Materiały źródłowe

• #1 Temporal Seizure – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK549852/

  Temporal lobe epilepsy is the commonest seizure disorder and affects approximately fifty million people worldwide. […] The etiology of temporal lobe seizures is extensive. The most common causes are: Hippocampal sclerosis, Infections, Tumors, Traumatic brain injury, Vascular anomalies, Genetic, Cryptogenic. […] MTLE is the most common form of epilepsy and is most commonly due to a neurodegenerative process known as hippocampal sclerosis (HS) found in the majority of patients diagnosed with this condition, upon histological evaluation. […] Aberrant neurological conduction, primarily due to the overactivity of stimulatory neurotransmitters such as glutamate or under activity of inhibitory neurotransmitters such as gamma-aminobutyric acid (GABA) with a primary focus in the temporal lobe results in epileptogenesis.

• #2 Temporal lobe epilepsy – Wikipedia

  https://en.wikipedia.org/wiki/Temporal_lobe_epilepsy

  In the field of neurology, temporal lobe epilepsy is an enduring brain disorder that causes unprovoked seizures from the temporal lobe. […] Temporal lobe epilepsy occurs from seizures arising within the temporal lobe. […] Approximately 80% of seizures in the temporal lobe begin in the mesial temporal region, frequently starting in or around the hippocampus. […] Hippocampal sclerosis occurs with severe CA1 and less severe CA3 and CA4 neuronal loss. […] Experimental research has shown that N-methyl-d-aspartate (NMDA) receptor activation causes neuronal cell loss, and electrical stimulation-induced animal models of temporal lobe epilepsy duplicate the cell loss pattern of temporal lobe epilepsy in humans. […] Repetitive seizures irreversibly damage interneurons leading to persistent loss of recurrent inhibition.

• #3 Mesial temporal sclerosis and epilepsy: a narrative review | Acta Epileptologica | Full Text

  https://aepi.biomedcentral.com/articles/10.1186/s42494-024-00172-5

  Mesial temporal sclerosis (MTS) stands out as a prevalent etiology of medically intractable temporal lobe epilepsy. […] The hippocampus has long been recognized as a structure that serves as both the primary site of epileptic seizures and as a region particularly vulnerable to secondary damage resulting from seizures or other brain injuries such as mesial temporal sclerosis (MTS). […] The characteristic gliosis, neuronal loss, and reorganization of the dentate gyrus and hippocampal circuits in MTS make it the second most common cause of temporal lobe epilepsy (TLE) in children. […] It has been recognized that the spread of seizures from remote areas of the cerebral cortex to the hippocampus is sufficient to disrupt synaptic connections in the mossy fibers. […] Severe damage, such as that caused by status epilepticus, can even result in macroscopic lesions in the hilus of the dentate gyrus and hippocampal subregions.

• #4 Temporal Seizure – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK549852/

  As noted, temporal lobe epilepsies arise through a myriad of etiologies, regardless of the focus of epileptogenic activity. […] Recent studies reveal a significant number of cases clustered in families or secondary to idiopathic genetic mutations. […] There has also been evidence regarding the role of astrocytes in the pathogenesis of epilepsy as well as interconnected epileptic networks.

• #5 Epilepsy and Seizures: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1184846-overview

  Seizures are paroxysmal manifestations of the electrical properties of the cerebral cortex. A seizure results when a sudden imbalance occurs between the excitatory and inhibitory forces within the network of cortical neurons in favor of a sudden-onset net excitation. […] The pathophysiology of focal-onset seizures differs from the mechanisms underlying generalized-onset seizures. Overall, cellular excitability is increased, but the mechanisms of synchronization appear to substantially differ between these 2 types of seizure and are therefore discussed separately. […] The electroencephalographic (EEG) hallmark of focal-onset seizures is the focal interictal epileptiform spike or sharp wave. The cellular neurophysiologic correlate of an interictal focal epileptiform discharge in single cortical neurons is the paroxysmal depolarization shift (PDS).

