Hematomyelia (spinal cord hemorrhage) is a bleeding of various etiology with the outpouring of blood into the substance and membranes of the spinal cord. Depending on the localization, hematomyelia is manifested by sudden symptoms of damage to certain segments of the spinal cord: motor and sensory disorders, impaired pelvic organ function, radicular pain syndrome. The main method by which hematomyelia is diagnosed is spinal cord MRI. Hematomyelia is treated with conservative (coagulants, neostigmine, nootropics, galantamine, etc.) or surgical (removal of hematoma, embolization and clipping of vascular malformation) methods.
Hematomyelia is an internal bleeding in which blood permeates the substance of the spinal cord or accumulates in the form of a hematoma. In the first case, the spilled blood spreads across the spinal cord, causing the death of nerve tissue in the anterior and posterior horns of the spinal cord, as well as compression of the motor and sensory pathways. In the second case, hematomyelia accompanied by the formation of a hematoma leads to compression of brain structures and spinal roots.
As a rule, hematomyelia leads to a partial lesion of the diameter of the spinal cord and is observed at the level of several spinal segments. Only in rare cases it is accompanied by a total lesion of the entire diameter of the spinal cord.
Hematomyelia may be accompanied by the outpouring of blood into the subarachnoid space of the spinal cord (subarachnoid hemorrhage) and the formation of shell hematomas (subdural, epidural). After stopping the bleeding, the spilled blood resolves or the formation of a chronic hematoma occurs, characterized by the presence of a capsule delimiting it. The spinal cells that died as a result of hematomyelia are not restored, but are replaced by glial tissue with the formation of cysts.
The most common cause of hematomyelia is spinal cord injury and damage to spinal vessels in spinal fractures. In second place are arterio-venous malformations of spinal cord vessels, in which hematomyelia develops as a result of thinning and rupture of the altered vascular wall. More rare causes of hematomyelia include pathological vascular changes in systemic vasculitis, disorders in hemorrhagic diathesis (thrombocytopenic purpura, hemorrhagic vasculitis, etc.), destruction of the vascular wall by a growing spinal cord tumor. In some cases, hematomyelia occurs as a complication of medical manipulations: epidural anesthesia or lumbar puncture.
Factors contributing to the development in neurology include severe somatic diseases (cirrhosis of the liver, decompensated hypertension, chronic renal failure, etc.), atherosclerosis, alcoholism, diseases with convulsive syndrome (epilepsy, encephalitis, meningitis, brain abscess, severe flu).
The clinical picture depends on the level of spinal cord injury and the size of the hemorrhage. Usually there is a sudden development of symptoms with an injury or after significant physical exertion (straining, lifting weights). Due to the development of an aseptic inflammatory reaction, hematomyelia may occur with a rise in temperature in the first few days after hemorrhage. Most often, with hematomyelia, there is a lesion of the posterior horns of the spinal cord, which is manifested by a violation of pain and temperature sensitivity while maintaining tactile and deep sensitivity, the pathways of which are located in the white matter of the posterior pillars.
When the anterior horns of the spinal cord are affected, peripheral (sluggish) paralysis develops, accompanied by a decrease in muscle tone, loss of tendon reflexes and atrophic muscle changes. The defeat of the conducting pyramidal pathways leads to the appearance of central (spastic) paralysis below the level of the lesion, for which an increase in muscle tone and tendon reflexes are typical. Depending on the prevalence of hematomyelia, sensory and motor disorders can be one- and two-sided.
Hematomyelia at the level of the upper cervical segments of the spinal cord (CI-CIV) is characterized by the spastic nature of paresis in both the upper and lower extremities. This is accompanied by a violation of urination according to the central type, i.e. urinary retention with intermittent incontinence. Possible radicular pain (sciatica) with irradiation in the back of the head.
Hematomyelia of the lower cervical segments (CV-CVII) and upper thoracic (ThI-ThII) is manifested by peripheral paresis in the arms and central paresis in the legs, sensitivity disorders and urination disorders. There may be miosis, drooping of the upper eyelid and enophthalmos (Gorner’s syndrome). Root pains are given to the upper extremities.
Hematomyelia of the thoracic segments (ThIII-ThXII) of the spinal cord is accompanied by central paresis of the lower extremities, urination disorder and shingling root pains. Hematomyelia at the level of lumbar thickening (LI-SII) leads to the development of peripheral paresis of the lower extremities with sensitivity disorders in them and in the perineum. Root pains radiate into the legs.
Hematomyelia of the cerebral cone (SIII-SV) proceeds without impaired movements in the extremities. Characterized by sensitivity disorders in the perineum, true incontinence of feces and urine. Hematomyelia with a lesion of the ponytail gives peripheral paralysis of the legs and impaired urination. In the early stages, it is characterized by an asymmetry of symptoms.
A vivid clinical picture and a thorough neurological examination allow a neurologist to diagnose spinal cord damage and determine the level of localization of pathological changes. However, it is not possible to accurately determine the nature of the pathological process in the spinal cord on the basis of clinical data. Lumbar puncture is of crucial importance in the diagnosis of hematomyelia. The presence of blood in the cerebrospinal fluid indicates in favor of bleeding, but is not always observed with hematomyelia. In addition, it should be borne in mind that blood can enter the cerebrospinal fluid from a vessel damaged during lumbar puncture.
The most reliable methods of hematomyelia diagnosis today are neuroimaging methods: CT and MRI of the spine. Angiography of spinal cord vessels can be used to detect arteriovenous malformations. Differential diagnosis of hematomyelia is performed with ischemic spinal stroke, acute myelitis, posttraumatic myelopathy, syringomyelia.
In the acute period of hematomyelia, conservative treatment is usually carried out. The patient needs complete rest. To stop bleeding with hematomyelia, coagulants are used: vikasol, epsilonaminocaproic acid. After 2-3 days, a comprehensive treatment is prescribed, aimed at restoring nerve functions lost due to hematomyelia. As a rule, it includes: neostigmine, galantamine, bendazole, nootropics and neuroprotectors. In order to prevent the development of secondary infection (cystitis, ascending pyelonephritis, congestive pneumonia), antibiotic therapy is recommended for hematomyelia. If urination is delayed, catheterization of the bladder is necessary. A patient diagnosed with hematomyelia should observe bed rest for 1.5 months. During this period, massage and physical therapy of paretic limbs are performed, urination is monitored and bedsores are prevented.
The presence of an extensive hematoma or arteriovenous malformation is an indication for surgical treatment of hematomyelia. It consists in a laminectomy and removal of a hematoma. In the case of arteriovenous malformation, clipping, microembolization or radical extirpation can be performed.
Hematomyelia is usually characterized by a regressive course, i.e. its symptoms decrease over time. In most cases, the resorption of the spilled blood leads to a gradual restoration of lost functions, which is noticeable already on the 7th-10th day of the disease. However, even against the background of adequate treatment, hematomyelia does not always end in complete recovery. Residual persistent disorders of the motor sphere and pelvic function can lead to disability of a patient who has undergone hematomyelia.
Hematomyelia of the upper cervical segments of the spinal cord can be complicated by ascending edema of the medulla oblongata and lead to death.