Occlusive Disease of Branches of the Aortic Arch

Occlusive Disease of Branches of the Aortic Arch

Occlusive Disease of Branches of the Aortic Arch From the Cardiovascular Surgical Section of the University of Illinois Hospitals and Presbyterian-St...

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Occlusive Disease of Branches of the Aortic Arch From the Cardiovascular Surgical Section of the University of Illinois Hospitals and Presbyterian-St. Luke's Hospital, Chicago Illinois

HUSHANG JAVID, M.D., PH.D., F.A.C.S. Clinical AlJ80ciate Professor of Surgery, UniverlJity of IUinoilJ: AlJsi8tant Attending Surgeon, Presbyterian-St. Luke's Hospital: Attending PhylJician in CardiovlllJcular Surgery, West Side Veterans Administration Hospital, Chicago and Hines Veterans Hospital, HineIJ, Illinois

of the large arteries arising from the arch of the aorta has been recognized as an entity for over 50 years. The early clinical manifestations of occlusive lesions of the carotid and subclavian systems are receiving belated attention as surgical means of treatment appear. Arteriosclerotic involvement of the aortic arch branches was clearly described by Broadbentl in 1875 and the frequency of atherosclerotic changes of the bifurcation of the carotid artery was emphasized by Chiari2 in 1905. Chiari thought the cerebral symptoms associated with these lesions were due to embolic phenomena. Advanced stages of occlusion of these branches were described by Takayasu17 in 1908. He described a syndrome characterized by loss of pulsation in the arteries of the upper extremity associated with syncope, visual disturbances, and changes in cerebral function. The majority of his patients were young Japanese women. As early as 1914 Hunt 7 recognized that atheromatous obstruction of the internal carotid artery in the neck can produce cerebral dysfunction when complicated by reduced collateral flow from the circle of Willis. Later in 1937, Moniz and co-workers15 first demonstrated by angiography occlusion of the cervical portion of the internal carotid artery. This technique allowed accurate diagnosis during life. Martorell and Fabre18 in 1944 and again in 19541' probably best described the clinical picture of occlusive lesions of the aortic arch branches. Since then this syndrome has frequently been referred to as the "Martorell syndrome." In recent years the segmental nature of these lesions has been OBSTRUCTION

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noted. Fisher5 in 1954 reported 45 cases of carotid artery occlusion among 432 autopsies on chronically disabled veterans. He found that in spite of severe involvement of the carotid bifurcation, the intracranial vessels were relatively free of disease. This, and other reports, led to the application of operative procedures that had proved effective in other segmental arterial occlusions. Subsequent studies by arteriography and clinical experience have revealed the importance of recognizing the lesions of the internal carotid artery in the pre-occlusive stage if the undesirable sequelae of cerebral ischemia are to be prevented. PATHOLOGY

The causes of occlusion of the aortic arch branches include syphilitic aortitis, nonspecific arteritis, healed dissecting aneurysm, trauma, tumor, congeriital vascular anomalies, and atherosclerosis. In our experience, the most common of these has been arteriosclerosis usually associated with occlusive lesions elsewhere. No evidence of inflammatory reaction such as fever, increased sedimentation rate, elevated white blood count, or elevated serum globulin level has been found in our cases. Arteriosclerotic occlusion of the branches of the aortic arch occur predominantly at their origins on the aortic arch, at the bifurcation of the innominate artery, or at the carotid bifurcation involving the proximal end of the internal carotid artery. In the majority of the cases the cervical portion of the internal carotid artery beyond the occluded segment appears normal without any indication of atheromatous involvement. When the narrowed segment becomes completely occluded the process extends well into the intracranial portion. This is in contrast to the less commonly seen occlusion of the common carotid artery which does not necessarily involve the distal segment. Patency of the internal carotid in the latter instance is probably maintained via collateral blood supply from the external carotid artery. CLINICAL FEATURES

The clinical manifestations of occlusions of the aortic arch branches are variable and depend upon the location and the extent of the lesion. For the sake of convenience this subject will be discussed under two headings: caroticovertebral occlusion and subclavian system occlusion. CaroticovertebralOcclusion

In our experience caroticovertebral occlusion has been predominantly a disease of the male sex, in the fifth and sixth decades of life. Blockage of the carotid artery usually begins with the formation of an atheromatous plaque at the bifurcation or at the origin of the carotid artery. The

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Ant. cere.~ral a. ,

-Int.. carotid a. -Ext.. carot.id a.

