Spinal cord compression

　　Tumors are the most common, accounting for more than 1/3 of the total number of spinal cord compression symptoms. Vertebral body dislocation, fractured fragments, hematoma inflammation, parasitic granuloma abscess, intervertebral disc herniation, spinal cord vascular malformation, and certain congenital spinal diseases can all cause spinal cord compression.

　　1. Tumor

　　(1) The majority originate from the spinal cord tissue itself and its accessory structures, including tumors from the spinal nerves, spinal meninges, spinal cord glial cells, spinal blood vessels, and adipose connective tissue around the spinal cord. Nearly half are schwannomas, followed by meningiomas. In addition, certain congenital tumors such as dermoid cysts, epithelioid cysts, and teratomas also occur. The spinal cord epidural adipose tissue is rich, so the occurrence of lipomas is also not uncommon. Tumors can occur at any part of the spinal canal, but schwannomas are most common in the thoracic segment, and congenital tumors are more common in the lumbar sacral region.

　　(2) Malignant tumors originating from the spine and other organs can also invade and metastasize to the spinal canal, affecting the spinal cord. Among them, malignant tumors of the lung, breast, kidney, and gastrointestinal tract are common, and there are also cases of lymphoma and leukemia invading the spinal cord and causing symptoms of spinal cord compression.

　　2, Inflammation

　　Bacterial infection foci in other parts of the body, the direct spread of purulent foci in adjacent tissues of the spinal canal through hematogenous spread, and direct implantation ('iatrogenic') and other pathways can all cause acute abscesses within the spinal canal or chronic true granulomas that compress the spinal cord, with the most common being extramedullary abscesses. Subdural and intramedullary abscesses are extremely rare. Non-bacterial infectious arachnoiditis, as well as arachnoiditis caused by bleeding, chemical agents such as intrathecal drug injection, and certain unknown causes, can cause adhesions between the spinal cord and inflammatory arachnoid, and in severe cases, the arachnoid can form cysts that compress the spinal cord. In addition, certain specific inflammatory conditions such as tuberculous parasitic granulomas can also cause spinal cord compression.

　　3, Injured spine

　　Spinal cord injury often occurs in conjunction with spinal cord injury. Spinal cord compression can also be caused by reasons such as fractures of vertebral bodies, pedicles, and laminae, subluxation of small joints, intervertebral disc herniation, and the formation of intraspinal hematoma, leading to spinal cord compression.

　　4, Spinal cord vascular malformation

　　It is often caused by congenital abnormalities in embryonic development. The cause of spinal cord dysfunction due to vascular malformations in the spinal cord, in addition to the compressive effect of the expanded and swollen malformed vessels, also includes ischemic damage to the spinal cord due to arteriovenous短路 and venous congestion.

　　5, Intervertebral disc herniation, also known as nucleus pulposus herniation

　　It also belongs to a relatively common cause of spinal cord compression, often due to overexertion or excessive extension and flexion of the spine.

　　6, Other

　　Certain congenital spinal diseases, such as basilar invagination, atlantoaxial ossification, spondylolisthesis, meningocele, spina bifida, scoliosis, and severe hypertrophic spondyloarthritis, can all cause spinal cord compression.

　　Symptoms and signs that appear with the progression of the disease, combined with the manifestations of the primary disease, often lead to complications such as pulmonary infection, urinary tract infection, and bedsores. It is easy to develop insufficient pulmonary function and inadequate ventilation and gas exchange when unable to get up for a long time, which can trigger atelectasis. At the same time, the deposition of toxins and impurities can easily lead to urinary tract infections; if lying down for a long time, it can lead to local pressure sores.