• #6

  https://scholars.duke.edu/publication/1662897

  Excitation-inhibition (E/I) imbalance is theorized as a key mechanism in the pathophysiology of epilepsy, with ample research focusing on elucidating its cellular manifestations. […] A broad decrease in the Hurst exponent is observed in pharmaco-resistant temporal lobe epilepsy (TLE), suggesting more excitable network dynamics. […] Connectome decoders point to temporolimbic and frontocentral cortices as plausible network epicenters of E/I imbalance. […] Furthermore, computational simulations reveal that enhancing cortical excitability in TLE reflects atypical increases in recurrent connection strength of local neuronal ensembles. […] Mixed cross-sectional and longitudinal analyses show stronger E/I ratio elevation in patients with longer disease duration, more frequent electroclinical seizures as well as interictal epileptic spikes, and worse cognitive functioning. […] This work provides in vivo evidence of a macroscale shift in E/I balance in TLE patients and points to progressive functional imbalances that relate to cognitive decline.

• #7 Temporal Lobe Epilepsy – Pathophysiology and Mechanisms – touchNEUROLOGY

  https://touchneurology.com/epilepsy/journal-articles/temporal-lobe-epilepsy-pathophysiology-and-mechanisms/

  Temporal lobe epilepsy (TLE) is a disorder of the nervous system due to unprovoked seizures originating from the temporal lobe. The main cause of TLE is neuronal hyperexcitability due to the presence of pathological changes in the temporal lobe of the brain such as neuronal loss, mutation, granule cell dispersion and malformations of cortical development. […] The ILAE defines HS as severe segmental loss of pyramidal neurons in the CA1 region, and less prominent neuronal loss can be seen in the areas CA3 and CA4. […] Experimental models show that activation of N-methyl-d-aspartate (NMDA) receptors can produce neuronal loss in TLE. […] Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter that inhibits neuronal firing by activating two different classes of receptors, GABAA and GABAB, through Cl-influx into the central nervous system. Therefore, damage of GABAergic interneurons will cause continuous unregulated neuronal firing, which will lead to seizures.

• #8 Temporal lobe epilepsy – Wikipedia

  https://en.wikipedia.org/wiki/Temporal_lobe_epilepsy

  Damage of GABAergic interneurons lead to loss of inhibition, uncontrolled neuronal firing, leading to seizures. […] The secondary epileptogenesis hypothesis is that repetitive seizures lead to interneuron loss, loss of glutamatergic principal neurons, axonal sprouting, and formation of new recurrent glutamatergic excitatory circuits leading to a more severe epilepsy. […] Mechanisms related to neuronal loss incompletely account for temporal lobe epilepsy as temporal lobe epilepsy may occur with only minimal neuronal cell loss. […] This KCC2 mutation prevents subicular neurons from potassium and chloride ion extrusion, leading to intracellular chloride accumulation, and positive -Aminobutyric acid (GABA) mediated currents. […] Accumulated chloride efflux through GABA receptors leads to neuronal depolarization, increased neuronal excitability and ultimately seizures.

• #9 Temporal Lobe Epilepsy – Pathophysiology and Mechanisms – touchNEUROLOGY

  https://touchneurology.com/epilepsy/journal-articles/temporal-lobe-epilepsy-pathophysiology-and-mechanisms/

  Mutation of the neuron-specific type 2 K+/Cl cotransporter (KCC2) in some of the subicular pyramidal cells, which leads to loss of function, is one of the causes of HS-associated MTLE. […] An increase in intracellular Cl concentration causes efflux of Cl through GABA receptors, resulting in depolarisation and hyperexcitability, and subsequently leading to seizures. […] Granule cell dispersion (GCD) in the dentate gyrus is observed in HS, which may be a consequence of enhanced proliferation of granule cell precursors as a result of seizures. […] GCD causes neuroplasticity of granule cell axons into their own dendritic field, a reorganisation process known as mossy fibre sprouting. […] This then creates de novo recurrent excitatory circuits, and thus increases excitation that can reduce the threshold for granule cell synchronisation, resulting in epilepsy due to the increase in excitatory signals.