Vert.ebral a.

Fig. 1. Caroticovertebral system.

arterial lumen is gradually narrowed and the blood flow is reduced. Because of its gradual development, the onset of the disease is usually insidious. Since each cerebral hemisphere receives blood from both internal carotid and basilar arteries through the circle of Willis (Fig. 1), the symptoms resulting from occlusion of a single carotid artery will obviously depend upon the efficiency of its collateral circulation. In young individuals or those with adequate collateral circulation, few or no symptoms may result. In older individuals, however, the functional deficit may be severe, particularly during any period of depressed blood pressure or if the patient becomes anemic. The frequent occurrence of extracranial carotid occlusion in patients dying of cerebral vascular accidents has been well established by Fisher, Samuel and others.5. 16 It is generally estimated that about 25 per cent of these patients have lesions of the carotid artery now thought to be correctable. It has also been shown that when occlusion of the internal carotid artery becomes complete, surgical intervention proves ineffective. 4 • 6 It is therefore quite important to recognize the various clinical aspects of this disease in the pre-occlusive stage. Atherosclerotic lesions

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also occur in the vertebral artery which supplies blood to the brain stem, cerebellum and cerebral hemisphere through the circle of Willis. The importance of atheromatous involvement of the cervical portion of the vertebral artery was emphasized in a recent study by Hutchinson and Yates. 8 Significant changes were found in the vertebral arteries in 19 of 48 postmortem examinations on patients who died of various cerebrovascular accidents. There was complete occlusion of the vertebral artery in three cases while in ten others the lumen was reduced to half on cross section. Simultaneous lesions of the carotid and vertebral arteries were noted in 30 per cent of the patients. Diminution of blood flow in the vertebral artery may produce manifestations of basilar artery insufficiency characterized by vertigo, visual disturbances (central), occipital headache, speech disorders, generalized weakness and lack of coordination. In our experience, the symptoms of patients with cerebral circulatory insufficiency due to caroticovertebral occlusion can be classified into three categories. Category I. Patients in this group experience intermittent attacks of dizziness and/or fainting associated with a temporary episode of unilateral sensory loss and muscle weakness. Blurring of vision or temporary blindness on the side of occlusion occurs in the majority of patients. Disturbance of speech occurs when the dominant hemisphere is affected. These patients usually recover spontaneously after a short period of time without evidence of residual involvement. Between attacks no neurological abnormality can be detected. Episodic loss of function which is supposedly ischemic is not due to any fresh vascular obstruction but to a temporary failure of compensatory mechanism. The cause of this transient deficit is not well understood. Alteration in blood pressure, changes in local CO 2 concentration and intramural hemorrhage resulting in cerebral vascular spasm have been suggested. None of these, however, offers an altogether satisfactory explanation of the clinical picture observed. Where changes in the position of the head produce symptoms of ischemia, it is possible that movements of the cervical spine may temporarily obstruct a narrowed and diseased vertebral artery which is the major collateral supply. Category II. These patients usually have a longer history of intermittent cerebral ischemia. In addition, they present a picture of stroke with adequate recovery leaving some residual weakness of the arm and possibly aphasia, if the dominant hemisphere was affected. There is often some evidence of mental deterioration such as anxiety, clouded memory, and lack of ambition. Category III. This group is the most difficult to diagnose and is often mistaken for brain tumor or encephalitis. The symptoms are slowly progressive over a period of months. Often the complaints at the onset are

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Arteriosclerotic Lesions of t.he Carotid System (Site of occlusion)

15



Complete occlusion Iii Part.ial occlusion

No. of pat.i.ent.s Fig. 2.

varied and consist of headache, dizziness, loss of efficiency, impairment of memory, and generalized muscle weakness. Visual disturbance is common in this group and may include visual field defects such as homonymous hemianopsia, marked fall in retinal artery pressure, and in some cases presence of microaneurysms of the retinal arteries. These patients usually have multiple occlusions of the carotid and vertebral systems. DIAGNOSIS

