Chapter 24. Vertebral Artery

At the completion of this chapter, the reader will be able to:

1. Describe the anatomy and distribution of the vertebral artery.

2. Describe the four commonly recognized portions of the vertebral artery.

3. Outline the causes of vertebral artery occlusion or compromise.

4. Recognize the characteristics of vertebral artery occlusion or insufficiency.

5. Describe various special tests used to assess the patency of the vertebrobasilar system and their diagnostic value.

The vertebral artery (VA), a component of the vertebrobasilar artery (VBA) system, supplies 20% of the blood to the brain (primarily the posterior cranial fossa), with the remaining 80% being supplied by the carotid system.1 The first studies of the VA were recorded as far back as 1844.2 Since that time, recognition of the importance of the VA has continued to grow, and it is now discussed in more detail than any other artery by physical therapists. For this reason, the VA is afforded its own chapter. To fully comprehend its significance, a review of its anatomy and function is in order.

The VBA system consists of three key vessels: two VAs and one basilar artery. The basilar artery is formed by the two VAs joining each other at the midline (Fig. 24-1).

Along its course, the artery can be viewed as having four portions: proximal, transverse, suboccipital, and intracranial.3,4

Proximal Portion

This portion runs from the origin of the artery to its point of entry to the cervical spine. The VA usually originates from the posterior surface of the subclavian artery, but it can also originate from the aortic arch and common carotid artery.5

The VA runs vertically, slightly medial, and posteriorly lateral to the longus colli and medial to the anterior scalene muscles to reach the transverse foramen of the lower cervical spine, although its exact direction is dependent on its exact point of origin. Its anomalous origin in this region has been suggested as a potential factor increasing the chance of blood flow compromise due to compression by the longus colli or scalene muscles.

In approximately 88% of individuals, the artery enters the transverse foramen of C6, but it has been shown to enter as far superior as the transverse foramen of C4.6

Transverse Portion

The second portion of the VA runs from the point of entry at the spinal column to the transverse foramen of C2 (Fig. 24-2). As already described, the origin of this part of the artery is typically at the C6 level, but this may vary between individuals and even from side to side in the same individual.

Throughout this section of the spinal column, the artery travels vertically in a true canal called the transverse canal (TC). The TC is formed by the bony transverse foramina at each spinal level and the overlying anterior and posterior intertransverse muscles, the scaleni, and the longus colli muscle. The dimension of the TC is proportionate to the diameter of the artery which itself is variable. Within the TC, the artery is surrounded by a periosteal sheath that is adherent to the boundaries of the canal and affords protection for the artery. However, the artery is in close proximity to the uncinate processes of each vertebral body on its medial aspect and is prone to compression from osteophyte formation or subluxation from the zygapophyseal joint.4,7 The VA in the transverse foramen is also adjacent to the anterior spinal roots. Arterial enlargement by an intramural hematoma or a dissecting aneurysm may cause radiculopathy by compressing or stretching the spinal root.8

Anomalies in this portion of the artery, which can include looping within the intervertebral foramina, can occur because of an abnormal origin of the artery from the aorta.9

The proximal and suboccipital portions of the artery are more elastic and less muscular than the transverse part.10 This variation is believed to be an adaptation to the greater mobility required in the proximal and transverse portions of the artery.

Suboccipital Portion

This portion of the artery extends from its exit at the axis (C2) to its point of penetration into the spinal canal. This portion can be further subdivided into four parts:

1. Within the transverse foramen of C2 (see Fig. 24-2). This portion lies in a complete bony canal formed by the two curves of the transverse foramen of C2. The inferior curve is almost vertical, whereas the superior curve is more horizontal and orientated laterally.

2. Between C2 and C1 (see Fig. 24-2). The second part runs vertically upward to the transverse foramen of C2. Throughout its journey, it is covered by the intertransversarii, the levator scapulae muscle, and the inferior oblique capitis muscle. Compression of the VA may occur in conditions in which these muscles have increased tone or loss of flexibility.11 It is also at this level that the VA is subjected to the most mechanical stress, as more than 50% of cervical spine rotation occurs here.

