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Neocortical Temporal Lobe Epilepsy  [PDF]
Eduard Bercovici,Balagobal Santosh Kumar,Seyed M. Mirsattari
Epilepsy Research and Treatment , 2012, DOI: 10.1155/2012/103160
Abstract: Complex partial seizures (CPSs) can present with various semiologies, while mesial temporal lobe epilepsy (mTLE) is a well-recognized cause of CPS, neocortical temporal lobe epilepsy (nTLE) albeit being less common is increasingly recognized as separate disease entity. Differentiating the two remains a challenge for epileptologists as many symptoms overlap due to reciprocal connections between the neocortical and the mesial temporal regions. Various studies have attempted to correctly localize the seizure focus in nTLE as patients with this disorder may benefit from surgery. While earlier work predicted poor outcomes in this population, recent work challenges those ideas yielding good outcomes in part due to better localization using improved anatomical and functional techniques. This paper provides a comprehensive review of the diagnostic workup, particularly the application of recent advances in electroencephalography and functional brain imaging, in neocortical temporal lobe epilepsy. 1. Introduction Neocortical temporal lobe epilepsy (nTLE) is a rather newly recognized entity that is different than the well-known entity of mesial temporal lobe epilepsy (mTLE) although not as well characterized [1]. The documented cases of patients with nonlesional neocortical temporal lobe seizure origin are not as rare as previously reported. In one study, out of 31 patients seizure-free more than 18 months after temporal lobectomy, only 3 patients (9.6%) were found to have NTLE [2]. More recently, Schramm et al. [1] demonstrated 62/581 of the temporal lobe epilepsy (TLE) cases as being neocortical. With better structural-functional imaging modalities as well as invasive monitoring, more of these cases are being described. Unfortunately, the nomenclature is inconsistent in the literature, often being dubbed as nonlesional, extrahippocampal, or lateral neocortical. For the purpose of this review, we will use the term nTLE. Recognition of nTLE is important because these patients may either be considered nonsurgical candidates or undergo extensive surgeries due to the poor localization of their seizure focus. Lesional nTLE cases are often not reported in the literature as compared to the nonlesional cases because they may be less likely to be admitted to an epilepsy monitoring unit (EMU) for video-electroencephalography (EEG) telemetry unless the lesion is closely associated with eloquent cortex, thereby limiting surgical resection or may be unamenable to surgery. Thus, the reported prevalence of nTLE is low. Therefore, it is difficult to know the prognosis of nTLE
Temporal Lobe Epilepsy in Children  [PDF]
Katherine C. Nickels,Lily C. Wong-Kisiel,Brian D. Moseley,Elaine C. Wirrell
Epilepsy Research and Treatment , 2012, DOI: 10.1155/2012/849540
Abstract: The temporal lobe is a common focus for epilepsy. Temporal lobe epilepsy in infants and children differs from the relatively homogeneous syndrome seen in adults in several important clinical and pathological ways. Seizure semiology varies by age, and the ictal EEG pattern may be less clear cut than what is seen in adults. Additionally, the occurrence of intractable seizures in the developing brain may impact neurocognitive function remote from the temporal area. While many children will respond favorably to medical therapy, those with focal imaging abnormalities including cortical dysplasia, hippocampal sclerosis, or low-grade tumors are likely to be intractable. Expedient workup and surgical intervention in these medically intractable cases are needed to maximize long-term developmental outcome. 1. Introduction The temporal lobe plays a vital role in epilepsy and is the most frequent lobe involved in focal onset seizures. Temporal lobe epilepsy in children and infants has clear clinical features which make it distinct from the fairly homogeneous syndrome seen in adults. Reported studies of temporal lobe epilepsy (TLE) in children are heavily biased towards those with medically intractable epilepsy, and few studies focus on cohorts who are newly diagnosed. This paper will address pediatric-specific aspects of TLE, including clinical semiology in young children, pediatric epilepsy syndromes involving the temporal lobe, medical and surgical management, associated psychiatric and cognitive disorders, and long-term outcomes. 