Clinical Testing for Cervical Mechanical is orders which Produce Ischemic Vertigo

WENDY ASPINALL, MHSc, DipManTher, DipPT'

The primary purpose of this paper is to outline the reasons for certain questions to be considered during the subjective examination if dizziness is a complaint. A gradual progression of clinical tests performed during the physical examination is proposed to detect vertebral artery signs and symptoms. The tests themselves create a risk as they are all applying stress to the vertebral artery. This progression will produce minimal vertebral artery signs and symptoms, by applying first the test which requires the least stress on the vertebral artery. These clinical tests are based on a pathological mechanical rationale. It is proposed that this clinical judgment process of testing for ischemic vertigo, will enable the clinician to select the most appropriate assessment and treatment techniques for patients with either cervical or upper quadrant syndromes. The upper quarter consists of the head, neck, and upper extremities including the clavicles and scapula. Upper quadrant syndromes involve both a spinal and peripheral dysfunction which are pathologically related.

Orthopaedic manipulative therapy is being used extensively in many countries. Due to the development of this approach, many upper quadrant syndromes are being assessed and treated by this method. The literature on incidents and accidents of cervical manipulation has been reviewed from 1947 to 1986 and approximately 58 cases were reported (8). The primary level of arterial damage was at the atlantoaxial segment of the vertebral artery. Neurological symptoms which progressed to permanent deficit or death were reported following manipulative thrust techniques (6, 8). These techniques were performed by chiropractors, osteopaths, medical practitioners, physiotherapists, and untrained personnel. Forty-four of the cases were treated by chiropractors. Dizziness is not an uncommon clinical symp tom for patients with cervical and upper quadrant syndromes. In many cases this produces a problem in the clinical judgment process, as to whether to treat or even assess using a manipulative therapy approach. In some cases dizziness may be ' Orthopaedic ManipulativePhysiotherapist.Cllnlcal Instructor and Consultant. Toronto. Ontarlo. Canada.
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produced during the treatment or following the treatment session, again causing a problem in the judgment process as to the treatment progression. It has been suggested that transient deficits of vertebral artery signs and symptoms are probably more frequent occurrences following mobilizations and manipulations, than those more serious complications documented in the literature (8). This statement is also an opinion of the author of this paper. The purpose of this paper is to outline the reasons for certain questions to be considered during the subjective examination if dizziness is a complaint. A gradual progression of clinical tests performed during the physical examination is proposed to detect vertebral artery signs and symptoms. These clinical tests are based on a pathological mechanical rationale. It is proposed that clinicians applying this clinical judgment process will be able to both assess and treat patients with cervical and upper quadrant syndromes appropriately, and avoid creating even a transient deficit related to the vertebral artery.
ETIOLOGIES OF VERTIGO OR DIZZINESS

Peripheral causes of vertigo or dizziness are the most frequently encountered in clinical practice. These causes are summarized in Table 1, and
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TABLE 1
Peripheral etiologies of vertigo' Peripheral vestibulopathy-labyrinthitis 'Benign" positional vertigo Post-traumatic vertigo Mhieres syndrome Vestibulotoxic drugs Other focal peripheral disease-bacterial infection

