INTRODUCTION	Section 2 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Background: 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 is the most common sequela of nonfatal car injuries. Whiplash is one of the most poorly understood disorders of the spine, and the severity of the trauma often is not correlated with the seriousness of the clinical problems (Riley, 1995). A history of neck injury is a significant risk factor for chronic neck pain (Croft, 2001). Pretorque of the head and neck increases facet capsular strains, supporting its role in the whiplash mechanism (Winkelstein, 2000).

The Quebec Taskforce on Whiplash-Associated Disorders has suggested the following system for classifying the severity of cervical sprains (Spitzer, 1995): 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.

Pathophysiology:

Relevant anatomy and physiology

Consistent with known biologic models, injury to bony, articular (disks and facets), nerve (including root and spinal cord), and soft tissues of the cervical spine (ligament, tendon, muscle) 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 recruitment of surrounding muscles 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 whiplash-like loads of combined shear, bending, and compression forces; this mechanism provides a mechanical basis for injury caused by whiplash loading (Siegmund, 2001).

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 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 both 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 (Anderson, 2001).

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 (Igarishi, 2004).

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 (Bogduk, 2002). 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 recruitment of surrounding muscles to splint the injured muscle.

Classic mechanism of whiplash injury

A collision in any direction can cause chronic whiplash (Ferrari, 2001).

In a clinical review, Barnsley et al described the classic whiplash scenario in which the patient's car was struck from behind (ie, rear ended) (Barnsley, 1993). 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 (Pearson, 2005). Direct facial impact has shown a flexion motion of the upper or middle cervical spine with extension of the lower cervical spine (Fukushima, 2006).

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 (Kumar, 2005).

When a rear impact is offset to the subject's left, it results in not only increased electromyographic activity in both sternocleidomastoids, but also the splenius capitis contralateral to the direction of impact bears part of the force, thus causing injury (Kumar, 2004). 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 visa versa (Kumar, 2005). 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 (Kumar, 2005).

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, suggesting genetic, hormonal, structural, or tolerance differences from males (Stemper, 2004).

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 occurred at C5-6 and C6-7 also occurred with head-turned impact (Panjabi, 2006). Head-turned rear impacts up to 8 G do not typically injure the alar, transverse, and apical ligaments (Maak, 2006).

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 stenotic foramen, the risk greatly increases to include C3-4 through C6-7 (Tominaga, 2006).

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 (Ito, 2004). 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 (Tropiano, 2004).

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 (Anderson, 2001). 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 (Cusick, 2001).

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 (Kumar, 2002).

The risk of whiplash injury in motor vehicle collisions increases when subjects are surprised and unprepared for the impact (Siegmund, 2003).

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 a peak of 4.5-5 G of vertical or axial acceleration and 1.5 G of lateral acceleration over approximately 100 ms on both. 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 suggest 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 (Freeman, 2005).

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, as a result 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 injury to the spinal cord that results in quadriparesis (Ino, 2004).

Postmortem studies have shown that ligamentous injuries are common after whiplash injuries, but disk herniation is a rare event (Mercer, 1999).

In 1 study, 33% of patients with whiplash injury had disk herniations with medullary or dura impingement over 2-year follow-up after injury (Pettersson, 1997).

In another study, whiplash-type distortions are associated with a 16% incidence of diskoligamentous injuries. On 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 (Jonsson, 1994).

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 (Barnsley, 1994).

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 cord signs.

MRI or CT myelography are necessary for the diagnosis (Chen, 2000).

Frequency:

• In the US: 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% (Dreyer, 1998).

  Estimates indicate that more than 1 million whiplash injuries occur each year due to automobile accidents. Barnsley et al estimate that the annual incidence of symptoms due to whiplash injury is 3.8 cases per 1000 population (Barnsley, 1994). Freeman et al cautiously estimate that 6.2% of the US population, or 15.5 million individuals, have late whiplash syndrome (Freeman, 1999).

• Internationally: 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 also 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 13.5% of women.

Age: The average age of patients with a whiplash injury is the late fourth decade.

	CLINICAL	Section 3 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

History: The most common symptoms of cervical disorders are suboccipital headache, ongoing or motion-induced neck pain, or both. Other symptoms associated with cervical strain include the following:

• Neck pain

• At the time of accident, neck pain may be minimal, with an onset of symptoms during the subsequent 12-72 hours.

• Nonspecific neck and shoulder pain (a variety of cervical radiculopathies) may indicate an injury to a disk in the upper cervical spine (Chen, 2000).

• Headache

• Headache is a frequent symptom of cervical strain.

• Neck structures play a role in the pathophysiology of some headaches, but the clinical patterns have not been defined adequately.

• Increased muscle hardness (determined by palpation) is significantly increased in patients with chronic tension-type headaches.

