Updated: Jul 15, 2009
Cervical strain is one of the most common musculoskeletal problems encountered by generalists and neuromusculoskeletal specialists in the clinic.
One cause of cervical strain is termed cervical acceleration-deceleration injury; this is frequently called whiplash injury.
Whiplash, one of the most common sequela of nonfatal car injuries, is one of the most poorly understood disorders of the spine, and the severity of the trauma is often not correlated with the seriousness of the clinical problems.1 A history of neck injury is a significant risk factor for chronic neck pain.2 Pretorque of the head and neck increases facet capsular strains, supporting its role in the whiplash mechanism.3
The Quebec Taskforce on Whiplash-Associated Disorders has suggested the following system for classifying the severity of cervical sprains4 :
Related eMedicine topics:
Cervical Facet Syndrome
Cervical Spine Sprain/Strain Injuries
Cervical Strain
Neck Trauma
Related Medscape topic:
Resource Center Spinal Disorders
Relevant anatomy and physiology
Consistent with known biologic models, injuries to bony, articular (disks and facets), nerve (including root and spinal cord), and soft (ligament, tendon, muscle) tissues of the cervical spine are the most likely sources of dysfunction and pain. Cervical strain is produced by an overload injury to the muscle-tendon unit because of excessive forces on the cervical spine. The cause is thought to be the elongation and tearing of muscles or ligaments. Secondary edema, hemorrhage, and inflammation may occur.
Many cervical muscles do not terminate in tendons but attach directly to the periosteum. Muscles respond to injury by contracting, with surrounding muscles recruited in an attempt to splint the injured muscle. Myofascial pain syndrome, which is thought to be the resultant clinical picture, may be a secondary tissue response to disk or facet-joint injury.
Facet capsular ligaments have been shown to contain free (nociceptive) nerve endings, and distending these ligaments by administering facet joint injections has produced whiplash-like pain patterns in healthy individuals. The cervical facet capsular ligaments may be injured under whiplashlike loads of combined shear, bending, and compression forces; this mechanism provides a mechanical basis for injury caused by whiplash loading.5
Chronic pain associated with cervical strains is most likely to affect the zygapophysial (facet) joints, intervertebral disks, and upper cervical ligaments. The C2-3 facet joint is the most common source of referred pain in patients with a dominant complaint of headache (60%). The C5-6 region is the most common source of cervical, axial, and referred arm pain. Cervical facet joint pain is typically a unilateral, dull, and aching neck pain with occasional referral into the occiput or interscapular regions. The cervical facet joints can be responsible for a substantial portion of chronic neck pain. The cervical facet joints refer pain overlapping with both myofascial and diskogenic pain patterns.
Neuroanatomic studies reveal that the facet joint is richly innervated and contains free and encapsulated nerve endings. The facet capsule is richly innervated with C fibers and A-delta fibers. Many of these nerves are at a high threshold and likely to indicate pain. Local pressure and capsular stretch can mechanically activate these nerves. These neurons can be sensitized or excited by naturally occurring inflammatory agents, including substance P and phospholipase A.
Physiologic changes in the spinal cord, particularly the pain complexes of the dorsal horn, implicate excitatory amino acids, such as substance P, glutamate, gamma-aminobutyric acid (GABA), and N -methyl-D-aspartate (NMDA), as well as other factors that sensitize the dorsal horn in chronic pain. The mechanism is massive input of noxious stimuli from cervical spine injury.6
In lumbar spine studies, inflammatory cytokines are found at high levels in facet joint tissue when a degenerative disorder is present. Facet joints are covered by hyaline cartilage and enclosed with synovium and joint capsules. This basic structure is found throughout the spine and in the joints of the arms and the legs.7
According to Bogduk, results of postmortem studies, biomechanical studies, and clinical studies converge to suggest that the zygapophysial joints are injured in cases of whiplash. Clinical studies have shown that pain in the zygapophysial joint is common in patients with chronic neck pain after whiplash injury.8 Injury was sustained to cervical facet capsular ligaments as a result of the combined shear, bending, and compression load levels that occur in rear-end impacts.9
An overload injury to the muscle-tendon unit produces cervical strain because of excessive forces on the cervical spine. This injury is accompanied by elongation and tearing of muscles or ligaments, secondary edema, hemorrhage, and inflammation. Many cervical muscles attach directly to bone (periosteum), and the muscle response to injury is contraction, with surrounding muscles recruited to splint the injured muscle.
