Spinal cord diseases

 

Neurological symptoms associated with the anatomical structure of the spinal cord and spine

Knowledge of the anatomical structure of the spinal cord (segmental principle) and the spinal nerves extending from it allows neuropathologists and neurosurgeons in practice to accurately determine the symptoms and syndromes of damage. During a neurological examination of the patient, going down from top to bottom, they find the upper limit of the onset of a disorder of sensitivity and motor activity of the muscles. It should be remembered that the vertebral bodies do not correspond to the spinal cord segments located below them. The neurological picture of spinal cord injury depends on the damaged segment.

During its formation and development, the spinal cord grows more slowly than the spine. In adults, the spinal cord ends at the level of the body of the first lumbar L1 vertebra. The nerve roots departing from it will go down further to innervate the limbs or pelvic organs.

The clinical rule used in determining the level of damage to the spinal cord and its nerve roots:

• the cervical roots (except for the C8 root) leave the spinal canal through the holes above the corresponding vertebral bodies
• thoracic and lumbar roots leave the spinal canal under the vertebrae of the same name
• the upper cervical segments of the spinal cord lie behind the vertebral bodies with the same numbers
• the lower cervical segments of the spinal cord lie one segment above the corresponding vertebra
• the upper thoracic segments of the spinal cord lie two segments higher
• the lower thoracic segments of the spinal cord lie three segments higher
• the lumbar and sacral segments of the spinal cord (the latter form the conus medullaris) are localized behind the Th9-L1 vertebrae

To clarify the distribution of various pathological processes around the spinal cord, especially in spondylosis, it is important to carefully measure the sagittal diameters (lumen) of the spinal canal. The diameters (lumen) of the spinal canal in an adult is normally:

• at the cervical level of the spine - 16-22 mm
• at the thoracic level of the spine - 16-22 mm
• at the level of the lumbar vertebrae L1-L3 - about 15-23 mm
• at the level of the lumbar vertebrae L3-L5 and below - 16-27 mm

 

Neurological syndromes of spinal cord diseases

With a lesion of the spinal cord at one level or another, the following neurological syndromes will be detected:

• loss of sensitivity below the level of his spinal cord injury (level of sensitivity disorders)
• weakness in the limbs innervated by the descending nerve fibers of the cortico-spinal path from the level of the spinal cord injury

Sensory disturbances (hypesthesia, paresthesia, anesthesia) may appear in one or both feet. Sensory disturbance can spread upward, mimicking peripheral polyneuropathy. In the event of a complete or partial interruption of the cortico-spinal and bulbospinal pathways at the same level of the spinal cord, the patient develops paralysis of the muscles of the upper and/or lower extremities (paraplegia or tetraplegia). In this case, symptoms of central paralysis are revealed:

• muscle tone is increased
• deep tendon reflexes are increased
• revealed by the pathological symptom of Babinsky

During the examination of a patient with spinal cord injury, segmental disorders are usually found:

• a band of changes in sensitivity near the upper level of sensory conduction disorders (hyperalgesia or hyperpathy)
• hypotension and muscle atrophy
• isolated loss of deep tendon reflexes

The level of conduction-type sensory disorders and segmental neurological symptoms roughly indicate the localization of the transverse spinal cord lesion in the patient. An accurate localizing sign is pain felt along the midline of the back, especially at the thoracic level. Pain in the interscapular region may be the first symptom of spinal cord compression in a patient. Radicular pain indicates the primary localization of the lesion of the spinal cord in the area of its outer masses. When the cone of the spinal cord is affected, pain is often noted in the lower back.

In the early stages of transverse spinal cord injury in the extremities, there may be a decrease in muscle tone (hypotension) rather than spasticity due to spinal shock in the patient. Spinal shock can last for several weeks. It is sometimes mistaken for an extensive segmental lesion. Later, the patient's tendon and periosteal reflexes become elevated. In transverse lesions, especially those caused by infarction, paralysis is often preceded by short clonic or myoclonic convulsions in the limbs. Another important symptom of transverse spinal cord injury is a dysfunction of the pelvic organs, manifested in the form of retention of urine and feces in the patient.

