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PubMed1997

[Nicotine and worsening myasthenia].

We report a case of myasthenia gravis worsened by a nicotine transdermal system, in a man who usually was smoking fourty cigarettes per day without any worsening of his symptomatology. He noted an increased bilateral ptosis, total ophtalmoplegia, difficulty in chewing and generalized weakness two hours after application of a nicotine transdermal system, the symptoms improving after he removed it. Cholinergic receptors involved in myasthenia gravis are nicotinergic, and their number at the neuromuscular junction is reduced in myasthenia gravis. That leads to a "functional overdosage" after application of the nicotine transdermal system similar to the cholinergic crisis. This case can be compared with myasthenia syndromes described during the Second World War in tobacco chewers without any muscle impairment.

Administration, Cutaneous↗

PubMedDate not supplied

Drug-induced neuromuscular blockade and myasthenia gravis.

Myasthenia gravis is an uncommon disorder of the neuromuscular junction resulting in weakness of all striated voluntary muscles. Therapeutic advances have increased patients' age and survival. Older patients with myasthenia gravis may have additional medication needs. Numerous drugs have experimental and clinical evidence of neuromuscular blockade. A MEDLINE search of the English literature from 1966 to the present pertinent to drug-induced myasthenia gravis was performed. Additional literature was obtained from reference citations of relevant articles. Drugs with several reports of neuromuscular blockade were assessed for causality by a recognized probability scale. Prednisone was most commonly implicated as aggravating myasthenia gravis, and D-penicillamine was most commonly associated with myasthenic syndrome. The greatest frequency of drug-induced neuromuscular blockade was seen with aminoglycoside-induced postoperative respiratory depression. However, drugs most likely to impact myasthenic patients negatively are those used in the treatment of the disease. These include overuse of anticholinesterase drugs, high-dose prednisone, and anesthesia and neuromuscular blockers for thymectomy.

Drug-Related Side Effects and Adverse Reactions↗

PubMed2002

Thymectomy for Myasthenia Gravis.

No Class I studies of the effectiveness of thymectomy for myasthenia gravis (MG) have been performed. Most Class II studies comparing outcomes in MG patients with and without thymectomy demonstrated higher MG remission and improvement rates in patients undergoing thymectomy. However, these Class II studies were also consistently confounded by important differences between MG patients in surgical and nonsurgical groups. Myasthenia gravis patients undergoing thymectomy were younger, more often women and were more likely to have severe myasthenia. The authors of this paper cannot determine from these Class II studies whether the observed association between thymectomy and improved MG outcomes was a result of a thymectomy benefit or was merely a result of the multiple differences in baseline characteristics between the surgical and nonsurgical groups. The authors concluded that the benefit of thymectomy in non-thymomatous autoimmune MG has not been conclusively established. Thus, for patients with non-thymomatous autoimmune myasthenia gravis, thymectomy should only be considered an option to increase the probability of remission or improvement. The quality standards subcommittee of the American Academy of Neurology recently adopted this position.

Journal Article↗

PubMed2006

[Myasthenia gravis and pregnancy: clinical course and management of delivery and the postpartum phase].

OBJECTIVES: To study influences of pregnancy on the time-course of myasthenia gravis (MG) and of MG on pregnancy, delivery, postpartum and newborn. METHODS: We retrospectively collected data from 100 women affected with MG, hospitalized between 1994 and 2003 in departments of Neurology of Lille University Hospital. RESULTS: Eighteen patients had a total of 36 pregnancies, occurring 7.2 years on average after MG onset. MG exacerbation occurred in 7 patients (26 percent) during pregnancy and in 4 (14.8 percent) during postpartum. One patient died of acute respiratory failure during postpartum. Delay between the onset of MG and pregnancy was the only variable significantly associated with MG exacerbation: 5.8 years when exacerbation and 9.5 years when no exacerbation (p=0.03). Seven miscarriages, two therapeutic abortions and no death at birth were reported. Levels of anti-acetylcholine receptor antibodies were abnormal in 3 of 27 newborns (11 percent), but only one (3.7 percent) developed seronegative transient neonatal myasthenia gravis. DISCUSSION: During pregnancy, the clinical course of MG is variable but exacerbations were associated with a shorter delay between MG diagnosis and pregnancy. The risk of transient neonatal myasthenia gravis is relatively small but exists even when the parturient has stable MG without elevated levels of anti-acetylcholine receptor antibodies. CONCLUSION: Our study confirms pregnancy is more difficult to manage at the beginning of MG. Given the unpredictable course of MG during pregnancy, we recommend women affected with MG to begin a pregnancy when the disease is stable.

