Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Repetitive transcranial magnetic stimulation (rTMS) has been used as a potential therapeutic tool in various neurological and psychiatric diseases including depression, Parkinson disease, spinocerebellar degeneration, epilepsy, urinary incontinence, movement disorders, chronic pain, migraine and chronic tinnitus, etc. Several reports showed the therapeutic effects of rTMS as a treatment of depression and Parkinson disease (PD), whereas others found no significant effects. It is by now not yet fully understood whether rTMS has a therapeutic effect on those diseases. The controversy arises from the differences of the stimulation parameters and evaluation methods of the effects in those studies. The Japanese multi-center, double blinded, sham stimulation controlled trial in 85 patients with PD showed an efficacy in both the rTMS-treated and sham stimulated patients. This result does not prove the efficacy of the rTMS in PD; on the other hand, it does not rule out the efficacy. Possible mechanism of favorable effects of rTMS is related to increasing the release of dopamine in the mesolimbic and mesostriatal system. The other Japanese multi-center, double blinded, sham stimulation controlled trial in 99 patients with spinocerebellar degeneration revealed significant therapeutic effects of rTMS in 51 patients with SCA6. We studied the effects of rTMS on seizure susceptibility in rats which prevented the development of status epilepticus of pentylenetetrazol-induced convulsions. This finding suggests the possibility of therapeutic use of rTMS in epilepsy. Further studies should be performed aiming to reveal the optimal stimulation parameters, and are necessary to reveal the therapeutic role of the rTMS in neurological and psychiatric diseases.
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PMID:[Clinical applications of transcranial magnetic stimulation for the treatment of various neurological diseases]. 1644 38

The clinical efficacy of lidocaine for convulsive status epilepticus in 53 convulsive episodes was examined in 37 children (17 males, 20 females). Mean age of patients receiving lidocaine was 3 years 7 months (SD 3y 5mo). Lidocaine administration achieved control of status epilepticus in 19 of 53 convulsive episodes (35.8%). Seizures ceased within 5 minutes of lidocaine administration in all 19 patients who were responsive to the drug. Regarding aetiology of status epilepticus and types of seizures, there was no statistical difference in effectiveness. Mild decrease of oxygen saturation, monitored by pulse oximetry, was observed in one patient, which improved by oxygenation using a mask. Lidocaine is a useful anticonvulsive agent; however, the response rate to lidocaine appears to be quite low, as less than half of the seizures were effectively controlled by lidocaine. Favourable properties of the drug include prompt responses, less alteration of consciousness, and fewer adverse effects, including less respiratory depression.
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PMID:Intravenous lidocaine for status epilepticus during childhood. 1648 99

Benzodiazepines are an important class of drugs in the management of acute pediatric seizure disorders such as status epilepticus. They are used both in the community and in the hospital; however, one of their major side effects is respiratory depression. If ventilation is needed for benzodiazepine-induced respiratory depression during seizure management, pressures to facilitate extubation may lead to the use of the specific reversal agent for this class of drugs, flumazenil. Three cases of seizure recurrence after flumazenil use in this context are reported, and the pharmacology is discussed. Irrespective of pressure to extubate such children, physicians must be alert to the potential risk of flumazenil in the clinical scenario.
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PMID:Danger of flumazenil use in pediatric status epilepticus. 1662 99

