Clark H. Millikan

The Pathogenesis of Transient Focal Cerebral Ischemia

The pathogenesis of certain types of focal cerebral ischemia, particularly episodes of focal cerebrovascular insufficiency, is not fully understood. Atherosclerosis, a relatively static process, commonly occurs without producing any neurologic phenomena. However, such episodes rarely occur in cerebral vascular systems unaffected by atherosclerosis. Atherosclerosis plus some transitory pathophysiologic event would explain the clinical events. A list of such events includes vasospasm, transitory systemic hypotension, kinking and external compression of vessels, transitory hypoglycemia, temporary shunts, and thrombosis and multiple emboli. The roles of polycythemia and anemia are mentioned. Evidence is presented that incriminates thrombosis or embolus formation (or both) as the process, secondary to atherosclerosis or associated with atherosclerosis, that produces the focal cerebral ischemia.

Treatment of progressing stroke.

Adequate management of a patient with progressing stroke should include the following. (1) Understanding of the pathophysiologic mechanisms causing cerebral infarction. (2) prompt diagnosis. When the possibility of progressing stroke is considered by the physician, it automatically becomes the priority diagnosis. (3) Prompt clinical and laboratory evaluation should be initiated. (4) Prompt institution of anticoagulant treatment unless contraindicated is appropriate. Heparin followed by coumadin is used most commonly. (5) If there is not prompt cessation of progression over the next 1--3 hr (following adequate anticoagulation), the patient should have a repeat CAT scan, and in many instances, a carotid angiogram to investigate the possibility of misdiagnosis or that an ulcerated atherosclerotic plaque is present releasing emboli not affected by anticoagulation. (6) If any progression occurs, the question of antiedema treatment should be raised.

Reassessment of Anticoagulant Therapy in Various Types of Occlusive Cerebrovascular Disease

Precise use of categorical terms and definitions is mandatory in discussing the use of anticoagulants in treating occlusive cerebrovascular disease. The components of the temporal profile of the disease are described. Six reports have appeared which describe the results of anticagulant therapy in transient cerebral ischemic attacks. From these six studies it is concluded that anticoagulant therapy significantly decreased the risk of cerebral infarction in patients who had attacks of transient focal cerebral ischemia. In the few carefully performed investigations of the use of anticoagulant for acute progressing stroke the evidence points to the lack of progression in patients receiving treatment when compared to individuals not getting such drugs. There continues to be a definite difference of opinion about the results of anticoagulant therapy in completed stroke. If anticoagulant is to be administered on a long-term basis, it must be considered dangerous and every effort made to control the level of anticoagulant action precisely. Hypertension must be effectively controlled.

Relationship of degree of atherosclerosis of internal carotid system in the brain of women to age and coronary atherosclerosis.

Cerebral infaretion currently is the third leading cause of death in the United States. Since atherosclerosis of the cerebral arteries is the basis for the majority of strokes, the authors undertook to define more accurately the distribution of such atherosclerosis, its relation to coronary atherosclerosis, and its relation to such other factors as hypertension, obesity, and cerebral infarction. The results of their study are presented here.

Syndrome of Intermittent Insuffiency of the Basilar Arterial System

TRANSIENT EPISODES of focal neurologic abnormalities occurring in the middle or older age groups and attributed variously to so-called vasospasm or small strokes are common and have been known to neurologists for many years. Despite considerable study, the exact pathogenesis of these has not been made clear. It is not the purpose of this communication to deal at length with data concerning the causation of these transient states of dysfunction of the central nervous system, although ischemia is assumed to be the factor fundamental to the actual production of symptoms. Rather, we wish to point out that there is a group of patients who, for one reason or another, have transient episodes presumably due to insufficient blood 00w through various portions of the basilar arterial system. These phenomena have never been adequately grouped. This complex of periodic transient symptoms might be termed “the syndrome of intermittent insufficiency of the basilar arterial system.”’ Although in some cases the diagnosis can only be suspected, in many instances the diagnosis can be made if one is alert to the possibility. It is our impression that these periodic phenomena due to insufficiency of the basilar artery may be more common than is generally believed. It also appears that this symptom complex is a common historic feature in patients who succumb to closure of the basilar artery by thrombosis. Once the diagnosis of occlusion of the basilar artery is established, serious neurologic abnormalities are usually present and the prognosis is grave. If treatment is to be adequate, it must in a sense be preventive or anticipatory, since there is no replacement for infarcted cerebral tissue. The first requisite for any treatment is early diagnosis. The transitory episodes under discussion may occur for months or years. They may be brief, lasting several minutes, or they may last several hours. Most last about 15 to 30 minutes. Between these spells the patient is well. Examination between the episodes reveals normal findings, while during an attack objective abnormalities are demonstrable. Although there are instances in which minor residual neurologic difficulty remains, we have chosen to look on most

