Monograph 22

Cervical Spine Trauma

By R. C. Schafer, DC, PhD, FICC
Manuscript Prepublication Copyright 1997

Copied with permission from   ACAPress

Common Injuries and Disorders of the Cervical Spine
Emergency Care
Initial Assessment
Posttraumatic Roentgenographic Clues
Injury of the Cervical Nerve Roots
  Contributing and Complicating Factors
  Motor Aberrations
  Interpreting Sensory Irregularities
Subluxation-Induced Reflex Syndromes

Neurovascular Implications of Upper Cervical Subluxations
  The Vertebral Arteries
  The Vertebral and Deep Cervical Veins
  Cerebrospinal Circulation
  The Medulla Oblongata
  The Vital Vagus

Classic Effects of Severe Cervical Trauma
  Planes of Force and Their Consequences
  Fractures and Dislocations of the Atlas
  Fractures and Dislocations of the Axis
  Severe C3–C7 Injuries
  Spinal Cord Injury
Vertebral Artery Abnormalities
Cervicothoracic Tunnel Compression Syndromes
  Clinical Features
  Clinical Maneuvers and Tests
Vertebrobasilar System Patency Tests
  Maigne's Test
  DeKleyn's Test
  Hautant's Test
Structural Characteristics of the Cervical Region
  The Upper Cervical Spine
  The Occipitocervical ligaments
  The Lower Cervical Area

  The Upper Cervical Area
  The Lower Cervical Area
  The Transitional Cervicothoracic Area

Applied Anatomy of the Cervical Plexus
The Brachial Plexus
The Cervicothoracic Junction Area

Clinical Management Electives In Cervical Strain/Sprain/IVD Lesion

Extension Strain/Sprain (Whiplash Syndrome)
  Case Management Flexion Strain/Sprain Mechanisms
  Case Management
  Lateral Flexion Strain/Sprain
Occipital and Cervical Subluxation Syndromes
  Functional Anatomy Relative to Cervical Subluxations
  Further Clinical Implications

Cervical Spondylosis
  Clinical Implications
  Clinical Findings
  Case Management and Prognosis

Reversal of the Normal Cervical Curve
  Clinical Findings
  Case Management and Prognosis
Traumatic Brachial Plexus Traction
  Bikele's Test
  Supine Tension Test
  Case Management
The Stinger Syndrome
  Clinical Findings
Subluxation Induced Torticollis
  Clinical Findings
Effects of Cervical Area Hypertonicity

Trigger-Point Syndromes

Barre-Lieou Syndrome
  Clinical Findings
  Barre-Lieou Test

Cervical Disc Disorders
  Disc Encroachment
  Disc Degeneration
  Clinical Findings
  Case Management
Traumatic Cervical Scoliosis
  Effect of a Flattening Curve
  The Self-Stabilization Factor
  Disc Reactions in Cervical Scoliosis
  Effect of Lateral Tilt in Cervical Scoliosis
Cervical Rib Syndromes
  Case Management
Posttraumatic Headaches of Cervical Origin

Posttraumatic Rehabilitation Goals
  Postural Strength and Balance
  Dynamic and Static Proprioception
  Cervical Receptor Input
  Normal Cervical Righting Mechanisms
  Cervical Strength Development
  Rehabilitation Therapy Following Cervical Trauma

References and Bibliography

The cervical spine provides structural stability and support for the cranium, and a flexible and protective column for movement and balance adaptation, along with housing of the spinal cord and vertebral arteries. It also allows for directional orientation of the eyes and ears. Nowhere in the spine is the relationship between the osseous structures and the surrounding neurologic and vascular beds as intimate or subject to disturbance as it is in the cervical region.


Whether induced by trauma or not, cervical subluxation syndromes may be reflected in total body habitus. IVF insults, and the effects of articular fixations can manifest throughout the motor, sensory, and autonomic nervous systems. Many peripheral nerve symptoms in the shoulder, arm, and hand will find their origin in the cervical spine, as may numerous brainstem disorders.

Common Injuries and Disorders of the Cervical Spine

Cervical spine injuries can be classified as

(1)   mild   (eg, contusions, strains);
(2)   moderate   (eg, subluxations, sprains, occult fractures, nerve contusions, neurapraxias);
(3)   severe   (eg, axonotmesis, dislocation, stable fracture without neurologic deficit); and
(4)   dangerous   (eg, unstable fracture-dislocation, spinal cord or nerve root injury).

Spasm of the sternocleidomastoideus and trapezius can be due to strain or irritation of the sensory fibers of the spinal accessory nerves as they exit with the C2–C4 spinal nerves. The C1 and C2 nerves are especially vulnerable because they do not have the protection of an IVF. Radicular symptoms are rarely evident unless an IVD protrusion or rupture is present.


Because of its great mobility, relatively small structures, and weight-bearing role, the cervical spine is a frequent site of severe spinal nerve injury and subluxation/fixations. A large variety of cervical contusions, Grade 1–3 strains and sprains, subluxations, disc syndromes, dislocations, and fractures will be seen as the result of trauma.

The most vulnerable segments to injury are the axis and C5–C6 according to accident statistics. Surprisingly, the atlas is the least involved of all cervical vertebrae. In terms of segmental structure, the vertebral arch (50%), vertebral body (30%), and IVD (30%) are most commonly involved in severe cervical trauma. While the anterior ligaments are only involved in 2% of injuries, the posterior ligaments are involved in 16% of injuries.


In the emergency-care situation, the patient with spinal cord injury must be treated as if the spinal column were fractured, even when there is no external evidence. Immediate and obvious symptom of spinal cord injury parallel those of fractures of the spinal column. The establishment of an adequate airway takes priority over all other concerns except for spurting hemorrhage.

In general, trauma anteriorly to the neck implies soft-tissue damage and possible airway obstruction; trauma posteriorly suggests cervical spine and cord damage; and lateral trauma indicates possible vascular and musculature damage. Due to relative head weight to neck strength and other anatomic differences, neck injury is more critical in the very young.


If there are no severe complaints or recognizable signs of major disability, ask the patient to conduct mild slow active movements if able to do so without discomfort. If slight straight axial compression on the head produces unilateral or bilateral radiating root pain, deep injury must be suspected and precautions taken immediately. After the neck has been evaluated, check possible injury to other parts of the body.

Knee and ankle reflexes can be tested, but the neck should not be moved. Stabilize the neck before assessment of severity. A collapsed patient should never be asked to sit or stand until major disability has been ruled out. The first point in accurate analysis is knowing the mechanism of injury. Without moving the patient, check vital signs and palpate for swelling, deep tenderness, deformity, and throat cartilage stability. When logical, another person should apply gentle bilateral traction on the cervical area via the skull during palpation.

Are there bleeding, spasm, pain, motion restrictions, sensory changes, signs of shock? Limb weakness or dysesthesia indicates nerve root compression. Injuries of the upper airway or alimentary canal feature ventilation abnormalities, stridor, a bubbling wound, subcutaneous emphysema, hoarseness and dysphagia, bloody sputum, nosebleed, bloody vomitus, or unexplained wound tenderness. Injuries to the cervical nerves are suggested by deviation of the tongue, drooping mouth corner, sensory deficits, and Horner's syndrome. Cervical fractures are commonly associated with severe pain, spasm, and joint stiffness.

Vascular injuries feature vigorous bleeding, absent superficial artery pulsations, an enlarging or pulsatile hematoma, and stroke signs. If there is any suggestion of injury to the carotid artery, palpation should be avoided. Such an injury should be suspected if there is a diagonal erythematous contusion on the side of the neck. Palpation may encourage complete carotid occlusion.


On standard lateral and A-P views, the anterior and posterior soft tissues deserve unusually detailed inspection. Signs of widened retrotracheal space, widened retropharyngeal space, displacement of the prevertebral fat stripe, laryngeal dislocation, or tracheal displacement should be sought. Abnormal vertebral alignment may be shown by a loss of the normal lordotic curve or even an acute kyphotic hyperangulation, vertebral body displacement, abnormal dens position, widened interspinous space, or rotation of the vertebral bodies. Abnormal joints may portray unusual IVD-space symmetry or widening of an apophyseal joint space. It is easy to miss lower cervical fractures because they are often obscured on lateral views by the subject's shoulders if proper precautions are not taken.


Neural dysfunction associated with either acute or chronic subluxation syndromes basically manifest as abnormalities in sensory interpretations and/or motor activities. These disturbances may be through one of two primary mechanisms: direct nerve or nerve root disorders or of a reflex nature.

Contributing and Complicating Factors   The common subluxation picture is rarely pure. It is often superimposed on subclinical processes in the mature patient such as weak or scarred tissue, vertebral instability, osteochondrophytic ridges at the uncovertebral joints, apophyseal thickening and exostosis. Canal encroachment can occur by a buckling ligamentum flavum, spinal stenosis, posterior vertebral body spurs, disc protrusions, dura and dentate thickening, arachnoid cysts, dura and arachnoid adhesions, and ossification of the posterior longitudinal ligament.

Loss of disc space, especially in the lower cervical area, may contribute as a source of chronic irritation to an already inflamed root by altering the angulation of involved IVF tunnels. The sequence of inflammation, granulation, fibrosis, adhesion formation, and nerve root stricture may follow, along with a loss in root mobility and elasticity. Fortunately for children, these degenerative changes are not as pronounced during youth.

Motor Aberrations   Nerve root insults from subluxations may manifest as disturbances in motor reflexes and/or muscular strength. Examples include the deep tendon reflexes such as seen in the reduced biceps reflex when involvement occurs between C5 and C6; or the reduced triceps reflex when involvement occurs between C6 and C7. These reflexes must be compared bilaterally to judge whether hyporeflexia is unilateral. Unilateral hyperreflexia is pathognomonic of an upper motor neuron lesion. Prolonged and/or severe nerve root irritation may also produce trophic changes in the tissues supplied.

Interpreting Sensory Irregularities   When direct nerve root involvement occurs on the posterior root of a specific neuromere, it manifests as an increase or a decrease in sensitivity over the dermatome. A typical example is foraminal occlusion or irritating factors exhibited clinically as hyperesthesia, particularly on the dorsal and lateral aspects of the thumb and radial side of the hand, when involvement occurs between C5 and C6. Another example is on the dorsum of the hand, the index and middle fingers, and the ventroradial side of the forearm, thumb, index and middle fingers, when involvement occurs between C6 and C7.

In other instances, nerve root involvement may cause hypertonicity and the sensation of deep pain in the muscles supplied by the neuromere. For example, in C6 involvement, there is deep pain in the biceps. In C7 lesions, there is deep pain in the triceps and supinators of the forearm. Direct pressure near the nerve root or along its distribution may be particularly painful. The pioneer chiropractic art of nerve tracing would be well to acquire.


It is generally accepted that certain spinosomatic and spinovisceral syndromes may result from cervical subluxation complexes. For example, if the involvement is in the C1–C4 area, the cervical portion of the sympathetic chain or the 9th–12th cranial nerves (as they exit from the base of the skull and pass into their compartments within deep cervical fascia) may be involved. The syndrome may include

(1) suboccipital or postocular migraine;
(2) greater occipital nerve extension neuralgia;
(3) mandibular, cervical, auricular, pectoral, or precordial neuralgia;
(4) paroxysmal torticollis;
(5) congestion of the upper respiratory mucosa, paranasal sinuses, or eustachian tube with hearing loss;
(6) cardiorespiratory attacks;
(7) ocular muscle malfunction;
(8) pathologic hiccups;
(9) scalenus anticus syndrome; or
(10) painful spasm in the suboccipital area.

Phillips describes that if a subluxation produces a stretching of the paravertebral musculature, there is a continuous barrage of afferent impulses in the Group Ia fibers. "These afferent impulses monosynaptically bombard the alpha motor neurons causing the paravertebral musculature to go into tetany. There is a cessation of this afferent barrage when the stretch is released. The muscle stretching also initiates afferent impulses in the Group II afferents from flower spray endings, which may reinforce the spastic muscle condition." He explains that trauma to facet joints, disturbed articular relationships, spasms of closely related muscles, and overlying trigger points --all the result of a subluxation-- inaugurate a barrage of flexor-reflex afferent impulses via the Group II–IV fibers that converge on the internuncial pool in lamina 7 of the spinal cord. "This abundant supply of flexor-reflex afferent impulses excites the alpha motor neurons through multisynaptic connections causing an excess of excitation of paravertebral muscles resulting in spasm."


Aside from nerve root dysfunction, subluxation complexes in the cervical spine, especially the upper region, can have serious neurovascular consequences. Function of the vertebral arteries, the vertebral veins and deep cervical veins, cerebrospinal circulation, the caudad medulla oblongata, and the vital vagus nerve may be disturbed.

The artery and vein supplying a spinal nerve course within the IVF between the nerve and the fibrous tissue in the anterior portion of the foramen. Deprived mobility of any one or more segments of the spine correspondingly influences area circulation, and the partial anoxia effected is likely to have a harmful influence on nerve function. Because of the vessels' position, it is unlikely that circulation to the nerve would be disrupted without first irritating or compressing the nerve because the arteries and veins are much smaller, the blood pressure within their lumen makes them somewhat resistant to compression, and nerve tissue is much more responsive to encroachment irritation.

The Vertebral Arteries

Janse explains that any cervical subluxation (particularly atlantal, axial, or occipital) producing muscle spasm may produce unilateral or bilateral constriction of the vertebral arteries resulting in circulatory impairment. A large number of equilibrium, cardiac, respiratory, cranial nerve, extrapyramidal, vagal, visual, and auditory symptoms may follow.

The vertebral nerve (sympathetic) courses along the vertebral artery within the arterial foramen of the cervical transverse processes. Irritation to this nerve can occur from mechanical irritation to the vertebral artery anywhere along its course producing symptoms of a vasomotor nature; eg, headache, vertigo, tinnitus, nasal disturbances, facial pain, facial flushing, and pharyngeal paresthesias. Cailliet points out that although sympathetic fibers have not been found along the cervical roots, surgical decompression of an entrapped nerve root relieves symptoms attributed to the sympathetics. The mechanism for this effect is unclear.

The Vertebral and Deep Cervical Veins.   Spasm of suboccipital muscles may cause a decided impediment of venous drainage from the suboccipital area via vertebral and deep cervical veins. The result is passive congestion with consequent pressure on the sensory nerves in the area. This is often perceived by the patient as unilateral or bilateral pain and a throbbing discomfort. The site may be palpated as knotty lumps within suboccipital muscles. The condition appears to be of a reflex nature that is more common among people under mental tension or those who work closely with their eyes over long periods.

Cerebrospinal Circulation.   Constriction in the connecting area between the cerebral subarachnoid space and the vertebral canal can impair the escape of cerebrospinal fluid into the inferior vertebral canal. This results in increased intracranial pressure. An atlanto-occipital subluxation may cause the dura mater of the cisterna cerebellaris to press against the posterior medullary velum and partially occlude the foramina of Luschka and Magendie and thus interfere with flow from the 4th ventricle. The increased intraventricular fluid accumulation can thus produce a variety of symptoms such as deep-seated stubborn "internal pressure" headaches, nausea, a tendency toward projectile vomiting, bizarre and unusual visual disturbances, and protopathic ataxia.

