Search

Objective Ideal heart valve solutions aim to provide thrombosis-free durability. A scaffold-based polycarbonate urethane urea tissue-engineered heart valve designed to mimic native valve microstructure and function was used. This study examined the acute in vivo function of a stented tissue-engineered heart valve in a porcine model. Methods Trileaflet valves were fabricated by electrospinning polycarbonate urethane urea using double component fiber deposition. The tissue-engineered heart valve was mounted on an AZ31 magnesium alloy biodegradable stent frame. Five 80-kg Yorkshire pigs underwent open tissue-engineered heart valve implantation on cardiopulmonary bypass in the pulmonary position. Tissue-engineered heart valve function was echocardiographically evaluated immediately postimplant and at planned study end points at 1, 4, 8, and 12 hours. Explanted valves underwent biaxial mechanical testing and scanning electron microscopy for ultrastructural analysis and thrombosis detection. Results All 5 animals underwent successful valve implantation. All were weaned from cardiopulmonary bypass, closed, and recovered until harvest study end point except 1 animal that was found to have congenital tricuspid valve dysplasia and that was euthanized postimplant. All 5 cases revealed postcardiopulmonary bypass normal leaflet function, no regurgitation, and an average peak velocity of 2 m/s, unchanged at end point. All tissue-engineered heart valve leaflets retained microstructural architecture with no platelet activation or thrombosis by scanning electron microscopy. There was microscopic evidence of fibrin deposition on 2 of 5 stent frames, not on the tissue-engineered heart valve. Biaxial stress examination revealed retained postimplant mechanics of tissue-engineered heart valve fibers without functional or ultrastructural degradation. Conclusions A biodegradable elastomeric heart valve scaffold for in situ tissue-engineered leaflet replacement is acutely functional and devoid of leaflet microthrombosis.

Highly proliferative cells depend heavily on glycolysis as a source of energy and biological precursor molecules, and glucose uptake is a useful readout of this aspect of metabolic activity. Glucose uptake is commonly quantified by using flow cytometry for cell cultures and positron emission tomography for organs in vivo. However, methods to detect spatiotemporally resolved glucose uptake in intact tissues are far more limited, particularly those that can quantify changes in uptake over time in specific tissue regions and cell types. Using lymph node metabolism as a case study, we developed an optimized method to detect dynamic and spatially resolved glucose uptake in living tissue by combining ex vivo tissue slice culture with a fluorescent glucose analogue. Live slices of murine lymph node were treated with the glucose analogue 2-[N-(7-nitrobenz-2-oxa-1,3-dia-xol-4-yl)amino]-2-deoxyglucose (2-NBDG). Incubation parameters were optimized to differentiate glucose uptake in activated versus naive lymphocytes. Regional glucose uptake could be imaged at both the tissue level, by widefield microscopy, and at the cellular level, by confocal microscopy. Furthermore, the glucose assay was readily multiplexed with live immunofluorescence labelling to generate maps of 2-NBDG uptake across tissue regions, revealing highest uptake in T cell-dense regions. The signal was predominantly intracellular and localized to lymphocytes rather than stromal cells. Finally, we demonstrated that the assay was repeatable in the same slices, and imaged the dynamic distribution of glucose uptake in response to ex vivo T cell stimulation for the first time. We anticipate that this method will serve as a broadly applicable, user-friendly platform to quantify dynamic metabolic activities in complex tissue microenvironments.

Highly proliferative cells depend heavily on glycolysis as a source of energy and biological precursor molecules, and glucose uptake is a useful readout of this aspect of metabolic activity. Glucose uptake is commonly quantified by using flow cytometry for cell cultures and positron emission tomography for organs in vivo. However, methods to detect spatiotemporally resolved glucose uptake in intact tissues are far more limited, particularly those that can quantify changes in uptake over time in specific tissue regions and cell types. Using lymph node metabolism as a case study, we developed a novel assay of dynamic and spatially resolved glucose uptake in living tissue by combining ex vivo tissue slice culture with a fluorescent glucose analogue. Live slices of murine lymph node were treated with the glucose analogue 2-[N-(7-nitrobenz-2-oxa-1,3-dia-xol-4-yl)amino]-2-deoxyglucose (2-NBDG). Incubation parameters were optimized to differentiate glucose uptake in activated versus naïve lymphocytes. Regional glucose uptake could be imaged at both the tissue level, by widefield microscopy, and at the cellular level, by confocal microscopy. Furthermore, the assay was readily multiplexed with live immunofluorescence labelling to generate maps of 2-NBDG uptake across tissue regions, revealing highest uptake in T cell-dense regions. The signal was predominantly intracellular and localized to lymphocytes rather than stromal cells. Finally, we demonstrated that the assay was repeatable in the same slices, and imaged the dynamic distribution of glucose uptake in response to ex vivo T cell stimulation for the first time. We anticipate that this assay will serve as a broadly applicable, user-friendly platform to quantify dynamic metabolic activities in complex tissue microenvironments.

