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Flash Brain Anatomy

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Preface to the Second Edition

The aim of this second edition of Magnetic Resonance in Epilepsy is to update readers about this rapidly changing field and its application to human epilepsy. We have retained in part the organization of the first edition with the first three chapters devoted to an introduction to principles that we feel are needed to more fully understand the context of neuroimaging findings. The first chapter is an introduction to epilepsy, written largely for those not familiar with the field. Chapter 2 similarly deals with the principles of MR in a way that is intended to provide an overview of major issues that allow the non-physicist an understanding of how MR works. We hope this will help in understanding the specific findings of later chapters. We felt that Chapter 3 by Henry Duvernoy was a masterpiece in the first edition. There it dealt primarily with the anatomy of the hippocampus and temporal lobe. As the focus of MR has increasing expanded to deal with issues of abnormalities beyond the...

What Should Be Modeled

Epilepsy accounts for a significant portion of the disease burden worldwide (Murray and Lopez, 1994). The economic, social, and personal costs of this disorder are due largely to uncontrolled seizures (Begley et al., 2000), which underscores the need for more research into new approaches for the diagnosis, treatment, and prevention of epilepsy and its consequences. Although one could argue that research on human epilepsy ideally should be carried out on humans with epilepsy, this approach is not always possible or practical (Engel, 1998). Obvious ethical constraints exist, particularly those associated with the invasive techniques often needed to pursue important investigative questions. It is difficult to control for clinical variables, and control data can be impossible to obtain. Statistical analysis frequently requires larger populations than can be obtained from most clinical practices. Finally, the cost of carrying out research projects on patients would be prohibitive....

Benzodiazepine Receptors And Membrane Excitability

In the 1970s use of radioactively labeled benzodiazepine derivatives allowed the detection of specific nanomolar benzodiazepine receptor sites in brain membrane (15-17). These sites have a very high affinity for the benzodiaz-epines, binding in low (nanomolar) concentration ranges. Binding to these receptors is reversible, saturable, and stereospecific. Nanomolar benzodiazepine receptors have now been identified in human brain, where they are widely distributed. The specific membrane protein that accounts for the majority of nanomolar benzodiaz-epine binding has a molecular weight of approximately 50,000 daltons and has been purified from animal and human brain (18).

The Issue of Secondary Epileptogenesis

How these observations in animal models relate to the origins of human epilepsy and to the secondary effects of seizures seen in the human brain remains controversial. Morrell used the criteria of unequivocal evidence of independent interictal or ictal epileptiform discharges in the hemisphere contralateral to a well defined tumor to demonstrate the phenomenon of the mirror focus in humans. He showed an incidence of up to 36 of what he called 'secondary epileptogenesis,' with 15 of patients having clinical attacks arising from this focus. While the demonstration of secondary epileptogenesis in humans is indirect, many epileptologists would accept the possibility of secondary epileptogenesis in their patients. It is possible that this phenomenon is the basis of the well-described 'dual pathology' of hippocampal sclerosis in patients with a tumor or other lesion elsewhere. The alternative view is that damage occurs bilaterally at the time of the original epileptogenic insult and that...

Seizureinduced Brain Damage

Therefore we can only conclude with some speculations (and opinions) - that sometimes seizures damage the brain but do not always do so. Furthermore, hippocampal sclerosis may occur as a primary lesion that is the consequence of unknown insults, but hippocampal sclerosis can also arise as a secondary lesion (like kindling) as a consequence of seizures originating elsewhere. In this latter instance, even if the initial seizures arise elsewhere, the hippocampus may become the primary seizure focus later in life. It is our opinion that the noninvasive techniques of MR investigation of the human brain that are described in this book provide the means whereby these issues can be more fully addressed.

