acute transverse myelitis
Introduction
Introduction to acute transverse myelitis Acute transverse myelitis (ATM) refers to acute myelopathy caused by various causes and traversal damage of spinal cord involving several segments. The main pathological changes were inflammation, demyelination and necrosis of the spinal cord. basic knowledge The proportion of illness: 0.001% - 0.007% Susceptible people: no special people Mode of infection: non-infectious Complications: urinary incontinence, acne, pneumonia, medullary paralysis
Cause
Causes of acute transverse myelitis
(1) Causes of the disease
The causes of this disease are diverse and are mainly found in the following aspects:
1. Infection: 20% to 40% is caused by viral infection, most commonly in herpes simplex virus type II, varicella-zoster virus and enterovirus. In recent years, HIV-1 and human (tropic) T lymphocyte virus type I The myelopathy associated with (HTLV-1) began to receive attention.
Domestic scholars have detected herpes simplex virus type 2 antibodies in the CSF of this disease, and detected their specific DNA by PCR. Bohr et al (1999) also used the same method to detect the RNA sequence of enterovirus in CSF. Cases of AIDS complicated with acute myelitis, cerebrospinal fluid PCR confirmed herpes zoster virus, after treatment with acyclovir (acyclovir), symptoms completely recovered (Lionnet, 1996), suggesting that direct damage to the spinal cord may be the main cause Other common pathogens causing this disease include various bacteria, spirochetes, fungi, mycoplasmas, and parasites.
2. Vascular disease: Myelitis caused by spinal cord blood supply disorder is also called acute necrotizing myelitis, which is often secondary to vascular inflammatory lesions such as connective tissue disease, sarcoidosis, malignant tumor, and infection.
3. Associated with demyelinating diseases: Partial multiple sclerosis (MS), acute disseminated encephalomyelitis and other demyelinating diseases can be the first symptom of acute transverse spinal cord injury.
4. Primary: refers to non-specific acute spinal cord injury of unknown cause, which may be induced by overwork and spinal trauma. Some patients have upper respiratory tract infection, diarrhea or vaccination history 1 to 2 weeks before the disease.
(two) pathogenesis
1. Infection: It is speculated that the infection route is:
1 The virus that has been lurking in the spinal ganglia for a long time, when the body's resistance declines, it spreads retrogradely along the nerve root to the spinal cord and causes disease.
2 other parts of the infection are caused by viremia, and then spread to the spinal cord through the blood circulation. In addition, the necrotic inflammatory reaction of the blood vessel wall caused by viral infection and its antibody-mediated immune response damage are also important mechanisms leading to the disease. An autopsy report of AIDS complicated with HTLV-1 myelopathy found extensive axonal destruction and loss of myelin in the lateral column of the spinal cord, and spinal cord hardening, hyaline degeneration and necrosis.
2. Vascular disease: due to fibrillar or hyaline degeneration and necrosis of small arteries, leading to stenosis or occlusion of the lumen, causing spinal cord ischemia, and anti-phospholipid antibody syndrome, this disease can be used as the first symptom and has a recurrent tendency .
3. Related to demyelinating diseases: Deng Rongkun et al (1984) compared the pathological changes of this disease with optic neuromyelitis, and found that the two are basically the same, and because some pathogenesis is very similar to MS, it has been proposed that multiple sclerotic spinal cord Diagnosis of inflammation.
4. Primary: Speculated to be associated with autoimmune changes induced after infection.
Pathological changes:
Damage can invade any segment of the spinal cord, the most common chest spinal cord, generally showing spinal cord swelling, soft texture, soft membrane congestion, opacity or inflammatory exudate attachment, spinal cord gray, white matter boundary is unclear, microscopic examination : soft meningeal and intramedullary vasodilatation, hyperemia, inflammatory cell infiltration around the blood vessels, swelling of nerve cells, nuclear translocation and cell fragmentation, dissolution, severe spinal cord softening, necrosis and cavity formation, visible in the white matter Swelling of the sheath, loss and axonal degeneration, disappearance of advanced nerve cell atrophy, scar formation at the lesion site, and finally spinal cord atrophy and thinning.
Prevention
Acute transverse myelitis prevention
Common secondary to rheumatic diseases, sarcoidosis, malignant tumors, infections, etc., it should prevent rheumatism and infection and other induced causes.
For patients with acute phase, complications such as urinary tract infections, hemorrhoids, and pneumonia should be prevented.
Complication
Complications of acute transverse myelitis Complications, urinary incontinence, acne, pneumonia, medullary paralysis
Urinary incontinence, hemorrhoids and urinary tract infections, respiratory muscle paralysis, hypostatic pneumonia, dry skin and no sweat, low skin temperature, finger (toe) nail brittle fracture, Horner sign, bulbar palsy.
