The etiology of seizures after cardiac transplantation.
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Biomedical subjects
Publications and source records attributed to M A Silver.
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Fourteen patients with 58 severe forearm muscle belly lacerations had muscle repair using tendon grafts. At mean follow-up of 14 months, results of manual muscle testing (N = 58) were: grade 5, 42%, grade 4, 14%, grade 3, 9%, grade 2, 9%, grade 1, 12%, and grade 0, 15%. Mean grip strength of the injured extremity, in pounds per square inch, was 33.5 compared with 83.4 on the noninjured side. Tendon excursion and joint mobility were maintained, and there were no postoperative complications. Tendon grafting of severe muscle lacerations is an effective method to overcome extensive defects.
The efficacy of OKT*3 monoclonal antibody in reversing acute cardiac allograft rejection was investigated in 10 cardiac transplant recipients aged 5 to 57 years (mean 34 +/- 18) and treated with the same induction and maintenance immunosuppression. Serial endomyocardial biopsies, right heart catheterization, and echocardiograms were performed for rejection surveillance. After intensified immunosuppression with equine antithymocyte globulins and steroids, nine patients showed persistent rejection (lymphocytic infiltration and myocyte necrosis). Conventional immunosuppression was contraindicated in one patient. OKT*3 (5 mg by intravenous push daily for 14 days) resulted in complete resolution of rejection in nine of 10 patients (90%). After therapy with OKT*3 mean right atrial and pulmonary arterial wedge pressure were significantly lower (9.1 +/- 4.0 vs 4.8 +/- 2.0 mm Hg and 13.4 +/- 4.3 vs 8.0 +/- 3.3 mm Hg, respectively; p less than .05). Cardiac index was doubled in two patients with rejection-induced cardiac dysfunction (1.5 vs 3.2 and 1.6 vs 2.7 liters/min/m2). Only two patients developed antibodies to OKT*3. Fever, nausea and headache occurred with the first three doses of OKT*3 and did not recur. One patient developed aseptic meningitis. OKT*3 effectively reverses refractory cardiac allograft rejection before the development of irreversible graft dysfunction. Patients who do not develop antibodies to OKT*3 can be retreated with this drug. Adverse reactions to OKT*3 are self-limited.
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The area, weight and 4 linear variables were measured in each aortic valve cusp in 100 necropsy patients with normally functioning aortic valves, and the volume of each sinus of Valsalva and the aortic area at the sinotubular junction were determined in the same patients. The sums of the aortic valve cuspal areas, cuspal weights and sinus of Valsalva volumes increased with age (p less than 0.001) and with heart weight (p less than 0.001). All 3 variables (cuspal area, cuspal weight and sinus of Valsalva volume) also increased with age and heart weight relative to each other. The luminal area of aorta at the sinotubular junction also increased with age and heart weight and it also increased as the sum of the aortic valve cuspal areas and weights and sinus of Valsalva volumes increased. In only 16% of the 100 patients were the 3 aortic valve cusps of similar size (less than 5% difference in area between cusps); in 51%, 1 cusp was of different size than the other 2, and in 33% of patients all 3 cusps were of different sizes.
Twenty of 59 hands (34%) of patients with carpal tunnel syndrome had abnormalities in sensibility testing of both median and ulnar nerves by either two-point discrimination, Semmes-Weinstein monofilament testing, or both. Before surgery, 53% of patients complained of paresthesias and/or numbness in ulnar nerve distribution. Eighty percent of the hands had abnormal Semmes-Weinstein monofilament testing of the ulnar nerve. Thirty-five percent had abnormal two-point discrimination. Forty-one percent had abnormal electromyographic testing of the ulnar nerve. All hands had median nerve decompression alone. Guyon's canal was not released. After surgery, 89% of patients had improvement in paresthesias and/or numbness of the ulnar nerve. Ninety-four percent had improvement in Semmes-Weinstein monofilament testing. Eighty-six percent had improvement in two-point discrimination. Patients with a residual abnormality in ulnar nerve sensibility also had continued abnormality in median nerve sensibility. A significant percentage of patients with carpal tunnel syndrome also have signs and symptoms of ulnar nerve compression. Most improved with carpal tunnel release alone.
Serum neuroleptic levels were measured by radioreceptor assay in 24 schizophrenic patients maintained on fluphenazine decanoate. Clinical state was assessed at the time of neuroleptic level measurement and during the subsequent 6 months. Patients with persistent psychotic symptoms were on higher doses of fluphenazine decanoate than those in remission and had higher neuroleptic levels. Patients who relapsed during the 6 months after neuroleptic levels were measured did not differ in dose from those who stayed in remission but tended to have lower serum neuroleptic levels. These observations suggest that persistent psychotic symptoms in neuroleptic-maintained patients cannot be accounted for solely by inadequate treatment. Furthermore, in remitted patients serum neuroleptic levels may be a determinant of outcome.
