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. Rats with spontaneous recurrent seizures (SRS) were obtained by injection of kainic acid (KA; 10 mg/kg SC) to drug-naive rats that regularly developed wet-dog shakes followed by complex partial seizures and status epilepticus. Three to five weeks later, the rats with manifest SRS were selected. 2. The SRS rats were challenged with KA (10 mg/kg SC). The seizures induced in SRS rats by KA were similar to SRS regarding their clinical stage and duration (mean duration of seizures: 44 sec and 43 sec, respectively). The frequency of seizures was, however, increased compared with the frequency of SRS in control, vehicle-treated SRS rats (mean frequency of seizures: 12.9 and 0.4 per 3 hr, respectively). The KA-induced seizures in SRS rats differ behaviorally from KA-induced seizures in naive rats-namely, neither wet-dog shakes nor the status epilepticus could be induced. 3. Repeated injection of an equal dose of KA, applied to the SRS rats 1 day after the previous KA challenge, did not induce seizures. The loss of seizure susceptibility to KA was only temporary, as shown after a 7-day drug-free period, when the repeated injection of KA regained its seizure-triggering capacity. 4. The results indicate that reactivity to the seizure-inducing agent kainic acid changes in rats with spontaneous recurrent seizures.
Gen Pharmacol 1998 Sep
PMID:The effects of kainic acid in rats with spontaneous recurrent seizures. 970 17

1. Imidazole 4-acetic acid (IMA) is a naturally occurring metabolite in brain, although it is unclear what biochemical pathways are involved in its biosynthesis and breakdown. Some evidence, however, suggests that IMA is an oxidation product of histamine. 2. The compound has pronounced neuropharmacological properties, many of which are consistent with an activation of GABA(A) receptors. Indeed, IMA is able to displace [3H]GABA from GABA(A) sites in a potent manner. 3. IMA displays definite partial agonist characteristics as an enhancer of benzodiazepine binding to the GABA(A) receptor complex in membrane preparations. In addition, it has an affinity for GABA(C) receptors, where it seems to act as an antagonist, and perhaps as a weak partial agonist. A third recognition site for IMA in brain is the I1-imidazoline receptor. 4. Parenteral administration to experimental animals leads to a sleep-like state which can often be accompanied by seizures. In addition, central application of IMA has been associated with a dose-related reduction in arterial pressure and sympathetic nervous discharge. 5. No specific receptor site or uptake system for IMA has yet been discovered, adding uncertainty to its role in central nervous system function. Yet the possibility cannot be overlooked that IMA plays a role in regulating blood pressure.
Gen Pharmacol 1998 Oct
PMID:Pharmacology and function of imidazole 4-acetic acid in brain. 979 7

The effects of drugs affecting GABA and glutamic acid receptors on theophylline-induced seizures were investigated in mice. Theophylline elicited tonic seizures in mice in a dose dependent manner. Muscimol, DABA and AOAA significantly prolonged the onset and significantly decreased the incidence of theophylline-induced seizures. Baclofen significantly delayed the onset of the tonic seizures induced by theophylline. Bicuculline and picrotoxin significantly shortened the onset and significantly increased the incidence of seizures induced by a low dose of theophylline and also significantly antagonized muscimol-attenuating effect against theophylline seizures. N-methyl-DL-aspartic acid significantly shortened the onset and significantly increased the incidence of seizures elicited by a low dose of theophylline. D-(-)-2-amino-phosphonopentanoic acid effectively delayed the onset and significantly decreased the incidence of seizures elicited by theophylline and also significantly antagonized the potentiating effect of N-methyl-DL-aspartic acid on seizures induced by a low dose of theophylline. Dextromethorphan and ketamine profoundly shortened the onset of theophylline-induced seizures. Clonidine effectively prolonged the onset and significantly decreased the incidence of theophylline-induced seizures. These data indicate that GABA(A) and N-methyl-D-aspartic acid receptors may mediate theophylline-elicited tonic seizures in mice.
Gen Pharmacol 1999 Mar
PMID:Gamma-aminobutyric acid and glutamic acid receptors may mediate theophylline-induced seizures in mice. 1021 93

