Positional Compression of the Vertebral Arteries

Normal Anatomy, Sites of Compression, and Symptoms

The vertebral artery (VA) is divided into four segments, termed V1–V4. The V1 or ostial segment arises from the subclavian artery and enters the transverse foramen of the C6 vertebra in most cases. Compression of the artery in this location may be due to fibrous bands or the anterior scalene muscle or tethering between the arterial origin and the transverse foramen of the C6. The V2 or transverse segment extends from the entry into the vertebral foramen, to the transverse foramen of the axis. Positional compression of the VA is the most common at the C1–C2 region due to the extreme mobility of this segment and at the subaxial cervical spine, which can occur from osteophytes at the transverse foramina, hypertrophy of the uncinate processes, or facets or cervical disc rupture. The V2 segment is surrounded by a venous plexus. This segment courses vertically until the C3 vertebra exits this vertebra’s transverse foramen, then bends horizontally and laterally along the base of the axis and then turns upward to enter the transverse foramen of the axis. The V3 or suboccipital segment begins at the transverse foramen of the axis and ends at the dura mater of the foramen magnum. The course of this segment is the most complex and is the most mobile segment during head turning and therefore is potentially most vulnerable to being stretched and compressed during head movement. The V4 segment refers to the segment of the VA between the entry through the dura and the end of the artery at the vertebrobasilar junction.

Symptoms of rotational vertebrobasilar insufficiency (VBI) include syncope or near syncope, dizziness, vertigo, visual disturbances, drop attacks and motor, and sensory and cranial nerve deficits that are induced when the head is turned to a particular side. ¹^, ²^, ³^, ⁴ With true rotational VBI, these symptoms may resolve promptly once the head is returned to the neutral position. Symptoms that persist or occur after the head has returned to neutral have been called “bow hunter’s stroke” after the description of a lateral medullary stroke occurring in a patient with posterior circulation infarction after target practice. ⁵ There is also a syndrome called beauty parlor stroke that has been described in patients after having their hair washed with their head in extreme extension. ⁶ These conditions most likely arise from arterial injury and dissection and thromboembolic phenomenon. It is also likely that chiropractic manipulation can cause injury to the VA on rare occasions which may manifest as immediate or delayed thromboembolic events. ⁶

Extrinsic compression of the VA by osteophytes or at the highly mobile C1–C2 segment during head rotation has been documented in cadaveric specimens and in patients ( ▶ Fig. 38.1). ⁴ Unilateral complete VA flow obstruction can occur in healthy people with head turning but VBI symptoms usually don’t occur because the contralateral VA may provide the necessary compensation to perfuse the basilar artery during transient compression of either artery. Most patients with positional VBI have one patent VA and a contralateral VA stenosis/occlusion due to congenital hypoplasia, atherosclerosis, or other causes or the VA may not connect to the basilar artery due to an absent segment between the posterior inferior cerebellar artery and the VB junction. If the posterior communicating arteries are robust and can provide adequate collateral circulation, then even temporary occlusion of a single isolated VA may not cause ischemic symptoms. A model of the cervical spine and VA in a (left) neutral position and when the head is turned to the right showing that the VA is stretched by the forward projection of the C1 transverse foramen as the head ( ▶ Fig. 38.1).

Fig. 38.1 (Left) Illustration of a plastic model that shows the vertebral artery passing through the transverse foramen of C1 in the neutral position and also (right) with the head turned to opposite side illustrating the mechanism of stretching of the vertebral artery at this location between the exit from the bone at C2 and the posterior part of the ring of the foramen at C1. This is the rationale for removing the posterior portion of the transverse foramen of C1 to prevent the stretching and occlusion of the lumen of the artery.

38.2 Diagnosis

Our experience suggests that the specific clinical symptoms in positional VB ischemia are very consistent and can predict which patients will have true transient arterial obstruction and neurological symptoms from blood flow reduction. ² Symptoms are most commonly associated with head turning, but may also be associated with head flexion or extension. Patients with the true disorder, usually report that they can reliably reproduce the symptoms by moving their head into a certain position and holding it there for a brief period of time (usually about 5–7 seconds) before the symptoms begin. Normally, patients will return their head to a neutral position as soon as symptoms begin, in order to avoid more severe symptoms or syncope. Symptoms include generalized weakness, dizziness, vertigo, diplopia, disorientation, and even altered level of consciousness.

Patients who report milder symptoms when they turn their head in different directions or inconsistently with flexion or extension or while looking up and cannot reproduce the symptoms in an office setting usually don’t have VB flow obstruction or ischemia and often have vestibular disorders or nonspecific entities. We reported two patients with adolescent stretch syncope and were able to document a transient decrease in cerebral blood flow that was most likely due to a combination of stretching of the first or ostial segment of the VA and Valsalva maneuver. ³ Our patients experienced symptoms only with extreme postural positions and therefore were not advised to have surgical treatment.

Another syndrome characterized by presyncopal symptoms to be distinguished from VBI is Eagle’s syndrome or variations of it. Eagle’s syndrome describes odynophagia and neck and face pain secondary to compression of the carotid artery and other structures in the upper neck and pharynx by an abnormally large styloid process. ⁷ Other neurological conditions and cardiopulmonary status of the patient are also important to assess as causes of syncope/presyncope/dizziness prior to conducting more invasive, definitive diagnostic studies. Transcranial Doppler (TCD) ultrasonography, dynamic cerebral angiography, including the cervical VA and computed tomography angiography (CTA) of the neck and head are the key diagnostic tools when suspecting positional VBI.

TCD is an inexpensive, noninvasive first diagnostic tool. Dynamic TCD allows monitoring of hemodynamic changes with the patient’s symptoms. In patients with positional VBI, the blood flow velocity in the posterior cerebral arteries decreases with head rotation to at least 50% of the patient’s baseline with the head in the neutral position. Moreover, a reactive hyperemic response of at least 10% above the baseline occurs when the patient resumes the neutral position and the symptoms disappear. ² These findings are consistently reproducible in patients with true rotational VBI ( ▶ Fig. 38.2, Video 38.1). Monitoring is done with bilateral fixed probes, which minimizes motion artifacts and allows for simultaneous recordings of both posterior cerebral arteries. TCD can also be invaluable in the operating room to help confirm complete decompression of the VA by detecting normal posterior cerebral artery flow velocities while performing passive head turning maneuvers. This technique, however, is limited to patients who are supine and when their head is not fixed and it is safe to rotate their head around when they are intubated under general anesthetic. TCD is also valuable to document resolution of positional blood flow reductions, postoperatively.

Fig. 38.2 (Left) Illustration of a diagram of the simultaneous transcranial Doppler recording of both posterior cerebral arteries. (Right) Spectral and outline of the posterior cerebral artery velocity profile initially in a neutral position and then with head turned, with accompanying velocity drop in a symptomatic patient, followed by return of the head to a neutral position and a hyperemic response in the velocity profile, confirming that there was a period of cerebral ischemia.

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