Chapter 24. Diseases of the spine

Degenerative diseases of the spine include osteochondrosis, spondylosis and spondyloarthrosis. Osteochondrosis is based on the primary pathology of the nucleus pulposus, spondylosis - on the pathological process in the fibrous ring and anterior longitudinal ligament. As a rule, spondyloarthrosis develops due to static spinal abnormalities associated with osteochondrosis, scoliosis, or as an independent disease of the intervertebral joints. During outpatient visits, 80% of patients complain of spinal pain. An in-depth study of this pathology is required for a doctor of any specialty.

Osteochondrosis

Etiology

Spinal osteochondrosis is based on degeneration of the intervertebral disc with subsequent involvement of adjacent vertebral bodies in the process, as well as changes in the intervertebral joints and ligamentous apparatus. Affecting patients at the peak of their working age, osteochondrosis leads to significant occupational inactivity. More than 70% of the total number of sickness certificates issued by neurologists account for various clinical manifestations of osteochondrosis. About 10% of patients become disabled.

Osteochondrosis is a polyetiological disease. The main causes of its development and progression are:

• injuries (consequences of fractures and ligament damage);
• microtraumas (spinal concussion, repetitive movements, prolonged forced posture);
• developmental anomalies (unfused arch, lumbarization, sacralization, tropism of articular processes, etc.), causing spinal instability;
• rheumatoid lesion (especially in advanced osteochondrosis);
• autoimmune disorders (occurrence of autoantibodies in intervertebral discs in collagenosis);
• vascular disorders (changes in the disk trophic due to microcirculatory disorders).

Anatomical and physiological features

The intervertebral disc is considered as a semi-joint, in which the nucleus pulposus (containing fluid similar to synovial one) is compared with the joint cavity, the hyaline plates of the vertebral bodies are compared with articular surfaces, and the fibrous ring is perceived as a joint capsule. The vertebral segment possesses its own ligamentous apparatus (Fig. 24.1).

Fig. 24.1. Intervertebral disc and vertebral segment. 1 - supraspinal ligament; 2 - lower articular process; 3 - interspinous ligament; 4 - spinous process; 5 - upper articular process; 6 - flaval ligament; 7 - posterior longitudinal ligament; 8 - vertebral body; 9 - anterior longitudinal ligament; 10 - fibrous ring; 11 - nucleus pulposus; 12 - Luschka aperture(Uncovertebral joints); 13 - hyaline plate; 14 - facet joint

The thoracic spine is fixed by the ribs, it is almost immobile. The maximum load falls on the middle and lower thoracic spine, while intervertebral discs of the lower thoracic spine bear the greatest dynamic loads.

Sympathetic fibers emerging from the spinal cord as part of the anterior roots form sympathetic trunks. In the upper thoracic spine, anastomosis of the cervical and thoracic sympathetic trunks occurs with the formation of a stellate ganglion, from which the main branch and afferent branches spring to the spine, esophagus. The abdominal nerve passes through the diaphragm with sympathetic fibers from the middle and lower thoracic sympathetic ganglia and is included in the solar plexus.

The vasomotor nerves of the lower extremities originate from the three lower thoracic and two upper lumbar segments (Th₁₀-L₂), anastomosing with the distal parts of the sympathetic chain. Blood supply to the spinal cord, its mid-thoracic region is carried out from a single artery that follows the 5th or 6th thoracic root. Arterial blood flow in the mid-thoracic region is not independent, as it is contingent on the anterior spinal system of two adjacent pools. The blood supply is supplemented by a thin anterior radicular-spinal artery, approaching Th_5-7 from the lumbar enlargement artery.

These anatomical features determine the polymorphism of the thoracic spine osteochondrosis clinical manifestations.

Pathogenesis and classification

The intervertebral disc degeneration begins with the depolymerization of glycosaminoglycans in the nucleusi pulposus; collagen destruction occurs in the protein-polysaccharide complex, depending on the increased activity of cathepsins and chondrocytes themselves, which are significantly influenced by autoimmune processes. The proliferation of chondrocytes is accompanied by the accumulation of lactic acid, which increases the hyaluronidase penetration and collagen destruction. The same process disrupts the metabolism of the synovial membrane in the vertebral and other joints. Production of synovial fluid decreases; the cartilage nutrition is disrupted. First, the nucleus pulposus swells, then it dries out, the disc flattens, and the fibrous ring starts to herniate. Fissures and tears appear in the dystrophically altered collagen fibers of the fibrous ring. The nucleus pulposus "seeps" through these fissures, which results in the herniated intervertebral disc outside the fibrous ring (Fig. 24.2). If this formation loses its connection with the disk, it becomes its sequester.

Fig. 24.2. Herniated intervertebral disc with compression of the spinal cord and roots: 1 - fissures in the fibrous ring; 2 - disc displacement

The following types of herniated intervertebral discs are distinguished:

• median (central) - located anteriorly from the posterior longitudinal ligament along the midline;
• paramedian (posterolateral) - located near the median line, develop partly behind the posterior longitudinal ligament, and partly exterior to it;
• lateral (foraminal) - located exterior to the posterior longitudinal ligament.