Epilepsy Patient and Family Guide Second Edition

Summary Epilepsy Patient and Family Guide is an updated resource that addresses all aspects (psychosocial, financial, legal, and medical) of epilepsy to help adult patients with epilepsy or parents of children with epilepsy understand the disorder and to enable them to better cope with the problems it causes. It is written in a style that the general reader can easily follow. The first section is entitled Medical Aspects of Epilepsy and consists of six chapters that cover topics including (1) brain anatomy and epilepsy, (2) seizures and epileptic syndromes, and (3) seizure provoking factors. The second section is entitled Diagnosis and Treatment of Epilepsy and is divided into seven chapters that (1) describe the health care team for a patient with epilepsy, (2) discuss how epilepsy is diagnosed, (3) discuss providing first aid for seizures, (4) summarize the

Resective Surgical Treatment Of Epilepsy

The second half of the 19th century witnessed the first modern neurosurgical procedures to alleviate pharmacoresistant seizures. However, epilepsy surgery progressed in a stepwise fashion rather than at a steady pace, because concerns with efficacy and safety, as well as the development of AEDs during the 20th century, have often challenged the procedure. The attainment of the current situation, where epilepsy surgery has a firm place in the neurological therapeutic armamentarium, depended on a number of advances in functional neuroanatomy, neurophysiology, and neuroimaging. The introduction of high-resolution MRI in the past decade has now simplified presurgical evaluation sufficiently for some patients to make surgical treatment for epilepsy a reality in the developing world.

Understanding Seizure Disorders

Summary Understanding Seizure Disorders, an 11-minute video produced by the Epilepsy Foundation of America, examines the human brain and uses testimonials from persons with epilepsy and videotapes of persons having seizures to explain epilepsy. Epilepsy is defined as seizures that are not related to an explained cause and which tend to recur over time in an unpredictable fashion. There are two types of seizures Generalized and partial. In a generalized seizure, the electrical disturbance affects the entire brain all at once. In a partial seizure, only one part of the brain is affected at the start the electrical disturbance may remain localized or spread throughout the brain. Partial seizures may be characterized by strange changes in sense of taste or smell or feeling of movement outside the body or back in time. Some people experience only one kind of seizure, while others experience several kinds. Doctors can attempt to determine the cause and treatment for seizures by (1) taking...

Avanzini and S Franceschetti

As in the case of many other pathological conditions, experimental models made a major contribution to our understanding of epileptogenesis. The term 'experimental models' should be restricted to animals presenting spontaneous or experimentally induced epileptic seizures, whereas in vitro or computer models are more properly called models of epileptogenic mechanisms. This is not just a question of semantics because the relevance of experimental results to the advances made in our understanding of epilepsy depends on how suitably the experiment has been designed for its purpose. Operationally, it is enough to say that an experimental preparation should only be referred to as a model (of epilepsy, of seizures, of epileptogenic mechanisms) if it faithfully reproduces the clinical and EEG characteristics of human epilepsies or seizures, or the biological changes that are known to be associated with them. Over the last few years, animal experiments have been effectively supplemented by...

Physiological expression of drug resistance proteins

The precise localization of MDR1 normally in the blood-brain barrier has been an area of some debate. The prevailing opinion is that expression is within the endothelial cells, MDR1 contributing to the blood-brain barrier 29 . An alternative school proposes that expression occurs on astrocytic end-feet 30 . Whilst the latter is unlikely to be the case in normal human brain, glia may affect MDR1 expression and activity 31 . The importance of MDR1 in the function of the blood-brain barrier has been demonstrated by the generation of knockout mice lacking the murine orthologues of MDR1. Such mice develop normally and are viable, but brain penetration of a number of drugs (e.g. domperidone, loperamide and ivermection) is increased, with possible neurotoxicity 32 . MDR1 is thus likely to have an important physiological function. It is likely that normal human cerebral parenchyma (glia, neurones) lacks MDR1 expres MRP1 has been less well studied. Its expression in human brain has been shown...

Evidence for overexpression of drug resistance proteins in human epilepsy

A few studies have demonstrated increased expression of the drug transport proteins MDR1 and MRP1 in pathological human brain tissue. Tishler et al. first reported increased endothelial and glial MDR1 protein and mRNA expression in surgically-resected brain tissue from patients with refractory temporal lobe epilepsy 34 , Using engineered cell lines overexpressing MDR1 in vitro, they demonstrated that phenytoin was a transport substrate for MDR1, albeit with low affinity, making MDR1 overexpression a plausible