• Facet joints and intervertebral disk damage have been implicated in the pathology of headaches due to neck injury (Anderson, 2001).

• No specific pathology on imaging or diagnostic studies has been correlated with cervicogenic headaches (Heldeman, 2001).

• Shoulder, scapular, and/or arm pain

• Visual disturbances (eg, blurred vision, diplopia)

• Tinnitus

• Dizziness: This may result from injury to facet joints that are supplied with proprioceptive fibers that when injured can cause confused vestibular and visual input to the brain (Anderson, 2001).

• Concussion

• Neurologic symptoms: These may include weakness or heaviness in the arms, numbness, and paresthesia.

• Difficulty sleeping due to pain

• Disturbed concentration and memory

• Late whiplash syndrome includes symptoms such as headache, vertigo, disturbances in concentration and memory, difficulty swallowing, and impaired vision. These cognitive impairments remain poorly understood.

• Many patients with these changes have abnormal results on single photon emission CT (SPECT) scans or P300 event-related potentials (Lorberboym, 2002).

• Bladder or bowel dysfunction: These may be symptoms of complication of myelopathy (spinal cord involvement).

Physical: 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.

• Observation of the patient's general appearance: This may yield information about pain behavior, verbal or nonverbal.

• Spinal examination

• During the postural assessment, the clinician may note the following findings: stiffness of the neck, forward head, flexed neck, rounded shoulders, asymmetry of the neck or shoulders, neck tilt or rotation, and 1 shoulder higher or tighter than the other.

• Palpation may reveal rigidity (loss of motion or postural abnormality), spasm tightness, muscle hardness, crepitation, swelling, enlargement of joints, tenderness, tender points, and trigger points. Palpation of the zygapophysial joints may be helpful in determining the painful joints either because of osteoarthritis or posttraumatic irritation of the joint capsule.

• ROM: Decreased active and passive ROM may be noted. Impaired cervical ROM (particularly in the sagittal plane) is useful in distinguishing between asymptomatic persons and those with persistent whiplash-associated disorders (Dall'Alba, 2001). Special methodology for measuring cervical ROM compared chronic whiplash and healthy subjects. Using mean coefficient of variation (MCV) and total cervical range of motion (TCROM), the TCROM was significantly lower and the MCV was significantly higher in injured patients as compared with healthy individuals (Prushansky, 2006).

• After acute whiplash injury, neck mobility is significantly reduced, but mobility is similar between patients with whiplash injury and in control subjects after 3 months (Kasch, 2001).

• Special maneuvers: Cervical neurocompression may cause parascapular or arm pain by narrowing the neural foramen (causing nerve root compression) or by causing pressure on the facet joints.

• Neurologic examination

• Mental status: Mood disturbance, such as anxiety or depressive affect, may be noted.

• Motor function: If cervical radiculopathy is present, the strength or bulk of the upper extremities may be decreased. If myelopathy is present, weakness of upper and lower extremities may be noted.

• Circumference: The dominant arm and forearm is usually slightly larger than the nondominant side.

• Reflexes: In cervical radiculopathy, muscle stretch reflexes (MSRs) may be decreased in a myotomal pattern in the affected upper limb; however, they should remain normal in the lower limbs. By contrast, in cervical myelopathy (cervical spinal cord involvement), the MSRs arising from a given level of the cord may be decreased in the upper limbs; however, MSRs in the lower limbs may be increased, with spasticity of the lower extremities, a positive Babinski sign, and a positive Hoffman sign.

• Sensation: If cervical radiculopathy is present, pain or 2-point discrimination of light tough may be reduced in a radicular pattern in the upper extremities.

• Coordination: With radiculopathy or myelopathy, coordination may be decreased in the involved upper extremity.

• Gait: In cases of cervical myelopathy, the patient's gait pattern may be abnormal as a result of spasticity. The presence of spasticity implies an upper motor neuron dysfunction, in contrast to injury to the peripheral nerves.

• Provocative maneuvers: The Spurling test uses cervical extension and lateral bending while the examiner applies a downward axial load). This test may provoke (reduce) radicular symptoms in a patient with cervical radiculopathy.

Causes:

• Common traumatic events or factors that may lead to cervical strain/sprain injuries include motor vehicle accidents, lifting or pulling heavy objects, awkward sleeping positions, unusual upper-extremity work, and prolonged static positions.

• Flexion/extension injuries may precipitate a myeloradiculopathic presentation in a patient with cervical spondylosis. Nerve root or spinal cord compression may occur from neural ischemia due to the preexisting stenosis that accompanies cervical spondylosis. Flexion-extension injuries, blows to the head, or neck injury while lifting heavy objects may precipitate an acute exacerbation of cervical spondylosis.

• Repetitive or abnormal postures may contribute to cervical sprains and strains.