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

1. Despite advances in the art and science of fluid balance, exertional heat illness -- even life-threatening heat stroke -- remains a threat for some athletes today. 2. Risk factors for heat illness include: being unacclimatized, unfit, or hypohydrated; certain illnesses or drugs; not drinking in long events; and a fast finishing pace. 3. Heat cramps typically occur in conditioned athletes who compete for hours in the sun. They can be prevented by increasing dietary salt and staying hydrated. 4. Early diagnosis of heat exhaustion can be vital. Early warning signs include: flushed face, hyperventilation, headache, dizziness, nausea, tingling arms, piloerection, chilliness, incoordination, and confusion. 5. Pitfalls in the diagnosis of heat illness include: confusion preventing self-diagnosis; the lack of trained spotters; rectal temperature not taken promptly; the problem of "seek not, find not;" and the mimicry of heat illness. 6. Heat stroke is a medical emergency. Mainstays of therapy include: emergency on-site cooling; intravenous fluids; treating hypoglycemia as needed; intravenous diazepam for seizures or severe cramping or shivering; and hospitalizing if response is slow or atypical. 7. The best treatment is prevention. Tips to avoiding heat illness include: rely not on thirst; drink on schedule; favor sports drinks; monitor weight; watch urine; shun caffeine and alcohol; key on meals for fluids and salt; stay cool when you can; and know the early warning signs of heat illness.
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PMID:Treatment of suspected heat illness. 969 24

We report a case of dystonia with a partial deletion of the short arm (p) of chromosome 18 and androgen insensitivity. Neurologic findings in the 18p syndrome are reported to include mental retardation, seizures, incoordination, tremor, and chorea. A 15-year-old girl with a denovo 18p deletion [karyotype 46, XY, del (18)(p11.1)] developed progressive asymmetric dystonia. She had oromotor apraxia and partial expressive aphasia since childhood, and she was able to partially communicate through elementary sign language. At the age of 15 years, she developed subacute and progressive choreic movements of the right arm, severe dystonic posturing of the left arm, and spastic dystonia in both legs. Her response to parenteral or oral benzodiazepines, oral trihexyphenidyl, benztropine mesylate, baclofen, and L-dopa were brief and inadequate. The response to intrathecal baclofen has been sustained over 18 months. In all likelihood, the 18p deletion syndrome affecting this patient is significant in the pathogenesis of her acquired dystonia. Chronic intrathecal baclofen therapy via pump has been effective in this case and should be considered as a treatment modality in carefully selected patients with dystonia.
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PMID:Progressive dystonia in a child with chromosome 18p deletion, treated with intrathecal baclofen. 1007 26

A group of 185 patients with brain atrophy found in CT is presented. The purpose of the study was to call attention to the the significance, frequency and clinical signs of brain atrophy. All patients were divided into two groups: 78 cases with secondary brain atrophy associated with other diseases of central nervous system and 107 cases of "primary" brain atrophy. The last one was an only finding without any other pathological lesions in the brain. Depending on the localisation, three groups of brain atrophy were isolated: generalized, subcortical and cortical. The clinical picture was analysed in the group of "primary" brain atrophy. In the studied group the most frequent cause of hospitalisation were epileptic seizures, the next one: headache, one-side hemiparesis or hemihypaesthesia, dizziness and incoordination. Neurological examination showed that one-side signs were observed very often in generalized brain atrophy. In the group of patients with cortical brain atrophy most patients were without any neurological signs. The analysis of the relationship between the clinical examination and "primary" brain atrophy found in CT, showed lack of characteristic, typical signs, which could be connected with brain atrophy. The problem of difficulty in the diagnosis of brain atrophy is stressed aesthesia. The definition and the significance of brain atrophy should be verified in diagnosis and the conclusions after finding brain atrophy have to be very careful.
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PMID:[Clinical symptomatology of primary brain atrophy]. 1046 19

