Abstracts
Identifieur interne : 000C43 ( Istex/Corpus ); précédent : 000C42; suivant : 000C44Abstracts
Auteurs : Cornelia CremensSource :
- Journal of geriatric psychiatry and neurology [ 0891-9887 ] ; 1991-01.
English descriptors
- KwdEn :
- Anorexia, Basal, Basal ganglia, Brain damage, Calcification, Dementia, Dyskinesia, Early recognition, Elderly patients, Family history, Fluidity, Ganglion, Geriatr psychiatry, Geriatrics, Hydergine, Neuroleptic, Neuroleptic therapy, Older patients, Oral form, Oral physostigmine, Physical examination, Physostigmine, Platelet, Platelet membrane fluidity, Weight loss.
- Teeft :
- Anorexia, Basal, Basal ganglia, Brain damage, Calcification, Dementia, Dyskinesia, Early recognition, Elderly patients, Family history, Fluidity, Ganglion, Geriatr psychiatry, Geriatrics, Hydergine, Neuroleptic, Neuroleptic therapy, Older patients, Oral form, Oral physostigmine, Physical examination, Physostigmine, Platelet, Platelet membrane fluidity, Weight loss.
Url:
DOI: 10.1177/089198879100400114
Links to Exploration step
ISTEX:1958AF7B14B1D76D99C32A73C75CE860039B6FA6Le document en format XML
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<contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Cremens</surname><given-names>Cornelia</given-names></name><degrees>MD</degrees></contrib></contrib-group>
<pub-date pub-type="ppub"><month>01</month><year>1991</year></pub-date><volume>4</volume><issue>1</issue><fpage>57</fpage><lpage>59</lpage><custom-meta-wrap><custom-meta xlink:type="simple"><meta-name>sagemeta-type</meta-name><meta-value>Journal Article</meta-value></custom-meta><custom-meta xlink:type="simple"><meta-name>search-text</meta-name><meta-value>57 Abstracts SAGE Publications, Inc.1991DOI: 10.1177/089198879100400114 Cornelia Cremens MD 'Failure to thrive' in the elderly: Diagnosis and management. Palmer RM Geriatrics 1990;45:47-55. Failure to thrive (FTT), a term familiar to pediatri- cians, describes an insidious decline in the elderly's prior level of functioning. As defined in this article and by other authors, FTT is "a gradual decline in physical and/or cognitive function, usually accompanied by weight loss, reduced appetite, and social withdrawal, that occurs without immediate explanation." FTT has recently been reported to be common in the institutionalized/hospitalized elderly and is often initially encountered by primary care physicians. FTT reflects gradual and subtle decline due to physiologic, psychosocial, and environmental factors. Etiologies of FTT most commonly appear to be dementia, depression, delirium, drug reactions, and chronic diseases. The article discusses a systematic and comprehensive evaluation process that encompasses four areas: a multidimensional assessment of the physical, functional, psychological, and social domains; a targeted history and physical examination; an interview of the patient's family members or caregivers; and selected laboratory studies. Early recognition and management of FTT can reduce the risk of further functional deterioration, hospitalization, or nursing home placement. Management of FTT is directed at the etiology and relative impact of the contributing factors. Probably the most important element is the continuity of care provided by the patient's primary care physician. Ergot mesylates for Alzheimer's disease: A year-long double-blind trial of 3 mg vs 12 mg daily. Jenike MA, Albert M, Baer L, et al. Int J Geriatr Psychiatry 1990;5:375-380. Several classes of drugs have been used to treat dementia of the Alzheimer's type. The most commonly used and studied neurotropic is Hydergine, which consists of three hydrogenated alkaloids of ergot. The article outlines a year-long double-blind study of 25 patients, comparing the use of high (12 mg/day) versus low (3 mg/day) dosages of Hydergine. Seventeen of the 25 patients completed the full-year study and suffered no problematic side effects. Four patients were dropped from the study due to compliance problems. The group identified patients who might benefit most from Hydergine by studying both behavioral and cognitive change. No difference was detected between the low and high dosages of Hydergine on a number of complex memory function tests. The data demonstrated that low-dose therapy was sufficient. There were no significant between-group differences in recogni- tion memory, incidental memory, naming ability, figure drawing, mood, or other psychiatric symptoms. Due to the small sample size, conclusions are considered preliminary. Despite treatment with Hydergine, Alzheimer patients declined cognitively on four measures during the year of the study. High-dose Hydergine had no benefit over low-dose in the measures assessed by this study, and it did not halt the progression of the disease. Further studies need to be performed to determine if Hydergine alone or in combination with other medications might slow the course of the illness. Platelet membrane fluidity, family history, severity and age of onset in Alzheimer's disease. Eagger S, Hajimohammadreza I, Fletcher K, et al. Int J Geriatr Psychiatry 1990;5:395-400. Alzheimer's disease is currently impossible to diagnose with certainty during life without a brain biopsy. This has led to the search for peripheral manifestations of the disease. Platelet membrane fluidity is increased in AD patients, whereas in normal aging, alterations in fluidity occur in the opposite direction. Increased platelet membrane fluidity has been reported to be a stable familial trait, possibly inherited in an autosomal dominant fashion, and has been postulated as a genetic marker for AD. This study assessed the frequency and extent of platelet membrane changes in