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Cervical Spine Trauma

By R. C. Schafer, DC, PhD, FICCManuscript Prepublication Copyright 1997

Copied with permission from ACAPress

BackgroundCommon Injuries and Disorders of theCervical Spine

PrevalenceEmergency Care

Initial AssessmentPosttraumatic Roentgenographic Clues

Injury of the Cervical Nerve RootsContributing and Complicating Factors

Motor AberrationsInterpreting Sensory Irregularities

Subluxation-Induced Reflex Syndromes

Neurovascular Implications of Upper

Cervical SubluxationsThe Vertebral ArteriesThe Vertebral and Deep Cervical Veins

Cerebrospinal CirculationThe Medulla Oblongata

The Vital Vagus

Classic Effects of Severe Cervical TraumaPlanes of Force and Their Consequences

Fractures and Dislocations of the AtlasFractures and Dislocations of the Axis

Severe C3C7 InjuriesSpinal Cord Injury

Vertebral Artery AbnormalitiesCervicothoracic Tunnel Compression

SyndromesOrigin

Clinical FeaturesClinical Maneuvers and Tests

Occipital and Cervical Subluxation

SyndromesFunctional Anatomy Relative to Cervical

SubluxationsFurther Clinical Implications

Cervical SpondylosisClinical ImplicationsEtiology

Clinical FindingsCase Management and Prognosis

Reversal of the Normal Cervical CurveClinical Findings

Case Management and PrognosisTraumatic Brachial Plexus Traction

Bikele's Test

Supine Tension TestCase Management

The Stinger SyndromeClinical Findings

ComplicationsSubluxation Induced Torticollis

Clinical FindingsEffects of Cervical Area Hypertonicity

Trigger-Point SyndromesManagement

Barre-Lieou SyndromeClinical Findings

Barre-Lieou Test


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Vertebrobasilar System Patency TestsMaigne's TestDeKleyn's Test

Hautant's Test

Arthrokinematics

Structural Characteristics of the CervicalRegion

The Upper Cervical SpineThe Occipitocervical ligaments

The Lower Cervical Area

KinematicsThe Upper Cervical Area

The Lower Cervical AreaThe Transitional Cervicothoracic Area

Applied Anatomy of the Cervical PlexusThe Brachial PlexusThe Cervicothoracic Junction Area

Clinical Management Electives In

Cervical Strain/Sprain/IVD Lesion

CommentaryExtension Strain/Sprain (Whiplash

Syndrome)Mechanisms

KinematicsEffects

Case Management Flexion Strain/SprainMechanisms

EffectsCase Management

Lateral Flexion Strain/Sprain

Cervical Disc DisordersDisc EncroachmentDisc Degeneration

Clinical FindingsCase Management

Traumatic Cervical ScoliosisEffect of a Flattening Curve

The Self-Stabilization FactorDisc Reactions in Cervical Scoliosis

Effect of Lateral Tilt in Cervical ScoliosisCervical Rib Syndromes

DifferentiationCase Management

Posttraumatic Headaches of Cervical Origin

Posttraumatic Rehabilitation Goals

Postural Strength and BalanceDynamic and Static ProprioceptionCervical Receptor Input

Normal Cervical Righting MechanismsCervical Strength Development

Rehabilitation Therapy Following CervicalTrauma

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 fordirectional orientation of the eyes and ears. Nowhere in the spine is therelationship between the osseous structures and the surrounding neurologic


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and vascular beds as intimate or subject to disturbance as it is in the cervicalregion.

BACKGROUND

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

Common Injuries and Disorders of the CervicalSpine

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 withoutneurologic 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 orirritation of the sensory fibers of the spinal accessory nerves as they exit withthe C2C4 spinal nerves. The C1 and C2 nerves are especially vulnerable

because they do not have the protection of an IVF. Radicular symptoms arerarely evident unless an IVD protrusion or rupture is present.

Prevalence

Because of its great mobility, relatively small structures, and weight-bearingrole, the cervical spine is a frequent site of severe spinal nerve injury andsubluxation/fixations. A large variety of cervical contusions, Grade 13 strainsand sprains, subluxations, disc syndromes, dislocations, and fractures will beseen as the result of trauma.

The most vulnerable segments to injury are the axis and C5C6 according toaccident statistics. Surprisingly, the atlas is the least involved of all cervical

vertebrae. In terms of segmental structure, the vertebral arch (50%), vertebralbody (30%), and IVD (30%) are most commonly involved in severe cervicaltrauma. While the anterior ligaments are only involved in 2% of injuries, theposterior ligaments are involved in 16% of injuries.


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EMERGENCY CARE

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 externalevidence. Immediate and obvious symptom of spinal cord injury parallel thoseof fractures of the spinal column. The establishment of an adequate airwaytakes priority over all other concerns except for spurting hemorrhage.

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

INITIAL ASSESSMENT

If there are no severe complaints or recognizable signs of major disability, askthe patient to conduct mild slow active movements if able to do so withoutdiscomfort. If slight straight axial compression on the head producesunilateral or bilateral radiating root pain, deep injury must be suspected andprecautions taken immediately. After the neck has been evaluated, checkpossible 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 shouldnever be asked to sit or stand until major disability has been ruled out. Thefirst point in accurate analysis is knowing the mechanism of injury. Withoutmoving the patient, check vital signs and palpate for swelling, deeptenderness, deformity, and throat cartilage stability. When logical, anotherperson should apply gentle bilateral traction on the cervical area via the skullduring palpation.

Are there bleeding, spasm, pain, motion restrictions, sensory changes, signs ofshock? Limb weakness or dysesthesia indicates nerve root compression.Injuries of the upper airway or alimentary canal feature ventilationabnormalities, stridor, a bubbling wound, subcutaneous emphysema,hoarseness and dysphagia, bloody sputum, nosebleed, bloody vomitus, orunexplained wound tenderness. Injuries to the cervical nerves are suggested

by deviation of the tongue, drooping mouth corner, sensory deficits, and


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Horner's syndrome. Cervical fractures are commonly associated with severepain, spasm, and joint stiffness.

Vascular injuries feature vigorous bleeding, absent superficial arterypulsations, 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 erythematouscontusion on the side of the neck. Palpation may encourage complete carotidocclusion.

POSTTRAUMATIC ROENTGENOGRAPHIC CLUES

On standard lateral and A-P views, the anterior and posterior soft tissuesdeserve 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 oreven 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 symmetryor widening of an apophyseal joint space. It is easy to miss lower cervicalfractures because they are often obscured on lateral views by the subject'sshoulders if proper precautions are not taken.

INJURY OF THE CERVICAL NERVE ROOTS

Neural dysfunction associated with either acute or chronic subluxationsyndromes basically manifest as abnormalities in sensory interpretationsand/or motor activities. These disturbances may be through one of twoprimary mechanisms: direct nerve or nerve root disorders or of a reflexnature.

Contributing andComplicating FactorsThe common subluxation picture is rarely pure. It is often superimposed onsubclinical 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,


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disc protrusions, dura and dentate thickening, arachnoid cysts, dura andarachnoid adhesions, and ossification of the posterior longitudinal ligament.

Loss of disc space, especially in the lower cervical area, may contribute as asource 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, thesedegenerative changes are not as pronounced during youth.