The Medulla Oblongata.   The medulla extends well into the lower reaches of the foramen magnum and the ligament ring connecting it with the atlas, thus any type of occipital or atlantal subluxation may potentially affect this portion of the brain stem. Bilateral posterior shifting of the occiput or atlas can induce pressure in the pyramids or adjacent olivary bodies producing a syndrome of upper-motor-neuron involvement characterized by a degree of spastic paralysis or ataxia. A lateral shift of the occiput may cause pressure on the tubercle of Rolando producing pain in trigeminal nerve distribution, headache, sinus discomforts, ocular neuralgia, and aches in the jaw.

The Vital Vagus.   As the vagus lies almost in immediate contact with the transverse process of the atlas, rotary subluxation of the atlas may induce pressure that can produce a broad range of symptoms. The syndrome may include nasal and sinus congestion, swallowing and speech difficulties, cardiac arrhythmias, functional coronary artery spasm, gastric and intestinal colic, and/or other symptoms of vagal disturbance.


Planes of Force and Their Consequences

It was briefly brought out earlier that knowing the mechanism of injury is important to accurate diagnosis. This section will confirm this truth.

Compression Forces.   Excessive compression forces on the neck commonly lead to facet jamming and fixation, isolated or multiple fractures of the atlantal ring, or vertical, oblique, and/or bursting fractures of the lower cervical bodies.

Hyperextension Forces.   The effects of forceful posterior bending may include sprain of the anterior ligaments, wedging of the posterior anulus and vertebral body, posterior subluxation, horizontal fracture of the anterior arch of the atlas, fracture of the anteroinferior margin of a vertebral body, compression of the posterior arch and associated structures, posterior bilateral or unilateral dislocation, spinous process fracture, and/or traumatic spondylolisthesis.

Hyperflexion Forces.   Excessive anterior bending may produce sprain of the posterior ligaments, compressive wedging of the anterior anulus and vertebral body, anterior subluxation, anterior bilateral or unilateral dislocation with locked facets, and/or spinous process avulsion. Abnormal widening of a spinous interspace on a lateral roentgenograph should arouse suspicion of ruptured posterior ligaments.

Lateral Hyperflexion Forces.   The effects of excessive lateral bending include transverse process fracture, uncinate process failure, lateral dislocation-fracture of the odontoid process, lateral wedging of the anulus and vertebral body, and/or brachial plexus injury.

Hyperrotary Forces.   Exorbitant segmental rotation about the longitudinal axis produces anterior or posterior ligament torsion overstress, rotary subluxation, spiral loosening of the nucleus pulposus, and/or unilateral or bilateral atlas-axis dislocation. The traumatic stress involved invariably include shear forces.

Shear Forces.   Flagrant shearing forces can disrupt the anterior or posterior ligaments, displace the end-plates, produce anterior or posterior subluxation or dislocation, create anterior or posterior fracture displacement of the dens, and/or cause anterior compressive fracture of the anterior ring of the atlas or vertebral body.

Fractures and Dislocations of the Atlas

Atlanto-occipital dislocations, often bilateral, are usually quickly incompatible with life. Any severe subluxation in the upper cervical area can lead to quadriplegia or death, often with little warning and few symptoms to differentiate it initially from a mild strain/sprain. Thus, it is always better to be especially cautious (and be accused of being too concerned in mild injuries) to insure against a possible disaster. Signs and symptoms vary from subtle to severe pain and gross motor involvement. Tenderness may be acute over the posterior atlas, aggravated by mild rotation and extension.

Fractures and Dislocations of the Axis

Odontoid fractures are often produced by severe forces directed to the head, and the direction of force usually determines the direction of displacement. Suboccipital tenderness may be present. A severe extension force may fracture the odontoid at its base, with possible odontoid posterior displacement. The danger of cord pressure is great. Open-mouth views, flexion-extension x-ray views, or tomography may be necessary for accurate determination.

Severe C3–C7 Injuries

Cervical fractures and dislocations are often the result of a severe fall, an automobile accident, a football pile-up, or a trampoline or gymnastic mishap. Bruises on the face, occiput, and shoulders may offer clues to the mechanism of injury. Seek signs of vertebral tenderness, limitation in movement, muscle spasm, and neurologic deficits. As in upper-cervical damage, careful emergency management is necessary to avoid paralysis and death. Severe fracture or dislocation of any cervical vertebra requires immediate orthopedic referral. Nevertheless. keep in mind that overdiagnosing instability of C2 on C3 is a common error.

Compression or flexion damage is sometimes seen, but extension injuries (eg, whiplash) are more common. Spinous process fractures usually occur at the C6 or C7 level after acute flexion or a blow to the flexed neck producing ligamentous avulsion. There is an immediate "hot" pain in the area of the spinous process that is increased by mild neck flexion. Again, any injury to C6 or C7 can be difficult to view on film because of overlapping structures.

Spinal Cord Injury

There are direct and indirect classes of cephalad spinal cord injuries. Direct injury to the cord, the nerve roots, or both, may be from impact forces or shattered bone fragments. The cord may be crushed, pierced, or cut. These types of injury are generally associated with an open wound. Indirect injury to the cord can be caused by the disturbance of tissues near the spine by violent forces such as falls, crushes, or blows.

When the cervical cord is injured, there is loss of sensation and flaccid paralysis cephally. The lower limbs exhibit spastic paralysis. If the space in which the spinal fluid flows between the spinal cord and the surrounding vertebral column is either compressed or enlarged, severe headache occurs. Posttrauma penile erection strongly suggests either cervical or thoracic cord injury.

Many cervical cord injuries are caused by extreme flexion where subluxation or fracture/dislocation occurs. Hemorrhage arises at the site with the same reaction as brain injury (liquefaction, softening, disintegration). Congenital fusions and stenosis may predispose a child to spinal cord trauma during a sporting activity.


Vertebral artery abnormalities such as deflection and arteriosclerosis must be determined before any form of cervical manipulation or adjustment is performed. Also, arteriosclerosis is no longer thought of as an "old person's disease." Autopsy studies of young soldiers killed in the Viet Nam War showed well established systemic arteriosclerosis in the majority of the 18–21-year age group.

The vertebral artery is a captive vessel from C6 upward. Extremes of rotation and flexion occur at the upper cervical region, but the four normal curves in the vertebral artery help to compensate for neck movements. Deflection may be caused by any tensile stretching of the artery during neck trauma. In later years, deflection is commonly associated with bony spurs from covertebral joints or grossly hyperplastic posterior vertebral articulations from arthrosis.

Smith explains that extension of the cervical spine allows the tip of the superior articular process of the posterior joint to glide forward and upward. If sufficiently hyperplastic, forced motion may cause encroachment on the vertebral arteries and/or the IVFs. Deflection of the artery and any resulting symptoms are exaggerated by rotation and/or extension of the neck. As a result of pressure against the artery, there may be temporary lessening in the volume of blood flow. Atheromatous changes may also occur within the vascular wall. Symptoms include headache, vertigo, nausea, vomiting, nystagmus, and suboccipital tenderness, which may be provoked by cervical extension. Sometimes symptoms are aggravated by dorsal extension and relieved by forward flexion with cervical traction.


The cervicothoracic junction is a unique area that receives far less attention than it deserves in all the healing arts. It is a common site of developmental anomalies; it is a major site of arterial, lymphatic, and neurologic traffic; and it presents the juncture of the highly mobile cervical spine with the very limited thoracic spine. This latter point is biomechanically significant.

Several cervicotrhoracic syndromes fall in the class of neurovascular compression syndromes (also termed thoracic outlet or inlet syndromes), each of which may produce the symptom complex of radiating pain over the shoulders and down the arms, atrophic disturbances, paresthesias, and vasomotor disturbances. These features, however, do not necessarily indicate the specific cause of the problem.

Origin.   Trauma to the head, neck, or shoulder girdle is a common factor. In some cases, poor posture, anomalies, or muscle spasm or contractures may be involved. Reduced tone in the muscles of the shoulder girdle, by itself, has been shown to allow depression of the clavicle that narrows the thoracic outlet and compresses the neurovascular bundle. Subluxation syndromes (eg, retrolisthesis) may also initiate these and other disturbances of the shoulder girdle.

Cervical pathology such as spinal canal or IVF encroachment by a buckling ligamentum flavum, spinal stenosis, or spurs should be a consideration. Degenerating dura and dentates become thickened, dura and arachnoid adhesions become prevalent, and osteochondrophytes may develop from the borders of the canal or foramen --all of which tend to restrict the cord and/or nerve roots during cervical motion.

Osteochondrophytes near the foramen can readily compress the vertebral artery against the nerve root. Differential diagnosis must exclude a cervical rib etiology (rare), infectious neuritis, banding adhesions, arthritis of the shoulder joint, clavicle fracture callus, bifid clavicle, cervical arthritis, subacromial bursitis, 1st rib subluxation and posttraumatic deformities, spinal or shoulder girdle malignancies, Pancoast's tumor of the lung apex, and heart disease. Aneurysm of the subclavian artery is rare.

Anatomical Considerations.   Working above and behind to produce shoulder abduction and retraction (eg, painting a ceiling, repairing a ceiling fixture) produces temporary clavicle encroachment on the brachial plexus and presses the subclavian artery against the scalenus medius. For many years, symptoms were attributed to costoclavicular compression from shoulder depression. However, postmortem stress tests have shown the following:

1.   When the arm is depressed, the clavicle moves inferior and anterior, and this widens the space between the clavicle and 1st rib.

2.   When the shoulder is depressed, the upper and middle trunks of the brachial plexus are stretched tightly over the tendinous edge of the scalenus medius and the lower trunks are pulled into the angle formed by the 1st rib and the scalenus medius tendon. Most symptoms found on shoulder depression will be the result of this traction. There is no compression of the subclavian artery against either scaleni.

3.   When the shoulder is retracted, the clavicle does not impinge the subclavian vein but the tendon of the subclavius muscle compresses the vein against the 1st rib. The middle third of the clavicle pushes the neurovascular bundle against the anterior scalenus medius, and this causes compression if a space-occupying lesion is also present (eg, cervical rib, extrafascial band).

Clinical Features.   Symptoms usually do not occur until after the ribs have ossified. Two groups of manifestation are seen: those of scalenus anticus syndrome and those due to cervical rib pressure. The symptoms of cervical rib and scalenus syndrome are similar, but the scalenus anticus muscle is the primary factor in the production of neurocirculatory compression whether a cervical rib exists or not.

Symptoms usually arise from compression of the lower cords of the brachial plexus and subclavian vessels such as numbness and pain in ulnar nerve distribution. Pain is worse at night because of pressure from the recumbent position, and its intensity varies throughout the day. Arm fatigue and weakness, finger cramps, numbness, tingling, coldness of the hand, areas of hyperesthesia, muscle degeneration in the hand, a lump at the base of the neck, tremor, and/or discoloration of the fingers are characteristic. Work and exercise accentuate symptoms, while rest and elevation of the extremity relieve symptoms. Adson's and other similar compression signs will usually be positive.

Neural vs Circulatory Symptoms.   Compression of nerve tissue results in numbness, pain, paralysis, and loss of function. Compression of vascular structures results in moderate pain and swelling. Obstructed circulation results in clotting within the vessels with possible consequent infarction in the tissues supplied. These unilateral phenomena are somewhat limited to the cervicobrachial distribution.

Clinical Maneuvers and Tests

Posttrauma radiographs should be taken before performing a neurologic or orthopedic test. It is important to rule out possible conditions that would be aggravated by any testing procedure.

Passive Cervical Compression Tests.   Two tests are involved. First, with the patient sitting, the examiner stands behind the patient. The patient's head is laterally flexed and rotated slightly toward the side being examined. The examiner places interlocked fingers on the patient's scalp and gently presses caudally. If an IVF is narrowed, the maneuver will insult the foramen by compressing the disc and further narrowing the foramen, causing pain and reduplication of other related symptoms. In the second test, the patient's neck is extended by the examiner who then places interlocked hands on the patient's scalp and gently presses caudally. If an IVF is narrowed, this maneuver mechanically compromises foraminal diameters bilaterally and causes pain and reduplication of other related symptoms described earlier.

Active Cervical Rotary Compression Test.   The sitting patient should be observed while voluntarily laterally flexing his head toward the side being examined. With the neck so flexed, the patient is instructed to rotate his chin toward the same side, which narrows the IVF diameter on the side of concavity. Pain or reduplication of other symptoms suggests a narrowing of one or more IVFs.

Shoulder Depression Test.   With the patient sitting, the examiner stands behind the subject. The patient's head is laterally flexed away from the side being examined. The doctor stabilizes the patient's shoulder with one hand and applies pressure alongside the patient's head with the palm of the other hand; stretching the dural root sleeves and nerve roots or aggravating radicular pain if the nerve roots adhere to the foramina. Extravasations, edema, encroachments, and conversion of fibrinogen into fibrin can result in interfascicular, foraminal, and articular adhesions and inflammation restricting fascicular glide and the ingress and egress of the foraminal content. Thus, pain and reduplication of other symptoms during the test suggest adhesions between the nerve's dura sleeve and other structures in and about the involved IVFs.

Cervical Distraction Test.   With the patient sitting, the examiner stands to the side of the patient and places one hand under the patient's chin and the other hand under the base of the occiput. Slowly and gradually the patient's head is lifted to remove weight from the cervical spine. This maneuver elongates the IVFs, decreases the pressure on the joint capsules around the facet joints, and stretches the paravertebral musculature. If the maneuver decreases pain and relieves other symptoms, it is a probable indication of narrowing of one or more IVFs, cervical facet syndrome, or spastic paravertebral muscles.

Spurling's Test.   This is a variation of the passive cervical compression test. The patient's head is turned to the maximum toward one side and then laterally flexed to the maximum. A fist is placed on the patient's scalp, and a moderate blow is delivered to it by the other fist. The patient's position produces reduced IVF spaces, and the blow causes a herniated disc to sharply bulge further into the IVF space or to aggravate an irritated nerve root, thus increasing the symptoms.

Adson's Test.   With the patient sitting, the examiner palpates the radial pulse and advises the patient to bend his head obliquely backward to the opposite side being examined, to take a deep breath, and to tighten the neck and chest muscles on the side tested. This maneuver decreases the interscalene space and increases any existing compression of the subclavian artery and lower components (C8 and T1) of the brachial plexus against the 1st rib. Marked weakening of the pulse or increased paresthesiae are signs of pressure on the neurovascular bundle, particularly of the subclavian artery as it passes between or through the scaleni musculature, thus indicating a probable cervical rib. 1st rib, or scalenus anticus syndrome.

Wright's Test.   With the patient sitting, the radial pulse is palpated from the posterior in the downward position and as the arm is passively moved through an 180 arc. If the pulse diminishes or disappears in this arc or if neurologic symptoms develop, it suggests pressure on the axillary artery and vein under the pectoralis minor tendon and coracoid process or compression in the retroclavicular space between the clavicle and 1st rib, and thus be a hyperabduction syndrome.

Eden's Test.   With the patient sitting, the examiner palpates the patient's radial pulse and instructs the patient to pull the shoulders backward firmly, throw the chest out in a "military posture," and hold a deep inspiration as the pulse is examined. The test is positive if weakening or loss of the pulse occurs, suggesting pressure on the neurovascular bundle as it passes between the clavicle and the 1st rib, and thus a costoclavicular syndrome.


