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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors found moderate to severe depression in 60% of a group of schizophrenic patients experiencing acute decompensations (N=30). The course of the depression was followed over an 8-week period8,during which patients were treated with depot fluphenazines. There was a statistically significant reduction in depression that closely paralleled the correction of the cognitive disorder. The authors discuss problems in identifying and quantifying depression during acute schizophrenic decompensation and suggest that the Hamilton scale anxiety/depression factor and the BRPS depression factor may be useful diagnositc tools.
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PMID:Depression and the reintegration phase of acute schizophrenia. 1 Jul 42

Cognitive impairment is a significant health problem for the elderly and is associated with severe negative consequences: higher morbidity and mortality and a diminished capacity to care for self. The accurate diagnosis of acute confusion, dementia, and depression depends on the routine, systematic, and comprehensive assessment of cognition, best achieved through the use of a mental status questionnaire and a behavioral rating scale. Nonspecific clinical features, atypical and variable presentations of symptomatology, and the frequent coexistence of acute confusion, dementia, and depression make an accurate diagnosis of the specific form of cognitive impairment difficult. The primary cognition disorder in acute confusion is that of attention, memory with dementia, and mood with depression.
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PMID:Diagnostic dilemma: cognitive impairment in the elderly. 143 Sep 3

A neurological outpatient department studied 323 consecutive referrals for suspected dementia: 135 (41.8%) were not demented. Of the patients 12.1% had diffuse cognitive disorder; 10.2% circumscribed memory disorder; 0.9% other circumscribed cognitive disorder, 14.2% psychiatric disorder, and 4.3% were judged to be normal. Of the nondemented, 44.1% had a potentially treatable cause for their cognitive symptoms; in 27.4% it was depression. The total of demented patients was 188 (58.2%): 38.8% had primary degenerative dementia; 37.2% vascular dementia including combined degenerative and vascular dementia; and 23.4% had a specific cause. Patients with specific cause were significantly younger than those with other causes of dementia. A potentially treatable cause was found in 10.7% of all demented patients, the most common being metabolic disorders, meningioma, hydrocephalus, subdural haematoma, and depressive pseudodementia.
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PMID:Suspected dementia: evaluation of 323 consecutive referrals. 342 23

Eighty-seven patients with definite multiple sclerosis (MS) were examined neurologically and administered the Mini-mental State examination (MMS) to assess cognitive disability at the beginning and end of a one-year study. A CT scan was performed in 37. A group of 16 patients with stable spinal cord injuries (SCI) were studied in a similar manner. Of the MS patients, 47% had a mean General Health Questionnaire (GHQ) score in the abnormal range. This was a higher rate than in SCI patients (P = 0.004). Mean depression scores were similar in MS and SCI patients, but MS patients with brain involvement were more depressed than those with cord lesions only (P = 0.05). Depression score was unrelated to functional disability but was correlated with the degree of neurological impairment (P = 0.03). Euphoric patients were more likely to have brain involvement (P = 0.006), to have progressive MS (P less than 0.0001), and to have enlarged ventricles (P = 0.04) and were more impaired cognitively (P = 0.04) than noneuphoric patients. These results suggest that depression in MS patients is partly determined by the presence of brain involvement, but that it is also an emotional reaction to the disorder. Euphoria and cognitive disorder are reflections of brain involvement.
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PMID:Structural brain correlates of emotional disorder in multiple sclerosis. 373 Aug 6

Cognitive therapy is based on the premise that cognition, the process of acquiring knowledge and forming beliefs, is a primary determinant of mood and behavior. After reviewing the basic theories of cognitive therapy, the authors discuss its application to the treatment of depression. They theorize that cognitive therapy can improve depressive mood and behavior by focusing on the depressed patient's cognitive disorder. This disorder includes impaired learning and memory function and a systematic negative bias in thinking. The authors note the encouraging results of preliminary outcome studies of this new treatment of depression; such results, they conclude, warrant further development and testing of cognitive therapy.
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PMID:Cognitive therapy of depression: theory and practice. 664 58