3. In the transverse foramen of C1 (see Fig. 24-2). In its third part, the suboccipital portion of the VA bends posteriorly and medially in the transverse foramen of C1 in which it is completely enclosed.

4. Between the posterior arch of the atlas and its entry into the foramen magnum (see Fig. 24-2). On exiting from the transverse foramen of C1, the artery and the nerve of C1 wind behind the mass of the superior articular process of the atlas (C1) to cross the posterior arch of the atlas in a groove in which the artery is held by a restraining ligament. Anomalies in this portion of the artery include ossification of the restraining ligament of the atlantal groove, turning this into a complete bony tunnel. From the medial end of this groove, the artery runs forward, inward, and upward to pierce the posterior atlantooccipital membrane. The artery penetrates the dura mater on the lateral aspect of the foramen magnum about 1.5 cm lateral to the midline of the neck. This upper portion of the extracranial VA is relatively superficial and covered only by the trapezius, semispinalis capitis, and rectus capitis muscles. Having unyielding bone beneath it, and only muscles above, the artery is vulnerable to direct blunt trauma at this part of its course, whereas in the remainder of its course, it is threatened more by penetrating trauma or disease processes such as osteophytosis or atherosclerosis.12,13

Although the artery is affected by cervical motion in the lower cervical region, it is affected even more between C2 and the occipital bone.14

In addition, because the transverse foramen of C1 is more lateral than that of C2, the artery must incline laterally between the two vertebrae. At this point, the artery is vulnerable to impingement from the following:

• Cervical extension at the craniovertebral joints, such as that which occurs with a forward head posture.11
• Excursion of the transverse mass of C1 during rotation. Approximately 50% of the cervical axial rotation occurs between C1 and C2; hence, there is a large excursion of the transverse mass of C1 with rotation. The artery is stretched during this process and the size of the lumen can be reduced.14,16 Any reduction in the size of the lumina is more profound in the presence of arterial disease.
• The atlantoaxial membrane. Ossification of this membrane can occur.

Intracranial Portion

This portion of the VA that runs from its penetration of the dura mater into the arachnoid space at the level of the foramen magnum to the formation of the basilar artery by the midline union of the two arteries at the lower border of the pons (Fig. 24-1).

After its penetration of the cranium, the VA inclines medially toward the medulla oblongata. It courses up the front of the medulla to reach the lower border of the pons, where the artery from each side unites with its partner to form the basilar artery. A major change in the structure of the VA occurs as it becomes intracranial.4 The tunica adventitia and tunica media become thinner, and there is a gross reduction in the number of elastic fibers in these coats.10 This decrease in elasticity can result in the distortion of the VA during cervical extension and rotation.14,16,19

Branches

Intracranially, the VA first generates small meningeal branches that supply the bone and dura mater of the cerebellar fossa. It is possible that ischemia of these tissues, which occurs with VA occlusion, could be responsible for the suboccipital pain that often accompanies damage to the artery.15

Spinal Branches8

Each of the vertebral arteries gives off single branches (Fig. 24-1), which fuse to form the anterior spinal artery (ASA) that descends in the median anterior fissure and is additionally supplied by anterior radicular arteries (typically two to four). While the ASA is bilaterally derived, the anterior radicular arteries may arise exclusively or predominately from one VA. This helps to explain how a unilateral insufficiency of the VA may cause bilateral spinal cord infarction.