• #10 Expression of Nav1.5 in the pathogenesis of temporal lobe epilepsy | Cellular and Molecular Biology

  https://cellmolbiol.org/index.php/CMB/article/view/2784

  To investigate the expressions of Nav1.5 mRNA at different time points in a rat model of temporal lobe epilepsy (TLE), and to assess the potential contribution of Nav1.5 to epileptogenesis. […] The expressions of Scn5a mRNA in the hippocampus during the latent and chronic periods were significantly higher than in the control group (p 0.05), but there were no significant differences in the corresponding expressions between the two different time points in the latent and chronic period groups (p 0.05). […] The expression peaked 30 days post-SE, and was sustained for 60 days. […] Immunohistochemical staining showed that expression levels of Nav1.5 in the CA3 region during latent and chronic periods were significantly higher than those in control group (p 0.05), and the expressions peaked at day 30. […] These results show that Nav1.5 might be involved in the pathogenesis of TLE.

• #11 Temporal lobe epilepsy – Wikipedia

  https://en.wikipedia.org/wiki/Temporal_lobe_epilepsy

  Dentate gyrus granule cell dispersion refers to a granule cell layer that is widened, poorly demarcated, or accompanied by granule cells outside the layer (ectopic granule cells). […] A hypothesis is that granule cell dispersion may disrupt the normal mossy fiber pathway connecting granule cells and CA3 pyramidal cells leading to mossy fiber sprouting and new excitatory networks capable of generating seizures. […] Focal cortical dysplasia is a brain malformation that may cause temporal lobe epilepsy. […] This malformation may cause abnormal cortical layers (dyslamination), occur with abnormal neurons (dysmorphic neurons, balloon cells) and may occur with a brain tumor or vascular malformation. […] An abnormality of the MTOR pathway leads to hyperexcitable glutamate mediated neurons leading to seizures.

• #12 Temporal Lobe Epilepsy – Pathophysiology and Mechanisms – touchNEUROLOGY

  https://touchneurology.com/epilepsy/journal-articles/temporal-lobe-epilepsy-pathophysiology-and-mechanisms/

  Focal cortical dysplasia (FCD) is a subtype of MCD which causes chronic medically refractory epilepsy in the paediatric population, and is a frequent cause of epilepsy in adults. […] FCD can cause hyperactivation of the rapamycin (mTOR) pathway, which is involved in regulation of protein and lipid synthesis, cell growth, and metabolism. […] TSC2 mutation causes hyperexcitability of glutamate-mediated neurons which will lead to seizures. […] In conclusion, the pathophysiology of TLE is complex and not well-understood; to-date there are several pathological findings in TLE. However, thorough understanding of the mechanism of the disease is crucial in developing new pharmacological therapies.

• #13

  https://link.springer.com/article/10.1007/s00221-023-06557-1

  Clarifying the underlying mechanisms of epileptogenesis is important in preventing the progression of chronic epilepsy. […] In epilepsy, the mTOR (mammalian target of rapamycin) pathway plays a critical role in mediating the mechanism of epileptogenesis. […] We found that apigenin-pretreatment had a significant inhibitory effect on neural cell death, spontaneous seizure spikes, aberrant neurogenesis, mTOR hyperactivity, and aberrant mossy fiber sprouting. […] Overall, these results suggest that apigenin has an antiepileptogenic effect and may be a useful target for inhibiting mTOR hyperactivity in epilepsy.

• #14

  https://aesnet.org/abstractslisting/the-role-of-the-entorhinal-cortex-in-the-pathogenesis-of-temporal-lobe-epilepsy–a-quantitative-mri-study

  Reciprocal glutamatergic pathways of the entorhinal cortex (EC) connect the hippocampus to the surrounding cortex. Damage to the EC is associated with increased risk of seizure generation. Neuronal loss of layer III of the EC has been reported in surgical specimens from patients with temporal lobe epilepsy (TLE). […] The pattern of atrophy demonstrated raises questions about the role of the EC in the pathogenesis of TLE. Further elucidation of these questions requires larger studies and clinical correlation.

