Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nineteen of 42 (45.2%) patients were socially phobic when and only when depressed. Each of these patients met diagnostic criteria for primary depression (Research Diagnostic Criteria) and major depression (DSM-III-R). Every subject had three or more distinct episodes of depression. Eight of the 9 men (88.9%) and 11 of the 33 women (33.3%) were socially phobic when depressed (p = 0.004). Patients with recurrent wintertime episodes of major depression (p = 0.036) and a past history of alcohol or drug abuse were more likely to be socially phobic (p = 0.0001). The authors suggest the 19 socially phobic patients with primary depression should be regarded as having secondary social phobia. Secondary social phobia may be an important source of comorbidity in patients with primary depression.
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PMID:Secondary social phobia in patients with major depression. 146 45

Regional cerebral blood flow was investigated in 14 patients with major depression diagnosed according to the DSM-III-R criteria (six patients with single and eight patients with recurrent episodes) and in ten healthy volunteers. The mean ages of the patients and the controls were 33.5 +/- 2.7 and 31.6 +/- 2.6 years, respectively. The severity of the depression was assessed using the 17-item Hamilton Depression Scale (mean: 23.2 +/- 1.5). None of the patients was under medication. After administration of 500 MBq technetium-99m hexamethylpropylene amine oxime, a single photon emission tomography study was performed and then transaxial, sagittal and coronal slices were obtained. For the semiquantitative analysis of the data, the ratios of the mean counts/pixel to the whole slice were calculated for 24 regions on three consecutive transaxial slices in the orbitomeatal plane. Additionally, left/right and frontal/occipital ratios were calculated. Both sides of the temporal region had a significantly decreased cerebral blood flow (CBF) when compared to the controls. The left/right ratio of the prefrontal region was also significantly lower in the patients than in the controls. The Hamilton score had a negative correlation with blood flow in the anterofrontal and left prefrontal regions. According to our results, regional CBF seems to be decreased in the left prefrontal and in both temporal regions in major depression. The severity of depression is correlated with the reduction in CBF in the regions of the anterofrontal and left prefrontal cortex.
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PMID:Assessment of changes in regional cerebral blood flow in patients with major depression using the 99mTc-HMPAO single photon emission tomography method. 146 56

Personality traits in euthymic elderly subjects with and without past histories of major depressive episodes were assessed using the Structured Clinical Interview for DSM-III-R and the Social Adjustment Scale-SR. Recovered depressed subjects were characterized by significantly more personality traits from DSM-III-R Clusters B and C than controls, and they exhibited differences in social adjustment, as well. Subjects who have recovered from depressive episodes may show significant differences in personality and social adjustment that might represent residua of past depression, a trait characteristic, or a risk factor for recurrence.
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PMID:Personality in recovered depressed elderly. 147 5

Although more than 20 factor analytic studies have been published on the Beck Depression Inventory (BDI), only Steer and co-workers (1987) have used a sample composed exclusively of patients diagnosed with depression. The component structure found in their study of depressed patients differs in important respects from the structure summarised in several reviews. The main aim of the present study was to investigate whether this structure could be confirmed with the BDI responses of an independent sample of 139 patients diagnosed with DSM-III Major Depressive Episode. Three principal components were extracted and rotated to maximum congruence with a target based on the results of Steer et al. (1987). The significance of the fit to this target was then evaluated by rotating the same matrix of loadings to 5000 random permutations of the target. The fit was found to be highly significant, though some possible improvements could be identified ad hoc. An alternative factor structure for the BDI, derived from covariance structure analysis by Tanaka and Huba (1984), was also tested but could not be confirmed.
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PMID:Components of major depression examined via the Beck Depression Inventory. 147 38

At least three categories of atypical depression have been described. The hysteroid dysphoria is characterized by repeated episodes of depressed mood in response to feeling rejected, and a craving for sweets and chocolate. Two other issues are characterized by a cyclical occurrence of changes of mood and appetite, i.e., the late luteal phase dysphoric disorder (DSM-III-R, appendix), or "the premenstrual syndrome" (PMS), and the major depression with seasonal pattern (DSM-III-R), or seasonal affective disorder (SAD). The reactive mood changes are frequently accompanied by features as hypersomnia, lethargy and increased appetite, particularly with a preference for carbohydrates. Central serotonin pathways participate in the regulation of mood and behavioural impulsivity, and modulate eating patterns qualitatively and quantitatively. Depressives with PMS og SAD benefit, in general, from treatments with serotonin potentiating drugs, suggesting that brain serotonin plays a role in the pathophysiology. Ingestion of carbohydrates increases the plasma ratio of tryptophan to other large neutral amino acids in man and animal, and the serotonin synthesis in the rat brain. Based on these findings it has been suggested that the excessive carbohydrate intake by patients with PMS and SAD reflects a self-medication that temporarily relieves the vegetative symptoms via an increased central serotonergic activity.
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PMID:Serotonin, carbohydrates, and atypical depression. 148 May 61

