Anatomy and physiology of spinal cord

Clinical manifestations of damage to different parts of the spinal cord

Characterization of spinal cord disease

Overview

Cause and pathogenesis

pathology

clinical manifestations

Auxiliary inspection

diagnosis

Differential diagnosis

treat

prognosis

definition

Cause

Pathogenesis

clinical manifestations

Auxiliary inspection

diagnosis

Differential diagnosis

treat

prognosis

Chapter 16 Spinal Cord Diseases Overview The spinal cord is an important part of the central nervous system. It is the downward extension of the brainstem. Its upper end is at the level of the foramen magnum and the medulla oblongata. Then, the lower end reaches the lower edge of the first lumbar vertebra to form the conus medullaris. The spinal cord is divided into 31 segments from top to bottom and sends out 31 pairs of spinal nerves, including the neck (C) There are 8 pairs of nerves, 12 pairs of thoracic (T) nerves, 5 pairs of lumbar (L) nerves, 5 pairs of medullary (S) nerves, and 1 pair of caudal (Co) nerves. The spinal cord is slightly flattened anteriorly and posteriorly Cylindrical in shape, with varying thicknesses throughout its entire length, it has two enlarged parts: neck enlargement (C, ~T) and waist enlargement (L, ~S), which respectively control the upper and lower limbs. of nerve roots. The interior of the spinal cord is composed of gray matter and white matter, which contain a large number of nerve cell nuclei and ascending and descending conduction tracts respectively, which provide various movement and Primary sensory center and important reflex center. The anatomical structure and physiological functions of the spinal cord are detailed in Section 1 of Chapter 2 [Clinical manifestations of spinal cord injury] They are mainly movement disorders, sensory disorders, sphincter dysfunction and other autonomic nervous system dysfunctions. The first two have a significant impact on the level of spinal cord lesions. The positioning is very helpful 1. Incomplete spinal cord damage is based on the location of the damage, such as the anterior horn, posterior horn, near the central canal, lateral horn, anterior funiculus, posterior funiculus, lateral funiculus, etc. Different symptoms and signs occur: Damage to one side of the spinal cord can cause Brown-Seq uard syndrome, which manifests as damage to For ipsilateral upper motor neuron paralysis below the plane, deep sensory impairment, and contralateral pain and temperature impairment, see Chapter 2, Section 1 for details. 2. Transverse spinal cord damage, bilateral upper motor neuron paralysis, total sensory loss, and sphincter dysfunction below the affected segment. In the acute phase of severe transverse injury, spinal shock occurs, manifesting as peripheral paralysis, which usually lasts for 2 to 4 weeks before reflex activity Movement gradually recovered and transformed into central paralysis. Determining the level of transverse spinal cord damage is mainly based on the level of sensory impairment, reflex changes and segments. Sexual symptoms, such as radicular pain or radicular distribution sensory disturbance, segmental muscle atrophy, loss of tendon reflexes, etc. High neck, enlarged neck, enlarged chest, enlarged waist, Damage to each spinal cord segment and cauda equina of the conus medullaris has different symptoms and signs respectively. Please see Chapter 2, Section 1 for details. [Characterization of spinal cord diseases After locating the disease and its anatomical level, the nature of the lesion can be roughly inferred, and then through special clinical examinations and laboratory examinations The cause of the disease can be diagnosed. 1. Judging from the location of the lesion on the cross-section of the spinal cord (1) Posterior root: neurofibroma, radiculitis (herpes zoster), posterior disc protrusion, secondary spinal stenosis (2) Posterior roots and posterior cords: spinal cord tumors, myelopathy, multiple sclerosis, spinal vascular lesions (3) Posterior cord, spinocerebellar tract and lateral cord: hereditary ataxia (4) Posterior and lateral cords: subacute combined degeneration and tuberculous meningomyelitis (5) Lateral cords and anterior horns: amyotrophic lateral sclerosis, ossification of the posterior longitudinal ligament, cervical spondylosis (6) Anterior horn and anterior root: poliomyelitis, Japanese encephalomyelitis, anterior spinal artery syndrome (7) Central gray matter and anterior horn of the spinal cord: syringomyelia, spinal cord hematoma, spinal cord hyperextension injury, and intramedullary tumors. (8) Spinal cord hemisection: extramedullary spinal cord tumors, spinal cord injury, spinal tuberculosis (9) Spinal cord transection: spinal cord trauma, transverse myelitis, advanced spinal cord compression, epidural swelling, metastatic cancer, tuberculosis, etc. 2. Judgment based on the anatomical level of the lesion (1) Intramedullary lesions: myelitis, spinal vascular disease, vascular malformation, myelopathy caused by metabolism or vitamin deficiency, syringomyelia Ependymoma, astrocytoma, angioreticuloma 371

