Arch aortography and cerebro vascular insufficiency

Clin. Radiol. (1966) 17, 330-345

A R C H A O R T O G R A P H Y A N D C E R E B R O V A S C U L A R I N S U F F I C I E N C Y *

DAVID SUTTON and E. RHYS DAVIES

From the Radiologieal Department, St. Mary's Hospital, London, W.2

A prospective survey of 330 arch aortograms performed to investigate patients with suspected cerebrovascular insufficiency is analysed to assess the functional importance of extracranial vascular disease. A detailed statistical analysis of the extracranial arterial obstructive lesions is presented. Extracranial atheromatous stenosis or occlusions are often associated with clinical cerebrovascular insufficiency and the lesions are often multiple. Nevertheless extensive arterial disease may be present with minor (or no) symptoms. The critical factors in determining whether or not symptoms occur are the haemodynamic state and the adequacy of the collateral pathways. The functional integrity of the Circle of Willis is of major importance in this respect.

THE association between permanent neurological deficit and internal carotid occlusion is well established. More recently, interest has been centred on transient carotid insufficiency due to internal carotid stenosis. This is characterised clinically by attacks of contralateral paraesthesiae and weakness of the limbs with or without speech defect or monocular blindness.

One of us (D.S.) was concerned with the first angiographic diagnosis of atheromatous internal carotid stenosis as a cause of cerebral dysfunction and this led to the first successful surgical cure (Eastcott, Pickering & Rob, 1954).

Over the past ten years at St. Mary's Hospital, this diagnosis has been confirmed by direct common carotid arteriograms in 307 cases. Of 502 arteries investigated, 121 were occluded and 205 stenosed. In about 4 0 ~ of the cases undergoing bilateral investigation, lesions were present on both sides. Cases investigated by arch aortography are analysed separately below.

The total number of cases operated on at St. Mary's Hospital is now well over 200 and the clinical and surgical aspects have been published in detail elsewhere (Eastcott et al., 1954; Edwards, Gordon & Rob, 1960; Kenyon & Thompson, 1965). In such carotid studies, the correlation between the symptoms and the lesion is good. It is generally accepted that the symptoms arise as a result of interference with cerebral blood flow. Some workers however consider that they are due to small platelet emboli (Ross-Russell, 1963; Gunning, Picketing, Robb Smith & Russell, 1964).

Also important are those cases in whom carotid occlusion is not associated with a neurological deficit (Willis, 1664). We have now seen many cases

TABLE 1

SYMPTOMS COMMONLY SEEN IN BASILAR INSUFFICIENCY (AFTER WILLIAMS AND WILSON,

1962).

Visual changes Hallucinations Hemianopia or field defect Diplopia

Vertigo Visceral Sensations Ataxia Drop attacks or weakness Hemiplegia Headaches Facial sensations and tingling extremities Deafness and auditory hallucinations Disorded consciousness

of bilateral carotid occlusions which were quite unexpected. We have also seen many cases where bilateral angiography has shown obstructive lesions on the symptomless side as well as on the side predicted by the unilateral symptoms.

In recent years the whole concept of carotid insufficiency has undergone change. It has been enlarged to include the vertebro-basilar system and the great arteries of the thorax. This was the result of pathological studies which emphasised the frequency of atheroma of the vertebral arteries and of multiple lesions (Hutchinson & Yates, 1957; Dickinson, 1961). Thus 'vertebrobasilar insufficiency' is now a widely accepted clinical diagnosis. However, its clinical manifestations are more pro- tean than those of carotid insufficiency because of the functional diversity of the brain substance

* Paper presented at the Radiological Section, Royal Society of Medicine, January, 1966.

330

A R C H A O R T O G R A P H Y A N D C E R E B R O V A S C U L A R I N S U F F I C I E N C Y 331

supplied by the vertebrobasilar system and the syndrome is therefore much less clearly defined.

Table 1 lists the symptoms of vertebrobasilar insufficiency described by Williams & Wilson (1962). It is important to note that the only presenting symptoms occurring in more than 10~ of their cases was vertigo which occurred in about 50 ~ .

In established cases the most frequent symptoms were visual disturbances, vertigo, and disordered consciousness.

Another aspect of eerebrovascular insufficiency has been elaborated recently following the report of a case of left subclavian occlusion with the left vertebral acting as a collateral to the left arm (Contorni, 1961). This was achieved by reversed flow in the left vertebral artery. The phenomenon was later described graphically as the 'subclavian steal' (Reivitch, Holling, Roberts & Toole, 1961). Over 100 of these cases have now been reported (Patel & Toole, 1965), including a series of 20 cases from this hospital (Irvine, Luck & Jacobey, 1965).

It has also become clear that lesions of the intra- thoracic great vessels such as the innominate and common carotid arteries, may lead to or aggravate cerebrovascular insufficiency.

There are many problems raised by these concepts and we have attempted to investigate the following in a prospective survey of arch aortographic material over the past 3 years.

We attempted to answer the following questions: 1. What is the incidence and nature of significant

extracranial lesions in cerebrovascular insufficiency?