• #15 SciELO Brazil – Entorhinal cortex involvement in human mesial temporal lobe epilepsy Entorhinal cortex involvement in human mesial temporal lobe epilepsy

  https://www.scielo.br/j/anp/a/MKPRy8ppZ75ChsXdNn3JyCN/?lang=en

  Entorhinal cortex involvement in human mesial temporal lobe epilepsy (Abstract). Dissertation. Marseille, 2001 […] There is some evidence that mesial temporal structures other than the hippocampus participate in seizure generation. In particular, an increasing number of studies demonstrate the involvement of the entorhinal cortex (EC) in the TLE pathogenesis. […] The role of the EC in human MTLE seizures genesis has rarely been directly studied. This study aimed at determining the respective role of the EC and other temporal lobe structures in the genesis of MTLE seizures. […] Results strongly suggested that the activity of the EC was secondarily triggered by the hippocampus or in some cases the amygdala. […] These seizures appeared to be initiated by interactions between the EC and one of the other mesial structures (amygdala or hippocampus). The entorhinal cortex was found to play a leader role suggesting that it is involved in the initiation of the ictal discharge. […] The entorhinal cortex is involved in MTLE seizure generation in different ways. It appears to be a key structure in seizures that start with rapid discharges arising from mesial structures.

• #16 Pathophysiogenesis of Mesial Temporal Lobe Epilepsy: Is Prevention of Damage Antiepileptogenic?

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4101766/

  Overall, the above mentioned histopathological changes are supposed to occur after the initial precipitating injury and are suspected to contribute to epileptogenesis. […] A crucial point is whether the prevention of structural changes, i.e. lesions, could be of help or not in preventing mesial TLE after a primary precipitating injury potentially able to cause hippocampal sclerosis. […] Most of the studies on TLE focused essentially on changes occurring in the hippocampal formation. […] However, lines of evidence suggest that other extrahippocampal regions are involved in TLE and could contribute to seizure generation. […] Evaluation of patients affected by TLE without hippocampal sclerosis demonstrated the occurrence of volumetric reductions in regions such as entorhinal and perirhinal cortices, thalamus and amygdala.

• #17 Pathophysiogenesis of Mesial Temporal Lobe Epilepsy: Is Prevention of Damage Antiepileptogenic?

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4101766/

  These findings were also supported by histological analyses of human epileptic tissue that showed the presence of selective neuronal loss and synaptic reorganization within extrahippocampal structures, independently of hippocampal sclerosis. […] The piriform cortex was recently outlined as a region relevant for partial seizures also in patients, so that the pathophysiological mechanisms involved in damaging this region could be important targets for preventive therapies. […] The presence of injuries to astroglial network has been found even after early diazepam administration. […] The contribution of astrocytes in modulating epileptogenesis and ictogenesis could be greatly altered in presence of brain lesions, such as those observed in TLE. […] Overall, studies have shown that blood-brain barrier leakage could be implicated in induction of seizures and progression of epilepsy.

• #18

  https://www.ncbi.ncbi.grantome.com/grant/NIH/R01-NS070824-05S1

  One of the most common types of epilepsy – mesial temporal lobe epilepsy (MTLE) – is characterized by spontaneous and recurrent partial seizures. […] Recent studies have suggested that a deficiency in glutamine synthetase in the hippocampus is implicated in the generation of seizures in MTLE (Eid et al. Lancet 2004;363: 28-37). […] The hypothesis is that a deficiency in glutamine synthetase leads to chronic high concentrations of glutamate in astrocytes and the extracellular space of the hippocampus with particularly high glutamate levels in individuals suffering from severe seizures and extensive brain damage. […] The hypothesis is that such triggers cause a transient surge in extracellular glutamate in the hippocampus with „spontaneous” seizures as the ultimate consequence. […] The hypothesis is that restoration of glutamine synthetase in the hippocampus leads to cessation of seizures even in the presence of extensive brain pathology.

