• H Openshaw.
• Department of Neurology, City of Hope National Medical Center, Duarte, CA 91010-3000, USA.
• Biol. Blood Marrow Transplant. 1997 Oct 1; 3 (4): 202-9.

AbstractPeripheral neuropathy after bone marrow transplantation can produce motor disability with significant morbidity and mortality, particularly when the neuropathy occurs within the first few months of the transplant. Most of these severe neuropathies have demyelinating features on electrophysiologic tests and histopathology, characteristic of immunologically-mediated neuropathies. The specific immune mechanism is uncertain. It is possible that cyclosporin, FK-506, and interferon-alpha may all trigger immunologically mediated neuropathies in rare patients. Transplants in patients with pre-existing demyelinating neuropathy may result in abrupt exacerbation of the neuropathy. Other causes of severe neuropathies include high-dose cytosine arabinoside and critical illness polyneuropathy. Less severe neuropathies with primarily sensory deficits may result from etoposide conditioning, thalidomide treatment for graft-versus-host disease, and the chemotherapeutic agents cisplatin and paclitaxel when used at high-dose with peripheral stem cell support. When encountering patients with disabling motor neuropathies, transplant physicians must identify (with the aid of nerve conduction tests) those neuropathies that are likely to be immunologically mediated and then empirically add or alter immunosuppressant therapies. Unfortunately, experience has been too limited to suggest specific regimens or the optimal sequence of immunosuppressant therapies.

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