SUBJECTIVE EXAMINATION The subjective examination of the clinical evaluation of a patient complaining of dizziness can be very informative regarding the etiology of the symptom. Patients complain of dizziness, a term which describes a host of symptoms such as unsteadiness, imbalance, floating, or light headedness. True dizziness or vertigo refers to a definite illusion of environmental spin or a self-rotation (1, 4). It is necessary to elicit the set of symptoms actually experienced by careful history taking. Peripheral causes of vertigo are more common than central etiologies (1, 6). Therefore, the features of peripheral etiologies such as labyrinthitis versus vertebrobasilar artery dysfunction, a central type of dizziness, should be considered. Peripheral vestibulopathy is characterized by a single or recurrent sudden episode of vertigo lasting from hours to a few days, and not associated with hearing loss. The vertigo may be evoked by head movements rather than head positions. The dizziness of benign positional vertigo, which is one of the peripheral etiologies, rarely lasts longer than 60 sec and occurs when a certain posture of the head is assumed (1, 6). In vertigo of other causes, changes in position may also intensify the symptoms. Vertigo immediately following head trauma may be produced if the calcareous deposits that lie on the vestibular receptors are displaced to new and sensitive regions of the ampulla of the posterior canal (1, 6). This may cause the receptors to be more susceptible to stimulation in certain head positions, producing a benign positional vertigo. When the symptoms are delayed, the mechanism may be hemorrhage into the labyrinth, producing serious labyrinthitis. Vestibulotoxic drug induced vertigo is caused by agents which are presumed to injure the peripheral end organ. Among such agents are the aminoglycosides, streptomycin and gentamycin. These drugs are selectively concentrated in the endolymphatic fluid and produce irreversible injury to vestibular hair cells (11). The most common symptoms associated with eighth nerve tumors, which is a central cause of vertigo, are progressive hearing loss and tinnitis, symptoms unlikely to occur with vertebrobasitar vascular dysfunction (1, 7). Before deciding that the signs and symptoms are due to vertebrobasilar artery dysfunction, one should seek additional signs of brain stem involvement. The posterior circulation supplies blood to the medulla, pons, cerebellum, mesencephalon, thalamus, occipital lobes, and portions of the temporo-occipital and parieto-occipital junctions. The most common defects with dysfunction in this system are disorders of motor function such as
177

' From Troost (17).

TABLE 2
Central causes of vertigo' Demyelinating disease Tumors Seizures Vertebrobasilar artery dysfunction Cervical or reflex vertigo

' From Troost (18).

TABLE 3
Systemic causes of vertigo or dizziness' Drugs Anticonvulsants, hypnotics. antihypertensives, alcohol, analgesics, tranquilizers Diabetes and hypothroidism

Hypotension Endocrine Disease

' From Troost (17).

result from dysfunction of the vestibular end organ-semicircular canals, utricle, and saccule. Vertebrobasilar insufficiency is a central cause of ischemic vertigo. Dysfunction of the vestibular portion of the eighth nerve and the vestibular nuclei within the brain stem and their central connections, is a central cause of vertigo or dizziness. A more frequent central cause is cervical or reflex vertigo. Dizziness can be caused by a disturbance of the tonic neck reflexes from a distortion of the normal afferent input to the vestibular nucleus from the neck. One mechanism appears to be derived from a disturbance of the proprioceptive contribution of the sternocleidomastoid muscle to body orientation in space (3). Another mechanism may be from dysfunction of the cervical joints (21). The essential difference between ischemic and reflex vertigo is that reflex vertigo is not accompanied by other features of brain stem ischemia or cardiovascular disease (1). Symptoms relate chiefly to spatial disorientation, postural dizziness at times expressed as a disagreeable movement within the head rather than true vertigo such as objects spinning around the patient (16). The central causes are summarized in Table 2. Certain drugs and medical conditions are systemic causes of dizziness. Systemic causes include disorders that secondarily affect peripheral and/or central vestibular structures to produce vertigo (Table 3).
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weakness, clumsiness, or paralysis. If the occipital lobes are the site of ischemia, visual loss will occur. Ataxia may occur because of labyrinthine or cerebellar ischemia (1, 7). The belief that dizziness is a more or less required symptom before posterior circulation dysfunction can be diagnosed is incorrect, because isolated symptoms may occur without dizziness (1). On the other hand, such symptoms may not always accompany dizziness due to posterior circulation dysfunction (1). Acute severe dizziness mimicking labyrinthine disease has been an early symptom of acute cerebellar infarction in the distal territory of the posterior inferior cerebellar artery (1, 7). To differentiate this condition from labyrinthine disease. particular attention is directed to the type of nystagmus which is present. In the peripheral etiologies there is a unidirectional nystagmus with increase of the fast phase during gaze to the opposite side of the lesion. With central causes the nystagmus direction is changing and also more prominent to the side of the lesion (4). It is important that every attempt be made to determine the type and quantity of medication being taken by the patient. Frequently the reduction in medication will produce a decreased incidence of dizziness. The condition of the patient's general health is an important question. Hypotension may produce dizziness following a change from the recumbent or sitting posture to an erect position, but not the reverse. Diabetes and hypothyroidism predispose the patient to rapid development of atherosclerotic occlusive disease. At times gastrointestinal distress, depletion of certain electrolytes, or physical exhaustion may also produce dizziness. These characteristics of peripheral versus central positional vertigo are summarized in Table 4, and features of individual etiologies should be carefully considered when questioning the patient

