Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0085584 (encephalopathy)
18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The epileptogenicity of caffeine and aminophylline was studied in rats. Intraperitoneal administration of caffeine produced an immediate excitation and seizures followed by an encephalopathy. A progression from encephalopathy to seizures was observed following aminophylline administration. During the development of behavioral seizures, the EEGs showed a progression from fast activity isolated or bursts of spikes and/or sharp waves to full-blown epileptiform discharges. A wide spectrum of cardiac arrhythmias was observed during and following the seizures. Epileptiform activities ranging from isolated or bursts of spikes and/or sharp waves to continuous epileptiform discharges were observed following local application of the drugs to the cerebral cortex.
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PMID:Caffeine- and aminophylline-induced seizures. 747 2

The clinical course is described of a 28-year-old woman who was severely ill following ingestion of a Do-Do tablet (which consists of ephedrine, caffeine and theophylline), 24 h after discontinuing phenelzine treatment. Signs and symptoms were delayed for 8 h after which she developed encephalopathy, neuromuscular irritability, hypotension, sinus tachycardia, rhabdomyolysis and hyperthermia. Her illness was complicated by pneumonia and adult respiratory distress syndrome (ARDS). The management of monoamine oxidase inhibitor (MAOI) toxicity, which can arise from interactions and overdoses, is discussed. It should be remembered that, despite the increase in use of alternative and safer antidepressants, MAOI interactions still occur and unless they are managed appropriately, are potentially fatal. Patients need to be warned that restrictions apply for up to 2 weeks after stopping the medication, and doctors need to be aware that serious interactions can occur in this time period.
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PMID:Dangerous monoamine oxidase inhibitor interactions are still occurring in the 1990s. 764 Aug 30

The majority of patients with acute liver failure (ALF) die waiting for orthotopic liver transplantation (OLT). No other treatment modality is shown to improve survival. This study was conducted to assess the safety and feasibility of hepatocyte transplantation (HT) and subsequent engraftment and function of donor cells. Functional and structural integrity of cryopreserved and thawed human hepatocytes were assessed by their morphological characteristics, induction of P-4501A1 transcription, and survival in vivo by xenotransplantation into rats. Five patients with severe ALF underwent intrasplenic (4 patients) and/or intrahepatic (2 patients) HT through angiography under cyclosporine immunosuppression. All patients had grade III to IV encephalopathy and factor V levels less than 0.5 U/mL, were ventilator and dialysis dependent, and were not OLT candidates. Three of the 5 patients who survived 48 hours after HT had substantial improvement in encephalopathy scores, arterial ammonia levels, and prothrombin times. Clinical improvement was paralleled by an increase in aminopyrine and caffeine clearances. All 3 patients lived substantially longer than expected based on clinical experience after HT (12, 28, and 52 days) but eventually died. Postmortem examination showed the presence of transplanted hepatocytes in liver and spleen by light microscopy and fluorescent in situ hybridization (FISH). Cryopreserved and thawed human hepatocytes can be transplanted into recipients with ALF with some acceptable but definite complications. Engraftment of donor hepatocytes was proven by histological examination and FISH by both transjugular biopsy and at autopsy. Improvement in brain edema, encephalopathy grade, and clearance of antipyrine and caffeine suggested function, albeit with a 24- to 72-hour delay posttransplantation.
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PMID:Hepatocyte transplantation in acute liver failure. 1064 76

Cerebral palsy is the most prevalent cause of persisting motor function impairment with a frequency of about 1/500 births. In developed countries, the prevalence rose after introduction of neonatal intensive care, but in the past decade, this trend has reversed. A recent international workshop defined cerebral palsy as "a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain." In a majority of cases, the predominant motor abnormality is spasticity; other forms of cerebral palsy include dyskinetic (dystonia or choreo-athetosis) and ataxic cerebral palsy. In preterm infants, about one-half of the cases have neuroimaging abnormalities, such as echolucency in the periventricular white matter or ventricular enlargement on cranial ultrasound. Among children born at or near term, about two-thirds have neuroimaging abnormalities, including focal infarction, brain malformations, and periventricular leukomalacia. In addition to the motor impairment, individuals with cerebral palsy may have sensory impairments, cognitive impairment, and epilepsy. Ambulation status, intelligence quotient, quality of speech, and hand function together are predictive of employment status. Mortality risk increases incrementally with increasing number of impairments, including intellectual, limb function, hearing, and vision. The care of individuals with cerebral palsy should include the provision of a primary care medical home for care coordination and support; diagnostic evaluations to identify brain abnormalities, severity of neurologic and functional abnormalities, and associated impairments; management of spasticity; and care for associated problems such as nutritional deficiencies, pain, dental care, bowel and bladder continence, and orthopedic complications. Current strategies to decrease the risk of cerebral palsy include interventions to prolong pregnancy (eg, 17alpha-progesterone), limiting the number of multiple gestations related to assisted reproductive technology, antenatal steroids for mothers expected to deliver prematurely, caffeine for extremely low birth weight neonates, and induced hypothermia for a subgroup of neonates diagnosed with hypoxic-ischemic encephalopathy.
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PMID:Diagnosis, treatment, and prevention of cerebral palsy. 1898 5

