An 18-year-old male patient presented to the neurosurgical clinic with the weakness of both lower limbs and inability to walk for the past 3 months. He had been operated in December of 2011, 4 months prior to presentation at another hospital to relieve paraplegia due to spinal cord compression. He regained full neurological function following the surgery for a period of 5 days after which he progressively declined until he lost function in both legs again. During this period, he underwent regular rehabilitative physiotherapy. Neurological examination showed spastic paraparesis with increased tone in both lower limbs. Power was 0/5. Deep tendon reflexes were 3+ bilaterally in the lower limbs. The sensory level was T12/L1. He was continent for urine and stool and anal tone was normal. A magnetic resonance imaging (MRI) with multi planar imaging of the spine done at presentation showed extensive epidural masses appearing slightly hyperintense on T1-weighted (T1W) image and isointense to adjacent bone on T2-weighted (T2W) image, involving the posterior aspect of the spinal canal at the level of T6–T11. Similar lesions were seen extending from L2 to L5. These masses were indenting the spinal cord from its posterior aspect and displacing it anteriorly. Maximum compression was seen at the level of T9–T10 with almost complete obliteration of the spinal canal and extension into the intervertebral foramina with nerve root compression. All vertebral bodies showed low to intermediate signal intensity signifying replacement of fatty marrow with hematopoietic tissue. There were no other abnormalities with the intervertebral discs or paravertebral tissue. Review of his available record from the first surgery revealed homozygous beta thalassemia major diagnosed in 1995, treated with regular blood transfusions and iron chelation. Unfortunately, the patient had lost his imaging studies done during his first surgery but reports if the studies were available. His laboratory work showed the following to be outside of normal limits; Hb% 8.5 g%, platelets 130,000/mm3, total bilirubin raised to 2.0 mg/dl (normal value up to 1.0 mg/dl), and alanine aminotransferase raised to 59 IU/L (normal up to 40 IU/L). An ultrasound of the abdomen done, at the time, showed moderately enlarged liver and spleen with no focal lesions, discounting the presence of EMH in these organs. An MRI done prior to the first surgery showed a single extra dural mass extending from T6 to L3, which appeared isointense to hyperintense on T1W and isointense on T2W. The location was posterior and toward the left side with displacement of the spinal cord anteriorly and toward the right. Subtle widening of the left exit canal was noted. Postcontrast images showed the lesion to be heterogeneously enhancing. These scans were unfortunately not available to the patient, but the radiology report was. The patient had undergone open surgery, and three “extradural tumor” specimens had been removed from level T2 to L3. Histopathology revealed normal bone with EMH and no evidence of granulomatous inflammation or malignancy. The patient was offered repeat surgery since he had shown complete resolution after his first surgery. The patient was placed in prone position with pads and gel foams to achieve a more comfortable position and to prevent pressure necrosis. A dorsal midline skin incision was made exactly over the previous incision. Bilateral laminectomies were done from T4 to T10 with sparing of the facet joints. The affected tissue appeared to be a dark reddish color and moderately adherent to the dura mater of the spinal cord. The masses were peeled away completely from the dura with ease, and no inadvertent durotomy was experienced. Blood loss was about 600 ml with the patient receiving packed cells during surgery. He had an uneventful recovery postoperatively with no complications. He was discharged on postoperative day 5. Histopathology of the resected tissue revealed bony trabecule with intervening hematopoietic tissue showing hypercellularity with erythroid and myeloid precursors and megakaryocytes. There was no evidence of malignancy. Follow-up at 1 month showed improved strength in both lower limbs (4+/5) with 2+ reflexes, and he was able to walk with support. He was referred to the Institute of Radiology and Nuclear Medicine, Peshawar, where he underwent two cycles of low dose radiotherapy in January 2013 to prevent recurrence. Follow-up at 2 years in October 2014 revealed he had completely recovered strength in both lower limbs and was able to walk without support and was able to function independently. He returned to his job as a computer operator for a private company during this time. MRI done at this time showed no evidence of residual mass or spinal cord compression.