mesial temporal lobe

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. Abbreviation: MTS. Thus, the investigator must evaluate potential sex differences in their animal models of epilepsy. Hippocampus. Epileptic FVB/N mice predominantly exhibited frequent HVSWs, but only infrequent HPDs, whereas NMRI mice exhibited both HVSWs and HPDs. Age at onset Late childhood or adolescence. There is pronounced dispersion of the granule cell layer and sprouting of mossy fibers, resulting in recurrent excitatory connections. 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. Occasionally, the mice may also present with generalized seizures (roughly 1–2 times per day). In line with this theory we found that ablation of adult neurogenesis using focal brain irradiation is associated with accelerated, kindling epileptogenesis in the rat-kindling model for TLE (Raedt et al., 2007). The second part addresses the clinical characteristics, in particular the natural evolution of the illness, the different aetiologies and the diagnostic relevance of the ictal semiology. Temporal lobe epilepsy (TLE) is the most common form of adult localization-related epilepsy. HS in temporal lobe epilepsy. Memory loss 3.3. There is limited research on the effects of sex in animal models of epilepsy. ), Strain Effects on Expression of Seizures and Epilepsy, Models of Seizures and Epilepsy (Second Edition), Riban et al., 2002; Twele et al., 2016a,b, Post-Status Epilepticus Models: Electrical Stimulation, Gorter et al., 2015; Norwood et al., 2010; Sloviter et al., 2007; Stables et al., 2003, Galanopoulou et al., 2013; Lidster et al., 2016; Pitkänen et al., 2013; Simonato et al., 2014; Sloviter, 2009; Stables et al., 2003, Norwood et al., 2010; Sloviter et al., 2007, Animal Models of Acquired Epilepsy and Tauopathies, Epilepsy is a common accompaniment of tauopathies, both related to primary neurodegenerative diseases, such as AD, and in acquired epilepsies, such, Gheyara et al., 2014; Holth et al., 2013; Zheng et al., 2014, Gheyara et al., 2014; Holth et al., 2013; Li et al., 2014. So the role of both processes in the genesis of MTLE remains controversial. Frances S. Cho, ... Jeanne T. Paz, in Models of Seizures and Epilepsy (Second Edition), 2017. Besides neuron-specific alterations, changes in glial function caused by aberrant activation and proliferation of astrocytes and microglia can promote increased excitability and seizures (Devinsky et al., 2013). It remains an unresolved question whether granule cell dispersion is a developmental defect or the result of epileptic seizure activity. Mesial temporal lobe epilepsy is the most common of the medically refractory chronic epilepsies. Neuropharmacology 139, 150–162. What causes temporal lobe epilepsy? Sufferers from LTLE comprise less than 10% of patients with TLE. Dispersion of granule cells, or the widening of the granule cell layer, is another typical phenomenon in TLE and is correlated with the severity of hippocampal neuronal loss and the extent of mossy fiber sprouting. Unable to process the form. Quantitative analysis of parvalbumin-immunoreactive cells in the human epileptic hippocampus. Care is taken that stimulation intensity is not too high and does not produce the tissue-damaging hydrolysis at the electrode tips that is caused by the higher stimulus intensities in the conventional electrogenic models. Some symptoms of a temporal lobe seizure may be related to these functions, including having odd feelings — such as euphoria, deja vu or fear.Temporal lobe seizures are sometimes called focal seizures with impaired awareness. (C and D) GAD67 mRNA stain of the CA1 in control (control) and pilocarpine-treated (pilocarpine) rats (D). Further studies will require careful determination of perivascular/perisynaptic AQP4 expression ratios in a variety of conditions. 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). 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). Recently a number of CDEs that define several post-SE models have become available (www.EPITARGET.eu). An aura or far-away look 1.2. Most patients present with complex partial temporal lobe epilepsy. Electroencephalography (EEG) has an important role in the diagnosis and classification of epilepsy. Paul Koch, Gordon Baltuch, in Neuromodulation (Second Edition), 2018. Simple focal seizures are the initial non-febrile seizures followed by In addition, 17β-estradiol can acutely suppress GABAergic inhibition of the hippocampus of female rats through a sex-specific molecular signaling pathway involving the estrogen receptor ERα (Tabatadze et al., 2015). Temporal lobe epilepsy (TLE) is a chronic neurological condition characterized by recurrent seizures (epilepsy) which originate in the temporal lobe of the brain with progressive neurological disabilities, including cognitive deficit, anxiety and depression.. Macroanatomy and microanatomy of the temporal lobe. 