Although cerebrovascular accidents are extremely rare following cervical manipulation, a few cases have been reported that justify special evaluation before cervical manipulation. Four clinical tests are described below to evaluate the patency of the vertebrobasilar system. These tests are helpful but not definitive in themselves.

Maigne's Test   The examiner places a sitting patient's head in extension and rotation. This position is held for about 15–40 seconds on each side. A positive sign is indicated by nystagmus or other symptoms of vertebrobasilar ischemia.

DeKleyn's Test   The patient is placed supine on an adjusting table, and the head rest is lowered. The examiner extends and rotates the patient's head, and this position is held for about 15–40 seconds on each side. A positive sign suggests the same as that in Maigne's test.

Hautant's Test   The examiner places a sitting patient's upper limbs so that they are abducted forward with the palms turned upward (supinated). The patient is instructed to close his eyes, and the examiner extends and rotates the patient's head. This position is held loosely for about 15–40 seconds on each side. A positive sign is for one or both arms to drop into a pronated position.


Many injuries of the cervical spine can be attributed to the small curved vertebral bodies, the wide range of movement in many planes, and the more laterally placed intervertebral articulations that require nerve roots to leave the spinal canal in an anterolateral direction. There is greater space within the cervical canal than below, but this space is occupied by cord enlargement to accommodate the brachial and cervical plexuses. The segmental function of these plexuses is shown in Table 1.

Table 1   Segmental Function of Cervical Nerves




Motor to head and neck extensors, infrahyoid, rectus capitis anterior and lateral, and longus capitis.


Sensory to lateral occiput and submandibular area; motor, same as C1 plus longus colli.


Sensory to lateral occiput and lateral neck, overlapping C2 area; motor to head and neck extensors, infrahyoid, longus capitis, longus colli; levator scapulae, scaleni, and trapezius.


Sensory to lower lateral neck and medial shoulder area; motor to head and neck extensors, longus coli, levator scapulae, scaleni, trapezius, and diaphragm.


Sensory to clavicle level and lateral arm (axillary nerve); motor to deltoid, biceps, biceps tendon reflex. Primary root in shoulder abduction, exits between C4-C5 discs.


Sensory to lateral forearm, thumb, index and half of 2nd finger (sensory branches of musculocutaneous nerve); motor to biceps, wrist extensors, brachioradialis tendon reflex. Primary root in wrist extension, exits between C5-C6 discs.


Sensory to second finger; motor to wrist flexors, finger extensors, triceps, triceps tendon reflex. Primary root in finger extension, exits between C6-C7 discs.


Sensory to medial forearm (medial antebrachial nerve), ring and little fingers (ulnar nerve); motor to finger flexors, interossei; no reflex applicable. Primary root in finger flexion, exits between C7-T1 discs.


Sensory to medial arm (medial brachial cutaneous nerve); motor to interossei; no reflex applicable. Primary root in finger abduction, exits between T1-T2 discs.


In the healthy cervical (or lumbar) spine displaying a moderate degree of lordosis, a good share of weight bearing is on the zygapophyses because the line of cumulative loading of compressive forces is posterior to the center of the vertebral bodies. This produces considerable articular jamming that tends to restrict a wide range of rotation. That is, the rotary motion occurring at the zygapophyses does so on firmly compressed facets. Fortunately, there is some structural adaptation for this. For the normal adult spine, the cervical discs average 3 mm in thickness, there is a 2:5 disc/body ratio, a 4:7 nucleus/anulus ratio, and the nucleus sits in a position that is slightly posterior to the center of the disc. In addition, the surface area of the cervical facets is larger in proportion to the surface area of the vertebral body than at any other region of the spine. This design contributes greatly to the overall segmental base of support in the neck. In fact, the weight-bearing surfaces of the facets are more than half (67%) that of the centrum. In addition, the superior facets below the axis face posterosuperior and medial to compensate for the normal anteroinferior tilt of the vertebral bodies.

The more the cervical curve flattens, the more superimposed weight is shifted to the discs. With the shift of normal compressive force normally at the posterior toward the anterior of the vertebral motion unit, the discs are forced to carry more weight and assume a greater responsibility in cervical stability. In time, this unusual compressive force on the nucleus can produce degenerative anular thinning, spurs, eburnation, and Schmorl's nodes. The posterior joints become relatively lax and predispose retropositioning and posterior subluxations. Add the disruptive forces of trauma, and this noxious situation is greatly increased.

The Upper Cervical Spine

The spinal canal of the upper cervical region is relatively large to accommodate the cervical enlargement of the cord. The pedicles, apophyseal joints, uncinate processes, and transverse processes have characteristics peculiar and specific to the cervical spine.

The Atlas.   The atlas can be considered a sesamoid between the occiput and axis that serves as a biomechanical washer or bearing between the occipital condyles and the axis. The absent body of the atlas is represented by its anterior arch and the dens of the axis, and the inner aspect of the anterior arch contains a facet for the dens. An IVD does not exist between the occiput and the atlas, nor does the atlas exhibit IVFs or a distinct spinous process.

The Axis.   The inferior facets of the atlas fit the superior facets of the axis like epaulets on sloping shoulders. The plane is about 110 to the vertical. To allow maximum rotation of the upper cervical complex without stress to the contents of the vertebral canal, the instantaneous axis of rotation is placed close to the spinal cord (ie, near the atlanto-odontoid articulation).

The C2–C3 Interface.   Rotation of C2 on C3 is limited by a mechanical blocking mechanism that protects the vertebral artery from excessive torsion. The anterior tip of the superior articular process of C3 impinges on the lateral margin of the foramen transversarium of C2. This blocking mechanism is also found in the subjacent cervical vertebrae.

The Occipitocervical Ligaments

It is well to be able to mentally picture the upper cervical ligament complex for serious sprains in this area can occur. The cross-shaped cruciate ligament completely secures the odontoid process. Its main portion is the triangular bilateral transverse ligament, which passes posteriorly on the dens and connects to the lateral masses of the atlas, transversing in front of the spinal cord. Its main function is to restrict anterior translation of the atlas. There are also two vertical bands. One rides from the dens upward to the basiocciput, and the other extends from the dens posteriorly down to the body of the axis. Because these ligaments are usually tough, the odontoid usually fractures prior to ligament failure. In addition, accessory atlantoaxial ligaments extend superiorly and laterally from the base of the inferior vertical cruciate and join the base of the dens with the inferomedial aspect of the lateral mass of C1. Anterior to the upper arm of the cruciate are the apical and alar ligaments.

The Lower Cervical Region

Nature has made many structural adaptations in the mid- and lower-cervical region. The laminae are slender and overlap, and this shingling increases with age. The osseous elevations on the posterolateral aspect forming the uncovertebral pseudojoints tend to protect the spinal canal from lateral IVD herniation, but hypertrophy of these joints added to IVD degeneration can readily lead to IVF encroachment. The IVDs are broader anteriorly than posteriorly to accommodate the cervical lordosis.

The Articular Facets.   The middle and lower cervical articular processes incline medially in the coronal plane and obliquely in the sagittal plane so that they are near a 45 angle to the vertical. Their bilateral articular surface area, which shares a good part of head weight with the vertebral body, is about 67% of that of the vertebral body.

The Capsular Ligaments.   The short, thick, dense capsular ligaments bind the articulating processes of each vertebral motion unit, enclosing the articular cartilage and synovial tissue. Their fibers are firmly bound to the periosteum of the superior and inferior processes and arranged at a 90 angle to the plane of the facet. This allows maximum laxity when the facets are in a position of rest. They normally allow no more than 2–3 mm of movement from the neutral position per segment, and possibly provide more cervical stability than any other ligament. Capsulitis from overstretch in acute subluxation is common. The posterior joint capsules enjoy an abundance of nociceptors and mechanoreceptors, far more than any other area of the spine. Within the capsule, small tongues of meniscus-like tissue flaps project from the articular surfaces into the synovial space. They are infrequently nipped in severe jarring at an unguarded moment during the end of extension, rotation, or lateral bending, establishing a site of apophyseal bursitis.

The Lower Cervical Perivertebral Ligaments.   The five lower, relatively similar, cervical vertebrae have eight intervertebral ligaments: four posterior and four anterior in terms of the motion unit. The anterior ligaments are the anterior longitudinal ligament, the anulus fibrosus, the posterior longitudinal ligament, and the intertransverse ligament. The posterior ligaments are the ligamentum flavum, the capsular ligaments, and the interspinous and supraspinous ligaments.

The Intervertebral Foramen.   The boundaries of the cervical IVFs are designed for motion rather than stability as compared with the thoracic and lumbar regions. The greatest degree of functional IVF diameter narrowing occurs ipsilaterally in lateral bending with simultaneous extension.


The head may be flexed forward so the chin strikes the sternum or thrown sideward so that the ear strikes the shoulder and the neck can still be within the normal range of motion. It is most rare, however, that the occiput strikes the back and does not exceed normal cervical extension.

The Upper Cervical Area

Movements in the cervical spine are relatively free because of the saddle-like joints. The cervical spine is most flexible in flexion and rotation. The latter occurs quite freely in the upper cervical area and is progressively restricted caudally. The specific ranges of cervical motion differ among so many authorities that any range offered here should be considered hypothetical depending on individual planes of articulation, other variances in structural design (eg, congenital, aging degeneration, posttraumatic), and soft-tissue integrity. This variance in opinion is also true for the centers of motion.

Upper-Cervical Instability.   Moderately strong soft-tissue connections exist in the occiput-atlas-axis complex. Bone, muscle, tendon, ligament, fascia, and lymph node abnormalities tend to restrict motion, while tissue tears and lax ligaments without associated muscle spasm may allow too much motion. Stability is provided the C1–C2 joint by paravertebral ligaments and muscle attachments. When weakening of these supports occurs (eg, trauma, postural stress, rheumatoid arthritis), a dangerous state of instability arises. Each infant presents a considerable degree of cervical instability because of the relatively large head weight superimposed on the small underdeveloped spine.

Extension and Flexion.   Considerable cervical motion is concentrated in specific spinal areas. About half of flexion and extension occurs at the atlanto-occipital joints, with the other half distributed among the remaining cervical joints. Inasmuch as the nucleus of the disc is nearer the anterior of a complete cervical vertebra, A-P motion is more discernible at the spinous process than at the anterior aspect of the vertebral body.

Active motion.   Regional active cervical flexion and extension motions are tested by having the patient raise and lower the chin as far as possible without moving the shoulders. Note smoothness of motion and degree of limitation bilaterally.

Passive motion.   Passive cervical flexion and extension are examined by placing the hands on the sides of the patient's skull and rolling the skull anteroinferior so that the chin approximates the sternum and posterosuperior so that the nose is perpendicular to the ceiling.

Rotation.   Approximately half of cervical rotation takes place at the atlantoaxial joints about the odontoid process, with the remaining half distributed almost evenly among the other cervical joints. During rotation, the odontoid represents a peg encased within a fairly enclosed ring or a stake surrounded by a horseshoe.

Active Rotation.   Regional active rotary motion is tested by having the patient move his nose as far as possible to the left and right without moving his shoulders. Note the smoothness of motion and degree of limitation bilaterally.

Passive Rotation.   Passive rotation is examined by placing the hands on the patient's skull and turning the head first to one side and then to the other so that the chin is in line with the shoulder.

Note:   If a complete fixation occurs between C1 and C2, the remaining cervical segments commonly become hypermobile in compensation. Thus, gross inspection of neck rotation (or other motions) should never be used to evaluate the function of individual segments.

Lateral Flexion.   Cervical lateral bending is essentially performed by the unilateral contraction of the neck flexors and extensors with motion occurring in the coronal plane. Such side-bending is accompanied by rotational torsion below C2 and distributed fairly equally in the normal cervical joints. That is, when the cervical spine as a whole bends laterally, it also tends to rotate anteriorly on the side of the concavity so that the vertebral bodies arc further laterally than the spinous processes.

The Lower Cervical Region

The lower cervical IVDs contain an exceptional amount of elastin, which allows the IVDs to conform to the many possible planes of movement. Excessive flexion is limited by ligament and muscle restraints on the separating posterior arches. Overextension is limited by bony apposition. Other factors include the resistance of the anular fibers to translation, the stiffness property of the anulus relative to its vertical height, and the physical barrier produced by the uncinate processes that are fully developed in late adolescence. Major joint movements and their innervation are shown in Table 2.

Table 2   Major Joint Movements and Their Innervation

Segments Joints Movement/Roots
C2-T1 Scapulae Elevation and retraction (C2-5)
    Depression and protraction (C5-T1)
C5-T1 Shoulder Abduction (C5-6)
    Abduction and flexion (C5-T1)
    Extension (C5-8)
C5-T1 Elbows Extension (C6-T1)
    Flexion (C5-6)
C6-T1 Wrists Flexion (C7-T1)
    Supination, pronation, extension (C6-7)
C6-T1 Fingers Extension (C6-8)
    Flexion (C7-T1)

Lower-Cervical Instability.   Subtle instability is rarely obvious in the ambulatory patient. The most important stabilizing agents in the mid- and lower-cervical spine are the anulus fibrosus, the anterior and posterior ligaments, and the area muscles, especially, which serve as important contributing stabilizers. On dynamic palpation, any segmental motion exceeding 3 mm should arouse suspicions of lack of ligament restraint.

Neurologic Insults.   There is a rough correlation between the degree of structural damage present and the extent of neurologic deficit. This is more true in the lower cervical area than in the upper region where severe damage may appear without overt neurologic signs. In either case, it's doubtful that a deficit would exhibit without an unstable situation existing. It is not unusual for a patient to display a neurologic deficit without static displacement; ie, the vertebral segment has rebounded back into a normal position of rest.

Segmental Angulation.   Angulation of one vertebral segment on a lateral roentgenograph more than 11 greater than an adjacent vertebra that is not chronically compressed indicates instability and pathologic displacement. While conservative traction may reduce the associated displacement, it is doubtful in severe cases that a normal resting position can be guaranteed without surgical fusion. But this should be considered as a final alternative.

Facet Action.   In the middle and lower cervical areas, A-P motion is a distinctly gliding translation. During flexion and extension, the superior vertebra's inferior facets slide anterosuperior and posteroinferior on the inferior vertebra's superior facets. During full flexion, the facets may be almost if not completely separated. Consequently, an adjustment force is usually contraindicated in the fully flexed position. The center of motion is often described as being in the superior aspect of the body of the subjacent vertebra. Some pivotal tilting of the superior facets, backward in extension and forward in flexion, is also normal near the end of the range of motion. The facets also tend to separate (open) on the contralateral side of rotation and lateral bending. They approximate (jam) during extension and on the ipsilateral side of rotation and lateral bending. Likewise, the foramina normally open on flexion, narrow on extension, and close on the concave side of lateral flexion. Because of the anterosuperior slant of the lower cervical facets, an inferior facet that moves downward must also slide posterior, and vice versa.

Adjustment Precautions.   Any corrective adjustment must consider the state of the cervical curve, planes of articulation, facet tilting, and degree of facet opening, as well as any underlying pathologic process involved, and applying just enough force to overcome the resistance of the fixation. Here, again, knowledge of the mechanism of trauma and the ability to mentally picture the state of hidden tissues are underscored.