2. Epidemiology The overall incidence of new-onset epilepsy in children ranges from 33 to 82 per 100,000 children per year, and approximately half- to two-thirds of these children have focal-onset seizures [1–6]. However, the exact incidence of TLE is not known, as the specific lobe of onset is not specified in most incidence studies. Compared to adults, focal seizures in children are more likely to arise from extratemporal foci. Simon Harvey et al. identified 63 children with new-onset TLE over a 4-year period in the state of Victoria, Australia (population 4.4 million) [7]. In our 30-year cohort of new-onset epilepsy in children, 276/468 (59%) had nonidiopathic focal epilepsy. Of these, 20 (7.2%) had a focal lesion on MRI in the temporal region (10: mesial temporal sclerosis, 1: malformation of cortical development, 2: ischemia/gliosis, 1: tumour, and 4: vascular malformation), while 17 (6.1%) had normal imaging and a single focus of epileptiform discharge in the temporal region. Therefore, it was determined that TLE was responsible
Neuropathology of Temporal Lobe Epilepsy  [PDF]
Fahd Al Sufiani,Lee Cyn Ang
Epilepsy Research and Treatment , 2012, DOI: 10.1155/2012/624519
Abstract: Pathologic findings in surgical resections from patients with temporal lobe epilepsy include a wide range of diagnostic possibilities that can be categorized into different groups on the basis of etiology. This paper outlines the various pathologic entities described in temporal lobe epilepsy, including some newly recognized epilepsy-associated tumors, and briefly touch on the recent classification of focal cortical dysplasia. This classification takes into account coexistent pathologic lesions in focal cortical dysplasia. 1. Introduction Temporal lobe epilepsy (TLE) is the most common form of focal epilepsy [1]. In medical centers where epilepsy surgery is performed, neuropathologists often encounter temporal lobe resection specimens. Most patients scheduled for surgical resection present with intractable focal epilepsy and are selected for surgery based on clinical, electrophysiology, and neuroimaging criteria. The pathologic findings in these resected specimens represent different groups of conditions such as hippocampal sclerosis (HS), malformative lesions, tumors, ischemic lesions, old traumatic injuries, and inflammatory lesions. The objective of this paper is to outline the pathologic entities associated with TLE, while highlighting the recent classification of focal cortical dysplasia (FCD) and some recently described neoplastic entities. 2. Hippocampal Sclerosis, Temporal Lobe Sclerosis, and Amygdaloid Sclerosis Hippocampal sclerosis, also known as Ammon horn sclerosis, is a common pathologic finding in surgical specimens from patients with TLE [2]. Although often used interchangeably with HS, the term “mesial temporal sclerosis” (MTS) is more appropriate for cases in which significant pathologic changes involve not only the hippocampus but also the amygdala and entorhinal cortex. The incidence of HS is variable in different studies, ranging from 48% to 73% [2–4]. Whereas the pathogenesis of HS is unknown, its occurrence after prolonged febrile seizures in early life has been implicated [5]. According to the International League Against Epilepsy (ILAE) Commission Report, HS is defined as neuronal loss and gliosis in hippocampal area CA1 (Sommer sector) and area CA4 (endplate/hilus/end folium) [6]. Histologically, the segmental loss of pyramidal neurons in area CA1 is severe, with less prominent neuronal loss in areas CA3 and CA4 (Figures 1(a) and 1(b)). The term “end folium sclerosis” is reserved for cases with neuronal loss and gliosis restricted mainly to area CA4. In approximately 50% of HS cases, granule cell dispersion in the dentate gyrus
Temporal Lobe Epilepsy Semiology  [PDF]
Robert D. G. Blair
Epilepsy Research and Treatment , 2012, DOI: 10.1155/2012/751510
Abstract: Epilepsy represents a multifaceted group of disorders divided into two broad categories, partial and generalized, based on the seizure onset zone. The identification of the neuroanatomic site of seizure onset depends on delineation of seizure semiology by a careful history together with video-EEG, and a variety of neuroimaging technologies such as MRI, fMRI, FDG-PET, MEG, or invasive intracranial EEG recording. Temporal lobe epilepsy (TLE) is the commonest form of focal epilepsy and represents almost 2/3 of cases of intractable epilepsy managed surgically. A history of febrile seizures (especially complex febrile seizures) is common in TLE and is frequently associated with mesial temporal sclerosis (the commonest form of TLE). Seizure auras occur in many TLE patients and often exhibit features that are relatively specific for TLE but few are of lateralizing value. Automatisms, however, often have lateralizing significance. Careful study of seizure semiology remains invaluable in addressing the search for the seizure onset zone. 1. Introduction Epilepsy has been recognized since antiquity. It affects millions of people worldwide and remains one of the most common and frightening neurological conditions. The word is derived from the