Complications of carotid manipulation

PALPATION, massage, and compression of the carotid arteries in the neck are commonly considered to be innocuous procedures. In practice, massage often means compression. In our experience, such manipulation of the carotid arteries has produced serious complications. It is our purpose to report 4 such instances and to discuss the pathogenesis of these complications. Interest in the effects of manipulation of the carotid arteries is not new. When the ancients named the main vessels to the brain, they chose “karotis,” from the Creek word meaning “deep sleep,” because they recognized the effects of external pressure on these vessels.’ The ancient Assyrians reportedly used carotid compression as a means of analgesia in their rites of circumcision. Parry* in 1799 detected cardiac slowing from pressure on the carotid arteries. Weiss and Baker3 in 1933 clearly outlined the clinical syndromes associated with hyperactivity of the carotid sinus. They described faintness, syncope, and convulsive movements occurring as a result of carotid massage but detected no irreversible neurologic changes in the patients tested. After it was recognized that, occasionally, patients have spontaneous episodes of syncope because of hypersensitivity of the carotid sinus, some physicians massaged the carotid sinus of every patient they examined. Not until 1941 was it recorded that irreversible neurologic damage could result from this maneuver. Marmor and Sapirsteid reported on a patient 53 years old whose pulse slowed immediately after compression of the right carotid sinus. This was followed in a few seconds bv generalized clonic twitching and syncope. The syncope lasted about ten seconds, and the patient then seemed perfectly normal. Several minutes later, he became unresponsive and manifested weakness of the limbs of the right side. Six hours later, he had spasticity of all limbs. At necropsy, there were recent hemorrhagic infarcts of both frontal lobes. The vessels of the circle of Willis were moderately stenotic. Askeyj in 1946 reported several examples of untoward reactions from carotid-sinus stimulation that were observed by members of the California Heart Association. Hemiplegia de-

Reversed Blood Flow in the Vertebral Arteries

Excerpt In 1961, Baker (1), Toole (2), and Fields (3) each showed arteriograms in which it was observed that, when the subclavian artery was severely narrowed or occluded proximal to the origin of ...

Effect of Anticoagulants on Experimental Cerebral Infarction: Clinical Implications

Cerebral infarction is attended by extravasation of blood in varying degrees. The present study was undertaken to learn whether anticoagulant therapy increases the extravasation and thereby diminishes or negates possibly favorable therapeutic effects. A series of experiments on dogs is described and the clinical implications are discussed.

Stroke: 1970-1977

The idea for the journal Stroke was conceived in a private conversation between Dr Irving S. Wright, first chairman of the Coordinating Committee for a Nationwide Stroke Program, and Dr Clark H. Millikan, second chairman of that committee, which took place during the Fifth Princeton Conference on Stroke, January 5–7, 1966. They enthusiastically agreed that there was a need for such a journal. It seemed likely that the Coordinating Committee for a Nationwide Stroke Program would become the Stroke Council of the American Heart Association (AHA). Such a council would provide a logical administrative structure on which to found the journal. In December 1966, the Central Committee of AHA approved the request for council status for Stroke , and the AHA Board of Directors took final official action on January 14, 1967, with Clark H. Millikan as chairman of the new Stroke Council . The Stroke Council met in New York City on January 27, 1967. Among many items on the agenda, the council discussed the pros and cons of starting a professional journal: Stroke . Dr Millikan was empowered to appoint a committee to further study the need for such a journal. He appointed Drs A.B. Baker, Alfred P. Fishman, John W. Goldschmidt, John S. Meyer, and James L. O’Leary, with Irving S. Wright as chairman. Dr Millikan was a member ex officio. This committee met May 8, 1967 at the AHA office in New York City; staff present included Campbell Moses, MD (Executive Director of AHA), John A. Hagan, and Fanny L. Bluh as recorder. After full discussion, the committee “approved in principle the establishment of a journal in the field of cerebrovascular disease with a representative administration cognizant of the interests of the American Heart Association, the American Neurological Association, and the American Academy of Neurology.” On …

Current indications for the use of anticoagulant drugs in cerebrovascular disease.

Considerable variation exists in the interplay of the factors influencing the occurrence of strokes and their final outcome. A final statement about the usefulness of anticoagulant drugs in the treatment of cerebrovascular disease must await further study. The current indications for their use include: (1) intermittent insufficiency of the basilar arterial system, (2) intermittent insufficiency of the internal carotid system, (3) thrombosis within the basilar arterial system, (4) recurrent cerebral emboli associated with a likely cardiac source and (5) possibly, recurrent cerebral thromboses.