Question 1

Which of the following statements regarding posturally induced symptoms is true?

A.  The mechanism for ischemia is the restriction of flow by external compression of the artery.

B.  The mechanism for ischemia is embolization from the damaged wall (dissection) or thrombus overlying the endothelial lining of the artery at the site of trauma.

C.  Both mechanisms may exist.

Question 2

Which of the following statements are correct?

A.  When dynamic symptomatic compression of the vertebral artery is demonstrated, angioplasty (with or without stent) is never indicated.

B.  Angioplasty of a stenosed or dissected vertebral artery at the suboccipital level is likely to result in rupture of the artery or formation of an arteriovenous fistula.

C.  Angioplasty and stenting of the distal vertebral artery is successful in stenosing lesions caused by external compression.

34.3  Commentary

In patients with low-flow ischemia secondary to extrinsic compression of the artery, the clinical picture is repetitive and can be induced by manipulating the patient’s head in the trigger position. Those patients who develop vertigo and nystagmus immediately as the head is moved to a particular trigger position should be considered as having Benign Positional Vertigo caused by an osteolith displaced in one of the semicircular canals.9 Patients with symptoms occurring with head rotation or extension generally experience symptoms a few seconds after inducing the trigger posture should have a dynamic arteriogram to show the anatomic lesion (extrinsic compression) at the same time as the patient experiences symptoms. Patients with low-flow symptoms (repetitive) and no evidence of embolization (negativeMRI)mayshowdeformity/compressionofonevertebralarterybutanormalcontralateral vertebral artery during head rotation or extension. If the contralateral, undisturbed artery is of normal size and empties normally into the basilar artery, then the role of the compression of one vertebral artery causing the symptoms is doubtful. The suboccipital approach permits access to the vertebral artery from the transverse process of C2 to the foramen magnum. The techniques used to relieve compression at the suboccipital level are laminectomy, or laminectomy plus bypass. Vertebrobasilar ischemia of postural origin is generally the consequence of mechanical compression of the vertebral artery by osteophytes (and occasionally ligaments) in its extracranial trajectory. The mechanism for symptoms is generally low flow in a dominant vertebral artery that cannot be compensated for by flow from a contralateral hypoplastic

orabsentvertebralartery.Thiscompressionisseenveryrarelyinthefirstsegment(origin–C6) caused by the tendon of the longus colli. External compression by vertebral osteophytes is usually observed in the second and third segments of the artery. In the second segment (C6– C2),thearteryisusuallycompressedbyosteophytes,andthesymptomsgenerallyappearwith rotation of the neck. In the third segment (C2–C0), the compression occurs in the pars atlanticaofthearterybetweenC1andtheforamenmagnum.Thearteryiscompressedbetweenthe sharp upper edge of the lamina of C1 below and the occipital ridge above when the head is rotated in hyperextension. [Q1: C]

The ischemic symptoms are usually the consequences of low flow through a dominant vertebral artery because of complete or near-complete occlusion at the latter by compressing osteophyte. Less frequently, the ischemic effects may be embolic from the mural thrombi that develop at the site of repetitive trauma on the artery by the offending osteophyte. In other cases, the artery may dissect at the point of repetitive traumatic compression, which may result in occlusion and/or distal embolization. Symptoms in patients with vertebrobasilar ischemia from the low-flow mechanism are repetitive and can be reproduced every time the neck is brought to the trigger position. Patients with vertebrobasilar ischemia of embolic origin usually present with a clinical stroke or TIA in different areas. MRI in the low-flow group is usually normal, but in the embolic group it may show cerebellar, brainstem or occipital infarctions. An arteriogram is needed to outline precisely the point of compression and to discern the possibility of a dissection and/or tandem lesions. It is also important to outline the entire course of the opposite vertebral artery to establish whether it is complete, normal or hypoplastic, and whether at the time of the provocative dynamic arteriogram the opposite vertebral artery fills the basilar artery normally while the patient has symptoms. The latter would suggest that the mechanism of symptoms is not low flow.

There is no role for angioplasty, with or without stent, in the treatment of extrinsic compression of the vertebral artery. Balloon dilation of the thin-walled vertebral artery against the hard bony prominence of an osteophyte is likely to result in the rupture of the arterial wall and the formation of a false aneurysm or an arteriovenous fistula. If the compression of the vertebral artery is limited to the V2 segment (C6–C2), then the single or multiple elements of compression are bypassed by reconstructing the artery to the level of C1. This is done through an anterior approach.8 In dynamic compression at the suboccipital level, the approach is posterior1 and the treatment consists of a laminectomy, with or without bypass. If a bypass is chosen at this level its inflow is obtained from the high cervical carotid. The latter is exposed by moving aside the cranial nerves that block access to the internal carotid when approached posteriorly. [Q2: A, B]

References

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9.Heidenreich KD, et al. Strategies to distinguish benign paroxysmal positional vertigo from rotational vertebrobasilar ischemia. Ann Vasc Surg. DOI: 10.1016/j.avsg.2009.09.018.