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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Findings from computed tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET), and single photon emission computed tomography (SPECT) studies of patients with depression suggest that this mood disorder is associated with regional brain dysfunction. The various elements of depression--dysphoria, anhedonia, helplessness, and sad affect--are all closely associated with changes in cerebral blood flow and/or metabolism in the frontal-temporal cortex and caudate nucleus. A compelling convergence of information from psychiatric and neurologic investigations indicates that depression is mediated by a restricted set of brain structures.
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PMID:The neuroanatomy of depression. 827 May 93

This study compared patients across 5 psychiatric diagnostic groups: Depression, Mania, Schizophrenia, Schizoaffective Disorder, and Psychosis NOS, all of whom are psychotic. Differences in overall cognitive profiles and in dysfunctional memory mechanisms, as well as the effect of psychosis on cognitive functioning were explored using the Neurobehavioral Cognitive Status Examination (NCSE), a brief screening instrument. Results indicated pronounced deficit in memory and abstract reasoning associated with schizophrenic illness, which is not secondary to psychosis and points to localized brain dysfunction. Both encoding and postencoding memory mechanisms were affected. Results support a hypothesis of progressive dysfunction associated with the severity and chronicity of the illness. Implications of findings in aiding diagnostic determination, patient management and rehabilitation are discussed.
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PMID:A comparison of cognitive profiles in schizophrenia and other psychiatric disorders. 877 46

In large families with affective illness, identification of a biological variable is needed that reflects brain dysfunction at an earlier point than symptom development. Eye movement disorder, a possible vulnerability marker in schizophrenia, is less clearly associated with affective illness, although a subgroup of affective disorders shows smooth-pursuit eye movement disorder. The auditory P300 event-related potential may be a useful marker for risk to schizophrenia, but a role in bipolar illness is less certain. The distribution of these two biological variables and their association with symptoms in two multiply affected bipolar families is described. In a single, five-generation family identified for linkage studies through two bipolar I (BPI) probands, 128 members (including 20 spouses) were interviewed. The 108 related individuals had diagnoses of BPI (7), bipolar II (2), cyclothymia (3), or major depressive disorder (19). Eight others had generalised anxiety (1), minor depression (5), intermittent depression (1), or alcoholism (1). Sixty-nine subjects had no psychiatric diagnosis. P300 latency (81) and eye tracking (71) were recorded from a subgroup of relatives within the pedigree. Eye tracking was abnormal in 11 of 71 relatives (15.5%) and was bimodally distributed. In these 11 relatives, clinical diagnoses included minor depression (1), alcoholism (1) and generalised anxiety disorder (1). P300 latency was normally distributed and did not differ from controls. In a second family in which five of seven siblings have BPI illness, P300 latency and eye movement disorder were found in affected relatives and in some unaffected offspring. In these large families, clinical diagnoses of general anxiety, alcoholism and minor depression, when associated with eye tracking abnormality, may be considered alternative clinical manifestations of the same trait that in other relatives is expressed as bipolar illness.
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PMID:Implications of comorbidity for genetic studies of bipolar disorder: P300 and eye tracking as biological markers for illness. 886 53

A wide variety of neuropsychiatric syndromes are associated with right brain dysfunction, including mania, depression, psychosis, hallucinations, personality changes, anxiety, dissociative states, and altered sexual behavior. This review summarizes the anatomic relationships reported between specific neuropsychiatric syndromes and localized right brain lesions. Information is derived from individual case studies and case series. Most neuropsychiatric syndromes are found to be associated with damage to the limbic system. Disruption of body schema and interpersonal functions mediated primarily by the right hemisphere contributes to the neuropsychiatric disability associated with right hemisphere injury. Nonlesion biologic and sociocultural influences including a family history of psychiatric disorder, personal psychiatric history, and the presence of cerebral atrophy increase the vulnerability to neuropsychiatric morbidity following right brain damage. Investigation of the secondary neuropsychiatric disorders occurring with right brain dysfunction contributes to understanding the pathophysiology of idiopathic psychiatric syndromes.
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PMID:Neuropsychiatric manifestations of right hemisphere lesions. 912 5

Chronic fatigue and chronic fatigue syndrome (CFS) have become increasingly recognized as a common clinical problem, yet one that physicians often find difficult to manage. In this review we suggest a practical, pragmatic, evidence-based approach to the assessment and initial management of the patient whose presentation suggests this diagnosis. The basic principles are simple and for each aspect of management we point out both potential pitfalls and strategies to overcome them. The first, and most important task is to develop mutual trust and collaboration. The second is to complete an adequate assessment, the aim of which is either to make a diagnosis of CFS or to identify an alternative cause for the patient's symptoms. The history is most important and should include a detailed account of the symptoms, the associated disability, the choice of coping strategies, and importantly, the patient's own understanding of his/her illness. The assessment of possible comorbid psychiatric disorders such as depression or anxiety is mandatory. When the physician is satisfied that no alternative physical or psychiatric disorder can be found to explain symptoms, we suggest that a firm and positive diagnosis of CFS be made. The treatment of CFS requires that the patient is given a positive explanation of the cause of his symptoms, emphasizing the distinction among factors that may have predisposed them to develop the illness (lifestyle, work stress, personality), triggered the illness (viral infection, life events) and perpetuated the illness (cerebral dysfunction, sleep disorder, depression, inconsistent activity, and misunderstanding of the illness and fear of making it worse). Interventions are then aimed to overcoming these illness-perpetuating factors. The role of antidepressants remains uncertain but may be tried on a pragmatic basis. Other medications should be avoided. The only treatment strategies of proven efficacy are cognitive behavioral ones. The most important starting point is to promote a consistent pattern of activity, rest, and sleep, followed by a gradual return to normal activity; ongoing review of any 'catastrophic' misinterpretation of symptoms and the problem solving of current life difficulties. We regard chronic fatigue syndrome as important not only because it represents potentially treatable disability and suffering but also because it provides an example for the positive management of medically unexplained illness in general.
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PMID:Chronic fatigue syndrome. A practical guide to assessment and management. 921 87

