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- Börjesson, L., et al.
(författare)
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Comparison between fMRI and Wada test
- 2004
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Ingår i: Epilepsia. - : Wiley-Blackwell. - 0013-9580 .- 1528-1167. ; 45:Suppl. 3, s. 84-84
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Language lateralisation in patients with epilepsy is more often atypical compared to a normal population. The Wada procedure for testing language and memory has some shortcomings; it is invasive and there is always a risk that the patient becomes too sedated, leading to difficulties in performing the tests. fMR1have shown promising results, showing good correlation to the Wadaprocedure concerning language-lateralisation. The aim of this studywas to investigate if fMRI could be used to determine which hemisphere was language dominant and compare the fMR1 results with the Wada-tests with a focus on patients with a complicated lateralisation.Method: 4 subjects were tested and they had a heterogeneous (I left handed, I ambidexter and 2 right handed) lateralisation and one had a severe dyslexia. A standard Wada procedure was used and compared with a fMRl investigation using a language paradigm.Results: The patients studied showed different language lateralisation patterns (2 left hemisphere and 2 bilateral). In two patients the two tests were fully concordant, in the others the fMRI showed a more bilateral pattern.Conclusion: fMR1 adds valuable information in the pre-surgical investigation for patients with a complex language lateralisation.
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| 2. |
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| 3. |
- Igelström, Kajsa, 1980-, et al.
(författare)
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Inhibition of hippocampal excitability by citalopram
- 2012
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Ingår i: Epilepsia. - : Wiley-Blackwell Publishing Inc.. - 0013-9580 .- 1528-1167. ; 53, s. 2034-2042
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Preclinical data have suggested that selective serotonin reuptake inhibitors (SSRIs) may have anticonvulsant properties, and some SSRIs are known to modulate ion channels in vitro. We screened citalopram, fluoxetine, and sertraline for anticonvulsant actions in mouse hippocampal slices, and studied the effects of citalopram on active membrane properties and repetitive action potential firing.Methods: To enable testing of antiepileptic effects and target modulation in a single experimental system, we used the simplistic low‐Ca2+ model, which is strongly dependent on the intrinsic excitability of CA1 pyramidal neurons. Field potentials and whole‐cell currents were recorded from brain slices, and SSRIs were bath‐applied.Key Findings: We found that citalopram, fluoxetine, and sertraline inhibited epileptiform activity recorded from area CA1. The effect of citalopram was more potent and less variable than that of fluoxetine and sertraline. The anticonvulsant action of citalopram was accompanied by marked slowing of action potential rise and decay, and robust inhibition of repetitive firing. This depression of membrane excitability appeared to be mediated in part by inhibition of a sustained potassium current.Significance: These findings confirm that SSRIs can have anticonvulsant effects in the hippocampus, and further suggest that citalopram may exert these effects at least in part by inhibition of voltage‐gated ion currents.
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| 4. |
- Igelström, Kajsa, 1980-
(författare)
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Preclinical antiepileptic actions of selective serotonin reuptake inhibitors – implications for clinical trial design
- 2012
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Ingår i: Epilepsia. - : Elsevier. - 0013-9580 .- 1528-1167. ; 53, s. 596-605
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Tidskriftsartikel (refereegranskat)abstract
- Selective serotonin reuptake inhibitors (SSRIs) can reduce seizure frequency in humans, but no large‐scale clinical trials have been done to test the utility of SSRIs as potential antiepileptic drugs. This may be caused in part by a small number of reports on seizures triggered by SSRI treatment. The preclinical literature on SSRIs is somewhat conflicting, which is likely to contribute to the hesitance in accepting SSRIs as possible anticonvulsant drug therapy. A careful review of preclinical studies reveals that SSRIs appear to have region‐specific and seizure subtype–specific effects, with models of chronic partial epilepsy being more likely to respond than models of acute generalized seizures. Moreover, this preclinical profile is similar to that of clinical antiepileptic drugs. These observations suggest that SSRIs are promising antiepileptic agents, and that clinical trials may benefit from defining patient groups according to the underlying pathology.
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| 5. |
- Klatt, Juliane, et al.
