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Neurobiology of Epilepsy: Neurosurgical Management Therapy

Case Report | DOI: https://doi.org/10.31579/2578-8868/019

Neurobiology of Epilepsy: Neurosurgical Management Therapy

  • Scott Maya 1

1 Department of Neurobiology, Iran

*Corresponding Author: Scott Maya,Department of Neurobiology, Iran

Citation: Scott Maya, Michael Alain ,Neurobiology of Epilepsy: Neurosurgical Management Therapy, J Neuroscience and Neurological Surgery. Doi: 10.31579/2578-8868/019

Copyright: © 2017 Scott Maya, This is an open-access article distributed under the terms of The Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Received: 28 March 2017 | Accepted: 12 April 2017 | Published: 20 April 2017

Keywords: tranumatic brain injury;nuerological degenerative diseases

Abstract

Epilepsy is a complex disease with diverse clinical characteristics that preclude a singular mechanism. One way to gain insight into potential mechanisms is to reduce the features of epilepsy to its basic components: seizures, epileptogenesis, and the state of recurrent unprovoked seizures that defines epilepsy itself. A common way to explain seizures in a normal individual is that a disruption has occurred in the normal balance of excitation and inhibition. The fact that multiple mechanisms exist is not surprising given the varied ways the normal nervous system controls this balance. In contrast, understanding seizures in the brain of an individual with epilepsy is more difficult because seizures are typically superimposed on an altered nervous system. The different environment includes diverse changes, making mechanistic predictions a challenge. Understanding the mechanisms of seizures in an individual with epilepsy is also more complex than understanding the mechanisms of seizures in a normal individual because epilepsy is not necessarily a static condition but can continue to evolve over the lifespan. Using temporal lobe epilepsy as an example, it is clear that genes, developmental mechanisms, and neuronal plasticity play major roles in creating a state of underlying hyper excitability. However, the critical control points for the emergence of chronic seizures in temporal lobe epilepsy, as well as their persistence, frequency, and severity, are questions that remain unresolved.

Introduction

Seizures and epilepsy have been documented since the earliest civilizations, before much was understood about the nervous system at all. Most individuals with epilepsy were thought to be possessed, and the word “seizure” is derived from that notion, implying that gods take hold or “seize” a person at the time a convulsion occurs. Fortunately, these conceptions about individuals with epilepsy have changed, and the current definition of a seizure has little religious connotation. A general definition for the word “seizure” is a period of abnormal, synchronous excitation of a neuronal population. Seizures typically last seconds or minutes but can be prolonged and continuous in the case of status epilepticus. Importantly, the clinical manifestations vary, and some seizures may not involve muscular contractions (convulsions) at all.

A seven-year-old boy, the first child of young and healthy parents without any family history of epilepsy, with an extensive defect of the right hemisphere, operated on three times due to treatment-resistant seizures present since the age of one. Previous pharmacotherapy included all antiepileptic medicines available on the Polish market, at the highest possible doses, in different regimens, including 2–5 drugs, without any spectacular results (some of the drugs increased the seizures or caused aggression). Complex partial seizures, of changing morphology, were present every day, in the number ranging from a few to a few dozens a day. The development of the boy was severely retarded. Neurological examination showed severe spastic paresis of the left limbs.

The first surgery, performed at the age of 4, consisted in removing (according to the SPECT and EEG image) the pallium of the right parietal lobe and in undercutting the cortex of the temporal, right occipital, and frontal lobe in the parasagittal area. Histopathological examination showed a cortical dysplasia with multiple balloon-like cells. Four months later, after an infection, there appeared seizures of the upper limb. Attempted modifications of the pharmacological treatment did not result in any clinical improvement. In the second neurosurgical procedure, performed on the basis of the SPECT and EEG image, the frontal lobe was exposed, up to its base. With incision of the borderline of the cortex and the white matter, the pallium was removed up to the frontal horn of the right lateral ventricle.

There was an improvement which persisted for a few months. Afterwards, there appeared seizures of a new type: psychomotor with vegetative symptoms. EEG was suggestive of focus formation in the left hemisphere, in the pre-frontal/frontal area. Callosotomy was performed – 2/3 of corpus callosum were incised in the front. Due to a widened ventricular system and an enlarged porencephalic cyst following hemispherectomy, a drainage system was implanted between the porencephalic cyst and the peritoneal cavity. In the next 2 years, the child’s condition was good.

A next acute infection led to seizures with a clinically defined onset within deep frontal areas. There followed developmental regress as well. One more change of antiepileptic treatment failed again. An MRI was carried out with the use of volumetric thin-slice T1-weighted images.

Next, in the interictal period, a SPECT examination was performed with the use of the 99mTc-labelled ethyl cysteinate dimer (99mTcECD).

For fusion and postprocessing, the following software was used: PMOD (Biomedical Image Quantification PMOD Technologies) with PFUS (Flexible Image Matching and Fusion Tool) and a program for a quantitative analysis of counts in the region of interest, so called VOI Constructor (Volume of Interest Constructor).

Owing to the method of interpolation, SPECT images were not only adjusted to the anatomical MRI image, but also made uniform with respect to spatial resolution, and divided into the same number of transverse sections, with exactly the same thickness of each section as in the MRI (so called corregistered data).

In the fused MRI and SPECT image, in the obtained transverse, sagittal and coronary sections, the location of the lesions was determined, in which the initially visually evaluated perfusion defect overlapped with the grey matter of the cortex measuring at least 0.5 cm3. A mean number of counts in the anatomically-adjusted region was compared with a mean number of counts within the brain, which was accepted as a reference value, defining the border between a normal and a decreased brain perfusion. The mean count in the anatomically-adjusted region was also compared with the mean count in a corresponding region in the other hemisphere (a difference of >15% was assumed as a verification of the deficit).

Discussion

Noninvasive tests visualizing brain activity can be divided into those carried out during an epileptic seizure (ictal SPECT) or interictally (interictal SPECT and other: MRI, CT, PET). From among the ‘other’ ones, PET reveals the highest sensitivity in the detection of the seizure-onset foci in patients with temporal lobe epilepsy (84%), while the sensitivity of SPECT (interictal) amounts to 66%, and of MRI to 55%. In nontemporal lobe epilepsy, the highest sensitivity is revealed by interictal SPECT (60%); MRI and PET – 43% and 33%, respectively. However, the highest sensitivity of all has ictal SPECT – 90% in the temporal epilepsy and 81% in the nontemporal one. SPECT carried out during an epileptic seizure shows foci of hyperperfusion. In the interictal period, perfusion deficits correspond to them.

Inability to show structural changes makes the MRI examination of the brain inappropriate for planning the resection of seizure-onset foci. It is the same with multiple lesions, e.g. in tuberous sclerosis, or in case of one but extensive lesion, when it is not known which part of it is responsible for seizures, and removal of the whole lesion is impossible. Detection of a focus of abnormal perfusion/metabolism in SPECT, on the other hand, is insufficient to plan a neurosurgical procedure, due to inadequate spatial resolution of this method.

References

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