We propose that cerebrovascular disease may predispose, precipitate, or perpetuate some geriatric depressive syndromes. The "vascular depression" hypothesis is supported by the comorbidity of depression, vascular disease, and vascular risk factors and the association of ischemic lesions to distinctive behavioral symptoms. Disruption of prefrontal systems or their modulating pathways by single lesions or by an accumulation of lesions exceeding a threshold are hypothesized to be central mechanisms in vascular depression. The vascular depression concept can generate studies of clinical and heuristic value. Drugs used for the prevention and treatment of cerebrovascular disease may be shown to reduce the risk for vascular depression or improve its outcomes. The choice of antidepressants in vascular depression may depend on their effect on neurologic recovery from ischemic lesions. Research can clarify the pathways to vascular depression by focusing on the site of the lesion, the resultant brain dysfunction, the presentation of depression and time of onset, and the contribution of nonbiological factors.
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PMID:'Vascular depression' hypothesis. 973 12

It has been suggested that recombinant interleukin-2 (rIL-2) may cause pyschological and psychiatric problems, although the effects of rIL-2 on its own have not been well documented. To evaluate these effects, 17 patients with advanced colorectal cancer took part in a randomised, parallel group study of rIL-2 with chemotherapy (5-fluorouracil and leucovorin) versus chemotherapy alone. Patients were assessed regularly by means of various psychometric tests including the Hospital Anxiety and Depression Scale, the Mood Rating Scale, the Mini-Mental State Examination, the Digit Symbol Substitution Test, the Trail-Making Test and the Benton Revised Visual Retention Test. Rigorous discontinuation criteria were applied to ensure that the effect of time-related variables did not influence the results. Compared with patients who were given chemotherapy alone, patients receiving immunochemotherapy reported reduced energy, impaired confidence, higher depressed mood and more confusion. Immunochemotherapy was rated as more distressing than chemotherapy alone and patients reported a greater incidence of appetite impairment, weight loss, poor concentration and fever. Cognitive assessments indicated that brain dysfunction can be caused by rIL-2. Compared with the control group, patients receiving immunochemotherapy showed significant impairment on Trail Making Test B and the Digit Symbol Substitution Test. One patient developed repeated transient psychotic episodes associated with rIL-2 infusions and another regularly became confused. These effects were not due to sleep deprivation or pyrexia. Treatment with rIL-2 should not be discarded on psychosocial grounds, although in each case the psychological morbidity and adverse effects on quality of life need to be balanced carefully against potential therapeutic benefits.
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PMID:The psychological and psychiatric effects of rIL-2 therapy: a controlled clinical trial. 945 48

