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MSK 2 > 1d - CSpine WAD > Flashcards

1d - CSpine WAD Flashcards

1
Q

what is whiplash

A

acceleration-deceleration mechanism of injury to neck

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2
Q

what are 3 MOIs for whiplash

A

MVC
sporting injury
fall

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3
Q

frontal impact vs rear end collision and the Cspine

A

frontal impact - head goes into hyperflexion then followed by hyperextension

rear end collision - hyperext followed by hyperflex

*side note: side impact can also lead to WAD, but she doesn’t provide info other than a pic

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4
Q

what are 6 structures that could potentially be injured in a WAD

A

facet joints
intervertebral discs
ms
ligaments
neuro structures
TMJ

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5
Q

what are 3 causes of neck pain w movement coordination impairments

A

traumatic (ie whiplash)
clinical instability/hypermob
postural dysfunction/syndrome

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6
Q

how can facet joints be potentially injured in a WAD

A

injury to joint capsule (strain)
c-spine meniscoids

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7
Q

how can intervertebral discs be potentially injured in a WAD

A

tears in anterior longitudinal ligament and rim lesions of anterior annulus fibrosus

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8
Q

how can ms be potentially injured in a WAD

A

fatty infiltrates of neck ms develop b/w 4wk-3mo s/p
- only in those w severe pain and disability

widespread fatty infiltrates in neck ms of pts w chronic whiplash

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9
Q

how can neurological structures be potentially damaged in a WAD

A

potential for trauma to:
- nerve roots
- dorsal root ganglion

mild TBI/concussion

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10
Q

what forces do hyperext and hyperflex exert on neck ms during a whiplash injury

A

horizontal shear forces

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11
Q

how does muscle imaging present after a whiplash injury

A

little evidence of tissue damage & poor correlation of imaging w s/sx

some ms fatty infiltration

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12
Q

how can WAD be classified

A

acute (<12wks) vs chronic (>12wks)
Grades 0-IV

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13
Q

what are the typical WAD grades seen in PT to treat

A

2 and 3

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14
Q

what setting are grades 0-IV for WAD seen in

A

less in clinic, more in research

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15
Q

WAD grade 0 clinical presentation

A

no complaint ab neck
no physical sign(s)

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16
Q

WAD grade I clinical presentation

A

neck pain, stiffness, or tenderness only

no physical sign(s)

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17
Q

WAD grade II clinical presentation

A

neck pain AND msk signs

msk signs:
- dec ROM
- point tenderness

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18
Q

WAD grade III clinical presentation

A

neck pain AND neuro signs

neuro signs:
- dec or absent tendon reflexes
- weakness
- sensory deficits

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19
Q

WAD grade IV clinical presentation

A

neck pain AND fx or dislocation

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20
Q

what is the difference b/w WAD grades II and III

A

III has neuro signs, II doesn’t

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21
Q

whiplash vs WAD

A

whiplash = MOI
WAD = wide range of disorders associated w whiplash MOI

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22
Q

what are the 3 most common complaints of those w persistent problems after a whiplash trauma

A

pain
dizziness
unsteadiness

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23
Q

when does most of the recovery occur after a whiplash injury

A

first 2-3mo after

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24
Q

what are poor outcome predictors following whiplash (11)

A

high NDI
pre-injury neck pain
neck pain at inception
high catastrophizing
female
WAD 2 or 3
high baseline pain intensity
HA at inception
less than college ed
no seatbelt used in accident
LBP at inception

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25
Q

what NDI score is a predictor of poor outcomes following whiplash

A

> 14.5 / 50

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26
Q

what baseline pain intensity is a predictor of poor outcomes following whiplash

A

> 5.5 / 10

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27
Q

why would less than a college education be a predictor of poor outcomes following whiplash

A

type of work likely doing
less flexibility w schedule and ability to take time off if not feeling well

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28
Q

what score indicates a presence of psych distress/PTSD that is a predictor of poor prognosis following WAD

A

33 + on impact of events scale

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29
Q

what are 2 predictors of poor prognosis following WAD

A

presence of psychological distress/PTSD
- high pain catastrophizing

cold hyperalgesia

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30
Q

what are 5 things that have no effect on outcome after WAD

A

angular deformity of neck
impact direction
seating position
awareness of collision
vehicle speed

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31
Q

what are 3 common trajectories for clinical recovery after WAD

A

complete recovery
mild sx
chronic pain and disability

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32
Q

what are 5 tools to assess for chronicity of WAD

A

high NDI
PTSD scales
PDS
IES
TSK

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33
Q

what is the PDS

A

post-traumatic stress diagnostic scale
- questions ab trouble sleeping, irritability, difficulties concentrating, being overly alert, easily startled

