[Levodopa-responsive parkinsonism-dystonia due to a traumatic injury of the substantia nigra].
نویسندگان
چکیده
3. Kuroki S, Saida T, Nukina M, Yoshioka M, Seino J. Three patients with ophthalmoplegia associated with Campylobacter jejuni. Pediatr Neurol. 2001;25:71—4. 4. Willison HJ, Yuki N. Peripheral neuropathies and anti-glycolipid antibodies. Brain. 2002;125:2591—625. 5. Kaida K, Kusunoki S. Antibodies to gangliosides and ganglioside complexes in Guillain—Barré syndrome and Fisher syndrome: mini-review. J Neuroimmunol. 2010;223:5—12. 6. Nagashima T, Koga M, Odaka M, Hirata K, Yuki N. Continuous spectrum of pharyngeal—cervical—brachial variant of Guillain—Barré syndrome. Arch Neurol. 2007;64:1519— 23. 7. Koga M, Yoshino H, Morimatsu M, Yuki N. Anti-GT1a IgG in Guillain—Barré syndrome. J Neurol Neurosurg Psychiatry. 2002;72:767—71. 8. Kaida K, Kamakura K, Ogawa G, Ueda M, Motoyoshi K, Arita M, et al. S. GD1b-specific antibody induces ataxia in Guillain—Barré syndrome. Neurology. 2008;71:196—201. 9. Odaka M, Yuki N, Hirata K. Anti-GQ1b IgG antibody syndrome: clinical and immunological range. J Neurol Neurosurg Psychiatry. 2001;70:50—5. 10. Santos-García D, Llaneza M, Macias M, Fuente-Fernández R. Multiple cranial neuropathy associated with herpes simplex virus infection and anti-GM2 immunoglobulin M antibodies. J Clin Neuromuscul Dis. 2009;10:199—201. 11. Susuki K, Koga M, Hirata K, Isogai E, Yuki N. A Guillain—Barré syndrome variant with prominent facial diplegia. J Neurol. 2009;256:1899—905. 12. Ortiz N, Sabaté MM, García N, Santafe MM, Lanuza MA, Tomas M, et al. Effect of anti-GM2 antibodies on rat sciatic nerve: electrophysiological and morphological study. J Neuroimmunol. 2009;208:61—9. 13. Korinthenberg R, Schessl J, Kirschner J, Mönting JS. Intravenously administered immunoglobulin in the treatment of childhood Guillain—Barré Syndrome: a randomized trial. Pediatrics. 2005;116:8—14.
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ورودعنوان ژورنال:
- Neurologia
دوره 27 3 شماره
صفحات -
تاریخ انتشار 2012