Background: Recommendations by the Lancet Commission on Global Surgery regarding surgical care in low- and middle-income countries (LMICs) require development to address the needs of children. The Global Initiative for Children’s Surgery (GICS) was founded in 2016 to identify solutions to problems in children’s surgery by utilizing the expertise of practitioners from around the world. This report details this unique process and underlying principles. Methods: Three global meetings convened providers of surgical services for children. Through working group meetings, participants reviewed the status of global children’s surgery to develop priorities and identify necessary resources for implementation. Working groups were formed under LMIC leadership to address specific priorities. By creating networking opportunities, GICS has promoted the development of LMIC-LMIC and HIC-LMIC partnerships. Results: GICS members identified priorities for children’s surgical care within four pillars: infrastructure, service delivery, training and research. Guidelines for provision of care at every healthcare level based on these pillars were created. Seventeen subspecialty, LMIC chaired working groups developed the Optimal Resources for Children’s Surgery (OReCS) document. The guidelines are stratified by subspecialty and level of health care: primary health center, first-, second- and third-level hospitals, and the national children’s hospital. The OReCS document delineates the personnel, equipment, facilities, procedures, training, research and quality improvement components at all levels of care. Conclusion: Worldwide collaboration with leadership by providers from LMICs holds the promise of improving children’s surgical care. GICS will continue to evolve in order to achieve the vision of safe, affordable, timely surgical care for all children.

The blood flow pathway within a device, together with the biomaterial surfaces and status of the patient’s blood, are well-recognized factors in the development of thrombotic deposition and subsequent embolization. Blood flow patterns are of particular concern for devices such as blood pumps (i.e. ventricular assist devices, VADs) where shearing forces can be high, volumes are relatively large, and the flow fields can be complex. However, few studies have examined the effect of geometric irregularities on thrombus formation on clinically relevant opaque materials under flow. The objective of this study was to quantify human platelet deposition onto Ti6Al4V alloys, as well as positive and negative control surfaces, in the region of defined crevices (~50–150 µm in width) that might be encountered in many VADs or other cardiovascular devices. To achieve this, reconstituted fresh human blood with hemoglobin-depleted red blood cells (to achieve optical clarity while maintaining relevant rheology), long working optics, and a custom designed parallel plate flow chamber were employed. The results showed that the least amount of platelet deposition occurred in the largest crevice size examined, which was counterintuitive. The greatest levels of deposition occurred in the 90 µm and 53 µm crevices at the lower wall shear rate. The results suggest that while crevices may be unavoidable in device manufacturing, the crevice size might be tailored, depending on the flow conditions, to reduce the risk of thromboembolic events. Further, these data might be used to improve the accuracy of predictive models of thrombotic deposition in cardiovascular devices to help optimize the blood flow path and reduce device thrombogenicity.

