Search PubMed⌕ Search

PubMed · 10963478

Epilepsy surgery in developing countries.

Abstract

Epilepsy surgery (ES) is a well-accepted treatment for medically intractable epilepsy patients in developed countries, but it is highly technology dependent. Such technology is not usually available in developing countries. For presurgical evaluation, magnetic resonance imaging (MRI) and electroencephalogram recording while videotaping the patient have been important. High technology equipment will, in conjunction with MRI, identify approximately 70% of ES candidates. Introducing ES into developing countries will require determining the candidates that are appropriate for the existing medical infrastructure. This article reviews ES and its possible introduction into conditions existing in developing countries. The authors address (a) the types of patients to be considered for resective ES (some patients require a fairly standard series of noninvasive studies: others will require extensive invasive studies), (b) ways to determine which patients might be appropriate for the existing situation (unilateral mesial temporal lobe epilepsy detected with MRI, epilepsy with a circumscribed MRI lesion, hemispheric lesions, circumscribed MRI detected neuronal migration, and development disorders), (c) surgical procedures (local resection, functional hemispherectomy, multiple subpial transections, corpus callosotomy, and implantation of a vagal nerve stimulator), (d) special considerations for introducing ES into developing countries (medical infrastructure, technology, seizure monitoring systems, selective intracarotid/carotid Amytal testing, and surgical equipment), and (e) the limitations, realistic expectations, personnel requirements, and educational function for selected professionals. Delivery of the technology and expertise to perform ES in developing regions of the world is a realizable project, but it would be limited by available technology and existing medical infrastructure. It should be possible in most areas to train local personnel and thereby leave a lasting legacy.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P D Williamson, B C Jobst. 2000. Epilepsy surgery in developing countries.. https://doi.org/10.1111/j.1528-1157.2000.tb01546.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Histone H3K9 methyltransferases regulate cortical growth by coordinating heterochromatin formation and neural progenitor dynamics.

DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.

Cerebral Cortex↗

A locus for bilateral perisylvian polymicrogyria maps to Xq28.

Polymicrogyria (PMG) is one of a large group of human cortical malformations that collectively account for a significant percentage of patients with epilepsy, congenital neurological deficits, and intellectual disability. PMG is characterized by an excess of small gyri and abnormal cortical lamination. The most common distribution is bilateral, symmetrical, and maximal, in the region surrounding the sylvian fissures, and is known as "bilateral perisylvian polymicrogyria" (BPP). Most cases are sporadic, although several families have been observed with multiple affected members, usually following an X-linked inheritance pattern. Here we report the first genetic locus for BPP mapped by linkage analysis in five families. Linkage places the critical region for BPP at Xq28 (LOD score 3.08 in Xq28, distal to DXS8103 by multipoint analysis). We suggest that this region contains a gene that is necessary for correct neuronal organization and that the identification of this gene will both enhance our understanding of normal cortical development and accelerate the identification of other genes responsible for PMG.

Cerebral Cortex↗

The validity of the inter- and/or intrahemispheric deficit hypothesis as an explanation of the co-occurrence of motor and language impairments.

From an initial cohort of 15 children, between the ages of 5 and 10 years, who had expressive oral language problems, 4 were shown in an earlier study to be both motor and language impaired. Two explanatory hypotheses were proposed to account for this communality: (a) cerebellar deficit; (b) inter- and/or intrahemispheric deficit. In order to explore the validity of the latter explanation, the same group of children, together with a matched control group, were required to carry out two sensory matching tests designed to tap inter- and intrahemispheric information processing abilities: hand-hand and foot-hand. The results, discussed in the light of Liederman's shielding model, provided more support for the hypothesis of an interhemispheric information processing problem from left to right rather than an intrahemispheric problem.

Cerebral Cortex↗