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Myasthenia gravis (MG) is the most common disorder of the neuromuscular junction. Myasthenia crisis, defined as respiratory failure requiring mechanical ventilation in MG, is a common life-threatening complication that occurs in approximately 15% to 20% of patients with MG during their life time. The advent of effective mechanical ventilation, specialized neurointensive care units and the widespread use of immunotherapies have substantially altered the prognosis of myasthenic crisis. Early intubation and mechanical ventilation is perhaps the most important step in the management of myasthenic crisis. The authors favor an orotracheal approach for intubation, and placement of small bore duodenal tubes that may help decrease the risk of aspiration and may be more comfortable than regular nasogastric tubes for the patient. Plasma exchange may be more effective than the intravenous immunoglobulin in the treatment of myasthenic crisis involving respiratory failure. A randomized trial is required to confirm the superior efficacy of plasma exchange compared with intravenous immunoglobulin. In the acute setting, the role of immunosuppression and intravenous/intramuscular pyridostigmine and the newer agents such as tacrolimus remains limited and at times controversial. The therapy should be tailored at an individual basis using best clinical judgment.

SUMMARYPrevious studies relating systolic time intervals and measures of cardiac performance have suggested that the time intervals may be useful indices of myocardial contractility. To explore this possibility, systolic times and left ventricular (LV) performance and contractility were measured nearly simultaneously in 14 normal subjects and 56 patients with cardiac disease. Preejection period (PEP) and the ratio of PEP to LV ejection time (LVET) changed significantly with acute inotropic influences (exercise and isoproterenol), were normal in patients with right or left ventricular overloads in whom cardiac index and ejection fraction were depressed but contractile element velocity at peak dP/dt and the Frank-Levinson contractility index were normal, and were significantly abnormal in patients with either clinically evident or occult LV decompensation in whom the measures of contractility were reduced. Correlations of PEP and PEP/LVET with measures of both performance and contractility were insignificant for patients with valvular disease, shunts, or cor pulmonale and significant but weak for the entire series. However, in subjects with either normal left ventricles or cardiac disease confined to the left ventricle, PEP and PEP/LVET exhibited good correlations with measures of pump function and excellent correlations with measures of contractility. These results indicate that the systolic times are a valid measure of contractility which should prove useful in comparing patients with cardiac pathology confined to the LV myocardium and in following patients with extramyocardial hemodynamic lesions of constant severity.

A small proportion of patients who present within 3 hours of symptom onset receive thrombolytic therapy. The observation that patients with more severe neurologic deficits and subsequently worse in-hospital outcomes appear to present early after symptom onset to the hospital may have implications for clinical studies.

PND occurs in nearly one fifth of patients with intracerebral hemorrhage. Higher diastolic blood pressure at the scene, intraventricular extension, and radiologically evident herniation seem to be associated with PND. Prospective studies are needed to evaluate the efficacy of Emergency Medical Services interventions to reduce this early clinical deterioration.

We observed a high rate of tolerability among patients with intracerebral hemorrhage who were treated with intravenous nicardipine using mean arterial pressure goals defined by American Heart Association guidelines within 24 hrs of symptom onset.

To examine the influence of preexistent diabetes mellitus on left ventricular performance and coronary blood flow responses to acute ischemia, mild normoglycemic diabetes was induced in nine mongrel dogs after three doses of alloxan, (20 mg/kg, iv), at monthly intervals. Hemodynamic measurements and coronary blood flow (85 Kr clearance) were obtained before and after the onset of ischemia. This was produced by oc-clusion of the proximal left anterior descending coronary artery via a balloon-type catheter in nine intact anesthetized diabetic dogs and 10 nondiabetic dogs. During the 1st hour of ischemia in the diabetic group, the end-diastolic pressure rose from 7 ± 1.1 (mean ± SE) mm Hg to 23.8 ± 2. 3 without a significant increase of end-diastolic volume. In controls end-diastolic pressure rose from 8.6 ± 1.1 mm Hg to 15.3 ± 1.4, and end-diastolic volume was significantly increased, so that the ratio of end-diastolic pressure and volume was significantly higher in the diabetic group (/•< 0.005). Although indices of contractility did not differ, stroke volume and work reductions were significantly greater in diabetics , despite the fact that coronary blood flow was reduced to a similar extent. Size of the ischemic areas appeared comparable as judged by distribution of dye injected distal to the occlusion. Since potassium loss and sodium gain in the inner and outer layers of ischemic tissue did not differ between the two groups, the intensity of ischemia seemed similar. Glycogenolysis was unimpaired in the diabetic ischemic muscle but triglyceride levels remained elevated. Morphologically the diabetic myocardium was characterized by a diffuse accumulation of periodic acid-Schiff-positive glycoprotein in the interstitium, which was thought to limit diastolic filling of the ischemic ventricle and to contribute to the substantial reduction of ventricular performance. ALTHOUGH the influence of acute regional ischemia on left ventricular function has been well defined in the previously normal animal. lt2 the response of the ventricle affected by a chronic metabolic or structural abnormality has not been described. Acute myocardial infarction has been reportedly associated with a greater incidence of pump failure and higher mortality in diabetes mellitus. 3 Although the increased mortality from cardiac disease complicating diabetes mellitus has been traditionally attributed to accelerated atherosclerosis of the coronary arteries. 4 this is a disputed issue since recent evidence in studies using more quantitative methods and age-matched controls has shown that the complicated lesions of atheroscle-rosis may occur to only a slightly greater extent in diabetics. 5 In a previous study from this laboratory. 6 we observed altered myocardial function in chronic diabetes mellitus in dogs, associated with accumulation of periodic acid-Schiff (PAS)-positive glycoprotein in the myocardial interstitium without coronary obstructive lesions; this morphological abnormality also has been observed in man ?• 8 To examine the response of ...

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