Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical definition of transient ischemic attacks (TIAs), besides the ischemic pathogenesis is based (i) upon 24 h. duration and (ii) complete reversibility. The limit of 24 h. has been chosen arbitrarily and episodes clearing completely after more than 24 h. do exist. In addition TIAs lasting less than 5 min. would have a higher incidence of subsequent completed stroke. Complete reversibility has also been disregarded: ischemic attacks leaving slight neurological deficits or showing an hypodense area at CT scanning have been shown to have the same significance at TIAs. Different clinical definitions and classifications account for very different natural history features reported in the literature. Transient attacks may be conveniently assessed under the label of Reversible Ischemic Attacks (RIA) covering attacks of 24 h. duration (TIA) and attacks of more than 24 h. duration (Protracted Transient Ischemic Attacks. PTIA). Terms such a RIND or PRIND (Reversible Ischemic Neurological Deficit or Prolonged Reversible Ischemic Neurological Deficit) should be disregarded since they are too general terms covering both cases with 24 and more than 24 h. duration. TIAs and PTIAs should be characterized by a complete clinical regression and normal CT, to avoid relevant wrong diagnostic statements (transient attacks in cases of lacunar stroke, hemorrhages, tumours); where clinical regression is partial and/or CT shows low attenuation areas the case should be labelled as one with partial non progressing stroke (PNS) or minor stroke. The question however arises whether TIA, PTIA or PNS significantly differ from each other from the clinical, prognostic and therapeutic standpoint or, on the contrary, any attempt to differentiate them on these grounds should be considered futile as suggested be Caplan (1983).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Point of view. Transient ischemic attacks. Is a reassessment needed?]. 408

Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease. During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index. To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis. Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet produced, after 12 wk, a progressive increase of heart rate and size, circulation time, and venous pressure, and a ventricular diastolic gallop. Normal values were restored within 7 wk after interrupting alcohol. These several studies suggest that the cumulative effects of repeated ingestion of ethanol in intoxicating doses can produce diminished LV function before clinical evidence of cardiac abnormality, or heart disease not necessarily related to malnutrition.
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PMID:Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy. 430 60

In view of the variables that obscure the pathogenesis of cardiomyopathy, a study was undertaken in mongrel dogs fed ethanol as 36% of calories for up to 22 mo. Both the experimental and control groups maintained body weight, hematocrit, plasma vitamin, and protein levels. Left ventricular function was evaluated in the intact anesthetized dog using indicator dilution for end-diastolic and stroke volume determinations. During increased afterload with angiotensin, the ethanol group exhibited a larger rise of end-diastolic pressure (P<0.01), whereas end-diastolic and stroke volume responses were significantly less than in controls. Preload increments with saline elicited a significantly higher end-diastolic pressure rise in the ethanol group (P<0.01). No hypertrophy, inflammation, or fibrosis was present and it was postulated that the enhanced diastolic stiffness was related to accumulation of Alcian Blue-positive material in the ventricular interstitium. To evaluate myocardial lipid metabolism, [1-(14)C]oleic acid was infused systemically. Plasma specific activity and myocardial lipid uptake were similar in both groups. There was a significantly increased incorporation of label into triglyceride, associated with a reduced (14)CO(2) production, considered the basis for a twofold increment of triglyceride content. In addition, diminished incorporation of [(14)C]oleic acid into phospholipid was observed accompanied by morphologic abnormalities of cardiac cell membranes. Potassium loss and sodium gain, like the lipid alteration, was more prominent in the subendocardium. Thus, chronic ethanol ingestion in this animal model is associated with abnormalities of ventricular function without evident malnutrition, analogous to the preclinical malfunction described in the human alcoholic.
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PMID:Myocardial function and lipid metabolism in the chronic alcoholic animal. 436 46

