[Depressive disorder(depressive episode, recurrent depressive disorder)].
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Studies in non-Hispanic whites have documented higher rates of hearing loss in adults with depression versus those without depression. Data from the Hispanic Health and Nutrition Examination Survey were used to investigate associations between depression and bilateral hearing loss in Cuban-American, Mexican-American, and Puerto Rican adults 20-74 years of age. Pure tone thresholds were calculated by averaging thresholds obtained at 500, 1000, and 2000 Hz separately for each ear. Hearing loss was defined as bilateral pure tone average threshold levels greater than 25 db. Lifetime history of a major depressive episode was assessed by the Diagnostic Interview Schedule, and depressive symptoms were assessed by the Center for Epidemiologic Studies Depression Schedule. Prevalence of overall hearing loss was consistently lower in Hispanics with a history of major depressive disorder than among those without such a history. Odds of hearing impairment was significantly greater among Puerto-Ricans reporting more depressive symptoms versus fewer symptoms. However, no such associations were found among Mexican-Americans or Cuban-Americans. In conclusion, despite the findings in Puerto Ricans with depressive symptoms short of major depression, hearing impaired Hispanics overall do not appear at increased risk of major depressive disorder.
Electroencephalography (EEG) can be a valuable technique to assess electrophysiological changes related to dementia. In patients suspected of having dementia, the EEG is often quite informative. The sensitivity of the EEG to detect correlates of psychiatric disorders has been enhanced by means of quantitative methods of analysis (quantitative EEG). Quantitative features are extracted from, at least, 2 minutes of artifact-free, eyes closed, resting EEG, log-transformed to obtain Gaussianity, age-regressed, and Z-transformed relative to population norms (Neurometrics database). Using a subset of quantitative EEG (qEEG) features, forward stepwise discriminant analyses are used to construct classifier functions. Along this vein, the main objective of this experiment is to distinguish profiles of qEEG, which differentiate depressive from demented patients (n = 125). The results showed that demented patients present deviations above the control group in variables associated to slow rhythms: Normed Monopolar Relative Power Theta for Cz and Normed Bipolar Relative Power Theta for Head. On the other hand, the deviation below the control group occurs with the variable associated to alpha rhythm: Normed Monopolar Relative Power Alpha for P3, in dementia. Using this method, the present investigation demonstrated high discriminant accuracy in separating Primary Degenerative Dementia from Major Depressive Disorder (Depression).
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Depressive states are a prevalent condition in mental disorders other than depressive disorders, which raises the question of whether or not depression in non-depressive disorders and depressive disorders has the same clinical and biological meaning. The aim of this study was to test the hypothesis that depression in schizophrenia spectrum disorders and depressive disorders does have the same characteristics regarding gender distribution and family history of mood disorders in first-degree relatives. The study sample was made up of 660 psychotic patients who were assessed for alternative definitions of depressive states. The pattern of gender distribution and family antecedents of mood disorders in those patients having depressive symptoms or syndromes was very similar to that reported in depressive disorders, and more specifically to depression in patients with schizophrenia spectrum disorders. These data support the hypothesis that depressions in schizophrenia spectrum disorders do have the same biological meaning as in depressive disorders.
Depressive disorders are of high clinical and economic relevance in outpatient and inpatient care. For the treatment of depression effective measures are available. However, these methods often are not used because depressive disorders are underdetected or underestimated in their severity. To improve diagnostic and therapeutic processes in the last years different national and international organizations developed guidelines for diagnosis and treatment of depressive disorders (e. g. AHCPR, APA, German Association of Psychiatrists). These guidelines differ substantially in their goals, content, size, specifically in their methodological quality. The Association of the Scientific Medical Societies in Germany (AWMF) and the German Agency for Quality in Medicine (AQUMED) developed a checklist to evaluate the methodological quality of guidelines. This manual was used to describe and analyze the most relevant and actual six guidelines for diagnosis and treatment of depressive disorders. Recommendations for further improvement and implementation of these guidelines are given.
The isoprenoid pathway produces digoxin, an endogenous membrane Na(+)-K+ ATPase inhibitor and regulator of neurotransmitter transport. The objective of the study was to relate digoxin status and hemispheric dominance to the pathogenesis of psychiatric disorders--bipolar mood disorder, major depressive disorder, and schizophrenia. The following parameters were assessed in bipolar mood disorder during the manic phase and depressive phase of the illness as well as in major depressive disorder, and schizophrenia: HMG CoA reductase activity, tryptophan and tyrosine catabolic patterns, red blood cell (RBC) Na(+)-K+ ATPase activity, and serum magnesium. These parameters were compared to individuals of differing hemispheric dominance. The levels of serum digoxin and HMG CoA reductase activity were found to be decreased in the depressive phase of bipolar mood disorder and major depressive disorder with a corresponding increase in RBC Na(+)-K+ ATPase activity and serum magnesium levels. There was increase in tyrosine and tyrosine catabolites, and a reduction in tryptophan and its catabolites, in the serum in the depressive phase of bipolar mood disorder and major depressive disorder. The neurotransmitter patterns and digoxin levels in the depressive phase of bipolar mood disorder/major depressive disorder correlated with those in right-handed/left hemisphere dominant individual. The neurotransmitter patterns and digoxin levels in the manic phase of bipolar mood disorder and schizophrenia correlated with those in left-handed/right hemisphere dominant individuals. Digoxin status and hemispheric dominance could correlate with the pathogenesis of psychiatric disorders--schizophrenia, major depressive disorder, and bipolar mood disorder.