372 Chapter 16 Spinal Cord Diseases (2) Extramedullary intradural lesions: schwannoma, meningioma. (3) Epidural lesions: spinal tumors, metastases, fatty hemangiomas, thick tumors, etc. Chapter 1 acute myelitis Acute myelitis (acute myelitis) refers to acute transverse myelitis inflammatory lesions caused by autoimmune reactions after various infections. Also known as acute transverse myelitis, it is the most common clinical myelitis, characterized by paralysis of the limbs below the level of the lesion and sensory impairment of conductive tracts. It is characterized by obstruction and urinary and defecation disorders. 【Cause and pathogenesis The cause is unknown and includes different clinical syndromes such as postinfectious and postvaccination myelitis, demyelinating myelitis (acute Multiple sclerosis), necrotizing myelitis and paraneoplastic myelitis, etc. Most patients have fever and shortness of breath 1 to 4 weeks before the onset of spinal cord symptoms. Symptoms of viral infection such as respiratory tract infection and diarrhea, but no viral antibodies were detected in the cerebrospinal fluid, and no virus was isolated from the spinal cord and cerebrospinal fluid. It is speculated that It can be related to the autoimmune response after viral infection and is not caused by direct infection. It is non-infectious inflammatory myelitis (my elit is of non-in- fec tio us inflammatory type) 【pathology】 The disease can affect any segment of the spinal cord, but it is most common in the thoracic cord (T 3-) because the blood supply there is not as abundant as elsewhere. Rich, easily affected; followed by cervical cord and lumbar cord. Acute transverse myelitis is usually limited to 1 segment, with multiple foci converging or multiple segments scattered. It is less common in lesions; if there are more than 2 scattered lesions in the spinal cord, it is called disseminated myelitis. Swelling and texture of the spinal cord in the affected segment can be seen with the naked eye. Becoming soft, the pia mater is congested or has inflammatory exudates. The cut surface shows softening of the spinal cord, unclear edges, and unclear boundaries between gray matter and white matter. under the mirror It can be seen that the blood vessels in the pia mater and spinal cord are dilated and congested, and the perivascular inflammatory cells are infiltrated, mainly lymphocytes and plasma cells. inner gray matter nerves Cell swelling, Nissl body dissolution, and cell fragmentation, dissolution, and disappearance may occur; myelin loss and axonal degeneration in the white matter, and collagen can be seen in the lesions Plasma cell proliferation. When the spinal cord is severely damaged, it can soften and form a cavity. [Clinical manifestations] This disease can occur at any age, but is more common in young adults. There is no significant difference in the incidence rate between men and women. Upper respiratory tract symptoms often occur 1 to 2 weeks before onset of illness Infection, symptoms of gastrointestinal infection, or history of vaccination. Trauma, fatigue, cold, etc. are the triggers of the disease. Acute onset, low fever at onset Nerve root pain in the affected area, numbness and weakness in the limbs, and bandage sensation in the affected segment; there are also patients who suddenly develop paralysis and phlegm without any other symptoms. big Movement disorders below the affected level, sensory loss, and bladder and rectal sphincter dysfunction often occur within hours or days. thoracic spine Myelitis is the most common, especially in the T segment, followed by cervical cord and lumbar cord. 1. Movement disorder has an acute onset and rapidly progresses. The early stage is the spinal shock stage, with paralysis of the limbs, reduced muscle tone, and loss of tendon reflexes. Loss, pathological reflex negative. Generally, it lasts for 2 to 4 weeks before entering the recovery period. Muscle tension and tendon reflexes gradually increase, pathological reflexes appear, and limb muscles Strength recovery often begins at the distal end of the lower limb and then gradually moves upward. The length of the spinal shock period depends on the severity of the spinal cord injury and the presence or absence of pulmonary Complications such as genital infections, urinary tract infections, and pressure ulcers. Severe spinal cord injury often results in increased flexor muscle tone. Irritation in any part of the lower limbs or A full bladder can cause flexion reflexes and pain in the lower limbs, accompanied by symptoms such as sweating, piloerection, and automatic discharge of urine and feces. This is called a general reflex and is often mentioned. Indicates poor prognosis. 2. Sensory disorder: loss of all sensation below the lesion segment, with hyperesthesia or banding sensation at the upper edge of the sensory loss level; mild Patients with the disease may not feel the plane clearly. As the disease recovers, the sensory level gradually decreases, but it is slower and worse than the recovery of motor function. 3. The early manifestation of autonomic nervous system dysfunction is urinary retention. During the spinal shock stage, the bladder capacity can reach 1000 ml, showing atonic nerves. Due to excessive bladder filling, filling urinary incontinence may occur. As spinal cord function recovers, bladder capacity shrinks and urine fills to 300 to 400 ml means spontaneous urination is called reflex neurogenic bladder, and overflow urinary incontinence occurs. Little or no sweating below the lesion level, Skin desquamation and edema, brittle fingernails and hyperkeratosis, etc. There may be episodic excessive sweating, skin flushing, and reflexes above the lesion level. Bradycardia, etc., is called autonomic dysreflexia (autonomic dysreflex i a). 【Auxiliary inspection】 1. Cerebrospinal fluid examination. The neck compression test is unobstructed. In a few cases, severe spinal edema may cause incomplete obstruction. Cerebrospinal fluid pressure is normal, external

