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Each of these factors renders neonatal seizures more difficult to treat, and therapy has been a vexing area for recent advances in this seizure category. Conversely, specific metabolic disorders have very special therapeutic considerations in the clinical setting of neonatal seizures which require a high index of clinical suspicion and rapid intervention for a successful outcome. The prototype is pyridoxine dependency, although pyridoxal 5\u2032\u2010phosphate dependency is a recently recognized but treatable neonatal epilepsy that deserves earmarked distinction. Clinicians must remain vigilant for these possibilities, including atypical cases where apparent seizure\u2010free intervals may occur. Folinic acid\u2010dependent seizures are allelic with pyridoxine dependency. Serine\u2010dependent seizures and glucose transporter deficiency may present with neonatal seizures and have specific therapy. A vital potassium channel regulated by serum ATP\/ADP ratios in the pancreas and brain may be mutated with a resultant neuroendocrinopathy characterized by development delay, epilepsy, and neonatal diabetes (DEND). This requires oral hypoglycaemic therapy, and not insulin, for neurological responsiveness. The startle syndrome of hyperekplexia, which mimics neonatal epilepsy, has been associated with laryngospasm and sudden death but is treated with benzodiazepines.<\/jats:p>","DOI":"10.1007\/s10545-009-1045-8","type":"journal-article","created":{"date-parts":[[2009,2,22]],"date-time":"2009-02-22T05:42:51Z","timestamp":1235281371000},"page":"204-213","source":"Crossref","is-referenced-by-count":35,"title":["New treatment paradigms in neonatal metabolic epilepsies"],"prefix":"10.1002","volume":"32","author":[{"given":"P. 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