Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ideal antiepileptic drug (AED) should correct the aberrant pathophysiology of epileptogenesis without interfering with normal neurotransmission A new group of drugs with antiepileptic efficacy, without sedative properties, would be an exciting prospect. Theoretical considerations and results from experimental animal models of epilepsy have put forward the possibility that calcium (Ca2+) antagonists may form such a group. The initiation of epileptogenic activity in the neuron is thought to be connected with the phenomenon known as "intrinsic burst firing", which is activated by an inward Ca2+ current. Ca2+ is described as the primary mediator of "excitotoxic" neuronal damage. Both necrotic and apoptotic cell death is associated with Ca2+ entry into the cells during status epilepticus. The Ca2+ channel blockers depressed epileptic depolarizations of neurons. In this review, we present anticonvulsant effects of cinnarizine, flunarizine, nifedipine, nimodipine, nicardipine, amlodipine, isradipine, niguldipine, diltiazem, verapamil and dantrolene in animal models of seizures. Also, a detailed analysis of interactions between Ca2+ blockers and AEDs was performed. Clinical trials in intractable epilepsy support to a certain degree antiepileptic properties of Ca2+ antagonists.
Pol J Pharmacol
PMID:Calcium modulation in epilepsy. 1504 75

We present a 43-year-old man with recurrent episodes of Hashimoto's encephalopathy who was diagnosed with autoimmune thyroiditis in childhood. Encephalopathy started with subacute dementia followed by extrapyramidal and psychiatric symptoms of insidious onset. He had also status epilepticus which occurred within the first year of the disease. The patient was in euthyreosis, but increased levels of antithyroid antibodies were found. MRI of the brain was normal. Electroencephalography was initially normal and later showed diffuse slowing with generalized theta/delta activity. The cerebrospinal fluid examination revealed a high level of protein which decreased when remission of the disease was achieved. After other etiology was excluded Hashimoto's encephalopathy was diagnosed. Almost complete clinical recovery after steroid administration was observed. Attempts of prednisone withdrawal led to recurrence of neurological and psychiatric symptoms. The diagnosis of Hashimoto's encephalopathy should be considered in each case with subacute encephalopathy associated with high levels of antithyroid antibodies (despite normal thyroid function) and in the absence of other brain diseases.
Neurol Neurochir Pol
PMID:[Hashimoto's encephalopathy. Case report and literature review]. 1504 70

The purpose of this paper is to present the problem of the diagnosis of psychogenic pseudoepileptic seizures from the clinician's point of view and to stress some difficulties which neurologist, psychiatrist and general practitioner can be faced. In epilepsy centers from 10 to 20% of patients with diagnosis of drug resistant epilepsy had psychogenic pseudoepileptic seizures. Diagnosis of psychogenic pseudoepileptic seizures can be established on clinical symptomatology, several EEG recordings, long term EEG videotape recording and some neurological tests evaluating post-seizure reflexive responsiveness. In differential diagnosis examination of simple defensive reactions, provocation of seizure or its arrest using suggestion with placebo may be very helpful. Author stress the consequences from false diagnosis. Prolonged pseudoepileptic seizures very often are treated as status epilepticus including general anesthesia.
Pol Merkur Lekarski 2003 Dec
PMID:[Psychogenic pseudo-epileptic seizures: diagnostic difficulties]. 1505 68

Topiramate, a new anticonvulsant, has been reported to possess neuroprotective effects in both in vivo and in vitro experiments. In the present study, the effect of topiramate (40 and 80 mg/kg ip) on the fully developed kainate-induced status epilepticus was evaluated in the rat. Injection of kainate (15 mg/kg ip) evoked recurrent limbic seizures which lasted several hours. Topiramate injected 1.5 h after kainate administration had no effect on the seizures and mortality of the animals. Biochemical study revealed that at 80 mg/kg ip, topiramate significantly attenuated the kainate-induced lipid peroxidation in the piriform cortex and showed similar tendency in the frontal cortex. Besides the central nervous system, the kainate-induced seizures evoked significant changes in immunoreactivity, such as reduction in thymus weight and the proliferative activity of splenocytes, and the splenocyte-increased production of interleukin-10, but not interferon-gamma. Topiramate did not affect the kainate-induced reduction in thymus weight, but attenuated changes in the proliferative activity of splenocytes. It is concluded that topiramate, when given during the fully developed kainate-induced status epilepticus in rats, has no effect on seizures, but attenuates lipid peroxidation in piriform cortex and prevents certain changes in immunoactivity.
Pol J Pharmacol
PMID:Effect of topiramate on the kainate-induced status epilepticus, lipid peroxidation and immunoreactivity of rats. 1559 43

