Spinal Cord Injury, Compression and Acute Myelopathy

Talha Nazir1, Awais Khan2

1 King Edward Medical University, Lahore, Pakistan

2 Assistant Professor, Department of Neurology, University of Arizona

Special thanks to Hafiz Muhammad Junaid mjunaid2611@gmail.com for graphic design work

Introduction

  • The annual incidence of spinal cord injury in United States is 54 per million and almost 17,730 new cases of SCI are being reported annually.
  • The traumatic spinal cord injury often results from a gunshot wound (10.4%), accidental trauma to head, neck and back region (31.5%), falling (25.3%) and spinal sports injuries (4.3%).
  • Non-traumatic spinal cord injuries can have a range of etiologies like degenerative changes, infections (Staph. Aureus and Mycobacterium tuberculosis), malignancy of spine (Primary: multiple myelomas, Metastasis: prostate in male and breast in females are common etiologies), inflammation or congenital abnormalities

Anatomy

Meninges and Spaces

    • Three membranes that cover the spinal cord from outward to inward (dura mater, arachnoid mater and pia mater) are known as meninges.
    • The space between the bony framework of the spinal vertebral column and the thick dura mater surrounding the spinal cord is known as epidural space.
    • The space between the dura mater and pia mater is known as subarachnoid space (contains CSF).

Vertebral column

    • An adult spine has S-shaped curve, cervical as well as lumbar regions has concave with more mobility, besides thoracic plus sacral regions have a convex curve. Consisting of 33 vertebrae (7 cervical, 12 thoracic, five lumber, five bones fused to form the sacrum and four fused to form coccyx).
    • Vertebrae consist of the body (anterior) and arch (posterior) surrounding a vertebral foramen (contain spinal cord and meninges). The vertebral arch is made up of pair of pedicles (sides) and laminae which gives the spinous process at their junction.

Intervertebral disc

    • Between two vertebral bodies (except C1 and C2), the discs which serves as the support for spine. It is covered with the annulus that surrounds nucleus pulposus. It functions as the shockwave absorbers for bones of spine.

Spinal Cord

    • Spinal cord originates from brainstem, pass through foramen magnum and continues distally through cervical and thoracic regions of the spinal column before terminating as a tapering structure known as the conus medullaris. Spinal cord ends at the level of L1 or L2 in adults and L3 in children.
    • The cross-sectional structure of spinal cord consists of grey matter and white matter.
    • Gray matter which is organized as an H- shaped body of cell bodies. The anterior horn (motor nuclei) and the dorsal horn (sensory nuclei) of both sides are connected with grey commissure.
    • White matter which is organized into anterior, posterior and lateral columns (thoracic region only) comprise many ascending and descending tracts (Fig. 1)
    • Spinal cord comprises of the 31 total nerve root sections (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal).
    • Nerves from the lower spinal segment exit terminal to the conus medullaris and form the cauda equine.

Blood supply

    • Anterior spinal arteries (anterior 2/3rd)
    • Posterior spinal arteries (posterior 1/3rd)
    • Segmental arteries reinforce the anterior and posterior arteries at each intervertebral foramen

Figure 1: Ascending and Descending Tracts of Spinal Cord

Acute traumatic spinal cord injury

Pathophysiology

    • Primary injury (immediate) is due to trauma or and hemorrhage in the spinal cord that lead to ischemia, necrosis, and neuronal damage.
    • Secondary injury (days to weeks), followed by primary injury, is due to inflammatory cascade that leads to edema, free radical formation, apoptosis, and release of neurotransmitters

Complete spinal cord transection

    • Common causes include fracture of vertebrae, penetrating injury and expanding tumor.
    • Bilateral at level of the lesion: Flaccid paralysis and atrophy
    • Bilateral below the level of lesion:
      • Spastic paralysis and absent superficial reflexes (corticospinal tract)
      • Loss of the pain and temperature sensations (Lateral spinothalamic tract)
      • Loss of light touch and pressure sensations two to three levels below due to different levels of decussations (anterior spinothalamic tract)
      • Loss of the vibration, two-points discrimination and proprioception (posterior column).

