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)

Cell-mediated and humoral immunity was studied in 74 patients with acute cerebral vascular disease. During the first two days after the onset of disease marked changes of cell-mediated immunity were observed, manifested as a decrease in total lymphocyte count in the peripheral blood, decrease in number of T lymphocytes, depression in lymphocyte blastogenesis and production of the migration inhibition factor, and a delayed-type skin reactivity. The changes were most evident in patients with severe lesions of brain tissue resulting from primary cerebral haemorrhage and cerebral infarction with fatal outcome. In the group of patients with cerebral infarction with improvement of neurological symptoms the immunological changes were not so pronounced as in the two above-mentioned groups, the smallest changes being found in patients with subarachnoid haemorrhage. We suppose that the depression in the immunne function was caused by severe stress during the course of disease. Impairment of the immune function may increase susceptibility to infection. The humoral immune response was not so evidently changed, and the observed increase of IgA in the sera was probably present before the stroke. In cases with good clinical course some improvement in the immunological parameters was observed, but full recovery did not occur until 3 weeks after the onset of disease.
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PMID:Immunological observations on patients with acute cerebral vascular disease. 52 39

Despite reports of studies linking menopausal estrogen therapy with endometrial cancer in 1975, physicians have persisted in considering menopause a condition needing medication--with estrogens. To assess the risks and benefits, NIH held a conference on estrogen usage in postmenopausal women. A panel of physicians heard the therapeutic, epidemiologic, and sociologic evidence and summarized the findings in a final report. It was agreed that estrogen therapy will be effective in combating vasomotor flushes (hot flashes) and vaginal atrophy and dryness. Evidence to justify estrogen use for coronary vascular disease and depression does not exist. Further evidence is needed to deterine whether estrogen therapy will decrease osteoporosis-related fractures. The risk of endometrial cancer increases 4-8-fold following 2-4 years of continuous estrogen usage. It was concluded that estrogens should be prescribed in the lowest effective dosages and for short terms, not exceedng 2-4 years. Cyclic progestin administration and yearly curettage sampling for endometrial cancer might reduce the risk of developing endometrial cancer while on estrogen therapy.
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PMID:Estrogen prescribing practices scrutinized at NIH conference. 52 51

Four patients with systemic lupus erythematosus (SLE) are described in whom there were major psychiatric complications. Two of these patients had cerebral lupus with psychiatric manifestations of the disease together with other features of disease activity and responding to treatment with high dose steroids. The first of these had had a ten-year history of recurrent episodes of depression before other features of the disease became evident; in the second patient recurrent psychotic episodes occurred after the onset of typical multi-system disease. The third patient had had a minor cerebro-vascular accident four years before other features of SLE became manifest, and cerebral deterioration later on in her life was probably due to hypertensive cerebro-vascular disease secondary to the renal disease of SLE. The fourth patient, a young man, had had recurrent episodes of depression and aggressive behaviour for several years and committed suicide at the age of 33.
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PMID:Psychiatric problems in systemic lupus erythematosus. 127 47

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

Changes in brain structure have been demonstrated in elderly patients suffering affective disorder. Enlarged ventricles are associated with cognitive impairment and higher mortality. Depressed subjects also may show a greater degree of cortical atrophy and subcortical white matter, and basal ganglia lesions seem to be commoner than in age-matched controls. The abnormalities demonstrated are not as severe as those found in degenerative dementias such as Alzheimer's disease, and at present there is no evidence to suggest they are progressive. There is a convincing association with vascular disease, although further neuropathologic correlates are needed. Functional imaging methods are just beginning to be applied to elderly populations and, in affective disorder, findings are similar to those in younger patient groups. The results from different groups vary due to technologic differences and the clinical heterogeneity of the patients studied. Depression, however, may be accompanied by decreased and mania by increased cerebral blood flow or metabolism. Evidence also appears to be mounting of a state-dependent frontostriatal dysfunction in depression. Challenges for the future include replicating such results using larger diagnostically homogeneous patient groups and differentiating the findings from those in other disorders such as schizophrenia and basal ganglia disorders.
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PMID:Imaging and affective disorder in the elderly. 160 Apr 77

Type II (non-insulin dependent) diabetes is associated with a high incidence of vascular disease that causes morbidity and mortality. The principal organs affected by this process are the heart, brain and lower limbs. For many years it has been proposed that depression of the fibrinolytic system, which acts to maintain patency of blood vessels, may contribute to the development of vascular disease. A number of pharmacological agents have been shown to enhance circulating fibrinolytic activity of which metformin is perhaps the most interesting because of its low incidence of serious side effects. Early studies with metformin demonstrated an increase in global fibrinolytic activity in patients with coronary artery disease, peripheral vascular disease and diabetes. Recent studies using assays specific for the components of the fibrinolytic system have shown that the effects of metformin are to cause a fall in plasma levels of the fibrinolytic inhibitor, plasminogen activator inhibitor-1 (PAI-1). There is evidence to suggest that the relationship between depressed fibrinolysis and vascular disease is due to high levels of PAI-1, and reasons to believe that a lowering of PAI-1 may be beneficial in this respect. Further studies are warranted to evaluate the long term effects of metformin warranted to evaluate the long term effects of metformin on the incidence of vascular disease in diabetic patients.
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PMID:The effects of metformin on the fibrinolytic system in diabetic and non-diabetic subjects. 193 71