Classic mechanism of whiplash injury
A collision in any direction can cause chronic whiplash.10
In a clinical review, Barnsley and colleagues described the classic whiplash scenario in which the patient's car has been struck from behind (ie, rear ended).11 This type of accident typically occurs in the following manner:
Frontal impact causes middle C2-3 to C4-5 and lower C6-7 and C7-T1 injury.12 Direct facial impact has shown a flexion motion of the upper or middle cervical spine, with extension of the lower cervical spine.13
The forces involved in an impact speed of 20 mph (32 km/h) cause the human head to reach a peak acceleration of 12 G during extension. If the head is in slight rotation, a rear impact forces the head into further rotation before extension, prestressing various cervical structures, such as the capsules of the zygapophysial joints, intervertebral disks, and the alar ligament complex. These structures are thus rendered susceptible to injury. Muscle injury may be less likely after low-velocity impacts with head rotation at the time of impact than they are in other mechanisms.14,15,16,17,18
When a rear impact is offset to the subject's left, it not only results in increased electromyographic activity in both sternocleidomastoids, it also the causes the splenius capitis contralateral to the direction of impact to bear part of the force, thus causing injury. Which muscle responds most to a whiplash-type injury is determined by the direction of head rotation. The sternocleidomastoid on the right responds most with the head rotated to the left, and vice versa. Measures to prevent whiplash injury need to account for the symmetric muscle response caused by victims looking to the right or left at the time of collision.
Lower cervical facet joints respond with a shear plus distraction mechanism in the front and shear plus compression in the back. In studies, females were more likely to be injured than were males, possibly owing to sex-related genetic, hormonal, structural, or tolerance differences.19
Head-turned rear impact also causes significantly greater injury at C0-1 and C5-6 as compared with head-forward rear and frontal impacts. Multiplanar injury that occurs at C5-6 and C6-7 has also been found to occur with head-turned impact.20 Head-turned rear impacts up to 8 G do not typically injure the alar, transverse, and apical ligaments.21
Head-turned impact also causes dynamic cervical intervertebral narrowing, indicating potential ganglion compression even in patients with a nonstenotic foramen at C5-6 and C6-7. In patients with a stenotic foramen, the risk greatly increases to include C3-4 through C6-7.22
A rear-end collision is most likely to injure the lower cervical spine, with intervertebral hyperextension at a peak acceleration of 5 G and above.23,24 The first substantial increase in intervertebral flexibility occurs at C56 following 5-G acceleration. At accelerations faster than this, the injuries spread to the surrounding levels (C4-5 to C4-T1). The 2 injury phases during whiplash are (1) hyperextension at C5-6 and C6-7 and mild flexion at C0-4 and (2) hyperextension of the entire cervical spine.25
An instantaneous change occurs in the pivot point at C5-6, causing a jamming effect of the inferior facet of C5 on the superior facet of C6.6 The nonphysiologic kinematic responses that occur during a whiplash impact may induce stresses in upper cervical neural structures or in lower facet joints. The result may be compromise sufficient to elicit neuropathic or nociceptive pain.26
The muscular component of the head-neck complex plays a central role in the abatement of higher acceleration levels; it may be a primary site of injury in the whiplash phenomenon. Muscle responses are greater with faster accelerations than with slower ones.27 Cervical muscle strains induced during a rear-end impact are greater than the injury threshold that had previously been reported for a single stretch of active muscle, with larger strains in the extensor muscles being consistent with clinical reports of pain in the posterior cervical region after the occurrence of a rear-end impact.28
The risk of whiplash injury in motor vehicle collisions increases when subjects are surprised and unprepared for the impact.29
One of the most important studies of cervical spine injury is of a case series of roller coaster injuries. The roller coaster studies have shown, over approximately 100 ms, a peak of 4.5-5 G of vertical or axial acceleration and 1.5 G of lateral acceleration. During the 19-month study period, 656 neck and back injuries were studied. The injuries included disk herniations, bulges, and compression fractures. The results of the study suggested that a minimum threshold of significant spine injury is not established. The greatest explanation for injury from traumatic loading of the spine was thought to be individual susceptibility to injury, which is an unpredictable variable.30
Complications
Cervical myeloradiculopathy is a complication of flexion/extension injuries in patients with underlying spondylosis. Cervical disks may become painful as part of the degenerative process, because of of repetitive microtrauma or a single excessive load. Pain due to a disk injury may result from annular tears with inflammation or compression of the local nervous or vascular tissue.
