1d - CSpine WAD Flashcards
what is whiplash
acceleration-deceleration mechanism of injury to neck
what are 3 MOIs for whiplash
MVC
sporting injury
fall
frontal impact vs rear end collision and the Cspine
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
what are 6 structures that could potentially be injured in a WAD
facet joints
intervertebral discs
ms
ligaments
neuro structures
TMJ
what are 3 causes of neck pain w movement coordination impairments
traumatic (ie whiplash)
clinical instability/hypermob
postural dysfunction/syndrome
how can facet joints be potentially injured in a WAD
injury to joint capsule (strain)
c-spine meniscoids
how can intervertebral discs be potentially injured in a WAD
tears in anterior longitudinal ligament and rim lesions of anterior annulus fibrosus
how can ms be potentially injured in a WAD
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
how can neurological structures be potentially damaged in a WAD
potential for trauma to:
- nerve roots
- dorsal root ganglion
mild TBI/concussion
what forces do hyperext and hyperflex exert on neck ms during a whiplash injury
horizontal shear forces
how does muscle imaging present after a whiplash injury
little evidence of tissue damage & poor correlation of imaging w s/sx
some ms fatty infiltration
how can WAD be classified
acute (<12wks) vs chronic (>12wks)
Grades 0-IV
what are the typical WAD grades seen in PT to treat
2 and 3
what setting are grades 0-IV for WAD seen in
less in clinic, more in research
WAD grade 0 clinical presentation
no complaint ab neck
no physical sign(s)
WAD grade I clinical presentation
neck pain, stiffness, or tenderness only
no physical sign(s)
WAD grade II clinical presentation
neck pain AND msk signs
msk signs:
- dec ROM
- point tenderness
WAD grade III clinical presentation
neck pain AND neuro signs
neuro signs:
- dec or absent tendon reflexes
- weakness
- sensory deficits
WAD grade IV clinical presentation
neck pain AND fx or dislocation
what is the difference b/w WAD grades II and III
III has neuro signs, II doesn’t
whiplash vs WAD
whiplash = MOI
WAD = wide range of disorders associated w whiplash MOI
what are the 3 most common complaints of those w persistent problems after a whiplash trauma
pain
dizziness
unsteadiness
when does most of the recovery occur after a whiplash injury
first 2-3mo after
what are poor outcome predictors following whiplash (11)
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
what NDI score is a predictor of poor outcomes following whiplash
> 14.5 / 50
what baseline pain intensity is a predictor of poor outcomes following whiplash
> 5.5 / 10
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
what score indicates a presence of psych distress/PTSD that is a predictor of poor prognosis following WAD
33 + on impact of events scale
what are 2 predictors of poor prognosis following WAD
presence of psychological distress/PTSD
- high pain catastrophizing
cold hyperalgesia
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
what are 3 common trajectories for clinical recovery after WAD
complete recovery
mild sx
chronic pain and disability
what are 5 tools to assess for chronicity of WAD
high NDI
PTSD scales
PDS
IES
TSK
what is the PDS
post-traumatic stress diagnostic scale
- questions ab trouble sleeping, irritability, difficulties concentrating, being overly alert, easily startled
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
what is the TSK
Tampa scale for kinesiophobia
- measures fear of reinjury d/t movement
what are 6 things to consider when doing an exam of WAD
- assess risk factors for chronicity
- assess transverse and alar ligs
- neuro exam/CN testing
- quantitative sensory testing
- dx tests
- MOI - direction and speed of impact
why should transverse and alar ligs be assessed in a WAD exam
trauma
what is a consideration w the use of dx testing for a WAD exam
conventional imaging may not identify a structural cause of WAD
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
what is measured during quantitative sensory testing
sensory threshold / thermal pain threshold with regard to:
- warm
- cool
- hot
- cold sensations
what thermal sensation is often more helpful when recording sensory threshold in QST
cold
what is the ice application test
hold bag of ice against skin for 10sec
screens for cold hyperalgesia
how are the results of the ice application test interpreted
cold hyperalgesia >5/10 pain
not cold hyperalgesia <1/10
how are mechanical pressure pain thresholds measured
use pressure algometer over neck, nerves, and remote sites (leg)
what test results can indicate central sensitization
combo of cold hyperalgesia and dec pressure pain threshold
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
what type of pain is chronic WAD associated with
central sensitization
what is a theory to why pts develop chronic pain
pain perceiving system is altered
- hypersensitive, low pain threshold
what literature is available for predicting outcomes of WAD
not good research available (unlike research on prognosis)
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
what are components of the biopsychosocial model
bio
- mechanical
- inflammatory
- neural
psych
- personality
- catastrophizing
- coping
