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EXMD3070 > WK2 & 3 - Intro to SCI > Flashcards

WK2 & 3 - Intro to SCI Flashcards

1
Q

What is the number of spinal nerves and vertebrae for each region?

A

Cervical - 8 pair spinal nerves, 7 vertebrae

Thoracic - 12 pair spinal nerves, 12 vertebrae

Lumbar - 5 pair spinal nerves, 5 vertebrae

Sacral - 5 pair spinal nerves, 5 vertebrae (fixed)

Coccyx, 1 pair spinal nerves

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2
Q

Cord, column and nerves dont all line up. T or F?

A

T

At level of T12 there is Vertebral column at T12, spinal cord at L3 and spinal nerves for T12, L1/2/3

Upper border L2 vertebra and termination of cord (segment Co1)

At L3 there is vertebral column L3, Cauda equina (spinal nerves L3 - Co1), actual cord unaffected

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3
Q

What is the basic segmental structure of grey matter?

A

Signals are transferred from ventral horn, through spinal nerves to targeted area

Return from dorsal root of spinal nerve to dorsal root ganglion to white matter of spinal cord

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4
Q

What is the segmental innervation of shoulder ABD, ADD, Flex, Ext, IR and ER?

A

C5-6
C5-8
C5-7
C6-8
C5-8
C5-6

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5
Q

What is the segmental innervation of elbow flex, ext?

A

C5-6
C7-8

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6
Q

What is the segmental innervation of wrist flex and ext?

A

C6-8

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7
Q

What is the segmental innervation of finger and tumb movements?

A

C7-T1

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8
Q

What is the segmental innervation of trunk abdominals and spinal ext?

A

T5-L1
C1-L5

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9
Q

What is the segmental innervation of hip flex, ext, abd, add?

A

L1-L3
L5-S2
L4-S1
L2-L4

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10
Q

What is the segmental innervation for knee ext, flex and ankle dorsi and plantar?

A

L2-L4
L5-S2
L4-S1
S1-S2

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11
Q

what happens with injury to Lumbar nerves?

A

L1-L5

  • result in some function loss in hips/legs
  • little/no voluntary control of bowel/bladder, can manage with special equipment
  • depending on leg strenght, may need wheelchair and walk in braces
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12
Q

What happens to damage of sacral nerves?

A

S1-S5

  • result in some loss of function in hips/legs
  • little/no voluntary control of bowel/bladder but can be managed
  • most likely able to walk
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13
Q

What happens to injury of thoracic nerves?

A

T6-T12
* affects trunk muscles (abs and back) depending on injury level
* usually results in paraplegia, normal UL movement
* fair-good ability to control/balance trunk while seated
* should be able to cough productively (if ab muslces intact)
* little/no voluntary control of bowel/bladder but can be managed
* most likely to use a manual wheelchair
* can learn to drive modified car
* some can stand in standing grame, others may walk in braces

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14
Q

What happens to injury of high cervical nerves?

A

C1-C4
* most severe
* paralysis in arms, hands, trunk and legs,
* independent breathing, bladder, bowel??
* speech impairment
* complete assistance with ADLs
* potential use of powered wheelchairs with special controls
* requires 24hr personal care

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15
Q

What happens to injury of low cervical nerves?

A

C5-C8

  • corresponding nerves control arms/hands
  • may be able to speak normally/breath independently
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16
Q

What happens when C5 nerve is injured?

A

can raise arm / bend elbow, some / total paralysis of wrists, hands,
trunk and legs,

can speak / use diaphragm with weakened breathing,

assistance with most ADLs – moving independently with power wheelchair

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17
Q

What happens when C6 nerve is injured?

A

Affected wrist EXT, paralysis in hands, trunk and legs (typically)

Speak + use diaphragm with weakened breathing, can move in/out of
wheelchair/bed with assistive equipment, may be able to drive an adapted vehicle,

little/no voluntary control of bowel/bladder, but may be
able to manage with special equipment.

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18
Q

What happens to injury of C7 nerve?

A

Nerves control elbow EXT and some finger EXT, most can straighten arm and have normal shoulder movement,

can complete ADLs independently, may need assistance with difficult tasks,

may be able to drive an adapted vehicle

Little/no voluntary control of
bowel/bladder, but may be able to manage independently with
special equipment

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19
Q

What happens with injury to C8 nerve?

A

Nerves control some hand movement – can grasp/release objects, with difficult tasks

may be able to drive an adapted vehicle

little/no voluntary control of bowel/bladder, but may be
able to manage independently with special equipment.

