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)

Electroconvulsive therapy, which is used to treat refractory major depression in humans increases seizure threshold and decreases seizure duration. Moreover, the expression of brain derived neurotrophic factor induced by electroshocks (ECS) might protect hippocampal cells from death in patients suffering from depression. As temporal lobe epilepsy is linked to neuronal damage in the hippocampus, we tested the effect of repeated ECS on subsequent status epilepticus (SE) induced by lithium-pilocarpine and leading to cell death and temporal epilepsy in the rat. Eleven maximal ECS were applied via ear-clips to adult rats. The last one was applied 2 days before the induction of SE by lithium-pilocarpine. The rats were electroencephalographically recorded to study the SE characteristics. The rats treated with ECS before pilocarpine (ECS-pilo) developed partial limbic (score 2) and propagated seizures (score 5) with a longer latency than the rats that underwent SE alone (sham-pilo). Despite this delay in the initiation and propagation of the seizures, the same number of ECS- and sham-pilo rats developed SE with a similar characteristic pattern. The expression of c-Fos protein was down-regulated by repeated ECS in the amygdala and the cortex. In ECS-pilo rats, c-Fos expression was decreased in the piriform and entorhinal cortex and increased in the hilus of the dentate gyrus. Neuronal damage was identical in the forebrain areas of both groups, while it was worsened by ECS treatment in the substantia nigra pars reticulata, entorhinal and perirhinal cortices compared to sham-pilo rats. Finally, while 11 out of the 12 sham-pilo rats developed spontaneous recurrent seizures after a silent period of 40+/-27 days, only two out of the 10 ECS-pilo rats became epileptic, but after a prolonged latency of 106 and 151 days. One ECS-pilo rat developed electrographic infraclinical seizures and seven did not exhibit any seizures. Thus, the extensive neuronal damage occurring in the entorhinal and perirhinal cortices of the ECS-pilo rats seems to prevent the establishment of the hyperexcitable epileptic circuit.
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PMID:Electroshocks delay seizures and subsequent epileptogenesis but do not prevent neuronal damage in the lithium-pilocarpine model of epilepsy. 1099 2

We report on a case of a 45-year-old man in an episode of major depression with psychotic features treated with bilateral electroconvulsive therapy (ECT). At the eighth treatment, he manifested unilateral, prolonged, nonconvulsive seizure activity on the left side, which lasted 351 seconds longer than seizure activity on the right, and was terminated with intravenous diazepam. This is the first report of a unilateral prolonged seizure. Its occurrence following bilateral ECT was particularly noteworthy. This case also highlights the importance of two-channel EEG recording during ECT. Without two recording channels we doubt that this event would have been detected, perhaps resulting in nonconvulsive status epilepticus.
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PMID:A unilateral, prolonged, nonconvulsive seizure in a patient treated with bilateral ECT. 1173 33

Psychiatric disorders frequently occur in patients with epilepsy, but the relationship between epilepsy and psychopathology is poorly understood. Frequent comorbidities in epilepsy patients comprise major depression, anxiety disorders, psychosis and cognitive dysfunction. Animal models of epilepsy, such as the pilocarpine model of acquired epilepsy, are useful to study the relationship between epilepsy and behavioral dysfunctions. However, despite the advantages of mice in studying the genetic underpinning of behavioral alterations in epilepsy, mice have only rarely been used to characterize behavioral correlates of epilepsy. This prompted us to study the behavioral and cognitive alterations developing in NMRI mice in the pilocarpine model of epilepsy, using an anxiety test battery as well as tests for depression, drug-induced psychosis, spatial memory, and motor functions. In order to ensure the occurrence of status epilepticus (SE) and decrease mortality, individual dosing of pilocarpine was performed by ramping up the dose until onset of SE. This protocol was used for studying the consequences of SE, i.e. hippocampal damage, incidence of epilepsy with spontaneous recurrent seizures, and behavioral alterations. SE was terminated by diazepam after either 60, 90 or 120 min. All mice that survived SE developed epilepsy, but the severity of hippocampal damage varied depending on SE length. In all anxiety tests, except the elevated plus maze test, epileptic mice exhibited significant increases of anxiety-related behavior. Surprisingly, a decrease in depression-like behavior was observed in the forced swimming and tail suspension tests. Furthermore, epileptic mice were less sensitive than controls to most of the behavioral effects induced by MK-801 (dizocilpine). Learning and memory were impaired in epileptic mice irrespective of SE duration. Thus, the pilocarpine-treated mice seem to reflect several of the behavioral and cognitive disturbances that are associated with epilepsy in humans. This makes these animals an ideal model to study the neurobiological mechanisms underlying the association between epilepsy and psychopathology.
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PMID:Behavioral alterations in the pilocarpine model of temporal lobe epilepsy in mice. 1771 5