Greek word which means to “seize” or “take hold of.” Epilepsy encompasses a heterogeneous group of disorders with various manifestations including seizures in addition to other signs, symptoms, and features that define a phenotype. The taxonomy and terminology of epilepsy has undergone a number of changes over the years. An early classification system generated confusion and heated discussion over equating the term “complex partial seizures” (CPSs) and “temporal lobe epilepsy” (TLE) [1]. The 1981 classification of epileptic seizures represented a consensus at that time [2]. A further revision was the Classification of Epilepsies and Epileptic Syndromes accepted in 1989 [3]. Yet another modification and change in philosophy was initiated by the Executive Committee of the International League Against Epilepsy (ILAE) which took office in 1997. The ILAE task force published the Revised Terminology and Concepts for Organization of the Epilepsies in 2010 [4]. Temporal lobe seizures are the most frequent site of origin of partial seizures. They represent approximately two thirds of the intractable seizure population coming to surgical management. Jackson in the 19th Century [5] was the first to link seizures characterized by a “dreamy state” to lesions near the uncus in the temporal lobe (hence the term “uncinate fits”). Gibbs and
Temporal Lobe Epilepsy in the Elderly  [PDF]
L. E. Morillo
Epilepsy Research and Treatment , 2012, DOI: 10.1155/2012/641323
Abstract: The incidence of epilepsy has bimodal distribution peaking at the extremes of life. Incidence is greater in younger and older age groups (Hauser et al., 1993, Sidenvall et al., 1993, Forsgren et al., 1996, and Olafsson et al., 2005). As the world population ages more elders with epilepsy will be identified. In the high-income countries with longer life expectancy, the number of elders with epilepsy will be even higher. CPSs account for 40% of all seizure types in the elderly (Hauser et al., 1992); however, the proportion with temporal lobe epilepsy (TLE) is uncertain. 1. Causes The specific causes of TLE in the elderly have not been clearly disclosed. With advancing age underlying coexisting factors are more likely to be identified, and the proportion of people classified as idiopathic is less when compared to the younger age groups. Nonetheless, up to half of elderly patients with epilepsy go without an identified cause. In the under 65-year age group, head trauma, brain tumors, and CNS infections are common associations. Etiology of seizures veers towards a cerebrovascular origin in the elderly [6]. Dementing illnesses have also taken their place as a significant etiology [7]. Idiopathic TLE has been reported in adults with familiar history of epilepsy (mean age of onset: 25.5; range: 11–45 years). This group was also found to have a better prognosis [8]. Similar reports in elderly patients are missing. There are however case reports of mesial temporal lobe sclerosis (MTS) in elderly persons with new onset seizures. These accounts highlight the challenging differential diagnosis overlap with primary cognitive disorders and nonparaneoplastic limbic encephalitis [9]. New onset TLE has also been reported without evidence of MTS [10]. The etiology of hippocampal damage is discussed in a retrospective study of 38 patients with adult onset TLE [11]. The median age at onset was 37.8 years (range: 21.0 to 78.7 years). A total of seven patients, 60 years and older, were included in this report. In all cases, the common features encompass frequent CPSs (range <1 to 600 seizures per month) developing over one year (defined as the median time from the initial onset of seizures to the time of assessment). Based on MRI evidence of hippocampal atrophy, history of causative events, concomitant disease, cerebrospinal fluid results, and autoantibodies patients were classified in one of four etiologic categories; secondary hippocampal sclerosis (HS); idiopathic HS; definite limbic encephalitis (LE) and MRI defined possible LE. Eleven patients met secondary HS criteria.
Catastrophic Childhood Temporal Lobe Epilepsy  [cached]
Giancarlo Di GENNARO,Antonio SPARANO,Addolorata MASCIA,Fabio SEBASTIANO
Journal of Neurological Sciences , 2005,
Abstract: Focal epilepsy, more frequently of extratemporal type, in children can present with a rapidly progressing course of intractable, severe epilepsy, associated to cognitive regression or stagnation. We present a typical example of such a patient with focal seizures due to a temporal lobe cortical lesion of developmental origin. Brain MRI revealed abnormalities in the right temporal lobe and Video-EEG monitoring revealed episodes clinically characterized by epileptic spasms followed by automotor seizures, with EEG findings suggestive of a right temporal lobe focus. Surgical resection resulted in excellent outcome.
