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Ettore Beghi - One of the best experts on this subject based on the ideXlab platform.

  • treatment of first tonic Clonic Seizure does not affect mortality long term follow up of a randomised clinical trial
    Journal of Neurology Neurosurgery and Psychiatry, 2011
    Co-Authors: M Leone, Alessandra Solari, Roberto Vallalta, Ettore Beghi
    Abstract:

    Background Information on the effects of early treatment of Seizures on mortality is scarce. The authors assessed the survival of patients with a first generalised tonic–Clonic Seizure, randomised to immediate treatment (treated) versus treatment only in the event of Seizure recurrence (untreated), over a 20-year period. Methods The authors followed 419 patients. The median follow-up was 19.7 years (range 0.2–21.5) for a total of 7867 person-years. Results 40 persons (9.6%) died during follow-up, 19 (8.9%) treated and 21 (10.3.%) untreated. The probability of surviving was 100% at 1 year, 97% (95% CI 95% to 99%) at 5 years, 94% (91–97) at 10 years and 91% (87–95) at 20 years in treated patients and 100%, 98% (95–100), 97% (94–99) and 89% (85–94), respectively, in untreated patients (p=0.7). After adjustment for treatment of first Seizure and putative risk factors (gender, age, Seizure type, previous uncertain Seizures, family history of Seizures, pre-, peri- and postnatal risk factors, remote aetiological factors for epilepsy, abnormal neurological examination, CT or MRI abnormalities, EEG abnormalities and acute treatment), only the presence of aetiological factors for epilepsy predicted a higher mortality (HR 3.4, 95% CI 2.5 to 4.3%; p Conclusion Starting antiepileptic treatment immediately after the first generalised tonic–Clonic Seizure or only after Seizure recurrence did not affect survival over the following 20 years.

  • treatment of the first tonic Clonic Seizure does not affect long term remission of epilepsy
    Neurology, 2006
    Co-Authors: M Leone, Alessandra Solari, Ettore Beghi
    Abstract:

    We followed 419 patients with a first, unprovoked, primarily or secondarily generalized tonic-Clonic Seizure, randomized to immediate antiepileptic treatment or to treatment only in the event of Seizure recurrence. The probability of achieving a 2-year remission was 72 vs 57% at 3 months, 84 to 79% at 3 years, and 85 to 86% at 10 years (p = NS). The probability of entering 5-year remission was 47 to 40, 58 to 58, and 64 to 64% (p = NS). Early treatment does not affect the long-term prognosis of epilepsy.

  • risk factors for a first generalized tonic Clonic Seizure in adult life
    Neurological Sciences, 2002
    Co-Authors: M Leone, Ettore Beghi, E Bottacchi, E Morgando, R Mutani, R Cremo, Ravagli L Ceroni, I Floriani
    Abstract:

    To evaluate risk factors for a first generalized tonic-Clonic Seizure (GTCS) in adults (=15 years), we performed a multicenter, case-control study involving eleven first-referral neurological departments in north-western Italy. The study enrolled 278 patients with a first GTCS, and 556 age- and sex-matched hospital controls. Cases and controls were interviewed through a questionnaire (inter-rater and index-proxy agreement varied between 75% and 100% for the different questions). Risk factors significantly associated with a first GTCS were: severe head trauma (odds ratio 9.9; 95% confidence limits 2.0–67.1), siblings with Seizures (5.7; 1.7–21.4), alcohol intake >50 grams/day (4.9; 3.1–7.9), history of stroke (3.8; 1.8–8.0), complications of delivery (2.7; 1.5–5.1), other relatives with Seizures (2.4; 1.3–4.6), sleep deprivation (2.4; 1.4–4.1), low gestational age (1.9; 1.1–3.4), mild-moderate head trauma (1.8; 1.2–3.0), and low birth weight (1.6; 1.0–2.7). Genetic and late acquired factors and life habits are major risk factors for a first GTCS in adults, while pre- and perinatal events play only a minor role.