Tizanidine, an alpha-2 adrenergic agonist, is a centrally active muscle relaxant and a spasmolytic drug. The aim of our study was to investigate the activity of tizanidine on maximal electroshock seizures (MES) in mice. In the first part of the study, convulsive current 50 (CC 50) value to produce seizures was found. Then, tizanidine was given intraperitoneally (IP) at the doses of 0.5, 1, and 2 mg/kg, and orally (PO) at the doses of 5, 10, 20, 40 mg/kg. We found that tizanidine at the doses of 1 and 2 mg/kg IP and 40 mg/kg PO caused a significant protection against MES. In the second part of the study, after pretreatment with yohimbine, an alpha-2 adrenergic receptor blocker, at the dose of 2 mg/kg, anticonvulsant effect of tizanidine is diminished. We concluded that the mode of action of the anticonvulsant effect of tizanidine may be mediated by the central alpha-2 adrenergic receptors.
Gen Pharmacol 1999 Apr
PMID:The effect of tizanidine on maximal electroshock seizures (MES) in mice. 1032 94

A district-wide epilepsy audit in general practice showed that levels of seizure frequency recording were too low to evaluate the quality of control of epilepsy. A repeat audit after multi-faceted interventions showed an improvement in seizure frequency recording of 13.2% (CI = 8.9 to 17.6) from 54.7% to 68%. This illustrates the difficulties of evaluating quality of care using routine records and the problems of implementing changes in general practice.
Br J Gen Pract 2000 Mar
PMID:Can district-wide audits improve primary care epilepsy management? An audit of seizure frequency recording. 1075 Feb 38

The "Controlled Arch System", coupled with a proper diagnosis and treatment plan, should produce excellent occlusion and esthetics for your patients from their Mixed Dentition growth period onward. The authors have offered a method of Phase I treatment for children of Mixed Dentition age that can be outlined as follows: 1. Fit maxillary and mandibular Functional Orthopedic appliances to produce whatever transverse expansion of the arches is needed, then distalize the maxillary 6 year molars to a super Class I relation, according the measurements assessed by the Sim Model Analysis. 2. On removal of the Functional Orthopedic appliances, upper and lower Fixed-Removable Lingual Arches are fitted to stabilize teeth and bone. 3. As needed, fit maxillary and mandibular 2 x 4 or 2 x 6 fixed Straightwire appliances with Nickel Titanium wires, utilizing pinched molar hook/stops to establish molar anchorage to level, align and rotate permanent incisors (and lower permanent canines, if erupted). 4. When alignment of the permanent incisors is completed, the FRLAs are left in place as "insurance" appliances to insure that no loss of arch width or arch length occurs. The FRLAs are left in place for up to two years as retainers. 5. Be sure to inform parents and patients that Phase II comprehensive fixed Straightwire treatment is almost certain to be needed during adolescence when the 28 permanent teeth have erupted. 6. Use of this "Controlled Arch System" not only simplifies and shortens the duration of orthodontic treatment, but also can dramatically lower the percentage of extraction cases in an orthodontic practice.
J Gen Orthod 1999
PMID:The controlled arch system: a new method of straightwire treatment. 1080 51

It is essential that both the neurologist and the psychiatrist be aware of the neurology drug-psychotropic drug interactions because neurologists prescribe many psychotropic medications and psychiatric consultants often recommend the use of psychotropic drugs for neurology patients. Six methods of examining drug-drug interactions were employed: 1) PubMed (MEDLINE); 2) Hanston's Drug Interaction Analysis and Management Text (July 2001 quarterly updated version); 3)Drug Interactions Facts (quarterly updated version through July 2001); 4) Micromedex Drug-dex; 5) American Hospital Formulary Service Drug Information; 6) Food and Drug Administration (MedWatch) Dear Doctor Letters and new labeling. Over eighty important interactions of significance level 1 (major), or significance level 2 (minor) were found. Furthermore, over one-third of the neurologist's most commonly administered medications were those also employed by the psychiatrist, but not necessarily for the same reason, e.g., carbamazepine, for seizure control (neurologist) or mood stabilization (psychiatrist).
Gen Hosp Psychiatry
PMID:Neurologic drug-psychotropic drug update. 1222 Jul 95

