The vertebrobasilar arterial system supplies the brain-stem, occipital lobes, and medial aspects of the temporal lobes. Symptoms arising from ischaemia causing loss of function in one or more of these segments can produce a complex of symptoms (Table 1) 188 which may be due to causes other than thromboembolism, especially when they occur in isolation. Because of the uncertainty of the diagnosis, surgery has played a far less prominent role in the management of vertebrobasilar transient ischaemic attacks than is the case for those in the carotid distribution. Nevertheless, epidemiological data from the Mayo Clinic in the 1970s suggested that the risk of stroke after a vertebrobasilar transient ischaemic attack was similar to that of patients with a similar attack in the carotid distribution. Thus identification of patients who might benefit from surgery is of considerable importance, although this has proved to be extremely difficult.

Obstruction of the origin of a single vertebral artery, usually by atheroma, should not result in distal ischaemia of the vertebrobasilar circulation if the contralateral vertebral artery is normal. In general, stenosis of the origins of both vertebral arteries is necessary to produce vertebrobasilar ischaemia; even then ischaemia may not occur if the internal carotid artery on each side is normal, along with a normal circle of Willis with intact posterior communicating arteries. However, there is often associated carotid bifurcation disease and intracerebral disease which, in association with disease of the origins of the vertebral arteries, can result in poor perfusion of the hindbrain. It should also be remembered that an intact so-called normal circle of Willis is found in only about 50 per cent of individuals.

In contrast to transient ischaemic attacks associated with stenoses of the internal carotid artery, those due to vertebrobasilar ischaemia are most often haemodynamic in origin. Whether it is also possible to produce temporary obstruction or kinking of the vertebral arteries in patients with cervical spondylosis by rotation of the neck is uncertain; although obstruction of a vertebral artery by osteophytes has been demonstrated, this should not result in symptoms unless there is associated disease in the contralateral vertebral artery.

A rather uncommon, but better defined, cause of vertebrobasilar ischaemia is the syndrome known as subclavian steal. In this condition there is a significant stenosis or even complete obstruction of the origin of the left subclavian artery, such that when the patient uses the left arm blood passing up the right vertebral artery passes into the left vertebral artery to feed the subclavian artery distal to the obstruction (Fig. 1) 301.

In addition, stenosis or occlusion of the origin of the innominate artery may be associated with steal down the right vertebral artery and internal carotid artery (innominate steal), causing symptoms associated with either vertebrobasilar ischaemia or carotid distribution ischaemia, or a combination of both.

Vertebrobasilar transient ischaemic attacks are difficult to diagnose unless several symptoms occur together during an attack or in separate attacks. Vertigo is the most common symptom of vertebrobasilar ischaemia, but is more often due to other causes, such as disorders of the vestibule (it is important to establish that the patient is having true vertigo). Transient episodes of ataxia are also not uncommon. Other symptoms include diplopia, dysphagia, dysarthria, and drop attacks. The drop attacks are a striking phenomenon when the patient recalls just dropping to the ground without any prewarning symptoms, perhaps, but usually not, losing consciousness transiently, and then recovering immediately. Tingling and numbness of the face and mouth or, indeed, half the body may occur, as also may transient hemiparesis.

Visual loss is the second most frequent symptom after vertigo and is quite variable, ranging from reduced vision in one half field, perhaps accompanied by positive scotomata, to impairment of vision on both sides. Bilateral impairment of vision ranges from total blindness to a generalized mistiness of vision; positive or negative scotomata may occur as spots or moving lights which may be coloured.

The innominate steal or subclavian steal syndromes are classically produced by exercise of the arm on the appropriate side. Apart from bruits in the root of the neck these syndromes will be associated with a distinct pressure gradient between the arms on each side (at least 20 mmHg). However, it must be stressed that the presentation of patients with innominate or subclavian steal is not classical and the association of symptoms with a radiological finding is often difficult. A differential diagnosis of vertebrobasilar ischaemia includes the same causes as outlined in the differential diagnosis of carotid artery transient ischaemic attacks (Section 7.8.1) 49.

