Spinal Cord Injury Flashcards
Organization of the vertebral column
VERTEBRAE 7 cervical 12 thoracic 5 lumbar 5 fused sacral 3/4 fused coccygeal
NERVES
Named for the vertebrae where they exit
8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal
C1-C7 nerves exit ABOVE the corresponding vertebrae
C8 and on exit BELOW the corresponding vertebrae
Intervertebral disks
Allow for flexibility and movement. Contain the nucleus pulposus (inner) and annulus fibrosus (outer)
Support in the spinal cord
provided by longitudinal ligaments connecting the bones: anterior, posterior longitudinal; supraspinal, interspinal, and ligamentus flavum.
Ligaments are not as strong on the backside–herniation more likely backwards
Major elements of central nervous system organization
- White matter (internal in the brain, external on the SC) contain axons while Grey matter contains cells bodies (soma)
- Efferent neurons move from the motor cortex=> SC => muscles. Most cross at medulla oblongata (contralateral)
- Afferent: Sensory receptors => SC => sensory cortex. Some cross (contralateral) some don’t (ipsilateral)
Nerves innervating the ANS
PNS: cerebral and sacral nerves
SNS: T1 to L4ish
Causes of Spinal injury
Serious injury: car crashes, falls, gunshots/stab wounds, sports injuries (diving).
Less serious: lifting, minor falls
Plegia
Paralysis monoplegia = one limb hemiplegia = both limbs on one side paraplegia = both upper OR both lower limbs quadriplega/tetriplegia = all four limbs
Paresis
Weakness. Can be ipsilateral (same side) or contralateral.
Muscle Tone related terminology
Hypotonia = less than normal tone flaccidity = absent tone Hypertonia = excessive tone (ie drug addicted babies) Spasticity = stiff, awkward movements Rigidity = immoveable stiffness Tetany = intermittent tonic spasms (Paroxysmal)
Vertebral column injuries
Fracture = fragmentation of the bone: pedicle, lamina, process Dislocation = displacement of the vertebral body Subluxation = partial dislocation
Types of vertebral injuries
Flexion
extension
compression
axial rotation (ie in shaken baby syndrome)
Extent of injury d/o location and severity
Patho of SCI (initial)
- Mechanical disruption of the neurons - vertebrae can grip onto them
- injury-related ischemia and hypoxia => local infarction / necrosis of neural tissue
- development of micro-hemorrhages or edema which interrupt neuronal function
Patho of SCI (Secondary)
Progressive neurologic damage due to initial injury
- some can be reversible*
- Vascular damage leads to ischemia, vascular permeability, edema
- Neuronal injury leads to loss of reflexes below the level of injury (spinal shock)
Prevention of Secondary effects/damage
Immediate immobilization and steroids
Types of SCI
- incomplete transection: partial preservation of sensory and motor function (central cord, anterior cord, brown sequard, conus medullaris)
- Complete transection: absence of sensory and motor function (leads to quadriplegia above T1/ paraplegia below T1)
Effects of SCI at or above C5
Respiratory paralysis b/c diaphragm doesnt work, quadriplegia
Effects of SCI C5-C6
- Paralysis of legs, wrists, and hands
- weak shoulder abduction and elbow flexion
- loss of brachioradialis reflex
Effects of SCI C6-C7
- Paralysis of legs, wrists, hands
- shoulder and elbow flexion usually possible
- loss of biceps jerk reflex
Effects of SCI C7-C8
Paralysis of legs and hands
Effects of SCI C8-T1
- Homer’s syndrome (constricted pupil, ptosis, facial anhidrosis)
- Paralysis of legs
Effects of SCI T11-T12
Paralysis of leg muscles above and below the knee
Effects of SCI T12-L1
Paralysis below the knee
Effects of SCI at the Cauda Equina
- Hyporeflex or areflexic paresis of the lower extremities
- Usually pain or hyperesthesia in the nerve roots (increased sensitivity)
- Loss of bowel and bladder control
Effects of SCI S3- S5 or Conus medullaris at L1
Complete loss of bowel and bladder control
Central Cord Syndrome
Damage to central gray or white matter of cord. Can happen in osteoperosis/ bone degradation or trauma.
