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)

The diagnostic evaluation of dementia is directed toward the identification of treatable causes. It can be facilitated by classification of the dementia into one of four categories: attentional, amnestic, cognitive, and intentional. Intentional dementia reflects dysfunction of frontal lobe systems, components of which include the frontal cortex, basal ganglia, thalamus, limbic structures, and subcortical white matter. Disorders that affect one or more of these components and produce intentional dementia include Binswanger's disease, Parkinson's disease, Huntington's disease, HIV infection, closed head injury, normal pressure hydrocephalus, neoplasms, syphilis, vitamin B12 deficiency, multiple sclerosis, and a number of uncommon degenerative and acquired syndromes. Depression may resemble intentional dementia. Guidelines for diagnosis and management are discussed.
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PMID:Multi-infarct dementia, subcortical dementia, and hydrocephalus. 203 8

In the absence of pathognomonic clinical features, the clinical diagnosis of Alzheimer's disease (AD) remains one of exclusion of other dementias. We investigated the clinical diagnoses among 394 neuropathologically confirmed AD cases in a dementia brain bank. Most patients were correctly diagnosed as AD (348 or 88%). Among the misdiagnosed patients, AD was mistaken for a primary depressive disorder in 14, multi-infarct dementia in 13, Parkinson's disease in nine, and alcoholic dementia in four. The number of misdiagnosed AD patients did not differ between physician specialties but was greater among AD patients with agitation, depression, paranoia, or delusions. This retrospective study suggests that the diagnostic sensitivity for AD is high among a cross-section of practicing physicians and that an important factor in mistaking AD for another illness is unfamiliarity with the potential psychiatric symptoms of AD.
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PMID:Neuropathologically confirmed Alzheimer's disease: clinical diagnoses in 394 cases. 205 48

Dopamine-3-O-sulfate (DA-3-O-S) and dopamine-4-O-sulfate (DA-4-O-S) are important end products of L-dopa metabolism. Therefore they may give indications of disturbances in the peripheral metabolism of catecholamines, when measured in urine samples of patients with Parkinson's disease (PD). In addition, information about the reliability of DA sulfatation after L-dopa therapy may be of significance for its role in the elimination of DA from the peripheral nervous system. Although DA-3-O-S appears to be the predominant sulfo-conjugate in urine, there are no changes in PD nor in depression syndrome compared to controls with or without other neurological disorders. By contrast, DA-4-O-S is significantly decreased in de novo PD subjects. However, a similar reduction is notable in patients with other neurological disorders. In depressed persons the loss of this compound was less pronounced as compared to de novo PD. Treatment with combined L-dopa therapy caused increased excretion of DA-3-O-S, while changes in DA-4-O-S were only marginal. It is concluded that urinary DA-3-O-S cannot be used as marker for PD, while DA-4-O-S is significantly reduced in a variety of neurological disorders and in particular in de novo PD. Further studies are necessary to elucidate its role as possible peripheral marker to distinguish preclinical PD and depression syndrome.
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PMID:Urinary dopamine sulfate: regulations and significance in neurological disorders. 208 10

We report here on the coexistence of dementia and depression in a community population aged 75 years and older. Complete information about mood and cognition was available for 286 cognitively intact subjects selected for assessment because of their low scores on the Mini-Mental State, and for 158 mildly and moderately demented subjects. Severely demented subjects, who were incapable of providing information, were excluded. Five percent (8/158) of demented subjects also fulfilled criteria for major depressive disorder Diagnostic and Statistical Manual of Mental Disorders, third edition (DSM-III) compared with 9% (27/286) of cognitively intact subjects. No substantial differences existed in the symptoms reported by demented depressives and nondemented depressives, but subjects who suffered from both disorders were so markedly apathetic that their depression might easily have been overlooked had specific enquiries not been made. Depression was particularly associated with dementia secondary to multi-infarct and Parkinson's disease. When reviewed one year later, 2 of the 18 surviving depressed, nondemented subjects showed evidence of dementia. Both presented unusual diagnostic difficulties, however, and no evidence emerged that large numbers of elderly people will be misclassified in community surveys that include a mental state examination, cognitive testing, and an informant interview.
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PMID:Coexisting depression and dementia in a community survey of the elderly. 210 Dec 97

The authors established the appearance of pain in 54 (68.3%) patients suffering from Parkinson's disease (PD) with levodopa treatment, and in 16 (76.2%) PD patients without treatment. Pain preceded the motor disorders in 39% of PD patients. Pain involved most often the upper (72.2%) and the lower limbs (68.1%), as well as the paravertebral (45.8%) and the neck regions (15.2%). It was located more frequently in joints (54.0%) than in muscles (28.1%). The frequency of pain was higher in PD patients with depression (20.17%) than in those without depression (11%). At the same time, the pain was noted in 61.9% of depressive patients without treatment, as compared to 35.4% depressive PD patients following treatment. The authors discussed the potential pathophysiological mechanism of pain in PD patients.
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PMID:[Pain in patients with Parkinson disease]. 213 2