Motor Aberrations

Nerve root insults from subluxations may manifest as disturbances in motorreflexes and/or muscular strength. Examples include the deep tendon reflexes

such as seen in the reduced biceps reflex when involvement occurs between C5and C6; or the reduced triceps reflex when involvement occurs between C6and C7. These reflexes must be compared bilaterally to judge whetherhyporeflexia is unilateral. Unilateral hyperreflexia is pathognomonic of anupper motor neuron lesion. Prolonged and/or severe nerve root irritation mayalso produce trophic changes in the tissues supplied.

Interpreting Sensory Irregularities

When direct nerve root involvement occurs on the posterior root of a specificneuromere, it manifests as an increase or a decrease in sensitivity over thedermatome. A typical example is foraminal occlusion or irritating factorsexhibited clinically as hyperesthesia, particularly on the dorsal and lateralaspects 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 indexand middle fingers, and the ventroradial side of the forearm, thumb, indexand 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. Forexample, 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 pressurenear the nerve root or along its distribution may be particularly painful. Thepioneer chiropractic art of nerve tracing would be well to acquire.


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SUBLUXATION-INDUCED REFLEX SYNDROMES

It is generally accepted that certain spinosomatic and spinovisceral syndromesmay result from cervical subluxation complexes. For example, if the

involvement is in the C1C4 area, the cervical portion of the sympathetic chainor the 9th12th cranial nerves (as they exit from the base of the skull and passinto their compartments within deep cervical fascia) may be involved. Thesyndrome may include (1) suboccipital or postocular migraine; (2) greateroccipital nerve extension neuralgia; (3) mandibular, cervical, auricular,pectoral, or precordial neuralgia; (4) paroxysmal torticollis; (5) congestion ofthe upper respiratory mucosa, paranasal sinuses, or eustachian tube withhearing loss; (6) cardiorespiratory attacks; (7) ocular muscle malfunction; (8)pathologic hiccups; (9) scalenus anticus syndrome; or (10) painful spasm inthe suboccipital area.

Phillips describes that if a subluxation produces a stretching of theparavertebral musculature, there is a continuous barrage of afferent impulsesin the Group Ia fibers. "These afferent impulses monosynaptically bombardthe alpha motor neurons causing the paravertebral musculature to go intotetany. There is a cessation of this afferent barrage when the stretch isreleased. The muscle stretching also initiates afferent impulses in the Group IIafferents from flower spray endings, which may reinforce the spastic musclecondition."He explains that trauma to facet joints, disturbed articularrelationships, spasms of closely related muscles, and overlying trigger points -

-all the result of a subluxation-- inaugurate a barrage of flexor-reflex afferentimpulses via the Group IIIV fibers that converge on the internuncial pool inlamina 7 of the spinal cord. "This abundant supply of flexor-reflex afferentimpulses excites the alpha motor neurons through multisynaptic connectionscausing an excess of excitation of paravertebral muscles resulting in spasm."

NEUROVASCULAR IMPLICATIONS OF UPPERCERVICAL SUBLUXATIONS

Aside from nerve root dysfunction, subluxation complexes in the cervicalspine, especially the upper region, can have serious neurovascularconsequences. Function of the vertebral arteries, the vertebral veins and deepcervical veins, cerebrospinal circulation, the caudad medulla oblongata, andthe vital vagus nerve may be disturbed.


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The artery and vein supplying a spinal nerve course within the IVF betweenthe nerve and the fibrous tissue in the anterior portion of the foramen.Deprived mobility of any one or more segments of the spine correspondinglyinfluences area circulation, and the partial anoxia effected is likely to have aharmful influence on nerve function. Because of the vessels' position, it is

unlikely that circulation to the nerve would be disrupted without firstirritating or compressing the nerve because the arteries and veins are muchsmaller, the blood pressure within their lumen makes them somewhatresistant to compression, and nerve tissue is much more responsive toencroachment irritation.

The Vertebral Arteries

Janse explains that any cervical subluxation (particularly atlantal, axial, or

occipital) producing muscle spasm may produce unilateral or bilateralconstriction of the vertebral arteries resulting in circulatory impairment. Alarge number of equilibrium, cardiac, respiratory, cranial nerve,extrapyramidal, vagal, visual, and auditory symptoms may follow.

The vertebral nerve (sympathetic) courses along the vertebral artery withinthe arterial foramen of the cervical transverse processes. Irritation to thisnerve can occur from mechanical irritation to the vertebral artery anywherealong 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 fibershave not been found along the cervical roots, surgical decompression of anentrapped nerve root relieves symptoms attributed to the sympathetics. Themechanism for this effect is unclear.

The Vertebral and Deep Cervical Veins

Spasm of suboccipital muscles may cause a decided impediment of venousdrainage from the suboccipital area via vertebral and deep cervical veins. The

result is passive congestion with consequent pressure on the sensory nerves inthe area. This is often perceived by the patient as unilateral or bilateral painand a throbbing discomfort. The site may be palpated as knotty lumps withinsuboccipital muscles. The condition appears to be of a reflex nature that ismore common among people under mental tension or those who work closely

with their eyes over long periods.


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CerebrospinalCirculation

Constriction in the connecting area between the cerebral subarachnoid spaceand the vertebral canal can impair the escape of cerebrospinal fluid into the

inferior vertebral canal. This results in increased intracranial pressure. Anatlanto-occipital subluxation may cause the dura mater of the cisternacerebellaris to press against the posterior medullary velum and partiallyocclude the foramina of Luschka and Magendie and thus interfere with flowfrom the 4th ventricle. The increased intraventricular fluid accumulation canthus produce a variety of symptoms such as deep-seated stubborn "internalpressure" headaches, nausea, a tendency toward projectile vomiting, bizarreand unusual visual disturbances, and protopathic ataxia.

TheMedulla Oblongata

The medulla extends well into the lower reaches of the foramen magnum andthe ligament ring connecting it with the atlas, thus any type of occipital oratlantal subluxation may potentially affect this portion of the brain stem.Bilateral posterior shifting of the occiput or atlas can induce pressure in thepyramids or adjacent olivary bodies producing a syndrome of upper-motor-neuron involvement characterized by a degree of spastic paralysis or ataxia. Alateral shift of the occiput may cause pressure on the tubercle of Rolandoproducing 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 ofthe atlas, rotary subluxation of the atlas may induce pressure that can producea broad range of symptoms. The syndrome may include nasal and sinuscongestion, swallowing and speech difficulties, cardiac arrhythmias,functional coronary artery spasm, gastric and intestinal colic, and/or othersymptoms of vagal disturbance.

CLASSIC EFFECTS OF SEVERE CERVICALTRAUMA


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Planes of Force and Their Consequences

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

Compression Forces. Excessive compression forces on the neckcommonly lead to facet jamming and fixation, isolated or multiple fractures ofthe atlantal ring, or vertical, oblique, and/or bursting fractures of the lowercervical bodies.

Hyperextension Forces. The effects of forceful posterior bending mayinclude sprain of the anterior ligaments, wedging of the posterior anulus and

vertebral body, posterior subluxation, horizontal fracture of the anterior archof the atlas, fracture of the anteroinferior margin of a vertebral body,

compression of the posterior arch and associated structures, posteriorbilateral or unilateral dislocation, spinous process fracture, and/or traumaticspondylolisthesis.

