Seminars in clinical neuropsychiatry最新文献

{"title":"Brain imaging in posttraumatic stress disorder.","authors":"G. Villarreal, C. King","doi":"10.1053/SCNP.2001.21840","DOIUrl":"https://doi.org/10.1053/SCNP.2001.21840","url":null,"abstract":"This is a review article of neuroimaging studies in post-traumatic stress disorder (PTSD). Findings from structural, biochemical, and functional studies are summarized. Magnetic resonance imaging (MRI) volumetric studies have consistently reported decreased hippocampal volumes in PTSD. Proton magnetic resonance spectroscopy studies report decreased N-acetyl aspartate (NAA) ratios and absolute concentrations in the medial temporal lobe. Although still controversial, these findings from volumetric and spectroscopic studies are thought to represent decreased neuronal density of the hippocampus. Functional imaging studies document different patterns of limbic and paralimbic structure activation in PTSD compared with controls. Of theoretical importance are findings of failure to activate the anterior cingulate as well as amygdala activation during symptom provocation studies. Also, increased amygdala activation was found with a behavioral task targeted to this structure. A neurobiological model is presented that takes into account findings from neuroimaging studies in PTSD as well as animal studies of fear conditioning. This model proposes that central to symptom mediation is a dysfunction of the anterior cingulate, with a failure to inhibit amygdala activation and/or an intrinsic lower threshold of amygdala response to fearful stimuli. The model further proposes that hippocampal atrophy is a result of the chronic hyperarousal symptoms mediated by amygdala activation.","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"6 2 1","pages":"131-45"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58315940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prefrontal changes and treatment response prediction in depression.","authors":"Ian A. Cook, A. Leuchter","doi":"10.1053/SCNP.2001.21844","DOIUrl":"https://doi.org/10.1053/SCNP.2001.21844","url":null,"abstract":"A continuing challenge in the treatment of depression is how to determine whether an effective drug has been selected for a particular patient, given that individuals will respond to some antidepressants but not others. The factors that contribute to response for each person have been examined from a variety of perspectives, both psychological and physiological. Advances in neuroimaging and in quantitative electroencephalography (QEEG) have made it possible to examine features of brain activity that are associated with response. A new QEEG measure, cordance, is correlated with regional cortical perfusion, and has been used with retrospective and prospective studies to evaluate specific findings that are predictive of clinical response in major depression. We present here a series of depressed subjects treated with antidepressants of different classes; decreases in prefrontal activity were seen as early as 48 hours into treatment in responders and were absent in nonresponders. These findings suggest a role for the prefrontal region in mediating response to medications with different mechanisms of action and raise the possibility of using new QEEG measures to identify changes in brain activity that are predictive of clinical outcome from antidepressant treatment.","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"6 2 1","pages":"113-20"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58315967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Images of the mind.","authors":"Joel Yager, John Lauriello","doi":"10.1053/SCNP.2001.21829","DOIUrl":"https://doi.org/10.1053/SCNP.2001.21829","url":null,"abstract":"","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"6 2 1","pages":"79-81"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46478893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Starving the brain: structural abnormalities and cognitive impairment in adolescents with anorexia nervosa.","authors":"D. Katzman, B. Christensen, A. Young, R. Zipursky","doi":"10.1053/SCNP.2001.22263","DOIUrl":"https://doi.org/10.1053/SCNP.2001.22263","url":null,"abstract":"Anorexia nervosa (AN) is one of the most common chronic illnesses afflicting adolescent girls and is associated severe medical complications. The structural abnormalities found in the brain of adolescents with AN are among the earliest and most striking physical consequences. In the past, it had been assumed that the brain abnormalities found in patients with AN reverse with weight-recovery. Recent evidence has shown that not all of these changes are completely reversible with weight recovery. To date, very little is known about the functional significance of these brain abnormalities. Several studies have shown that cognitive dysfunction is also a common feature of AN. Although current evidence suggests that there may be some degree of improvement in cognition with weight-recovery, it is unclear whether cognition recovers fully or equally across all neuropsychological domains. Furthermore, it