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70 Cards in this Set

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What is the prevalence of spinal cord injury in the US?
What is the m:f ration for spinal cord injury?
What is the most common level of spinal cord injury at hospital discharge?
What is the most common reason of spinal cord injuries?
motor vehicle accidents
Describe ASIA classification of injuries.
A: complete injury (no sensory or motor under lesion)
B: sensory but no motor fxn @ S4-S5
C: motor fxn preserved under LOI & >50% of them have <3/5 strength.
D: motor fxn preserved below LOI & @ least 50% >3/5
Where does the spinothalamic tract cross & what is its main fxn?
Pain & temp sensation. Crosses: ventral white matter of cord, ascending one level as they cross.
What is the fxn and where does the ascending dorsal white columns cross?
Fxn: proprioception, light touch.
Cross: medulla (via medial lemniscus) then go to thalamus
Where does the descending corticospinal fibers cross & what is the main fxn?
Cross @ medulla-->become lateral corticospinal tract. Small pt don't cross & descend in anterior corticospinal tract.
What are the symptoms of anterior cord syndrome?
Variable loss of motor & pain/temp w/ preserved proprioception & light touch.
Prognosis for motor recovery is poor.
What are the causes of anterior cord syndrome?
retropulsed disk/vertebral fragments, aortic clamping during surgery, lesions in anterior spinal artery
What is the most common incomplete injury?
Central Cord Syndrome
What are the symptoms of someone w/ central cord syndrome?
UE > LE weakness & sacral sparing. These pts are 'walking quads'==>50% ambulate
How does one get central cord syndrome?
They're cervical level lesions (not much room around there so easy to get pinching & older pts get cervical canal narrowing, cord compression also anterior & posterior w/ bulging ligamentum flavum)
What are the causes of Brown-Sequard syndrome?
stab wounds, tumors
What are the symptoms of Brown-Sequard syndrome?
Hemisection of cord causes ipsilateral motor loss & proprioception, contralateral (spinothalamic tracts cross over) loss of pain/temp. Prognosis for ambulation is 90%.
What symptoms do you get with conus medullaris syndrome?
Saddle anesthesia + bladder/anal sphincter/erectile dysfunction due to S2-S4.
-Reflexes: hyporeflexic: anal (S2-4), bulbocavernosus (S2-4), ankle DTR (S1,S2) b/c LMN problem.
-Poor prognosis for recovery
What is traumatic conus?
L1/L2 fracture of disc herniation--accompanied by injury to lumbosacral N roots & LE weakness.
What is Cauda Equina Syndrome?
Neural Canal compression (similar to traumatic conus syndrome) w/ fractures of pelvis/sacrum/spine below L2. LMN purely (areflexia, radicular pain, flaccid paralysis).
-Presents like multiple radiculopathies.
What is the clinical pictures of Cauda Equina syndrome?
Purely LMN promblem: bladder/bowel areflexia & erectile dysfxn, saddle anesthesia, flaccid LE weakness, radicular pain, reflexes may be lost, some regeneration/sprouting is possible.
What is syringomyelia?
Gradual enlargement of fluid-filled cyst in central cord at level of injury.
50% prevalence, 5% neurologic decline esp in cervical spine.
How do you treat syringomyelia?
Diuresis, positioning; tapping is only temporary, syrinoperitoneal shunting is possible.
What are the symptoms of syringomyelia?
Weakness, numbness, respiratory decline, & pain expands rostrally, caudally.
What is Virchow's triad of DVT?
Stasis, Intimal injury (vasoactive amines), hypercoagulability (altered clotting factors)
When are you at highest risk of getting a DVT?
In 1st 2 weeks post injury.
What treatment should be done for DVT in spinal cord injuries?
12 wks of prophylactic treatment of complete injury, 8 wks for incomplete injuries.
How is DVT diagnosed?
Duplex ultrasonagraphy.
What is in a differential diagnosis of DVT?
HO, infection, dependent edema, fracture, hematoma.
Where are pressure ulcers most commonly found?
Sacrum & ischium, trochanters, heels.
What is the tx for pressure ulcers?
necrotic tissue debridement, UV light, laser radiation, U/S, hyperbaric O2, Estim, proteins, vitamins C,A, Zinc.
What are risk factors for pressure ulcers?
Incontinence (skin maceration), age, elevated temperatures, nutritional deficits, insensate skin (pt can't feel pain or temp)
What is the mechanism of forming pressure ulcers?
Pressure & SHEAR. 70 mm Hg for 2 hrs-->ischemia, even less w/ added shearing forces.
How is heterotopic ossification diagnosed?
bone scan, XR, Alk Phos (serum marker for bone growth);
How is heterotopic ossification treated?
ROM, biphosphonate, NSAIDS, surgery.
What is heterotopic ossification?
Medullary & cortical bone forming around jts-->deposition of periarticular bone typically below LOI-->may limit ROM, fuse joints, alter positioning, increase pressure ulcer risk (b/c of inc Ca around the jts)
What are the symptoms of immobilization hypercalcemia?
Lethargy, fatigue, nausea, cramping, polydipsia. Eventually osteopenia below LOI, increase in bone resorption in first 6 months, exceeding kidney excretion ability.
