Whiplash Associated Disorder

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1 Whiplash Associated Disorder The pathology Whiplash is a mechanism of injury, consisting of acceleration-deceleration forces to the neck. Mechanism: Hyperflexion/extension injury Stationary vehicle hit from behind Side & head on collisions also common Injury occurs when muscles are unable to compensate for the rapidity of head & torso movement & physiological limits of cervical structures are exceeded hyperextension occurs first followed by hyperflexion Hyperextension occurs first as body & vehicle are propelled forward leaving head stationary. As inertia overcome head & neck move into flexion hyperextension phase is the most damaging hyperflexion phase is limited by chin-chest or forehead-steering wheel Sporting accident Falling off ladders/horse etc Phases of injury related to pathology During the hyperextension phase the anterior structures, the intervertebral disc, anterior longitudinal ligament and anterior muscles can be damaged or torn and posterior structures compressed. During the hyperflexion phase- the dens may impact against the atlas, and the atlanto-occipatal joint, posterior ligaments and zygapophyseal joints can be involved. The alar and transverse ligaments and tectorial and posterior atlanto-occipital membranes can also be damaged. 1

2 Although a whiplash injury was previously thought to be predominantly a soft tissue injury to the structures surrounding the cervical spine, more recent evidence suggests that the cervical facet capsular ligament is probably the primary anatomic site for whiplash injury. Seigmund et al 2001 suggest that the risk of facet capsular ligament injury is more related to individual differences than to the magnitude of the loads to which an individual is exposed. Other structures can be involved; these include ligament tissue, muscle tissue, fascia and tendons. In more severe cases there can be damage to discs and nerves. In these cases further investigation and intervention may be necessary. Whiplash can also be a risk factor of vascular accident There is a high incidence of chronic pain of more than 3 months following a whiplash injury which is associated with disturbances in motor function, generalized sensory hypersensitivity likely as a result of sensitized pain pathways within the central nervous system and psychological distress. The prevalence of cervical facet joint pain in patients with chronic pain after whiplash has been determined as 54% to 60%. In 1995, the Que bec Task Force on Whiplash associated Disorders (WAD) used the term WAD to describe the symptoms that can result from this type of injury. This cluster of symptoms includes neck pain, along with other symptoms of the injury such as dizziness and pain in other parts of the body. The Quebec Classification of WAD can be seen in the table below: Grade 0 Grade I no neck complaints and no physical signs injuries involving complaints of neck pain, stiffness or tenderness, but no physical signs. 2

3 Grade II Grade III Grade IV neck complaints accompanied by decreased range of motion and point tenderness neck complaints accompanied by neurologic signs such as decreased or absent deep tendon reflexes, weakness and/or sensory deficits. (MRI may show nerve involvement or disc lesion) injuries in which neck complaints are accompanied by fracture or dislocation Other symptoms such as deafness, dizziness, tinnitus, headache, memory loss, dysphagia, and temporomandibular joint pain can be present in all grades. Signs and Symptoms Subjective findings client will report a specific incident of injury such as RTA onset of pain often hours after injury- pain may be felt at the time of trauma which settles and then returns with stiffness hours later. Severe pain from the time of trauma that does not settle may be an indication of a more serious pathology such as fracture or dislocation Anyone can suffer from a WAD may report having x-ray which will be normal onset of pain a few hours later or the following morning may have disturbed sleep disturbance to hobbies and ADLs may report headaches and dizziness (dizziness is usually cervicogenic and rarely vascular) look out for psychological factors in PMH as well as present yellow flags Psychosocial factors are a determinant of chronic pain following acute injury 3

4 Objective findings Common to have reduced ROM of the cervical spine Tenderness on palpation of the muscles Joint stiffness Myofascial trigger points Neurodynamic testing may be positive (especially in cases longer than 3 months) Whiplash and chronic pain (Nijs Et al) Central sensitization is defined as an augmentation of responsiveness of central neurons to input from unimodal and polymodal receptors (Meyer et al 1995). Central sensitization leads to increased responsiveness to a variety of peripheral stimuli including mechanical pressure, chemical substances, light, sound, cold, heat, and electrical stimuli. One of the main characteristics of central sensitization in patients with musculoskeletal pain is a generalized rather than a localized decrease in their pressure pain threshold. Here, generalized implies more than a segmental spreading of the symptom area, in that it means that the increased sensitivity is localized at sites segmentally unrelated to the primary source of nociception. It is important to consider these changes in the central pain processing mechanisms in clients that report symptom aggravation with manual therapy, decreased pain threshold and have poor treatment progress. Central sensitization is not linked to psychological distress. Management- dependent on stage of injury 0-2 weeks Ice Analgesia Education, Active exercises? early mobilisation- evidence is debatable advice on self management and return to normal activity as soon as possible 2-12 weeks after injury Postural training Deep neck flexor retraining Trigger point release METs Deep transverse frictions Advice on heat/ice 4

5 Cervical stretches Cervical and scapulothoracic rehabilitation Endurance retraining superficial muscular Proprioceptive cervical rehabilitation Joint manipulations Education 12 weeks following injury (chronic stage) Treatment as above Central sensitization may be an influence in poor treatment progress CBT may be required Plan B After 6 weeks of treatment if there is no significant improvement or persisting neurological symptoms, referral to an orthopaedic consultant is required. References Meyer RA, Campbell JN, Raja SN. Peripheral neural mechanisms of nociception. In: Wall PD, Melzack R, editors. Textbook of pain. 3rd ed. Edinburgh: Churchill Livingstone; p Jo Nijs a,b,c,*, Boudewijn Van Houdenhove d, Rob A.B. Oostendorp Recognition of central sensitization in patients with musculoskeletal pain: Application of pain neurophysiology in manual therapy practice Manual Therapy 15 (2010) M Sterling, G Jull, B Vicenzino, J Kenardy - Characterization of acute whiplash-associated disorders Spine, journals.lww.com GP Siegmund, BS Myers, MB Davis, HF Bohnet - Mechanical evidence of cervical facet capsule injury during whiplash: a cadaveric study using combined shear, compression, and extension loading Spine, journals.lww.com 5

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