Depression (differential diagnoses)

About: Depression (differential diagnoses) is a research topic. Over the lifetime, 56557 publications have been published within this topic receiving 2048357 citations.

Handbook of depression

Abstract: Gotlib, Hammen, Introduction. I.Descriptive Aspects of Depression. Kessler, Epidemiology of Depression. Boland, Keller, Course and Outcome of Depression. A.M. Nezu, C.M. Nezu, K.S. McClure, Zwick, Assessment of Depression. Ingram, Siegle, Contemporary Methodological Issues in the Study of Depression: Not Your Father's Oldsmobile. Klein, Durbin, Shankman, Santiago, Depression and Personality. Johnson, Kizer, Bipolar and Unipolar Depression: A Comparison of Clinical Phenomenology and Psychosocial Predictors. II.Vulnerability, Risk, and Models of Depression. Wallace, Schneider, McGuffin, Genetics of Depression. Thase, Jindal, Howland, Biological Aspects of Depression. Davidson, Pizzagalli, Nitschke, The Representation and Regulation of Emotion in Depression: Perspectives from Affective Neuroscience. Goodman, Depression and Early Adverse Experiences. Abramson, Alloy, Hankin, Haeffel, MacCoon, Gibb, Cognitive Vulnerability - Stress Models of Depression in a Self-Regulatory and Psychobiological Context. Joiner, Depression in Its Interpersonal Context. Monroe, Hadjiyannakis, The Social Environment and Depression: Focusing on Severe Life Stress. III. Prevention and Treatment of Depression. Munoz, Le, Clarke, Jaycox, Preventing the Onset of Major Depression. Gitlin, Pharmacological Treatment of Depression. Hollon, Haman, Brown, Cognitive-Behavioral Treatment of Depression. Weissman, Markowitz, Interpersonal Psychotherapy for Depression. Beach, Jones, Marital and Family Therapy for Depression in Adults. Kaslow, E.B. McClure, Connell, Treatment of Depression in Children and Adolescents. IV.Depression in Specific Populations. Tsai, Chentsova-Dutton, Understanding Depression Across Cultures. Nolen-Hoeksema, Gender Differences in Depression. Lewinsohn, Essau, Depression in Adolescents. Powers, Thompson, Gallagher-Thompson, Futterman, Depression in Later Life: Epidemiology, Assessment, Impact, and Treatment. Stolberg, Clark, Bongar, Epidemiology, Assessment and Management of Suicide in Depressed Patients. Hammen, Gotlib, Closing Comments and Promising Directions for the Next Decade.

Mental health, educational, and social role outcomes of adolescents with depression

Abstract: BACKGROUND: This study used longitudinal data to examine the extent to which young people with depression in mid adolescence (ages 14-16) were at increased riskof adverse psychosocial outcomes in later adolescence and young adulthood (ages 16-21). METHODS: Data were gathered during a 21-year longitudinal studyof a birth cohort of 1265 children. Measures included assessments of DSM-III-R major depression (at age 14-16); psychiatric disorders, educational achievement, and social functioning (at age 16-21); social, familial, and individual factors; and comorbid disorders. RESULTS: Thirteen percentof the cohort developed depression between ages 14 and 16. Young people with depression in adolescence were at significantly (P<.05) increased riskof later major depression, anxiety disorders, nicotine dependence, alcohol abuse or dependence, suicide attempt, educational underachievement, unemployment, and early parenthood. These associations were similar for girls and boys. The results suggested the presenceof 2 major pathways linking early depression to later outcomes. First, there was a direct linkage between early depression and increased riskof later major depression or anxiety disorders. Second, the associations between early depression and other outcomes were explained by the presenceof confounding social, familial, and individual factors. CONCLUSIONS: Young people having early depression were at increased risk of later adverse psychosocial outcomes. There was a direct linkage in which early depression was associated with increased risk of later major depression and anxiety disorders. Linkages between early depression and other outcomes appeared to reflect the effectsof confounding factors Language: en

Paraneoplastic limbic encephalitis: neurological symptoms, immunological findings and tumour association in 50 patients.