The paired posterior spinal arteries (PSAs) originate superiorly from the vertebral arteries or posterior inferior cerebellar arteries (PICAs). The PSAs are also supplied by posterior radicular arteries (usually two or three), which themselves arise exclusively or predominately from one VA, again demonstrating how a unilateral VA dissection can lead to bilateral spinal cord infarction. The PSAs supply the posterior one-fifth to one-quarter of the spinal cord including the posterior columns, the posterior (dorsal) horns, and parts of the corticospinal and spinothalamic tracts. The ASA is the exclusive arterial supply to the gray matter of the cord. The watershed area between the PSA and ASA encompasses the anterior (ventral) horns and part of the corticospinal and spinothalamic tracts.

Muscular Branches

The muscular branches arise from the suboccipital part of the artery as it winds around the superior articular process of the atlas. They supply the deep suboccipital muscles and anastomose with the occipital and cervical arteries.

Posterior Inferior Cerebellar Artery

The PICA (see Fig. 24-1) is the largest branch of the VA, usually being formed opposite to the medulla oblongata about 1 cm below the formation of the basilar artery. It supplies, either directly or indirectly, the medulla and the cerebellum and, via the PSAs, the posterior (dorsal) portion of the spinal cord.

Basilar Artery

The formation of the basilar artery at the lower border of the pons marks the termination of the VA. The basilar artery runs in a fissure on the anterior surface of the pons (see Fig. 24-1). Directly and indirectly, the basilar artery supplies the pons, the visual area of the occipital lobe, the membranous labyrinth, the medulla, the temporal lobe, the posterior thalamus, and the cerebellum.

Collateral Circulation

Fortunately, there is an inherent redundancy in the vascular supply to the brain. The posterior and anterior vessels, and the vessels stemming from the internal carotid arteries, form an anastomotic network via the circle of Willis. Thus, occlusion of the left VA may be compensated for by perfusion of the right VA, the occipital artery, the ascending and deep cervical arteries, and the internal carotid arteries.21,22 In fact, there is evidence that suggests that blood flow velocity and blood flow volume can increase in the arteries to compensate for occlusion in another vessel.23 It is worth considering that palpation of the carotid pulse would give the clinician information regarding the ability of the carotid to perform its normal function, and if the pulse appears excessively strong, this could be an indication that the carotid artery is compensating for loss of VA flow.24,25

Damage and occlusion of the vertebral arteries are felt to occur because of the close proximity of the VA and the bony and ligamentous structures of the cervical spine.26 Trauma to this area may lead to thrombosis, dissection, transection, transmural hematoma, pseudoaneurysm, and spasm of the VA. VA insufficiency may also occur because of atherosclerotic involvement of the artery, sickle cell disease (see Chapter 5), rheumatoid arthritis, arterial fibroplasias, an arteriovenous fistula, and a number of congenital syndromes.

Whatever the cause of VA compromise, the diagnosis requires a high index of suspicion for prompt recognition and intervention. Vertebrobasilar insufficiency (VBI) is associated with signs and symptoms of focal neurologic compromise that are of sudden onset and brief duration and relate to the specific areas that are normally supplied by the vessels.

Occlusion

The VA is subject to occlusion from external and internal causes.

External Causes

Extracranial Compression

Extracranial compression of the VA may cause neurologic symptoms depending on the acuteness of the occlusion or the presence of underlying pathologic conditions such as atherosclerosis, sickle cell disease, fibromuscular dysplasia, rheumatoid arthritis, or osteogenesis imperfecta.

Many blood flow studies have demonstrated a change (reduction) in blood flow in the contralateral VA during cervical rotation.27–30 Other studies, however, have found no change in blood flow.31,32

What is known is that the greatest mechanical stress affecting the contralateral artery occurs at a position of cervical rotation and extension. Furthermore, if this position is sustained, the arterial flow takes longer to return to normal.32

In addition to the C1–2 portion, the VA is vulnerable to compression in the portion that courses through the transverse foramen from C6 to C1. Because of its fixation to the spine in this segment, subluxations of one vertebral body on another may exert undue tension and traction on the artery. Positions of the cervical spine can cause compression of the VA.19,33 Rotation–extension–traction appears to be the most stressful, followed by rotation–extension, rotation alone, side flexion alone, extension alone, and then flexion.19,33,34

If the main restraint to atlantoaxial rotation, the alar ligament, is ruptured, then the degree of C1–2 rotation has been shown to increase by 30%.35 Insufficiency of the alar ligament has been shown to follow a rear-end collision in motor vehicle accidents, and it may also exist because of a congenital defect of the dens.36 Other contributing factors to the preponderance of lesions occurring at the second cervical joint level are the fixation of the periosteal sheath of the artery to the dura mater, the superficiality of the artery in this region, and the hard neural arch beneath the artery.

