Spinal
Cord
Injury
Too big a topic for 30 minutes……………..
• Goals:
• Demographics
• Mechanisms of Injury & Pathophysiology
• Presentation & Diagnosis including common spinal cord syndromes
Special Added Attraction: Neuroanatomy
• Management
• Little Fun
• Won’t Cover
• Bony spinal injuries
• Imaging
• SCIWORA
Review!
Who gets spinal cord injuries
and how?
What is the cost and frequency?
Risk Factors
• Young male most likely victim
• Males 77-80%
• Alcohol involved in at least 25%
• Underlying spinal diseases
•
•
•
•
Cervical spondylosis
Atlantoaxial instability
Osteoporosis
Spinal arthropathies- ankylosis spondylitis or rheumatoid arthritis
Spinal Cord Injury Facts
• Direct medical expenses accrued over the lifetime of one patient- $500K- $2
million
• Traumatic Spinal Cord Injury (TSCI)
• Incidence 2010- 40 per million per year or approx. 12,400 annually
• 2005- approx. 250,000 living survivors of TSCI in USA
• Causes TSCI in US:
•
•
•
•
•
MVA 48%
Falls 16%
Violence (GSW, SW, etc) 12%
Sports accidents 10%
Other 14%
Patients with spinal cord injuries are sick!
What are the mechanisms of
injury?
Primary vs Secondary Injury?
Pathophysiology
• Most produced in association with injury to vertebral column
• Fracture of one or more bony elements
• Dislocation at one or more joints
• Tearing of ligaments
• Disruption and/or herniation of the intervertebral disc
Pathophysiology: Primary vs Secondary Injury
• Primary Injury- immediate effect of trauma
• Forces of compression, contusion, shear injury to cord
• Secondary Injury:
• Begins within minutes & evolves over hours
• Complex & incompletely understood
• Mechanisms
•
•
•
•
•
•
Ischemia
Hypoxia
Inflammation
Edema
Excitotoxicity
Apoptosis
• Clinically manifest by neurologic deterioration over first 8-12 hrs in patient who initially present with
incomplete cord syndrome
• Spinal cord edema develops within hours of injury
• Maximal day 3-6
• Begins to recede after day 9
• Gradually by replaced hemorrhagic necrosis
Clinical Presentation
How do you assess the severity of spinal cord injury?
Clinical Presentation
• Typically pain at site of spinal fx
• Patients with TSCI often have associated brain & systemic injuries
that may limit patient’s ability to report localized pain
• Approx 50% TSCI’s involve cervical cord and present with
quadriparesis or quadriplegia
• Severity of spinal cord syndromes classified using American Spinal
Injury Association (ASIA) Scale
• This is the “Stroke Scale” for Spinal Injury
Terms
• Sacral Sparing
• Sensory sacral sparing includes sensation preservation (intact or impaired) at the anal mucocutaneous
junction (S4-S5 dermatome) on one or both sides for light touch or pin prick or deep anal pressure (DAP)
• Motor sacral sparing includes presence of voluntary contraction of external anal sphincter on digital rectal
exam
• Bulbocavernosus Reflex
• Pull on foley or gently pinch penis or clitoris and monitor anal contraction
• If reflex is intact, the anal sphincter will contract
• Presence of the reflex indicates an incomplete lesion
• Anal Wink (anocutaneous reflex)
• Contraction of anal sphincter in response to pinprick stimulus of perineum
• Deep Anal Pressure
• Examiner’s finger inserted and gentle pressure applies to anorecal wall
• Alternatively, pressure can be applied by using thumb to gently squeeze the anus against the inserted index
finger.
• Consistently perceived pressure should be graded as being present or absent (YES or NO)
American Spinal Injury Association (ASIA)
Complete Cord Injury (ASIA Grade A)
• Rostral zone of spared sensory levels (C5 and higher dermatomes spared
with C5-6 fx-dislocation), reduced sensation in the next caudal level, & no
sensation in levels below, including NONE in sacral segments S4-S5
• Reduced muscle power in level immediately below injury followed by complete
paralysis more caudally
• Acute stage- reflexes absent, no response to plantar stimulation, muscle tone
flaccid
• Male w/ complete lesion may have priapism
• Bulbocavernosus reflex usually absent
• Urinary retention and bladder distention occur
Incomplete Cord Injury (ASIA grades B-D)
• Various degrees of motor function in muscles controlled by levels of spinal
cord caudal to injury
• Sensation partially preserved in dermatomes below area of injury’
• Sensation often preserved to a greater extent than motor function because
sensory tracts are located in more peripheral, less vulnerable areas of the
cord
• Bulbocavernosus reflex and anal sensation often present
• Incidence of incomplete vs complete has increased over last 50 yrs
Neuroanatomy of the Spinal Cord
Spinal Cord anatomy
• Cross-sectional anatomy — The spinal cord contains the gray matter, the
butterfly-shaped central region, and the surrounding white matter tracts.