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. mesial temporal sclerosis. Other hearing-related effects include: Thus there is a subpopulation of patients with refractory mesial temporal epilepsy for whom resective surgery is not an option, but who may respond to epileptogenic disruption via hippocampal DBS. Lip smacking 2.3. Mesial temporal lobe epilepsy (MTLE) is often discussed as a separate entity because it is quite distinct from its lateral counterpart in terms of etiology, semiology, imaging, and electrophysiologic characteristics. Neuronal cell loss involves both glutamatergic excitatory neurons and GABAergic inhibitory interneurons in the dentate gyrus and the hippocampus proper. Temporal lobe epilepsy (TLE) comprises 30%–35% of all epilepsies and is the most common form of refractory symptomatic epilepsy (Spencer, 2002). Although most changes in hippocampal neurogenesis in case of seizures suggest a proepileptic role, a recent study has shown that epilepsy-generated mature granule neurons in the granule cell layer are suppressed, as they receive less excitatory drive and more inhibitory input when compared to new granule neurons generated in physiological conditions (Jakubs et al., 2006). The mesial surfaces are those closest to the midline of the dental arch. Mesial temporal lobe epilepsy (MTLE) is the most common form of focal, pharmacoresistant epilepsy in adults and is often associated with hippocampal sclerosis. Granule cell dispersion is mainly observed in TLE patients who experience febrile convulsive seizures in early infancy, suggesting an initial precipitating event as a trigger for the development of granule cell dispersion (Houser, 1990; Lurton et al., 1998). Not all people who experience temporal lobe seizures experience auras. Other possible auras include hallucinations of sounds, voices, people, smells, and tastes. After the seizure: 3.1. Ping Zheng, ... Terence J. O’Brien, in Models of Seizures and Epilepsy (Second Edition), 2017. However, seizures themselves can cause or aggravate HS (Sutula et al., 2003). Together, these changes then pathologically rewire the network, as is particularly evident in HS (see Temporal lobe epilepsy) (Pitkanen and Lukasiuk, 2011). Learn more. Developed by renowned radiologists in each specialty, STATdx provides comprehensive decision support you can rely on - Mesial Temporal Sclerosis 12.4B. Severe neuron loss in the anterior hippocampus has been associated with anterior focal EEG ictal onsets. Introduction. Our recent studies revealed a potential link from expression of group I metabotropic glutamate receptors (i.e., mGluR1 and mGluR5) in somatostatin-expressing oriens-lacunosum moleculare (O-LM) interneurons to their vulnerability to excitotoxicity. Such asymptomatic localized disturbances may spread to recruit anatomically contiguous gray matter, creating a larger abnormality leading to the clinical manifestations of a seizure with changes in consciousness, motor control, sensory perception, behavior, and/or autonomic dysfunction (Davenport, 1998). Since the accompanied shrinkage of the hippocampus makes it necessary to reimplant the electrodes in order to record chronic hippocampal EEG seizures, this model is very labor-intensive, fact that may explain the hesitation to use or further develop this model by other research groups. see Mesial temporal lobe epilepsy radiosurgery. 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). The DHPG-induced slow oscillations are insensitive to the sodium channel blocker tetrodotoxin (TTX, 1 μM). MTLE is the most common type of epilepsy and is often characterized by the sense of an aura immediately preceding the seizure. A clear seizure-free latent period was only observed in male NMRI mice, but not in female NMRI, B6, or FVB/N mice. Patients suffering from TLE can have simple partial seizures in which they remain conscious. This protocol also leads to recurrence of spontaneous seizures (Norwood et al., 2010). However, confirmation that this plays a causal, rather than associative relationship, with human epilepsy awaits the results of clinical trials that specifically target tau-based mechanisms. 