The patient came to the clinic 23-December-2008 complaining of difficult walking due to weak both lower limbs more the right  for two years and numbness both lower limbs with progressive course.

The patient suffered RTA 3 years ago with wedge fracture of D12. The patient receiving Xatral for prostatic hypertrophy for the last 2 months. The patient has Polio of the right lower limb since childhood.

MRI of the lumbar spine with MRMyelography was performed 17-December-2008 showing the wedging of D12 and severe stenosis at this level with malacia of the spinal cord at this level.

On examination: the patient  has exaggerated scoliotic stance. SLRS was 20 degrees right side with bilateral sciatica. He had weak dorsi and planterflexion both feet 4/5 with weak right quadriceps muscle 3/5 and adductors of the knees 4/5 and abductors of the right knee 3/5 and left knee 4/5.He has hypalgesia both lower limbs below the knees with signs of cauda equina syndrome more pronounced in the right side. Babinski was positive both sides with clonus both feet.

Using image-intensifier, theD11-12 level was identified and decompressive laminectomy of D11 and D12 was performed. The spinous processi of D11 and D12 were destroyed and replaced by cartilaginous structures, but the lamina were stable. After decompression the bony alignments were checked another time for stability. There was no epidural fat at the exposed dural sheath.  Routine closure of the wound with water-tight multilayer stitching.

Smooth postoperative recovery and the power of the left leg normalized with slight improvement of the power of the right lower limb.

The patient suffered RTA 3 years ago and he was not diagnosed at that time. The spinous processi were completely destroyed, which was found during surgery. The wedged old fracture was stable.

The malacia of the spinal cord could be due to the direct injury to the spine, or due to the repetitive microtrauma with progressive stenosis.

The progressive course of deterioration mostly related with callus formation around the facet joints, which caused secondary canal stenosis with escalation of the clinical manifestations.