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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present studies characterize working memory capabilities in the El mouse model of epilepsy using a species-typical social recognition memory task. As the El mouse exhibits a stress hyper-reactivity phenotype, the impact of hypertonic saline consumption, a memory modulatory treatment, upon social recognition performance was also examined. The hypotheses under test were: (1) that seizure susceptible El mice would perform poorly in the short-term working memory task relative to seizure resistant ddY controls, and (2) that the behavioral and neural responses to stressor exposure would be atypical in El mice. Results revealed a short-term working memory deficit and altered reactivity to social, environmental, and physiological stressors in El mice. In Experiment 1, El mice exhibited poor sociability and decreased olfactory investigation times, both anxiogenic-like traits, compared to ddY controls. In Experiment 2, El mice exhibited poor working memory performance compared to capable performance in ddY controls. Social recognition memory in ddY mice was abolished, however, by salt-loading whereas El mice were unaffected by exposure to this physiological stressor. In Experiment 3, all salt-loaded mice exhibited enhanced brain stress neuropeptide (corticotropin releasing factor-CRF) content, and salt-loaded El mice exhibited a 70% reduction in handling-induced seizures. These findings suggest that El mice exhibit high emotionality as well as atypical reactions to stressor exposure, and that these characteristics impact social working memory performance and seizure susceptibility.
Seizure 2007 Jan
PMID:Short-term social recognition memory deficit and atypical social and physiological stressor reactivity in seizure-susceptible El mice. 1711 13

The effects of centrally administered tripeptide fragment CRF(4-6) of corticotropin-releasing factor on convulsive activity in outbred albino rats were investigated. The peptide CRF(4-6) (icv; 6, 30, 150 nmol/head) causes dose-dependent increase in total EEG power in 1-40 Hz frequency range as a reflection of tripeptide-induced various epileptiform EEG signs such as single peaks and spike trains without external convulsion. Higher doses of CRF(4-6) (icv; 150, 225, 300 nmol per animal) induce tonicoclonic seizures. Switching to convulsive activity occurs at CRF(4-6) dose of 150 nmol per animal: injection of this dose leads only to EEG paroxysmal activity under habitual conditions and induces pathological locomotor activation under stressing conditions. Thus, CRF(4-6) similarly to full-length corticotropin-releasing factor induces epileptiform activity in rats.
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PMID:[Epileptogenic activity of tripeptide corticotropin-releasing factor fragment (CRF(4-6))]. 1728 74

The El mouse strain provides a non-induced model of idiopathic, multifactorial epilepsy in which seizures are elicited in response to stressful environmental stimuli such as tail suspension handling. In the present studies, genetically seizure susceptible El and non-susceptible ddY control mice were exposed to tail suspension, foot-shock and social stressors in order to test the hypothesis that neural and physiological responses to such stimuli would be exaggerated in the El strain. The first experiment assessed neural cell density, stress neuropeptide (corticotropin releasing factor--CRF) levels, and plasma corticosterone activation in El and ddY mice in an unhandled control condition or following exposure to tail suspension or foot-shock stressors. The second experiment assessed brain electroencephalographic activity using telemetrically monitored skull surface electrodes in El and ddY mice exposed to tail suspension or social interaction stressors. Assessment of El mouse brains revealed higher cell counts in amygdala and elevated CRF peptide content in the paraventricular thalamic nucleus relative to ddY controls. El mice exhibited significantly elevated plasma corticosterone levels 60 min following exposure to tail suspension and foot-shock stressors relative to ddY controls. Finally, El mice exhibited significantly elevated brain electroencephalographic (1-4 Hz) activity in response to tail suspension, but not social interaction, relative to ddY controls. These results indicate that potentiated neural, endocrine and physiological activation arises in the El strain following exposure to a known seizure trigger stimulus, involuntary tail suspension handling. The findings support a diathesis-stress hypothesis in which genetically seizure susceptible El mice exhibit a multifaceted hyperreactivity to noxious environmental stimuli.
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PMID:Neural, endocrine and electroencephalographic hyperreactivity to human contact: a diathesis-stress model of seizure susceptibility in El mice. 1732 61

