Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149958 (complex partial seizures)
 2,563 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kainic acid (KA 4-14 mg/kg) administered intraperitoneally (i.p.) produces automatisms (scratching until third postnatal week, "wet dog" shakes thereafter), and clonic and tonic-clonic seizures in rats aged 7, 12, 18, 25, and 90 days. Administration of carbamazepine (CBZ) i.p. (25 or 50 mg/kg), phenobarbital (PB 20-80 mg/kg), clonazepam (CZP 0.2 or 1 mg/kg), or valproate (VPA 200 mg/kg) influenced neither incidence nor latency of automatisms. Clonic seizures that are regularly observed after the third postnatal week in controls were either abolished or substantially suppressed by any of the aforementioned antiepileptic drugs (AEDs). Tonic-clonic seizures observed in the first 3 postnatal weeks were suppressed only by solvent [including propyleneglycol (PEG), ethanol, and water]; the effect of AEDs on tonic-clonic seizures was proconvulsant instead. The automatisms were most resistant to AED therapy. These results induce some doubts about the adequacy of the KA model for identifying AEDs effective against complex partial seizures, but forthcoming AEDs that suppress automatisms in the KA rat model might also be active against human complex partial seizures.
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PMID:Action of antiepileptic drugs against kainic acid-induced seizures and automatisms during ontogenesis in rats. 146 81

Stereotactic surgery was performed in Wistar rats and stainless steel injection chemitrode were inserted in bilateral amygdala (AM). Stainless steel screws were placed on the dura over bilateral motor cortex (Cx). One week after the surgery, rats were placed in the recording chamber. Kainic acid (KA) injection was performed into the left AM and focal AM seizure status was induced. Seizures evolved into limbic seizure status during 3 days. Seven days after the first KA injection, KA was injected into the right AM. The limbic seizure status was elicited again, however, these seizures subsided within 3 days. About 3 week after the first KA injection, spontaneous limbic seizures developed. Three ictal EEG patterns were seen (1) Bilateral independent seizures, (2) Synchronous ictal discharge over the bilateral AM, and (3) Switch of lateralized ictal activity from one to the other AM. The histological study demonstrated bilateral hippocampal cell loss and hippocampal atrophy. These changes are very similar to those observed in human intractable complex partial seizures with bilateral mesial temporal focus. The result suggests that this model will be a good tool in order to resolve intractability of complex partial seizure in patients with bilateral temporal focus.
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PMID:[Experimental bilateral focus model of complex partial seizure: clinical, electrophysiological and pathological studies]. 931 Sep 98

Kainic acid-induced multifocal status epilepticus in the rat is a model of medically intractable complex partial seizures and neurotoxicity. The exact mechanisms of kainic acid epileptogenic and neurotoxic effects are unknown, but enhanced glutamate release seems to be an important factor. PNU-151774E ((S)-(+)-2-(4-(3-fluorobenzyloxy) benzylamino) propanamide, methanesulfonate) is a broad-spectrum new anticonvulsant with Na+ channel-blocking and glutamate release inhibiting properties. We have examined the effect of pretreatment with this compound on both seizure activity and hippocampal neuronal damage induced by systemic injection of kainic acid in rats. Lamotrigine, a recently developed anticonvulsant with similar glutamate release inhibitory properties, was tested for comparison, together with diazepam as reference standard, on the basis of its anticonvulsant and neuroprotectant properties in this animal model. PNU-151774E, lamotrigine (10, 30 mg/kg; i.p.) and diazepam (20 mg/kg; i.p.) were administered 15 min before kainic acid (10 mg/kg; i.p.). In the vehicle-treated group, kainic acid injection caused status epilepticus in 86% of animals. Hippocampal neuronal cell loss was 66% in the CA4 hippocampal area at 7 days after kainic acid administration. Diazepam inhibited both seizures and neurotoxicity. Lamotrigine reduced hippocampal neuronal cell loss at both doses, even when it did not protect from seizures, although it showed a trend toward protection. On the other hand PNU-151774E protected from both hippocampal neurodegeneration and status epilepticus. Thus, these data support the concept that seizure prevention and neuroprotection might not be tightly coupled. Glutamate release inhibition may play a major role in neuroprotection, but an additional mechanism(s) of action might be relevant for the anticonvulsant activity of PNU-151774E in this model.
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PMID:PNU-151774E protects against kainate-induced status epilepticus and hippocampal lesions in the rat. 983 Dec 89