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.. 12.4D; see the Table 1 of a review by Alexander et al., 2016, presenting interneuron loss in detail in TLE). Temporal lobectomy is a surgical procedure to remove the brain tissue in the temporal lobe that is causing the seizures. The aberrantly sprouted mossy fibers preferentially innervate glutamatergic granule cells, primarily creating a recurrent excitatory feedback circuitry, thus mossy fiber sprouting is believed to be an excitatory phenomenon (Buckmaster et al., 2002; Scharfman et al., 2003; Wuarin and Dudek, 1996). (A and B) Nissl stain of normal human hippocampus (A) and damaged hippocampus due to hippocampal sclerosis (B). There is still a lot of debate about the mechanisms underlying development and intractability of TLE, but it is generally believed that limbic structures such as the hippocampus, the amygdala, and the temporal neocortex play crucial roles. [4] PMID: 32119319 We report on 3 patients with mesial temporal lobe epilepsy as the first, predominant clinical indication, and in 2 of the patients so far the sole clinical symptom of the disease. Neuroscience 149, 131–143. 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. One of the most common findings is scarring in the temporal lobe. NMRI mice were more sensitive to the antiseizure effect of carbamazepine than FVB/N mice (Twele et al., 2016b). Dentate gyrus. 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). The sprouted fibers form excitatory synapses primarily onto other granule cells, likely contributing to hyperexcitability and spontaneous seizures (Scharfman et al., 2003). A number of those changes contribute to spontaneous seizures, whereas others prevent hippocampal circuits from seizures. 12.3C for an example of PVBC in the dentate gyrus), surviving basket cells in TLE remain hypoactive, resulting in hyperexcitability in the dentate gyrus (also known as “the dormant basket cell hypothesis”), along with interneuron loss. 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. 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. First, from epilepsy surgery it is evident that best seizure control (up to 80%) in TLE is obtained when a large part of the hippocampus is included in the temporal lobe surgery (Engel, 1996). Recurrent excitation and the development of seizures have been associated with aberrant mossy fiber sprouting in ### Case histories. {"url":"/signup-modal-props.json?lang=us\u0026email="}. We report on 3 patients with mesial temporal lobe epilepsy as the first, predominant clinical indication, and in 2 of the patients so far the sole clinical symptom of the disease. Electrophysiological studies on human hippocampal slices and experimental studies in animal models for TLE confirm this by showing that the extent of mossy fiber sprouting correlates with the excitability of the hippocampus (Cavazos et al., 1991; Franck et al., 1995). The temporal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. Moreover, the mesial temporal lobes tend to be the site of origin of close to 80% of all TLEs. 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. Jan A. Gorter, Erwin A. van Vliet, in Models of Seizures and Epilepsy (Second Edition), 2017. 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. (2012) proposed that the intrahippocampal mouse model of mesial TLE is suited as a model of difficult-to-treat focal seizures. Mesial temporal lobe epilepsy is the most common form of human epilepsy, and its pathophysiological substrate is usually hippocampal sclerosis, the most common epileptogenic lesion encountered in patients with epilepsy. Mesial temporal lobe epilepsy is the most common form of human epilepsy, and its pathophysiological substrate is usually hippocampal sclerosis, the most common epileptogenic lesion encountered in patients with epilepsy. Mesial temporal lobe epilepsy is often associated with changes or abnormal findings on MRI (magnetic resonance imaging). The transsylvian-transcisternal approach is a good way to access the mesial structures while preserving the lateral and basal temporal structures. The dendritic tree of the granule cells of the dentate gyrus also exhibits morphological plasticity. Methods: We retrospectively reviewed the video electroencephalography recordings, SPECT studies, and MR images of 32 MTLE patients and of a … These results suggest that activation of group I mGluRs in O-LM interneurons generates intrinsic, sodium channel-independent oscillations. Mesial temporal lobe. The temporal lobe is one of the four major lobes of the cerebral cortex. Similarly, the blood–brain barrier (BBB) is pivotal for neuronal functioning by maintaining brain homeostasis. Sex Males = females. 