373 Chapter 16 Spinal Cord Diseases Appearance is colorless and transparent, cell number and protein content are normal or slightly increased, mainly lymphocytes, sugar and chloride are normal 2. Electrophysiological examination (1) Visual evoked potential (VEP): normal, which can be used as a basis for differentiation from neuromyelitis optica and multiple sclerosis. (2) Lower limb sensory evoked potential (SEP): the amplitude can be significantly reduced. (3) Abnormal motor evoked potential (MEP) can be used as an indicator to judge efficacy and prognosis. (4) Electromyography: can be normal or show denervation changes 3. Imaging examination and spine X-ray are normal. If the spinal cord is severely swollen, MRI will show that the spinal cord in the diseased area is thickened and the spinal cord in the diseased segment is thickened. There are multiple patchy or diffuse T-hyperintensities with uneven intensity and possible fusion (Figure 16-1). Some cases may always be normal. Figure 16-1 MRI manifestations of acute myelitis A.T-weighted image shows localized thickening of the spinal cord at the upper thoracic level, showing lower signal; B.T 2-weighted image shows higher signal in the corresponding segment Signal [Diagnosis and differential diagnosis] 1. Diagnosis is based on acute onset, history of infection or vaccination before illness, rapid onset of clinical manifestations of transverse spinal cord damage, and results. With the combination of cerebrospinal fluid examination and MRI examination, the diagnosis is not difficult. 2. Differential diagnosis requires identification of the following diseases (1) Neuromyelitis optica: It is a demyelinating disease. In addition to the symptoms of transverse myelitis, there is also vision loss or abnormal VEP. Optic neuropathy can occur before, at the same time, or after spinal cord symptoms (2) Spinal vascular disease 1) Ischemic: Anterior spinal artery occlusion syndrome is easily confused with acute myelitis. Root pain and short-term pain may occur at the corresponding location of the lesion. Paraplegia, loss of pain and temperature sensation, and urinary and defecation difficulties occurred for a period of time, but deep sensation was preserved. 2) Hemorrhagic: Spinal cord hemorrhage is rare and is mostly caused by trauma or spinal vascular malformation. It has an acute onset and is accompanied by severe back pain, limb paralysis and Retention of urine and feces. Bloody cerebrospinal fluid may be present, and MRI examination is helpful in diagnosis. (3) Subacute necrotizing myelitis (sub acute necrotizing myelitis): more common in men over 50 years old, and slowly progressively worsens Weakness of both lower limbs, hyperreflexia of tendons, and positive pyramidal tract signs are often accompanied by muscle atrophy and decreased sensation below the level of the lesion. As the disease progresses Symptoms gradually worsen and lead to complete paraplegia, urinary and defecation difficulties, obvious muscle atrophy, reduced muscle tone, and weakened or absent reflexes. cerebrospinal fluid protein Increased, mostly normal cell count. Lipiodol myelography shows dilated blood vessels on the surface of the spinal cord. This disease may be a thrombotic disease of the spinal cord Phlebitis, spinal angiography can confirm the diagnosis. (4) Acute spinal cord compression: Spinal tuberculosis or metastatic cancer causes damage to the vertebral body, which suddenly collapses and compresses the spinal cord, leading to acute transverse spinal cord compression. damage. Spinal imaging examination can show changes such as vertebral body destruction, intervertebral space narrowing, or cold swelling of the vertebral body. In addition to spinal imaging examination for metastatic cancer, A whole body bone scan can be done.