The investigation of patients with putative vertebrobasilar ischaemia is still based largely on angiography. An aortic arch study with selective viewing of both vertebral arteries and both carotid arteries, together with intracerebral views is required. The demonstration of stenoses at the origin of the vertebral artery does not necessarily confirm a diagnosis of vertebrobasilar ischaemia, and there is a lack of adequate functional tests of vertebrobasilar ischaemia. Duplex scanning of the vertebral arteries allows examination of the arteries in different positions of the neck. This, along with transcranial Doppler and duplex scanning of the circle of Willis, is likely to allow more precise definition of the relevance of extracerebral vascular disease, in particular vertebral disease, to symptoms compatible with a diagnosis of vertebrobasilar transient ischaemia.

Angiography remains an essential investigation for vertebrobasilar ischaemia, whatever the proposed cause might be. It demonstrates stenoses or occlusions of the origin of the left subclavian artery and the innominate artery, and also shows retrograde flow down the left vertebral in a subclavian steal syndrome (Fig. 2) 302, and down the right carotid and vertebral in an innominate steal syndrome. Reverse flow can also be detected by duplex scanning the appropriate arteries in comparison with the contralateral side.

In the presence of symptoms compatible with vertebrobasilar ischaemia, appropriate lesions demonstrable on angiography, such as bilateral vertebral artery stenoses, left subclavian artery stenosis with reverse flow down the left vertebral artery, or innominate artery stenosis with reverse flow down the common carotid and vertebral arteries on the right side, can be considered an indication for surgery. However, patients in whom a diagnosis can be reached of vertebrobasilar ischaemia due to a surgically correctable lesion are relatively few. The steal syndromes are the most clear-cut diagnoses, but even here the diagnosis often remains speculative and is only confirmed by a satisfactory outcome following surgical correction of the defect.

A stenosis of the origin of the vertebral artery may be approached directly and an endarterectomy performed at the origin or preferably through the subclavian artery (Fig. 3) 303. Alternatively the vertebral artery can be divided distal to the lesion and reimplanted into the common carotid artery (Fig. 4) 304. These procedures are performed through a transverse incision in the root of the neck, after division of the sternomastoid.

Although the original approach to a stenosis of the origin of the subclavian artery was via a left anterolateral thoracotomy with endarterectomy of the artery and closure with a patch, this is rarely performed today. The current operations of choice do not involve opening the chest. A graft, prosthetic or vein, is inserted end-to-side between the common carotid artery and the subclavian artery distal to the origin of the vertebral artery (Fig. 5) 305. An approach which avoids clamping the common carotid artery involves running a graft, vein or prosthetic, from the axillary artery on the contralateral side subcutaneously just below the sternal notch to the axillary artery on the affected side (Fig. 6) 306. Finally the subclavian artery may be divided proximal to the origin of the vertebral artery and anastomosed end-to-side to the common carotid artery (Fig. 7) 307.

Although it is possible to perform an endarterectomy directly on the origin of the innominate artery, the simplest approach is to run a Dacron graft off the arch of the aorta and anastomose it end-to-end to the distal innominate artery at its bifurcation (Fig. 8) 308. The innominate artery and its origin from the arch of the aorta is best approached by a median sternotomy.

In the presence of complex disease, such as stenoses of the subclavian and innominate arteries, reconstruction can be satisfactorily performed with a bifurcated Dacron graft, the legs of the graft being anastomosed to the distal innominate artery and left subclavian artery distal to the stenosis but proximal to the vertebral artery.

Surgery for vertebrobasilar ischaemia, which now rarely involves opening the chest, can be performed with minimal morbidity. However, it is much more difficult to evaluate the efficacy of surgery in terms of relief of symptoms because of the varied nature of the symptom complex. Nevertheless with careful selection of patients, the outcome can be favourable. The outcome of surgery for innominate or subclavian artery steals in terms of symptom relief is much better in general than for vertebral artery surgery. If severe bilateral carotid stenoses are present in a patient with symptoms of vertebrobasilar ischaemia, the most appropriate procedure might well be a carotid endarterectomy.

Alpers BJ, Berry RG, Paddison RM. Anatomical studies of the circle of Willis in normal brain. Arch Neurol Psychiatr 1959; 81: 409–18.

Cartlidge NEF, Whisnant JP, Elveback LR. Carotid and vertebro-basilar transient cerebral ischaemic attacks: a community study, Rochester, Minnesota. Mayo Clinic Proc 1977; 52: 117–20.

Morris PJ. Surgery of vertebrobasilar disease. In: Warlow C, Morris PJ, eds. Transient Ischaemic Attacks. New York: Marcel Dekker 1982: 297–309.