Cord compression after whiplash due to physiologic extension loading is not likely. However, individuals with a narrow spinal canal have an increased risk of quadriparesis-causing injury to the spinal cord.24
Postmortem studies have shown that ligamentous injuries are common after whiplash injuries, but disk herniation is a rare event.31
In one study, 33% of patients with whiplash injury had disk herniations with medullary or dura impingement over 2-year follow-up after injury.32
In another study, whiplash-type distortions were associated with a 16% incidence of diskoligamentous injuries. On magnetic resonance imaging (MRI), most patients with severe, persisting, radiating pain had large disk protrusions that were confirmed as herniations at surgery. Neck and radiating pain were alleviated with early disk excision and fusion.33
Strain or tears of the anterior annulus and the alar portions of the posterior longitudinal ligament (when stretched by a bulging disk) are possible causes for diskogenic pain after whiplash injury. Injuries of the zygapophysial joint found in clinical and cadaveric studies include fracture, bleeding, rupture or tear of the joint capsule, fracture of the subchondral plate, contusion of the intra-articular meniscus, and fracture of the articular surface.34
Upper cervical disk protrusions as a result of cervical strain injury may result in nonspecific and shoulder pain. Motor weakness or reflex or sensory abnormalities may be limited or nonspecific. Radiculopathy is more likely than are cord signs.
MRI or computed tomography (CT) myelography are necessary for the diagnosis.35
Almost 85% of all neck pain is thought to result from acute or repetitive neck injuries or from chronic stresses and strain. Dreyer and Boden showed that, in the general population, the 1-year prevalence rate for neck and shoulder pain is 16-18%.36
Estimates indicate that more than 1 million whiplash injuries occur each year due to automobile accidents. Barnsley and colleagues estimated that the annual incidence of symptoms due to whiplash injury is 3.8 cases per 1000 population.34 Freeman and co-investigators cautiously estimated that 6.2% of the US population, or 15.5 million individuals, have late whiplash syndrome.37
The annual incidence in Switzerland is 0.44 cases per 1000 population. In Norway, a rate of 2 cases per 1000 population has been reported. The approximate annual incidence in Western countries is 1 case per 1000 population.
Chronic neck pain, regardless of its cause, is identified in 9.5% of men and in 13.5% of women.
On average, patients with a whiplash injury are in their late fourth decade.
The most common symptoms of cervical disorders are suboccipital headache and/or ongoing or motion-induced neck pain. Other symptoms associated with cervical strain include the following:
The physical examination is a vital part of the diagnosis of cervical stress and strain injuries. Various signs and symptoms may be noted during the physical examination.
Cervical Radiculopathy
Factitious Disorder
Polymyalgia Rheumatica
Traumatic Brain Injury: Definition,
Epidemiology, Pathophysiology
Cervical herniated disk
Cervical myelopathy
Cervical osteoarthritis
Infection or osteomyelitis
Inflammatory rheumatologic disease
Malingering
Psychogenic pain disorder
Referred pain from cardiothoracic structures
Tumor or malignancy of cervical spine
Vascular abnormality of cervical structures
Early rehabilitation helps to prevent chronic pain and disability. Passive modalities include the application of heat, ice, electrical stimulation, massage, myofascial release, and traction. Passive modalities are often used to decrease pain or inflammation and to facilitate participation in an active rehabilitation program, which often involves stretching and strengthening. Extended use of passive modalities without a more active program is generally inappropriate.
