Biomedical subjects

Martha Morrell

Publications and source records attributed to Martha Morrell.

4 recordsLinked to original sources

PubMed2006

Brain stimulation for epilepsy: can scheduled or responsive neurostimulation stop seizures?

PURPOSE OF REVIEW: Scheduled and responsive direct brain stimulation may be an effective and safe therapy for medically intractable epilepsy. RECENT FINDINGS: Scheduled stimulation (open loop) has been provided via electrodes implanted in thalamic nuclei, the cerebellum and the hippocampus using devices commercially available for treatment of tremor and Parkinson's disease. Small pilot trials suggest that seizure frequency is reduced in some patients with intractable epilepsy. Responsive stimulation requires systems that detect abnormal electrographic activity and provide stimulation (closed loop). Studies in inpatients and outpatients suggest that abnormal electrographic discharges can be detected before there is evolution into a clinical seizure, and that focal stimulation of the epileptogenic region terminates electrographic seizures and reduces the frequency of clinically evident seizures. SUMMARY: Direct brain stimulation appears to be safe and may be efficacious in treating medically intractable epilepsy. The optimal location (deep brain or cortical) and characteristics of the stimulation (frequency, current, duration), and whether stimulation should be focal or responsive are still to be determined. If ongoing studies of a deep brain stimulator and of a cranially implanted responsive neurostimulator demonstrate effectiveness, then neurostimulation may become available as adjunctive therapy for medically intractable epilepsy.

Animals↗

PubMed2005

Experimental Electrical Stimulation Therapy for Epilepsy.

Electrical stimulation of the nervous system is an attractive possible therapy for intractable epilepsy, but only stimulation of the vagus nerve has been subjected to large, controlled, and completed clinical trials. Controlled trials are in progress for intermittent cycling stimulation of the anterior nuclei of the thalamus, and for cortical stimulation at a seizure focus, responsive to detection of seizure onset. Anecdotal experience has been gathered with stimulation of cerebellum, centromedian thalamus, subthalamus, caudate, hippocampus, and brainstem. All stimulation of the central nervous system for epilepsy must be considered experimental.

Journal Article↗

PubMed2003

Seizure-free days observed in randomized placebo-controlled add-on trials with levetiracetam in partial epilepsy.

PURPOSE: We examined the effect of adjunctive levetiracetam (LEV; 1,000 to 3,000 mg/day) on the number of seizure-free days gained per quarter in adult patients with refractory partial-onset epilepsy. METHODS: The treatment effect was studied in a meta-analysis using individual patient data of a subpopulation of patients (n = 846) emerging from the three randomized, double-blind, placebo-controlled, phase III trials (n = 904). RESULTS: Adding LEV effectively increased the number of days without seizures by 5.19 days per quarter [95% confidence interval (CI), 3.63-6.76; p = 0.0001; titration and stable dose periods]. CONCLUSIONS: LEV adjunctive treatment shows a clear benefit in terms of seizure-free days gained for patients with refractory epilepsy. This gain is significant for the pooled and for each LEV dose compared with placebo.

Adult↗

PubMed2003

Endocrine and metabolic responses to long-term monotherapy with the antiepileptic drug valproate in the normally cycling rhesus monkey.

An association between epilepsy and reproductive disturbances with an apparent increase in a polycystic ovarian syndrome (PCOS) has been reported. Whether this association can be attributed to epilepsy itself or is related to antiepileptic drug therapy, in particular valproate (VPA), remains controversial. We studied effects of a long-term VPA treatment on cycling monkeys, postulating that, if VPA monotherapy were to promote abnormal endocrine and metabolic parameters that are characteristic of PCOS, changes in cyclicity would be readily demonstrated. After a 2-month control, a 12- to 15-month VPA monotherapy was initiated in 7 regularly cycling rhesus monkeys. Overall mean levels of VPA were 88.7 +/- 4.0 (SE) microg/ml. Mean body weight increased progressively during VPA treatment from 8.5 +/- 0.5 kg before treatment to 9.6 +/- 0.7 kg in the last week of treatment (P < 0.05). Monkeys continued to have regular ovulatory menstrual cycles throughout VPA monotherapy. Length of the cycles was 28 +/- 0.58 d in control and 28.4 +/- 1.18 d in the last 3 months of VPA treatment. Follicular and luteal lengths and peak preovulatory estradiol and integrated luteal progesterone levels did not differ between control and treatment. Ovaries from VPA-treated monkeys showed histological evidence of ovulation, and none had characteristic features of PCOS. Endocrine PCOS markers, such as increased early follicular LH/FSH ratio and androgen levels were not different in control and VPA treatment cycles. LH and 17-hydroxyprogesterone responses to GnRH agonist challenges and the insulin response to glucose tolerance tests were similar in control and VPA groups. Lipid profiles were not affected by VPA treatment. The data indicate that a 12- to 15-month therapeutic exposure to VPA does not induce cyclic hormonal or morphological ovarian abnormalities or characteristics of the PCOS when administered to nonepileptic normally cycling nonhuman primates.

Animals↗