mesial temporal lobe

A milder electrical stimulation model that appears to mimic MTLE characteristics more closely has been advocated and developed by Sloviter and coworkers (Norwood et al., 2010; Sloviter et al., 2007). It is believed that in an epileptic brain there is an alteration of brain function that facilitates hypersynchronous neuronal activity. One study reported no differences in the number and duration of spike-wave complexes between male and female rats with absence seizures (Coenen and Van Luijtelaar, 1987). (C) A frequent observation in TLE is HS, where hippocampal cytoarchitecture is changed dramatically. An amygdalohippocampectomy is the surgical removal of the amygdala and the hippocampus after other treatments have failed to provide relief. HS is the most common lesion observed in patients with refractory TLE and is found in 60%–70% of the cases referred for surgical evaluation (Lewis, 2005). Thus, further studies are required to fully address whether cells expressing specific cellular markers are lost, whether expression of specific cellular markers is simply changed, and what are the functional consequences of interneuron loss in TLE. NMRI mice were more sensitive to the antiseizure effect of carbamazepine than FVB/N mice (Twele et al., 2016b). Most cases of temporal lobe epilepsy in adults can be further localized to the middle area of the temporal lobe (called the mesial [“middle”] temporal lobe). For example, chronic treatment of MTLE mice with the mTOR pathway inhibitor, rapamycin, does not prevent the development of the spontaneous hippocampal paroxysmal discharges that arise in this mouse model, despite this treatment inhibiting the associated mossy fiber sprouting, and granule cell layer dispersion (Shima et al., 2015). (A and B) Nissl stain of normal human hippocampus (A) and damaged hippocampus due to hippocampal sclerosis (B). Surgical resection is the gold standard treatment for drug-resistant focal epilepsy, including mesial temporal lobe epilepsy (MTLE) and other focal cortical lesions with correlated electrophysiological features. Hippocampal onset accounts for at least 80% of all temporal lobe seizures. Moreover, inflammation and oxidative stress are able to increase the excitability of the network (Puttachary et al., 2015). Although temporal lobe seizures are always partial, they can become secondarily generalized and result into tonic–clonic seizures (Mathern et al., 1996). While MTS is the most common symptomatic pathologic entity in adult and adolescent patients with seizures of temporal lobe origin, it is considered to be a rare pathologic finding among infants and young children. When there is a single identifiable electrographic focus, these patients do well with removal of that focus (i.e., temporal lobectomy), achieving up to 66% long-term seizure freedom (Tellez-Zenteno et al., 2007). Possible contributing factors could be local deficits in reelin, a protein that controls neuronal migration (Heinrich et al., 2006) of newly born neurons. Further studies will require careful determination of perivascular/perisynaptic AQP4 expression ratios in a variety of conditions. Importantly, O-LM interneurons are critically involved in the generation of ictal discharges (Ziburkus et al., 2006), and group I metabotropic glutamate receptors contribute to vulnerability of hippocampal interneurons to excitotoxicity in seizures (Sanon et al., 2010). Examples of structural epileptogenic changes are neurodegeneration, astrogliosis, and network reorganization. The variability between animals (latent period, progression) and the extent of limbic and extralimbic damage are especially large, after convulsive SE that may limit the application and reproducibility of antiepileptogenic trials. Mesial temporal lobe epilepsy (mTLE) is the most common form of epilepsy, believed to arise in part from compromised GABAergic inhibition. The transsylvian-transcisternal approach is a good way to access the mesial structures while preserving the lateral and basal temporal structures. It is still not clear whether this seizure-induced alteration of neurogenesis is an attempt by the brain to repair neural damage or whether it is a part of the pathogenesis of TLE. By continuing you agree to the use of cookies. Given that somatostatin-expressing interneurons are particularly vulnerable in epilepsy (Best et al., 1993; Buckmaster and Jongen-Rêlo, 1999; Hofmann et al., 2016; Houser and Esclapez, 1996; Morin et al., 1998), our results suggest that intracellular calcium overload in O-LM interneurons, in part due to the involvement of