This prospective study presents the prevalence and risk factors of malnutrition in 49 consecutive stroke patients on the rehabilitation (Rehab) service and at 2- to 4-month follow-up. Malnutrition was diagnosed using biochemical and anthropometric data. Stroke patients, on admission to Rehab, have a very high prevalence of malnutrition. Malnutrition, 49% on admission, declined to 34%, 22%, and 19% at 1 month, 2 months, and follow-up, respectively. Dysphagia, 47% on admission, was associated with malnutrition (p = .032) and significantly declined over time. Using logistic regression, predictors of malnutrition on admission involved acute service tube feedings (p = .002) and histories of diabetes (p = .027) and prior stroke (p = .013). Tube feedings, associated with malnutrition on admission (p = .043), were more prevalent in brain stem lesion patients. Patients tube fed > or = 1 month during rehabilitation or at home were not malnourished. Malnutrition was associated with advanced (> 70 years) age at 1 month (p = .002) and weight loss (p = .011) and lack of community care (p = .006) at follow-up. Early and ongoing detection and treatment of malnutrition are recommended during rehabilitation of stroke patients both on the service and at follow-up.
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PMID:Malnutrition in stroke patients on the rehabilitation service and at follow-up: prevalence and predictors. 771 30

Of all strokes 75% occur in people over age 65, and the incidence of stroke rises with age. Because swallowing problems often result, the elderly stroke patient is at risk for dysphagia and its complications. Acute and chronic swallowing problems are associated with many complications including dehydration, malnutrition, aspiration, pneumonitis, depression and even death. These complications make swallowing problems in the aged stroke patient an important focus for nursing attention. Nurses must be aware of the complexity of normal swallowing mechanisms, knowledgeable about the aged stroke patient's risk for dysphagia, aware of the importance of early detection and treatment of dysphagia and confident about their role in dysphagia assessment and treatment regimen. This information can be used in the assessment, treatment and rehabilitation of the elderly dysphagic stroke patient.
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PMID:Dysphagia in the elderly stroke patient. 807 79

Protein malnutrition remains a problem throughout much of the Caribbean region. In Antigua 5-7% of children are malnourished, and 15% of children aged 17-19% are obese and at risk for diabetes, hypertension, and stroke later in life. Problems of malnutrition are exacerbated by the high cost of fruits and vegetables and nonnutritious imports from the US of fatty fast foods that are high in sugar, fat, and additives. Nutrition education is introduced in home economic courses in schools and in parental education efforts. The Caribbean Food and Nutrition Institute has a pilot education project operating in elementary and secondary schools. The aim is to study the nature, extent, and quality of snacking among children aged 9-11 years of age. The study involves 20 children who keep a log of foods consumed in the course of a day. Snacks are considered to be all food consumed between meals or after the evening meal. Nonbasic foods are identified as those not fitting the basic six food groups. Findings show that every child eats between meals. 60% of the children eat between breakfast and lunch. 41% of all energy is obtained from foods consumed as snacks between lunch and dinner, and 8% of all energy is obtained from morning snacks. Principal snack foods include soft drinks, fresh fruit and unsweetened fruit juices, sweets and chocolates, sugar, and based products (listed in highest to lowest frequency of consumption). Over 33% of daily energy intake, almost 50% of carbohydrate intake, and almost 66% of added sugar are obtained from snacks. Daily consumption averages 61 g of sugar and ranges from 8 to 101 g. 33% of average energy intake is obtained from meals.
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PMID:Children's eating habits: a question of balance. 818 96