There has been much debate about the nosologic forms of electrical status epilepticus during sleep (ESES) that can occur in a number of syndromes. The pathogenesis of ESES is unknown, and the natural course is variable. It is debatable whether these age-specific epileptic syndromes belong to the same spectrum of disorders with different severity but a common denominator of sleep-related hypersynchronization of generalized paroxysmal epileptic discharges. This report describes 18 children with medically refractory seizures, gradual deterioration in language skills, fine-motor incoordination, behavioral changes, psychologic and intellectual regression of different degrees, and the ESES phenomenon. Most exhibited clinical and electroencephalographic responses to intravenous or oral benzodiazepines, especially if initiated within the first 2 years of seizure onset. Seizure remission was nearly complete with cessation of seizures and marked improvement in language and fine-motor skills, behavior, and intellectual function in those with an idiopathic etiology. Therapeutic trials with benzodiazepines should be given to all children with the ESES phenomenon. Sleep electroencephalographic monitoring is recommended in all young children with epilepsy and language or psychologic deterioration so that the brain dysfunction can be reversed at a critical and vulnerable period of early life.
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PMID:Spectrum of epileptic syndromes with electrical status epilepticus during sleep in children. 1091 29

The activity-guided fractionation of the ethanol extract of leaves of Annona diversifolia Saff., led to the isolation of palmitone (16-hentriacontanone) as the only anticonvulsant active compound. This aliphatic ketone was highly effective to diminish pentylenetetrazole (PTZ)-induced clonic-tonic seizures and toxicity. Also, it produced a prolongation of the latency for onset of seizures and a reduction of the death rate produced by 4-aminopyridine (4-AP) and bicuculline (BIC). However, it was inactive to inhibit the kainic acid (KA)- and strychnine (STC)-induced seizures. Palmitone did not produce motor incoordination and loss of righting reflex which are used as signs of neurological impairment. Palmitone (ED50 = 1.85 mg/kg) proved to be a more potent antiepileptic drug against the PTZ-induced seizures than etosuximide (ED50 = 59.6 mg/kg), sodium valproate (ED50 = 63 mg/kg), and carbamazepine (ED50 > 300 mg/kg) and it was only four-fold less potent than diazepam (ED50 = 0.48 mg/kg). The pharmacological profile of palmitone suggests that this compound could be acting on the GABAergic inhibitory system.
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PMID:Anticonvulsant properties and bio-guided isolation of palmitone from leaves of Annona diversifolia. 1130 59

Glycine receptors (GlyRs) are pentameric ligand-gated ion channels that inhibit neurotransmission in the adult brainstem and spinal cord. GlyR function is potentiated by ethanol in vitro, and a mutant GlyR subunit alpha(1)(S267Q) is insensitive to the potentiating effects of ethanol. To test the importance of GlyR for the actions of ethanol in vivo, we constructed transgenic mice with this mutation. Under the control of synapsin I regulatory sequences, transgenic expression of S267Q mutant GlyR alpha(1) subunits in the nervous system was demonstrated using [(3)H]strychnine binding and immunoblotting. These mice showed decreased sensitivity to ethanol in three behavioral tests: ethanol inhibition of strychnine seizures, motor incoordination (rotarod), and loss of righting reflex. There was no change in ethanol sensitivity in tests of acute functional tolerance or body temperature, and there was no change in ethanol metabolism. Transgene effects were pharmacologically specific for ethanol, compared with pentobarbital, flurazepam, and ketamine. These results support the idea that glycine receptors contribute to some behavioral actions of ethanol and that ethanol sensitivity can be changed in vivo by transgenic expression of a single receptor subunit.
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PMID:Transgenic expression of a mutant glycine receptor decreases alcohol sensitivity of mice. 1180 13

