The obsessive-compulsive disorders spectrum concept has grown in recent years because of the common clinical features, such as obsessive thinking and compulsive rituals, biological markers, presumed etiology, and treatment response, that these disorders may share with obsessive-compulsive disorder (OCD). This concept has important implications in regard to diagnosis, nosology, neurobiology, and treatment of a wide group of diverse disorders affecting up to 10% of the population. New insights in central nervous system (CNS) mechanisms that drive the repetitive behaviors of the obsessive-compulsive spectrum disorders have heightened interest in the spectrum in researchers, clinicians, and those involved in drug development.

An important approach in neuropsychiatry centers on employing a dimensional classification of psychopathology. Psychiatric phenomena often fall on a continuum. A dimensional approach allows for the classification of patients who fall at the border of classical entities or who are otherwise atypical. Diagnostic categories are considered along a spectrum if there is considerable overlap in symptoms and in etiology, as demonstrated by familial linkage biological markers, and pharmacological dissection. Categorical and dimensional approaches to the OCD spectrum could have significant implications for diagnosis, nosology, neurobiology, and treatment of a wide group of disorders affecting a sizable percentage of the population.

Recent interest has focused on spectrums in movement disorders, affective disorders, schizophrenia, epileptic and impulsive disorders, and obsessive-compulsive disorders (which we will examine here); in addition, there has been interest in the overlap between these spectrums. Viewing disorders in terms of overlapping spectrums provides researchers and clinicians a framework with which to better understand and treat these disorders.

This chart review examined the effects of effort on neuropsychological assessment and test performance patterns among genuine and exaggerating patients, with and without neurological findings, as aids to diagnosing symptom exaggeration. The sample consisted of 561 consecutive patients involved in compensation claims. With a flexible neuropsychological test (NPT) battery, the claims were assessed over 2 days. The sample included 303 patients evaluated for traumatic brain injury, 55 patients with neurological disease, and 203 patients assessed for other conditions (eg, depression or chronic pain). An average of 38 ability measures per patient were used to generate an overall NPT domain score. Composite scores were also computed for symptom validity tests, self-report measures of psychiatric symptoms, and memory complaint inventory. Seven NPT cognitive subdomain scores were multiply regressed onto the symptom validity test composite, accounting for 45% of its total variance. Patients were also assigned to Genuine or Exaggerator groups based on symptom validity test performance. The NPT for Exaggerating patients averaged 1.43 standard deviations below that of Genuine patients, suggesting that NPT scores for most Exaggerating patients are underestimates of their true ability. Factor analysis results differed between these groups. As a result, clinicians might avoid falsely identifying genuine patients as exaggerating by incorporating their self-reports of psychiatric symptoms and memory complaints into the diagnostic process.

Body dysmorphic disorder (BDD) has a significant impact on the patients’ quality of life (QOL). This is an initial literature review of QOL in patients with BDD, examining the extent of QOL impairments, the impact of psychiatric comorbidity on QOL, and the effect of treatment on QOL in BDD. Studies were identified through PubMed, MEDLINE, and PsycINFO searches from 1960–2011 using the keywords: “quality of life,” “body dysmorphic disorder,” “dysmorphophobia,” and “body image.” Studies included in this review were selected using specific criteria by two authors reaching consensus. Most BDD research studies have used symptom severity measures mainly to study BDD and its treatments. BBD with or without comorbidities is significantly associated with poor QOL and functioning. Studies show that treatment of BDD, either by psychopharmacological treatments such as selective serotonin reuptake inhibitors (SSRIs) or cognitive behavior therapy, might have positive effects on QOL, although these results need to be replicated in larger studies. In conclusion, QOL could add significant value to the assessment of BDD if used as one of the primary measures in research and clinical work in BDD, by providing more information and clearer understanding on the impact of the illness on satisfaction with activities of daily life and overall sense of wellbeing before and after treatment.

Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder which effects an estimated 3% to 5% of children. Despite estimates that ADHD persists in 30% to 70% of adults having had the disorder in childhood, ADHD in adulthood remains controversial. This report summarizes current thinking in the diagnosis and etiology of adult ADHD. Most theories posit that ADHD is related to anomalies in frontal lobe function and dopaminergic transmission. However, there is debate as to whether ADHD is a unitary disorder with different manifestations, a syndrome, or multiple disorders. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, classifies ADHD into inattention, hyperactivity-impulsivity, and combined subtypes. Although problems with cognition are core ADHD symptoms, self reporting has not been a reliable predictor of neuropsychological test performance. Nevertheless, we suggest that a performance-based diagnosis, including empirically derived, age-sensitive neuropsychological tests, provides the best hope of dissociating ADHD from psychiatric disorders with similar symptoms. We also describe the promise of new neuroimaging technologies, such as functional magnetic resonance imaging, in elucidating the pathophysiology of ADHD and similar psychiatric disorders.

Worldwide, patients with common mental disorders, such as depression and anxiety, have a tendency to present first to primary care exhibiting idiopathic physical symptoms. Typically, these symptoms consist of pain and other physical complaints that remain medically unexplained. While in the past, traditional psychopathology emphasized the relevance of somatic presentations for disorders, such as depression, in the last few decades, the “somatic component” has been neglected in the assessment and treatment of psychiatric patients. Medical specialties have come up with a variety of “fashionable” labels to characterize these patients and the new psychiatric nomenclatures, such as the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, attempt to classify these patients into a separate “somatoform disorders” category. These efforts fall short, and revisionists are asking altogether for the elimination of “somatoform disorders” from future nomenclatures.

This review emphasizes the importance of idiopathic physical symptoms to the clinical phenomenology of many psychiatric disorders, offers suggestions to the diagnostic conundrum, and provides some hints for the proper assessment and management of patients with these common syndromes.

Traumatic grief is a common and debilitating syndrome whose clinical presentation is well recognized but whose diagnostic criteria have only recently been delineated. Though it shares features with major depressive disorder, adjustment disorder, and posttraumatic stress disorder, none of these subsume the criteria set for traumatic grief, and the diagnostic overlap is limited in community samples. Furthermore, diagnosis of traumatic grief appears to have prognostic value for clinical course and treatment response among bereaved individuals. In the absence of empirically supported treatments of pathological grief, a new, manualized treatment for traumatic grief symptoms has been developed and is currently undergoing testing in a randomized controlled trial. The conceptual basis for Traumatic Grief Treatment (TGT) is presented, the structure of the treatment is outlined, and the primary clinical strategies employed are described.

Schizophrenia and obsessive-compulsive disorder (OCD) have historical, clinical, and epidemiological links. The clinical use of atypical neuroleptics (ie, dual serotonin-dopamine antagonists) to treat both conditions sheds a new light on them. We report the first two cases of obsessive-compulsive symptoms (OCS) induced by quetiapine in schizophrenia patients. A case of successful augmentation by quetiapine in refractory OCD is also presented. A review of the literature on OCS induced by atypical neuroleptics follows. This paradoxically induced OCD symptomology in schizophrenia patients administered atypical neuroleptics is discussed from new pathophysiological and clinical perspectives. The discussion emphasizes the prognostic implications of OCS in schizophrenia and available therapies for this comorbidity.

Medical students from New York City were integrally involved in the response by health professionals to aid the families of victims of the September 11, 2001, attacks on the World Trade Center. The present study was performed to investigate the emotional impact of this involvement on medical students from the Mount Sinai School of Medicine in New York City. One hundred fifty-seven students responded to a mail survey that explored their personal and professional involvement in the disaster as well as their psychiatric symptoms in the week after the event and at the time of the survey (3.5 months after the event). Findings suggested a differential emotional impact on female students and on students involved in less supervised and more emotionally intense activities. However, involvement in the relief effort, per se, did not contribute to psychiatric symptomatology. It may have been associated with enhanced professional self-esteem among the students. These findings have implications for future planning of psychiatric response to disasters.

Behavioral and psychological symptoms of dementia pose significant challenges in the management of patients with Alzheimer's disease. Neuropsychiatric symptoms are associated with cognitive decline, highly impaired activities of daily living, and frontal lobe pathology. Moreover, behavioral and psychological symptoms can diminish patient quality of life, increase caregiver distress, and accelerate nursing home placement. Although these symptoms are often associated with the later stages of Alzheimer's disease, a high percentage of individuals with mild cognitive impairment or mild Alzheimer's report symptoms as well. This article provides an overview of behavioral and neuropsychiatric symptoms associated with Alzheimer's disease and discusses nonpharmacologic and pharmacologic approaches to the management of such symptoms. For patients with severe behavioral and psychological symptoms of dementia, pychotropic agents may be warranted, whereas approved therapies for Alzheimer's, including cholinesterase inhibitors and the N-methyl-D-aspartate receptor antagonist memantine, may be appropriate in less severe cases.

