Whiplash Associated Disorders


Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle collisions, but can also occur during sport (diving, snowboarding) and other types of falls. The impact may result in bony or soft-tissue injuries (whiplash injury), which in turn may lead to a variety of clinical manifestations called Whiplash Associated Disorders (WAD)[1]. It is estimated that about 30% to 50% of patients who sustain a symptomatic whiplash injury are going to report chronic, and potentially more widespread symptoms, classified as WAD[2]. WAD is a good example of a medical condition where there is often an apparent disconnect between the magnitude of injury and the magnitude of disability[2].

Clinically Relevant Anatomy

Whiplash and whiplash-associated disorders (WAD) affect a variety of anatomical structures of the cervical spine, depending on the force and direction of impact as well as many other factors[3][4][5]. Causes of pain can be any of these tissues, with the strain injury resulting in secondary oedema, haemorrhage, and inflammation:

Whiplash Injuries.jpg


Several lesions may occur, depending on the movement of the head during the accident. These lesions ranks from severe to moderate to slight. Hyperextension is the most common mechanism, followed by hyperflexion and lateral flexion.[6]

Severe Lesions

Hyperextension and distraction of the neck may rupture the anterior longitudinal ligament and also some discs. A ruptured disc can lead to backward displacement of the vertebra lying above it (the upper facets then slide downwards on the lower) with damage to the spinal cord as a result. Spinal cord injuries after motor vehicle accidents occur most often in young car users in the 15–24 year age group.

Pure hyperextension may also lead to compression of the spinal cord in those cases where retrolisthesis or spinal stenosis already existed. Compression fractures of the posterior elements may occur in other cases.

Hyperflexion injury may lead disruption of posterior ligaments and occasionally facet joint luxation and/or to fractures of the vertebral body (most fractures of the atlas and of the axis are the result of motor vehicle accidents).

Less likely, lesions of veins, arteries, neural structures, oesophagus and retropharyngeal tissues may occur.[6]

Other Lesions

Less severe lesions which may involves the intervertebral discs, the zygapophyseal joints, the cervical ligaments and muscles are much more frequent. These lesions may occur in isolation but are more often combined and therefore are sometimes difficult to recognize. The common complaint is neck pain.[6]

Discodural and Discoradicular Interactions

According to recent retrospective studies, the occurrence of disc lesions after whiplash injury is quite high and one prospective study indicates the value of clinical diagnosis. Most disc lesions are ruptures of the anterior annulus fibrosus and endplate avulsions.

As the result of the hyperextension element during the trauma the disc may have fissured. The subsequent flexion or hyperflexion element causes displacement of disc material in a posterior direction. Davis et al describe a number of posterolateral disc lesions with radicular symptoms as the result of a hyperextension whiplash trauma. These herniations seemed to develop only after the acute phase and it took a few weeks for the radicular symptoms to manifest. In postmortem studies, Taylor et al describe the intervertebral disc as the most frequently damaged structure.[7] Jónsson et al[8] also confirmed the large number of disc lesions after whiplash, and during surgery were able to confirm the findings from magnetic resonance imaging (MRI).

Posterocentral protrusions lead to central, bilateral or unilateral pain in a multisegmental distribution: pain in the neck, upper scapular area and trapezius. On examination, a symmetrical (mimicking a full articular pattern) or asymmetrical pattern of limitation is evident. In acute cases the picture may be torticollis-like.[6]

Facet Joint Problems

Whiplash may also lead to problems at the level of the zygapophyseal joint capsules.[9] Lord et al undertook a placebo-controlled prevalence study after whiplash and found that chronic cervical facet joint pain was common.[10]

Pain which is usually localized is felt unilaterally. A convergent or divergent motion pattern may occur, although any asymmetrical pattern is compatible.[6]

Ligamentous Lesions

Minor lesions can occur when ligaments can become overstretched, or may become adherent as the result of post-traumatic immobilization. They manifest with vague stretching pain felt at the end of range of those movements that stretch the ligament.