- Most affects motor function of upper extremities. Paresis or paralysis, loss of fine motor function
- Less effect on LE motor fxn, bowel, bladder, sexual fxn.
- Recovery: Can become ambulatory and control bowel and bladder, but often incapable of detailed work with hands.
Anterior Cord Syndrome
Infarction of anterior spinal artery. Damages anterior 2/3 of cord.
Most affected: loss of motor fxn, loss of pain and temp sensation. Reduction/loss of local reflexes and LMNs of the anterior horn.
Less affected: Posterior 1/3 of cord, which conveys position, vibration, and touch.
Recovery: tend to do poorly
Brown-Sequard Syndrome
Damage to a hemi-section of the anterior and posterior cord.
Most affected:
- loss of voluntary motor fxn from the corticospinal tract.
- Ipsilateral proprioception lost.
- Contralateral pain and temp sensations (below the lesion) lost.
Recovery: Can improve to point of ambulation and bowel and bladder control.
Conus Medullaris Syndrome
Damage to the CM or the Sacral cord and lumbar nerve roots w/in neural canal.
Most affected:
- flaccid bowel, bladder, and sexual function (ED, saddle anesthesia, Urinary and fecal incontinence, hypotonic anal sphincter, abnormal bulbocavernosus and anal wink reflexes)
- motor fxn in legs and feet: Distal leg paresis
Less affected: reflexes are preserved if only CM is involved. May not have sensory impairment
Cauda Equina Syndrome
Damage to lumbosacral nerve roots w/in the canal
Most affected: patterns of asymmetric flaccid paralysis, sensory impairment, pain
Neuro exam for SCI
Should include:
- Mental status and speech
- cranial nerves
- Central and peripheral sensory fxn
- Motor fxn
- Cranial and peripheral reflexes
- cerebellar fxn and gait
Diagnostics: X-Ray
Provides detail of the bone structures in the spine.
- USED to rule out instability, tumors, fractures
- Does NOT capture disc and nerve root structures.
- Can’t be used to diagnose lumbar disc herniation/nerve pinching.
Diagnostics: CT
Useful for imaging large disc herniations (but can miss smaller ones)
Diagnostics: CT with Myelogram
Use a radiopaque dye into the sac around the nerve roots to light them up.
- good info about nerve roots.
- sensitive for nerve impingement and can pick up subtle lesions.
Diagnostics: MRI
- Most useful imaging study available for spine surgery (but expensive!)
- Aids in assessment of certain conditions by providing detail of the disc and nerve roots
- Provides refined detail of spine anatomy
Diagnostics: EMG
Electromyography (more rare)
Like EKG but for nerves–assesses electrical activity
- used to distinguish neuropathy (nerve degeneration) from radiculopathy (nerve root compression)
Diagnostics: SSEP
Somatosensory Evoked Potentials (more rare)
- assesses speed of electrical conduction across spinal cord
- if it’s pinched the electrical signals will travel slower
- used to monitor SC during surgery
SCI: Early Management
Immediate goal to reduce neuro deficits and prevent additional losses.
- immobilize with neck collars and back boards
- log roll and secure head
- Cervical traction for cervical injury
- Bedrest and log rolling for thoracic and lumbar injury
- high dose methylprednisone w/in 8 hrs to stabilize (but watch out for pneumonia)
Alterations in Spinal reflexes: UMN lesions
- affected by any injury at or above T12
- results in spastic paralysis of affected skeletal muscles groups and muscles that control bowel, bladder, sexual fxn.
- Can still have a reflex arc but lack control
Alterations in Spinal reflexes: LMN lesions
- With injuries below T12
- Result from damage to the peripheral nerves
- Causes flaccid paralysis (no reflex arc) of involved skeletal and muscle groups
Spinal or Neurogenic Shock
often the first complication of injury
- State of areflexia
- loss of most/all spinal reflexes below injury level
- manifestations: flaccid paralysis, lack of reflexes and autonomic fxn.
