In the study of cardiac abnormalities responsible for the development of cerebral embolism two-dimensional echocardiography was performed on 350 patients with ischemic cerebrovascular disease. The results were compared with those obtained from 350 controls without any history of stroke. Atrial fibrillation was detected on ECG in 115 cases (33%) of the patients and in 35 cases (10%) of the controls (p less than 0.001). The structural cardiac diseases observed in stroke patients were: rheumatic heart disease (RHD) in 37, congestive cardiomyopathy (CCM) in 7, hypertrophic cardiomyopathy (HCM) in 19, mitral annulus calcification (MAC) in 29, mitral valve prolapse (MVP) in 9, and myocardial infarction (MyI) in 10 patients. Controls were found to have these lesions in 11, 2, 3, 12, 4 and 9 patients respectively. RHD (p less than 0.001), HCM (p less than 0.01) and MAC (p less than 0.01) were significantly more frequent in patients with ischemic cerebrovascular disease, but not MyI, CCM or MVP. Intracardiac thrombi were diagnosed in 29 cases of patients and in 4 cases of controls (p less than 0.001). Our data suggested that nonrheumatic heart diseases such as MAC and HCM could also be considered as causes of embolic stroke. The reasons for the variable frequencies of cardiac abnormalities reported in the literature for stroke patients are discussed.

In 14 stroke patients showing angiographic recanalization of the occluded internal carotid artery or middle cerebral arterial axis, the postrecanalized angiograms demonstrated several findings that have been considered to be generally rare in cerebral infarction. These findings principally consisted of narrowing of arterial caliber in six cases (43 percent), mass effect in eight cases (57 percent) and capillary blush in five cases (36 percent).

SUMMARY In order to understand the mechanism of clinical worsening in patients with cerebral infarction, attention was focused on the changes in cerebral angiograms obtained repeatedly before and after neurological deterioration. Among 212 stroke patients with minor neurological deficits, incomplete hemiparesis progressed to complete hemiplegia in 15 patients several days after the beginning of symptoms. On admission, 3 had internal carotid artery occlusion, 2 had stenosis of the internal carotid artery, 5 had occlusion of the middle cerebral arterial trunk, 2 had occlusion of the middle cerebral arterial branch, and 3 had no angiographical ly visible occlusion. The changes between the first and the second angiograms were of different varieties: another recurrent occlusion, progression of occlusion, new occlusion in the cerebral arteries opacified through the collateral pathway, recanalization of the initially occluded artery, and no change. Such different patterns of pathophysiological events show that the mechanism of neurological worsening in infarcted patients is not uniform. Based on the results from the present study, several problems which arose during the investigation and the somewhat vague definition of "progressing stroke" currently in use are discussed.

The authors review 15 patients with acute cerebellar infarction accompanied by obstructive hydrocephalus. These patients were among 1700 consecutive patients with acute cerebrovascular disease who were examined by angiography and also, except for the initial 320 cases. by computerized tomography (CT) scan. The CT scans were helpful in diagnosis and management of the patients. It demonstrated cerebellar mass lesions as being low density, isodense, or high density, according to the amount of hemorrhage into the infarcted area. Such cerebellar mass lesions caused acute compression of the posterior fossa. The clinical picture was determined mainly by the extent of the initially infarcted area in the vertebrobasilar territory and the speed of enlargement of the subsequently developing cerebellar mass lesion. Suboccipital decompressive surgery was performed in 10 patients and was generally beneficial. The postoperative prognosis depended mainly on the presence or absence of coexisting brain-stem infarction. Five patients who were managed conservatively died during the acute stage. Prompt and correct diagnosis of this illness is required to ensure adequate therapy.

SUMMARY Ophthalmic artery blood flow in 5 patients with internal carotid artery occlusion of sudden onset was monitored by an ultrasonic Doppler flowmeter to investigate the possible relationship to spontaneous recanalization of the occluded artery. The occluded internal carotid arteries of 2 patients were confirmed angiographically to recanalize and the reversed flow of their ophthalmic arteries changed to physiological flow after the recanalization. The ophthalmic artery blood flow remained reversed in 2 patients whose occluded internal carotid arteries did not recanalize on the follow up angiograms. In the other patient, whose ophthalmic artery blood flow was not detected by the ultrasonic Doppler flowmeter in the acute stage, physiological flow through the ophthalmic artery was detected later. The occluded internal carotid artery did not recanalize and this physiological ophthalmic artery blood flow was filled through the circle of Willis.AN OCCLUDED major cerebral artery spontaneously recanalizes in about 40% of acute patients and the spontaneous recanalization frequently produces hemorrhagic infarction.