Chronic obstructive pulmonary disease (COPD) affects over 16 million people in the United States and is a major cause of disability and death worldwide. Its prevalence and mortality are increasing disproportionately among the elderly, women, African-Americans, persons of lower socioeconomic status, and the populations of developing countries in which tobacco is aggressively marketed. In contrast to other major chronic diseases such as heart disease and cancer, medical treatments for COPD have not made decisive inroads into its morbidity or death rates over the last 20 years, resulting in continuing efforts to reduce disability in patients with established disease. Depression is a source of increased disability in COPD, and, as in other chronically ill patient populations, is often unrecognized and untreated in the primary and specialty care sectors. Nearly half of all patients experience some depressive symptoms and at least one-fifth have had one or more major depressive episodes, frequently of long duration. Evidence from randomized controlled trials supports the thesis that patients with mild depression improve with multidisciplinary rehabilitation, whereas patients with major depression may require specific pharmacotherapy to achieve significant improvement in mood disorder and day-to-day function. In addition to its impact on disability, depression may contribute indirectly to the etiology and progression of COPD through its relationship to addictive smoking. Mood disorder in adolescence and early adulthood contributes to early smoking and failure to quit, even after the onset of respiratory disease in later life. Patients with a history of major depression are more likely to fail in smoking cessation programs and to develop a major depressive episode when they do stop. This relationship calls for psychiatrically informed intervention models to improve long-term abstinence rates. The functional impairments associated with COPD are themselves potential promoters of depressive morbidity and chronicity, acting through complex causal pathways. Progressive hypoxia due to respiratory insufficiency leads to structural brain changes and neurocognitive deficits that impair day-to-day function and reduce adaptive potential; and oxygen therapy, as now practiced, offers minimal neurocognitive and mood benefits to most patients. Limited data from studies of experimental hypoxia in animals suggest that relatively mild lack of oxygen impairs the function and plasticity of critical neurotransmitter systems implicated in both cognition and mood, although current practice standards withhold oxygen therapy until late in the course of disease when the damaging effects of hypoxia on the brain have become well established. Neuropsychiatric approaches to the prevention, delay, and treatment of brain dysfunction should be a primary objective of research to improve patient outcomes. A comprehensive relational model that links pulmonary disease, hypoxia, neurocognitive impairment, and structural brain disease with depression provides a useful framework for the design of such studies. The near-term research agenda should include three components: (1) practical methods for improving physician and patient recognition of depression and neurocognitive impairment as targets for intervention; (2) additional trials of standard antidepressant treatment approaches for both major and minor depression; and (3) tests of the hypothesis that late-onset depression in patients with COPD is a marker for the presence of neurocognitive deficits and structural brain changes. The long-range research agenda must aim at preventive interventions designed to forestall brain deterioration. Controlled clinical trials of supplemental oxygen in patients with mild hypoxia and minimal cognitive deficits are needed to determine whether early treatment can reverse or moderate decline, reduce the incidence and chronicity of depression, and improve response to antidepressant treatment. Novel neuroprotective therapies such as antioxidant supplementation and modulation of monoaminergic neurotransmission, coupled with overall improvements in long-term respiratory disease management that minimize episodes of increased systemic oxidative stress, should be considered for multisite trials designed to define optimal treatment and prevention.
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PMID:Depression and Chronic Obstructive Pulmonary Disease: Treatment Trials. 1008 98

Although memory deficits are associated with major depressive disorder, few studies have identified which patient characteristics predict impairment. Because recurrent depression appears related to more severe cerebral dysfunction, the present study tested whether recurrent depressed individuals have worse memory function than first-episode depressed individuals. Two groups of young-adult, nonpsychotic, depressed inpatients (20 single episode [SE] and 46 recurrent episode [RE]) were administered the California Verbal Learning Test within a broader battery of neuropsychological tests. The groups were equivalent in age, education, estimated IQ, severity of depression, and demographic composition. The RE group demonstrated memory deficits relative to both the SE group and published norms, but no other significant difference was found across the battery. Data indicate that abnormal memory performance is associated with recurrent depression, whereas memory deficits are not prominent in first-episode depressed individuals.
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PMID:Relative memory deficits in recurrent versus first-episode major depression on a word-list learning task. 1052 64

Hypoglycemia can cause brain dysfunction, brain injury, and death. The present study seeks to broaden current information regarding mechanisms of hypoglycemic brain injury by investigating a novel etiology. The cat's high resistance to brain injury from hypoglycemia suggested that additional influences such as respiratory depression might play a facilitating role. Three groups of cats were exposed to fasting and insulin-induced hypoglycemia (HG; n = 6), euglycemic respiratory depression (RD; n = 5), and combined hypoglycemic respiratory depression (HG/RD; n = 10). The HG animals were maintained at <1.5 mmol (mean 1 mmol) serum glucose concentration for 2 to 6.6 hours. The respiratory depression was associated with PaO2 and PaCO2 values of approximately 50 mm Hg for 1 hour and of approximately 35 and approximately 75 mm Hg, respectively, for the second hour. Magnetic resonance diffusion-weighted imaging estimated brain energy state before, during, and after hypoglycemia. The hypoglycemic respiratory depression exposures were terminated either to euglycemia (n = 4) or to hyperglycemia (n = 6). Brain injury was assessed after 5 to 7 days of survival. Cats exposed to hypoglycemia alone maintained unchanged diffusion coefficients; that is, they lacked evidence of brain energy failure and all six remained brain-intact. Only 1 of 5 euglycemic RD but 10 of 10 HG/RD cats developed brain damage (HG and RD vs. HG/RD, P < 0.01). This difference in brain injury rates suggests injury potentiation by hypoglycemia and respiratory depression acting together. Three injury patterns emerged, including activation of microglia, selective neuronal necrosis, and laminar cortical necrosis. Widespread activation of microglia suggesting damage to neuronal cell processes affected all damaged brains. Selective neuronal necrosis affecting the cerebral cortex, hippocampus, and basal ganglia was observed in all but one case. Instances of laminar cortical necrosis were limited to cats exposed to hypoglycemic respiratory depression treated with hyperglycemia. Thus, treatment with hyperglycemia compared with euglycemia after hypoglycemic respiratory depression exposures significantly increased the brain injury scores (24 +/- 6 vs. 13 +/- 2 points; P < 0.05). This new experimental hypoglycemia model's contribution lies in recognizing additional factors that critically define the occurrence of hypoglycemic brain injury.
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PMID:Hypoglycemic brain injury: potentiation from respiratory depression and injury aggravation from hyperglycemic treatment overshoots. 1061 96


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