Late clinical and hemodynamic observations are described in 6 patients who had either tricuspid valve anuloplasty (TVA) (2 patients) or tricuspid valve replacement (TVR) (4 patients) 5 to 132 months earlier for Ebstein's anomaly of the tricuspid valve unassociated with right ventricular outflow obstruction. Of the 6 patients, 4 had improved postoperatively by 1 New York Heart Association functional class and 2 had improved by 2 functional classes. The cardiothoracic ratio decreased 5 to 12 months after either TVR or TVA in all 6 patients (from a mean of 0.72 to 0.62). Repeat cardiac catheterization 5 to 12 months after TVA or TVR disclosed that the right atrial mean pressure had increased from a median of 4.0 to 10.5 mm Hg (p = 0.05); the right ventricular peak systolic pressure had increased from 19.0 to 31.5 mm Hg (p = 0.02); the right ventricular end-diastolic pressure had increased from 5.0 to 9.0 mm Hg (p = 0.05); the systemic arterial peak systolic pressure had increased from 115 to 123 mm Hg (p = 0.03); and the cardiac index had increased (in all 4 patients in whom both pre- and postoperative values were available) from 1.7 to 2.9 liters/min/m2 (p = 0.06). Thus, the tricuspid valve operations in our 6 patients with Ebstein's anomaly were associated with a decrease in symptoms of cardiac dysfunction, a decrease in cardiac size, an increase in cardiac index and an increase in right ventricular and right atrial pressures. The elevation of the right atrial pressures postoperatively may have resulted from increased right ventricular filling pressures, persistent tricuspid regurgitation or bioprosthetic stenosis.
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A Hancock porcine bioprosthesis (PB) was simultaneously implanted in each of 6 patients aged 30 to 64 years (mean 45) in the tricuspid and mitral valve positions and both PBs were explanted 62 to 140 months (mean 102) later. Cuspal degenerative changes occurred in all 12 PBs. In 5 patients, the changes were more extensive on the PBs in the mitral position than in those in the tricuspid position. Cuspal calcific deposits, as determined by radiographs of the explanted bioprostheses, occurred in 5 PBs in the mitral position and in 3 in the tricuspid position: 1 patient with calcific deposits in the PB in the mitral position had no calcific deposits in the corresponding PB in the tricuspid position; 1 patient had heavy calcific deposits in the PB in the mitral position and only mild deposits in the PB in the tricuspid position; and 3 patients had similar but mild calcific deposits in both PBs. Cuspal tears occurred in 5 of the 6 PBs in the mitral position and in no PB in the tricuspid position. Thrombus was observed on the ventricular aspects of the bioprosthetic cusps in 1 PB in the mitral position and in 4 PBs in the tricuspid position. Thus, in our 6 patients, the degenerative changes were more extensive in the PBs in the mitral position than in those in the tricuspid position. These observations indicate that wear characteristics of simultaneously implanted PBs vary according to the site of implantation.
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A patient is described who postoperatively developed a clinical syndrome characteristic of toxic shock syndrome following amputation of a previously injured finger. A small stitch abscess was identified which grew Staphylococcus aureus. The patient became ill within 12 hours of surgery, suggesting that a small inoculum of a toxic shock-producing strain of S. aureus can produce the clinical syndrome.
A within-subjects design was used to assess age changes in cerebellar Purkinje neurons. Four groups of naive male Sprague-Dawley rats, aged 3, 10, 20, and 28 months. underwent single cell recording for electrophysiological assessment of Purkinje cell firing patterns, followed by perfusion for glyoxylic acid induced catecholamine fluorescence. Cerebellar sections were photographed first by fluorescence microscope for catecholamines, and 2-3 weeks later for quantification of lipofuscin autofluorescence. Finally, these same tissues were treated with cresyl violet and photographed a third time to permit quantitative estimates of age changes in the number of Nissl staining Purkinje neurons. Electrophysiological studies revealed significant effect of age on a number of Purkinje cell firing parameters: in particular, increasing numbers of aberrant, very slow-firing cells were encountered in older animals. These cells showed normal climbing fiber mediated burst activity, but spontaneous simple spike firing rates 3-5 times less than normal. Rats exhibiting the highest numbers of such abnormal cells also exhibited the poorest Nissl staining. Conversely, good Nissl staining of Purkinje neurons in an old rat was a reliable predictor of relatively normal Purkinje cell firing. Lipofuscin was found to accumulate measurably in Purkinje neurons by 20 months of age, and to increase significantly thereafter. Deposition of the substance occurred almost exclusively at the apical pole of the soma. Our data suggest, however, that accumulation of lipofuscin in Purkinje neurons, as well as its reported accumulation in the inferior olive, is not a primary cause of electrophysiological dysfunction. There was no apparent age change in glyoxylic acid induced catecholamine fluorescence nor, in separate pharmacological studies, could any senescent alteration in cerebellar catecholamine levels be found.