• The spinal cord gray matter, which contains the neuronal cell bodies, is made
up of the dorsal and ventral horns, each divided into several laminae
Spinal Cord Anatomy
• Ventral Horn:
• Contains motor nuclei of the spinal cord
• Also contains interneurons mediating information
from other descending tracts of the pyramidal and
extrapyramidal motor systems.
• Dorsal Horn:
• Entry point of sensory information into the CNS.
• Processes sensory information
• Modulates pain transmission through spinal and
supraspinal regulatory circuits.
Efferent Motor Tracts
• Pyramidal:
• Originate in cerebral cortex
• Carry motor fibers to spinal cord & brainstem
• Corticospinal Tract (CST): voluntary control of muscles of body
• To ipsilateral musculature
• Anterior Corticospinal Tract (15-20%): ends in cervical & upper
thoracic cord
• Lateral Corticospinal Tract (80-85%):
• Crosses in medulla & terminates in ventral horn.
• From ventral horn goes to spinal nerve and muscles
•
Corticobulbar Tract: voluntary control of muscles of face
• Extrapyramidal
•
•
•
•
•
Originate in brainstem & carry fibers to spinal cord
Responsible for involuntary & automatic control of muscular function such as muscle to ne,
balance, posture, & locomotion
Tectospinal tract: mediates reflex postural movements of the head in response to visual and/or
acoustic input
Vestibulospinal: balance, posture, antigravity muscles
Reticulospinal:
•
•
•
Medial Reticulospinal: increases tone & facilitates voluntary movements
Lateral Reticulospinal: decrease tone & inhibits voluntary movements
Rubrospinal: via red nucleus ?fine motor hand
Afferent Sensory Tracts
• Dorsal Column Medial Lemniscal (DCML)Pathway:
• Ipsilateral fine touch (tactile sensation), vibration, & proprioception
• In brainstem it is transmitted thru the medial lemniscus
• Enter cord into dorsal horn and then go to ipsilateral Dorsal Columns
• Dorsal Columns = Posterior Columns
• Fasciculus cuneatus: cervical/thoracic- lateral localization/orientation
• Fasciculus gracilis: lumbar/sacral- medially localization/orientation
• Spinothalamic:
• Enter cord and cross midline (anterior(aka ventral) commissure)
then go to contralateral Anterior STT or Lateral STT
• Anterior Spinothalamic: contralateral crude touch & pressure
• Sensations not accurately localized (itch & tickle)
• Lateral Spinothalamic: contralateral pain & temperature
• Cervical medial localization/orientation
• Sacral lateral localization/orientation
• Spinocerebellar Tracts: The dorsal and ventral spinocerebellar tracts carry inputs mediating unconscious
proprioception directly to the cerebellum
• Spinoreticular tract carries deep pain input to the reticular formation of the brainstem
Spinal Cord Blood supply
• A single anterior and two posterior spinal
arteries supply the spinal cord
• Anterior spinal artery supplies anterior 2/3 of the cord
• Posterior spinal arteries primarily supply the dorsal columns
• Anterior & Posterior spinal arteries arise from vertebral arteries in neck
• Various radicular arteries branch off the thoracic and abdominal aorta to
provide addition blood supply to the spinal arteries
• Artery of Adamkiewcz (aka Great Ventral Radicular Artery)
• Largest & most consistent of radicular branches
• Supplies the Anterior Spinal Artery
• Enters spinal cord anywhere btn T5 &L1 (usually T9-T12)
• Anterior Spinal Artery uninterrupted along the entire length of
the spinal cord in most
• In others, it is discontinuous, usually in midthoracic segment
• These individuals more susceptible to vascular injury
• The primary watershed area of the spinal cord in most people is in the
midthoracic region
Location of lesion in central cord syndrome
Central Cord Syndrome
• Characterized by loss of pain and temp sensation in the
distribution of one or several adjacent dermatomes at the site of the
spinal cord lesion
• As a central lesion enlarges, encroachs on medial aspect of the
corticospinal tracts or on the anterior horn gray matter, producing
weakness in the analgesic areas.
• There are usually no bladder symptoms.
• Due to disruption of crossing spinothalamic fibers in the ventral
commissure.
• Dermatomes above & below the lesion have normal pain & temp
sensation, creating the so-called “suspended sensory level”
• Vibration & proprioception ( Dorsal Columns) are often spared.
• Most frequently result of hyperextension injury in
patients with long-standing cervical spondylosis.
Get disproportionately greater motor impairment in
upper compared with lower extremities, bladder
dysfunction, and a variable degree of sensory loss
below the level of injury
Location of lesion in Brown-Sequard syndrome
Brown-Sequard Syndrome
• A lateral hemisection syndrome involves the
dorsal column, corticospinal tract, and
spinothalamic tract unilaterally.
• Produces ipsilateral weakness, loss of
vibration, & proprioception & contralateral
loss of pain and temperature . The
unilateral involvement of descending
autonomic fibers does not produce bladder
symptoms.