374 Chapter 16 Spinal Cord Diseases (5) Acute epidural swelling: The clinical manifestations are similar to acute myelitis, but there are purulent lesions and a history of infection. Tenderness, spinal canal obstruction, increased white blood cells in peripheral blood and cerebrospinal fluid, and significantly increased cerebrospinal fluid protein content. MRI can help diagnose (6) Acute inflammatory demyelinating polyneuropathy: flaccid paralysis of the limbs, terminal sensory impairment, and may be accompanied by cranial nerve damage. Sphincter dysfunction is rare, and even if it occurs, it usually recovers within a few days to a week in the acute phase. (7) Human T lymphotropic virus type 1 associated myelopathy (HT LV-1 associated myelopathy, HAM); is a human T lymphocyte Myelopathy related to immune abnormalities caused by chronic infection with cell type 1 virus is clinically characterized by slowly progressive paraplegia. 【treat】 Acute myelitis requires early diagnosis, early treatment, and careful care. Early rehabilitation training is also very important for the prognosis. 1. General treatment, enhanced care, and prevention of various complications are the prerequisites for ensuring functional recovery. (1) People with high cervical myelitis and dyspnea should take oxygen in time to keep the respiratory tract open, and use effective antibiotics to control infection. Tracheotomy and artificial assisted respiration if necessary (2) People with urinary disorders should keep a sterile urinary catheter and release the drainage tube every 4 to 6 hours. When bladder function is restored, residual urine volume Do not catheterize when the volume is less than 100 ml to prevent bladder contraction and volume reduction. (3) Keep the skin clean, turn over, pat the back, and suction on time, and use air cushions or soft cushions in areas prone to pressure to prevent pressure sores. redness of skin The area can be gently rubbed with 10% ethanol or warm water, and 3.5% benzoin alcohol can be applied. If ulcers are formed, the dressing should be changed in time and a pressure ulcer patch should be applied. 2.Drug treatment (1) Corticosteroids: In the acute phase, high-dose methylprednisolone short-course pulse therapy can be used, intravenous infusion of 500 to 1000 mg, every Once a day for 3 to 5 days, it is possible to control the progression of the disease. Dexamethasone 10 to 20 mg can also be used as an intravenous infusion, once a day for 7 to 14 days. For one course of treatment. After using the above drugs, switch to oral prednisone at 1 mg per kilogram of body weight or 60 mg daily for adults for 4 to 6 weeks. Gradually reduce the dose and discontinue the drug. (2) High-dose immunoglobulin: The daily dosage can be calculated as 0.4 g/kg. The dosage for adults is generally about 20 g per time. Intravenous drip, every Once a day, use for 3 to 5 days as a course of treatment. (3) Vitamin B family: Contributes to the recovery of nerve function. Commonly used vitamin B, 100 mg, intramuscular injection; vitamin B, 500~ 1000 ug, intramuscular injection or intravenous administration, 1 to 2 times a day. (4) Antibiotics: Select antibiotics based on the results of etiological examination and drug sensitivity test to treat respiratory and urinary system infections in a timely manner. Avoid aggravating the condition. Antiviral drugs include acyclovir, ganciclovir, etc. (5) Others: Vasodilators, such as nicotinic acid and nimodipine, can be used in the acute phase. Neurotrophic drugs, such as adenosine triphosphate, citicoline Alkali, efficacy undetermined. People with arthritis in both lower limbs can take baclofen 5~10 mg, 2~3 times a day. 3. In the early stage of rehabilitation treatment, paralyzed limbs should be maintained in functional positions to prevent limb and joint pain and joint shrinkage, and promote muscle strength recovery. and perform passive, active exercises and local limb massage. 【Prognosis】 The prognosis depends on the degree of acute spinal cord damage and complications. If there are no serious complications, the disease will basically recover within 6 months and the child will be healthy. Take care of yourself. Six months after complete paraplegia, the electromyogram still shows denervation changes, MRI shows extensive intramedullary signal changes, and the range of lesions involves the spinal cord. Those with multiple and diffuse medullary segments have a poor prognosis. Complicated urinary system infections, pressure ulcers, and pulmonary infections often affect recovery and leave sequelae. acutely Ascending myelitis and high cervical myelitis have a poor prognosis, and they can die from respiratory and circulatory failure in the short term. Section 2 Spinal Cord Compression Compressive myelo path y is a group of spinal cord compression syndrome caused by space-occupying lesions in the spinal canal or vertebrae. As the disease progresses, spinal cord hemisection syndrome, transverse damage, and spinal canal obstruction occur, and spinal nerve roots and blood vessels may be affected to varying degrees. [Cause and pathogenesis] 1.Cause (1) Tumors: common, accounting for more than 1/3 of the disease, and most originate from spinal cord tissue and adjacent structures. Located within the extramedullary dura mater

