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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three hundred one patients were examined for suicidal plans during the acute hospital period following stroke and at 3, 6, 12, and 24 months' follow-up. It was found that 6.6% of patients developed suicidal plans during the initial in-hospital evaluation (acute-onset suicidal plans) and 11.3% of patients developed suicidal plans at 3, 6, 12, or 24 months' follow-up (delayed-onset suicidal plans). The development of both acute and delayed-onset suicidal plans was strongly related to the existence of depressive disorders, especially major depression, and to a prior history of stroke. Acute-onset suicidal plans were also related to premorbid alcohol abuse. Acute-onset suicidal patients had more anterior lesion location and delayed-onset suicidal patients had more posterior stroke lesions. Delayed-onset suicidal plans were not related to alcohol abuse but tended to be associated with greater physical impairment and poorer social support during the acute poststroke period. These data suggest that the etiology of these two types of suicidal plans may be different with acute onset related to biological mechanisms and delayed onset related to psychological mechanisms.
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PMID:Suicidal plans in patients with stroke: comparison between acute-onset and delayed-onset suicidal plans. 914 75

We report 8 patients with the acquired immunodeficiency syndrome (AIDS) and intracerebral haemorrhage. There were 7 men and 1 woman (mean age 37.2 years) with a mean CD4 count of 81.2/mm3. Alcohol abuse was recorded in 7 patients, intravenous drug use in 4, homosexual activity in 2, thrombocytopaenia in 1 and severe hypertension in 1. There were 5 lobar and 3 deep haemorrhages. Potential aetiologies of intracerebral haemorrhage included cerebral toxoplasmosis (n = 2), thrombocytopenia (n = 2), hypertension (n = 1) and cerebral tuberculosis (n = 1). Data of these patients were compared with those of 30 AIDS inpatients without brain haemorrhage matched by age and sex and no statistically significant differences in risk factors for AIDS except for alcohol abuse (> 80 g/day) (p = 0.045) were found. Causes of brain haemorrhage in AIDS patients are heterogeneous. The relationship between both conditions may be explained by the effect of several predisposing factors to stroke in association with AIDS-related complications. Intracerebral haemorrhage is a late and serious complication of AIDS (mortality 62.5%). The frequency of intracerebral haemorrhage in AIDS (1.0%) is higher than that expected in a general population of young adults.
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PMID:Intracerebral haemorrhage in AIDS. 968 62

Although the treatment of acute ischemic stroke has improved, the greatest reductions in stroke mortality and morbidity may possibly be achieved through more effective prevention strategies. Toward this goal, risk factor profiles for initial and recurrent stroke have been identified through longitudinal epidemiologic studies. Nonmodifiable risk markers for initial ischemic stroke include age, sex, family history, and race/ethnicity. Modifiable risk factors for first ischemic stroke include hypertension, cardiac disease (particularly atrial fibrillation), diabetes, hyperlipidemia, cigarette smoking, alcohol abuse, physical inactivity, asymptomatic carotid stenosis, and transient ischemic attack. As improved acute treatments increase survival after a first stroke, the threat of increased morbidity from stroke recurrence will have greater significance. The risk and specific determinants of early and late stroke recurrence are the subject of ongoing investigations. Age, stroke syndrome, hypertension, cardiac disease (particularly congestive heart failure), hyperglycemia, and alcohol abuse have been identified as predictors of late stroke recurrence. Now that many risk factors are established, greater emphasis should be placed on identifying high stroke-risk patient populations for intensive risk factor modification and antithrombotic treatments. Better understanding and management of stroke risk factors will undoubtedly improve our ability to prevent first and recurrent ischemic stroke.
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PMID:Identifying patient populations at high risk for stroke. 974 29