(författare)
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The EPILEPSIAE database : An extensive electroencephalography database of epilepsy patients
- 2012
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Ingår i: Epilepsia. - : Wiley-Blackwell. - 0013-9580 .- 1528-1167. ; 53:9, s. 1669-1676
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Tidskriftsartikel (refereegranskat)abstract
- From the very beginning the seizure prediction community faced problems concerning evaluation, standardization, and reproducibility of its studies. One of the main reasons for these shortcomings was the lack of access to high-quality long-term electroencephalography (EEG) data. In this article we present the EPILEPSIAE database, which was made publicly available in 2012. We illustrate its content and scope. The EPILEPSIAE database provides long-term EEG recordings of 275 patients as well as extensive metadata and standardized annotation of the data sets. It will adhere to the current standards in the field of prediction and facilitate reproducibility and comparison of those studies. Beyond seizure prediction, it may also be of considerable benefit for studies focusing on seizure detection, basic neurophysiology, and other fields.
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| 7. |
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| 8. |
- Ottosson, Nina, et al.
(författare)
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Synthetic resin acid derivatives selectively open the hK(V)7.2/7.3 channel and prevent epileptic seizures
- 2021
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Ingår i: Epilepsia. - : Wiley-Blackwell. - 0013-9580 .- 1528-1167. ; 62:7, s. 1744-1758
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Tidskriftsartikel (refereegranskat)abstract
- Objective About one third of all patients with epilepsy have pharmacoresistant seizures. Thus there is a need for better pharmacological treatments. The human voltage-gated potassium (hK(V)) channel hK(V)7.2/7.3 is a validated antiseizure target for compounds that activate this channel. In a previous study we have shown that resin acid derivatives can activate the hK(V)7.2/7.3 channel. In this study we investigated if these channel activators have the potential to be developed into a new type of antiseizure drug. Thus we examined their structure-activity relationships and the site of action on the hK(V)7.2/7.3 channel, if they have unwanted cardiac and cardiovascular effects, and their potential antiseizure effect. Methods Ion channels were expressed in Xenopus oocytes or mammalian cell lines and explored with two-electrode voltage-clamp or automated patch-clamp techniques. Unwanted vascular side effects were investigated with isometric tension recordings. Antiseizure activity was studied in an electrophysiological zebrafish-larvae model. Results Fourteen resin acid derivatives were tested on hK(V)7.2/7.3. The most efficient channel activators were halogenated and had a permanently negatively charged sulfonyl group. The compounds did not bind to the sites of other hK(V)7.2/7.3 channel activators, retigabine, or ICA-069673. Instead, they interacted with the most extracellular gating charge of the S4 voltage-sensing helix, and the effects are consistent with an electrostatic mechanism. The compounds altered the voltage dependence of hK(V)7.4, but in contrast to retigabine, there were no effects on the maximum conductance. Consistent with these data, the compounds had less smooth muscle-relaxing effect than retigabine. The compounds had almost no effect on the voltage dependence of hK(V)11.1, hNa(V)1.5, or hCa(V)1.2, or on the amplitude of hK(V)11.1. Finally, several resin acid derivatives had clear antiseizure effects in a zebrafish-larvae model. Significance The described resin acid derivatives hold promise for new antiseizure medications, with reduced risk for adverse effects compared with retigabine.
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| 9. |
- Öhman, Inger, et al.
(författare)
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Topiramate kinetics during delivery, lactation, and in the neonate : Preliminary observations
- 2002
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Ingår i: Epilepsia. - : Wiley. - 0013-9580 .- 1528-1167. ; 43:10, s. 1157-1160
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: To study the pharmacokinetics of topiramate (TPM) during delivery, lactation, and in the neonate. Methods: TPM concentrations in plasma and breast milk were measured with fluorescence polarization immunoassay (FPIA) in five women with epilepsy treated with TPM during pregnancy and lactation. Blood samples were obtained at delivery from mothers, from the umbilical cord, and from the newborns on three occasions (24, 48, and 72 h) after delivery. Blood and breast milk also were collected from mothers 2 weeks, and 1 and 3 months postpartum. Blood samples also were drawn from the infants during breast-feeding. Three of the mother-infant pairs were studied both at delivery and during lactation, two contributed with data from delivery only. Results: The umbilical cord plasma/maternal plasma ratios were close to unity, suggesting extensive transplacental transfer of TPM. The mean milk/maternal plasma concentration ratio was 0.86 (range, 0.67-1.1) at 2-3 weeks after delivery. The milk/maternal plasma concentration ratios at sampling 1 and 3 months after delivery were similar (0.86 and 0.69, respectively). Two to 3 weeks after delivery, two of the breast-fed infants had detectable (>0.9 ╡M) concentrations of TPM, although below the limit of quantification (2.8 ╡M), and one had an undetectable concentration. Conclusions: Our limited data suggest free passage of TPM over the placenta and an extensive transfer into breast milk. Breast-fed infants had very low TPM concentrations, and no adverse effects were observed in the infants.
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