Symptom
Acute transverse myelitis symptoms Common symptoms Dyspnea urinary incontinence Meningeal irritation Sensory sensation Sensation Spirometry Shock Cough skin Dry spinal cord intermittent break
Acute onset, often first back pain, chest and abdomen belt sensation and lower limb numbness, after the rapid development of spinal cord injury below the plane, feeling and dysfunction, mostly peak in hours to days, 70% ~75% are found in the thoracic marrow, followed by the cervical spinal cord, the lumbar spinal cord, and the medullary pulp are the least seen. The level, extent and severity of spinal cord damage vary depending on the cause.
At the beginning of the disease, it is often manifested as spinal shock. The sputum is tachycardia. After 3 to 4 weeks, it becomes spasmodic. The muscle strength begins to recover from the distal to the proximal end. The length of the shock period is related to the degree of spinal cord damage and the number of complications. A small number of patients with spinal cord softening and necrosis due to blood supply disorders, after the shock period, the limbs will still be in a long-term retarded state, and the prognosis is poor.
The sensory disturbance is a conduction beam type, and various sensations below or below the lesion level are reduced or disappeared. Some of the sensory allergy areas or band-like sensation abnormalities in the upper edge of the sensory disappearance area are 1 or 2 segments, and the lesions are different. There may be spinal cord hemisection damage, and very few have no sensory disturbances.
In the early stage of the disease, there was defecation and retention. The shock stage was mainly urinary incontinence. After the spinal cord function recovered, the bladder detrusor showed rhythmic contraction. 50% recovered urinary function within 2 to 3 weeks. Other autonomic symptoms included Dry skin, no sweat, low skin temperature, finger (toe) nail crack, Horner sign and so on.
Part of the spinal cord lesions can progress rapidly from the lower segment to the high position. The sputum begins in the lower limbs within a few hours to several days, involving the waist, chest, and neck in turn, and finally affects the medulla, dyspnea, drinking water, coughing, and speech. It is called ascending myelitis, and the prognosis is poor. A few lesions involve the spinal cord or spinal nerve roots, and meningeal irritation occurs.
According to the acute onset, rapidly progressing lower extremity paralysis or quadriplegia, conduction beam sensation and dysfunction, spinal MRI showed segmental swelling and scattered spots, patchy abnormal signals, if there is infection or vaccination before the disease History should consider this disease.
Examine
Examination of acute transverse myelitis
1. Peripheral blood: The white blood cell count is normal, and mild to moderate elevation if there is infection.
2. Cerebrospinal fluid examination: CSF pressure is mostly normal, a few due to spinal cord swelling caused by mild obstruction of the spinal canal, the appearance of colorless and transparent, the number of cells may be normal or mild to moderately elevated depending on the cause, most of them are lymphocytes The protein is normal or slightly elevated, and glucose and chloride are normal.
3. PCR detection of CSF and blood bacterial or viral DNA or RNA; enzyme-linked immunosorbent assay for detection of pathogenic bacteria antibodies; CSF pathogen culture or animal inoculation methods to find the source of infection.
4. ESR, antiphospholipid antibody, rheumatism series, anti-double-stranded DNA antibody, lupus belt test, etc., have differential diagnostic value.
5. Spinal MRI can show the location, extent and nature of spinal cord lesions early.
6. Neurophysiological examination.
Diagnosis
Diagnosis and diagnosis of acute transverse myelitis
The exact diagnosis should be based on the cause of the disease. Polymerase chain reaction (PCR) can be used to detect bacterial or viral DNA or RNA in CSF and blood, enzyme-linked immunosorbent assay (ELISA) for detection of pathogenic bacteria, CSF pathogen culture or animal inoculation, etc. Method to find the source of infection.
For patients with recurrent acute transverse myelitis, routine evoked potentials such as visual and somatosensory, MRI of the brain and spinal cord should be examined to observe the presence or absence of extraspinal lesions, to exclude multiple sclerosis, and to perform ESR, antiphospholipid antibodies. Check to exclude antiphospholipid antibody syndrome; for young women should be rheumatoid series, anti-double-stranded DNA antibodies, lupus belt test to exclude SLE and other autoimmune diseases; for patients with suspected primary spinal cord vascular disease, feasible myelography Or selective spinal angiography to confirm the diagnosis.
The disease should also be differentiated from epidural abscesses, spinal tuberculosis, spinal cord tumors, and Guillain-Barré syndrome.
