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

In a case series study we evaluated 53 composite-materials workers in an aerospace plant who filed workers' compensation claims for illness allegedly related to phenol-formaldehyde resin exposure. Symptoms ranged from mucosal and skin irritation to depression and cognitive impairment. Certain health practitioners implying they had immunologic dysfunction and organic brain injury, led workers to believe they were chemically poisoned. Industrial hygiene evaluation failed to show levels of chemicals above permissible levels. Thorough evaluation by our multidisciplinary panel failed to find significant objective abnormalities by physical exam and laboratory testing. Thirty-nine percent of the workers had sensory irritation and/or skin complaints that generally resolved rapidly with removal from exposure. Psychiatric diagnoses (including major depression and/or panic attacks) were made in 74% of the workers, but only 26% of these had antecedent disease. Fourteen (26%) had multiple somatic complaints that generally persisted despite removal from exposure, but they also had long histories of significant pre-existing psychological illness. Detailed neuropsychologic testing failed to show any definite evidence or organic brain dysfunction in any of the workers tested. We speculate that sensory irritation from low-level volatile organic compounds with autonomic arousal, reinforced by the belief they were "chemically poisoned," led to psychogenic illness.
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PMID:Depression and panic attacks related to phenol-formaldehyde composite material exposure in an aerospace manufacturing plant. 183 99

1. In a multicenter, placebo-controlled, double-blind clinical trial in 155 elderly patients with cognitive decline, glycosaminoglycan polysulfate was found to be a therapeutically effective agent in the treatment of old age dementias. 2. Treatment with glycosaminoglycan polysulfate in the daily dosage of 600 LRU, administered on the basis of a divided dosage schedule for 12 weeks, was significantly superior to an inactive placebo on several outcome measures including the Wechsler Memory Scale-Russell Revision (Easy Paired Associates Learning and Immediate Visual Reproduction), Mini Mental State Examination, the Sandoz Clinical Assessment Geriatric (Cognitive Dysfunction and Depression), Hachinski Dementia Scale, Brief Psychiatric Rating Scale (Confusion and Depressive Withdrawal) and Global Improvement Scale of the Clinical Global Impression. 3. Adverse effects with glycosaminoglycan polysulfate were few and mild. The drug was equally well tolerated and equally effective in the two major dementias of old age, i.e., primary degenerative and multi-infarct. The number of abnormal laboratory test readings remained essentially unchanged from pre-treatment to post-treatment.
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PMID:Glycosaminoglycan polysulfate in the treatment of old age dementias. 186 17

The relationship between depression and dementia is complex. Transient emotional disturbances and long-lasting depressive disorders may occur as psychological reactions to the loss of mental abilities or as behavioural manifestations of brain injury. On the other hand, major depressive disorder of late onset or of a recurrent type may be superimposed on dementing illness. Depression, particularly in elderly individuals, can manifest itself as a reversible syndrome of dementia that responds favourably to antidepressant treatment. It is not known whether the dementia syndrome of depression represents a quantitative intensification of minor cognitive impairments that can be observed in a large proportion of depressed patients. It also remains doubtful whether dementia in depressed patients has to be considered as an epiphenomenon of pervasive melancholic illness. An alternative explanation would look at such conditions as manifestations of a specific brain dysfunction. Major depression associated with cognitive impairment in stroke patients might be regarded as an example of a reversible dementia dysfunction.
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PMID:Depressive disorders and dementia: the clinical view. 189 74

