3. YaCes PO, Hutchinson EC: Cerebral infarction: The role of the extracranial arteries. Special Report series No. 33 Medical Research Council, London. H. M. Stationery Office, 1961, pp 1-95 4. Millikan CH, Siekert RG: Studies in cerebrovascular disease. IV. The syndrome of intermittent insufficiency of the carotid arterial system. Mayo Clin Proc 30: 186-191, 1955 5. Fisher CM: Observations of the fundus oculi in transient monocular blindness. Neurology (Minneap) 9: 333-347, 1959 6. Eastcott HHG, Pickering GW, Robb CG: Reconstruction of internal carotid artery in patient with intermittent attacks of hemiplegia. Lancet 2: 994-996, 1954 7. Fisher CM: The use of anticoagulants in cerebral thrombosis. Neurology (Minneap) 8: 331-332, 1958 8. Hass WK, Fields WS, North RR, et al: Joint study of extracranial arterial occlusion. II. Arteriography, techniques, sites and complications. JAMA 203: 961-986, 1968 9. Kuller L: Formal discussion. In: McDowell FH, Brennan RW (eds): Cerebral Vascular Diseases, Eighth Conference, New York, Grune & Stratton Inc. pp 19-22, 1973 10. Kuller L: The transient ischemic attack. A critical review of anticoagulant and surgical therapy. Current Concepts Cerebrovascular Disease-Stroke 9: 23-26, 1974 11. Genton E, Barnett HJM, Fields WS, et al: XIV. Cerebral ischemia. The role of thrombosis and antithrombotic therapy. Stroke 8: 150-175, 1977 12. Whisnant JP, Matsumoto N, Elveback LR: Transient cerebral ischemic attacks in a community: Rochester, Minnesota, 1955 through 1969. Mayo Clin Proc 48: 194-198, 1973 13. Millikan CW: Treatment of occlusive cerebrovascular disease. In: Siekert RG (ed) Cerebrovascular Survey Report for Joint Council Subcommittee on Cerebrovascular Disease, National Institute of Neurological and Communicative Disorders and Stroke and National Heart and Lung Institute (revised). Rochester, Minnesota, Whiting Press Inc. pp 213-242, 1976

BACKGROUND:The efficacy of carotid endarterectomy in patients with asymptomatic carotid stenosis has not been confirmed in randomized clinical trials, despite the widespread use of operative intervention in such patients.METHODS:We conducted a multicenter clinical trial at 11 Veterans Affairs medical centers to determine the effect of carotid endarterectomy on the combined incidence of transient ischemic attack, transient monocular blindness, and stroke. We studied 444 men with asymptomatic carotid stenosis shown arteriographically to reduce the diameter of the arterial lumen by 50 percent or more. The patients were randomly assigned to optimal medical treatment including antiplatelet medication (aspirin) plus carotid endarterectomy (the surgical group; 211 patients) or optimal medical treatment alone (the medical group; 233 patients). All the patients at each center were followed independently by a vascular surgeon and a neurologist for a mean of 47.9 months.RESULTS:The combined incidence of ipsilateral neurologic events was 8.0 percent in the surgical group and 20.6 percent in the medical group (P < 0.001), giving a relative risk (for the surgical group vs. the medical group) of 0.38 (95 percent confidence interval, 0.22 to 0.67). The incidence of ipsilateral stroke alone was 4.7 percent in the surgical group and 9.4 percent in the medical group. An analysis of stroke and death combined within the first 30 postoperative days showed no significant differences. Nor were there significant differences between groups in an analysis of all strokes and deaths (surgical, 41.2 percent; medical, 44.2 percent; relative risk, 0.92; 95 percent confidence interval, 0.69 to 1.22). Overall mortality, including postoperative deaths, was primarily due to coronary atherosclerosis.CONCLUSIONS:Carotid endarterectomy reduced the overall incidence of ipsilateral neurologic events in a selected group of male patients with asymptomatic carotid stenosis. We did not find a significant influence of carotid endarterectomy on the combined incidence of stroke and death, but because of the size of our sample, a modest effect could not be excluded.