Active treatment refers to therapeutic exercises that are aimed at improving the patient's strength, endurance, flexibility, posture, and body mechanics. The goal is to obtain an independent home program or community fitness program at the conclusion of formal physical therapy. The typical therapy prescription is recommended 3 times per week for 4-8 weeks.
Scientific evidence for the physiotherapeutic management of whiplash is sparse. An early, active strategy is recommended to improve functions, increase activity, and prevent chronicity.52 In patients with whiplash-associated disorders caused by a motor vehicle collision, treatment with frequently repeated active submaximal movements combined with mechanical diagnosis and therapy is more effective in reducing pain than is a standard program of initial rest, use of a soft collar, and gradual self-mobilization.53
In patients with whiplash-associated disorders, active intervention is more effective than standard intervention in reducing pain intensity and sick leave, as well as in retaining/regaining total ROM. Appropriately trained healthcare professionals can start and support active intervention, that is, frequently repeated, active cervical rotation, which can be followed, if needed, by assessment and intervention according to the McKenzie protocol.54 Strength and endurance training for 12 months are effective for decreasing pain and disability in women with chronic, nonspecific neck pain. Stretching and fitness training are commonly advised for patients with chronic neck pain, but stretching and aerobic exercising alone are less effective than strength training.55
Specific neck exercises for the management of chronic neck pain, including active activation of the deep neck muscles and dynamic strengthening, may significantly improve disability scores.56 Consistent evidence (from 2 randomized, controlled trials) supports mobilization as an effective, noninvasive intervention for acute whiplash-associated disorders.57,58
In examining the costs and consequences of 2 types of intervention after whiplash trauma in automobile crashes, active intervention using physical therapy was found to be less costly and more effective than short-term immobilization using a cervical collar followed by a gradual self-exercise program taught by a leaflet.59
Another study questioned the efficacy of therapeutic interventions. The report found that 1 year after whiplash injury, a strategy employing immobilization, "act-as-usual," or mobilization had a similar effect to the other 2 methods in terms of pain prevention, disability, and work capability.60
Occupational therapy may be indicated unless a concurrent problem involves a distal upper-extremity function or ergonomic factors in causation. A workstation ergonomic evaluation may be indicated if biomechanical stresses of work activity are factors in the causation or exacerbation of the condition.
The degree of neck pain or dysfunction can be evaluated by using standardized scales. The choice of a scale should be tailored according to the target population and the purpose of evaluation. The Neck Disability Index is useful for evaluating groups of patients, and the Patient Specific Scale is an effective tool for assessing individual patients.61
Upon review of several randomized, controlled trials and epidemiologic studies regarding medical and surgical interventions, published since 1993, moderate evidence exists in support of radiofrequency neurotomy. Evidence for steroid injections, botulinum treatments, and cervical diskectomy is conflicting or unclear.57,58
Early and appropriate treatment with analgesics for pain relief, with anti-inflammatory agents for inflammation, with muscle relaxants for spasms, and with aids for sleep disturbance, are the mainstay pharmaceutical therapies for cervical sprain/strain injuries.
Pain control is essential to high-quality patient care. Nonnarcotic analgesics ensure patient comfort and promote pulmonary toilet. These medications have sedating properties, which are beneficial for patients who have traumatic injuries.
DOC for treatment of pain in patients with documented hypersensitivity to aspirin or NSAIDs or in patients with upper GI disease or who are taking oral anticoagulants
1000 mg PO qid
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 doses in 24 h
Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity can occur in patients with chronic alcoholism, with various dose levels of acetaminophen; severe or recurrent pain or high or continued fever may indicate serious illness
These agents are indicated for the medical treatment of moderate to severe pain.
For relief of moderate to severe pain. Dose available with 2.5, 5, 7.5, 10 mg of hydrocodone. Total daily dose of acetaminophen should be considered; not to exceed 4 g/d. Individualize dose from qd to q4h, depending on degree of pain, effect of pain on patient's lifestyle, and need to keep blood levels of analgesic at therapeutic dose consistently or only intermittently.