375 Chapter 16 Spinal Cord Diseases The most common one is schwannoma. Glioblastoma is the most common tumor in the spinal cord. Metastatic tumors are more common in the epidural. Malignant tumors of the spine can be Invasion of the spinal cord along the venous plexus around the spinal canal, lymphoma and leukemia are rare (2) Inflammation: non-specific inflammation of the spinal cord, tuberculous cerebrospinal meningitis, severe spinal stenosis, repeated injection of drugs into the spinal canal, and multiple intervertebral Disc lesions, repeated surgeries, and spinal anesthesia can cause arachnoid adhesions or compress blood vessels, affecting blood supply, causing spinal cord and nerve root involvement. Symptoms: Tuberculosis and parasites can cause chronic granulomas, arachnoiditis, arachnoid cysts, etc.: Hematogenous spread of purulent inflammation can cause acute epidural or subdural swelling (3) Spinal trauma: such as fractures, dislocations and intraspinal hematoma formation. (4) Spinal degenerative diseases: such as intervertebral disc herniation, posterior longitudinal ligament calcification and ligamentum flavum hypertrophy, etc., can lead to spinal stenosis (5) Congenital diseases: such as facial depression, circumvertebral occipitalization, cervical fusion malformation, spinal vascular malformation, etc. (6) Blood diseases: Patients with thrombocytopenia and other coagulation disorders may cause epidural hematoma and spinal cord compression after lumbar puncture. 2. Pathogenesis: In the early stage of spinal cord compression, it can be compensated by displacement, drainage of cerebrospinal fluid and surface venous blood flow. Although the appearance is obvious, Changes, but the nerve conduction path is not interrupted, and there may be no manifestations of neurological involvement; bone resorption may occur in later stages of compensation, causing local vertebrae to The canal is enlarged and there are usually obvious neurological symptoms and signs. The nature and speed of lesions produced by spinal cord compression can influence compensatory mechanisms To the degree of exertion, acute compression usually does not have sufficient time to compensate, and the spinal cord injury is serious; in chronic compression, the compensatory mechanism can be fully exerted, and the injury is relatively severe. For milder cases, the prognosis is better. The location of the lesion also affects the consequences of the injury. For example, if intramedullary lesions directly invade the nerve tissue, symptoms will appear earlier; Due to the obstruction of the dura mater, extradural space-occupying lesions cause less pressure on the spinal cord than intradural lesions; arterial compression and insufficient blood supply can cause spinal cord degeneration. Rhomboid contraction, venous compression and congestion lead to spinal cord edema. [Clinical manifestations] 1. Acute spinal cord compression Acute onset, rapid progression, often complete loss of spinal cord function within hours to days. multiple expressive ridges Transverse spinal cord damage, spinal cord shock, flaccid paralysis below the level of the lesion, loss of various sensations and reflexes, and retention of urine and feces 2. Chronic spinal cord compression progresses slowly, and early symptoms and signs may not be obvious. It can usually be divided into three stages: ① Root pain stage: superficial Present symptoms include nerve root pain and meningeal irritation; ② Partial spinal cord compression period: may manifest as spinal cord hemisection syndrome: ③ Complete spinal cord compression period: Symptoms and signs of complete transverse spinal cord damage occur. The three phases of performance are not completely separate, often overlap, and