Patients with upper cervical injuries are at increased risk of developing what condition?
Acute & chronic pneumonia (b/c can't clear out secretions)
In someone w/ an upper cervical injury, in what position should they be in to increase their vital capacity?
Supine, abdominal binder in upright (to prevent stretching of abdomen & dropping of diaphragm.)
Complication after SCI that results in increased BP, bradycardia, and profuse sweating above the lesion?
Autonomic Dysreflexia
What is the most common levels involved and causes of Autonomic Dysreflexia?
T6 & above. Bladder distention, UTI, bowel impaction, pressure ulcer, ingrown toenails.
With neurogenic GI complications, whats the difference between UMN and LMN bowel?
UMN: longer transit times, peristalsis altered, increased sphincter tone; LMN: slowed stool propulsion, external anal sphincter (EAS) tone lost which causes impaired urge
Related to GU spinal levels, explain S2-4 and T10-L2
Sympathetic (T10-L2) relaxation; Parasympathetic (S2-4) detrusor contraction.
What are the GU effects of a suprasacral SCI?
DSD (detrusor sphincter dyssynergia) lack of sphincter relaxation during bladder contraction (urinary retention and reflux into kidneys causing kidney failure).
Compare complete vs incomplete sexual dysfunctions from SCI in men?
complete: reflexogenic erections, no psychogenic erections, rare ejaculation; incomplete: both reflexogenic/psychogenic erections, ejaculation more common. Infertility is common (retrograde ejaculation)
What are negative predictors of motor recovery?
hemorrhage and length of cord edema on MRI
what are the different types of head trauma injuries?
traumatic brain injury = head injury = head trauma: closed or penetrating (dura compromised) head injury, focal or diffuse (missile injuries), and nontraumatic brain injury
what are three causes of nontraumatic brain injury?
hypoxic ischemic encephalopathy (HIE), toxic, infectious
What is the leading cause of death in children and elderly >75
What are risk factors for TBI?
low SES, drugs/EtOH, history of TBI, MVA, falls (children, elderly), violence (20-50yo)
What are pre-injury predictors of recovery from TBI?
employment status, educational level, hty substance abuse, age < 60
What are post-injury predictors of recovery from TBI?
effect on cognitive, behavioral, social support, litigation (all effecting employment outcome)
In severe, moderate, and mild, what is the % mortality and % recover to moderate disability?
severe >50% mortality, ~30% recover to moderate disability; moderate <10% mortality, ~70% recover; mild ~95% recover.
What are and where do contusions occur?
hemorrhagic bruises on gyri. Frontal or temporal lobes.
Coup vs. Contra-Coup. How injured? Where is the brain damage?
Coup - moving object (damage: directly underneath); Contra-coup - moving head (damage: occurs on opposite side of impact)
Which primary injury would not be seen on CT (requires MRI) and hallmark is shearing of corpus callosum?
Diffuse Axonal Injury
What would occur in late primary injury?
cascade of glutamate/aspartate release; enzyme-linked Ca channels; increased enzymatic activity -> "self destruct"
What would be the tx for secondary injury with ICP > 20mmHg?
mannitol, hyperventilation, hypertonic Na, hypothermia, craniotomy, craniectomy
What are measuring systems for recovery?
MMSE, Functional Independence Measure (self-care, hygiene), Rancho Los amigos scale (more neuromuscular than cognitive)
What is the difference in seizure tx at the >24hrs after a TBI?
>24hrs need anticonvulsants. Immediate sezures w/in 24hrs tx, but not related to chronic
How long and what drugs would you use for AED prophylaxis?
2 wks at most. Carbemazepine, valproic acid better than phenobarbitol or phenytoin
What is the type of hydrocephalus commonly found in TBI patients?
Generally communicating/non-obstructive (defect CSF reabsorption)
Define hydrocephalus ex vacuo
A hydrocephalic condition resulting from the loss or atrophy of brain tissue.
What are the neuromuscular complications from TBI with UMN syndrome?
spasticity, contractures, movement disorders (rigidity, tremor, ataxia, myoclonus, ballism, chorea), weakness
What drug would best tx UMN syndrome in TBI patients?
What drug would be used to treat movement disorders in UMN syndrome?
Dopamine agonists
What is the difference in HO between TBI and SCI patients?
TBI: UE=LE. Whereas SCI: hips/knees
How would you tx HO in TBI pt?
Etidronate, NSAIDs, radiation, surgery when "cool" on bone scan
What is the difference between vegetative state and coma related to sleep?
Coma has no sleep/wake cycles in transient state; Vegetative state has sleep/wake cycles
What is of concern in moderate TBI pt recovery?
structured sensory integration. Control of agitation and restlessness (electrolyte imbalances, seizures, sleep disturbances, MSK injury & pain, Posttraumatic hydrocephalus, environmental overload)
Which drugs would you use for least effect on sleep architecture?
Trazadone, Ambien, Chloralhydrate
What drugs would you use and avoid for agitation?
r/o medical causes FIRST, then adjust env stimuli. Stay away from sedatives and antipsychotics. AEDs, central antihypertensives, Bblockers, stimulants