The purpose of the study was to perform an open, prospective study on various aspects of PGB effectiveness in Bulgarian patients with drug-resistant epilepsy. It was open, prospective and was performed with the participation of patients with epilepsy who attended the Clinic of Neurology at the University Hospital in Plovdiv, Bulgaria for a regular examination in cases of unsatisfactory seizure control or for adverse events from treatment. Patients completed diaries about seizure frequency, severity, and adverse events. There were regular documented visits at 3 or 6 months during the first year of treatment with pregabalin (PGB) and at 6 months or 1 year afterwards, with dynamic assessment of seizure frequency, severity, adverse events, and EEG recordings. PGB was applied as add-on treatment in 47 patients (24 males, mean age 34 years) with long duration of epilepsy, manifested with predominantly severe and very frequent partial, a combination of partial and generalized or generalized tonic-clonic seizures, refractory to the prescribed, usually combined treatment with a variety of AEDs. There was relatively mild, stable though, dynamic improvement of seizure severity, satisfactory seizure frequency reduction in 43.5% of participants, stable mean seizure frequency reduction (48-51%) from the 6-th to the 24-th month of the study, as well as a high and stable responder rate (58.7-62.5%) during the same period. New seizure types (generalized tonic-clonic, generalized atonic) appeared in 2 patients. The final clinical efficacy was higher in patients without seizure clusters or status epilepticus in the disease course. EEG improvement was found in a small percentage of patients (less than a third) and it did not correlate with clinical findings and their dynamics. Adverse events (dizziness/vertigo, sleepiness, memory impairment, increased weight, diplopia, lymphadenomegaly, impaired concentration, gastro-intestinal discomfort, transient leucopenia, rash, nausea, anxiety) were reported in 25.53% of patients. They were usually severe and became a cause of treatment termination in 12.8% of patients. In conclusion, PGB treatment is associated with: low and stable improvement of seizure severity, good and stable reduction of seizure frequency, a possibility of seizure control worsening, possible appearance of new seizure types, rare EEG dynamics, acceptable safety and tolerability.
{"title":"Various aspects of Pregabalin effectiveness as add-on therapy in patients with refractory epilepsy","authors":"E. Viteva","doi":"10.14800/MCE.1616","DOIUrl":"https://doi.org/10.14800/MCE.1616","url":null,"abstract":"The purpose of the study was to perform an open, prospective study on various aspects of PGB effectiveness in Bulgarian patients with drug-resistant epilepsy. It was open, prospective and was performed with the participation of patients with epilepsy who attended the Clinic of Neurology at the University Hospital in Plovdiv, Bulgaria for a regular examination in cases of unsatisfactory seizure control or for adverse events from treatment. Patients completed diaries about seizure frequency, severity, and adverse events. There were regular documented visits at 3 or 6 months during the first year of treatment with pregabalin (PGB) and at 6 months or 1 year afterwards, with dynamic assessment of seizure frequency, severity, adverse events, and EEG recordings. PGB was applied as add-on treatment in 47 patients (24 males, mean age 34 years) with long duration of epilepsy, manifested with predominantly severe and very frequent partial, a combination of partial and generalized or generalized tonic-clonic seizures, refractory to the prescribed, usually combined treatment with a variety of AEDs. There was relatively mild, stable though, dynamic improvement of seizure severity, satisfactory seizure frequency reduction in 43.5% of participants, stable mean seizure frequency reduction (48-51%) from the 6-th to the 24-th month of the study, as well as a high and stable responder rate (58.7-62.5%) during the same period. New seizure types (generalized tonic-clonic, generalized atonic) appeared in 2 patients. The final clinical efficacy was higher in patients without seizure clusters or status epilepticus in the disease course. EEG improvement was found in a small percentage of patients (less than a third) and it did not correlate with clinical findings and their