• CAUSES: knife or bullet injuries &
demyelination are most common causes.
Rarer causes include spinal cord tumors, disc
herniation, infarction & infections.
Location of lesion in Anterior (Ventral) Cord Syndrome
Anterior (ventral) cord syndrome
• Relatively rare historically related to decreased blood
supply
• usually includes tracts in the anterior two-thirds of
the spinal cord,
• Corticospinal tracts, Spinothalamic tracts, and
descending autonomic tracts to the sacral centers for
bladder control
• Corticospinal tracts injury produce weakness and
reflex changes. Spinothalamic tract deficit
produces bilateral loss of pain & temp sensation.
• Tactile, position, & vibratory sensation as normal since
controlled by DORSAL COLUMNS
• Urinary incontinence is usually present
• Causes: spinal cord infarction, intervertebral disc
herniation, and radiation myelopathy.
Location of lesion in posterior (dorsal) cord syndrome
Dorsal (posterior) cord syndrome
• Bilateral involvement of dorsal columns,
corticospinal tracts, & descending autonomic
tracts to bladder control centers in sacral cord
• Dorsal column symptoms include gait
ataxia and paresthesias
• Corticospinal tract dysfunctions produces
weakness
• Acute: muscle flaccidity & hyporeflexia
• Chronic: muscle hypertonia and hyperreflexia
• Extensor plantar responses and urinary
incontinence may also be present
• CAUSES: MS,tabes dorsalis, Friedreich ataxia,
subacute combined degeneration, vascular
malformations, epidural and intradural
extramedullary tumors, cervical spondylotic
myelopathy, and atlantoaxial subluxation.
Cauda Equina Syndrome
• Involves lumbosacral nerve roots of cauda equine
& may spare the cord itself
• Injury to the nerve roots will classically produce
flaccid paralysis of muscles of lower limbs
(muscles affected depend on level of injury)
and areflexic bowel & bladder.
• Often asymmetric
• All sensory modalities are similarly impaired & may
be partial or complete loss of sensation
• Sacral reflexes, bulbocavernosus & anal wink,
will be absent
• Causes: intervertebral disc herniation, epidural abscess, epidural
tumor, intradural extramedullary tumor, lumbar spine spondylosis,
and a number of inflammatory conditions including spinal
arachnoiditis, chronic inflammatory demyelinating polyneuropathy,
and sarcoidosis
Conus medullaris syndrome
• Similar to Cauda Equina but injury is more rostral in cord (L1 & L2 area)
• Most commonly due to thoraco-lumbar bony injury
• Depending on level of lesion, may manifest with mixed picture of upper
motor neuron (due to conus injury) and lower motor neuron symptoms
(due to nerve root injury).
• Some cases difficult to clinically distinguish from cauda equina injury
• Sacral segments may occasionally show preserved reflexes (ie
bulbocavernosus & anal wink) with higher lesions of conus medullaris
• There is early and prominent sphincter dysfunction with flaccid paralysis
of the bladder and rectum, impotence, and saddle (S3-S5) anesthesia.
• Leg muscle weakness may be mild if the lesion is very restricted and
spares both the lumbar cord and the adjacent sacral and lumbar nerve
roots.
• Causes: disc herniation, spinal fracture, and tumors
Transient Paralysis & Spinal Shock
• Immediately after SCI, may be a physiological loss of all spinal cord function
caudal to level of injury with flaccid paralysis, anesthesia, absent bowel &
bladder control, loss of reflex activity
• In males, especially those with cervical cord injury, priapism may develop.
• May also be bradycardia & hypotension not due to causes other than the
spinal cord injury.
• May be secondary to loss of K from injured cells & accumulation in the
extracellular space causing decreased axonal transmission
Initial Evaluation & Management
• ABCDE
• Capnography
• High cervical injuries may require intubation
• Hypoxia in face of cord injury can adversely affect outcome
• Hypotension- hypoperfusion can adversely affect outcome
• Detailed neuro exam ASAP (ASIA format useful)
Glucocorticoids for Rx of TSCI?
• Still controversial?
• Not recommended at HFH
• “Steroids and Spinal Cord Injures: Steroids are NOT
indicated for spinal cord injury”
• HFH Trauma Practice Guidelines p.35
Prognosis for TSCI• Initial ASIA Grade A (Complete TSCI)
• 10-15% improve
• 3% improve to ASIA Grade D
• <10% will be ambulatory at 1 year
• Initial ASIA Grade B:
• 54% recover to C or D
• 40% regain some ambulatory ability
• Initial ASIA Grade C:
• 62% able to ambulate independently
• Initial ASIA Grade D:
• 97% able to ambulate independently
• Most recovery for patients with incomplete TSCI takes place in first 6 months
The Beer ?
Who is this?
Frank Netter MD
“The Michelangelo of Medicine”
1906-1991