I. Concept and pathological changes of discogenic cervical and low back pain
In recent years, many scholars have conducted in-depth research on the neuroanatomical biochemistry and biomechanics before and after intervertebral disc degeneration or injury, and people gradually realize that in the absence of disc herniation, lesions occurring inside the intervertebral disc can also cause cervical and low back pain
– This is called discogenic cervical and low back pain.
The pathological changes in discogenic cervical and lumbar pain are twofold: one manifests as an internal fracture of the disc annulus fibrosus, which is a tear in the inner, inner layer of the annulus fibrosus, and the other is the appearance of inflammatory granulation bands on top of the tear (discitis).
(intervertebral discitis), these pathological changes are called intradiscal disorders (IDD).
II. Pathogenesis of discogenic cervical and low back pain
1, the stimulation of intravertebral disc chemicals
In recent years, many studies have shown that the process of disc degeneration or injury can produce a large number of inflammatory mediators or degeneration products, and the stimulation of these chemicals on peripheral nerve fibers can make the nerve tissue in a hypersensitive state, which can cause pain under slight external stimulation.
2, the emergence of the posterior edge of the intervertebral disc fiber ring fissure
With the degeneration of the intervertebral disc, fissures gradually occur from the nucleus pulposus to the outer layer of the annulus fibrosus, and on the basis of the fissures, granulation tissue invades and inflammatory cells exude, forming an inflammatory granulation zone at the posterior edge of the annulus fibrosus of the intervertebral disc. In the process of producing inflammation, growth factors related to healing and growth also appear, and these growth factors act to cause degeneration and inflammation of the disc, further aggravating discogenic pain.
3, changes in mechanical pressure within the disc
At present, it is believed that due to the very high content of inflammatory mediators in the degenerated intervertebral disc, the injury receptors at the sinus nerve terminals are in a hypersensitive state under the action of inflammatory mediators, thus the pain threshold to mechanical pressure decreases, and nerve impulses can be generated under slight mechanical pressure stimulation.
Third, discogenic lower back pain
It is an extremely common clinical condition, accounting for 39% to 40% of cases, and is caused by various diseases within the intervertebral disc (e.g. degeneration, endplate injury, etc.) stimulating pain receptors within the disc. Loss-of-function lower back pain, which is not clinically associated with radiculopathy and has no radiological evidence of nerve root compression, can be described as chemically mediated discogenic pain.
1. Diagnosis
There is no gold standard for diagnosis, but it is generally believed that the following conditions must be met: (1) recurrent lower back pain symptoms lasting >6 months. (2) The persistent lower back pain is aggravated in sitting position without radicular symptoms. (3) Positive discogram or MR showing typical lesions with low signal in the disc and high signal in the posterior part of the annulus fibrosus.
The presentation of MR of discogenic low back pain with a lesioned disc showing low signal on T2-weighted images, i.e., black disc syndrome, along with a high signal area at the posterior edge of the fibrous annulus, such MR highly supports the diagnosis of discogenic low back pain, but requires a combination of clinical manifestations and positive discography findings.
A, Recurrent symptoms of lower back pain, but the duration is less than 6 months
B, persistent lower back pain aggravated in sitting position, presenting radicular symptoms
C, positive discography or MR performance typical of the lesion disc high signal, posterior to the fibrous ring