Hyperflexion Forces. Excessive anterior bending may produce sprainof the posterior ligaments, compressive wedging of the anterior anulus and

vertebral body, anterior subluxation, anterior bilateral or unilateraldislocation 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 bendinginclude transverse process fracture, uncinate process failure, lateraldislocation-fracture of the odontoid process, lateral wedging of the anulus and

vertebral body, and/or brachial plexus injury.

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

Shear Forces. Flagrant shearing forces can disrupt the anterior orposterior ligaments, displace the end-plates, produce anterior or posteriorsubluxation or dislocation, create anterior or posterior fracture displacement


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of the dens, and/or cause anterior compressive fracture of the anterior ring ofthe atlas or vertebral body.

Fractures and Dislocations of the Atlas

Atlanto-occipital dislocations, often bilateral, are usually quickly incompatiblewith life. Any severe subluxation in the upper cervical area can lead toquadriplegia or death, often with little warning and few symptoms todifferentiate 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 tosevere pain and gross motor involvement. Tenderness may be acute over theposterior 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 fracturethe odontoid at its base, with possible odontoid posterior displacement. Thedanger of cord pressure is great. Open-mouth views, flexion-extension x-ray

views, or tomography may be necessary for accurate determination.

Severe C3C7 Injuries

Cervical fractures and dislocations are often the result of a severe fall, anautomobile accident, a football pile-up, or a trampoline or gymnastic mishap.Bruises on the face, occiput, and shoulders may offer clues to the mechanismof injury. Seek signs of vertebral tenderness, limitation in movement, musclespasm, and neurologic deficits. As in upper-cervical damage, carefulemergency management is necessary to avoid paralysis and death. Severefracture or dislocation of any cervical vertebra requires immediate orthopedicreferral. Nevertheless. keep in mind that overdiagnosing instability of C2 onC3 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 theC6 or C7 level after acute flexion or a blow to the flexed neck producingligamentous avulsion. There is an immediate "hot" pain in the area of thespinous process that is increased by mild neck flexion. Again, any injury to C6or C7 can be difficult to view on film because of overlapping structures.


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Spinal Cord Injury

There are direct and indirect classes of cephalad spinal cord injuries.Directinjury 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. Thesetypes of injury are generally associated with an open wound.Indirect injury tothe cord can be caused by the disturbance of tissues near the spine by violentforces such as falls, crushes, or blows.

When the cervical cord is injured, there is loss of sensation and flaccidparalysis cephally. The lower limbs exhibit spastic paralysis. If the space in

which the spinal fluid flows between the spinal cord and the surroundingvertebral 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 subluxationor fracture/dislocation occurs. Hemorrhage arises at the site with the samereaction as brain injury (liquefaction, softening, disintegration). Congenitalfusions and stenosis may predispose a child to spinal cord trauma during asporting activity.

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BRAL ARTE

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ALITIE

SVertebral artery abnormalities such as deflection and arteriosclerosis must bedetermined before any form of cervical manipulation or adjustment isperformed. Also, arteriosclerosis is no longer thought of as an "old person'sdisease." Autopsy studies of young soldiers killed in the Viet Nam War showed

well established systemic arteriosclerosis in the majority of the 1821-year agegroup.

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 inthe vertebral artery help to compensate for neck movements. Deflection maybe caused by any tensile stretching of the artery during neck trauma. In lateryears, deflection is commonly associated with bony spurs from covertebraljoints or grossly hyperplastic posterior vertebral articulations from arthrosis.

Smith explains that extension of the cervical spine allows the tip of the


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superior articular process of the posterior joint to glide forward and upward. Ifsufficiently hyperplastic, forced motion may cause encroachment on the

vertebral arteries and/or the IVFs. Deflection of the artery and any resultingsymptoms are exaggerated by rotation and/or extension of the neck. As aresult of pressure against the artery, there may be temporary lessening in the

volume of blood flow. Atheromatous changes may also occur within thevascular wall. Symptoms include headache, vertigo, nausea, vomiting,nystagmus, and suboccipital tenderness, which may be provoked by cervicalextension. Sometimes symptoms are aggravated by dorsal extension andrelieved by forward flexion with cervical traction.

CERVICOTHORACIC TUNNEL COMPRESSIONSYNDROMES

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

Several cervicotrhoracic syndromes fall in the class of neurovascularcompression syndromes (also termed thoracic outlet or inlet syndromes), eachof which may produce the symptom complex of radiating pain over the

shoulders and down the arms, atrophic disturbances, paresthesias, andvasomotor disturbances. These features, however, do not necessarily indicatethe specific cause of the problem.

Origin

Trauma to the head, neck, or shoulder girdle is a common factor. In somecases, poor posture, anomalies, or muscle spasm or contractures may beinvolved. Reduced tone in the muscles of the shoulder girdle, by itself, has

been shown to allow depression of the clavicle that narrows the thoracic outletand compresses the neurovascular bundle. Subluxation syndromes (eg,retrolisthesis) may also initiate these and other disturbances of the shouldergirdle.

Cervical pathology such as spinal canal or IVF encroachment by a bucklingligamentum flavum, spinal stenosis, or spurs should be a consideration.Degenerating dura and dentates become thickened, dura and arachnoid


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adhesions become prevalent, and osteochondrophytes may develop from theborders of the canal or foramen --all of which tend to restrict the cord and/ornerve roots during cervical motion.

Osteochondrophytes near the foramen can readily compress the vertebral

artery against the nerve root. Differential diagnosis must exclude a cervical ribetiology (rare), infectious neuritis, banding adhesions, arthritis of the shoulder

joint, clavicle fracture callus, bifid clavicle, cervical arthritis, subacromialbursitis, 1st rib subluxation and posttraumatic deformities, spinal or shouldergirdle malignancies, Pancoast's tumor of the lung apex, and heart disease.

Aneurysm of the subclavian artery is rare.

AnatomicalConsiderations. Working above and behind to produce shoulderabduction 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, symptomswere 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, andthis widens the space between the clavicle and 1st rib.

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

3. When the shoulder is retracted, the clavicle does not impinge thesubclavian vein but the tendon of the subclavius muscle compresses the veinagainst the 1st rib. The middle third of the clavicle pushes the neurovascular

bundle against the anterior scalenus medius, and this causes compression if aspace-occupying lesion is also present (eg, cervical rib, extrafascial band).

Clinical Features

Symptoms usually do not occur until after the ribs have ossified. Two groupsof manifestation are seen: those ofscalenus anticus syndrome and those dueto cervical rib pressure. The symptoms of cervical rib and scalenus syndromeare similar, but the scalenus anticus muscle is the primary factor in the


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should be observed while voluntarily laterally flexing his head toward the sidebeing examined. With the neck so flexed, the patient is instructed to rotate hischin toward the same side, which narrows the IVF diameter on the side ofconcavity. Pain or reduplication of other symptoms suggests a narrowing ofone or more IVFs.

Shoulder Depression Test. With the patient sitting, the examinerstands behind the subject. The patient's head is laterally flexed away from theside being examined. The doctor stabilizes the patient's shoulder with onehand and applies pressure alongside the patient's head with the palm of theother hand; stretching the dural root sleeves and nerve roots or aggravatingradicular pain if the nerve roots adhere to the foramina. Extravasations,edema, encroachments, and conversion of fibrinogen into fibrin can result ininterfascicular, 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 suggestadhesions between the nerve's dura sleeve and other structures in and aboutthe involved IVFs.

