Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study investigated the effect of dextromethorphan and 6,7-dinitroquinoxaline-2,3-dione (DNQX) pre-treatment on the development of cocaine- and lidocaine-induced seizures. The dopaminergic action of cocaine was also studied. The NMDA antagonist dextromethorphan and the non-NMDA (AMPA/kainate) antagonist DNQX both significantly decreased the intensity of the seizure response to intravenous convulsant doses of cocaine and lidocaine individually (20 mg/kg) and in combination (5 mg/kg each). The incidence of seizures in rats receiving cocaine or lidocaine individually was significantly reduced by pre-treatment with dextromethorphan but not DNQX. Haloperidol did not have an effect on the incidence or intensity of seizures induced by cocaine or lidocaine, alone or in combination. The results suggest that local anesthetic-induced convulsive seizures are mediated by excitatory glutamate transmission through both NMDA and non-NMDA receptor systems.
 ...
PMID:Decreased cocaine- and lidocaine-induced seizure response by dextromethorphan and DNQX in rat. 918 30

The effects of selective dopaminergic agonists and antagonists on epileptic activity were tested in rats using the lithium/pilocarpine seizure model. Systemic administration of the D1 agonist SKF-38,393 reduced the latency of onset of forelimb clonus with rearing, whereas the D1 antagonist SCH-23,390 and the D2 agonist B-HT 920 prevented the convulsive activity in a dose-dependent manner. Mixed agonists like apomorphine offered partial protection. Haloperidol (D1, D2 blocker, with antimuscarinic property) reduced the threshold for convulsions. The effects of SKF-38,393 and B-HT 920 could be partially blocked by pretreating the rats with SCH-23,390 and sulpiride, respectively. Neither D1 nor D2 antagonists could alter the limbic stereotypies induced by lithium/pilocarpine. These results indicate that dopamine receptor subtypes exert opposite effects on the regulation of convulsive activity. Lipid peroxidation levels (MDA formed) in rat brain homogenates were found to be concomitant with the development of epileptiform activity.
 ...
PMID:Dopaminergic modulation of lithium/pilocarpine-induced status epilepticus in rats. 941 31

In the past few years, literature has accumulated describing manifestation of seizures following administration of certain antidepressants. Such reports are of particular importance because depression is a frequent psychiatric problem associated with epilepsy. Therefore, in the view of the fact that NMDA receptor antagonists have been reported to reduce behavioural deficits and have been shown to be anticonvulsant, it was considered imperative to study their antidepressant effect using shock-induced depression model in mice. Presentation of inescapable foot shock significantly reduced ambulation and rearing in the open field arena and increased immobility duration in the FST. Pretreatment with imipramine, MK 801 and ketamine significantly prevented the effect of shock. Also, the combination of imipramine with either of the NMDA antagonists antagonised the effect of shock. Haloperidol, prazosin and ketanserin pretreatment modified the effect of these agents. These findings suggest an antidepressant effect of the NMDA receptor antagonists, and a complexity of neurotransmitter mechanisms, which are responsible for the occurrence of behavioural effects in shock-induced depression model.
 ...
PMID:Interaction between N-methyl-D-aspartate receptor antagonists and imipramine in shock-induced depression. 1078 52

Passive avoidance reflex was shown to be differently reproduced in rats. The reproduction was more stable in rats with a higher level of learning. Amnestic effects induced seizures were shown to depend on relationships between the intensity of learning and the intensity of seizures. Unconditioned stimuli acting as a reminder decreased the amnestic effects of seizures. Learning process significantly reduced the seizure severity. A dissociated convulsive state was reproduced with the aid of a pharmacological reminder of anxiety formed in the course of learning. Haloperidol produced anxiety and suppressed amnestic effects of seizures, facilitated conditioning in rats with a low level of learning.
 ...
PMID:[Pharmacological reminder of the emotional condition facilitates the amnestic memory trace retrieval]. 1088 20