patients. Platelet membrane fluidity was determined in three groups of subjects: 15 Alz- heimer's patients with a first-degree family history; 16 Alz- heimer's patients with no family history; and 22 healthy controls. Platelet membrane fluidity changes were found to be the same in both AD groups, but none of the controls had increased platelet membrane fluidity. The severity of AD, as measured by the Mini-Mental State Examination and the Cambridge Cognitive Index scores, correlated well with membrane fluidity for the non-family history group but not for the family history group. No apparent association between increased platelet membrane fluidity and age of onset of AD was noted. This study did not find evidence of increased platelet membrane fluidity as a peripheral marker for familial AD. Idiopathic basal ganglia calcification presenting as hypomania. Wylie KR, Harris SJ. Int J Geriatr Psychiatry 1990 ;5 :401- 402. Idiopathic basal ganglia calcification (IBGC), also known as Fahr's disease, is characterized by four criteria: bilateral basal ganglia calcification; extrapyramidal disturbance ; neuropsychiatric abnormalities; and normal serum 58 calcium-phosphate levels. IBGC involves nonatheroscle- rotic symmetrical calcification of cerebral vessels of certain areas of the brain, usually the basal ganglia, dentate nucleus, cerebellar cortex, and cerebral cortex. Movement disorders of the parkinsonian or chorea type are present in 20% to 30% of the patients. Neuropsychiatric manifestations are either schizophrenic-like psychosis or dementia. The paper presents a 64-year-old woman with hypomanic psychosis who later went on to develop subcortical dementia and. parkinsonian movement disorders. Computed tomography revealed bilateral calcifications in the basal ganglia. Parathyroid disease and other causes of calcification were ruled out. Only one prior case of organic mood disorder of the manic type had been reported in association with IBGC. Treatment is palliative, because the course appears to be progressive. Oral physostigmine as treatment for dementia of the Alzheimer type: A long-term outpatient trial. Jenike MA, Albert MS, Baer L. Alzheimer Dis Assoc Disord 1990;4:226-231. Abnormalities in the cholinergic system in Alz- heimer's disease (AD) and their association with memory deficits in controls has led to various pharmacologic treatment hypotheses. Initial research used choline or other precursors of acetylcholine in an attempt to increase the extracellular concentration. However, results were disappointing. Further attempts were made to inhibit the breakdown of acetylcholine in AD brains by using a cho- linesterase inhibitor, such as physostigmine. One obstacle to treatment with physostigmine was the unavailability of an oral form of the drug. However, a few years ago an oral form became available for research purposes. This study compared six AD patients treated with oral physostigmine for 9 to 27 months with six control AD patients matched for sex, age, and initial degree of dementia not given physostigmine. Although the sample size was small, all controls' Dementia Rating Scale scores declined, while of the six treated patients, two patients had increased scores and one patient's score dropped only 2 points. One question was whether the drug was absorbed into the central nervous system or not in the nonresponders. Second, had the dementia in the nonresponders damaged the cholinergic and serotonergic cells to such a degree that the physostigmine could not be used. Finally, without postmortem documentation, the possibility of misdiagnosis could not be eliminated. Large-scale studies with long-term follow-up will be necessary to evaluate the effect, if any, of physostigmine on the symptoms and course of AD. Data generated on these six patients clearly demonstrates the safety of oral physostigmine in long-term trials. Anorexia in older patients: Its meaning and management. Mor- ley JE. Geriatrics 1990;45:59-66. Increasing evidence suggests that a major risk factor for mortality in older individuals is low weight. This article reviewed major causes of weight loss in the elderly with regard to social, psychological, medical, and age-related issues. Social causes include isolation, poverty, and inability to shop for oneself. Institutionalized elderly can no longer choose their own food, and they are not as com- fortable while eating. Psychological causes include depression, bereavement, alcoholism, dementia, late-life paranoia, late-life mania, loss of sense of control, anorexia ner- vosa, and excessive burdens of life. Medical causes were divided into four categories: increased metabolism, anorexia, swallowing problems, and malabsorption. Age-related causes are related to multidimensional factors of aging such as decrease in olfaction, deteriorating vision, and poor dentition. Management of geriatric anorexia includes early recognition of malnutrition, identification of treatable causes, detection of social factors, active treatment of dysphagia, avoidance of special medical diets, identification of abnormal attitudes toward food, evaluation of food likes and dislikes, aggressive maintenance of food intake, and active prevention programs aimed at increasing elderly awareness of the dangers of being underweight. Assessing competency in the elderly. Janofsky JS. Geriatrics 1990;45:45-48. This paper provides guidelines that help the geriatri- cian understand the clinical and legal concepts behind competency. Recommendations follow on how to manage a patient who is clearly not competent to make medical decisions. In addition, the author delineates recommendations that may be given to an elderly person on how to preplan