The use of flexion-extension magnetic resonance imaging for evaluating signal intensity changes of the cervical spinal cord.

J Neurosurg Spine. 2009 Apr; 10(4): 366-73Guppy KH, Hawk M, Chakrabarti I, Banerjee AThe authors present 2 cases involving patients who presented with myelopathy. Magnetic resonance imaging of the cervical spine showed spinal cord signal changes on T2-weighted images without any spinal cord compression. Flexion-extension plain radiographs of the spine showed no instability. Dynamic MR imaging of the cervical spine, however, showed spinal cord compression on extension. Compression of the spinal cord was caused by dynamic anulus bulging and ligamentum flavum buckling. This report emphasizes the need for dynamic MR imaging of the cervical spine for evaluating spinal cord changes on neutral position MR imaging before further workup for other causes such as demyelinating disease.

Senescence mechanisms of nucleus pulposus chondrocytes in human intervertebral discs.

Spine J. 2009 Jun 18; Kim KW, Chung HN, Ha KY, Lee JS, Kim YYBACKGROUND CONTEXT: The population of senescent disc cells has been shown to increase in degenerated or herniated discs. However, the mechanism and signaling pathway involved in the senescence of nucleus pulposus (NP) chondrocytes are unknown. PURPOSE: To demonstrate the mechanisms involved in the senescence of NP chondrocytes. STUDY DESIGN/SETTING: Senescence-related markers were assessed in the surgically obtained human NP specimens. PATIENT SAMPLE: NP specimens remaining in the central region of the intervertebral disc were obtained from 25 patients (mean: 49 years, range: 20-75 years) undergoing discectomy. Based on the preoperative magnetic resonance images, there were 3 patients with Grade II degeneration, 17 patients with Grade III degeneration, and 5 patients with Grade IV degeneration. OUTCOME MEASURES: We examined cell senescence markers (senescence-associated beta-galactosidase [SA-beta-gal], telomere length, telomerase activity, p53, p21, pRB, and p16) and the hydrogen peroxide (H(2)O(2)) content as a marker for an oxidative stress in the human NP specimens. METHODS: SA-beta-gal expression, telomere length, telomerase activity, and H(2)O(2) content as well as their relationships with age and degeneration grades were analyzed. For the mechanism involved in the senescence of NP chondrocytes, expressions of p53, p21, pRB, and p16 in these cells were assessed with immunohistochemistry and Western blotting. RESULTS: The percentages of SA-beta-gal-positive NP chondrocytes increased with age (r=.82, p