Specific patterns of atherosclerotic lesions in patients with ischemic cerebrovascular disease have emerged from analysis of arteriograms in approximately 7500 patients in three large-scale multicentered clinical trials, for which I have had the privilege of being the coordinator. In each of these trials aortocranial arteriography was a requisite for entry. The first of these was the Joint Study of Extracranial Arterial Occlusion, which included 23 institutions in the United States and the Institute of Neurology in Montevideo, Uruguay. The primary objective of this study was to determine the role of reconstructive arterial surgery in the prevention of stroke. It soon became apparent that among whites in North America the predominant lesion was atherosclerotic stenosis situated at the extracranial bifurcation of the common carotid artery. Lesions at this location were deemed appropriate and readily accessible for carotid endarterectomy. Among persons of similar European background, living in Uruguay, Argentina, and Southern Brazil, cerebral ischemic symptoms occurred in approximately 35% as a consequence of dilatation, elongation, and kinking of the extracranial arteries. Kinking was considered an indication for reconstructive arterial surgery. Among North American blacks admitted to the Joint Study, it was noted that the offending lesions were more often found in the carotid siphon, at the origin of the middle cerebral artery, or at both locations. Lesions of this nature are virtually unknown among West Africans of the same ethnic origin.

Two patients with transient ischemic attacks and subsequent minor cerebral infarction had repair of very tight carotid stenosis, 4 and 5 weeks respectively after their stroke. Each developed intracerebral hemorrhage when hypertension was uncontrolled during the post-operative period. Hypertension is a significant complication of carotid endarterectomy, and may be a prominent factor in the development of intracerebral hemorrhage post-carotid endarterectomy.

A revival of interest in antithrombotic agents for the treatment of ischemic cerebrovascular disease has resulted in the widespread use of oral anticoagulants for the prophylaxis and therapy of the ischemic variety of stroke, and has generated enthusiasm for the use of platelet-suppressant agents such as aspirin, dipyridamole, and sulfinpyrazone. In delineating the several clinical types of focal ischemic disease and outlining the causes of cerebral ischemia and infarction, the study group considers the problems of data interpretation in the face of inconsistent terminology. The basic mechanisms of hemostasis and thrombogenesis are concisely detailed. Finally, the study group critically reviews extensive earlier reports of clinical trials of anticoagulants, platelet function suppressants, and thrombolytic agents, and reassesses according to present-day statistical standards the significance of the results. The information contained in this report should familiarize the reader with sufficient data to permit him to utilize antithrombotic agents under a variety of circumstances and to appreciate the contraindications and potential dangers in their use.

Among 6,534 patients admitted to the study, 17% showed evidence of subclavian or innominate arterial occlusion or stenosis of 30% or more. Only 168 fulfilled the criteria of "subclavian steal" and more than 80% of these had associated lesions of other extracranial vessels. Differences were noted in operative mortality for various surgical procedures, and complications were higher when the thorax was opened. Mortality and morbidity from stroke were exceedingly high in the surgical group. No significant differences in survival were noted between the medically and surgically treated groups. Patients with subclavian artery disease only did not have strokes during the follow-up period whether they were treated medically, surgically, or not at all.

An analysis was made of 5,593 white and 911 black patients in the Joint Study of Extracranial Arterial Occlusion to determine the difference in clinical and arteriographic manifestations of ischemic stroke in the two groups. Black patients were found to have a higher frequency of occlusive disease of the intracranial arteries, whereas white patients were more likely to have lesions in the extracranial arteries. Blacks differed from whites in their neurologic manifestations, with a lower incidence of transient ischemic symptoms and a greater frequency of completed stroke. Severe hypertension was noted in 40% of the black patients and only 26% of the white patients. In general, the age of blacks on admission was younger than that of whites.

This is a superb little volume describing an important, but hitherto poorly understood, aspect of vascular anatomy. The frequent occurrence of anomalies in the aortocranial arteries is of importance to persons in the several medical disciplines concerned with both normal and abnormal cerebral circulation. The embryology of the arteries of the head and neck is reviewed in detail and provides an excellent background for understanding the role of morphologic variants which may persist into postnatal life. There is profuse illustration employing roentgenograms, line drawings, schematic diagrams, and photographs made during surgery. The book also includes an extensive bibliography which provides historical background for much of the descriptive anatomy. This reviewer finds only one criticism in the organization of the monograph, namely, that it is somewhat discursive in respect to correlation of embryology, pathologic anatomy, radiographic anatomy, and certain clinical features. Attention is focused on the extracranial arteries and those intracranial

For 80% of 4,748 patients with cerebrovascular insufficiency, complete four-vessel examinations were made. Although the primary purpose was localization of surgically accessible extracranial lesions, intracranial studies were also obtained in a high percentage of cases. The overall grave complication rate was 1.2%. A test of interinstitutional comparability of x-ray interpretation revealed greatest agreement when lesions compromised more than 50% of the arterial lumen.