Cervical Distraction Test. With the patient sitting, the examinerstands to the side of the patient and places one hand under the patient's chinand the other hand under the base of the occiput. Slowly and gradually thepatient's head is lifted to remove weight from the cervical spine. Thismaneuver elongates the IVFs, decreases the pressure on the joint capsules

around the facet joints, and stretches the paravertebral musculature. If themaneuver decreases pain and relieves other symptoms, it is a probableindication of narrowing of one or more IVFs, cervical facet syndrome, orspastic paravertebral muscles.

Spurling's Test. This is a variation of the passive cervical compressiontest. The patient's head is turned to the maximum toward one side and thenlaterally flexed to the maximum. A fist is placed on the patient's scalp, and amoderate blow is delivered to it by the other fist. The patient's positionproduces 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, thusincreasing the symptoms.

Adson's Test. With the patient sitting, the examiner palpates the radialpulse and advises the patient to bend his head obliquely backward to theopposite side being examined, to take a deep breath, and to tighten the neck


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and chest muscles on the side tested. This maneuver decreases theinterscalene space and increases any existing compression of the subclavianartery and lower components (C8 and T1) of the brachial plexus against the 1strib. Marked weakening of the pulse or increased paresthesiae are signs ofpressure on the neurovascular bundle, particularly of the subclavian artery as

it passes between or through the scaleni musculature, thus indicating aprobable cervical rib. 1st rib, or scalenus anticus syndrome.

Wright's Test. With the patient sitting, the radial pulse is palpated fromthe posterior in the downward position and as the arm is passively movedthrough an 180 arc. If the pulse diminishes or disappears in this arc or ifneurologic symptoms develop, it suggests pressure on the axillary artery and

vein under the pectoralis minor tendon and coracoid process or compressionin 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'sradial 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 thepulse is examined. The test is positive if weakening or loss of the pulse occurs,suggesting pressure on the neurovascular bundle as it passes between theclavicle and the 1st rib, and thus a costoclavicular syndrome.

VERTEBROBASILAR SYSTEMPATENCY TESTS

Although cerebrovascular accidents are extremely rare following cervicalmanipulation, a few cases have been reported that justify special evaluation

before cervical manipulation. Four clinical tests are described below toevaluate the patency of the vertebrobasilar system. These tests are helpful butnot definitive in themselves.

Maigne's Test

The examiner places a sitting patient's head in extension and rotation. Thisposition is held for about 1540 seconds on each side. A positive sign isindicated by nystagmus or other symptoms of vertebrobasilar ischemia.

DeKleyn's Test


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The patient is placed supine on an adjusting table, and the head rest islowered. The examiner extends and rotates the patient's head, and thisposition is held for about 1540 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 abductedforward with the palms turned upward (supinated). The patient is instructedto close his eyes, and the examiner extends and rotates the patient's head. Thisposition is held loosely for about 1540 seconds on each side. A positive sign isfor one or both arms to drop into a pronated position.

ARTHROKINEMATICS

Many injuries of the cervical spine can be attributed to the small curvedvertebral bodies, the wide range of movement in many planes, and the morelaterally placed intervertebral articulations that require nerve roots to leavethe spinal canal in an anterolateral direction. There is greater space within thecervical canal than below, but this space is occupied by cord enlargement to

accommodate the brachial and cervical plexuses. The segmental function ofthese plexuses is shown in Table 1.

Table 1 Segmental Function of Cervical Nerves

Segment Function

CERVICAL PLEXUS (C1C4)

C1 Motor to head and neck extensors, infrahyoid, rectus capitis anterior

and lateral, and longus capitis.

C2 Sensory to lateral occiput and submandibular area; motor, same as C1plus longus colli.

C3 Sensory to lateral occiput and lateral neck, overlapping C2 area; motorto head and neck extensors, infrahyoid, longus capitis, longus colli;

levator scapulae, scaleni, and trapezius.


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C4 Sensory to lower lateral neck and medial shoulder area; motor to head

and neck extensors, longus coli, levator scapulae, scaleni, trapezius,and diaphragm.

BRACHIAL PLEXUS (C5T1)

C5 Sensory to clavicle level and lateral arm (axillary nerve); motor to

deltoid, biceps, biceps tendon reflex. Primary root in shoulderabduction, exits between C4-C5 discs.

C6 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 wristextension, exits between C5-C6 discs.

C7 Sensory to second finger; motor to wrist flexors, finger extensors,

triceps, triceps tendon reflex. Primary root in finger extension, exitsbetween C6-C7 discs.

C8 Sensory to medial forearm (medial antebrachial nerve), ring and little

fingers (ulnar nerve); motor to finger flexors, interossei; no reflexapplicable. Primary root in finger flexion, exits between C7-T1 discs.

T1 Sensory to medial arm (medial brachial cutaneous nerve); motor tointerossei; no reflex applicable. Primary root in finger abduction, exits

between T1-T2 discs.

STRUCTURAL CHARACTERISTICS OF THECERVICAL REGION

In the healthy cervical (or lumbar) spine displaying a moderate degree oflordosis, a good share of weight bearing is on the zygapophyses because theline of cumulative loading of compressive forces is posterior to the center ofthe vertebral bodies. This produces considerable articular jamming that tends

to restrict a wide range of rotation. That is, the rotary motion occurring at thezygapophyses does so on firmly compressed facets. Fortunately, there is somestructural adaptation for this. For the normal adult spine, the cervical discsaverage 3 mm in thickness, there is a 2:5 disc/body ratio, a 4:7 nucleus/anulusratio, and the nucleus sits in a position that is slightly posterior to the center ofthe disc. In addition, the surface area of the cervical facets is larger inproportion to the surface area of the vertebral body than at any other region of


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the spine. This design contributes greatly to the overall segmental base ofsupport in the neck. In fact, the weight-bearing surfaces of the facets are morethan half (67%) that of the centrum. In addition, the superior facets below theaxis face posterosuperior and medial to compensate for the normalanteroinferior tilt of the vertebral bodies.

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

The Upper Cervical Spine

The spinal canal of the upper cervical region is relatively large toaccommodate the cervical enlargement of the cord. The pedicles, apophyseal

joints, uncinate processes, and transverse processes have characteristicspeculiar and specific to the cervical spine.

The Atlas. The atlas can be considered a sesamoid between the occiput andaxis that serves as a biomechanical washer or bearing between the occipitalcondyles and the axis. The absent body of the atlas is represented by itsanterior arch and the dens of the axis, and the inner aspect of the anterior archcontains a facet for the dens. An IVD does not exist between the occiput andthe 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 likeepaulets on sloping shoulders. The plane is about 110 to the vertical. To allowmaximum rotation of the upper cervical complex without stress to the

contents of the vertebral canal, the instantaneous axis of rotation is placedclose to the spinal cord (ie, near the atlanto-odontoid articulation).

The C2C3 Interface. Rotation of C2 on C3 is limited by a mechanical blockingmechanism that protects the vertebral artery from excessive torsion. Theanterior tip of the superior articular process of C3 impinges on the lateralmargin of the foramen transversarium of C2. This blocking mechanism is also


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found in the subjacent cervical vertebrae.

