The “Unusual Suspects” in Spinal Pain

About 81% of patients with neck or low back pain will either have a joint (facet) or disc problem causing their pain; treat both, combined with therapy aimed at the soft tissues and we almost have all your bases covered. But what about the 10-20% of cases that seem to be unresponsive to conservative treatment or even more invasive interventions like injections or surgery.  In this newsletter I would like to briefly touch on a few lesser known pain generators of the spine. Identifying how they present is key in diagnosing and treating these cases

Vertebral endplate

The vertebral endplate is present on either side of each vertebra in the spine, and is thought to be one of the weakest links of the spine.  The end plate has extensive nerve supply making it very sensitive to injury.  These injuries typically happen with vertical loading mechanisms that cause disc injury, think falling straight down on you behind, dropped weight on your head or car accident injuries. Typical presentation is pain along the midline of the spine worsened by stationary positions and transitions from seated to standing.  This can occur with or without apparent disc injury.  We can confirm injury to the endplate when MR imaging demonstrates Modic changes (inflammation in the bone) or Schmorles nodes, although the presence of these findings is not essential for diagnosis.

Thecal Sac Compression

The thecal sac is a combination of tissues that covers and protects the spinal cord and nerves. The front side of the thecal sac (also the side facing the disc) is more densely innervated by nerves than the back of it. Pain from this region is often triggered by either physical compression by an injured disc or inflammatory irritation (discussed more below). We can pick this up on physical examination when a test called a straight leg raise test reproduces pain in the lower back but does not cause any leg pain. Recent studies suggest that this maneuver causes stretching of the thecal sac, known conveniently as the “thecal tension sign” and could indicate irritation near the structure.

Inflammatory Chemical Mediators
Acute injury to the spinal tissue often brings about an inflammatory response. This is followed by release of inflammatory mediators including cytokines, TNF-α, neurotropins and interlukens.  These chemicals play a role in amplifying the pain signal coming from the injured tissue as well as other structures around it. For example, a disc herniation can be “leaky” of these inflammatory chemicals and cause irritation of the nerve roots and the feeling of radiating pain to the arms or legs, even in the absence of true nerve “pinch”. In fact the same can occur in an injured and leaky facet joint, producing radiating symptoms even in the absence of disc injury!

Granulation Tissue

Ok, so we are talking about the disc again here, BUT…in this case we are not discussing acute injury to the disc itself but rather the changes in the disc tissue that follow an injury. The occurrence of disc injuries typically takes route from the inside out. This means the nucleus tears through the inner layers of tough fiber ring and makes its way outwards. Pain is not perceived until the tear reaches the outer one-third of the annulus which is innervated by nerve fibers.  The healing process of this tear involves “plugging” it with what we call granulation tissue which does not exhibit the properties of full tensile collagen making it weaker and more susceptible to reinjury. More importantly, the deposition of granular tissue comes with deeper infiltration of the nerves into the disc, and increased expression of pain receptors, making the disc more sensitive and recording pain more frequently.