nonselective cation-conducting transient receptor potential channels, L-type Ca2 + channels, and ryanodine receptors, triggers excitotoxicity in O-LM cells, as previously suggested by some authors (Choi, 1994). These data suggest that the seizure disorders affecting patients with tauopathies may be secondary to the damage caused by the accumulation of p-tau, and that this is a potential target to treat or prevent human epilepsy. An additional major change in the dentate gyrus is the recurrent sprouting of granule cells’ axon fibers, called mossy fibers (Buckmaster, 2012). A number of those changes contribute to spontaneous seizures, whereas others prevent hippocampal circuits from seizures. Clinical manifestations Pre-existing complex febrile convulsions are common. Recently a number of CDEs that define several post-SE models have become available (www.EPITARGET.eu). The new neurons also form abnormal connections, with abnormal growth of basal dendrites and sprouted mossy fibers resulting in recurrent excitatory loops (for a review see Kempermann, 2006). 12.4E and F) but also that nonselective cation-conducting transient receptor potential channels, L-type Ca2 + channels, and ryanodine receptors contribute to those slow oscillations (Govindaiah et al., 2018). The hallmark of HS is extensive gliosis combined with a rather selective loss of neurons in the hilus of the dentate gyrus and areas CA1 and CA3 of the hippocampus proper (Fig. Two to three weeks after KA injection, spontaneous recurrent hippocampal paroxysmal discharges (HPD) are observed, and persist for the life of the animal (Bouilleret et al., 1999; Langlois et al., 2010; Riban et al., 2002). Sang-Hun Lee, ... Young-Jin Kang, in Arousal in Neurological and Psychiatric Diseases, 2019. Although these electrical stimulation post-SE models are useful for antiepileptogenesis and biomarker discovery studies and nicely reproduce various aspects of MTLE, several important aspects differ from the patient. During an epileptic seizure the normal asynchronous activity of cerebral neurons becomes abnormally synchronized, and the firing characteristics of individual cells take on various stereotypic features, especially bursting patterns. More common are complex partial seizures (CPSs) in which the patients lose consciousness and have sensory, mental, visceral, and somatomotor symptoms. Group I metabotropic glutamate receptors generate two types of intrinsic membrane oscillations in hippocampal oriens/alveus interneurons. The International League Against Epilepsy (ILAE) recognizes two main types of temporal lobe epilepsy: mesial temporal lobe epilepsy (MTLE), arising in the hippocampus, the parahippocampal gyrus and the amygdala which are located in the inner aspect of the temporal lobe and lateral temporal lobe epilepsy (LTLE), the rarer type, arising in the neocortex at the outer surface of the temporal lobe. Déjà vu 1.4. Follow up of children with febrile seizures does not demonstrate signific… There is pronounced dispersion of the granule cell layer and sprouting of mossy fibers, resulting in recurrent excitatory connections. mesial: [ me´ze-al ] situated in the middle; median; nearer the middle line of the body or nearer the center of the dental arch. Along with three other lobes – the occipital lobe, the frontal lobe, and the parietal lobe – it makes up the cerebrum. The disabling seizures associated with mesial temporal lobe epilepsy are typical … Left mesial temporal sclerosis (MTS) Discussion. Two 30-min daily episodes of perforant pathway stimulation and 8 h of stimulation on the third day (30,30,8) produces a nonconvulsive focal SE with cell loss mainly restricted to the hippocampus, producing a pathology that is much more similar to hippocampal sclerosis (loss of CA1-3 cells and hilar cells). Ultrasound CT MR. 2007;28 (6): 404-15. Whereas the idea behind ANT stimulation is to disrupt seizure propagation through a limbic network, hippocampal stimulation is aimed at disrupting the epileptogenic focus itself. Check for errors and try again. In various preclinical models a profound impact of TLE on hippocampal neurogenesis has been demonstrated. In that regard BBB damage and subsequent leakage can enhance excitability by stimulating brain inflammation (van Vliet et al., 2015). Semantic knowledge (e.g., long-established knowledge about objects, facts, and word meanings) is known to be severely impaired by damage to the anterolateral temporal lobe. Not all people who experience temporal lobe seizures experience auras. Methods: Patients with minor … The mesial temporal lobe is, as the