remains unknown whether the reported functional consequences are associated with these structural brain changes. This article will review the current literature on structural brain abnormalities and cognitive dysfunction in adolescents with AN.","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"6 2 1","pages":"146-52"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58315568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proton magnetic resonance spectroscopy (H-MRS) studies of schizophrenia.","authors":"L. Rowland, J. Bustillo, J. Lauriello","doi":"10.1053/SCNP.2001.21838","DOIUrl":"https://doi.org/10.1053/SCNP.2001.21838","url":null,"abstract":"Proton magnetic resonance spectroscopy ((1)H-MRS) is a noninvasive technique that can quantify biochemical compounds in the brain. (1)H-MRS has been used to investigate neural structures implicated in the pathology of schizophrenia. The majority of research has revealed reduced N-acetylaspartate (NAA), an index of neuronal integrity, in frontal and temporal regions of medicated and chronically ill patients with schizophrenia. This review summarizes basic principles of (1)H-MRS, studies of frontal, temporal, subcortical, and cerebellar regions in schizophrenia. Technical and study design limitations are also discussed.","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"113 1","pages":"121-30"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58315721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prefrontal-subcortical and limbic circuit mediation of major depressive disorder.","authors":"A. Brody, M. Barsom, Robert G. Bota, S. Saxena","doi":"10.1053/SCNP.2001.21837","DOIUrl":"https://doi.org/10.1053/SCNP.2001.21837","url":null,"abstract":"Substantial progress has been made in elucidating the pathophysiology of major depressive disorder (MDD) using functional and structural brain imaging. In functional imaging studies comparing MDD subjects to normal controls at baseline, dorsolateral prefrontal cortex (DLPFC) activity has been found to be decreased and ventrolateral prefrontal cortex (VLPFC) activity has been found to be increased in MDD. Other regions found abnormal in baseline studies include the anterior cingulate gyrus (AC), temporal lobe, and basal ganglia. Studies examining mood state change (using sleep deprivation, sadness-induction, and tryptophan depletion) and changes from pre- to posttreatment have generally shown improvement of these abnormalities with improved MDD symptoms and worsening of these abnormalities with worsening symptoms. In structural imaging studies, decreased frontal lobe, hippocampal, and basal ganglia volumes are the most commonly reported findings. Several associations can be made between clinical features of MDD and brain function: (1) active sad thoughts/sadness with both decreased DLPFC and dorsal AC activity and increased VLPFC and ventral AC activity (2) psychomotor retardation with decreased left prefrontal activity (3) anxiety with increased left AC activity (4) impaired episodic memory with left prefrontal and medial temporal dysfunction and (5) impaired sustained attention with right prefrontal and parietal dysfunction.","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"6 2 1","pages":"102-12"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58315377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain-behavior relationships in obsessive-compulsive disorder.","authors":"S. Saxena, R. Bota, A. Brody","doi":"10.1053/SCNP.2001.21833","DOIUrl":"https://doi.org/10.1053/SCNP.2001.21833","url":null,"abstract":"Advances in neuroimaging have led to a greater understanding of brain-behavior relationships in obsessive-compulsive disorder (OCD). This article provides an updated review and analysis of the structural and functional neuroimaging studies in OCD published to date and discusses how evidence from various types of neuroimaging studies has been synthesized to generate and test hypotheses regarding these relationships. We also review the basic science literature on the functional neuroanatomy of cortico-basal ganglia-thalamo-cortical circuits and integrate this information with neuroimaging data in OCD, to present a theoretical model of brain mediation of OCD symptoms and response to treatment. Taken together, neuroimaging studies indicate that OCD symptoms are mediated by hyperactivity in orbitofrontal-subcortical circuits, which may be attributable to an imbalance of tone between direct and indirect striato-pallidal pathways. Serotonergic drugs may ameliorate OCD symptoms by changing the relative balance of tone through the indirect versus direct orbitofrontal-subcortical pathways, thereby decreasing activity in the overall circuit that exists in the symptomatic state.","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"6 2 1","pages":"82-101"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1053/SCNP.2001.21833","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58315236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stress, medical illness, and depression.","authors":"L. Slimmer, J. Lyness, E. Caine","doi":"10.1053/SCNP.2001.9554","DOIUrl":"https://doi.org/10.1053/SCNP.2001.9554","url":null,"abstract":"In