Incomplete spinal cord syndromes

    • Central Cord syndrome
      • Involvement of cervical spines is the most common presentation. Elderly people are the high-risk population (hyperextension injury and fall)
      • Associated with cervical spondylosis, syringomyelia and neuromyelitis optica.
      • Symptoms are due to compression of spinothalamic and corticospinal tracts.
      • Upper extremities are affected more than lower extremities due to the central location of nerves.
      • Bladder dysfunction and some sensory loss.
      • Cruciate paralysis: Rare condition involving cervico-medullary junction. Commonly due to trauma to C1 and C2 vertebrae with the involvement of upper limbs only.
      • Syringomyelia: Formation of cyst within the spinal cord (syrinx) that can expand and destroy the spinal cord. Lower cervical and upper thoracic spine are commonly locations.
      • Symptoms include bilateral loss of pain and temperature sensations in specific dermatomes (Cape like distribution).
      • Associated with Chiari malformation.
    • Brown Sequard syndrome (hemisection of spinal cord)
      • Common etiologies include penetrating injury and expanding tumor of cervical spine (most common).
      • Ipsilateral at the level of lesion: Hypotonic paralysis (anterior grey horn) and anesthesia (posterior grey horn)
      • Ipsilateral below the level of lesion:
        • Spastic paralysis and loss of superficial reflexes (corticospinal tract)
        • Loss of vibration, two-point discrimination and proprioception (Posterior column)
      • Contralateral below the level of lesion:
        • Loss of pain and temperature sensations (Lateral spinothalamic tract)
        • Loss of fine touch and pressure sensations two to three levels below due to different levels of decussations (anterior spinothalamic tract)
    • Anterior cord syndrome:
      • Anterior 2/3rd of spinal cord is affected due to a range of etiologies like ischemia (anterior spinal artery occlusion and severe hypotension), trauma, disc herniation and multiple sclerosis.
      • Bilateral at level of lesion: Flaccid paralysis (Anterior grey horn)
      • Bilateral below the level of injury:
        • Spastic paralysis (corticospinal tracts)
        • Loss of pain, temperature, light touch and pressure sensation (anterior and lateral spinothalamic tracts)
      • Dorsal column: Sensations of two-point discrimination, vibration and proprioception are preserved bilaterally.
    • Posterior cord syndrome:
      • Posterior 1/3rd of spinal cord is affected
      • Common causes include MS, trauma, and hyperextension injury.
      • Ipsilateral loss of vibration, two points’ discrimination and proprioception.
      • Pain, temperature, fine touch and pressure sensations (anterior and lateral spinothalamic tract) and motor functions (corticospinal tract) are intact.

Cauda equina syndrome

    • Injury at the level of L2 or below due to various etiologies like disc herniation or compression due to tumor or abscess.
    • LMN, sensory and autonomic nerves are involved.
    • Common symptoms include pain radiating to legs, bladder and anal dysfunction, saddle anesthesia, impotence (male) and loss of ankle and knee reflexes.
    • Conus medullaris syndrome: Injury between T12 to L2. Spontaneous pain is not common and loss of motor function and saddle anesthesia is symmetrical. Conus medullaris syndrome may be associated with cauda equina syndrome.
    • Treatment: Surgical

Spinal shock syndrome

    • Transient depression or loss of entire functions below level of the lesion.
    • Anal sphincter reflex testing is used for diagnosis except in patient with lower spinal cord injury(S2-S4).
    • Reflexes are absent
    • Many patients recover in 24 hours, while others may take one to four weeks

Figure 2: Spinal Cord Transection Syndromes

Table 1: Upper Motor Neuron Lesion vs Lower Motor Neuron Lesion

Table 2: Localization of lesions (Cervical Region)

Table 3: Localization of lesions (Thoracic and Lumbosacral Region)

Table 4: ASIA Impairment Scale

(https://asia-spinalinjury.org/wp-content/uploads/2016/02/International_Stds_Diagram_Worksheet.pdf)

Physical examination

Motor system

▪ Bulk: Compare both sides. Atrophy in LMN lesions.

