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.
Pathogenesis
- 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 and has minimal role in acute conditions.
- CT scans have replaced the role of plain radiographs in the setting of multiple trauma due to their specificity and accuracy.
- Plain x-ray film is indicated in 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 CT is inconclusive.
- MRI is recommended for all patients who have new-onset urinary symptoms with associated back pain.
- Patients who present with a tumor history should undergo MRI-enhanced imaging.
- 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
All the patients with acute spinal cord compression must be admitted. The mainstay of treatment includes surgery for most of the cases except for compression caused by metastasis. The treatment in such cases is mostly palliative. Antibiotics are indicated in cases of compression caused by an epidural abscess.
Antibiotics
- Preferred regimen (1): vancomycin 15-20 mg/kg IV q8-12h and metronidazole 500 mg IV q6h and cefotaxime 2 g IV q6h
Maintaince of fluid volume
- Goal is to mainatain systotic bp above 100 mmhg and an adequate urine output (0.5 mL/kg/hour) using volume resuscitation, and vasopressors.
- Preffered regimen: volume resuscitation using fluid replacement with isotonic crystalloid solution to a maximum of 2 L is the initial treatment of choice.
- Alternative regimen : Dopamine 1-50 micrograms/kg/minute IV q8h.
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 repositioning of the patient for the prevention of pressure ulcers every 2 hours
Surgery
| Cause of compression | Prefered treatment | Adjuvant therapy |
|---|---|---|
| Trauma | Decompressive/stabilization surgery of vertebral column | + |
| Disk herniation | Laminectomy | + |
| Metastasis | Corticosteroids + radiation therapy | + |
| Epidural asbcess | CT guided aspiration of abscess + Antibiotics | + |
Differential
| Disease/Condition | Differentiating Signs/Symptoms | Differentiating Tests | |
|---|---|---|---|
| CSF Findings | Other diagnostic tests | ||
| Transverse myelitis | Febrile illness preceding the symptoms
LE >UE |
Pleocytosis
↑Total protein |
Focal demyelination on MRI |
| Guillain-Barre syndrome (GBS) | History of gastroenteritis or influenza-like illness
Ascending paralysis Loss of deep tendon reflexes Respiratory muscle weakness requiring ventilation |
Albumin-cytologic dissociation
↑Total protein |
EMG shows decreased conduction
Seropositive for Campylobacter jejuni (50% cases) |
| HIV-related myelopathy | History of HIV infection
Paraparesis, spasticity or ataxia (or both) coupled with dementia |
Nonspecific | ELISA + followed by confirmation with Westeren blot. |
| Amyotrophic lateral sclerosis (ALS) | Combination of UMN and LMN
Muscle weakness and stiffness as the initial symptoms |
Nonspecific | Fibrillation potentials and positive sharp waves, with fasciculation potentials on EMG |
| Multiple sclerosis | Mimic clinical symptoms of spinal, compression, however, all cases involve the brain.
Presents with multiple episodes separated by space with self-resolution Visual symptom (neuromyelitis optica) distinct for MS |
↑ IgG and oligobands | MRI brain shows areas of demyelination. |
| Diabetic neuropathy | History of diabetes mellitus.
Pain and loss of sensation in the feet in a glove-and-stocking distribution. Bladder dysfunction may be present due to autonomic neuropathy. |
Nonspecific | EMG shows reduction in sensory nerve conduction and a decrease in amplitude. |
| Polymyositis | Symmetrical weakness of shoulder and pelvic girdles. | Nonspecific | EMG include spontaneous fibrillations, low-amplitude short-duration polyphasic motor potentials
Muscle biopsy shows immune cell infiltration and destruction of muscle fibers |
| Hereditary muscular dystrophy | Proximal and distal muscle weakness
Without sensory changes in the initial stages. |
Nonspecific | MRI and EMG/nerve conduction studies will show only myopathic changes |
Prognosis
- 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 its complete, quadriparesis and with no sensory preservation. Recovery is <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. Recovery is >50%.
Complications
- Pressure ulcers
- Deep vein thrombosis
- Urinary tract infections
- MRSA infection
- Pulmonary embolism