Adenosine is an endogenous modulator that has an inhibitory effect on neuronal activity. The aim of this work was to investigate the role of aminophylline, an adenosine receptor antagonist, on the long-term effects of status epilepticus (SE) in the developing brain. Four groups of rats at the postnatal age of 12 days were intraperitoneally administered with saline, aminophylline (50 mg/kg), lithium-pilocarpine (Li-PC) (3 mEq/kg-60 mg/kg), and Li-PC plus aminophylline, respectively. The four groups were tested for spatial memory using the Morris water maze task at P80 and motor performance by the Rotarod test at P100. The brains were then analyzed with cresyl violet stain for histological lesions and evaluated for mossy fiber sprouting with the Timm stain. At the acute stage, all rats subjected to Li-PC developed SE and no seizures were elicited in the saline-treated or aminophylline-treated rats. The seizure duration was longer in the Li-PC plus aminophylline group (346.9+/-32.7 min) as compared with that in the Li-PC group (265.2+/-9.8 min). The difference of mortality was not significant. Rats without seizures exhibited no motor imbalance, spatial deficits, or morphological changes. The rats with Li-PC-induced SE demonstrated spatial memory deficits without motor incoordination or morphological changes. However, the rats subjected to Li-PC plus aminophylline exhibited motor impairment and morphological changes, including neuronal cell loss in CA1 area and increased mossy fiber sprouting in CA3 area. In addition, the rats of Li-PC plus aminophylline had greater spatial memory deficits than that seen in rats with Li-PC. We concluded that an adenosine receptor antagonist, such as aminophylline, had synergistic effects on the SE-induced long-term deficit of cognition and motor performance in the developing brain. The present study may provide experimental evidence and lead to novel therapeutic interventions.
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PMID:Aminophylline exacerbates status epilepticus-induced neuronal damages in immature rats: a morphological, motor and behavioral study. 1207 43

We reported previously a model of polyglutamine repeat disorders with insertion of 146 CAG repeats into the murine hypoxanthine phosphoribosyl transferase locus (Hprt(CAG)146; Ordway et al. [1997] Cell 91:753-763), which does not normally contain polyglutamine repeats. These mice develop an adult-onset neurologic phenotype of incoordination, involuntary limb clasping, seizures, and premature death. Histologic analysis demonstrates widespread ubiquinated neuronal intranuclear inclusions (NIIs). We now report characterization of the age of onset of behavioral abnormalities, correlated with the time course of occurrence of NIIs in several brain regions, and the occurrence of NIIs in non-neuronal tissues. Onset of behavioral abnormalities occurred at approximately 22 weeks of age. There was variable time course of expression of NIIs in several brain regions. Assessment of several non-neuronal tissues revealed nuclear inclusions in hepatocytes and choroid plexus epithelium. Gamma-aminobutyric acid (GABA)/benzodiazepine receptors, dopamine D1-like and D2-like receptors, and type 2 vesicular monoamine transporter (VMAT2) binding sites were assayed before and after the onset of behavioral abnormalities. GABA/benzodiazepine receptors were unchanged either before or after the onset of behavioral abnormalities in any region analyzed, whereas striatal D1-like and D2-like receptors were diminished after but not before the onset of symptoms. Dorsal striatal VMAT2 binding sites were decreased before the onset of behavioral changes. Mitochondrial electron transport chain components were assayed with histochemical methods before and after the onset of behavioral changes. There was no change in behaviorally presymptomatic or symptomatic animals. Hprt(CAG)146 mice did not exhibit increased susceptibility to the mitochondrial toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Hprt(CAG)146 mice are a useful model for studying polyglutamine repeat disorders.
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PMID:Hprt(CAG)146 mice: age of onset of behavioral abnormalities, time course of neuronal intranuclear inclusion accumulation, neurotransmitter marker alterations, mitochondrial function markers, and susceptibility to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. 1294 82