Neurogenic dysphagia results from sensorimotor impairment of the oral and pharyngeal phases of swallowing due to a neurologic disorder. The symptoms of neurogenic dysphagia include drooling, difficulty initiating swallowing, nasal regurgitation, difficulty managing secretions, choke/cough episodes while feeding, and food sticking in the throat. If unrecognized and untreated, neurogenic dysphagia can lead to dehydration, malnutrition, and respiratory complications. The symptoms of neurogenic dysphagia may be relatively inapparent on account of both compensation for swallowing impairment and diminution of the laryngeal cough reflex due to a variety of factors. Patients with symptoms of oropharyngeal dysphagia should undergo videofluoroscopy of swallowing, which in the case of neurogenic dysphagia typically reveals impairment of oropharyngeal motor performance and/or laryngeal protection. The many causes of neurogenic dysphagia include stroke, head trauma, Parkinson's disease, motor neuron disease and myopathy. Evaluation of the cause of unexplained neurogenic dysphagia should include consultation by a neurologist, magnetic resonance imaging of the brain, blood tests (routine studies plus muscle enzymes, thyroid screening, vitamin B12 and anti-acetylcholine receptor antibodies), electromyography/nerve conduction studies, and, in certain cases, muscle biopsy or cerebrospinal fluid examination. Treatment of neurogenic dysphagia involves treatment of the underlying neurologic disorder (if possible), swallowing therapy (if oral feeding is reasonably safe to attempt) and gastrostomy (if oral feeding is unsafe or inadequate).
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PMID:Dysphagia associated with neurological disorders. 820 77

The annual incidence of cerebrovascular disease in children is 2.5/100,000 and cerebral infarction is being increasingly recognised in neonates. Deficiency of proteins C and S and their roles in thrombosis have only recently been recognised. Immunologic and functional assays of these proteins now make it possible to determine whether deficiency of them is associated in any particular case of childhood cerebrovascular accident (CVA). We describe two patients, both presenting with stroke in childhood, who were found to be deficient, one in protein C and one in protein S.
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PMID:Protein C and S deficiency causing childhood stroke. 823 61

A 27-year-old woman suffered from a sudden onset of slight paralysis of the right side of her body and the inability to express herself by speech, writing, or signs. She was admitted to the National Rehabilitation Hospital in Washington, D.C., in the US. 6 months prior to these events, she had been in a motor vehicle accident and had since experienced headaches and generalized musculoskeletal pain. The only drug she took was an oral contraceptive (OC), which she took irregularly. Health workers could not arouse her upon admission. Clinical examination revealed symptoms consistent with a left hemispheric stroke. Cerebral computed tomography and magnetic resonance imaging revealed a left temporoparietal infarct. Her free protein S was only 27% on admission and 14% 11 days after admission (normal range, 55-125%). Over the next 72 hours, her physical condition deteriorated, entailing focal motor seizures, right Babinski's sign, loss of pain reflex response on her right side, and complete paralysis of the right side of her body. The left middle cerebral artery appeared to be constricted, which physicians first believed was caused by vasculitis but later found was the result of emboli. The patient developed right femoral vein deep thrombosis. The physicians treated her initially with heparin and followed with warfarin therapy. Nevertheless, embolus. Health workers placed a filter in her inferior vena cava and continued warfarin therapy. She did not experience any more thrombotic or embolic episodes during the rest of her hospital stay. OCs reduce circulating levels of free protein S which, along with activated protein C, inhibits clotting. OCs likely reduced her already existing low levels of free protein S. Deficiency of free protein S was likely responsible for the cerebral infarction and her thrombotic and embolic episodes.
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PMID:A case of cerebral infarction in association with free protein S deficiency and oral contraceptive use. 823 70

Obesity is a common form of malnutrition among the elderly. Excessive weight gain is associated with decreased physical activity and a progressive decline in caloric requirements for weight maintenance. Obesity increases the risk of myocardial infarction, stroke, hypertension, noninsulin-dependent diabetes, osteoarthritis of the lower extremities and several types of cancer. Specific guidelines are recommended for weight-loss programs used in the elderly. While calories from dietary fats and carbohydrates are restricted, a protein intake of approximately 70 g per day is desirable. Exercise is an important part of the weight-loss program and contributes to a general sense of well-being. Limitation of motion may necessitate innovative forms of exercise for elderly patients.
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PMID:Treatment of obesity in the elderly. 846 13


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