The intracerebral administration of phenytoin using controlled-release polymers reduces experimental seizures in rats.

Purpose: An alternative strategy for the treatment of intractable seizures may be to administer anticonvulsants directly into the brain near the site of a seizure focus using controlled-release polymers. We describe the pharmacokinetics of a phenytoin-ethylene-vinyl acetate (EVAc) controlled-release polymer and report the reduction of seizures in a cobalt-induced rat model of epilepsy with the intracerebral delivery of phenytoin using surgically implanted polymers.

Methods: In the pharmacokinetics study, the drug release rate of 50%-loaded phenytoin-EVAc polymers (n=3) was determined in vitro over 15 weeks initially and then several months later (over a 2-week period after 1 year of in vivo release).

Intrauterine repair of experimental surgically created dysraphism.

The paralysis seen in children with myelomeningocele has been attributed to congenital myelodysplasia. Clinical and pathological data, however, suggest that the paralysis may be due in part to a spinal cord injury caused by exposure of the neural tube to the intrauterine environment. This possibility has been supported by experimental data obtained using a fetal rat model of surgically created dysraphism.

Craniocervical decompression for cervicomedullary compression in pediatric patients with achondroplasia.

The congenital osseous abnormalities associated with achondroplasia include stenosis of the foramen magnum and the upper cervical spinal canal. In the pediatric achondroplastic patient, such stenosis may lead to cervicomedullary compression with serious sequelae, including paresis, hypertonia, delayed motor mile-stones, and respiratory compromise. Using a standardized protocol the authors have treated 15 young achondroplastic patients with documented cervicomedullary compression by craniocervical decompression and duroplasty.

Biphasic action of dextrorphan on penicillin induced bursting in rat hippocampal slice.

Effects of dextrorphan (DX), a metabolite of the over-the-counter antitussive, dextromethorphan, were investigated in rat hippocampal slices exposed to the epileptogenic agent penicillin. At 50 microM and 100 microM concentrations dextrorphan suppressed late components of the epileptiform CA1 field potential elicited by afferent electrical stimulation, and partially suppressed the intracellularly recorded paroxysmal depolarization shift. These effects were not due to non-specific changes in cell excitability, since resting cell membrane potential, input resistance, and the ability of cells to fire action potentials in response to direct depolarizing current were unaffected.

The paralysis associated with myelomeningocele: clinical and experimental data implicating a preventable spinal cord injury.

Paralysis seen in children with myelomeningocele has been attributed to congenital myelodysplasia. We suspected that paralysis may be due in part to a spinal cord injury caused by exposure of the neural tube to the amniotic fluid. This hypothesis was tested using a fetal rat model of surgically created dysraphism.