Neurotoxicity is a well-recognized sequela of cyclosporine, and the most common complications are tremor and altered mental status. Cyclosporine neurotoxicity can occur in one in 10 patients after liver transplantation. Behavioral signs include acute psychosis, restlessness, wide mood swings with inappropriate crying and laughing, cortical blindness, visual hallucinations, stupor, and akinetic mutism. Additionally, seizures, extrapyramidal symptoms, action myoclonus, and quadriparesis have been reported. In patients with neurological signs, cyclosporine levels are usually outside the normal range, and after lowering the dose or withholding administration, neurotoxicity clears in most cases. MRI abnormalities are consistent with cortical or white matter high-signal changes and may relate to demyelination or edema.y Although the mechanism of cyclosporine neurotoxicity has not been fully elucidated, one theory suggests that hypocholesterolemia may result in upregulation of the low-density lipoprotein receptors, which increases intracellular transport of cyclosporine. Access may be particularly high in the white matter with a relatively high density of low-density lipoprotein receptors. Another theory implicates endothelin, a potent vasoconstrictive neuropeptide, in combination with breakdown of the blood-brain barrier, resulting in local ischemia. Other possible etiological mechanisms of cyclosporine neurotoxicity include hypomagnesemia, hypertension, aluminum overload, and high-dose methylprednisolone administration. y , y Both the clinical manifestations and the neuro-imaging abnormalities of cyclosporine neurotoxicity usually resolve with a reduction or discontinuation of cyclosporine. y , y


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