Tomida M, Yamamoto T, Matsuzawa Y, Nakazima S, Uemura K
Department of Neurosurgery, Fujinomiya City General Hospital.
No Shinkei Geka. 1994 Jun;22(6):589-92.
A 35-year-female developed tetraparesis following a period of back pain, urinary retension and paraparesis. She was admitted to our hospital on September 22, 1990. Neurological examination revealed tetraparesis with a sensory level at C3. Deep tendon reflexes were hyperactive in all four extremities with bilateral Hoffmann and Babinski reflexes. Spinal MR imaging demonstrated cavity formation within the cervical cord, extending from C2 to C6 without any anomalies at the craniocervical junction including Chiari malformation. The cavity was not enhanced with Gd-DTPA. Cerebrospinal fluid (CSF) examination revealed no abnormality. Although a syringo-subarachnoid shunt was performed on October 18, 1990, her symptoms did not improve. On December 17, 1990, she developed optic neuritis in the right eye and her paraparesis deteriorated. Delayed metrizamide CT scans showed another syrinx from Th3 to Th9. Repeated CSF contained 37 cells/mm3, protein 88 mg% and sugar 49 mg%. CSF oligoclonal bands were present and the CSF myelin basic protein was 6.6 ng/ml (normal < 4). A pulse therapy of steroid improved her vision and paraparesis. However, she developed paraparesis again on October 29, 1991. A brain T2-weighted MR image demonstrated multiple periventricular high signal intensity spots. Her paraparesis improved again with steroid. MR images in September, 1992 revealed a cord atrophy and disappearance of the cavity. Based on these clinical courses and radiological findings, a definite diagnosis of multiple sclerosis (MS) was made. We think MS may have caused the syringomyelia.