dynamics. Adverse events (dizziness/vertigo, sleepiness, memory impairment, increased weight, diplopia, lymphadenomegaly, impaired concentration, gastro-intestinal discomfort, transient leucopenia, rash, nausea, anxiety) were reported in 25.53% of patients. They were usually severe and became a cause of treatment termination in 12.8% of patients. In conclusion, PGB treatment is associated with: low and stable improvement of seizure severity, good and stable reduction of seizure frequency, a possibility of seizure control worsening, possible appearance of new seizure types, rare EEG dynamics, acceptable safety and tolerability.","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"454 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76771195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Intractable epilepsy afflicts approximately 25% of children with epilepsy. Because antiepileptic medications (AEDs) share similar mechanisms of action aimed at affecting neuronal ion channels or neurotransmitter receptors, it is not surprising that the likelihood of additional AEDs resulting in significant seizure reduction is low with risks outweighing potential benefit. In addition, it is unclear if AEDs can modify the underlying process promoting seizures. Intravenous immunoglobulins (IVIg) and prednisone have been used as alternative therapies in children with intractable epilepsy after multiple AEDs have been tried unsuccessfully. Recent evidence has suggested that neuroinflammation may play a role in epileptogenesis giving credence to the use immune modulatory agents in refractory epilepsy. In this research highlight, we will discuss our recent study examining and comparing the use of IVIg and prednisone in treating intractable pediatric epilepsy.
{"title":"The Use of Intravenous Immunoglobulins and Prednisone in the Treatment of Intractable Pediatric Epilepsy","authors":"R. Tang-wai","doi":"10.14800/MCE.1571","DOIUrl":"https://doi.org/10.14800/MCE.1571","url":null,"abstract":"Intractable epilepsy afflicts approximately 25% of children with epilepsy. Because antiepileptic medications (AEDs) share similar mechanisms of action aimed at affecting neuronal ion channels or neurotransmitter receptors, it is not surprising that the likelihood of additional AEDs resulting in significant seizure reduction is low with risks outweighing potential benefit. In addition, it is unclear if AEDs can modify the underlying process promoting seizures. Intravenous immunoglobulins (IVIg) and prednisone have been used as alternative therapies in children with intractable epilepsy after multiple AEDs have been tried unsuccessfully. Recent evidence has suggested that neuroinflammation may play a role in epileptogenesis giving credence to the use immune modulatory agents in refractory epilepsy. In this research highlight, we will discuss our recent study examining and comparing the use of IVIg and prednisone in treating intractable pediatric epilepsy.","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89410883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The epileptic encephalopathies (EE) are a family of severe brain disorders manifesting early in life and characterized by spasms and/or intractable seizures. The relentless seizure activity impacts both cognitive and behavioral development in the patient . Many patients do not respond to typical anti-epileptic therapies and can experience early death. Of late, several novel mutations in newly revealed genes have been associated with the EEs. Through the efforts of such groups as the Epi4K and EuroEPINOMIC-RES consortiums, the Epilepsy Phenome/Genome Project and the Deciphering Developmental Disorders Study, de novo variants have surfaced in such genes as GABRB3, ALG13, GRIN1, NEDD4L, DNM1 and others . Whole-exome sequencing of patients has revealed 9 DNM1 variants . This research highlight describes our study of the mouse Dnm1 EE model to illustrate how certain classes of de novo variants may give rise to EEs and emphasize the contribution of specific neuronal populations to the comorbid phenotypes. Dynamin-1, the product of the DNM1 gene, is a large GTPase required for synaptic vesicle recycling in neurons . The highly brain specific Dynamin-1 is expressed during synaptogenesis through adulthood and undergoes alternative splicing resulting in the regulated expression of several splice variants.
