Treatment of spinal cord edema

Myelitis is an inflammation of the spinal cord. Myelitis is primary and secondary. Primary myelitis is caused by neurotropic viruses. Secondary myelitis is much more common than primary and occurs with common infectious diseases: influenza, typhoid, measles, etc. Infectious agents and their toxins penetrate the spinal cord through the lymphatic and blood vessels and cause more or less pronounced inflammatory and dystrophic changes. In viral myelitis, the spinal cord, roots and nerve trunks are affected to varying degrees.
Myelitis, as a rule, develops sharply: the temperature rises, chills appear, general malaise, meningeal symptoms are often expressed (see Meningitis). In the blood there is leukocytosis, a shift of the leukocyte formula to the left, accelerated ROE. Within a few hours or 1-2 days after the onset of the disease, there are symptoms of spinal cord injury that depend on the level of the lesion. In this case the defeat of the entire diameter of the spinal cord is more often noted.
Symptoms of myelitis are composed of paralysis (see Paralyzes, pareses), sensitivity disorders, violations of pelvic organs and trophic disorders.
With the localization of the inflammatory process inthe region of the upper cervical segments spastic paralysis of the four limbs and violation of all kinds of sensitivity are observed. When the cervical thickening of the spinal cord is affected, flaccid paralysis of the hands and spastic paralysis of the legs are noted with disorders of all kinds of sensitivity below the level of the lesion. With defeat at the level of the thoracic segments there is a spastic paralysis of the legs with sensitivity disorders below the level of the affected segments of the spinal cord. With lesions at the level of the lumbar spinal cord thickening, a limp paralysis of the legs is noted. At the onset of the disease, urine retention and constipation occur, which are then replaced by incontinence of urine and feces. Pressure ulcers may develop later. swelling of the feet, increased sweating. The pressure of the cerebrospinal fluid is increased, the number of cells and protein in it is increased. The neurological symptomatology reaches its maximum during the first days of the disease and persists for several weeks or months. Reverse development with myelitis occurs slowly and gradually. First, the sensitivity and function of the pelvic organs is restored, and later, movements in the limbs.
The forecast depends on the localization and severity of the process. Perhaps the recovery, improvement, stabilization of the state, the growth of painful phenomena. The lack of improvement within six months of the disease is a poor prognostic sign. The prognosis in cases of an ascending process and with the addition of pneumonia worsens. cystitis, pyelonephritis. extensive bedsores.
Differentiation should be made with poliomyelitis. multiple sclerosis. trauma of the spinal cord and especially with spinal stroke, leading sometimes to the development of brain necrosis and paralysis of the limbs.
Treatment is carried out in a hospital. Assign antibiotics and sulfonamides in the usual dosages, intravenously administered 40% solution of hexamethylenetetramine (urotropine) for 8-10 ml, 40% glucose solution for 15-20 ml. From the first days of the disease, it is very important to follow careful skin care in order to prevent bedsores. It is necessary to monitor the cleanliness of bed linen. Under the protruding parts of the body should be put a rubber circle or cotton-gauze rings. Several times a day, the skin is wiped with camphor alcohol, often changing the position of the patient. With the appearance of pressure sores, irradiation with quartz is prescribed, treated with a 5% solution of potassium permanganate. impose ointment dressings (Vishnevsky ointment, sulfadimezinovaya or sintomitsinovaya emulsion). When the urine retention is repeated catheterization of the bladder in conditions of strict asepsis. The bladder is washed with 2% solution of boric acid, potassium permanganate (0.1. 200), silver nitrate (1. 2000). When cystitis or pyelocystitis is prescribed, levomycetin (0.5 g 4 times a day), biomycin (0.2 g 4-5 times), plentiful drink. For the prevention of contractures from the first days of development of paralysis, it is necessary to monitor the position of the limbs, laying them in the desired position with the help of pouches with sand. Already in the early period should be used passive, and then active gymnastics and massage.
For the purpose of improving motor functions,proserin. dibazol, vitamins of group B. To reduce muscle tone with spastic paralysis apply mulliktin 0,02 g 2-3 times a day. After 2 months from the onset of the disease, it is advisable to use iontophoresis with iodine, diathermy to the area of ​​the lesion. In some cases, orthopedic treatment is indicated.

