Tonic syndrome in spinal pathology

Mechanism of development of reflex syndromes

Reflex pain syndromes develop due to irritation of receptors in the affected spinal segment. The deformed annulus fibrosus, joint-ligament apparatus, periosteum, and, primarily, the posterior longitudinal ligament become the foci of pathological impulses.

Pathogenesis of the myotonia reflex:

1. The pain impulse is transmitted via Luschka's sinuvertebral nerve, which branches off from the spinal ganglion and returns into the spinal canal.
2. The signal travels along the posterior root into the spinal cord.
3. Switching occurs in the anterior and lateral horns of the spinal cord.
4. The efferent impulse reaches the striated muscles, causing their persistent spasm.

In addition to muscle tension, this reflex arc triggers vasomotor and visceral reactions. Prolonged pathological impulses lead to neuroosteofibrosis — dystrophy of the fibrous tissues of ligaments and tendons at their attachment sites to bones.

Classification of reflex vertebrogenic syndromes

Depending on the level of the lesion and the structures involved, three main groups of reflex syndromes are distinguished:

• Musculoskeletal tonic. At the lumbosacral level, these include symphyseal and abdominal syndromes (pubalgia, abdominalgia, "symphyso-sternal syndrome"), as well as vertebrogenic iliopsoas syndrome. In the legs, the spasm involves hip abductors ("gluteal-tract syndrome"), adductors, hamstring muscles, and the tibialis anterior muscle. They are frequently accompanied by painful spasms — crampi.
• Neurodystrophic (myosclerotomal). Manifest as tissue dystrophy. Examples: trochanteritis (lesion of the greater trochanter area), knee epicondylitis, periarthrosis of the foot and ankle, metatarsalgia. Due to connective tissue induration, secondary entrapment syndromes (compression of lower limb nerves) can occur.
• Neurovascular (angiopathic). Include lower limb vascular dystonia (predominantly vasospasm or vasodilation), local and general vasodistonia, restless legs syndrome, as well as subpyriform intermittent claudication syndrome and lower limb occlusive vascular disease syndrome.

Structure of pain syndrome in osteochondrosis

The clinical picture of degenerative changes of the spine has a complex structure and consists of a combination of several syndromes:

1. Reflex — described above, associated with receptor irritation.
2. Compression — caused by physical compression of spinal canal structures (herniated protrusion, edge of a displaced vertebra, or posterior osteophyte). Depending on the compressed element, the following develop:
3. Radiculopathy (nerve root compression).
4. Myelopathy (spinal cord compression).
5. Radiculomyeloischemia (compression of feeder vessels).
6. Myoadaptive — secondary changes in the muscles of the trunk and limbs. They arise as an adaptation to spinal deformity caused by chronic pain.

Pathobiomechanics and disc degeneration

Intervertebral disc degeneration against the background of ongoing loads inevitably leads to a decrease in the height of the intervertebral space and a change in the distribution of dynamic forces.

This provokes discogenic pathobiomechanical syndromes, which manifest as:

• Functional blocks of joints.
• Regional postural muscle imbalance.
• Formation of a non-optimal motor stereotype.

Upon ruptures of the hyaline cartilage endplate, disc tissue can penetrate into the spongy bone of the vertebral body, forming intravertebral hernias. Simultaneously, chronic irritation of bone tissue stimulates osteophyte growth.

Class and exam questions

What else to study on this topic

• Topical diagnosis of sensory and motor disorders in radiculopathies.
• Mechanisms of formation of intravertebral disc hernias.
• Clinical presentation and diagnosis of subpyriform intermittent claudication syndrome.
• Features of local and referred reflex syndromes of the cervical spine.
• Biomechanics of the formation of non-optimal motor stereotypes.

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.