bubble_chart Overview

Spinal cord compression is a group of disorders caused by space-occupying lesions within the spinal canal that compress the spinal cord. Clinically, it is characterized by complete or incomplete transverse spinal cord damage and spinal canal obstruction.

bubble_chart Etiology

Generally, the causes of disease are divided into three categories:

(1) Spinal diseases are most commonly caused by trauma and subcutaneous nodes, followed by metastatic tumors and herniation of intervertebral disc.

(2) Spinal membrane diseases are mostly caused by extramedullary intradural tumors. Conditions such as arachnoiditis, hematomas due to vascular malformations, abscesses, and metastatic tumors can all lead to spinal cord compression.

(3) Spinal cord diseases are frequently caused by spinal cord tumors, such as neurofibromas and spinal gliomas. Other causes include hemorrhage and syringomyelia.

Systemic diseases like leukemia and lymphoma can also cause compression.

The aforementioned disease causes can result in direct or indirect spinal cord compression and circulatory disturbances. Acute spinal cord compression obstructs venous return, leading to uncompensated spinal edema and severe damage to neural pathways, with symptoms peaking rapidly and manifesting as acute transverse spinal cord injury. If the spinal cord is compressed gradually, collateral circulation develops, spinal edema is less pronounced, and the clinical presentation is progressive transverse spinal cord injury. Intramedullary space-occupying lesions directly invade nerve fibers, causing early and severe symptoms. Due to spinal cord compression, cerebrospinal fluid circulation and absorption are affected, leading to varying degrees of spinal canal obstruction.

bubble_chart Pathological Changes

Softening, edema, or depressed deformation, infiltration, and destruction of the spinal cord can be observed, along with degeneration, rupture, necrosis, and demyelination of nerve cells and fibers within the spinal cord. Due to varicose veins on the surface of the spinal cord and protein exudation, the protein content in the cerebrospinal fluid increases.

bubble_chart Clinical Manifestations

Acute spinal cord compression is often caused by epidural abscesses, massive herniation of intervertebral discs, or traumatic hematomas. The symptoms resemble those of acute myelitis and are frequently accompanied by spinal shock. Clinically, chronic-onset, progressively worsening extramedullary intradural tumors are more common. The evolution of symptoms is as follows:

(1) Nerve root symptoms In the early stages of the lesion, irritation of the posterior root leads to spontaneous, radiating pain in its distribution area (often unilateral), known as radicular pain. The pain may be stabbing, cutting, burning, or manifest as a "band-like sensation" in the corresponding segment. It is often more severe at night and unbearable. Coughing, sneezing, bending, twisting, or exertion can exacerbate the pain, while changing posture may alleviate it. Examination may reveal localized hyperesthesia.

As the lesion progresses, the posterior root is destroyed, reducing radicular pain and causing hypoesthesia or anesthesia in the corresponding area. If the lesion affects the ventral anterior root of the spinal cord, fasciculations and muscle atrophy may occur in that segment. Nerve root symptoms may persist for a long time, providing significant diagnostic value for lesion localization.

(2) Symptoms of incomplete transverse damage As the lesion continues to develop, one side of the spinal cord is compressed, affecting its three major conduction tracts to varying degrees. Damage to the spinothalamic tract (already crossed) results in contralateral pain and temperature sensation loss below the lesion level, progressing upward. Damage to the posterior column (uncrossed) causes ipsilateral deep sensory impairment below the lesion. Damage to the pyramidal tract (already crossed) leads to ipsilateral upper motor neuron paralysis, characterized by increased muscle tone, hyperreflexia, and positive pathological reflexes. At this stage, patients complain of unilateral leg weakness that worsens gradually, requiring a cane for walking. This unilateral spinal cord damage is called Brown-Sequard syndrome. Additionally, damage to the anterior and posterior horns at the affected segment may manifest as corresponding sensory, motor, and reflex impairments, such as muscle atrophy and fasciculations.

(3) Symptoms of complete transverse damage If the disease cause is not resolved, compression may spread from one side to the other, leading to complete spinal cord compression and spinal canal blockage. Clinically, this manifests as total loss of sensation, motor function, and sphincter dysfunction below the lesion level. Paralyzed limbs may exhibit dry skin, desquamation, reduced sweating, or anhidrosis.