during the subjective examination. Evaluation of the findings of the subjective examination may permit the clinician, in some situations, to form an opinion based on an intellectual hypothesis of whether the patient has peripheral, systemic, or central causes to account for their complaints. Despite the intellectual hypothesis on the causes of dizziness, clinical testing for vertebral artery symptoms should be pursued during the physical examination. These tests should also be included even if no such symptoms of dizziness or vertigo are suggested by patients when they present with cervical or upper quadrant syndromes. Symptoms may not be provoked unless certain cervical movements and or positions are stressed. Such movements and positions may be used during an orthopaedic manual therapy assessment to localize the musculoskeletal lesion. It is therefore essential that the vertebral artery be taken into consideration.
CLINICAL TESTS RELATED TO PATHOLOGICAL SYNDROMES

Cervical mechanical disorders of ischemic vertigo will be discussed in relationship to four parts of the vertebral artery and the appropriate clinical tests applied in a progressive order. It is recommended by the author that throughout all testing procedures, the cervical positions should be held for a minimum of 10 sec. Before progressing to the next test, a minimum of a 10-sec waiting period should be provided to recognize any latent symptoms. It may be necessary to repeat the testing procedures and/or accelerate the speed of testing dependent on the subjective report of the aggravating factor. In all tests, the patient's eyes should be observed for nystagmus and subjective symptoms of dizziness. In order to apply the least required stress on the vertebral artery to produce symptoms, a progressive order of clinical tests is suggested.

TABLE 4
Characteristics of peripheral versus central vertigo'
Symptm or Sign
Peripheral Central

Latency Fatigability Adaptation with repetition of provocative maneuver Intensity Nausea Nystagmus direction Reproducibility Assoc~ated symptoms Diplopia Drop attacks Dysarthria Dysphagia
-

3-45 seconds Yes Yes Severe Severe Fixed Inconsistent None

None No No Mild Rare Changing More consistent Yes NIB Not with reflex vertigo

' From Troost (1 7).

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Testing procedures are performed first in the sitting, followed by the lying position. It is the author's opinion that less range of movement is achieved in the sitting position due to the effect of muscle tone and joint compression factors. Positioning for the vertebral artery tests in the upper and lower cervical spine should be performed individually. It is not biomechanically possible to achieve the end of active and/or passive range in both areas of the cervical spine concomitantly (20). Examining both areas of the cervical spine separately may allow for a clinical differentiation of the areas of the cervical spine which are producing mechanical disorders causing ischemic vertigo. Therefore, treatment planning and safety precautions may be appropriately applied.
Vertebral Artery-Area

It is therefore important, in the author's opinion, to commence clinical testing of the vertebral artery by active cervical rotation in sitting. The longus colli and scalene muscles rotate the cervical spine and thereby squeeze the vertebral artery on the side contralateral to the rotation. This test may reproduce symptoms if areas two and three of the vertebral artery (described below) are involved. Tests which require the least stress on the vertebral artery for areas two and three should then be performed to assist in localizing the problem.
Vertebral Artery-Area