Parkinson's disease is predominantly a dopamine deficiency syndrome, which is produced in the brain by the loss of cells located in a small area in the ventral midbrain called the substantia nigra. Complete unilateral dopamine lesions, based on the administration of toxic substances (ie, 6-hydroxy-dopamine in rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice and primates) have been extremely useful in testing strategies of replacement. For example, the functional and biochemical impact of the transplanted ventral mesencephalic dopaminergic progenitors has been characterized to a large extent, using the complete lesion model in rats. Over the last decade, however, studies addressing the ability of neurotrophic factors to protect injured dopamine cells prompted researchers to make available partial and progressive lesion models to allow a window of opportunity to interfere the disease progression. Recent findings relating a-synuclein with Parkinson's disease pathology have opened new possibilities to develop alternative models based on the overexpression of this protein using recombinant adeno-associated viral vectors, which is valuable not only for helping to better understand its involvement in the disease process, but also to more closely resemble the neurodegeneration found in Parkinson's disease.

Intervention in the progression of schizophrenia is an effort not just to deter psychosis but also to protect the brain from physiologic deterioration. Neurodegeneration is believed to result from neurochemical dysregulation during the onset of schizophrenia. Deterioration accrued over recurring psychotic episodes causes cumulative loss of cell processes, loss of gray matter volume, and apoptosis. Neurodegeneration ultimately results in persistent symptomology and functional impairment. Functional decline occurs early in the course of schizophrenia, and the symptoms that emerge during the prodromal stage may derail the normal adolescent neurodevelopment. Both first-episode psychosis and the prodrome may be opportunities to forestall neurodegeneration. Unfortunately, people with schizophrenia often experience a long duration of untreated psychosis. Treatment of first-episode psychosis with antipsychotic agents shows robust response. However, early-stage patients have very high rates of medication noncompliance. Treatment in the prodrome may offer the best chance to delay the onset of illness, mitigate its severity after onset, or even prevent onset of symptoms entirely. Nonpharmacologic treatments during the prodrome, such as education, treatment for substance use, and cognitive-behavioral therapy, are low-risk interventions that are potentially beneficial. Pharmacologic interventions during the prodrome are also effective in delaying onset of illness, but carry the risk of adversely affecting patients who are false positives for prodromal schizophrenia.

In this Expert Roundtable Supplement, Jeffrey A. Lieberman, MD, provides an overview of the neurobiological basis of neurodegeneration and the concept of neuroprotection. Next, Peter F. Buckley, MD, reviews the importance of first-episode psychosis, including duration of untreated illness and medication adherence. Finally, Diana O. Perkins, MD, MPH, reviews treatment strategies for prodromal schizophrenia.

Introduction: Pathological love (PL)–behavior characterized by providing repetitive and uncontrolled care and attention to the partner in a romantic relationship–is a rarely studied condition, despite not being rare and causing suffering. This study aims at investigating impulsivity, personality, and characteristics related to the romantic relationship in this population.

Methods: Eighty-nine individuals (50 with PL; 39 individuals with no psychiatric disorder) were compared regarding impulsivity, personality, type of attachment, satisfaction with romantic relationship, and love style.

Results: Individuals with PL have higher levels of impulsivity (P<.001; Barratt Impulsiveness Scale), higher self-transcendence, that is, are more unconventional and hold sense of communion with a wider reality (P<.001; Temperament and Character Inventory) and keep dissatisfactory romantic relationships (P<.001; Adapted Relationship Assessment Scale).

Conclusion: Individuals with PL present personality traits and relationship aspects that must be taken into account in devising assessment and therapeutic strategies for this population.

This review begins with a description of some problems that recently have beset an influential circuit model of fear conditioning and goes on to look at neuroanatomy that may subserve conditioning viewed in a broader perspective, including not only fear but also appetitive conditioning. The column will then focus on basal forebrain functional-anatomical systems, or macrosystems, as they have come to be called. Yet, more specific attention is then given to the relationships of the dorsal and ventral striatopallidal systems and extended amygdala with the dopaminergic mesotelencephalic projection systems, culminating with the hypothesis that all macrosystems contribute to behavioral conditioning.