Biomedical subjects

Douglas R Labar

Publications and source records attributed to Douglas R Labar.

3 recordsLinked to original sources

PubMed2006

Hormone replacement therapy in women with epilepsy: a randomized, double-blind, placebo-controlled study.

PURPOSE: Previous reports have suggested that hormone replacement therapy (HRT) could increase seizure activity in women with epilepsy. We sought to determine whether adding HRT to the medication regimen of postmenopausal women with epilepsy was associated with an increase in seizure frequency. METHODS: This was a randomized, double-blind, placebo-controlled trial of the effect of HRT on seizure frequency in postmenopausal women with epilepsy, taking stable doses of antiepileptic drugs (AEDs), and within 10 years of their last menses. After a 3-month prospective baseline, subjects were randomized to placebo, Prempro (0.625 mg of conjugated equine estrogens plus 2.5 mg of medroxyprogesterone acetate or CEE/MPA) daily, or double-dose CEE/MPA daily for a 3-month treatment period. RESULTS: Twenty-one subjects were randomized after completing baseline. The subjects' ages ranged from 45 to 62 years (mean, 53 years; SD, +/-5), and the number of AEDs used ranged from none to three (median, one). Five (71%) of seven subjects taking double-dose CEE/MPA had a worsening seizure frequency of at least one seizure type, compared with four (50%) of eight taking single-dose CEE/MPA and one (17%) of six taking placebo (p = 0.05). An increase in seizure frequency of the subject's most severe seizure type was associated with increasing CEE/MPA dose (p = 0.008). An increase in complex partial seizure frequency also was associated with increasing CEE/MPA dose (p = 0.05). Two subjects taking lamotrigine had a decrease in lamotrigine levels of 25-30% while taking CEE/MPA. CONCLUSIONS: CEE/MPA is associated with a dose-related increase in seizure frequency in postmenopausal women with epilepsy. CEE/MPA may decrease lamotrigine levels.

Anticonvulsants↗

PubMed2002

Antiepileptic drug use during the first 12 months of vagus nerve stimulation therapy: a registry study.

Understanding interrelationships between antiepileptic drugs (AEDs) and vagus nerve stimulation (VNS) therapy can guide research into epilepsy treatment. A constant cohort of patients with data available at baseline and 12 months were drawn from the VNS patient outcome registry and analyzed for changes in AEDs and seizure rates. Of the 1,407 patients, group 1 (n = 896) took fewer (n = 228) or the same (n = 668) AEDs at 12 months compared to baseline. Group 2 (n = 511) took additional (n = 251) or different (n = 260) AEDs. Median seizure rate reductions after 12 months of VNS therapy were 58% in group 1 and 55% in group 2. The number of and specific AEDs remained unchanged for 668 patients and dosages remained the same for 269 (40%) of these patients. The most commonly discontinued drugs were topiramate (n = 115), tiagabine (n = 78), carbamazepine (n = 62), lamotrigine (n = 56), and gabapentin (n = 52). Changes in seizure rates were not significantly different among patients who added levetiracetam (n = 151), zonisamide (n = 71), or oxcarbazepine (n = 46) to VNS. Changes in seizure rates were not significantly different among patients whose baseline AEDs were carbamazepine (n = 273), lamotrigine (n = 238), valproate (n = 201), topiramate (n = 190), or phenytoin (n = 151). Our results suggest the following: (a) patients commonly stay on the same AEDs during 12 months of treatment with VNS; (b) the registry cohort who had reduced AEDs by month 12 did not appear to experience any seizure exacerbation; and (c) no specific AED shows promise of unique additive antiepileptic effects in combination with VNS.

Adult↗

PubMed2002

Cerebral activation during vagus nerve stimulation: a functional MR study.

PURPOSE: To study the short-term effects of vagus nerve stimulation (VNS) on brain activation and cerebral blood flow by using functional magnetic resonance imaging (fMRI). METHODS: Five patients (three women, two men; mean age, 35.4 years) who were treated for medically refractory epilepsy with VNS, underwent fMRI. All patients had a nonfocal brain MRI. The VNS was set at 30 Hz, 0.5-2.0 mA for intervals of activation of 30 s on and 30 s off, during which the fMRI was performed. Statistical parametric mapping (SPM) was used to determine significant areas of activation or inhibition during vagal nerve stimulation (p < 0.05). RESULTS: VNS-induced activation was detected in the thalami bilaterally (left more than right), insular cortices bilaterally, ipsilateral basal ganglia and postcentral gyri, right posterior superior temporal gyrus, and inferomedial occipital gyri (left more than right). The most robust activation was seen in the thalami (left more than right) and insular cortices. CONCLUSIONS: VNS-induced thalamic and insular cortical activation during fMRI suggests that these areas may play a role in modulating cerebral cortical activity, and the observed decrease in seizure frequency in patients who are given VNS may be a consequence of this increased activation.

Adult↗