Objectives The present study compared physical, mechanical, and biologic characteristics of 4 clinically available surgical sealants for cardiovascular repair. Methods BioGlue (Cryolife Inc, Kennesaw, Ga), PreveLeak (Mallinckrodt Pharmaceuticals, St Louis, Mo), Tridyne VS (BD, Franklin Lakes, NJ), and Coseal (Baxter Healthcare Corporation, Westlake Village, Calif) were compared for the following properties: hydrated swelling, cytocompatibility, burst strength, biaxial stretching (elasticity), and in vitro degradation. Results Sealants showed a wide range of swelling upon hydration. By gravimetric and volumetric measurement, swelling was greatest for Coseal followed by Tridyne VS, BioGlue, and PreveLeak. Tridyne VS was the most cytocompatible based on Alamar Blue assay results, supporting 85% cell survival compared with 36% to 39% survival with the other sealants. All sealants withstood pressure above mean arterial pressure (70-110 mm Hg) and physiologic systolic blood pressure (90-140 mm Hg) in an ex vivo arterial flow burst model; lowest peak pressure at failure was PreveLeak at 235 ± 48 mm Hg, and highest peak pressure at failure was BioGlue at 596 ± 72 mm Hg. Biaxial tensile testing showed no differences in elasticity between ex vivo porcine aorta and carotid arteries and Tridyne VS or Coseal, and BioGlue and PreveLeak were significantly stiffer. In vitro degradation time for Coseal was 6 days and 21 days for Tridyne VS. No degradation was observed in BioGlue or PreveLeak for 30 days. Conclusions Although all sealants withstood supraphysiologic arterial pressure, there were differences in characteristics that may be important in clinical outcome. Coseal degradation time was short compared with other sealants, whereas BioGlue and PreveLeak showed a significant compliance mismatch with native porcine carotid artery. Tridyne VS was significantly more cytocompatible than the other 3 sealants.

We have previously reported that botulinum neurotoxin type A (BoNT/A)-specific T-cell responses occur in a majority of patients treated with botulinum neurotoxins (BoNT). In this study, we first determined if T-cell responses against BoNT/A and tetanus toxin (TeNT) differ between cervical dystonia (CD) patients and other movement disorder cases. Secondly, we have examined in CD cases the treatment parameters that may have an effect on the T-cell responses against BoNT/A. We found that T-cell responses to BoNT/A were significantly higher in patients with CD than in those with other movement disorders. An increase in TeNT T-cell response in CD was observed when compared to un-treated controls. CD patients who were injected with BoNT/B mounted higher responses to BoNT/A than patients treated with BoNT/A only. Frequent injections (more than 2.1/year) were associated with a significantly higher T-cell response to BoNT/A in CD. T cell responses to BoNT/A did not differ between CD patients who had clinically responsive and non-responsive status at the time of enrollment.

An unanticipated discovery was made while examining genetics of the immune response in patients treated with botulinum neurotoxin (BoNT), which included cervical dystonia (CD) patients. Initial examination of HLA DQA1:DQB1 frequencies revealed an unexpectedly high number of DQA1*0102:DQB1*0604 homozygotes (hz) in the CD patients. We typed the BoNT-treated CD Caucasian subset for HLA-DRB1, DQA1, and DQB1 and succeeded in typing HLA-DRB1, -DQA1, and -DQB1 for 75 of the patients. Two statistical methods found the DQB1 locus associated with CD and one method found a probable association of DQB1*0604. Examination of the allele and haplotype pairing indicated that DQB1*0604 hz comprised most to all of the positive association. Other than this genotype, one other allele, DQB1*0504 contributes to the association of the DQB1 locus. These findings indicate a probable infectious and/or autoimmune component in some CD patients. However, longer distance associations within an extended and conserved DQB1*0604 bearing haplotype leave a possibility that a locus proximal to DQB1 might be involved.

We theorise that in some cases Attention Deficit Hyperactivity Disorder (ADHD) predisposes to narcolepsy and hypersomnia, and that there may be a shared pathophysiology with various addictions [Reward Deficiency Syndrome (RDS)]. Reticence to acknowledge such connections may be due to a narrow nosological framework. Additionally, we theorise that the development of narcolepsy on a baseline of ADHD/RDS leads to an additional assault on the dopaminergic reward system in such individuals. In this study, we propose to test these hypotheses by using a combination of broad genetic screening, and neuroimaging with and without pharmacological intervention, in those with pure ADHD, pure narcolepsy, and the combined ADHD-narcolepsy phenotype. Results of this proposed study may reveal a common pathophysiology of ADHD, narcolepsy and RDS, and perhaps an additional compromise to the reward system in those with combined ADHD-narcolepsy. If the evidence supports the hypothesis that indeed there is a shared pathophysiology for narcolepsy with RDS and thus its subtype ADHD, early intervention/preventative treatment amongst those with ADHD may be beneficial with the putative dopaminergic compound KB220Z™.