Unilateral occlusion of the VA rarely results in a neurologic deficit because of the collateral supply through the contralateral vertebral and PICAs.37

After the primary tear of the intima, blood flows into the arterial wall between the intima and the media causing intramural hematoma and thickening of the vessel wall. Subintimal hemorrhage can produce various degrees of stenosis; subadventitial hemorrhage can cause a pseudoaneurysm. Tearing of the artery is not always related to remarkable trauma, and so this aspect may not appear in the history unless the symptoms appear immediately following the injury. The presence of a pseudoaneurysm has been a commonly noted angiographic feature following sudden head and neck movements. In this injury, the two internal coats of the VA are torn from the tunica adventitia, which under the influence of arterial pressure slowly balloons out and sometimes ruptures.

Extracranial Dissection

Extracranial VA dissection (vertebrobasilar infarction) is recognized with increasing frequency as a cause of stroke, and spontaneous dissections of the carotid and vertebral arteries are well-recognized causes of stroke in young and middle-aged adults.44–47 Traumatic dissection can also occur in the extracranial part of the internal carotid arteries, often after only moderate blunt trauma.48

Postmortem studies have shown that neurologic deficits, or even death, have followed posterior neck injuries by up to 8 days after the accident.49,50 The most common clinical findings are brain stem or cerebellar ischemic symptoms preceded by severe neck pain, occipital headache, or both. Occasionally, these patients report radicular symptoms.45

Spinal manipulation, in particular manipulation of the upper spine, has been associated with serious adverse occurrences, including dissection of the vertebral51 and internal carotid artery,52 resulting in strokes53 and death.54 However, the evidence implicating cervical manipulations with these serious consequences is conflicting, especially in light of the fact that even normal neck movements have been associated with spontaneous dissections. The reciprocal finding of increased blood flow through the carotid artery during VA occlusion was made by Stern,55 who demonstrated that the flow rate in the contralateral carotid artery increased by one and a half to two times with experimental occlusion of the VA. These alterations in the flow rates following an occlusion of the parallel artery serve as an apparent safety mechanism and may explain why more patients are not injured during cervical manipulation.

Frisoni and Anzola58 concluded that VA dissection at the atlantoaxial joint with intimal tear, intramural bleeding, or pseudoaneurysm leading to thrombosis or embolism is the mechanism for VBI when associated with chiropractic manipulation. The same study found that possible risk factors for VBI after neck motion are VA size asymmetry, anomalous course of VA, atherosclerosis, osteoarthritis, and vertebral ligament laxity.58 However, despite the reports of 115 cases of cerebrovascular accidents after manipulation in English language publications during the period of 1966–1998 (198 articles), there is virtually no detailed information on the magnitude of forces that were exerted or the type of procedure used. It has even been suggested that, in many cases, cervical manipulation may have been administered to patients who already had a spontaneous dissection in progress.59

Internal Causes

Atherosclerosis and Thrombosis

Atherosclerosis of the extracranial part of the VA primarily affects the proximal and transverse portions, leaving the suboccipital part relatively free. Atherosclerosis in the transverse portion of the artery occurs at any level between C2 and C6 and tends to occur at levels of the artery opposite osteophytic spurs. Castaigne et al.60 investigated 44 patients with VBA occlusions and found that the cause in almost 90% of cases was atherosclerosis, mostly affecting the proximal and intracranial portions of the artery. Approximately 40% of the patients in this study had concomitant carotid stenosis.

