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This paper reports two patients, each of whom presented with a neurological deficit following extra cranial vascular trauma without complete vascular occlusion. It is suggested that in each case embolism occurred from the damaged intima.

Chorea is a major criterion in diagnosis of rheumatic fever. When it occurs in a child without other signs of rheumatic fever and when other less common causes are ruled out, rheumatic fever prophylaxis is indicated. Other neurologic concerns in rheumatic fever are cerebral embolism from the heart and possible direct cerebral effects.

Cerebral Embolism: Clinical Course, Prognostic Signs, and Effects of Anticoagulation Ther¬ apy. Dr. Charles E. Wells. The clinical courses of 97 episodes of cerebral embolism occurring in 82 patients have been ana¬ lyzed. Sixty-three episodes occurred in patients who were not given anticoagulants, and 34 epi¬ sodes occurred in patients who were treated with anticoagulants. In the untreated groups 70% of the patients had rheumatic heart disease and 17% had arterio¬ sclerotic or hypertensive cardiovascular disease. Forty-seven per cent were found to be in normal sinus rhythm when examined after the onset of the embolie phenomena. The onset was most fre¬ quent in the morning hours. Headache was a fea¬ ture of onset in 25%, and in half of these it was of high intensity. Seizures occurred at the onset in 12.5%. The laboratory findings were nonspecific. Twenty-five of the episodes ended in death, and 35% resulted in severe permanent neurologic dys¬ function. A further study was made to determine what factors allow prediction of a good or a poor result

Seven cases of puerperal hemiplegia were seen at the Peking Union Medical College Hospital within a period of four years. Six of the patients were Chinese women. Two cases were apparently due to cerebral hemorrhage, two to cerebral thrombophlebitis, and three to cerebral embolism. Puerperal hemiplegia from brain hemorrhage usually comes on during or shortly after labor, probably always as the result of a coexisting toxemia of pregnancy. The mechanism of the hemorrhage is best explained on the ground that the toxemias of pregnancy produce structural damage to the vessel walls which become so weakened that the elevated blood pressure and the bearing-down efforts incident to labor cause rupture. Puerperal hemiplegia from cerebral thrombosis, possibly the most common type of the condition, occurs most often in the second or third week of the puerperium. It is probably always secondary to a pelvic infection, although the latter may be so slight as to escape detection. In many instances the cerebral thrombosis is preceded by a toxemia of pregnancy and it is suggested that here, as in cerebral hemorrhage, vessel damage may play an important etiologic role. Certain changes in the colloidal state of the blood further augment the tendency to thrombosis in the puerperium. Puerperal hemiplegia from cerebral embolism may be due either to detached cardiac vegetations or to emboli of pelvic origin. The former probably represents a coincidence not directly related to the puerperal state. The mechanism by which detached pelvic thrombi may reach the brain through the pulmonary capillaries is obscure, but numerous necropsy studies attest its occurrence and its actuality must be conceded. Although the seven cases of this report all survived, the prognosis of puerperal hemiplegia is usually grave. Cerebral hemorrhage occurring during labor is particularly likely to prove fatal. Patients who survive the apoplectic seizure seldom escape a certain degree of permanent paralysis.

A case of silent congenital mitral regurgitation presenting with cerebral embolism is described. There was marked deficiency of the anterior mitral cusp. The patient has undergone successful mitral valve replacement.

The clinical events surrounding cerebral embolism have received scant attention from neurologists. Although various aspects of experimentally produced cerebral embolism have been pursued, most studies dealing with the clinical event in man have been written by cardiologists primarily interested in the origin of the embolus itself or by pathologists predominantly concerned with its end state. This situation has developed no doubt because the pathophysiology of the disorder appears obvious; i.e., a solid fragment is broken away, usually from a thrombus in the left auricle of the heart, passes into a cerebral vessel, obstructs blood flow through that vessel, and results in infarction of the region distal to the point of occlusion. The difficulty which neuropathologists have encountered in trying to explain why some of these infarcts are pale and some hemorrhagic reveals that the matter is not always so clear-cut. A more detailed clinical study of these patients reveals, likewise