Between July 1, 1961, and June 30, 1965, 4,748 patients with signs and symptoms of ischemic cerebrovascular disease were admitted to various institutions for prospective investigation. The mean age for the group was 60 years. Two thirds were below 65 years of age. A significantly larger proportion of nonwhites were in the age group below 55. Eighty-four percent were white, and men outnumbered women 2:1. Interinstitutional differences in clinical status of patients were noted, particularly between vascular surgical and neurologic services. Complete arteriographic studies showing intracranial and extracranial circulation were accomplished in 80%. Twenty-five percent of the patients had no lesions demonstrated or had surgically inaccessible lesions only. The remainder had surgically accessible lesions, both with or without inaccessible lesions. A higher proportion of patients with surgically accessible lesions was noted among whites.

Abstract Arteriographic studies were carried out in nine patients with presumed thoracic outlet syndrome. The examinations were always done with the affected upper limb in the positions in which symptoms were experienced. In seven patients, the injections were made with the symptomatic arm in 90 deg. abduction and the head and neck in neutral position, turned to one side and then the other. Narrowing or complete obstruction of the subclavian artery occurred in all of these patients with at least one of the positions tested. In two patients, extrinsic compression was observed when the “symptomatic arm” was held in downward traction. Since compression of neural and vascular structures in the thoracic outlet may occur in asymptomatic individuals, arteriography was performed in the same manner in 22 controls who were being studied because of cerebrovascular insufficiency. In the control group, turning the head and neck toward the abducted arm did not cause the compression of the subclavian artery seen in the symptomatic group. From these observations we have concluded that neurovascular compression in the thoracic outlet is related to the size of the costoclavicular space. The anterior scalene muscle may contribute to the production of symptoms by further narrowing the space in some patients. Resection of a segment of the first rib and scalenotomy is considered the most suitable treatment.

I MPROVED techniques 1,7'17'2~ and new contrast media s,14 ,2~ .2~ have extended the horizons of cerebral angiography and made possible complete visualization of the vertebrobasilar system. The published reports of saccular aneurysms of the posterior fossa are principally from necropsy nlaterial or from a combination of cases identified either angiographically or at postmortem (Table 1). We are reporting s cases of aneurysms of the posterior fossa, each diagnosed anglographically.

ANGIOGRAPHY OF THE POSTERIOR CERVICOCRANIAL CIRCULATIONJORGE WEIBEL, M.D. and WILLIAM S. FIELDS, M.D.Audio Available | Share

COMPLETE occlusion of the basilar artery has for many years been generally accepted as fatal or productive of severe neurological deficit. This concept stems principally from the fact that published case reports have been obtained almost entirely from postmortem studies and correlated retrospectively with the clinical manifestations. In this report of living patients in whom basilar artery occlusion was considered to have been demonstrated arteriographically, the extent of neurological deficit is shown to be dependent upon the adequacy of collateral circulation. When collateral pathways are available and patent, maintenance of function is possible. Cervicocranial panarteriography has made it possible to demonstrate not only normal patterns of blood flow in living patients but also the collateral pathways which bypass arterial occlusion. Information regarding the pathological involvement of the arterial tree and the effectiveness of collateral circulation will assist in planning therapy and in predicting the outcome following occlusion. For accurate localization

THE ANASTOMOSES of the blood vessels of the brain are of two kinds: the normal blood vessel connections and those remaining as remnants of embryologic maldevelopment. Many can be visualized in the living by angiography, but others require demonstration only through anatomic studies. When the vascular system is examined in the complicatedly folded adult brain, a maze of vessels coursing in all directions can be seen. It is quite evident that, in order to present understandable data pertaining to this system and the anastomoses in particular, an orderly and methodical approach to the problem must be put forth. To do this, the brain and its vascular network will have to be reduced to a basic unit and the development to the final pattern followed through its various stages.