Chronic Post-Traumatic Neck Pain

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The majority of patients sustaining whiplash injuries to the cervical spine either don't have symptoms or recover. A minority of patients have persistent symptoms, and this area is now moderately well understood due to research in biomechanics, pathology, and diagnostic blocks. The persistent pain is thought to arise from injuries to the anulus fibrosus or zygapophysial joints. The zygapophyseal joints are the most clinically relevant structural cause of chronic post-traumatic neck pain because there is a proven treatment.


See also: Category:Cervical Spine Anatomy

The cervical disc are very different to lumbar discs. The annulus is non-concentric, and only well-developed in the anterior aspect of the disc. It is more of an interosseous ligament which is non-load bearing.


Studies have consistently shown that the facet joints are implicated 50-60% of the time in chronic post-traumatic neck pain when identified via concordant comparative medial branch blocks.

Prevalence Studies of Pain Sources in Chronic Neck Pain
Study Patients Blocks Relief Proportion
Barnsley 1995[1] Whiplash Concordant comparative MBB 100% 54%
Lord 1996[2] Whiplash Placebo-controlled MBB 100% 60%
Speldewinde 2001[3] Variety Concordant comparative MBB โ‰ค 1/10 36%
Manchikanti 2002[4] Variety Concordant comparative MBB 75% 60%
Yin 2008[5] Variety Concordant comparative MBB 100% 55%
Yin 2008[5] Variety Provocative discography 7/10

(pain not relief)



Biomechanics of Whiplash

Whiplash is an inertial event, not a result of a direct force. It can occur in a motor vehicle accident or even during a fall. With motor vehicle accidents it has traditionally referred to a rear-end impact, but it now is also used with side and front impacts. In experimental studies, asymptomatic patients develop neck pain with impacts at speeds of greater than 10km per hour.

Whiplash is a compression injury, not a flexion-extension or acceleration-deceleration injury. There are two phases.[6]

Phase I: Following impact, the trunk is first thrust upwards and forward into the neck. During the deformation, the lower cervical segments extend, while the upper segments flex. This results in a sigmoid deformation of the cervical spine at about 110ms after impact. The anterior annulus fibrosis is distracted, and the facet joints are impacted. As the trunk continues forward, the head drops, and the upper segments extend. The entire cervical spine has extended at the end of this phase.

Phase II: The trunk and upper neck drop down, and the head returns to a normal position over the base of the neck. Importantly, a flexion phase does not occur.

There can be abnormal motion within individual segments even when the total range of motion is within normal limits, however C6-7 and C7-T1 can exceed normal limits. In normal cervical extension, the axis of rotation is found in the vertebral body below the one that is moving. The moving vertebra translates posteriorly during extension, and the inferior articular process of the vertebra above glides along the superior articular process of the vertebra below. During whiplash, the axis of rotation is located in the moving vertebra itself. There is no posterior translation of the moving vertebra, only extension (posterior sagittal rotation). The vertebral bodies are separated, the inferior articular process of the vertebra above is driven into the superior articular process of the vertebra below (phase I), and the anterior capsules of the facet joints are strained beyond normal physiological limits (phase II). The strain is greatest in the C4-5 disc at low accelerations, while at higher accelerations there is strain in the C3-4, C5-6, and C6-7 discs.

The biomechanics of whiplash predict certain injuries which have been corroborated with pathological studies (see pathology section). Laboratory studies on whiplash in living individuals have been conducted between 2 - 10 km/hr, as ethical considerations limit any greater speeds. At these low speeds some patients developed symptoms lasting up to two weeks.


The majority of patients subject to whiplash do not have any injury. Specific tissue damage seen are tears of the anterior anulus fibrosis, strain or tears of the facet joint capsules (rim lesions and avulsions), and impaction injuries of the facet joints. Impaction injuries include contusions of the intra-articular meniscoids with intra articular haemorrhage, and subchondral and transarticular fractures.[6]

Rim lesions are the most common disc injury. They are a horizontal annular tear at the vertebral rim, without tearing the anterior longitudinal ligament. They are often a multilevel injury. Anterior disc injuries vary from small rim lesions to partial avulsion of the anterior longitudinal ligament.

Disc avulsions are the separation of the disc from the vertebral body along the disc-vertebral junction. They are the most common severe disc injury in subjects under the age of 55 years. There is variable extent of anterior longitudinal ligament damage. The anterior muscles are usually left intact.

With acute zygapophyseal joint injuries there is often haemarthrosis. The bleeding can come from a ruptured synovial fold, damaged articular surface, or a zygapophyseal joint fracture. Haemarthrosis is often multi-level.