Responses of the right cervical sympathetic nerve and the systemic arterial pressure to vertebral and carotid embolism were examined in rabbits anesthetized with α-chloralose and the following results were obtained: (1) Vertebral embolism resulted in a marked rise of blood pressure, while carotid embolism resulted a fall.(2) Hypertension produced by vertebral embolism was converted to hypotension by carotid embolism, whereas hypotension produced by carotid embolism to hypertension by vertebral embolism.(3) Hypertension produced by vertebral embolism disappeared on administration of hexamethonium or tetraethyl-ammonium chloride immediately after the rise of blood pressure, whereas it became more marked following the administration of the latter after several minutes indicating increased circulating vasopressor substances. After administration of either hexamethonium or phenoxybenzamine, vertebral embolism caused only a slight rise in blood pressure.(4) The action potentials of the cervical and renal sympathetic nerves increased usually at the onset of hypertension in vertebral embolism, whereas they decreased at the onset of hypotension in carotid embolism.In conclusions, the increased sympathetic activity participated in hypertension produced by vertebral embolism, while the decreased sympathetic activity in hypotension produced by carotid embolism. It was supposed that sympathetic function was dominant in the portions supplied by the vertebral arteries, whereas sympathetico-inhibitory function in the portions supplied by the internal carotid arteires.

Since the introduction of artificial pneumothorax in the treatment of pulmonary tuberculosis occasional cases of air embolism complicating this form of therapy have been reported in the literature. Bruns reported thirteen cases of air embolism with four deaths, occurring during a nine year period in approximately 12,700 pneumothorax treatments. Reyer and Kohl noted ten cases with five deaths in a "series of many thousand insufflations during a period of about four years." The latter observers believe that many of those cases of pleural shock reported in the literature are, in reality, mild cases of cerebral embolism especially since the sign and symptoms in both conditions are very similar. It is quite probable that this complication is more frequent than is generally recognized. This may be due to the fact that if a fatal termination does not occur, the condition is overlooked or called pleural shock or else this type or case is not reported in the literature. The infrequency of necropsies on cases dying from air embolism and the definite proof of the cause of death warrants the recording of this case.

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In a discussion of old and new concepts of cerebral embolism, two cases are used to illustrate the phathophysiology of atheroembolism in producing intermittent and lasting neurologic deficits. Emboli are due to both cardiogenic and noncardiogenic sources. The onset is characteristically abrupt, but premonitory warnings may occur. The risk of recurrent embolism must be weighed against the risk of anticoagulant therapy, which may cause lethal hemorrhage into the infarcted area. Definitive therapy may require surgical intervention. It seems likely that embolism occurs more frequently than has been previously stated, and these patients should be identified to permit appropriate medical and surgical therapy.

In 220 operations for prolapse of the uterus in 212 patients, the average age was 45.8 years, the average parity 4.2, 192 patients (87.3 per cent) were postmenopausal or were sterilized. Twenty-five (11.4 per cent) were first degree prolapse, 73 (33.2 per cent) were second degree prolapse, and 122 (55.4 per cent) were third degree prolapse. Eleven types of operations were employed. Based on the immediate and remote results, four of these seem best suited to meet particular indications, namely, Gilliam suspension with vaginal reconstruction, the Watkins interposition operation, the Murphy extrafascial fixation operation, and the LeFort vaginal occlusion operation. There were four deaths (1.8 per cent). One was from cardiac dilatation and shock, one from lobar pneumonia, one from cerebral embolism and one from hemorrhage and shock. End-results by personal examination were obtained after 148 operations (69 per cent). One hundred twenty-seven (85.8 per cent) were successful, 9 (6.1 per cent) were partially successful and 12 (8.1 per cent) were failures. Combining the cured and improved groups, 136 (91.9 per cent) were successful.

This is a report of a case of coronary and cerebral embolism occurred in a patient with mitral steno-insufficiency. Clinical diagnosis of coronary and cerebral embolism was made by evidences of left hemiplegia and myocardial infarction shown by electrocardiogram. Clinical diagnosis was confirmed at autopsy and postmortem coronary angiography disclosed the location of the coronary embolus.

Fourteen women taking oral contraceptives were admitted during a five-year period because of acute cerebrovascular lesions. A diagnosis of major cerebral embolism was established in four of them. No source of embolism was found, and thorough investigation failed to reveal any predisposing illness. Cerebral embolism was a probable diagnosis in several of the remaining 10 patients. A comparison was made with the strokes occurring in women not taking contraceptive pills in corresponding age groups.