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19
Q

What happens with injury to C8 nerve?

A

Nerves control some hand movement – can grasp/release objects, with difficult tasks

may be able to drive an adapted vehicle

little/no voluntary control of bowel/bladder, but may be
able to manage independently with special equipment.

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20
Q

What is the segmental function of white matter?

A

Lat corticospinal tract = skilled voluntary movement

Dorsal columns = fine touch and proprioception

Spinocerebellular tract = muscle and joint receptors

Spinothalamic tract = pain, temp, coarse touch, pressure

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21
Q

What are the main causes of injury?

A
  • 46% land crashes
  • 29% unprotected land transport users
  • 36% falls (low = 14%, hgih = 21%)
  • 7% water-related
  • 1% football (inc. rugby codes)
  • 80% male
  • largest case number 25-34y (21%), followed by 55-84y (18%)
    *level of injury: 55% Cx spine, 43% incomplete quadraplegia
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22
Q

What is a congenital SCD?

A

Spina Bifida = the spine if bifid = SC doesn’t develop normally

3 types:
1. spina bifida occulta (hidden)
2. meningocele (meninges herniation)
3. myelomeningocele (nerve meninges herniation)

23
Q

What is the difference between meningocele and myelomeningocele?

A

Meningocele involves defect of POS elements of the spine with extrusion of meninges and cerebrospinal fluid (CSF) without involvement of neural elements.

Myelomeningocele involves extrusion of meninges, CSF, and functional neural elements such as nerve or spinal cord contents.

24
Q

Provide examples of SCI from disease or infection.

A
  • sub-acute combined degeneration
  • cysts or tumours
  • poliomyelitis/ post-polio syndrome
25
Q

What are the effects of spinal cord damage?

A

Inc. interruption of:
* sensory/afference nervous system
* motor/efferent nervous system
*ANS

Extent of impairment (paralysis/paresis) depends on…
* level/completeness of lesion

26
Q

Define Paraplegia

A

Complete or partial loss of function in trunk and lower limbs. Damage occurs to spine below 1st thoracic segment

27
Q

Define tetraplegia (sometimes quadriplegia).

A

Complete or partial loss of function in upper limb, trunk and lower limbs. Damage occurs to spine at or above the 1st thoracic segment

28
Q

What is the ASIA Impairment Scale (AIS) Score?

A

American Spinal Injury Association Impairment Scale: Standardised Neurological examination used by rehab team to assess sensory and motor levels affected by SCI.

29
Q

Explain the Grades of the ASIA Impairment Scale.

A

Grade A: Impairment complete. No motor/sensory function left below injury level
Grade B: Impairment incomplete. Sensory function but no motor preserved below neurologic
level (1st normal level above injury level). Some sensation preserved in S4 & S5.
Grade C: Impairment incomplete. Motor function preserved below neurologic level, but > half of key muscles have muscle grade <3 (i.e.not strong enough to move
against gravity)
Grade D: Impairment incomplete. Motor function preserved below neurologic level, and half of the
key muscles have a muscle grade of 3 or more (i.e., joints can move against gravity).
Grade E: patient’s functions normal. All motor/sensory functions are unhindered.

30
Q

What is the most common neurologic category of SCI in Aus?

A
  • Incomplete Tetra (52%)
  • Complete para - tx (16%).
  • Incomplete para - tx (13%)
  • Complete tetra (11%)
31
Q

What is the mechanism behind the stretch reflex after SCI?

A

EXAMPLE
Activation of patellar reflex sends signal via afferent fibres through the peripheral nerve onto the cell body of the alpha motor neuron. This transfers signal via peripheral nerve using efferent fibres to the muscle spindle of intrasfusal fibres to trigger a contraction = shortening of tendon attached to quads.

32
Q

What is the definition and mechanism of poor thermoregulation?

A

Reduced ability to tolerate extremes in temperature and to perform exercise in hot or humid environments

Mechanism:
SCD (through ANS damage), may affect vasomotor, sudomotor and piloerector responses.
VASOMOTOR
– Sub-lesion: Inability for superficial capillaries to vasodilate – blood cannot get to surface to aid cooling
– Supra-lesion: lower than normal BV in Ex muscles, less volume available for cooling.
* Sudomotor: Decreased rate/surface area for sweating below injury = reduced capacity to dissipate
heat.
* Piloerector: In cold – decreased piloerection, with poor superficial vasoconstriction + reduced
shivering response reduced ability to retain heat.