These injuries are predicted on biomechanical studies, and are found on careful analysis of the cervical spines of those deceased in motor vehicle accidents by focusing on sublethal cervical spine injury patterns. None of the lesions in the autopsy studies were visible on post-mortem radiography.

Other rare injuries attributed to whiplash, normally seen with more significant forces than seen with the above pathology, include disruption of transverse and/or alar ligaments, prevertebral haematoma, perforation of oesophagus, tears of the sympathetic trunk, damage to the recurrent laryngeal nerve, spinal cord injury, perilymph fistula, thrombosis or traumatic aneurysm of the vertebral or internal carotid arteries, anterior spinal artery syndrome, and cervical vertebral fracture.

Cervical vertebral fractures in whiplash are very rare, and are difficult to detect by conventional investigations. The majority involve the upper cervical vertebrae. Fracture patterns include fractures of the odontoid process, laminae and articular processes of C2, and fracture of the occipital condyles.

A useful text on cervical spine pathology is James Taylor's The Cervical Spine: An atlas of normal anatomy and the morbid anatomy of ageing and injuries.


The zygaphophyseal joints are an important source of nociception following chronic post-traumatic neck pain. Lord et al found that the ZA joints below C2-3 are the cause of neck pain after whiplash in 49-60% of 68 cases[8]. The prevalence of third occipital nerve headache among 100 whiplash patients was 27% and among those with dominant headache the prevalence was as high as 53%.[9] Barnsley found that the ZA joints cause 54% of neck pain after whiplash among 50 patients, mostly C2-3 and C5-6[10] Manchikanti et al found that in the general chronic spine patient population, the ZA joints cause 55% of chronic cervical spine pain among 255 cervical spine pain patients.[11]

There are sensory axons in C1, C2, and C2 spinal nerves that converse on dorsal horn neurons that also receive trigeminal afferents largely from the ophthalmic division. The convergence allows pain mediated in the C1, C2, or C3 nerves to be perceived in regions innervated by the trigeminal nerve (cervical - trigeminal referral). Can also have cervical - cervical referral.

Clinical Assessment


Assess for red flags. The hallmark symptom of whiplash is neck pain. There is often somatic referred pain to the head in the case of injury to the upper cervical segments; or to the posterior upper limb girdle or anterior chest wall in the case of injury to the lower cervical segments. Other that pain, there can be other lesser symptoms, and these are more variable in their prevalence.

Paraesthesias: this could indicate a cervical radiculopathy, or a thoracic outlet compression as a result of spasmed scalene muscles.

Weakness: Cervical radiculopathy is more likely if the weakness is in a myotomal distribution. More commonly, a global subjective weakness can occur as a result of pain inhibition reflexes. The nociceptive afferent input from a painful area inhibits the efferent motor neuron pools of the muscle that moves that region. A greater upper motor neuron drive is required to overcome the segmental inhibition.

Dizziness: Bogduk believes that this is due to derangement of tonic neck reflexes via the spinovestibular pathway, and disturbed function of the cervical muscles as a result of pain. Other authors conceptualise this as abnormal sensory input with sensory mismatch, where there cervical inputs are dominant over vestibular inputs due to pain or stiffness. There are no validated methods of diagnosing cervical dizziness.

Visual Disturbance: Patients may complain of visual problems which is not a reduction in visual acuity but more akin to difficulty focusing. The mechanism of this is thought to be due to increased sympathetic pupil dilator tone through the spinociliary reflex due to neck pain, which results in compensatory increased drive for pupil constriction with a side effect being increased accommodation. If this occurs in an asymmetrical manner, the individual may perceived their vision as blurred.

Tinnitus: One possible theory is inner ear damage

Cognitive Impairment: It is thought that this is due to memory or concentration disturbance as a result of pain or side effects of analgesics. The evidence supporting traumatic brain injury in whiplash is inconclusive.

Back Pain: The cause is unknown.


There is no proven diagnostic value in the physical examination. There is good reliability of tenderness over the facet joints, but it lacks validity. Testing for gross range of motion has not been tested for reliability and lacks validity. Provocation of neck pain with various movements may be seen but this is also not diagnostic of a specific pain source.

In the case of paraesthesias, cervical radiculopathy is suggested in the presence of dermatomal numbness, myotomal weakness, or loss of reflexes. Thoracic outlet compression is suggested if the paraesthesias coincides with pain flares, and if it is in a "glove" distribution due to compression the C6, C7, and C8 roots of the brachial plexus.