Depressive disorders are a common problem in late life, requiring consistent and reliable screening by clinicians. Such screening should be based upon the most recent criteria available to facilitate diagnostic and nosologic agreement. This study presents a new screening instrument for geriatric depressive disorders based upon DSM-III-R criteria and the known differences in the display of depression that occur among older persons. The Older Adult Health and Mood Questionnaire (OAHMQ) is a 22-item questionnaire with sound psychometric properties and high validity. Its validation included comparisons with diagnostic assessments by geriatrically-trained psychiatrists and psychologists, and factor analysis. Using a three-part division of "normal," "clinically significant depressive symptoms," and "probable major depression," its sensitivity is .80 and its specificity is .87 for major depression, and .92 and .87, respectively, for any depressive disorder. Separate scoring of affective symptoms versus other symptoms of depression (i.e., physiologic, cognitive, or behavioral) can be useful for diagnostic and research purposes.
Depressive disorders are a heterogeneous group of conditions in terms of their etiology, symptom composition and outcome, which has resulted in difficulties in the definition of the axial depressive syndrome and its clinical forms. This gives rise to a number of problems regarding their definition and delimitation from other mental disorders and from normality. As a result, changing and to some extent overlapping definitions of depressive disorders have been proposed over time. A definition of axial depressive syndrome is proposed based on the differentiation between disturbances of mood and affect. The two main classificatory approaches (categorical and dimensional) are examined with regard to their appropriateness in classifying depressive disorders. Although the two approaches possess pros and cons, the dimensional approach has a number of characteristics that makes it more appropriate than the categorical approach for classifying mental disorders in general and depressive disorders in particular. A multidimensional model for classifying depressive disorders is proposed. The model includes etiological, symptomatological and course/outcome components, each of which is composed of a number of dimensions that have clinical and therapeutical relevance.
Depressive disorders are more common in the relatives of depressed probands than in the population at large, and there is compelling evidence that the familial aggregation of bipolar disorder and severe unipolar depression is at least partly due to genetic factors. However, the evidence concerning 'non-endogenous' depression is less clear, and family environment probably plays a stronger role. Much current research is focused on two areas: firstly, the mode of inheritance of manic-depressive illness, with the use of molecular biological techniques to detect and localise major genes; and secondly, the ways in which familial predisposition and environmental insults combine to produce depressive disorder.
Depression is associated with elevated rates of cardiovascular morbidity and mortality. This elevation seems to be due to a significantly increased risk of coronary artery disease and myocardial infarction and, once the ischemic heart disease is established, sudden cardiac death. Recent data suggest that the increased rates of cardiovascular disease in patients with depression may be the result of one or more still-unrecognized underlying physiological factors that predispose a patient to both depression and cardiovascular disease. Two possibly related factors that may have a causal relation with both depressive disorders and cardiovascular disease are an omega-3 fatty acid deficiency and elevated homocysteine levels. We present the available data connecting cardiovascular disease, depression, omega-3 fatty acids, and homocysteine. In addition, we suggest research strategies and some preliminary treatment recommendations that may reduce the increased risk of cardiovascular mortality in patients with major depressive disorder.
The authors evaluated the trait/state issues of harm avoidance in depressive-spectrum disorders and its predictive potential for antidepressant response. Subjects with Diagnostic and Statistical Manual of Mental Disorders (4th edn; DSM-IV) major depressive disorder (n = 39), dysthymic disorder (n = 37), depressive personality disorder (n = 39), and healthy control subjects (n = 40) were evaluated with the Temperament and Character Inventory and the 17-item Hamilton Depression Rating Scale (HDRS-17) at baseline and after a 12 week antidepressant treatment period. Higher harm avoidance scores predicted lesser improvement in subjects with dysthymic disorder and major depressive disorder, as determined by lesser decrease in HDRS-17 scores. Mean harm avoidance scores in depressed subjects were consistently greater than those in healthy controls, controlling for age, gender and diagnosis. Mean harm avoidance scores decreased significantly in all depressive-spectrum disorders after treatment, but still remained higher than harm avoidance scores in control subjects. The present study reports that harm avoidance is a reliable predictor of antidepressant treatment in subjects with major depressive disorder and dysthymic disorder and that harm avoidance is both trait- and state-dependent in depressive-spectrum disorders.