Occlusive lesions of the carotid systems commonly occur in two areas. The more common site is the origin of the internal carotid artery just beyond the bifurcation. In our series of 25 patients, the internal carotid artery was involved in 15. The proximal end of the common carotid artery is less often involved and was affected in only ten individuals. Segmental lesions of the common carotid artery below the bifurcation were seen in combination with other lesions in four patients (Fig. 2). In contrast with the lesions of the internal carotid artery, partial or complete occlusions of the common carotid artery can readily be diagnosed by physical examination. The diagnosis should be considered in the presence of episodic neurological symptoms, particularly when associated with diminished or absent carotid pulsations in the neck or with a systolic murmur or thrill in the supraclavicular region. In patients whose complaints are indicative of diminished cerebral circulation, the exact location and extent of the internal carotid involvement can best be determined by angiography. It is possible, however, to suspect its presence on the basis of the clinical findings. A careful examination of the neck may sometimes reveal a. markedly

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rigid and enlarged carotid bifurcation associated with a thrill under the angle of the jaw. Palpation of the internal carotid pulsations through the neck or tonsillar fossae should be attempted as it may be of help in the diagnosis of some patients. However, this is not consistently successful because transmitted pulsation from the external carotid artery makes this examination unreliable. The superficial temporal artery pulsation may be diminished in advanced carotid bifurcation lesions thereby confirming the clinical impression. Presence of bruit in the neck has been of great help in suspecting lesions of the internal carotid artery. A bruit was absent in only two of our patients with partial occlusion of the internal carotid artery. These two individuals had rather extensive involvement of both common and internal carotid arteries. Bruit was the result of an atheromatous plaque at the bifurcation with insignificant degree of stenosis in two cases. In order to determine frequency of carotid artery disease, in a hospital population over the age of 45, auscultation of the neck was done routinely on patients admitted to the vascular service. Bruit over the carotid artery was noted in 15 persons among 300 examined. None of these, however, came into the hospital primarily for cerebral dysfunction. Six of the 15 admitted on specific questioning occasional dizziness, headache, and episodic blurring of vision associated with some weakness of the opposite extremity. A continuous bruit was noted in two of our patients, both of whom had marked narrowing of the artery with absence of pulsation distal to the involved segment. We have regarded the continuous murmur as a sign of marked reduction of the poststenotic arterial pressure due to inadequate collateral circulation. Carotid Compression. Compression of the normal or less involved carotid will result in syncope and sometimes convulsive movements of the same side when contralateral occlusion is present. Syncope due to carotid sinus syndrome or insufficiency of the vertebral artery flow should be considered. Ophthalmodynamometric Studies. Diastolic pressure of the central retinal arteries may be determined by ophthalmodynamometer. This method allows pressure measurements of the ophthalmic artery, which is the first branch of the internal carotid artery. Any decrease in pressure may be indicative of carotid occlusion. This test is not infallible, however. Two of our patients with symptoms of cerebral ischemia and demonstrated partial internal carotid occlusion were found to have equal pressure readings in both eyes. This was considered to be due to adequate collateral circulation through the circle of Willis. The marked differences between the central retinal artery pressures of the two eyes has been considered by us as diagnostic of an occlusive process. Differential diagnosis of carotid thrombosis, embolism, or cerebral

Occlusive Disease oj Branches oj the Aortic Arch Table 1.

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Differential Diagnosis of Vascular Causes of Stroke HEMORRHAGE

EMBOLISM

THROMBOSIS

Onset ................. Sudden Associated findings ..... Hypertension

Sudden Cardiac lesion

Headache .............. Severe

Absent or mild (early phase) None

Gradual Occlusive lesions elsewhere Absent or mild (early phase) None

Usually clear

Usually clear

Normal Clear Normal

Normal Clear Normal

Nuchal rigidity .........

