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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neuro-oncology 1 (1983), S. 125-130 
    ISSN: 1573-7373
    Keywords: somatosensory evoked potential ; misonidazole ; radiosensitizer ; demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Spinal and cortical somatosensory potentials were recorded weekly in rats treated with misonidazole at a dose of 300 mg/ kg/ day until clinical signs of severe neurotoxicity developed. After sacrifice, the brains, spinal cords and sciatic nerves were examined. All treated rats developed necrotic brain stem lesions identical to those previously described by Griffin and by us. Two rats had mild demyelination of spinal cord white matter tracts, but only one of these rats had changes in the SEPs. Interestingly, changes in the cervical and cortical SEP from this rat were only transient. We conclude that misonidazole neurotoxicity in the rat predominantly affects the brain stem nuclei adjacent to the fourth ventricle without involving the lemniscal pathways that are situated ventromedially in the brain stem. Therefore, somatosensory evoked potentials (SEPs) are not useful for the diagnosis of MISO neurotoxicity.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-7373
    Keywords: misonidazole ; radiosensitizer ; central neurotoxicity ; brain stem ; auditory evoked potential ; diagnosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Central neurotoxicity produced in rats by daily administration of 300 mg/ kg of misonidazole (MISO) 5 times/ week for 4–5 weeks (total dose = 6.0 gm/ kg) was evaluated weekly with brain stem auditory evoked potentials (BAEPs). Compared to untreated control rats, all treated rats had a prolongation of the I–IV interpeak latency (p 〈 0.005) at a mean of 13.2 ± 2.7 days at a cumulative dose of approximately 4.0 gm/ kg of MISO per rat. In some rats, the I–III and I–II interwave latencies were prolonged and waves III and IV were lost. Control rats did not show any significant alteration in BAEP latency or amplitude. Histopathologic examination of the brain stems of treated rats showed that necrotic lesions were present primarily in the nuclei of the tegmentum of the fourth ventricle, with scattered nuclear involvement in the cerebellar roof nuclei, inferior olive, and nucleus of the spinal tract of the trigeminal nerve. The cerebral cortex appeared to be normal in all treated rats. Changes in BAEPs caused by central neurotoxicity correlated with the histopathologic findings. We conclude that BAEPs are a sensitive method for evaluating MISO central neurotoxicity in the rat model.
    Type of Medium: Electronic Resource
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