Cord Injury Too big a topic for 30 minutes Goals Demographics Mechanisms of Injury amp Pathophysiology Presentation amp Diagnosis including common spinal cord syndromes ID: 494837
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Slide1
Spinal Cord InjurySlide2
Too big a topic for 30 minutes……………..Goals:Demographics
Mechanisms of Injury & PathophysiologyPresentation & Diagnosis including common spinal cord syndromes
Special Added Attraction:
Neuroanatomy Review!
ManagementLittle FunWon’t CoverBony spinal injuriesImagingSCIWORASlide3
Who gets spinal cord injuries and how?What is the cost and frequency?Slide4
Risk Factors Young male most likely victimMales 77-80%Alcohol involved in at least 25%
Underlying spinal diseasesCervical
spondylosis
Atlantoaxial
instabilityOsteoporosisSpinal arthropathies- ankylosis spondylitis or rheumatoid arthritisSlide5
Spinal Cord Injury Facts Direct medical expenses accrued over the lifetime of one patient- $500K- $2 millionTraumatic Spinal Cord Injury (TSCI)
Incidence 2010- 40 per million per year or approx. 12,400 annually2005- 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%Slide6
Patients with spinal cord injuries are sick!Slide7
What are the mechanisms of injury?Primary vs Secondary Injury?Slide8
PathophysiologyMost produced in association with injury to vertebral columnFracture of one or more bony elementsDislocation at one or more joints
Tearing of ligamentsDisruption and/or herniation of the intervertebral discSlide9
Pathophysiology: Primary vs Secondary Injury Primary Injury- immediate effect of traumaForces of compression, contusion, shear injury to cord
Secondary Injury: Begins within minutes & evolves over hours
Complex & incompletely understood
Mechanisms
IschemiaHypoxiaInflammationEdemaExcitotoxicityApoptosisClinically 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 Slide10
Clinical PresentationHow do you assess the severity of spinal cord injury?Slide11
Clinical PresentationTypically pain at site of spinal fx
Patients with TSCI often have associated brain & systemic injuries that may limit patient’s ability to report localized painApprox
50% TSCI’s involve cervical cord and present with
quadriparesis
or quadriplegiaSeverity of spinal cord syndromes classified using American Spinal Injury Association (ASIA) ScaleThis is the “Stroke Scale” for Spinal Injury Slide12
TermsSacral SparingSensory 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
ReflexPull on foley or gently pinch penis or clitoris and monitor anal contractionIf reflex is intact, the anal sphincter will contractPresence of the reflex indicates an incomplete lesionAnal 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) Slide13
American Spinal Injury Association (ASIA)Slide14
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 cauda
l level, &
no
sensation in levels below, including
NONE in sacral segments S4-S5Reduced muscle power in level immediately below injury followed by complete paralysis more caudallyAcute stage- reflexes absent, no response to plantar stimulation, muscle tone flaccidMale w/ complete lesion may have priapismBulbocavernosus reflex usually absentUrinary retention and bladder distention occurSlide15
Incomplete Cord Injury (ASIA grades B-D)Various degrees of motor function in muscles controlled by levels of spinal cord caudal to injurySensation 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
yrsSlide16
Neuroanatomy of the Spinal CordSlide17
Spinal Cord anatomyCross-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
Slide18
Spinal Cord AnatomyVentral 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 informationModulates pain transmission through spinal and supraspinal
regulatory circuits. Slide19
Efferent Motor TractsPyramidal:
Originate in cerebral cortexCarry motor fibers to spinal cord & brainstem
Corticospinal Tract (CST)
: voluntary control of muscles of body
To ipsilateral musculatureAnterior Corticospinal Tract (15-20%): ends in cervical & upper thoracic cordLateral Corticospinal Tract (80-85%):Crosses in medulla & terminates in ventral horn.From ventral horn goes to spinal nerve and musclesCorticobulbar Tract: voluntary control of muscles of faceExtrapyramidalOriginate 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 handSlide20
Afferent Sensory TractsDorsal Column Medial Lemniscal
(DCML)Pathway:
Ipsilateral fine touch (tactile sensation), vibration, & proprioception
In brainstem it is transmitted thru the medial lemniscusEnter cord into dorsal horn and then go to ipsilateral Dorsal ColumnsDorsal Columns = Posterior ColumnsFasciculus cuneatus: cervical/thoracic- lateral localization/orientationFasciculus
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 brainstemSlide21
Spinal Cord Blood supplyA single anterior and two posterior spinal arteries supply the spinal cord
Anterior spinal artery supplies anterior 2/3 of the cordPosterior 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 branchesSupplies the Anterior Spinal ArteryEnters 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
regionSlide22Slide23
Location of lesion in central cord syndromeSlide24
Central Cord SyndromeCharacterized 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 Slide25
Location of lesion in Brown-Sequard syndromeSlide26
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.Slide27
Location of lesion in Anterior (Ventral) Cord SyndromeSlide28
Anterior (ventral) cord syndromeRelatively rare historically related to decreased blood supplyusually
includes tracts in the anterior two-thirds of the spinal cord,
Corticospinal
tracts, S
pinothalamic 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.Slide29
Location of lesion in posterior (dorsal) cord syndrome Slide30
Dorsal (posterior) cord syndromeBilateral involvement of dorsal columns, corticospinal tracts, &
descending autonomic tracts to bladder control centers in sacral cordDorsal column symptoms include gait ataxia and
paresthesias
Corticospinal
tract dysfunctions produces weaknessAcute: muscle flaccidity & hyporeflexiaChronic: muscle hypertonia and hyperreflexiaExtensor plantar responses and urinary incontinence may also be presentCAUSES
:
MS,tabes
dorsalis
,
Friedreich
ataxia,
subacute
combined degeneration, vascular malformations, epidural and
intradural
extramedullary
tumors, cervical
spondylotic
myelopathy, and
atlantoaxial
subluxation.Slide31
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 asymmetricAll sensory modalities are similarly impaired & may be partial or complete loss of sensationSacral 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 Slide32
Conus medullaris syndrome
S
imilar to
Cauda
Equina but injury is more rostral in cord (L1 & L2 area)Most commonly due to thoraco-lumbar bony injuryDepending 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 Slide33Slide34
Transient Paralysis & Spinal ShockImmediately 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 activityIn 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 transmissionSlide35
Initial Evaluation & ManagementABCDECapnography
High cervical injuries may require intubationHypoxia in face of cord injury can adversely affect outcome
Hypotension-
hypoperfusion
can adversely affect outcomeDetailed neuro exam ASAP (ASIA format useful)Slide36
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 Slide37
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 abilityInitial ASIA Grade C:62% able to ambulate independentlyInitial ASIA Grade D:97% able to ambulate independentlyMost recovery for patients with incomplete TSCI takes place in first 6 monthsSlide38
The Beer ?Who is this? Slide39
Frank Netter MD“The Michelangelo of Medicine”1906-1991