this review, we present potential pathways through which medical illness may act as a stress-related catalyst of major depression. We will consider available evidence and discuss biological, psychological, and psychosocial theories, individually and in their interplay, in an attempt to better understand the potential roles of stress in mediating the relationships between medical illness and mood disorder. We will use the specific example of major depression occurring after acute myocardial infarction to illustrate the application of our theoretical framework.","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"6 1 1","pages":"12-26"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58316939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging, stress, and affective disorders.","authors":"L. Blake","doi":"10.1053/SCNP.2001.20881","DOIUrl":"https://doi.org/10.1053/SCNP.2001.20881","url":null,"abstract":"The interaction between aging, stress, and affective disorders has interested researchers for many years. Many stressful events occur as a part of aging. The majority of elderly people seem to tolerate this fairly well, but constant uncontrollable stress can lead to changes in the functioning of the hypothalamic-pituitary-adrenal axis. There are also age-related changes in the sensitivity of the hypothalamic-pituitary-adrenal axis, which have little clinical effect on healthy subjects, but may be more significant in the presence of an affective disorder. Stress is a more important predictor of depression in the elderly than are genetic factors. Attempts to minimize stress and the stress response in the elderly may improve treatments of affective disorders in this population.","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"6 1 1","pages":"27-31"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58315096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel animal models of affective disorders.","authors":"Eva E. Redei, N. Ahmadiyeh, A. Baum, David A. Sasso, Jennifer L. Slone, L. C. Solberg, Claire C. Will, Andreja Volenec","doi":"10.1053/SCNP.2001.20882","DOIUrl":"https://doi.org/10.1053/SCNP.2001.20882","url":null,"abstract":"Is there an appropriate animal model for human affective disorders? The traditional difficulties in accepting animal models for psychopathology stem from the argument that there is no evidence for concluding that what occurs in the brain of the animal is equivalent to what occurs in the brain of a human. However, if one models any or some core aspects of affective disorder, this model can become an invaluable tool in the analysis of the multitude of causes, genetic, environmental, or pharmacological, that can bring about symptoms homologous to those of patients with affective disorders. Animal models can also allow the study of the mechanisms of specific behaviors, their pathophysiology, and can aid in developing and predicting therapeutic responses to pharmacologic agents. Although animals exhibit complex and varied social and emotional behaviors for which well-validated and standardized measures exist, an understanding that a precise replica of human affective disorders cannot be expected in a single animal model is crucial. Instead, a good animal model of a human disorder should fulfill as many of the four main criteria as possible: (1) strong behavioral similarities, (2) common cause, (3) similar pathophysiology, and (4) common treatment. An animal model fulfilling any or most of these criteria can be used to elucidate the mechanisms of the specific aspect of the model that is homologous to the human disorder. A wide range of animal models of affective disorders, primarily depression, has been developed to date. They include models in which \"depressive behavior\" is the result of genetic selection or manipulation, environmental stressors during development or in adulthood, or pharmacologic treatments. The assessment of these animal models is based either on behavioral tests measuring traits that are homologous to symptoms of the human disorder they model, or behavioral tests responsive to appropriate pharmacologic treatments. The goal of this review is to focus on relatively recent developments of selected models, to aid in understanding their strengths and weaknesses, and to help those choosing the difficult task of developing novel animal models of affective disorders. The ideal animal model of affective disorders of the future would be an endogenous, genetic model that reiterates the essential, core aspects of the human disease and responds to the standard regimens of therapy. Because complex diseases have been approached from the genetic startpoint by using rodent models, a genetic model of affective disorder would open up possibilities for genetic analysis of polygenic traits that seem to underlie these disorders.","PeriodicalId":79723,"journal":{"name":"Seminars in clinical neuropsychiatry","volume":"6 1 1","pages":"43-67"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58315152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}