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The phenotype is thought to arise due to deficits in cerebral energy production during and after fetal development, the accumulation of the potentially neurotoxic guanidinoacetate and other guanidino compounds, and possible abnormalities in ongoing neural signaling associated with abnormalities in the creatinephosphocreatine system (88)

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Possible association of CAG repeat polymorphism in KCNN3 encoding the potassium channel SK3 with oxaliplatin-induced neurotoxicity

PMID: 28753539 7 Biochemical, Molecular, and Clinical Characterization of Patients With Primary Carnitine Deficiency via Large-Scale Newborn Screening in Xuzhou Area

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