Two patients in whom coronary embolism occurred in association with primary myocardial disease are presented. In addition to coronary embolism, multiple systemic embolism occurred in both patients. In Patient 1, cerebral embolism preceded coronary embolism by a short period of time, and death resulted from myocardial infarction and cardiogenic shock. In Patient 2, the patient survived the episode of coronary embolism, but had episodes of precordial pain for some months following coronary embolism, and continued to have multiple systemic emboli. It is suggested that some instances of angina and sudden death in primary myocardial disease may be due to coronary embolism.

RECENT clinical reports have stressed beneficial effects resulting from the use of anticoagulant drugs in thrombosis of the basilar and carotid arteries1 2 3 4 and in thromboembolic cerebrovascular disease.5 , 6 It was concluded that this type of treatment improves transient symptoms due to intermittent ischemia, decreases the occurrence of cerebral embolism and thrombosis but does not alter the course of cerebral infarction once established.7 How anticoagulant drugs cause benefit in cerebrovascular disease is not fully understood. Clinical and experimental evidence indicates that after a delay such treatment may result in recanalization of a thrombosed vessel. More rapid improvement occurring within the first week . . .

Of nine patients who have had triple valve replacements for organic rheumatic triple valve disease two died in the postoperative period from inadequate myocardial reserve, and a third died four months later from cerebral embolism originating from clot on the left atrial wall. The remainder are well and, except for one, leading normal lives. Though cardiac transplantation has been recommended and used successfully for triple valve disease by Cooley, it is suggested that the long-term outlook today of triple valve replacement is likely to be better than that of transplantation.

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1. 1. Prompt surgical intervention is vital in cases of perforated gastric and duodenal ulcer. 2. 2. If the period between perforation and operation is twelve hours or less, the mortality should be practically nil under favorable conditions and in the absence of unavoidable complications. In this series of cases the elapsed time averaged only six hours. 3. 3. In about 90 per cent of the cases the perforation was on the anterior wall. 4. 4. Operation should consist of simple closure with chromic catgut and suture of the omentum over the site of perforation. Immediate radical operation such as partial gastrectomy is unjustifiable. 5. 5. Intraperitoneal drainage is not necessary or desirable in the early cases. 6. 6. There was only one death in this series and that was due to an unavoidable complication, cerebral embolism on the ninth day.

A 24 year old woman presented with evidence of possible cerebral embolism following a transient episode of temporoparietal headache and sudden inability to move her left arm and leg. The electromyographic studies were within normal limits, but the electrocardiogram revealed junctional rhythm with no evidence of atrial activity. Her condition was diagnosed as persistent atrial standstill, a rare arrhythmia; only 19 other case reports could be retrieved from the literature.

To the Editor:— The use of anticoagulants in the management of cerebal embolism has been highly controversial, and after studying some of the literature, I have concluded that the evidence is contradictory to your editorial statement that therapy should probably be promptly instituted rather than waiting several days ( 201 :877, 1967). The rationale for prompt use of anticoagulants is based primarily on the study of Carter, 1 in which he reported a significantly higher recovery rate in those patients who were promptly treated. Subsequent reports by other investigators were less enthusiastic however, and Carter himself has modified his earlier approach, delaying anticoagulants for three weeks. 2 Neuropathologists are familiar with the frequent occurrence of hemorrhagic infarction following cerebral embolism, as shown both in experimental animals and at autopsy. Fisher and Adams 3 reported a 51% incidence of hemorrhagic infarction in 123 cases of fatal cerebral embolism. They demonstrated fragmentation of

Chicago, Dec. 11, 1902. To the Editor: —Referring to the notice inThe Journal, December 6, concerning suit brought against me for damages, allow me to state the facts: During an operation by Dr. Lemke in the year 1898 his patient had a cerebral embolism, followed by a partial hemiplegia. Shortly after that a lawsuit was commenced against Dr. Lemke, and I was included in the suit, on account of the supposed financial relations between Dr. Lemke and myself. I was not present at the time Dr. Lemke operated, and had nothing to do with the case. The case was tried two weeks ago, and when the plaintiff had completed his evidence, and without the presentation of witnesses and without a defense on the part of Dr. Lemke or myself, the judge instructed the jury to return a verdict in favor of the defendants, thus exonerating Dr. Lemke from any

A case of fatal cerebral embolism complicating transseptal left heart catheterization is presented. Some of the previously reported complications of this procedure are reviewed. Fatal cerebral embolism must now be added to the list of potential hazards of this procedure.