• #19 Temporal lobe epilepsy: etiology, fisiopathogeny and magnetic resonance imaging

  https://inis.iaea.org/search/search.aspx?orig_q=RN:36090807

  In many cases of acquired lesions seizures are related to the excitotoxicity mediated by glutamate as a possible trigger of the process. […] Besides, neuronal division has been demonstrated in the hippocampus, which could explain a neurogenic mechanism in the development of the seizures. […] The pathologic molecular findings in cortical malformations and the function of the glial cells in the neuronal homeostasis, contribute with data that sustain the neuro genesis of the seizures. […] The knowledge derived from areas as molecular biology, genetic and electrophysiology of isolate neurons and astrocytes, contributes to understand the pathologic mechanism of the seizures.

• #20 Pathophysiogenesis of Mesial Temporal Lobe Epilepsy: Is Prevention of Damage Antiepileptogenic?

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4101766/

  The observation coming from clinical studies supporting the view that microglia are persistently activated after a brain injury makes these glial cells a crucial player in triggering a complex cascade of events that definitely leads to a persistent inflammatory state. […] The role of autoimmunity in epilepsy has been recently reviewed by addressing a number of epileptic syndromes associated with immunological alterations and responding to immunomodulatory agents. […] Although these reports are suggestive for a role of neuroinflammation in TLE, more evidence is required to draw definite conclusions. […] The most severe type of epilepsy in adults, TLE, is characterized by complex pathological changes whose relationship with refractoriness to therapy is unclear. […] Research on the use of antiepileptic drugs as neuroprotective agents, apart from limited cases such as diazepam, turned out to be frustrating, mainly because of the limited results on epileptogenesis or, even, for the absence of consistent findings. […] These findings suggest that new pharmacological tools can be taken into consideration as promising neuroprotective molecules and/or add on treatments in pharmacoresistant epilepsy.

• #21 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20201014/Amino-acid-produced-by-the-brain-could-prevent-temporal-lobe-epileptic-seizure.aspx

  Temporal lobe epileptic seizures are debilitating and can cause lasting damage in patients, including neuronal death and loss of neuron function. […] Their research indicates that an amino acid known as D-serine could work with the mechanism to help prevent epileptic seizures, thereby also preventing the death of neural cells that accompanies them. […] When FSU receptors allow too much calcium to enter neurons, TLE patients experience epileptic seizures as neurons become overstimulated from the influx. The overstimulation, or hyperexcitability, is what causes neurons to die, a process known as excitotoxicity. […] The research team also found that the amino acid D-serine blocks these receptors to prevent excess levels of calcium from reaching neurons, thereby preventing seizure activity and neuronal death.

• #22 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20201014/Amino-acid-produced-by-the-brain-could-prevent-temporal-lobe-epileptic-seizure.aspx

  Kumar’s research points to neuroinflammation as the cause for diminished D-serine levels in the entorhinal cortex of the brain. D-serine is typically produced by glial cells, but neuroinflammation experienced as part of TLE causes cellular and molecular changes in the brain that can prevent it from being produced. […] The important thing is that we’ve outlined the basic bread-and-butter mechanisms of why D-serine works. What we’ve established is the discovery of the receptors, discovery of the antagonist for these receptors (D-serine), how it works and how to prevent the emergence of TLE. The mechanisms and pathophysiology are as relevant to the animal model as they are to human beings, and that’s where the excitement lies.

• #23 Adult-onset temporal lobe epilepsy suspicious for autoimmune pathogenesis: Autoantibody prevalence and clinical correlates | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0241289

  Temporal lobe adult-onset seizures (TAOS) related to autoimmunity represent an increasingly recognized disease syndrome within the spectrum of epilepsies. […] In this context, certain autoantibodies (autoABs) were often associated with limbic encephalitis (LE). […] Here, we aimed to gain insights into (a) the distribution of neurological autoABs (neuroABs, defined as autoABs targeting neuronal surface structures or onconeuronal ABs or anti-glutamate acid decarboxylase 65 (GAD65) autoABs) in a large consecutive TAOS patient cohort, to characterize (b) clinical profiles of seropositive versus seronegative individuals and to find (c) potential evidence for other autoABs. […] Serological testing in a large consecutive TAOS patient series revealed seropositivity for anti-GAD65 autoABs as the most frequent neuroAB.