Botulinum toxin type A (Dysport) has been shown in European studies to be a safe and effective treatment for cervical dystonia. This multicenter, double-blind, randomized, controlled trial assessed the safety and efficacy of Dysport in cervical dystonia patients in the United States. Eighty patients were randomly assigned to receive one treatment with Dysport (500 units) or placebo. Participants were followed up for 4 to 20 weeks, until they needed further treatment. They were assessed at baseline and weeks 2, 4, 8, 12, 16, and 20 after treatment. Dysport was significantly more efficacious than placebo at weeks 4, 8, and 12 as assessed by the Toronto Western Spasmodic Torticollis Rating Scale (10-point vs. 3.8-point reduction in total score, respectively, at week 4; P < or = 0.013). Of participants in the Dysport group, 38% showed positive treatment response, compared to 16% in the placebo group (95% confidence interval, 0.02-0.41). The median duration of response to Dysport was 18.5 weeks. Side effects were generally similar in the two treatment groups; only blurred vision and weakness occurred significantly more often with Dysport. No participants in the Dysport group converted from negative to positive antibodies after treatment. These results confirm previous reports that Dysport (500 units) is safe, effective, and well-tolerated in patients with cervical dystonia.

Norman Geschwind had a profound effect on behavioral neurology, not only on the basis of his research and theories expressed during his lifetime, but also through the impact that he had on colleagues privileged to train under him or have their work personally influenced by him. My work falls into the latter category. Novel associations between brain function/structure and behavior characterized his professional contributions, and offer a model for those who follow in his footsteps. He correctly predicted that like aphasic disorders, developmental dyslexia might be associated with deficits in color naming expressed currently as deficits in Rapid Automatized Naming. He stimulated anatomic research regarding patterns of asymmetry and microscopic architecture leading to the establishment of the Orton Dyslexia Neuropathology Laboratory at Beth Israel Hospital, Boston. He predicted an association between autoimmune disorders and reading disorders, an association that proved to be of genetic origin. He further predicted that reading disorders, like language disorders, would be cross-cultural and, similarly, their mechanism of production would be cross-cultural, although affected perhaps by the structure of the language to be learned. His suspicion that the clinical impression of male gender preponderance in dyslexia was accurate and carried biologic significance has recently been reconfirmed by colleagues at the Mayo Clinic in Rochester, Minnesota. Finally, with respect to dyslexia, one should not be surprised that since affect is influenced by brain architecture, developmental disorders characterized by altered brain architecture might be associated with affective or other psychiatric phenomena. My own work suggests that the altered neuroanatomy in dyslexia may be accompanied by altered clinical neurophysiology, offering the possibility that in some developmental disorders, behaviors, including academic aptitude and cognitive function, might benefit from medications designed originally to lower the risk of clinical seizures. Perhaps Geschwind’s greatest lesson is to not assume that all we have been taught as dogma is truth. Rather, we must have a willingness to make clear perceptions and draw conclusions that come closer to the reality of the causal relationship between brain and behavior.

Immunoresistance (Ab+) to botulinum toxin type A (BTX-A) has been a serious concern since the introduction of BTX-A in the treatment of dystonia and other disorders associated with abnormal muscle contractions. We studied seven patients who developed Ab+ and later reverted to antibody-negative (Ab-) status. These seven patients, six women (mean age, 56 years; range, 41-80 years), with an average duration of dystonia for all patients of 197 months (range, 84-360 months), received a total mean cumulative dose of 1659 units (U) (range, 810-1975 U), with an average dose of 207 U per visit. All of these patients became unresponsive to BTX-A treatment and became Ab+ as determined by mouse bioassay. Their response to BTX-A after they reverted to Ab- was analyzed. The average latency between the initial BTX-A treatment and development of Ab+ was 27 months (range, 1543 months). The average duration between the detection of Ab+ status and subsequent reversal to Ab- status was 30 months (range, 10-78 months). Six of these Ab- patients were reinjected with BTX-A, and all six benefited from repeat injections comparable with their earlier response. Three patients lost their clinical response to subsequent injections and were found to be again Ab+. Two of the five patients who became immunoresistant to BTX-A received botulinum toxin type F (BTX-F) injections and one patient received a single session of BTX-B with improvement in their symptoms. In conclusion, this unique group of patients who were Ab+ and became Ab- responded favorably to repeat BTX-A injections, but some lost the benefit with subsequent injections. These observations suggest that the anamnestic immunologic response to BTX-A can wane, but can be reactivated by repeat BTX-A treatments. The presence of antibodies did not interfere with the response to BTX-F or BTX-B injections, thus confirming the antigenic specificity of various BTX serotypes.

