spinal cord injury

Spinal Spinal Cord Cord

InjuryInjury

Joselito B. Diaz, MD, Joselito B. Diaz, MD, FPNAFPNA

College of Rehabilitation SciencesCollege of Rehabilitation Sciences

Spinal cord

• Continuation of the medulla• Commences at the foramen

magnum and extends to the level between L1 and L2 vertebrae

• 31 segments– 8 cervical– 12 thoracic– 5 lumbar– 5 sacral– 1 coccygeal

Relationship of spinal cord segments to vertebral numbers

Vertebrae Spinal segment

Cervical vertebrae Add 1

Upper thoracic vertebrae Add 2

Lower thoracic vertebrae (7-9) Add 3

Tenth thoracic vertebra L1 and 2 cord segments

Eleventh thoracic vertebra L3 and 4 cord segments

Twelfth thoracic vertebra L5 cord segment

First lumbar vertebra Sacral and coccygeal cord segments

Spinal cord

• Posterior roots convey sensory inputs while the anterior roots conduct efferent axons to the innervate skeletal muscles

• Arterial blood supply comes from the anterior spinal and 2 posterior spinal arteries

• Anterior spinal artery supplies all the cord except the dorsal horn and posterior column

Sectional Organization of the Spinal Cord

Spinal cord (descending tracts)

• Lateral and anterior corticospinal tract – convey axons from the motor cortex

• Vestibulospinal tract – convey axons from the lateral vestibular nucleus; facilitate activity of extensor muscles

• Reticulospinal tract – transmit autonomic axons and respiratory motor fibers; facilitate or inhibit voluntary movement

• Rubrospinal tract – facilitate activity of flexor muscles

• Tectospinal tract – arise in the superior colliculus, serves as efferent pathway for spinal-visual reflexes

Motor pathway

Spinal effector Mechanism

Spinal cord (ascending tracts)

• Lateral spinothalamic tract – carry pain and temperature sensation

• Anterior spinothalamic tract – pathways for crude touch and pressure

• Posterior columns – consists of two tracts which convey position, discriminative touch and vibration sense– Fasciculus gracilis and cuneatus

• Spinocerebellar tract – convey propioceptive sensation to the cerebellum

Somesthetic System

CL

T

L

S

T

C

S

Corticospinal tract

Spinothalamic tract

CLT S

Dorsal column

SCI Classification

• Tetraplegia – results from injury in the cervical spinal cord

• Paraplegia – results from injury in the thoracic, lumbar or sacral segments

• The neurological level is the most caudal spinal segment that retains normal motor and sensory function on both sides of the body

• The rectal area is examined digitally– A complete lesion is defined as the absence of

sensory or motor function in the lower sacral segment

– Incomplete lesion if either sensory or motor function is present and known as sacral sparing

• ASIA defines the Zone of Partial Preservation as up to 3 segments caudal to the level of a complete injury, in which impaired sensory or motor function is found

• If any function is found more than 3 segments below the level, the lesion is incomplete

Mechanisms of Injury

1. TRAUMA TO THE SPINE AND SPINAL CORD• 10-14% of spinal fractures and dislocations result in

SCI• Fracture-dislocation, pure fracture and pure dislocation

(3:1:1)• Direct blow to the spine is a relatively uncommon cause

of serious spinal cord injury except for bullets, sharpnel and stab wounds

• Mechanisms:– Vertical compression of the spinal column to which

anteroflexion is added• The adjacent cervical vertebrae are forced together at the level of

maximum stress and the anteroinferior edge of the upper vertebral body is driven into the one below, sometimes splitting it in two. The posterior part of the fractured body is displaced backward and compresses on the cord


– Vertical compression and retroflexion (hyperextension)

• Stress is mainly on the posterior elements, which may fractured, and on the anterior ligaments. This allows for displacement of one vertebral body on the adjacent one.