Muscular Lesions

Muscular lesions which are mostly anterior are described in clinical studies, on echography( the use of ultrasound as a diagnostic aid), in experiments in animals and in postmortem studies. Muscles, especially their occipital insertions, can be strained during injury. The subsequent pain will be quite localized and can be reproduced during either contraction or stretching.[6]


WAD is considered to be "the most common nonhospitalised injury resulting from a road traffic crash".[11] Based on several studies, we can conclude that the prevalence of WAD depends on the country or the part of the world. For example, the prevalence per 100,000 inhabitants is of 70 in Quebec, 106 in Australia and 188–325 in the Netherlands.
But according to the study of Versteegen, in which he studied patients with neck pain following a car accident in the last ten years, the prevalence per 100,000 inhabitants increased significantly from to 3.4 in 1974 to 40.2 in 1994. A study by Richter also shows an increase in prevalence of 20% between 1985 and 1997. The increase is due in part to a higher number of cars on the roads, which in turn can lead to more accidents. However, this increase in prevalence is also due to the fact that there is a greater public awareness of WAD and therefore those affected are more likely to consult their doctor and therefore the number of patients seeking healthcare for whiplash is on the rise[12][13].

The risk that patients develop WAD after an accident with acceleration-deceleration mechanism of energy transfer of the neck depends on a variety of factors:

  • severity of the impact, however, it is difficult to obtain objective evidence to confirm this[12].
  • neck pain present before the accident is a risk factor for acute neck pain after collision[13].
  • women seem to be slightly more at risk of developing WAD.
  • Age is also important; younger people (18-23) are more likely to file insurance claims and/or are at greater risk of being treated for WAD[14][15].

JD Cassidy and Scholton-Peeters demonstrated in their studies that 14 to 42 % of the whiplash patients are at risk of developing chronic complaints (longer than 6 months) and that 10 % of those have constant severe pain. The number of people worldwide who suffer from chronic pain is between 2 and 58 %, but lies mainly between 20 and 40%[13]. If patient still have symptoms 3 months after the accident they are likely to remain symptomatic for at least two years, and possibly for much longer[15]. 50% of people with injury from whiplash will have a full recovery, 25% may have mild levels of disability and the rest moderate to severe pain and disability[11]

There are many prognostic factors that determine the evolution of WAD and the likelihood that it will evolve into chronic pain.

  • Pre-collision self-reported unspecified pain, high psychological distress, female gender and low educational level predicted future self-reported neck pain[16].
  • no postsecondary education, older age, female gender, history of previous neck pain, baseline neck pain intensity greater than 55/100, presence of neck pain at baseline, presence of headache at baseline, catastrophising, WAD grade 2 or 3, and no seat belt in use at the time of collision[17].[11]
  • If the patient was out of work before the accident, sick-listed, or had social assistance, this can also be associated with a negative evolution following whiplash trauma. Illness notification before the accident can also be associated with neck pain in the future[16].
  • Baseline disability has a strong association with chronic disability, but psychological and behavioural factors are also important[18].
  • Cold pain threshold, neck ROM, headache, posttraumatic stress symptoms, hyperarousal symptoms (PDS), initial high Neck Disability Index (NDI)[11]

Whiplash Clinical Prediction Rule

A Clinical Prediction Rule (CPR) is a tool that helps to predict outcome, for example the possibility of a person to have moderate/severe pain and disability or have full recovery after a whiplash injury.[11] CPRs are used mostly in the following circumstances:[11]

  • complex decision-making
  • uncertainty
  • cost saving possibilities with no compromise to patient care

According to Howell, chronic neck pain following a whiplash-type injury could be predicted with the use of the Neck Disability Index (NDI). She found correlations with pain, disability and driving task scores with whiplash associated disorder (WAD) patients. Also, she reported that active cervical range-of-motion (CROM) reductions were common and important clinical outcome measures related to clinical prognosis of neck disability[19]

The CPR for WAD suggests the following:[11]

  • Probability for chronic moderate/severe disability with older age (≥35), initial high levels of neck disability (NDI≥40) and symptoms of hyperarousal
  • Probability for full recovery with younger age (≤35) and initial low levels of neck disability (NDI≤32)

Clinical Prediction Rule Algorithm

Ritchie et al found this CPR to be reproducible and accurate when used following whiplash due to a motor vehicle collision[20]

Clinical Presentation

Whiplash-associated disorders, is a complex condition with varied disturbances in motor, sensorimotor, and sensory functions and psychological distress[21][22]. The most common symptoms are sub-occipital headache and/or neck pain that is constant or motion-induced[23]. There may be up to 48 hrs delay of symptom onset from the initial injury[24].