Marked (early phase) Sensorium ............. Drowsy to comatose Spinal fluid Pressure ............. Increased Color ............... Red Protein .............. Maybe elevated

hemorrhage remains as much of a challenge today as it was 50 years ago. While is it impossible to set forth rigid rules, Table 1 may serve as a guide for the clinical differentiation in patients who enter the hospital with cerebral vascular accidents. If the cause of stroke cannot be determined by clinical picture, cerebral angiography is indicated. Angiography. Advances in medical and surgical treatment of vascular lesions of the brain have made the accurate diagnosis in cases of cerebrovascular accident essential. It becomes a matter of considerable practical importance to be able to differentiate between patients with stroke due to cerebral artery thrombosis and those with stroke due to internal carotid occlusion. In a recent report by Kuhn,!l no mortality or morbidity was experienced in cerebral angiography of 100 patients with stroke due to various causes. Percutaneous carotid angiography under local anesthesia is satisfactory in patients with cerebrovascular accidents. Five to 10 cc. of 50 per cent Hypaque (sodium diatrizoate) solution may be injected through a standard 18 gauge Cournand needle. General anesthesia may be necessary in apprehensive individuals. We have not used angiography in patients with occlusion of the proximal portion of the common carotid and subclavian arteries. In our opinion it is indicated only when involvement of the internal carotid or the vertebral artery is suspected. SURGICAL TREATMENT

The aim of surgical therapy is re-establishment of vigorous unobstructed blood flow to the brain. This, in addition to relieving the symptoms of cerebral ischemia, will, in our opinion, prevent progression of the disease in the carotid artery and delay the obliterative process in the cerebral arteries. Three methods have been used for this purpose;

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Fig. 3 (Case I). A, Preoperative carotid angiogram demonstrating partial occlusion of internal carotid artery. B, Angiogram taken 6 months after operation. Graft patent and functioning. C, Operative view showing arteriosclerotic involvement of the carotid bifurcation. D, Bridging of defect created by excision of carotid bifurcation with autogenous vein graft.

namely, vascular replacement, thromboendarterectomy and by-pass graft. Replacement is often necessary when the artery is secondarily invaded by a malignant neck tumor. In this series it was used in only one patient. CASE I (J.Q.). This 44 year old man was admitted to the hospital in December 1955 with a history of repeated attacks of left-sided headache associated with weakness of the arm and aphasia. Percutaneous carotid angiography revealed narrowing of the proximal end of the left internal carotid artery (Fig. 3, A). At operation a lesion of the carotid bifurcation was noted which was at first

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considered to be a carotid body tumor (Fig. 3, C). This lesion was totally excised and the defect was bridged by a segment of autogenous long saphenous vein graft (Fig. 3, D). Pathological examination of the excised artery revealed arteriosclerotic involvement of the carotid bifurcation. An arteriogram made 6 months after operation revealed satisfactory patency of the autogenous vein graft (Fig. 3, B).

Endarterectomy has proved highly successful in pre-occlusive arteriosclerotic lesions of the carotid bifurcation. These patients all have been shown to have segmental lesions. The blood flow into the common carotid artery is not affected and the internal carotid artery distal to the involved segment shows no gross evidence of intimal thickening. In a series of 11 patients treated by endarterectomy for partial occlusion of the internal carotid artery, pulsatile flow was established in all. Nine of these patients have remained asymptomatic during a follow-up period of from three months to one and one-half years. One patient continues to have slight aphasia; another has weakness of the right arm. These symptoms, however, have diminished gradually in the postoperative course. Supportive measures such as hypothermia and temporary shunts were used only in patients who developed syncope on compression of the affected carotid artery or in those who demonstrated significant blood flow through the narrowed segment at operation. CASE II (V.D.). This 59 year old painter was treated in 1956 with bilateral lumbar sympathectomy for arterial insufficiency of the lower extremities. In January 1959 he noted a sudden attack of numbness and weakness of the right hand while painting. After a few minutes normal sensation and strength returned but a dull left-sided headache persisted for several hours after the episode. In the ensuing 2 months he had several similar attacks. When first seen examination revealed strong carotid pulsation bilaterally but the left carotid bifurcation was found, on palpation, to be markedly rigid and a thrill could be felt over it. On auscultation a systolic bruit was audible under the left angle of the jaw. Compression of the right carotid artery for 5 seconds resulted in syncope, while compression of the other side produced dizziness and numbness of the right hand after 5 minutes. Slight weakness was initially noted on the right side. This disappeared in 24 hours. Anticoagulant therapy was administered over a 1 month period. During this time he had several more attacks of right-sided weakness now associated with transient blindness of the left eye. Surgical treatment was decided upon. Under general anesthesia, a left internal carotid thromboendarterectomy was performed together with preoperative and postoperative angiography (Fig. 4). This patient has remained asymptomatic in the past 6 months.