Twenty-seven medication-free, depressed patients (Research Diagnostic Criteria, endogenous subtype) were administered a comprehensive battery testing memory and other cognitive functions before and after a series of bilateral, brief-pulse electroconvulsive therapy (ECT) administered according to a dosage-titration procedure (8.9 +/- 1.981 treatments). A subset of patients (N = 14) were reexamined at 1 month and 6 months after the conclusion of the treatment. Anterograde (verbal and visuospatial tasks), as well as retrograde (famous and personal events), memory function was significantly impaired at the end of the ECT series. By 1 month follow-up, performance had improved to pre-ECT (depression) levels on both anterograde and retrograde tasks and exceeded these by 6 months. The memory deficits induced by ECT were not a consequence of generalized cognitive impairment. Furthermore, depression and ECT were shown to independently affect memory, and recovery from depression was not a consequence of the amnestic action of the treatment. The results generally confirm previous reports regarding the nature of ECT-induced memory impairment, in a different language and culture. They suggest that long-term effects of the treatment on memory are even less prominent than previously observed.
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PMID:Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. 191 54

In the study of dementia four distinct categories of instruments can be distinguished: instruments to examine cognitive dysfunction, to measure the severity of dementia, to assess disturbances in daily behaviour, and instruments to make a differential diagnosis of dementia. The Cambridge Examination for Mental Disorders of the Elderly (CAMDEX), published in 1988, incorporates these four categories in a single comprehensive interview schedule. Items related to the diagnosis of clouded/delirious state, depression and other psychiatric symptoms are also included. The Dutch version (CAMDEX-N) and accompanying software for data analysis and for scientific research were developed. Items were added to the section on physical and neurological examination, and to the section on ancillary investigations. The software can be adapted to future developments in dementia research.
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PMID:[CAMDEX-N: the Dutch version of the Cambridge Examination for Mental Disorders of the Elderly with automatic data processing]. 192 99

Current knowledge of cognitive dysfunction in Parkinson's disease (PD) has largely been obtained from studies of chronically treated patients in whom effects of disease chronicity, treatment, depression and dementia are confounding factors. Studies of untreated patients have examined few cognitive domains and relationships between cognition, depression and motor disability have been incompletely explored. Accordingly, we studied 60 consecutive patients with newly diagnosed, untreated, idiopathic PD and 37 matched, healthy control subjects; no subject had clinical dementia or depression. All subjects received tests of specific processes of memory and cognition, including working memory, verbal and non-verbal short- and long-term memory, language, visuospatial capacity, set-formation and shifting and sequencing. Patients also received quantitative global clinical measures of severity of dementia, depression and motor disability. The PD group as a whole showed deficits in immediate recall of verbal material, language production and semantic fluency, set-formation, cognitive sequencing and working memory and visuomotor construction. However, this group was unimpaired in immediate memory span, long-term forgetting, naming, comprehension and visual perception. Language deficits and more severe frontal lobe impairments were confined to those PD patients scoring abnormally on a Mini Mental State examination. Motor disability correlated strongly with severity of depression but weakly with cognitive impairment. Cognitive sequencing, set-formation and set-shifting deficits tended to associate with depression, but otherwise there was no association between cognition and depression. The results indicate dissociation of cognition and motor control in early PD which suggests that cognitive dysfunction is largely independent of frontostriatal dopamine deficiency underlying motor disability. Some, but not all, of the frontal lobe deficits of chronic disease are detectable in early, untreated PD. The pathogenesis of the cognitive deficits shown here appears to involve extrastriatal dopamine systems or non-dopaminergic pathology. Longitudinal study is necessary to determine whether increasing disease duration exacerbates the early cognitive deficits and affects new cognitive domains, in addition to producing increasing motor disability.
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PMID:Cognitive impairment in early, untreated Parkinson's disease and its relationship to motor disability. 193 36

Hearing impairment is one of the most common causes of disability in the elderly. In addition to its obvious adverse effects on communication, hearing impairment has been associated with impaired mobility, cognitive impairment, and depression. Treatment of hearing impairment can reduce symptoms of depression and improve quality of life in hearing impaired patients. Yet in the Framingham cohort, although 41% of those 65 years of age and older admitted to hearing difficulty, only 10% had ever used a hearing aid. This article discusses the epidemiology of hearing problems in the elderly, types of hearing loss, the adverse effects of hearing loss, the benefits and drawbacks of hearing aids, and the role of the primary care physician in helping hearing impaired.
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PMID:Hearing impairment and the elderly patient. 194 71

