| 1. |
- Peltola, J, et al.
(författare)
-
Interleukin-6 and interleukin-1 receptor antagonist in cerebrospinal fluid from patients with recent tonic-clonic seizures.
- 2000
-
Ingår i: Epilepsy Res. - Tampere Univ Hosp, Dept Neurol, FIN-33101 Tampere, Finland. Tampere Univ Hosp, Dept Clin Microbiol, FIN-33101 Tampere, Finland. Univ Tampere, Sch Med, FIN-33101 Tampere, Finland. Dept Neurosci, Uppsala, Sweden. : ELSEVIER SCIENCE BV. - 0920-1211 .- 1872-6844. ; 41:3, s. 205-11
-
Tidskriftsartikel (refereegranskat)
|
|
| 2. |
- Pålhagen, Sven, et al.
(författare)
-
Rufinamide : A double-blind, placebo-controlled proof of principle trial in patients with epilepsy
- 2001
-
Ingår i: Epilepsy Research. - 0920-1211 .- 1872-6844. ; 43:2, s. 115-124
-
Tidskriftsartikel (refereegranskat)abstract
- Objective: This was the first proof of principle clinical trial assessing the efficacy and safety of rufinamide as adjunctive therapy in epileptic patients. The pharmacokinetic (PK) profile of rufinamide was also determined. Methods: Fifty patients with diagnoses of partial or primary generalized tonic-clonic seizures were enrolled in this 28-day double-blind, placebo-controlled, weekly rising dose (400-1600 mg/day) trial. PK profiles were obtained after administration of single-dose rufinamide prior to and after the Double-blind phase. Results: In the evaluable patient population, seizure frequency decreased by 41% in the rufinamide group and increased by 52% in the placebo group (P = 0.040). Thirty-nine percent (39%) of rufinamide-treated and 16% of placebo-treated patients experienced reduction in seizure frequency of at least 50% relative to baseline (P = 0.096). Safety: Treatment-emergent adverse events (AEs) consisted mainly of neurologic signs and symptoms commonly associated with antiepileptic drugs (AEDs). Pharmacokinetics: At steady state, rufinamide reached a peak plasma concentration with a mean time (Tmax) of 3.4 h and a mean half-life (t1/2) of 7.3 h. No autoinduction of rufinamide metabolism occurred. Rufinamide did not influence the plasma concentration of carbamazepine, phenytoin or valproate when added to these single AED regimens. Conclusion: Rufinamide has been shown, in this proof of principle trial, to be safe and effective in reducing seizure frequency in epileptic patients with no relevant influence on the metabolism of other AEDs. © 2001 Elsevier Science B.V.
|
|
| 3. |
- Persson, Håkan, et al.
(författare)
-
Carbamazepine affects autonomic cardiac control in patients with newly diagnosed epilepsy.
- 2003
-
Ingår i: Epilepsy Research. - : Elsevier BV. - 0920-1211 .- 1872-6844. ; 57:1, s. 69-75
-
Tidskriftsartikel (refereegranskat)abstract
- Previous studies indicate that epilepsy patients may have impaired autonomic cardiovascular control in the interictal state although it is unclear whether the observed reduction in cardiovascular responses is due to the epilepsy and the interictal epileptogenic discharges, or to the treatment with antiepileptic drugs. Spectral analysis of heart rate variability makes it possible to partly separate the sympathetic components, low frequency (LF), from the vagal components, high frequency (HF) of autonomic cardiac control. We used spectral analysis of heart rate variability to assess the effect of carbamazepine (CBZ) on autonomic cardiac control in patients with newly diagnosed epilepsy. Fifteen adult outpatients with newly diagnosed seizures/epilepsy underwent 24 h ambulatory EKG recordings before and after commencement of CBZ treatment. Total power as well as low frequency (LF), very low frequency (VLF) and high frequency (HF) power in heart rate variability was calculated. When analysing the full 24 h recordings, patients had significantly lower standard deviation of RR-intervals (P=0.0015), total power (P=0.0010), LF (P=0.0002), VLF (P=0.0025) and HF (P=0.0139) during treatment with CBZ than before. The results were very similar for daytime and night time recordings. Our observations demonstrate that CBZ may suppress both parasympathetic and sympathetic functions in newly diagnosed patients with epilepsy. The possible implications of our results for sudden unexpected death in epilepsy are discussed.
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
|
|