Weakness from cervical radiculopathy versus weakness secondary to pain may be deduced as follows. With upper limb movement the levator scapulae and rhomboid scapula muscles stabilise the shoulder girdle, and this muscle action results in compression forces being transmitted to the neck thereby causing pain. This can be detected by comparing upper limb strength in sitting to that in a supine position. In sitting the scapula muscles are active, and so weakness may be detected due to pain inhibition. In the supine position the shoulder girdle can be braced in order to isolate the arm from the shoulder girdle and avoid transmitting compression forces to the neck. In this way upper limb strength can be assessed more accurately without aggravating the neck pain.



Autopsy studies have found that current imaging techniques are not high enough resolution to detect the lesions described in the pathology section. Pathology like rim lesions, disc avulsions, and haemarthroses may or may not be seen if MRI is done soon after injury. MRI is most often done in the subacute and chronic stage and so it is usually normal.

Therefore for most patients, imaging will be normal or simply show "cervical spondylosis," or facet joint osteoarthritis. Normal imaging does not exclude a nociceptive source of pain, indeed normal imaging is expected in those with chronic post-traumatic neck pain. Yet the injury may still be clinically relevant and cause ongoing problems.

CT scintigraphy is used a lot in New Zealand. It is good for picking up small occult fracture and tumours etc. It does not however show pain, only increased blood flow. It tends to miss cases where there is pain arising from soft tissue damage for example capsular tears.

Medial Branch Blocks

Main article: Cervical Facet Joint Precision Treatment
The cervical medial branches.

The two most common joints to be positive (by a long shot) are the C2-3 and C5-6 facet joints.[12]

C1-2 (Atlanto-axial joint)

The C1-2 cannot be blocked by medial branch blocks. Therefore it is blocked via the lateral atlanto-axial joint block. This is potentially hazardous as it is close to the vertebral artery and dural sac. There is a very small risk of hitting the C2 nerve (~4%). The C2 ventral ramus is closely related to the posterior capsule of the lateral atlanto-axial joint, assumes a variable relationship to the cavity of the joint, some authors report that it runs exactly parallel to the line of the joint, while others illustrate it running below. Most often the nerve runs across the capsule, behind the superior articular process of C2, and less often behind the inferior articular process of C1. The variability means there is no guaranteed trajectory to avoid the C2 ventral ramus. The recommended technique is to place the needle on a bony target above or below the lateral aspect of the joint. This is to reduce the risk of hitting the dural sac, C2 dorsal ganglion, vertebral artery, and over-penetration. Once the needle hits bone, advance the needle very slowly.

C2-3 (Third occipital nerve)

This is the most useful diagnostic intervention for chronic cervicogenic pain, because the C2-3 joint is the most common source of pain. There are two medial branches of the C3 dorsal ramus. There is the deep medial branch which contributes to the innervation of the C3-4 joint, and the superficial branch which is the third occipital nerve and innervates the C2-3 joint and also semispinalis capitis and a small area of skin in the suboccipital area. The nerve crosses the joint, but is quite variable in its distribution, and the needle placement reflects the variability, with three small volume injections along the distribution. It is easy to miss the nerve even if the needle locations are correct. Testing the expected patch of numbness is a good way of checking that you have anaesthetised the nerve. Injecting contrast can be helpful. Ultrasound guided injections can also be done.


This is an uncommon source of pain on its own.

Provocative Discography

Provocative discography is hardly ever done in New Zealand. There is a very high false positive rate. Discography should never been done unless medial branch blocks have been done and are negative. Even though C5/6 has the highest incidence of degenerative change, there are still high rates of positive discs at other levels. C3/4, C4/5, and C5/6 are the most common with similar incidences of positive tests.

The diagnosis of cervical discogenic pain can be made when all the following criteria are met:

  1. Cervical facet joint pain has been excluded with medial branch blocks
  2. Disc stimulation has been performed with correct technique
  3. Disc stimulation reproduces concordant pain
  4. Disc stimulation reproduces pain of at least 7/10 in intensity
  5. Disc stimulation of adjacent discs does not reproduce pain.

Discitis is a a rare risk at just under 1%.


The treatment of whiplash amounts to the treatment of neck pain. All lesser symptoms, except perhaps tinnitus, can be due to secondary pain responses.


