Sandbox spinalcord
Causes
Common causes of acute spinal cord compression include
- Trauma is a leading cause of acute spinal cord compression
- Primary or secondary metastatic spinal tumor
- Vertebral compression fractures due to osteomalacia, osteoporosis, corticosteroid therapy
- Intervertebral disk herniation
- Epidural abscess
- Epidural hematoma
Risk factors
Common risk factors in the development of spinal cord compression include
- 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
Pathophysiology
Anatomy
- The spinal cord extends from the foramen magnum down to the level of the first and second lumbar vertebrae.
- 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.
Pathogenisis
- 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 stretching or from pressure.
- It initiates a cascade of events in the gray matter and white matter, and results in hypoperfusion and eventually hemorrhagic necrosis.
- The extent of necrosis depends on the severity of the trauma, concomitant compression, perfusion pressures and blood flow, and administration of pharmacological agents.
- 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.
Dissemination
Hematogenous spread
Genetic Factors
Associated conditions
Lesions may develop gradually or acutely and be complete or incomplete. Incomplete lesions often present as distinct syndromes as follows:
Sensory dysfunction | Motor dysfunction | Sphincter dysfunction | |
---|---|---|---|
Central cord syndrome | Sensory loss is very rare | Upper extremity weakness
distal muscles are involved more than proximal |
|
Brown-Séquard syndrome | Ipsilateral position and vibration sense loss
Contralateral pain and temperature sensation loss |
Motor loss ipsilateral to cord lesion | |
Anterior cord syndrome | Loss of pin and touch sensation
Vibration, position sense preserved |
Motor loss or weakness below the level of compression | |
Transverse cord syndrome | Loss of sensation below level of compression | Loss of voluntary motor function below the level of compression | Sphincter control lost |
Conus medullaris syndrome | Saddle anesthesia
Sensory loss may range from patchy to complete transverse pattern |
Weakness may be of upper motor neuron type | Sphincter control impaired |
Cauda equina syndrome |
Epidemiology and Demographics
Epidemiology
Incidence
- The annual incidence of spinal cord compression is estimated to be about 11,000 new cases/yr in the United States
- The worldwide incidence of spinal cord compression varies from 8 to 246 cases per million inhabitants per year.
Prevelance
- The global prevalence of spinal cord injury (SCI) has been reported to vary from 236 to 1,298 per million inhabitants.
- In United States the prevalence is estimated to be 171,000 persons.
Demographics
Gender
Spinal cord compression is more commonly seen in males than females
Age
It is more common in 40's
Race
No racial predilection
Symptoms
Symptoms of spinal cord compression depends on the anatomic level involved in compression and can be discussed as follows
Type of spinal
involvement |
Symptoms |
---|---|
Cervical | Headache
Neck, shoulder or arm pain Loss of sensation over the upper extremities Motor weakness of neck, shoulder, and arm |
Thoracic | Pain in the chest and/or back
Loss of sensation below the level of the compression Paralysis of respiratory muscles |
Lumbosacral | Low back pain that may radiate down the legs
Weakness in the legs and feet Loss of sensation in the legs and feet Bladder and bowel problems Sexual dysfunction Foot drop Decreased or absent reflexes in the legs |
Laboratory findings
Spinal cord compression is diagnosed based on clinical history and imaging studies. Other lab studies like CBC, CSF, clotting studies and electrolyte exam helpful in excluding infection as a cause.
- CBC shows increased neutrophil count in cases of infection.
- ESR and CRP are elevated
- Blood and CSF cultures are positive in case of an epidural abscess or osteomyelitis.
- Tumor biopsy positive for malignant cells if compression of spinal cord is due to malignancy
- Urodynamic studies reveal reduced bladder contractility and sphincter dysfunction.
X-ray spine
- Plain radiographs are useful in assessing mechanical stability of the spine in trauma cases.
- Multidetector CT with sagittal and coronal sections have been overtaken the role of plain radiographs, especially in the setting of multiple trauma.
- Plain x-ray film is indicated in all patients presenting with chronic back pain as an initial symptom
CT Spine
- MRI and CT imaging are preferred diagnostic modalities in confirming the diagnosis
- CT spine is preferred for detection of spinal canal abnormalities.
- Anteroposterior, lateral, views are required to show the alignment of bone structures.
- CT guidance is employed in surgical aspiration and diagnosis of infection or drainage of an epidural abscess.
- CT-guided biopsy of suspected tumors helps in confirmation of the diagnosis.
MRI Spine
- MRI is the study of choice when there is incomplete paralysis or under other circumstances where direct visualization of neural or ligamentous structures is clinically necessary.
- MRI is the best imaging method for evaluation of neural tissue.
- MRI has largely replaced CT scanning in the noninvasive evaluation of patients with painful myelopathy because of its superior soft-tissue resolution and multiplanar capability.
- Urgent MRI is recommended for all patients who have new-onset urinary symptoms with associated back pain or sciatica.
- Patients who present with a tumor history should undergo CT- or MRI-enhanced imaging.
- Plain radiographs of the entire spine should then be performed, followed by CT or MRI with and without contrast enhancement.
- Epidural abscess is best detected by MRI.
Treatment
First line treatment | Adjuvant | ||
---|---|---|---|
Acute traumatic spinal cord compression |
|
Prophylaxis for venous thromboembolism
Prevention of stress ulcers
Supportive therapies
|
|
- Patients with a spinal cord injury should be immobilized first with a cervical collar and backboard/head strap. The choice of treatment options depends upon the cause of the compression.The patient can be grouped into the following categories for treatment:
- Acute traumatic spinal cord compression
- Intervertebral disk compression (cauda equina syndrome)
- Spinal cord compression due to metastasis
- Compression of spinal cord due to epidural abscess (infection)
The goal of treatment is
- To prevent further deterioration of the disease.
- To relieve the patient from pain.
- To restore functional ability.
Medical treatment
The mainstay of treatment for an acute spinal compression is surgery. Medical treatment aids as an adjuvant.
It includes:
Corticosteroids=
- Preferred regimen: Methylprednisone 30 mg/kg intravenously as a bolus given over 15 minutes followed by 5.4 mg/kg/hour intravenous infusion for 24 hours (if <3 hours since injury) or for 48 hours (if 3-8 hours since injury)<
Prophylaxis for venous thromboembolism
- Preferred regimen: Enoxaparin 40 mg subcutaneously q24h
- Alternative regimen (1): Heparin 5000 units subcutaneously q8-12h
- Alternative regimen (2): IVC filter (in patients with contraindications to anticoagulation)
Prevention of stress ulcers
- Preferred regimen (1): Omeprazole 40 mg orally q24h
- Preferred regimen (2): Cimetidine 300 mg orally/intravenously q6h
- Preferred regimen (3): Famotidine 40 mg orally q24h (or) 20 mg intravenously q12h
Supportive therapies
- Nutritional support
- Compression stockings or pneumatic intermittent compression
- Bladder catheterization
- Frequent position changing for the prevention of pressure ulcers every 2 hours