Abortion, Therapeutic↗

PubMed2005

Overexpression of IFN-induced protein 10 and its receptor CXCR3 in myasthenia gravis.

Myasthenia gravis (MG) and its animal model, experimental autoimmune MG (EAMG), are autoimmune disorders in which the acetylcholine receptor (AChR) is the major autoantigen. Microarray technology was used to identify new potential drug targets for treatment of myasthenia that would reduce the need for the currently used nonspecific immunosuppression. The chemokine IFN-gamma-inducible protein 10 (IP-10; CXCL10), a CXC chemokine, and its receptor, CXCR3, were found to be overexpressed in lymph node cells of EAMG rats. Quantitative real-time PCR confirmed these findings and revealed up-regulated mRNA levels of another chemoattractant that activates CXCR3, monokine induced by IFN-gamma (Mig; CXCL9). TNF-alpha and IL-1beta, which act synergistically with IFN-gamma to induce IP-10, were also up-regulated. These up-regulations were observed in immune response effector cells, namely, lymph node cells, and in the target organ of the autoimmune attack, the muscle of myasthenic rats, and were significantly reduced after suppression of EAMG by mucosal tolerance induction with an AChR fragment. The relevance of IP-10/CXCR3 signaling in myasthenia was validated by similar observations in MG patients. A significant increase in IP-10 and CXCR3 mRNA levels in both thymus and muscle was observed in myasthenic patients compared with age-matched controls. CXCR3 expression in PBMC of MG patients was markedly increased in CD4(+), but not in CD8(+), T cells or in CD19(+) B cells. Our results demonstrate a positive association of IP-10/CXCR3 signaling with the pathogenesis of EAMG in rats as well as in human MG patients.

Adolescent↗

PubMed1965

MYASTHENIA GRAVIS: ANESTHETIC AND SURGICAL MANAGEMENT OF THE PATIENT UNDERGOING THYMECTOMY.

Experience in the anesthetic and surgical management of 25 patients with myasthenia gravis is recorded. These are subdivided into two groups: those operated on during the period 1950-1958 and those operated on during the period 1959-1964. The purpose of this paper is to indicate improvement in mortality and morbidity due to three major advances: (1) use of the decamethonium diagnostic test in a myasthenia gravis clinic; (2) improvements in assessment and management of respiratory insufficiency; and (3) avoidance of anticholinesterase treatment in the immediate and early postoperative recovery period.Fourteen patients with myasthenia gravis, including five with thymoma and two who were refractory to medication, were in the second (1959-1964) group. There were no deaths and no myasthenic or cholinergic crises. Three prophylactic tracheostomies were performed. No emergency bronchoscopies or tracheostomies were required.

Anesthesia↗

PubMed2003

[Severe neonatal myasthenia with arthrogryposis].

Maternal myasthenia gravis has been associated with the presence of neonatal myasthania and sometimes fetal congenital anomalies. The purpose of this paper is to present an infant with multiple deformations born to a mother with myasthenia gravis. The infant presented with arthrogryposis multiplex and pulmonary hypoplasia. The new born died within the first day of life. Twenty-seven other cases of neonatal myasthenia with arthrogryposis have been reported. Twenty-two of them were stillborn or died. The surviving children needed ventilatory assistance for a long period.

Adult↗

PubMed2005

[Myasthenia gravis and pregnancy].

We retrospectively analyzed the course and outcome of pregnancy in a group of 26 women with myasthenia gravis. Premature births were noted in 7.9% of pregnancies, the rate of cesarean section was 15.8%. Neonatal myasthenia was observed in 10 children born by 5 women (16% of the mothers). There were three neonatal deaths: two due to neonatal myasthenia, one in a child born with multiple congenital anomalies. Transient exacerbation of MG symptoms was observed during four pregnancies (10.5%). MG is not associated with increased risk for MG patient and the newborn. Giving birth to one child with transient MG increases the risk of transient MG in consecutive pregnancies.

Adult↗

PubMed1975

Corticosteroid-induced mediastinal widening in myasthenia gravis.

Corticosteroid-induced mediastinal widening with simulated focal lymphadenopathy was found in a patient having myasthenia gravis. To my knowledge, this is the first report of such changes occurring in a patient having myasthenia gravis. As the use of corticosteroids in the treatment of myasthenia gravis becomes more common, this association can be expected to occur more often. Reemphasis of this phenomenon should help to avoid unnecessary surgical intervention in these patients.

Humans↗

PubMed1984

Myasthenia gravis in monozygotic twins. Clinical follow-up nine years after thymectomy.

