A 67-year-old female presented with complains slowly progressing bilateral leg weakness with associated chronic low back pain. There was no bowel or bladder involvement. On examination, motor and sensory exams were normal. Lab work was unremarkable. Magnetic resonance imaging (MRI) was performed which demonstrated anterior displacement of the spinal cord with an associated kink at T6 level with cerebrospinal fluid (CSF) pulsation artifacts in the posterior subarachnoid space []. High-resolution thin slice T2-weighted imaging demonstrated subtle small focus of herniated cord through the dural defect []. The findings favored spinal cord herniation instead of a posterior arachnoid cyst. To confirm the findings, a CT myelogram was performed which showed anterior cord kink at T6 with complete opacification of CSF posterior to the kinked and anteriorly displaced spinal cord confirming spinal cord herniation and excluding arachnoid cyst [].
A 52-year-old male fell 10 years before presentation from a scaffolding. Immediately after this fall, he noticed a diffuse sensibility loss in his right leg, which did not improve. Remarkably, he did not notice temperature changes or pain in that leg. Gradually, the strength in his left leg diminished. In recent years, this has clearly been progressive. In his lower left leg, he noticed paresthesias. He had a normal erectile function, but was unable to ejaculate.\nOn neurological examination, his left leg was slightly paretic. Vital and gnostic sensibility loss were present on the right side below T8. Within the L4 dermatoma on the left side, the vital sensibility was lost. The reflexes of both legs were pathologically increased with a Babinski’s sign on both sides. Radiological examination revealed a herniation of the SC at T4–T5 (Figure ).\nDuring surgery, the dura was opened after a midline approach with laminectomy T4 and T5. The dentate ligaments were transected on both sides, allowing some manipulation of the SC. On the ventral side, a defect of the dura was seen, along with many adhesions from the dura to the SC. These were sharply transected from both sides. Finally, the SC was freed from the dural defect and a mass originating from the ventral part of the SC was developed from the dural defect (Figure ). To prevent re-herniation, an artificial graft was gently placed in front of the SC covering the defect and was fixated laterally to the dural sleeve. Throughout the entire surgery, MEPs, SSEPs, and D-waves were monitored. During manipulation, the signals diminished twice. After waiting for several minutes, the signals returned to a normal level. Post-operatively, the patient did not notice any new complaints. The neurology is his right leg remained unaltered three months after surgery, whereas the symptoms in his left leg had improved.