Two

One

The first part of the vertebral artery is a portion between the subclavian artery and the sixth cervical vertebrae. An extrinsic mechanical disorder in this part of the artery is the obliteration of vertebral artery flow at the level of the vertebral foramen of the sixth cervical vertebrae by the contraction of the longus colli muscle and/or the scalene muscle (10). An anomalous origin of the vertebral artery has been reported, which may increase the chance of obliteration in some cases (13). An anomalous course of the artery between the fascicles of either the longus colli or the scalenius anterior may also decrease the blood flow (10). This reduction in the flow of blood is usually compensated for by an increased flow through the other carotid and vertebral artery. If, however, the vertebral artery flow is decreased and the carotid flow is not compensating, then rotation of the head will completely arrest the flow of blood through the vertebral artery (10). The acute reduction of cerebral blood flow could conceivably be enough to manifest itself clinically as dizziness. The occurrences of these anomalies are infrequent but variations in the caliber of the vertebral artery are common (1). When marked inequality occurs, the basilar artery becomes supplied virtually entirely by the dominant vertebral artery (1). Certain thoracic outlet syndromes which involve shortening of the anterior scalene muscle may produce vertebral artery symptoms. Fascia1 bands which connect these two muscles have been reported as a possible cause that might obstruct the vertebral artery on cervical rotation (9). These bands may be tensed by an abnormal position of the clavicle, produced from either upper quadrant postural or dysfunction syndromes. In such cases vertebral artery symptoms may be observed.
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The second portion of the vertebral artery, which we will discuss, traverses through the transverse foramen of each cervical vertebrae from C6 to C1. It is in this area that the extrinsic mechanical complications caused by osteophyte formation of cervical spondylosis or even subluxation of a zygapophyseal joint may produce blood flow decrease and therefore, vertebral artery symptoms. The development of osteophytes on the anterior third of the lateral part of the uncinate portion of the vertebrae displace the anteromedial part of the artery producing a tortuous appearance (13). The most common sites of these displacements are between the fourth, fifth, and sixth vertebrae (13). This displacement by uncinate osteophytes may predispose the vessel to the formation of atherosclerotic plaques. This may also be a reason for the incidence of cervical spondylosis and cerebrovascular atherosclerosis to occur concomitantly in the same age group. Comparison of films taken before and after rotation of the neck, show that severe stenosis of the vertebral artery created by osteophytes may become completely obstructed when the head is rotated fully. Stretching of the vertebral artery over an uncinate osteophyte occurs on the opposite side to the rotation of the head. However. compressive forces are more severe on the same side due to pressure of the vertebral artery against the osteophyte (13). It is important to test passive cervical rotation bilaterally in sitting, where muscle activity and joint compression will influence the effect on a positive test. If no symptoms are reproduced, the same tests should be performed in lying when more range may be available due to decreased muscle activity and decreased joint compression. The vertebral arteries do not normally come into contact with the zygapophyseal joints even during the most extensive movements of the spine. The vertebral artery may be affected by intermittent contact with the zygapophyseal joints during movements of the spine if the transverse diameter of the zygapophyseal joint is increased, or the cervical movements are abnormal in regard
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to the quality or excessive range of movement (5). Enlargement of the transverse diameter of the articular surfaces can occur with arthrosis being the most frequent cause. Transient contacts between the artery and bone margins of the enlarged zygapophyseal surface may result in injury to the vasa vasorum, which is the nerve supply of the vertebral artery, with subsequent degeneration and scar formation of the arterial wall (5). The second area of the vertebral artery is more or less rigid, being maintained in the foramen transversarium. The artery may be angled at this level during movements of the spine, so that its lumen temporarily becomes almost completely reduced by enlarged zygapophyseal joints (5). Patients with cervical spondylosis may at times complain of dizziness on cervical flexion. Osteophytes on the anteromedial margin of the inferior articular surface of the zygapophyseal joints extend over the posterolateral segment of the foramen transversaria. These osteophytes may compress the vertebral artery on cervical flexion (5). If no symptoms are reproduced with overpressure to the mid and lower cervical spine in flexion, traction should be added to this position. This will pull on the artery and pull it across the osteophytes and that might create symptoms. It is the author's opinion that this traction procedure of vertebral artery testing is essential if traction is to be considered in the treatment program. If dizziness is produced, traction should not be used as a treatment. Osteophytes on the upper articular surfaces may compress the vertebral arteries during cervical extension (5). To test for this extrinsic mechanical cause, active cervical extension followed by overpressure into extension of the mid and lower cervical spine should be performed in sitting. If no symptoms are reproduced this test may be progressed to the lying position, where more range may be available. Syndromes such as unilateral subluxations of the zygapophyseal joints producing an altered quality or excessive range of movement may coexist with osteophytes at the margins of the uncovertebral joints at the same level (5). Passive rotation combined with extension of the mid and lower cervical spine may compress the vertebral artery in the narrow space between the two affected joints. Using a passive combined movement of extension and rotation is a natural progression to test for symptoms. This test should first be performed in sitting and then in the lying position. If this combined movement produces symptoms, it would incriminate a specific level in the cervical area. The involved level can be determined by positioning the patient in cervical flexion combined with the symptom-free rotation. Stabilizing each cervical level by fixing the inferior articular process and spinous process of the caudal
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vertebrae prevents rotation at that level. Extend and rotate the level above the stabilization toward the symptomatic side until symptoms are produced. By proper identification and to attempt relief, treatment can be focused above or below the level producing vertebral artery symptoms.
Vertebral Artery-Area Three