Motor Dysfunction:

  • One of the most common clinical characteristics is a restricted range of motion of the cervical spine. This finding may reflect underlying disturbances in motor function due to the initial peripheral nociceptive input caused by injured anatomical cervical structures. Further research of such potential mechanisms in WAD is necessary[3][21].
  • Another characteristic is altered patterns of muscle recruitment in both the cervical spine and shoulder girdle regions. This is clearly shown to be a feature of chronic WAD[21][25][26][27].
  • Mechanical cervical spine instability[24]

Sensorimotor Dysfunction

  • Loss of balance
  • Disturbed neck influenced eye movement control[24]
  • Sensorimotor dysfunction is greater in patients who also report dizziness due to the neck pain[21][28][29].

Sensory Dysfunction: Sensory Hypersensitivity to a Variety of Stimuli

  • Psychological distress
  • Post traumatic stress[21]
  • Concentration and memory problems[28][29]
  • Sleep disturbances[30]
  • Anxiety[28]
  • Depression[28] is common in WAD patients. There are different types we can distinguish:
    • Initial depression: this can be associated with greater neck and low back pain severity, numbness/tingling in arms/hands, vision problems, dizziness, fracture[31]
    • Persistent depression: this can be associated with older age, greater initial neck and low back pain, post-crash dizziness, anxiety, numbness/tingling, vision and hearing problems[31]

Degeneration Cervical Muscles

  • Neck stiffness[28][29]
  • Fatty infiltrate may be present in the deep muscles in the suboccipital region and the multifidi may account for some of the functional impairments such as: Proprioceptive deficits, Balance loss, Disturbed motor control of the neck[32][23][25][26][28][27][29]

Other Symptoms

The following symptoms may also occur[24][28]

  • Tinnitus
  • Malaise
  • Disequilibrium/Dizziness
  • Thoracic, temporomandibular, facial, and limb pain

It is important to carry out thorough spinal and neurological examinations in patients with WAD to screen for delayed onset of the cervical spine instability or myelopathy[24]. Whiplash can be an acute or chronic disorder. In acute whiplash, symptoms last no more than 2-3 months, while in chronic whiplash symptoms last longer than three months. Patients with acute WAD experience widespread pressure hypersensitivity and reduced cervical mobility[33]. Various studies indicate that there can be a spontaneous recovery within 2-3 months[34] According to the Quebec Task Force of WAD (QTF-WAD), 85% of the patients recover within 6 months[35].

In addition, according to a follow-up study by Crutebo et al. (2010), some symptoms were already transient at baseline and symptoms such as neck pain, reduced cervical range of motion, headache, and low back pain, decreased further over the 6 months period. They also investigated the prevalence of depression and found that at baseline this was around 5% in both women and men, whereas post traumatic stress and anxiety were more common in women (19.7% and 11.7%, respectively) compared to men (13.2% and 8.6%). The majority of all reported associated symptoms were mild at both baseline and during follow-up[36].


QTFC (Quebec Task Force Classification)[29]

The Quebec Task Force was a task force sponsored by a public insurer in Canada. This Task Force developed recommendations regarding the classification and treatment of WAD, which were used to develop a guide for managing whiplash in 1995. An updated report was published in 2001. Each of the QTFC grades corresponds to a specific treatment recommendation[25].

QTFC Grade Clinical presentation
  • No complaint about neck pain
  • No physical signs
  • Neck complaints of pain, stiffness or tenderness only
  • No physical signs
  • Neck complaint
  • Musculoskeletal signs including
    • decreased ROM
    • point tenderness
  • Neck complaint
  • Musculosceletal signs
  • Neurological signs including:
    • decreased or absent deep tendon reflexes
    • muscle weakness
    • sensory deficits
  • Neck complaint and fracture or dislocation

MQTFC (Modified Quebec Task Force Classification)[25]

classification grade

Physical and psychological impairments present
  • No complaints about neck pain
  • No physical signs
  • No complaints of pain, stiffness or tenderness only
  • No physical signs
  • Neck complaint
  • Motor impairment
    • decreased ROM
    • altered muscle recruitment patterns (CCFT)
  • Sensory Impairment
    • local cervical mechanical hyperalgesia
  • Neck complaint
  • Motor impairment
    • decreased ROM
    • altered muscle recruitment patterns (CCFT)
  • Sensory Impairment
    • local cervical mechanical hyperalgesia
  • Psychological impairment
    • elevated psychological distress (GHQ, TAMPA)
  • Neck complaint
  • Motor impairment
    • decreased ROM
    • altered muscle recruitment patterns (CCFT)
    • increased JPE
  • Sensory Impairment
    • local cervical mechanical hyperalgesia
    • generalized sensory hypersensitivity (mechanical, thermal, ULNT)
    • Some may show SNS disturbances
  • Psychological impairment
    • elevated psychological distress (GHQ, TAMPA)
    • elevated levels of acute posttraumatic stress (IES)
  • Neck complaint
  • Motor impairment
    • decreased ROM
    • altered muscle recruitment patterns (CCFT)
    • increased JPE
  • Sensory Impairment
    • local cervical mechanical hyperalgesia
    • generalized sensory hypersensitivity (mechanical, thermal, ULNT)
    • Some may show SNS disturbances
  • Neurological signs of conduction loss including:
    • decrease or absent deep tendon reflexes
    • muscle weakness
    • sensory deficits
  • Psychological impairment
    • elevated psychological distress (GHQ, TAMPA)
    • elevated levels of acute post traumatic stress (IES)
WAD IV Fracture or dislocation

