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

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	Immobilization of the patient along with decompressive surgery Maintenance of volume and blood pressure	IV corticosteroids Prophylaxis for venous thromboembolism First line low-molecular-weight heparin, enoxaparin: 40 mg subcutaneously once daily Second-line unfractionated heparin 5000 units subcutaneously every 8-12 hours Compression stockings or pneumatic intermittent compression Prevention of stress ulcers Omeprazole: 40 mg orally once daily Cimetidine: 300 mg orally/intravenously every 6 hours Famotidine: 40 mg orally once daily; 20 mg intravenously every 12 hours Supportive therapies Nutritional support Bladder catheterization Frequent position changing for the prevention of pressure ulcers every 2 hours.

• 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	MRI brain shows areas of demyelination.
Diabetic neuropathy
Polymyositis
Hereditary muscular dystrophy
Peripheral neuropathy

1

Approximately one third of patients report a. Most have leg weakness of varying degrees of severity. The arms are involved in a minority of cases.

Associated illnesses include multiple sclerosis, rheumatoid arthritis, HIV infection, and sarcoidosis.

CSF analysis shows with a modest number of lymphocytes and increase in .

MRI shows with possible enhancement at the appropriate level. Lyme titers are occasionally found to be high. [41]

2

Two-thirds have aweeks before onset of neurologic symptoms. It is frequently severe and presents with features which are similar to those of spinal cord compression (SCC), as an initially with weakness in the legs that spreads to the upper limbs and the face, along with complete . Autonomic signs may be present in some variations. May develop progressive .

Typical CSF findings include , that is, an elevated protein level (100-1000 mg/dL) without an accompanying increased cell count. A sustained increased WBC count may indicate an alternative diagnosis such as infection.

In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing. [42]

Nearly 40% of patients are i. [43]

3

or high-risk behaviors (IV drug use, HIV-infected blood transfusion, unprotected sex).

Signs and symptoms referable to the spinal cord lesions, including often accompanied by .

testing should be ordered when HIV testing is indicated. False-negatives may occur during window period immediately after infection and before antibodies to HIV have developed. A positive result should be confirmed with a Western blot or second ELISA. The window period can be reduced to 2 to 4 weeks by using fourth-generation tests and those that include IgM antibodies to HIV.

CSF, microbiologic, and spinal imaging studies may be inconclusive or . [44] [45]

4

Presents as a symptoms and signs.

Approximately 60% of ALS patients experience . The neurologic exam usually shows evidence of muscle weakness (localized or widespread, depending on the extent of the disease). The exam also reveals muscle atrophy. The muscles may be so stiff that, when the neurologist moves them, they continue to move abnormally afterward. When the neurologist tests the knee jerk reaction, the movement is abnormally quick (hyperreflexia).

EMG testing is a significant part of the diagnosis. The current criteria define a positive EMG when signs of active denervation include . [46]

5

Can , in almost .

Has a variable (i.e., neurologic symptoms result from lesions in different CNS sites) and time. Common symptoms include progressive limb weakness, gait difficulty,.

In the setting of acute paraparesis, . NMO is thought to be a distinct entity from MS by many neurologists. It has a relapsing course (80% to 90%), and predominantly affects females. [47]

Brain

CSF exam shows raised .

If NMO suspected (optic neuritis, myelitis, longitudinal cord lesion on MRI), NMO-IgG seropositivity. [47]

6

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.

Nerve conduction studies show reduction in sensory nerve conduction velocity and a decrease in amplitude.

7

Symmetrical weakness of shoulder and pelvic girdles.

Elevated muscle enzyme levels (e.g., CK), often with a positive ANA titer.

Characteristic changes in EMG include increased needle insertional activity, spontaneous fibrillations, low-amplitude short-duration polyphasic motor potentials, and complex repetitive discharges.

Diagnosis is confirmed with muscle biopsy, indicating immune cell infiltration and destruction of muscle fibers.

8

Severe proximal and distal muscle weakness without sensory changes from an early age.

MRI and EMG/nerve conduction studies will show only myopathic changes and no SCC.

9

Peripheral neuropathy and neuropathies due to diabetes or thyroid disease may be difficult to differentiate from neurologic symptoms of compression neuropathies.

Nerve conduction studies and EMG are helpful in confirming neuropathy and characterizing the neuropathy, that is, demyelinating, axonal, polyneuropathy, mononeuropathy multiplex, radiculopathy, or plexopathy.