Coupling Patterns.   During lateral bending, the vertebral bodies tend to rotate toward the concavity while the spinous processes swing in a greater arc toward the convexity. Note that this is exactly opposite to the coupling action in the lumbar spine. During cervical bending to the right, for example, the right facet of the superior vertebra slides down the 45 plane toward the right and posterior and the left facet slides up the 45 incline toward the left and anterior. This coupling phenomenon is seen in circumstances in which an unusual ratio of axial rotation and lateral bending produces a subluxation or unilateral facet dislocation.

The amount of cervical rotation coupled with lateral flexion varies with the segmental level. At C2, there is 1 of rotation with every 1.5 of lateral flexion. This 2:3 ratio changes caudally so that the degree of coupled rotation decreases. For example, at C7, there is 1 of rotation for every 7.5 of lateral flexion, a 2:15 ratio.

Ranges of Motion.   All cervical vertebrae from C2 to C7 partake in flexion, extension, rotation, and lateral flexion, but some segments (eg, C5) are more active than others. In the C3–C7 area, flexion and extension occur as slight gliding translation of the upper on the lower facets, accompanied by disc distortion. The site of greatest flexion is near the C4–C5 level, while extension movement is fairly well diffused. This fact likely accounts for the high incidence of arthritis at the midcervical area. Rotation in this region is greatest near the C5–C6 level, slightly less above and considerably less below. Lateral bending in greatest near the C2–C3 level and is diminished caudally. The arc of lateral motion is determined by the planes of the covertebral joints.

The Transitional Cervicothoracic Area

The lateral gravity line of the body falls anterior to the mid thoracic region. With fatigue, there is a tendency for thoracic kyphosis to increase. Thus, when cervical alignment is poor, equal concern must be given to reduce an exaggerated thoracic kyphosis because the positions of the cervical and thoracic regions are interrelated; ie, a thoracic kyphosis is usually accompanied by a compensatory cervical lordosis, and vice versa.

In the cervicothoracic area, normal movement is somewhat similar to that in the lumbosacral area insofar as the type of stress (not magnitude of load) to which both areas are subjected is similar. L5 is relatively immobile on the sacrum and C7 is relatively immobile on T1. Most movement in the cervicothoracic junction is at C6–C7 and primarily that of rotation.

Note: The use of examining A-P and lateral patient posture with a plumbline was common in pioneer chiropractic. Because this practice has been generally discontinued, some basic structural correlations can be easily overlooked.


The dura of the spinal cord is firmly fixed to the margin of the foramen magnum and to the 2nd and 3rd cervical vertebrae. In other spinal areas, it is separated from the vertebral canal by the epidural space. Since both the C1 nerve and the vertebral artery pass through this membrane and both are beneath the superior articulation of the atlas and under the overhanging occiput, atlanto-occipital distortion can produce traction of the dura mater producing irritation of the artery and nerve unilaterally and compressional occlusion contralaterally. De Rusha feels that this helps us understand those cases of suboccipital neuralgia where a patient upon turning his head to one side increases the headache and vertigo that are relieved when the head is turned to the opposite side.

There is also a synapse between the upper cervical nerves and the trigeminal nerve, which also supplies the dura mater. This may explain why irritation of C1 results in a neuralgia not only confined to the base of the skull but is also referred to the forehead or eye via the supraorbital branch of the trigeminal. The greater occipital (C2) nerve does not tend to do this. It exits between the posterior arch of the atlas and above the lamina of the axis, referring pain to the atlanto-occipital area and sometimes to the vertex of the scalp.

The superficial sensory cutaneous set of the cervical plexus (C1–C4) is frequently involved in subluxations of the upper four segments (see Table 3), particularly when there are predisposing spondylitic degenerative changes. Janse describes four resultant neuralgias:

(1) lesser occipital neuralgia, involving the posterior area of the occipitofrontalis muscle, mastoid process, and upper posterior aspect of the auricle;
(2) greater auricular neuralgia, extending in front and behind the auricle, skin over the parotid gland, paralleling the distribution of the auriculotemporal branch of the trigeminus and easily misdiagnosed as chronic trifacial neuralgia;
(3) cervical cutaneous neuralgia, involving the area of the middle third of the platysma to the midline, possibly extending from the chin to the sternum;
(4) supraclavicular neuralgia. Depending on which rami are affected, the neuralgia may involve the suprasternal area, pectoral area, or deltoid area. Thus, sternoclavicular and acromioclavicular neuralgias may originate in the spinal levels of the supraclavicular nerve.

Table 3   Nerve Function of the Cervical Plexus (C1–C4)

Nerve Function
Lesser occipital Sensory to skin behind ear and mastoid process.
Greater auricular Sensory to skin over parotid, jaw angle, ear lobe, and front of mastoid process.
Cervical cutaneous Sensory to skin over anterolateral portion of neck.
Supraclaviculars Sensory to skin over medial infraclavicular area, pectoralis major and deltoid.
Muscular branches Motor to capitus anterior and lateralis, longus capitus, longus colli, hyoid muscles, sternocleidomastoideus, trapezius, levator scapulae, scalenus medius.
Phrenic Sensory to costal and mediastinal pleura and pericardium. Motor to diaphragm.

De Rusha suggests that dysphagia and dysarthria may at times be due to upper cervical involvement rather than a CNS situation. The C1 joins the hypoglossal nerve supplying the intrinsic muscles of the tongue. It then descends to join the descending cervical that is derived from C2 and C3. A loop of nerves, the ansi hypoglossi, which supplies muscles necessary for deglutition and speaking, is arises from C1–C3.

Irritative lesions involving the cervical articulations may in turn irritate the sympathetic nerve plexuses ascending into the cranium via the vertebral and carotid arteries. Some cases of visual and aural symptoms are related to upper-cervical distortion where the arch of the atlas snugly hugs the occiput, thus possibly irritating the sympathetic plexus near the vertebral artery as well as partially compressing the vessel. To appreciate this, note that the visual cortical area of the occipital lobe requires an ideal blood supply dependent on the sympathetics ascending the great vessels of the neck, and this holds true for the inner ear as well.

To test this syndrome, De Rusha suggests having the supine patient read some printed matter while the examiner places gentle traction on the skull, separating the atlanto-occipital articulations. A positive sign occurs when the patient, often to his surprise, experiences momentarily enhanced visual acuity or reduced tinnitus.


See Table 4 for review. Many features of brachial plexus involvement manifest in the upper extremities and have been described in previous papers in this series.

Table 4   Nerve Function of the Brachial Plexus (C5–T1)

Nerve Function
Radial Motor for wrist and thumb extension; sensory to dorsal webspace between thumb and index finger.
Ulnar Motor for little finger abduction; sensory to distal ulnar aspect of little finger.
Median Motor for thumb opposition and abduction; sensory to distal radial aspect of index finger.
Axillary Motor to deltoid muscle; sensory to lateral arm and deltoid patch on upper arm.
Musculo-cutaneous Motor to biceps muscle; sensory to lateral forearm.


The area of cervicothoracic transition is a complex of prevertebral and postvertebral fascia and ligaments subject to shortening. It offers a multitude of attaching and crossing muscles such as the longus colli, trapezius, scaleni, sternocleidomastoid, erector spinae, interspinous and intertransverse, multifidi and rotatores, splenius capitis, splenius cervicis, semispinalis capitis, semispinalis cervicis, longissimus capitis, longissimus cervicis, and the levator costarum and scapula --all subject to spastic shortening and fibrotic changes that tether normal dynamics.


1.   Stage of Acute Inflammation and Active Congestion

The major goals are to control pain and reduce swelling by vasoconstriction, compression, and elevation; to prevent further irritation, inflammation, and secondary infection by disinfection, protection, and rest; and to enhance healing mechanisms. Common electives include:

Disinfection of open skin (eg, scratches, abrasions, etc)
Cold packs
Ice massage
Vapocoolant spray
Pressure bandage
Protection (padding)
Indirect therapy (reflex therapy)
Meridian therapy
Spondylotherapy (upper dorsal)
Mild pulsed ultrasound
Pulsed alternating current
Foam/padded appliance
Plaster cast
Rigid appliance
Indicated diet modification and nutritional supplementation.

2.   Stage of Passive Congestion

The major goals are to control residual pain and swelling, provide rest and protection, prevent stasis, disperse coagulates and gels, enhance circulation and drainage, maintain muscle tone, and discourage adhesion formation. Common electives include:

Indirect articular therapy (reflex therapy)
Alternating superficial heat and cold
Pressure bandage
Protect lesion (padding)
Light nonpercussion vibrotherapy
Mild passive exercise of adjacent joints
Mild surging alternating current
Mild pulsed ultrasound
Meridian therapy
Foam/padded appliance
Rigid appliance
Plaster cast
Orthopedic pillow
Indicated diet modification and nutritional supplementation.

3.   Stage of Consolidation and/or Formation of Fibrinous Coagulant

The major goals are the same as in Stage 2 plus enhancing muscle tone and involved tissue integrity and stimulating healing processes. Common electives include:

Mild articular adjustment technics
Moist superficial heat
Moderate active range-of-motion exercises
Meridian therapy
Alternating traction
Sinusoidal current
High-volt therapy
Interferential current
Spondylotherapy (upper dorsal)
Mild transverse friction massage
Mild proprioceptive neuromuscular facilitation techniques
Rest and Immobilization
Foam/padded appliance
Semirigid appliance
Orthopedic pillow
Indicated diet modification and nutritional supplementation.

4.   Stage of Fibroblastic Activity and Potential Fibrosis

At this stage, causes for pain should be corrected but some local tenderness likely remains. The major goals are to defeat any tendency for the formation of adhesions, taut scar tissue, and area fibrosis and to prevent atrophy. Common electives are:

Prudent deep heat
Articular adjustment technics
Spondylotherapy (upper dorsal)
Local vigorous vibromassage
Transverse friction massage
Active range-of-motion exercises without weight bearing
Motorized alternating traction
Negative galvanism
Sinusoidal and pulsed muscle stimulation
High-volt therapy
Interferential current
Meridian therapy
Proprioceptive neuromuscular facilitation techniques
Flexible foam/padded appliance
Orthopedic pillow
Indicated diet modification and nutritional supplementation.

5.   Stage of Reconditioning

Direct articular therapy for chronic fixations
Progressive remedial exercise
Passive stretching
Isometric static resistance
Isotonics with static resistance
Isotonics with varied resistance
Orthopedic pillow
Indicated diet modification and nutritional supplementation.


Traumatic overextension of the neck is not the most common cervical injury, but it's certainly the most publicized. Forceful extension produces tearing of the anterior longitudinal ligament that may coexist with an avulsion fracture at the anterior vertebral bodies. Pedicle fracture or severe posterior subluxation may also occur. Tenderness will usually be shown along the lateral musculature. Upper extremity pain or numbness and restricted cervical motion at an interspace during flexion-extension may exhibit. Symptoms may be prolonged without demonstrable evidence.

Mechanisms.   Other than those occurring in automobile accidents, the forces in whiplash are usually administered from below upward; eg, an uppercut to the chin or a blow to the forehead while running forward. This is in contrast to the compressive type of hyperextension or hyperflexion injury where the force is usually from above downward. Thus, knowing the direction of force, even if the magnitude is unknown, is important in analyzing the effects. A facial injury usually suggests an accompanying extension injury of the cervical spine as the head is forced backward either by an external force or as a defensive maneuver.

Kinematics.   In whiplash resulting from a mild automobile collision, the cervical injury is due to indirect trauma from acceleration-deceleration forces. If the head does not strike something, the damage is produced solely by inertia forces. The body moves at the same speed as the automobile. If the automobile is struck from the rear, the unrestrained head is whipped backward, because the head is not restrained by the seat, and then rebound forward. If the automobile is struck from the front or hits a relatively immovable object, the head is thrown forward and then rebound backward. Thus, the inertia force displaces the head in the direction opposite to the automobile's acceleration. The first movement is that of translation producing a shearing force at the base of the neck because the bending moment is greatest at that point.

The rebound can be caused by several factors. In a front-end collision, for example, there is an initial flexion elongation of the cervical spine after impact that is followed by rebound extension. The rebound is produced by the rapid deceleration of the automobile, the impact from the seat, and the stretch reflex produced in the elongated neck and upper dorsal muscles. This reflex can be quite severe. Because it occurs when the neck is at its full range of movement, the pull generates considerable compression as well as extension.

Effects.   When the head is violently thrown backwards (eg, whiplash), the damage may vary from minor to severe tearing of the anterior and posterior longitudinal ligaments. This flattens the cervical curve in about 80% of cases, and a degree of facet injury must exist even if not evident on film. Stretching to the point of hematoma can occur in the scalene muscles, sternocleidomastoideus, longus capitis, and longus cervicis.

Severe cord damage may occur that is usually attributed to momentary pressure by the dura, ligamentum flavum, and laminae posteriorly, even without roentgenologic evidence. Even without any cord deficit, severe damage to the nerve roots may occur as the facets jam and close on the IVFs, especially if fracture occurs. Incidence is highest at the C4–C6 area. Severe stretching of the vertebral arteries, sympathetic trunk, nerve root, and spinal cord attachments to some degree is inevitable.

Cailliet points out that it is difficult to visualize a sprain causing rupture of the ligaments of a joint without causing some derangement of the opposing joint surfaces, which by definition is an orthopedic subluxation. If a whiplash injury is considered a severe sprain, an orthopedic subluxation injury must be assumed to have occurred even if it has been spontaneously reduced. Such subluxations may occur during the initial movement and/or the rebound movement, and it is not unusual to have manifestations of a flexion sprain superimposed on manifestations of an extension sprain. In the typical whiplash injury, whether it be from hyperextension or hyperflexion or both, the effects of traumatic elongation and compression are compounded by underlying fixations, arteriosclerosis, spondylosis, ankylosing spondylitis, etc.

Case Management.   Treatment of mild or moderate injuries not exhibiting severe neurologic trauma requires reduction of subluxation, mobilization of fixations, physiotherapeutic remedial aid of soft-tissue injury, a custom-fit nonflexible supporting collar for several weeks depending on the clinical symptoms and signs, and graduated therapeutic exercises. Continuous traction, which reduces the cervical lordosis, may be helpful in extension injuries after the acute stage, but it would usually be contraindicated where the cervical curve has reversed (eg, flexion strain). The previously described template offers several beneficial electives.

Flexion Strain/Sprain

Slight anterior subluxation is usually not serious, but neurologic symptoms may appear locally or extend down the arm.

Mechanisms.   An occipital blow usually suggests an accompanying flexion injury of the anterior cervical spine and posterior soft tissues as the skull is forced forward. Excessive flexion may also be a part of whiplash; ie, superimposed on an excessive extension injury.

Effects.   The posterior paraspinal tissues are overstretched, the facets are sprung open, and the process of bleeding, edema, fibrosis, and adhesions is initiated. Fractures of end-plates may be difficult to assess early. Disc degeneration and posttraumatic osteoarthritis may follow, which lead to spondylosis.

Case Management.   Management is similar to that of extension injuries except that the period of necessary immobilization is often shorter (6–8 weeks).

Lateral Flexion Strain/Sprain.   Traumatic brachial plexus traction syndromes have been described in an earlier paper of this series. These injuries usually occur when the head is not only severely flexed sideward but also flexed forward and downward below the shoulder.