2. What is the distribution of the lesions and how often are multiple arteries involved?

3. What is the relationship of the site of the lesions to the ischaemic areas of brain and the clinical symptoms?

4. Why do identical lesions produce severe symptoms in one patient, and none in another?

MATERIAL

We have now performed arch aortography in over 700 patients. The arch aortograms of 330 patients, all with a clinical diagnosis of cerebro vascular insufficiency have been analysed. These patients were seen in the three years between January 1963 and December 1965. Seventy-five per cent of them were male, and 25 % female (Fig. 1) reflecting the higher incidence of atheroma in males. TECHNIQUE.--This has been modified over the years and will no doubt be modified further in the

100

NUMBER OF

PATIENTS

50

F--]NO LESION

j~/ ] ATHEROMA ONLY

I LOCALIZED LESION

F

30 40 50 60 AGE OF PATIENTS IN YEARS

Fro. 1

Age and sex distribution of the 330 investigated patients.

70 80

future. Our present technique is to attempt, where possible, percutaneous trans-femoral catherisation of the aortic arch. Even though many of these patients suffer from severe vascular atheromatous disease this was possible in about 90 ~ of the cases. Where trans-femoral catheterisation was not possible owing to severely atheromatous or kinked iliac arteries, the right trans-axillary approach was used. This usually succeeds but can also fail were there is severe atheroma of kinking of the subclavian artery, or where there is an anomalous right subclavian artery. In isolated cases we have used a left trans-axillary approach, and in one case a trans- carotid approach.

We prefer to use the smallest type of large-lumen catheter possibly and therefore prefer polythene (P.E. 240) to the thicker radiopaque catheters. The catheter tips are tapered to allow insertion through small puncture holes and 4 or 5 side holes are made near the tip of the catheter. The catheter tip is screened into position in the ascending aorta using an image intensifier. Forty ml. of contrast medium are injected using a Talley pump at a pressure of about 100 lbs. per square inch. This usually delivers the contrast medium in about 2 seconds.

The patient is placed in the left anterior oblique position and 16 films are taken on a 14 in. × 14 in. Schonander film changer at a rate of 4 films per second.

The contrast medium we have used throughout this series is Triosil 75 ~ . We have now used this in about 500 arch aortograms with no complications. Since it has proved so safe in our hands we continue to use it though there are no doubt other media equally safe.

ANAESTHESIA.---With a few isolated exceptions of

332 CLINICAL RADIOLOGY

very difficult or nervous patients, all our examina- tions have been performed under local anaesthesia. Usually however, the patient is pre-medicated with Pethidine 25 mg. and Phenergan 25 mg. Patients tolerate the examination very well provided they are warned just before the major injection is made, to expect the feeling of heat.

COMPLICATIONS.--We reported the first series of percutaneous catheter arch aortograms 12 years ago

(Sutton, 1954). This was before the development of selective arterial techniques and a trans-carotid approach was then used. Contrast media were then much more toxic and included 7 0 ~ Diaginol which has now been largely abandoned. Modern techniques and contrast media are of course much safer. In the present series of 330 cases, there was one death attributable to the procedure. This patient is illustrated in fig. 16 and death was due to

~ ~ ~ PRESENT BOSNIAK, M. A. SERIES

330 CASES 100 CASES

73.6 ~o 69 ~o A

B ?~"~~" 18.4~ 16%

13/~/~~~ 5.6% 6%

1.2% i%

AUTOPSY REPORTS

1902 WHITE 399 NEGRO

70 % 56 %

22 ,% 36 ~o

6%

2?/00

FIG. 2

Anatomy of the aortic arch and its great branches. (A)--Normal arrangement. (B and c)--Common origin of innominate and left common carotid. In (n) the two vessels arise in common, in (c) the left common carotid arises from the innominate. (D)--Origin of the left vertebral from the aortic arch. (E)--Anomalous right subclavian artery arising distally on the arch.


thrombosis of a stenosed left internal carotid artery which apparently occluded about six hours after the arteriogram.

It is probable that patients with stenosed arteries are always at some risk of developing a thrombosis if blood pressure should fall markedly and these patients need careful observation from this point of view.

The only other significant complications was a patient who developed ischaemia of the leg following trans-femoral catheterisation. The dorsalis pedis pulse disappeared and the foot became cold and white. The patient responded rapidly to conserva- tive treatment and the pulse re-appeared within three hours. However, the danger of thrombosis following traumatic catheterisation in atheromatous arteries is well known, and emphasises that the procedure should only be carried out by skilled workers conversant with all the risks involved.

RADIOGRAPHIC FINDINGS A. Anatomical Features.--The main anatomical

variations of the arch have been compared with those of an earlier aortographic series (Bosniak, 1964), and with the autopsy series reported in the literature (Fig. 2).