Minimal hepatitis encephalopathy (MHE) is a liver cirrhosis complication that does not show symptoms of overt hepatitis encephalopathy (OHE) but can be detected using specific complementary neuropsychological and neurophysiological evaluations. Patients with MHE show abnormalities in cognitive functions, which can increase the risk of automobile accidents. The aim of this study was to compare the cognitive functioning of patients with MHE to patients with other liver disease and to compare their driving abilities, using a driving simulator and the Stim(2) software. Thirty-eight participants, who were not diagnosed with OHE but were diagnosed with chronic hepatitis and liver cirrhosis, took part in the study. The results indicate that patients with MHE show reduced level of cognitive functioning, which may affect their ability to drive safely. We cautiously predict that any future guidelines based on this knowledge may help reduce the incidence of traffic accidents caused by drivers with decreased with driving abilities.
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PMID:Impairment of driving ability and neuropsychological function in patients with MHE disease. 1936 22

Sepsis, necrotizing enterocolitis (NEC), and chronic lung disease (CLD) in preterm neonates are associated with significant mortality and morbidity, including long-term neurodevelopmental impairment and socioeconomic burden. Safe and effective drugs for the prevention and treatment of these conditions are urgently needed. Pentoxifylline, a synthetic theobromine derivative, is a non-steroidal immunomodulating agent with unique hemorrheologic effects which has been used in a range of infectious, vascular, and inflammatory conditions in adults and children. The unique properties of pentoxifylline explain its potential benefits in preterm neonates with sepsis, NEC, and CLD, conditions characterized by activation of the inflammatory cytokine cascade, free radical toxicity, and impaired microcirculation. Pentoxifylline has anti-inflammatory properties resulting from inhibition of erythrocyte phosphodiesterase. It lowers blood viscosity and improves microcirculation and tissue perfusion. As a phosphodiesterase inhibitor, pentoxifylline downregulates pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-6, and interferon-gamma. Methylxanthines, including caffeine, theophylline, and theobromine are relatively non-toxic drugs; of these, theobromine is the least toxic. Pentoxifylline-related significant adverse events are thus very rare. Unlike other methylxanthines, pentoxifylline does not have significant cardiac and bronchodilating effects at therapeutic doses. Although it is contraindicated in adults with recent cerebral hemorrhage due to its effect on platelets, red blood cells, and plasma fibrinogen levels, no significant adverse effects including thrombocytopenia and bleeding have been reported in critically ill preterm neonates with sepsis or NEC after treatment with pentoxifylline. Based on data from pilot randomized trials and observational studies, our systematic review suggests that pentoxifylline may reduce mortality and/or morbidity in preterm neonates with sepsis, NEC, and CLD. Results of experimental studies also indicate that pentoxifylline may potentially be beneficial in meconium aspiration syndrome and hypoxic ischemic encephalopathy. Given the substantial burden of sepsis, NEC, and CLD in high-risk preterm neonates, and the findings of this systematic review, pentoxifylline needs to be evaluated urgently as a preventative and therapeutic agent for these conditions in randomized controlled trials that can detect minimal clinically significant effect sizes. Further clinical and experimental studies are also necessary to evaluate whether pentoxifylline is safe and effective in meconium aspiration syndrome and hypoxic ischemic encephalopathy.
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PMID:Pentoxifylline in preterm neonates: a systematic review. 2079 59

The market value for energy drinks is continually growing and the annual worldwide energy drink consumption is increasing. However, issues related to energy drink ingredients and the potential for adverse health consequences remain to be elucidated. This aim of the present paper is to review the current knowledge on putative adverse effects of energy drinks, especially in youths. There are many energy drink brands in the worldwide market, even if only few brands are available in France. Although the energy drink content varies, these beverages often contain taurine, caffeine, vitamins B and carbohydrates. These drinks vary widely in both caffeine content (80 to 141 mg per can) and caffeine concentration. Except caffeine, the effects of energy drink ingredients on physical and cognitive performances remain controversial. Researchers identified moderate positive effects of energy drinks on performances, whereas others found contrary results. The adverse effects of energy drink can be related to either the toxicity of ingredients or specific situations in which energy drinks are used such as ingestion in combination with alcohol. Although the issue of taurine-induced toxic encephalopathy has been addressed, it is likely that the risk of taurine toxicity after energy drink consumption remains low. However, whether the prolonged use of energy drinks providing more than 3g taurine daily remains to be examined in the future. The consumption of energy drinks may increase the risk for caffeine overdose and toxicity in children and teenagers. The practice of consuming great amounts of energy drink with alcohol is considered by many teenagers and students a primary locus to socialize and to meet people. This pattern of energy drink consumption explains the enhanced risk of both caffeine and alcohol toxicity in youths. Twenty five to 40% of young people report consumption of energy drink with alcohol while partying. Consumption of energy drinks with alcohol during heavy episodic drinking is at risk of serious injury, sexual assault, drunk driving, and death. However, even after adjusting for alcohol consumption, students who consume alcohol mixed with energy drinks had dramatically higher rates of serious alcohol-related consequences. It has been reported that the subjective perceptions of some symptoms of alcohol intoxication are less intense after the combined ingestion of the alcohol plus energy drink; however, these effects are not detected in objective measures of motor coordination and visual reaction time.
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PMID:[Risks of energy drinks in youths]. 2092 66

