Osteochondrosis of the spine: neurologic complications

Beginning with Hildebrandt (1933), who proposed the term “osteochondrosis of the intervertebral disc” to define an extensive degenerative process affecting not only the cartilage but also the subchondral part of adjacent vertebrae, this term has become widely used in the works of morphologists, radiologists and clinicians.

The term "osteochondrosis of the spine" (OP) refers to a primarily developing degenerative process in the intervertebral discs, which in turn leads to the secondary development of reactive and compensatory changes in the bone-ligament apparatus of the spine.

The intervertebral discs, which together make up about 1/4 of the length of the entire spine, play a major role in the biomechanics of the spine: they act as ligaments and unique joints, and are also buffers that soften the shocks that fall on the spine. At the same time, a certain importance is given to the nucleus pulposus, which has a high degree of hydrophilicity, the water content of which reaches 83%. The extraordinary hydrophilicity of the nucleus significantly exceeds the hydrophilicity of other tissues of the human body.

During the process of degeneration, the discs lose moisture, the nucleus dries out and disintegrates into separate fragments, the fibrous ring loses its elasticity, softens, becomes thinner, and cracks, ruptures and fissures appear in the disc, streaking the disc in various directions. At first, cracks form only in the inner layers of the ring and sequesters of the nucleus, penetrating the crack, stretch and bulge the outer layers of the ring. When cracks spread through all layers of the ring, either individual sequesters of the nucleus or the entire nucleus fall out into the lumen of the spinal canal through this defect. In these cases, the integrity of the posterior longitudinal ligament may be compromised.

Due to the defectiveness of the nucleus pulposus, it is now subject to not only tangential but also vertical loads. All this, firstly, causes the prolapse of the fibrous ring beyond the disk, and secondly, contributes to its instability. In addition, due to the loss of elastic properties, the fibrous ring cannot hold the nucleus pulposus or its fragments, which creates conditions for herniation.

At a certain stage of development of degenerative changes, a bulging of the disc may form without a rupture of the fibrous ring, which is designated by the term "protrusion" of the disc. The bulging area of the disc becomes vascularized, fibrous tissue grows in it, and in later stages calcification is observed. In cases where a rupture of the fibrous ring occurs with its exit beyond part or all of the pulpous nucleus, which is more often observed in young people after an acute injury, a "prolapse or herniation of the disc" is already judged.

Depending on the direction of prolapse or hernia, the following types are distinguished:

• anterior and lateral, mostly asymptomatic;
• posterior and posterolateral, penetrating the spinal canal and intervertebral openings and often causing compression of the spinal cord and its roots;
• central prolapses (Schmorl's nodes), in which disc tissue penetrates through the degeneratively altered area of the hyaline plate into the spongy mass of the vertebral body, forming depressions of various shapes and sizes in it; they are a radiological finding without clinical manifestations.

With disc degeneration and the convergence of the vertebral bodies, there is also a displacement of the facets of the intervertebral joints and vertebral bodies, and the mechanism of their movements changes. Disc degeneration is accompanied by secondary changes in the vertebral bodies, which consist of two simultaneously occurring processes:

• degenerative-dystrophic changes in the subchondral bone, which occur only after the disintegration and disappearance of the hyaline plates of the disc;
• reactive bone tissue neoplasm in the vertebral bodies, expressed in sclerosis of the subchondral bone tissue with the formation of marginal bone growths - osteophytes. These arthritic bone growths are designated by the term "spondylosis".

The developing deforming arthrosis in the form of proliferation of the articular surfaces of the spine in places of greatest loads is designated by the term "spondyloarthrosis or osteoarthrosis". Osteophytes located in the lumen of the spinal canal, as well as protrusions and prolapses of hernias, can cause symptoms of compression of the spinal cord and its roots.