33
Q

What are some strategies and solutions to poor thermoregulation?

A
  • Strict adherence to usual heat management procedures
  • i.e. consume fluids regularly, seek shade, wear light clothing, use sunscreen
  • Sweat can be produced artificially (spray bottles)
  • Extra precautions in cold.
34
Q

Define and explain mechanism of orthostatic/postural hypotension.

A
  • Drop in BP caused by changes in body position
  • Sx: light-headedness/dizziness. Can cause fainting.
  • PW SCI more likely than general pop. to be affected
  • Lack of normal resting muscle tone (i.e. flaccid musculature) + impaired vasomotor function = reduced capacity to counteract effects of gravity in blood distribution.
  • Leads to pooling of blood in periphery with sittingup/standing
  • May reduce cerebral blood flow and/or reduce absolute BP which leads to
    Sx described.
35
Q

What are some strategies and solutions ot orthostatic/posturla hypotension?

A
  • pre-participation screening
    Encourage affected people to:
    -move in controlled manner wen changing posture
    -breathing deploy, slowly and evenly during Ex
    -use abdominal binder to assist venous return

If client becomes affected:
- move into supine position + elevate feet&legs
- monitor BP if possible
- seek help if person appears distressed/loses consciousness

36
Q

Define and explain mechanism of exterional hypotension.

A
  • Drop in BP accompanying PA
    Sx: light headedness or dizziness - fainting??
  • Normal vasodilation occurs, vasoconstriction in non-Ex limbs may not.
  • Coupled with decreased Ex SV from reduced venous return, SBP may decrease by 10-20mmHg
37
Q

What are some strategies and solutions to exertional hypotension?

A

*pre-participation screening
* Gradual intro to increases in PA, particularly for
previously sedentary
*Sx may decrease over time
* Monitor BP in early stages of program (if possible)

38
Q

Define and explain mechanism of contracture.

A

Complete/high resistance to passive stretch of a muscle resulting from fibrosis of connective tissue of
muscles/joints.

  • Lack of voluntary movement, joints not regularly moved through full ROM.
  • Micro-structural changes in connective tissue take place (fibrosis).
  • Movement made more difficult = less movement = more structural changes.
  • Osseous changes may eventually take place at the joint.
39
Q

What are some strategies and solutions to contracture?

A

Prevention: regular movement of all joints through full ROM.
May affect/prevent front lying and limit appropriate postural adjustments for some Ex and activities.

40
Q

Define Neurologically Limited HRMax.

A
  • Lesions of T1-T5 may have muted HR response to Ex
  • A lesion above T1 may have Hrmax110 – 130 bpm

=decreased physical work capacity

41
Q

What is the mechanism of neurologically limited HRmax?

A
  • Absence of external stimulus, inherent HR is ~110-130 bpm (set by SA node)
  • To increase neurologically = sympathetic innervation
  • Sympathetic innervation of heart comes from T1-T5
  • Injury to T1-T5 = mute sympathetic drive.
  • Injuries above T1 = HR only elevated by withdrawal of vagal (PNS) innervation. Complete withdrawal of parasympathetic tones allows heart to
    beat at inherent rate (~110-130 bpm)
42
Q

What are some strategies and solutions for neurologically limited HRmax?

A

HR may not be good indicator of Ex intensity
RPE is a valid indicator
Make some allowances for decreased physical work capacity, esp. initial stages.

43
Q

Define and explain mechanism of bowel/bladder dysfunction

A

SCD frequently = loss of voluntary control of bowel/bladder function, and loss of sensory feedback
* Management carried out according to routine due to loss of sensory feedback.

Neural innervation of bowel/bladder arises S2-S4, therefore many
people with SCD = disruption of bowel/bladder function.

44
Q

What are some methods of bladder management?

A
  • Intermittent Clean Self Catheterisation (ICSC): Common, requires manual dexterity and good hygiene
  • Supra-pubic pressure: this + ICSC used several times a day
  • In-Dwelling Catheter (IDC): semi-permanent; drains from bladder to legbag, emptied prior to Ex.
  • External Collection Devices (e.g. Urodome): condom-like receptable used by males,
    emptied prior to exercise.
  • aided by suppositories/laxitives- carried out 1-3x/day
45
Q

What are some strategies for bowel/bladder management?