A high incidence of depressive symptoms has been observed in patients with Parkinson's disease (PD). PD involves a loss of central monoamines, and a decrease of monoamines has been implicated in depression; therefore, it is possible that depressive symptoms in PD result from the loss of endogenous neurotransmitters. However, it is equally possible that depressive symptoms represent a reaction to the chronic disabling course of PD. By comparing depressive symptoms in PD patients to those in matched patients with other chronic disabling diseases not involving a loss of central monoamines, it may be possible to decide between these alternatives. Thus, depressive symptoms were assessed in 45 patients with PD and 24 disabled controls that did not differ from the PD subjects on a measure of functional disability. Results showed that PD subjects obtained significantly higher total scores on the Beck Depression Inventory (BDI) than controls. PD subjects scored significantly higher than controls on BDI items grouped to reflect cognitive-affective and somatic depressive symptoms. The BDI scores of PD subjects were not reliably related to age, sex, duration of PD, or clinical ratings of PD symptom severity or functional disability. Self-rated disability and the number of recent medical problems were the greatest predictors of depressive symptoms. These findings supported the hypothesis that depressive symptoms in PD may not represent solely a reaction to disability.
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PMID:Depressive symptoms in Parkinson's disease: a comparison with disabled control subjects. 214 Jun 82

The dexamethasone suppression test (DST) has been suggested as an effective tool for differentiating between depression and dementia. After administering 1 mg dexamethasone, we measured cortisol, ACTH, and beta-endorphin levels in 32 nondepressed patients with idiopathic Parkinson's disease (PD) (14 also with dementia) and 20 healthy, age-matched controls. Four of the 20 controls, 9 of the 18 with PD alone, and 8 of the 14 with PD and dementia were dexamethasone nonsuppressors (cortisol value greater than or equal to 5 micrograms/100 ml). PD patients without dementia (nonsuppressors) showed higher basal plasma values of cortisol (22.06 +/- 5.30 micrograms/100 ml) compared with the suppressors (13.38 +/- 3.30 micrograms/100 ml). Plasma ACTH and beta-endorphin responded in a coupled way to dexamethasone challenge. Higher basal levels of both peptides were found among PD patients (demented and nondemented), nonresponders to DST. Thus, the DST does not appear to be effective in differentiating between depression and dementia in PD. In addition, PD nonsuppressors showed higher basal values of plasma ACTH, beta-endorphin, and cortisol (similar to patients with major depression). This suggests that although the depression is clinically undetectable, both disorders may share some pathophysiological features at the hypothalamic hypophyseal adrenal level.
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PMID:Cortisol, ACTH, and beta-endorphin after dexamethasone administration in Parkinson's dementia. 215 5

Depression is the most commonly encountered mental change in patients with Parkinson's disease. However, its cause is controversial and little is known about its natural history. Some view depression as reactive to the physical disability inherent to Parkinson's disease; however, others view the depressive disorder as the direct result of underlying biochemical changes caused by the disease process. Abnormalities within the serotonin metabolic pathway have been observed in depressed patients with Parkinson's disease and may help to explain why this form of depressive disorder is so common and persistent. Other forms of depression share this biochemical alteration. Attempts to alleviate depression with serotonin agonists have proven successful. Current research efforts are exploring biological aspects of depression in Parkinson's disease and the epidemiology of this disorder as a model of depression in the elderly, medically ill patient.
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PMID:Depression in the patient with Parkinson's disease. 219 9

Social support, depressive symptoms, and three methods of coping were assessed in 45 patients with Parkinson's disease (PD) and 24 comparably disabled controls. The PD subjects employed significantly fewer cognitive and behavioral coping strategies compared with the controls. Fewer depressive symptoms were related to increased cognitive coping in PD subjects. Behavioral coping strategies were associated with lesser depression among controls. Avoidance coping methods showed a marginally significant positive association with depressive symptoms in PD subjects. Social support was related to the significant coping predictors in each group, but was not related to depressive symptoms. Although correlational, these results might suggest that active (cognitive and behavioral) coping strategies are superior to avoidance strategies in attenuating the affective distress expected from chronic deteriorative illnesses.
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PMID:Coping, social support, and depressive symptoms in Parkinson's disease. 220 63

This study compares the performance of Parkinson's disease patients with age-matched controls on semantic and letter-initial verbal fluency tests. An analysis of variance revealed that Parkinsonian patients showed impaired word production. However when the covariates of age, present verbal ability (Mill Hill Synonyms) and severity of depression (Geriatric Depression Screening Scale) were included in an analysis of covariance, the significant effect of Parkinson's disease on verbal fluency disappeared. Instead, age and present verbal ability were revealed to be the significant sources of between subject variation in total verbal fluency performance; results indicated that increased age and lower present verbal ability resulted in poorer performance on the verbal fluency tests. Depression score was not a significant source of between subject variation. The results are discussed in relation to those recently reported by Gurd and Ward (1989).
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PMID:Verbal fluency in Parkinson's disease. 221 85


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