The patient  is a physician came to the clinic 22-August-2004 complaining of ataxic gait with weal upper left limb with lesser degree of the left lower limb and hypalgesia of the ulnar distribution of the left upper limb with loss of sensation of the right lower limb below the knee. These complains as he claimed persisted for 4 months.

The patient  is a known hypertensive for 4 years in angiotec and under treatment with kemadrine and clopixol for schizophrenia  for several years, which he refused to give details about it.

On examination: The patient is unable to stand for Romberg test with severe weak flexion and extension of the left hand and the left triceps muscle. There is weak both feet muscles 4/5 and the left quadriceps muscle 4/5. The deep tendon reflexes are exaggerated in the left side of the body with mild dysarthria and flattening of the left nasolabial fold. Rossolimo and Hoffmann are positive in the left side and Babinski positive left side. There is loss of sensation for pin=brick below the right knee and the ulnar distribution of the left upper limb.

The clinical manifestations were of Brown-Sequard syndrome with left C5-6 involvement.  Suspicion about multiple sclerosis or transverse myelitis, for what MRI of the brain with MRI of the cervical spine were requested.

The patient came back 15-December-2004 with severe deterioration of his condition with increasing weakness of his four limbs with inability to walk. He brought with him the MRI investigations. MRI of the brain was almost normal, but the MRI of the cervical spine showed massive malacia of the spinal cord, partially old and partially edematous extending from C4 down to C7 with severe compression of the spinal cord due to extruded disc C5-6.

Considering that the malacia was more wide spread than the compressive lesion, still suspicion about transverse myelitis  or compression of the anterior spinal artery or arteriitis  remained.

Considering his severe deterioration, it was explained to the patient, that he needs surgery to remove the compression and that the morphologic changes of the spinal cord will remain, but his improvement is related to the nature of the pathologic changes of the spinal cord.

The patient was operated  and discectomy of the C5-6 was achieved with decompression of the dura at that level using the high-speed drill and micro-instrumentations. The dura was very thin and transparent, that the spinal cord could be seen through it. Smooth postoperative recovery. 

The patient  came to the clinic 28-December-2004: the wound clean. The power of the legs became normal  and power of the left hand normalized, but still weak left triceps muscle. The hypalgesia of the left upper limb disappeared , but the sensory deficit of the right lower limb still the same. The patient still unable to walk without help and there is gait disturbance.

The patient came 16-January-2005  with walking difficulty and upon examination of the power of the four limbs are 5/5 , but there is hypalgesia of the right side of the body below the right nipple. Hoffmann sign was positive in both sides. MRI of the cervical spine was requested.

The patient came 30-January-2005  with MRI of the cervical spine, showing good alignment of the cervical spine with mild regression of the the edematous part of the malacia and the usual reactionary changes of the endplates after surgery. Due to use of the high-speed drill the debris of the metal showing some artifacts, which could mimic compression at that level, but in the saggital views there is no compression.

The patient then came 27-March-2005 with new MRI of the cervical spine and MRI of the brain. The morphologic changes were the same. The patient still walking with difficulty, but the power of the four limbs were 5/5  and there is hypalgesia below the nipples both sides with preservation of sensation of the feet. The patient complained of urgency and frequency and constipation. The patient after that disappeared.

The patient  has severe compression at the cervical spine at C5-6 level with Brown-Sequard syndrome functionally copying the morphologic site. It is hard to tell if the patient has transverse myelitis at that level or coincidental arteritis at that level. If the surgeon is not sure about the nature of the lesion, the presence of compression must be eliminated, whatsoever the essential causative factor playing in the disease. At least, the compression must be resolved to prevent the multifactorial dilemma.

The patient got improvement of his upper limbs, which could be explained by surgery. (resolution of the radicular problems), which justify the role of surgery.

The patient in 09-January-2007 hold a claim against me to the Jordanian Medical Association, reporting, that he went to USA in Minnesota, where he was (reoperated?) 27-May-2005  and as he reporting grafting with fixation of C4-6 was done after what, he continued to deteriorate as claiming with paraplegia of both lower limbs with loss of urination and defecation control.

Now the situation is out of science and the legal portion of the problem taking precedence.

 More investigations must be done to explore his real problem and to see if any possible treatment must be provided to prevent further deterioration.