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First published on May 12, 2008
Journal of Child Neurology 2008, doi:10.1177/0883073808315617

Article

Leucoencephalopathy, Transverse Myelopathy, and Peripheral Neuropathy in Association With Glutamic Acid Decarboxylase-65 (GAD) Antibodies in Children With Cancer

Davonna S. Ledet, MS1, Rupert Handgretinger, MD2, Tulio E. Bertorini, MD3, Gregory A. Hale, MD4, Raul C. Ribeiro, MD5, and Raja B. Khan, MD6*

1 Division of Neurology, St Jude Children’s Research Hospital, Memphis, Tennessee
2 Department of Bone Marrow Transplant, St Jude Children’s Research Hospital
3 Department of Neurology, University of Tennessee, Memphis, Tennessee
4 Department of Bone Marrow Transplant, St Jude Children’s Research Hospital, Memphis, Tennessee
5 Department of Oncology, St Jude Children’s Research Hospital, Memphis, Tennessee
6 Divisions of Neurology and Neuro-Oncology, St Jude Children's Research Hospital, and Department of Neurology, University of Tennessee, Memphis, Tennessee

* To whom correspondence should be addressed. E-mail: rkhan{at}neuroclinic.org.


  Abstract
Neurologic toxicity may occur as a direct effect of cancer and its therapy or indirectly because of a dysfunctional immune system. The authors report the development of axonal neuropathy, myelopathy, and leucoencephalopathy associated with glutamic acid decarboxylase-65 (GAD) antibodies in 4 children with progressive cancer who were heavily pretreated. Three patients with refractory leukemia and 1 with Ewing sarcoma developed paraplegia with sensory level and dorsal column dysfunction. Three developed leucoencephalopathy and 1 died of neurologic disease. All had high serum titers of GAD antibodies during the progressive phase of the illness, and the antibody levels returned to normal with the stability of the neurologic disease. Three survivors are showing gradual recovery. This syndrome of central and peripheral nervous system toxicity may have resulted from chemotherapy toxicity or from immune dysfunction, as suggested by the high GAD antibody titers.


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