the boundaries are unclear. The main signs and symptoms of chronic spinal cord compression are as follows: (1) Nerve root symptoms: The lesions are small, and the compression has not yet reached the spinal cord, causing only irritation of the spinal nerve roots. Its main manifestation is root pain or focal movement disorder. The location of pain is fixed and limited to the dermatome area where the affected nerve root is distributed. The pain was so severe that it was described as electric It feels like hitting, burning, cutting or tearing. Actions that increase abdominal pressure such as coughing, defecation and straining can make the pain worse. Changing the body position can make the pain worse. Symptoms are relieved or worsened, and sometimes there is a banding sensation in the corresponding segment. As the disease progresses, nerve root symptoms can change from one side and intermittent to bilateral. Side, persistence. Hypersensitive bands can be found in the early stages, and segmental sensory loss in the later stages. Patients with lesions located on the ventral side of the spinal cord may have no radicular pain symptoms Symptoms of anterior root irritation may appear in the early stage, manifested as muscle bundle movements of the corresponding controlled muscle groups, and later muscle weakness and muscle atrophy may occur. These early symptoms The distribution location is very valuable for the localization and diagnosis of spinal cord compression. (2) Sensory impairment: Involvement of the spinothalamic tract results in decreased or absent pain and temperature sensation in the contralateral body that is 2 to 3 segments below the level of the lesion. If it is lost, the symptoms will be obvious in those with high pressure level. The sensory conduction fibers of the spinal cord have a certain order, which is helpful for the identification of intramedullary and intramedullary lesions. extramedullary disease Sensory disorder develops from the distal end of the lower limb upward to the compressed segment: in the early stage of intramedullary disease, dissociative sensory impairment occurs in the area dominated by the diseased segment, which causes and spinothalamic tract, the sensory impairment develops downward from the lesion segment, and the sellar area (S-) sensation is preserved until it is finally affected, which is called "saddle avoidance" Involvement of the posterior cord produces reduced or absent ipsilateral deep sensation below the level of the lesion. Later stage shows transverse spinal cord damage, with various lesions below the level of Sensation is missing. (3) Movement disorder: compression of the pyramidal tract on one side causes paralysis of the limbs on the same side below the lesion, increased muscle tone, hyperreflexia of tendons, and Pathological signs appear; in the early stage of bilateral pyramidal tract compression, the lower limbs show extension-like traction paralysis, and in the later stage, they show flexion-like painful paralysis and phlegm. anterior horn of spinal cord And pressure on the anterior root can cause flaccid paralysis of the muscles controlled by the diseased segment, accompanied by muscle fascicles and muscle atrophy. (4) Abnormal reflexes: When the posterior root, anterior root or anterior horn of the compressed segment is affected, the tendon reflex of the diseased segment is weakened or absent; the abdominal wall reflex and The Ticui reflex is absent; pyramidal tract involvement causes hyperreflexia and pathological reflexes on the ipsilateral side below the level of damage. (5) Autonomic symptoms: sphincter dysfunction appears early in intramedullary lesions, and urinary retention and defecation occur in early lesions above the cone.