Genetically proved monozygotic female twins in whom myasthenia gravis developed in their 20s initially had their disease well controlled with anticholinesterase medication. Because of increasing resistance to medication, twin 1 had her thymus removed, after which the symptoms decreased. Predicated on the improvement in her sister and the need for increasing medication to allay symptoms, and after proof of monozygosity, twin 2 also underwent thymectomy, with subsequent symptomatic improvement. The twins were followed up nine and six years after thymectomy, respectively. Monozygotic twins with myasthenia gravis are generally young women, with onset of disease in one occurring within one to three years of the other. Reports of only one affected twin may be misleading because of inadequate documentation of monozygosity, absence of long-term observation, or both. Serial investigations of the "uninvolved" twin in a monozygous pair and proof of monozygosity should be obtained to aid in early diagnosis and treatment of this illness, as well as to study the pathogenesis of myasthenia gravis prior to symptom onset.

Adult↗

PubMed1993

Coping with myasthenia gravis and implications for psychotherapy.

The aim of this study was to investigate psychosocial influences and mechanisms of coping to establish indications for psychotherapy in patients with myasthenia gravis. We investigated clinical symptoms, personality, psychopathology, and coping in 44 patients with myasthenia gravis. The patients' personalities were not characteristically altered, and in 29.5% (13/44) of them, preexistent, long-term psychiatric disturbances (according to International Classification of Diseases criteria) were present, which corresponds to the prevalence in the average population. In general, coping was characterized by an attitude of calmness and acceptance, which is attributable to effective medical treatment and could be considered an unspecific mode of coping with chronic diseases of moderate severity. Four women had undergone psychotherapy because of neurotic symptoms that were unrelated to myasthenia gravis. At the end of psychotherapy, their myasthenic symptoms had greatly improved or disappeared. Psychotherapeutic techniques may be helpful in patients with neurotic or reactive psychiatric symptoms, but there is no general implication for psychotherapy in myasthenic patients, especially if there is adequate "somatic" therapy.

Adaptation, Psychological↗

PubMed1979

Orbicularis fatigue: the 'peek' sign of myasthenia gravis.

Three patients with myasthenia gravis demonstrated a distinctive sign of orbicularis fatigue. After momentary opposition on gentle sustained lid closure, the lid margins separated, resulting in widening of the palpebral fissure and scleral exposure. The patient thus appeared to "peek" at the examiner. The "peek" sign was not observed in 200 control patients and in 49 of 50 patients with facial weakness secondary to a spectrum of neuromuscular disorders. Three of 25 patients with myasthenia gravis displayed this sign, and in one patient it was the major diagnostic finding. The presence of the "peek" sign suggests the diagnosis of myasthenia gravis.

Adult↗

PubMed1976

Audiotympanometric findings in myasthenia gravis.

Myasthenia gravis can be a difficult diagnostic and therapeutic problem. Our study on six patients consisted of pure-tone audiograms, tympanometry, and acoustic reflex tests. Positive findings in the myasthenia gravis patients prior to medication included hyperacusis and increase in the intensity of sound required to elicit an acoustic reflex. Following medication, the hyperacusis lessened and the intensity of sound required to elicit the acoustic reflex decreased. During follow-up of two of the patients we encountered cholinergic (overdosage) crisis in one patient and myasthenic (underdosage) crisis in the other patient. Muscle weakness can be a common factor in both conditions. The acoustic reflex test can differentiate between the two types of crises. We believe audiotympanometric tests can aid in diagnosis and treatment of myasthenia gravis patients.

Acoustic Stimulation↗

PubMed1991

The association of pauciarticular juvenile arthritis and myasthenia gravis.

We encountered two children with fluorescent antinuclear antibody-positive pauciarticular juvenile arthritis who later developed myasthenia gravis. Acetylcholine receptor binding, blocking, and modulating antibodies, retrospectively tested on frozen serum, yielded negative results before the onset of myasthenic symptoms but all yielded strongly positive results coincident with the onset of weakness. In both children, myasthenia gravis responded to thymectomy, and one child had a beneficial response to plasmapheresis. Although, to our knowledge, only two patients with juvenile arthritis and myasthenia gravis have been described in the past, the presence of two additional children with both diseases in a single clinic population suggests that the association may be more prevalent than previously suspected.

Adolescent↗

PubMed1997

Remission of myasthenia gravis caused by proteinuria in nephrotic syndrome.

