Disease symptoms
Cold, overexertion, and trauma are often the triggers for the onset of the disease. Spinal cord symptoms occur rapidly, mostly numbness and tingling in both lower extremities, and back pain in the corresponding part of the lesion. The lesioned segment has a fasciculated sensation around the torso. It progresses to a peak within 2-3 days with paralysis of the limbs below the level of the lesion, sensory loss and sphincter deficits. If the onset is rapid and the lesion is extensive and severe, the paralyzed limb has low muscle tone and loss of tendon reflexes, which is considered spinal shock. The general shock period is about 2 to 4 weeks. If pneumonia, urinary tract infection or decubitus ulcer occurs, it can be prolonged to several months, which affects the prognosis. If there are no important comorbidities, the recovery period will be entered after 3 to 4 weeks. Usually, basic recovery is achieved 3-6 months after the onset of the disease, but a few cases have sequelae of varying degrees.
Etiology
The exact etiology of this disease is not known. Most cases of myelitis are autoimmune reactions caused by viral infections, or inflammation of the spinal cord due to poisoning or allergies. The etiology is mainly influenza virus, herpes zoster virus, rabies virus, poliovirus, etc. In recent years, there are reports of myelitis caused by hepatitis virus. There are still some patients with unknown causes, but they often have some symptoms of upper respiratory tract infection before the disease. Transverse myelitis is the most common clinical condition, with lesions mainly in the thoracic segment, followed by the cervical segment, and less commonly in the lumbar and sacral segments. It manifests as limb paralysis, sensory loss, and bladder and rectal dysfunction below the level of the spinal cord lesion.
Pathology
The pathological changes are inflammation and degeneration, mainly manifested by edema, degeneration, inflammatory cell infiltration, exudation, swelling of nerve cells in the soft spinal membrane and spinal cord, and in severe cases, spinal cord softening, necrosis, hemorrhage, nerve cell atrophy in the chronic phase, neuromyelin loss, axonal degeneration, and neuroglial cell proliferation. Cerebrospinal fluid examination in the acute phase of the disease may have a mildly increased white blood cell count and protein content.
Diagnosis
Physical signs.
1, motor disorders: mainly manifested as upper motor neuron palsy below the lesion segment. However, in acute cases, the early stage may be a transient flaccid paralysis, called spinal shock. After a few days to weeks, typical signs such as hyperactive tendon reflexes, increased muscle tone and pathological reflexes gradually appear. The corresponding muscles of the lesioned segment show lower motor neuron palsy, but most of them have no typical signs. The motor deficits are mostly symmetrical, but may also involve one side or both sides to varying degrees. If the lesion is high, respiratory muscle paralysis and swallowing difficulties may occur.
2.Sensory impairment: hypoesthesia or loss of sensation below the lesion segment. Both superficial and deep senses are involved to varying degrees, but the severity is not necessarily symmetrical bilaterally. If only one side of the spinal cord is involved, it will show the absence of pain and temperature sensation in the contralateral limb below the level of the lesion, and the absence of deep sensation on the same side. In the junction area between normal sensation and sensory loss, there is often a nociceptive hypersensitivity area.
3, vegetative symptoms: in the acute stage, there is mostly urinary retention or constipation, and in those who have passed the spinal shock period, urinary incontinence gradually appears, and some cases eventually become autonomic bladder. With different damage segments, other phytonadic dysfunction may appear, such as Horner’s syndrome, abnormal vasodilation, sweat secretion and nutrition disorders, and abnormal visceral function.
Diagnosis by imaging.
1, myelography: diffuse swelling of the spinal cord is common, or may be normal. It is mainly used in cases with atypical clinical manifestations and to differentiate from other diseases. Acute phase examination may lead to aggravation of the disease.
2, spinal cord CT: often used in combination with myelography. Mild thickening of the spinal cord and inhomogeneous density can be seen.
3, spinal cord MRI: swelling of the spinal cord can be seen, and there are mostly inhomogeneous long T1 and long T2 signals.
Blood picture: mostly no abnormal changes, acute phase and co-infection can be seen in the increased white blood cell count and increased neutrophil ratio. Pressure is mostly normal, but decreases if spinal cord swelling causes significant incomplete obstruction. Protein quantification is often mildly elevated, with an increase in gamma globulin. The cell count is mildly increased or normal, with a predominantly monocytic classification. These changes are most often seen in the acute phase.
