Different pharmacoresistance of focal epileptic spasms, generalized epileptic spasms, and generalized epileptic spasms combined with focal seizures

Takahashi, Yukitoshi; Ota, Akiko; Tohyama, Jun; Kirino, Tomoko; Fujiwara, Yumi; Ikeda, Chizuru; Tanaka, Shigeki; Takahashi, Junya; Shinoki, Toshihiko; Saito, Hiroshi; Inoue, Tetsuyoshi; Fujita, Hiroshi; Bonno, Motoki; Nagao, Masayoshi; Kaneko, Hideo

doi:10.1002/epi4.12560

Cited by 4 publications

(3 citation statements)

References 20 publications

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“…Our patients, consistent with previous findings, suggest a potential association between focal onset seizures and early onset in ESwoH. [6,7,9] Although previous reports indicate that in patients with IESS, the occurrence of focal onset seizures is associated with resistance to pharmacological treatments, [11]…”

Section: Discussionsupporting

confidence: 92%

“…Among these, 17 patients (25%) had concurrent focal onset seizures coincided with ES, [6,7,9] a ratio higher than that in the general population of IESS. [11] Previous reports included six patients of ESwoH with early onset up to three months of age (Supplementary Table 1), and three of those patients had focal onset seizures (50%). Our patients, consistent with previous findings, suggest a potential association between focal onset seizures and early onset in ESwoH.…”

Section: Discussionmentioning

confidence: 99%

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Three Patients of the Early Onset Epileptic Spasms without Hypsarrhythmia

Ohshiro,

Okanishi,

Ohta

et al. 2024

Neuropediatrics

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Introduction: Epileptic spasms without hypsarrhythmia occur when patients do not display hypsarrhythmia on EEG at the onset and throughout the clinical course. We report three patients of epileptic spasms in patients with early onset, all of whom experienced other types of seizures. Case reports: We detail three patients (two boys and one girl) of epileptic spasms without hypsarrhythmia, occurring between one and three months of age, with no abnormalities detected on neurometabolic analysis and brain MRI. Long-term video-EEG monitoring revealed epileptic spasms with focal onset seizures in two patients, and epileptic spasms followed by generalized tonic-clonic seizures in one patient. Hypsarrhythmia was never observed in repeated EEG examinations. Two patients achieved seizure freedom and improved development through treatment with topiramate alone or in combination with valproate, without requiring hormonal therapies or vigabatrin. The remaining patient achieved seizure freedom following administration of antiseizure medications, including topiramate, after a trial of ACTH therapy. Conclusion: We report the cases of three patients with early onset epileptic spasms without hypsarrhythmia. All patients achieved seizure freedom after topiramate treatment. Topiramate may be considered as a relatively effective anti-seizure medication for early onset epileptic spasms without hypsarrhythmia.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Three Patients of the Early Onset Epileptic Spasms without Hypsarrhythmia

Ohshiro,

Okanishi,

Ohta

et al. 2024

Neuropediatrics

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“…Epilepsy is a complex multifactorial disease, and it is difficult to perform an effective treatment because of pharmacoresistance [ 6 , 36 , 37 ]. In recent years, the research of epilepsy has been focused on discovering new therapeutic targets.…”

Section: Discussionmentioning

confidence: 99%

Blockade of Kv1.3 Potassium Channel Inhibits Microglia-Mediated Neuroinflammation in Epilepsy

Zhang

Liang

Zhang

et al. 2022

IJMS

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Epilepsy is a chronic neurological disorder whose pathophysiology relates to inflammation. The potassium channel Kv1.3 in microglia has been reported as a promising therapeutic target in neurological diseases in which neuroinflammation is involved, such as multiple sclerosis (MS), Alzheimer’s disease (AD), Parkinson’s disease (PD), and middle cerebral artery occlusion/reperfusion (MCAO/R). Currently, little is known about the relationship between Kv1.3 and epilepsy. In this study, we found that Kv1.3 was upregulated in microglia in the KA-induced mouse epilepsy model. Importantly, blocking Kv1.3 with its specific small-molecule blocker 5-(4-phenoxybutoxy)psoralen (PAP-1) reduced seizure severity, prolonged seizure latency, and decreased neuronal loss. Mechanistically, we further confirmed that blockade of Kv1.3 suppressed proinflammatory microglial activation and reduced proinflammatory cytokine production by inhibiting the Ca2+/NF-κB signaling pathway. These results shed light on the critical function of microglial Kv1.3 in epilepsy and provided a potential therapeutic target.

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