The variation which was seen most often was a common origin for the innominate and the left common carotid artery. Obvious cases are recognised readily, but it is sometimes difficult or even impossible to distinguish minor degrees, even in the oblique position, because of overlapping. About one fifth of our cases had this anomaly, but it is commoner in Negroes, being present in 36 ~ of reported autopsy series among Negroes. This predilection may account for the rather higher incidence in Bosniak's series, because an unspecificd proportion of his cases were Negroes, whereas less than 1 ~o of ours were. The main importance of this anomaly is that in the presence of an innominate lesion it calls for operation under hypothermia, since a clamp on the innominate artery may impair flow up the left common carotid (Irvine et al., 1965).

The remaining anomalies show a fairly consistent

Fro. 3 Fro. 4 Fro. 3--Both internal carotid arteries are occluded at their origins ( ~ ). The right vertebral is narrowed by osteophytes at 5/6 cervical vertebrae. Fic. 4 - -The left common carotid is occluded at its origin ( ~. ). There is a stenosis at the origin of the right subclavian

( ~ ) and the right vertebral fills poorly (~-~).

334 C L I N I C A L R A D I O L O G Y

incidence and are also of importance. Thus the left vertebral arises from the aortic arch in 5-6 % of patients so that its origin can only be shown in these cases by arch aortography, and not by subclavian catheterisation. Further, a patient with a proximal left subclavian occlusion will be saved from a subclavian steal if the vertebral is anomalous. We have now seen several such cases.

The aberrant right subclavian artery (Fig. 10) present in 1-2% of patients is also important because it may be a cause for right transaxillary catheterisation failing to enter the ascending aorta. B. Extracranial Pathology--The patients can be divided into 4 groups according to the radiographic findings:

Group 1 . - -One hundred and fifty seven cases (47.6 %) with a localised stenosis or occlusion of at least one extracranial artery. More than one artery was involved in as many as 44 % of this group. The localisation of the lesions was as follows:

(a) Carotid Occlusions. The commonest site of

occlusion was immediately distal to the origin of the internal carotid. Occasionally the occlusion was bilateral (Fig. 3).

In a smaller number of cases, the common carotid was occluded. Again the occlusion was usually just beyond the origin of the artery (Fig. 4). We have however seen one case in which the left common carotid artery was occluded midway between its origin and its bifurcation (Fig. 5).

This illustration also shows collateral filling of the internal carotid by retrograde flow down the external carotid. This is one of the important collateral pathways to which we shall refer later, and which has not been previously illustrated in atheromatous common carotid occlusion.

In a very few cases, common carotid occlusion was bilateral, as in a 60 year old man whose only symptom was giddiness on extending his neck. Even this symptom was only elicited by direct questioning when he attended the hospital because of intermittent claudication. His vertebral arteries

FIG. 5 FIG. 6

FIG. 5--Subtraction print. The left common carotid is occluded at its mid point (~--). Its bifurcation is filling from collaterals (~+) between the occipital branches of the external carotid and the muscular branches of the left vertebral, which is large. FIG. 6 - Both common carotids are occluded at their origins ( $ ). Both vertebrals are large but irregular. Incidentally there is atheroma at

the origin of the left coronary, and narrowing of the left subclavian as it crosses the first rib.


FIG. 7 FIG. 8

Fro. 7--Subtraction ,erint. The right internal carotid is stenosed just beyond its origin ( j" ). The right vertebral is small, and the left is irregular. Incidentally, the left common carotid and the innominate arise in common. FIG. 8 The left vertebral is

occluded at its origin. Note that the right common carotid is tortuous.

were also narrowed (Fig. 6), and he illustrates well the ability of some patients to compensate very adequately for severe arterial disease.

(b) CarotidStenosis. The commonest sites corres- ponded to those of occlusion i.e. the origins of either the internal carotid (Fig. 7) or the common carotid. Sometimes there was severe atheroma of the common carotid beyond its origin.

(c) Vertebral Occlusion. In this series, vertebral occlusion was always at the origin of the artery, and unilateral, as in Fig. 8. One patient, outside this series with bilateral vertebral occlusion at the base of the skull, has been reported elsewhere (Sutton, 1962).

(d) Vertebral Stenosis. This type of lesion was most common at the origin of the artery (Fig. 9). Less commonly the artery was stenosed in the proximal part of its course in the vertebral canal (Fig. 6). Sometimes the vertebral arteries are tortuous and deviated by osteophytes (Fig. 3). We have not regarded these as lesions unless the artery was also narrowed by the osteophytes. Nevertheless

osteophytes are important because they may cause basilar insufficiency by compressing the vertebral arteries when the head is turned or the neck extended (Brain, 1957).

(e) Multiple Lesions. More than one artery was affected in 44 ~ of the cases with localised lesions, and both the carotid and vertebral systems were involved in 25 ~ (Figs. 3, 6 and 7).

(f) Innominate and Subclavian Lesions. Subclavian stenosis proximal to the origin of the vertebral artery may cause cerebral ischaemia by reducing forward flow in the vertebral (Fig. 10). In innominate stenosis flow may be reduced in the right common carotid also. Multiple stenotic lesions may also be present in the thorax (Fig. 10).