Vertebral subluxations are difficult to classify under normal categories of injury because they can involve bone, joint, muscle, fascia, ligament, capsule, disc, nerve, cord, spinal fluid, and vascular tissues. Inasmuch as all freely movable articulations are subject to subluxation, the atlanto-occipital diarthrosis is no exception. The stress at this point is unusual when one considers that the total weight of the cranium is supported by the ring of the atlas about 1/20th the circumference of the skull and a variety of spinal muscles, subject to spasm, have their attachments on the occiput.

Aside from direct trauma, disturbances in the upper-cervical area usually arise from muscular spasm of one or more of the six muscle bundles having attachments on the occiput, atlas, or axis. Unequal tension and ultimate fibrotic changes within the perivertebral structures can readily influence the delicate nerve fibers and vascular and axoplasmic flow. The vertebral artery is frequently involved by compression of the overlying muscles in the suboccipital triangle. West points out that the vertebral artery can be completely occluded during postmortem studies just by turning the head backward and to the opposite side

Functional Anatomy Relative to Cervical Subluxations

The artery and vein supplying a spinal nerve course within the foramen between the nerve and the fibrous tissue in the anterior portion of the opening. It is unlikely that circulation to the nerve would be disrupted without first irritating or compressing the nerve because the arteries and veins are much smaller, blood pressure within the lumen makes them not easily compressed, and nerve tissue is much more responsive to encroachment irritation. Nevertheless, loss of mobility of any one or more segments of the spine correspondingly influences its circulation.

Without the massing effects of motion, collateral microcirculation and CSF flow along the nerve root is hampered. The resulting partial anoxia, venous congestion, and stagnant lymph and CSF have a harmful influence on nerve function. This is one reason why attaining the highest degree of normal mobility possible after trauma is so important in chiropractic rehabilitation. Mobility reflects a joint that is free of stasis, binding adhesions, taut scar tissue, compression impingement, etc.

Once a vertebra loses its ideal relationship with contiguous structures (subluxation) and becomes fixed or restricted at some point (fixation) in its normal range of motion, it's no longer competent to fully participate in ideal coordinated spinal dynamics. The affected area becomes the target for unusual stress, weight-bearing and traumatic. In addition to the attending circulatory, neuromechanical, and static changes in the involved area, there is disturbed reflex activity that can manifest as changes in superficial and deep reflexes, hyperkinesia, pupillary changes, excessive lacrimation, tremors and spasms.

Add to factors explained above anomalies in the cervical area that can predispose subluxations from minor overstress. The weight of the head along with activity demands may contribute to chronic degenerative spondylosis often superimposed on asymptomatic anomalies. A vicious cycle is seen where subluxation contributes to degenerative processes and these processes contribute to subluxation. This poses the question when pain fades, "When can the patient be discharged?" But a better question would be, "How long should periodic check-ups be continued to monitor an asymptomatic patient?" There is no life that is void of stress.

Further Clinical Implications.   Neurologic disturbances may result from muscular and fibrotic changes along the cranial nerve pathways that emit from the skull and pass intimately between and under suboccipital fasciculi. Five of the cranial nerves are thus vulnerable: the facial, glossopharyngeal, vagus, spinal accessory, and hypoglossal. In addition, circulatory impairment of major and minor nerves of the neck may alter the function of those cranial nerves that do not exit from the skull proper (eg, the olfactory, optic, oculomotor, trochlear, trigeminal, abducens, and auditory) but which are contained within the cranium and remote from direct vertebral subluxation encroachment effects. We should not overlook the fact that it is essentially muscle that produces and maintains the subluxation. Concern must be given to why the subluxation is produced. Perpetuation may be only by a self-generating reflex.

Due to the interlocking arrangement of the articular processes, a straight posterior subluxation is an anatomical impossibility unless there is a fracture of the articular processes. The body of any vertebra follows the plane of the articular surfaces in movement. If a spinous process moves left, it does so by inscribing an arc toward the superior and anterior while simultaneously the right transverse process moves inferiorly and somewhat posteriorly. It is thus improbable for an individual vertebra to be rotated straight right or left on its longitudinal axis. A typical vertebra cannot be subluxated without an articular process moving either superiorly or inferiorly; thus it can be said that superiority or inferiority attends every posterior/anterior subluxation.

If subluxation of a vertebra occurs in a superior direction, the contents of the intervertebral foramen become compressed. Anatomic disrelationship by elongating the short diameter of the intervertebral foramen will cause indirect pressure upon the nerve trunk from compression between the fibrous tissue in the anterior portion of the foramen. If there is movement in an inferior direction, enlargement of the foramen occurs. Because the nerve sheath is firmly anchored by tissues connecting it to the borders of the foramen, a stretching effect is exerted on the nerve sheath, altering its shape. It can thus be appreciated that enlarging the intervertebral foramen can cause as much trouble as a reduction in the size of the intervertebral foramen. In addition, it's impossible to subluxate a vertebra between C2 and L5 inclusive without changing the shape of the IVD in compensation.


Three not infrequent diseases of the cervical spine with biomechanical implications are spondylosis, rheumatic spondylitis, and ankylosing spondylitis. In each of these conditions, severe subluxation is a cardinal manifestation. Cervical spondylosis invariably has a traumatic origin. This may be from a blow to the neck, a whiplash injury, a fall, or years of poor neck posture (eg, typing, overhead work). It's prevalence in the late degenerative stage is likely due to inadequate posttraumatic rehabilitation

Cervical spondylosis is a chronic condition in which there is progressive degeneration of the IVDs leading to secondary changes in adjacent vertebrae, including the posterior apophyseal joints. It is the result of direct trauma (ie, disc injury), occupational stress, aging degeneration, or found in association with and adjacent to congenitally defective vertebrae.

Clinical Implications.   Spondylosis may produce compression of either the nerve root or spinal cord. During the degenerative process, intradisc pressure decreases, the anulus protrudes, and the end plates approximate due to reduction of disc thickness. As the disc protrudes, it loosens the attachment of the posterior longitudinal ligament and this allows the anulus to extrude into the cavity formed between the posterior vertebral body and the ligament. This portion of the anulus, in time, becomes fibrous and then calcifies. It is for this process that posterior osteophytes prevail in the cervical and lumbar regions, while anterior spurs are more common to the dorsal spine.

Etiology.   Jeffreys sees a correlation of cervical spondylosis to carpal tunnel syndrome, lateral humeral epicondylitis, cervical stenosis, and low-back and/or lower extremity osteoarthritis. Pre-existing spinal stenosis, a thickened ligamentum flavum, a protruding disc, and spur formation not uncommonly complicate the picture of cervical spondylosis. There is almost no correlation between the degree of perceived pain in the neck and the degree of arthritic changes noted in early x-ray films. The weight of the head in faulty posture (eg, exaggerated dorsal kyphosis and cervical lordosis) along with activity stress may contribute to chronic degenerative spondylosis often superimposed on asymptomatic anomalies. Again we may see a vicious cycle in which subluxation contributes to degenerative processes, and these processes contribute to subluxation fixation.

Clinical Findings.   The onset is usually rapid and insidious but may be subjectively and objectively asymptomatic. The classic picture is one of a middle-aged person with greatly restricted cervical motion with marked muscle spasm, positive cervical compression test, insidious neck and arm pain and paresthesia aggravated by sneezing or coughing, acute radiculopathy from disc herniation, and usually some muscle weakness and fasciculations. A general rule states that central herniation produces local neck pain while lateral herniation produces upper extremity pain.

Whiting lists the manifestations that develop in spondylosis to also include neck crepitus, subjective or objective; local neck tenderness; headaches; neck pain radiating to the scapulae, trapezius, upper extremities, occiput, or anterior thorax; extremity muscle weakness; paresthesia of the upper and/or lower extremities; dizziness and fainting; impaired vibration sense at the ankle; hyperactive patellar and Achilles reflexes; and positive Babinski responses. From this one can see why the diagnosis is made from roentgenologic findings. The Davis series may suffice, but special views, tomography, myelography, or discography may be necessary for firm diagnosis.

Because of the constant weight of the head, postural strains, occupational insults, degrees of congenital anomalies, and posttraumatic or postinfection effects with or without associated disc involvement, the development of chronic degenerative spondylosis offers some distinct progressive characteristics:

(1) flattening of the cervical spine from muscle spasm and adhesion development,
(2) A-P fixation and restricted mobility,
(3) thinning of the atlanto-occipital and atlantoaxial articular plates resulting in motion restriction,
(4) middle and lower cervical disc wearing and thinning which narrows the IVFs,
(5) disc weakness encouraging nuclear shifting and herniation contributing to nerve encroachment,
(6) osseous lipping and spurs with extensions into the IVFs, and
(7) infiltration and ossification of paravertebral ligaments adding to inflexibility and pain upon movement.

Case Management and Prognosis.   Whiting brings out that it is fortunate that most people with cervical spondylosis are asymptomatic because there is no correction per se. Initial treatment is aimed at reducing symptoms of neurologic and vasomotor involvement or treating the soft-tissue injury superimposed on the pre-existing spondylosis. A trial of conservative treatment with emphasis on postural alignment may be preferred in cases demonstrating signs of either cervical radiculopathy and/or myelopathy.

Patients suffering with symptoms of radiculopathy related to cervical spondylosis tend to improve regardless of the treatment regimen. Unfortunately, the degenerative changes of the IVDs, vertebral bodies, and associated diarthrodial joints are permanent and, in most cases, progressive. Treatment is therefore aimed at reducing symptoms and future attacks by proper case management and prophylaxis. Traction and stretching exercises are highly beneficial in the postacute stage.

Exacerbation of symptoms is quite common, and months or years may elapse between attacks. With age and the gradual increase in degenerative changes, attacks are more closely spaced, and recovery from each attack is prolonged. Any trauma superimposed on silent cervical spondylosis can result in permanent partial disability of the cervical spine with symptoms far out of proportion to the severity of the injury.


In contrast to the primary thoracic kyphosis that is a structural curve, the cervical and lumbar anterior curves are functional arcs produced by their wedge-shaped IVDs and they normally flatten in the nonweightbearing supine position. Likewise, they quickly adapt to changes involving the direction of force. A pathologic straightening of the normal anterior curve of the cervical spine, as viewed in a lateral weight-bearing x-ray film, results in mechanical alteration of normal physiologic and structural integrity. The normal vertical A-P line of gravity, as viewed laterally with a plumbline, falls approximately through the odontoid and touches the anterior border of T2. As the cervical spine tends to flatten in the erect position, the gravity line passes closer to the center of the cervical discs.

Clinical Findings.   Cervical flattening is usually the result of paraspinal spasm secondary to an underlying injury, irritation, or inflammatory process. The acute clinical picture is often torticollis. Other manifestations include headaches (occipital, occipital-frontal, supraorbital), vertigo, tenderness elicited on lateral C4–C6 nerve roots, neuritis involving branches of the brachial plexus due to nerve-root pressure, hyperesthesia of one or more fingers, and loss or lessening of the biceps reflex on the same or contralateral side. In rare instances, the triceps reflex may be involved. One or more symptoms are frequently aggravated by an abnormal position of the head such as during reading in bed, an awkward sleeping position, or long-distance driving.

The typical radiographic findings include loss of the normal lordotic curve by the straightened cervical spine (78% cases), anterior and posterior subluxation on flexion and extension views, narrowing of IVD spaces at C4–C6 in 46% of cases, discopathy at the affected vertebral level as the injury progresses, and osteoarthritic changes that are often accompanied by foraminal spurring.

A flattened cervical spine in the erect posture somewhat resembles a normal spine during flexion. To appreciate the mechanisms involved, it is well here to review the biomechanics involved. The nucleus of the disc serves as a fulcrum during flexion and return extension. When the spine is subjected to bending loads during flexion, half the disc on the convex side suffers tension, widens, and contracts, while the other half of the disc on the concave side suffers compression, thins, and bulges. Concurrently, the nucleus bulges on the side of tension and contracts on the side of compression, which increases tension on the adjacent anulus. This creates a self-stabilizing counteracting flexion force to the vertebral motion unit that aids a return to the resting position.

Case Management and Prognosis.   Specific correction of offending vertebral subluxations should be accomplished. Adjunctive care includes massage and methods to reduce muscle spasm such as ultrasound, diathermy, hydrocollator packs, reflex spinal techniques, and a rolled towel placed under the neck in the supine position to increase the cervical curve. The individual should be instructed to sleep without a pillow. Cervical muscle re-education is quite helpful.

Prognosis is excellent if the condition is treated early and the case is not complicated by fracture or dislocation, but guarded if injury is severe. In cases of minimal cervical discopathy, at least symptomatic relief can be expected. Prognosis is poor in advanced degenerative osteoarthritis.


The branches of the brachial plexus in the shoulder lie just anterior to the glenohumeral joint. The axillary nerve runs just below the joint. In brachial plexus trauma, the entire plexus or any of its fibers may be injured. These injuries may be divided into three general types: total-arm palsies, upper-arm palsies (most common), and lower-arm palsies. Motor disturbances are the main feature as sensory loss is obscured by overlapping innervation.

The term Erb's palsy refers to the effects of a stretch injury or avulsion of the upper roots of the brachial plexus. In contrast, Klumpke's palsy means the effects of a stretch injury or avulsion of the lower roots of the brachial plexus.

Bikele's Test.   The sitting patient is asked to raise the involved arm laterally to a horizontal and slightly backward position. Flex the elbow, and laterally flex the neck to the opposite side. If active extension of the elbow, which stretches the brachial plexus, produces resistance and increased cervicothoracic radicular pain, the test is said to be positive for a nerve root or spinal cord inflammatory process (eg, brachial neuritis, meningitis).

Supine Tension Test.   The patient is placed supine so that the scapula is fixed. Have the patient laterally flex the neck to the opposite side of involvement. Abduct the humerus to about 45 , externally rotate the arm, extend the elbow, and extend the wrist. This maneuver places tension on the brachial plexus and its peripheral branches and thus helps to elicit signs of a lesion. The neurologic signs in brachial radiculopathy are shown in Table 5.

Case Management.   Provide support in the functional position, apply cold initially and correct any subluxations/fixations found. Once the acute symptoms are controlled, massage, interferential therapy, lower cervical and upper thoracic galvanic stimulation, ultrasound, moist heat, acupuncture, and progressive exercises to reduce cervicothoracic postural distortions are common recommendations.

Referral for suture is recommended in complete tears, and some improvement can be hoped for. The prognosis is usually hopeless for full recovery following avulsion from the cord. Fortunately, most injuries are a neurapraxia, and full recovery can be anticipated in time. If the lesion is due to simple stretching, contusion, or partial tearing, the prognosis is good for conservative therapy and complete recovery can be expected in most cases.

Table 5   Neurologic Signs in the Brachial Radiculopathies

Major Sensory Disorder
Major Motor Disorder
Reflex Changes
Nerve Root



(+/- Reflexes)
C5 Lateral arm Biceps, supraspinatus, Biceps
    infraspinatus, deltoid  
C6 Lateral forearm and thumb Brachioradialis Brachioradialis
C7 Middle finger Triceps Triceps
C8 Little finger Wrist and finger flexors None
T1 Medial forearm Intrinsic hand muscles Finger flexors


Albright describes the "stinger" syndrome as an apparently mild brachial plexus injury reflecting a transient radiculopathy at the time of impact. Football "spearing" and head butting are common causes. The injury usually occurs when the neck is forcibly hyperextended and laterally flexed, and symptoms can usually be precipitated in this position during examination.