{"title":"Separation of seizures from comorbidities in the Fitful mouse model of DNM1epileptic encephalopathy","authors":"R. Boumil, S. Asinof","doi":"10.14800/MCE.1028","DOIUrl":"https://doi.org/10.14800/MCE.1028","url":null,"abstract":"The epileptic encephalopathies (EE) are a family of severe brain disorders manifesting early in life and characterized by spasms and/or intractable seizures. The relentless seizure activity impacts both cognitive and behavioral development in the patient . Many patients do not respond to typical anti-epileptic therapies and can experience early death. Of late, several novel mutations in newly revealed genes have been associated with the EEs. Through the efforts of such groups as the Epi4K and EuroEPINOMIC-RES consortiums, the Epilepsy Phenome/Genome Project and the Deciphering Developmental Disorders Study, de novo variants have surfaced in such genes as GABRB3, ALG13, GRIN1, NEDD4L, DNM1 and others . Whole-exome sequencing of patients has revealed 9 DNM1 variants . This research highlight describes our study of the mouse Dnm1 EE model to illustrate how certain classes of de novo variants may give rise to EEs and emphasize the contribution of specific neuronal populations to the comorbid phenotypes. Dynamin-1, the product of the DNM1 gene, is a large GTPase required for synaptic vesicle recycling in neurons . The highly brain specific Dynamin-1 is expressed during synaptogenesis through adulthood and undergoes alternative splicing resulting in the regulated expression of several splice variants.","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"62 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76914584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Epilepsy as a common neurological disorder appears the sudden onset and self-termination in the cerebral cortical ictal discharges and tonic muscle contractions within a few minutes. The seizure onset is believed to be initiated by the synchronous activity of excitatory neurons and the weakness of inhibitory synapses. Current medications to suppress the seizure onset are applying exogenous reagents to enhance inhibitory synaptic transmission and block spike generation. After the treatments, many epileptic patients become insensitive to original medications and the pathogenesis in the elevated ratio of cortical excitation to inhibition is still present. The reasons for lack of long-term medical efficiency may include that the medical treatment is not neuron-specific and the seizure self-termination has not been taken into account. Therefore, new therapeutic strategies against epilepsy remains to be explored based on strengthening the endogenous mechanisms of seizure self-termination in a neuron-specific manner. We review the potential mechanism of seizure self-termination and give our thought in anti-epilepsy by strengthening endogenous seizure self-termination in different neuronal compartments.
{"title":"Neuron-specific mechanisms for epilepsy self-termination","authors":"Jin-Hui Wang, Wei Lu, Bo Wen","doi":"10.14800/MCE.716","DOIUrl":"https://doi.org/10.14800/MCE.716","url":null,"abstract":"Epilepsy as a common neurological disorder appears the sudden onset and self-termination in the cerebral cortical ictal discharges and tonic muscle contractions within a few minutes. The seizure onset is believed to be initiated by the synchronous activity of excitatory neurons and the weakness of inhibitory synapses. Current medications to suppress the seizure onset are applying exogenous reagents to enhance inhibitory synaptic transmission and block spike generation. After the treatments, many epileptic patients become insensitive to original medications and the pathogenesis in the elevated ratio of cortical excitation to inhibition is still present. The reasons for lack of long-term medical efficiency may include that the medical treatment is not neuron-specific and the seizure self-termination has not been taken into account. Therefore, new therapeutic strategies against epilepsy remains to be explored based on strengthening the endogenous mechanisms of seizure self-termination in a neuron-specific manner. We review the potential mechanism of seizure self-termination and give our thought in anti-epilepsy by strengthening endogenous seizure self-termination in different neuronal compartments.","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"67 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76700837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sonia Alonso-Alonso, Carmen Freire-Cobo, M. Vázquez-Illanes, Manuel Freire, G. Sierra-Paredes
SourceURL:file:///Macintosh%20HD/Users/cruz/Desktop/mol-cell-epi/MOL-CEL.doc We have previously shown that in vivo disruption of F-actin filaments induces acute and chronic seizures in rats and mice. On these basis, we have studied the effect of latrunculin A microperfusion in the mice hippocampus on seizure patterns, actin filaments and NMDA receptors. Latrunculin A (8 mg/ml) was perfused for three consecutive days into the mice hippocampus using microdialysis probes with continuous EEG and video monitoring. After microdialysis experiments, F-actin depolymerization and synaptic and extrasynaptic NR1 protein levels were investigated. Intrahippocampal latrunculin A microdialysis induced partial seizures during the third day of perfusion, and the animals started showing spontaneous partial seizures one month after treatment. Increased levels of extracellular glutamate via microdislysis probes induced seizures in treated mice. F-actin levels were significantly decreased, while NMDA receptor density increased both in synaptic and non-synaptic locations. These results support the hypothesis that actin disruption might be not just a consequence but also a possible cause of epileptic seizures. Actin depolymerization-induced seizures are related to an increase in synaptic and extrasynaptic NMDA receptors and to changes in the extracellular environment. We propose a new experimental model in mice to study the biochemical changes that may lead to chronic seizures, and a method for testing new antiepileptic drugs.