Physiopathogenetic Interrelationship between Nocturnal Frontal Lobe Epilepsy and NREM Arousal Parasomnias  [PDF]
Péter Halász,Anna Kelemen,Anna Sz?cs
Epilepsy Research and Treatment , 2012, DOI: 10.1155/2012/312693
Abstract: Aims. To build up a coherent shared pathophysiology of NFLE and AP and discuss the underlying functional network. Methods. Reviewing relevant published data we point out common features in semiology of events, relations to macro- and microstructural dynamism of NREM sleep, to cholinergic arousal mechanism and genetic aspects. Results. We propose that pathological arousals accompanied by confused behavior with autonomic signs and/or hypermotor automatisms are expressions of the frontal cholinergic arousal function of different degree, during the condition of depressed cognition by frontodorsal functional loss in NREM sleep. This may happen either if the frontal cortical Ach receptors are mutated in ADNFLE (and probably also in genetically not proved nonlesional cases as well), or without epileptic disorder, in AP, assuming gain in receptor functions in both conditions. This hypothesis incorporates the previous “liberation theory” of Tassinari and the “state dissociation hypothesis” of Bassetti and Terzaghi). We propose that NFLE and IGE represent epileptic disorders of the two antagonistic twin systems in the frontal lobe. NFLE is the epileptic facilitation of the ergotropic frontal arousal system whereas absence epilepsy is the epileptic facilitation of burst-firing working mode of the spindle and delta producing frontal thalamocortical throphotropic sleep system. Significance. The proposed physiopathogenesis conceptualize epilepsies in physiologically meaningful networks. 1. Concept of Nocturnal Frontal Lobe Epilepsy (NFLE) From the eighties several observations had been published reporting on events characterized by a storm of dystonic/dyskinetic movements involving both sides of the body, accompanied by bizarre vocalisation, arising from sleep. Patients preserved consciousness during or retained it immediately after the attacks which were preceded usually by EEG/polygraphic microarousals appearing during NREM sleep in clusters. Since interictal and even ictal EEG was meager in epileptiform signs, at the beginning it was held to be a sleep disorder named “nocturnal paroxysmal dystonia” [1, 2]. It was recognized from the beginning that the attacks exhibited a variation in degree of motor components from “minimal” to “major” symptomatology. Later it turned out that several patients with similar symptoms have MRI lesions in the frontal lobe [3] and both the scalp EEG data and the data derived from intracerebral studies pointed to frontomedial or orbitofrontal origin [4, 5]. The spectrum of symptoms of these surgical cases compared to unlesional ones
Perirhinal cortex and temporal lobe epilepsy  [PDF]
Giuseppe Biagini,Philip de Guzman,Massimo Avoli
Frontiers in Cellular Neuroscience , 2013, DOI: 10.3389/fncel.2013.00130
Abstract: The perirhinal cortex—which is interconnected with several limbic structures and is intimately involved in learning and memory—plays major roles in pathological processes such as the kindling phenomenon of epileptogenesis and the spread of limbic seizures. Both features may be relevant to the pathophysiology of mesial temporal lobe epilepsy that represents the most refractory adult form of epilepsy with up to 30% of patients not achieving adequate seizure control. Compared to other limbic structures such as the hippocampus or the entorhinal cortex, the perirhinal area remains understudied and, in particular, detailed information on its dysfunctional characteristics remains scarce; this lack of information may be due to the fact that the perirhinal cortex is not grossly damaged in mesial temporal lobe epilepsy and in models mimicking this epileptic disorder. However, we have recently identified in pilocarpine-treated epileptic rats the presence of selective losses of interneuron subtypes along with increased synaptic excitability. In this review we: (i) highlight the fundamental electrophysiological properties of perirhinal cortex neurons; (ii) briefly stress the mechanisms underlying epileptiform synchronization in perirhinal cortex networks following epileptogenic pharmacological manipulations; and (iii) focus on the changes in neuronal excitability and cytoarchitecture of the perirhinal cortex occurring in the pilocarpine model of mesial temporal lobe epilepsy. Overall, these data indicate that perirhinal cortex networks are hyperexcitable in an animal model of temporal lobe epilepsy, and that this condition is associated with a selective cellular damage that is characterized by an age-dependent sensitivity of interneurons to precipitating injuries, such as status epilepticus.
Temporal lobe epilepsy in childhood: review article
Franzon, Renata C.;Guerreiro, Marilisa M.;
Journal of Epilepsy and Clinical Neurophysiology , 2006, DOI: 10.1590/S1676-26492006000200006
Abstract: introduction: the authors present a review article on temporal lobe epilepsy in childhood. methods: we performed a search in the literature. results: the main etiologies of temporal lobe epilepsy in childhood are developmental tumors and focal cortical displasia, besides temporal medial sclerosis. the clinical features may be variable particularly in children younger than six years of age. epilepsy may present with generalized seizures. electroencephalographic findings are also variable and show a functional dysfunction of several brain areas besides temporal lobes, especially frontal lobes. conclusion: recent advances demonstrate that temporal lobe epilepsy in childhood present with great etiologic, clinical and electroencephalographic diversity.
Epilepsy and Adult Neuropsychiatry: Behavioral Symptoms Related to Frontal Lobe Epilepsy and Juvenile Myoclonic Epilepsy  [PDF]
Emre BORA
N?ropsikiyatri Ar?ivi , 2008,
Abstract: Psychiatric symptoms are common in epilepsy. It is generally accepted that temporal lobe epilepsy is more strongly associated with psychiatric comorbidity and some epilepsy specific syndromes such as interictal dysphoric disorder, interictal psychosis and personality change were defined. However the specificity of these syndromes are still questionable and evidence regarding the relationship between psychiatric syndromes and extratemporal focuses such as the frontal lobe is increasing. Another epilepsy syndrome, Juvenile myoclonic epilepsy, is thought to be associated with impulsive personality disorders. This article reviews the evidence regarding the association of frontal lobe epilepsy and juvenile myoclonic epilepsy with behavioral syndromes.(Archives of Neuropsychiatry 2008; 45: 48-52)
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