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.
A 48-year-old female presented 3 years after being thrown against a wall with a sequela of traumatic brain injury (TBI) with cerebral palsy, worsening myelopathy, and gait ataxia. She initially utilized a walker for ambulation, but progressed to wheelchair bound by the time of presentation [].\nShe underwent MRI studies of the brain and spine, plus EMG and NCV of the lower extremities. The thoracic MRI showed a ventral thecal sac irregularity with accompanying distortion of the ventral cord, consistent with “tethering;” cervical and lumbar studies were unremarkable []. The CT myelogram was suggestive of ventral dural tear and spinal cord herniation at the T7-8 levels and a diffuse ventral subdural fluid collection extending from T1 to T10 [].\nWe performed a T7-T8 laminectomy and unilateral facetectomy with removal of the right T7 pedicle and transverse process, exposing the T7-8 nerve roots []. After using ultrasounds to confirm the level, the right T7 nerve root was ligated. Using microsurgical technique, the dural defect was approached from the right side intra- and extradurally. Once the dural defect was identified, it was repaired with onlay and inlay DuraGen (Integra LifeSciences, Princeton, NJ, USA) and, after weighing the risk and benefits, we reinforced with DuraSeal (Integra LifeSciences, Princeton, NJ, USA) to minimize risk of postoperative CSF leak.\nPostoperatively, the patient went to rehab and within 2 months, she was ambulating with assistance using a walker. Her strength continued to improve at her 4-month and 1-year neurosurgical follow-up visits []. She is now ambulating independently with a walker. On repeat, MRI at 4 months postoperatively demonstrates postsurgical changes with a well-circumscribed right paraspinal fluid collection with minimal mass effect on the spinal cord []. There was no clinical or radiographic evidence of recurrent herniation, and the patient did not experience clinical signs or symptoms of CSF leak.