(1) In dialysis patients with chronic renal failure, hyperphosphataemia can cause osteorenal dystrophy, leading to bone pain, fractures and excess cardiovascular mortality. In addition to a low-phosphorus diet and dialysis, phosphorus chelators are usually needed to control blood phosphorus levels. The first choice is calcium carbonate, and sevelamer is an alternative. (2) Lanthanum carbonate, a phosphorus chelator, is now also licensed for the treatment of hyperphosphataemia in dialysis patients with chronic renal failure. (3) In addition to three dose-finding placebo-controlled studies, clinical evaluation includes 2 comparative randomised unblinded trials: one 6-month trial versus calcium carbonate and a 2-year trial versus other phosphorus chelators. During these trials, lanthanum was no more effective than the comparators in terms of effects on the mortality rate, incidence of fractures, or blood phosphorus level. (4) During these trials, adverse events attributed to treatment were more frequent with lanthanum than with the other phosphorus chelators. The main problems were gastrointestinal disorders (nausea, vomiting, diarrhoea, constipation and abdominal pain), headaches, seizures, and encephalopathy. (5) The accumulation of lanthanum in the bones and brain is troubling. The known long-term adverse effects of aluminium, another trivalent cation with weak gastrointestinal absorption, suggest that caution is also required with lanthanum. (6) In practice, when a phosphorus chelator is needed to treat hyperphosphataemia in dialysis patients with chronic renal failure, calcium carbonate is the first choice and sevelamer remains the best alternative.
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PMID:Lanthanum: new drug. Hyperphosphataemia in dialysis patients: more potential problems than benefits. 1745 39

Posterior reversible encephalopathy (PRES) is a recently described syndrome, defined by clinical and neuroimaging features. Chronic kidney disease patients may be especially vulnerable to this syndrome because they are frequently exposed to several of its possible causes, including uremia and hypertension. In its most severe form, PRES can manifest clinically as seizures, coma or death. However, if properly diagnosed and treated, this syndrome can be completely reversible. Therefore, neuroimaging methods, especially brain magnetic resonance is fundamental for its diagnosis because it shows brain edema in characteristic pattern, and excludes causes of seizures or coma. An important example is the case of a young hypertensive chronic kidney disease patient on peritoneal dialysis, brought to the emergency room comatous with generalized tonic-clonic seizures; the cerebral magnetic resonance imaging features were impressive. Anti-hypertensive therapy and hemodialysis allowed complete recovery. The reversibility of this syndrome depends on timely diagnosis and therapy and therefore it should be kept in mind in the differential diagnosis of seizures. or coma in chronic kidney disease patients.
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PMID:[Posterior reversible encephalopathy syndrome (PRES) and chronic kidney disease]. 1804 48

Extracellular nucleotides and nucleosides act as signaling molecules involved in a wide spectrum of biological effects. Their levels are controlled by a complex cell surface-located group of enzymes called ectonucleotidases. There are four major families of ectonucleotidases, nucleoside triphosphate diphosphohydrolases (NTPDases/CD39), ectonucleotide pyrophosphatase/phosphodiesterases (E-NPPs), alkaline phosphatases and ecto-5'-nucleotidase. In the last few years, substantial progress has been made toward the molecular identification of members of the ectonucleotidase families and their enzyme structures and functions. In this review, there is an emphasis on the involvement of NTPDase and 5'-nucleotidase activities in disease processes in several tissues and cell types. Brief background information is given about the general characteristics of these enzymes, followed by a discussion of their roles in thromboregulatory events in diabetes, hypertension, hypercholesterolemia and cancer, as well as in pathological conditions where platelets are less responsive, such as in chronic renal failure. In addition, immunomodulation and cell-cell interactions involving these enzymes are considered, as well as ATP and ADP hydrolysis under different clinical conditions related with alterations in the immune system, such as acute lymphoblastic leukemia (ALL), B-chronic lymphocytic leukemia (B-CLL) and infections associated with human immunodeficiency virus (HIV). Finally, changes in ATP, ADP and AMP hydrolysis induced by inborn errors of metabolism, seizures and epilepsy are discussed in order to highlight the importance of these enzymes in the control of neuronal activity in pathological conditions. Despite advances made toward understanding the molecular structure of ectonucleotidases, much more investigation will be necessary to entirely grasp their role in physiological and pathological conditions.
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PMID:NTPDase and 5'-nucleotidase activities in physiological and disease conditions: new perspectives for human health. 1880 12