Radanov et al Classification[37]

In addition, a classification based on subjective complaints and formal testing of self-estimated cognitive impairment, divided attention, and speed of information processing was suggested by Radanov and co-workers[37]

  • Lower cervical spine syndrome (LCS) accompanied by cervical and cervicobrachial pain.
  • Cervicoencephalic syndrome (CES) characterized by headache, fatigue, dizziness, poor concentration, disturbed accommodation, and impaired adaptation to light intensity.

In comparison with the QTF classification, this system of classification incorporates neuropsychological symptoms[38].

Differential Diagnosis

Diagnostic Procedures

Clinical diagnosis

WAD can be diagnosed based on the mechanism of the injury and clinical presentation of the patient, [25][43]. There are no specific neuropsychological tests that can diagnose WAD[43]. However, there are several psychological symptoms, as described above, that are associated with WAD. In addition, a whiplash profile has been developed with high scores on sub-scales of somatisation, depression and obsessive compulsive behaviour in patients with WAD[14].

Radiographic Diagnosis

Whiplash injury is most often not identified radiologically in the acute phase[44] . The most common radiographic findings are[45]:

  • preexisting degenerative disease
  • slight loss of the normal lordotic curve of the cervical spine
  • kyphotic angle at the time of injury due to hypermobility and secondary to muscle spasm

MRI is not indicated at the time of initial presentation because of the high false positive results[46].

CT and MRI are generally used by patients with suspected spinal cord or disc injury, fracture or ligamentous injury. They may also be indicated in patients with long term persistent arm pain, neurological deficits, or clinical signs of nerve root compression[46]

X-ray should be routinely used for the patients with WAD grade III and IV. If the X-ray gives positive results for fracture or dislocation, the patient should be immediately referred to an emergency department or to a specialist surgeon[5].

Canadian C-Spine Rule (CCR) is an algorithm to determine the necessity for cervical spine radiography in alert and stable patients with trauma and cervical spine injury[47].

Outcome measures


The assessment of individuals with WAD should follow the normal cervical examination.


The subjective history should specifically include information about:

  • prior history of neck problems (including previous whiplash)
  • prior history of long-term problems (injury and illness)
  • current psychosocial problems (family, job-related, financial)
  • symptoms (location + time of onset)
  • mechanism of injury (e.g. sport, motor vehicle)

Outcome Measures

  1. General Health Questionnaire (CHQ)
  2. Visual Analogue Pain Scale
  3. Neck Disability index


Physical examination is required to identify signs and symptoms and classify WAD according to the QTF-WAD[53].

Inspection and palpation.

During palpation, stiffness and tenderness of the muscles may be observed. These physical symptoms are present in grade 1, 2 and 3. Trigger points may also be observed in grade 2 and 3 WAD. The number of active trigger points may be related to higher neck pain intensity, the number of days since the accident, higher pressure pain hypersensitivity over the cervical spine, and reduced active cervical range of motion[33].

ROM testing.

In grade 1 WAD, there are no physical signs, so there will be no decreased ROM. In grades 2 and 3, a decreased ROM can be identified by testing the neck flexion, extension, rotation and 3D movements[33][53].

Neurological examination

To distinguish grade 3 from grade 2, neurological examination is needed. Patients with grade 3 have symptoms of hypersensitivity to a variety of stimuli. These can be subjectively reported by patients, and may include allodynia, high irritability of pain, cold sensitivity, and poor sleep due to pain.

Objectively, the results of the neurological examination are hyporeflection, decreased muscles force and sensory deficits in dermatome and myotome. These responses may occur independently of psychological distress. Other physical tests for hypersensitivity include pressure algometers, pain with the application of ice, or increased bilateral responses to the brachial plexus provocation test.