Few signaling molecules have the potential to influence the developing mammal as the nucleoside adenosine. Adenosine levels increase rapidly with tissue hypoxia and inflammation. Adenosine antagonists include the methylxanthines caffeine and theophylline. The receptors that transduce adenosine action are the A1, A2a, A2b, and A3 adenosine receptors (ARs). In the postnatal period, A1AR activation may contribute to white matter injury in the preterm infant by altering oligodendrocyte (OL) development. In models of perinatal brain injury, caffeine is neuroprotective against periventricular white matter injury (PWMI) and hypoxic-ischemic encephalopathy (HIE). Supporting the notion that blockade of adenosine action is of benefit in the premature infant, caffeine reduces the incidence of bronchopulmonary dysplasia and CP in clinical studies. In comparison with the adverse effects on the postnatal brain, adenosine acts via A1ARs to play an essential role in protecting the embryo from hypoxia. Embryo protective effects are blocked by caffeine, and caffeine intake during early pregnancy increases the risk of miscarriage and fetal growth retardation. Adenosine and adenosine antagonists play important modulatory roles during mammalian development. The protective and deleterious effects of adenosine depend on the time of exposure and target sites of action.
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PMID:Adverse and protective influences of adenosine on the newborn and embryo: implications for preterm white matter injury and embryo protection. 2122 31

When asked to address the above question, findings that appeared to be among the most relevant included (1) interventions in the delivery room directed at supporting the physiological transition from intrauterine to extrauterine life rather than actively intervening in it; (2) recent data suggesting that keeping extremely low-gestational age neonates at a pulse oximeter saturation (SpO(2)) of 91-95% would increase their chances of survival compared with aiming for lower SpO(2) values; (3) using caffeine citrate in infants <1250 g with apnoea of prematurity improves neurodevelopmental outcome; (4) injecting antivascular epithelial growth factor into the vitreous seems to be an effective treatment for retinopathy of prematurity and (5) moderate hypothermia for perinatal hypoxic-ischaemic encephalopathy increases the likelihood of survival without neurological impairment. Here, data that support these recent changes in approach will be presented and discussed.
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PMID:What are the main research findings during the last 5 years that have changed my approach to clinical practice? 2186 86

Patients with early infantile epileptic encephalopathy (EIEE) are at increased risk for sudden unexpected death in epilepsy (SUDEP). De novo mutations of the sodium channel gene SCN8A, encoding the sodium channel Na_v1.6, result in EIEE13 (OMIM 614558), which has a 10% risk of SUDEP. Here, we investigated the cardiac phenotype of a mouse model expressing the gain of function EIEE13 patient mutation p.Asn1768Asp in Scn8a (Na_v1.6-N1768D). We tested Scn8a^N1768D/+ mice for alterations in cardiac excitability. We observed prolongation of the early stages of action potential (AP) repolarization in mutant myocytes vs. controls. Scn8a^N1768D/+ myocytes were hyperexcitable, with a lowered threshold for AP firing, increased incidence of delayed afterdepolarizations, increased calcium transient duration, increased incidence of diastolic calcium release, and ectopic contractility. Calcium transient duration and diastolic calcium release in the mutant myocytes were tetrodotoxin-sensitive. A selective inhibitor of reverse mode Na/Ca exchange blocked the increased incidence of diastolic calcium release in mutant cells. Scn8a^N1768D/+ mice exhibited bradycardia compared with controls. This difference in heart rate dissipated after administration of norepinephrine, and there were no differences in heart rate in denervated ex vivo hearts, implicating parasympathetic hyperexcitability in the Scn8a^N1768D/+ animals. When challenged with norepinephrine and caffeine to simulate a catecholaminergic surge, Scn8a^N1768D/+ mice showed ventricular arrhythmias. Two of three mutant mice under continuous ECG telemetry recording experienced death, with severe bradycardia preceding asystole. Thus, in addition to central neuron hyperexcitability, Scn8a^N1768D/+ mice have cardiac myoycte and parasympathetic neuron hyperexcitability. Simultaneous dysfunction in these systems may contribute to SUDEP associated with mutations of Scn8a.
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PMID:Cardiac arrhythmia in a mouse model of sodium channel SCN8A epileptic encephalopathy. 2779 Nov 49


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