In cadavers with no history of arterial disease, radiographs have demonstrated that cervical rotation combined with extension creates a marked narrowing of the vertebral artery lumen at the level of the atlas and axis on the contralateral side. Traction, when added in this extended and rotated position, created bilateral occlusion of the vertebral artery (2). Bony anomalies in the occiput, atlas-axis area are common. If the arch of the atlas is excessively large, compression of the vertebral artery by the atlanto-occipital membrane could occur when the head on neck is hyperextended (12). Vertebral artery symptoms may be reproduced by testing active upper cervical extension. If no symptoms are produced, overpressure to upper cervical extension is added in sitting. Then this test is repeated in lying, to gain greater range of extension. This may be a reason why some patients with a forward head postural syndrome or a flexion dysfunction in the craniovertebral area may suffer from vertebral artery symptoms, due i, this : extrinsic mechanical cause. The upper portion of the vertebral artery is in direct contact with the obliquus capitis inferior and the intertransversarius muscles as it passes between the two foramina transversaria of the atlas and axis. The artery then passes through a slit of the atlanto-occipital membrane as it travels medially and ventrally in the groove of the atlas (11). Compression of the vertebral artery may take place in conditions where these muscles have increased tone or loss of flexibility. In this case, clinical testing needs to involve passive upper cervical rotation combined with flexion. This will produce the patient's symptoms. Hypermobility or subluxations in the craniovertebral area can be produced by pathological conditions such as rheumatoid arthritis and congenital anomalies. These in turn may produce vertebral artery symptoms. Overpressure to passive cervical rotation combined with extension in the upper cervical spine should be accomplished to see whether the symptoms can be reproduced. The tests are performed first in the sitting and then in the lying position. The need to passively rotate the atlas on the axis before coupling it with upper cervical extension is necessary to achieve full end range at this level, and stress the vertebral artery to its maximum. If no symptoms are produced, traction may be added to the upper cerviJOSPT 11.5 November 1989

ASPINALL

cal spine in the combined position of rotation and extension to check for occlusion. It is suggested that these vertebral artery tests not be performed on patients with a medical history of rheumatoid arthritis.
Vertebral Artery-Area Four

vertebral artery dysfunction are summarized in Table 5 and 6.