As a result, the biomechanics of the vertebral bodies adjacent to the affected vertebral motor segment (VMS) are disorganized, and the support capacity of the spine loses its consistency and rhythm. The affected VMS itself acquires a non-physiological, often fixed, position, most often kyphotic. This entails hyperlordosis and hypermobility of the overlying VMS, which initially act as compensatory, but subsequently can contribute to the detection and intensification of the dystrophic process with its consistent spread to an increasing number of VMS.

Instability in the PDS is one of the most common pathomorphological substrates of neurological syndromes. Most often, instability is detected at the level of segments C ₄ _ ₅ and L ₄ _ ₅.

Segmental instability occurs as one of the early manifestations of the dystrophic process in any of the constituent elements of the SDS, leading to a disruption of its harmonious function, and is manifested by excessive mobility between the elements of the SDS. As a result, an excessive degree of flexion and extension in the SDS is possible, as well as slipping forward or backward.

In the pathogenesis of instability, the main role is played by the dystrophy of the fibrous ring, which loses its elasticity and its own fixation ability. The slippage of the overlying vertebral body relative to the underlying one is facilitated by ruptures of the fibrous ring, loss of turgor by the nucleus pulposus, and involvement of the posterior sections of the spinal joints, in particular the intervertebral joints, in the dystrophic process, which is accompanied in severe cases of instability by the development of extension subluxation in them. In addition, constitutional weakness of the ligamentous apparatus predisposes to subluxation.

Due to excessive mobility in the PDS, a series of successive structural, biomechanical and reflex changes develop:

• a bevel of the anterior-superior angle of the body of the underlying vertebral body is formed;
• a “traction spur” is formed;
• formation of neoarthrosis in the area of contact between the articular process and the arch.

Due to compensatory reflex tension of segmental muscles, at a certain stage, fixation of the segment in one or another pose (kyphosis, hyperlordosis) may occur. These changes are caused by both pathogenetic and sanogenetic mechanisms. The predominance of the latter may lead to fibrotization of the disc and, thus, the elimination of instability. Fixation of the PDS is also facilitated by the development of intervertebral spondyloarthrosis. However, with non-fixed instability, both reflex and reflex-compression, compression-reflex and, rarely, compression syndromes may develop.

This depends on the following situations and relationships between the tissues of the PDS and the neurovascular formations during instability:

• excessive mobility in the segment determines irritation of receptors both in the fibrous ring and in the disc-associated sections of the anterior and posterior longitudinal ligaments; and in the capsules of the intervertebral joints;
• the development of subluxation according to Kovacs at the cervical level causes trauma to the vertebral artery with its autonomic plexus. The latter is possible with excessive movements in the PDS, certain motor loads and the absence of subluxation in the joint;
• a pronounced subluxation in the intervertebral joint may be accompanied by a displacement of the apex of the articular process towards the intervertebral opening and cause its narrowing, which under certain conditions can lead to compression of the root and radicular artery;
• significant posterior slippage in combination with some additional factors (congenital narrowness of the canal, compensatory development of posterior marginal bone growth) can lead to narrowing of the spinal canal and serve as a condition for the development of compression or vascular spinal syndrome.

Pathological effects (irritative or compressive) are possible not only as a result of direct contact between the altered bone-cartilaginous structures of the spinal joint and the vascular-nerve formations, but also due to the reduction of the spaces in which these formations are located. In particular, we are talking about the intervertebral openings and the spinal canal.

Narrowing of the intervertebral foramen may be caused by the following changes in the tissues of the intervertebral foramen:

• a decrease in the height of the interbody space due to disc dystrophy (the vertical size of the opening decreases accordingly);
• marginal bone growths of a deforming type in the area of the intervertebral joints (the horizontal size of the opening is mainly narrowed);
• uncovertebral growths, marginal bone growths of the bodies and disc herniation at the lumbar and thoracic levels;
• dystrophically altered yellow ligament.