▪ Tone:

▪ Spastic paralysis (UMN lesion)

▪ Cog-wheel rigidity (Lesion of basal ganglia)

▪ Flaccid paralysis (LMN and sensory pathway lesions, cerebellar dysfunction and spinal shock)

▪ Power: Common terminologies are Monoplegia (one limb involvement), Paraplegia (both lower limbs involvement), Diplegia (both upper limbs involvement), Quadriplegia (Both upper and lower limbs involvement).

▪ Reflexes: Reflex arc is made up of afferent (sensory) and efferent (motor) limbs. Each reflex arc represents specific spinal nerve roots.

Sensory system

▪ Pain and temperature (lateral spinothalamic tract)

▪ Light touch and pressure (anterior spinothalamic tract)

▪ Sense of position and localization (spinocerebellar tract)

▪ Vibration and two-point discrimination (posterior column)


Table 5: Grading of Muscle Power

Table 6: Nerve Root values for reflexes

Table 7: Important points to consider during examination

Table 8: Acute Spinal Injury Management Steps

Workup

▪ Blood: CBC, Serum electrolytes, ABGs, LFTs, Serum amylase and lipase, Coagulation studies, blood typing and screening for alcohol

▪ Complete Urine and toxicology

▪ Chest X-ray

▪ ECG

▪ PFTs

▪ Imaging: CT/MRI spine

Management

ABCs

▪ Airway can be maintained by the suction of secretions and by Chin Lift or Jaw thrust maneuver. Airway Support can also be given via endotracheal intubation, cervical stabilization as well as cricothyroidotomy.

▪ Goals:

▪ Prevention of atelectasis

▪ Removal of respiratory secretions

▪ Prevention of respiratory infections.

▪ Increased oxygen delivery to the spinal cord

▪ Monitor:

▪ Respiratory rate, use of accessory muscles and paradoxical chest movements.

▪ Respiratory mechanics (NIF, FVC and TV)

▪ Oxygen saturation

▪ Changes in secretions

▪ Temperature

▪ Breathing adequately (15L/min oxygen) is required to maximize patient oxygenation and carbon dioxide elimination.

▪ Monitor respiratory rate and effort.

▪ Atelectasis can be prevented by using higher tidal volume (10-15ml.kg).

▪ Use diaphragmatic pacer in quadriplegics during the weaning process.

▪ Ventilated patients:

▪ Pneumonia can be prevented by following VAP (Ventilator-associated pneumonia) protocol.

▪ Assist coughing every 4 hours

▪ Nebulized with 2.5mg Albuterol every 4 hours

▪ Non-ventilated patients:

▪ Spirometry every 1-2 hours

▪ Assist coughing

▪ EZ-PAP every 4 hours

▪ Nebulized with 2.5mg Albuterol every 4 hours

▪ Circulatory collapse requires to be quickly recognized and managed. A high bore of (14- or 16-gauge) IV line must be maintained. Fluid bolus using crystalloid must be administered as per confined protocols in shocks.

▪ Goals:

▪ Prevention of bradycardia

▪ Prevention of hypotension (MAP > 85mmHg and MAP > 65mmHg in incomplete and complete SCI, respectively.

▪ Stabilize hemodynamic parameters

▪ Hypotension:

▪ Fluid challenge: 2L normal saline

▪ 0.05mcg/kg/min norepinephrine if BP doesn’t improve

▪ Check for serum cortisol if BP is still low. Start 100mg IV hydrocortisone every 8 hours.

▪ Bradycardia:

▪ Assess airway blockage

▪ 0.5mg IV atropine if HR<40

▪ Consider albuterol, caffeine or external pacemaker for refractory bradycardia

▪ DVT prophylaxis:

▪ LMW heparin (5000 units SQ)

▪ IV filter in high-risk patients.

