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- Chaplin, John, 1955
(author)
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Vocational assessment and intervention for people with epilepsy
- 2005
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In: Epilepsia. - : Wiley. ; 46:s1, s. 55-56
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Journal article (peer-reviewed)abstract
- Employment restrictions have been experienced by many people with epilepsy. In many cases, the restrictions are unjustified and based on stigma or a stereotypical image of the person with epilepsy. Unjustifiable restrictions are a form of discrimination and lead to unemployment and underemployment. Unfortunately, much of the research in this area has been difficult to interpret because of differences in the definition of "people with epilepsy" and differences in the definition of "employment restrictions or problems." I report on an attempt to develop a classification structure and examine some survey results collected by the IBE Employment Commission from professionals and people with epilepsy concerning the sources of employment restrictions and possible methods to overcome these restrictions.
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- Ben-Menachem, Elinor, 1945
(author)
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Pregabalin pharmacology and its relevance to clinical practice.
- 2004
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In: Epilepsia. - : Wiley. - 0013-9580 .- 1528-1167. ; 45 Suppl 6, s. 13-8
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Research review (peer-reviewed)abstract
- Pregabalin is a potent ligand for the alpha-2-delta subunit of voltage-gated calcium channels in the central nervous system that exhibits potent anticonvulsant, analgesic, and anxiolytic activity in a range of animal models. In addition, pregabalin has been shown to be a highly effective adjunctive therapy for partial seizures in clinical trials. Potent binding to the alpha-2-delta site reduces depolarization-induced calcium influx with a consequential modulation in excitatory neurotransmitter release. Pregabalin has no demonstrated effects on GABAergic mechanisms. Pregabalin demonstrates highly predictable and linear pharmacokinetics, a profile that makes it easy to use in clinical practice. Absorption is extensive, rapid, and proportional to dose. Time to maximal plasma concentration is approximately 1 h and steady state is achieved within 24-48 h. These characteristics reflect the observed onset of efficacy as early as day two in clinical trials. High bioavailability, a mean elimination half life (t(1/2)) of 6.3 h, and dose-proportional maximal plasma concentrations and total exposures predict a dose-response relationship in clinical practice and allow an effective starting dose of 150 mg/day in clinical practice without need for titration. Administration with food has no clinically relevant effect on the amount of pregabalin absorbed, providing for a dosing regimen uncomplicated by meals. Pregabalin does not bind to plasma proteins and is excreted virtually unchanged (<2% metabolism) by the kidneys. It is not subject to hepatic metabolism and does not induce or inhibit liver enzymes such as the cytochrome P450 system. Therefore, pregabalin is unlikely to cause, or be subject to, pharmacokinetic drug-drug interactions--an expectation that has been confirmed in clinical pharmacokinetic studies. However, dose adjustment may be necessary in patients with renal insufficiency. Thus, the pharmacological and pharmacokinetic profiles of pregabalin provide a predictable basis for its use in clinical practice.
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- Ahnlide, Jan Anders, et al.
(author)
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Does SISCOM contribute to favorable seizure outcome after epilepsy surgery?
- 2007
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In: Epilepsia. - : Wiley. - 0013-9580 .- 1528-1167. ; 48:3, s. 579-588
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Journal article (peer-reviewed)abstract
- Purpose: To assess the additional value of subtraction ictal single-photon emission computed tomography (SPECT) coregistered to MRI (SISCOM) for localization of the epileptogenic zone in patients with drug-resistant epilepsy scheduled for invasive video-EEG (VEEG) before epilepsy surgery by a descriptive study from clinical practice. Methods: Forty-nine consecutive epilepsy patients between January 2000 and March 2006 were included. Thirty-six of the 49 patients were offered surgery, and 34 underwent resective surgery during the study period. Localizing and outcome data are presented from 31 patients with a follow-up period of >= 12 months. Successful ictal SPECT was performed in 26 patients, and SISCOM showed significant hyperperfusions with 3.5 SD above reference. Twenty patients had SISCOM-guided electrode placement, invasive monitoring, and 1-year postsurgical follow-up data. Two independent epileptologists evaluated whether SISCOM results (a) altered the hypothesis and extended the strategy for electrode placement at invasive recording, or (b) were confirmatory of other localizing data and did not alter the strategy. We defined that SISCOM had an impact on seizure outcome if the seizure-onset zone was seen in electrodes overlying a brain region with a significant hyperperfusion. When SISCOM was concordant with ictal onset in the extended electrodes, SISCOM was considered a prerequisite for the outcome at postoperative follow-up. Results: SISCOM findings altered and extended the strategy for electrode placement at invasive recording in 15 patients (group A). SISCOM was a prerequisite for seizure outcome in all six patients with favorable outcomes. Nine patients had poor results from surgery in this group; SISCOM was concordant with invasive VEEG in six patients, and discordant with invasive VEEG in three patients. SISCOM findings were confirmatory with other localizing data and did not alter the strategy at invasive recording in five patients (group B). Two patients had favorable surgical outcomes. In this group, three patients had poor results; SISCOM and other localizing findings were concordant with invasive VEEG in one patient and discordant with invasive VEEG in two patients. Conclusions: SISCOM is valuable for the identification of the epileptogenic zone in patients with drug-resistant epilepsy scheduled for invasive VEEG. SISCOM analysis was either a prerequisite for favorable result or concordant with other localizing methods in all patients with favorable seizure outcome at 1 year of follow-up [40%; confidence interval (CI), 19-64).