Anxiety in the elderly is often mixed with depression, and successful antidepressant treatment will often also eliminate the anxiety. For specific symptoms of generalized anxiety, benzodiazepines are important therapeutic agents. Selection of an appropriate benzodiazepine is guided by pharmacokinetic properties of individual drugs. Long half-life benzodiazepines usually are not preferred for older patients because of cumulative toxicity. Among the short half-life drugs, high-potency compounds (e.g., lorazepam, alprazolam) may be more toxic than low-potency compounds (e.g., oxazepam). Although confirming controlled data are lacking, clinical experience suggests that dependence, rebound symptoms, and memory impairment may be more intense with lorazepam and alprazolam. Clinicians should endeavor to use benzodiazepines for short periods when treating the elderly. Long-term use has been reported effective and nonhazardous, but subtle and gradual cognitive impairment may occur in other patients over time. Buspirone has also been reported as an effective, nontoxic antianxiety compound for older patients, but more experience and comparative research data are needed.
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PMID:Anxiety in the elderly: treatment strategies. 197 20

Nineteen cases are described, including 12 cases from three different families and 7 nonfamilial cases, in which multisystem neurological disease was associated with acanthocytosis in peripheral blood and normal plasma lipoproteins. Mild acanthocytosis can easily be overlooked, and scanning electron microscopy may be helpful. Some neurologically asymptomatic relatives with significant acanthocytosis were identified during family screening, including some who were clinically affected. The mean age of onset was 32 (range 8-62) yrs and the clinical course was usually progressive but there was marked phenotypic variation. Cognitive impairment, psychiatric features and organic personality change occurred in over half the cases, and more than one-third had seizures. Orofaciolingual involuntary movements and pseudobulbar disturbance commonly caused dysphagia and dysarthria that was sometimes severe, but biting of the lips or tongue was rarely seen. Chorea was seen in almost all symptomatic cases but dystonia, tics, involuntary vocalizations and akinetic-rigid features also occurred. Two cases had no movement disorder at all. Computerized tomography often demonstrated cerebral atrophy. Caudate atrophy was seen less commonly, and nonspecific focal and symmetric signal abnormalities from the caudate or lentiform nuclei were seen by magnetic resonance imaging in 3 out of 4 cases. Depression or absence of tendon reflexes was noted in 13 cases and neurophysiological abnormalities often indicated an axonal neuropathy. Sural nerve biopsies from 3 cases showed evidence of a chronic axonal neuropathy with prominent regenerative activity, predominantly affecting the large diameter myelinated fibres. Serum creatine kinase activity was increased in 11 cases but without clinical evidence of a myopathy. Postmortem neuropathological examination in 1 case revealed extensive neuronal loss and gliosis affecting the corpus striatum, pallidum, and the substantia nigra, especially the pars reticulata. The cerebral cortex appeared spared and the spinal cord showed no evidence of anterior horn cell loss. Two examples of the McLeod phenotype, an X-linked abnormality of expression of Kell blood group antigens, were identified in a single family and included 1 female. The genetics of neuroacanthocytosis are unclear and probably heterogeneous, but the available pedigree data and the association with the McLeod phenotype suggest that there may be a locus for this disorder on the short arm of the X chromosome.
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PMID:Neuroacanthocytosis. A clinical, haematological and pathological study of 19 cases. 199 79

A 72 years-old man presented with melancholia with delusions, possibly resulting from multiple lacunar infarcts in the basal ganglia. This case is akin to the syndrome of psychic akinesia and compulsive activity, resulting from lenticular nucleus lesions or frontal lobe lesions. We suggest that melancholia could be a consequence of a certain type of stereotyped mental activity and we would compare this stereotyped mental activity to stereotyped verbal activity in aphasia. Cognitive impairment might then be a cause of depression.
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PMID:[Delusional melancholia and multiple lacunar infarcts of the basal ganglia]. 201 83


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