Narrowing of the spinal canal due to degenerative changes may be caused by:

• posterior disc herniations;
• posterior marginal bone growths of the vertebral bodies;
• hypertrophied yellow ligament;
• slipped vertebral body with severe instability;
• cicatricial-adhesive changes in the epidural tissue and membranes of the spinal cord.

Narrowing of the spinal canal is accompanied mainly by compression or compression-reflex effects.

Sanogenetic mechanisms are naturally aimed at eliminating the narrowing and are associated with the possibility of reducing hernial protrusions, improving circulation in the spinal canal, and resorption of dystrophically altered tissues.

Disturbances in biomechanical relationships in the kinematic chain of the spine in combination with other pathogenetic mechanisms contribute to the development of the myodiscoordination process in the muscles of the PDS, spine and limbs. In this case, complex synergistic reciprocal and other reflex processes develop with a violation of the statokinetics of the spine. First of all, its configuration changes due to changes in the tone of the muscles of the spine, which seek to compensate for the insufficiency of the PDS function - lordosis is smoothed out or a kyphotic position in the department develops, and in some cases, due to the transfer of support to the leg of the unaffected side, a scoliotic position occurs. Multi-articular muscles of the back and small intersegmental muscles participate in the formation of these changes. At a certain stage, these compensatory mechanisms are sufficient. However, with prolonged tonic tension of the muscles, dystrophic changes develop in them. In addition, due to the formation of a pathological reflex ring, muscle tension from a sanogenetic mechanism turns into its opposite - a pathological contracture. As a result, the loads not only on the muscles of the spine change, but also on the muscles of the limbs functioning in new conditions, which leads to myoadaptive postural and vicarious myodystonic and myodystrophic changes in them.

Due to dystonic and dystrophic changes, muscles become a source of pathological afferentation addressed to the same segments of the spinal cord that innervate the affected PDS, as well as to the polysegmental interneuronal apparatus when the muscles of the entire spine and limbs are involved in the process.

Thus, a pathogenetic ring is created that supports, aggravates and develops the pathological process in osteochondrosis of the spine. The emergence of new biomechanical conditions and the pathological state of such an important motor organ as the spine leads to a limitation of mobility not only of its individual parts, but also of general motor activity, which contributes to the disruption of adequate activity of motor-visceral reflexes, which are of great importance for optimal metabolic and trophic support of motor activity.

Most often, neurological complications of osteochondrosis of the spine occur in the cervical and lower lumbar regions.

The main factors in the development of neurological complications in cervical osteochondrosis of the spine are the following.

1. Relatively constant compression of the spinal cord, its roots with their autonomic fibers, the vertebral artery with its sympathetic plexus and the ligamentous apparatus of the spine with its innervation apparatus.

• In the cervical region, disc herniation is relatively rare; most often, only a disc protrusion forms here.
• Compression syndromes are the result of posterior bone osteophytes. Uncovertebral joints are not true, they are prone to deforming arthrosis; in this case, osteophytes are directed either backwards, into the intervertebral foramen, affecting the nerve roots, or outwards, causing compression of the vertebral artery or its sympathetic plexus.
• Narrowing of the intervertebral foramen in the anterior section usually occurs due to uncovertebral bone growths, in its posterior section - due to spondyloarthrosis of the intervertebral joints, subluxation according to Kovacs and thickening of the yellow ligament, and a decrease in the vertical size of the disc leads to a decrease in this size of the intervertebral foramina due to the convergence of the bodies of adjacent vertebrae.
• Unfavorable circumstances include the departure of the spinal cord roots in this section at a right angle to it (and not vertically, as at other levels), a small length of the radicular nerve (no more than 4 mm), and the lack of elasticity and sufficient mobility of the radicular cuffs.
• Naturally, under pathological conditions, there is a disruption of blood and lymph circulation within the narrowed intervertebral openings with the development of venous congestion, edema resulting in scarring, and clinical manifestation of irritative and degenerative radicular symptoms.
• Possibility of compression effects on the spinal cord from the yellow ligament. With increased loads, thickening of the yellow ligament with fibrosis gradually develops, and with a sharp hyperextension of the cervical region (especially sudden), conditions are created for pinching the ligament between the vertebral arches and for pressure on the posterior sections of the spinal cord.

