Spinal Cord Injury Flashcards
clinical effects of complete spinal cord injury
all voluntary movement and sensory gone
reflex function in all segments are suspeded
definition of level of injury
most caudal segment with normal sensation and muscle strength of 3/5 or better with the level immediately above 5/5
complete vs incomplete lesion
complete: no preservation of any motor or sensory function
incomplete: any residual motor or sensory function more than 3 segments below the level of injury
signs of incomplete cord injury
any sensation or voluntary movement in LE
sacral sparing (anus sensation, perineum, voluntary anal contraction)
preservation of sacral reflexes not counted
what is spinal shock
profound loss of all spinal reflexes below level of injury + complete paralysis and anesthesia
NOT THE SAME AS COMPLETE CORD INJURY
presentation of spinal shock
flaccid paralysis
areflexia
hypotonic paralysis of bowel and bladder
hypotension, anhidrosis, flushed warm peripheral skin
hypotension without compensatory tachy (if high cervical lesion)
triad of neurogenic shock
hypotension
bradycardia
hypothermia
more common in injuries above t6 due to secondary disruption of sympathetic outflow from t1-l2
t/f less complete lesions and slow developing lesions result in little to no spinal shock
true
mechanisms of spinal cord injury
vertical compression
hyperflexion
rotational
hyperextension
characteristics of vertical compression
creates axial node on vertebra –> vertebral body is compressed –> burst fracture
usually in lumbar
characteristics of hyperreflexion injury
causes wedge fractures and stretched interspinous ligaments
characteristics of rotational injuries
shearing injury that causes fracture
results in tearing of posterior ligamentous structures and displacement of vertebrae
characteristics of hyperextension injury
causes a disruption in the anterior longitudinal ligament or buckling of ligamentum flavum into spinal canal
can rupture intervertebral discs
asia impairment scale
table 4
pathology in acute paraplegia syndrome
squeezing or shearing in spinal cord –> destruction of gray and white matter + hemorrhage –> traumatic necrosis
healing –> gliotic focus or cavitation + hemosiderin and iron
in months/years: progressive cavitation happens (traumatic syringomyelia or fluid build up) –> delayed central or incomplete transverse cord syndrome
t/f in most traumatic lesions, the lateral parts suffer greater injury
false, the central parts
features of cord injury in c1-c3
vasomotor and respiratory collapse = ventilator support
features of cord injury in c4-c5
quadriplegia/tetraplegia with preserved respiratory function
complete paralysis below the neck
features of cord injury in c5-c6
sparing of shoulder muscles with partial paralysis of arm and hands
loss of biceps and brachioradialis reflexes
paralysis of lower body
features of cord injury in c7 and c8
c7: biceps sparing, loss of triceps reflex
c8: triceps sparing, paralyzed fingers and wrist flexion
high vs low cervical cord injury
table 6
features of t6 injury
paraplegia (xiphoid process)
features of t9 injury
paralysis of lower abdominal muscles
loss of superficial abdominal reflexes
(+) beevor sign
high vs low thoracic cord injury
high: spares UE, impaired breathing, ileus, paraplegia
low: spares abdominal muscles, normal breathing,
lumbar cord injury (l1)
paraplegia
incomplete injuries of spinal cord
central cord syndrome
anterior spinal cord syndrome (anterior 2/3)
posterior spinal cord syndrome (posterior column)
brown sequard syndrome (hemisection)
most common type of incomplete spinal cord injury
central cord syndrome - symmetrical incomplete quadriparesis, disproportionately affecting ue
tracts affected in central cord syndrome
cervical corticospinal
cervical lateral spinothalamic
pathophysio of ccs
fall forward and hit chin = hyperextension
usually with preexisting narrowing of spinal canal
spinal cord rubs against disc osteophyte = anterior compression
inward buckling of ligamentum flavum = posterior compression
clinical presentation of ccs
loss of pain and temperature in the distribution level of the injury
expansion of lesion = weakness at level of sensory loss
syringomyelia in ccs
fluid filled cavitation in the cord
- loss of pain and temp sensation (cape-like sensory loss)
- suspended sensory loss
- weakness of muscles in arms with atrophy and hyporeflexia
- later: cst involvement with brisk reflexes in legs, spasticity and weakness
etiology of syringomyelia in ccs
trauma
chiari type 1 malformation
clinical presentation of syringomyelia
central cord syndrome (arms weaker than legs)
dissociated sensory loss
areflexic weakness in ue
management of syringomyelia
syringo-subarachnoid shut
another type of lesion that can have similar presentation with ccs
intramedullary tumor
clinical presentation of anterior spinal cord syndrome
bilateral muscle weakness (cst)
bilateral loss of pain and temp sensation (stt)
urinary incontinence (descending autonomic tracts)
posterior column sparing
etiology of ascs
anterior spinal artery infarction 2/3 (thromboembolism, trauma, vertebral burst fracture)
intervertebral disc herniation
radiation myelopathy
spinal metastasis (fracture or sc compression)
cervical spine injury w/ wedge and burst fractures (bone compressing)
progression of symptoms in ascs
back pain numbness of limbs difficulty walking urinary urgency paralysis
least favorable prognosis in all of syndromes
ascs
preservation of some sensory or motor function below the level of injury are good prognostic factors
clinical presentation of posterior spinal cord syndrome
loss of proprioception and vibration sense
no weakness
bladder dysfunction
clinical presentation of brown sequard syndrome
ipsilateral: weakness, lmn symptoms at level, umn symptoms below, loss of proprioception, vibrationi, light touch, and tactile sense
contralateral findings: loss of pain and temperature sensation
etiology of brown sequard syndrome
knife or bullet
ms
tumor
t/f cauda equina syndrome is part of incomplete cord injuries
false
clinical presentation of cauda equina syndrome
radicular pain in sciatic distribution that worsens with coughing or sneezing
severe radicular sensory deficits in legs and saddle area
lmn deficit: flaccid paresis of le with areflexia, urinary and fecal incontinence, impaired sex
clincial presentation of conus syndrome
detrusor areflexia with urinary retention and overflow incontinence fecal incontinence impotence saddle anesthesia loss of anal reflex
management for conus syndrome
open surgery to remove disk that comes out
clinical presentation of poliomyelitis
lower motor neuron weakness (invasion of anterior horn cells)
flaccid paralysis
atrophy
areflexia
