alcoholism/opuch

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Baclofen-induced edema in alcohol use disorders.

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[Relationship between the Expression of α-syn and Neuronal Apoptosis in Brain Cortex of Acute Alcoholism Rats].

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OBJECTIVE To observe the changes of expression of α-synuclein （α-syn） and neuronal apoptosis in brain cortex of acute alcoholism rats and to explore the mechanism of the damage caused by ethanol to the neurons. METHODS The model of acute alcoholism rat was established by 50% alcohol gavage. The

Bilateral putaminal hemorrhage with cerebral edema in hyperglycemic hyperosmolar syndrome.

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Bilateral putaminal hemorrhages rarely occur simultaneously in hypertensive patients. The association of intracerebral hemorrhage with cerebral edema (CE) has been rarely reported in diabetic patients. We present a patient with bilateral putaminal hemorrhage (BPH) and CE during the course of

Brain damage due to episodic alcohol exposure in vivo and in vitro: furosemide neuroprotection implicates edema-based mechanism.

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Adult rats intubated with a single dose of ethanol (alcohol; approximately 5 g/kg) for 5 to 10 successive days incur neurodegeneration in the entorhinal cortex, dentate gyrus, and olfactory bulbs accompanied by cerebrocortical edema and electrolyte (Na+, K+) accumulation. The brain damage is not

[Congestive heart failure due to chronic alcoholism (author's transl)].

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In rare instances, chronic alcoholism leads to the congestive heart failure which is characteristic of alcoholic beriberi with edema. The affected patients is usually a young man with longstanding alcoholic intoxication and often with neurologic features. Onset is often sudden, with dyspnea on

[Differential diagnosis of a macrocytic, hyperchromic anemia following alcohol abuse and simultaneous therapy with triamterene and cotrimoxazole].

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METHODS A 50-year-old woman was admitted to our emergency room because of progressive weakness. She collapsed the night before admission. Skin and mucosa were pale, she denied major infections or bleedings. An alcohol abuse was known for many years. Because of edema she received a therapy with

Damage of hippocampal neurons in rats with chronic alcoholism.

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Chronic alcoholism can damage the cytoskeleton and aggravate neurological deficits. However, the effect of chronic alcoholism on hippocampal neurons remains unclear. In this study, a model of chronic alcoholism was established in rats that were fed with 6% alcohol for 42 days. Endogenous hydrogen

Decision support tool for early differential diagnosis of acute lung injury and cardiogenic pulmonary edema in medical critically ill patients.

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BACKGROUND At the onset of acute hypoxic respiratory failure, critically ill patients with acute lung injury (ALI) may be difficult to distinguish from those with cardiogenic pulmonary edema (CPE). No single clinical parameter provides satisfying prediction. We hypothesized that a combination of

Intramyocardial small-vessel disease in chronic alcoholism.

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A morphologic study of the small (50 to 200 micron) intramyocardial coronary arteries was performed. The cases chosen for study were selected from a relatively young group of patients without clinical evidence of alcoholic cardiomyopathy or pathologic evidence of large coronary artery disease, in

[Alcohol abuse as a risk factor for ARDS].

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Morbidity and mortality rates of ARDS (acute respiratory distress syndrome) are high in patients with a history of chronic alcohol abuse. In addition to susceptibility to lung infection, alteration of local cellular functions in the lung has recently been proposed as a new mechanism of exacerbation

Cessation of Smoking and Alcohol Addiction Following Thalamic Hemorrhage.

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BACKGROUND We describe a case of thalamic intracerebral hemorrhage leading to cessation of smoking. METHODS A 53-year-old female presented to the emergency department with right-sided weakness and dysarthria. Initial systolic blood pressure was 220 mm Hg. Computed tomography scan showed a left

Alcohol abuse and pulmonary disease.

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ARDS is a severe form of lung injury characterized by increased permeability of the alveolar capillary membrane, diffuse alveolar damage, the accumulation of proteinaceous interstitial and intra-alveolar edema, and the presence of hyaline membranes. These pathological changes are accompanied by

Double-Blind Randomized Clinical Trial of Prazosin for Alcohol Use Disorder.

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OBJECTIVE Current medications for alcohol use disorder do not target brain noradrenergic pathways. Theoretical and preclinical evidence suggests that noradrenergic circuits may be involved in alcohol reinforcement and relapse. After a positive pilot study, the authors tested the α-1 adrenergic

[Rapid improvement of callosal edema by thiamine administration in Marchiafava-Bignami disease: a case report].

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Marchiafava-Bignami disease (MBD) associated with chronic alcoholism is a fatal disorder characterized by demyelination of the corpus callosum. A 62-year-old Japanese man, a heavy drinker for his last over 10 years, was admitted to our hospital because of acute onset of speech disturbance. The first

Alcohol abuse promotes changes in non-synaptic epileptiform activity with concomitant expression changes in cotransporters and glial cells.

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Non-synaptic mechanisms are being considered the common factor of brain damage in status epilepticus and alcohol intoxication. The present work reports the influence of the chronic use of ethanol on epileptic processes sustained by non-synaptic mechanisms. Adult male Wistar rats administered with

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