• #24 Adult-onset temporal lobe epilepsy suspicious for autoimmune pathogenesis: Autoantibody prevalence and clinical correlates | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0241289

  These data support the potential presence of so far unrecognized autoABs in patients with TAOS. […] The criteria of limbic syndrome have been recently defined in a strict manner. […] Here, we report on a large consecutive series of patients newly referred to a large Epilepsy Center over more than three years suffering from temporal lobe adult-onset seizures (TAOS) with clinical findings suggestive of an autoimmune origin. […] Our present study goes beyond serological testing for neurological ABs by analyzing neuroAB negative patients but screening positive for autoABs putatively targeted against not yet characterized protein structures. […] The use of additional screening tests (IIFT / immunoblots) may be regarded supportive and complementary to specific autoAB tests in individuals with clinical characteristics of possible autoimmune encephalitis seropositive in screening assays but negative for specific neuronal or onconeuronal autoABs with the perspective to define new forms of autoAB related (limbic) encephalitis. […] The present data point to the importance of considering autoimmune mechanisms in patients with the leading symptom of adult onset temporal seizures may encourage further research on this topic and the development of tailored treatments.

• #25 Molecular Mechanisms behind Initiation of Focal Seizure in Temporal Lobe Epilepsy: Computational Study | IntechOpen

  https://www.intechopen.com/chapters/72555

  Epilepsy is a noncommunicable disease of the brain that affects people of all ages. The chapter aims to identify protein targets and their mechanism of action behind temporal lobe epilepsy. […] The most appropriate route for initiation of seizure was observed to be route 3. It describes the dysregulated signal transduction from adenosine A1 receptor (ADORA1) to gamma-aminobutyric acid (GABA) B receptor 1 (GABBR1). This causes electrical imbalance and hyper-excitation of neurons that lead to focal seizure. […] The downregulation of GABA causes electrical imbalance in the brain and hence leads to focal seizure. […] The interactions were later segregated into smaller routes to understand the flow of information inside the brain during a seizure. […] The starting point for the current study of routes was finalized to be adenosine A1 receptor (ADORA1), while the last (effector molecule) was chosen to be gamma-aminobutyric acid B receptor 1 (GABBR1), we have limited our hypothesis between these two proteins.

• #26 Identification and validation of diagnostic biomarkers for temporal lobe epilepsy related to ferroptosis and potential therapeutic targets | Scientific Reports

  https://www.nature.com/articles/s41598-025-89390-6

  Ferroptosis pathway activation is potentially correlated with temporal lobe epilepsy (TLE). […] However, the diagnostic significance and mechanism of ferroptosis-related genes (FRGs) in TLE require further investigation. […] It can be inferred that the activation of the ferroptosis pathway is potentially related to epilepsy and the death of hippocampal neurons. […] Notably, research on ferroptosis induced by aberrant iron metabolism and distribution has highlighted hippocampal neuronal death as a potential cause of the onset and progression of mTLE with cognitive defect. […] These studies suggest that ferroptosis may play a significant role in the development of mTLE, and activation of the ferroptosis pathway may offer novel perspectives for early diagnosis and therapeutic improvement of mTLE.

• #27 Identification and validation of diagnostic biomarkers for temporal lobe epilepsy related to ferroptosis and potential therapeutic targets | Scientific Reports

  https://www.nature.com/articles/s41598-025-89390-6

  Nevertheless, the diagnostic significance of ferroptosis-related genes (FRGs) in mTLE and their mechanism of action require further investigation. […] The accumulation of ROS exacerbates the neuronal loss caused by epileptic seizures in TLE. […] Oxidative stress is one of the main pathophysiological causes of TLE. […] Moreover, oxidative stress, increased ROS, and iron overload lead to severe lipid peroxidation, a hallmark of ferroptosis. […] Therefore, exploring diagnostic biomarkers of ferroptosis in TLE can help clarify the mechanisms underlying this disease and identify potential therapeutic targets. […] Previous studies have not elucidated the genes dependent on ferroptosis in TLE neurons. […] The gene and protein expression levels were confirmed in animal tissue samples. […] These findings indicate the potential of these biomarkers as a novel focus for identifying TLE, and targeted therapy against these genes could effectively improve TLE symptoms. […] Our investigation revealed that the differentially expressed FRGs (CBS, SHMT1, RIN3, QDPR, and PLPP4) in TLE have high diagnostic value and could serve as new biological markers for early TLE diagnosis, offering fresh insights into its pathogenesis and treatment.