Percentage of subjects reported as recovered versus time in those cohorts with less than 3 weeks inception time, greater than 80% follow-up and a validated outcome measure (includes 7 data points from 3 cohorts).[13]
Individuals with worse initial symptoms are more likely to have worse outcomes.[14]

One systematic review was not able to definitively establish which factors are important in predicting poor outcomes due to variation in measuring and reporting prognostic associations. In a narrative review of the literature they found the following.[13]

  • High initial neck pain and disability are indicators of poor prognosis
  • Generalised psychological distress such as anxiety and depression are poor prognostic factors
  • Female gender and older age do not appear to be related to poor outcome
  • Crash related factors including direction and estimated speed of impact do not appear to be related to poor outcome

Recovery rates vary across cohorts likely due to variations in measures. They only found homogeneity of the data when they limited the analysis to the highest quality data (which was only 7 data points from 3 cohorts, versus 67 data points from 33 cohorts for the entire dataset) they found that most patients recover within the initial few months, but a significant portion do not and continue to have pain and disability for years.[13] One often sited cohort study found good recovery after the first year, but then it tails off. At 24 months 14% have not fully recovered, and 4% are severely affected.[15]

See Ritchie et al for a recent in depth review and discussion about recovery trajectories after whiplash injury.[16]


  • There is good evidence from biomechanical and post-mortem studies that various structures can be injured during whiplash.

Important Articles


  1. โ†‘ Barnsley et al.. The prevalence of chronic cervical zygapophysial joint pain after whiplash. Spine 1995. 20:20-5; discussion 26. PMID: 7709275. DOI.
  2. โ†‘ Lord et al.. Chronic cervical zygapophysial joint pain after whiplash. A placebo-controlled prevalence study. Spine 1996. 21:1737-44; discussion 1744-5. PMID: 8855458. DOI.
  3. โ†‘ Speldewinde et al.. Diagnostic cervical zygapophyseal joint blocks for chronic cervical pain. The Medical journal of Australia 2001. 174:174-6. PMID: 11270757. DOI.
  4. โ†‘ Manchikanti et al.. Prevalence of cervical facet joint pain in chronic neck pain. Pain physician 2002. 5:243-9. PMID: 16902649.
  5. โ†‘ 5.0 5.1 Yin & Bogduk. The nature of neck pain in a private pain clinic in the United States. Pain medicine (Malden, Mass.) 2008. 9:196-203. PMID: 18298702. DOI.
  6. โ†‘ 6.0 6.1 Bogduk. On cervical zygapophysial joint pain after whiplash. Spine 2011. 36:S194-9. PMID: 22020612. DOI.
  7. โ†‘ Kaneoka, K., Ono, K., Inami, S., Ochiai, N., & Hayashi, K. (2002). The Human Cervical Spine Motion During Rear-Impact Collisions. Journal of Whiplash & Related Disorders, 1(1), 85โ€“97. DOI
  8. โ†‘ Lord et al.. Chronic cervical zygapophysial joint pain after whiplash. A placebo-controlled prevalence study. Spine 1996. 21:1737-44; discussion 1744-5. PMID: 8855458. DOI.
  9. โ†‘ Lord et al.. Third occipital nerve headache: a prevalence study. Journal of neurology, neurosurgery, and psychiatry 1994. 57:1187-90. PMID: 7931379. DOI. Full Text.
  10. โ†‘ Barnsley et al.. The prevalence of chronic cervical zygapophysial joint pain after whiplash. Spine 1995. 20:20-5; discussion 26. PMID: 7709275. DOI.
  11. โ†‘ Manchikanti et al.. Prevalence of facet joint pain in chronic spinal pain of cervical, thoracic, and lumbar regions. BMC musculoskeletal disorders 2004. 5:15. PMID: 15169547. DOI. Full Text.
  12. โ†‘ Cooper et al.. Cervical zygapophysial joint pain maps. Pain medicine (Malden, Mass.) 2007. 8:344-53. PMID: 17610457. DOI.
  13. โ†‘ 13.0 13.1 13.2 Kamper et al.. Course and prognostic factors of whiplash: a systematic review and meta-analysis. Pain 2008. 138:617-629. PMID: 18407412. DOI.
  14. โ†‘ Sterling et al.. Compensation claim lodgement and health outcome developmental trajectories following whiplash injury: A prospective study. Pain 2010. 150:22-28. PMID: 20307934. DOI.
  15. โ†‘ Radanov et al.. Long-term outcome after whiplash injury. A 2-year follow-up considering features of injury mechanism and somatic, radiologic, and psychosocial findings. Medicine 1995. 74:281-97. PMID: 7565068. DOI.
  16. โ†‘ Ritchie & Sterling. Recovery Pathways and Prognosis After Whiplash Injury. The Journal of orthopaedic and sports physical therapy 2016. 46:851-861. PMID: 27594661. DOI.
  • Kaneoka, K., Ono, K.,. Motion Analysis of Human Cervical Vertebrae During Low-Speed Rear Impacts by the Simulated Sled. Journal of Crash Prevention and Injury Control. 1999 Sep;1(2):87โ€“99. DOI
  • Kaneoka et al.. Motion analysis of cervical vertebrae during whiplash loading. Spine 1999. 24:763-9; discussion 770. PMID: 10222526. DOI.