Spinal cord compression

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Spinal cord compression develops when the spinal cord is compressed by bone fragments from a vertebral fracture, a tumor, abscess, ruptured intervertebral disc or other lesions. It is regarded as a medical emergency independent of its cause and requires prompt diagnosis and treatment to prevent long-term disability due to irreversible spinal cord injury.^[1]

The spinal cord extends from the foramen magnum down to the level of the first and second lumbar vertebrae. The cord is protected by the vertebral column, which is mobile and allows for movement of the spine. It is enclosed by the dura mater and the vessels supplying it. The spinal cord and nerve roots depend on a constant blood supply to perform axonal signaling. Conditions that interfere, either directly or indirectly, with the blood supply will cause malfunction of the transmission pathway. Injury to the spinal cord or nerve roots arises from direct trauma, compression by bone fragments, hematoma, or disc herniation or ischemia. The tissue responses by gliosis, demyelination, and axonal loss. This results in injury to the white matter (myelinated tracts) and the gray matter (cell bodies) in the cord with loss of sensory reflexes (pinprick, joint position sense, vibration, hot/cold, pressure) and motor function.^{[2][3][4][5][6]}

Common causes of spinal cord compression include trauma, primary or metastatic spinal tumor, intervertebral disk herniation, epidural abscess, and epidural hematoma. ^{[7][8][9][10]}

Acute spinal cord compression presents with sudden onset of paralysis along with back pain, it must be differentiated from other diseases with similar presentation such as muscle weakness and back pain. Transverse myelitis, GBS (Gullian-Barrie syndrome), HIV-myopathy, diabetic neuropathy, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS) and peripheral neuropathies are some of the diseases to be considered in the differential.^{[11][12][13][14][15][16][17][18][19]}

Trauma is the main cause of acute spinal cord compression followed by compression due to metastasis. The annual incidence rates of spinal cord compression due to trauma is estimated to be approximately 8-246 cases per 100,000 population. Men are more commonly affected with spinal cord compression than females. The male to female ratio is approximately 4 to 1.^[20][21]

The most important risk factors in the development of spinal cord compression are cervical spondylosis, atlantoaxial instability, congenital conditions (tethered cord), osteoporosis, ankylosing spondylitis, and rheumatoid arthritis with cervical spine involvement.^[1]

Spinal cord compression is an emergency condition that needs immediate treatment. If left untreated it leads to permanent damage to nerve roots and paralysis. Complications that can develop as a result of spinal cord compression include pressure ulcers, deep vein thrombosis, urinary tract infections, MRSA infection, pulmonary embolism. Prognosis is poor if the syndrome is complete (quadriparesis and with no sensory preservation), and recovery is less than 5%. The mortality rate for 1 year after injury in patients with complete lesions can be 100%. On the contrary, the prognosis is much better for the incomplete cord syndromes with some preserved sensory function with recovery rate greater than 50%.^{[22][23][24][25]}

Back pain is the most common presenting symptom in almost all acute cases of spinal cord compression. Symptoms of spinal cord compression depend upon the anatomic level involved. All cases of spinal cord compression present with sensory, motor and autonomic dysfunction. Sensory symptoms include altered sensation below a certain level (e.g. pinprick, touch, vibration, temperature), hemi-sensory loss. Motor symptoms include hemiplegia or hemiparesis (sparing the face), paraplegia or paraparesis, tetraplegia or tetraparesis. Autonomic symptoms include constipation, urinary retention, dizziness (due to hypotension), cold, shivering, and drowsiness (due to hypothermia), erectile dysfunction, abdominal pain and distension (due to ileus), and syncope (due to bradycardia).^[26][27][1]

The most significant physical examination findings in acute cases is point tenderness of back. Other physical examination findings include paralysis of limbs below the level of compression, decreased sensation below the level of compression, Lhermitte’s sign (intermittent shooting electrical sensation), hyperreflexia, and upward plantar reflex (Babinski sign).^[1]

Spinal cord compression is diagnosed based on clinical symptoms and imaging studies. Laboratory studies play a minimal role in diagnosing spinal cord compression expect in assessing the patient’s condition preoperatively for surgery and to exclude any infection.^[28]