The specific involvement of the delta-opioid receptor in the control of nociception was explored by investigating the pharmacological activity in vivo of a selective, orally active, and centrally penetrant delta-opioid agonist. [8R-(4bS*,8aalpha,8abeta,12bbeta)]7,10-dimethyl-1-methoxy-11-(2-methylpropyl)oxycarbonyl 5,6,7,8,12,12b-hexahydro-(9H)-4,8-methanobenzofuro[3,2-e]pyrrolo[2,3-g]isoquinoline hydrochloride (SB-235863) is a new pyrrolomorphinan with high affinity (Ki = 4.81 +/- 0.39 nM) for the delta-opioid receptor, full agonist activity, and binding selectivity versus the mu- and kappa-opioid receptors of 189-fold and 52-fold, respectively. Perorally administered SB-236863 was inactive in the rat tail-flick and hot-plate tests of acute pain response, but potently reversed thermal hyperalgesia in rats resulting from a carrageenan-induced inflammatory response. This activity could be blocked by the delta-opioid antagonist naltrindole (3 mg/kg s.c.), but selective mu- and kappa-opioid antagonists were ineffective. Naltrindole (1 microg i.c.v.) also blocked the activity of 10 mg/kg (p.o.) SB-235863, showing that the compound activates delta-opioid receptor sites in the central nervous system. SB-235863 was additionally effective at reversing chronic hyperalgesia in the Seltzer rat model of partial sciatic nerve ligation after peroral administration. These data show that the delta-opioid receptor plays a selective role in regulating evoked and lasting changes in nociceptive pain signaling. Classical side effects of mu- and kappa-opioid receptor activation (slowing of gastrointestinal transit and motor incoordination, respectively) were not observed after administration of 70 mg/kg (p.o.) SB-235863, nor was evoked seizure activity affected. These results suggest a selective and limited role of delta-opioid receptors in the modulation of nociception.
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PMID:Evidence for a selective role of the delta-opioid agonist [8R-(4bS*,8aalpha,8abeta, 12bbeta)]7,10-Dimethyl-1-methoxy-11-(2-methylpropyl)oxycarbonyl 5,6,7,8,12,12b-hexahydro-(9H)-4,8-methanobenzofuro[3,2-e]pyrrolo[2,3-g]isoquinoline hydrochloride (SB-235863) in blocking hyperalgesia associated with inflammatory and neuropathic pain responses. 1455 Dec 88

Epilepsy is a sequel of depolarizing neuronal event with recurrent seizures. Neuronal membrane disorder is the main cause of epileptogenesis. The epileptic process is initiated and progressing due to the membrane inability to maintain balanced changing of the electrochemical gradient, which is physiologically necessary for intracerebral signal transfer. Membrane ion channels are deranged, which may be congenital or acquired. To date, only a few specific genetically caused ion channel aberrations in some less common epileptic syndromes have been identified, however, the main pathophysiologic sequence of events at the cellular level remains obscure. Synaptic dysregulation of epileptic neuronal groups with unbalanced inter-relationship of excitatory and inhibitory complements within the epileptic focus has been only partly elucidated. Therefore, the treatment of epilepsy remains fortuitous to a great extent because idopathic epileptogenesis is stochastically unpredictable. We do not yet know why, how and when the epileptic process begins, and vice versa, why the process may occasionally be completely silent in a continuously overstrained interaction system. What link in the excitation neuronal system is weakest: membrane instability, neurotransmitter incoordination, or something else? Yet, in two thirds of the individuals prone to epilepsy, monotherapy with so-called channel antiepileptics with selective action on membrane ion exchange and/or antiepileptics with neurotransmitter modulation will stop the manifestation of epilepsy but not the longterm proneness to epileptogenesis. In the remaining one third of sufferers the epilepsy is refractory to any therapeutic attempts. Therefore, antiepileptic treatment is a highly complex, individualized procedure in which only the observational predictors have been positively defined to date, i.e. clinical manifestation and electroencephalography specificity. They make the basis for balanced evaluation of the real extent of action of the antiepileptics available.
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PMID:[Epilepsy--an ongoing challenge]. 1581 53


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