34  Vertebrobasilar Ischemia: Embolic and Low-Flow Mechanisms	351

with local symptoms (pain) and evidence of dissection but without central manifestations of ischemia (central nervous system deficits or MR evidence of infarction). Patients with massive infarction are not anticoagulated to avoid intraparenchymal bleeding. There is no indication for wire-catheter-stent manipulation of a dissected vertebral. In patients who are anticoagulated appropriately and continue to have intermittent symptoms, the dissected vertebral artery is considered to be the source of emboli. [Q3: A] In these circumstances, and if technically feasible, the dissected segment is excluded and bypassed.7,8

34.2 

Vertebrobasilar Ischemia: Low-Flow Mechanism

A 62-year-old woman with a healthy lifestyle presented with a history of dimming of the visual field and passing out when she turned her head to the extreme right. Three months before, she had been evaluated elsewhere with a history suggestive of amaurosis fugax and bouts of imbalance and vertigo when she turned her head to the right. A carotid endarterectomy had been performed at another institution.

She continued to have severe vertebrobasilar symptoms with head turning. She had a myocardial revascularization 20 years ago, at which point she stopped smoking.

On examination, the patient appeared healthy, with normal and equal (124/80 mmHg) blood pressure in both brachial arteries. Neurological examination under resting conditions was normal. Her neck was silent. When her head was turned to the right, the patient developed dimming of vision, loss of balance, and a sensation of passing out. The arteriogram available from the previous operation carried out elsewhere showed a clearly dominant large left vertebral artery, but we could not see clearly the distal segment of the vessel. The right vertebral artery was small and diseased severely to a preocclusive level throughout its second segment. There was no evidence of posterior communicating arteries. Because the symptoms were repetitive and induced posturally, the patient was scheduled for a dynamic arteriogram. First, we obtained a view with a selective subclavian injection of the dominant left vertebral in the neutral position, which was normal. Following this, the patient’s head was turned to the right; when she became symptomatic, the contrast injection was repeated (Fig. 34.4). This revealed a severe compression of the vertebral artery as it crossed over the posterior lamina of C1, the segment known as the pars atlantica.

The patient underwent exploration of the suboccipital space with dissection and exposure of the vertebral artery where it crossed the lamina of C1. The compression mechanism was between the sharp upper edge of the lamina and the occipital bone. A laminectomy was carried out to provide space for the artery to pass from the exit of the transverse foramen of C1 to the foramen magnum without bony compression (Fig. 34.5). The artery was examined by palpation and direct duplex interrogation; we could find no element of plaque or stenosis in the lumen once the artery was freed and the laminectomy completed. The patient became asymptomatic. Full-range motion of the neck no longer caused syncope or vertigo.

352	R. Berguer

Fig. 34.4  Selective injection of a left subclavian artery while the patient is experiencing symptoms with her head turned to the right. The single, dominant vertebral artery is severely compressed above C1 in its pars atlantica

Fig. 34.5  Three-dimensional reconstruction of a CT scan of the craniocervical junction. The lamina of C1 has been removed