Seizure disorders and epilepsy represent neurologic conditions that commonly are seen among patients requiring dental treatment. When dentists possess a working knowledge of seizures, in addition to an understanding of updated therapies for seizure management and oral complications associated with pharmacological therapy, they are able to treat patients with these disorders more effectively. Neurologic consultations and selecting an appropriate venue for treatment may need to be addressed prior to treatment, depending on the level of seizure control. Laboratory tests designed to evaluate medication levels, leukocyte counts, and clotting ability also may be required. Frequent recall visits may be necessary for seizure disorder patients who display adverse oral complications from medication, such as gingival hypertrophy, xerostomia, and oral yeast infections.
Gen Dent
PMID:Seizure disorders: update of medical and dental considerations. 1505 17

The aim of this study was to examine clinical characteristics in patients with psychogenic nonepileptic seizures and to analyze the Minnesota Multiphasic Personality Inventory (MMPI) profiles and their relation to psychopathology. Thirty patients with nonepileptic seizures confirmed through video-electroencephalography were included. A structured clinical interview (Structured Clinical Interview for DSM-III-R), a measure of personality variables (MMPI), and several structured interviews designed for collecting data on clinical and personal history were administered. Descriptive and comparative statistical methods were used. Of the sample, 67.7% met criteria for two or more simultaneous Axis I diagnoses, and 60% for an Axis II personality disorder. The most frequently elevated scales of the MMPI were Schizophrenia and Depression. There were multiple scale elevations in 12 profiles, the 91.7% of which had elevated "neurotic" and "psychotic" scales. The subgroup with personality disorders showed higher scores on the MMPI Paranoia and Hypomania scales, and the subgroup with traumatic experiences showed higher scores on the MMPI Hypomania scale. Our sample comprising patients with nonepileptic seizures showed a significant degree of psychopathology and absence of a unique character substrate. According to grades of clinical severity of pseudoseizures, several subgroups and different therapeutic implications may be defined.
Gen Hosp Psychiatry
PMID:Psychiatric disorders, trauma, and MMPI profile in a Spanish sample of nonepileptic seizure patients. 1523 27

Mutations in genes encoding neuronal voltage-gated sodium channel subunits have been linked to inherited forms of epilepsy. The majority of mutations (>100) associated with generalized epilepsy with febrile seizures plus (GEFS+) and severe myoclonic epilepsy of infancy (SMEI) occur in SCN1A encoding the NaV1.1 neuronal sodium channel alpha-subunit. Previous studies demonstrated functional heterogeneity among mutant SCN1A channels, revealing a complex relationship between clinical and biophysical phenotypes. To further understand the mechanisms responsible for mutant SCN1A behavior, we performed a comprehensive analysis of the single-channel properties of heterologously expressed recombinant WT-SCN1A channels. Based on these data, we then determined the mechanisms for dysfunction of two GEFS+-associated mutations (R1648H, R1657C) both affecting the S4 segment of domain 4. WT-SCN1A has a slope conductance (17 pS) similar to channels found in native mammalian neurons. The mean open time is approximately 0.3 ms in the -30 to -10 mV range. The R1648H mutant, previously shown to display persistent sodium current in whole-cell recordings, exhibited similar slope conductance but had an increased probability of late reopening and a subfraction of channels with prolonged open times. We did not observe bursting behavior and found no evidence for a gating mode shift to explain the increased persistent current caused by R1648H. Cells expressing R1657C exhibited conductance, open probability, mean open time, and latency to first opening similar to WT channels but reduced whole-cell current density, suggesting decreased number of functional channels at the plasma membrane. In summary, our findings define single-channel properties for WT-SCN1A, detail the functional phenotypes for two human epilepsy-associated sodium channel mutants, and clarify the mechanism for increased persistent sodium current induced by the R1648H allele.
J Gen Physiol 2006 Jan
PMID:Single-channel properties of human NaV1.1 and mechanism of channel dysfunction in SCN1A-associated epilepsy. 1730 47


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