Neurological management:

▪ Evaluate both motor and sensory system.

▪ Localize the level of the lesion.

▪ Use rotorest bed for patients who need immobilization and log roll method to transfer the patients.

▪ Neurosurgery should be done within 72 hours for immediate support (bilateral locked facet for incomplete SCI)

▪ Gastrointestinal management:

▪ Goals:

▪ Prevention of paralytic ileus

▪ Diet management

▪ NPO until bowel sounds return

▪ Clear NG tube every 4 hours

▪ Peptic ulcers prophylaxis: Proton pump inhibitors (20mg omeprazole)

▪ Constipation:

▪ Irritant suppository

▪ Digital stimulation

▪ Abdominal massage

▪ Use of assistive devices to improve bowel evacuation.

▪ Continence:

▪ Catheterization due to neurogenic bladder

▪ Prevent catheter-associated infections

▪ Measure total fluid intake and urine volume per day

▪ Skincare:

▪ Apply the appropriate collar (cervical).

▪ Initiate protocol to prevent pressure ulcers

Rehabilitation

▪ In the cervical spine, reduction can be achieved and maintained with traction, whereas in the thoracolumbar spine recumbency and appropriately positioned bolsters are used.

▪ Emphasize on respiratory management such as deep breathing, assisted cough, chest physiotherapy, and abdominal support should be given.

▪ Patient education, functional independence training including bed mobility, transfer and wheelchair mobility.

▪ Preservation plus strengthening of the existing function of muscle by a range of motion exercises.

▪ Restoration of fine motor abilities and the learning of adaptive methods for mobility.

▪ Stretching of muscles with spasm plus pelvic exercise for bowel and bladder control.

▪ Strollers, crutches and orthoses training is considered essential for providing ambulation in later phases

Acute Myelopathy

Pathology of spine and meninges covering the spinal cord is termed as myelopathy. Acute myelopathies can be classified as

Compressive myelopathies

Abscess related myelopathy

▪ The common causative organisms are staphylococcus aureus and mycobacterium tuberculosis

▪ Risk factors include IV drug abuse, diabetes, alcohol

▪ Fever and local tenderness that may progress to neurological deficit.

▪ Commonly involve thoracic and lumbar regions

▪ MRI is diagnostic (well-defined enhancement of perilesional area and edema)

▪ Treat with antimicrobial therapy and surgery

Vascular malformation:

▪ Vascular malformation can lead to compressive or non-compressive myelopathy

▪ Etiology

▪ Thrombosis: Aortic surgery, spinal angiography, embolism, and coagulative disorders

▪ Occlusion of arteries such as anterior spinal artery (Anterior spinal cord syndrome), posterior spinal artery (posterior spinal cord syndrome) and sub-commissural artery (brown Sequard syndrome) can lead to different presentations.

▪ AV fistula

▪ Venous infarct

▪ Spinal aneurysm

▪ Hemangioblastoma and cavernous malformation

▪ MRI

▪ Serpent like images

▪ Absence of flow signals

▪ CSF

▪ CSF is normal, but protein concentration may be higher in AV fistulas.

▪ Low cell content and absent oligoclonal bands

Management of compressive myelopathy

▪ Immobilization

▪ IV methylprednisolone

▪ Urgent surgical intervention

Non-compressive myelopathies

Transverse myelitis:

▪ Bilateral spinal cord dysfunction with a well-defined area of sensory loss during the first four weeks of presentation without any compression or disease and evidence of spinal inflammation (CSF pleocytosis, raised IgG)

▪ Peak incidence is during the 2nd and 4th decade of life.

▪ Perivascular and medullary infiltration of monocytes, lymphocytes (acute) and macrophages (subacute).

▪ MRI

▪ Central and focal high signal areas

▪ Involvement of three to four segments (thoracic spine is the most common)

▪ Diffuse enhancement on contrast medium (differentiate from other intramedullary tumors)

▪ Management

▪ IV corticosteroids (methylprednisolone, dexamethasone)

▪ Plasma exchange

▪ Immunosuppressive therapy for relapses

Infections related myelopathy

▪ Associated with blood-borne infections of lungs, skin and genitourinary system.