Partial occlusion of the origin of the vertebral artery has been treated by endarterectomy by DeBakey 4 and co-workers. In a series of six patients, a success rate of 50 per cent was reported. Endarterectomy of the proximal end of the carotid and innominate

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Fig. 4 (Case II). Operative angiogram showing partial occlusion of internal carotid artery. Excision of intima (shown above) results in satisfactory lumen.

arteries has been disappointing. Although it resulted in temporary success in a patient for one year,3 by-pass graft became necessary to reestablish the blood flow. By-pass Grafts. Lesions of the proximal end of the aortic arch branches are best treated with by-pass grafts (Fig. 5). The proximal anastomosis is made between the end of a 10 mm. crimped woven Dacron graft 9 , 10 and the side of the ascending aorta. Exposure of the aortic arch is accomplished through a longitudinal median sternotomy incision. The graft is tunneled under the clavicle and sternocleidomastoid muscle and the upper end is then anastomosed to the common carotid or the internal carotid artery depending on the extent and the location of the lesion. CASE III. P.M., a 55 year old man, was first admitted to the University of Illinois Hospitals in February 1954 for study of the cause of attacks of dizziness, blurring of vision, diplopia, clouded memory and weakness of all 4 extremities. These attacks had been experienced over a 3 year period prior to the admission. Arterial pulsations could not be detected in the right neck and the right upper extremity. The left radial pulse was markedly diminished and a systolic pressure of 80 rom. Hg was obtained in the left arm. The left carotid pulsation was satisfactory. Right innominate thromboendarterectomy was done in March 1954.3 This procedure produced a patent lumen in the artery which persisted for 1 year with subjective improvement. Subsequent occlusion of thromboendarterectomized segment was treated by implantation of a by-pass graft of crimped dacron, the patency of which has persisted for 16 months to the date of the present report. A third operation has been done in this patient consisting of a successful endarterectomy of the left internal carotid artery.

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Fig. 5. Procedure employed for aortocarotid by-pass graft.

In patients whose general condition does not justify thoracotomy, a by-pass graft between the subclavian artery and carotid artery can be done through the neck, if there is no interference with blood flow into the subclavian artery. Multiple lesions of the aortic arch branches may be treated in one stage, particularly if the subclavian and carotid arteries on the same side are involved. In such a situation the proximal end of a bifurcation graft is anastomosed to the side of the ascending aorta and the limbs of the graft are sutured to the sides of the involved vessels distal to the occluded segment. Re-establishment of blood flow to both carotids was accomplished in one patient with the aid of a bifurcation graft originating from the ascending aorta. This 50 year old woman had complete occlusion of the innominate and left subclavian arteries and marked narrowing of the left internal carotid artery which resulted in daily attacks of

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fainting followed by weakness in both arms and total blindness lasting for periods up to one hour. The presence of microaneurysms was noted on funduscopic examination. The immediate postoperative period was entirely satisfactory and anticoagulants were administered. Pulses were palpable in the neck bilaterally. On the sixth postoperative day the patient became comatose and died. Postmortem examination revealed diffuse cerebral hemorrhage. This case represents our only fatality in patients who had corrective surgery (Table 2). Table 2. NO.

