Intradural disc herniation at L4/5 level causing Cauda equina syndrome: A case report

Intradural disc herniation has been documented rarely and the pathogenesis remains unclear. The region most frequently affected by intradural lumbar disc herniations is L4-5 level, and the average age of intradural disc herniations is between 50 and 60 years. Although magnetic resonance imaging is a valuable tool in the diagnosis of this disease, it is still difficult to make a definite diagnosis preoperatively. In this report, we described a 58-year-old male patient who presented with intermittent pain of low back and radiating pain of the both lower extremities for 2 years as well as decreased muscle strength of the both legs and dysfunction of urinary and defecation for 1 month. Lumbar disc herniation was diagnosed during the first clinical examination in the local hospital. Magnetic resonance imaging revealed a mass disc filling almost the entire spinal canal at the L4/5 level and a stalk connecting the mass to the intervertebral disc was detected in the sagittal T2-weighted image. The massive lesion caused cauda equina compression, resulting in dysfunction of urinary and defecation. Considering the mass's volume, bilateral hemilaminectomy, and transforaminal lumbar interbody infusion were performed. During the surgery, we found a perforation in the ventral dura and major part of herniated disc was located in the intradural space through it. The disc was carefully dissected from the surrounding nerve roots and the ventral dura and then totally removed. The defect on the ventral dura was sutured to prevent cerebrospinal fluid leakage. The patient presented complete recovery of the radiculopathy and cauda equina syndrome and significant improvement of muscle strength of both legs at 12 months follow-up. The diagnosis of intradural disc herniations is very difficult and mainly based on intraoperative and histopathological results. Surgical intervention is only effective method to manage this disease and to relieve symptoms and prevent severe neurological deficits.