Cervical Facet Mediated Pain Katherine White, MD, Thomas H. Hudgins, MD, and Joseph T. Alleva, MD, MBA The Quebec Task Force on Whiplash-Associated Disorders defines whiplash as an acceleration-deceleration mechanism of energy transfer to the neck most often resulting from rear- or side-impact motor vehicle collisions; the impact often results in bony or soft-tissue injuries, which are referred to as whiplash injury. The varied symptoms arising from whiplash injury are termed whiplash associated disorders (WAD).1,2 The most common complaints after whiplash are neck pain, pain in the interscapular area, shoulder pain, arm pain with or without paresthesias, and headache. Somewhat less common, but potentially disabling symptoms include disturbances of concentration and memory, dizziness, visual disturbance, weakness or heaviness of the arms, depression, fatigue, and low back pain.3 Most people involved in rear-end collisions do not experience pain. Those who do experience pain often have spontaneous resolution of their symptoms in 3 to 6 months. However, there are those who develop chronic pain associated with whiplash. Chronic pain refers to pain persisting after the mechanical injury is presumed to have healed; it is not necessary to wait until 6 months to classify a patient as having chronic WAD, but it is generally considered that symptoms persisting 6 months from whiplash injury are chronic.1,2 Fifteen percent to 40 percent of patients who have acute neck pain after a motor vehicle collision will go on to develop chronic neck pain.4 Those patients who do experience chronic pain represent a financial burden from workdays lost, health care resources used, and litigation pending. Estimates have been as high as $29 billion in the United States alone.5 The etiology for whiplash is best described by discussing potential pain generators in the cervical spine. The 3 most common structures for generating pain after whiplash are the cervical zygapophyseal or facet
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joints, the cervical intervertebral disks, and soft tissues such as ligaments and muscles. Each will be addressed, but the focus of this section is on the facet joint and soft tissues. The energy transfer in motor vehicle collisions comes from the moving car to the struck car, through the frame to the seat and seat back of the car to the person sitting in the car. The collision causes the thorax to move forward relative to the head, causing nonphysiologic movements of the cervical spine and its structures.6 The lower cervical spine translates forward into extension with flexion of the head from occiput to C2 because of the head’s inertia. This causes a nonphysiologic S-curve. This upper cervical flexion and lower cervical extension then transitions into whole cervical spine extension and then flexion.7,8 Neither the flexion nor the extension is grossly out of the physiological range of motion; it is thought that the S-curve, which does not happen under normal circumstances, and the movement happening at the level of the cervical facet joints causes strain and shear forces that are responsible for pain-generating injuries.6,9 Failure of the facet capsule ligament occurs under the strain of shear and compressive forces, causing a pinching mechanism of the facet joints of the lower cervical spine. The nociceptive nerve endings in the facet capsule ligament are capable of pain generation when an injury occurs.9-12
Pain Generators In vivo studies have confirmed the facet joint as a potential source of pain with particular patterns of distribution based on the level of injury. With injections of contrast in healthy subjects, researchers were able to elicit pain in facet joints from C2-3 to C6-7. The distribution of pain was marked on the skin and recorded on a body diagram. The medial branches of the dorsal rami of the target joint were then blocked with a short-acting anesthetic to alleviate the pain. This and subsequent studies revealed a predictable pattern of distribution from the head to the cervical region, shoulder, and intrascapular region, that was reproducible and corresponded to the level of injury.13-15 In further studies using diagnostic joint injections to discern the prevalence of facet joint mediated pain after whiplash, it was shown that the facet joint is the etiology of neck pain 49%-60% of the time.5 Headaches responded to C2-3 facet joint blocks approximately 50% of the time.5,6 The facet joint is richly innervated with nociceptors and mechanore730
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ceptors; these nerves can be adversely affected by facet capsular strain.5,16 Inflammation of the facet joint can sensitize nociceptive neurons and lower the firing threshold, causing pain during “normal” motion, or peripheral sensitization. Similarly, disruption of mechanoreceptors can cause subtle proprioceptive disturbances and result in spinal instability or uncoordinated, painful cervical muscle contraction, and guarding.17,18
Anatomy The cervical spine is composed of 7 cervical vertebrae, intervertebral disks, zygapophyseal or facet joints, ligaments, muscle/fascia, neural structures, and vasculature. There are 14 facet joints in the cervical spine. They are true synovial joints and are composed of a fibrous capsule lined with synovium and hyaline cartilage between the bony structures. The capsule is richly innervated by nociceptors and mechanoreceptors that help with cervical spine proprioception. The orientation of the facet joint provides resistance to anterior translation and assists in weight-bearing. They are at a 45-degree angle, allowing flexion, extension, rotation, and limited translation. The atlantooccipital and atlanto-axial joints (C1 and C2) do not have facet joints. C2-3 is innervated by the medial branch of the C2 dorsal rami and the third occipital nerve or the medial branch of the C3 dorsal rami. C3-4 to C7-T1 are innervated by the medial branches of the cervical dorsal rami located above and below the joint.19
History and Physical Examination Whiplash is classified by severity as outlined by the Quebec Task Force and is based on patient symptoms and the presence or absence of physical signs. The numbering system is from 0 to 4, with 0 being no neck complaints or physical signs and 4 being neck complaints and fracture or dislocation. The grades most commonly encountered in the office setting are 1-3, and they are classified as follows: (1) neck complaint of pain stiffness or tenderness with no physical signs; (2) neck complaint and musculoskeletal signs including decreased range of motion and point tenderness; (3) neck complaint and neurological signs including decreased or absent deep tendon reflexes, weakness, and sensory deficits. Symptoms that may be associated with any grade injury include dizziness, tinnitus, headache, memory loss, depression, insomnia, dysphagia, and temporomandibular joint pain.1,2 Neck pain is often the most severe symptom and can be unilateral, DM, December 2009
