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Christian Senft - One of the best experts on this subject based on the ideXlab platform.
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dislocated pacemaker electrode simulating focal Epileptic State in a patient with subdural hematoma case report and review of the literature
World Neurosurgery, 2016Co-Authors: Sae-yeon Won, Jan Mersmann, Volker Seifert, Markus Bruder, Christian SenftAbstract:Background Due to demographic changes, the number of patients with traumatic brain injury carrying a cardiac resynchronization therapy device is increasing. One of the common complications of subdural hematoma (SDH) is epilepsy, whereas one of the most frequent early complications after cardiac resynchronization therapy device implantation is lead dislocation. The latter might then cause unintended skeletal muscle stimulation that might be misinterpreted in seizure-prone patients. Case Description An 86-year-old female patient with an initially conservatively treated SDH on the right side presented with a tonic muscle contraction in her left arm 2 weeks after the trauma not responding to antiEpileptic therapy. A computed tomography scan revealed residual hematoma on the right side with regular, time-dependent resorption. The muscle contraction was misdiagnosed as a focal Epileptic State leading to evacuation of the chronic SDH. Additionally, routine postoperative chest radiographs were performed. Postoperatively, the tonic muscle contraction in her arm persisted. Chest radiographs revealed a dislocation of the left ventricular electrode, which appeared retracted into the left subclavian vein, next to the plexus brachialis. After deactivating the electrode, the alleged focal State ceased. Conclusions In case of refractory treatment of epilepsy, dislocation of pacemaker electrodes is a, most certainly, rare but possible differential diagnosis. Confirmation of electrode position and function is easily and quickly feasible and will help prevent futile seizure-directed therapy.
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Dislocated Pacemaker Electrode Simulating Focal Epileptic State in a Patient with Subdural Hematoma-Case Report and Review of the Literature.
World neurosurgery, 2016Co-Authors: Sae-yeon Won, Markus G Bruder, Jan Mersmann, Volker Seifert, Christian SenftAbstract:Due to demographic changes, the number of patients with traumatic brain injury carrying a cardiac resynchronization therapy device is increasing. One of the common complications of subdural hematoma (SDH) is epilepsy, whereas one of the most frequent early complications after cardiac resynchronization therapy device implantation is lead dislocation. The latter might then cause unintended skeletal muscle stimulation that might be misinterpreted in seizure-prone patients. An 86-year-old female patient with an initially conservatively treated SDH on the right side presented with a tonic muscle contraction in her left arm 2 weeks after the trauma not responding to antiEpileptic therapy. A computed tomography scan revealed residual hematoma on the right side with regular, time-dependent resorption. The muscle contraction was misdiagnosed as a focal Epileptic State leading to evacuation of the chronic SDH. Additionally, routine postoperative chest radiographs were performed. Postoperatively, the tonic muscle contraction in her arm persisted. Chest radiographs revealed a dislocation of the left ventricular electrode, which appeared retracted into the left subclavian vein, next to the plexus brachialis. After deactivating the electrode, the alleged focal State ceased. In case of refractory treatment of epilepsy, dislocation of pacemaker electrodes is a, most certainly, rare but possible differential diagnosis. Confirmation of electrode position and function is easily and quickly feasible and will help prevent futile seizure-directed therapy. Copyright © 2016 Elsevier Inc. All rights reserved.
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Dislocated Pacemaker Electrode Simulating Focal Epileptic State in a Patient with Subdural Hematoma—Case Report and Review of the Literature
World Neurosurgery, 2016Co-Authors: Sae-yeon Won, Jan Mersmann, Volker Seifert, Markus Bruder, Christian SenftAbstract:Background Due to demographic changes, the number of patients with traumatic brain injury carrying a cardiac resynchronization therapy device is increasing. One of the common complications of subdural hematoma (SDH) is epilepsy, whereas one of the most frequent early complications after cardiac resynchronization therapy device implantation is lead dislocation. The latter might then cause unintended skeletal muscle stimulation that might be misinterpreted in seizure-prone patients. Case Description An 86-year-old female patient with an initially conservatively treated SDH on the right side presented with a tonic muscle contraction in her left arm 2 weeks after the trauma not responding to antiEpileptic therapy. A computed tomography scan revealed residual hematoma on the right side with regular, time-dependent resorption. The muscle contraction was misdiagnosed as a focal Epileptic State leading to evacuation of the chronic SDH. Additionally, routine postoperative chest radiographs were performed. Postoperatively, the tonic muscle contraction in her arm persisted. Chest radiographs revealed a dislocation of the left ventricular electrode, which appeared retracted into the left subclavian vein, next to the plexus brachialis. After deactivating the electrode, the alleged focal State ceased. Conclusions In case of refractory treatment of epilepsy, dislocation of pacemaker electrodes is a, most certainly, rare but possible differential diagnosis. Confirmation of electrode position and function is easily and quickly feasible and will help prevent futile seizure-directed therapy.