We enrolled and treated 122 patients with idiopathic cervical dystonia in a double-blind, placebo-controlled safety and efficacy study of botulinum toxin type B (BotB). Both A-responsive and A-resistant patients were enrolled. Patients received intramuscular injections of either BotB (2,500 U, 5,000 U, or 10,000 U) or placebo. The primary outcome measure of efficacy was the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS)-Total score at 4 weeks following study drug administration. Secondary measures of efficacy were TWSTRS-Severity, -Disability, and -Pain subscale scores, and Analog Pain Assessment, Investigator Global Assessment, Patient Global Assessment, and Sickness Impact Profile scores. Duration of effect was estimated with an intent-to-treat analysis of responders. Safety measures included clinical parameters, laboratory tests, and adverse events. The primary and most of the secondary analyses indicated a statistically significant treatment effect and a dose response. BotB is safe, well tolerated, and efficacious in the treatment of cervical dystonia at the doses tested.

Organic disorders, which secondarily affect learning, can be identified through careful history, physical examination, and laboratory investigation. Support for those developmental disorders of the nervous system called learning disabilities can be obtained through detailed family and personal developmental history, quantitative neurologic examination, and diagnostic studies. Social, emotional problems commonly complicate both groups of disorders but may be directly induced by anomalous brain development. An approach to distinguishing these differential mechanisms from primary psychiatric disorders is given.

The natural history of cervical dystonia (spasmodic torticollis) was investigated in a population-based study in Rochester, Minnesota. Eleven new cases were identified with onset during the 20-year period 1960–1979. The overall incidence rate was 1.2 per 100,000 person-years (95% confidence interval 0.5–1.9) with a female: male ratio of age-adjusted incidence rates of 3.6:1. A unitary etiology was not apparent: injury antedated onset in four of the 11 patients, whereas six had documented thyroid disease and four had diabetes. A family history of movement disorder was recorded for only one subject. Only one of the cases would have been classified as moderate in severity; the others were mild. In follow-up through 1993, progressive disability was noted in only two patients, and two others went into remission. Three cases of intracranial aneurysm were confirmed, two of which produced fatal subarachnoid hemorrhage. A third death was due to amyotrophic lateral sclerosis.

A short cut review was carried out to establish whether heat application was a comparable alternative to traditional painkillers in women with dysmenorrheal pain. Two randomized trials were directly relevant to the question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these papers are tabulated. The clinical bottom line was that heat application was an alternative to NSAIDs.

To the Editor: We read the article by Zuber et al, [1] dealing with the incidence of antibody formation after repetitive injections of botulinum toxin, with interest and concern. The article correctly points out that with repetitive injections there is a definitive incidence of sensitization that may render continued therapy with that immunotype ineffective. Recently, Hathaway and Dang [2] and Statkowski et al [3] reported significant numbers of cases in which sensitization had occurred. Hathaway …

Analysis of face pain is predicated on knowledge of the structures of the face, head, and neck that may generate this sensation. Of particular importance in this process are historical data; characteristics of the pain, as elicited in history taking, should lead to the definition of recognized syndromes that may threaten a patient's survival or function and for which appropriate intervention may bring relief. Among these syndromes are trigeminal neuralgia and neuropathy, cluster headache, cranial arteritis, nasopharyngeal carcinoma, and psychogenic face pain.

And a second point to be emphasized is that such underachievement, when encountered in written language, is often the result of an innate biologic predisposition in language learning of the individual. If the first point is not appreciated, any discussion of definition will be merely academic and have no impact on the practical world of delivery of educa tional services. If such appreciation is achieved, however, the second point, regarding the innate biologic predisposition to this disability, assumes its proper importance in determining the specific remedial methods that should be employed and in deciding to whom such services should be offered.

This paper represents a condensation of a 2-hour oral presentation that made extensive use of visual aids in color, many of which could not be reproduced. Several of the areas that received more elaboration in the oral presentation have been shortened in the interest of space.

Depression appears to be common in patients with tardive dyskinesia (TD), and we hypothesized that this refractory movement disorder might respond to antidepressant treatment. We treated 19 TD patients with tricyclic antidepressant therapy supplemented within two to three weeks with lithium carbonate. All patients fulfilled the Research Diagnostic Criteria for major depressive disorder, although seven of them denied being dys phoric. The Abnormal Involuntary Movement Scale and the Hamilton Rating Scale were used to measure dyskinesia and de pression, respectively. Of the 19 patients, 11 (58%) experienced moderate or marked improvement in both dyskinesia and de pression. The authors conclude that treatment with a tricyclic antidepressant and lithium may alleviate tardive dyskinesia in patients with depressive symptoms.