O~~

Carotid System Occlusions in 25 Patients

PATIENTS

LOCATION OF OBSTRUCTION

15

Internal carotid artery

10

DEGREE OF OBSTRUCTION

PROCEDURE

BLOOD FLOW RESTORED

Complete 2 Incomplete 13

Endarterectomy 2 Endarterectomy 11 By-pass graft 2

11 2

By-pass graft

10

Common carotid artery Complete 6 Incomplete 4

TOTALS

10

MORTALITY

o

23

Subclavian Artery System Occlusion

The significant role that arteriosclerosis plays in the occlusive arterial lesions of the upper extremity has recently been recognized. Although occlusion of the terminal branches has formerly been identified with Buerger's disease, it is now evident that some of these as well as the proximal lesions are primarily arteriosclerotic. In a review of 78 patients who were subjected to operation for vascular insufficiency of the upper extremity, the causative factor was arteriosclerosis in 24 cases. Six of these patients had occlusion of the proximal portion of the subclavian artery and were subjected to direct arterial surgery. Onset of the disease was insidious in all patients with proximal occlusion. Intermittent claudication of the upper extremity was experienced by five patients. Pain, when present, was usually confined to the fingertips or hand and was ischemic in type, unlike compressive lesions which cause pain along the distribution of C8 and Tl. SURGICAL TREATMENT

Although dorsal sympathectomy has been advocated for occlusive disease of the upper extremity, a review of our cases indicates that signficant residual manifestations of vascular insufficiency persist if restoration of pulsation is not achieved. By-pass graft or endarterectomy is indicated whenever possible to restore pulsation. Table 3 summarizes our experi-

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, A

~

IS

Fig. 6. By-pass graft between ascending aorta and the axillary artery.

ence with by-pass grafts in occlusion of the proximal end of the subclavian artery. No instance of failure of the graft has occurred in four patients, the pulses in the extremities having been restored. All symptoms were relieved in three of the patients while the fourth (W.P.) continues to show some evidence of pain along the brachial plexus distribution. The deep cyanosis of the fingertips which prior to operation had suggested ischemia in two cases was relieved immediately following operation. In two patients who had segmental disease of the right subclavian artery it was necessary to pass the prosthesis from the aorta within the chest to the brachial artery (Fig. 6). In order to pass the 10 mm. lumen Dacron tube through the chest wall, a tortuous course over the first rib was avoided by producing a new extrapleural opening in the anterolateral portion of the first interspace. The graft, after it emerged from the chest, was positioned so that abduction and elevation of the shoulder allowed the graft to pivot on the point of emergence without

H USHANG J AYID

124 Table 3.

Subclavian System Occlusions

LOCATION OF OBSTRUCTION

DEGREE OF OBSTRUCTION

PROCEDURE

RESULT

AGE

SEX

G.M.

55

M

Left subclavian origin

Complete

Aorticosubclavian by-pass

Excellent

J. DeR.

63

M

Right subclavian at Complete innominate bifurcation

Aorticobrachial by-pass through first interspace

Excellent

s.

60

F

1. Right subclavian at Complete Aorticobrachial innominate bifurcation by-pass through 2. Right internal carotid Mild and first interspace incomplete

Excellent

51

F

Left subclavian at origin

Excellent

PATIENT

R.

W.P.

Complete at origin

Left common carotid to left subclavian by-pass and excision of cervical rib

constriction. Within the chest the graft followed a retropleural course without contact with the lung. This route of passage of the graft apappeared to be advantageous in comparison to a course over the top of the first rib. In one patient (G.M.) the obstructed portion of the left subclavian artery was by-passed from an approach made entirely within the left chest; in another case (W.P.) a by-pass graft between the left common carotid artery and the subclavian artery was performed through the neck. In the remaining two patients, endarterectomy of both the subclavian and brachial arteries was done. DISCUSSION

In this group of patients, only a few presented symptoms and signs of a single lesion affecting only one of the branches of the aortic arch. Most had lesions at multiple locations. The division into caroticovertebral and subclavian system obstruction is, therefore, only one of convenience and the clinical features of the two should be considered together in an attempt to add to the development of the clinical entity, which has been described by others. The ideal candidate for carotid or vertebral artery surgery falls into Category I described previously. The symptoms of transient cerebral ischemia in this group have been entirely reversible in contrast to those in Category III whose neurologic changes may persist after surgery. In the latter group, however, re-establishment of pulsatile blood flow may hinder further progression of the occlusive process. Complete occlusion of the internal carotid artery at the bifurcation is