{"title":"Partial seizures induced by latrunculin A microperfusion in the mouse hippocampus: Role of extracellular glutamate and NMDA receptors","authors":"Sonia Alonso-Alonso, Carmen Freire-Cobo, M. Vázquez-Illanes, Manuel Freire, G. Sierra-Paredes","doi":"10.14800/MCE.608","DOIUrl":"https://doi.org/10.14800/MCE.608","url":null,"abstract":"SourceURL:file:///Macintosh%20HD/Users/cruz/Desktop/mol-cell-epi/MOL-CEL.doc We have previously shown that in vivo disruption of F-actin filaments induces acute and chronic seizures in rats and mice. On these basis, we have studied the effect of latrunculin A microperfusion in the mice hippocampus on seizure patterns, actin filaments and NMDA receptors. Latrunculin A (8 mg/ml) was perfused for three consecutive days into the mice hippocampus using microdialysis probes with continuous EEG and video monitoring. After microdialysis experiments, F-actin depolymerization and synaptic and extrasynaptic NR1 protein levels were investigated. Intrahippocampal latrunculin A microdialysis induced partial seizures during the third day of perfusion, and the animals started showing spontaneous partial seizures one month after treatment. Increased levels of extracellular glutamate via microdislysis probes induced seizures in treated mice. F-actin levels were significantly decreased, while NMDA receptor density increased both in synaptic and non-synaptic locations. These results support the hypothesis that actin disruption might be not just a consequence but also a possible cause of epileptic seizures. Actin depolymerization-induced seizures are related to an increase in synaptic and extrasynaptic NMDA receptors and to changes in the extracellular environment. We propose a new experimental model in mice to study the biochemical changes that may lead to chronic seizures, and a method for testing new antiepileptic drugs.","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79581974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective ：To investigate the abnormality of mossy fiber sprouting (MFS) and glial fibrillary acidic protein (GFAP) as well as neuronal loss in rats hippocampus during subclinical seizures following hypoxic cerebral insult. Methods ：Rats were assigned randomly into the control (n=12) and hypoxia group (n=91). Hypoxia was induced by treating the mice with 8% oxygen-nitrogen mixture gas, while control rats were treated with room air followed by the same procedures. According to the EEG records of epileptic discharges, hypoxia group rats were further divided into subclinical seizures group and non-subclinical seizures group. The changes in neuropathology, MFS in hippocampus and the expression of GFAP in cortex and hippocampus were examined by Nissl staining, Timm staining, immunohistochemistry staining and western-blot analysis, respectively. Results : 23.08% (21/91) rats exposed to hypoxia present subclinical seizures. Compared with non-subclinical seizures and control group, these mice showed significant neuronal loss of hippocampal CA1 and CA3 region as well as temporal cortex(P＜0.05) Also, as MFS scores in the hippocampal CA3 region increased (P<0.05), a higher expression of GFAP was detected, especially in hippocampal area (P＜0.05). However, the MFS score within inner molecular layer (IML) of the dentate gyrus (DG) was not significantly different among three groups mentioned above (P＞0.05). Conclusion ：In this study, we found the onset of subclinical seizures occurred following hypoxic brain injury in rats. Also, rats with epileptic discharges showed distinct neuronal loss, MFS in hippocampal CA3 subfield, and up-regulation of GFAP expression, which we proposed to be attributed to subclinical seizures following hypoxic cerebral damage.