Wolfgang Löscher - One of the best experts on this subject based on the ideXlab platform.
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Commonalities and differences in extracellular levels of hippocampal acetylcholine and amino acid neurotransmitters during status Epilepticus and subsequent epileptogenesis in two rat models of temporal lobe epilepsy.
Brain research, 2019Co-Authors: Sebastian Meller, Claudia Brandt, Wiebke Theilmann, Jochen Klein, Wolfgang LöscherAbstract:Chemically or electrically induced status Epilepticus (SE) in rodents is a commonly used method for induction of epilepsy. Structural and functional changes in the hippocampus play a pivotal role in epileptogenesis induced by SE. Although cholinergic mechanisms have long been thought to play an important role in the onset and propagation of Epileptic seizures, not much is known about the potential role of acetylcholine (ACh) in ictogenesis and epileptogenesis in SE models of temporal lobe epilepsy. Here we used in vivo microdialysis to determine extracellular levels of ACh and, for comparison, several amino acid transmitters in the ventral hippocampus during SE, epileptogenesis, and the chronic Epileptic State in two rat models of SE-induced epilepsy. SE was either induced by lithium-pilocarpine or by sustained electrical stimulation of the basolateral amygdala (BLA). ACh increased during SE in both models. Pretreatment with the muscarinic receptor antagonist scopolamine before BLA stimulation reduced SE severity and duration. In contrast to ACh, no consistent changes in amino acid levels were found during SE in the two models. During epileptogenesis and the chronic Epileptic State, the only commonalities found in both models were a decrease in ACh in Epileptic rats during the chronic Epileptic State and a decrease in aspartate during epileptogenesis. The data demonstrate complex, model-dependent alterations in extracellular levels of ACh and amino acid neurotransmitters and only few commonalities. Thus, data originating from only one model of post-SE epilepsy should not be generalized but may have a limited translational value for understanding ictogenesis or epileptogenesis.
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the enigma of the latent period in the development of symptomatic acquired epilepsy traditional view versus new concepts
Epilepsy & Behavior, 2015Co-Authors: Wolfgang Löscher, Lawrence J. Hirsch, Dieter SchmidtAbstract:A widely accepted hypothesis holds that there is a seizure-free, pre-Epileptic State, termed the "latent period", between a brain insult, such as traumatic brain injury or stroke, and the onset of symptomatic epilepsy, during which a cascade of structural, molecular, and functional alterations gradually mediates the process of epileptogenesis. This review, based on recent data from both animal models and patients with different types of brain injury, proposes that epileptogenesis and often subclinical epilepsy can start immediately after brain injury without any appreciable latent period. Even though the latent period has traditionally been the cornerstone concept representing epileptogenesis, we suggest that the evidence for the existence of a latent period is spotty both for animal models and human epilepsy. Knowing whether a latent period exists or not is important for our understanding of epileptogenesis and for the discovery and the trial design of antiepileptogenic agents. The development of antiepileptogenic treatments to prevent epilepsy in patients at risk from a brain insult is a major unmet clinical need.