　　The clinical manifestations of spinal cord compression syndrome vary due to the nature of the lesion, the location of the lesion, the speed of development, and the extent of involvement. For example, spinal cord tumors usually develop slowly and gradually; vertebral metastatic cancer and extramedullary abscesses often cause acute compression symptoms; the symptoms of spinal cord compression caused by spinal tuberculosis can be either slow or acute. Generally speaking, the development process of clinical symptoms is as follows:

　　Symptoms of spinal nerve root compression

　　The pain, often burning, tearing, or piercing, may result from compression of one or more posterior roots of the spinal nerves and can radiate to the corresponding dermatomes. The pain may worsen during activities such as moving the spine, coughing, or sneezing, and can be relieved by changing the body position. This primary radicular pain symptom is often of significant diagnostic significance. Conditions such as spinal epiduralitis, extramedullary tumors, particularly neurofibromas, and vertebral canal collapse caused by various etiologies can lead to prominent radicular pain. Sensory hyperesthesia or abnormal areas can often be found at the site of radicular pain, and if the function is impaired, it can cause segmental sensory dullness. If the lesion is located on the ventral side of the spinal cord, it can stimulate and damage the anterior roots of the spinal nerves, causing segmental muscle spasms and atrophy.

　　2. Symptoms of spinal cord compression

　　1. Motor impairment. When the anterior horn of the spinal cord is compressed, segmental hypomotor neuron paralysis symptoms may occur, manifested as muscle atrophy, weakness, and muscle tremors in the limbs or trunk under the control of the damaged anterior horn. When the corticospinal tract is damaged, it causes spastic paralysis below the level of compression of the limbs, with increased muscle tone, hyperactive tendon reflexes, and positive pathological reflexes. In chronic lesions, they usually start from one side and then affect the other side; in acute lesions, they often affect both sides simultaneously, and there is a stage of spinal cord shock in the early stage (flaccid paralysis of the limbs below the lesion), which usually takes about 2 weeks to gradually transition to spastic paralysis. If the lesion is in the lumbar sacral segment, the symptoms of upper motor neuron damage will not appear.

　　2. Sensory impairment. When the lesion damages the spinothalamic tract and posterior tract, it causes a fasciculate sensory impairment below the level of damage in the body. If the ascending sensory conduction tract on one side is damaged first, it manifests as the impairment of deep sensation below the level of damage on the same side of the body and superficial sensation on the opposite side; when the lesion develops to transverse damage of the spinal cord, there is impairment of both deep and superficial sensations below the level of damage. In extramedullary compressive lesions, the impairment of pain and temperature sensation often starts from the lower limbs and extends to the level of compression; in intramedullary compressive lesions, the impairment of pain and temperature sensation often extends downward from the level of compression. The level of sensory impairment often has great reference value for the localization of the lesion.

　　3. Abnormal reflexes. If the reflex arc at the site of the lesion is damaged, the normal physiological reflexes within that segment are weakened or disappear, which is helpful for localization diagnosis. When one side of the pyramidal tract is damaged, the tendon reflexes below the same side of the lesion site become hyperactive, the abdominal wall reflex and cremasteric reflex become slow or disappear, and the pathological sign is positive; when both sides of the pyramidal tract are not affected, abnormal reflexes and pathological signs appear on both sides below the lesion site.

　　4. Autonomic nerve dysfunction: Below the level of the lesion, the skin is dry and sweat is less, the nails are rough, and the limbs are edematous. In the early stage of chronic compression lesions above the lumbar sacral cord, urgency of urination is not easy to control; if it is an acute shock phase with rapid damage, the functions of automatic urination and defecation are lost, and then it transitions to incontinence of urine and feces. Lesions in the lumbar sacral cord manifest as urinary and fecal retention. Bladder dysfunction appears earlier in intramedullary lesions than in extramedullary lesions. Lesions in the upper cervical cord can produce Horner's syndrome.

　　5. During the process of chronic compression of the spinal cord, there can be a development process from hemisectional damage to transverse damage, which is more easily seen in extramedullary tumors. Hemisectional damage refers to the impairment of deep sensation and pyramidal tract signs below the level of damage on the same side and superficial sensory impairment on the opposite side (spinal hemisection syndrome); transverse damage refers to the impairment of both deep and superficial sensations, pyramidal tract, and autonomic nerve dysfunction below the level of damage.

　　3. Spinal symptoms

　　The lesion site may have signs such as tenderness, percussion pain, deformity, limited activity, etc.