{"title":"Mossy fiber sprouting in rats hippocampus of subclinical seizures following hypoxic brain injury","authors":"Xiu Chen","doi":"10.14800/MCE.300","DOIUrl":"https://doi.org/10.14800/MCE.300","url":null,"abstract":"Objective ：To investigate the abnormality of mossy fiber sprouting (MFS) and glial fibrillary acidic protein (GFAP) as well as neuronal loss in rats hippocampus during subclinical seizures following hypoxic cerebral insult. Methods ：Rats were assigned randomly into the control (n=12) and hypoxia group (n=91). Hypoxia was induced by treating the mice with 8% oxygen-nitrogen mixture gas, while control rats were treated with room air followed by the same procedures. According to the EEG records of epileptic discharges, hypoxia group rats were further divided into subclinical seizures group and non-subclinical seizures group. The changes in neuropathology, MFS in hippocampus and the expression of GFAP in cortex and hippocampus were examined by Nissl staining, Timm staining, immunohistochemistry staining and western-blot analysis, respectively. Results : 23.08% (21/91) rats exposed to hypoxia present subclinical seizures. Compared with non-subclinical seizures and control group, these mice showed significant neuronal loss of hippocampal CA1 and CA3 region as well as temporal cortex(P＜0.05) Also, as MFS scores in the hippocampal CA3 region increased (P<0.05), a higher expression of GFAP was detected, especially in hippocampal area (P＜0.05). However, the MFS score within inner molecular layer (IML) of the dentate gyrus (DG) was not significantly different among three groups mentioned above (P＞0.05). Conclusion ：In this study, we found the onset of subclinical seizures occurred following hypoxic brain injury in rats. Also, rats with epileptic discharges showed distinct neuronal loss, MFS in hippocampal CA3 subfield, and up-regulation of GFAP expression, which we proposed to be attributed to subclinical seizures following hypoxic cerebral damage.","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"34 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81493213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neurological diseases occupy a major chunk of the burden of Non Communicable disease all over the world. Epilepsy is one of the most important Neurological diseases in India. It has complex etiology and is characterized by recurrent seizures. The study was conducted to To study the clinicosocial profile of the epilepsy patients under study and to find out the predictors of seizure free status in them. A descriptive cross sectional study carried out in Neuromedicine OPD involving 315 diagnosed epilepsy patients selected by systematic random sampling. The selected patients and their caregivers were interviewed with the predesigned, pretested semistructured proforma. Data were compiled and analysed using SPSS software. Majority of the study subjects was in the age group of 16-30 years with completed primary education and were unskilled labours and belonged to class IV and V of Prasad’s economic status scale. Almost twenty four percent (23.8per cent) has their onset of fits between 11 to 15 years. Mean duration of epilepsy was 7.93 ± 6.44 years for males and 9.84 ± 7.96 years for females and the difference was not statistically significant ( p= 0.99). Family history of epilepsy was present in 14.3per cent cases. Almost 35.0per cent had complex partial seizure, 30.2per cent simple partial seizure and 26per cent had generalized tonic-clonic seizure. About 15.0per cent of the total participants reported to have some precipitating or provocating factors. Regarding the treatment received by the study subjects, 55.2per cent were on monotherapy and 44.8per cent on polytherapy.Family history of epilepsy and presence of addiction were found to be significant predictors of seizure free status in the study population .