– Whiplash or recoil injury• Sudden forward flexion of the neck followed by retroflexion• Transient posterior dislocation of a vertebral body or

retropulsion of the intervertebral disc into the spinal canal

– High velocity missile penetrates the vertebral canal and damages the spinal cord directly


• Most common sites of vertebral injuries– 1st and 2nd cervical vertebrae– 4th to 6th cervical vertebrae– T11 to L2 vertebrae

• Most mobile portions and the regions in which the cervical and lumbar enlargements greatly reduce the space between neural and bony structures


2. Radiation injury of the spinal cord

• Well recognized sequela of radiation therapy– Transient radiation myelopathy– Delayed progressive radiation myelopathy

3. Spinal cord injury due to electric currents and lightning

4. Myelopathy following lumbar puncture


5. Spinal tumors6. Demyelinating diseases (MS, transverse

myelitis)7. Infectious myelitis including Pott’s disease8. Degenerative joint diseases e.g. cervical spondylosis

9. Vascular diseases of the spinal cord– Infarction – Hemorrhage of the spinal cord and spinal canal– Vascular malformations

10. Hereditary disorders e.g. familial spastic paraplegia

11. Congenital disorders e.g. tethered cord

Clinical syndromesComplete cord transection

syndrome– Caused by fracture

dislocation of the vertebral column, bullet or stab wound, or an expanding tumor

– Bilateral flaccid paralysis and muscular atrophy at the level of the lesion

– Bilateral spastic paralysis below the level of the lesion

– Bilateral loss of all sensation below the level of the lesion (pain and temperature loss 1-2 segments below the lesion)

– Loss of voluntary bowel and bladder control

Clinical syndromesCentral cord syndrome

– Generally occur in the cervical area

– Occurs in elderly with DJD in the neck following hyperextension injury; syringomyelia

– Greater UE spastic weakness than LE

– Segmental loss of pain and temperature

– Bilateral atrophic, areflexic paralysis due to involvement of the AHC

– Bilateral loss of all sensations below the level of the lesion with characteristic “sacral sparing”

Clinical syndromesBrown-Sequard syndrome

– Lateral hemisection of the cord e.g. bullet, knife wound, expanding tumor

– Ipsilateral spastic paralysis below the injury

– Ipsilateral loss of vibration and position sense

– Contralateral loss of pain and temperature 1 or 2 segments below the injury

– Ipsilateral flaccid paralysis at level of injury (AHC)

– Ipsilateral paresthesia/radiculopathy/ anesthesia in the segment of the lesion (dorsal root)

– Simple touch maybe unimpaired

Clinical syndromesAnterior cord syndrome

– Thrombosis of the anterior spinal artery, herniated intervertebral disc, cord contusion during vertebral fracture or dislocation

– Bilateral flaccid paralysis at the level of the lesion

– Bilateral spastic paralysis and loss of pain and temperature sense below the lesion

– Intact position and vibration sense

Clinical syndromesPosterior cord syndrome

– Thrombosis of the posterior spinal artery or vertebral artery dissection (uncommon)

– Surgery or trauma to the spine

– Bilateral loss of position and vibration sense below the lesion

– Motor function and sense of pain and temperature preserved

Stages in Complete Transection

• Spinal shock– Lasts 1-6 weeks, average of 3 weeks– Due to loss of excitatory descending

influences, the findings below the lesions are:• Loss of somatic sensation• Loss of visceral sensation• Loss of motor function• Loss of muscle tone• Loss of reflex activity


• Stage of Minimal Reflex Activity– 3-6 weeks– Characterized by:

• Bulbocavernous reflex (heralds its onset)• Weak flexor responses to nociceptive stimuli

which begin distally and later proximal


• Stage of Flexor Muscle Spasm (Spasticity)– 6-16 weeks– Characterized by:

• Increasing tone in flexor muscles• Stronger flexor response to nociceptive stimuli which

progressively involve more proximal muscle group• Triple flexion response – flexion at hip, knee and ankle with

mild nociceptive stimulus or• Mass reflex response – mild stimulus leads to powerful

bilateral triple response (due to spread of afferent impulses from one segment to the next and continue to fire even after the stimulus withdrawal)


• Stage of alternate flexor and extensor spasticity– More than 4 months– Both flexor and extensor spasms occur, but

within relative short time, extensor muscle tone may be so great that patient can momentarily support his weight in standing position