2. Microtraumatization of the spinal cord, its membranes, roots, vascular system and ligamentous apparatus of the spine that periodically occurs over a long period of time during movements of the spine.

• Reid's (1960) studies of the dynamic relationships between the spinal cord and spine in normal conditions revealed significant mobility of the spinal cord and dura mater in the oral and caudal directions during flexion and extension movements of the head and spine. During flexion, the length of the spinal canal (mainly in the C2-Th1 region) can increase to 17.6% and, accordingly, the spinal cord is stretched and slides upward along the anterior surface of the canal. Naturally, under conditions of instability of the cervical vertebrae (disks), the tension of the spinal cord and roots can increase and traumatization of nerve formations is especially evident with unevenness of the anterolateral sections of the spinal canal due to the presence of osteophytes and subluxation. During forced flexion of the neck in the presence of a posterior osteophyte, the brain is stretched above it, increasing compression and traumatization of brain tissue. Osteophytes can have a periodic effect (as a result of microtraumas during changes in the position of the vertebrae) on the nerve formations embedded within the posterior longitudinal ligament and the dura mater, which manifests itself in pain and, probably, reflex phenomena. In this sense, the subluxation of the vertebra, which often develops, is also important. Traumatization of the spinal cord increases if there is instability of the discs, and during flexion and extension movements, one vertebra slides and shifts along the surface of another.
• Osteophytes formed in the area of the uncovertebral joint, directed into the intervertebral foramen and towards the spinal canal, can cause the syndrome of damage to the vertebral artery and its sympathetic plexus.

Compression of the vertebral artery with its sympathetic plexus may be relatively constant, and may also occur periodically at times of change in the position of the head and neck. Irritation of sympathetic fibers or circulatory disturbance in the vertebral artery system of a mechanical or reflex nature often occurs with changes in the position of the head and neck.

Subluxation according to Kovacs is of certain importance for the development of vertebral artery syndrome. In such patients, forward deviation of this artery is observed mainly in the position of neck extension.

3. Vascular ischemia and its significance in the clinical syndrome of brain compression in cervical spondylosis.

Compression of the anterior spinal artery system may be a consequence of the direct impact of a posterior osteophyte or disc herniation, as well as the compressive effect of these formations at the moment of changing the position of the neck.

4. Involvement of the peripheral and central parts of the autonomic nervous system in the pathological process.

Reflex effects of pathological impulses emanating from the spinal cord, its roots with their autonomic fibers, the spinal nerve, which is a branch of the stellate ganglion, and the ligamentous elements of the spine with its innervation apparatus, are manifested by a variety of sympathetic and neurodystrophic disorders.

In the initial stage of the disease, posterior osteophytes or a bulging disc often cause only compression and stretching of the anterior and posterior longitudinal ligaments; in this case, the rest of the ligamentous apparatus of the spine may also be involved in the pathological process. The ligamentous apparatus of the spine, primarily the anterior and posterior longitudinal ligaments, as well as the dura mater, are innervated mainly by the sympathetic sensory branches of the sinuvertebral nerve (recurrent meningeal nerve), consisting of a meningeal branch extending from the posterior root and a branch from the communicating branch of the border sympathetic column.

Nerve endings have been identified both in the posterior (due to the sinuvertebral nerve) and in the anterior longitudinal ligaments, and there is reason to believe that irritation of these ligaments manifests itself as pain in the back of the neck with irradiation to the suboccipital, interscapular regions and to both shoulders.

Thus, a degenerated cervical disc can be considered, on the one hand, as a source of pain manifestations, and on the other hand, pathological impulses that, switching through the central nervous system, cause reflex disorders in the neck, shoulder girdle and hand.

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