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The enigma of the latent period in the development of symptomatic acquired epilepsy — Traditional view versus new concepts
Epilepsy & Behavior, 2015Co-Authors: Wolfgang Löscher, Lawrence J. Hirsch, Dieter SchmidtAbstract:A widely accepted hypothesis holds that there is a seizure-free, pre-Epileptic State, termed the "latent period", between a brain insult, such as traumatic brain injury or stroke, and the onset of symptomatic epilepsy, during which a cascade of structural, molecular, and functional alterations gradually mediates the process of epileptogenesis. This review, based on recent data from both animal models and patients with different types of brain injury, proposes that epileptogenesis and often subclinical epilepsy can start immediately after brain injury without any appreciable latent period. Even though the latent period has traditionally been the cornerstone concept representing epileptogenesis, we suggest that the evidence for the existence of a latent period is spotty both for animal models and human epilepsy. Knowing whether a latent period exists or not is important for our understanding of epileptogenesis and for the discovery and the trial design of antiepileptogenic agents. The development of antiepileptogenic treatments to prevent epilepsy in patients at risk from a brain insult is a major unmet clinical need.
Dieter Schmidt - One of the best experts on this subject based on the ideXlab platform.
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the enigma of the latent period in the development of symptomatic acquired epilepsy traditional view versus new concepts
Epilepsy & Behavior, 2015Co-Authors: Wolfgang Löscher, Lawrence J. Hirsch, Dieter SchmidtAbstract:A widely accepted hypothesis holds that there is a seizure-free, pre-Epileptic State, termed the "latent period", between a brain insult, such as traumatic brain injury or stroke, and the onset of symptomatic epilepsy, during which a cascade of structural, molecular, and functional alterations gradually mediates the process of epileptogenesis. This review, based on recent data from both animal models and patients with different types of brain injury, proposes that epileptogenesis and often subclinical epilepsy can start immediately after brain injury without any appreciable latent period. Even though the latent period has traditionally been the cornerstone concept representing epileptogenesis, we suggest that the evidence for the existence of a latent period is spotty both for animal models and human epilepsy. Knowing whether a latent period exists or not is important for our understanding of epileptogenesis and for the discovery and the trial design of antiepileptogenic agents. The development of antiepileptogenic treatments to prevent epilepsy in patients at risk from a brain insult is a major unmet clinical need.
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The enigma of the latent period in the development of symptomatic acquired epilepsy — Traditional view versus new concepts
Epilepsy & Behavior, 2015Co-Authors: Wolfgang Löscher, Lawrence J. Hirsch, Dieter SchmidtAbstract:A widely accepted hypothesis holds that there is a seizure-free, pre-Epileptic State, termed the "latent period", between a brain insult, such as traumatic brain injury or stroke, and the onset of symptomatic epilepsy, during which a cascade of structural, molecular, and functional alterations gradually mediates the process of epileptogenesis. This review, based on recent data from both animal models and patients with different types of brain injury, proposes that epileptogenesis and often subclinical epilepsy can start immediately after brain injury without any appreciable latent period. Even though the latent period has traditionally been the cornerstone concept representing epileptogenesis, we suggest that the evidence for the existence of a latent period is spotty both for animal models and human epilepsy. Knowing whether a latent period exists or not is important for our understanding of epileptogenesis and for the discovery and the trial design of antiepileptogenic agents. The development of antiepileptogenic treatments to prevent epilepsy in patients at risk from a brain insult is a major unmet clinical need.
Sae-yeon Won - One of the best experts on this subject based on the ideXlab platform.
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dislocated pacemaker electrode simulating focal Epileptic State in a patient with subdural hematoma case report and review of the literature
World Neurosurgery, 2016Co-Authors: Sae-yeon Won, Jan Mersmann, Volker Seifert, Markus Bruder, Christian SenftAbstract:Background Due to demographic changes, the number of patients with traumatic brain injury carrying a cardiac resynchronization therapy device is increasing. One of the common complications of subdural hematoma (SDH) is epilepsy, whereas one of the most frequent early complications after cardiac resynchronization therapy device implantation is lead dislocation. The latter might then cause unintended skeletal muscle stimulation that might be misinterpreted in seizure-prone patients. Case Description An 86-year-old female patient with an initially conservatively treated SDH on the right side presented with a tonic muscle contraction in her left arm 2 weeks after the trauma not responding to antiEpileptic therapy. A computed tomography scan revealed residual hematoma on the right side with regular, time-dependent resorption. The muscle contraction was misdiagnosed as a focal Epileptic State leading to evacuation of the chronic SDH. Additionally, routine postoperative chest radiographs were performed. Postoperatively, the tonic muscle contraction in her arm persisted. Chest radiographs revealed a dislocation of the left ventricular electrode, which appeared retracted into the left subclavian vein, next to the plexus brachialis. After deactivating the electrode, the alleged focal State ceased. Conclusions In case of refractory treatment of epilepsy, dislocation of pacemaker electrodes is a, most certainly, rare but possible differential diagnosis. Confirmation of electrode position and function is easily and quickly feasible and will help prevent futile seizure-directed therapy.