It is important to know that these neurological symptoms do not necessarily indicate peripheral nerve compression and may be a reflection of altered central nociceptive processes[53].

These findings may be important for the differential diagnosis of acute whiplash injury. A poorer outcome is generally predicted in patients with higher initial pain and disability as well as hypersensitivty (e.g. cold hyperalgesia)[53][54].

“In recent years, there has also been extensive research undertaken demonstrating movement, muscle, and motor control changes in the neck and shoulder girdles of patients with neck pain, including WAD. Study findings include inferior performance on tests of motor control involving the cervical flexor, extensor and scapular muscle groups when compared to asymptomatic control participants; changes in muscle morphology of the cervical flexor and extensor muscles; loss of strength and endurance of cervical and scapular muscle groups; and sensorimotor changes manifested by increased joint re-positioning errors, poor kinaesthetic awareness, altered eye movement control, and loss of balance. Detailed information on the clinical assessment of cervical motor function is available elsewhere. The rationale for the evaluation of such features is to plan an individualised exercise program for each patient based on the assessment findings.” [53].

Medical Management

Steroid Injections

The cervical facet joint can be a source of pain in individuals with chronic WAD. Animal studies have demonstrated that cervical facet joint injury may be responsible for hypersensitivity and increased neuronal excitability.
Pain from the cervical facet joint can be medically managed using steroid injections to the specific zygopopsyal joints. Steroid injections can be used to treat acute and chronic WAD. However, there are conflicting findings on the possible outcomes from such treatment.[55][56][57]
Pettersson et al. suggests that a high dose of methyl-prednisolone therapy given to the patient within 8h after injury minimises the chance of developing chronic WAD. It is not often used because of the practical difficulties of this treatment (8h limitation, 23-h infusion, need for hospitalisation, cost).[57]

Radiofrequency Neurotomy

The nociception input from the cervical facet joint can be modulated via radiofrequency neurotomy (RFN).
The radiofrequency neurotomy is a neuroablative procedure used to interrupt nociceptive pathways and uses heat generated by radio waves to target specific nerves (medial branch emitted by dorsal ramus) and temporarily interfere with their ability to transmit pain signals from the facet joints. The RNF can improve the pain, disability widespread hyperalgesia to pressure and thermal stimuli, nociceptive flexor reflex threshold, and brachial plexus provocation responses as well as increased neck range of motion one month and up to 3 months after the RFN[58]. A prospective study with chronic WAD patients who underwent CRFN treatment, showed an improvement in 70% of patients based on a number of parameters including Neck Disability Index and cervical range of motion[59][60] .

Botulin Toxin Treatment

Botulinum Toxin-A (BTX-A) decreases muscle spasm that contribute to both pain and dysfunction. Pain and range of motion with patients with chronic grade 2 WAD improves 2 to 4 weeks post treatment[61][62].
The effect of the Botulinum toxin lasts nearly 8-12 weeks. Most patients treated with Botulinum toxin require repeated injections over many years[63].
Other interventions are sterile water injections, saline injections, dextrose, lidocaine intra-articular injections and epidural blood patch therapy. However, it is not clear whether these treatments are actually beneficial. Further research is required to determine the efficacy and the role of invasive interventions in the treatment of chronic WAD.[64]

Surgical interventions

A study by Jonsson et al. (1994) found that 20% of patients had a protrusion of a cervical disc of grade 3 or grade 4 on MRI which correlated with neurological findings after a whiplash injury[8]. Such patients might need to undergo anterior cervical discectomy[5]. After the discectomy, the surgeon might need to permanently stabilise the cervical spine. This can be achieved using artificial cervical disc or fusion of the cervical vertebrae[65].

Cervical discectomy and anterior cervical fusion can also be used to treat chronic WAD if the non-invasive treatments (including multimodal physical therapy) did not provide satisfactory results[56]. Indications for surgery include severe and prolonged headache, neck and radicular pain if the symptoms identified during the clinical examination are in agreement with the radiographic findings[16].

Physical Management

Management approaches for patients with WAD are poorly researched. Very often these patients do not fit into treatment categories as defined for other cervical pain problems due to multiple factors, and even within the WAD group there are multiple variances which warrant individualised treatment approaches[26].