Clinical Findings.   The condition is initially felt as a painfully severe electrical shock-like dysesthesia extending from the shoulder to the fingertips. This feeling passes within a few moments and is replaced by sensations of numbness and upper extremity weakness that may last from a few seconds to several minutes.

A common site of injury is at the C5 or C6 root level, and because of this, the most persistent sign will be weakness of the proximal shoulder muscles. An initial attack rarely leaves residual neurologic symptoms. Repetitive injuries of this nature, however, tend to have a cumulative effect that may lead to axonotmesis and chronic muscle weakness that may require up to 3 years for full recovery.

Complications.   The most common lesion associated with the stinger syndrome is cervical sprain with traumatic compression neuritis. Infrequently, an acute cervical disc rupture or a spontaneously reduced hyperextension dislocation may be associated. These later disorders are far more serious and usually require hospitalization until the severity of the injury can be properly assessed.


Initial examination must be conducted with special care. Traumatic dislocations of upper cervical vertebrae cause a distortion of the neck much like that of torticollis. A rotary fracture-dislocation of a cervical vertebra, especially of the atlas on the axis or the axis on C3, will produce neck rigidity and a fast pulse. Fever is absent. Local and remote trigger points are frequently involved. Even in mildly suspicious cases, the neck should always be x-rayed in two or more planes before it is physically examined.

The most common direct cause is that from irritating cervical subluxation (eg, trauma, rotational overstress, unilateral chilling, unbalanced lifting, instability). Subluxation may also be an asymptomatic complicating factor to those etiologic factors mentioned above. Barge states that the structural cause of torticollis is a rotatory vertebral malposition and abnormal disc wedging, where the nucleus of an involved disc has been forced to shift away from compressive forces. The patient's symptoms are often self-limiting with time and rest that allow the disc to expand in its nonweightbearing (decompressed) state and the vertebral facets to be relieved of their jammed position.

It can be theorized, however, that if the neck does not achieve this subluxation correction through disc imbibition a rotatory scoliosis is produced in adaptation so that the victim may at least have a straight eye level. But, as the now chronic subluxation has not been fully corrected, it can serve as a focus for morbid neurologic and degenerative processes, especially at the zygapophyses, covertebral joints, and IVFs.

Clinical Findings.   Regardless of the cause of torticollis, the neck is rigid and tender, the head tilts laterally toward the side of spasticity, and the chin is usually rotated to the contralateral side. Special care must be taken to determine the etiology and differentiate its many possible causes. Besides traumatic causes, torticollis may have an inflammatory, a congenital, or a neuropathic origin, or be the effect of various superimposed factors.

The pain associated with acute torticollis is attributed essentially to zygapophyseal capsulitis and covertebral joint inflammation. This can generally be confirmed by palpation and should not be confused with the pain of stretching rigid muscles on the side of the concavity.


Overuse is a common cause for taut muscles that fail to relax on rest. Excessive hypertonicity of a muscle, confirmed by palpatory tone and soreness, will tend to subluxate/fix its site of osseous attachment. Below is a listing of common problem areas in the neck.

  1. Splenius capitis.   Increased tone tends to pull the C5–T3 spinous processes lateral, superior, and anterior and to subluxate the occiput inferior, medial, and posterior.

  2. Scalenus anterior.   Hypertonicity tends to pull the C3–C6 transverse processes inferior, lateral, and anterior and the 1st rib superior and medial.

  3. Scalenus medius.   Excessive tone tends to pull the C1–C7 transverse processes inferior, lateral, and anterior and the 1st rib superior and medial.

  4. Scalenus posterior.   Hypertonicity tends to pull the C4–C6 transverse processes inferior, lateral, and anterior and the 2nd rib superior and medial.

  5. Obliquus capitis superior.   Abnormal tone tends to roll the occiput anterior and inferior and pull the atlas posterior and superior to produce a lateral occiput tilt and condyle jamming.

  6. Obliquus capitis inferior.   Excessive tone tends to produce a rotary torque of the atlas-axis motion unit.

  7. Rectus capitis posterior major.   Hypertonicity tends to pull the occiput posterior, inferior, and medial and the spinous of the axis superior, lateral, and anterior. Strong hypertonicity will lock the occiput and axis so that they appear to act as one unit even though they are not contiguous.

  8. Interspinales.   Excessive tone found between the spinous processes tends to hyperextend the involved vertebral motion units.

  9. Sternocleidomastoideus.   Abnormal tone tends to pull the sternum and clavicle posterior and superior and the occiput inferior and anterior.

  10. Upper trapezius.   Hypertonicity tends to pull the occiput posteroinferiorly, the C7–T5 spinous processes laterally, and the shoulder girdle medially and superiorly.


The muscle fascia of the posterior neck is a common site for trigger point development. The cervical and suprascapular areas of the trapezius, usually a few inches lateral to C7, frequently refer pain and deep tenderness to the lateral neck (especially the submastoid area), temple area, and angle of the jaw. The sternal division of the sternocleidomastoideus refers pain chiefly to the eyebrow, cheek, tongue, chin, pharynx, throat, and sternum. The clavicular division refers pain mainly to the forehead (bilaterally), back of and/or deep within the ear, and infrequently to the teeth.

Other common trigger points involved in "stiff neck" are in the levator scapulae, the splenius cervicis lateral to the C4–C6 spinous processes, and the splenius capitis over the C1–C2 laminae. These points are often not found unless the cervical muscles are relaxed during palpation.

Management.   Peripheral inhibitory afferent impulses can be generated to partially close the pre-synaptic gate by deep massage, acupuncture, or transcutaneous nerve stimulation. Ultrasound is not as beneficial. Most authorities feel deep sustained manual pressure on trigger points is the best method, but a few others prefer very strong short-duration pressure (1–2 seconds), but keep in mind that deep pressure is contraindicated in any patient receiving anti-inflammatory drugs (eg, cortisone). Subcutaneous hemorrhage may result.


The vertebral nerve has its origin in the middle cervical sympathetic ganglion, and it offers vasomotor control over the vertebral artery. The Barre-Lieou syndrome is thought to be the result of vertebral nerve irritation causing circulatory impairment in the area of the cranial nuclei, especially those of the trigeminal and auditory nerves.

Clinical Findings.   The Barre-Lieou syndrome frequently occurs from trauma to the cervical spine. An underlying cervical arthritis and/or an IVD lesion (possibly related to spondylosis) are often present. Although the symptomatology is generally considered nonspecific, Kimmel describes the common features to be earache, eye pain, facial vasomotor disturbances, headache, temporary blurred vision, tinnitus, and vertigo. Dysphagia, phonation defects, and laryngeal and pharyngeal paresthesias are often associated. If chronic cervical arthritis is the cause of sympathetic irritation, especially in the midcervical area, corneal hyperesthesia and small persistent ulcers usually appear that are confined to the exposed conjunctiva.

Barre-Lieou Test.   The sitting patient is asked to slowly but firmly rotate the head first to one side and then to the other. Crawford reports that transient mechanical occlusion of the vertebral artery may be precipitated by simply turning the head, and this phenomenon is attributed to the compressive action of the longus colli and scalene muscles on the vertebral artery just before coursing through the IVF of C6. A positive sign exhibits if dizziness, faintness, nausea, nystagmus, vertigo, and/or visual blurring result, suggesting blockage (eg, buckling) of the vertebral artery.


Grieve describes the clinical picture of cervical disc disorders as typically "a hard osseocartilaginous spur produced by the disc together with the adjacent margins of the vertebral bodies." Furthermore, contends Cailliet, "the mechanism by which pain and disability originate in the neck region can be considered broadly to result from encroachment of space or faulty movement in the region of the neck through which the nerves or blood vessels pass." This encroachment and/or faulty movement commonly comprise apophyseal subluxation with osteophyte formation, contributing to or superimposed on disc degeneration and/or protrusion. This occurs most frequently in the C4–C6 area (ie, at the apex of the cervical curve).

Disc Encroachment

Aggression of a disc on the spinal canal or an IVF as seen in the lumbar region is not often seen in the cervical area. This is due to several factors. First, the posterior longitudinal ligament completely covers the posterior aspect of the disc and not just its central aspect as in the lumbar region. This ligament is also stronger and thicker (double-layered) in the cervical area. Next, the thickness of the cervical disc is so designed that it is wider anteriorly and narrower posteriorly, and horizontally wider and stronger in its posterior aspect. This tends to somewhat minimize posteriorly directed movement of the nucleus. Also, the dorsolateral disc herniation necessary for nerve root compression is minimized by the lips of the covertebral joints, which form a hard wall between the anulus and the exiting nerve.

Disc Degeneration

The cervical spine is readily subject to degenerative disc disease owing to its great mobility and because it serves as a common site for various congenital defects. Bone changes are more common posteriorly in the upper cervicals and anteriorly in the lower cervicals. Cervical degenerative changes can be demonstrated in about half the population at 40 years of age and 70% of those at 65 years, many of which may be asymptomatic. Various determinants, individually or in combination, may be involved in initiating the process. These factors include trauma, postural and occupational stress, biochemical abnormalities (eg, hydration, mucopolysaccharide, collagen, lipid changes), biologic changes (eg, aging), autoimmune responses, psychophysiologic effects (eg, the sodium retention of depression), and genetic predisposition (eg, identical development in twins).

Clinical Findings.   IVDs below C3 exhibit a higher incidence and the greatest severity of herniation. The C5 disc is the most frequently involved, followed by the C6 disc. The C2 disc is the least frequently involved. In acute disorders, interspace narrowing, straightening of the cervical curve, and instability may be the only roentgenographic signs present. Instability will be evident as aberrant segmental movement by comparing lateral films made during full flexion and extension.

If the overt protrusion is central, cord signs and symptoms display such as lower extremity spasticity and hyperactive reflexes. Sensory changes are rarely evident. The gait may be ataxic. If the protrusion is posterolateral, the nerve root will be involved rather than the cord.

Lhermitte's Sign.   With the patient seated, flexing of the patient's neck and hips simultaneously with the patient's knees extended may produce sharp pain radiating down the spine and into the upper or lower extremities. When pain is brought out, it suggests irritation of the spinal dura mater by a protruding cervical disc, a tumor, a fracture, or multiple sclerosis.

Chronic Disorders.   Several structural changes arise in chronic disorders. The vertebral bodies involved become elongated, the normal cervical lordosis flattens, the anterosuperior angle of the vertebral bodies becomes rounded, the involved body interspace narrows, the total height of the neck is reduced, and the inferior apophyseal facet above tends to subluxate posteriorly on the superior facet below and erode the lamina. Posterior osteophytes form at the disc attachment peripherally, often compromising the IVFs and vertebral canal. This may be noted by narrowing of the A-P dimension of the spinal canal in lateral films and foraminal encroachment on oblique films. These signs frequently occur at the C6–C7 level.

Anterior osteophytes are considered the result of abnormal ligament stress rather than part of the disc degeneration process. They frequently occur below the C4 level, as do alterations of the covertebral joints.

Neurovascular Signs

The specific neurovascular manifestations of acute cervical disc herniation are:

C2 disc protrusion: (C3 nerve root level)   posterior neck numbness and pain radiating to the mastoid and ear. The reflexes test normal.

C3 disc protrusion: (C4 nerve root level)   posterior neck numbness and pain radiating along the levator scapulae muscle and sometimes to the pectorals. The reflexes are normal.

C4 disc protrusion: (C5 nerve root level)   lateral neck, shoulder, and arm pain and paresthesia, deltoid weakness and possible atrophy, and hypesthesia of C5 root distribution over the middle deltoid area (axillary nerve distribution). The reflexes test normal.

C5 disc protrusion: (C6 nerve root level)   pain radiating down the lateral arm and forearm into the thumb and index finger, hypesthesia of the lateral forearm and thumb, and decreased biceps reflex, biceps and supinator weakness.

C6 disc protrusion: (C7 nerve root level)   pain radiating down the midforearm to the middle fingers, hypesthesia of the middle fingers, decreased triceps and radial reflexes, and triceps and grip weakness.

C7 disc protrusion: (C8 nerve root level)   possible pain radiating down the medial forearm and hand, ulnar hypesthesia, intrinsic muscle weakness of the hand. However, these symptoms are uncommon. The reflexes are normal.

These characteristics vary depending on the direction of the disc bulge; eg, on the nerve root, IVF vessels, spinal cord, or combinations of involvement. In some acute and many chronic cases, numbness may manifest without pain. In acute disorders, these cervical signs may be confused with those of shoulder or elbow bursitis, epicondylitis, or subluxation, especially when no local cervical symptoms exist.

Autonomic Involvement

Vague autonomic symptoms may be exhibited such as dizziness, blurred vision, and hearing difficulties. These can usually be attributed to involvement of the plexus around the vertebral artery or intermittent disruption of the blood flow.

Vertebral Artery Compression. Associated subluxation and osteophyte development can produce vertebral artery compression, especially if a degree of arteriosclerosis exists. Symptoms of unsteadiness, dizziness, and fainting occur especially when the head is rotated contralaterally.

Case Management.   Mobilization of a restricted facet, repositioning of a malpositioned nucleus, and/or reduction of a protruded anulus are the goals of the primary therapy. Adjustive treatment consists of specific positioning performed with manual or mechanical traction at the involved vertebral motion units to free impinged synovial fringes, reduce articular and disc displacements, and mobilize areas of fixation. This should not be performed with the neck in extension, and extreme care must be taken to avoid joint, nerve, cord, or vascular insult.

Adjunctive therapy includes immobilization of the neck with a cervical brace, heat (diathermy, ultrasound, infrared, moist hot packs) to reduce pain from muscle ischemia, trigger point therapy, and periodic bed rest with cervical traction by an orthopedic pillow. Gross vibrations (eg, long-distance automobile riding) and neck hyperextension (eg, overhead work) must be avoided. Goodheart feels that nutritional supplementation with 140 mg of manganese glycerophosphate six times daily is helpful. Isometric exercises during rehabilitation to lengthen the cervical spine and strengthen the cervical muscles are extremely beneficial.

Referral for radical treatment is generally made if one of the following occurs:

(1) conservative treatment fails to produce remission of symptoms;
(2) attacks reappear after a short period; or
(3) severe nerve root compression with paralysis develops, indicated by muscle wasting and/or a significant persistent sensory deficit.


Whether symptomatic or not, traumatic cervical scoliosis is something quickly recognized by a chiropractor using a plumbline but rarely noticed by an allopath. When viewed from the back, the vertical lateral line of gravity passes through the occipital protuberance and the vertebrae's spinous processes. In cervical scoliosis, the midcervical spinous processes, especially, tend to deviate laterally from this line. That is, in the common rotary cervical scoliosis, the spinous processes tend to rotate toward the convex side of the lateral curve, the vertebral bodies rotate toward the concave side, and the discs and articular facets are subjected to abnormal stretching forces as they open on the side of convexity. Compressive forces occur on the side of concavity. This type of cervical scoliosis is usually the compensatory effect of a lower scoliosis to the other side and a common cause of recurring episodes of idiopathic torticollis.