Bloodbrain Barrier And Dc Shift

Occlusion of the left middle cerebral artery in rats with duration between 1.2 and 3.7 minutes is followed by suppression of EEG amplitude and the occurrence of multiple DC shifts (Iijima et al., 1992). The number of these shifts declined after MK-801 injection, produced to a decrease in the volume of ischemically injured tissue. Anoxic depolarization producing slow DC shift is closely associated with a massive intracellular calcium elevation possibly due to activation of NMDA (N-methyl-D-aspartate) receptors (Heinemann et al., 1977). Vanhatalo and co-authors studied whether similar changes may also contribute to the generation of ictal DC shifts in the epileptic brain (Vanhatalo et al., 2003c). They showed that hemodynamic changes in the human brain are associated with marked DC shifts that cannot be accounted for by intracortical neuronal or glial currents. DC shifts were also elicited by changes in artificial ventilation, causing end-tidal CO2 variations within a 2-5 range....

Secondbysecond Lglutamate Measurements In The Mammalian Central Nervous System

Release and clearance, alterations in either aspect of neurotransmission without compensation can lead to altered resting concentrations. We believe glutamate neurotransmission is altered in the moments preceding an ictal event and continues through the time course of the actual seizure. To us, seizure is the classic neurological example of a possible consequence following breakdown of compensatory mechanisms. Coupling second-by-second monitoring of extracellular glutamate levels obtained via our glutamate-sensitive MEA with new prediction algorithms, we will likely be able to convert real-time fluctuations in resting glutamate (independent variable) into output commands (dependent variable) for computer-controlled therapeutic intervention targeted at seizure termination. A different type of merged MEA-computational modeling technology has utility as a biomimetic hippocampal prosthesis for maintenance of normal communication through the trisynaptic circuit during hippocampal...

Drug resistance in epilepsy human epilepsy

The basis of drug resistance in human epilepsy is not understood. Parallels with resistance in cancer suggest that drug resistance proteins may have a role. To examine this possibility, we have studied human brain tissue containing pathologies capable of causing refractory epilepsy. Using immunohistochemistry for P glycoprotein (Pgp) and multidrug resistance-associated protein 1 (MRP1), we examined both pathological tissue and control tissue. We demonstrate expression of Pgp and MRP1 in glia from cases of malformation of cortical development studied both before and after the onset of epilepsy, as well as in cases of hippocampal sclerosis and dysembryoplastic neuroepithelial tumours. In one particular type of malformation, we also demonstrate that dysplastic neurons express MRP1. The pattern of immunolabelling suggests overexpression is concentrated particularly around vessels in most of the pathologies. The timing shows that expression may be constitutive in some...

Advantages And Limitations Of The Zebrafish Model

Zebrafish Advantage

seizure resistant zebrafish mutants. This research program is based on a fundamental question of how to identify genes that prevent, or protect, an individual from developing epilepsy. Because larval zebrafish are a pediatric epilepsy model, perhaps these types of studies could lead to new therapies for the large number of children suffering with medically intractable forms of epilepsy. Although it is too early to speculate on how data from zebrafish will be extrapolated to human pediatric epilepsy disorders, especially considering the vast complexity of the human brain in relation to the relative simplicity of the zebrafish CNS, it is safe to predict that the process of discovery will lead to novel insights.

The Role Of Microelectrodes In Epilepsy Therapy And Hippocampal Repair

FIGURE 33.7 Photograph of Spencer-Gerhardt electrode (SG-2), showing flexible shaft for chronic compatibility and optimal placement of MEA tip (magnified image) into human brain. Lower left panel image taken during second-by-second glutamate recordings in anesthetized non-human primate. Studies conducted in operating room (OR) equipped for human surgeries to mimic closely stringent OR requirements as we prepare for human recordings. Lower right diagram characteristic fluctuations in resting glutamate (top trace) recognized as signature of impending seizure, which triggers local application of drug to terminate seizure onset. FIGURE 33.7 Photograph of Spencer-Gerhardt electrode (SG-2), showing flexible shaft for chronic compatibility and optimal placement of MEA tip (magnified image) into human brain. Lower left panel image taken during second-by-second glutamate recordings in anesthetized non-human primate. Studies conducted in operating room (OR) equipped for human surgeries to mimic...