1-2 tab or cap PO q4-6h prn
Do not exceed the following doses of hydrocodone bitartrate:
<2 years: 1.25 mg PO q4-6h prn
2-12 years: 5 mg PO q4-6h prn
>12 years: 10 mg PO q4-6h prn
Phenothiazines may decrease analgesic effects; toxicity can increase with concurrent CNS depressants or tricyclic antidepressants
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Tablets contain metabisulfite, which may cause hypersensitivity; caution in patients dependent on opiates (substitution may result in acute opiate-withdrawal symptoms); caution in severe renal or hepatic dysfunction; alcohol intake may result in excessive sedation or liver toxicity; dependency may occur with use of hydrocodone
Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional nonsteroidal anti-inflammatory drugs (NSAIDs). Ongoing analysis of cost avoidance of GI bleeds will further define the populations for whom COX-2 inhibitors are most beneficial.
COX-1 is important for platelet aggregation, regulation of blood flow in the kidney and stomach, and regulation of gastric acid secretion. Inhibition of COX-1 may contribute to NSAID GI toxicity. COX-2 is considered an inducible isoenzyme, being induced during pain and inflammatory stimuli. Celecoxib inhibits primarily COX-2. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek the lowest dose for each patient.
200 mg PO bid
Not established
Coadministration with fluconazole may increase plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease celecoxib plasma concentrations
Documented hypersensitivity to sulfonamides
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing patient to fluid retention; severe heart failure and hyponatremia, because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction or abnormal liver laboratory results
These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well; these include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation and various cell-membrane functions.
Nonacidic NSAID rapidly metabolized after absorption to a major active metabolite that inhibits cyclooxygenase enzyme, which in turn inhibits inflammation.
1000-2000 mg PO qd
Not established
Probenecid may increase toxicity of NSAIDs; coadministration with ibuprofen may decrease effects of loop diuretics; coadministration with anticoagulants may prolong PT (watch for signs of bleeding); NSAIDs may increase serum lithium levels and risk of methotrexate toxicity (eg, stomatitis, bone marrow suppression, nephrotoxicity)
Documented hypersensitivity; active peptic ulcer disease, hepatic impairment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Elderly patients may require decreased doses; caution in hepatic and renal impairment
These medications are indicated for the relaxation of increased muscle tone, spasm, and rigidity associated with cervical strain syndromes.
Indicated for treating muscle spasm in patients with cervical strain. Centrally acting muscle relaxant metabolized in the liver and excreted in urine and feces.
2-8 mg PO tid; may give in small dose at night, eg, 2-4 mg, to help decrease spasms that interfere with sleep
Not established
May interact with alcohol (increase somnolence, stupor) and oral contraceptives (which decrease its clearance); can cause increased hypotensive effects with concurrent diuretics
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal impairment
Short-acting medication that may have depressant effects at the spinal cord level.
350 mg PO tid/qid
Not established
Increases toxicity of alcohol, CNS depressants, MAOIs, clindamycin, phenothiazine
Documented hypersensitivity; acute intermittent porphyria
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal and hepatic impairment
Skeletal muscle relaxant that acts centrally and reduces motor activity of tonic somatic origins, influencing alpha and gamma motor neurons. Structurally related to tricyclic antidepressants and thus has some of their disadvantages.
20-40 mg/d PO divided bid/qid; not to exceed 60 mg/d
Not established
Coadministration with MAOIs and tricyclic antidepressants may increase toxicity; may have additive effect with concurrent anticholinergics; may enhance effects of alcohol, CNS depressants, and barbiturates
Documented hypersensitivity; patients who have taken MAOIs within last 14 d
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients with angle-closure glaucoma, and urinary hesitance
Reduces nerve impulse transmission from spinal cord to skeletal muscle.