Group 2--Subclavian Steal. Twenty six cases (7"9 %). These cases form a separate group because of their unique haemodynamics. The common feature to all the cases is the occlusion of the subclavian or innominate artery proximal to the origin of the vertebral artery, with consequent retrograde flow in the vertebral. In two thirds of our cases, the


FIG. 9 FIG. 10

FIG. 9--The origin of the right vertebral is severely stenosed ( T ). There is also stenosis of the left subclavian proximal to the vertebral origin (+-). FIG. 10--Aberrant right subclavian which appears to arise in common with the left subclavian. Note the narrowing of the right common carotid and left subclavian origins and the atheroma of

the arch of the aorta.

occlusion was on the left (Fig. 1 la and b), and in the remaining third, on the right. Two of the latter group are of particular interest because the occlusion was in the innominate artery, and there was retrograde flow in the right carotid system as well as in the vertebral (Fig. 12a and b). Under these circumstances it is not surprising that symptoms of carotid insufficiency were the dominant clinical feature in one case. The post-operative arteriograms of this case is illustrated in Fig. 12c.

Seventy five per cent of cases with subclavian steal had other lesions as well, e.g. carotid stenosis (Fig. 11). This suggests that the symptoms are not always due to the subclavian steal.

Group 3--Simple Atheroma. Sixty five cases (18.8 %). These cases had atheroma of the proximal parts of the major branches of the arch without any evidence of occlusion or stenosis. Mild degrees of atheroma, which would be visible at operation or in a pathological specimen cannot be seen radiologi- cally in large vessels, and it is likely that the incidence of atheroma has been underestimated.

Group 4--No Extraeranial Lesion. Eighty five cases (25.7 %). None of these cases had any evidence

of an extracranial lesion. Routine intracranial studies were not carried out on these patients and it was not possible to demonstrate how often intracranial lesions were present.

DISCUSSION

SITE OF LESION.--The distribution of the 93 occluded arteries is summarised in Fig. 13. The occlusions were nearly always at the origins of the arteries, and 51.5 % were at the origin of the internal carotid or vertebral arteries. A further 18.5 % were at the origin of the common carotids. Occlusions were twice as common in the carotid system as in the vertebral system.

Fig. 14 shows the distribution of 170 stenoses. Internal carotid stenosis alone accounted for 52% of these, and vertebral stenosis for 44 %. Common carotid stenosis was relatively much less common than common carotid occlusion. In general, occlusion was commoner than stenosis in the proximal parts of the great vessels.

I t is clear from the diagrams that occlusions and stenoses tend to occur at the same sites. Two theo-

A R C H A O R T O G R A P H Y 2 A N D CEREBRO V A S C U L A R I N S U F F I C I E N C Y 337

FIG. llA FIG. l ib

FIG. 11A~The left subclavian is occluded just beyond its origin. There is also narrowing of the left internal carotid near its origin, and of the right vertebral in the vertebral canal. FIG. 11B--A later film in the same series, showing reversed flow in the left vertebral which is supplying the left subclavian. This is an example

of the 'subclavian steal' phenomenon.

ties have been put forward to explain this. Firstly the developmental theory (Dalith, 1963). Points of structural deficiency are said to occur where the foetal arteries fuse or become obliterated during the transition from the embryonic arches to the adult aortic arch. Among such points are the origins of the innominate, right subclavian, and both internal carotids. 4 7 . 5 ~ of all occlusions, and 5 4 ~ of all stenoses were at these sites, but approximately one half of all lesions were at other sites, and the theory does not cover these.

Secondly, the mechanical theory (Stehbens, 1959). It has been shown experimentally that turbulence in a liquid is maximal at an S bend (e.g. the carotid syphon), or where a branch comes off the main stem at right angles (e.g. the origins of the left common carotid, innominate, left subclavian and both vertebrals). In the same way turbulence might be expected at the junction of the innominate and left common carotid when they arise in common, because the angle between them is then nearly a right angle. I t is interesting that both our cases of innominate occlusion had such a common origin (Fig.

12). Thus increased turbulence can be expected at all the sites where stenosis and occlusion are common, but until a causal relationship can be shown to exist between turbulence and atheroma, the role of the former must remain in some doubt.

CLINICAL DIFFERENTIATION OF SUBCLAVIAN STEAL. - - T h e subclavian steal is potentially reversible by surgery, and therefore it is important to differenti- ate it f rom other causes of cerebral ischaemia which it resembles symptomatically. Among the suggested methods is the onset of cerebral symptoms when the appropriate a rm is exercised. When this occurs it is undoubtedly suggestive, but we have seen so many cases without this association that i t must be considered an unreliable sign.

A further important clinical observation is the inequality of the systolic blood pressure in the arms. This was found to be the most important single sign in all the cases so far reported (Patel & Toole, 1965). We have compared these differences in our four groups of patients (Fig. 15). Some inequality was not uncommon, even in the absence of subclavian occlusion. However, it was usually mini-


FIG. 12A

FIG. 12c

mal, and the inequality tended to be greatest in the group with subclavian steal.