Differential diagnosis
1.Spinal cord tumor: it can compress the spinal cord and cause motor sensory disorder, and in severe cases, spinal cord transection syndrome. However, in most cases, the disease progresses slowly and spinal shock is not obvious. Myelography, CT and other examinations can be clear.
2, extramedullary occupying lesions in the spinal canal: local hematomas, tumors, abscesses, etc. can compress the spinal cord and cause clinical manifestations similar to those of myelitis. However, the radicular pain is more obvious, the abnormal curvature of the spine is easy to see, and the symptoms and signs are more obvious asymmetrical, or may be accompanied by the manifestation of the primary disease, such as high fever of epidural abscess. Imaging examination can confirm the diagnosis.
3, Green-Barre syndrome: motor disorders are similar to those seen in the acute phase of myelitis when spinal shock is present. However, sensory impairment is relatively mild and transient, urinary retention is mostly inconspicuous, and there is often no nociceptive hypersensitivity band. Cerebrospinal fluid cell count is normal. protein cell separation occurs after 1 to 2 weeks.
4.In some cases, myelitis is the first manifestation of multiple sclerosis. Therefore, it is important to pay attention to the comprehensive examination of patients with myelitis, especially fundus and brain signs. Intracranial imaging is performed when necessary.
Classification
1.Etiological classification
(1) Infectious myelitis
(1) Viral myelitis: acute anterior spinal cord poliomyelitis.
(2) bacterial myelitis: septic myelitis, tuberculous myelitis.
(3) Spirochete myelitis: syphilitic myelitis, spinal leptospirosis.
④Parasitic myelitis: malaria, schistosomiasis, trichinella, toxoplasma, etc.
⑤ Infection and post-inoculation myelitis.
(2) Myelitis of unknown cause.
2, clinical type classification
(1) Acute myelitis
①Acute anterior spinal cord poliomyelitis
(2) acute non-specific myelitis: acute transverse myelitis, acute ascending myelitis, acute disseminated encephalomyelitis.
(2) chronic myelitis: chronic viral myelitis, tuberculous myelitis, syphilitic myelitis, sarcoidosis myelitis, subacute necrotizing myelitis, etc.
Treatment
No special treatment.
I. General treatment
1, the acute stage should be bed rest, give a diet rich in calories and vitamins. Or give ATP, coenzyme A, adenosine, cytidylcholine and other drugs to promote the recovery of neurological function. A small amount of fresh plasma infusion from healthy people can also help improve the patient’s immune function, which is beneficial to the prevention of infection and recovery.
2. Turn the patient regularly, keep the skin clean and dry, and pay attention to massage the pressurized parts to prevent the occurrence of decubitus ulcers.
3.If urinary retention is severe, catheterization is required. A sterile catheter can be left in place and urine is released once every 3 to 4 hours to prevent bladder contracture. Pay attention to the prevention of urinary tract infection during the period of indwelling catheterization. For those who have difficulty in defecation, clean enema or laxative should be used in time.
Adrenal corticosteroids
The current belief is that myelitis is related to autoimmunity and can be treated with adrenal corticosteroids. The first is to use hydrocortisone 5-10mg/kg daily, added to 5%-10% glucose soluble tuck intravenously, once a day. 1 to 2 weeks later, reduce the amount as appropriate, or change to prednisone oral, and gradually reduce the stop.
Third, other therapies
1, plasma exchange: can remove the patient’s plasma auto-circulating antibodies and immune complexes and other harmful substances, for critically ill patients can relieve the symptoms, hormone treatment is not effective may also be effective. Generally once a day, 7 days as a course of treatment.
2.UV irradiation oxygenated self-blood transfusion: Take 150-200m1 of the patient’s own whole blood and transfuse it after oxygenated UV irradiation. 1～2 times a week for 3～5 weeks. It can promote the recovery of spinal cord function.
Fourth, the recovery period treatment
1.Start functional exercise as early as possible, pay attention to keep the limb in a functional position to prevent contracture or deformity of the affected limb.
Patients with contracture or deformity should be given physiotherapy and physical therapy to further strengthen training, or small doses of Valium or Antan can be given orally to relieve muscle tone.