Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prognostic value of early neonatal continuous electroencephalographic recordings in hypoxic ischaemic encephalopathy was evaluated. Thirty seven full term infants with hypoxic ischaemic encephalopathy were studied. The electroencephalogram (EEG) was recorded using four or eight channel Oxford Medilog recorders and was started as soon as possible after birth. The recordings were initially visually analysed and divided into four categories: three in relation to the grade of discontinuity of the background activity (continuous, discontinuous, and maximum depression) and an additional fourth category to include status epilepticus. The EEGs with discontinuous activity were then analysed by computer to obtain a more objective assessment of discontinuity. The results were related to neurological outcome. Continuous background activity was associated with a normal outcome in all but the three infants who had continuous, but asymmetrical EEGs and who developed contralateral hemiplegia. In the eight infants with discontinuous activity, the outcome appeared to be related to the grade of continuity and the presence of clear convulsions on the EEG. The 10 infants with maximum depression and status epilepticus had severe impairment. These preliminary results suggest that continuous recording of EEGs could be used routinely in term infants with hypoxic ischaemic encephalopathy. Computer analysis can improve the value of this technique, allowing the identification of infants who might benefit from early therapeutic intervention.
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PMID:Prognostic value of continuous electroencephalographic recording in full term infants with hypoxic ischaemic encephalopathy. 797 86

Recent experiments have indicated that recurrent inhibition in the dentate gyrus, as measured with paired-pulse tests, is reduced following the induction of status epilepticus. Also, a loss of cells in the hilus has been reported, and it has been suggested that the two effect might be related. In this experiment, we have monitored paired-pulse depression and counted cells in the hilus in animals that have been kindled well beyond the typical stage 5 criterion. Responses evoked in the dentate gyrus by paired-pulse stimulation of the perforant path were monitored before and after kindling of the perforant path. One group of animals served as controls and received no kindling stimulations. Another group was kindled to 4 stage 5 seizures and then allowed to recover for 2 months. A third group was kindled to 44 stage 5 seizures and then allowed to recover for at least 5 weeks. Paired-pulse tests were taken at 1 week intervals during the kindling and recovery phases. Paired-pulse inhibition increased during kindling, peaked after 4 stage 5 seizures, remained enhanced throughout the additional 40 stage 5 seizures, and recovered towards baseline over a period of about 5 weeks. Upon completion of this phase of the experiment, cell counts were taken in the hilar regions of the Nissl stained brain sections. There was a significant reduction in number of cells in the tissue from kindled animals, compared to controls, but there was no significant difference between the 2 kindled groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of kindling beyond the 'stage 5' criterion on paired-pulse depression and hilar cell counts in the dentate gyrus. 817 49

The amino acids L-glutamate and L-aspartate have been shown to be excitatory neurotransmitters in mammalian central nervous systems. Antagonists acting selectively at excitatory amino acid receptors have shown antiepileptic properties in several animal models. We report the results of the first therapeutic trial of the competitive NMDA antagonist, D-CPP-ene (SDZ EAA-494), in eight patients with intractable complex partial seizures. All patients withdrew prematurely because of side-effects, including poor concentration (8), sedation (7), ataxia (6), depression (3), dysarthria (2), amnesia (2) and unilateral choreo-athetosis in a patient with contralateral Sturge-Weber syndrome. Seizures were unchanged in four patients and worse in three. A further patient with apparent improvement in seizures in the first week developed complex partial status epilepticus on withdrawal of DCPP-ene. EEG on treatment (5) or in the immediate post-treatment period (2) showed slowing of background activity and, in five cases, an increase in epileptiform activity. Serum concentrations of DCPP-ene were found to be unpredictable and higher than expected from pharmacokinetic data on normal subjects. There was no clear relationship between serum concentrations and the severity of side-effects. Preliminary experience with DCPP-ene in patients with refractory partial seizures is not promising. Evaluation of related compounds is warranted.
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PMID:The excitatory amino acid antagonist D-CPP-ene (SDZ EAA-494) in patients with epilepsy. 826 15

Three children with refractory status epilepticus, unresponsive to intravenous administration of diazepam, phenytoin, and lidocaine, received pentobarbital therapy and were monitored by electroencephalography (EEG). They required mechanical ventilation and vasopressor therapy. Intravenous pentobarbital therapy was successful and without distinct sequelae in all 3 patients, and could be incrementally discontinued without breakthrough seizures after 12-65 hours of a burst-suppression or complete suppression pattern on EEG. Obtaining a suppression pattern was important for controlling status epilepticus in children as well as adults. We suggest that 12 hours after a burst-suppression pattern is obtained, tapering of pentobarbital should be attempted to avoid serious complications of extended pentobarbital anesthesia (e.g., respiratory depression, hypotension, pneumonia).
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PMID:Pentobarbital therapy for status epilepticus in children: timing of tapering. 853 84