  • treatment of first tonic Clonic Seizure does not improve the prognosis of epilepsy
    Neurology, 1997
    Co-Authors: Massimo Musicco, Ettore Beghi, Alessandra Solari, F Viani
    Abstract:

    It is widely agreed that after two or more Seizures patients should be given antiepileptic treatment, but there is still controversy about the treatment of patients after a first unprovoked Seizure. In a multicenter, randomized, open trial, patients with a first tonic-Clonic Seizure were randomized to immediate treatment (carbamazepine, phenytoin, phenobarbital, or sodium valproate) or to treatment only after another Seizure. Fifty-two(24%) of the 215 patients randomized to immediate treatment and 85 (42%) of the 204 randomized to delayed treatment experienced Seizure recurrence during follow-up. Age, acute treatment of the Seizure with benzodiazepines, remote etiologic factors, and EEG abnormalities were significant predictors of relapse. Of the immediately treated patients, 87% had no Seizures for a year and 68% had no Seizures for 2 years, whereas only slightly fewer initially untreated patients (83% and 60%) achieved these endpoints. Patients treated after the first Seizure and those treated after Seizure relapse had the same time-dependent probability of achieving 1 and 2 Seizure-free years. None of the variables that were prognostic predictors of relapse was significantly associated with the probability of having 1 or 2 years of Seizure control. Anticonvulsants in patients presenting a first tonic-Clonic Seizure reduce the risk of relapse; however, 50% of patients who are not treated will never experience a second Seizure. Moreover, the probability of long-term remission is not influenced by treatment of the first Seizure.

  • alcohol use is a risk factor for a first generalized tonic Clonic Seizure the alc e alcohol and epilepsy study group
    Neurology, 1997
    Co-Authors: M Leone, Ettore Beghi, E Bottacchi, E Morgando, R Mutani, R Cremo, G Amedeo, M Gianelli, Ravagli L Ceroni
    Abstract:

    We performed a multicenter case-control study to estimate whether chronic alcoholism and alcohol consumption are risk factors for developing a first generalized tonic-Clonic Seizure (GTCS). We studied 237 first-Seizure patients (158 men, 79 women) matched to 474 hospital controls for center, sex, age (+/-5 years), and weekday of the Seizure. The risk of first GTCS in alcoholics was greater than in non-alcoholics for men (odds ratio, 6.8; 95% confidence limits, 3.6-13.0) and women (6.8, 1.6-32.6). The odds ratio (both sexes) was 1.2 (0.8-1.8) for an average daily intake of absolute alcohol of 1 to 25 g/day and rose with the amount of alcohol consumed daily: 1.3 (0.8-2.1) for 26 to 50 g/day, 3.0 (1.7-5.4) for 51 to 100 g/day, 7.9 (2.9-21.9) for 101 to 200 g/day, and 16.6 (1.9-373.4) for >200 g/day. Our study provides evidence of a powerful association between alcohol use, alcoholism, and the first GTCS.

Ahmad Reza Dehpour - One of the best experts on this subject based on the ideXlab platform.

  • Effects of Modafinil on Clonic Seizure Threshold Induced by Pentylenetetrazole in Mice: Involvement of Glutamate, Nitric oxide, GABA, and Serotonin Pathways
    Neurochemical Research, 2018
    Co-Authors: Erfan Bahramnjead, Soheil Kazemi Roodsari, Payam Etemadi, Iraj Aghaei, Nastaran Rahimi, Ahmad Reza Dehpour
    Abstract:

    Epilepsy is the third most common chronic brain disorder. Modafinil is an awakening agent approved for narcolepsy. In addition to its clinical uses some reports revealed that modafinil was associated with some alterations in Seizure threshold. The purpose of this study was to clarify the effect of acute administration of modafinil in Clonic Seizure threshold (CST) induced by pentylenetetrazole in mice and the involvement of glutamate, nitric oxide, gamma amino butyric acid (GABA), and serotonin systems in this feature. Modafinil at 80 and 150 mg/kg showed anti- and pro-convulsant effects respectively and expressed maximum anti- and pro-convulsant activities at 30 min after injection. Both modulatory effects were blunted by pretreatment of l -NAME [nonspecific nitric oxide synthase (NOS) inhibitor; 10 mg/kg, i.p.], 7-nitroindazole (a neuronal NOS inhibitor; 40 mg/kg, i.p.), and aminoguanidine (an inducible NOS inhibitor; 50 mg/kg, i.p.). Injection of the NOS precursor l -arginine (60 mg/kg, i.p.) before modafinil did not change the anti-convulsant effect, while thoroughly reversed the pro-convulsant one. Our experiments displayed that administration of diazepam (a GABA_A receptor agonist; 0.02 mg/kg, i.p.) and MK-801 (a NMDA receptor antagonist; 0.05 mg/kg, i.p.) before different doses of modafinil significantly increased CST. Finally, pretreatment of citalopram (a selective serotonin reuptake inhibitor; 0.1 mg/kg, i.p.) did not modify the convulsant activities of modafinil. Therefore, nitric oxide system may mediate anti-convulsant activity, while glutamate, nitric oxide, and GABA pathways may involve in pro-convulsant property. Serotonin receptors have no role on convulsant effects of modafinil.