legal matters to maximize autonomy should they become incompetent at some future time. According to this author, informed consent requires that a patient understand the medical procedure being proposed, that consent is voluntary, and that the patient is competent to give consent. Due to the potential for declining cognitive functioning with increasing age, elderly patients are at risk of becoming incompetent and thereby unable, according to the law, to give consent. Advance directives, such as a living will and durable power of attorney, allow competent patients to guide their doctors and others concerned with their health care choices if they are not able to make their own choices in the future. Tardive dyskinesia: Managing a common neuroleptic side effect. Jeste DV, Krull AJ, Kilbourn K. Geriatrics 1990;45:49-58. Neuroleptics are useful agents commonly prescribed in elderly patients to treat psychotic and severe behavioral symptoms. With the continuing growth of the over-65- year-old population, the number of older patients prescribed neuroleptics may be expected to increase. Unfortunately, older patients are at high risk of developing side effects, especially tardive dyskinesia (TD). This article discusses the conditions under which TD might arise during or after neuroleptic therapy, how to make a differential diagnosis, and how best to approach treatment. Careful assessment prior to initiating treatment, as well as close monitoring during treatment with both the patient and the families involved, can prevent severe side effects. Risk factors in the elderly include a high cumulative neuroleptic exposure, mood disorder, brain damage, and early extrapyramidal reactions to treatment. TD usually develops gradually, with choreoathetoid movements in the orobuc- colingual areas in 80% of the patients. If TD is suspected, the patient and family should be informed, indications for 59 continued neuroleptic therapy evaluated, and a complete work-up for dyskinetic movements ordered. Differential diagnoses include: drug-induced parkinsonism, Hunting- ton's disease, Wilson's disease, drug-induced dyskinesia, toxin-induced dyskinesia, hyperthyroidism, edentulous dyskinesia, and spontaneous dyskinesia. Once the diagnosis of TD is made, taper the dose and ultimately discontinue the neuroleptic if the risk of halting treatment is not high. If discontinuing therapy is not possible, then switch to a lower-potency agent at the minimal effective dose. The decision to continue therapy should be discussed with the patient and the family to evaluate the ongoing risk. From disease to delirium: Managing the declining elderly patient. McCabe M. Geriatrics 1990;45:28-31. Many geriatric patients have concomitant physical and psychiatric illnesses, but at times it may be difficult to determine which is primary. Delirium, a transient syndrome of acute onset that presents with psychiatric symp- toms that are usually the manifestation of an organic disorder, is often unrecognized by health professionals. Delirium is a manifestation of a cerebral dysfunction; however, its pathophysiology is often unknown. Factors that predispose the elderly to its development include sensory impairment, brain damage, reduced homeostatic regulatory reserve, psychosocial stresses, the presence of chronic illnesses, and age-related physiologic changes. Differential diagnosis includes dementia, depression, psychotic states, and anxiety. The hallmark of delirium is inattentiveness, which can be evaluated using the digit span test and the letter recognition test. Comprehensive laboratory studies are suggested, due to the extensive etiologic possibilities. However, the tests can be narrowed after the complete history and physical examination have been reviewed. Treatment includes correcting the underlying cause, providing a supportive environment, and assuring the pa- tient's safety. The recognition and diagnosis of delirium are important because of the reversibility and because of the high mortality if untreated.</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Abstracts</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Abstracts</title></titleInfo><name type="personal"><namePart type="given">Cornelia</namePart><namePart type="family">Cremens</namePart><namePart type="termsOfAddress">MD</namePart></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Sage Publications</publisher><place><placeTerm type="text">Sage CA: Thousand Oaks, CA</placeTerm></place><dateIssued encoding="w3cdtf">1991-01</dateIssued><copyrightDate encoding="w3cdtf">1991</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><relatedItem type="host"><titleInfo><title>Journal of geriatric psychiatry and neurology</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0891-9887</identifier><identifier type="eISSN">1552-5708</identifier><identifier type="PublisherID">JGP</identifier><identifier type="PublisherID-hwp">spjgp</identifier><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>57</start><end>59</end></extent></part></relatedItem><identifier type="istex">1958AF7B14B1D76D99C32A73C75CE860039B6FA6</identifier><identifier type="ark">ark:/67375/M70-G5H8BP3V-7</identifier><identifier type="DOI">10.1177/089198879100400114</identifier><identifier type="ArticleID">10.1177_089198879100400114</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-0J1N7DQT-B">sage</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/1958AF7B14B1D76D99C32A73C75CE860039B6FA6/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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|clé= ISTEX:1958AF7B14B1D76D99C32A73C75CE860039B6FA6
|texte= Abstracts
}}
| This area was generated with Dilib version V0.6.32. |  |