It is well recognized that epileptic patients are at higher risk for acute or chronic psychotic states than non-epileptic subjects. Here we present intracranial depth electrode recordings during a psychotic episode in a 20-year-old woman who was referred for presurgical evaluation. Unrelated to her seizures, she presented acoustic hallucinations and delusions and became agitated for a duration of 18-24 hours. During this period, a new unusual pattern of sharp slow waves was seen semi-rhythmically every 2-3 sec from left anterior neocortical temporal areas. Her condition responded well to a treatment with Haloperidol, but not with Benzodiazepines. Ictal and interictal scalp- and depth-EEG recordings outside the psychotic episode as well as MRI-based volumetry, PET, SPECT and neuropsychological testing gave evidence of bilateral temporal and frontal dysfunction. This case report suggests that psychosis in epileptic patients may be based on a bilateral cerebral dysfunction linked together in a pathological network, but with a focal (here: left temporal) driving mechanism.
 ...
PMID:Left temporal rhythmic electrical activity: a correlate for psychosis? A case report. 1090 37

Two patients are described who had frequent epileptic seizures, one with primary generalized, the other with partly complex type, in whom after treatment EEG pattern became normal but acute psychotic disturbances appeared. In the literature this phenomenon is known as "forced normalization". The term is not precise since it reduces it to only EEG changes leaving aside seizures and psychosis as alternative of seizures. The condition occurs usually in young persons who previously had no psychotic changes, but had frequent daily seizures, usually generalized of absence type, treated usually with suximide, but in some cases the syndrome was observed in other types of epilepsy treated with other drugs. The incidence of the syndrome is estimated at 1%. Haloperidol is the treatment of choice, but sometimes psychotic episodes were so intense that anticonvulsants had to be withdrawn, as this occurred in one of the reported cases.
 ...
PMID:[Forced normalization]. 1110 4

1. Several neuroleptics inhibited the 3 microM gamma-aminobutyric acid induced-chloride current (GABA-current) on dissociated rat dorsal root ganglion neurons in whole-cell patch-clamp investigations. 2. The IC(50) for clozapine, zotepine, olanzapine, risperidone and chlorpromazine were 6.95, 18.26, 20.30, 106.01 and 114.56 microM, respectively. The values for the inhibitory effects of neuroleptics on the GABA (3 microM)-current, which were calculated by the fitting Hill's equations where the concentrations represent the mean therapeutic blood concentrations, were ranked clozapine>zotepine>chlorpromazine>olanzapine>risperidone. These inhibitory effects, weighted with the therapeutic concentrations of neuroleptics, were correlated with the clinical incidences of seizure during treatment with neuroleptics. 3. Clozapine reduced the picrotoxin-inhibiton, and may compete with a ligand of the t-butylbicyclophosphorothionate (TBPS) binding site. 4. Haloperidol and quetiapine did not affect the peak amplitude of the GABA (3 microM)-current. However, haloperidol reduced the clozapine-inhibition, and may antagonize ligand binding to TBPS binding site. 5. Neuroleptics including haloperidol and quetiapine enhanced the desensitization of the GABA (3 microM)-current. However, haloperidol and quetiapine at 100 microM inhibited the desensitization at the beginning of application. 6. Blonanserin (AD-5423) at 30 and 50 microM potentiated the GABA (3 microM)-current to 170.1+/-6.9 and 192.0+/-10.6% of the control current, respectively. Blonanserin shifted GABA concentration-response curve leftward. Blonanserin only partly negatively interacted with diazepam. The blonanserin-potentiation was not reversed by flumazenil. Blonanserin is not a benzodiazepine receptor agonist. 7. The various effects of neuroleptics on the GABA-current may be related to the clinical effects including modifying the seizure threshold.
 ...
PMID:The effects of neuroleptics on the GABA-induced Cl- current in rat dorsal root ganglion neurons: differences between some neuroleptics. 1190 69