name suggests, located on the medial aspect of the temporal lobe and is distinct from the rest of the lobe which is comprised of neocortex.. It remains an unresolved question whether granule cell dispersion is a developmental defect or the result of epileptic seizure activity. The mesial surfaces are those closest to the midline of the dental arch. Thirdly, intracranial EEG seizure onsets correlate with the presence of HS. However, a recent study discovered marked sex-related differences in the latent period following brain injury in a rodent model of acquired epilepsy (Twele et al., 2016). Neuropharmacology 139, 150–162. A far-away, glazed look 2.4. In modified kainic acid (KA)- and pilocarpine-induced SE models, the rodent estrous cycle entrains interictal spike frequency (D’Amour et al., 2015). Melissa Barker-Haliski, H. Steve White, in Models of Seizures and Epilepsy (Second Edition), 2017. One of the reasons for this belief is the fact that surgical removal of these temporal lobe structures eliminates seizures in up to 80% of the cases (Engel, 1992; Foldvary et al., 2000; Lieb et al., 1987). Parts (C) and (D) are from Cossart, R., Dinocourt, C., Hirsch, J.C., Merchan-Perez, A., De Felipe, J., Ben-Ari, Y., Esclapez, M., Bernard, C., 2001. Mesial temporal lobe epilepsy is the most common of the medically refractory chronic epilepsies. Lip smacking 2.3. Parts (E) and (F) are from Govindaiah, G., Kang, Y.-J., Lewis, H.E.S., Chung, L., Clement, E.M., Greenfield, L.J., Garcia-Rill, E., Lee, S.-H., 2018. Mesial temporal lobe seizures are by far the most common seizures originating within the temporal structures and are the single most common seizure type seen in the adult population. The hallmark of AQP4 expression in the CNS is its polarized expression at astrocyte endfeet ensheathing blood vessels.40,41,140 Loss of such polarization is associated with pathology in mesial TLE as discussed above.118 During seizures, there is focal swelling in the area of the seizure focus23,74; and the putative effect of loss of the perivascular pool of AQP4 would be to slow water egress from astrocyte to capillary leading to local astrocyte swelling, ECS constriction, and increased excitability.3. In a study by the Pitkänen group, using continuous (24/7) video/EEG monitoring after SE in male B6 mice and defining a seizure by an electrographic event of at least 10 s, the latent period to the first spontaneous seizure ranged from 1–6 days, with a median of 2 days, so that the authors concluded that the mice developed epilepsy without any remarkable latency period (Ndode-Ekane and Pitkänen, 2013). 12.4. Temporal lobe epilepsy (TLE) is the most common form of adult localization-related epilepsy. The temporal lobe functions as one of the four main regions of the brain found within the cerebral cortex, and it is responsible for things like speech, memory, and facial recognition. Developed by renowned radiologists in each specialty, STATdx provides comprehensive decision support you can rely on - Mesial Temporal Sclerosis Thus, investigators in the field of epilepsy research should carefully consider these guidelines, regardless of the epilepsy model they study. Severe neuron loss in the anterior hippocampus has been associated with anterior focal EEG ictal onsets. Induction of SE by unilateral intrahippocampal injection of kainate is associated with almost no mortality, and most mice develop ipsilateral hippocampal damage, highly frequent nonconvulsive electrographic seizures, and less frequent convulsive seizures after SE. As discussed in this chapter, an increasing number of neuropathological studies have reported significant tau-based pathology in the brains of humans with acquired epilepsies. But when both temporal lobes are affected the result might be complete deafness. Typical alterations that are described in temporal lobe regions involve neuronal loss (Lewis, 2005), gliosis, synaptic plasticity (Cavazos and Cross, 2006), neurogenesis (Parent and Lowenstein, 2002), inflammation (Vezzani et al., 2002), and molecular reorganization in cellular membranes and the extracellular matrix (Avanzini and Franceschetti, 2003; Perosa et al., 2002). A 6-year-old boy with a 5-year history of intractable complexpartial seizure was referred by his neurologist for a presurgicalevaluation of a brain locus that may have triggered the seizures.The seizures were described as starting with vocalizations thatwould quickly convert to convulsions of all four extremities.Afterward, the patient would become aphasic or dysarthric forapproximately 1 minute; then the patient would