The Occipitocervical Ligaments

It is well to be able to mentally picture the upper cervical ligament complex forserious sprains in this area can occur. The cross-shaped cruciate ligamentcompletely secures the odontoid process. Its main portion is the triangular

bilateral transverse ligament, which passes posteriorly on the dens andconnects to the lateral masses of the atlas, transversing in front of the spinalcord. Its main function is to restrict anterior translation of the atlas. There arealso 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 fracturesprior to ligament failure. In addition, accessory atlantoaxial ligaments extend

superiorly and laterally from the base of the inferior vertical cruciate and jointhe 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-cervicalregion. The laminae are slender and overlap, and this shingling increases withage. The osseous elevations on the posterolateral aspect forming theuncovertebral pseudojoints tend to protect the spinal canal from lateral IVDherniation, but hypertrophy of these joints added to IVD degeneration canreadily lead to IVF encroachment. The IVDs are broader anteriorly thanposteriorly to accommodate the cervical lordosis.

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

The Capsular Ligaments. The short, thick, dense capsular ligaments bind thearticulating processes of each vertebral motion unit, enclosing the articularcartilage and synovial tissue. Their fibers are firmly bound to the periosteumof the superior and inferior processes and arranged at a 90 angle to the planeof the facet. This allows maximum laxity when the facets are in a position ofrest. They normally allow no more than 23 mm of movement from the


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neutral position per segment, and possibly provide more cervical stability thanany other ligament. Capsulitis from overstretch in acute subluxation iscommon. The posterior joint capsules enjoy an abundance of nociceptors andmechanoreceptors, far more than any other area of the spine. Within thecapsule, small tongues of meniscus-like tissue flaps project from the articular

surfaces into the synovial space. They are infrequently nipped in severe jarringat an unguarded moment during the end of extension, rotation, or lateral

bending, establishing a site of apophyseal bursitis.

The Lower CervicalPerivertebral Ligaments. The five lower, relativelysimilar, cervical vertebrae have eight intervertebral ligaments: four posteriorand four anterior in terms of the motion unit. The anterior ligaments are theanterior longitudinal ligament, the anulus fibrosus, the posterior longitudinalligament, and the intertransverse ligament. The posterior ligaments are theligamentum flavum, the capsular ligaments, and the interspinous and

supraspinous ligaments.

The Intervertebral Foramen. The boundaries of the cervical IVFs are designedfor motion rather than stability as compared with the thoracic and lumbarregions. The greatest degree of functional IVF diameter narrowing occursipsilaterally in lateral bending with simultaneous extension.

KINEM

ATICSThe head may be flexed forward so the chin strikes the sternum or thrownsideward so that the ear strikes the shoulder and the neck can still be withinthe normal range of motion. It is most rare, however, that the occiput strikesthe 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 latteroccurs quite freely in the upper cervical area and is progressively restrictedcaudally. The specific ranges of cervical motion differ among so manyauthorities that any range offered here should be considered hypotheticaldepending on individual planes of articulation, other variances in structuraldesign (eg, congenital, aging degeneration, posttraumatic), and soft-tissueintegrity. This variance in opinion is also true for the centers of motion.


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Upper-Cervical Instability. Moderately strong soft-tissue connections exist inthe occiput-atlas-axis complex. Bone, muscle, tendon, ligament, fascia, andlymph node abnormalities tend to restrict motion, while tissue tears and laxligaments without associated muscle spasm may allow too much motion.

Stability is provided the C1C2 joint by paravertebral ligaments and muscleattachments. When weakening of these supports occurs (eg, trauma, posturalstress, rheumatoid arthritis), a dangerous state of instability arises. Eachinfant presents a considerable degree of cervical instability because of therelatively large head weight superimposed on the small underdeveloped spine.

Extension and Flexion. Considerable cervical motion is concentrated inspecific 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 thanat the anterior aspect of the vertebral body.

Active motion. Regional active cervical flexion and extension motions aretested by having the patient raise and lower the chin as far as possible withoutmoving the shoulders. Note smoothness of motion and degree of limitation

bilaterally.

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

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

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

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


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

Lateral Flexion. Cervical lateral bending is essentially performed by theunilateral contraction of the neck flexors and extensors with motion occurringin 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 rotateanteriorly on the side of the concavity so that the vertebral bodies arc furtherlaterally than the spinous processes.

The Lower Cervical RegionThe lower cervical IVDs contain an exceptional amount of elastin, whichallows the IVDs to conform to the many possible planes of movement.Excessive flexion is limited by ligament and muscle restraints on theseparating posterior arches. Overextension is limited by bony apposition.Other factors include the resistance of the anular fibers to translation, thestiffness property of the anulus relative to its vertical height, and the physical

barrier produced by the uncinate processes that are fully developed in lateadolescence. Major joint movements and their innervation are shown in Table

2.

Table 2 Major JointMovements and TheirInnervation

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)


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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- andlower-cervical spine are the anulus fibrosus, the anterior and posteriorligaments, and the area muscles, especially, which serve as importantcontributing stabilizers. On dynamic palpation, any segmental motionexceeding 3 mm should arouse suspicions of lack of ligament restraint.

Neurologic Insults. There is a rough correlation between the degree ofstructural damage present and the extent of neurologic deficit. This is moretrue in the lower cervical area than in the upper region where severe damagemay appear without overt neurologic signs. In either case, it's doubtful that a

deficit would exhibit without an unstable situation existing. It is not unusualfor a patient to display a neurologic deficit without static displacement; ie, thevertebral segment has rebounded back into a normal position of rest.

Segmental Angulation. Angulation of one vertebral segment on a lateralroentgenograph more than 11 greater than an adjacent vertebra that is notchronically compressed indicates instability and pathologic displacement.

While conservative traction may reduce the associated displacement, it isdoubtful 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 distinctlygliding translation. During flexion and extension, the superior vertebra'sinferior facets slide anterosuperior and posteroinferior on the inferior

vertebra's superior facets. During full flexion, the facets may be almost if notcompletely separated. Consequently, an adjustment force is usuallycontraindicated in the fully flexed position. The center of motion is often


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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 forwardin flexion, is also normal near the end of the range of motion. The facets alsotend 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 onflexion, narrow on extension, and close on the concave side of lateral flexion.Because of the anterosuperior slant of the lower cervical facets, an inferiorfacet that moves downward must also slide posterior, and vice versa.

AdjustmentPrecautions. Any corrective adjustment must consider the state ofthe cervical curve, planes of articulation, facet tilting, and degree of facetopening, as well as anyunderlying 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 rotatetoward the concavity while the spinous processes swing in a greater arc towardthe convexity. Note that this is exactlyopposite to the coupling action in thelumbar spine. During cervical bending to the right, for example, the right facetof the superior vertebra slides down the 45 plane toward the right andposterior 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 ratioof axial rotation and lateral bending produces a subluxation or unilateral facetdislocation.

The amount of cervical rotation coupled with lateral flexion varies with thesegmental 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 rotationdecreases. For example, at C7, there is 1 of rotation for every 7.5 of lateralflexion, a 2:15 ratio.