Lithium-pilocarpine status epilepticus (SE) resulted in delayed changes of single cortical interhemisperic (transcallosal) responses in immature rats. Low-frequency stimulation inducing depression and/or potentiation was studied to analyze possible dynamic changes in cortical responses. Status was elicited in 12-day-old (SE12) or 25-day-old (SE25) rats. Control siblings received saline instead of pilocarpine. Interhemispheric responses were elicited by stimulation of the sensorimotor region of the cerebral cortex 3, 6, 9, 13, or 26 days after status. A series of 5 biphasic pulses with intensity equal to twofold threshold were used for stimulation. The interval between pulses was 100, 125, 160, 200 or 300 ms, eight responses were always averaged. Peak amplitude of the first positive, first negative and second positive waves was measured and responses to the second, third, fourth and fifth pulse were compared with the first one. Animals after status epilepticus as well as lithium-paraldehyde controls exhibit a frequency depression at nearly all the intervals studied. An outlined increase of responses in SE rats in comparison with the controls three days after SE stayed just below the level of statistical significance. In addition, animals in the SE12 group exhibited potentiation of responses at this interval after SE. With longer intervals after SE, the relation between SE and control animals changed twice resulting in a tendency to lower amplitude of responses in SE than in control rats 26 days after SE. Rats in the SE25 group exhibited higher responses than controls 13 days after status, but this difference was not present at the longest interval after SE. Low-frequency stimulation did not reveal increased cortical excitability as a long-lasting consequence of status epilepticus induced in immature rats. In addition, the outlined differences between SE and control rats changed with the time after SE.
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PMID:Depression and/or potentiation of cortical responses after status epilepticus in immature rats. 1692 71

Acute repetitive seizures are a predictable component of a patient's seizure disorder, historically distinct from the patient's other epileptic seizures in type, frequency, severity, or duration, and with an onset easily recognized by caregiver and physician. Onset has a consistent predictable component (such as aura or prodrome, which may be a convulsive or nonconvulsive symptom, or characteristic single or multiple seizures) that is predictably and temporally linked to subsequent seizures. Typically there is recovery between seizures. Episodes may or may not progress to a prolonged seizure or to status epilepticus but may be predictable for each patient based on history. Acute repetitive seizures may include any type of epileptic seizure and may occur at any age. Other terms for acute repetitive seizures include cluster, serial, recurrent, or crescendo seizures. Treatment should only be administered by caregivers who in the opinion of the prescriber are capable of monitoring the clinical response and recognize when the response is such that immediate professional evaluation or care is necessary. Caregivers must be comfortable so that they feel capable of recognizing when and how to treat. The prescriber and caregiver should have a written plan on when to treat and what to observe and do after treatment. The most immediate treatment for out of hospital care and the only US Food and Drug Administration-approved product for acute repetitive seizures is rectal diazepam gel administered at a dose of 0.2 to 0.5 mg/kg, depending on age and weight (Class I evidence). Treatment may produce central nervous system depression. Oral, buccal, and sublingual benzodiazepines (lorazepam, diazepam) are also used for treatment but only if the risk of aspiration is not a concern and recognizing that absorption time will be increased (Class III evidence). Nasal benzodiazepine products, available in some countries, are not yet available in the United States.
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PMID:Identification and treatment of acute repetitive seizures in children and adults. 1758 5

Synaptic plasticity is thought to be a key mechanism of information storage in the CNS. Different forms of synaptic long-term potentiation have been shown to be impaired in neurological disorders. Here, we show that metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD), but not NMDA receptor-dependent LTD at Schaffer collateral-CA1 synapses, is profoundly impaired after status epilepticus. Brief application of the group I mGluR agonist (R,S)-3,5-dihydroxyphenylglycine (100 microM; 5 min) induced mGluR LTD in control, but not in pilocarpine-treated rats. Experiments in the presence of selective inhibitors of either mGluR5 [2-methyl-6-(phenylethynyl)-pyridine] or mGluR1 [7-(hydroxyimino)cyclopropachromen-carboxylate ethyl ester and (S)-(+)-alpha-amino-4-carboxy-2-methylbenzeneacetic acid] demonstrate that loss of mGluR LTD is most likely attributable to a loss of mGluR5 function. Quantitative real-time reverse transcription PCR revealed a specific downregulation of mGluR5 mRNA, but not of mGluR1 mRNA in the CA1 region. Furthermore, we detected a strong reduction in mGluR5 protein expression by immunofluorescence and quantitative immunoblotting. Additionally, the scaffolding protein Homer that mediates coupling of mGluR5 to downstream signaling cascades was downregulated. Thus, we conclude that the reduction of mGluR LTD after pilocarpine-induced status epilepticus is the result of the subtype-specific downregulation of mGluR5 and associated downstream signaling components.
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PMID:Loss of metabotropic glutamate receptor-dependent long-term depression via downregulation of mGluR5 after status epilepticus. 1833 Apr 67

