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MSK 2 > 1d - CSpine WAD > Flashcards

1d - CSpine WAD Flashcards

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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
what NDI score is a predictor of poor outcomes following whiplash
>14.5 / 50
26
what baseline pain intensity is a predictor of poor outcomes following whiplash
> 5.5 / 10
27
why would less than a college education be a predictor of poor outcomes following whiplash
type of work likely doing less flexibility w schedule and ability to take time off if not feeling well
28
what score indicates a presence of psych distress/PTSD that is a predictor of poor prognosis following WAD
33 + on impact of events scale
29
what are 2 predictors of poor prognosis following WAD
presence of psychological distress/PTSD - high pain catastrophizing cold hyperalgesia
30
what are 5 things that have no effect on outcome after WAD
angular deformity of neck impact direction seating position awareness of collision vehicle speed
31
what are 3 common trajectories for clinical recovery after WAD
complete recovery mild sx chronic pain and disability
32
what are 5 tools to assess for chronicity of WAD
high NDI PTSD scales PDS IES TSK
33
what is the PDS
post-traumatic stress diagnostic scale - questions ab trouble sleeping, irritability, difficulties concentrating, being overly alert, easily startled
34
what is the IES
revised impact of events scale - self report, 3-6wks s/p - subjective distress caused by traumatic events - similar hyperarousal Qs as PDS
35
what is the TSK
Tampa scale for kinesiophobia - measures fear of reinjury d/t movement
36
what are 6 things to consider when doing an exam of WAD
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
37
why should transverse and alar ligs be assessed in a WAD exam
trauma
38
what is a consideration w the use of dx testing for a WAD exam
conventional imaging may not identify a structural cause of WAD
39
what is quantitative sensory testing (QST)
clinical method to measure response to sensory stim and used as indicator of neural function or altered pain sensitivity
40
what is measured during quantitative sensory testing
sensory threshold / thermal pain threshold with regard to: - warm - cool - hot - cold sensations
41
what thermal sensation is often more helpful when recording sensory threshold in QST
cold
42
what is the ice application test
hold bag of ice against skin for 10sec screens for cold hyperalgesia
43
how are the results of the ice application test interpreted
cold hyperalgesia >5/10 pain not cold hyperalgesia <1/10
44
how are mechanical pressure pain thresholds measured
use pressure algometer over neck, nerves, and remote sites (leg)
45
what test results can indicate central sensitization
combo of cold hyperalgesia and dec pressure pain threshold
46
what is nociplastic pain
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
what type of pain is chronic WAD associated with
central sensitization
48
what is a theory to why pts develop chronic pain
pain perceiving system is altered - hypersensitive, low pain threshold
49
what literature is available for predicting outcomes of WAD
not good research available (unlike research on prognosis)
50
what is SIT
stress inoculation training - CBT approach that facilitates problem solving and coping strategies to manage stress-related anxiety when combined w exercise, good outcome
51
what are components of the biopsychosocial model
bio - mechanical - inflammatory - neural psych - personality - catastrophizing - coping social - family - work - legal
52
what are 3 common sx associated w WAD
referred shoulder girdle or UE pain nonspecific concussive s/sx heightened affective distress
53
what are nonspecific concussive s/sx that can be associated w WAD
dizziness/nausea HA, concentration/memory difficulties confusion hypersensitivity to: - mechanical - thermal - acoustic - odor - light stimuli
54
what does deficits in strength and endurance in neck ms indicate in WAD
inc fatty infiltrates in ms
55
what impairment do expected WAD exam findings substantiate
movement coordination impairments
56
what 3 tests are expected to be (+) in an WAD exam
cranial cervical flex neck flex ms endurance pressure algometry
57
what in a WAD exam will provoke pain (5)
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
what impairments and deficits are noted in a WAD exam (5)
movement coordination neck ms strength/endurance proprioception postural balance/control - EO or EC altered ms activation patterns
59
what are palpable changes in a WAD exam
taut band of skeletal ms nodules palpable w/i ms
60
acute: education and HEP if prognosis for quick and early recovery