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. Moreover, inflammation and oxidative stress are able to increase the excitability of the network (Puttachary et al., 2015). Background:In the surgical treatment of temporal lobe epilepsy with mesial temporal lobe tumor, whether to remove the hippocampus aiming for a better seizure outcome in addition to removing the tumor is a dilemma.Two pediatric cases treated successfully with tumor removal alone are presented. Unlike patients with MTLE, there are no reported large series of patients with well-documented lateral temporal lobe seizure origin. Histological studies on tissue obtained surgically from patients with intractable and unilateral TLE reveal specific changes which could underlie hyperexcitability of the removed structures. Axons and somatodendritic compartment are shown in black and red, respectively. From Darby and Walsh, 1994. 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. Mesial temporal lobe epilepsy (MTLE), the most common epilepsy in adults, is generally intractable and is suspected to be the result of recurrent excitation or inhibition circuitry. The mesial temporal lobe, also known as the medial 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 composed of neocortex. Hippocampal onset accounts for at least 80% of all temporal lobe seizures. 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). The hypothesis on TLE development covers three phases: an initial precipitating insult of the brain, such as head trauma, status epilepticus, stroke, inflammation, or febrile seizures, initiates a cascade of events; a period of epileptogenesis during which several processes (either molecular or structural) occur; and chronic epilepsy characterized by the occurrence of recurrent seizures. Dendritic but not somatic GABAergic inhibition is decreased in experimental epilepsy. • Familial mesial temporal lobe epilepsy cannot be distinguished from nonfamilial cases on the basis of clinical, EEG, or MRI findings. Methods: Patients with minor … 1-3 The etiology of MTS is still not fully understood. Sclerosis can extend to other mesiotemporal regions such as the amygdala and the entorhinal, perirhinal, and temporopolar cortex (Hermann et al., 2002; Jutila et al., 2001; Salmenpera et al., 2001; Wieser, 2004; Yilmazer-Hanke et al., 2000). In rat primary hippocampal neurons, estrogen affects abnormal epileptiform bursting activity in a dose-dependent manner via modulation of the potassium channel Kv4.2 (Zhang et al., 2015). Figure 81.3. In the dentate hilus, there is also significant loss of excitatory mossy cells and interneurons. Note that there are fewer GAD67 mRNA-positive cells in the stratum oriens in pilocarpine-treated rats, compared with control. The condition called mesial temporal sclerosis is closely related to temporal lobe epilepsy, a type of partial (focal) epilepsy in which the seizure initiation point can be identified within the temporal lobe of the brain. 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). The MTLE mouse is characterized by an initial neurotoxic event, that is, a unilateral intrahippocampal injection of KA into the dorsal hippocampus that induces nonconvulsive SE lasting several hours. 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). Kindled seizure models are certainly superior to acute models from the perspective of modeling epilepsy. An additional major change in the dentate gyrus is the recurrent sprouting of granule cells’ axon fibers, called mossy fibers (Buckmaster, 2012). In a normal brain the spread of bursting activity is prevented by intact hyperpolarization and a region of surrounding inhibition, created by inhibitory neurons. Wolfgang Löscher, in Models of Seizures and Epilepsy (Second Edition), 2017. By contrast, in most surgical patients with poor seizure control, no hippocampal pathology or only mild damage can be demonstrated (e.g., amygdalar sclerosis) (Mathern et al., 1995; Miller et al., 1994). Abnormal neurogenesis in response to seizures seems not to be limited to animal models for TLE. In this patient it was a left sided temporal sclerosis. In human TLE, hippocampal sclerosis is evident in the dentate, CA3, and CA1 with selective cell loss and gliosis as shown in Fig. 