2016
DOI: 10.1212/wnl.0000000000002467
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Pearls & Oy-sters: Tacrolimus neurotoxicity presenting as an isolated brainstem lesion

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Cited by 8 publications
(3 citation statements)
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“…The drug has high lipophilicity, which facilitates its passage through blood-brain barrier to the brain, leading to cerebral vasodilatation and vasogenic edema [9]. Moreover, it can exert a direct neurotoxic effect, cytotoxic edema, direct endothelial damage, vasoconstriction, demyelination, or inhibition of the expression of drug-efflux pumps [10]. Radiologically, although the commonest presentation is described under the term of posterior reversible encephalopathy syndrome, several MRI studies have shown that imaging characteristics are variable and more heterogenous than commonly perceived [11].…”
Section: Discussionmentioning
confidence: 99%
“…The drug has high lipophilicity, which facilitates its passage through blood-brain barrier to the brain, leading to cerebral vasodilatation and vasogenic edema [9]. Moreover, it can exert a direct neurotoxic effect, cytotoxic edema, direct endothelial damage, vasoconstriction, demyelination, or inhibition of the expression of drug-efflux pumps [10]. Radiologically, although the commonest presentation is described under the term of posterior reversible encephalopathy syndrome, several MRI studies have shown that imaging characteristics are variable and more heterogenous than commonly perceived [11].…”
Section: Discussionmentioning
confidence: 99%
“…Isolated cases of brain stem involvement have also been reported. 13 , 14 In one study, 2/5 patients with tacrolimus toxicity had no reversal of white matter abnormalities upon discontinuation, even in the context of clinical improvement. 15 This appears similar to case 1 in which white matter lesions persisted after medication discontinuation.…”
Section: Discussionmentioning
confidence: 99%
“…Combined with a wide range in half-life (3.5–40.5 hours), normal plasma levels may not accurately reflect a patient's tacrolimus burden. 14 , 16 Studies have also found different genetic predispositions to drug pharmacokinetics that may increase susceptibility to CNS penetration, and presumably, optic nerve damage. 17 One case series suggested that transient breakdown in the blood-brain barrier due to graft-versus-host disease (GVHD) may also allow for increased CNS penetration.…”
Section: Discussionmentioning
confidence: 99%