A
  • Adults responsible for bowel/bladder care
  • children/teens should familiarise procedure and talk with parents/carers. Encourage children to void prior to PA
  • some reuqire assistance accessing toilets (esp. not wheelchair accessible), practitioner/teacher prepared for this instance
46
Q

Define and explain mechanisms of reduced awareness of injury.

A

People with SCI have reduced/absent sensation = can sustain unaware injuries

Causes:
* external (noxious stimuli - burns/collisions/falls/friction)
* internal (no regular postrual adjustments, blood flow to soft tissue covering bony prominences. esp. sitting/lying)

  • injury goes undetected = untreated = escalation of consequences
    *recovery slow due to poor circulation
47
Q

What are some strategies/solutions to external causes of reduced awareness of injury?

A

Protective equipment:
– Socks in swimming pools = prevent scraping on tiles
– Shin guards in semi-contact situations
Fall / collision: use methods other than p+ to evaluate
seriousness of injury.
– Did it look bad?
– Q’s like “do you feel funny?”, “do you feel sick / faint?”
– Take time to observe / examine injury sites.

48
Q

What are decubitus ulcers?

A

Decubitus Ulcers (Pressure
Sores)
– Absence of afferent input from pressure receptors
– Pressure can be applied to soft-tissue for long periods without discomfort (e.g. over bony prominences)
– Occlusion of blood from area
– Chronic: hypoxic and necrotic soft tissue damage

49
Q

What are some strategies/solutions for decubitus ulcers?

A

Prevent: encourage regular checks (esp. if trying new equipment/technique).
Most require precaution/assistance.
Know warning signs – treat red areas seriously.
If suspicious, med attention should be sought. Until assessed, minimize pressure on area.

50
Q

Provide a definition of autonomic dysreflexia/hyperreflexia.

A
  • Life-threatening event affecting people with lesions above T6 major sympathetic splanchnic outflow
  • A noxious stimulus can = massive, unmediated sympathetic discharge that
    increases BP (e.g. 300/160mmHg)
  • Can cause blindness, stroke or death unless promptly relieved
51
Q

Explain pathway of sensing painful stimuli.

A
  1. Lower sensory neurons sense pain - transmit stimuli to SC - at SCI level, signal is prevented from reaching cerebral cortex
  2. As signal travels up SC - stimulates major splanchnic sympathetic outflow (T6-L2) = large-scale vasoconstriction in concerned organs. Causes hypoertension, headache, blurred vision, anxiety and below SCI, pallor, sweating and gooseflesh
  3. Barorecptors in aortic arch/carotids sense hypertension and signal brain
  4. brain signals SC above lesion level, normal responses to maintain homeostasis occur- sympathetic inhibition (vasodilation of blood vessels) and parasympathetic stimulation of heart via vagus nerve (CN X) = bradycardia.
    HOWEVER, signal for sympathetic inhibition or sacral parasympathetic stimulation cannot pass across lesion. In so, areas below lesion level, initial sympathetic reflex goes unchecked
52
Q

What are symptoms of dysreflexia/hyperreflexia?

A
  • Throbbing, pounding headache.
  • Sudden rise in BP.
  • Blurred vision.
  • Bradycardia.
  • Below SCI – pallor, sweating and gooseflesh.
  • Above SCI – flushed appearance.
53
Q

What are strategies and solutions for autonomic dysreflexia/hyperreflexia?

A
  • pre-participation screening
    if yes - usual management?
  • get upright
    *000
  • eliminate noxious stimulus if possible (e.g. check catheter)
54
Q

Define involuntary movement/spasms.

A
  • Muscles below complete SCI level=paralysed, however, involuntary movement possible.
  • Spastic paralysis = involuntary movements (spasms)
  • People affected by spastic paralysis have less muscle atrophy, can be protective against pressure sores.
  • If severe, can also be disadvantaged in PA – often triggered by changes in position= can interrupt transfers, sitting up and lying down.
55
Q

What are the mechanisms of involuntary movement/spasms?

A
  • In complete SC lesion lessens ability of brain
    communication with periphery
  • Some involuntary movement (e.g. spinal reflexes) do not
    require input from brain

E.G. stretch reflex

56
Q

What are some strategies/solutions for involuntary movement/spasms?

A
  • useful pre-participation q’s (triggers? whats expected? hinderance or useful? med management?
  • be aware of significant LL atrophy and increased injury risk
  • some people can deliberately induce it and use it to assist with activities e.g. induce extensor spasm in legs to assist them to transfer

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