Neuropsychiatric symptoms are recognized to occur in a significant percentage of systemic lupus erythematosus patients and to be a leading cause of morbidity and mortality in lupus. The aim of the present study is to investigate neuropsychiatric symptoms in the patients with lupus nephritis without chronic renal failure. We studied 74 patients (4 male, 70 female) with SLE without chronic renal failure. Disease activity was assessed by the European Consensus Lupus activity Measurement (ECLAM). Renal biopsies disclosed type V lesions in 23 patients, type IV--in 34, type III--in 3, type II--in 11, type I--in 3 patients. Two control groups are used--with rheumatoid arthritis (96 patients) and 63 healthy subjects. The most frequent clinical manifestations are cognitive dysfunction (52.94%), headache (29.41%), psychoses (17.65%), epileptic seizures (20.59%) etc., and the most common cognitive deficit is related to impairment of the memory. The tests for cognitive disorders and nuclear magnetic resonance are the methods of investigation, by which the nervous system injuries are most early detected in the course of the disease. The presented study describes the correlations between the immunologic deviations (antiribosomal P-antibodies, aPL, aSm, aC1q), MMP-9, AT III and the NP injuries.
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PMID:Neuropsychiatric lupus in patients with lupus glomerulonephritis. 1892 62

Triphasic waves are seen in the electro-encephalogram of adult patients with toxic-metabolic encephalopathies of various origins. Levetiracetam is a broad spectrum anti-epileptic drug with renal elimination and no hepatic metabolism. We describe the case of encephalopathy with triphasic waves concomitant with levetiracetam accumulation in a patient with chronic renal failure. The condition was reversible after down-titration of levetiracetam with no change of the renal function. Other causes of metabolic encephalopathy were excluded. Moreover, this patient suffered from a probable cortical myoclonus that relapsed after cessation of the drug but was well controlled by a low dosage adapted to the renal failure. In cases of metabolic encephalopathy with triphasic waves in a patient with renal failure taking levetiracetam, it is important to exclude toxic accumulation of levetiracetam among other causes.
Seizure 2009 Jun
PMID:Levetiracetam accumulation in renal failure causing myoclonic encephalopathy with triphasic waves. 1920 20

Despite adequate antidepressant monotherapy, the majority of depressed patients do not achieve remission. Even optimal and aggressive therapy leads to a substantial number of patients who show minimal and often only transient improvement. In order to address this substantial problem of treatment-resistant depression, a number of novel targets for antidepressant therapy have emerged as a consequence of major advances in the neurobiology of depression. Three major approaches to uncover novel therapeutic interventions are: first, optimizing the modulation of monoaminergic neurotransmission; second, developing medications that act upon neurotransmitter systems other than monoaminergic circuits; and third, using focal brain stimulation to directly modulate neuronal activity. We review the most recent data on novel therapeutic compounds and their antidepressant potential. These include triple monoamine reuptake inhibitors, atypical antipsychotic augmentation, and dopamine receptor agonists. Compounds affecting extra-monoamine neurotransmitter systems include CRF(1) receptor antagonists, glucocorticoid receptor antagonists, substance P receptor antagonists, NMDA receptor antagonists, nemifitide, omega-3 fatty acids, and melatonin receptor agonists. Focal brain stimulation therapies include vagus nerve stimulation (VNS), transcranial magnetic stimulation (TMS), magnetic seizure therapy (MST), transcranial direct current stimulation (tDCS), and deep brain stimulation (DBS).
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PMID:Emerging targets for antidepressant therapies. 1950 41

A gas chromatography-mass spectrometric method was developed that allowed the accurate, highly sensitive and specific quantification of F(2)-isoprostanes (F(2)-IsoPs) in different tissues and body fluids. Measurement of F(2)-IsoPs in isolated rat brain mitochondria, HaCaT keratinocytes, human plasma, and microdialysates of human skin has established the occurrence of oxidative stress in a variety of model systems and disease states. F(2)-IsoPs correlated with other markers of lipid peroxidation (e.g., TBARS, HETEs) in experimental models of oxidative stress. F(2)-IsoPs were elevated about 100-fold after iron/ascorbate-induced oxidative stress and 2- to 4-fold after pentylenetetrazol (PTZ)-induced seizures, in hemodialysis patients with end stage renal disease, in psoriasis patients, in HaCaT keratinocytes, and in microdialysates of human skin following UVB irradiation.Both human and experimental studies have indicated associations of F(2)-IsoPs and inflammatory conditions. Anti-inflammatory drugs such as diclofenac did not only suppress the prostaglandin but also the F(2)-IsoP pathway.Microdialysis allows the "near-in vivo" measurement of prostanoid mediators, released in the interstitial space of the dermis under inflammatory conditions.
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PMID:F(2)-isoprostanes: sensitive biomarkers of oxidative stress in vitro and in vivo: a gas chromatography-mass spectrometric approach. 1978 91


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