gerstmann-straussler-scheinker disease/ödéma

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Pathogenesis of hepatic encephalopathy and brain edema in acute liver failure.

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Neuropathologic investigations in acute liver failure (ALF) reveal significant alterations to neuroglia consisting of swelling of astrocytes leading to cytotoxic brain edema and intracranial hypertension as well as activation of microglia indicative of a central neuroinflammatory response. Increased

Encephalopathy and cerebral edema in the setting of acute liver failure: pathogenesis and management.

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Cerebral edema is a potential life-threatening complication in patients with acute liver failure who progress to grade III/IV encephalopathy. The incidence is variably reported but appears to be most prevalent in those patients with hyperacute liver failure as opposed to subacute forms of liver

Diffusion-weighted imaging abnormalities in wernicke encephalopathy: reversible cytotoxic edema?

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BACKGROUND Wernicke encephalopathy (WE) is a metabolic disorder of the central nervous system resulting from vitamin B(1) deficiency. The exact mechanisms underlying the pathogenesis of the lesions in WE are not completely understood. Vitamin B1 deficiency is associated with intracellular and

Fulminant encephalopathy with marked brain edema and bilateral thalamic lesions.

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We encountered two children with acute encephalopathy associated with unique clinical manifestations. Both the patients had status epilepticus at onset and neuroimaging studies revealed marked brain edema and bilateral thalamic lesions. Although they were treated with steroids and immunoglobulin,

Drug-Related Hyponatremic Encephalopathy: Rapid Clinical Response Averts Life-Threatening Acute Cerebral Edema.

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BACKGROUND Drug-induced hyponatremia characteristically presents with subtle psychomotor symptoms due to its slow onset, which permits compensatory volume adjustment to hypo-osmolality in the central nervous system. Due mainly to the syndrome of inappropriate antidiuretic hormone secretion (SIADH),

Increased toll-like receptor 4 in cerebral endothelial cells contributes to the astrocyte swelling and brain edema in acute hepatic encephalopathy.

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Astrocyte swelling and the subsequent increase in intracranial pressure and brain herniation are major clinical consequences in patients with acute hepatic encephalopathy. We recently reported that conditioned media from brain endothelial cells (ECs) exposed to ammonia, a mixture of cytokines (CKs)

Effect of body temperature on brain edema and encephalopathy in the rat after hepatic devascularization.

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Brain edema is a fatal complication of fulminant hepatic failure and its pathogenesis remains unclear. To determine its presence in a model of ischemic hepatic failure, rats were subjected to a portacaval anastomosis followed by hepatic artery ligation. Brain water was measured using the sensitive

Roles of changes in active glutamine transport in brain edema development during hepatic encephalopathy: an emerging concept.

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Excessive glutamine (Gln) synthesis in ammonia-overloaded astrocytes contributes to astrocytic swelling and brain edema, the major complication of hepatic encephalopathy (HE). Much of the newly formed Gln is believed to enter mitochondria, where it is recycled to ammonia, which causes mitochondrial

Cytotoxic Edema in Posterior Reversible Encephalopathy Syndrome: Correlation of MRI Features with Serum Albumin Levels.

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OBJECTIVE Posterior reversible encephalopathy syndrome is a clinicoradiologic entity with typical MR imaging showing predominant vasogenic and occasional cytotoxic edema. It is unclear whether MR imaging correlates with levels of serum albumin. We determined potential risk factors for development of

Extracellular edema and glial response to it in the cerebellum of suckling rats with low-dose lead encephalopathy. An electron microscopic and immunohistochemical study.

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Newborn rats were exposed to daily intraperitoneal injections of 10 mg lead nitrate per kg body weight for the first 15 postnatal days. The growth and mortality of the lead-exposed animals did not differ from their control litter-mates, injected with vehicle only. In our previous studies, focal

Brain edema dynamics in patients with overt hepatic encephalopathy A magnetic resonance imaging study.

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The aim of our study was to investigate the dynamics of brain water content assessed by magnetic resonance imaging (MRI) applications in patients with cirrhosis and overt episodic hepatic encephalopathy (HE). METHODS Twenty-four patients with cirrhosis and overt HE, 9 healthy controls and 9 controls

[Acute reversible encephalopathy with brain edema and serial seizures in pseudohypoparathyroidism].

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A 16 year old patient with the typical clinical signs of Albright's hereditary dystrophia developed series of epileptic seizures with loss of consciousness, tonic muscle contractions and bite of the tongue. After termination of the seizures there was coma without focal neurological signs. CT scan

[Fulminating meningitis caused by Haemophilus influenzae with rapid progression of severe brain edema similar to acute encephalopathy].

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We report a 4-year-old boy with fulminating meningitis caused by Haemophilus influenzae (Hib). He suddenly developed fever, vomiting and then somnolence. As bacterial meningitis was suspected, treatment with antibiotics was started at 12 hours after the onset. However, there was a rapid progression

Management of concomitant metabolic encephalopathy and meningioma with vasogenic edema and impending herniation.

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UNASSIGNED Altered mental status describes impaired mental functioning ranging from confusion to coma and indicates an illness, either metabolic or structural in nature. Metabolic causes include hypothyroidism, hyperuremia, hypo/hyperglycemia, hypo/hypernatremia, and encephalopathy. The structural

Non-Immune Hydrops, Hypotonia, Encephalopathy, and Liver Failure with Novel Compound Heterozygous AHCY Mutations.

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A late-preterm infant with a prenatal diagnosis of non-immune hydrops was born with hypotonia, poor respiratory effort, chylothorax, encephalopathy, coagulopathy, progressive hepatic failure, and refractory pulmonary hypertension. Life support was withdrawn at 7 days of life due to multisystem organ

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