Atherosclerosis may, as with any other artery, produce signs and symptoms resulting from ischemia of the tissues supplied by the artery distal to the occlusion. However, if the contralateral artery is not occluded, and is of good caliber, the condition may be asymptomatic.

Thrombosis can occur at any level of the VA but is more common in the suboccipital and intracranial portions than in the transverse part.61

Arterial Fibrodysplasia

This condition is a nonatheromatous, noninflammatory segmental angiopathy of unknown etiology. It occurs in less than 1% of all patients receiving cerebral angiograms, but it is the third most frequent structural lesion affecting the VA following atherosclerosis and dissection.62 Arterial fibrodysplasia is believed to be hereditary, affecting mainly young and middle-aged female patients.

Klippel–Trenaunay Syndrome

Klippel–Trenaunay syndrome consists of a constellation of anomalies including capillary malformation, varicose veins or venous malformations, and hypertrophy of both bony and soft tissues primarily involving limbs and to a much lesser degree, intra-abdominal, thoracic, or facial structures.63,64 The vascular abnormalities commonly occur in the lower extremity but have been observed in other areas as well (head, neck, buttocks, abdomen, chest, and oral cavity). Klippel–Trenaunay syndrome is theorized to result from a mesodermal abnormality.65 The syndrome is diagnosed on the basis of presence of any two of the three aforementioned features and any intervention is based on the severity of these features.

Arteriovenous Fistulas

An arteriovenous fistula is an abnormal communication between the extracranial VA, or one of its muscular or radicular branches, and an adjacent vein. It has variable causes, including traumatic dissections or dissecting aneurysms, and may occur spontaneously as a result of the existing disease, such as fibromuscular dysplasia, or as a congenital condition. Most spontaneous arteriovenous fistulas occur at the level of C2–3 and come directly from the VA through what is believed to be a tiny rupture in the wall of the artery.66,67 Although rare, progressive myelopathy from an intracranial arteriovenous fistula can occur.68 In these cases, endovascular embolization, either alone or followed by surgery, is the intervention of choice.

The Clinical Manifestations of Vertebrobasilar Insufficiency

The clinical manifestations of VBI are difficult to distinguish from other causes of brainstem ischemia (see later) and can include any or all of the following: dizziness, visual disturbance, drop attacks (a sudden loss of postural tone without loss of consciousness), ataxia, dysarthria, dysphagia, hemiplegia, hemianesthesia, nausea, and ringing in the ears. Indeed, no single consistent pattern of neurologic signs and symptoms is pathognomonic for VA insufficiency. The most common presenting symptoms are vertigo, nausea, and headache that can be subtle, intermittent, and even chronic in nature.11,69–71

Vertigo

Vertigo or dizziness is a commonly reported symptom in the physical therapy clinic.11,70,71 Owing to the different areas of the brain that the VA and its branching arteries supply, dizziness, although the most common and usual symptom of VBI, is rarely an isolated symptom, especially in advanced stages of the condition. Tatlow and Bammer16 proved that the cause of the vertigo in patients with VBI was cervical rather than vestibular. This was accomplished by placing symptomatic patients into a Stryker bed to determine whether the vertigo symptoms were being elicited by the movement of the entire body or by the movement of the head relative to the torso. Each patient who was secured within the Stryker bed had the entire body rotated up to a full 360 degrees en bloc (without movement of the head and neck relative to the torso), and the patients reported no symptoms. However, when the torso was fixed in a still position but the head and neck was moved relative to the torso, symptoms were reproduced.

Nausea

Nausea is the accompanying symptom for many different conditions including VBI.

Headache

The headache associated with VBI is typically a unilateral occipital headache with associated vertigo and nausea.40 The pain is usually sharp and acute in its onset located on the same side as the insufficiency.