Cognitive disorders associated with HIV infection may be due to focal lesions (lymphoma, toxoplasmosis, progressive multifocal leukoencephalitis, etc.), metabolic encephalopathy (e.g. hepatic insufficiency) or psychiatric disorders (depression). In the absence of such causes a "cognitive and motor syndrome associated with HIV infection" has been defined on clinical criteria (Working group of the American Academy of Neurology, 1991). This syndrome is not consistently associated with any specific lesion. Neither the multifocal encephalitis of HIV or CMV infection nor the diffuse leukoencephalopathy associated with HIV are the only causes. The existence of a neocortical neuronal loss has been suggested by several retrospective studies, but our prospective study has not shown cortical or subcortical atrophy. Measurement of neuronal density in Brodmann's areas 4,9 and 40 has not revealed a significant loss either global, by layer, or by column. The only constant lesion was gliosis of the cortex and white matter. Neuronal loss, therefore, is not indispensable to the occurrence of cognitive disorders in AIDS. The mechanism of dementia might be: dysfunction of cortical neurons (dendritic abnormalities, virus/neurotransmitter competition); subcortical dysfunction, as suggested by the high density of microglial nodules in that region; white matter lesions which could be due to abnormalities in the blood-brain barrier. The expression of cell adhesion molecules (VCAM-1, VLA-4, ICAM-1 and LFA-1) by endothelial cerebral cells is not significantly different in AIDS patients, demented or not, and in patients with multiple sclerosis. In contrast, the expression of VCAM-1 by astrocytes is significantly increased in demented AIDS patients compared with non demented ones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[HIV and dementia: neuropathology]. 747 30

Criteria for the diagnosis of ICD-10 Mild Cognitive Disorder (MCD) were applied to a sample of 897 community dwelling elderly participants. Criterion A (the presence of a physical disorder) was met by 44%, Criterion B (report of a cognitive disorder) by 17%, Criterion C (an abnormality in quantified cognitive assessments) by 60%, and Criterion D (exclusion on basis of dementia and other conditions) by 74%. A total of 36 cases (4%) met all four criteria. Correlations between Criteria A and B, and B and C were weak (r = 0.18), and the correlation between Criteria A and C was almost zero (r = 0.02). This suggests that no syndrome exists. Membership of MCD was predicted by a report that memory or intelligence interfered with daily life but not by performance on cognitive tests or by a report of physical illness. Cases of MCD had higher anxiety, depression and neuroticism scores than normal elderly, but did not differ substantially on tests of cognitive functioning. These findings call into question the validity of the ICD-10 diagnosis of MCD.
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PMID:ICD-10 mild cognitive disorder: epidemiological evidence on its validity. 779 46

In Parkinson's disease, mental disturbances frequently accompany the typical motor disorder. Subcortical dementia develops in 10 to 20% of patients. Contrary to the dementia of Alzheimer's type, the apraxia-aphasia-amnesia syndrome is uncommon. Depression and specific impairment of speech, visuospatial functions, and memory are present in an important proportion of patients. As a principal feature of cognitive disorder, deficit of executive functions can be characterised by decreased mental flexibility and inability to cope with changing external conditions. Further, psychiatric complications of pharmacological treatment of Parkinson's disease are briefly described. Finally, presumed pathophysiological mechanisms of cognitive dysfunction are characterized involving dopaminergic and non-dopaminergic changes and complex interactions on the subcortico-cortical level.
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PMID:[Mental dysfunction in Parkinson's disease]. 868 66

During the terminal phase of illness, many geriatric patients develop psychiatric complications that subsequently have profound effects on their quality of life. Effective treatment requires the skills of a physician who is experienced in the recognition, assessment, and management of psychiatric complications of terminal care. Specialized knowledge is required, because even the most common psychiatric symptoms (anxiety, depression, and cognitive disorder) may be difficult to diagnose and treat. Recognition and management are complicated by the fact that these symptoms can arise as a consequence of other symptoms, for example, as a direct result of the disease and its treatment, or as a reflection of underlying psychosocial issues. In many instances, the use of pharmacologic agents, either alone or in combination with psychotherapeutic interventions, provides reasonable control of psychiatric symptoms. Here, too, specialized knowledge is required in order to know which regimens are likely to yield the most benefits with the least risk of toxicity. Fortunately, a considerable body of knowledge has accumulated over the last few years regarding the management of psychiatric symptoms in terminal care. The challenge for the future is to make sure that this information is applied in the routine clinical care of the terminally ill geriatric patient.
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PMID:Psychiatric symptom management in terminal care. 879 51

Data from a two-wave longitudinal study of an elderly community sample were used to assess whether cognitive complaints either predict subsequent cognitive decline or reflect past cognitive decline. Cognitive complaints and cognitive functioning were assessed on two occasions three and a half years apart. Cognitive complaints at Wave 1 were found not to predict future cognitive change on the Mini-Mental State Examination, an episodic memory test or a test of mental speed. Similarly, cognitive complaints at Wave 2 were unrelated to past cognitive changes on these tests after statistically controlling for the effects of anxiety and depression. Furthermore, cognitive complaints did not predict either mortality (after controlling for anxiety and depression) or future dementia. These results are evidence against the inclusion of cognitive complaints in diagnostic criteria for proposed disorders such as age-associated memory impairment, mild cognitive disorder and ageing-associated cognitive decline.
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PMID:Do cognitive complaints either predict future cognitive decline or reflect past cognitive decline? A longitudinal study of an elderly community sample. 912 13


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