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34
Q

what is the IES

A

revised impact of events scale
- self report, 3-6wks s/p
- subjective distress caused by traumatic events
- similar hyperarousal Qs as PDS

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35
Q

what is the TSK

A

Tampa scale for kinesiophobia
- measures fear of reinjury d/t movement

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36
Q

what are 6 things to consider when doing an exam of WAD

A
  1. assess risk factors for chronicity
  2. assess transverse and alar ligs
  3. neuro exam/CN testing
  4. quantitative sensory testing
  5. dx tests
  6. MOI - direction and speed of impact
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37
Q

why should transverse and alar ligs be assessed in a WAD exam

A

trauma

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38
Q

what is a consideration w the use of dx testing for a WAD exam

A

conventional imaging may not identify a structural cause of WAD

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39
Q

what is quantitative sensory testing (QST)

A

clinical method to measure response to sensory stim and used as indicator of neural function or altered pain sensitivity

40
Q

what is measured during quantitative sensory testing

A

sensory threshold / thermal pain threshold with regard to:
- warm
- cool
- hot
- cold sensations

41
Q

what thermal sensation is often more helpful when recording sensory threshold in QST

A

cold

42
Q

what is the ice application test

A

hold bag of ice against skin for 10sec
screens for cold hyperalgesia

43
Q

how are the results of the ice application test interpreted

A

cold hyperalgesia >5/10 pain
not cold hyperalgesia <1/10

44
Q

how are mechanical pressure pain thresholds measured

A

use pressure algometer over neck, nerves, and remote sites (leg)

45
Q

what test results can indicate central sensitization

A

combo of cold hyperalgesia and dec pressure pain threshold

46
Q

what is nociplastic pain

A

pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing activation of peripheral nociceptors or evidence of dz or lesion of somatosensory system causing pain
- pain no longer coupled to noxious stim
- lower pain thresholds d/t altered central pain processing

47
Q

what type of pain is chronic WAD associated with

A

central sensitization

48
Q

what is a theory to why pts develop chronic pain

A

pain perceiving system is altered
- hypersensitive, low pain threshold

49
Q

what literature is available for predicting outcomes of WAD

A

not good research available (unlike research on prognosis)

50
Q

what is SIT

A

stress inoculation training
- CBT approach that facilitates problem solving and coping strategies to manage stress-related anxiety

when combined w exercise, good outcome

51
Q

what are components of the biopsychosocial model

A

bio
- mechanical
- inflammatory
- neural
psych
- personality
- catastrophizing
- coping
social
- family
- work
- legal

52
Q

what are 3 common sx associated w WAD

A

referred shoulder girdle or UE pain
nonspecific concussive s/sx
heightened affective distress

53
Q

what are nonspecific concussive s/sx that can be associated w WAD

A

dizziness/nausea
HA, concentration/memory difficulties
confusion
hypersensitivity to:
- mechanical
- thermal
- acoustic
- odor
- light stimuli

54
Q

what does deficits in strength and endurance in neck ms indicate in WAD

A

inc fatty infiltrates in ms

55
Q

what impairment do expected WAD exam findings substantiate

A

movement coordination impairments

56
Q

what 3 tests are expected to be (+) in an WAD exam

A

cranial cervical flex
neck flex ms endurance
pressure algometry

57
Q

what in a WAD exam will provoke pain (5)

A
  1. midrange motion -> inc w end-range positions
  2. point tenderness
    - myofascial trigger points
    - hyperirritable spot
  3. painful on compression or ms contraction
  4. referred pain pattern distant from spot
  5. neck and referred pain reproduced by provocation of involved cervical segments
58
Q

what impairments and deficits are noted in a WAD exam (5)

A

movement coordination
neck ms strength/endurance
proprioception
postural balance/control
- EO or EC
altered ms activation patterns

59
Q

what are palpable changes in a WAD exam

A

taut band of skeletal ms
nodules palpable w/i ms

60
Q

acute: education and HEP if prognosis for quick and early recovery

A

education:
- remain active
- return to normal non-provocative activities
- reassure that recovery is expected in first 2-3 mo
minimize collar use

HEP:
- pain-free cervical ROM
- postural re-ed
- body mechanics for ADLs, work, and rest activities