We studied the association between preceding psychiatric disorders and Parkinson's disease (PD) using a case-control design. We used the medical records-linkage system of the Rochester Epidemiology Project to identify 196 subjects who developed PD in Olmsted County, Minnesota, during the years 1976-1995. Each case was matched by age (+/-1 yr) and sex to a general population control. We reviewed the complete medical records of cases and control subjects to detect preceding psychiatric disorders. The frequency of psychiatric disorders was higher in cases than in control subjects; the odds ratio was 2.2 for anxiety disorders (95% confidence interval [95% CI] = 1.4-3.4; p = 0.0003), 1.9 for depressive disorders (95% CI = 1.1-3.2; p = 0.02), and 2.4 for both anxiety disorders and depressive disorders occurring in the same individual (95% CI = 1.2-4.8; p = 0.02). When we restricted analyses to disorders present 5 years or more before the onset of motor symptoms of PD, the association with depressive disorders lost statistical significance. However, the association with anxiety disorders remained significant for disorders present 5, 10, or 20 years before onset of motor symptoms. Our results suggest that anxiety disorders and depressive disorders are associated with PD and that the causative process or the risk factors underlying PD are present many years before the appearance of motor symptoms.
BACKGROUND: The aim was to examine basic performance on attention and memory tasks in treatment-naive children and adolescents with anxiety disorder or depressive disorder and in healthy subjects under drug-free conditions. METHODS: Basic neurocognitive performance on attention and verbal memory tasks was examined in children and adolescents with emotional disorders, between 6 and 17 years of age. A total of 34 children with an anxiety disorder, 31 children with a depressive disorder, and 33 healthy controls were assessed with a comprehensive neuropsychological test battery. All children were treatment-naive at the time of testing. Five different computerised attention tasks and the Rey Auditory-Verbal Learning Test were administered. RESULTS: A significant effect of diagnosis was found for verbal memory but not for attention. LIMITATIONS: The large age range and inclusion of different diagnoses resulted in rather inhomogeneous groups. CONCLUSION: The present study provided evidence for an undisturbed attentional performance in both patient groups and a dissociation in memory functioning between anxious and depressed children. Memory impairment was found to be specifically associated with childhood depression.
The study investigated biases in selective attention to emotional face stimuli in generalized anxiety disorder (GAD) and depressive disorder, using a modified probe detection task. There were 4 face types: threatening, sad, happy, and neutral. Measures of attentional bias included (a) the direction and latency of the initial eye movement in response to the faces and (b) manual reaction time (RT) to probes replacing the face stimuli 1,000 ms after their onset. Results showed that individuals with GAD (without depressive disorder) were more likely to look first toward threat faces rather than neutral faces compared with normal controls and those with depressive disorder. They also shifted their gaze more quickly toward threat faces, rather than away from them, relative to the other two groups. There were no significant findings from the manual RT data. Implications of the results for recent theories of clinical anxiety and depression are discussed.
Depressive disorders are of great medical and political significance. Despite improvements in the treatment of depressive patients, the potential for guideline-oriented diagnosis and therapy as well as better co-operation between different levels of care is evident. This study is part of the German Research Network on Depression and Suicidality. The study is conducted in Southern Baden, North Rhine and Munich. The objective is to develop a quality management program for primary care physicians and psychiatrists. A comprehensive continuous medical education concept as well as quality management measures were developed, implemented and evaluated. A total of 66 physicians (43 primary care physicians and 23 psychiatrists) participated. They documented the diagnostic and treatment measures provided to depressive patients before and after the intervention that had been implemented in the intervention regions of Southern Baden and North Rhine. Effects regarding guideline orientation and implementation of stepped-care treatment are analysed with an intervention/control group design and prepost data measurement.
The aims of the present study was (a) to examine the relationship between parental bonding and various personality disorders, when the effect of a lifetime depressive disorder was statistically controlled for, and (b) to examine the relationship between parental bonding and a lifetime depressive disorder when the effects of various personality disorders were accounted for. The study included 135 psychiatric outpatients and 41 healthy controls. The patients were diagnosed according to DSM-III-R axis I and axis II. Results indicated that obsessive-compulsive personality disorder was associated with reports of lower levels of paternal care and higher levels of paternal overprotection, while cluster B personality disorder was associated with reports of high parental overprotection. Avoidant, dependent, and cluster A personality disorders were not associated with abnormal parental bonding. Lifetime depressive disorders were associated with reports of low maternal care and high maternal overprotection when the effect of a personality disorder was accounted for.
Depressive disorders belong to the most frequent diseases worldwide showing a lifetime prevalence of up to 20%. Moreover they are one of the leading causes for the amount of years lived with disability. Increasing knowledge about the pathological mechanisms underlying depressive syndromes is obtained by using modern neurobiological research-techniques. Thereby some older theories that have been the basis of emotion-research for decades--like the monoamine hypothesis--have been strengthened. In addition new aspects of the pathological processes underlying depressive disturbances have been unraveled. In this review established models and recent findings will be discussed, to bridge various research-fields, ranging from genetics, epigenetics and morphological changes to the functional consequences of depression. Finally therapeutic implications that could be derived from these results will be presented, showing up putative possibilities for diagnosis and treatment of depressive syndromes.