Effect of a Flattening Curve

Cervical scoliosis is often mechanically predisposed by flattening rather than exaggeration of the cervical lordosis. This is common during youth. As described previously, the posterior joints become relatively lax during flattening of the cervical spine. This encourages retropositioning and posterior subluxations that are frequently the first step toward cervical scoliosis.

The Self-Stabilization Factor

When a cervical disc is loaded unilaterally, the disc initially becomes wedge-shaped and the normally parallel vertebral plateaus form an angle. This vertically stretches the anular fibers opposite the weight-bearing side, but this action is quickly counteracted by forces transmitted laterally from the resilient nucleus to help the disc return to its normal shape. This self-stabilization factor is the product of a healthy nucleus and anulus working as a mechanical couple.

Disc Reactions in Cervical Scoliosis

Rotary forces must be considered. Because the apposing layers of anular fibers run alternately oblique in opposite directions, the oblique disc fibers angled toward the direction of twist become stretched when a vertebra rotates. The oblique fibers running against the direction of rotation tend to relax.

The greatest tension from stretch occurs centrally where the fibers are nearly horizontal. This increases nuclear pressure by compression proportional to the degree of rotation. If severe, the nucleus can be dislodged from its central position.

Effect of Lateral Tilt in Cervical Scoliosis

Cervical scoliotic rotation is also associated with a lateral tilt that increases the distance between the lateral margins of the vertebral bodies on the convex side of the curve. This stretches the anulus laterally, which produces a contraction of that part of the disc and a compensatory bulging of its contralateral (thinned) aspect. If the anular filaments become stretched or weakened and the disc loses some of its stiffness property, the nucleus may shift from its central position so that the vertebral segment is unable to return to its normal position. A firmly locked rotational subluxation can result. Thus, vertebral tilting as seen in subluxations with disc wedging alters the relationship of apposing articular surfaces to produce a change in the direction of compressive forces on these joints and the nucleus of the disc. Besides tilting, severe rotation produces abnormal jamming compression forces on ipsilateral facets and stretching tension forces on contralateral opened facets.

If continuous compression is applied to any active and mobile joint, cartilaginous erosion followed by arthritis can be expected. When continuous stretching is applied to any active and mobile synovial joint, capsulitis can be expected. When scoliotic rotation takes place evenly among the cervical segments and the cervical nuclei hold their relatively central position in the discs, the situation is usually asymptomatic even if erosion and arthritis are evident on roentgenographs. However, when a nucleus fails to hold its central position and shifts laterally away from the point of maximum compression, the superimposed vertebra will be encouraged to present a fixed subluxation.


Anomalous development of extra ribs in the cervical region may be a single unilateral rib, be bilateral, or be multiple bilaterally. The condition is usually seen at C7, and the cause is a variation in the position of the limb buds. The bone(s) may vary from a small nubbin to a fully developed rib. A small rudimentary rib may give rise to more symptoms than a well-developed rib because of a fibrous band attached between the cervical rib and sternum or 1st thoracic rib.

A cervical rib arising from C7 and ending free or attached to the T1 rib appears as an angular fullness that may pulsate owing to the subclavian artery above it. It is often encountered when percussing the apex of the lung. The bone can be felt behind the artery by careful palpation in the supraclavicular fossa and demonstrated by roentgenography. It rarely produces symptoms, but pain or wasting in the arm and occasionally thrombosis may occur. Additional features are described below.

Differentiation.   The etiologic theories of the cervicobrachial syndrome are compression of nerve trunks, trauma to nerve trunks, injuries to the sympathetic and vasomotor nerves, trauma to the scalenus anterior muscle, embryologic defects, postural or functional deficits, narrowing of the upper thoracic cap as a result of adjacent infections or anatomic defects, acute infection producing myositis, intermittent trauma to the subclavian artery, or a cervical rib.

Symptoms arise at age 12 or later, after the ribs have ossified. The 4th and 5th decades mark the highest incidence, probably because of regressive muscular changes. Two groups of symptoms are seen, those of the scalenus anticus syndrome and those due to cervical-rib encroachment pressure. The symptoms of cervical rib and scalenus syndrome are similar, and the scalenus anticus muscle is the primary factor in the production of neurocirculatory compression whether a cervical rib is present or not.

Symptoms are usually from compression of the lower cord of the brachial plexus and subclavian vessels such as numbness and pain in ulnar nerve distribution. Pain is worse at night because of pressure from the recumbent position. Pain of varying intensity, tiredness and weakness of the extremity, finger cramps, numbness, tingling, coldness of the hand, areas of hyperesthesia, muscle degeneration in the hand, a lump at the base of the neck, tremor, and discoloration of the fingers are characteristic. Work and exercise accentuate symptoms, while rest and elevation of the extremity relieve symptoms. Adson's and similar signs are positive.

Trauma is a common precipitating factor in sports. Aneurysms of the subclavian artery are rare. Differential diagnosis must exclude infectious neuritis, shoulder or cervical arthritis, subacromial bursitis, deformities, and cardiac disease. Compression of nerve tissue results in numbness, pain, paralysis, and loss of function. Compression of vascular structures produces moderate pain, edema, swelling, and obstruction of circulation resulting in clotting within the vessels with possible infarction in the tissues supplied. These unilateral phenomena are limited to the cervicobrachial distribution.

Case Management.   It has been Claypool's experience that palliative relief can be obtained in some cases by correction of posture, gentle manipulation of the upper thoracic and lower cervical spine, cervical traction, and other relaxing physiotherapy. Those cases not responding to conservative treatment require surgery, and those cases treated conservatively usually show a recurrence of symptoms periodically.


Investigation of headaches of cervical origin begins after possible brain or cord injury has been ruled out. It must also be kept in mind that posttrauma examination may reveal a subclinical entity (eg, brain tumor, aneurysm).

Markovich, the renowned neurologist, found that the most common headache is the type caused by neuromuscular skeletal imbalance. He points out that "the head in the human species has changed its position from the quadruped to the erect, thereby changing the basic relationship between the cervical spine and the head, with its important functional structures, and the rest of the body." He calls attention to the delicate interaction and highly sensitive biofeedback or servo-mechanisms that continually make adjustments in body balance, vision, pressure, and hearing with head and neck posture. "These regulatory, homeostatic mechanisms can be disturbed by a variety of conditions, originating at any level, including the inflammation and/or irritation of the cephalic projection of the upper cervical nerves (cervico-occipital neuralgias)."

Sustained contraction of muscles at the occipitocervical area appears to generate a type of "ischemic irritation" that includes the entrapment of the C2 nerves (greater and lesser occipital) as they pierce thick muscle and ascend to the back of the head to supply the posterior scalp, temples, and ear lobes, sending branches to the top of the head, the back of the eye, and the angle of the jaw.

The attending doctor should keep in mind that a patient may not exhibit a specific picture. For example, vascular migraine may be superimposed on occipitocervical neuralgia or episodes may be interposed, depending on the causes involved.


Although segmental spasm or instability may not be detectable by observation, it usually becomes evident by alert dynamic palpation. Careful localization of motion and muscle strength is necessary before prescribing any exercise program to assist postural realignment.

Postural Strength and Balance

Besides strengthening damaged soft tissues, one goal of posttraumatic exercise is to correct habitual postural problems that may be part of the problem. Because the center of gravity of the head lies anterior to the occipital condyles, definite force must be applied by the posterior muscles of the neck to hold the head erect. In addition, several groups of muscles are attached directly or indirectly to the anterior part of the head, and their function adds to the force of gravity to increase the load on the posterior cervical muscles. Gelb feels that the most important anterior neck muscles are the masticatory and supra- and infra-hyoid groups, which form a chain to the hyoid and mandible to which they attach, joining the head to the shoulder girdle anteriorly.

Deformed cervical posture can be associated with or without neck pain. As described previously, the deformity may be an exaggerated curve, flattening, occipital tilt, rotation, and areas of complete or partial segmental fixation. If pain arises, deviation may be toward or away from the site of pain, depending on the primary site of irritation. Remember that spinal stability is essentially under the control of neuromuscular mechanisms rather than ligaments.

Dynamic and Static Proprioception

The abundant proprioceptors of the vertebral column enable the brain to know where each segment is and what it is doing at any given time without visual confirmation. Impulse data are specifically relayed about the degree of muscle tension and/or the length of muscles via the muscle spindles and Golgi tendon organs. Tension messages are moved through fast-conducting nerves from annulospiral endings and through higher threshold nerves from flower spray receptors in the muscle spindle. The less complex Golgi tendon organs near the musculotendinous junctions discharge impulses initiated by either muscle contraction or stretch. Other receptors near the articular surfaces relate messages about facet motion speed and direction of motion.

In postural realignment, Gelb points out that restoring muscles to their physiologic resting length is a three-dimensional concept requiring placing the origin and insertion of muscles in a correct three-dimensional relationship. Lieb shows several full spine x-ray films of severe spinal distortions greatly improved solely through improvement of dental occlusion. If the temporomandibular joint has such a proprioceptive influence on posture, it is no wonder that chiropractors who specialize in solely upper-cervical or sacral correction exhibit a similar abundance of such before-and-after exhibits because each spinal segment is richly endowed with equal or greater receptors than that of the jaw.

Cervical Receptor Input

The apophyseal joints of the cervical spine are richly innervated with mechanoreceptors and afferent fibers, endowed more than any other spinal region. Activity of the cervical articular receptors exerts significant facilitatory and inhibitory reflex effects on the muscles of the neck and both the upper and lower extremities.

Wyke shows that the patterns of "normal cervical articular mechanoreceptor reflexes are profoundly distorted when cervical articular nociceptive afferent activity is added to that derived from the normally functioning cervical mechanoreceptors." To underscore this point, he reports that:

Manipulation of the head on the neck can produce coordinated flexion and extension movements on the paralyzed arm and leg of a hemiplegic patient.

Arm movement control in the absence of visual aid is considerably affected by rotation of the head.

Induced unilateral local anesthesia of the cervical joints in healthy subjects produces severe postural instability, dizziness, nystagmus, and muscle incoordination.

These signs and symptoms are similar to those experienced by some patients suffering from cervical spondylosis, ankylosing spondylitis, and gross fixations, and some while wearing an orthopedic cervical collar.

Normal Cervical Righting Mechanisms

Several head extensors arise from the lower cervical and upper thoracic vertebrae that exert an oblique posteroinferior pull on the occiput. If the line of pull falls behind the atlanto-occipital joint, a rotary movement results that tilts the occiput posteriorly and lifts the face so that the neck is hyperextended. However, if this posterior rotation of the head is inhibited by the cervical flexors (which is normal), the oblique pull has a posterior translatory component when the head is anterior to the midline. This serves to bring the head back toward the vertical gravity line and into normal alignment. In addition, the longus group exerts a bowstring action on the anterior cervicals that assists in axial extension of the neck.

Thus, the extensors essentially serve to return the head to the midline following flexion, but axial extension is really completed by a straightening of the cervical lordosis produced by segmental flexion. If this segmental flexion did not occur during extension, the face would rest in the neutral position pointing superiorly. Simultaneously, the thoracic extensors tend to straighten the dorsal curve so that the alignment of the entire cervicothoracic region is improved.

Flexion fixation of the lower cervicals elongates the posterior upper-thoracic soft tissues with adaptive shortening of the anterior elements (eg, anterior longitudinal ligament, anterior disc anulus, pectorals, intercostals). This is often seen in aging where it is contributed to by degeneration of the normally fibroelastic ligamentum nuchae, which helps to resist anterior deviation of the head. If this chronic flexion state occurs, cervical extension to the midline following flexion is fairly limited to increasing the cervical lordosis with little axial extension of the neck by segmental flexion. The neck angles forward, and the jaw juts out as the occiput rolls backward.

Cervical Strength Development

With two exceptions, specific isotonic exercises will not be described here as the literature abounds with many good regimens. However, the rationale behind isotonic cervical exercises following trauma deserves attention.

Weak Extensor Strength.   Clinical development of the trapezius, semispinalis capitis, splenius group, and erector spinae should be made if weak extension strength is evident. Only in the thoracic region do the erector spinae act solely as erectors. Their contraction in the cervical region produces hyperextension with posterior rotation of the occiput so that the chin points upward. Hyperextension, viewed as hyperlordosis, may be a manifestation of extensor hypertonicity or weak prevertebral muscles.

Weak Flexor Strength.   If weak neck flexion is evident, emphasis should be on developing the sternocleidomastoideus, longus group, and rectus capitis anterior and lateralis. The longus group and rectus capitis group are direct antagonists to the posterior cervical muscles. They principally serve to right the neck after extension but have some activity in flexion from the neutral position. Hyperflexion, viewed as a flattened or kyphotic cervical curve, may be a manifestation of prevertebral hypertonicity, weak extensors, or a posteriorly displaced disc nucleus.

Rehabilitation Therapy Following Cervical Trauma

Fisk describes the reflex response to pain as an increase in isometric muscle activity by the small gamma fibers and a decrease in isotonic activity for continuous resting (splinting) an irritated area. This functional inactivity tends to reduce impulses from the large fibers of muscle and joint proprioceptors so that the spinal cord's theoretical "gate" is kept open. Because prolonged inactivity leads to muscle weakness and atrophy, shortening of related connective tissues, and deterioration of articular cartilage, restoring motion and strength of a stressed region is an important clinical and biomechanical objective.

Grieve states that posttraumatic soft-tissue changes secondary to joint derangement or irritability become progressively prominent with age --mild during youth, severe in the elderly. The periarticular connective tissues adapt by shortening on one side of the joint and lengthening on the other, resulting in a relatively permanent lateral flexion accompanied by a degree of rotation. This makes chronic subluxations difficult to hold in a corrected position. However, prior to this chronic state is the state of prolonged isometric contraction described above, which is readily amenable if comprehensive therapy is applied. Gillet and others have confirmed this.

During the posttraumatic acute stage where there is neural excitation from the inflamed area, temporary impulse activity over the large-fibered proprioception circuits can be encouraged by movement, pressure, stretching, heat, and cold stimuli. However, heat at this stage increases swelling and movement provokes spasm, and thus are contraindicated. The logical alternative is to apply isometric exercises soon after the danger of recurrent hemorrhage has passed. This offers stretching without motion that increases circulation without engorgement and activates the large-fiber circuits, allowing a more rapid recovery. Even in chronic disorders, vigorous active motion increases intradisc pressure and can aggravate inelastic degenerated soft tissues. This would not be true for isometric exercises.

Following are several isometric exercises recommended by Fisk for the cervical spine that can readily be modified to meet varying clinical situations. They are designed to increase strength, but they also teach the patient the different perceptions of contraction and relaxation (eg, helpful in controlling chronic tension). As the head is held in the neutral position, these exercises are not contraindicated even in cases of uncomplicated hypermobility or arthritis if the patient is carefully instructed. Two or three exercise bouts daily are recommended.

Resisted Flexion Sitting.   The patient sits erect with the head straight and is instructed to place clasped hands against the forehead, breathe normally, and attempt to push the head forward against the resisting hand contact. This position should be held for about 7 seconds; then the patient relaxes for several seconds and repeats the exercise until fatigued.