Abstract: Paraneoplastic limbic encephalitis (PLE) is a rare disorder characterized by personality changes, irritability, depression, seizures, memory loss and sometimes dementia. The diagnosis is difficult because clinical markers are often lacking, and symptoms usually precede the diagnosis of cancer or mimic other complications. The frequency of antineuronal antibodies in patients with PLE has not been investigated. We examined the neurological symptoms and the causal tumours in 50 patients with PLE to determine the utility of paraneoplastic antibodies and other tests. The diagnosis of PLE required neuropathological examination or the presence of the four following criteria: (i) a compatible clinical picture; (ii) an interval of <4 years between the development of neurological symptoms and tumour diagnosis; (iii) exclusion of other neuro-oncological complications; and (iv) at least one of the following: CSF with inflammatory changes but negative cytology; MRI demonstrating temporal lobe abnormalities; EEG showing epileptic activity in the temporal lobes. Of 1047 patients with neurological symptoms, whose sera or CSF were examined for paraneoplastic antibodies, 79 had the presumptive diagnosis of limbic encephalitis, dementia, cognitive dysfunction, or confusion. Fifty of these patients fulfilled our criteria for PLE. Pathological confirmation was obtained in 12 patients. The commonly associated neoplasms were of the lung (50%), testis (20%) and breast (8%). Neurological symptoms preceded the cancer diagnosis in 60% of patients (by a median of 3.5 months). Twenty-five of 44 (57%) patients with MRI studies had signal abnormalities in the limbic system. Thirty (60%) patients had antineuronal antibodies (18 anti-Hu, 10 anti-Ta, 2 anti-Ma), and 20 were antibody-negative or had uncharacterized antibodies (n = 4). The combination of symptoms, MRI findings and paraneoplastic antibodies established the diagnosis of PLE in 78% of the patients. Patients with anti-Hu antibodies usually had small-cell lung cancer (94%), multifocal neurological symptoms (78%) and a poor neurological outcome. Patients with anti-Ta (also called anti-Ma2) antibodies were young men with testicular tumours (100%), frequent hypothalamic involvement (70%) and a poor neurological outcome. In the group of patients without anti-Hu or anti-Ta antibodies, the tumour distribution was diverse, with cancer of the lung the most common (36%); 57% had positive MRI. Fifteen of 34 (44%) patients with a median follow-up of 8 months showed neurological improvement. Treatment of the tumour appeared to have more effect on the neurological outcome than the use of immune modulation. Improvement was observed in 38% of anti-Hu patients, 30% of anti-Ta patients and 64% of patients without these antibodies.

Stressful life events, genetic liability, and onset of an episode of major depression in women.

Abstract: Objective This study was undertaken to clarify how genetic liability and stressful life events interact in the etiology of major depression. Method Information about stressful life events and onset of major depressive episodes in the past year was collected in a population-based sample of female-female twin pairs including 2,164 individuals, 53,215 person-months of observation, and 492 onsets of depression. Results Nine "personal" and three aggregate "network" stressful events significantly predicted onset of major depression in the month of occurrence, four of which predicted onset with an odds ratio of > 10 and were termed "severe": death of a close relative, assault, serious marital problems, and divorce/breakup. Genetic liability also had a significant impact on risk of onset of depression. For severe stressful events, as well as for 10 of the 12 individual stressful events, the best-fitting model for the joint effect of stressful events and genetic liability on onset of major depression suggested genetic control of sensitivity to the depression-inducing effects of stressful life events. In individuals at lowest genetic risk (monozygotic twin, co-twin unaffected), the probability of onset of major depression per month was predicted to be 0.5% and 6.2%, respectively, for those unexposed and exposed to a severe event. In those at highest genetic risk (monozygotic twin, co-twin affected), these probabilities were 1.1% and 14.6%, respectively. Linear regression analysis indicated significant Genotype by Environment interaction in the prediction of onset of major depression. Conclusions Genetic factors influence the risk of onset of major depression in part by altering the sensitivity of individuals to the depression-inducing effect of stressful life events.