Case 2- A 28-year-old male presented with neck, mid-back, and lumbar pain resulting from a traumatic injury in 1981 when the vehicle he was driving was rear-ended by a truck.

He could only work for short periods of time for the following 4-5 years due to neck, back, and leg pain. Analgesic and anti-inflammatory medication was the only form of therapy given at that time, with little effect. A 1988 consultation from a neurosurgeon led to a magnetic resonance imaging (MRI) and prescription medications. Again there was little in the way of improvement. In January 1992 he presented for chiropractic consultation with a pain level of 8/10 taking medications and using alcohol for pain relief. Sensory examination suggested an L1 hypoalgesia of both lower extremities, left greater than right. Vibratory sense was impaired in both legs, greater in the left. Because of the pain he had stopped working 2 months prior to consultation. SLR caused low back pain at 40 on the right and 30 on the left. He exhibited bilateral muscle spasm of the cervical and thoracolumbar spine with a decrease in range of motion of at least 50% in the cervical spine and 45% in the lumbar spine. He was experiencing daily mild to moderate headaches. Another MRI was obtained indicating a segmental hemivertebrae at the T7 level which may be partially fused to the T6 vertebral body. The disc space of T7-T8 was markedly narrowed with small posterior osteophytic spurs present. There was an angled kyphosis at this level and the spinal cord was draped over the angulated area.. Axial images showed that there was compression of the spinal cord in the AP dimension, with large amount of the epidural fat present and attenuation of the subarachnoid space surrounding the spinal cord. The lumbar spine showed a loss of lordosis and six non-rib-bearing vertebral bodies in the lumbar spine. Decreased disc space was seen at L2-L3 and L3-L4 Schmorl's type invaginations were note at the inferior endplate of L4, with bilateral posterior concavities noted at L5. Mild anterior spondylosis was also noted in the lumbar region. The cervical spine was straightened with mild spondylotic changes.

The patient underwent manipulation without anesthesia in an office setting for 3 months. Pain and muscle contraction limited full joint mobilization. The patient underwent the MUA procedure in the cervical and lumbar region which was carried out over 3 consecutive days with the patient under general anesthesia. Due to the angulation of the cord at the hemivertebral level, MUA was not attempted at he thoracic spine level per the request of the neurosurgeon. The patient also received physical therapy 3 times per day in the form of interferential current, ultrasound, moist heat, and massage in the cervical spine and lumbar spine. Post-MUA pain level was at a 2/10. Thirty days post-MUA the pain level was 3/10. His SLR was negative for back pain at 80 with hamstrings tightness. Braggard's sign was negative. Radicular signs and symptoms continued due to the above-mentioned thoracic spine angulations. His gait improved and he was able to toe walk on right and left. Lumbar range of motion was 80% of normal and cervical spine range of motion was 90% of normal. His headaches were occasional.

Follow-up office care consisted of manipulation without anesthesia to the cervical and lumbar spine with physical therapy, at a decreasing rate for a month with follow up visits to the neurosurgeon. This procedure decreased pain and increased range of motion in his cervical and lumbar spine. At 12 months post-MUA, his pain level was between 3/10 and 4/10. Some stiffness had returned to his neck and low back. Due to his osseous hemivertebra compression on the cord, the sensory deficit to his lower extremities persisted. Surgical removal of the hemivertebra with fixation of the segments of the thoracic spine was then performed. This surgical procedure was successful in restoring normal sensations to the lower extremities. Following the procedure he wore a thoracic brace for approximately 1 year.