Thirteen patients with moderately severe myasthenia gravis participated in a double-blind study using either 100 mg of prednisone or an equivalen numbder of placebo tablets on alternate days. Anticholinesterase therapy was continued on a demand basis. At the end of 6 months the code was broken. Seven patients were on placebo and three of these had improved to such a degree that steroid therapy was not indicated. Four of these patients ultimately were started on prednisone and improved. Of the six patients on prednisone, three showed no improvement and three were improved. At the end of 2 years, the seven patients still taking prednisone were on maintenance dosage of this drug. Three of this group had experienced relapses when the dosage was cut to 15 to 25 mg on alternate days, and they again improved when the prednisone dosage was increased. No statistical evaluation is possible because of the small number of patients. It can be stated that seven patients improved with steroid therapy. Conversely, not all patients treated with alternate-day prednisone improved. Finally, any evaluation of treatment of myasthenia gravis must take into consideration the potential for spontaneous improvement, as demonstrated by three of the patients treated with placebo.

An anatomic pattern of (1) temporal lobe symmetry and (2) left more than right frontosylvian cortical anomalies has been documented in a small number of children with developmental disorders of reading. These alterations occur during embryogenesis and are the direct result of neither genetic factors nor perinatal stress. Underperformance in reading, writing, and other linguistic skills as well as visuo-spatial excellence may result from these changes. Related brain mechanisms may influence disorders affecting attention, arithmetic, and nonverbal learning. The suspected association between depressed mood and certain learning disorders raises the possibility of joint cause. Future work in learning disorders must define affective state precisely, specifically characterize learning disorder, and wisely apply technology to reveal anatomic, physiological, and metabolic correlates.

The logotype of the Mayo institution depicts three shields representing clinical service, research, and education. An approach to current trends and issues in medicine related to educational underachievement (referred to in the United States as “specific learning disabilities”) can be organized into these same three categories of service, research, and education. These concerns are appropriate not only in medicine but also in the fields related to the diverse behaviors underlying unexpected school failure. Physicians have made and will continue to make important contributions to the recognition of academic underachievement and particularly to clarification of the relationship of underachievement to biologic determinants. The views that follow are in part influenced by my experiences and those of my colleagues at the Mayo Clinic involved in the Learning Disabilities Assessment Program.

In previous reports,l.2 a relationship between suscepti­ bility to tardive dyskinesia (TO) and the presence of major affective disorders was described. In another study. Rosenbaum and associates 3 found that these patients also had the endocrinologic abnormalities usually associated with primary affective disorders. Rosenbaum and associates4 have reported that use of a tricyclic antidepressant agent plus lithium is effica­ cious in therapy of depressed patients with tardive dyskinesia with or without dysphoria. An account of this treatment in 19 such patients appears elsewhere in this issue of Psychosomatics. The following is a brief case history ofa patient who was treated for depression and dyskinesia with electroconvulsive therapy and maintained on amitriptyline and lithium therapy. C8MNPOI1 A 74-year-old married woman dated the onset of her de­ pressive illness and TO to the appearance of severe pain in her low back region four years previously. Muscle relaxant medication was administered at that time, and one morning after this treatment had been started she awakened with the involuntary movements of the face, trunk, arms. and legs she currently exhibited. Gradually a pa«ern of 1i«le sleep.

Elevated amounts of antibodies specific for acetylcholine receptors were detected in 87 percent of sera from 71 patients with myasthenia gravis but not in 175 sera from individuals without myasthenia gravis, including those with other neurologic or autoimmune disease. Antireceptor antibodies were not directed at the acetylcholine binding site of the receptor. Presence or titer of antibody did not appear to correlate with age, sex, steroid therapy, or duration of symptoms. Myasthenia gravis patients with only ocular symptoms had lower antibody titers, while the majority of titers in myasthenia gravis patients with thymoma exceeded the median titer of the myasthenia gravis group as a whole. Assay of antireceptor antibody should prove a useful test in the diagnosis of myasthenia gravis.