CLINICAL EVALUATION DURING AND FOLLOWING TREATMENT

The fourth area of the vertebral artery is the terminal part as it enters the foramen magnum to merge with the vertebral artery on the opposite side to form the basilar artery. The vertebral artery passes anterior to the alar ligament of the atlas and enters the vertebral canal. It pierces the spinal dura and passes upward into the posterior cranial fossa through the foramen magnum (19). It is in this area that intrinsic mechanical causes, such as atherosclerotic plaques or stenosis, can reduce the arterial flow of the vertebral artery or other cerebral connecting vessels (7). This predisposes the individual to transient vertebral artery attacks when the collateral circulation is reduced.
FINAL PROGRESSIVE TESTING PROCEDURES

Even though symptoms of vertebrobasilar ischemia are not produced during the physical examination, one must continually evaluate the effect of treatment in producing such symptoms both during and following the treatment session. No prior testing can truly simulate treatment procedures. In addition, if cervical range initially was decreased, testing for vertebral artery signs and symptoms should be applied to the new range before further treatment.
CONCLUSION

To avoid minor or major transient deficits during or following treatment utilizing mobilizations and manipulations, further vertebral artery testing should be done if symptoms are not reproduced with the tests discussed so far. The following tests seek to simulate some of the stresses which will be imposed on the cervical structures during treatment. These vertebral artery tests are passive accessory mobilizations which apply a greater stress to the joint structures and vertebral artery at the end of the available range. Passive accessory mobilizations may be used as treatment techniques and should therefore be selected to test for vertebral artery signs and symptoms prior to their application as treatment techniques. Passive accessory movements performed in the combined position of extension and rotation to both the upper, mid, and lower cervical spine are performed to stress the vertebral artery to its maximum. An example of testing the low cervical levels would be with the patient supine and the low cervical spine held in a position of combined extension and left rotation. An oscillatory anterior/ posterior movement applied to the left transverse process of the sixth cervical vertebrae would increase rotation to the left between the sixth and seventh cervical vertebrae. The same principle would be used in both the upper and mid cervical spine. Prior to manipulation, the position should be sustained for a minimum of 10 sec and then released for 10 sec to ensure that there are no latent symptoms before proceeding with the manipulative thrust. The clinical tests outlined for
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The literature on vertebral artery complications suggests a number of factors to consider, such as legal issues, elements of unpredictability, and risks of clinical testing (8). Efficient charting provides the resource for a clinical judgment process. Reviewing these charts will provide further knowledge regarding this testing approach. It must be realized that there is always an element of unpredictability. The area of the vertebral artery shown to be most susceptible to occlusion under normal circumstances is in the occipital, atlanto/axial area. The position of comTABLE 5
Progressive clinical tests for production of vertebral artery signs and symptoms

Area one X Area two X X

X

Vertebral Artery Area

Pos~t~on S~tt~ng Lying

Test Mid & Lower Cervtcal Sptne

-

X X
X X

X X
X

Active cervical rotation Active cervical rotation Passive cervical rotat~on Active cervical extension Passive cervical extension Passive cervical extension with rotation Passive segmental extension with rotation Passive cervical flexion Cervical flexion with traction Accessory oscillatory anterior/posterior movement-transverse processes C2-7 in combined extension and rotation Sustained manipulation position

CLINICAL TESTING FOR CERVICAL DISORDERS

TABLE 6
Progressive clinical tests for production of vertebral artery signs and symptoms
Vertebral Artery Area Sittmg Ly~ngTest Upper Cervcal Spme

Area three

X X

Active cervical rotation Passive cervical rotation Active cervical extension Passive cervical extension Passwe cervical rotation with extension Cervical rotation with extension and traction Cervical rotation with flexion Accessory oscillatory anteriorlposterior movernent-transverse processes C1-2 in combined rotation and extension Sustained manipulation position