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. All … Moreover, the mesial temporal lobes tend to be the site of origin of close to 80% of all temporal lobe … The intrahippocampal kainic acid (KA) mouse model of, Bouilleret et al., 1999; Langlois et al., 2010; Riban et al., 2002, Bouilleret et al., 1999; Riban et al., 2002, ). 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). Similarly, Badaut et al. 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). Our objective was to demonstrate common patterns of ictal cerebral blood flow changes in a group of patients with mesial temporal lobe epilepsy (MTLE) using the technique of composite subtraction ictal SPECT coregistered to MRI (SISCOM). These interneurons are also known to be vulnerable to excitotoxicity in TLE (Fig. 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). Group I metabotropic glutamate receptors generate two types of intrinsic membrane oscillations in hippocampal oriens/alveus interneurons. The treatment is predominantly surgical [2] , [3] , [4] . see Mesial temporal lobe epilepsy radiosurgery. Recurrent excitation and the development of seizures have been associated with aberrant mossy fiber sprouting in The granule cell layer (G) of the dentate gyrus (DG) sends projections, called mossy fibers, toward the CA3 layer. However, we recently reported that the latent period after kainate-induced SE before onset of spontaneous recurrent seizures varies as a function of mouse strain and sex (Twele et al., 2016a). Unaware of surroundings 3. 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 ). (C) A frequent observation in TLE is HS, where hippocampal cytoarchitecture is changed dramatically. Along with three other lobes – the occipital lobe, the frontal lobe, and the parietal lobe – it makes up the cerebrum. A 24 h stimulation protocol in mice (applied under anesthesia) also leads to hippocampal sclerosis and spontaneous seizures (Kienzler et al., 2009). This observation suggests that the new neurons adjust their functional status to their local network environment, and therefore might help to compensate for pathological excitation in epileptic seizures. This was substantiated in a subsequent study by the same group (Rantala et al., 2015), in which the first generalized convulsive seizure was observed 1–2 days after intrahippocampal injection of kainate in male B6 mice. 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. mesial: [ me´ze-al ] situated in the middle; median; nearer the middle line of the body or nearer the center of the dental arch. found loss of polarization of AQP4 expression on astrocyte endfeet following subarachnoid hemorrhage (SAH) and in peritumoral tissue130; thus, posttraumatic epilepsy and tumor-associated epilepsy142 could be associated with alterations in AQP4 expression and distribution. posterior inferior cerebellar artery (PICA), anterior inferior cerebellar artery (AICA), persistent carotid-vertebrobasilar artery anastomoses, persistent proatlantal intersegmental artery, internal carotid artery venous plexus of Rektorzik, 1. Examples of structural epileptogenic changes are neurodegeneration, astrogliosis, and network reorganization. • Some families have a benign outcome, whereas others have a more heterogeneous presentation, including refractory patients. It may look like the hippocampus on one side, or both, has shrunk or is smaller. Although temporal lobe seizures are always partial, they can become secondarily generalized and result into tonic–clonic seizures (Mathern et al., 1996). This is very rare. 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. 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). 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Foci after resection, and transvestite and transsexual behaviour experience auras by subsequent studies, so that Guillemain et.! Of group I mGluRs in O-LM interneurons generates intrinsic, sodium channel-independent oscillations and... To excitotoxicity in TLE resulting in recurrent excitatory connections exist ( Walczak, 1995.! Not all people who experience temporal lobe seizures channel blocker tetrodotoxin ( TTX 1! Mri findings brain homeostasis fully understood Steve White, in models of seizures information about and! Bilateral seizure foci, or develop contralateral foci after resection, and the hippocampus term five. Have a benign outcome, whereas NMRI mice, but only infrequent HPDs whereas.
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