Status epilepticus (SE) is one of the most common neurologic emergencies in children, adolescents, and young adults. SE may be due to acute neurologic conditions such as meningitis, encephalitis, or stroke, complicated febrile seizures, intractable epilepsy, degenerative diseases, intoxication, or may be the first manifestation of epilepsy. Initial treatment of convulsive SE is usually with an intravenous benzodiazepine (BZD) [lorazepam (LZP) or diazepam (DZP)], phenobarbital (PB), or phenytoin (PHT). LZP is less likely to cause respiratory depression than DZP and is therefore preferred. Sequelae and risk for recurrence of SE are primarily related to the underlying cause. Refractory SE (RSE) is most often symptomatic of an acute neurologic condition or neurodegenerative disease. Treatment for RSE is difficult, usually requiring intensive support of vital functions. Reported treatments for RSE include very high dose PB, continuous infusions of pentobarbital or BZDs (DZP, midazolam), lidocaine, inhalation anesthesia, and propofol. Outcome is related to underlying cause. Nonconvulsive SE may present as confusion or may mimic psychiatric illness. Response to BZDs is usually rapid but may not be sustained. Rapid initiation of oral or rectal valproate may be useful. Epilepsia partialis continua (EPC) is almost always due to an acute or chronic destructive lesion. Surgical treatment may be the only effective modality in some children with EPC. Acute treatment of breakthrough seizures and clusters of seizures at home with rectal BZDs (usually DZP, 0.2-0.5 mg/kg) may prevent progression to SE in some children and adolescents and reduce the need for visits to emergency facilities.
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PMID:Status epilepticus and acute repetitive seizures in children, adolescents, and young adults: etiology, outcome, and treatment. 864 55

The apparent diffusion coefficient of brain water was decreased by frontal cortical electroshock, usually but not always associated with brief epileptic afterdischarge detectable at the parietal cortex. Previous studies have shown that status epilepticus causes similar larger decreases, which are largely reversible by the termination of seizure discharge with pentobarbital. Cerebral blood flow is elevated in these conditions, and biochemical energy failure does not occur. The brain water diffusion coefficient also decreases in spreading depression, without depletion of energy stores. All of these findings may be due in part to the reduction of brain extracellular space caused by cell swelling, which occurs to some degree in all three conditions. However, major biological differences between brain activation and brain ischemia and new evidence for increased cytosolic viscosity in the latter both suggest that other mechanisms deserve further investigation. Use-dependent motility of dendritic spines and other phenomena that may allow direct detection of neural activity by diffusion-weighted NMR imaging are of special interest.
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PMID:Diffusion-weighted NMR imaging changes caused by electrical activation of the brain. 873 72

A failure of early paired pulse depression often precedes the onset of intermittent spontaneous seizures in animal models of status epilepticus. In the present study, changes in the strength of early and late paired pulse depression of dentate granule cell field potentials were compared in the unanesthetized rat during the initiation of a single afterdischarge (AD) evoked by perforant path stimulation (0.1 ms pulse duration, 5 Hz, 12-18 s duration, 50-1000 microA). Late paired pulse depression was measured by sequential changes in the population spike (PS) amplitude during 5 Hz stimulation (200 ms interpulse interpulse interval, IPI). When 5 Hz stimulation triggered an AD, the population spike (PS) was initially depressed and then increased to above pre-train values, indicating a loss of late paired pulse depression by the middle of the train. Early paired pulse depression was measured by inserting paired pulses (20 ms IPI) at spaced intervals throughout the 5 Hz train. In contrast to late paired pulse depression, early paired pulse depression remained at maximum strength until an abrupt failure was detected coincident with AD initiation. Two experimental treatments shown to increase the strength of late paired pulse depression, administration of the N-methyl-D-aspartate antagonist, MK-801 (0.25 mg/kg, i.p.), and the development of kindled seizures, produced an increase in AD thresholds and in the initial depression in the PS amplitude during 5 Hz stimulation. Together, these results suggest that a failure of late paired pulse depression may be a precipitating event in AD initiation triggered by 5 Hz stimulation in the unanesthetized rat.
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PMID:Changes in dentate granule cell field potentials during afterdischarge initiation triggered by 5 Hz perforant path stimulation. 881 48

