Requiring a Cardiac Pacemaker in a Patient on

Tacrolimus is an immunosuppressive agent that inhibitscytokine synthesis and blocks T-cell development. It was introduced into clinical use at the University of Pitts-burgh in 1989 for liver rescue purposes, but has since be-come the standard immunosuppresant for almost all solid organ transplants. Neuropsychiatric adverse effects of tacrolimus therapy can be mild (headache, tremors, night-mares, vertigo, dysesthesiae, photophobia, mood distur-bances) or severe (bilateral optic neuropathy, akinetic mutism, seizures, encephalopathy).1 However, the exact mechanism of neurotoxicity of this drug remains unclear. Severe neurologic adverse effects can be seen in 21–32% of patients and can have a significant impact on the mor-bidity of transplant recipients.2 Guillain–Barré syndrome (GBS) is an acute, frequently severe, and fulminant polyradiculoneuropathy that is au-toimmune in nature. Miller Fisher syndrome (MFS) is a variant of GBS that presents as rapidly evolving ataxia and areflexia of limbs without weakness and ophthalmoplegia, often with pupillary abnormalities.3 The MFS variant ac-counts for approximately 5 % of all GBS cases. Anti-GQ1b immunoglobulin (Ig) G antibodies are found in>90 % of patients with MFS, and titers of IgG are highest early in the course. These antibodies are not found in other forms of GBS unless there is extraocular motor nerve involve-ment. The recognition of this syndrome is important as, despite its alarming nature, the course and outcome (after removing the offending cause and with early initiation of treatment with intravenous immunoglobulin or plasma-pheresis) are optimistic