{"title":"Neuroepidemiology of epileptic seizures: A study from a tertiary care setting of Eastern India","authors":"Abhik Sinha","doi":"10.14800/MCE.524","DOIUrl":"https://doi.org/10.14800/MCE.524","url":null,"abstract":"Neurological diseases occupy a major chunk of the burden of Non Communicable disease all over the world. Epilepsy is one of the most important Neurological diseases in India. It has complex etiology and is characterized by recurrent seizures. The study was conducted to To study the clinicosocial profile of the epilepsy patients under study and to find out the predictors of seizure free status in them. A descriptive cross sectional study carried out in Neuromedicine OPD involving 315 diagnosed epilepsy patients selected by systematic random sampling. The selected patients and their caregivers were interviewed with the predesigned, pretested semistructured proforma. Data were compiled and analysed using SPSS software. Majority of the study subjects was in the age group of 16-30 years with completed primary education and were unskilled labours and belonged to class IV and V of Prasad’s economic status scale. Almost twenty four percent (23.8per cent) has their onset of fits between 11 to 15 years. Mean duration of epilepsy was 7.93 ± 6.44 years for males and 9.84 ± 7.96 years for females and the difference was not statistically significant ( p= 0.99). Family history of epilepsy was present in 14.3per cent cases. Almost 35.0per cent had complex partial seizure, 30.2per cent simple partial seizure and 26per cent had generalized tonic-clonic seizure. About 15.0per cent of the total participants reported to have some precipitating or provocating factors. Regarding the treatment received by the study subjects, 55.2per cent were on monotherapy and 44.8per cent on polytherapy.Family history of epilepsy and presence of addiction were found to be significant predictors of seizure free status in the study population .","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"33 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84256752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Psychogenic non-epileptic seizures (PNES) is a relevant differential diagnosis in epilepsy clinics because of its high prevalence and impact on patient’s lives and health care services. An approach to the diagnosis and treatment of PNES is important, and many issues make the subject challenging. Video electroencephalography (VEEG) is considered the gold-standard for PNES diagnosis but there is still risk for false positive and false negative results, both with potential dire consequences. VEEG should be planned and analyzed with caution, as well as paired with other clinical variables in order to increase its predictive value. The frequent coexistence of epilepsy among PNES patients makes diagnosis and treatment even more complex. The clinician should always mind that possibility, which has important implications for diagnosis and treatment of the PNES. Patients’ understanding and acceptance of the disorder as well as health care professionals’ attitude towards the patients have impact on prognosis. Proper and coherent communication is important for patients’ acceptance of diagnosis, treatment, and prognosis.
{"title":"A review of the clinical approach and challenges to psychogenic non-epileptic seizures","authors":"P. Gordon, R. L. Marchetti","doi":"10.14800/MCE.369","DOIUrl":"https://doi.org/10.14800/MCE.369","url":null,"abstract":"Psychogenic non-epileptic seizures (PNES) is a relevant differential diagnosis in epilepsy clinics because of its high prevalence and impact on patient’s lives and health care services. An approach to the diagnosis and treatment of PNES is important, and many issues make the subject challenging. Video electroencephalography (VEEG) is considered the gold-standard for PNES diagnosis but there is still risk for false positive and false negative results, both with potential dire consequences. VEEG should be planned and analyzed with caution, as well as paired with other clinical variables in order to increase its predictive value. The frequent coexistence of epilepsy among PNES patients makes diagnosis and treatment even more complex. The clinician should always mind that possibility, which has important implications for diagnosis and treatment of the PNES. Patients’ understanding and acceptance of the disorder as well as health care professionals’ attitude towards the patients have impact on prognosis. Proper and coherent communication is important for patients’ acceptance of diagnosis, treatment, and prognosis.","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"15 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81782822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sensing, modeling, and neuromodulation technologies are profoundly advancing the practice of epilepsy surgery. Chronically implanted neural monitoring technologies developed for seizure termination and seizure prediction have each been found to be useful in unintended applications, specifically for the planning of resective surgery. We review and summarize the use of chronic monitoring in an unanticipated context in which it was found to be invaluable in