Ranges ofMotion. All cervical vertebrae from C2 to C7 partake in flexion,extension, rotation, and lateral flexion, but some segments (eg, C5) are moreactive than others. In the C3C7 area, flexion and extension occur as slightgliding translation of the upper on the lower facets, accompanied by discdistortion. The site of greatest flexion is near the C4C5 level, while extensionmovement is fairly well diffused. This fact likely accounts for the highincidence of arthritis at the midcervical area. Rotation in this region is greatestnear the C5C6 level, slightly less above and considerably less below. Lateral

bending in greatest near the C2C3 level and is diminished caudally. The arc


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of lateral motion is determined by the planes of the covertebral joints.

The TransitionalCervicothoracic 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, whencervical alignment is poor, equal concern must be given to reduce anexaggerated thoracic kyphosis because the positions of the cervical andthoracic regions are interrelated; ie, a thoracic kyphosis is usuallyaccompanied by a compensatory cervical lordosis, and vice versa.

In the cervicothoracic area, normal movement is somewhat similar to that inthe 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 thesacrum and C7 is relatively immobile on T1. Most movement in thecervicothoracic junction is at C6C7 and primarily that of rotation.

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

APPLIED ANATOMY OF THE CERVICAL PLEXUS

The dura of the spinal cord is firmly fixed to the margin of the foramenmagnum and to the 2nd and 3rd cervical vertebrae. In other spinal areas, it isseparated from the vertebral canal by the epidural space. Since both the C1nerve and the vertebral artery pass through this membrane and both are

beneath the superior articulation of the atlas and under the overhangingocciput, atlanto-occipital distortion can produce traction of the dura materproducing irritation of the artery and nerve unilaterally and compressionalocclusion contralaterally. De Rusha feels that this helps us understand those

cases of suboccipital neuralgia where a patient upon turning his head to oneside increases the headache and vertigo that are relieved when the head isturned to the opposite side.

There is also a synapse between the upper cervical nerves and the trigeminalnerve, which also supplies the dura mater. This may explain why irritation ofC1 results in a neuralgia not only confined to the base of the skull but is also


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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 theposterior arch of the atlas and above the lamina of the axis, referring pain tothe atlanto-occipital area and sometimes to the vertex of the scalp.

The superficial sensory cutaneous set of the cervical plexus (C1C4) isfrequently 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 occipitalneuralgia,involving the posterior area of the occipitofrontalis muscle, mastoidprocess, and upper posterior aspect of the auricle; (2) greater auricularneuralgia,extending in front and behind the auricle, skin over the parotidgland, paralleling the distribution of the auriculotemporal branch of thetrigeminus and easily misdiagnosed as chronic trifacial neuralgia; (3) cervicalcutaneous 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, theneuralgia may involve the suprasternal area, pectoral area, or deltoid area.Thus, sternoclavicular and acromioclavicular neuralgias may originate in thespinal levels of the supraclavicular nerve.

Table 3 Nerve Function of the Cervical Plexus(C1C4)

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, longuscapitus, longus colli, hyoid muscles,

sternocleidomastoideus, trapezius, levator scapulae,scalenus medius.

Phrenic Sensory to costal and mediastinal pleura and


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pericardium. Motor to diaphragm.

De Rusha suggests that dysphagia and dysarthria may at times be due toupper cervical involvement rather than a CNS situation. The C1 joins thehypoglossal nerve supplying the intrinsic muscles of the tongue. It thendescends to join the descending cervical that is derived from C2 and C3. Aloop of nerves, the ansi hypoglossi, which supplies muscles necessary fordeglutition and speaking, is arises from C1C3.

Irritative lesions involving the cervical articulations may in turn irritate thesympathetic nerve plexuses ascending into the cranium via the vertebral andcarotid 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 wellas partially compressing the vessel. To appreciate this, note that the visualcortical area of the occipital lobe requires an ideal blood supply dependent onthe sympathetics ascending the great vessels of the neck, and this holds truefor the inner ear as well.

To test this syndrome, De Rusha suggests having the supine patient read someprinted 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 acuityor reduced tinnitus.

THE BRACHIAL PLEXUS

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

Table 4 Nerve Function of the Brachial Plexus(C5T1)

Nerve Function


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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 CERVICOTHORACIC JUNCTION AREA

The area of cervicothoracic transition is a complex of prevertebral andpostvertebral fascia and ligaments subject to shortening. It offers a multitudeof 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 levatorcostarum and scapula --all subject to spastic shortening and fibrotic changes

that tether normal dynamics.

CLINICALMANAGEMENT ELECTIVES INCERVICAL STRAIN/SPRAIN/IVD LESION

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, andsecondary infection by disinfection, protection, and rest; and to enhancehealing mechanisms. Common electives include:

Disinfection of open skin (eg, scratches, abrasions, etc)CryotherapyCold packs


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Ice massageVapocoolant sprayPressure bandageProtection (padding)Indirect therapy (reflex therapy)

Iontophoresis/phonophoresisAuriculotherapyMeridian therapySpondylotherapy (upper dorsal)Mild pulsed ultrasoundPulsed alternating currentRestBedrestFoam/padded applianceImmobilization

BracePlaster castRigid applianceIndicated diet modification and nutritional supplementation.

2. Stage ofPassive Congestion

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

Indirect articular therapy (reflex therapy)Alternating superficial heat and coldPressure bandageProtect lesion (padding)Light nonpercussion vibrotherapyMild passive exercise of adjacent jointsMild surging alternating currentMild pulsed ultrasoundMeridian therapyPhonophoresisRestBedrestFoam/padded applianceImmobilizationBrace


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Rigid appliancePlaster castOrthopedic pillowIndicated diet modification and nutritional supplementation.

3. Stage of Consolidation and/or Formation of FibrinousCoagulant

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

Mild articular adjustment technicsMoist superficial heatThermowraps

Spray-and-stretchModerate active range-of-motion exercisesMeridian therapy

Alternating tractionSinusoidal currentUltrasoundPhonophoresisMicrowave

VibromassageHigh-volt therapyInterferential currentSpondylotherapy (upper dorsal)Mild transverse friction massageMild proprioceptive neuromuscular facilitation techniquesRest and ImmobilizationFoam/padded applianceSemirigid applianceOrthopedic pillowIndicated 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 tendernesslikely remains. The major goals are to defeat any tendency for the formation ofadhesions, taut scar tissue, and area fibrosis and to prevent atrophy. Commonelectives are:


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Prudent deep heatArticular adjustment technicsSpondylotherapy (upper dorsal)Local vigorous vibromassageTransverse friction massage

Spray-and-stretchActive range-of-motion exercises without weight bearingMotorized alternating tractionNegative galvanismUltrasoundSinusoidal and pulsed muscle stimulationHigh-volt therapyInterferential currentMeridian therapyProprioceptive neuromuscular facilitation techniques

Flexible foam/padded applianceOrthopedic pillowIndicated diet modification and nutritional supplementation.

5. Stage of Reconditioning

Direct articular therapy for chronic fixationsProgressive remedial exercisePassive stretchingIsometric static resistanceIsotonics with static resistanceIsotonics with varied resistancePlyometrics

AerobicsOrthopedic pillowIndicated diet modification and nutritional supplementation.