• Stage of predominant extensor spasticity– More than 6 months– Characterized by:

• Complete paralysis below lesion• Marked extensor spasticity• Loss of somatic/visceral sensation• Increased MSR• Bilateral Babinski• Clonus in both lower extremities• Bowel and bladder incontinence• Reflex spinal sweating in response to noxious

stimuli

ASIA’s Adaptation of Frankel’s Classification

Class Degree

A Complete All motor and sensory is absent below the zone of partial preservation

B Incomplete, preserved sensory only

Preservation of any demonstrable, reproducible sensations. Voluntary motor function is absent

C Incomplete, preserved motor, non-functional

Preservation of voluntary motor function which is minimal and performs no useful purpose (MMT grade <3)

D Incomplete, preserved motor, functional

Preservation of voluntary motor function which is useful functionally (MMT grade ≥3)

E Normal Return of all motor and sensory functions but one may still have abnormal reflexes

Complications of SCI

• Neurogenic bladder– UMN type – lesion above S2 level– LMN type – lesion at S2-S4– Cystometry offers the best diagnostic tool for

differentiation UMN from LMN– Reflex tests to differentiate

Reflex test UMN LMN

Bulbocavernous +++ -

External rectal sphincter

Spastic Lax

Anocutaneous Anal wink -


• Long term indwelling or suprapubic catheter complications– UTI (most common morbidity)– Epididymo-orchitis– Urethral diverticuli– Vesicovaginal or penoscrotal fistula– Bladder calculi

• Intermittent catheterization program – retraining the bladder to function on its own


• Methods of stimulating micturition– Stroking or tapping the upper medial thigh– Alternate hot and cold compress– Sound of water from the faucet– Gentle pulling of the pubic hair– Insertion of gloved finger into the anus to relax the

sphincter

• Residual urine determination– %RU = [RU/(RU+VU)] x 100

• If %RU is < 20%, trial with catheter out• If %RU is > 20%, reinsert indwelling catheter or continue

ICP


• Neurogenic bowel– Decreased intestinal activity– Diarrhea caused by fecal impaction– Bowel program

• Food– High residue diet– Fruits

• Fluid intake– 8-12 liters

• Stool softeners• Timing

– Postprandial (gastrocolic reflex)– Assists: suppositories, digital stimulation, laxatives– Regularity: early morning/evening

• Positioning– Sitting down (physiologic position)


• Autonomic hyperreflexia– Complication in lesions above T6– Signs and symptoms

• Pilomotor erection• Hypertension• Headache• Pallor• Dyspnea• Sweating

– Management:• Since bladder distention is the most frequent cause, urinary

drainage should be established immediately• Rule out causes from the intestinal tract

• Cold extremities below the level of lesion• Bradycardia• Flushing above the level of lesion• Hot above the level of lesion


• Spasticity– Aggravated by noxious stimuli below the

level of the lesion e.g. skin lesions, ischemic muscle areas or irritation from the bowel and bladder

– 3 characteristic patterns• Increased myotatic reflexes• Resistance to passive range of motion• Clonus and Babinski

Complications of SCIModified Ashworth Scale for Grading SpasticityGrade Description

0 No increase in muscle tone

1Slight increase in muscle tone manifested by a check & release or by minimal resistance at the end of the ROM when the affected parts is moved in flexion or extension

1+Slight increase in muscle tone manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM

2More marked increase in muscle tone, through most of the ROM but the affected parts easily moved

3 Considerable increase in muscle tone, passive movement difficult

4 Affected parts rigid in flexion or extension


• To allow good circulation to insensitive muscles, self-stretching exercises are recommended

• If spasticity interferes with functional activity, medications should be given– Diazepam, baclofen, tizanidine, dantrolene

• Neurological procedures– Botulinum toxin injection– Intrathecal alcohol block, rhizotomy,

myelotomy


• Pressure ulcers (decubitus ulcers, bed sores, pressure sores)– Area of unrelieved pressure over a defined

area, usually over a bony prominence, resulting in ischemia, cell death and tissue necrosis