　　4. Vertebral canal obstruction

　　Compressive spinal cord disease can cause incomplete or complete obstruction of the subarachnoid cavity of the spinal cord. It is manifested as a decrease in cerebrospinal fluid pressure during lumbar puncture, lack of normal fluctuations in cerebrospinal fluid pressure with respiration and pulse, and Quincke test showing incomplete or complete obstruction. The appearance of cerebrospinal fluid may be pale yellow or yellow, with increased protein content. After lumbar puncture, it is often accompanied by exacerbation of neurological symptoms. Extra caution should be taken during lumbar puncture in patients suspected of having high cervical cord lesions to avoid exacerbation of symptoms and respiratory muscle paralysis.

　　The prevention of spinal cord compression mainly involves preventing various primary diseases from compressing and damaging the spinal cord. It is advocated to relieve spinal cord compression by early surgery; in treatment, it should be as early as possible to select nerve nutrition and metabolism drugs such as B vitamins, vitamin E, cytidine diphosphate choline ATP coenzyme A, and nerve growth factors, and other drugs or partially improve the function of the spinal cord.

　　Spinal cord compression is a common disease of the nervous system. It is a group of intraspinal lesions with space-occupying characteristics. There are obvious progressive clinical manifestations of spinal cord compression, with the development and expansion of the cause, the spinal cord, spinal nerve roots, and their supplying blood vessels are compressed and become increasingly severe, which will seriously affect the patient's quality of life and ability to work. Then, what kind of laboratory tests are needed for spinal cord compression? The following experts introduce the laboratory tests needed for spinal cord compression.

　　1. Laboratory examination

　　Cerebrospinal fluid examination refers to the determination of cerebrospinal fluid dynamics and routine, biochemical examination is an important method for diagnosing spinal cord compression.

　　1. Dynamic changes in cerebrospinal fluid

　　When compressive lesions cause subarachnoid blockage of the spinal cord, intracranial pressure cannot be transmitted to the subarachnoid space below the blockage level, resulting in low pressure in the subarachnoid space below the blockage level, sometimes even undetectable. Occasionally, normal or even elevated pressure may be observed, which mostly belongs to cases with partial or no blockage. In completely blocked cases, the pressure is generally low, and there is no fluctuation in the cerebrospinal fluid level. Pathological changes in cerebrospinal fluid pressure are of great significance for the diagnosis of spinal cord compression and subarachnoid blockage. The dynamic examination of cerebrospinal fluid generally has three results: ① No blockage in the subarachnoid space of the spinal cord; ② Partial blockage; ③ Complete blockage, with the possibility of needle penetration into the tumor during lumbar puncture in cases of caudal spinal cord lesions (tumors). At this time, cerebrospinal fluid cannot be obtained. If there is fluid, it may be tumor cyst fluid, which is generally yellowish and sticky. The pressure is not affected by the dynamic test and should not be mistaken for complete blockage of the subarachnoid space. At this time, it should be chosen to puncture the previous or two vertebral spaces again. If cerebrospinal fluid is obtained, it can be used to judge the location of the lesion. The size of the tumor is the main factor causing subarachnoid blockage, but whether there is adhesion around the tumor also has an important impact. In addition, the cavity of the thoracic vertebra is narrower than that of the lumbar and lower cervical segments. A tumor of the same size can cause complete blockage earlier in the thoracic segment than in the lumbar segment, or the cervical segment.

　　2. Cerebrospinal fluid cell count

　　The cerebrospinal fluid cell count is generally within the normal range. In cases of inflammatory lesions, there is often an increase in white blood cells; in cases of tumor hemorrhage and necrosis, there may be an increase in red blood cells and white blood cells.

　　3. Cerebrospinal fluid color and protein content

　　The cerebrospinal fluid is colorless and transparent with low protein content, and pale yellow to orange yellow with high protein content. The quantitative content per hundred milliliters ranges from several hundred milligrams to more than 1g. It can self-coagulate when left aside, known as the self-coagulation phenomenon. The amount of protein in cerebrospinal fluid with spinal cord compression is related to the degree of subarachnoid space obstruction, the duration of obstruction, and the height of the obstruction level. Generally, the more complete the obstruction, the longer the duration of obstruction, the lower the obstruction level, and the higher the protein content. Tumor compression has a higher protein content than non-tumor compression, especially neurinoma, which often grows in the subarachnoid space, and its cerebrospinal fluid protein content is also higher than that of other types of tumors. The increase in cerebrospinal fluid protein content due to spinal cord compression can also be caused by compression of the spinal cord supply vessels, leading to congestion and hypoxia, which increases the permeability of the vascular wall and the amount of protein exudation; it can also be due to subarachnoid space obstruction, which prevents the cerebrospinal fluid on the distal side from participating in normal circulation, resulting in the absorption of a small amount and concentration.