COMMENTARY

Extension Strain/Sprain (Whiplash Syndrome)

Traumatic overextension of the neck is not the most common cervical injury,but it's certainly the most publicized. Forceful extension produces tearing of


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the anterior longitudinal ligament that may coexist with an avulsion fractureat the anterior vertebral bodies. Pedicle fracture or severe posteriorsubluxation may also occur. Tenderness will usually be shown along the lateralmusculature. Upper extremity pain or numbness and restricted cervicalmotion 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 areusually administered from below upward; eg, an uppercut to the chin or a

blow to the forehead while running forward. This is in contrast to thecompressive type of hyperextension or hyperflexion injury where the force isusually from above downward. Thus, knowing the direction of force, even if

the magnitude is unknown, is important in analyzing the effects. A facialinjury usually suggests an accompanying extension injury of the cervical spineas the head is forced backward either by an external force or as a defensivemaneuver.

Kinematics

In whiplash resulting from a mild automobile collision, the cervical injury isdue to indirect trauma from acceleration-deceleration forces. If the head doesnot strike something, the damage is produced solely by inertia forces. The

body moves at the same speed as the automobile. If the automobile is struckfrom the rear, the unrestrained head is whipped backward, because the head isnot restrained by the seat, and then rebound forward. If the automobile isstruck from the front or hits a relatively immovable object, the head is thrownforward and then rebound backward. Thus, the inertia force displaces thehead in the direction opposite to the automobile's acceleration. The firstmovement is that of translation producing a shearing force at the base of theneck 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 impactthat is followed by rebound extension. The rebound is produced by the rapiddeceleration of the automobile, the impact from the seat, and the stretch reflexproduced in the elongated neck and upper dorsal muscles. This reflex can bequite severe. Because it occurs when the neck is at its full range of movement,the pull generates considerable compression as well as extension.


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Effects

When the head is violently thrown backwards (eg, whiplash), the damage mayvary from minor to severe tearing of the anterior and posterior longitudinal

ligaments. This flattens the cervical curve in about 80% of cases, and a degreeof facet injury must exist even if not evident on film. Stretching to the point ofhematoma can occur in the scalene muscles, sternocleidomastoideus, longuscapitis, and longus cervicis.

Severe cord damage may occur that is usually attributed to momentarypressure by the dura, ligamentum flavum, and laminae posteriorly, even

without roentgenologic evidence. Even without any cord deficit, severedamage to the nerve roots may occur as the facets jam and close on the IVFs,especially if fracture occurs. Incidence is highest at the C4C6 area. Severe

stretching of the vertebral arteries, sympathetic trunk, nerve root, and spinalcord attachments to some degree is inevitable.

Cailliet points out that it is difficult to visualize a sprain causing rupture of theligaments of a joint without causing some derangement of the opposing jointsurfaces, which by definition is an orthopedic subluxation. If a whiplash injuryis considered a severe sprain, an orthopedic subluxation injury must beassumed to have occurred even if it has been spontaneously reduced. Suchsubluxations may occur during the initial movement and/or the reboundmovement, and it is not unusual to have manifestations of a flexion sprain

superimposed on manifestations of an extension sprain. In the typicalwhiplash injury, whether it be from hyperextension or hyperflexion or both,the effects of traumatic elongation and compression are compounded byunderlying fixations, arteriosclerosis, spondylosis, ankylosing spondylitis, etc.

CaseManagement

Treatment of mild or moderate injuries not exhibiting severe neurologictrauma 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 clinicalsymptoms and signs, and graduated therapeutic exercises. Continuoustraction, which reduces the cervical lordosis, may be helpful in extensioninjuries after the acute stage, but it would usually be contraindicated wherethe cervical curve has reversed (eg, flexion strain). The previously describedtemplate offers several beneficial electives.


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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 theanterior cervical spine and posterior soft tissues as the skull is forced forward.Excessive flexion may also be a part of whiplash; ie, superimposed on anexcessive 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 andposttraumatic osteoarthritis may follow, which lead to spondylosis.

CaseManagement

Management is similar to that of extension injuries except that the period of

necessary immobilization is often shorter (68 weeks).

Lateral Flexion Strain/Sprain

Traumatic brachial plexus traction syndromes have been described in anearlier paper of this series. These injuries usually occur when the head is notonly severely flexed sideward but also flexed forward and downward below theshoulder.

OCCIPITAL AND CERVICAL SUBLUXATIONSYNDROMES


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Vertebral subluxations are difficult to classify under normal categories ofinjury because they can involve bone, joint, muscle, fascia, ligament, capsule,disc, nerve, cord, spinal fluid, and vascular tissues. Inasmuch as all freelymovable articulations are subject to subluxation, the atlanto-occipitaldiarthrosis 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 theatlas about 1/20th the circumference of the skull and a variety of spinalmuscles, subject to spasm, have their attachments on the occiput.

Aside from direct trauma, disturbances in the upper-cervical area usually arisefrom muscular spasm of one or more of the six muscle bundles havingattachments on the occiput, atlas, or axis. Unequal tension and ultimatefibrotic changes within the perivertebral structures can readily influence thedelicate nerve fibers and vascular and axoplasmic flow. The vertebral artery isfrequently involved by compression of the overlying muscles in the

suboccipital triangle. West points out that the vertebral artery can becompletely occluded during postmortem studies just by turning the head

backward and to the opposite side

Functional Anatomy Relative to CervicalSubluxations

The artery and vein supplying a spinal nerve course within the foramenbetween the nerve and the fibrous tissue in the anterior portion of the

opening. It is unlikely that circulation to the nerve would be disrupted withoutfirst irritating or compressing the nerve because the arteries and veins aremuch smaller, blood pressure within the lumen makes them not easilycompressed, and nerve tissue is much more responsive to encroachmentirritation. Nevertheless, loss of mobility of any one or more segments of thespine correspondingly influences its circulation.

Without the massing effects of motion, collateral microcirculation and CSFflow along the nerve root is hampered. The resulting partial anoxia, venouscongestion, and stagnant lymph and CSF have a harmful influence on nerve

function. This is one reason why attaining the highest degree of normalmobility possible after trauma is so important in chiropractic rehabilitation.Mobility reflects a joint that is free of stasis, binding adhesions, taut scartissue, 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


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normal range of motion, it's no longer competent to fully participate in idealcoordinated spinal dynamics. The affected area becomes the target for unusualstress, weight-bearing and traumatic. In addition to the attending circulatory,neuromechanical, and static changes in the involved area, there is disturbedreflex 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 canpredispose subluxations from minor overstress. The weight of the head along

with activity demands may contribute to chronic degenerative spondylosisoften superimposed on asymptomatic anomalies. A vicious cycle is seen wheresubluxation contributes to degenerative processes and these processescontribute to subluxation. This poses the question when pain fades, "Whencan the patient be discharged?" But a better question would be, "How longshould 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 alongthe cranial nerve pathways that emit from the skull and pass intimately

between and under suboccipital fasciculi. Five of the cranial nerves are thusvulnerable: the facial, glossopharyngeal, vagus, spinal accessory, and

hypoglossal. In addition, circulatory impairment of major and minor nerves ofthe neck may alter the function of those cranial nerves that do not exit fromthe skull proper (eg, the olfactory, optic, oculomotor, trochlear, trigeminal,abducens, and auditory) but which are contained within the cranium andremote from direct vertebral subluxation encroachment effects. We should notoverlook the fact that it is essentially muscle that produces and maintains thesubluxation. 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 fractureof the articular processes. The body of any vertebra follows the plane of thearticular surfaces in movement. If a spinous process moves left, it does so byinscribing an arc toward the superior and anterior while simultaneously theright transverse process moves inferiorly and somewhat posteriorly. It is thusimprobable for an individual vertebra to be rotated straight right or left on itslongitudinal axis. A typical vertebra cannot be subluxated without an articular