Resisted Extension Sitting.   The patient sits erect with the head straight and is instructed to clasp the hands behind the head above the cervical spine. The patient is then asked to breathe normally, keep the head straight, and attempt to push the head back against the resisting hands. This position should be held for about 7 seconds. Then the patient relaxes for several seconds and repeats the exercise several times until fatigued.

Resisted Extension Supine.   The above exercise can also be conducted in the supine position by having the patient lie face up on a firm surface. A small firm pillow or cushion should be placed under the neck to support the head. The patient is instructed to firm the head against the pillow and firmly tuck the chin in while breathing normally. This position should be held for about 7 seconds; then the patient relaxes for several seconds and repeats the exercise until fatigued.

Resisted Flexion Prone.   In the alternative prone position, the patient lies face down with his forehead on a large folded towel to allow breathing in this position. The patient is instructed to tuck the chin in and firm the forehead against the towel while breathing normally. Pressure should be held for about 7 seconds; then the patient relaxes for several seconds and repeats the exercise until fatigued.

Resisted Lateral Flexion Sitting.   The patient sits erect with the head straight and places the right hand over the right ear with the fingers extending over the scalp. The patient is then asked to breathe normally and attempt to bend the neck toward the side of contact while resisting the effort with the contact hand. Again, this position should be held for about 7 seconds. Then the patient relaxes for several seconds and repeats the exercise about five times. The hand positions are then interchanged, and the exercise is conducted for the other side.

Resisted Sidebending Laterally Recumbent.   This exercise can also be conducted in the lateral recumbent position. The patient lies on the side with the underside of the face against a firm pillow so that the spine is straight. The patient firms the head against the pillow while breathing normally. This position is held for about 7 seconds; then the patient relaxes for several seconds and repeats the exercise a few times. The patient is then instructed to lie on the other side and to repeat the exercise.

Resisted Rotation Sitting.   The patient sits erect with the head straight and is instructed to place the right hand on the right temple, and then asked to breathe normally and attempt to look over the right shoulder while resisting the movement with the hand contact. This position is also held for about 7 seconds. Then the patient relaxes for several seconds and repeats the exercise until fatigued. After a short rest, the left hand is applied to the left temple and the exercise is conducted for the left side. This exercise can also be done in the supine position.

Two mild active isotonic exercises can be incorporated into the regimen when pain begins to diminish. These involve related shoulder and scapular muscles that are often chronically tensed following cervical trauma.

Shoulder-Shrugging.   The patient stands or sits erect with the head straight, the neck aligned vertically, and the arms hanging loosely at the sides. The patient is asked to breathe normally, elevate the shoulders as far as possible for several seconds, hold this position while the shoulders are retracted as far as possible for several seconds, and then to drop the shoulders in the retracted position and hold them there for several seconds. The patient then relaxes for several seconds and repeats the exercise for a few minutes until fatigued.

Arm Circling.   Have the patient stand erect with the head straight, the arms hanging loosely at the sides, and the feet slightly apart to widen the base of support. The patient is instructed to breathe normally, flex forward at the waist (when low-back pain is absent), and then bring the arms back and up in an arc from the anterior to the posterior as far as can be comfortably managed. This arm circling should be repeated without resting intervals for as many times as fatigue will allow.


Albright JA, Brand RA: The Scientific Basis of Orthopaedics. New York, Appleton-Century-Crofts, 1979.

Anderson LD, D'Alonzo RT: Fractures of the Odontoid Process of the Axis. Journal of Bone and Joint Surgery, 56A:1663, 1924.

Andreoli G: Neurological Implications of Sports Injuries. New England Journal of Chiropractic, Winter 1979.

Arthur PB: General Management of On-Field Injuries. ACA Journal of Chiropractic, August 1979.

Barge FH: Torticollis. Davenport, Iowa, Bawden Bros, Inc, 1979.

Basmajian JV (ed): Therapeutic Exercise, ed 3. Baltimore, Williams & Wilkins, 1978.

Bhalla K, Simmons EH: Normal Range of Intervertebral Joint Motion of the Cervical Spine. Canadian Journal of Surgery, 12:181-187, 1969.

Brunarski DJ: Functional Considerations of Spinal Manipulative Therapy. ACA Journal of Chiropractic, May 1980.

Bryan EC: The Traumatic Cervical Root Syndrome. ACA Journal of Chiropractic, April 1967.

Burt HA: Effects of Faulty Posture. Proceedings of the Royal Society of Medicine, 43:187, 1950.

Cailliet R: Neck and Arm Pain. Philadelphia, F.A. Davis, 1964.

Claypool DS: Cervical Rib. Roentgenological Briefs, American Council on Chiropractic Roentgenology. Date unknown.

Colson JHC: Progressive Exercise Therapy, ed 3. Bristol, England, John Wright & Sons, 1975.

Conley RN: Stress Evaluation of Cervical Spinal Mechanics. Journal of Clinical Chiropractic, Special Edition, 1:3, 1974.

Copass MK, Eisenberg MS: The Paramedic Manual. Philadelphia, W.B. Saunders Company, 1980, Chapter 2.

Corwin JM: personal correspondence. Oakland, California, June-October 1981.

Coventry MB: Anatomy of the Intervertebral Disk. Clinical Orthopaedics, 67:9, 1969.

Cowen AR: Emergency Care of Spinal Injuries: A Field Approach for Chiropractic Physicians. ACA Journal of Chiropractic, June 1979.

Craig TT (ed): Comments in Sports Medicine. Chicago, American Medical Association, 1973, pp 18-20.

Craton E: Occipital-Atlantal Articulation Redefined. The Texas Chiropractor, February 1978.

Crawford JP, et al: Vascular Ischemia of the Cervical Spine: A Review of Relationship to Therapeutic Manipulation. Journal of Manipulative and Physiological Therapeutics, 7(3):149-154, September 1984.

Cyriax E: Some Common Postural Deformities and Their Treatment by Exercise and Manipulation. British Journal of Physical Medicine, June 1938.

Cyriax JC, RG: Textbook of Orthopaedic Medicine. Baltimore, Williams & Wilkins, 1977, Vol II.

Daniels L, Worthingham C: Therapeutic Exercise, ed 2. Philadelphia, W.B. Saunders, 1977.

de Reuck AVS, Knight J (eds): Myotactic, Kinesthetic, and Vestibular Mechanisms. Boston, Ciba Foundation Symposium, Little-Brown, 1967.

De Rusha JL: Upper Cervical Technic Correlated with Neurodiagnosis. ACA Journal of Chiropractic, September 1961.

Dolan JP, Holladay J: First-Aid Management: Athletics, Physical Education, Recreation, ed 4. Danville, NY, Interstate Printers & Publishers, 1974.

Ebel JN: Reflex Relationships of Paravertebral Muscles. American Journal of Physiology, 200:5, May 1961.

Farkas A: The Pathogenesis of Idiopathic Scoliosis. Journal of Bone and Joint Surgery, 36:617, 1954.

Ferlic D: The Range of Motion of the "Normal" Cervical Spine. Bulletin of John Hopkins Hospital, 110:59, 1962.

Fielding JW: Cineroentgenography of the Normal Cervical Spine. Journal of Bone and Joint Surgery, 39A:1280, 1957.

Fisk JW: The Painful Neck and Back. Springfield, IL, Charles C. Thomas, 1977.

Gehweiler JA Jr, et al: The Radiology of Vertebral Trauma. Philadelphia, W.B. Saunders, 1980.

Gelb H: Patient Evaluation. In Gelb H (ed): Clinical Management of Head, Neck and TMJ Pain and Dysfunction. Philadelphia, W.B. Saunders, 1977.

Goodheart GJ: Applied Kinesiology, eds 2–9. Detroit, published by author, 1964–1971.

Goodheart GJ: Collected Published Articles and Reprints. Montpelier, Ohio, Williams County Publishing, 1969.

Granit R: The Basis of Motor Control. New York, Academic Press, 1970.

Grice A: Preliminary Evaluation of 50 Sagittal Cervical Motion Radiographic Examinations. Journal of the Canadian Chiropractic Association, 2:1, 1977.

Grieve GP: Common Vertebral Joint Problems. New York, Churchill-Livingstone, 1981.

Guthrie-Smith OF: Rehabilitation, Reeducation, and Remedial Exercises. Baltimore, Williams & Wilkins, 1943.

Hahl M: Normal Motions in the Upper Portion of the Cervical Spine. Journal of Bone and Joint Surgery, 46:1777, 1964.

Haldeman, S: The Pathophysiology of the Spinal Subluxation. In Goldstein M (ed): The Research Status of Spinal Manipulative Therapy. Washington, DC, Government Printing Office, NINCDS Monograph No. 15 DHEW Publication No. (NIH) 76-998, Stock No. 017-049-00060-7, U.S. 1975.

Henderson DJ: Significance of Vertebral Dyskinesia in Relation to the Cervical Syndrome. Journal of Manipulative and Physiological Therapeutics, 2:1, 1979.

Iversen LD, Clawson DK: Manual of Acute Orthopaedic Therapeutics. Boston, Little, Brown, and Company, 1977.

Jackson R: The Cervical Syndrome, ed 2. Springfield, Illinois, Charles C. Thomas, 1958.

Jackson RB: The Neurovascular Compression Syndromes. ACA Journal of Chiropractic, March--May 1963.

Jahn WT: Acceleration-Deceleration Injury. Journal of Manipulative and Physiological Therapeutics, 1:2, June 1978.

Janse J: The Integrated Purpose and Function of the Nervous System: A Review of Classical Literature. Journal of Manipulative and Physiological Therapeutics, 1(3), September 1978.

Janse J: Principles and Practice of Chiropractic. Lombard, Illinois, National College of Chiropractic, 1976.

Jefferson G: Discussion of Spinal Injuries. Proceedings of the Royal Society of Medicine, 21:625, 1928.

Jeffreys E: Disorders of the Cervical Spine. Boston, Butterworths, 1980.

Jirout J: Changes in the Atlas-Axis Relations on Lateral Flexion of the Head and Neck. Neuroradiology, 6:215, 1973.

Jirout J: The Influence of Postural Factors on the Dynamics of the Cervical Spine: A Comparison of the Reaction of Vertebrae on Lateroflexion in Sitting and in Recumbency. Neuroradiology, 4:239-244, 1972.

Jirout J: Patterns of Changes in the Cervical Spine on Lateroflexion. Neuroradiology, 2:164, 1971.

Jochumsen OH: The Curve of the Cervical Spine. ACA Journal of Chiropractic, August 1970.

Kapandji IA: The Physiology of the Joints, ed 2. New York, Churchill-Living stone, 1974, Vol III.

Kellgren JH: Observations on Referred Pain Arising from Muscle. Clinical Science, 3:175, 1938.

Korr IM: The Spinal Cord as Organizer of Disease Processes: Some Preliminary Perspectives, Journal of the American Osteopathic Association, September 1976.

Lawson SM, Crawford AH: Traction in the Treatment of Spinal Deformity. Orthopedics, 6(4):447-451, April 1983.

Lieb MM: Oral Orthopedics. In Gelb H (ed): Clinical Management of Head, Neck and TMJ Pain and Dysfunction. Philadelphia, W.B. Saunders, 1977.

MacEwen GD: A Look at the Diagnosis and Management of Scoliosis, Orthopaedic Review, 3:9, 1974.

Markovich SE: Painful Neuro-Muscular Dysfunction Syndromes in the Head: A Neurologist's View. American Academy of Cranio-Mandibular Orthopedics Meeting, New Orleans, September 1976.

Martinez JL, Garcia DJ: A Model for Whiplash. Journal of Biomechanics, 1, 1968, pp 23-32.

McKenzie JA: The Dynamic Behavior of the Head and Cervical Spine During "Whiplash." Journal of Biomechanics, 4:477-490, 1971.

Nelson WA: personal correspondence, San Francisco, California, 1980.

Panjabi MM, et al: Cervical Spine Mechanics as a Function of Transection of Components. Journal of Biomechanics, 8:327-336, 1975.

Phillips RB: The Irritable Reflex Mechanism. ACA Journal of Chiropractic, January 1974.

Phillips RB: Upper Cervical Biomechanics. ACA Journal of Chiropractic, October 1976.

Pierce WV: The Fifth Cervical Key, The Digest of Chiropractic Economics, 25:1, July/August 1982.

Reed RC: On Field Management of Athletic Injuries. ACA Journal of Chiropractic, July 1981.

Rehberger LP: Reversal of the Normal Cervical Curve, Roentgenological Briefs, Des Moines, IA, Council on Roentgenology of the American Chiropractic Association, date not shown.

Schafer RC: Chiropractic Management of Sports and Recreational Injuries, ed 2. Baltimore, Williams & Wilkins, 1986, pp 314–332.

Schafer RC: Chiropractic Physical and Spinal Diagnosis. Oklahoma City, Associated Chiropractic Academic Press, 1980, Chapter VIII.

Schafer RC: Clinical Biomechanics: Musculoskeletal Actions and Reactions, ed 2. Baltimore, Williams & Wilkins, pp 299–339.

Schafer RC: "Hot Shots" and Brachial Plexus Traction. Journal of the American Chiropractic Association, September 1982.

Schafer RC: Physical Diagnosis. Arlington, Virginia, American Chiropractic Association, 1988, pp 528–568.

Sharpless SK: Susceptibility of Spinal Roots to Compression Block. In Goldstein M (ed): The Research Status of Spinal Manipulative Therapy. Washington, DC, U.S. Government Printing Office, NINCDS Monograph No. 15, DHEW Publication No. (NIH) 76-998, Stock No. 017-049-00060-7, 1975.

Smith DM: Vertebral Artery. Roentgenological Briefs, Council on Roentgenology of the American Chiropractic Association. Date not shown.

Stish EE: Anthropokinetics. Journal of Health, Physical Education, and Recreation, 35:33, November-December 1964.

Travell J: Myofascial Trigger Points: Clinical View. In Bonica JJ, Albe-Fessard D (eds): Advances in Pain Research and Therapy. New York, Raven Press, 1976.

Turner EA: Spondylosis–Spondylitis–Spondylolysis. Roentgenological Briefs, American Council on Chiropractic Roentgenology. Date not shown.

Wax M: Procedures in Elimination of Trigger Points in Myofascial Pain Syndromes. ACA Journal of Chiropractic, October 1962.

West HG: Vertebral Artery Considerations in Cervical Trauma. ACA Journal of Chiropractic, December 1968.

White AA III, Panjabi MM: Clinical Biomechanics of the Spine. Philadelphia, J.B. Lippincott, 1978.

Whiting RJ: Cervical Spondylosis. Roentgenological Briefs, American Council on Chiropractic Roentgenology. Date not shown.

Wyke BD: Articular Neurology and Manipulative Therapy. In Aspects of Manipulative Therapy, Proceedings of Multidisciplinary International Conference on Manipulative Therapy, Melbourne, Lincoln Institute of Health Sciences, Carlton, Victoria, Australia, August 1979, pp 67-72.

Yashon D: Spinal Injury. New York, Appleton-Century-Crofts, 1978.

Zatzkin HR: The Roentgen Diagnosis of Trauma. Chicago, Year Book, 1965.

Zuidema GD, et al: The Management of Trauma, ed 3. Philadelphia, W.B. Saunders, 1979.

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