We examined the relationship between the pre-senile/senile depressive state and silent cerebral infarction using MRI. The subjects studied were 56 patients 50 years of age or older with a depressive state who underwent MRI and who were hospitalized and treated at the Department of Psychiatry or the Department of Neurology of Hiroshima Prefectural Hospital. We made a diagnosis of depression in patients who fulfilled the criteria of DSM-III-R for major depression. Patients in whom apoplectic attacks had occurred, or who had local neurologic symptoms or a history of evident cerebrovascular disorders, were not included in the study. Silent cerebral infarction was observed with pre-senile onset in 60.3% of patients with a pre-senile depressive state, and the complication rate was significantly higher than for cases with juvenile onset (20%). For patients with a senile depressive state, the complication of silent cerebral infarction was found in 53.6% of cases of pre-senile onset and in 100% of cases of senile onset. These rates were remarkably higher than the age-related complication rate of silent cerebral infarction in normal persons reported hitherto, we therefore suspect that nearly half of patients with depressive state of pre-senile onset and most of patients with that of senile onset might have an organic-depressive state complicated by silent cerebral infarction. Both perforating-type infarcts and cortical-type infarcts were found, suggesting that infarct-related foci of depressive states were polyphyletic. When we divided the depressive states complicated by cerebral infarction into 2 subtypes, those complicated by a perforating-type infarct and those by a cortical-type infarct, and compared the 2 types, we found possible differences in clinical symptoms and course between the subtypes. These differences seem worthy of further study. Among cortical-type lesions, parietal lesions were predominant, followed by frontal and then temporal lesions in incidence. There were significantly more left frontal lesions than right frontal lesions. Infarcts of both the parietal lobe and left frontal lobe may be related to the depressive state. Compared with cases not complicated by cerebral infarction, those with perforating- and mixed-type cerebral infarction were complicated with PVH significantly more frequently, similarity in risk factors and pathology between perforating-type cerebral infarction and PVH was suggested by these results.
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PMID:[Clinical study of correlation pre-senile, senile depressive state with silent cerebral infarction--MRI findings and its distribution]. 148 5

Depression among elderly people with reversible cognitive loss often manifests with concomitant vascular disease and can also precede the development of nonvascular degenerative dementia. Little is known about etiological factors for reversible or irreversible dementias in older depressed people. The amino acid homocysteine (HC), which is both a vascular disease risk factor and a precursor of the excitotoxic amino acids cysteine and homocysteic acid, could play a role in the pathophysiology of such individuals. Twenty-seven depressed elderly acute inpatients by DSM-III-R criteria had significantly higher plasma homocysteine levels and lower cognitive screening test scores than did 15 depressed young adult inpatients. HC was highest in the older patients who had concomitant vascular diseases (n = 14). HC was lowest in the older depressives who had neither vascular illnesses nor dementia (n = 8), comparable to the young adult depressives. Higher HC correlated significantly with poorer cognition only in the nonvascular geriatric patients (rs = -0.53). The findings extend earlier work showing higher HC in vascular patients from general medical populations, and also suggest a possible metabolic factor in certain dementias associated with late-life depression.
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PMID:Plasma homocysteine in vascular disease and in nonvascular dementia of depressed elderly people. 148 29

Meta-analyses of the worldwide paroxetine database assessed the efficacy of this compound in the treatment of both DSM-III defined melancholia and hospitalised patients with severe depression (HAMD > or = 25). The analysis for melancholia included 178 paroxetine treated patients and 66 patients treated with placebo. Paroxetine was significantly superior to placebo in the treatment of melancholia and a clear dose-response relationship was established. The meta-analysis for severely depressed hospitalised patients included 109 paroxetine treated patients and 107 patients treated with a tricyclic/tetracyclic control. Paroxetine and active controls showed comparable efficacy in the treatment of severely depressed hospitalised patients.
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PMID:Paroxetine in the treatment of melancholia and severe depression. 148 27

We examined the validity in various settings of two questionnaires for assessment of Typus melancholicus, F-list and Kasahara's scale, and characterological differences between the questionnaires, based on data in 69 patients with unipolar depression and 386 normal controls without a history of depression. The questionnaires were performed on both groups. In addition, a diagnosis of DSM-III-R personality disorders was done for the patient group. Our results demonstrated that Kasahara's scale has much more stable validity in various settings for distinction between personalities of the two groups, and that high scorers in Kasahara's scale have more obsessionality and less personality instability than those in F-list. Such differences between the questionnaires suggested that a direct international comparison of premorbid personality of unipolar depressive patients is needed.
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PMID:Differences between two questionnaires for assessment of typus melancholicus, Zerssen's F-list and Kasahara's scale: the validity and relationship to DSM-III-R personality disorders. 148 44

Controversy continues over the characteristics of beta-endorphin secretion in depression. Beta-endorphin plasma levels were measured in 30 drug-free male patients with a DSM-III-R major depressive disorder and 21 healthy controls. Depressed patients displayed significantly lower beta-endorphin plasma levels in baseline conditions, after the single dose metyrapone test, and after the dexamethasone suppression test. The activation of hypothalamic-pituitary-adrenal (HPA) axis in depression might be due, at least in part, to low levels of beta-endorphin. These results suggest that HPA axis dysregulation in depression may involve peptides other than ACTH.
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PMID:Beta-endorphin responses to metyrapone and dexamethasone in depressed patients. 149 94


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