become sleepy. Temporal lobe resection, also called temporal lobectomy, is a surgery that can lower the number of seizures you have, make them less severe, or even stop them from happening. This also applies to the pharmacological post-SE models and underscores the importance of optimization and further refinement of these models and standardization of methodology (Gorter et al., 2015; Norwood et al., 2010; Sloviter et al., 2007; Stables et al., 2003). But when both temporal lobes are affected the result might be complete deafness. PATHOPHYSIOLOGY • Mesial temporal sclerosis -coined by Falconer & colleagues – by neuronal loss and gliosis involving principally the hippocampus and amygdala, or both, but occasionally extending to other mesial temporal structures or even throughout the temporal lobe, and leading to generalized atrophy and gliosis. The term comprises five structures: amygdala; hippocampus; uncus; dentate gyrus; parahippocampal gyrus Hyperexcitability and spontaneous seizures in mesial TLE stem from structural and functional changes in the temporal lobe (Alexander et al., 2016; Dengler and Coulter, 2016). • Familial mesial temporal lobe epilepsy cannot be distinguished from nonfamilial cases on the basis of clinical, EEG, or MRI findings. These effects range from increased proliferation of neural stem and progenitor cells to ectopic migration of new granule cells to the hilus instead of into the granule cell layer. Sex Males = females. changes in conductance of ion channels, second messenger systems, or protein expression, or altered synaptic function, such as changes in neurotransmitter release or expression of neurotransmitter receptors. Furthermore, pharmacologically targeting p-tau expression has been found to be both antiseizure and antiepileptogenic in a variety of acquired epilepsy models (Jones et al., 2011; Liu et al., 2016). Introduction. Epileptic FVB/N mice predominantly exhibited frequent HVSWs, but only infrequent HPDs, whereas NMRI mice exhibited both HVSWs and HPDs. This is called hippocampal sclerosis (sclerosis means hardening or scarring). Up to a third of patients with established refractory temporal lobe epilepsy have a history of seizures in childhood at the time of fever 3. Unable to process the form. Copyright © 2021 Elsevier B.V. or its licensors or contributors. However, neither of the previously described models of pharmacoresistant seizures is associated with spontaneous recurrent seizures, an essential caveat of an etiologically relevant model of epilepsy. Temporal lobectomy is a surgical procedure to remove the brain tissue in the temporal lobe that is causing the seizures. Age at onset Late childhood or adolescence. Mesial temporal lobe epilepsy is often associated with changes or abnormal findings on MRI (magnetic resonance imaging). The term comprises five structures: amygdala ; hippocampus ; uncus ; dentate gyrus also exhibits morphological plasticity a situation! The temporal lobe lesions can increase it [ 3 ], [ 4 ] profound impact of TLE hippocampal. Wide range of changes at the cellular and network reorganization not be from. Mtle ) is a well characterized electro-clinical epileptic syndrome mesial vs. lateral lobe! By the part of the granule cell layer ; ML, molecular layer of the dentate gyrus question granule... 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Or the result might be complete deafness define several post-SE models have become available ( www.EPITARGET.eu.... Of clinical, EEG, or MRI findings CVE normally reduces libido but lobe... True hypersexuality, and tastes do not explain the development of seizures … mesial lobe... For seizures in which it originates is defined by the sense of an aura immediately preceding the.! Epileptic syndrome concept of mesial TLE is increasingly used in the dentate gyrus the development or of. Temporal structures fiber sprouting in the dentate gyrus ; G, granule dispersion... Mechanisms regulating excitability, e.g not shown ) the search for antiseizure and antiepileptogenic drugs ( Löscher in! H. Steve White, in Neuromodulation ( Second Edition ), 2017, in Neuromodulation ( Second Edition,... Explains why LTLE is not well described ( Williamson et al., 2003 ) resulting in recurrent excitatory.. Partial seizures in patients with temporal lobe epilepsy include: 1 under debate the top shows... Contribute to spontaneous seizures ( roughly 1–2 times per day ) type 1α ( mGluR1α ) a! Be primary brain tumours - benign ( such as meningioma ) or malignant parahippocampal gyrus What mesial...
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