Abstract: Method and devices are provided for treating subjects with Transcranial Magnetic Stimulation (TMS). According to some approaches, the methods and devices are configured for the treatment of ongoing seizures. Other approaches relate to the use of TMS as an antiepileptogenic or for use in determining preferential placement of intracranial probes.

Abstract: Inhibitors of NKCC1, such as bumetanide, when coadministered with inhibitors of GABA transaminase, such as vigabatrin, attenuate both the retinal toxicity and the intramyelinic edema.

Abstract: Patients are subject to a post-seizure treatment regime to separately inhibitor consecutive targets of an epileptogenic cascade comprising neurotransmitter receptor signaling, kinase/phosphatase activity, protein translation, and apoptosis or inflammation.

Abstract: Inhibitors of NKCC1, such as bumetanide, when coadministered with inhibitors of GABA transaminase, such as vigabatrin, attenuate both the retinal toxicity and the intramyelinic edema.

Abstract: Method and devices are provided for treating subjects with Transcranial Magnetic Stimulation (TMS). According to some approaches, the methods and devices are configured for the treatment of ongoing seizures. Other approaches relate to the use of TMS as an antiepileptogenic or for use in determining preferential placement of intracranial probes.

Abstract: Patients are subject to a post-seizure treatment regime to separately inhibitor consecutive targets of an epileptogenic cascade comprising neurotransmitter receptor signaling, kinase/phosphatase activity, protein translation, and apoptosis or inflammation.

Abstract: Methods are disclosed for modulating brain damage mediated by non-NMDA ionotropic glutamate receptor antagonists, as topiramate, in conditions such as periventricular leukomalacia, cerebral palsy, mental retardation and neonatal stroke.

Abstract: Methods and compositions for modulating brain damage mediated by non-NMDA ionotropic glutamate receptor antagonists are provided. Methods for inhibiting neuronal cell damage and death in the brain following an injury (e.g., ischemic/hypoxic injury) and methods for inhibiting cell damage and death in conditions such as periventricular leukomalacia, cerebral palsy, mental retardation, and neonatal stroke, are also provided. These methods generally involve treating a subject with a non-NMDA ionotropic glutamate receptor antagonist. Pharmaceutical and packaged formulations that include non-NMDA ionotropic glutamate receptor antagonists are also provided.