social
- family
- work
- legal
what are 3 common sx associated w WAD
referred shoulder girdle or UE pain
nonspecific concussive s/sx
heightened affective distress
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
what does deficits in strength and endurance in neck ms indicate in WAD
inc fatty infiltrates in ms
what impairment do expected WAD exam findings substantiate
movement coordination impairments
what 3 tests are expected to be (+) in an WAD exam
cranial cervical flex
neck flex ms endurance
pressure algometry
what in a WAD exam will provoke pain (5)
- midrange motion -> inc w end-range positions
- point tenderness
- myofascial trigger points
- hyperirritable spot - painful on compression or ms contraction
- referred pain pattern distant from spot
- neck and referred pain reproduced by provocation of involved cervical segments
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
what are palpable changes in a WAD exam
taut band of skeletal ms
nodules palpable w/i ms
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
what is an important consideration if prognosis is good
don’t over treat
when should you follow up/check in w acute WAD w early recovery prognosis
f/u visit in 1wk
- monitor for acceptable progress
acute/subacute: education if prognosis for prolonged recovery
advice to remain active
counseling on ADLs
acute/subacute: exercise if prognosis for prolonged recovery
active cervical ROM
isometric low-load strengthening DNF/E ms
acute/subacute: manual therapy if prognosis for prolonged recovery
cervical mobilization or manip
acute/subacute: physical agents if prognosis for prolonged recovery
ice
heat
TENS
acute/subacute: supervised exercise if prognosis for prolonged recovery
active cervical ROM/stretching
strength, endurance, NM exer
postural, coordin, scap stabil
what are 5 components of acute/subacute WAD w prognosis for prolonged recovery
education
exercise
manual therapy
physical agents
supervised exercise
education for chronic >3mo post WAD (3)
encouragement
reassurance
pain management
individualized progressive exercise for chronic >3mo post WAD (4)
- low load, endurance, flexibility, functional training
- cervico-scap-thoracic strength using CBT
- vestib rehab, eye-head-neck coordination
- NM coordination elements
what are 5 interventions for chronic >3mo post WAD
- education
- manage similar to prolonged recovery prognosis
- cervical mobilization
- individualized progressive exercise
- TENS
what are 3 conditions that fit into neck pain w movement coordination impairment category
WAD
postural dysfunction
cervical hypermobility
- clinical instability
what causes postural dysfunction/syndrome
results from sustained end range positions and postures
- end range stress or static loading of normal tissues
what can happen from postural dysfunction progression over time
lead to tissue dysfunction and derangement
common hx for postural dysfunction
gradual onset
common sx for postural dysfunction
dull aching pain
sustained positions/poor posture
sx better w exercise
key tests and measures for postural dysfunction
MMT
ms length assessment
ergonomic assessment
what are the 3 main interventions for postural dysfunction
posture correction
- reposition head to neutral posture
self treatment
aerobic conditioning
what is the focus of interventions for postural dysfunction
postural correction
what are self-treatment interventions for postural dysfunction
stretching
- pec ms
strengthening
- scap ms
- deep neck flexor ms
what is the significance of fixing the posture/ergonomics of someone w postural dysfunction
pts are usually fine
- just need another 2-4wks
what is a piece of education for students w postural dysfunction
backpack use
- 20% of BW up to max of 25#
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
describe how a change in neutral zone impacts cervical hypermobility
end range puts tension on passive structures
what are sx of cervical hypermobility
fatigue
inability to hold head up
shaking, lack of control
sharp pain
- possible w sudden movments
what are characteristics of sx of cervical hypermobility
frequent episodes of acute attacks
unpredictable sx
what are aggravating vs relieving factors for cervical hypermobility
aggravating:
- intolerance to prolonged static posture
relieving:
- external support (ie hands, collar)
- self manipulation
why does self manipulation relieve sx of cervical hypermobility
inc mechanoreceptor input into joint
- temporary
what pt population is cervical hypermobility
younger pts, w more movement
what is a risk factor for cervical hypermobility to screen for
pts w systemic hypermobility
- Beighton ligamentous laxity >/=4
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
what is 1 test for poor coordination/NM control in cervical hypermobility
CCFT
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
what is a reason for motion to not be smooth w movement in cervical hypermobility
ms guarding
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
what are 4 interventions for cervical hypermobility
- strengthening exercises
- DNF and DNE
- scap stabilization - posture ed
- mobilize hypomobile regions prox and distal
- motor control/proprioception exercise (tracking exercises w laser)