bilateral, or midline. Pain is often referred to the trapezius muscle, shoulder, interscapular area, arm, and possibly the face.4,20 On examination, the most common finding is decreased range of motion at the cervical spine. Studies have shown that patients with whiplash have significantly decreased cervical axial range of motion. It is thought that patients with whiplash remain in a “neutral zone.” They are either unable or unwilling to go to normal range of motion secondary to pain or the fear of pain.21 It is important to note that decreased range of motion is not specific to chronic neck pain caused by acceleration-deceleration injury; the finding of cervical muscle dysfunction and guarding/fear of movement is common to all patients with chronic neck pain, and it does not suggest a particular etiology of pain generation.22 Arm pain in the chronic setting may represent radiculopathy from disk herniation and neural root impingement. It is important to ask the patient about neurologic symptoms such as paresthesias, weakness, and/or impairment of fine motor coordination of the hand. Headache is also a common symptom and is generally accepted to be cervicogenic. It originates in the occiput and radiates forward to the frontal region and crown of the head. Generally, unilaterally, it can involve either side of the head and vary from side-to-side in the same patient. It is thought that the pain can be attributed to prolonged neck positioning from guarding, C2-C3 disk or facet pathology, or from the atlanto-occipital joint.4,6
Diagnosis During the acute phase, patients with pain, neurologic deficit, distracting injury, and altered consciousness require plain radiographs to ensure spinal stability.22 Patients who are ambulatory, lack pain or tenderness, and have at least 45 degrees of range of motion do not require imaging.23 Cervical spine instability is defined by 3.5 mm or more of sagittal translation on lateral flexion/extension views or more than 11 degrees of rotation in the sagittal plane on plain films.24 Magnetic resonance imaging is not a predictor of chronic symptoms during the acute phase and is unnecessary at this time in a neurologically intact individual.25,26 If the patient has persistent arm pain, neurologic deficits, or clinical signs of nerve root compression that is presumed to be secondary to impingement from a herniated disk, magnetic resonance imaging would be warranted if surgery were being considered.4 732
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Treatment Acute Initial treatment consists of reassurance that there is a positive natural history of spontaneous recovery from whiplash. Patients should be encouraged to return to their usual activities without restriction or fear of incurring further injury despite the pain. In fact, it has been shown that immobilization and rest have adverse affects on outcome. There is benefit to patients resuming their activities immediately after whiplash injury. There is no benefit conferred by the use of soft-collar orthosis. Those patients who were instructed to “act as usual” had decreased subjective symptoms of pain, stiffness, memory and concentration deficits, as well as improved visual analog scale measurements of pain at 6 months after injury when compared to patients who were given time off work and immobilized in a soft neck collar for 14 days.27,28 Prescribing a specific home exercise program is beneficial for reducing whiplash injury pain. It has been shown that early active intervention with 1 instructional visit with physical therapy is superior to initial immobilization with a soft collar.29 The first line of oral medications for neck pain from whiplash injury includes nonsteroidal anti-inflammatory drugs, opioid analgesics, and muscle relaxants.4 It is generally best to try different nonsteroidal antiinflammatory drugs sequentially, looking for a favorable response. If there seems to be a component of central sensitization or a neuropathic etiology of the patient’s pain, it may be worthwhile to try a more centrally acting medication such as gabapentin or pregabalin. A study of intravenous steroids administered within 8 hours from injury showed decreased pain at 1 week and decreased number of sick days taken, but no correlation with decreased pain at 6 months.30 A short course of oral steroids, Medrol dose pack, is effective in reducing radicular pain due to a herniated disk.
Chronic Physical therapy for chronic neck pain from whiplash focuses on the neck and shoulder area, increasing endurance, stretching to improve range of motion, and body mechanics training to help patients overcome pain avoidance and fear of engaging in unsupervised exercise.4 More invasive interventions in the chronic phase of whiplash injury include radiofrequency nerve ablation, anesthetic and steroid injections to the facet joints, epidural steroid injections, and trigger point botulinum toxin injections. DM, December 2009
There are no studies to date showing significant clinical or functional benefit of botulinum toxin A trigger-point injections in treating WAD.4,31
Prognosis If the pain generator in the acute phase is from partial tear of soft tissues, there is no evidence that persistence of this injury would cause pain in the long term. Based on animal models and general observation, soft-tissue injuries should heal within 4-6 weeks.1,2 There does not appear to be a psychological, personality-based, or sociodemographic profile that predicts prognosis following whiplash injury. Other studies on the psychological symptoms of whiplash reveal a characteristic profile of patients with whiplash injury that show heightened somatisation, obsessive-compulsive, and depression subscales of a psychological symptom checklist called the SCL-90 R, the McGill Pain Questionnaire, and a visual analog pain scale. This particular profile was unable to be faked by people enrolled in the study who were instructed to answer questions as if they were trying to convince a clinician that they had whiplash.32 These studies and the dearth of literature showing statistically significant premorbid “profiles” of patients who develop chronic WAD should steer the clinician to take the whiplash patient’s complaints seriously and evaluate each patient with whiplash injury as an individual with valid complaints. While all symptoms may not be clearly linked to demonstrated pathology, the distress of chronic pain from any mechanism of injury is real and can be debilitating.
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