Combined electroencephalography and sonoencephalography.
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Biomedical subjects
Publications and source records attributed to B A Sandok.
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Records of 37 consecutive patients with acute brain infarction from vertebrobasilar artery disease, admitted to the cerebrovascular hospital service within 36 hours of the onset of symptoms, were studied to define the temporal profile of clinical events during the first week of illness. A stable course with unchanged neurologic deficit was found in 11% (4 patients). Progressive improvement in symptoms occurred in 35% (13 patients). Progressive disability occurred in 43% (16 patients). A remitting-relapsing course was noted in 11% (4 patients). In these latter 2 groups, stabilization of the clinical course occurred in the majority with 48 hours after the initial symptom; however, definite changes continued to develop up to 96 hours in a significant number of patients. Mortality at the conclusion of the first week was 27% for the entire group. This was 2.5 times greater than the 10.6% previously reported for a group of 179 patients with acute brain infarction due to carotid system disease who were concomitantly studied.
All patients 20 years old or older referred for echocardiographic examination and found to have mitral valve prolapse during the period January 1975 through December 1979 were included in the study. Of the 1,138 patients, two-thirds were women and one-third were men. Their average age was 48.4 years. Forty patients (3.5%) had histories of prior focal cerebrovascular ischemic events. In 26 of the 40 patients, no responsible mechanism other than mitra valve prolapse was identified, and in 4, the ischemic event occurred during an episode of bacterial endocarditis, a known complication of mitral valve prolapse. In 10 of the 26 patients, there was clinical information to suggest an embolic mechanism for the ischemic. A conservative estimate of the prevalence rate for cerebral infarction in this group of patients is four times greater than the rate expected in a normal population. This difference is likely due to the contribution of mitral valve prolapse in the pathogenesis of cerebral infarction.
Survivors of stroke are often left with severe mental and physical disabilities, which create a major social and economic burden. Many investigators have attempted to assess the role of rehabilitation in reducing such disability. Few controlled studies provide accurate assessment and documentation of benefit. Because of the presence of multiple variables and inadequate measures of outcome, it is difficult to design studies evaluating the effectiveness of rehabilitation for stroke. It is unclear how early rehabilitation should begin and what aspects of rehabilitation are important. Intensive rehabilitation is an expensive and limited resource; thus, the ability to identify the subgroup of patients with stroke who are likely to benefit is a critical issue. Although preliminary guidelines for the selection of patients who are appropriate for rehabilitation are given, no uniform criteria reliably differentiate patients who need rehabilitation from those who will recover spontaneously or do poorly. Controlled studies in the practice of rehabilitation for stroke will provide much useful information for patient management.
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In a case of fatal cerebral embolic infarction following aorto-coronary bypass graft (ACBG) surgery, postmortem examination revealed thrombosis of the vein grafts to the left circumflex and left anterior descending coronary arteries. Continguous with the thrombus in the graft to the circumflex artery was thrombotic material adherent to the aortic sutures and extending several millimeters into the lumen of the aorta. A nonadherent thrombus of similar histologic character was found in the right middle cerebral artery, associated with localized brain infarction. In addition to the risks of cerebral complication associated with other types of open-heart surgery, the location of the vein grafts in patients undergoing ACBG operations seems to offer a unique mechansim for the occurrence of systemic and cerebral embolism, which may be operational in other cases.
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In order to study the effects of septic embolism on the brain, silicone rubber emboli of various types were injected into the carotid arteries of 35 dogs. Pathologic and angiographic studies were performed to assess the resultant arterial and parenchymal lesions. Pure silicone rubber emboli (14 dogs) produced occasional intra-arterial thrombosis but no arteritis. Sterile and bacterially contaminated emboli containing a lead-chromate pigment (similar to those used in previous studies of septic embolism) (11 dogs) and pure silicone rubber emboli with transversely oriented canals (10 dogs), after brief placement in a bacterial suspension, were associated with intense inflammatory arteritis. This was accompanied by focal meningitis, subarachnoid hemorrhage, thrombosis, and cerebritis of the underlying cortex. The findings resembled those found in mycotic aneurysm. Aneurysmal dilatation was observed in one postmortem angiogram. In previous models of mycotic aneurysm, the inflammation attributed to bacterial contamination was probably due to the lead-chromate pigment used.
The effect of anticoagulation on lesions caused by cerebral emboli of different types was studied in 57 dogs. The resultant arterial and parenchymal lesions were assessed by pathologic and angiographic studies. Embolization with emboli that caused little or no inflammatory response in the artery (12 dogs) was not associated with hemorrhagic infarcts or with subdural or subarachnoid hemorrhage; furthermore, treatment with anticoagulants (9 dogs) did not change the character of the lesions. Embolization with emboli that caused arteritis, that is, bacterial contamination or presence of lead chromate in the embolus (21 dogs), was associated with hemorrhagic infarcts, focal subarachnoid hemorrhage, and increased incidence of acute subdural hemorrhage. Treatment with anticoagulants (16 dogs) was associated with a further increase in the incidence of subdural hemorrhage.