Whiplash-associated disorder is a debilitating and costly condition of at least 6-month duration. Although the majority of patients with whiplash show no physical signs[66], Studies have shown that as many as 50% of victims of whiplash injury (grade 1 or 2 WAD) will still be experiencing chronic neck pain and disability six months later. In most cases, symptoms are short lived. Only a substantial minority goes on to develop LWS (late whiplash syndrome), i.e. persistence of significant symptoms beyond 6 months after injury[67]. Available data suggest that the combination of the injury with psychological factors such as coping style and explanatory style may lead to chronic WAD[60].

Acute Whiplash

Treatment for acute whiplash can be delayed due to multiple social, economic, and psychological factors[44]. Psychological factors such as depression, anxiety, expectations for recovery, and high psychological distress have been identified as important prognostic factors for WAD patients[66].

Coping strategies such as diverting attention and increasing activity are related to positive outcomes[66]. Another review with a high evidence level recommends that patients suffering from acute WAD “act as usual” and do early, controlled, physical activity within their tolerance level[60][53].

Education provided by physiotherapists or general practitioners is important in preventing of chronic whiplash, and must be part of the biopsychosocial approach for whiplash patients. The most important goals of the interventions are:

  1. Reassuring the patient
  2. Modulating maladaptive cognition about WAD
  3. Activating the patient[66]

The target of education is removing therapy barriers, enhancing therapy compliance and preventing and treating chronicity[66].

There is strong evidence that to reduce pain, disability and improve mobility both verbal education and written advice are helpful. According to Meeus et al., in acute patients oral information is equally as efficient as an active exercise program[66].
In subacute or chronic patients, a programme integrating information, exercises and behavioural programmes, and a multidisciplinary programme, seem necessary. For more information on this refer to the section on chronic WAD.
In acute whiplash patients, a short oral education session is effective in reducing pain and enhancing mobility and recovery. Different types of education include[66]:

  1. Oral Education: there is strong evidence for providing oral education concerning the whiplash mechanisms and emphasising physical activity and correct posture. It has a better effect on pain, cervical mobility, and recovery, compared to rest and neck collars. Furthermore, studies show that oral education could be as effective as active physiotherapy and mobilisation.
  2. Educational video: A brief psycho-educational video shown at the patient's bedside seems to have a profound effect on subsequent pain and medical utilisation in acute whiplash patients, compared to the usual care[68][66][69].

According to the Whiplash book education and information given to the patient must contain the following information:

  • Reassurance that prognosis following a whiplash injury is good.
  • Encouragement to return to normal activities as soon as possible using exercises to facilitate recovery
  • Reassurance that pain is normal following a whiplash injury and that patients should use analgesia consistently to control this
  • Advice against using a soft collar[67]

More studies are required to provide firm evidence for the type, duration, format, and efficacy of education in the different types of whiplash patients[66][69]

Future research should be founded on sound adult learning theory and learning skill acquisition[68].

Different types of exercise can be considered for WAD, including ROM exercises, McKenzie exercises, postural exercises, and strengthening and motor control exercises. It is not clear which type of exercise is more effective or if specific exercise is more effective than general activity or merely advice to remain active[53].

Active treatment which consists of early active mobilisation that is applied gently and over a small ROM, and which is repeated 10 times in each direction every waking hour seems to be as effective at reducing the pain after the whiplash injury as on ROM. This exercise can also be given as homework[70].

In a randomised study by A. Söderlund et al., where the aim was to compare two different home exercise programs in acute WAD, the result was that a home exercise programme, including training of neck and shoulder ROM, relaxation and general advice, seems to be sufficient treatment for acute WAD patients when used on a daily basis[71].

Supported by several high and low quality studies, evidence-based therapy for acute WAD consists of early physical activity, mobilisation and education.

From this, we can conclude that there is strong evidence to suggest that exercise programs and active mobilisation significantly reduce pain in the short term and there is evidence that mobilisation may also improve ROM[72][73][74][75][70][69].

Spinal manual therapy is often used in the clinical management of neck pain. It is not easy to tease out the effects of manual therapy alone because most studies used it as part of a multimodal package of treatment.

Systematic reviews of the few trials that have assessed manual therapy techniques alone concluded that manual therapy, such as passive mobilisation, applied to the cervical spine may provide some benefit in reducing pain, but that the included trials were of low quality[53].

Patients with grades 1 and 2 2 WAD showed good results in a multimodal treatment program including exercises and group therapy, manual therapy, education and exercise. At their 6 months follow-up, 65% of subjects reported a complete return to work, 92% reported a partial or complete return to work, and 81% reported no medical or paramedical treatments over 6 months[76]

For the early management of WAD grades 1 and 2, general practitioner care includes advice to stay active and resumption of regular activities.

