A 33-year-old woman visited our hospital for slowly developing left leg weakness for 3 month without history of trauma. She also had progressive right side paresthesia which had developed six years ago. At that time, she had orthostatic headache and examinations to find cerebrospinal fluid (CSF) leakage were performed to rule out spontaneous intracranial hypotension (SIH) at another university hospital. However, there were no specific findings and orthostatic headache improved spontaneously. She has been suffering from nocturia and residual urine sense for five months with no sign of defecation disorder. Neurological examination revealed some indications of Brown-Sequard syndrome, such as decreased pain and temperature sensation (70/100) in the region below right T4 dermatome and muscular weakness (Grade IV) and a poor tactile and vibration sense (70/100) in the region below left T4 dermatome. Deep tendon reflex (DTR) was increased in both lower limbs. The blood test showed no specific finding. Initial MRI showed left antero-lateral displacement of the thoracic spinal cord in T3-4 with expanded subarachnoid space, but there was no abnormal signal change within the spinal cord (). With the diagnosis of ISCH, we performed T3 total laminectomy and found that spinal cord was herniated through the dural defect on the left antero-medial side of T3 level (). After reduction of herniated spinal cord into intra-dural space, we patched dural defect with Tacho-comb® both intradurally and extradurally (). Postoperatively, the patient's symptoms gradually alleviated. Decreased pain and temperature sensation improved by 90% and left side weakness was restored to full muscular strength after 10 days. Dysuria due to the neurogenic bladder was slowly cured and was fully recovered approximately 6 months later.
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.