X-ray spine plays a minimal role in diagnosing spinal cord compression. There are no x-ray findings associated with spinal cord compression.^[29]

CT spine is only indicated when MRI is not available. CT guidance is employed in surgical aspiration or drainage of an epidural abscess after the diagnosis confirmed by MRI.^[30]

MRI spine is diagnostic of spinal cord compression. Findings include extradural spinal hematoma, abscess or tumor, disc rupture, spinal cord hemorrhage, contusion or edema.^[31][32][33]

All the patients with acute spinal cord compression must be admitted. The mainstay of treatment includes surgery along with adjuvant therapy. In cases of compression caused by metastasis, the treatment is mostly palliative. Antibiotics are indicated in cases of compression caused by an epidural abscess. Dexamethasone (a potent glucocorticoid) in doses of 16 mg/day may reduce edema around the lesion and protect the cord from injury. It may be given orally or intravenously and is indicated in cases of compression caused by edema or acute inflamation.^[34][1]

Surgery is the mainstay of treatment in localized compression. Emergency radiation therapy (usually 20 Gray in 5 fractions) is the mainstay of treatment for malignant spinal cord compression. It is very effective as pain control and local disease control. Some tumors are highly sensitive to chemotherapy (e.g. lymphomas, small cell lung cancer) and may be treated with chemotherapy alone.^[35][1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

The spinal cord extends from the foramen magnum down to the level of the first and second lumbar vertebrae. The cord is protected by the vertebral column, which is mobile and allows for movement of the spine. It is enclosed by the dura mater and the vessels supplying it. The spinal cord and nerve roots depend on a constant blood supply to perform axonal signaling. Conditions that interfere, either directly or indirectly with the blood supply will cause malfunction of the transmission pathway. Injury to the spinal cord or nerve roots arises from direct trauma, compression by bone fragments, hematoma, or disk herniation or ischemia. The tissue responses by gliosis, demyelination, and axonal loss. This results in injury to the white matter (myelinated tracts) and the gray matter (cell bodies) in the cord with loss of sensory reflexes (pinprick, joint position sense, vibration, hot/cold, pressure) and motor function.^[1][2]

• The spinal cord extends from the foramen magnum down to the level of the first and second lumbar vertebrae.^[1][2]
• At L2 level spinal cord transforms into spinal roots and forms a cone-shaped structure called conus medullaris.
• The cord is protected by the vertebral column, which is mobile and allows for movement of the spine.
• It is enclosed by the dura mater and the vessels supplying it.
• The cord floats in the cerebrospinal fluid which acts as a buffer to movement and early degrees of compression.
• The cord substance contains a gray area centrally and is surrounded by white matter communication tracts, both ascending and descending.

• The spinal cord and nerve roots depend on a constant blood supply to perform axonal signaling.^[3][4][5]
• Conditions that interfere, either directly or indirectly, with the blood supply will cause malfunction of the transmission pathway.
• Injury to the spinal cord or nerve roots arises from direct trauma, compression by bone fragments, hematoma, or disc herniation or ischemia.
• It initiates a cascade of events in the gray matter and white matter and results in hypoperfusion.
• The following results in autonomic dysfunction leading to neurogenic shock ( triad of hypotension, bradycardia and peripheral vasodilation) and eventually hemorrhagic necrosis.
• The extent of necrosis depends on the severity of the trauma, concomitant compression, and blood flow.
• The tissue responses by gliosis, demyelination, and axonal loss.
• This results in injury to the white matter (myelinated tracts) and the gray matter (cell bodies) in the cord with loss of sensory reflexes (pinprick, joint position sense, vibration, hot/cold, pressure) and motor function.
• Rapid compression will result in the collapse of the venous system, resulting in vasogenic edema.
• Vasogenic edema exacerbates parenchymal pressure and may lead to rapid progression of dysfunction.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Common causes of spinal cord compression include trauma, primary or metastatic spinal tumor, intervertebral disk herniation, epidural abscess, and epidural hematoma.