▪ Etiologies can be classified and based on the causative organism

▪ CSF

▪ Pleocytosis

▪ Neutrophilia

▪ Increased protein

▪ Absent oligoclonal bands

▪ MRI

▪ Central high signal areas

▪ Spinal edema

▪ Management

▪ Appropriate antibiotics

▪ Surgical intervention (epidural abscess, subdural empyema etc.)

Multiple sclerosis:

▪ Autoimmune demyelination of nerves in brain and spinal cord. Associated with HLA-DR2. Symptoms include

▪ Relapsing and remitting symptoms. Common in women of 20 and 30 years old.

▪ Immune-mediated inflammation may lead to demyelination of axons in CNS (brain and spinal cord)

▪ Optic neuritis (associated with Marcus Gun pupil)

▪ Brainstem and cerebellar involvement (bilateral involvement is more common)

▪ Demyelination of pyramidal tract (spasticity)

▪ MRI

▪ Gold standard

▪ Periventricular plaques

▪ Multiple lesion in white matter

▪ McDonald’s criteria:

▪ Space: One or more than one lesion in two areas with or without enhancement (periventricular, infratentorial, juxtacortical and spinal cord)

▪ Time: One new white matter lesion as compared to the previous MRI with or without enhancement.

▪ CSF

▪ Raised IgG levels

▪ Oligoclonal bands (diagnostic)

▪ Management

▪ IV steroids for acute flares

▪ Prevent relapses by disease-modifying therapy (beta-interferon)

▪ Catheterization and anticholinergic drugs for neurogenic bladder

▪ Baclofen for spasticity

▪ TCAs (Tricyclic antidepressants) for pain

Neuromyelitis Optica

▪ Incidence is 0.4 per million in western population with a male to female ratio of 1:3

▪ Acute myelitis and optic neuritis along with two or more than two of the following

▪ Spinal cord lesion involving more than three segments

▪ IgG positive (aquaporin four antibodies)

▪ CSF:

▪ Raised protein

▪ Pleocytosis

▪ Absent oligoclonal bands

▪ MRI

▪ Central longitudinal lesion (confluent) involving more than three segments

▪ Spinal expansion in T1 (low signals) and T2 (high signals)

▪ Periventricular lesion in more than 60% of the patients (high aquaporin four concentration)

▪ Optic nerve lesion

▪ Management

▪ Acute

▪ IV methylprednisolone (100mg for 3-5days)

▪ Plasmapheresis (5-7 cycles)

▪ Chronic

▪ Immunosuppression (Rituximab, Mycophenolate mofetil, azathioprine)

▪ Change the drug or optimize the dose if patient relapses.

Workup for acute myelopathy

Step 1: Confirm the diagnosis of acute myelopathy

▪ History and physical examination

▪ Neurological deficit and involvement of bladder and bowel

Step 2: MRI (Gadolinium enhancement)

▪ To rule out a compressive myelopathy

Step 3: CSF analysis and confirm the presence of the lesion

▪ Step 3a: Define the infectious causes of myelopathy

▪ Pleocytosis

▪ Neutrophilia

▪ Increased protein

▪ Absent oligoclonal bands

▪ Step 3b: Define the inflammatory causes of myelopathy

▪ Raised IgG and oligoclonal bands (MS)

▪ IgG against aquaporin 4, raised proteins, pleocytosis and absent oligoclonal bands (Neuromyelitis Optica)

▪ Step 3c: Determine the location of the lesion

▪ Brain and spinal cord (MS)

▪ Spinal cord only (Transverse myelitis)

▪ Optic nerve and spinal cord (Neuromyelitis Optica)

Table 9: Etiologies of Compressive and Non-compressive Myelopathies

Table 10: Tumors causing Compressive Myelopathy

Table 11: Infections of Spinal cord

Bibliography

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