- can last minutes, hours, days, weeks but usually self limiting
(body may regain fxn)
Innervation for Ventilation (when functioning)
- Diaphragm innervated by phrenic nerves, C3-C5.
- Intercostals innervated by T1-T7
- Major muscles of expiration innervated by T6-T12
Ventilation dysfunction r/t level of injury
C1-C3 injury: Lack of respiratory effort, requires ventilation
C3-C5 injury: allows partial diaphragmatic fxn but ventilation is diminished
Below C5: ability to take a deep breath and cough is less impaired
Tools for meeting communication needs (patient is VERBAL)
- they made need intubation*
- Fenestrated tracheostomy tubes: provide airflow for vibration of the vocal cords
- talking tracheostomy tubes
- Diaphragmatic pacing
- Electrolarynx-type devices
- Mechanical ventilation w/ air leak (use vibration)
Tools for meeting communication needs (patient is NON-VERBAL)
- Communication boards or cards
- computerized scanning programs
- Mouth-stick control devices
ANS Dysfunction
- above level of injury - normal fxn*
- Ascending and descending transmission below injury is blocked: uncontrolled spinal and autonomic reflexes
- Biggest issues: Autonomic regulation of circulatory function and thermoregulation
- Higher the level of injury the more profound the effect (especially above T6) – watch for diaphragm, IC muscles, baroreceptors in carotids.
Vasovagal response
(Normal = vagus has inhibitory effect on HR/SNS)
Vagal stimulation => vasovagal response => bradycardia or asystole b/c SNS signal blocked
- If you need to deep tracheal suction, hyperoxygenate first in case they need O2
- Avoid rapid position change - if necessary to do so have anticholinergic drugs available to work against PNS
Autonomic Dysreflexia: Causes
(stimulation that would normally be non-threatening become life threatening)
- Visceral distension ie full bladder or rectum
- pain: pressure ulcers, ingrowns, dressing changes, operative procedures
- Visceral contractions: ejaculation, bladder spasms, uterine contractions
Autonomic Dysreflexia: Description
Patients can’t feel stimulus but signals are still being sent.
- Acute episode of exagg. SNS reflex response
- Characterized by: Hypertension, bradycardia, headache from vasodilation
- Does not occur until spinal shock has resolved and reflexes return (w/in 6 mo) but timing unpredictable and can occur throughout life
- T6 and above injuries
Autonomic Dysreflexia: Patho
Unregulated SNS activity =>
Vasospasm, hypertension, skin pallor, piloerection =>
baro-reflex mediated vagal bradycardia, vasodilation.
Skin flushed and profuse sweating above the injury (pallor below)
Postural Hypotension
- with injuries at T4-T6 and above*
- related to descending control of sympathetic outflow to blood vessels in the extremities and abdomen
- Blood pools without responding vasoconstriction => Low CO
- SIGNS: dizziness, pallor, sweating above injury level, bblurred vision, fainting.
- PREVENTION: change position slowly, promote venous return.