376 Chapter 16 Spinal Cord Diseases Secretion, reflex bladder appears in the late stage; urinary and fecal incontinence occurs in conus and cauda equina lesions. Vasomotor and sudomotor dysfunction below the level of the lesion may Less sweating, no sweating, dry skin and desquamation are seen, the nails (toes) lose their luster, the subcutaneous tissue is loose, and pressure ulcers (pressure ulcers) are prone to occur. There is a sympathetic ciliary spinal cord center in the gray matter lateral horn of Cs~T. Horner syndrome will occur when damaged, which is a valuable location. physical signs. (6) Symptoms of meningeal irritation: mostly caused by epidural lesions, manifesting as local spontaneous pain, throbbing pain in the spine, and limited movement such as neck resistance. and positive straight leg raising test. 【Auxiliary inspection】 In order to determine the segment, nature and degree of compression of the disease, in addition to clinical neurological symptoms and signs, it is often necessary to resort to appropriate Auxiliary inspection. 1. Cerebrospinal fluid examination, routine cerebrospinal fluid examination, biochemical examination and dynamic changes are very helpful in determining the degree of spinal cord compression and spinal cord compression. value. If a lesion causes blockage in the subarachnoid space of the spinal cord, the pressure below the level of blockage is very low or even undetectable, and the pressure may be partially blocked or not blocked. The pressure of patients with congestion is normal or even increased. The neck compression test can prove whether there is spinal canal defecation obstruction, but a normal test cannot rule out obstruction; if the pressure increases during neck compression A rapid rise and a slow fall after the pressure is relieved, or a slow rise and even slower fall indicate incomplete obstruction. In cases of severe spinal canal obstruction, cerebrospinal fluid protein-cell When the cells are separated, the number of cells is normal, and the protein content exceeds 10 g/L, the yellow cerebrospinal fluid will automatically coagulate after flowing out, which is called Froin's sign. Common memes The more complete the obstruction, the longer it lasts, and the lower the level of obstruction, the higher the protein content. Lumbar puncture to drain cerebrospinal fluid below the level of obstruction and cervical compression test It may cause displacement of space-occupying lesions and worsen symptoms, so attention should be paid. When epidural swelling is suspected, lumbar puncture should be avoided at the spinal tenderness area to avoid Prevent subarachnoid space infection. 2. Imaging examination (1) Spinal X-ray: Spinal fractures, dislocations, dislocations, tuberculosis, bone destruction and spinal stenosis can be found; pedicle deformation or spacing Widening, enlargement of the intervertebral foramen, depression of the posterior edge of the vertebral body, or bone destruction may indicate metastatic cancer (2) CT and MRI: can show spinal cord compression, and MRI can clearly show the nature, location and boundaries of lesions in the spinal canal (Figure 16-2). Figure 16-2 MRI shows extramedullary subdural mass compressing the cervical spinal cord A.T weighted image: B.T weighted image (3) Myelography: It can show the interface of spinal canal obstruction. When the spinal canal is completely obstructed, ascending angiography only shows the lower boundary of the compressive lesion. The shadow can show the upper limit of the lesion. Medical units without MRI or CT equipment can use this to help with diagnosis (4) Nuclide scan: Apply 10 mCi of Tc or I (sodium iodide) and inject it through lumbar puncture. Half an hour later, a full-length scan of the spinal cord can be performed more efficiently. Accurately determine the location of obstruction. Patients suffer less pain and have fewer adverse reactions [Diagnosis and differential diagnosis] 1. Diagnosis first determines whether the spinal cord injury is compressive or non-compressive; then determines the location and plane of spinal cord compression, and then analyzes the compression Whether it is located in the intramedullary, extramedullary dura or epidural and the degree of compression; finally determine the cause and nature of the compressive lesion.