The synthesis of DA Sutton et al. suggests that patients receiving high-intensity health care tend to experience poorer outcomes than those who receive fewer treatments for WAD and NAD[47].

Another interesting topic is the use of a collar. The use of a collar stands in contrast with what is indicated in most of the studies; activation, mobilisation and exercise. In a randomised study of Bonk et al. subjects were randomly assigned to a collar therapy group or to the exercise group. During a one week period participants had to record their average pain and disability in a diary, using the VAS scale. The results showed a significant difference between the groups, with positive effects on the prevalence of symptoms in the exercise therapy group compared to the collar group at six weeks. It is proven that early exercise therapy is superior to collar therapy in reducing pain intensity and disability for whiplash injury. Other studies also showed that exercise therapy gives a better pain relief than a soft collar[70][77][69].

Chronic Whiplash

There is a difference between a patient suffering from acute whiplash and a patient suffering from chronic whiplash. There is a suggestion that the injury in combination with psychological factors may lead to chronic WAD[60].

A multidisciplinary therapy with cognitive, behavioural therapy and physical therapy, including neck exercises is effective in the management of WAD patients with chronic neck pain[78][60][79]

When behavioural therapy is used in the therapy, it decreases the patient’s pain intensity in problematic daily activities. Therefore functional behavioural analyses can be used to adapt planning and treatment[80].

There is evidence that exercise programs have a positive result in reducing pain in the short term. Exercise programmes are the most effective noninvasive treatment for patients with chronic WAD, although many questions remain regarding the relative effectiveness of various exercise regimens. There is also evidence suggesting that coordination exercises should be added to the treatment to reduce neck pain.

Multidisciplinary therapy gives positive results according to the reductions of neck pain and sick leave reported[60].

This is also the therapy recommended by the Dutch clinical guidelines for WAD[81].

In patients with chronic WAD, negative thoughts are a very important factor. Self-efficacy, a measure of how well an individual believes he can perform a task or specific behaviour and emotional reaction in stressful situations, was the most important predictor of persistent disability in those patients[82].

Negative thoughts and pain behaviour can be influenced by specialists and physical therapists by educating patients with chronic WAD on the neurophysiology of pain. Improvement in pain behaviour resulted in improved neck disability and increased pain-free movement performance and pain thresholds according to a pilot study[83].

Michaleff et al. even found that simple advice is equally as effective as a more intense and comprehensive physiotherapy exercise programme[84].

In a case report of Ferrantelli J.R.et al., the patient underwent a Clinical Biomechanics of Posture Rehabilitation in which he received mirror-image cervical spine adjustments, exercises and traction to reduce head protrusion and cervical kyphosis. The first ten visits included regional bilateral long-lever cervical spinal manipulation to temporarily decrease pain and increase ROM, and there after the structural rehabilitation care started. This treatment consisted in mirror-image drop table adjustments, mirror-image handheld instrument adjustments, mirror-image isometric exercise and mirror-image extension-compression traction for the reduction of the abnormal anterior translation posture of the head. After 5 months, the patient’s chronic WAD symptoms were improved[85].

As Michaleff et al. say in their article, that we can conclude that an important health priority is the need to identify effective and affordable strategies to prevent and treat acute to chronic whiplash associated disorders[84].


Below is a listing of the various therapy techniques and studies with key evidence.


Quebec Task Force 1988 [86] Prolonged immobilization may increase scar tissue in the neck and reduce cervical mobility  2B
Mealey et al 1986 [87] Initial immobilization after whiplash injuries gave rise to prolonged symptoms. A more rapid improvement can be achieved by early active management without any consequent increase in discomfort 3A
Borchgrevink GE et al
2008 [88]
Advice to “act as usual” plus NSAIDs significantly improved some symptoms (including pain during daily activities, neck stiffness, memory, concentration, and headache) after 6 months compared with immobilisation plus 14 days' sick leave plus NSAIDs  1A
Teasell R.W. et al
2010 [89]
Immobilization with a soft collar is less effective than active mobilization and no more effective than advice to act as usual. Active mobilization is associated with reduced pain intensity and limited evidence that mobilization may also improve ROM, although it is not clear whether active mobilization is any more effective than advice to act as usual. 1A