Interhemispheric limbic connections

Phylogenetically, commissural fibres have constituted a major group of extrinsic connections joining the two hippocampi and their sub fields, but the connections are substantially reduced in the human brain. There are two components of the interhemispheric pathway the ventral hippocampal commissure, which carries fibres from the hippocampal formation, and the dorsal hippocampal commissure, which carries fibres from the entorhinal cortex, presubiculum and parahippocampal gyrus. In the subhuman primate, the ventral hippocampal commissure is greatly reduced and limited to the anterior hippocampus, while the dorsal commissure carries primarily presubicular and parahippocampal gyrus fibres to the contralateral entorhinal cortex (Amaral et al., 1984). In the human brain, dissection of The relative reduction of commissural interchange from lower animal to primate may provide the basis for the hemispheric specialization unique to the human brain, particularly relating to differences in verbal...

Surgical treatment of epilepsy due to cortical dysplasia

Eeg Findings Post Ictal Psychosis

Epilepsy surgery in cortical dysplasia is generally disappointing. The best outcome is reported following complete resection of focal cortical dysplasia (Taylor dysplasia), with short-term seizure-free rates of about 50 of cases, and there are no data about longer-term outcome. Resection of small areas of subcortical heterotopia also alleviate epilepsy in a reasonable number of cases. Other types of dysplasia, however, fare worse, and the comparatively poor outcome of all types of dysplastic lesion must reflect widespread epilepto-genesis which extends beyond the margins of the lesions visible on conventional MRI scanning. Furthermore, brain anatomy is often abnormal in patients with cortical dysplasia, and cortical mapping shows aberrant location of functional cortex, and surgical morbidity can be greater than is the case in surgery for other cortical lesions. In focal cortical dysplasia and subcortical heterotopia, a good outcome requires at least the complete resection of the...

Epilepsy secondary to multiorgan hereditary disorders

Genetic disorders of brain development encompass a wide range of conditions characterized by interruptions in the development of the human brain at various stages. While cortical developmental disorders usually cause epilepsy, it is unknown what proportion of epilepsy is attributable to disorders of brain development. In addition, except for some specific syndromes, there are no clinical features which distinguish these disorders. Generalized abnormalities of cortical development tend to present with generalized seizures while focal or multifocal malformations are most commonly associated with focal seizures. There are many classification schemes for cortical malformations.

Basic Mechanisms

Table 1-1 summarizes some important factors that may play a role for these developmental windows of increased susceptibility to seizures and in the development of epilepsy in the immature brain. In this table, factors A1 through A5 are operant in the normal and abnormal brain while factors B1 through B3 may be more specific for abnormal brains. The contribution of these factors in the pathophysiology of childhood seizures can be studied in animal models of seizures and, if available, in models of epilepsy. To study the age-related changes in seizure susceptibility in experimental animals, the investigator has to correlate the brain development of the animal to human brain development. Such correlations are difficult and should be viewed cautiously. Not all parameters studied follow similar developmental curves in animals and humans. This issue is very carefully reviewed in a recent article (7). Nevertheless, based on comparative ontogenetic studies of the rate of brain growth, an...

Neuronal Circuits

As well as these questions of basic neurotransmitters and receptors, it has become clear that the circuitry of the neurons may also be abnormal in patients with epilepsy (75-87). There is a form of reorganization, characterized by sprouting of axonal branches and terminals, that occurs as a result of seizures in human hippocampal tissue as well as in animal models (88, 89). Most of these studies show concurrent loss of cells associated with this axonal sprouting. It has been suggested that the sprouting axons replace the neurons at the synaptic sites where cell death has removed the presynaptic elements. This process appears to provide cells with additional recurrent excitatory feedback that can increase the excitability of the circuits. The discovery that neurogenesis can occur in the human brain has led to the idea that cellular proliferation (in addition to cell loss) may be part of the plastic process underlying epileptogenesis.