Common causes of acute spinal cord compression include ^[1]

• Trauma
• Tumor (primary or secondary)^[2]
  • Secondary tumors: lung cancer, breast cancer, prostate cancer, or renal cancer. Sarcoma, myeloma, leukemia, thyroid cancer, lymphoma, melanoma, and gastrointestinal malignancies can also cause spinal cord compression
• Intervertebral disk disease
• Scoliosis
• Vertebral compression fractures
• Epidural abscess
• Epidural hematoma^[3][4]

Less common causes are:

• Neurocysticercosis

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Acute spinal cord compression presents with sudden onset of paralysis along with back pain, it must be differentiated from other diseases with similar presentation such as muscle weakness and back pain. Transverse myelitis, GBS (Gullian-Barrie syndrome), HIV-myopathy, diabetic neuropathy, multiple sclerosis (MS), amyotrophic lateral sclerosis(ALS) and peripheral neuropathies are some of the diseases to be considered in the differential.^{[1][2][3][4][5][6][7][8][9]}

Acute spinal cord compression presents with sudden onset of paralysis along with back pain, it must be differentiated from other diseases with similar presentation such as muscle weakness and back pain. Transverse myelitis, GBS(Gullian-Barrie syndrome), HIV-myopathy, diabetic neuropathy, multiple sclerosis (MS), amyotrophic lateral sclerosis(ALS) and peripheral neuropathies are some of the diseases to be considered in the differential. The following table describes the differentiating signs and symptoms of other diseases from an acute spinal cord compression.^{[1][2][3][4][5][6][7][8][9]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Trauma is the main cause of acute spinal cord compression followed by compression due to metastasis. The annual incidence rates of spinal cord compression is estimated approximately to be 8-246 cases per 100,000 population. Men are more commonly affected with spinal cord compression than females. The male to female ratio is approximately 4 to 1

• The annual incidence rates of spinal cord compression due to trauma is estimated approximately to be 8-246 cases per 100,000 population.^[1][2]
• The annual incidence rates of spinal cord compression due to cancer-related in the US is approximately 20,000.
• The annual incidence rates of spinal cord compression due to epidural abscess in the US is approximately 2.8 cases per 10,000 hospital admissions

• The annual prevalence of spinal cord compression is estimated approximately 236 to 1,298 per million population.

Men are more commonly affected with spinal cord compression than females. The male to female ratio is approximately 4 to 1.

There is no racial predilection to spinal cord compression.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

The most important risk factors in the development of spinal cord compression are cervical spondylosis, atlantoaxial instability, congenital conditions (tethered cord), osteoporosis, ankylosing spondylitis, rheumatoid arthritis of the cervical spine.^[1]

Common risk factors in the development of spinal cord compression include: ^[1]

• Cervical spondylosis
• Atlantoaxial instability
• Congenital conditions (tethered cord)
• Osteoporosis
• Ankylosing spondylitis
• Rheumatoid arthritis of the cervical spine

Less common risk factors

• IV drug abuse
• Immunocompromised codition

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Spinal cord compression is an emergency condition that needs immediate treatment. If left untreated it leads to permanent damage to nerve roots and paralysis. Complications that can develop as a result of spinal cord compression include pressure ulcers, deep vein thrombosis, urinary tract infections, MRSA infection, pulmonary embolism. Prognosis is poor if the syndrome is complete (quadriparesis and with no sensory preservation), and recovery is less than 5%. The mortality rate for 1 year after injury in patients with complete lesions can be 100%. On the contrary, the prognosis is much better for the incomplete cord syndromes with some preserved sensory function with recovery rate greater than 50%.^[1][2][3][4]

Spinal cord compression is an emergency condition that needs immediate treatment. If left untreated it leads to permanent damage to nerve roots and paralysis.

Complications that can develop as a result of spinal cord compression include:

• Pressure ulcers
• Deep vein thrombosis
• Urinary tract infections
• MRSA infection
• Pulmonary embolism

• The factors that determine the prognosis of an acute spinal cord compression depends upon
  • Type of compression
  • Degree of paralysis
  • Sensory preservation
  • Time of presentation
• Prognosis is poor if the syndrome is complete (quadriparesis and with no sensory preservation), and recovery is less than 5%.
• The mortality rate 1 year after injury in patients with complete lesions can be 100%.
• On the contrary, the prognosis is much better for the incomplete cord syndromes with some preserved sensory function with recovery rate greater than 50%.^[1][2][3][4]

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