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
what is an important consideration if prognosis is good
don't over treat
62
when should you follow up/check in w acute WAD w early recovery prognosis
f/u visit in 1wk - monitor for acceptable progress
63
acute/subacute: education if prognosis for prolonged recovery
advice to remain active counseling on ADLs
64
acute/subacute: exercise if prognosis for prolonged recovery
active cervical ROM isometric low-load strengthening DNF/E ms
65
acute/subacute: manual therapy if prognosis for prolonged recovery
cervical mobilization or manip
66
acute/subacute: physical agents if prognosis for prolonged recovery
ice heat TENS
67
acute/subacute: supervised exercise if prognosis for prolonged recovery
active cervical ROM/stretching strength, endurance, NM exer postural, coordin, scap stabil
68
what are 5 components of acute/subacute WAD w prognosis for prolonged recovery
education exercise manual therapy physical agents supervised exercise
69
education for chronic >3mo post WAD (3)
encouragement reassurance pain management
70
individualized progressive exercise for chronic >3mo post WAD (4)
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
what are 5 interventions for chronic >3mo post WAD
1. education 2. manage similar to prolonged recovery prognosis 3. cervical mobilization 4. individualized progressive exercise 5. TENS
72
what are 3 conditions that fit into neck pain w movement coordination impairment category
WAD postural dysfunction cervical hypermobility - clinical instability
73
what causes postural dysfunction/syndrome
results from sustained end range positions and postures - end range stress or static loading of normal tissues
74
what can happen from postural dysfunction progression over time
lead to tissue dysfunction and derangement
75
common hx for postural dysfunction
gradual onset
76
common sx for postural dysfunction
dull aching pain sustained positions/poor posture sx better w exercise
77
key tests and measures for postural dysfunction
MMT ms length assessment ergonomic assessment
78
what are the 3 main interventions for postural dysfunction
posture correction - reposition head to neutral posture self treatment aerobic conditioning
79
what is the focus of interventions for postural dysfunction
postural correction
80
what are self-treatment interventions for postural dysfunction
stretching - pec ms strengthening - scap ms - deep neck flexor ms
81
what is the significance of fixing the posture/ergonomics of someone w postural dysfunction
pts are usually fine - just need another 2-4wks
82
what is a piece of education for students w postural dysfunction
backpack use - 20% of BW up to max of 25#
83
what causes cervical spine instability/hypermobility/altered motor control
active and neural cervical subsystem failure -> neutral zone inc relative to total range of motion and poor ms control in that zone
84
describe how a change in neutral zone impacts cervical hypermobility
end range puts tension on passive structures
85
what are sx of cervical hypermobility
fatigue inability to hold head up shaking, lack of control sharp pain - possible w sudden movments
86
what are characteristics of sx of cervical hypermobility
frequent episodes of acute attacks unpredictable sx
87
what are aggravating vs relieving factors for cervical hypermobility
aggravating: - intolerance to prolonged static posture relieving: - external support (ie hands, collar) - self manipulation
88
why does self manipulation relieve sx of cervical hypermobility
inc mechanoreceptor input into joint - temporary
89
what pt population is cervical hypermobility
younger pts, w more movement
90
what is a risk factor for cervical hypermobility to screen for
pts w systemic hypermobility - Beighton ligamentous laxity >/=4
91
how will movement present in cervical hypermobility (3)
poor coordination & NM control abnormal joint play (hyper) - shear (AP translatoric motion) motion not smooth thru range - segmental, hinging, pivoting
92
what is 1 test for poor coordination/NM control in cervical hypermobility
CCFT
93
what are 2 reasons for poor coordination/NM control in cervical hypermobility
lack of dissociation of cervical segments w movement dec neck ms endurance - flex and ext
94
what is a reason for motion to not be smooth w movement in cervical hypermobility
ms guarding
95
what are the 2 goals for the interventions for cervical hypermobility
enhance the function of spinal stabilizing subsystems - improve motor control dec stresses on involved spinal segments
96
what are 4 interventions for cervical hypermobility
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)

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