tebral artery will require a minimal addition of clinical tests. It is proposed that this clinical judgment process of clinical testing for ischemic vertigo will enable the clinician to select the most appropriate assessment and treatment techniques for patients with cervical and upper quadrant syndromes. 0 REFERENCES
1. Bogduk N: Cervcal causes of headache and dizziness. In: Grieve GP ( 4 ) . Modern Manual Therapy of the Vertebral Column. Ch 27. pp 289-302. New York: Church~ll L~v~ngstone. 1986 2. Brown BSTJ. Tatlow WFT. Radlographc studies of the vertebral arterles In cadavers. Rad~ology 81(1):80-88. 1963 3. Cohen LA: Role of eye and neck proprloceptlve mechansms in body orientat~on and motor coordmat~on. Neurophys~ol J 24:l-11. 1961 4. Coman WB: Dminess related to ENT conditions. In: Grieve GP (ed). Modem Manual Therapy of the Vertebral Column. Ch 28, pp 303-314 New York: Churchdl L~vmgstone. 1986 5. Constantin P. Lucretia C: Relations between the cervical spme and the vertebral arterles. ACTA Rad~ol 6:91-96. 1971 6. Fast A. Ztn~cola DF. Marin EL: Vertebral artery damage complicatIng cervcal man~pulat~on. Spine 12(9)-840-842. 1987 7. F~sherCM. Gore I. Okabe N. Wh~tePD: Atherosclerosis of the carot~d vertebral arter~es-extracran~al and ~ntracran~al. and J Neuropathol Exp Neurol 24:455-476. 1965 8. Grant R: D~zziness testmg and man~pulat~on the cervical spine. of In: Grant R (ed). Phys~cal Therapy of the Cerv~caland Thoracc Spme. Clincs In Phys~cal Therapy. Vol 17. Ch 7, pp 111-124. New York: Churchill Livmgstone. 1988 9. Hardin CA. Poser CM Rotational obstruction of the vertebral artery due to redundancy and extralummal cervcal fascia1 bands. Ann Surg 158.133-137, 1963 10. Husni EA: Mechanical occlusion of the vertebral artery. JAMA 196(6):101-104. 1966 11. Hybels RL: Drug tox~cityof the inner ear. Med Clin Nortt, Am 63 309-319. 1979 12. Okawara S. Nibbelink D: Vertebral artery occlusion following hyperextenslon and rotation of the head. Stroke 5:640-642. 1974 13. Sheehan S. Bauer RB. Meyer JS: Vertebral artery compression in cerv~cal spondylosis. Neurology 10:968-986. 1960 14. Tatlow WFT. Bammer HG: Syndrome of vertebral artery compresslon. Neurology 7:331-340. 1957 15. Toole JF. Tucker SH: Influence of head pos~tion upon cerebral c~rculat~on. AMA Arch Neurol 2:42-49. 1960 16. Travell JG. S~mons DG: Myofasc~al Pain and Dysfunction. London: W~ll~amsW~lk~ns. 8 1984 17. Troost BT: Dlzzmess and vertigo in vertebrobasilar disease. Part I. Stroke 11(3):301-303. 1980 18. Troost BT: Dmmess and vertlgo In vertebrobasilar disease. Part II. Stroke 11(4):413-415. 1980 19. Warw~ck . W~ll~ams (eds): Gray's Anatomy. 35th Ed. London: R PL Longman. 1973 20. Worth DR: Movements of the cervical spine. In: Grieve GP (ed). Modem Manual Therapy of the Vertebral Column Ch 7. pp 77-85. New York: Church~ll L~vmgstone.1986 21. Wyke B: Neurology of the Cervical Spmal Jomts. Physiotherapy 65.72-76.1979

bined extension and rotation of the upper cervical spine with and without the application of traction has been shown to occlude the artery (14. 15). If possible, one should avoid the application of high velocity thrust techniques as the effect of speed and amplitude on the vertebral artery cannot be pretested. The tests themselves create a risk as they are all applying stress to the vertebral artery. This building block approach to clinical testing, which has been suggested, should reduce the risk by minimizing vertebral artery signs and symptoms to be reproduced utilizing minimal stress on the vertebral artery. Most of the positions for vertebral artery testing are positions used during a spinal examination to test for the reproduction of pain and/or restriction. Therefore, the integration of these vertebral artery tests into a spinal examination procedure, producing progressive stress on the ver-

JOSPT 11.5 November 1989