1. This report examines alterations in presynaptic and postsynaptic processes mediated by gamma-aminobutyric acid-B (GABAB) receptors within hippocampal region CA1 in a model of chronic temporal lobe epilepsy (TLE). Intracellular recordings were obtained in pyramidal cells from combined hippocampal/parahippocampal control slices and slices obtained > or = 1 mo after a period of self-sustaining limbic status epilepticus (SSLSE) induced by continuous hippocampal stimulation. 2. Monosynaptic inhibitory postsynaptic potentials (IPSPs) were evoked by placement of the stimulating electrode in stratum pyramidale within 500 microns of the recording electrode in the presence of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione and D(-)-2-amino-5-phosphonovaleric acid. Control IPSPs exhibited early (GABAA-receptor-mediated) and late (GABAB-receptor-mediated) components. In contrast, post-SSLSE IPSPs displayed only a GABAA-receptor-mediated IPSP. Post-SSLSE IPSPs were completely eliminated by antagonists of the GABAA receptor (bicuculline methiodide and picrotoxin). In control tissue, GABAB receptor antagonists P-(3-aminopropyl)-P-diethoxymethyl-phosphinic acid (CGP 55845A), 3-N[1-(S)-(3,4-dichlorophenyl) ethyl]amino-2-(S)- hydroxypropyl-P-benzyl-phosphinic acid (CGP 35348), and 2-hydroxysaclofen eliminated the late component of the biphasic IPSP but had no discernible effect on IPSPs evoked in post-SSLSE CA1 pyramidal cells. 3. A paired pulse paradigm was employed to investigate the integrity of presynaptic GABAB-receptor-mediated inhibition of GABA release. To isolate pure GABAA-receptor-mediated responses, and thus facilitate comparison with post-SSLSE tissue, control neurons were penetrated with intracellular electrodes containing Cs2SO4/lidocaine, N-ethyl bromide (QX-314), and IPSPs were evoked employing the monosynaptic IPSP protocol. In controls, paired pulses [interpulse intervals (IPIs) of 70-1,500 ms] resulted in a diminution of the second early, GABAA-receptor-mediated chloride IPSP (IPSPA) relative to the first; maximum paired pulse depression (PPD) occurred at an IPI of 100 ms. GABAB receptor antagonists reduced PPD without affecting the amplitude of IPSPAs; the GABAB receptor agonist baclofen reduced the amplitude of both the first and second IPSPA and largely alleviated PPD. In contrast, no PPD was evident at any IPI in post-SSLSE neurons. Neither antagonists nor agonists of GABAB-receptor-mediated processes had an effect on either the degree of PPD or the amplitude of IPSPs. 4. To better approximate the pattern of CA1 pyramidal cell activation occurring during epileptiform activity. IPSPAs were evoked by trains of stimuli. In controls, mean monosynaptic IPSPA amplitude decreased by approximately 60% during a 3-Hz, 5-s train, with more than half the decline coming between the first and second IPSPs. In post-SSLSE, no significant IPSPA depression resulted from delivery of stimulus trains. Baclofen reduced the amplitude of control IPSPAs evoked during stimulus trains; both agonist and antagonists significantly lessened the degree of IPSP depression. These same agents altered neither IPSP amplitude nor the degree of use-dependent IPSP depression produced in post-SSLSE tissue during stimulus trains. 5. We conclude that a dysfunction of both presynaptic and postsynaptic GABAB-receptor-mediated processes occurs in hippocampal area CA1 in the post-SSLSE model of TLE. GABAB receptor agonists and antagonists had no effect on post-SSLSE CA1 pyramidal cell synaptic responses, whereas antagonists of the GABAA receptor completely eliminated IPSPs. Repetitive activation produced no use-dependent synaptic depression. The implications of these findings for the epileptogenic potential of post-SSLSE CA1 and the "dormant basket cell" hypothesis are discussed.
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PMID:Profound disturbances of pre- and postsynaptic GABAB-receptor-mediated processes in region CA1 in a chronic model of temporal lobe epilepsy. 887 Dec 36

A previously healthy 2 1/2-year-old girl developed status epilepticus followed by cortical blindness during intravenous N-acetylcysteine therapy for paracetamol ingestion. The child's vision was almost completely recovered during the 18 months follow-up period. We assume that the cortical blindness was a postictal sequela after prolonged seizure episode, most probably due to respiratory depression induced by N-acetylcysteine.
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PMID:Status epilepticus following intravenous N-acetylcysteine therapy. 896 81

An epileptic patient well controlled on valproic acid (VPA) developed a prolonged episode of status epilepticus 12 days after initiation of 75 mg of clomipramine (CMI) to treat depression. Serum level of VPA in the emergency room was unchanged from her previous levels; serum level of CMI was very elevated despite the relatively small dose of CMI. A pharmacokinetic interaction between VPA, an enzyme inhibitor, and CMI has not been described but seemed to have occurred in this patient. Decreased metabolism of CMI and its metabolites, increased free CMI fraction, and precipitation of a nonlinear saturation kinetic state has been described when CMI was used concomitantly with other highly protein-bound, enzyme-inhibiting compounds. This case provides reasonable evidence that the combination of VPA and CMI may result in elevation of levels of CMI and possibly of its metabolites and may precipitate seizures in patients with an underlying predisposition. The elevated serum level of CMI at the time of the seizures, despite the relatively small oral dose of the drug, suggests that VPA may have inhibited its metabolism and/or elimination.
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PMID:Status epilepticus associated with the combination of valproic acid and clomipramine. 902 50


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