Transverse spinal cord injury syndrome: causes, symptoms, diagnosis

Transverse spinal cord injuries involve one or more segments and completely or partially interrupt the spinal cord. Complete transection of the spinal cord at the cervical or thoracic level causes the following symptoms:

1. Complete, ultimately spastic, tetraplegia or, if only the legs are affected, lower paraplegia, which, in the case of complete damage, takes on the character of paraplegia in the flexed position;
2. Total conduction-type anesthesia below the level of the lesion;
3. Pelvic organ dysfunction;
4. Violation of vegetative and trophic functions (bedsores, etc.);
5. segmental flaccid paralysis and muscular atrophy due to involvement of the anterior horns at the level of one or more damaged segments.

The most common syndrome is incomplete (partial) transverse lesion.

Symptoms vary with spinal cord lesions at the upper cervical level (segments C1-C4), at the level of the cervical thickening, with lesions of the thoracic spinal cord, the upper lumbar region (L1-L3), the epicone (L4-L5, S1-S2) and the cone (S3-S5). Isolated lesions of the cone of the spinal cord are less common than in combination with lesions of the equine tail (in the latter case, severe radicular pain, flaccid paralysis of the lower limbs, anesthesia in them, urination disorders such as retention or "true" urinary incontinence are observed).

Lesions at the level of the lower sections of the spinal cord have their own clinical features. Thus, the epiconeus syndrome (L4 - S2) is characterized by damage to the muscles innervated by the sacral plexus with predominant damage to the peroneus muscle and relative preservation of the tibialis. Hip flexion and knee extension are preserved. Flaccid paralysis (varying in severity) of the muscles of the gluteal region, back of the thigh, lower leg and foot (defective hip extension and knee flexion, foot and toe movements). Achilles reflexes are lost; knee reflexes are preserved. Sensitivity disorders below the L4 segment. Functions of the bladder and rectum ("autonomous bladder") deteriorate.

Conus medullaris syndrome (S3 and more distal segments) is characterized by the absence of paralysis (with isolated conus lesion); the presence of saddle anesthesia, flaccid paralysis of the bladder and paralysis of the anal sphincter, absence of anal and bulbocavernous reflexes; tendon reflexes are preserved; pyramidal signs are absent.

Diseases that cause damage to only one half of the spinal cord result in the well-known Brown-Sequard syndrome, which is not discussed in detail here (in most cases, incomplete variants of Brown-Sequard syndrome are encountered).

In slowly developing lesions of the thoracic and cervical spine, the development of spinal automatism syndrome with protective reflexes is possible, which can be used to determine the lower boundary of the spinal process, for example, a tumor.

The main reasons for incomplete (partial) transverse damage:

1. Occlusion of the anterior spinal artery.
2. Pathology of the vertebrae (spine).
3. Extramedullary and intramedullary tumor (originating from spinal tissue, metastases, sarcoma, glioma, spinal angioma, ependymoma, meningioma, neurinoma).
4. Non-tumor compression (herniated disc, epidural abscess, epidural hemorrhage (hematoma), lumbar stenosis.
5. Myelitis, epiduritis, abscess, demyelinating diseases.
6. Radiation myelopathy.
7. Trauma with spinal cord contusion (contusion) and late traumatic compression of the spinal cord.

Anterior spinal artery occlusion

The anterior spinal artery, running along the ventral surface of the spinal cord, supplies the anterior two-thirds of the spinal cord via numerous sulcal-commisural arteries that enter the cord in a ventrodorsal direction. These arteries supply the anterior and lateral horns of the spinal cord, the spinothalamic, anterior corticospinal, and, most importantly, the lateral corticospinal tracts.

The most important point is the non-involvement of the posterior funiculi and posterior horns. Based on these anatomical relationships, the anterior spinal artery syndrome (identical to the central spinal lesion syndrome) is represented by the following symptoms): central lower paraparesis (sometimes monoparesis of the leg), which in the acute phase of the disease can be flaccid (spinal shock) with areflexia, but then, after several weeks, a gradual increase in muscle tone occurs according to the spastic type, hyperreflexia, clonus, Babinski's symptom, urinary retention develops, which gradually turns into urinary incontinence (hyperreflexive bladder), decreased pain and loss of temperature sensitivity. In contrast to impaired pain and temperature sensitivity, tactile sensitivity and the ability to localize an irritant are preserved, the same applies to vibration sensitivity. Radicular pain corresponding to the upper level of the lesion is often observed. Sometimes spinal cord infarction is preceded by transient ischemic spinal attacks.

The cause of occlusion may be embolism or a local atherosclerotic process. Less often, spinal infarction is caused by systemic diseases (for example, periarteritis nodosa). The disease begins acutely. Incomplete transverse lesion of the spinal cord occurs at the lower cervical or thoracic levels, where large feeding vessels flow into the anterior spinal artery. The age of patients is predominantly elderly (but not always). Signs of widespread atherosclerosis are revealed. There are no abnormalities in the X-ray examination. The cerebrospinal fluid is unchanged. Sometimes, as in cerebral stroke, the hematocrit is increased.

Infarction of the posterior spinal artery does not give a picture of transverse damage to the spinal cord.

A rare cause of spinal cord compression syndrome is venous infarction.

Spinal cord compression may be caused by spinal pathology (tumor, spondylitis, intervertebral disc prolapse) in which dysmorphic vertebral tissue, neoplastic or inflammatory tissue is introduced into the spinal canal. The anamnesis may indicate radicular pain at the level of the lesion preceding the acute development of symptoms, but such information may be absent. Quite often, the syndrome of incomplete transverse spinal cord lesion develops without any precursors. A neurological examination can only approximately determine the level of the lesion. Neurological examination can mainly be relied on to determine the transverse nature of the lesion, and not the level of spinal cord lesion. The reason for this is the so-called eccentric arrangement of the long ascending and descending fibers. Any lesion affecting the spinal cord in the direction from the outside to the inside will primarily affect these long fibers, so the first clinical manifestations usually occur in anatomical areas localized below the level of localization of the lesion itself.