The ingestion of one or two alcoholic drinks can affect heart rate, blood pressure, cardiac output, myocardial contractility, and regional blood flow. These actions generally are not clinically important. In the presence of cardiovascular disease, however, even such small quantities of alcohol might result in transient unfavorable hemodynamic changes. Moreover, alcohol abuse can produce cardiac arrhythmias, hypertension, cardiomyopathy, stroke, and even sudden death. In contrast, moderate alcohol use produces changes that have an overall favorable effect on atherosclerotic-related vascular diseases. Because cardiovascular disease due to atherosclerosis is the leading cause of death in Western society, this desirable effect of alcohol use outweighs its detrimental actions, resulting in favorable findings in population studies. Nevertheless, the body of evidence argues against encouraging alcohol use for its cardiovascular effects.
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PMID:Cardiovascular effects of alcohol. 975 45

Sialic acid (SA), N-acetylated derivatives of neuraminic acid, play a central role in the biomedical functioning of humans. The normal range of total sialic acid (TSA) level in serum/plasma is 1.58-2.22 mmol L-1, the free form of SA only constituting 0.5-3 mumol L-1 and the lipid-associated (LSA) forms 10-50 mumol L-1. Notably, considerably higher amounts of free SA are found in urine than in serum/plasma (approximately 50% of the total SA). In inherited SA storage diseases such as Salla's disease, SA levels are elevated many times over, and their determination during clinical investigation is well established. Furthermore, a number of reports describe elevated SA levels in various other diseases, tentatively suggesting broader clinical utility for SA markers. Increased SA concentrations have been reported during inflammatory processes, probably resulting from increased levels of richly sialylated acute-phase glycoproteins. A connection between increased SA levels and elevated stroke and cardiovascular mortality risk has also been reported. In addition, SA levels are slightly increased in cancer, positively correlating with the degree of metastasis, as well as in alcohol abuse, diabetes, chronic renal failure and chronic glomerulonephritis. Several different mechanisms are assumed to underlie the elevated SA concentrations in these disorders. The apparent non-specificity of SA to a given disease limits the potential clinical usefulness of SA determination. In addition, some non-pathological factors, such as aging, pregnancy and smoking, may cause changes in SA concentrations. The absolute increases in SA levels are also rather small (save those in inherited SA storage disorders); this further limits the clinical potential of SA as a marker. Tentatively, SA markers might serve as adjuncts, when combined with other markers, in disease screening, disease progression follow-up, and in the monitoring of treatment response. To become clinically useful, however, the existing SA determination assays need to be considerably refined to reduce interferences, to be specific for certain SA forms, and to be more easy to use.
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PMID:Occurrence of sialic acids in healthy humans and different disorders. 1035 98

Although epidemiological studies are limited by diagnostic uncertainties, they suggest that stroke increases the risk of dementia. The mortality rate is higher in vascular dementia (VaD) than in Alzheimer's disease (AD). Community-based studies have provided several consistent findings: (i) age dependence with prevalence rates doubling every 5 years, (ii) a higher frequency in men and (iii) nation-to-nation differences. The prevalence of VaD ranges from 2.2% in 70- to 79-year-old women, to 16.3% in men >80 years. One sixth of acute stroke patients have preexisting dementia. The incidence of VaD has been studied much less extensively than that of AD, and substantial variations in the incidence rates have been observed: annual incidence rates (per 100,000) range from 20 to 40 between 60 and 69 years of age and from 200 to 700 over 80. The incidence rate of VaD declined over the last 2 decades, probably as a consequence of effective stroke prevention. It is generally assumed that risk factors for VaD are those of stroke, with arterial hypertension as leading factor, followed by atherosclerotic disease, low education level, alcohol abuse and heart disease. Stroke characteristics, such as lacunar infarction and left-sided hemispheric lesions, are major determinants of VaD. The cerebrovascular lesions are likely to be the only cause of dementia in strategic infarcts, in lacunar state, in hereditary cystatin C amyloid angiopathy and in CADASIL. However, white matter changes, and associated Alzheimer pathology, which are both frequent in this age category, may also contribute to the cognitive decline.
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PMID:Epidemiology of vascular dementia. 1042 61

