A Practical Guide to Treatment of Childhood Absence Epilepsy

Kessler, Sudha Kilaru; McGinnis, Emily

doi:10.1007/s40272-019-00325-x

Cited by 74 publications

(58 citation statements)

References 64 publications

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“…There were no pronounced automatisms or myoclonia. CAE is an idiopathic, generalized epilepsy with a typical onset between 4-10 years of age (Kessler and Mcginnis, 2019). While affected children were generally believed to have a normal neurological and cognitive development, an increased risk of attention deficit and subsequent academic difficulties has been reported (Masur et al, 2013).…”

Section: Eeg-based Functional Network Analysis In Epilepsymentioning

confidence: 99%

The brain as a complex network: assessment of EEG‐based functional connectivity patterns in patients with childhood absence epilepsy

Leitgeb¹,

Šterk²,

Petrijan³

et al. 2020

Epileptic Disorders

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The human brain is increasingly seen as a dynamic neural system, the function of which relies on a diverse set of connections between brain regions. To assess these complex dynamical interactions, formalism of complex networks was suggested as one of the most promising tools to offer new insight into the brain's structural and functional organization, with a potential also for clinical implications. Irrespective of the brain mapping technique, modern network approaches have revealed fundamental aspects of normal brain-network organization, such as small-world and scale-free patterns, hierarchical modularity, and the presence of hubs. Moreover, the utility of these approaches, to gain a better understanding of neurological diseases, is of great interest. In the present contribution, we first describe the basic network measures and how the brain networks are constructed on the basis of brain activity data in order to introduce clinical neurologists to this new theoretical paradigm. We then demonstrate how network formalism can be used to detect changes in EEG-based functional connectivity patterns in six paediatric patients with childhood absence epilepsy. Notably, our results do not only indicate enhanced synchronicity during epileptic episodes but also reveal specific spatial changes in the electrical activity of the brain. We argue that the network-based evaluation of functional brain networks can provide clinicians with more detailed insight into the activity of a pathological brain and can also be regarded as a support for objective diagnosis and treatment for various neurological diseases.

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Section: Eeg-based Functional Network Analysis In Epilepsymentioning

confidence: 99%

The brain as a complex network: assessment of EEG‐based functional connectivity patterns in patients with childhood absence epilepsy

Leitgeb¹,

Šterk²,

Petrijan³

et al. 2020

Epileptic Disorders

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“…Children with CAE often suffer absence seizures during which children lose consciousness and stare blankly. Children with CAE have a risk for psychosocial and behavioral comorbidities and may develop persistent absence seizures or other types of epilepsy ( Kessler and McGinnis, 2019 ). CAE mostly occurs in school-age children, ranging from 6 to 12 years of age, and the morbidity of CAE is higher in females than in males.…”

Section: Introductionmentioning

confidence: 99%

“…Childhood absence epilepsy is considered primary generalized epilepsy. On electroencephalography (EEG), seizures are characterized by a highly recognizable pattern of generalized (bilateral, symmetric, and synchronous) 3-Hz spike and wave discharges (SWDs) ( Kessler and McGinnis, 2019 ). However, an increasing number of studies have found that CAE was more likely to have focal brain origins that were responsible for absence seizures ( Westmijse et al, 2009 ; Kim et al, 2011 ; Tenney et al, 2013 ; Rozendaal et al, 2016 ; Kokkinos et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Multifrequency Dynamics of Cortical Neuromagnetic Activity Underlying Seizure Termination in Absence Epilepsy

Sun

Gao

Miao

et al. 2020

Front. Hum. Neurosci.

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Purpose This study aimed to investigate the spectral and spatial signatures of neuromagnetic activity underlying the termination of absence seizures. Methods Magnetoencephalography (MEG) data were recorded from 18 drug-naive patients with childhood absence epilepsy (CAE). Accumulated source imaging (ASI) was used to analyze MEG data at the source level in seven frequency ranges: delta (1–4 Hz), theta (4–8 Hz), alpha (8–12 Hz), beta (12–30 Hz), gamma (30–80 Hz), ripple (80–250 Hz), and fast ripple (250–500 Hz). Result In the 1–4, 4–8, and 8–12 Hz ranges, the magnetic source during seizure termination appeared to be consistent over the ictal period and was mainly localized in the frontal cortex (FC) and parieto-occipito-temporal junction (POT). In the 12–30 and 30–80 Hz ranges, a significant reduction in source activity was observed in the frontal lobe during seizure termination as well as a decrease in peak source strength. The ictal peak source strength in the 1–4 Hz range was negatively correlated with the ictal duration of the seizure, whereas in the 30–80 Hz range, it was positively correlated with the course of epilepsy. Conclusion The termination of absence seizures is associated with a dynamic neuromagnetic process. Frequency-dependent changes in the FC were observed during seizure termination, which may be involved in the process of neural network interaction. Neuromagnetic activity in different frequency bands may play different roles in the pathophysiological mechanism during absence seizures.