　　It should be pointed out that when performing cerebrospinal fluid dynamic examination by lumbar puncture, due to the possible movement of the tumor position (such as neurinoma), it may cause sudden exacerbation of symptoms of spinal cord compression or increased pain, which must be estimated in advance.

　　It is not difficult to judge spinal cord lesions based on medical history and physical examination, but it is not easy to accurately determine the location, degree, and nature of the lesions. Although some valuable focal signs in clinical practice can be used for localization diagnosis, errors are still common. The judgment of the degree and nature of the lesions is often much larger than the actual situation, so it is generally necessary to conduct further examinations, especially before considering surgery or radiotherapy, and choosing appropriate auxiliary examinations is indispensable.

　　2. Imaging examination

　　1. Spinal X-ray imaging

　　The positioning includes anteroposterior view, lateral view, and oblique view when necessary. The focus of spinal injury observation is the presence of fractures, dislocations, luxations, and narrowing of intervertebral spaces. Benign tumors may show up in about 50% of cases, such as widened distances between vertebral pedicles, deformed or blurred vertebral pedicles, expanded intervertebral foramina, concave posterior edges of vertebral bodies, osteoporosis, and destruction. Metastatic tumors commonly show bone destruction. In the early stage of the disease, there may be no changes, but the incidence and severity of bone changes increase with the progression of the disease.

　　2. Magnetic Resonance Imaging (MRI)

　　It can clearly show the断层 images of different axes, provide a clearer anatomical structure level, and provide the most valuable information on the location, upper and lower margin boundaries, position, and nature of the spinal cord lesions, which is the most valuable tool for diagnosing spinal cord lesions.

　　3. CT

　　Tumors smaller than 5mm can be detected by high-resolution imaging, and the images are clear, able to accurately show the location and relationship of the tumor to the spinal cord.

　　4. Myelography

　　Medical units without MRI or CT equipment can use this to help with diagnosis.

　　5. Radionuclide Scanning

　　Using 99mTc or 10mCi of 131I (sodium iodide) is injected through lumbar puncture, and a full-length spinal cord scan is performed half an hour later, which can accurately judge the blocked location with less patient pain and fewer reactions.

　　The diet of patients with spinal cord compression should be reasonably balanced with grains, lean meat, fish, eggs, milk, various vegetables, and soy products, and the amount of each should not be excessive. This can supplement the various nutrients needed in the body.

　　The diet of patients with spinal cord compression should be given according to medical advice, and the diet should start with thin and soft food and gradually increase other foods as the body adapts. It is important not to consume too much oil, and to reasonably match sugar, fat, protein, minerals, vitamins, and other foods.

　　Patients with spinal cord compression should avoid foods and刺激性 food that are harmful to the condition, such as chili, especially patients in the acute stage and those with yin deficiency and fire hyperactivity should best avoid them.

　　Most cases of spinal cord compression require surgical treatment. Tumors growing outside the spinal cord can be removed, and benign tumors can be completely removed without recurrence. Tumors growing inside the spinal cord are difficult to completely remove, and surgical removal may worsen symptoms. Metastatic tumors cannot be completely removed, and the surgical outcome is not good.

　　An epidural abscess should be treated with emergency surgery to drain the pus in the spinal canal, and spinal tuberculosis should also be treated promptly with surgery to remove the focus of tuberculosis. If the cause of spinal cord compression cannot be removed, a part of the vertebral bone (vertebral plate) can be removed to widen the spinal canal and alleviate the degree of compression on the spinal cord, which is called decompression surgery. Malignant tumors can be treated with radiotherapy and antitumor drug therapy.