• #28 Temporal Lobe Epilepsy (TLE): Causes, Symptoms & Treatment

  https://my.clevelandclinic.org/health/diseases/17778-temporal-lobe-seizures

  Treatment for temporal lobe epilepsy may include: Antiseizure medications, Epilepsy surgery, Neurostimulation. […] Your healthcare provider may consider surgery if antiseizure medications aren’t successful or if a tumor causes epilepsy symptoms. […] Neurostimulation devices may be an option if medications aren’t successful or surgery isn’t a safe option. Neurostimulation uses an implanted device to deliver an electrical impulse to your temporal lobe. This treatment gradually reduces seizures over time.

• #29 Temporal Lobe Epilepsy (for Parents) | Nemours KidsHealth

  https://kidshealth.org/en/parents/temporal-lobe-epilepsy.html

  Kids with temporal lobe epilepsy have seizures that start in one of the temporal lobes of the brain. The seizures in temporal lobe epilepsy are focal seizures. Focal seizures begin in one area of the brain, and may or may not spread to other areas of the brain. Infections, brain injury, a tumor, genetic mutations, or changes in brain structure all can cause temporal lobe epilepsy. Babies who have a febrile seizure that lasts for 15 minutes or longer have a higher risk for developing the condition later on. Seizures usually get better with medicine. If medicines don’t control the seizures, doctors may recommend surgery or neurostimulation. In many cases, epilepsy surgery can lead to very good results for patients with temporal lobe epilepsy. […] It’s important to keep your child safe during a seizure.

• #30 Hippocampal low-frequency stimulation prevents seizure generation in a mouse model of mesial temporal lobe epilepsy | eLife

  https://elifesciences.org/articles/54518

  Mesial temporal lobe epilepsy (MTLE) is the most common form of focal, pharmacoresistant epilepsy in adults and is often associated with hippocampal sclerosis. Here, we established the efficacy of optogenetic and electrical low-frequency stimulation (LFS) in interfering with seizure generation in a mouse model of MTLE. […] We found that stimulation at 1 Hz for 1 hr resulted in an almost complete suppression of spontaneous seizures in both hippocampi. […] Furthermore, LFS for 30 min before a pro-convulsive stimulus successfully prevented seizure generalization. […] Taken together, our results suggest that hippocampal LFS constitutes a promising approach for seizure control in MTLE. […] In MTLE with hippocampal sclerosis, however, the efficacy of HFS is rather variable between patients.

• #31 New Drug Candidate to Treat TLE – BioTechniques

  https://www.biotechniques.com/drug-discovery-development/small-molecule-shows-promise-in-treating-temporal-lobe-epilepsy/

  A novel drug candidate to treat temporal lobe epilepsy (TLE) has been identified, which suppresses TLE-induced neuroinflammation and curbs seizures. […] Research has found that connexin-based gap junctions and hemichannels in brain glial cells in TLE play a role in neuroinflammation. […] The research team identified an organic molecule that selectively blocks connexin hemichannels in glial cells, called D4. Neuroinflammation and seizures can be exacerbated when glutamate and other molecules leak from reactive glial cells into the extracellular environment via hemichannels, a process that alters synapses. D4 is able to prevent this from occurring, thereby reducing neuroinflammation and curbing TLE seizures. […] We have found a very promising new drug candidate for treating epilepsy that works through a new mechanism blocking connexin hemichannels. Our findings also highlight the important involvement of neuroinflammation in neurological disorders such as epilepsy.

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