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anterior cord syndrome
- damage to corticospinal & spinothalamic tracts
- loss of motor function, pain, and temp sensation due to involvement of ant neural structures
- dorsal column is preserved (this spares proprioception & kinesthesia)
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causes for ant cord syndrome (which means it's an incomplete lesion)
- usually MVA or blow to back of head
- injury to ant cord and/or its vascular supply (the ASA)
- wedge fx of ant vert body due to compression, or fx of post elements
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2 causes of central cord syndrome
- cervical hyperextension
- degenerative narrowing of vertebral canal (often seen in elderly due to spinal stenosis)
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for central cord syndrome, first there's cervical hyperextension or degen narrowing of vertebral canal, and this results in...?
edema a/o bleeding into central grey matter, most commonly in cervical region
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how does central cord syndrome present?
- loss of UE function w relative sparing of LE (walking quad)
- these pts are often ambulatory but w greater falls risk 2/2 flaccid arms that can't use ADs or use arms for protection
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Brown Sequard Syndrome
- cord hemisection due to trauma w/split presentation
- one side loses motor function and position sense due to damage of lateral corticospinal tracts and dorsal columns
- other side loses pain and temp (beginning a few levels below lesion) due to damage to lat spinothalamic tract
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in Brown Sequard syndrome, the side where the lateral corticospinal tracts and dorsal columns are damaged lose what?
motor function and position sense
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in Brown Sequard syndrome, the side where the lateral spinothalamic tract is damaged loses what?
pain and temp (beginning a few levels below lesion)
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posterior cord syndrome - typically due to what?
due to compression and tumor rather than trauma
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what's damaged in posterior cord syndrom?
dorsal column
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when the dorsal column is damaged, causing posterior cord syndrome, how does pt present?
- loss of proprioception below lesion
- wide based gait
- tabes dorsalis
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cauda equina - what is it? presents how?
- LMN lesion
- flaccid paralysis
- absent DTRs
- myatrophy
- sensory loss
- bc it's PNS there's a better prognosis for recovery than in CNS injuries
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heterotopic ossification - what? where?
- formation of bone in extra-skeletal soft tissue
- it'll happen below level of injury both extraarticular and extracapsular
- occurs adjacent to large joints (esp hips and knees, but elbows, shoulder, spine are targets too)
- can cause functional limitations in 20% of pts
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if hyeterotopic ossification is likely to happen, you may see elevated levels of what in the blood?
alkaline phosphate
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heterotopic ossification can lead to waht?
- joint anklylosis
- may require surgical resection
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what's going on w cells to cause heterotopic ossification
multipotential connective tissue cells transform to osteoblasts and chondroblasts
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what to do for heterotopic ossification if it's early stage? if it's late?
- early - do PROM
- late - don't do PROM (it's contraindicated 2/2 risk of pathological fracture)
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why do SCI pts have higher incidence of osteoporosis?
- following SCI, bone resorption is greater than formation
- (can have this at same time as heterotopic growth)
- normally there's a good balance btwn bone formation by osteoblasts and bone resorption by osteoclasts
- this changes 2/2 changes mobility and lack of muscle contraction
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in addition to osteoporosis, increased bone resorption can lead to what?
- hypercalcuria which leads to renal calculi (kidney stones)
- these stones may not be felt by SCI pt --> autonomic dysreflexia
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a few ways to avoid osteoporosis in SCI pt
- spasticity
- FES (functional electrical stim)
- standing
- ambulation
- mobility
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syringomyelia (post-traumatic cystic myelopathy) - what is it?
- cavitation of central grey matter of spinal cord
- can occur 2 months to 20 years post injury
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syringomyelia (post-traumatic cystic myelopathy) - how does it present?
sensory loss, esp pain and temp loss, in UEs
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syringomyelia - what's it associated with?
- spinal tumors
- congenital abnormalities of the foramen magnum or base of skull
- arachnoiditis
- associated w late deterioration of function following SCI
- ass. most frequently w pain, local or radicular
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a nice quote describing syringomyelia
- Syringomyelia is a chronic, progressive neurological condition and is sometimes associated with other neurological disorders such as Arnold-Chiari Malformation, osteoporosis, and scoliosis.
- SM is characterised by a syrinx or pocket of fluid within the spinal cord. It results from an enlargement of the spinal cord due to excess fluid which builds up under pressure. The fluid is forced into the spinal cord causing debilitating effects.
- The causes and symptoms of SM are numerous and no two cases are alike.
- Common symptoms of SM can be motor impairment, severe pain, spacticity, numbness, weakness, and loss of sensitivity in the extremities.
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how to diagnose & treat syringomyelia
- diagnosis by history, confirmation by MRI
- tx: laminectomy and drainage or surgical shunting
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autonomic dysreflexia comes when there's a lesion where, and then a noxious sime where?
- lesion at T6 higher
- triggered by a noxius stim below level of lesion
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in autonomic dysrflexia,what's happening in the body?
there was a noxious stim below level of lesion that caused a massive uncompensated autonomic outflow above he lesion
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sypmtoms of autonic dysreflexia?
- severe HTN
- tachycardia
- sweating
- flushing
- HA (headache)
- piloerection
- shivering
can be lethal or severe
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what to do if your pt goes into autonomic dysreflexia
- sit pt up to lower the BP
- search for offending noxious stim (usually a kinked catheter)
- take BP
- (SCI systolic norm is 90-110, so 140-80 can mean significant HTN)
- if symptoms don't improve call for help aspa
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orthostatic hypotension happens in SCIs why? 3 influences
- loss of LE SNS influences that cause vasoconstriction, leaving the pt in LE vasodilation
- loss of LE muscle pump
- prolonged bedrest, which lead to venous stasis
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ways to prevent orthostatic hypotension
- pressure garments (TEDS/pressure stockings & abdominal binders)
- teach pt to valsava
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piloerection
goose bumps / hair standing up
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most simplistic tx for orthostatic hypotension and for autonomic dysreflexia
- OH: lay'em down
- AD: raise'em up
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resumption of upright pos in pt w orthostatic hypotension?
- it's difficult in early tx
- requires judicious BP monitering and much patience
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thermoregulation troubles in SCI pts
- loss of connection btwn hypthalamus & cord
- poikilothermia - inability to control temp below lesion (won't sweat or shiver)
- always present if there's a complete lesion
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SCI pts & DVTs/PEs? why are they at high risk?
- decreased LE mvmnt
- loss of LE muslce pump
- presence of hypercoagulable condition
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tx for DVTs/PEs for SCIs
- coumadin or heparin
- waering TEDs/stockings or other pressure garments
- daily mobilization
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what % of SCIs don't survive to get acute hospitalization
- 10-20%
- 750-1000 acute SCI deaths/year
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what percent of SCIs die in acute care
3%
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life expectancy for pts injured at 20y/o - tetra, low tetra, para
- tetra: 33
- low tetra: 39
- para: 44
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primary causes for SCI deaths
- respiratory/pneumonia
- suicide
- heart disease
- subsequent trauma
- septicemia
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secondary causes for SCI deaths
- chronic respiratory failure
- bladder dysfunction
- bowel dysfunction
- cachexia
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