Compression within (intramedullary) or around the spinal cord (extramedullary) can clinically manifest similarly. Therefore, one neurological examination of the patient is not enough to determine the localization of the spinal cord injury. The neurological signs that testify in favor of the localization of pathological processes around the spinal cord (extramedullary) include:

• radicular pain
• Brown-Séquard half spinal lesion syndrome
• symptoms of damage to peripheral motoneurons within one or two segments, often asymmetric
• early signs of cortico-spinal tract involvement
• a significant decrease in sensitivity in the sacral segments
• early and pronounced changes in cerebrospinal fluid (CSF)

Neurological signs that support the localization of pathological processes inside the spinal cord (intramedullary) include:

• hardly localized burning pains
• dissociated loss of pain sensitivity while maintaining muscular-articular sensitivity
• preservation of sensitivity in the perineum and sacral segments
• late arising and less pronounced pyramidal symptoms
• normal or slightly altered composition of cerebrospinal fluid (CSF)

A lesion inside the spinal cord (intramedullary), accompanied by the involvement of the most internal fibers of the spinothalamic pathways, but not affecting the outermost fibers that provide the sensitivity of the sacral dermatomes, will manifest itself in the absence of signs of damage. The perception of pain and temperature irritations in the sacral dermatomes (nerve roots S3-S5) will be preserved.

Brown-Séquard syndrome is a complex of symptoms of half lesion of the spinal cord diameter. Brown-Séquard syndrome is clinically manifested:

• on the side of the spinal cord injury - paralysis of the muscles of the arm and/or leg (monoplegia, hemiplegia) with loss of muscular-articular and vibration (deep) sensitivity
• on the opposite side - loss of pain and temperature (surface) sensitivity

The upper limit of pain and temperature sensitivity disorders in Brown-Séquard syndrome is often determined 1-2 segments below the site of spinal cord injury, since the fibers of the spinothalamic pathway, after the formation of a synapse in the dorsal horn of the spinal cord, pass into the opposite lateral cord, rising up. If there are segmental disorders in the form of radicular pain, muscle atrophy, extinction of tendon reflexes, then they are usually unilateral.

If the focus of the spinal cord lesion is limited to the central part or affects it, then it will mainly damage the neurons of the gray matter and segmental conductors, which produce their intersection at this level. This is observed with contusion during spinal cord injury, syringomyelia, tumors, and vascular lesions in the basin of the anterior spinal artery. With a central lesion of the cervical spinal cord, there are:

• arm weakness, which is more pronounced compared to leg weakness
• dissociated sensitivity disorder (analgesia, i.e. loss of pain sensitivity with distribution in the form of a “cape on the shoulders” and the lower part of the neck, without anesthesia, i.e. loss of tactile sensations, and with the preservation of vibration sensitivity)

Lesions of the cone of the spinal cord, localized in the region of the vertebral body L1 or below, compress the spinal nerves that make up the cauda equina. This causes peripheral (flaccid) asymmetric paraparesis with areflexia. This level of damage to the spinal cord and its nerve roots is accompanied by dysfunction of the pelvic organs (dysfunction of the bladder and intestines). The distribution of sensory disorders on the patient's skin resembles the outline of a saddle, reaches the L2 level, and corresponds to the innervation zones of the roots entering the cauda equina. Achilles and knee reflexes in such patients are reduced or absent. Often, patients notice pain radiating to the perineum or thighs.

With pathological processes in the area of the spinal cord cone, pain is less pronounced than with lesions of the cauda equina, and disorders of the intestinal and bladder functions occur earlier. Achilles reflexes are extinguished in this case. Compression processes can simultaneously capture both the cauda equina and the cone of the spinal cord, which causes a combined syndrome of lesions of peripheral motor neurons with increased reflexes and the appearance of a pathological Babinsky symptom.

With a lesion of the spinal cord at the level of the foramen magnum, patients develop muscle weakness in the shoulder girdle and arm, followed by weakness in the leg and arm on the opposite side. Volumetric processes of this localization sometimes give pain in the neck and back of the head, extending to the head and shoulders. Horner's syndrome is another evidence of a high cervical level (up to the Th1 segment) of the lesion.

Some diseases of the spine can cause sudden myelopathy without prior symptoms (such as a spinal stroke). These include epidural hemorrhage, hematomyelia, spinal cord infarction, prolapse (prolapse, extrusion) of the nucleus pulposus of the intervertebral disc, and subluxation of the vertebrae.

Chronic myelopathies occur with the following diseases of the spine or spinal cord:

• Spondylosis
• Lumbar spinal stenosis
• Degenerative and hereditary myelopathies
• Syringomyelia
• Tabes (tabes dorsalis)