Spinal Cord Injury

Main syndrome :
1. Complete/almost complete sensorimotor myelopathy yang meliputi most/all ascending
dan descending tract (transerse myelopathy)
2. Combined painful radicular dan tranverse cord syndrome
3. Hemicord (Brown-Sequard) syndrome
4. Ventral cord syndrome, sparing posterior coloumn function.
5. High cervical-foramen magnum syndrome
6. Central cord or syringomyelic syndrome
7. Syndrome of the conus medullaris
8. Syndrome of the cauda equina
Intramedullary : lession within the cord
Extramedullary : lession that compress the cord
The Syndrome of Acute Paraplegia or Quadriplegia due to Complete Transverse
Lesions of The Spinal Cord (Transverse Myelopathy)
Best considered in relation to trauma. Most frequent cause
Also as a result of infarction/hemorrhage and with rapidly advancing compressive,
necrotizing, demyelinative or inflammatory lesions (transverse myelitis)
Mechanism of Spine and Spinal Cord Injury
Walaupun bisa meliputi spinal cord saja, seringnya vetebral coloumn injured
pada saat yang sama. Dan biasanya ada head injury yang berkaitan.
Klasifikasi : fracture-dislocation, pure fractures, dan pure dislocation. (3:1:1)
Most spinal injury resulr of : force applied at a distance from the site of spinal
fracture and dislocation.
Mechanism dari ketiga jenis klasifikasi diatas hampir sama yaitu ;
1. vertical compression of spinal coloumn + anteroflexion
2. vertical compression + retroflexion (hyperextension)
Hal penting dalam vetebral injury :
1. structure of the bones at the level of injury
2. intensity, direction, and point of impact of the force.
Many spinal injury are due to blow to the head.
1. Cranium struck by hard object in high velocity skull fracture force injury
absorbe by elastic quality of the skull.
In slower velocity spine (most mobile portion) will be the part injured
2. If neck rigid and straight & force apllied quickly to the head atlas and
odontoid axis may break.
In slower velocity element of flexion or extension added.
3. Severe forward flexion injury (Head bent sharply forward when force is
applied) cervical vertebrae forced at maximum level of stress
4. Hyperextension injury (vertical compression with head in an extended
position).
- Stress mainly on posterior element. C4-C6 may be fractured
unilaterally/bilaterally & anterior ligament
- Commonly occur without apparent damage/misalignment of vertebrae in
radiology exam.
- Common in children.
5. Whip-lash or recoil injury most often of automobile accident.
- Occipitonuchal and SCM muscle & supporting structure of neck and head
afeect much more than spinal cord or roots.

- Quadriparesis rarely.
Most vetebral injury occur at level : C1-C2, C4-C5, T11-L2
Etiology spinal cord injury :
1. Motor vehicle accident
2. Falls
3. Gunshot/stab wounds
4. Diving accidents
5. Motorcycle accident
6. Crushing industrial injury
7. Birth injury
Fatal cases : associated with fracture-dislocation C1-C4 sudden respiratory
paralysis.
Nonfatal cases : fracture-dislocation mid and lower cervical spine
Incidency spinal cord injury 5 : 100.000 ; Male : female = 4 : 1
3500 die/year . 5000 left with complete/nearly complete loss of spinal function
per year.

Pathology of Spinal Cord Injury

Traumatic necrosis : destruction gray and white matter and variable amount of
hemorrhage.
Maximal at level of injury and one/two segment above and below it.
As lesion heals : leave gliotic focus/cavitation with variable amounts of hemosiderin
&iron pigment.
Traumatic syringomyelia (progressive caviation) may develop after months/years and
extend above main lession.
Most traumatic lession : central part spinal cord suffer greater injury than peripheral
parts.
Sometime, lesion retricted to anterior and posterior grat matter segmental
weakness & sensory loss in arm and few long tract sign Schneider
syndrome/Central cervical syndrome. (Transient phenomena, reverse after several
days)
Clinical Effect of Spinal Cord Injury
Disorder function of spinal cord injury
1. All voluntary movement body below the lesion, immediately&permanently lost.
2. All sensation from the lower part is abolished.
3. Reflex function in all segment of isolated spinal cord, suspended. (Spinal shock) Involve
tendon as well autonomic reflexes.
Riddoch, divide clinical effect of spinal cord trnsection into 2 stages.
1. Stage of Spinal Shock or Areflexia
Loss motor function : tetraplegia (lesion of C4-C5 or above) , paraplegia (lesion of
thoracic cord)
Immediate atonic paralysis of bladder&bowel, gastric atony, loss sensation below level
of spinal cord lession, muscular flaccidity, almost complete suppression of all spinal
segmental reflex activity below lesion result of sudden separation from higher level,
neural element below lesion fail to perform normal function.
Impaired control of autonomic function : vasomotor tone, sweating, piloerection lower
part of body, abolished.
Systemic hypotension may be severe and contribute to spinal cord damage.
Lower extremities : lose heat and swell
Skin : dry and pale, may develop ulceration.
Inhibitory influence from CNS loss spincther of bladder & rectum remain contracted

2.