61
Q

what is an important consideration if prognosis is good

A

don’t over treat

62
Q

when should you follow up/check in w acute WAD w early recovery prognosis

A

f/u visit in 1wk
- monitor for acceptable progress

63
Q

acute/subacute: education if prognosis for prolonged recovery

A

advice to remain active
counseling on ADLs

64
Q

acute/subacute: exercise if prognosis for prolonged recovery

A

active cervical ROM
isometric low-load strengthening DNF/E ms

65
Q

acute/subacute: manual therapy if prognosis for prolonged recovery

A

cervical mobilization or manip

66
Q

acute/subacute: physical agents if prognosis for prolonged recovery

A

ice
heat
TENS

67
Q

acute/subacute: supervised exercise if prognosis for prolonged recovery

A

active cervical ROM/stretching
strength, endurance, NM exer
postural, coordin, scap stabil

68
Q

what are 5 components of acute/subacute WAD w prognosis for prolonged recovery

A

education
exercise
manual therapy
physical agents
supervised exercise

69
Q

education for chronic >3mo post WAD (3)

A

encouragement
reassurance
pain management

70
Q

individualized progressive exercise for chronic >3mo post WAD (4)

A
  1. low load, endurance, flexibility, functional training
  2. cervico-scap-thoracic strength using CBT
  3. vestib rehab, eye-head-neck coordination
  4. NM coordination elements
71
Q

what are 5 interventions for chronic >3mo post WAD

A
  1. education
  2. manage similar to prolonged recovery prognosis
  3. cervical mobilization
  4. individualized progressive exercise
  5. TENS
72
Q

what are 3 conditions that fit into neck pain w movement coordination impairment category

A

WAD
postural dysfunction
cervical hypermobility
- clinical instability

73
Q

what causes postural dysfunction/syndrome

A

results from sustained end range positions and postures
- end range stress or static loading of normal tissues

74
Q

what can happen from postural dysfunction progression over time

A

lead to tissue dysfunction and derangement

75
Q

common hx for postural dysfunction

A

gradual onset

76
Q

common sx for postural dysfunction

A

dull aching pain
sustained positions/poor posture

sx better w exercise

77
Q

key tests and measures for postural dysfunction

A

MMT
ms length assessment
ergonomic assessment

78
Q

what are the 3 main interventions for postural dysfunction

A

posture correction
- reposition head to neutral posture

self treatment

aerobic conditioning

79
Q

what is the focus of interventions for postural dysfunction

A

postural correction

80
Q

what are self-treatment interventions for postural dysfunction

A

stretching
- pec ms
strengthening
- scap ms
- deep neck flexor ms

81
Q

what is the significance of fixing the posture/ergonomics of someone w postural dysfunction

A

pts are usually fine
- just need another 2-4wks

82
Q

what is a piece of education for students w postural dysfunction

A

backpack use
- 20% of BW up to max of 25#

83
Q

what causes cervical spine instability/hypermobility/altered motor control

A

active and neural cervical subsystem failure
-> neutral zone inc relative to total range of motion and poor ms control in that zone

84
Q

describe how a change in neutral zone impacts cervical hypermobility

A

end range puts tension on passive structures

85
Q

what are sx of cervical hypermobility

A

fatigue
inability to hold head up
shaking, lack of control
sharp pain
- possible w sudden movments

86
Q

what are characteristics of sx of cervical hypermobility

A

frequent episodes of acute attacks
unpredictable sx

87
Q

what are aggravating vs relieving factors for cervical hypermobility

A

aggravating:
- intolerance to prolonged static posture

relieving:
- external support (ie hands, collar)
- self manipulation

88
Q

why does self manipulation relieve sx of cervical hypermobility

A

inc mechanoreceptor input into joint
- temporary

89
Q

what pt population is cervical hypermobility

A

younger pts, w more movement

90
Q

what is a risk factor for cervical hypermobility to screen for

A

pts w systemic hypermobility
- Beighton ligamentous laxity >/=4

91
Q

how will movement present in cervical hypermobility (3)

A

poor coordination & NM control
abnormal joint play (hyper)
- shear (AP translatoric motion)
motion not smooth thru range
- segmental, hinging, pivoting

92
Q

what is 1 test for poor coordination/NM control in cervical hypermobility

A

CCFT

93
Q

what are 2 reasons for poor coordination/NM control in cervical hypermobility

A

lack of dissociation of cervical segments w movement

dec neck ms endurance
- flex and ext

94
Q

what is a reason for motion to not be smooth w movement in cervical hypermobility

A

ms guarding

95
Q

what are the 2 goals for the interventions for cervical hypermobility

A

enhance the function of spinal stabilizing subsystems
- improve motor control

dec stresses on involved spinal segments

96
Q

what are 4 interventions for cervical hypermobility

A
  1. strengthening exercises
    - DNF and DNE
    - scap stabilization
  2. posture ed
  3. mobilize hypomobile regions prox and distal
  4. motor control/proprioception exercise (tracking exercises w laser)

MSK 2 (20 decks)

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