Some useful information can be obtained from laboratory tests (e.g. ESR). Other necessary diagnostic tests may not be available at the time of admission (e.g. bone metabolism tests).

Additional studies are required to clarify the diagnosis. Traditional methods include radiography and neuroimaging in bone imaging mode, which allow us to detect destructive changes in the vertebrae due to local impact of a neoplasm or inflammatory process. In the absence of changes in radiography or neuroimaging, spinal scintigraphy is diagnostically valuable. Scintigraphic examination serves as a search method when the level of damage to the spinal column cannot be determined. When determining the level of damage, the degree of spinal cord compression and extraspinal impact are judged by the results of myelography in combination with CT.

Extramedullary or intramedullary tumor

For detection of extramedullary intradural space-occupying processes, myelography in combination with CT or MRI is the most informative. In such cases, the spinal column is often intact, while there is spinal cord compression. The advantage of myelography is its ability to visualize the localization of the pathological process well, in addition, it is possible to simultaneously take cerebrospinal fluid for examination and obtain diagnostically valuable information. The spectrum of extramedullary pathological processes is wide: from neurinoma or meningioma (usually located on the posterolateral surface of the spinal cord and requiring surgical intervention) to lymphoma, which is better amenable to radiation therapy, and arachnoid cyst.

Intramedullary spinal cord tumors are rare. The clinical picture is dominated not by pain, but by paresthesia, paraparesis, and urination disorders. With such symptoms, if there are any suggestions about neurological pathology, then the spinal form of multiple sclerosis is suspected first and foremost. However, this condition does not have multiple foci or a course with exacerbations and remissions. The progressive course of spinal pathology with the involvement of different systems (sensory, motor, vegetative) should be the basis for searching for a volumetric process.

Non-neoplastic spinal cord compression

A herniated disc at the cervical level usually leads to Brown-Sequard syndrome, but anterior spinal artery syndrome can also develop. No extraordinary impact is required for a herniation to occur: in most cases, it occurs in completely unremarkable situations, such as stretching (stretching the arms) while lying on the back. Among additional research methods, neuroimaging is the method of choice.

Epidural abscess is characterized by a syndrome of incomplete transverse spinal cord lesion of a progressive nature: local, almost unbearable pain and tension of the affected part of the spinal column; local tenderness; and inflammatory changes in the blood. In this situation, there is no time for additional studies, except for radiography and myelography. Urgent surgical intervention is required.

Epiduritis requires differential diagnosis with myelitis. MRI or myelography is of decisive diagnostic importance. Lumbar puncture is absolutely contraindicated if epiduritis is suspected.

Acute development of transverse cord injury syndrome in a patient receiving anticoagulants is most likely due to bleeding into the epidural space (epidural hematoma). Such patients should be promptly treated with anticoagulant antagonists, as this situation requires neuroimaging studies, myelography, and urgent surgical intervention.

Myelitis and multiple sclerosis

More or less complete transverse damage to the spinal cord occurs with an inflammatory (viral, paraneplastic, demyelinating, necrotizing, post-vaccination, mycoplasmic, syphilitic, tuberculous, sarcoidosis, idiopathic myelitis) process in the spinal cord. In other words, both viral and other etiologies of myelitis are possible; it often occurs as a post-infectious immune reaction, manifested as multifocal perivenous demyelination. This condition is sometimes difficult to differentiate from multiple sclerosis. A characteristic sign of the latter is the ataxic paraparesis syndrome. However, ataxic syndrome may be absent in the acute stage.

Myelitis occurs acutely or subacutely, often against the background of general infectious symptoms. Pain and paresthesia appear in the innervation zone of the affected roots; tetraplegia or lower paraplegia (paraparesis) join them, which are sluggish in the acute period. Disorders of the pelvic organs and trophic disorders (bedsores) are characteristic. The functions of the posterior columns are not always impaired.

Clarification of the etiology of myelitis requires a set of clinical and paraclinical studies, including cerebrospinal fluid examination, spinal cord MRI, evoked potentials of different modalities (including visual), serological diagnostics of viral infection, including HIV infection. In approximately half of cases of isolated inflammation of the spinal cord, the cause cannot be identified.

Radiation myelopathy

Radiation myelopathy may develop late (6-15 months) after radiation therapy for tumors in the chest and neck. Peripheral nerves are more resistant to this damage. Paresthesia and dysesthesia in the feet and Lhermitte phenomenon gradually appear; then weakness in one or both legs with pyramidal signs and symptoms of spinothalamic tract involvement develops. A picture of transverse myelopathy or Brown-Sequard syndrome occurs. Cerebrospinal fluid does not show noticeable deviations from the norm, except for a slight increase in protein content. MRI helps to see vascular foci of low density in the parenchyma of the spinal cord.

Spinal cord injury and late traumatic spinal cord compression

Diagnosis of acute spinal cord injury is not difficult, since the relevant anamnestic information is available. However, if the injury occurred many years ago, the patient may forget to inform the doctor about it, since he/she does not suspect that this injury may be the cause of the existing progressive spinal symptoms. Therefore, chronic vascular myelopathy due to compression injury of the vertebra may be difficult to diagnose without the help of radiography.

Other (rare) causes of spinal cord compression syndrome: cicatricial adhesive processes, hematomyelia, hematorrhachis, spinal syphilis (gumma), cysticercosis, cysts.