Mood disorders and major depression are frequently comorbid with epilepsy. While the nature of this comorbidity is not fully understood, multiple lines of evidence suggest that changes in serotonin (5-HT) neurotransmission may be an underlying mechanism. In this study, we tested the hypothesis that chronic epilepsy in rats can be associated with loss of 5-HT neurons in the dorsal raphe (DR) nuclear complex, the main source of 5-HT projections to the cerebral cortex, which would help to explain respective behavioral deficits. Epilepsy was induced using the kainate model of status epilepticus in adult Wistar rats. After a 3-month recovery period, all kainate-treated rats that had experienced status epilepticus showed spontaneous seizures and reduced sucrose preference (anhedonia), a core symptom of depression. No changes in the forced swim test were detected. The total numbers of 5-HT immunoreactive cells were estimated in all DR subdivisions of control and epileptic rats. Interestingly, epilepsy-related loss of 5-HT neurons (approximately 35%) was observed only in the interfascicular part of the DR complex, which is known to innervate brain regions involved in depression. These findings support the notion that mental health impairments observed in epilepsy may be related to loss of a specific population of the DR 5-HT neurons projecting to limbic brain areas.
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PMID:Altered taste preference and loss of limbic-projecting serotonergic neurons in the dorsal raphe nucleus of chronically epileptic rats. 2645 22

Mr. R, a 27 year old Hispanic male with history of traumatic brain injury (TBI) over ten years prior but no psychiatric history, presents to the psychiatric consultation service with recent onset of mutism, psychotic behavior and new diagnosis of epilepsy. The differential diagnosis is broad and includes both medical and psychiatric causes: post-ictal state, non-convulsive status epilepticus, delirium due to metabolic conditions, drugs, catatonia, conversion disorder, major depression with psychotic features, new onset schizophrenia or a combination of these possible diagnoses. We explore different medical causes that can present with symptoms of catatonia, as it is crucial to rule out a possible treatable medical cause.
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PMID:Consultation Dilemma Catatonia in a Patient with Prior TBI: MentaI or Medical Disorder? 2718 97

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.
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PMID:Psychotic symptoms as a complication of electroconvulsive therapy - a case report. 2845 92

Vilazodone hydrochloride is the first member in a new class of antidepressants called indolealkylamines and was approved for use in the United States in 2011 for major depressive disorder. It has a combined mechanism of action of a selective serotonin reuptake inhibitor and a partial agonist of serotonin 5-HT1A receptors. It has not been approved for use in the pediatric population, and toxicity from exploratory vilazodone ingestion has been rarely described to date. We describe 2 children with laboratory-confirmed vilazodone ingestions that led to significant toxicity including refractory status epilepticus in 1 patient and likely transient seizure activity in the other. Both patients required multiple doses of benzodiazepines; in the more severe case, barbiturates were added to control seizure activity. These children returned to baseline and had no prolonged neurologic complications. Pediatric experience with vilazodone is limited; however, the literature demonstrates 3 additional case reports of children experiencing seizure after vilazodone ingestion. With the 2 new cases presented here, it seems prudent to educate prescribers and families of the potential dangers of ingestion of vilazodone tablets by young children.
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PMID:Seizures After Pediatric Vilazodone Ingestion: A Case Series. 2859 Sep 88

Catatonia is a well-described clinical syndrome characterized by features that range from mutism, negativism and stupor to agitation, mannerisms and stereotype. Causes of catatonia may range from organic brain disorders to psychiatric conditions. Despite a characteristic syndrome, catatonia is grossly under diagnosed. The reason for missed diagnosis of catatonia in neurology setting is not clear. Poor awareness is an unlikely cause because catatonia is taught among conditions with deregulated consciousness like vegetative state, locked-in state and akinetic mutism. We determined the proportion of catatonia patients correctly identified by neurology residents in neurology emergency. We also looked at the alternate diagnosis they received to identify catatonia mimics. Twelve patients (age 22-55 years, 7 females) of catatonia were discharged from a single unit of neurology department from 2007 to 2017. In the emergency department, neurology residents diagnosed none of the patients as catatonia. They offered diagnosis of extrapyramidal syndrome in 7, meningitis in 2, and conversion reaction, acute psychosis/encephalopathy and non-convulsive status epilepticus in one each. Their final diagnosis at discharge was catatonia due to general medical condition in 6 (progressive supranuclear palsy in 2, post-status epilepticus, uremic encephalopathy, glioblastoma multiforme and tuberculous meningitis in one each), catatonia due to major depression in 4, schizophrenia and idiopathic catatonia in one each. Extrapyramidal syndrome appeared as common mimic of catatonia. The literature reviewed also revealed the majority of organic catatonia secondary to causes that are usually associated with extrapyramidal features. Therefore, we suggest that neurologists should consider catatonia in patients presenting with extrapyramidal syndromes.
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PMID:Why do neurologists miss catatonia in neurology emergency? A case series and brief literature review. 3114 76