Increasing emphasis has been placed on the detection and treatment of hazardous and harmful drinking disorders, particularly among patients who are seen in primary care settings. In this review, we summarize the epidemiology and health-related effects of hazardous and harmful drinking and discuss current methods for their detection and treatment. Hazardous drinking is defined as a quantity or pattern of alcohol consumption that places patients at risk for adverse health events, while harmful drinking is defined as alcohol consumption that results in adverse events (e.g., physical or psychological harm). Prevalence estimates range from 4% to 29% for hazardous drinking and from less than 1% to 10% for harmful drinking. Data from several recent large prospective studies suggest that alcohol consumption in quantities consistent with hazardous or harmful drinking may increase risk for adverse health events, such as hemorrhagic stroke and breast cancer. Existing screening instruments, such as the Michigan Alcoholism Screening Test (MAST) or the CAGE questionnaire, while excellent for detecting alcohol abuse or dependence, should not be used alone to screen for hazardous and harmful drinking. The Alcohol Use Disorders Identification Test (AUDIT) is currently the only instrument specifically designed to identify hazardous and harmful drinking. Treatment of these disorders in the form of brief interventions can be successfully accomplished in primary care settings, as demonstrated by a number of well-conducted randomized trials. Given its proven efficacy in the primary care setting, we recommend routine application of this treatment approach.
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PMID:Hazardous and harmful alcohol consumption in primary care. 1044 69

Alcohol consumption has been reported to have both beneficial and harmful effects on the incidence of stroke. Different drinking habits may explain the diversity of the observations, but this is still unclear. We reviewed recent clinical and epidemiological studies to find out whether alcohol intake could increase or decrease the risk for stroke. By a systematic survey of literature published from 1989 to 1997, we identified 14 case-control studies addressing alcohol as a risk factor for haemorrhagic and ischaemic stroke morbidity and fulfilling the following criteria: the type of stroke was determined by a head computerised tomography scan on admission or at autopsy; and alcohol consumption was verified using structured questionnaires or by personal interviews. In some studies, adjustment for hypertension abolished the independent role of alcohol as a risk factor. On the other hand, the studies covering even recent alcohol intake showed in many cases that heavy drinking is an independent risk factor for most stroke subtypes, and that the risk may decrease relatively rapidly after the cessation of alcohol abuse. In some studies, regular light to moderate drinking seemed to be associated with a decreased risk for ischaemic stroke of atherothrombotic origin. In conclusion, recent heavy alcohol intake seems to be an independent risk factor for all major subtypes of stroke. The ultimate mechanisms leading to the increased risk are unclear. The significance of alcohol as a risk factor has been demonstrated in young subjects because they are more often heavy drinkers than the elderly. Several factors to explain the beneficial effect of light to moderate drinking have been proposed.
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PMID:Alcohol intake and the risk of stroke. 1050 Dec 73