Myelitis (myelitis; from the Greek. myelos - brain) - an inflammatory disease of the spinal cord of infectious, toxic and traumatic etiology. With the development of the inflammatory process, only in the gray matter of the spinal cord is poliomyelitis (see); if the process is localized only in white matter, focal myelitis develops, and in the process, both in white and in gray matter, disseminated and necrotic myelitis occurs. MS Margulis (1940) distinguishes two subspecies of myelitis: focal M. with the phenomena of transverse lesion of the spinal cord (myelitis transversa) and disseminated M. in the form of disseminated foci along the spinal cord length. To disseminated M., he also includes opticomelitis. At present, M. is considered as an independent clinical-anatomical form. A special group is those cases when symptoms of cerebral lesions are attached to spinal phenomena - encephalomyelitis (see).
Etiology. Infectious M. and encephalomyelitis are described after various infections, endocarditis, pyelonephritis, rheumatism, etc. Purulent processes in the body can give purulent myelitis; syphilis and tuberculosis can cause both acute and chronic M. There are cases of M. and encephalomyelitis after various vaccinations (postvaccinal). In recent years, M. and encephalomyelitis have been described with toxoplasmosis. A significant number of M. is caused by neurotropic viruses. Toxic M. and encephalomyelitis can develop after acute and chronic poisoning with lead, carbon monoxide, and also sometimes during pregnancy and childbirth.
In the development of compression myelitis an important roleplay extramedullary tumors, tuberculosis lesions of the spine and meninges. In recent years, compression M. has been described with lesions of intervertebral discs, with Schmorl hernia. Traumatic M. may occur with penetrating wounds of the spine; with closed trauma of the spine, foci of softening with hemorrhages in the substance of the spinal cord are noted.

Pathological anatomy. Myelitic foci, especially in acute casesM. can be seen already with the naked eye. There is a general increase in volume, hyperemia and a milder consistency of the brain. The boundaries between white and gray matter are smoothed. MS Margulis distinguishes two forms of focal M. vascular-inflammatory and alterative by the nature of the process. The main form should be considered the first, when the process is dominated by a vascular inflammatory reaction of tissue with lymphoid infiltration around the vessels. In the area of ​​the lesion, the vessels are enlarged, small perivascular hemorrhages are noted, increased multiplication of glia, especially microglia in white matter. The essence of the pathological process in myelitis is the disintegration of nerve fibers with a lesion of the myelin sheath, and then of the axial cylinder. The centers of demyelination occupy various areas of white matter. Ganglion cells of the spinal cord in the foci of inflammation with phenomena of tigrolisis and atrophy. To the alterative form of focal acute M. belongs those cases when the foreground are hemorrhages and spinal cord infarctions on the basis of thrombosis of vessels of soft meninges or vasocorona.
With optometrielitis, along with changes in the spinal cordthe brain shows neuritis of the optic nerves with demyelination of their fibers, changes in the inflammatory character in the trunk, in the cerebellum and in the cerebral cortex, and also in the proteinaceous and choroidal membranes of the eye. In subacute necrotic M. describe necrosis with the predominant localization of them in a gray matter, but with a capture and white. With syphilitic myelitis, the inflammatory process first affects the membranes and vessels of the spinal cord, and its substance is affected again - hemorrhages develop and the tissues of the spinal cord soften. The phenomena of demyelination are most pronounced in syphilis in the posterior columns. With tuberculosis M. there may be a compression of the spinal cord by curdled masses that burst into the vertebral canal or that has resulted from tuberculosis of the dura mater. In the spinal cord can develop tuberculous tubercles with changes in blood vessels, cells and fibers of white matter.
Pathogenesis. Acute myelitis occurs in some caseshematogenous pathway with violation of the blood-brain barrier. In most cases, the lesion of the spinal cord with acute M. lymphogenous origin. On the nerves and roots, the infection reaches the epidural space, and from here, through the lymphatic pathways of the dura mater, the virus spreads to the subarachnoid spaces and the substance of the spinal cord.
Toxic M. has the character of degenerative changes. In these cases, it is often said not about M. but about myelosis (see Funicular myelosis).