Thirty-nine percent (33/83) of patients in this study present affective disorders in the chronic phase of ischemic cerebral vascular disease (ICV). The incidence of depression reaches its maximum in atherothrombotic infarcts (52%, 15/29) and in infarcts of cardiac embolic origin (71%, 5/7), and its minimum in lacunar infarcts (25%, 11/43). Affective disorders are more common (27%) in patients with previous history of depression (p = 0.005) and they are more common when the infarcts are extensive (87%, 7/8), they are located in the carotid territory (42%, 25/59), in the dominant cerebral hemisphere (60%, 20/33) and they are more frequent at cortical level (55%, 15/27) (p = 0.03), mainly when they produce a clinical situation with moderate (50%, 10/20) or severe (87%, 7/8) (p = 0.006) limitation. Our results demonstrate that affective disorders are frequent in the chronic phase of ischemic cerebral vascular disease and it is mandatory its correct diagnosis in order to perform an adequate treatment and to improve the clinical symptoms of these patients.
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PMID:[Affective disorders in the chronic phase of ischemic cerebrovascular disease]. 209 Oct 90

Vascular dementia results from ischemic injury to the brain. Depression is a frequent complication of cerebrovascular dementia (CVD) occurring in 25 to 80% of patients during the course of their illness. Depression is unrelated to the severity of intellectual compromise or to the co-existence of delusions. The symptom profile of depression in CVD is indistinguishable from that of late-onset idiopathic major depressive episodes. The frequency of depression differs with the subtype of CVD and is most common in disorders with lesions of the frontal lobes, either cortical or subcortical. In addition to lesion site, other contributors to depression in CVD include vascular disease of other organs, drug therapy of co-existing medical conditions, and psychological reactions to disability. The depression of CVD responds to treatment with antidepressant agents.
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PMID:Depression in vascular dementia. 322 47

Many disorders--including vascular disease, alcoholism, Huntington's disease, drug toxicity, metabolic disorders, brain tumors, depression, and other psychiatric disorders--can cause dementia. Moreover, 50% of all dementia patients have Alzheimer's disease. Guidelines have been established to define the types of dementia. A detailed history, which may note previous depression, and a physical examination are essential. Assessment of the patient's mental status and a neurological examination may help to distinguish other forms of dementia from Alzheimer's disease. Brain imaging and psychometric testing may also help to establish a diagnosis. Metabolic screening for reversible causes of dementia, such as thyroid disturbance or electrolyte-imbalance, is essential. Common features of Alzheimer's disease include memory loss; difficulty with problem solving, abstractions, and calculations; and language and visuospatial deficits. Delusions are common in the early phase of the disease. It is not yet possible to diagnose Alzheimer's disease with complete accuracy. Additional neurophysiological and biochemical markers for diagnosis must be developed.
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PMID:Dementia update: diagnosis and neuropsychiatric aspects. 328 27

Forty-four studies of regional cerebral blood flow (rCBF), fractional oxygen extraction (rOER) and oxygen consumption (rCMRO2) were made on twenty-five patients with recent internal carotid artery territory infarcts. The purpose was to study flow-metabolism relationships in the contralateral hemispheres, and to investigate whether contralateral rCMRO2 was depressed as a result of the recent infarcts. Two groups of controls were included for comparison--seventeen normal volunteers, and ten patients with proven extracranial cerebrovascular disease but without evidence of cerebral infarction. The results demonstrated that: contralateral hemispheric rCMRO2 was less variable than regional oxygen availability (the product of rCBF and arterial oxygen content). This was due, in part, to the effect of individual variations in PaCO2 on rCBF, but other uncontrolled factors, such as intracranial pressure, may have had influences. As a result, rCMRO2 did not correlate with rCBF; mean rCMRO2 in the contralateral hemispheres was 12% lower than normal (a significant difference), but was not different from the value found in patients with extracranial vascular disease in whom there was no evidence of infarction or ischemia; contralateral rCMRO2 did not correlate with the size of the infarct in the opposite hemisphere. It is concluded that rCMRO2 cannot be inferred from rCBF measurements in uncontrolled human studies (as frequently done in the past), and that depression of contralateral rCMRO2 may have preceded infarction in the opposite hemisphere, a consequence of the previous influences of diseases that predispose to stroke.
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PMID:No evidence for transhemispheric diaschisis after human cerebral infarction. 376 54


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