Neck pain disorders Flashcards
traumatic neck pain disorders
Whiplash associated disorders
Post traumatic headache
non traumatic neck pain disorders
cervicogenic headache
secondary headaches
PTH, WAD, cervicogenic
primary headaches
migraines, tension type, trigeminal autonomic cephalagia
Cervicogenic headache - criteria
non-traumatic
disorders of the Cx spine
- imaging of lesion of Cx or neck soft tissue.
- 2 of:
* temporal development with onset of Cx disorder/lesion
* improvement is parallel to that of Cx lesion/disorder
*decreased Cx ROM, headache way worse w provocative manoeuvres
* abolished by diagnostic blockade
- can’t be explained by other classifications
Cervicogenic headache - symtoms
- side-lock pain BUT can be bilateral
- provoked by neck muscle palpation + head mvmt
PAIN PRECEEDS HEADACHE
Cervicogenic headache - diary
time
type
duration
intensity + areas
triggers
signs and symptoms (vision, diziness..)
Cervicogenic headache - obj findings
limited ROM - active and passive
impaired neuromsk performance - head lift off, craniocervical flxn, axio-scap muscle function)
Headache reproduced with manual assessment (PAIVMs with 2/10 pain + stiffness)
WAD - classification
NON TRAUMAIC
- developed within 7days of event.
- associated w neck pain at time.
0- no complaint or physical signs
I- neck pain, stiffness or tenderness only. no physical signs
II - neck pain AND MSK signs (decreased ROM, point tenderness)
III- neck complaint AND neurological signs (impaired tendonreflexes, weakness or sensory deficit)
IV- neck complain AND fracture/dislocation
WAD - aetiology
structural changes:
- inflammatory changes + ischemia
- increase fatty infiltration
- decrease CSA of suboccipital muscles
- change from slow to fast muscle fibres
- mechanical disruption of joint surface and muscle
WAD - physical assessment
sensorimotor system:
- Cx spine proprioception
- balance
- occulomotor
- coordination
neurodynamic system:
- central sensitisation
WAD management
restoring whatever has deficit:
-pain
- mvmt
- neuromuscular
- sensorimotor
- neural mechanosensitivity
- fear avoidance, low self efficacy
Concussion - mechanism of injury
forces applied to brain at high magnitude (60-100G).
Brain is shaken around = damage.
Brain chemistry of consussion
K+ out, Ca2+ and Na2+ in.
overdrive of ion channels
energy crisis as brian is deprived of blood from inflammation, bv damage, limited space.. BUT ATP needed for ion channels = depressed brain function (drowsy/drunk effect).
impaire mitochondria function = more celllular dysfunction
structural changes to axons
Concussion presentation
somatic - headache
cognitive - feeling foggy, slowed rxn time
balance - gait instability
behavioural changes - moody, irritable, sad..
sleep/wake changes - drowsiness
symptoms can take up to 48h to show - hence importance of coming off field (death from re-injury = herniation)