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Dislocated Pacemaker Electrode Simulating Focal Epileptic State in a Patient with Subdural Hematoma-Case Report and Review of the Literature.
World neurosurgery, 2016Co-Authors: Sae-yeon Won, Markus G Bruder, Jan Mersmann, Volker Seifert, Christian SenftAbstract:Due to demographic changes, the number of patients with traumatic brain injury carrying a cardiac resynchronization therapy device is increasing. One of the common complications of subdural hematoma (SDH) is epilepsy, whereas one of the most frequent early complications after cardiac resynchronization therapy device implantation is lead dislocation. The latter might then cause unintended skeletal muscle stimulation that might be misinterpreted in seizure-prone patients. An 86-year-old female patient with an initially conservatively treated SDH on the right side presented with a tonic muscle contraction in her left arm 2 weeks after the trauma not responding to antiEpileptic therapy. A computed tomography scan revealed residual hematoma on the right side with regular, time-dependent resorption. The muscle contraction was misdiagnosed as a focal Epileptic State leading to evacuation of the chronic SDH. Additionally, routine postoperative chest radiographs were performed. Postoperatively, the tonic muscle contraction in her arm persisted. Chest radiographs revealed a dislocation of the left ventricular electrode, which appeared retracted into the left subclavian vein, next to the plexus brachialis. After deactivating the electrode, the alleged focal State ceased. In case of refractory treatment of epilepsy, dislocation of pacemaker electrodes is a, most certainly, rare but possible differential diagnosis. Confirmation of electrode position and function is easily and quickly feasible and will help prevent futile seizure-directed therapy. Copyright © 2016 Elsevier Inc. All rights reserved.
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Dislocated Pacemaker Electrode Simulating Focal Epileptic State in a Patient with Subdural Hematoma—Case Report and Review of the Literature
World Neurosurgery, 2016Co-Authors: Sae-yeon Won, Jan Mersmann, Volker Seifert, Markus Bruder, Christian SenftAbstract:Background Due to demographic changes, the number of patients with traumatic brain injury carrying a cardiac resynchronization therapy device is increasing. One of the common complications of subdural hematoma (SDH) is epilepsy, whereas one of the most frequent early complications after cardiac resynchronization therapy device implantation is lead dislocation. The latter might then cause unintended skeletal muscle stimulation that might be misinterpreted in seizure-prone patients. Case Description An 86-year-old female patient with an initially conservatively treated SDH on the right side presented with a tonic muscle contraction in her left arm 2 weeks after the trauma not responding to antiEpileptic therapy. A computed tomography scan revealed residual hematoma on the right side with regular, time-dependent resorption. The muscle contraction was misdiagnosed as a focal Epileptic State leading to evacuation of the chronic SDH. Additionally, routine postoperative chest radiographs were performed. Postoperatively, the tonic muscle contraction in her arm persisted. Chest radiographs revealed a dislocation of the left ventricular electrode, which appeared retracted into the left subclavian vein, next to the plexus brachialis. After deactivating the electrode, the alleged focal State ceased. Conclusions In case of refractory treatment of epilepsy, dislocation of pacemaker electrodes is a, most certainly, rare but possible differential diagnosis. Confirmation of electrode position and function is easily and quickly feasible and will help prevent futile seizure-directed therapy.
Jan Mersmann - One of the best experts on this subject based on the ideXlab platform.