Oxidative stress and mitochondrial dysfunction are acute consequences of status epilepticus (SE). However, the role of mitochondrial oxidative stress and genomic instability during epileptogenesis remains unknown. Using the kainate animal model of temporal lobe epilepsy, we investigated oxidative mitochondrial DNA (mtDNA) damage and changes in the mitochondrial base excision repair pathway (mtBER) in the rat hippocampus for a period of 3 months after SE. Acute seizure activity caused a time-dependent increase in mitochondrial, but not nuclear 8-hydroxy-2-deoxyguanosine (8-OHdG/2dG) levels and a greater frequency of mtDNA lesions. This was accompanied by increased mitochondrial H2O2 production and a transient decrease in mtDNA repair capacity. The mtBER proteins 8-oxoguanine glycosylase (Ogg1) and DNA polymerase gamma (Pol gamma) demonstrated elevated expression at mRNA and protein levels shortly after SE and this was followed by a gradual improvement in mtDNA repair capacity. Recurrent seizures associated with the chronic phase of epilepsy coincided with the accumulation of mtDNA damage, increased mitochondrial H2O2 levels, decreased expression of Ogg1 and Pol gamma and impaired mtDNA repair capacity. Together, increased oxidative mtDNA damage, mitochondrial H2O2 production and alterations in the mtBER pathway provide evidence for mitochondrial oxidative stress in epilepsy and suggest that mitochondrial injury may contribute to epileptogenesis.
 ...
PMID:Mitochondrial DNA damage and impaired base excision repair during epileptogenesis. 1829 98

Reversible posterior leukoencephalopathy (RPLE) is a unique clinicoradiological entity characterized by diverse neurological symptoms with bilateral posterior cerebral white matter edema. It is frequently associated with seizures but rarely with status epilepticus. Periodic lateralized epileptiform discharges (PLEDs) as an initial electrographic pattern in a patient with RPLE have never been reported. We discuss a 47-year-old woman with a newly diagnosed non-small cell carcinoma of the lung on etoposide who was admitted with encephalopathy. Initial EEG demonstrated PLEDs. She later developed nonconvulsive status epilepticus. Magnetic resonance imaging (MRI) revealed bilateral subcortical edema predominantly of the temporo-occipital lobes. Discontinuation of etoposide resulted in full clinical, electrical recovery within 10 days and significant radiological improvement within 15 days. Our case indicates the importance of identifying and addressing any modifiable etiologic factors of RPLE. We emphasize identification of the unique initial electrographic pattern of PLEDs, which may be a predisposing factor to status epilepticus or an indication of structural damage.
Neurol Neurochir Pol
PMID:Periodic lateralized epileptiform discharges: an initial electrographic pattern in reversible posterior leukoencephalopathy syndrome. 1836 64

Tuberculoma involving the cerebellopontine angle is very rare. Preoperative neuroradiological features of such lesions may mimic neoplastic lesions and postoperative histopathological study brings the ultimate diagnosis. Here we present a patient with a large tuberculoma at the cerebellopontine angle who had another small lesion at the right fronto-basal region and was managed by surgical excision of the cerebellopontine angle lesion along with post-surgical antitubercular therapy for 18 months. On the 14th postoperative day, the patient developed status epilepticus, left hemiplegia and left-sided complete hearing loss. Computed tomography showed right frontal oedema. Then he recovered his motor function slowly and incompletely but left-sided hearing loss remained unchanged. Magnetic resonance imaging of the brain at 18 months after surgery showed no residual lesion with right frontal cortical atrophy.
Neurol Neurochir Pol
PMID:Large cerebellopontine angle tuberculoma: a case report. 2258 4

The cortical laminar necrosis (CLN) is a permanent injury characterized by the selective delayed necrosis of the cerebral cortex, mainly of the third layer, and usually greater in the depths and sides of the sulci than over the crest of the gyri. The damage involves all cellular components - either neurons, glia cells and blood vessels - and results in a focal cortical band of pan-necrosis detectable in late sub-acute or chronic stages of reduced energy supply to the brain. The CLN has been described in different conditions as hypoxia, hypoglycemia and status epilepticus. At brain CT or MR scans it appears with pathognomonic highly hyperdense or T1-hyperintense lesions following the gyral anatomy of the cerebral cortex. We reported a case of CLN associated to myocardial infarct and discussed the underlying mechanisms.
Neurol Neurochir Pol
PMID:Cortical laminar necrosis following myocardial infarction. 2737 42

We report a patient who experienced atypical symptoms in the course of electroconvulsive therapy (ECT). During ECT treatment patient experienced psychotic symptoms which should be differentiated with prolonged delirium and nonconvulsive status epilepticus. 46-year-old female was referred to hospital with a diagnosis of major depressive disorder with no psychotic features in the course of recurrent depression. Despite several changes of pharmacological treatment no improvement was achieved, therefore it was decided to initiate ECT. Physical and neurological examination revealed no deviations from the norm. The results of other tests (CT and EEG) were normal. 4 bilateral, bitemporal ECT procedures were performed. The course of each procedure was typical, the same doses of anesthetic medication and pulse dose was administered throughout all of the procedures. The duration of seizure was 32-40 s. Despite this mental symptoms observed during the course of the treatment differed from known to the authors from both their own experience and from literature. Delusions of reference, persecution, agitation, oneiric delusions and olfactory hallucinations which appeared after the 4th ECT session maintained for 14 days and resolved after treatment with olanzapine. To the best of our knowledge, this is the first report on delusions of reference and persecution, oneiric delusions and olfactory hallucinations associated with the course of ECT.
Psychiatr Pol 2017 Feb 26
PMID:Psychotic symptoms as a complication of electroconvulsive therapy - a case report. 2845 92


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