Natural History of the Degenerative Cascade

Published on 11/04/2015 by admin

Filed under Orthopaedics

Last modified 11/04/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1264 times

4 Natural History of the Degenerative Cascade

Anatomy and General Mechanisms of Pain

In order to understand the degenerative cascade of the spine, it is of paramount importance to understand the normal function of the different structures and how they interrelate with each other. The facet joints are designed to bear approximately 10% to 30% of the load in the lumbar spine, depending on the patient’s position. The articular cartilage that bears such loads is supported by the subchondral bone. The subchondral bone also serves to provide nutrition to the articular cartilage. The facet joints are diarthrodial synovial joints that have a capsule. The capsules together with the ligaments constrain joint motion. The medial and anterior capsule is formed by a lateral extension of the ligamentum flavum. The capsules and ligaments are innervated by primary articular branches from larger peripheral nerves and accessory articular nerves. Such nerves consist of both proprioceptive and nociceptive fibers. They are monitored by the central nervous system, and may perceive excessive joint motion (potentially due to instability or an injury) as a noxious stimulus and mediate a muscular reflex to counteract such excursions. Nociceptive free nerve endings and mechanoreceptors have been isolated in the human facet capsules and synovium. Such nerve endings may perceive chemical stimuli or mechanical stimuli such as instability, trauma, or capsular distention as noxious stimuli. Joint effusions, commonly seen on MRIs, may prevent such reflexes due to capsular distention, similar to a distended knee joint and absent patellar reflex. Substance P, a pain-related neuropeptide, has been identified in synovium. Higher concentrations have been found in arthritic joints. Additionally, capsular free nerve endings have been found to become sensitized in arthritic joints. This has caused otherwise dormant nerve endings to become reactive to motion that was perceived as normal in nonarthritic conditions.

The intervertebral disc is another significant component of the degenerative cascade. The sinuvertebral nerve innervates the posterior and posterolateral aspect of the intervertebral disc, as well as the posterior longitudinal ligament (PLL) and the ventral aspect of the thecal sac. The lateral and anterior aspect of the disc is innervated by the gray ramus communicans. These free nerve endings have been found primarily in the outer one third of the annulus, and have been found to be immunoreactive for painful neuropeptides. Some complex endings have been identified within the annulus as well. The considerable overlap of the descending and ascending nerve endings with branches of the sinuvertebral nerves of the adjacent one to two discs makes identifying the exact pain generator even more difficult when performing clinical diagnostic tests. Leakage of such neuropeptides out of the disc in the presence of annular tears, onto the nearby dorsal root ganglion (DRG), can cause irritation of the DRG and become another source of pain. The PLL fibers are closely intertwined with the posterior annulus. The PLL has been identified to contain a variety of free nerve endings. Hence any irritation of the posterior annulus and disc can cause irritation of these nerve endings. Such irritation can be mechanical secondary to pressure from a herniated disc, abnormal motion from instability, or mechanical incompetence of the annulus. Irritants can also be chemical such as low pH fluids, cytokines, or neuropeptides that can leak out from the disc via annular tears.

Cortical bone, bone marrow, and periosteum have been found to be innervated by nerves containing nociceptive neuropeptides such as calcitonin, gene-related peptides, and substance P. Periosteal elevation, such as in cases of infection, tumor, or hematoma, can be painful. Periosteal tears in cases such as fractures, inflammation, or subsidence (e.g., in osteoarthritic conditions) can cause pain. Vascular congestion from bone infarcts or sickle cell can cause the intramedullary nerve fibers to initiate a painful response. Nociceptive nerve fibers have been identified in varying concentrations within the fibrous tissue of spondylolytic pars defects as well.

The spine is covered with muscles and tendons in which the main nociceptive nerve endings are unencapsulated. Pain may be mediated by chemical or mechanical conditions or both. The mechanonociceptive units may respond to disruption, stretch, or pressure. Direct injury can cause damage to the intrafascicular nerve fibers or cause a hematoma and edema, which can lead to a chemically mediated pathway. Such a pathway can begin by release of nociceptive sensitizing chemicals such as histamine, potassium, and bradykinin from the damaged tissues. This, in turn, can lead to altered vascular permeability and an influx of the inflammatory cells. It is through such neuropeptides that sensitization of the receptors occurs and, in combination with interstitial edema, this can cause primary muscular pain. At times, the mechanical effect of spasm of a major muscle group in and of itself can cause further trauma to the muscle, and potentiate the pain cascade.

Biochemical Changes

Buy Membership for Orthopaedics Category to continue reading. Learn more here