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- Akel, Sarah, et al.
(author)
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Neurofilament light, glial fibrillary acidic protein, and tau in a regional epilepsy cohort: High plasma levels are rare but related to seizures
- 2023
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In: Epilepsia. - 0013-9580. ; 64:10, s. 2690-2700
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Journal article (peer-reviewed)abstract
- Objective: Higher levels of biochemical blood markers of brain injury have been described immediately after tonic-clonic seizures and in drug-resistant epilepsy, but the levels of such markers in epilepsy in general have not been well characterized. We analyzed neurofilament light (NfL), glial fibrillary acidic protein (GFAP), and tau in a regional hospital-based epilepsy cohort and investigated what proportion of patients have levels suggesting brain injury, and whether certain epilepsy features are associated with high levels.Methods: Biomarker levels were measured in 204 patients with an epilepsy diagnosis participating in a prospective regional biobank study, with age and sex distribution correlating closely to that of all patients seen for epilepsy in the health care region. Absolute biomarker levels were assessed between two patient groups: patients reporting seizures within the 2 months preceding inclusion and patients who did not have seizures for more than 1 year. We also assessed the proportion of patients with above-normal levels of NfL.Results: NfL and GFAP, but not tau, increased with age. Twenty-seven patients had abnormally high levels of NfL. Factors associated with such levels were recent seizures (p = .010) and epileptogenic lesion on radiology (p = .001). Levels of NfL (p = .006) and GFAP (p = .032) were significantly higher in young patients (<65 years) with seizures & LE;2 months before inclusion compared to those who reported no seizures for >1 year. NfL and GFAP correlated weakly with the number of days since last seizure (NfL: r(s) = -.228, p = .007; GFAP: r(s) = -.167, p = .048) in young patients. NfL also correlated weakly with seizure frequency in the last 2 months (r(s) = .162, p = .047).Significance: Most patients with epilepsy do not have biochemical evidence of brain injury. The association with seizures merits further study; future studies should aim for longitudinal sampling and examine whether individual variations in NfL or GFAP levels could reflect seizure activity.
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- Avdic, Una, et al.
(author)
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Nonconvulsive status epilepticus in rats leads to brain pathology
- 2018
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In: Epilepsia. - : Wiley. - 0013-9580 .- 1528-1167. ; 59:5, s. 945-958
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Journal article (peer-reviewed)abstract
- Objective: Status epilepticus (SE) is an abnormally prolonged epileptic seizure that if associated with convulsive motor symptoms is potentially life threatening for a patient. However, 20%-40% of patients with SE lack convulsive events and instead present with more subtle semiology such as altered consciousness and less motor activity. Today, there is no general consensus regarding to what extent nonconvulsive SE (NCSE) is harmful to the brain, which adds uncertainty to stringent treatment regimes. Methods: Here, we evaluated brain pathology in an experimental rat and mouse model of complex partial NCSE originating in the temporal lobes with Western blot analysis, immunohistochemistry, and ex vivo diffusion tensor imaging (DTI). The NCSE was induced by electrical stimulation with intrahippocampal electrodes and terminated with pentobarbital anesthesia. Video-electroencephalographic recordings were performed throughout the experiment. Results: DTI of mice 7 weeks post-NCSE showed no robust long-lasting changes in fractional anisotropy within the hippocampal epileptic focus. Instead, we found pathophysiological changes developing over time when measuring protein levels and cell counts in extracted brain tissue. At 6 and 24 hours post-NCSE in rats, few changes were observed within the hippocampus and cortical or subcortical structures in Western blot analyses of key components of the cellular immune response and synaptic protein expression, while neurodegeneration had started. However, 1 week post-NCSE, both excitatory and inhibitory synaptic protein levels were decreased in hippocampus, concomitant with an excessive microglial and astrocytic activation. At 4 weeks, a continuous immune response in the hippocampus was accompanied with neuronal loss. Levels of the excitatory synaptic adhesion molecule N-cadherin were decreased specifically in rats that developed unprovoked spontaneous seizures (epileptogenesis) within 1 month following NCSE, compared to rats only exhibiting acute symptomatic seizures within 1 week post-NCSE. Significance: These findings provide evidence for a significant brain pathology following NCSE in an experimental rodent model.