Schnabel et al 2004 [90] Early exercise therapy is superior to the collar therapy in reducing pain intensity and disability for whiplash injury  2B
Binder A. 2008 [88] Instruction on mobilization exercises may be more effective than a soft collar at reducing pain at 6 weeks in people treated within 48 hours of a whiplash injury who all also took NSAIDs 1A
Schnabel M et al 2008 [88] Exercises significantly reduce the proportion of people with neck pain at 6 weeks compared with a soft collar and significantly reduce pain and disability at 6 weeks 1A


Binder A 2008 [88] Advice to "act as usual" plus NSAIDs may be more effective at 6 months than immobilization plus 14 days sick leave plus NSAIDs at improving neck stiffness in people with acute whiplash  1A
Borchgrevink GE et al 2008 [88] Advice to “act as usual” plus NSAIDs significantly improved some symptoms (including pain during daily activities, neck stiffness, memory, concentration, and headache) after 6 months compared with immobilisation plus 14 days' sick leave plus NSAIDs  1A
Yadla S et al
2008 [91]
Early mobilization and return to activity may offer the best chance for recovery. 1A
Teasell R.W. et al
2010 [89]
It does not appear that providing educational information during the acute phase provides a significant measurable benefit. There is some indication that oral and/or video presentation of educational information may be more effective than the distribution of pamphlets. 1A


Verhagen AP 2008 [88] Limited evidence that active and passive interventions seemed more effective than no treatment. Less convincing evidence about active interventions compared with passive ones  1A
Binder A 2008 [88] Instruction on mobilization exercises may be more effective than a soft collar at reducing pain at 6 weeks in people treated within 48 hours of a whiplash injury who all also took NSAIDs  1A
Lamb S et al 2013 [92] Physiotherapy is recommended by several clinical guidelines. Recommended treatments include manual therapy, exercise, advice, and recognition of anxiety and psychological problems  2A
Schnabel M et al 2008 [88] Exercises significantly reduced the proportion of people with neck pain at 6 weeks compared with a soft collar and significantly reduced pain and disability at 6 weeks  1A
Scholten – Peeters G et al 2008 [88] No significant difference between physiotherapy (exercise or mobilization) and usual care in pain intensity, headache, or work activities measured at 8, 12, 26, or 52 weeks 1A
Söderlund A 2008 [88] No significant difference between a regular exercise regimen versus the same exercise regimen plus instructions in disability or pain after 3 or 6 months
Binder A
2008 [88]
Multimodal treatment (postural training, psychological support, eye fixation exer- cises, and manual treatment) may be more effective at improving pain at 1 and 6 months in people with whiplash due to a road traffic accident in the previous 2 months  1A
Teasell R.W. et al
2010 [89]
Exercise programs are significantly more effective in reducing pain intensity over both the short and medium term. Conversely, supplemental exercise programs added to mobilization programs may not be any more beneficial than mobilization programs alone 1A
Drescher K et al
2008 [93]
Moderate evidence to support the use of postural exercises for decreasing pain and time off work in the treatment of patients with acute whiplash-associated disorders.
No evidence exists to support the use of postural exercises for increasing neck range of motion.
Conflicting evidence in support of neck stabilization exercises in the treatment of patients with acute whiplash-associated disorders.

Clinical Bottom Line

Whiplash associated disorders (WAD) are a result of a previous whiplash injury and has a variety of characteristics and symptoms. This clinical presentation can be divided into different grades, reported by The Quebec Task Force. This classification is widely used and gives recommendations about the possible therapy. When a patient has a WAD several anatomical tissues can be affected, depending on the force and direction of the impact. Some people are more likely to develop WAD than others. To diagnose WAD radiographic images are not the norm, unless it concerns a WAD Grade III and IV. It’s more useful to make a clinical diagnosis based on the clinical presentation and anamnesis. Depending on severity of the WAD different medical/surgical interventions are needed. The most common interventions are steroid injections, radiofrequency neurotomy, botulin toxin treatment, cervical discectomy and cervical fusion. Although there are a lot of medical interventions, a WAD can also be treated in a conservative way. The therapy of an acute whiplash should consist of education, where it’s made clear by the therapist to stay active and ‘act as usual’, and early physical activity and mobilization. For the management of chronic whiplash there is strong evidence that a multidisciplinary therapy is effective. This therapy also has to consist of an exercise program.


In 2017 Walton and Elliot proposed a new Integrated Model of Chronic WAD. This journal article will explain more on this model:

  1. Walton DM, Elliott JM. An integrated model of chronic whiplash-associated disorder. journal of orthopaedic & sports physical therapy. 2017 Jul;47(7):462-71.  


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