  • 5 ht3 receptor mediates the dose dependent effects of citalopram on pentylenetetrazole induced Clonic Seizure in mice involvement of nitric oxide
    Epilepsy Research, 2012
    Co-Authors: Borna Payandemehr, Pouya Ziai, Arash Bahremand, Reza Rahimian, Afsaneh Amouzegar, Mohammad Sharifzadeh, Ahmad Reza Dehpour
    Abstract:

    Summary Citalopram is a selective serotonin reuptake inhibitor (SSRI), widely used in the treatment of depressive disorders. It has been shown that citalopram affects Seizure susceptibility. Although the exact mechanism of these effects are not yet fully understood, recent data suggest that 5HT 3 receptors and nitric oxide (NO) might participate in the central effects of SSRIs. In this study in a mouse model of Clonic Seizure induced by pentylenetetrazole we investigated whether 5-HT 3 receptors are involved in the effects of citalopram on Seizure threshold. In our experiments, citalopram at lower doses (0.5 and 1mg/kg, i.p) significantly increased the Seizure threshold and at higher doses (≥25mg/kg) showed proconvulsive effects. Moreover, mCPBG (a 5-HT 3 receptor agonist) at low and non-effective doses augmented while non-effective doses of tropisetron prevented the anticonvulsive properties of citalopram. On the other hand, Low doses of nitric oxide synthase inhibitors l-NAME and 7-NI alone or in combination with lower doses of 5-HT 3 receptor agonist enhanced the anticonvulsive property of citalopram, while l-arginine (NO precursor) alone or in combination with tropisetron blocked the protective effect of citalopram. In summary, our findings demonstrate that 5-HT 3 receptor mediates the anticonvulsant properties of low doses of citalopram, whereas it seems that the proconvulsive effect is mostly mediated through the NO pathway and can be totally blocked by NOS inhibitors. This could propose a new approach toward finding the mechanism of citalopram activity, curtailing the adverse effects of citalopram and perhaps managing the convulsions as a vicious consequence of citalopram overdose.

  • morphine sensitization in the pentylenetetrazole induced Clonic Seizure threshold in mice role of nitric oxide and μ receptors
    Epilepsy & Behavior, 2011
    Co-Authors: Hamed Shafaroodi, Nazanin Baradaran, Leila Moezi, Siavash Dehpour, Tina Kabiri, Ahmad Reza Dehpour
    Abstract:

    Behavioral sensitization occurs after repeated administration of μ-opioid receptor agonists following a drug-free period. It seems that the changes in dopaminergic systems induced by μ-opioid receptor agonists play a crucial role in behavioral sensitization to opioids. Nitric oxide also plays a role in some behavioral effects of morphine, including sensitization to the locomotor-stimulating effect. This study investigated whether morphine sensitization appears in Seizure threshold and the possible role of μ-opioid receptor and nitric oxide in this sensitization. Sensitization was produced by daily injections of morphine (0.1, 0.5, 1, 5, 15, or 30 mg/kg), followed by a 10-day washout period. Then the challenge test was performed using morphine (0.1, 0.5, 1, 5, 15, or 30 mg/kg) in different groups. To assess Clonic Seizure threshold, pentylenetetrazole (PTZ) was administered intravenously. Subcutaneous administration of morphine (0.1 and 0.5 mg/kg) induced sensitization in PTZ-induced Clonic Seizures in mice. Intraperitoneal administration of L-NAME (20 mg/kg), a nonselective inhibitor of nitric oxide synthase, or naltrexone (10 mg/kg), an opioid receptor antagonist, along with morphine inhibited morphine-induced sensitization in PTZ-induced Seizure threshold. In conclusion, at low doses, morphine induces sensitization in PTZ-induced Clonic Seizures in mice probably as a result of the interaction with μ-receptors and nitric oxide.

  • A role for opioid system in the proconvulsant effects of sildenafil on the pentylenetetrazole-induced Clonic Seizure in mice.
    Seizure, 2011
    Co-Authors: Laleh Montaser-kouhsari, Borna Payandemehr, Taha Gholipour, Pouya Ziai, Pooneh Nabavizadeh, Abbas Ghasemi, Arash Bahremand, Mehdi Ghasemi, Ahmad Reza Dehpour
    Abstract:

    There are several lines of evidence that opioidergic and nitrergic systems could modulate the Seizure threshold. We previously have shown that sildenafil had proconvulsant effects in a model of Clonic Seizure induced by pentylenetetrazole (PTZ) or bicuculline. In the present study, we examined whether the opioid system participates in the action of sildenafil on the PTZ-induced Clonic Seizures in mice. Sildenafil (1, 5, 10 and 20 mg/kg, i.p.) significantly decreased the Seizure threshold in a dose-dependent manner, whereas morphine had both anticonvulsant and proconvulsant effects at low (0.5, 1, and 3 mg/kg, s.c.) and high (60 mg/kg, s.c.) doses. A sub-effective dose of sildenafil (5 mg/kg) combined with a dose of morphine (7.5 mg/kg) which was sub-effective for its proconvulsant effects significantly decreased the Seizure threshold. Although naltrexone at 0.5 and 1 mg/kg had no effect on the Seizure threshold, it significantly prevented both the proconvulsant effects of sildenafil as well as the anticonvulsant and proconvulsant effects of morphine on the PTZ-induced Seizure thresholds. Our data suggested a role for opioidergic system in the proconvulsant effects of sildenafil on the PTZ-induced Clonic Seizures in mice.

  • effect of acute and chronic photoperiod modulation on pentylenetetrazole induced Clonic Seizure threshold in mice
    Epilepsy Research, 2008
    Co-Authors: Pouya Tahsilifahadan, Noushin Yahyavifirouzabadi, Kiarash Riazi, Mohammad Hossein Ghahremani, Ahmad Reza Dehpour
    Abstract:

    Summary Changes in circadian rhythms have been shown to alter Seizure susceptibility and anticonvulsant properties of drugs. The present study attempts to elucidate the effect of acute and chronic light/dark (LD) cycle alterations on pentylenetetrazol-induced Clonic Seizure threshold (CST) in male NMRI mice. The acute effect was tested by comparing the effects of abrupt 6-h phase shifts that resulted in 6-h and 18-h photoperiods, during the 24-h period before CST determination, with the controls that were maintained on 12 h/12 h LD cycle. In order to test the effect of chronic LD cycle alteration on CST, three groups of mice were maintained on 12 h/12 h, 6 h/18 h and 18 h/6 h LD cycles for 2 weeks prior to CST testing. The effect of administration of exogenous melatonin (5, 10 and 20 mg/kg, i.p.) was also assessed on LD cycle related changes of CST. The results indicate that acute photoperiod change from 12 h/12 h to 18 h/6 h LD cycle lowers CST, while keeping animals under shorter photoperiod does not produce a significant effect. The pro-convulsant effect of acute increase in light period is reversed by a single injection of melatonin (10 and 20 mg/kg). Animals chronically maintained on both shorter and longer photoperiods show a significant decrease in CST compared to animals under 12 h/12 h LD cycle. However, in both groups chronic administration of melatonin (20 mg/kg) reversed the effect of LD cycle alteration on CST. In conclusion, our data demonstrate that acute increase and chronic modulation of the photoperiod increase Seizure susceptibility in mice. Moreover, the pro-convulsant effect of LD cycle alteration could be reversed by exogenous melatonin administration.

P. R. D. Humphrey - One of the best experts on this subject based on the ideXlab platform.

Carolyn A. Young - One of the best experts on this subject based on the ideXlab platform.

Ida Sarovapinhas - One of the best experts on this subject based on the ideXlab platform.

  • early treatment of a single generalized tonic Clonic Seizure to prevent recurrence
    JAMA Neurology, 1996
    Co-Authors: Ronit Gilad, Yair Lampl, Uri Gabbay, Yehiel Eshel, Ida Sarovapinhas
    Abstract:

    Background: The question of whether to start antiepileptic treatment after a single unprovoked Seizure remains controversial and has been the subject of much debate in the relevant literature. Objectives: To determine the rate of recurrence of a second attack after a single unprovoked epileptic Seizure by using 2 study groups of treated and untreated patients and, thus, to establish a treatment policy for these patients. Patients and Methods: A group of 91 patients with a single generalized tonic-Clonic Seizure were prospectively studied; 87 of these patients completed the study. The end point of the study was 36 months after the single attack or the occurrence of a subsequent epileptic attack. The patients were randomly divided into 2 groups: 45 patients who immediately received anticonvulsive treatment and 42 who remained untreated for the follow-up period. Patients in the treated group were given monotherapy with carbamazepine. The results of recurrences were statistically analyzed by using the Kaplan-Meier method. Results: Results indicated a significantly higher percentage of Seizure-free patients in the treated group compared with that in the untreated group ( P =.001). The treated men were proved to be less at risk for recurrent Seizures compared with treated women ( P P =.03, respectively). Conclusion: Treatment after a single unprovoked Seizure leads to a significant reduction in the risk of relapse of generalized tonic-Clonic epilepsy.