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Cervical Sprain and Strain

  • Author: Oregon K Hunter, Jr, MD; Chief Editor: Consuelo T Lorenzo, MD  more...
 
Updated: Dec 28, 2015
 

Background

Cervical strain is one of the most common musculoskeletal problems encountered by generalists and neuromusculoskeletal specialists in the clinical setting. Normal and straightened lordotic lateral cervical curves are shown in the images below.

Radiograph of the lateral cervical spine shows a n Radiograph of the lateral cervical spine shows a normal lordotic curve.
Radiograph of the lateral cervical spine shows str Radiograph of the lateral cervical spine shows straightening of the lordotic curve.

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 sprains[4] :

  • 0: No neck pain complaints, no physical signs
  • 1: Neck pain complaints, only stiffness or tenderness, no other physical signs
  • 2: Neck complaints and musculoskeletal signs (decreased range of motion [ROM] and point tenderness)
  • 3: Neck complaints and neurologic signs (weakness, sensory and reflex changes)
  • 4: Neck complaints with fracture and/or dislocation
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Pathophysiology

Relevant anatomy and physiology

Consistent with known biologic models, injuries to bony, articular (discs 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 disc 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 discs, and upper cervical ligaments. The C2-3 facet joint is the most common source of referred pain in patients with a dominant complaint of occipital 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 discogenic 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.[6]

Cervical extensor muscle function was studied in 15 individuals using muscle functional magnetic resonance imaging (mfMRI) during neck exercises, with and without experimentally induced pain. Function of the cervical extensor muscles was recorded at rest and after the performance of a cervical extension exercise. The authors reported instantaneous decrease in function of the deep and superficial cervical extensor muscle layers following a saline injection into the upper trapezius muscle. The authors conclude that early evaluation of cervical extensor muscle function is appropriate for patients with painful cervical spine injuries.[7]

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.[8]

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.[9]

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.[10] 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.[11]

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.[12]

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).[13] This type of accident typically occurs in the following manner:

  • At the time of impact, the vehicle suddenly accelerates forward. About 100 ms later, the patient's trunk and shoulders follow, induced by a similar acceleration of the car seat.
  • The patient's head, with no force acting on it, remains static in space. The result is forced extension of the neck, as the shoulders travel anteriorly under the head. With this extension, the inertia of the head is overcome, and the head accelerates forward.
  • The neck then acts as a lever to increase forward acceleration of the head, forcing the neck into flexion.

Frontal impact causes middle C2-3 to C4-5 and lower C6-7 and C7-T1 injury.[14] Direct facial impact has shown a flexion motion of the upper or middle cervical spine, with extension of the lower cervical spine.[15]

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 discs, 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.[16, 17, 18, 19, 20]

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.[21]

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.[22] Head-turned rear impacts up to 8 G do not typically injure the alar, transverse, and apical ligaments.[23]

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.[24]

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.[25, 26] 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.[27]

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.[8] 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.[28]

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.[29] 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.[30]

The risk of whiplash injury in motor vehicle collisions increases when subjects are surprised and unprepared for the impact.[31]

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 disc 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.[32]

Complications

Cervical myeloradiculopathy is a complication of flexion/extension injuries in patients with underlying spondylosis. Cervical discs may become painful as part of the degenerative process, because of repetitive microtrauma or a single excessive load. Pain due to a disc injury may result from annular tears with inflammation or compression of the local nervous or vascular tissue.

Spinal cord compression after whiplash due to physiologic extension loading is not likely. However, individuals with a narrow spinal canal, most commonly due to degenerative spinal stenosis, have an increased risk of quadriparesis secondary to the spinal cord compression.[26]

Postmortem studies have shown that ligamentous injuries are common after whiplash injuries, but disc herniation is a rare event.[33]

In one study, 33% of patients with whiplash injury had disc herniations with medullary or dura impingement over 2-year follow-up after injury.[34]

In another study, whiplash-type distortions were associated with a 16% incidence of discoligamentous injuries. On magnetic resonance imaging (MRI), most patients with severe, persisting, radiating pain had large disc protrusions that were confirmed as herniations at surgery. Neck and radiating pain were alleviated with early disc excision and fusion.[35]

Strain or tears of the anterior annulus and the alar portions of the posterior longitudinal ligament (when stretched by a bulging disc) are possible causes for discogenic 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.[36]

Upper cervical disc 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. Cervical radiculopathy is more likely than are pathologic signs of upper motor neuron or spinal cord myelopathy.

MRI or computed tomography (CT) myelography are necessary for the diagnosis.[37]

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Epidemiology

Frequency

United States

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%.[38]

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.[36] Freeman and co-investigators cautiously estimated that 6.2% of the US population, or 15.5 million individuals, have late whiplash syndrome.[39]

International

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.

Mortality/Morbidity

Mortality is rare unless severe trauma causes the cervical strain, with associated brain or spinal cord trauma, respiratory compromise, or vascular injury.

Morbidity includes cervical pain syndromes with associated symptoms. Disability in acute or chronic cervical strains is responsible for significant socioeconomic costs.

Low-energy collisions occurring at less than 6-9 mph (9.7-14.5 km/h) are thought to be unlikely to produce significant neck trauma.

Sex

Chronic neck pain, regardless of its cause, is identified in 9.5% of men and in 13.5% of women.

Age

On average, patients with a whiplash injury are in their late fourth decade.

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Contributor Information and Disclosures
Author

Oregon K Hunter, Jr, MD Physiatrist, Southeastern Rehabilitation Medicine, SIMED

Oregon K Hunter, Jr, MD is a member of the following medical societies: American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners Institute, American College of Legal 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 Examiners, North American Spine Society, American College of Occupational and Environmental Medicine, American Academy of Pain Management, American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Coauthor(s)

Michael D Freeman, MedDr, PhD, MPH Associate Professor of Forensic Epidemiology, CAPHRI School for Public Health and Primary Care, Maastricht University Medical Center

Michael D Freeman, MedDr, PhD, MPH 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, Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Milton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and Ohio Valley General Hospital

Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD Medical Director, Senior Products, Central North Region, Humana, Inc

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Acknowledgements

Martin K Childers, DO, PhD Professor, Department of Neurology, Wake Forest University School of Medicine; Professor, Rehabilitation Program, Institute for Regenerative Medicine, Wake Forest Baptist Medical Center

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

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Radiograph of the lateral cervical spine shows a normal lordotic curve.
Radiograph of the lateral cervical spine shows straightening of the lordotic curve.
MRI of the cervical spine shows disc protrusion.
 
 
 
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