377 Chapter 16 Spinal Cord Diseases (1) Longitudinal positioning: determined based on the lesion characteristics of each segment of the spinal cord (see Section 1 of this chapter). Early segmental symptoms such as nerve root pain, sensory Hypoaesthetic areas, tendon reflex changes and muscle atrophy, spinous process tenderness and throbbing pain, especially the sensory level, have the most positioning significance, MRI or spinal cord reconstruction Shadow can assist positioning (2) Lateral positioning: distinguish whether the lesion is located in the intramedullary, extramedullary, or epidural mater, see Table 16-1. Table 16-1 Differentiation of intramedullary, extramedullary intradural and epidural lesions Intramedullary disease extramedullary intradural lesions epidural lesions Start from one side more Early symptoms Mostly bilateral From one side, it soon progresses to both sides radicular pain Common in early stages, severe, with clear location Could there be early Rare, location unclear Conduction bundle, starting on one side sensory impairment Separation Mostly bilateral conduction bundles Develop from bottom to top, focusing on the tail Pain and temperature disturbance Bilateral development from bottom to top Develop from top to bottom, focusing on the head may have hemisection syndrome Common Rare rare, limited Rare segmental muscle weakness and atrophy Early appearance, widespread and obvious Appears early, mostly from one side Not obvious Appears early, mostly bilateral pyramidal tract sign appear early Late appearance sphincter dysfunction Appear later Spinal process tenderness and pain none More common common Spinal canal obstruction Appears late and is not obvious Appear early, obvious Appears earlier, obviously Increased cerebrospinal fluid protein Not obvious more obvious obvious Changes in spine X-rays may have obvious none Cup shape jagged myelographic filling defect Spinal cord enlargement MRI Spinal cord enlargement Extramedullary mass and spinal cord displacement Epidural mass and spinal cord displacement (3) Qualitative diagnosis: Tumors are the most common intramedullary and extramedullary intradural lesions. The lesions caused by spinal arachnoiditis are often asymmetrical and the symptoms Sometimes mild and sometimes severe, sensory disturbances are mostly radicular, segmental or patchy and irregularly distributed. Neck compression test may show obstruction and increased protein content; spinal canal Contrast imaging shows that the contrast agent is distributed in a drop-like or patchy shape. Epidural lesions are mostly metastatic cancer and herniated intervertebral discs (lumbar and lower cervical segments). transfer Cancer progresses rapidly, with obvious root pain and bone destruction. Acute compression is mostly caused by traumatic epidural hematoma or epidural thickening. The former progresses rapidly and the latter Patients often have symptoms and signs of infection. 2. Differential diagnosis (1) Acute myelitis: acute onset, usually with a history of infection or vaccination before the disease, and transverse spinal cord damage occurring within hours or days. The cerebrospinal fluid kinetic test in the acute phase generally shows no obstruction, cerebrospinal fluid leukocytes increase, mainly mononuclear and lymphocytes, and the protein content is normal. Or slightly increased, spinal cord MRI can help identify it. (2) Syringomyelia: The onset is hidden and the course of the disease is long. Early symptoms are more common in the lower cervical and upper thoracic spinal cord segments, and can also extend to the spinal cord. marrow. Typical manifestations include dissociated sensory disorder of the skin in the area controlled by the lesion segment, muscle atrophy in the area controlled by the lesion segment, and rarely radicular pain. Nutritional disorders changed significantly. MRI can show a long hole in the spinal cord. (3) Subacute combined degeneration: usually starts slowly, with signs of damage to the posterior cord, lateral cord and peripheral nerves of the spinal cord. vitamins in serum The diagnosis can be confirmed in patients with B deficiency and pernicious anemia. 【treat】 1. The principle of treatment for spinal cord compression is to remove the cause as soon as possible. Those who can undergo surgery should undergo surgery as soon as possible, such as removal of space-occupying tissue in the spinal canal. Lesions, laminectomy and dural sacrotomy. Malignant tumors or metastatic cancer can be treated with surgery, radiotherapy or chemotherapy. epidural thickening Laminectomy was performed to remove the thick swelling and long-term anti-infective treatment was performed. For spinal cord hemorrhage, supportive care is mainly used and surgical treatment is generally not used. If it is caused by For bleeding caused by vascular malformations, selective angiography can be used to identify the site, and surgery or interventional treatment can be considered. 2. Acute spinal cord compression requires seizing the opportunity and decompressing within 6 hours of onset. If the epidural is thick, emergency surgery should be performed and sufficient dosage should be given. Antibiotics and anti-tuberculosis treatment are given during radical surgery for spinal tuberculosis. 3. Paralyzed limbs should actively undergo rehabilitation treatment and functional training, and those who are bedridden for a long time should prevent and treat urinary tract infections, pressure ulcers, pneumonia and limb injuries. Complications such as Li shrinkage.

subtopic

【Prognosis】 There are many factors that influence the prognosis of spinal cord compression, such as the nature of the disease, the degree of spinal cord damage, and the timing of treatment. Extramedullary and intradural tumors are common They are benign and have a good prognosis with complete surgical resection; intramedullary tumors have a poor prognosis. Generally, the shorter the time of compression, the smaller the damage to spinal function and the more likely recover. Acute spinal cord compression has a poor prognosis because it cannot fully exert its compensatory function.