SUMMARY To study endocardial wall motion and thickness as indexes of infarction, we used two-dimensional echocardiography to examine regional percentages of systolic wall thickening (%Th) and endocardial motion (%EM) in infarcted canine hearts. Thirteen dogs were studied 48 hours after occlusion of the circumflex or left anterior descending coronary artery. Two-dimensional echocardiographic cross sections obtained every 16 msec at 1-cm intervals from apex to base in an open-chest, anesthetized preparation were analyzed with a computer-aided contouring system for quantification of segmental %EM and %Th at 16 equally spaced points per slice. Slices corresponding to each two-dimensional echocardiographic cross section were examined pathologically for evidence of infarction.Comparing histologically infarcted with distant normal zones in each slice, %Th and %EM both yielded clear separation with little overlap (-12.5% infarcted vs 37.4% normal for thickness; -11.3 vs 25.7% for motion, p << 0.001 for both). Endocardial motion was less precise than thickening, however, in distinguishing infarct from either distant normal zones or zones directly adjacent to infarct.Although wall thickening was useful in separating out true subendocardial infarct, change in systolic thickening was not accurate in detecting the transmural extent of infarction. In 827 individual two-dimensional echocardiographic segments with varying degrees of transmural involvement, segments with 1-20% extent of transmural infarction showed reduced thickening compared with noninfarcted segments (39.9 vs 15.2%, p < 0.001), whereas myocardial segments with 21-100% transmural infarction showed systolic thinning (-8.9 to -13.3%). There was no significant augmentation in the severity of systolic thinning as the extent of transmural infarction increased from 21% to 100%.We conclude that: (1) Wall motion abnormalities are less precise than thickening in discriminating between infarcted and noninfarcted zones and could lead to overestimation of infarct size. (2) There is an abrupt deterioration in systolic thickening in segments containing more than 20% transmural extent of infarction. (3) There is no significant augmentation in the degree of systolic thinning as the transmural extent of infarct increases from 21% to 100%. This "threshold" phenomenon may therefore preclude accurate estimation of infarct size by two-dimensional echocardiography. (4

SUMMARY In 1 year 6 patients with prosthetic heart valves (PHVs) treated with anticoagulants suffered intracranial hemorrhage. In 4, hemorrhage occurred into the site of a recent non-hemorrhagic infarction. In the others, both of whom had endocarditis, hemorrhages probably occurred as the result of rupture of a mycotic aneurysm. Five patients were treated with warfarin, 1 with heparin. In all patients the level of anticoagulant activity was greater than 1.5 times control. Five patients were in atrial fibrillation; 1 was hypertensive. The diagnosis of intracranial hemorrhage was made and its location and extent accurately determined by computed tomography (CT). Three patients underwent surgery and 2 are alive with only minor neurological deficits. Among the 3 patients who did not undergo surgery 2 died and 1 is alive with a moderate neurological deficit. The management of PHV patients with use of anticoagulants is discussed in terms of the mechanisms involved in intracranial bleeding. Emphasis is placed on prevention of emboli, discontinuation of anticoagulants once non-hemorrhagic infarction has occurred and the primacy of CT scan in diagnosis when hemorrhage is suspected. The special problems of anticoagulation in the presence of endocarditis are also discussed.A LARGE NUMBER of patients are now living with artificial non-organic prosthetic heart valves (PHVs). Although operative mortality and morbidity have been dramatically reduced, emboli and infection continue to be problems. In the absence of anticoagulants the frequency of

Visual hallucinations and bilateral symptoms were associated with dementia in our cohort of PD brain donors. No association between dementia and survival duration was found. Understanding the influence of dementia on the clinical phenotype of the disease and predicting its development is essential for the successful management of PD.

SUMMARY Seven patients with progressive supranuclear palsy were treated with lisuride. Mean age was 62 years (range, 52 to 68 years), and duration of disease was 4-4 years (range, 1 to 7 years). All seven had been treated with levodopa/carbidopa and three with bromocriptine; four had, at one time, shown a partial response to levodopa. One patient had also shown a partial response to bromocriptine. Lisuride was used alone in four patients, and combined with levodopa/carbidopa in three patients. Mean dose of lisuride was 2-5 mg (range, 1-5 to 5 0 mg). Mean duration of treatment was 4 months (range, 1 to 10 months). While two patients showed a reduction in rigidity, one in tremor and two in bradykinesia, in only one of them was there an overall improvement. It is postulated that the relative lack of response to lisuride may be due to a loss of both the dopaminergic and serotonergic receptors in progressive supranuclear palsy.Progressive supranuclear palsy is a multi-systems degeneration that is characterised by a supranuclear gaze palsy affecting eye movements more severely in the vertical than in the lateral plane

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