IT HAS long been known that serious consequences may follow trauma or ligation of the carotid artery. About 1798 Abernathy 1 ligated the common carotid artery in a patient who had been gored in the neck by an ox, in order to arrest bleeding from a lacerated left internal carotid artery; the right side was paralyzed, and the patient died thirty hours after ligation. The common carotid artery was ligated in England by Fleming and in America by Cogswell in 1803; in the first instance the patient survived, while the latter case ended fatally twelve days after operation. 2 For the treatment of aneurysm, ligation of the common carotid artery was first employed by Cooper 3 in 1805; hemiparesis developed on the eighth day, to be followed thirteen days later by death. However, in all fairness, it should be added that three years later this surgeon repeated the same procedure

This article deals with a review of the relevant literature on the theme: Complications to external cardiac massage. A special interest is taken in the possible neuropathological implications. Since the original article by Kouwenhotiven et al. appeared in 1960, detailed observations with adequate pathological anatomical documentation concerning embolism to the central nervous system as a consequence of the performed external cardiac massage are rare in the literature. A case of cerebellar embolism is reported in which external cardiac massage had been performed immediately prior to death; the relevant neuropathological techniques are emphasized.

IN the past decade lymphography has had increasing clinical acceptance, with rare complications and no previous report of cerebral embolism. The following fatal case calls attention to a hazard inherent in the intravasation of lipid. Case Report A 53-year-old woman with lymphosarcoma controlled for 5 years by radiation, nitrogen mustard and adrenocorticosteroids was admitted to the hospital because of pain in the left leg. Except for a 2-cm. inguinal node on the left, the superficial lymph nodes were no longer enlarged, and no abdominal masses were felt. Lymphography was done after other studies failed to account for the pain. Roentgenograms . . .

THE association of atrial fibrillation and arterial embolization is a well known clinical entity. However, this sequence in a patient with no clinical evidence of organic heart disease is exceedingly rare. Case Report A 49-year-old woman was admitted to the hospital on January 15, 1958, because of a left-sided hemiparesis of sudden onset, unassociated with loss of consciousness. For 2 years before admission, she had experienced frequent attacks of palpitation, which had been increasing in frequency and which seemed to be related to exercise, amount of coffee consumed (10 to 15 cups a day) and excessive smoking. There was no . . .

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A simple method of estimating the degree of independence has been used to investigate the functional disability initially and during recovery from hemiplegia in ninety-eight patients hospitalized for acute hemiplegia caused by thrombosis, hemorrhage or cerebral embolism. The degree of independence can be scored on a scale of 100. The use of such a scoring system measures the degree of improvement in independence and also focuses attention on what disabilities are in need of treatment. The overall mortality rate at the end of two years was 60 per cent. In the group with the lowest Score for Activities of Daily Living the mortality rate was 81 per cent. The majority of deaths during the follow-up period occurred in the first six months. Using the conventional methods of physical medicine and rehabilitation, little improvement in independence occurred after one month in those patients who did improve. Twenty per cent of all patients achieved complete independence.

THE TERM "cerebral embolism" has in the course of time acquired a fixed clinical meaning; in its usual connotation this diagnosis portrays an episode of sudden onset, often of rapid fatal termination. This conception of embolic disease of the brain, although deeply rooted in medical thinking, is inadequate. There is mounting indication that often cerebral embolism does not manifest itself as an acute process; this syndrome may, in fact, pursue a subtle, recurrent chronic course ultimately leading to progressive crippling of cerebral function. Cerebral embolism is usually thought of clinically as an acute catastrophic neurological complication occurring in patients with known active cardiac disease. All too familiar is the clinical picture of acute cerebral embolism: A patient with known myocardial infarction, convalescing favorably, is suddenly rendered hemiplegic. However, in some instances the onset of symptoms is insidious and slow. In patients who prove to have cerebral embolism often the cardiac

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Since the pioneer work of Head and Holmes,1the physiological and psychological aspects of central pain have been the subject of many studies. Central pain is of specific character: It is severe, it is of burning quality, it affects the whole personality and may cause changes in behavior, it is aggravated by emotional influences and sensory stimuli, and it is generally not alleviated by the usual analgetics. Frequently the pain does not leave the patient during the night and may be so severe as to lead to suicide. At times it is accompanied by vasomotor and trophic disturbances. In spite of numerous clinical and experimental investigations, complete understanding of the problem of central pain has not yet been achieved. Since the work of Dejerine and Roussy,2the thalamus and its cerebral connections are held responsible for the central pain sensation. The mechanism by which damage to the thalamus