the planning of surgery; this was observed in a pivotal study of a seizure detection and termination system. Monitoring of patients chronically in their normal ambulatory setting, as facilitated by this technology, allows unperturbed assessment of patients while on outpatient medication regimens and without the time and space constraints imposed by cost and infection risk inherent in subacute inpatient invasive monitoring. Five patients in the NeuroPace US pivotal trial underwent resective surgery which was subsequent to and enabled by chronic recordings from the implanted monitoring system. These resective surgeries were independent from the primary intended function of the implanted neural monitoring device. Chronic monitoring facilitated greater anatomical localization of the sources and allowed for a deeper understanding of the dynamic network behavior of interconnected seizure foci, thereby facilitating a substantially more sophisticated approach to resective surgery. In the NeuroPace trial, monitoring and analysis of chronic unlimited recording electrocorticography (CURE) from chronically implanted subdural and depth electrodes facilitated planning of resective surgery that resulted in near or complete seizure freedom in 4 patients. This series suggests that chronic recording of electrocorticographic signals is a therapeutic modality meritorious of further investigation. Note: This was analysis and study was performed on patients previously enrolled in the NeuroPace® RNS® Ststem Pivotal trial: http://clinicaltrials.gov/show/NCT00572195
{"title":"Chronic Recording Electrocorticography Guided Resective Epilepsy Surgery: Overview and Future Directions","authors":"D. Dilorenzo, E. Mangubat, M. Rossi, R. Byrne","doi":"10.14800/MCE.208","DOIUrl":"https://doi.org/10.14800/MCE.208","url":null,"abstract":"Sensing, modeling, and neuromodulation technologies are profoundly advancing the practice of epilepsy surgery. Chronically implanted neural monitoring technologies developed for seizure termination and seizure prediction have each been found to be useful in unintended applications, specifically for the planning of resective surgery. We review and summarize the use of chronic monitoring in an unanticipated context in which it was found to be invaluable in the planning of surgery; this was observed in a pivotal study of a seizure detection and termination system. Monitoring of patients chronically in their normal ambulatory setting, as facilitated by this technology, allows unperturbed assessment of patients while on outpatient medication regimens and without the time and space constraints imposed by cost and infection risk inherent in subacute inpatient invasive monitoring. Five patients in the NeuroPace US pivotal trial underwent resective surgery which was subsequent to and enabled by chronic recordings from the implanted monitoring system. These resective surgeries were independent from the primary intended function of the implanted neural monitoring device. Chronic monitoring facilitated greater anatomical localization of the sources and allowed for a deeper understanding of the dynamic network behavior of interconnected seizure foci, thereby facilitating a substantially more sophisticated approach to resective surgery. In the NeuroPace trial, monitoring and analysis of chronic unlimited recording electrocorticography (CURE) from chronically implanted subdural and depth electrodes facilitated planning of resective surgery that resulted in near or complete seizure freedom in 4 patients. This series suggests that chronic recording of electrocorticographic signals is a therapeutic modality meritorious of further investigation. Note: This was analysis and study was performed on patients previously enrolled in the NeuroPace® RNS® Ststem Pivotal trial: http://clinicaltrials.gov/show/NCT00572195","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90037177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Veena Jayant Khardenavis, Vikram Khardenavis, A. Deshpande
Although a specific definition is still lacking, the consensus seems to be that the increase in seizure frequency (at least twice the baseline) during specific phase of menstrual cycle of the female, is highly suspicious of a diagnosis of Catamenial epilepsy. Atleast 33% of females with medically refractory seizures in their reproductive age group have this underlying condition. Women with partial epilepsy are more prone to have catamenial epilepsy, however other epilepsy syndromes associated with catamenial epilepsy is also well known. The perimenstrual followed by periovulatory phases are the phases where the patient is susceptible to have clustering of seizures as a part of catamenial epilepsy. The low progesterone to estrogen ratio is a commonly observed biochemical finding during these times. Menopause is associated with drastic decrease in the frequency of catamenial epilepsy frequency. However, Acetazolamide,clobazam,hormonal therapy,GnRH analogues along with intermittent modification in the schedule of anti-epileptic medication( based on times of month when patient is most prone to have seizures) are some of the treatment options.
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