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- Azarbayjani, Faranak, et al.
(author)
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Embryonic arrhythmia by inhibition of HERG channels : a common hypoxia-related teratogenic mechanism for antiepileptic drugs?
- 2002
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In: Epilepsia. - : Wiley. - 0013-9580 .- 1528-1167. ; 43:5, s. 457-468
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Journal article (peer-reviewed)abstract
- PURPOSE: There is evidence that drug-induced embryonic arrhythmia initiates phenytoin (PHT) teratogenicity. The arrhythmia, which links to the potential of PHT to inhibit a specific potassium channel (Ikr), may result in episodes of embryonic ischemia and generation of reactive oxygen species (ROS) at reperfusion. This study sought to determine whether the proposed mechanism might be relevant for the teratogenic antiepileptic drug trimethadione (TMO). METHODS: Effects on embryonic heart rhythm during various stages of organogenesis were examined in CD-1 mice after maternal administration (125-1,000 mg/kg) of dimethadione (DMO), the pharmacologically active metabolite of TMO. Palatal development was examined after administration of a teratogenic dose of DMO and after simultaneous treatment with DMO and a ROS-capturing agent (alpha-phenyl-N-tert-butyl-nitrone; PBN). The Ikr blocking potentials of TMO and DMO were investigated in HERG-transfected cells by using voltage patch-clamping tests. RESULTS: DMO caused stage-specific (gestation days 9-13 only) and dose-dependent embryonic bradycardia and arrhythmia at clinically relevant maternal plasma concentrations (3-11 mM). Hemorrhage in the nasopharyngeal part of the embryonic palate (within 24 h) preceded cleft palate in fetuses at term. Simultaneous treatment with PBN significantly reduced the incidence of DMO-induced cleft palate, from 40 to 13%. Voltage patch-clamping studies showed that particularly DMO (70% inhibition), but also TMO, had Ikr blocking potential at clinically relevant concentrations. CONCLUSIONS: TMO teratogenicity, in the same way as previously shown for PHT, was associated with Ikr-mediated episodes of embryonic cardiac arrhythmia and hypoxia/reoxygenation damage.
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| 25. |
- Bastlund, JF, et al.
(author)
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Spontaneous epileptic rats show changes in sleep architecture and hypothalamic pathology
- 2005
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In: Epilepsia. - : Wiley. - 0013-9580 .- 1528-1167. ; 46:6, s. 934-938
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Journal article (peer-reviewed)abstract
- Purpose: The goal of the present study was to investigate the relationship between sleep, hypothalamic pathology, and seizures in spontaneous epileptic rats. Methods: Rats were implanted with radiotelemetry transmitters for measuring electrocorticogram (ECoG) and stimulation electrodes in the hippocampus. Epileptogenesis was triggered by 2 h of electical stimulation-induced self-sustained status epilepticus (SSSE). After SSSE, ECoGs were monitored over a 15-week period for the occurrence of interictal high-amplitude low-frequency (HALF) activity and spontaneous reoccurring seizures (SRSs). Results: Spontaneous epileptic rats showed clinical features of temporal lobe epilepsy (TLE), such as spontaneous seizures, interictal activity and neuronal cell loss in the dorsomedial hypothalamus, a region important for normal sleep regulation. Interestingly, epileptic rats showed disturbances in sleep architecture, with a high percentage of the seizures occurring during sleep. Conclusions: Therefore we conclude that a close association exists between epileptiform activity and alterations in sleep architecture that may be related to hypothalamic pathology.
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