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)

Of 178 patients with AD, at least one depressive symptom was reported by 63%, 24% were rated as being depressed by a trained observer, and 43% were considered depressed by their relatives. Ten per cent had a previous history of depression. Elevated mood was rare, occurring in only six patients (3.5%). Subjects with depressive symptoms had less cognitive impairment and less ventricular enlargement on CT compared with those without symptoms. Widening of the interhemispheric fissure was associated with symptoms of mania but was inversely related to presence of depressive symptoms.
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PMID:Psychiatric phenomena in Alzheimer's disease. III: Disorders of mood. 239 67

Loss of erection was reported in 53% of 55 male Alzheimer's disease patients with a mean age of 70.25. Loss of erection is not related to degree of cognitive impairment, age, or depression. Modal time of onset of erectile problems is concurrent with onset of Alzheimer's symptoms. Patients with erectile problems were not taking more medications overall than those without problems and had no greater overall incidence of concurrent physical problems. Thus, the evidence suggests that there may be an elevated incidence of erectile failure in patients with Alzheimer's disease as a primary problem not attributable to other age-related factors.
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PMID:The incidence and correlates of erectile problems in patients with Alzheimer's disease. 240 Feb 96

This paper discusses the definition of apathy, reviews its differential diagnosis, and proposes a classification for the conditions that may produce it. Apathy is defined as diminished motivation not attributable to diminished level of consciousness, cognitive impairment, or emotional distress. In its differential diagnosis, abulia, akinesia and akinetic mutism, depression, dementia, delirium, despair, and demoralization must be ruled out. Classification of apathy is organized in terms of its adaptive and functional consequences, its relationship to personality or to sociocultural or environmental events, and its association with psychiatric, neurological, and medical disorders. An approach to assessment and treatment is proposed.
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PMID:Differential diagnosis and classification of apathy. 240 72

We report EEG findings in 33 elderly patients with mixed symptoms of depression and dementia, followed longitudinally to confirm diagnosis. Two groups of patients, dementia with depressive features (mixed-DEM, group I, n = 23) and patients with depressive pseudodementia (mixed-DEP, group II, n = 10), were defined. In addition, we also included, for comparison purposes, 35 patients with probable AD without depressive features (group III), 23 patients with major depression without cognitive impairment (group IV), and 61 healthy elderly controls (group V). We found significant group differences on waking EEGs between those mixed patients who did well after treatment for depression (depressive pseudodementia) compared to patients having dementia with secondary depression. The differences paralleled those between the 'pure' groups of demented and depressed patients. In patients with either depression or depressive pseudodementia, the EEG was usually normal or showed only mild abnormalities. In contrast, the majority of patients with either dementia or dementia with secondary depression had abnormal EEGs, with approximately one-third having moderate (or severe) abnormalities. Although the EEG was usually normal or only mildly abnormal in patients with pseudodementia or depression, these groups (II and IV) did show a significant slowing of the dominant posterior rhythm compared to controls. They also had a higher percentage of generalized abnormal EEGs than controls and this difference was significant between group IV (depression) and controls.
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PMID:EEG findings in depressive pseudodementia and dementia with secondary depression. 246 95

Selegiline is a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B). It also inhibits the reuptake of catecholamines into the presynaptic nerve and enhances the synthesis of dopamine by blocking the presynaptic dopamine autoreceptors. Thanks to these properties it potentiates and prolongs the duration of action of levodopa. Several clinical trials have shown its efficacy as an adjuvant to levodopa therapy. Improvement in parkinsonian disability and reduction of fluctuations in disability can be achieved by adding selegiline to the prevailing levodopa therapy. End-of-dose type fluctuations, in particular, react favourably to selegiline. Side-effects of the therapy can be managed by reducing the dose of levodopa. According to preliminary studies selegiline may also have some benefit as monotherapy in de novo parkinsonian patients. High doses of selegiline have been found to have some antidepressant efficacy, especially in patients with nonendogenous depression. It may also have an effect on bradyphrenia and some symptoms of cognitive dysfunction and dementia. In animal models selegiline has been shown to prevent parkinsonism caused by MPTP and also to increase the life span of rats. Whether selegiline slows down the progression of Parkinson's disease needs further examination.
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PMID:Selegiline in the treatment of Parkinson's disease. 251 15