Nevertheless the inequality of the arm blood pressures may be quite misleading as in the case of a fifty year old man with episodic weakness of his right arm. This case illustrates very well some of the difficulties of diagnosis where multiple lesions are present and emphasises the necessity for first class technique in angiographic investigation. The

FIG. 12B

FIG. 12A--Occlusion of the origin of the innomina te artery. FIG. 12B--A later film, showing reversed flow in lhe r ight ver tebral and the r ight common carot id, which are filling the r ight subclavian. FIG. 12c - -Pos topera t ive film. All the vessels are now filling antegradely, and the innomina te and common carot id are lef t shown to have

a common origin.

systolic blood pressure was lower in the left arm and a clinical diagnosis of left subclavian steal was made. This diagnosis seemed to be supported by an arteriogram performed elsewhere. However since it was technically rather poor in contrast and detail we repeated it in order to show the detailed circulation better before planning surgery.

The right transaxillary route was chosen as a result of the information already available. The catheter entered the right vertebral artery, and an injection was made into it in an effort to show the subclavian steal in isolation from the other arteries. Contrast was seen on the screen passing up as far as the level of C2. From here it ran back into the subclavian and the patient complained of pain in his right arm (Fig. 16a). The catheter was with- drawn into the subclavian artery and an injection here not only failed to fill the vertebral but showed a streamline defect near the vertebral origin (Fig. 16b). Furthermore the catheter would not pass into the innominate. It was considered therefore that he had a right subclavian steal. This was then confirmed by arch aortography via the transfelno- ral route (Fig. 16c and d). There was also severe atheroma of the left subclavian artery which ac-

A R C H A O R T O G R A P H Y AND CEREBRO V A S C U L A R I N S U F F I C I E N C Y 339

counted for the lower blood pressure on this side and had misled the previous observers.

Clinically his attacks of left arm weakness were considered to be incompatible with uncomplicated right subclavian steal. This was supported by cerebral flow studies carried out at Guy's Hospital which showed a reduced cerebral flow on the right. A left carotid arteriogram was then done at St. Mary's Hospital, and this showed non-filling of the left middle cerebral artery (Fig. 16e).

1%1 8 % 1%

// . " ,Jh4o• l I M I ~ o I I

-o~~ 6'5% / / 8"50 / °J~ -

FIG. 13

The distribution of 93 occlusions,

1-5"/

/

,.

FIG. 14

The distribution of 170 stenoses.

This case illustrates two important points. Firstly, that careful arteriography is the only reliable way of making the diagnosis of subclavian steal; and secondly, that the clinical syndromes are extremely difficult to interpret when multiple lesions are present. The symptoms in this case were probably quite unassociated with the subclavian steal, and were due mainly to an intracerebral lesion.

CORRELATION OF CLINICAL SIGNS AND ARTERIAL LESIONS

PREVIOUS PATHOLOGICAL EVIDENCE. - -The association between cerebral ischaemia and general extracranial atheroma was originally based on pathological material, notably that reviewed by by Hutchinson & Yates (1957), and Dickinson (1961). Extracranial atheroma was found to be commoner than intracranial atheroma in patients dying from cerebrovascular disease, and it was estimated that between 40 % and 50 % of chronic cerebral ischaemia was due to extracranial atheroma. Multiple lesions were common and Hutchin- son & Yates found that if one carotid or vertebral artery was involved, there was an 80 % chance that at least one of the other main cerebral arteries was involved also.

On the other hand, the incidence of severe narrowing at autopsy in patients without clinically recognised cerebral ischaemia has been estimated at 40% in several series (Martin, Whisnant &

NUMBER OF

CASES

40- - - L

20-

0 20 40 60 B.E DI FFERENCE

STE NO SIS/OCCLUSION

40-

NUMBER OF 20-

CASES

0 20 40 60 B.P. DIFFERENCE

SUBCLAVIAN STEAL

40- L 40'

NUMBER NUMBER OF 20- OF 20-

EASES CASES

0 20 40 60 B.R DIFFERENCE ATHERONA

FIG. 15

Incidence and severity of unequal arm systolic blood pressure in each group.

0 20 40 60 B,,~ DIFFERENCE

NO LESION


FIG. 16A FIG. 16B

FrG. 16c FI~. 16D

FIG. 16A--Right vertebral injection. FIG. 16B--Right subclavian injection proximal to the origin of the vertebral which is not filling. FIG. 16c--Aortic root injection after transfemoral catheterisation. There is a right subclavian steal, and severeatheroma of the ]eft subclavian. FIG. 16D--A later film in the same series confirming the R. subclavian

steal.


FIG. 16E Left carotid arteriogram in the same patient. The middle cerebral

artery is occluded.

Sayre, 1960; Schwarz & Mitchell, 1961). Martin et al. (1960) found some evidence of less severe atheroma in all their cases.

It seems from this pathological evidence that despite the association between cerebral ischaemia and extracranial atheroma, some patients are able to compensate very adequately for severe narrowing or complete occlusion of at least one vessel.