In addition to those signs and symptoms already mentioned, the following have also been linked, both directly and indirectly, to VBI40,73,74:

• Wallenberg, Horner, and similar syndromes
• Bilateral or quadrilateral paresthesia
• Hemiparesthesia
• Scotoma (a permanent or temporary area of depressed or absent vision)
• Periodic loss of consciousness
• Lip/perioral anesthesia
• Hemifacial paralysis/anesthesia
• Hyperreflexia
• Positive Babinski, Hoffman, or Oppenheim signs
• Clonus
• Gait ataxia
• Dysphasia

Clinicians need to be aware of these signs and symptoms and consider VA dissection early in the differential diagnosis because of the potential devastating neurological consequences and to decrease morbidity and mortality.40

Subclavian Steal Syndrome

The subclavian steal syndrome involves a proximal subclavian artery obstruction and reversed vertebral flow with resultant siphoning of blood from the brain and cerebrovascular symptoms.75–77

The subclavian steal syndrome can produce cerebral symptoms such as a “drop attack.”78 Headache, dizziness, and vertigo can occur while walking and turning the neck to look to the side or up.79

Imaging Studies

Conventional angiography has long been the gold standard in the diagnosis of arterial and venous pathology in the neck. Angiography can show the arterial lumen and allows extensive characterization of dissections of the carotid and vertebral arteries.80 VA angiography is not, however, without risk. Magnetic resonance angiographic (MRA) techniques are less invasive and are replacing conventional angiography as the gold standard in the diagnosis of dissections of the carotid and vertebral arteries. MRA is highly sensitive and specific in identifying stenoses and occlusions and can show the intramural hematoma itself.81

Ultrasonographic techniques are useful in the initial assessment of patients who are thought to have a dissection of the carotid artery.82 Doppler sonography allows a direct visualization of the vascular tree while assessing blood flow velocity and pressure waveforms. Although the site of dissection generally is not seen, an abnormal pattern of flow is identified in more than 90% of patients.82

Physical Therapy Examination of the Vertebral Artery

Screening procedures to identify patients at risk for VBI prior to manual therapy interventions have been widely advocated and routinely used by physical therapists for many years, being first described by Maitland in 1968.83 It is widely recognized that passive therapeutic maneuvers applied to the cervical spine carry a small risk of developing iatrogenic stroke. This is especially pertinent with regard to cervical manipulations (high-velocity thrust or grade V techniques). It is therefore generally advised that all patients with neck pain receive a subjective screening examination for VBI and be evaluated for their ability to perform active neck movements.84 The initial test consists of having the patient rotate the head to each side while in the sitting position. The longus colli and scalene muscles rotate the cervical spine and can squeeze the VA on the side contralateral to the rotation.11 The presence of muscular compression of the artery can be further tested by combining cervical flexion with rotation to place the inferior oblique capitis on stretch.11 If dizziness is provoked with rotation, it is sometimes possible to implicate or exclude the vestibular apparatus of the inner ear as the source of dizziness.85 In a standing position, the clinician holds the patient's head steady as the patient turns the trunk while keeping the feet fixed, thus producing sustained end-range cervical spine rotation.86 Because the semicircular canal fluid is not disturbed by this test, a positive response theoretically excludes the labyrinth of the inner ear.85

Theoretically, patients with a negative subjective history and negative findings with the initial test should undergo additional passive physical examination procedures in the form of stress tests for the vertebrobasilar system to further assess the potential for VBI.87 Traditionally, this has involved the use of manual premanipulative tests to determine the appropriateness of a grade V technique.