Evaluating the clinical significance of cognitive dysfunction in patients who exhibit signs of both depression and dementia is one of the more formidable challenges in psychiatry. This article reviews cognitive dysfunction associated with depression, the concept of "pseudodementia," and the syndromal phenomenology of coexisting depression and Alzheimer's-type dementia. The state of the art in neuropsychologic, electroencephalographic, metabolic, and neuroradiographic techniques for evaluating dementia and depression syndromes will be discussed, as will implications for the treatment of such patients.
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PMID:Neuropsychological and biomedical assessment of depression-dementia syndromes. 252 Oct 82

The authors report a study of electroencephalographic (EEG) sleep predictors of two-year mortality in 26 elderly patients with mixed symptoms of depression and cognitive impairment. Patients who had died by two-year follow-up were characterized by significantly longer rapid eye movement (REM) sleep latencies at baseline, less robust REM sleep rebound following all-night sleep deprivation, and baseline apnea-hypopnea indexes greater than 3. Logistic regression analysis using the apnea-hypopnea index value and REM latency correctly predicted 77% of survivors and non-survivors. Survival time following initial measurements was significantly correlated with REM sleep time (r = 0.78, p less than .02) and duration of first REM sleep period (r = 0.75, p less than .02). The authors speculate that changes in these predictor variables may indicate impairment in the cholinergic control of cognitive function, REM sleep, and respiratory function.
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PMID:Predicting mortality in mixed depression and dementia using EEG sleep variables. 252 Oct 84

For the patient, the most important aspect of parkinsonism is the degree to which the disease interferes with daily living. The patient's self-report may be the only way in which such information can be obtained. Depression and cognitive impairment, however, may influence that self-report. In the present study, three ratings of disability, from the patient, a relative, and an independent observer, showed high levels of agreement. The patients' cognitive function made a small but significant contribution to the accuracy of their self-report judged against the relative's rating. Depression, however, played no role. Agreement between patients and relatives for individual items on the disability questionnaire was reasonably high. The results suggest that patients with parkinsonism can provide accurate self-report of their level of disability, even in the presence of depression and cognitive impairment.
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PMID:Accuracy of self-reported disability in patients with parkinsonism. 252 39

Forty-three depressed inpatients, referred for electroconvulsive therapy, and 30 manic patients were examined with clinical ratings and regional cerebral blood flow (rCBF) determinations. The depressed patients were mainly medication free, while most of the manic patients were medicated. Both patient groups showed a normal cerebral blood flow level and regional distribution compared with age- and sex-matched normal controls. In the depressed group and especially in the unipolar subgroup, a significant positive relationship was found between the mean rCBF and symptoms of depression and cognitive dysfunction. Eighteen of the depressed and 18 of the manic patients were reexamined in a euthymic state following treatment and recovery. Only minor and statistically nonsignificant flow changes were found in connection with the clinical improvement. In the manic patients, a significant negative relationship was found between neuroleptic dosage and rCBF.
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PMID:Regional cerebral blood flow in depression and mania. 256 33

A series of 195 cases of Wilson's disease were assessed retrospectively on a range of variables, including psychiatric, neurologic, and hepatic symptoms, and biochemical data as recorded at first admission to a specialist clinic. Ninety-nine patients (51%) were rated as displaying some evidence of psychopathologic features, and 39 (20%) had seen a psychiatrist before the diagnosis of Wilson's disease. The most common psychiatric features were abnormal behavior and personality change, although depression and cognitive impairment were also rated frequently. Schizophrenialike psychoses were rare, apparently occurring at no more than chance frequency. Psychiatric symptoms were related to neurologic rather than hepatic symptoms, and certain symptoms (incongruous behavior, irritability, and personality change) had a particularly significant relationship with bulbar and dystonic disorders but not with tremor. Psychiatric manifestations are important in Wilson's disease, and many of the psychopathologic features seem to have an organic basis.
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PMID:Wilson's disease. Psychiatric symptoms in 195 cases. 258 27


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