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dislocated pacemaker electrode simulating focal Epileptic State in a patient with subdural hematoma case report and review of the literature
World Neurosurgery, 2016Co-Authors: Sae-yeon Won, Jan Mersmann, Volker Seifert, Markus Bruder, Christian SenftAbstract:Background Due to demographic changes, the number of patients with traumatic brain injury carrying a cardiac resynchronization therapy device is increasing. One of the common complications of subdural hematoma (SDH) is epilepsy, whereas one of the most frequent early complications after cardiac resynchronization therapy device implantation is lead dislocation. The latter might then cause unintended skeletal muscle stimulation that might be misinterpreted in seizure-prone patients. Case Description An 86-year-old female patient with an initially conservatively treated SDH on the right side presented with a tonic muscle contraction in her left arm 2 weeks after the trauma not responding to antiEpileptic therapy. A computed tomography scan revealed residual hematoma on the right side with regular, time-dependent resorption. The muscle contraction was misdiagnosed as a focal Epileptic State leading to evacuation of the chronic SDH. Additionally, routine postoperative chest radiographs were performed. Postoperatively, the tonic muscle contraction in her arm persisted. Chest radiographs revealed a dislocation of the left ventricular electrode, which appeared retracted into the left subclavian vein, next to the plexus brachialis. After deactivating the electrode, the alleged focal State ceased. Conclusions In case of refractory treatment of epilepsy, dislocation of pacemaker electrodes is a, most certainly, rare but possible differential diagnosis. Confirmation of electrode position and function is easily and quickly feasible and will help prevent futile seizure-directed therapy.
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Dislocated Pacemaker Electrode Simulating Focal Epileptic State in a Patient with Subdural Hematoma-Case Report and Review of the Literature.
World neurosurgery, 2016Co-Authors: Sae-yeon Won, Markus G Bruder, Jan Mersmann, Volker Seifert, Christian SenftAbstract:Due to demographic changes, the number of patients with traumatic brain injury carrying a cardiac resynchronization therapy device is increasing. One of the common complications of subdural hematoma (SDH) is epilepsy, whereas one of the most frequent early complications after cardiac resynchronization therapy device implantation is lead dislocation. The latter might then cause unintended skeletal muscle stimulation that might be misinterpreted in seizure-prone patients. An 86-year-old female patient with an initially conservatively treated SDH on the right side presented with a tonic muscle contraction in her left arm 2 weeks after the trauma not responding to antiEpileptic therapy. A computed tomography scan revealed residual hematoma on the right side with regular, time-dependent resorption. The muscle contraction was misdiagnosed as a focal Epileptic State leading to evacuation of the chronic SDH. Additionally, routine postoperative chest radiographs were performed. Postoperatively, the tonic muscle contraction in her arm persisted. Chest radiographs revealed a dislocation of the left ventricular electrode, which appeared retracted into the left subclavian vein, next to the plexus brachialis. After deactivating the electrode, the alleged focal State ceased. In case of refractory treatment of epilepsy, dislocation of pacemaker electrodes is a, most certainly, rare but possible differential diagnosis. Confirmation of electrode position and function is easily and quickly feasible and will help prevent futile seizure-directed therapy. Copyright © 2016 Elsevier Inc. All rights reserved.
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Dislocated Pacemaker Electrode Simulating Focal Epileptic State in a Patient with Subdural Hematoma—Case Report and Review of the Literature
World Neurosurgery, 2016Co-Authors: Sae-yeon Won, Jan Mersmann, Volker Seifert, Markus Bruder, Christian SenftAbstract:Background Due to demographic changes, the number of patients with traumatic brain injury carrying a cardiac resynchronization therapy device is increasing. One of the common complications of subdural hematoma (SDH) is epilepsy, whereas one of the most frequent early complications after cardiac resynchronization therapy device implantation is lead dislocation. The latter might then cause unintended skeletal muscle stimulation that might be misinterpreted in seizure-prone patients. Case Description An 86-year-old female patient with an initially conservatively treated SDH on the right side presented with a tonic muscle contraction in her left arm 2 weeks after the trauma not responding to antiEpileptic therapy. A computed tomography scan revealed residual hematoma on the right side with regular, time-dependent resorption. The muscle contraction was misdiagnosed as a focal Epileptic State leading to evacuation of the chronic SDH. Additionally, routine postoperative chest radiographs were performed. Postoperatively, the tonic muscle contraction in her arm persisted. Chest radiographs revealed a dislocation of the left ventricular electrode, which appeared retracted into the left subclavian vein, next to the plexus brachialis. After deactivating the electrode, the alleged focal State ceased. Conclusions In case of refractory treatment of epilepsy, dislocation of pacemaker electrodes is a, most certainly, rare but possible differential diagnosis. Confirmation of electrode position and function is easily and quickly feasible and will help prevent futile seizure-directed therapy.