PURPOSE: To describe cortical hyperintensities in proton density-weighted images in six patients with presumed cyclosporine-induced neurotoxicity. METHODS: In six patients with clinical evidence of cyclosporine-related encephalopathy, MR imaging was performed after the onset of symptoms and signs (mean, 24 days after liver transplantation). Five of these patients had serial MR imaging for a period that varied from 2 to 20 months. Along with the imaging studies, the patients' clinical status was evaluated and various laboratory parameters, including blood pressure and levels of cyclosporine, cholesterol, and magnesium, were monitored. RESULTS: In all six patients, initial MR studies showed hyperintensity of several cerebral gyri that was unequivocal only on proton density-weighted images. Although in five patients these signal abnormalities were limited to the cortex, one patient had increased signal in the subjacent white matter as well. In one patient, the images were also remarkable for areas of cortical hyperintensities on T1-weighted images. In another patient, cortical enhancement occurred after administration of gadopentetate dimeglumine, with a normal cortical signal on the precontrast images. The abnormal cortical signal began to fade after cyclosporine reduction, but in two patients it remained visible for at least 20 months. The neurologic symptomatology associated with cyclosporine-induced neurotoxicity included seizures (three patients), speech disorder (three patients), and disturbance of consciousness (three patients). CONCLUSION: Cyclosporine-induced neurotoxicity occurring in patients after liver transplantation appears to affect the cerebral cortex preferentially. Because its MR equivalent resembles changes resulting from hypoxic injury or cortically centered vasculitis, we suspect the underlying mechanism may be a vascular injury that results in cortical hypoperfusion.
PURPOSE: To describe cortical hyperintensities in proton density-weighted images in six patients with presumed cyclosporine-induced neurotoxicity. METHODS: In six patients with clinical evidence of cyclosporine-related encephalopathy, MR imaging was performed after the onset of symptoms and signs (mean, 24 days after liver transplantation). Five of these patients had serial MR imaging for a period that varied from 2 to 20 months. Along with the imaging studies, the patients' clinical status was evaluated and various laboratory parameters, including blood pressure and levels of cyclosporine, cholesterol, and magnesium, were monitored. RESULTS: In all six patients, initial MR studies showed hyperintensity of several cerebral gyri that was unequivocal only on proton density-weighted images. Although in five patients these signal abnormalities were limited to the cortex, one patient had increased signal in the subjacent white matter as well. In one patient, the images were also remarkable for areas of cortical hyperintensities on T1-weighted images. In another patient, cortical enhancement occurred after administration of gadopentetate dimeglumine, with a normal cortical signal on the precontrast images. The abnormal cortical signal began to fade after cyclosporine reduction, but in two patients it remained visible for at least 20 months. The neurologic symptomatology associated with cyclosporine-induced neurotoxicity included seizures (three patients), speech disorder (three patients), and disturbance of consciousness (three patients). CONCLUSION:Cyclosporine-induced neurotoxicity occurring in patients after liver transplantation appears to affect the cerebral cortex preferentially. Because its MR equivalent resembles changes resulting from hypoxic injury or cortically centered vasculitis, we suspect the underlying mechanism may be a vascular injury that results in cortical hypoperfusion.