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Neuroscience > Week 3 - Spinal Cord Injuries > Flashcards

Week 3 - Spinal Cord Injuries Flashcards

1
Q

what are causes of spinal cord injuries?

A
  1. trauma (car accident, falls, sports, gunshots)
  2. alcohol
  3. cancer
  4. disease (transverse myelitis: autoimmune of long fiber tract)
  5. degenerative spine (myelopathy)
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2
Q

what are immeduate (acute) consequences of SCI?

A
  1. weakness
  2. sensory loss or abnormalities
  3. hypotension (from spinal cord ischemia)
  4. urinary retention (b/c lost ability to consciously relax)
  5. orthopaedic pain (broken neck/back, multiple fractures, pain meds may further decrease BP)
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3
Q

when would quadriparesis/plegia VS paraparesis/plegia occur?

A

quad: neck injury
para: injury caudal to T1

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4
Q

what does paraesthesia feel like?

A

sensory abnormality that feels like pins and needles

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5
Q

what are long-term (chronic) consequences of SCI?

A
  1. involuntary movements
  2. spastic or flaccid bladder paralysis
  3. decreased bowel motility
  4. sexual dysfunction
  5. increased risk for blood clots and pressure ulcers
  6. autonomic dysfunction
  7. metabolic disorders (diabetes, heart disease)
  8. musculoskeletal breakdown (rotator cuffs and carpal tunnel) and fractures (osteoporosis)
  9. psychosocial issues
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6
Q

what is the difference between spastic VS flaccid bladder paralysis

A

spastic (neurogenic): injury at or above T10

flaccid: injury below T12

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7
Q

what are the symptoms of spastic (neurogenic) bladder?

A

voluntary relaxation of external urethral sphincter is lost

  • bladder muscle (detrussor) contracts w/ continued filling
  • the harder the detrussor contracts, the stronger the sphincter contracts
  • urine flows in brief dribbles when detressor emptying pressure > sphincter closure pressure
  • incomplete bladder emptying –> chronic infections (main cause of death until 1940s)
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8
Q

how are bladder problems managed?

A
  1. intermittent catheterization (4-6x a day)
    - hard for C6 or higher quadriplegics and women
  2. condom catheter
    - poor solytion due to autonomic dysreflexia (chronic HTN)
  3. indwelling (Foleys)
    - infections, cosmetic appearance
  4. surgical options
    - suprapubic catheter (umbilicus) w/ or w/o valve
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9
Q

what are sexual dysfunction problems with SCI?

A

males: erection unlikely, ejaculation rare
- sperm viability (development and motility) severely impaired)
- fertility severely reduced

females: fertility largely unaffected
- delivery possible, but C-section recommended due to autonomic dysreflexia

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10
Q

how can pressure ulcers be prevented?

A

repositioning patient to prevent cutaneous ischemia (perfuse patches of skin)

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11
Q

what are autonomic dysfunction problems with SCI?

A
  • thermoregulation largely absent, esp. if above T10
  • -no sweating (overheat easily)
  • -limited vasoconstriction (conserving heat)
  • autonomic dysreflexia
  • -episodes of very bad HTN, but paradoxical b/c HR drops to 40 bpm
  • -occurs in response to strong afferent input:
  • –nociceptor (overly full bladder)
  • –bladder-emptying if “neurogenic bladder”
  • –strong cutaneous inputs
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12
Q

what is the gender-specific incidence of SCI?

A

75% males, 25% females

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13
Q

what are the most common areas for SCI?

A

over half are to C-spine

over half are neurologically incomplete

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14
Q

what is the ASIA handbook classifications?

A

American Spinal Injury Association
A: complete - no motor or sensory function below injury
B: incomplete - sensory (only) below injury, including S4-5) anal sensation
-may be able to become C
C: incomplete - sensation + limited motor function below injury level
D: incomplete - sensation + significant motor function below injury level
-can walk, but may need assisted devices
E: normal - sensory + motor function is normal

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15
Q

what are 3 broad approaches to SCI treatment?

A
  1. neuroprotection - protect surviving cells/axons, so they don’t succumb to toxic environment caused by injury
  2. neurorestoration - replace cells, provide neurotrophins, or establish a growth-permissive environment to promote regeneration and reestablishment of neural circuitry
  3. neurorehabilitation - strengthen existing (maybe atrophied) systems, retrain circuits, or develop alternative strategies to accomplish desired tasks
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16
Q

is there CPG for stepping in humans?

A

central pattern generator may exist, as spontaneous stepping movements possible in an incomplete C5 SCI

  • much better voluntary walking ability after 17 years of PT (improved from ~50 ft to ~500 ft in 45 min)
  • characterized by low gain (high threshold)
  • caused by arthritic degeneration and subluxation (spontaneous expression always associated with pathology)
  • could be halted by injecting lidocaine into joint capsule
17
Q

can involuntary CPG stepping be “trained” to improve voluntary walking in people with incomplete SCI?

A

no, b/c clear increased walking have treadmill training, but no evidence from neuropathy

  • better balance
  • stronger leg muscles
  • improved fitness
18
Q

what are interlimb reflex characteristics?

A

observed in all persons with chronic cervical SCI, unless total denervation of arms and hands; but not evident in able-bodied subjects, even when subjects make background contraction at time of stimulus

  • most common in distal upper limb muscles
  • rare in proximal upper limb muscles
  • response almost always excitatory in nature
  • minimum latency suggests (near) direct pathway between sensory afferent and cervical motoneuron
19
Q

when do interlimb reflexes appear following SCI?

A

months to years later

  • novel connections develop, or existing connections strengthen dramatically
  • regenerative sprouting create new connections between contralateral motoneurons
20
Q

what is the cause of interlimb reflexes? what are implications?

A

new growth within spinal cord caudal (below) to lesion

  • implications regarding prospects for reinnervation of motoneuron pools, should we learn how to get UMN axons to grow across injury locus
  • potential target cells already re-innervated
  • might be basis for autonomic dysreflexia
21
Q

what are components of autonomic dysreflexia? when is most likely seen?

A
  • substantial BP increase in response to sensory inputs, but unknown cause
  • typically after cervical or high thoracic SCI
  • incidence after complete SCI&raquo_space;> incomplete SCI
  • loss of inhibition from brain/brainstem regions
  • excessive sensory response to stimuli
  • excessive sympathetic response to normal afferent activity
  • excessive vascular response to normal sympathetic activity
22
Q

when is the onset of autonomic dysreflexia?

A

ill-defined after SCI

  • if early: pre-existing spinal circuit in all of us
  • if later: novel circuitry reflecting spinal cord or vascular plasticity

Neuroscience (39 decks)

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