Hepatic encephalopathy represents a reversible decrease in neurological function caused by liver disease. Overall incidence of seizures in hepatic encephalopathy varies between 2% and 33%. Non-convulsive status epilepticus may be particularly common in these patients. Psychiatric disturbances manifest as agitation, personality change, delusions, etc. Aims of seizure management include treatment of basic disease, correction of precipitant factors, imaging of head, and choice of a pharmacologically safe agent. It is important to consider non-convulsive status epilepticus and rule it out by an EEG. Absolute data for safety profile of drugs in liver disease is still not clear, as changes of pharmacokinetics make choice of drugs difficult. Free drug concentrations may be higher, making plasma concentration monitoring essential in such circumstances. A single seizure may not require therapy. However when started, antiepileptic drugs are usually discontinued early. Drugs with sedative effects are best avoided because of a risk of precipitating coma. Phenytoin and gabapentin are relatively preferred drugs; however, monitoring of drug levels is desirable. Management of agitation includes physical restraint and medication. Benzodiazepines are best avoided. Haloperidol is a safer choice in the presence of liver disease. Overall management of neuropsychiatric state aims at management of underlying pathology, the resolution of which leads to improvement in the clinical symptomatology.
 ...
PMID:Management of agitation and convulsions in hepatic encephalopathy. 1502 57

Fyn-mediated tyrosine phosphorylation of N-methyl-D-aspartate (NMDA) receptor subunits has been implicated in various brain functions, including ethanol tolerance, learning, and seizure susceptibility. In this study, we explored the role of Fyn in haloperidol-induced catalepsy, an animal model of the extrapyramidal side effects of antipsychotics. Haloperidol induced catalepsy and muscle rigidity in the control mice, but these responses were significantly reduced in Fyn-deficient mice. Expression of the striatal dopamine D(2) receptor, the main site of haloperidol action, did not differ between the two genotypes. Fyn activation and enhanced tyrosine phosphorylation of the NMDA receptor NR2B subunit, as measured by Western blotting, were induced after haloperidol injection of the control mice, but both responses were significantly reduced in Fyn-deficient mice. Dopamine D(2) receptor blockade was shown to increase both NR2B phosphorylation and the NMDA-induced calcium responses in control cultured striatal neurons but not in Fyn-deficient neurons. Based on these findings, we proposed a new molecular mechanism underlying haloperidol-induced catalepsy, in which the dopamine D(2) receptor antagonist induces striatal Fyn activation and the subsequent tyrosine phosphorylation of NR2B alters striatal neuronal activity, thereby inducing the behavioral changes that are manifested as a cataleptic response.
 ...
PMID:Fyn is required for haloperidol-induced catalepsy in mice. 1640 46

This report is about a 40-year-old man suffering from fluctuating catatonia as main symptom of long-lasting paraneoplastic encephalitis caused by a testicular neoplasm. With recurrence of a neoplasm initially diagnosed as seminoma after a 7-year symptom-free interval the patient suddenly developed various neurological and psychopathological symptoms including seizures, autonomic dysregulation, continuous anterograde short-term amnesia and predominantly a long-lasting complex catatonic syndrome with on-off phenomena. Repeated MRI scans of the brain showed no pathology; brain FDG-PET scans indicated a hypometabolism of the frontal cortex and the left temporal lobe. Eventually a paraneoplastic encephalitis was diagnosed. Repeated resections of tumour recurrences and plasmapheresis moderately alleviated catatonic symptoms. Haloperidol and lorazepam effectively relieved catatonic symptoms in contrast to various atypical antipsychotic drugs and diazepam. A series of 12 electroconvulsive treatments (ECT) temporarily improved residual catatonic symptoms such as catalepsy, stupor and mutism. Further neoplasm recurrences, however, reinforced catatonia until the tumour was successfully treated and the patient fully recovered. This case report illustrates the potential but also the limitations of various therapeutic approaches in organic catatonia due to paraneoplastic encephalitis.
 ...
PMID:Therapeutic strategies for catatonia in paraneoplastic encephalitis. 1785 66


<< Previous 1 2 3 4 5 Next >>