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

An open-label, randomized controlled study was conducted at a tertiary care teaching hospital to compare efficacy and safety of intravenous sodium valproate versus diazepam infusion for control of refractory status epilepticus. Forty children with refractory status epilepticus were randomized to receive either intravenous sodium valproate or diazepam infusion. Refractory status epilepticus was controlled in 80% of the valproate and 85% of the diazepam patients. The median time to control refractory status epilepticus was less in the valproate group (5 minutes) than the diazepam group (17 minutes; P < .001). None of the patients in the valproate group required ventilation or developed hypotension, whereas in the diazepam group 60% required ventilation and 50% developed hypotension after starting diazepam infusion. No adverse effects on liver functions were seen with valproate. It is concluded that intravenous sodium valproate is an effective alternative to diazepam infusion in controlling refractory status epilepticus in children and is free of respiratory depression and hypotension.
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PMID:Intravenous sodium valproate versus diazepam infusion for the control of refractory status epilepticus in children: a randomized controlled trial. 1794 Feb 45

The dentate gyrus, a region of the hippocampal formation, displays the highest level of plasticity in the brain and exhibits neurogenesis all through life. Dentate neurogenesis, believed to be essential for learning and memory function, responds to physiological stimuli as well as pathological situations. The role of dentate neurogenesis in the pathophysiology of temporal lobe epilepsy (TLE) has received increased attention lately because of its disparate response in the early and chronic stages of the disease. Acute seizures or status epilepticus immensely enhance dentate neurogenesis and lead to an aberrant migration of newly born neurons into the dentate hilus and the formation of epileptogenic circuitry in the injured hippocampus. Conversely, spontaneous recurrent seizures that arise during chronic TLE are associated with dramatically reduced dentate neurogenesis. In this review, we discuss the potential significance of enhanced but abnormal neurogenesis taking place shortly after brain injury or the status epilepticus towards the development of chronic epilepsy, and prospective implications of dramatically waned dentate neurogenesis occurring during chronic epilepsy for learning and memory function and depression in TLE. Furthermore, we confer whether hippocampal neurogenesis is a possible drug target for preventing TLE after brain injury or the status epilepticus, and for easing learning and memory impairments during chronic epileptic conditions. Additionally, we discuss some possible drugs and approaches that need to be evaluated in future in animal models of TLE to further understand the role of neurogenesis in the pathogenesis of TLE and whether modulation of neurogenesis is useful for treating TLE.
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PMID:Could hippocampal neurogenesis be a future drug target for treating temporal lobe epilepsy? 1804 63

The definition of status epilepticus (SE) has been reduced from 30 minutes to 5 minutes and this article questions if treatment should not be offered before reaching that window. After provision of first aid, benzodiazepines (BDZ) are the initial form of intervention, with either nasal or buccal midazolam being favored for nonprofessionals. Proper patient supervision, including admission to an intensive care unit for more difficult patients, is endorsed, and the need to warn nonprofessionals of the potential risk of respiratory depression is imperative. The article criticizes the use of phenytoin as the antiepileptic medication (AEM) with which to load patients, as it is no longer a first-line AEM, and argues in favor of using a first-line AEM such as valproate or carbamazepine, or preferably the AEM that previously proved efficacious in a patient with known epilepsy who was noncompliant. Alternative routes of administration of AEMs are discussed, and the use of blood level monitoring, as an adjunct to management, to protect against further episodes of SE, is supported. Touched on in this article are the use of some of the newer AEMs in the management of SE and exploration of treatment strategies that acknowledge that treatment must also include patient education that incorporates techniques to enhance compliance.
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PMID:An alternative perspective on the management of status epilepticus. 1826 47


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