In those cases in which the clinician is to perform cervical mobilizations of grade I–IV rather than a grade V thrust technique, the Australian Physiotherapy Association's Protocol for Premanipulative Testing of the Cervical Spine continues to be recommended, although this cannot be viewed as a prescriptive guideline.84 The protocol recommends that the clinician should maintain the immediate premobilization position for a minimum of 10 seconds to test the patency of the vertebrobasilar system. Others recommend assessing the patient's responses for a further 10 seconds to note any latent response.17,37 Clinical testing of the VA should stop once positive signs or symptoms are noted. Throughout the tests, the clinician should observe the patient's eyes for possible nystagmus or changes in pupil size and should have the patient count backward to assess his or her quality of speech. The patient is asked to report any changes in symptoms however insignificant he or she may feel the changes to be.

Unfortunately, it is not clear how sensitive these premanipulative protocols are.85,88 For example, studies by Haynes89 and Cote et al.,90 found these protocols to have poor predictiver value. Other studies have shown that the results of these tests are inconsistent91 and inaccurate, 92 suggesting that the VA tests have very little, if any, diagnostic value. In addition, many of these premanipulative screening protocols involve the same combination of positions that have been suspected of causing spontaneous arterial dissections (cervical extension and rotation).

Although one could argue that if the VA was damaged or compromised, the patient would surely have signs and/or symptoms indicating this, the logical question still becomes, “How does one proceed in the absence of certainty?”87 It would seem extremely prudent to avoid cervical thrust techniques on a patient with any degree of uncertainty. Even in the absence of any symptoms, it would be wise to either introduce the application of incrementally greater movements and loads or investigate VA flow using Doppler sonography or an MRA scan before performing a grade V technique in the cervical spine.93 In addition to the specific tests of blood flow, the clinician should use a combination of the patient's description of the symptoms and medical history, and those considerations in Table 24-1, before reaching a conclusion.94 Alternatively, the clinician should consider avoiding placing the patient's cervical spine in the extremes of rotation and side bending in both the examination and the subsequent intervention, which would obviate the need for these tests.

The following case study42 illustrates the problems associated when encountering a patient with a VBA insufficiency.

History

A 62-year-old woman with no history of vertigo or dizziness reported to the clinic for her scheduled physical therapy session for cervical degenerative joint disease. During the course of conversation, the patient reported experiencing dizziness after a shampoo treatment of her hair at a hairdressing salon. She had visited her hairdresser earlier that day and reported severe vertigo, occipital pain, difficulty in standing, and a periodic numbness of the right arm and leg. The patient also reported hypesthesia in a glove-and-stocking type of distribution.

Tests and Measures

Most of the findings of the physical therapy examination were negative. Although muscle stretch reflexes and muscle power were normal, disturbances of equilibrium were noted and nystagmus was present.95 Given the presence of the nystagmus, the patient was referred back to her physician for further testing.

Following MRA, a diagnosis was made of VBA insufficiency with cerebellar infarction caused by neck hyperextension in the hairdressing salon. The patient was treated conservatively with rest and medication, and the vertigo improved 1 week after injury, enabling the patient to walk without assistance.

Beauty parlor stroke syndrome was first described by Weintraub96 in 1993. Since then, various authors have reported similar cases.97,98 Because this syndrome is not recognized widely, a careful history is necessary in the presence of symptoms such as those described. Such symptoms are often thought to be nonspecific and might be attributed to neurosis, psychogenic headache, or menopause, particularly when imaging studies do not show specific findings. Routine radiography, computed tomography, and magnetic resonance imaging studies usually do not help to identify lesions in this syndrome. Special care is therefore necessary to evaluate the clinical findings during examination of the nervous and auditory systems. The most likely pathophysiologic mechanism of the beauty parlor stroke syndrome is stenosis of the VA caused by compression at the atlantooccipital junction. This compression leads to damage of the intima, thrombus formation, stenosis of the artery by fibrosis, or embolism followed by infarction of the brain stem or cerebellum.

• 1. From which artery does the VA normally arise?

• 2. What is the most common variation in the origin of the VA?

• 3. Describe the course of the third part of the artery (suboccipital).

• 4. List the branches generated directly by the basilar artery.

• 5. Which of the cranial nerves is (are) not vascularized by the VA?

Answers