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OKT3 neurotoxicity presenting as akinetic mutism.
Sean J Pittock1, Alejandro A Rabinstein, Brooks S Edwards
1Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Transplantation
|April 17, 2003
Summary
Muromonab-CD3 (OKT3) can cause severe neurotoxicity in heart transplant patients, presenting as a distinct neurologic syndrome. Discontinuation of OKT3 led to symptom resolution and imaging improvements, suggesting drug-induced encephalopathy.
Area of Science:
- Immunology
- Neurology
- Transplantation
Background:
- Muromonab-CD3 (OKT3), a monoclonal antibody targeting T lymphocytes, is a potent immunosuppressant for preventing allograft rejection in cardiac transplant recipients.
- Neurotoxicity is an uncommon side effect of OKT3, typically presenting as aseptic meningitis.
Observation:
- A severe neurologic syndrome, including akinetic mutism, blepharospasm, anomic aphasia, and delirium, was observed in an orthotopic heart transplant patient.
- Neuroimaging revealed meningeal enhancement on MRI and reduced tracer uptake on SPECT scans.
Findings:
- Discontinuation of OKT3 treatment resulted in the complete resolution of the patient's neuropsychiatric symptoms.
- Neuroimaging abnormalities normalized concurrently with the resolution of symptoms and the normalization of CD3+ lymphocyte counts.
Implications:
- Distinguishing drug-induced encephalopathy from other post-transplant neurologic complications can be challenging.
- MRI and cerebral perfusion studies like SPECT may aid in diagnosing OKT3-associated encephalopathy.
- Prospective SPECT studies are needed to better define the prevalence of OKT3-induced encephalopathy.