– Most important etiologic factor is localized ischemia due to excessive pressure

– Secondary factors: sensory loss, paralysis, joint contractures, spasticity, incontinence


• Sites of occurrence (depends on positioning of patient)– Ischial tuberosities (if in sitting position)– Greater trochanter (if in lateral decubitus

position)– Sacrum (if lying on back)– Heels– Others: knees, lateral malleoli, scapulae,

spinous process, occiput, head of fibula, ASIS and patella


Classification and Staging of Decubitus Ulcers

Stage Description

1Non-blanchable erythema not resolved in 30 minutes; epidermis intact; reversible with intervention

2Partial thickness loss of skin involving epidermis, possibly into dermis; may appear as blisters with erythema

3Full thickness destruction through dermis into subcutaneous tissue

4Deep tissue destruction through subcutaneous tissue to fascia, muscle, bone, or joint

http://images.search.yahoo.com/search/images/view?back=http%3A%2F%2Fimages.search.yahoo.com%2Fsearch%2Fimages%3Fp%3Ddecubitus%2Bulcers%26toggle%3D1%26cop%3Dmss%26ei%3DUTF-8%26js%3D1%26ni%3D18%26fr%3Dyfp-t-501%26b%3D1&w=250&h=183&imgurl=www.biomedrix.com%2Fimages%2FprogranX%2Fcase1%2Fcase1_4.jpg&rurl=http%3A%2F%2Fwww.biomedrix.com%2FprogranX%2Fcase1&size=13.0kB&name=case1_4.jpg&p=decubitus+ulcers&type=jpeg&no=14&tt=316&oid=94a9e4a371b33ef4&ei=UTF-8


• Prevention– Turning every 2 hours and inspecting skin– Relieve pressure– Spread weight

• Treatment– High protein, high vitamin– No pressure on the decubitus– Debridement of all devitalized tissues– Medications – Plastic surgical repair


• Cardiovascular complications – Orthostatic hypotension

• Seen in those with lesions above T6

– Edema of the lower extremities• Due to poor tissue turgor• Loss of compressible muscle force• Treatment: compressive stockings

– Thrombophlebitis with pulmonary embolism• Fatal in 2-5%• Treatment: prophylactic anticoagulation


• Respiratory complications– Pulmonary atelectasis– Pulmonary infection– Pulmonary edema

• Treatment: mechanical ventilation, tracheostomy, respiratory therapy (breathing exercises, postural drainage), antibiotics, etc


• Metabolic and Endocrinologic complications– Hypoproteinemia– Hormonal levels, including adrenal and sex

hormones, change immediately following injury but resolve within weeks or months

– Testicular atrophy with impaired spermatogenesis• Abnormal temperature regulation of the scrotum• Pituitary-gonadal feedback changes• Frequent infection of the urogenital tract

– Osteoporosis can lead to fractures– Immobilization hypercalcemia– Treatment: adequate hydration, reduced calcium

intake, trial with steroids or oral phosphatase, furosemide and mithramycin

Case • A 65 year old woman was admitted because of

progressive lower extremity weakness• HPI:

– Three months prior to admission, she started to experience moderately severe nape pain. This was followed a week after by numbness of right foot ascending to the right leg and thigh.

– Two months prior to admission, she also noted weakness of the right leg described as dragging of the right foot when walking. She also noticed ascending numbness on the left lower extremity.

– One month prior to admission, she was only able to walk with the help of a stick

– Five days prior to admission, she was no longer able to walk.

• Neurological exam– No cognitive impairment– Cranial nerve examination

• Left pupil: 3-4 mm RTL• Right pupil: 1-2 mm RTL, with mild ptosis

– Weak hand grip on both sides but power was normal on the proximal segments of the upper extremities

– Both lower limbs showed weakness with increased muscle tone, especially on the right

– Knee jerks and ankle jerks in both lower limbs were grossly exaggerated and there was bilateral extensor toe responses

– Loss of pain sensation below the nipple on both sides of the body

– Postural and vibration sense were impaired in both great toes

THANK YOU

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