PREVIOUS ANGIOGRAPHICAL EVIDENCE.--47"6% of our series had localised stenosis or occlusion of extracranial arteries, and 44 % of these had multiple lesions. A further 7.9 % had subclavian steal and 75 % of these had multiple lesions. In the only other comparable radiologieal series, 40 % of 305 cases of cerebrovascular insufficiency had extracranial lesions, and about one half of these had multiple lesions (DeBakey, Crawford & Shields, 1960). The incidence of subclavian steal is not mentioned. Seventy per cent of the lesions in this series were

in the internal carotid or vertebral arteries, compared with 77 % in our series.

In a smaller series of 152 cases investigated' by a combination of carotid arteriograms and brachial catheterisation (Bauer, Sheehan, Wechaler & Meyer, 1962), only 50 % of the lesions were at these sites, the remainder being more proximal at the origins of the great vessels from the arch.

In our material, carotid lesions were half as common again as vertebral lesions, a rather higher proportion than in a series of 100 cases investigated by Meyer, Sheehan & Bauer (1961). Carotid and vertebral arteries were equally affected in this series, but true comparison is difficult because only one half of Meyer's cases had arteriograms and the figures are based on a combination of radiological and pathological material.

The real clinical significance of the findings in the two major series can only be measured by comparison with a control series of patients without cerebral symptoms. This seemingly insurmountable diffi- culty has been overcome in a controlled investigation of 43 volunteer asymptomatic patients aged 40 to 65 from the Kansas State Penitentiary (Faris, Poser & Wilmore, 1963). Some kind of arterial lesion was said to be present in 23 men (53.6 %) and more than one artery was involved in 10 men (23-3 %). The control group of 68 patients with cerebral ischaemia had only minor radiological differences from the asymptomatic group.

SITE OF LESIONS.--Pathological studies have suggested that the site of arterial obstructions have little influence on the sites of cerebral ischaemia which are determined by the presence of intracranial arterial lesions (Dickinson, 1961). This view was supported by a study of 42 cerebral infarcts in 34 patients (McGee, McPhedran & Hoffman, 1962), Carotico-vertebral disease was prominent in 50% of these cases but usually some other factor such as intracranial disease, hypotension or embolus had been present as well.

TABLE 2 RELATIONSHIP BETWEEN THE CLINICAL SYNDROMES AND THE SITE OF THE RADIOLOGICAL LESIONS

Clinical Syndrome

42.1 16.0% 17.3%

Carotid insufficiency Basilar insufficiency Carotico-basilar insufficiency Ischaemia of arm only

Total 23.0%

Site of Radiological Lesions

Vertebral Both ] Subclavian steal

95% 16"5% 19.2%

I 23% 6.0% 8-8%

25.0% 13.5%

7"9%

Athooma Nil _ _ _

18"0% I 22"1% 88 23"0% / 29"7 ~ 187

7"7% ] 17-3% 51,

25-7% 330

Total no.

* Denotes a case of subclavian steal who had ischaernia of his arm without cerebral symptoms.


UI~. 17A Fm. 17n

FIG. 17A There is severe a the roma of both internal carotids. The r ight vertebral is occluded and the left vertebral tor tuous. This pat ient developed a r ight hemiplegia within 6 hours of the ar ter iogram and died on the next day. FIG. 17B--Postmor tem specimen showing occlusion of the left internal carot id at its origin (-~). F la . 1 7 c - - Circle of Willis. The occlusion has spread f rom the neck into the left anter ior cerebral artery. The left poster ior com- munica t ing artery is hypoplas t ic (<--), one of the commoner anomal ies of the circle of Willis. The r ight anter ior cerebral is

also small ( "~ ).

Fro. 17c

Because of these studies, we have compared the radiological lesions in each of the clinical groups in our series (Table 2). The table shows that patients with symptoms of carotid insufficiency were more likely to have a carotid lesion (42.1 ~ ) than a vertebral lesion (9.5 ~) . A smaller number had lesions of

both systems ( 6 ~ ) while 2 . 3 ~ had subclavian steal.

The correlation in patients with "basilar insufficiency" is less good. Only 5 2 ~ had a localised lesion and these lesions were fairly evenly divided between the carotid (16 ~ ) and vertebral arteries (16.5 ~) .


FiG. 18

Diagram to illustrate possible collateral pathways in cerebrovascular insufficiency. (A and B)--Posterior communicating and anterior communicating arteries of the Circle of Willis. (C)--Communicat ions between maxillary and ophthalmic artery. (D)--Communicat ion between muscular branches of the vertebral and the occipital artery. (E)--Communicat ion between the vertebral and ascending cervical arteries. (F)- - Communications between the inferior thyroid and superior thyroid arteries of the same and opposke sides. (G)--The vertebral artery providing retrograde flow to the subclavian (subclavian steal). (H)--Pial anastomoses between terminal branches of the anterior cerebral, middle cerebral, and posterior cerebral arteries. (J)--Pial anastomoses in the posterior fossa.

(K)--MeningeaI anastomoses and rete mirabile.

Not surprisingly, patients whose symptoms were referable to both basilar and carotid territories had the highest incidence of localised lesions (75%) with lesions of both systems in 25 %.

