Cortical neuroglia in experimental epilepsy

Abstract

Three different sites of aluminum hydroxide (alumina) application to sensorimotor cortex of monkey are compared: subdural, subarachnoid, and intracortical. The thin arachnoid membrane excludes subdural alumina from brain to prevent clinical or electrical seizures and histological changes. Subarachnoid alumina results in late onset of epilepsy (4–6 months), and seizures are often severe. This epileptic lesion spreads over the outermost cortex like an umbrella. Astrocyte reaction in the border zones results in thick pia-glial membranes, hypertrophied cells with increased filaments and microfilaments, greater number of processes, and increased numbers of cellular connections. The hypertrophic reaction is general in superficial cortex, but in deeper layers organized stripes or bands of giant hypertrophied astrocytes occur at depths where potassium electrode studies have shown increased potassium ions in extracellular spaces with seizures. Neuronal depopulation and neurofibrillary degeneration are not features of the subarachnoid model. Intracortical injections cause seizures in 6–8 weeks, but the lesions are an anatomical disarrangement. In addition to gliosis about the lesion, there are associated asymmetrically located stripes of reactive astrocytes far distant from the injection site. Astrocytes are thought to contribute to or cause the epileptic lesion. They appear to respond to the resulting hyperactivity in neurons, associated ion flux or transmitter release, by hypertrophic reaction in the epileptic focus.