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the posterior vertebral body and the ligament. This portion of the anulus, intime, becomes fibrous and then calcifies. It is for this process that posteriorosteophytes prevail in the cervical and lumbar regions, while anterior spursare 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 lowerextremity osteoarthritis. Pre-existing spinal stenosis, a thickened ligamentumflavum, a protruding disc, and spur formation not uncommonly complicatethe picture of cervical spondylosis. There is almost no correlation between thedegree of perceived pain in the neck and the degree of arthritic changes notedin early x-ray films. The weight of the head in faulty posture (eg, exaggerated

dorsal kyphosis and cervical lordosis) along with activity stress may contributeto chronic degenerative spondylosis often superimposed on asymptomaticanomalies. Again we may see a vicious cycle in which subluxation contributesto degenerative processes, and these processes contribute to subluxationfixation.

Clinical Findings

The onset is usually rapid and insidious but may be subjectively andobjectively asymptomatic. The classic picture is one of a middle-aged person

with greatly restricted cervical motion with marked muscle spasm, positivecervical compression test, insidious neck and arm pain and paresthesiaaggravated by sneezing or coughing, acute radiculopathy from disc herniation,and usually some muscle weakness and fasciculations. A general rule statesthat central herniation produces local neck pain while lateral herniationproduces upper extremity pain.

Whiting lists the manifestations that develop in spondylosis to also includeneck crepitus, subjective or objective; local neck tenderness; headaches; neckpain radiating to the scapulae, trapezius, upper extremities, occiput, or

anterior thorax; extremity muscle weakness; paresthesia of the upper and/orlower extremities; dizziness and fainting; impaired vibration sense at theankle; hyperactive patellar and Achilles reflexes; and positive Babinskiresponses. From this one can see why the diagnosis is made fromroentgenologic findings. The Davis series may suffice, but special views,tomography, myelography, or discography may be necessary for firmdiagnosis.


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Because of the constant weight of the head, postural strains, occupationalinsults, degrees of congenital anomalies, and posttraumatic or postinfectioneffects with or without associated disc involvement, the development ofchronic degenerative spondylosis offers some distinct progressive

characteristics: (1) flattening of the cervical spine from muscle spasm andadhesion development, (2) A-P fixation and restricted mobility, (3) thinning ofthe atlanto-occipital and atlantoaxial articular plates resulting in motionrestriction, (4) middle and lower cervical disc wearing and thinning whichnarrows the IVFs, (5) disc weakness encouraging nuclear shifting andherniation contributing to nerve encroachment, (6) osseous lipping and spurs

with extensions into the IVFs, and (7) infiltration and ossification ofparavertebral ligaments adding to inflexibility and pain upon movement.

CaseManagement andP

rognosisWhiting brings out that it is fortunate that most people with cervicalspondylosis are asymptomatic because there is no correction per se. Initialtreatment is aimed at reducing symptoms of neurologic and vasomotorinvolvement or treating the soft-tissue injury superimposed on the pre-existing spondylosis. A trial of conservative treatment with emphasis onpostural alignment may be preferred in cases demonstrating signs of eithercervical radiculopathy and/or myelopathy.

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

Exacerbation of symptoms is quite common, and months or years may elapsebetween 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 inpermanent partial disability of the cervical spine with symptoms far out ofproportion to the severity of the injury.


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REVERSAL OF THENORMAL CERVICAL CURVE

In contrast to the primary thoracic kyphosis that is a structural curve, thecervical and lumbar anterior curves are functional arcs produced by their

wedge-shaped IVDs and they normally flatten in the nonweightbearing supineposition. Likewise, they quickly adapt to changes involving the direction offorce. A pathologic straightening of the normal anterior curve of the cervicalspine, as viewed in a lateral weight-bearing x-ray film, results in mechanicalalteration of normal physiologic and structural integrity. The normal vertical

A-P line of gravity, as viewed laterally with a plumbline, falls approximatelythrough the odontoid and touches the anterior border of T2. As the cervicalspine tends to flatten in the erect position, the gravity line passes closer to thecenter of the cervical discs.

Clinical Findings

Cervical flattening is usually the result of paraspinal spasm secondary to anunderlying injury, irritation, or inflammatory process. The acute clinicalpicture is often torticollis. Other manifestations include headaches (occipital,occipital-frontal, supraorbital), vertigo, tenderness elicited on lateral C4C6nerve roots, neuritis involving branches of the brachial plexus due to nerve-root pressure, hyperesthesia of one or more fingers, and loss or lessening ofthe biceps reflex on the same or contralateral side. In rare instances, thetriceps 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 bythe straightened cervical spine (78% cases), anterior and posterior subluxationon flexion and extension views, narrowing of IVD spaces at C4C6 in 46% ofcases, discopathy at the affected vertebral level as the injury progresses, andosteoarthritic 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 toreview the biomechanics involved. The nucleus of the disc serves as a fulcrumduring flexion and return extension. When the spine is subjected to bendingloads 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 sufferscompression, thins, and bulges. Concurrently, the nucleus bulges on the sideof tension and contracts on the side of compression, which increases tension


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on the adjacent anulus. This creates a self-stabilizing counteracting flexionforce to the vertebral motion unit that aids a return to the resting position.

CaseManagement andP

rognosis

Specific correction of offending vertebral subluxations should beaccomplished. Adjunctive care includes massage and methods to reducemuscle spasm such as ultrasound, diathermy, hydrocollator packs, reflexspinal techniques, and a rolled towel placed under the neck in the supineposition to increase the cervical curve. The individual should be instructed tosleep 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 casesof minimal cervical discopathy, at least symptomatic relief can be expected.Prognosis is poor in advanced degenerative osteoarthritis.

TRAUMATIC BRACHIAL PLEXUS TRACTION

The branches of the brachial plexus in the shoulder lie just anterior to theglenohumeral joint. The axillary nerve runs just below the joint. In brachialplexus 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-armpalsies (most common), and lower-arm palsies. Motor disturbances are themain feature as sensory loss is obscured by overlapping innervation.

The termErb's palsy refers to the effects of a stretch injury or avulsion of theupper roots of the brachial plexus. In contrast,Klumpke's palsy means theeffects 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 armlaterally to a horizontal and slightly backward position. Flex the elbow, andlaterally flex the neck to the opposite side. If active extension of the elbow,

which stretches the brachial plexus, produces resistance and increasedcervicothoracic radicular pain, the test is said to be positive for a nerve root orspinal cord inflammatory process (eg, brachial neuritis, meningitis).

Supine Tension Test. The patient is placed supine so that the scapula is


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fixed.Have the patient laterally flex the neck to the opposite side ofinvolvement. 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 alesion. The neurologic signs in brachial radiculopathy are shown in Table 5.

Table 5 Neurologic Signs in the BrachialRadiculopathies

Major Sensory

DisorderMajor Motor

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