I remember in one the courses that they discussed why discs are more likely to herniate posteriorly and I’m having trouble puzzling it out now. It seems like if the spine is tonically extended and the diaphragm becomes a postural stabilizer, that the anterior spinal ligaments would be working harder to compensate. So why is it that the posterior spinal ligaments are weaker and more prone to herniations?
Thanks for your question about disc pathomechanics and the tendancy for discs to herniate posteriorly. You correctly mentioned the muscle tone in the L AIC pattern directing the spine into a state of spinal extension and the altered role of the diaphragm as a postural stabilizer of the spine (pulling it forward into extension) in this position. Your question then asked about the contributing influence of the anterior vs posterior spinal ligaments in this extended position without discussing the destructive forces being directed into the annulus fibrosis portion of the disc. This discussion would help you better understand the resulting disc pathologies as the nucleus pulposis herniates through the compromised peripheral support of the annulus fibrosis regardless of the tautness or laxity of the spinal ligaments.
When the muscle tone from the AIC pattern directs the pelvis forward into flexion and the lumbar spine backward into spinal extension, the compressive forces between the vertebral bodies is greatest at the posterior aspect of the disc. This posterior compression is further exacerbated by the compressive influence of spinal torsion forces present in the discs as the upper lumbar spine and lower thoracic spine counter rotate back to the left because of the right oriented sacral and lower lumbar spine position in the L AIC pattern. These sagittal and transverse compressive forces lead to posterior disc dehydration, weakening, tearing and an overall compromise to the posterior aspect of the annulus fibrosis. The over-compressed and weakened posterior disc gives way to the wide variety of posterior bulges, posterior protrusions, posterior extrusions, etc as the nucleus pulposis is more easily forced through the weaker posterior annulus fibrosis as compared to the anterior annulus fibrosis, which rarely allows the nucleus to herniate anteriorly.
PRI’s approach to inhibiting extension muscle tone and negating the torsional influence of left vs right dystonia with breathing techniques does 3 powerful things to promote healthy disc tissue and function: 1) decompresses the posterior disc as the abdominals are used during exhalation to flex a hyperextended spine toward neutrality 2) relieves the torsional compression forces on the discs as left vs right muscle tone is balanced and the spine is rotated back to neutral and 3) allows the diaphragm’s crura to pull vertically on the lumbar spine (instead of forward into more extension) which decompress the discs upon inhalation. This happens as the central tendon lowers during inhalation and the vertically positioned crura pull upwardly against the opposition of the properly positioned abdominal wall when the diaphragm and rib cage have been drawn down into a neutral spine state called Zone of Apposition. This approach allows decompressed tri-planar movement across the previously restricted lumbar spine with ample support from the diaphragm, abdominal wall and anti-gravity postural muscles.