Alterations in temperature Regulation
- Again related to SNS helping regulate*
- Central mechanisms for temp in hypothalamus
- Sympathetic effector responses below level of injury are disrupted (can’t conserve or dissipate heat)
- Higher level of injury = more disturbance
- Poikilothermy: assuming the external temperature
- Education: clothing choice and awareness of environment
Circulatory System Dysfunction
- Edema and DVT common b/c blood doesn’t return
- Low PVR, areflexia and hypotonia lead to incr. venous pressure and pooling
- Respond with Elevation and compression (AE Hose)
- Respond to DVT: low dose heparin, ROM, compression devices
Sensorimotor Dysfunction
- Isolated reflex activity and muscle tone no longer under control of higher centers
- Results in hypertonia/ spasticity below level of injury
- May be tonic (sustained) or clonic (intermittent)
- Occurs in injuries above T12 - below the response is damaged @ spinal cord or nerve level
- Stimuli: stretching, infection, distension, pressure
- Intervention: PROM, avoid stimuli, antispasmodics
Skin
- Skin injury is the most preventable complication from SCI*
- innervation by nerves in dermatomes
- SNS: control vasomotor and sweat glands, provide circulation, excretion, temp regulation
Factors of injury: pressure, shearing, trauma, irritation, sweat
Intervention: relieve pressure, encourage circulation, inspect for breakdown
Pain
- Diverse and unpredictable- could be none or lots*
- Mechanical/Fracture pain: Dull, aching, at level of injury (from soft tissue damage)
- Radicular or spinal nerve root pain: aching/shooting along distribution
- Visceral: poorly localized, burning. r/t bladder distension or UTI
- Central: diffuse burning sensationb elow level. Aggravated by touch, movement, distansion
Interventions: TENS, TCAs, Anticonvulsants, NSAIDs, PT
Bladder Function
In health: sensory signals from stretch receptors to voiding center to motor neurons
- SNS: detrusor relaxation (bladder filling)
- PNS: detrusor contraction (voiding)
- UMN injury: spastic bladder dysfunction. Lack awareness of filling/ voluntary control => incontinence
- LMN injury: flaccid bladder dysfxn. Lack awareness of filling and tone. Cannot void => retention and overflow.
Intervention: drainage, external collection, manual techniques
Bowel elimination
In health: SNS: T6-L3 = low motility and high sphincter tone.
PNS: S2-S4: high motility, low sphincter tone.
- Injuries S2-S4: flaccid fxn of defecation reflex = loss of voluntary control
- injuries above S2: spastic function of defectaion reflex => intrinsic contractile response intact but no defecation reflex.
Intervention: high fluid, high fiber diet, mobility, privacy, positioning, laxatives
Sexual fxn
In health: T11-L2: mental stimuli or psychogenic sexual response
S2-S4: sexual touch or reflexogenic sexual response
Spinal cord injury at any level: disrupts neural pathways.
- UMN lesion (T10 and higher): reflex sexual response to touch but not mental stimuli
- LMN lesion (T12 and below): reflex center may be damaged. No response to touch, may have mental stimuli.
Intervention: erectile aids, lubricants.
May still have fertility!
Herniated Disks- reasons
- Trauma (50%): microfractures or microtears
- Aging
- Degenerative disorders (ie osteoperosis)
Most common herniation
Posterior and oblique toward the intervertebral foramen.
L5 nerve impingement
Can cause weakness in extension of big toe and ankle. Numbness and pain on top of foot and pain into buttocks
S1 nerve impingement
May cause loss of ankle reflex or weakness in ankle push. Numbness and pain down the sole or outside of foot.
Lumbar disk herniation
most comon L4 to L5 or L5 to S1
Cervical Disk herniation
Most common = C6 to C7 and C5 to C6.
- C5 = shoulder pain, deltoid weakness, possibly some numbness in the shoulder. Bicep reflex may be reduced
- C6 = weak biceps and wrist extensors, pain/numbness down arm to thumb. Brachioradialis reflex may be diminished.
- C7 = pain/numbness down arm to middle finger. Tricep reflex may be diminished
- C8 = hand dysfunction (nerve to small muscles of the hand). pain/numbness to outside of little finger and impair reflex.
Disk herniations: Manifestations
- # 1 = pain
- intensified by coughing, sneezing, straining, stooping, standing, jarring
- radiating
- slight motor weakness
- paresthesias and numbness
- lowered reflexes
Disk herniations: management
- analgesics: NSAIDS or short term opioids
- Anti-inflammatories: steroids or cortisone injection
- Muscle relaxants
- conditioning exercise
- PT
- Chiropractic manipulation
- Education: corrected mechanics for lifting and protection
- Surgical indications: documented herniation, consisted pain or neuro deficit, failure to respond to other therapy, incontinence, foot drop