1.5 g PO qid for 2-3 d and decrease to 4-4.5 g/d in 3-6 divided doses
Not established
Increases toxicity of CNS depressants
Documented hypersensitivity; renal impairment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients with history of seizures
Disturbed sleep is often a significant symptom with cervical strain. If analgesics and muscle relaxants do not provide enough relief, medications such as low-dose antidepressants can be used. These agents have central and peripheral anticholinergic effects, as well as sedative effects.
Analgesic for certain types of chronic and neuropathic pain.
10-40 mg PO qhs (50-150 mg may be necessary in some individuals)
Children: 0.1 mg/kg PO qhs; increase, as tolerated, over 2-3 wk to 0.5-2 mg/d qhs
Adolescents: 25-50 mg/d PO initially; increase gradually to 100 mg/d in divided doses
Phenobarbital may decrease effects; coadministration with inhibitors of CYP2D6 enzyme system (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram
Documented hypersensitivity; use of MAOIs in past 14 d; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention; acute recovery phase after MI; prostate enlargement with urinary retention
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in elderly patients with cardiac disease, arrhythmias, urinary retention (particularly due to prostate enlargement), angle-closure glaucoma; history of hyperthyroidism, and renal or hepatic impairment
These agents are used for severe inflammation (eg, radiculopathy) caused by the release of inflammatory chemicals from disk injury. These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, they modify the body's immune response to diverse stimuli.
Indicated for treatment of severe pain and/or radiculopathy if inflammation is suspected.
2-60 mg/d PO in 1-4 divided doses followed by gradual reduction to lowest level that can maintain clinical response
Loading dose: 2 mg/kg IV
Maintenance dose: 0.5-1 mg/kg/dose IV q6h for up to 5 d
Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor for hypokalemia when used with concurrent diuretics
Documented hypersensitivity; viral, fungal or tubercular skin infections; labile diabetes, uncontrolled or severe hypertension, and active or recurrent PUD or gastritis
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications
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C-spine sprain, C-spine strain, acceleration/deceleration injury, acceleration-deceleration injury, cervical myofascial pain, cervical soft-tissue pain syndrome, cervical sprain, cervicobrachial strain, chronic cervical sprain, chronic cervical strain, chronic neck sprain, chronic neck strain, extension-flexion injury, extension/flexion injury, flexion-extension injury, flexion/extension injury, hyperflexion-hyperextension injury, hyperflexion/hyperextension injury, neck/shoulder girdle soft-tissue injury, neck sprain, neck strain, regional soft-tissue pain syndrome, WAD, whiplash-associated disorders, whiplash syndrome
Oregon K Hunter Jr, MD, Physiatrist, Southeastern Rehabilitation Medicine, SIMED
Oregon K Hunter Jr, MD is a member of the following medical societies: American Academy of Pain Management, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Legal Medicine, American College of Occupational and Environmental Medicine, American Congress of Rehabilitation Medicine, American Medical Association, Florida Medical Association, Florida Society of Physical Medicine and Rehabilitation, International Association for the Study of Pain, International Society of Physical and Rehabilitation Medicine, National Association of Disability Evaluating Professionals, and North American Spine Society
Disclosure: Nothing to disclose.
Michael D Freeman, PhD, MPH, DC, Clinical Associate Professor of Epidemiology, Department of Public Health and Preventive Medicine, Oregon Health Sciences University; Adjunct Associate Professor of Forensic Medicine and Epidemiology, Institute of Forensic Medicine, Faculty of Health Sciences at Aarhus University, Denmark
Michael D Freeman, PhD, MPH, DC is a member of the following medical societies: American Academy of Forensic Sciences, American Academy of Pain Management, American College of Epidemiology, Association for the Advancement of Automotive Medicine, North American Spine Society, and Sigma Xi
Disclosure: Nothing to disclose.
Martin K Childers, DO, PhD, Associate Professor, Department of Neurology, Wake Forest University Health Services
Martin K Childers, DO, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Congress of Rehabilitation Medicine, American Osteopathic Association, Christian Medical & Dental Society, and Federation of American Societies for Experimental Biology
Disclosure: Allergan pharma Consulting fee Consulting
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
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