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most frequently associated with propagating thrombosis of the artery into its intracranial portion. At operation complete evacuation and clearing of the internal carotid artery has proved to be impossible unless the operation was done within a few hours after the occlusion occurs. Greatest emphasis, therefore, should be placed on diagnosis of the lesion before the occlusion is complete. The presence of any of the signs of intermittent cerebral ischemia should cause suspicion of the presence of partial internal carotid occlusion. The presence of a bruit would appear to be the most important physical sign. Restoration of blood flow by surgical means has been demonstrated to be a feasible procedure in occlusive lesions of the aortic arch branches regardless of the extent of obstruction and in partial occlusions of the internal carotid and vertebral arteries. REFERENCES 1. Broadbent, W. H.: Absence of Pulsation in Both Radial Arteries, Vessels Being Full of Blood. Tr. Clin. Soc., London 8: 165, 1875. 2. Chiari, H.: tlber da~ Verhalten des Teilungswinkels der Carotis communis bei der Endarteritis chronica deformans. Verhandl. deutsch. path. Gesellsch. 9: 326, 1905. 3. Davis, J. B., Grove, W. J. and Julian, O. C.: Thrombic Occlusion of Branches of Aortic Arch. Martorell's Syndrome: Report of a Case Treated Surgically. Ann. Surg. 1,#: 124,1956. 4. DeBakey, M. E., Crawford, E. S., Cooley, D. A. and Morris, G. C. Jr.: Surgical Considerations of Occlusive Disease of Innominate, Carotid, Subclavian, and Vertebral Arteries. Ann. Surg. 149: 690, 1959. 5. Fisher, M.: Occlusion of Carotid Arteries; Further Experiences. Arch. Neurol. &. Psychiat. 72: 187, 1954. 6. Gurdjian, E. S. and Webster, J. E.: Thromboendarterectomy of ~rotid Bifurcation and Internal Carotid Artery. Surg. Gync. & Obst. 106: 421, 1958. 7. Hunt, J. R.: Role of Carotid Arteries in Causation of Vascular Lesions of Brain, with Remarks on Certain Special Features of Symptomatology. Am. J. M. Sc. 147: 704, 1914. 8. Hutchinson, E. C. and Yates, P. O. : The Cervical Portion of the Vertebral Artery: A Clinico-Pathological Study. Brain 79: 319, 1956. 9. Julian, O. C., Deterling, R. A., Bhonslay, S., Su, H. H., Dye, W. S. and LopezBelio, M.: Dacron Tube and Bifurcation Arterial Prostheses Produced to Specification. Surgery 41: 50-61, 1957. 10. Julian, O. C., Deterling, R. A., Dye, W. S., Bhonslay, S., Grove, W. J., Belio, M. L. and Javid, H.: Dacron Tube and Bifurcation Arterial Prostheses Produced to Specification: II. Continued Clinical Use and the Addition of Microcrimping. A.M.A. Arch. Surg. 78: 260-270,1959. 11. Kuhn, R. A.: Importance of Accurate Diagnosis by Cerebral Angiography in Cases of "Stroke". J.A.M.A. 169: 1867,1959. 12. Lin, P. M., Javid, H. and Doyle, E. J.: Partial Internal Carotid Artery Occlusion Treated by Primary Resection and Vein Graft. J. Neurosurg. 13: 650,1956. 13. Martorell, F. and Fabre, J.: El sindrome de obliteration de los trancos supraaorticos. Med. cUn. 2: 26, 1944. 14. Martorell, F. and Fabre, J.: El sindrome de obliteration de los trancos supraaorticos. Second Congress of International Society of Angiology. Lisbon, 271, 1954.

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15. Moniz, E., Lima, A. and de Lacerda, R.: Hemiplegies par thrombose de la carotide interne. Presse med. 45: 977, 1937. 16. Samuel, K. C.: Atherosclerosis and Occlusion of Internal Carotid Artery. J. Path. & Bact. 71: 391, 1956. 17. Takayasu, M.: Acta Soc. ophth. Jap. 12: 554,1908. 25 E. Washington Street Chicago 2, Illinois