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“…Different types of seizures require the use of different antiepileptic drugs: phenobarbital and phenytoin are often used as the first choice for treating epileptic seizures [33] . And for absence seizure, ethosuximide is often used as the primary therapeutic drug [34] . As a classic antiepileptic drug, VPA has a good therapeutic effect on many types of epilepsy.…”

Section: Discussionmentioning

confidence: 99%

Sodium valproate protects against neuronal ferroptosis in epilepsy via suppressing lysyl oxidase

Qin

Jia

et al. 2020

Preprint

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Background and purpose:Epilepsy is a chronic neurological disease that is characterized by repetitive seizures. Seizures-related complications such as cognitive deficits, anxiety and sleep disorders seriously impact the life quality of patients.Antiepileptic drugs are widely used for the treatment of epilepsy. Sodium valproate is served as the first-line antiepileptic drugs and possesses various pharmacological effects on the brain. Sodium valproate exerts neuroprotective effects in acute nervous system diseases such as ischemic brain damage by inhibiting oxidative stress.However, the mechanism of neuroprotection of sodium valproate in epilepsy is unclear. Lysyl oxidase (Lox) is a monoamine oxidase that acts on extracellular matrix collagen and elastin and it can promote accumulation of oxidative stress. Our previous studies have confirmed that Lox is involved in ferroptosis, a novel iron-dependent and lipid peroxidation-mediated cell death pathway, during epilepsy. In this study, we would like to investigate whether sodium valproate can exert neuroprotective effects on kainic acid-induced epileptic seizures by inhibiting Lox-mediated ferroptosis. Methods: Epileptic mouse models were established by intracranial injection of 250 ng/μl kainic acid on right hippocampus. Sodium valproate and ferroptosis inhibitors were administrated by intraperitoneal injecting. The epileptic behavior of the mice within 4 hours was recorded after intracranial injection of kainic acid. Mouse hippocampus was acquired to analyze the mRNA expression of prostaglandin-endoperoxide synthase 2 (PTGS2) and the production of 4-hydroxynonenal (4-HNE). In vitro, the protective effects of sodium valproate on glutamate-induced HT22 cell damage model was assessed by PI/Hoechst staining; The levels of PTGS2, 4-HNE and lipid ROS were analyzed by RT-qPCR, western blot and flow cytometry, respectively. RT-qPCR and Western blot analysis the mRNA and protein expression of Lox in the glutamate-induced HT22 cell damage model. The Lox overexpression model was established by intracranial injection of AAV on right hippocampus. Results: Pretreatment with sodium valproate and ferroptosis inhibitors could significantly alleviate the epileptic seizures in the kainic acid induced epilepsy mouse model. Western blot and RT-qPCR results showed that sodium valproate and ferroptosis inhibitors significantly inhibited the levels of 4-HNE and PTGS2. PI/Hoechst staining showed that 1 mM sodium valproate exerted protective effect on glutamate-induced HT22 cell injury model. There was no significant difference observed between sodium valproate and ferroptosis inhibitors co-intervention group and sodium valproate intervention group on glutamate-induced cell injury model. And sodium valproate could significantly inhibit the production of lipid reactive oxygen species and 4-HNE. The expression of Lox was significantly increased in the glutamate-induced HT22 cell injury model, which could be reversed by pretreatment of sodium valproate. And β -aminopropionitrile (a specific inh...

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A Practical Guide to Treatment of Childhood Absence Epilepsy

Cited by 74 publications

References 64 publications

The brain as a complex network: assessment of EEG‐based functional connectivity patterns in patients with childhood absence epilepsy

The brain as a complex network: assessment of EEG‐based functional connectivity patterns in patients with childhood absence epilepsy

Multifrequency Dynamics of Cortical Neuromagnetic Activity Underlying Seizure Termination in Absence Epilepsy

Sodium valproate protects against neuronal ferroptosis in epilepsy via suppressing lysyl oxidase

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