ERM proteins (ezrin and moesin) are expressed in germinal matrix cells, migrating cells, and radial glial fibers in the developing human brain (201), correlating with RhoA expression in proliferating and migrating cells in the developing rat brain (205). Dysfunction of tuberin and hamartin may perturb communication between ERM proteins and Rho GTPase to cause abnormal neuronal migration, polarity, and morphology, resulting in the formation of dysplastic cortex. Hamartin and tuberin are coexpressed within a population of abnormal neuroglial cells (206), and both TSC gene products and ERM proteins are also coexpressed within a subpopulation of abnormal neuroglial cells in TSC tubers (201). Abnormalities of radial glia have also been implicated in the pathogenesis of brain lesions of TSC (206a).

Figure 512

Destructive lesions, with the neuropathology appearance of regions of cystic encephalomalacia, are commonly encountered in corticectomies for epilepsy, especially in infants and children (162). They are presumed to represent sequelae of intrauterine, perinatal, or (rarely) postnatal brain infarcts (Figure 5-12) or hemorrhages, the etiology of which is multifactorial, extremely complex, and beyond the scope of this chapter. For excellent recent monographs on pathophysiologic mechanisms important in the evolution of destructive brain lesions in the developing human brain, including ones that may cause seizures, see the works by Kalimo (232) and Golden and Harding (232a).


The goal of this chapter is to provide an overview of the methods employed, useful experimental goals, and limitations of investigating human chronically epileptic brain tissue in vitro. Such tissue is often available in the course of epilepsy surgery, particularly for temporal lobe resection associated with intractable mesial temporal lobe epilepsy (MTLE) but also for lesionectomies and other types of epileptogenic foci. Human specimens can be maintained in vitro in a slice preparation, and thus they can be studied with many of the technical advantages applied to tissue from animal models. Because human brain slices do not really model epileptic phenomena in the human epileptic brain (i.e., this tissue cannot serve as a model of itself), the format of this chapter departs somewhat from that of the other chapters in this book. In particular we spend little time drawing comparisons to clinical seizure types, elaborating on the challenge of establishing an epilepsy model, or discussing...


A general limitation of all slice preparation models of epileptiform activity is their isolation from the distributed system that is presumably involved in seizure generation. This is an especially important consideration in dealing with human tissue because we ignore which brain region is actually responsible for seizure generation or even if there is a localized epileptogenic zone. At the clinical level, surgical procedures have been justified by their effective ends. However, it is not the case that if seizure activity is interrupted by removal of, for example, hippocampus, that result proves that the hippocampus is responsible for the seizure activity. That may be the case, or the hippocampus simply may have been a part (perhaps a normal part) of a larger seizure circuit. Thus when we remove a piece of tissue from the human brain, we do not know that tissue is epileptic. A major problem in interpreting data from human slice experiments is the absence of normal controls. Obviously,...


We studied formalin-fixed paraffin-embedded human brain tissue from neuro-pathological archives. The study was approved by the Joint Ethics Committee of the Institute of Neurology and the National Hospital for Neurology and Neurosurgery. All tissue was surplus to diagnostic requirements.

Future Work

Future work in this field will likely center on broader band recordings, higher spatial resolution systems, coupled with much broader spatial sampling. There will be better crafted and newer methods of modulating network output, either with electrical stimulation, local application of drugs, cooling or other technologies. It is likely that, in addition to detailed structural atlases of brain anatomy, there will be more detailed functional maps of brain activity and connectivity, perhaps even some form of 'wiring diagrams' that will help target diagnostic and therapeutic investigations. As mechanisms underlying waveforms of interest, such as high frequency oscillations, 'microseizures' and unit ensemble activity in epilepsy are elucidated, it is our hope that this progress should directly translate into better patient care and clinical outcome.

Caas Craas

Rats exposed to the antimitotic agent MAM on gestational day (G) 15 develop a neuronal migration disorder similar to the cortical dysplasias seen in the human brain. MAM-exposed suckling rats then undergo the AY model protocol as described previously. The result is that the animal presents with spontaneous, recurrent, atypical absence seizures that are characterized by bilaterally synchronous slow spike-wave discharges (SSWDs) with a frequency of 4 to 6 Hz (see Table 3). The MAM-AY-induced atypical absence seizures are refractory to ethosuximide and sodium valproate. Histologic examination of brains from MAM-treated rats showed hippocampal heterotopias in addition to atrophy and abnormalities of cortical lamination. The MAM-AY-treated rat represents a reproducible model

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