Detrusor of bladder & smooth muscle of rectum : atonic

Passive distention of bowel, feces retention, absence of peristaltis, genital relfexes
abolished/depressed.
Bulbocavernosus reflex : first to return
Stage of Heightened Reflex Activity
Neurologic state within several weeks/months after spinal injury.
Reflexes response stronger
Typical patters (triple flexion) : Babinski sign, fanning toe, flexion/slow withdrawal
movement of foot,leg, and thigh.
Achilles and patellar reflexes return.
Retention urine less complete, reflex defecation also begin.
After flexor response fully developed, overactivity of extensor muscle apeear after 6
months.
Extensor muscle first manifest : hip and thigh and later leg, some people spinal
standing.
Paraplegia in flexion (extreme flexion in hips & knee as in fetal position) most seen
in cervical lession than caudal one.
Flexor spasm more frequent with higher lesion.
Parathesia : most common being a dull, burning pain in lower back and abdomen,
buttocks, and perineum.
Overactivity neuron in isolated segment of spinal cord :
1. suprasegmental inhibitory influences removed by transection afferent sensory
impulse evoke phasic and tonic myotatic reflexes.
2. isolated neuron become hypersensitive to neurotransmitter.
Higher cervial lesion result in extreme&prolonged tonic spasm of legs due to release
tonic myotatic reflexes
Voluntary movement may develop for several minutes.
Segemental damage in low cervical/lumbar gray matter destroy inhibitory Renshaw
neuron release activity of remaining anterior horn cell spinal segmental spasticity
Any residual symptom persist after 6 months permanent
Enlarging cavity in proximal segment of the cord loss of motor & sensory function
above the lesion (after years of trauma)

Transient Cord Injury

Transient loss of motor and or sensory function of spinal cord that recover within

minutes/hour/several days.
Syndrome : bibrachial weakness, quadriparesis, paresthesia, dysesthesias, or sensory
symptom alone.
Mechanism
1. Cord undergoes elastic deformation when head struck at vertex/frontally cervical
spine compressed/hyperextended
2. Direct blowto spine or forcefull fall flat on the back
3. Sharp fall on the tip of coccyx
Most frequent in athletes in contact sports.

Central Cord Syndrome (Schneider Syndrome) and Cruciate Paralysis

In case of acute central cord damage, loss motor function more severe in upper limb
than lower one.
Bladder dysfunction with urinary retention and slight sensory loss.

Damage in central gray matter & interuption of crossing pain and thermal fiber
atrophic, areflexic, segmental loss of pain and thermal sensation
Cruciate paralysis : similar with central cord but weakness more selective, limited to
arms. Could be asymmetrical/unilateral. Sensory loss is inconsistent.
C1-C2 region

Examination and Management of Spine-Injured Patient

Diaphragmatic paralysis : lesion of C1-C3
Complete paralysis of arm & leg : fracture/dislocation C4-C5
Legs paralyzed but arm still can be abducted and flexed : C5-C6
Paralysis legs and only the hands : C6-C7
Lesion below L1 : cauda equina syndrome better prognosis than injury in lower
thoracic (involve cord and multiple roots)

Lesion of lower cervical cord may show sparin sensation down to nipple line
becasue contribution of C3 and C4 cutaneous brances of the cervical plexus (innervate
skin below the clavicle)
In all cases of spinal cord and cauda equina injury, prognosis better if there any
movement/sensation during first 48-72h.
Concern : avoide movement of cervical spine
Standard of American Spinal Injury Association to assign injury to a pint (Frankel Scale)
1. Complete : motor and sensory loss below the lession
2. Incomplete : some sensory preservation below the zone of injury
3. Incomplete : motor and sensory sparing, but patient is nonfunctional
4. Incomplete : motor and sensory sparing and the patient is functional (stand and
walk)
5. Complete functional recovery : reflexes may be abnormal
*Group 2,3,4 better prognosis than group 1
Management :
Methylprednisolone high dose (improvement both motor and sensory funcion)
Gm1 ganglioside (enhance recovery)
Radiologic examination : determine alighment of vertebrae and pedicle, fracture,
compression of spinal/cauda equina, bone debris in spinal canal, tissue damage wihtin
cord.
1. MRI 2. CT Scan
Surgical management
1. Advocate reduction and aligment of dislocated vetebrae by traction and
immobilization until skeletal fixation obtained than rehabilitation.
2. Early surgical decompression correction bony displacement removal of
herniated disc tissue & intra and extramedullary hemorrhage, often spine is fixed at
the same time by bone graft/other stabilization.
*Complete spinal cord lesion & hematoma no surgery
Greatest risk of spinal cord injury : first 10 days (when gastric dilataion, ileus, shock
and infection threat to life)
Aftercare : psychologic support, management bladder&bowel disturbance, care of skin
(prevent ulcer), prevention of pulmonary embolism and nutrition maintanance.
Bacteruria common.
Chronic pain give NSAID
Rehabilitation.

Radiation Injury of Spinal Cord

Delayed necrosis spinal cord and brain due to radiation therapy in thorax and nec.

Injury to the gray matter LMN syndrome

Spinal Cord Injury due o Electric Current and Lightning

Electric
Neurologic damage after delay 1 day to 6 weeks (1 week average)
Spinal athropic paralysis low voltage, from arm to arm (across the cervical cord) or
arm to leg
Immediately : pain adn paresthesias, milid weakness unilateral.
Lightning
Dangerous : 30 percent fatal cases
Unconsius
Disturbance of sensorimotor function (limb) may be cyanotic/cold.

Sumber : Adam and Victors Principle of Neurology 8th edition (pg 1049-1057)