Due to variations in lesion levels, clinical manifestations differ significantly. Intramedullary lesions typically lack radicular pain, exhibit milder spinal canal blockage, and feature downward-progressing sensory impairment with prominent dissociative sensory loss. Muscle atrophy at the compressed segment is pronounced, and sphincter dysfunction occurs early and severely. In advanced stages, the entire spinal cord is affected, presenting as transverse damage.

Epidural lesions are often malignant or metastatic tumors, progressing rapidly with severe radicular pain, localized spinal spontaneous pain, or marked tenderness. Movement is restricted, and transverse spinal cord damage develops quickly. X-ray examinations often reveal bone destruction.

bubble_chart Auxiliary Examination

1. Cerebrospinal fluid examination and Queckenstedt test: The main change in cerebrospinal fluid is an increase in protein content, which becomes more pronounced the lower the site of obstruction. If the protein level exceeds 10g/L (1000mg/dl), the fluid appears yellow and coagulates spontaneously after withdrawal, a phenomenon known as Froin's syndrome. The Queckenstedt test indicates complete or incomplete spinal canal obstruction. Lumbar puncture should never be performed at a site suspected of abscess to avoid introducing bacteria into the subarachnoid space, which could lead to purulent myelomeningitis.
2. X-ray examination: This helps assess the condition of the spine and spinal canal, including the presence of hyperostosis, destruction, spinal canal stenosis or dilation, and unilateral enlargement of intervertebral foramina.
3. Myelography: This clearly determines whether there is spinal canal obstruction and its level, playing a crucial role in diagnosing spinal cord compression.
4. CT or magnetic resonance imaging (MRI): Both are helpful in diagnosing this condition.

bubble_chart Diagnosis

1. Determine whether it is compression
   1. Based on the lesion starting from one side, early onset of radicular pain, and a chronic, progressively worsening history of spinal cord damage from incomplete to complete transverse impairment;
   2. elevated cerebrospinal fluid protein;
   3. if the Queckenstedt test shows complete or incomplete obstruction, it can be confirmed as spinal cord compression.
2. Determine the level and segment of the lesion: Based on signs, identify whether it is in the high cervical cord, cervical enlargement, thoracic cord, lumbar enlargement, conus medullaris, or cauda equina. After determining the segmental level of the lesion, further identify the layer within the plane—whether it is intramedullary, intradural extramedullary, or extradural. If surgery is planned, myelography or CT scans must also be performed for precise localization.
3. Determine the nature of the lesion (qualitative diagnosis): Based on medical history, disease progression, symptom characteristics, and targeted laboratory and auxiliary examinations, and through exclusion analysis on the basis of localization, the nature of the lesion can be preliminarily clarified.

bubble_chart Treatment Measures

1. Disease cause Treatment requires timely diagnosis and early surgery. Acute compression should be decompressed within 6 hours to relieve spinal cord compression and facilitate functional recovery.
2. Drug treatment Depending on the condition, antibiotics and anti-subcutaneous node therapy should be used reasonably in the early stage.
3. Radiotherapy or chemotherapy For a small number of patients who cannot undergo surgery, this therapy may be considered to achieve symptom relief.
4. For the treatment of the stage of convalescence paralysis, tuina, physiotherapy, acupuncture, and functional exercises can be performed.

bubble_chart Prognosis

The extent of relief from disease causation is related to the duration of compression and the degree of functional impairment. Intradural extramedullary tumors are mostly benign and easily removed by surgery, with a good prognosis. Intramedullary tumors have a poorer prognosis. Generally, shorter compression duration and less spinal cord functional damage result in a higher likelihood of recovery, and vice versa. Chronic compression cases, due to sufficient compensation, have a relatively better prognosis than acute compression.

bubble_chart Prevention

Strictly enforce safety production to prevent trauma-induced compression. Conduct regular surveys, and promptly treat any subcutaneous node disease found to prevent dissemination. Diagnose and treat radicular pain early to minimize functional impairment and sequelae.

bubble_chart Complications

Common urinary tract infections, bedsores, and lung infections.

bubble_chart Differentiation

1. Acute myelitis: In this disease, the cerebrospinal fluid protein content may be elevated, but not as significantly as in spinal cord compression. Myelography shows no spinal canal obstruction.
2. Certain extradural diseases such as pleuritis, angina, and renal stones may be confused with early radicular pain. However, abnormalities can be detected through chest X-rays, electrocardiograms, and renal X-rays. Additionally, cerebrospinal fluid protein levels are not elevated, and there is no spinal canal obstruction, making differentiation easier.