These results confirm the view that it is often impossible to relate a given clinical syndrome to a particular arterial lesion. In those cases where platelet emboli have been observed as the cause of the symptoms, the association is clear (Gunning et al., 1964). But in most cases it seems that the symptoms are the result of a complex effect on the cerebral blood flow.

Arteriography has shown that there is normally no mixing of the carotid and basilar blood, and that there are 3 points of 'no flow' in the Circle of Willis at the contiguous margins of these major streams. Williams & Wilson (1962), have elaborated this concept, pointing out that if the basilar pressure

gradient falls, the point of no flow will move proximally. If it happens to fall at the mouth of one of the basilar branches, the territory supplied by that branch becomes ischaemic. The variable poisition of the point of no flow under these circumstances is thought to explain the vari able symptoms of basilar insufficiency.

A further consideration is the effect of an obstructive lesion on the total cerebral blood flow. A stenosis of nearly 90 % is stated to be needed before the cerebral blood flow is reduced in otherwise healthy young people (Brice, Dowsett & Lowe, 1964) and it is generally accepted that occlusion of one carotid artery can occur without necessarily reducing cerebral blood flow in an otherwise healthy circulation (Gunning et al., 1964). It is obvious that the reason for the triviality or total absence of symptoms in these cases is the presence of a good collateral circulation.

TH E COLLATERAL CIRCULATION

CIRCLE OF WILLiS.--Theoretically the Circle of Willis is a perfect collateral system. Its potential cannot be defined better than in Willis' original description (1664 quoted by Symonds, 1955).

' If by chance one or two vessels should be stopt there might easily be found another passage in- stead of one of them, as for example if the carotid one side be obstructed then the vessel of the other side might provide for either province . . . . however if both sides should be stopt the offices of each might be supplied from the vertebrals.' However the potential of the Circle of Willis is

limited by the frequency of congenital anomalies. The most important ones are hypoplasfic posterior communicating (22%), anterior communicating (3 %), or anterior cerebral (2%) arteries (Alpers, Berry & Paddison, 1959). If one of the posterior communicating arteries is aplastic, a major extracranial obstruction may impair the circulation seriously or even fatally (Fig. 17).

Other important anomalies are total absence of one vertebral (Berk, 1961), and failure of fusion of the two vertebrals, one of them ending in the posterior inferior cerebellar artery (Thomas, Anderson, I-lain & Mesendino, 1959). These rare anomalies are vitally important when the left vertebral is to be sacrificed, as for example in the Blalock operation. Brain stem infarction has been recorded during cardio pulmonary bypass for V.S.D. as a result of sacrificing the only vertebral feeding the basilar (Thomas, Anderson, Hain & Mesendino, 1959).

OTHER C O L L A T E R A L S . - - S o m e of the alternative routes, such as that from the maxillary to the

344 CLINICAL RADIOLOGY

ophthalmic artery are well known (Fig. 18). Others, less well known, include those between the occipital artery and the muscular branches of the vertebral; between the ascending cervical branches of the subclavian and the muscular branches of the vertebral; and between the external carotid and the ascending cervical branches of the subclavian artery.

We have seen examples of common carotid occlusion with filling of the internal carotid at its origin from collaterals between the external carotid and the muscular branches of the vertebral (Fig. 5), a type of anastomosis not previously emphasised. The implications of this "carotid steal" in recon- structive surgery are clear.

We have previously published illustrations of pial anastomoses between the major branches of the internal carotid artery (Sutton, 1962). These were first shown angiographically by Kreig (1939) and their importance was emphasised by Mount & Taveras (1957).

Pial anastomoses in the posterior fossa appear to be rare but were shown angiographically in a case of basilar artery thrombosis investigated by us in 1963 (Fig. 19). The one other example so far published was recently reported by Weidner, Crandua, Hanafee & Tomiyasu (1965).

Of less importance in the present context are 1. anastomoses between the middle meningeal

and the meningeal branch of the internal carotid, and

2. the 'rete mirabile'. This represents embryonic communications between the external and internal carotid systems at the base of the skull which normally atrophy but can persist, particularly in infantile arterial obstructive lesions.

The considerable capacity of the cerebral circu. lation to provide a collateral circulation is illustrated by a patient whose arteriogram showed right vertebral occlusion and left subclavian occlusion (Fig. 20). The left vertebral arose from the aortic arch. He eventually died of left ventricular failure, and the astonishing feature of the autopsy was the congenital absence of both posterior communicating arteries, so that there was no possibility of any collateral supply through the Circle of Willis. Yet in life the left vertebral was not only the sole supply to the hind brain, but was also able to provide collaterals to the left arm.

Even in the presence of a good collateral circulation, patients with obstructive lesions have a precariously balanced cerebral circulation which may become insufficient (Denny, Brown, 1951).

vertebral is occluded and there is a theroma at the or igin of the left c o m m o n carotid. FIG. 20

ARCH AORTOGRAPHY AND CEREBRO VASCULAR INSUFFICIENCY 345

LESION

/ \ POOR COLLATERALS GOOD COLLATERALS

CARDIAC OUTPUT

ARTt~RIAL CONPRESSION BY NECK NOVENENT

FIG. 21 Diagram of the many factors that influence the severity of

symptoms.