Although there is general agreement that chronic ingestion of alcohol poses great risks for normal cardiovascular functions and peripheral-vascular homeostasis, a direct cause and effect between the real phenomena of alcohol-induced headache and risk of brain injury and stroke is not appreciated. "Binge drinking" of alcohol is associated with an ever-growing number of strokes and sudden death. It is becoming clear that alcohol ingestion can result in profoundly different actions on the cerebral circulation (e.g., vasodilation, vasoconstriction-spasm, vessel rupture), depending upon dose and physiologic state of host. Using rats, it has been demonstrated that acute, high doses of ethanol can result in stroke-like events concomitant with alterations in brain bioenergetics. We review recent in vivo findings obtained with 31P-NMR spectroscopy, optical reflectance spectroscopy, and direct in vivo microcirculatory studies on the intact brain. Alcohol-induced hemorrhagic stroke is preceded by a rapid fall in brain intracellular free magnesium ions ([Mg2+]i) followed by cerebrovasospasm and reductions in phosphocreatine (PCr)/ATP ratio, intracellular pH, and the cytosolic phosphorylation potential (CPP) with concomitant rises in deoxyhemoglobin (DH), mitochondrial reduced cytochrome oxidase aa3 (rCOaa3), blood volume, and intracellular inorganic phosphate (Pi). Using osmotic mini-pumps implanted in the third cerebral ventricle, containing 30% ethanol, it was found that brain [Mg2+]i is reduced 30% after 14 days; brain PCr fell 15%, whereas the CPP fell 40%. Such animals became susceptible to stroke from nonlethal doses of ethanol. Human subjects with mild head injury have been found to exhibit early deficits in serum ionized Mg (IMg2+); the greater the degree of early head injury (30 min-8 h), the greater and more profound the deficit in serum IMg2+ and the greater the ionized Ca (ICa2+) to IMg2+ ratio. Patients with histories of alcohol abuse or ingestion of alcohol prior to head injury exhibited greater deficits in IMg2+ (and higher ICa2+/IMg2+ ratios) and, unlike the subjects without alcohol, did not leave the hospital for at least several days. Women, for some unknown reason, exhibit a much higher incidence of morbidity and mortality from subarachnoid hemorrhage (SAH) than men. Data on 105 men and women with different types of stroke indicate that, on the average, a 20% deficit in serum IMg2+ is seen; total Mg (TMg) or blood pH is usually near normal. Women with SAH, however, exhibit much lower IMg2+ and higher ICa2+/IMg2+ ratios; the presence of ethanol in the blood is associated with even more depression in IMg2+ in SAH in women. It is possible that prior alcohol ingestion is, in large measure, responsible for a great deal of this unexplained higher incidence of SAH in women. It has recently been reported that the cyclical changes in estrogenic hormones appear to control the serum IMg2+ level in young women. A surge in estrogenic levels prior to SAH could thus precipitate, in part, the SAH. In other human studies, it has been shown that migraines and headache, dizziness, and hangover, which accompany ethanol ingestion, are associated with rapid deficits in serum IMg2+ but not in TMg. The former, and the alcohol-associated headache, can be ameliorated with IV administration of MgSO4. Premenstrual tension-headache (PTH) and its exacerbation by alcohol in women is also accompanied by deficits in IMg2+, and elevation in serum ICa2+/IMg2+; IV MgSO4 corrects the PTH and the serum deficit in IMg2+. Animal experiments show that IV Mg2+ can prevent alcohol-induced hemorrhagic stroke and the subsequent fall in brain [Mg2+]i, [PCr], pHi, and CPP. Other recent data indicate that alcohol-induced cellular loss of [Mg2+]i is associated with cellular Ca2+ overload and generation of oxygen-derived free radicals; chronic pretreatment with vitamin E prevents alcohol-induced vascular injury and pathology in the brain. (ABSTRACT TRUNCATED)
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PMID:Association of alcohol in brain injury, headaches, and stroke with brain-tissue and serum levels of ionized magnesium: a review of recent findings and mechanisms of action. 1054 55

The authors reviewed clinical records of 57 consecutive adults (age: 17-78, 63%--men) treated in the intensive care unit to convulsive SE that was refractory to first-line medication (BDZ,PB). They were divided into three groups: up to 30 (mean 21 years, 28%), between 31-50 (43 y, 32%) and above 50 (59 y, 40%), 58% had previously had epilepsy with prevalence in the youngest (85%). Among the oldest in whom epilepsy occurred de novo as much as 42% experienced it in the form of convulsive SE. Generalized SE was observed in 83% of cases; exclusively in patients up to 50 and in 61% of the oldest. The identifiable precipitating causes of SE were determined in 72% cases but in 25% there were two or more of them. Among previously epileptics leading etiologies for SE were: alcohol abuse, infection or drug withdrawal. Recent brain injury (stroke, neuro-infection, trauma) accelerated refractory seizures in epilepsy-free cases. Time to recovery varied from 0.5-2 (6%) to 2-6 or above 6 hrs (46% each) after continuous i.v. administration of BZD or chlormethiazole (53%) when ineffective. No side effects were noted. The commonest complications during SE were hyperthermia and transient dysregulation of circulatory or/and respiratory systems. Everyone was led out of SE. Overall mortality amounted to 12%. Among the deceased 71% were in the oldest group and everyone with recent brain lesion. This study highlights differences in the course of convulsive SE according to age and underlying etiology and the importance of intense care in therapeutic schedule. A more common chlormethiazole administration, a useful therapeutic tool in management of convulsive SE in adults had been discussed.
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PMID:[Convulsive status epilepticus--clinical analysis of patients treated iin the Neurological Clinics, Medical Academy in Lublin in the years 1986-1995]. 1076 Dec 41


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