system in patients with obsessive-compulsive disorder (OCD). However, the findings implicating serotonin (5-hydroxytryptamine [5-HT]) in the pathophysiology of OCD are increasing at a rate not found in any other psychiatric disorder. These abundant findings foster numerous complex questions that await answers. For example, which 5-HT receptor subtypes or other subcomponents of the 5-HT system are principally involved in OCD pathophysiology, and how do they interact with dysfunctions of other systems? In the search for answers to these critical questions, experimental pharmacology represents a key tool for approaching the complexity of the involvement of 5-HT in OCD, and also suggests new potential therapeutic targets. This article summarizes, in part, the presentations and the discussion of the symposium, “Experimental Pharmacology in OCD,” which was held during the Third International OCD Conference meeting in Madeira, Portugal, in September 1998.

ISSUE:Standards for the practice of medicine are increasingly being confused with standards for the sale and reimbursement of medicines. Authority for prescribing of psychotropic drugs, whether on-label or off-label, is determined by the standard of medical care set by practitioners, not by regulators of the pharmaceutical industry.