The cerebral arterioles may be maximally dilated already, and unable to counteract any further fall in perfusion pressure (Fazekas & A l m a n , 1965); if there is a fall in b lood pressure f rom any cause, or a reduction in cardiac output , cerebral ischaemia will occur. Temporary vertebral or carotid oblitera- tion by turn ing the head or extending the neck may diminish the total flow in the same way (Brain, 1957).

These concepts and the mult iple factors involved are il lustrated in Fig. 21.

REFERENCES ALPERS, B. J., BERRY, R. G., PADDISON, R. M. (1964). Arch.

Neurol. Psychiat., 81, 409. BAUER, R. B., SHEEHAN, S., WECHALER, N., MEYER, J. S.,

Neurology, 12, 698. BERK, M. E. (1961). Brit. J. Radiol., 34, 221. BOSNIAK, M. A. (1964). Amer. J. Roentgenol., 91, 1222. BRAIN, R. (1957). Lancet, ii, 857. BR/CE, J. G., DOWSETT, D. J., Low~, R. D. (1964). Brit. med.

J., ii, 1363.

CONTORNI, L. (1960). Minerva Chir., 15,268. DALITH, F (1963) J. Amer. med. Ass. 185, 82. DEBAKEY, i . E., CRAWFORD, E. S., FIELDS, W. S. (1961).

Ann. intern. Med., 163, 944. DENNY BROWN, n . (1951). Med. Clin. N. Amer., 35, 1457. DICKINSON, C. J. (1961). Brit. reed. J., ii, 858. EASTCOTT, H. H. G., PICKER/NG, G. W., ROB, C. G. (1954).

Lancet, ii, 994. EDWARDS, C. H., GORDON, N. S., ROB, C. (1960). Quart. J.

Med., 29, 67. FAR/S, A. A., POSER, C. M., WILMORE, D. W. (1963). Neuro-

logy, 13, 368. FAZEKAS, J., ALMAN, R. (1964). Arch. NeuroL, 11, 303. GUNNING, A., PICKERING, G., ROBB SMITH, A., RUSSELL, R.

(1964). Quart. J. Med., 33, 155. HUTCHINSON, E. C., YATES, P.O. (1957). Lancet, 1, 2. IRVlNE, W. T., LUCK, R. J., JACOBEY, J. A. (1965). Lancet, 1,

994. KENYON, J. R., THOMPSON, A. E. (1965). Lancet, 1, 1461. KREIG, W. (1939). Zbl. Chit., 66, 562. McGEE, D. A., McPrmDRAN, R. S., HOrFMAN, H. J. (1962).

Neurology, 12, 848. MARSHALL, J. (1964). Quart. J. Med., 33, 309. MARTIN, M. J., WHISNANT, J. P., SAYRE, J. P. (1960). Arch.

NeuroL, 3, 530. MEYER, J. S., SHEEHAN, S., BAUER, R. P. (1960). Arch.

NeuroL, 1, 27. MOUNT, L. A. (~ TAVERAS, J. M. (1957). Arch. Neurol.

Psychiat., 78, 235. PATEL, A., TOOLE, J. F. (1965). Medicine, 44, 289. REIVITCH, M., HOLL1NG, H. E., ROBERTS, B., TOOLE, J. F.

(1961). New Engl. J. Med., 265, 878. ROSS RUSSELL, R. W. (1963). Lancet, ii, 1354. SCHWARTZ, C. J., MITCHELL, J. R. A. (1961). Brit med. J.

(1961). ii, 1057. STEHEENS, W., E. (1959). Quart. J. exp. Physiol., 44, 110. SUTTON, D. (1962). Arteriography. Edinburgh & London:

E. & S. Livingstone. SYMONDS, C. (1955). Brit. med. J., i, 1t9. THOMAS, G. J., ANDERSON, K. N., HAIN, R. F., MESENDINO,

K. A. (1959). Circulation, 46, 747. V~rEIDNER, W., CRANDUA, P., HANAFFEE, W., TOMIYASU, U.

(1965). Amer. J. RoentgenoL, 95, 831. WILLIAMS, D., WILSON, T. G. (1962). Brain., 85, 741. WILLIS, J. (1664). Cerebri Anatome. London.

A d d e n d u m . - - S i n c e this paper was submit ted for publ ica t ion an excellent review of the cerebral collateral circulation has been published by Hawkins.

HAWKINS, T. D. (1966). Clin. Radiol., 17, 203.

N O T I C E

THE Nineteenth Annual Midwinter Radiological Conference, sponsored by the Los Angeles Radiological Society will be held at the International Hotel (adjacent Los Angeles Inter- national Airport), Los Angeles, California, on Saturday, January 28 and Sunday, January 29, 1967. The program

will include the following speakers: G. J. D'Angio, Benjamin Felson, Herbert J. Kaufmann, John W. Laws and Richard Lester. Conference reservations should be made through Richard R. Screiber, M.D., 2400 South Flower Street, Los Angeles, California, 90007.

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Arch aortography and cerebro vascular insufficiency

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