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Wakamoto H.,Ehime Rehabilitation Center for Children | Nagao H.,Ehime University
Neurology Asia | Year: 2011

People with epilepsy (PWE) can have cognitive and behavioral disturbances caused by many factors, including epileptic seizures, interictal electroencephalographic discharges, brain pathology, psychological factors, and side effects of antiepileptic drugs (AEDs). Recent studies suggest that factors other than seizures themselves play a crucial role in the cognitive dysfunction in PWE. Neuropsychologic deficits due to cognitive effects of interictal epileptic activity have been demonstrated (transitory cognitive impairment). With regard to the cognitive side effects of AEDs, new generation drugs have a less significant negative impact compared to older AEDs. PWE are more likely to have neuropsychiatric co-morbidities (depression, anxiety, and aggression), which should be attended to. Increasing evidence suggests that subtle cognitive and behavioral disorders can be seen in association with benign epilepsy of childhood with centrotemporal spikes.

Fukuda M.,Ehime University | Hino H.,Ehime University | Suzuki Y.,Ehime University | Takahashi H.,Ehime University | And 2 more authors.
Acta Neurologica Belgica | Year: 2014

Febrile seizures (FS) are recognized as an antecedent to the development of temporal lobe epilepsy with hippocampal sclerosis (TLE-HS), but it is unclear whether prolonged FS are a direct cause of TLE-HS. Here, we used a rat model of infantile FS to study the effects of inflammatory cytokines on seizure susceptibility and neuronal death in adults. Prolonged hyperthermia-induced seizures (pHS) were induced in male Lewis rats at post natal day (P) 10. Cytokines were administered twice intranasally, once immediately after pHS and once the following day. The effects of intranasal interleukin (IL)-1β or tumor necrosis factor (TNF) α were tested in rats undergoing a single episode of pHS (P10) and in rats undergoing repeated pHS (P10 and P12). Seizure susceptibility was tested at P70-73 by quantifying the seizure onset time (SOT) after kainic acid administration, and neuronal cell injury and gliosis in adulthood. SOT significantly reduced in rats receiving IL-1β together with repeated pHS, whereas no significant effects were seen in rats receiving IL-1β after a single pHS episode, or in rats receiving TNFα. Hippocampal neuronal cell loss was observed in the CA3 region of rats receiving IL-1β together with repeated pHS; however, there was no significant change in gliosis among each group. Our results are consistent with the hypothesis that excessive production of IL-1β after repeated prolonged FS can enhance adult seizure susceptibility and neuronal cell death, and might contribute to the development of TLE-HS. © 2013 Belgian Neurological Society.

Shigemi R.,Matsuyama Shimin Hospital | Fukuda M.,Ehime University | Suzuki Y.,Ehime University | Morimoto T.,Ehime Rehabilitation Center for Children | Ishii E.,Ehime University
Brain and Development | Year: 2011

We report a case involving a 15-year-old boy with MELAS (G13513A mutation) who developed several stroke-like episodes in a short period of time. Intravenous administration of l-arginine during the acute phase of the stroke-like episodes reduced symptoms immediately, and oral supplementation of l-arginine successfully prevented further stroke-like episodes. This is the first report on effective l-arginine therapy in MELAS associated with the G13513A mutation. © 2010 The Japanese Society of Child Neurology.

Fukuda M.,Ehime University | Suzuki Y.,Ehime University | Hino H.,Ehime University | Kuzume K.,Ehime Prefectural Niihama Hospital | And 2 more authors.
Epilepsia | Year: 2010

Theophylline-associated seizures (TAS) often progress to prolonged or treatment-resistant convulsions. Theophylline is a nonselective adenosine receptor antagonist. Adenosine is an endogenous anticonvulsant that can terminate seizures. Fever and young age have been reported to be risk factors for TAS. To elucidate the mechanism of TAS, we investigated the effect of theophylline and adenosine receptor ligands on hyperthermia-induced seizures in juvenile rats. The treatment dose of theophylline or control saline was injected intraperitoneally 1 h before hyperthermia-induced seizures. The seizure threshold in the theophylline group was significantly lower and seizure duration was significantly longer than those in the control group. The addition of a selective adenosine A1 receptor agonist and an adenosine kinase inhibitor completely counteracted the effects of theophylline. Moreover, a selective A1 antagonist caused a significantly longer seizure duration compared with the control. These findings suggest that blockage of the adenosine A1 receptor is the main cause of TAS. © 2009 International League Against Epilepsy.

Wakamoto H.,Ehime Prefectural Central Hospital | Wakamoto H.,Ehime Rehabilitation Center for Children | Takahashi Y.,Shizuoka Institute of Epilepsy and Neurological Disorders | Ebihara T.,Ehime Prefectural Central Hospital | And 4 more authors.
Brain and Development | Year: 2012

Acute encephalitis with refractory, repetitive partial seizures (AERRPS) is a neurologic syndrome characterized by extraordinarily frequent and refractory partial seizures, which immediately evolve into refractory epilepsy. To elucidate the pathophysiology of AERRPS, we performed an immunologic study of an affected boy, revealing decreased natural killer (NK) cell activity in the peripheral blood mononuclear cells. IgG antibodies against the glutamate receptor (GluR)ε2, ζ1, and δ2 subunits were all positive in both the serum and cerebrospinal fluid (CSF). There were raised plasma concentrations of interleukin (IL)-2, IL-6, IL-10, tumor necrosis factor-α, and interferon-γ as well as an extremely elevated CSF level of IL-6. These findings suggest that AERRPS is immune-mediated encephalitis, in which both autoimmunity and exaggerated cytokine production are involved. NK cell dysfunction may be the underlying abnormality in this AERRPS case, which might have contributed to the production of GluR autoantibodies. © 2012 The Japanese Society of Child Neurology.

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