Myasthenia gravis is caused by antibodies against acetylcholine receptors and is treated with inhibition or elimination of antibody production. We report a 43-year-old myasthenic female who was symptomatic until she developed proteinuria from nephrotic syndrome, which caused a marked drop in acetylcholine receptor antibody titer with remission of myasthenia. Treatment of the nephrotic syndrome produced exacerbation of her myasthenia and a rise in antibody level. This patient's improvement is the result of antibody elimination during proteinuria in nephrotic syndrome.

Adult↗

PubMed2000

Immunoglobulin treatment in refractory Myasthenia gravis.

Failure to induce and maintain remission in severe exacerbations of myasthenia gravis (MG), despite optimal care, is a common problem. We evaluated the efficacy and safety of high-dose intravenous immunoglobulin (IVIg) therapy in an open-label study of 10 patients with severe generalized myasthenia and an acute deterioration unresponsive to conventional therapy including high-dose corticosteroids, cyclosporine, and azathioprine. Intravenous Ig at a loading dose of 400 mg/kg was administered daily for 5 consecutive days, with maintenance IVIg treatment at a dose of 400 mg/kg, once every 6 weeks. Significant improvement occurred in all patients, beginning at 6 +/- 2 days of treatment as measured by the Osserman scale, fatigue variables, muscle strength, and respiratory function tests. No side effects were observed during induction of remission. Further IVIg treatments were highly efficacious in maintaining the remission. The severity of the disease decreased by 2.5 +/- 0.8 grades of the Osserman scale over a period of 1 year (P <0.001), in parallel with reduction of immunosuppressive therapy as well as a decrease in acetylcholine receptor antibody titers (P < 0.01). Intravenous Ig therapy seems to be highly potent for inducing rapid improvement in refractory myasthenia during acute deterioration as well as for maintaining remission.

Adult↗

PubMed1998

Modulation of the anti-acetylcholine receptor response and experimental autoimmune myasthenia gravis by recombinant fragments of the acetylcholine receptor.

Myasthenia gravis (MG) is a neuromuscular disorder of man caused by a humoral response to the acetylcholine receptor (AChR). Most of the antibodies in MG and in experimental autoimmune myasthenia gravis (EAMG) are directed to the extracellular portion of the AChR alpha subunit, and within it, primarily to the main immunogenic region (MIR). We have cloned and expressed recombinant fragments, corresponding to the entire extracellular domain of the AChR alpha subunit (H alpha1-210), and to portions of it that encompass either the MIR (H alpha1-121) or the ligand binding site of AChR (H alpha122-210), and studied their ability to interfere with the immunopathological anti-AChR response in vitro and in vivo. All fragments were expressed as fusion proteins with glutathione S-transferase. Fragments H alpha1-121 and H alpha1-210 protected AChR in TE671 cells against accelerated degradation induced by the anti-MIR monoclonal antibody (mAb)198 in a dose-dependent manner. Moreover, these fragments had a similar effect on the antigenic modulation of AChR by other anti-MIR mAb and by polyclonal rat anti-AChR antibodies. Fragments H alpha1-121 and H alpha1-210 were also able to modulate in vivo muscle AChR loss and development of clinical symptoms of EAMG, passively transferred to rats by mAb 198. Fragment H alpha122-210 did not have such a protective activity. Our results suggest that the appropriate recombinant fragments of the human AChR may be employed in the future for antigen-specific therapy of myasthenia.

Adoptive Transfer↗

PubMed1999

Normal human immunoglobulin suppresses experimental myasthenia gravis in SCID mice.

Serum IgM has been shown to participate in the control of IgG autoreactivity in healthy subjects. We have recently shown that an immunoglobulin preparation of pooled normal human IgM (IVIgM) contains anti-idiotypic antibodies against disease-associated IgG autoantibodies in autoimmune patients and protects rats from experimental autoimmunity. The aim of the present study was to asses the in vitro and in vivo immunomodulatory effects of IVIgM in comparison with IgG, in SCID mice reconstituted with thymic cells from a myasthenia gravis patient. Non-leaky SCID mice were injected i.p. with 60 x 10(6) thymic cells from a patient with myasthenia gravis and 1 day later boosted with 10(6) irradiated acetylcholine receptor (AchR)-expressing TE671 cells. On days 14, 21 and 28, mice were treated with IVIgM or with equimolar amounts of human serum albumin. The level of anti-AchR antibodies in the sera of three out of four IgM-treated animals was less than 1 nM. Further, there was a significant decrease in the loss of endplate AchR on the diaphragms of IgM-treated SCID mice. These findings indicate that pooled normal IgM exerts an immunoregulatory role in experimental myasthenia gravis, and suggests that IgM may be considered as an alternative approach in the therapy of autommune diseases.

Animals↗