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Find video protocols related to scientific articles indexed in Pubmed.
Clinical and serologic parallels to APS-I in patients with thymomas and autoantigen transcripts in their tumors.
J. Immunol.
PUBLISHED: 09-17-2014
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Patients with the autoimmune polyendocrine syndrome type I (APS-I), caused by mutations in the autoimmune regulator (AIRE) gene, and myasthenia gravis (MG) with thymoma, show intriguing but unexplained parallels. They include uncommon manifestations like autoimmune adrenal insufficiency (AI), hypoparathyroidism, and chronic mucocutaneous candidiasis plus autoantibodies neutralizing IL-17, IL-22, and type I IFNs. Thymopoiesis in the absence of AIRE is implicated in both syndromes. To test whether these parallels extend further, we screened 247 patients with MG, thymoma, or both for clinical features and organ-specific autoantibodies characteristic of APS-I patients, and we assayed 26 thymoma samples for transcripts for AIRE and 16 peripheral tissue-specific autoantigens (TSAgs) by quantitative PCR. We found APS-I-typical autoantibodies and clinical manifestations, including chronic mucocutaneous candidiasis, AI, and asplenia, respectively, in 49 of 121 (40%) and 10 of 121 (8%) thymoma patients, but clinical features seldom occurred together with the corresponding autoantibodies. Both were rare in other MG subgroups (n = 126). In 38 patients with APS-I, by contrast, we observed neither autoantibodies against muscle Ags nor any neuromuscular disorders. Whereas relative transcript levels for AIRE and 7 of 16 TSAgs showed the expected underexpression in thymomas, levels were increased for four of the five TSAgs most frequently targeted by these patients' autoantibodies. Therefore, the clinical and serologic parallels to APS-I in patients with thymomas are not explained purely by deficient TSAg transcription in these aberrant AIRE-deficient tumors. We therefore propose additional explanations for the unusual autoimmune biases they provoke. Thymoma patients should be monitored for potentially life-threatening APS-I manifestations such as AI and hypoparathyroidism.
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Fetal growth restriction and birth defects with newer and older antiepileptic drugs during pregnancy.
J. Neurol.
PUBLISHED: 01-22-2014
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The primary aim of this study was to assess the risks of fetal growth restriction and birth defects in children exposed prenatally to newer and older antiepileptic drugs, using an unselected epilepsy cohort. Deliveries recorded in the compulsory Medical Birth Registry of Norway 1999-2011 formed the study population. All 2,600 children exposed to antiepileptic drugs during pregnancy were compared to all 771,412 unexposed children born to women without epilepsy. Children of untreated mothers with epilepsy served as an internal control group. The main outcomes were small for gestational age birth weight and head circumference, and major congenital malformations. Children exposed to antiepileptic drugs had a moderate risk of growth restriction. Infants exposed to topiramate had a considerable risk of microcephaly (11.4 vs. 2.4 %; OR 4.8; CI 2.5-9.3) and small for gestational age birth weight (24.4 vs. 8.9 %; OR 3.1; 95 % CI 1.9-5.3). Carbamazepine, lamotrigine, levetiracetam, oxcarbazepine, gabapentin, and pregabalin had low malformation rates, whereas topiramate tended to have an elevated malformation rate. Valproate monotherapy was associated with a significant risk of birth defects (6.3 vs. 2.9 %; OR 2.5; CI 1.6-3.8), and specifically with septal heart defects and hypospadias. For mothers using valproate, the presence of major birth defect in one child was associated with a markedly increased risk for the siblings (42.9 vs. 6.7 %; OR 10.4; CI 2.3-46.7). Children of untreated mothers with epilepsy had malformation risk similar to the reference group. In conclusion, topiramate was associated with a substantial risk of fetal growth restriction, and possibly an increased malformation rate. Other newer-generation antiepileptic drugs had a low malformation rate. Valproate monotherapy had a significant malformation risk, especially in repeated pregnancies.
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Early child development and exposure to antiepileptic drugs prenatally and through breastfeeding: a prospective cohort study on children of women with epilepsy.
JAMA Neurol
PUBLISHED: 09-25-2013
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Exposure to antiepileptic drugs during pregnancy is associated with adverse effects on psychomotor development.
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Psychiatric comorbidity and social aspects in pregnant women with epilepsy - the Norwegian Mother and Child Cohort Study.
Epilepsy Behav
PUBLISHED: 08-13-2013
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The objective of this study was to investigate psychiatric disease and social aspects in young women with epilepsy before and during pregnancy.
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Exposure to antiepileptic drugs in utero and child development: a prospective population-based study.
Epilepsia
PUBLISHED: 04-23-2013
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Antiepileptic drugs may cause congenital malformations. Less is known about the effect on development in infancy and childhood. The aim of this study was to examine whether exposure to antiepileptic drugs during pregnancy has an effect on early child development.
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Anti-voltage-gated potassium channel Kv1.4 antibodies in myasthenia gravis.
J. Neurol.
PUBLISHED: 11-02-2011
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Myasthenia gravis (MG) is an autoimmune disease characterized by skeletal muscle weakness mainly caused by acetylcholine receptor antibodies. MG can be divided into generalized and ocular, and into early-onset (<50 years of age) and late-onset (?50 years of age). Anti-Kv1.4 antibodies targeting ?-subunits (Kv1.4) of the voltage-gated potassium K(+) channel occurs frequently among patients with severe MG, accounting for 18% of a Japanese MG population. The aim of this study was to characterize the clinical features and serological associations of anti-Kv1.4 antibodies in a Caucasian MG population with mild and localized MG. Serum samples from 129 Caucasian MG patients with mainly ocular symptoms were tested for the presence of anti-Kv1.4 antibodies and compared to clinical and serological parameters. There were 22 (17%) anti-Kv1.4 antibody-positive patients, most of them women with late-onset MG, and all of them with mild MG. This contrasts to the Japanese anti-Kv1.4 antibody-positive patients who suffered from severe MG with bulbar symptoms, myasthenic crisis, thymoma, myocarditis and prolonged QT time on electrocardiography, despite equal anti-Kv1.4 antibody occurrence in both populations. No other clinical or serological parameters influenced anti-Kv1.4 antibody occurrence.
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Investigation for RAPSN and DOK-7 mutations in a cohort of seronegative myasthenia gravis patients.
Muscle Nerve
PUBLISHED: 09-14-2011
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Myasthenia gravis (MG) is an autoimmune disease. Patients without detectable antibodies against the nicotinic acetylcholine receptor or the muscle-specific tyrosine kinase are referred to as seronegative MG (SNMG). Because late-onset congenital myasthenic syndromes (CMSs) due to RAPSN or DOK7 mutations may be mistaken for SNMG, we investigated their frequency in a nationwide SNMG cohort.
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Arthrogryposis multiplexa congenita: an epidemiologic study of nearly 9 million births in 24 EUROCAT registers.
Eur. J. Obstet. Gynecol. Reprod. Biol.
PUBLISHED: 07-13-2011
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To examine the occurrence of arthrogryposis multiplex congenita (AMC) in Europe and to identify possible risk factors.
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Lambert-eaton myasthenic syndrome; pathogenesis, diagnosis, and therapy.
Autoimmune Dis
PUBLISHED: 05-26-2011
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Lambert-Eaton Myasthenic Syndrome (LEMS) is a rare disease with a well-characterized pathogenesis. In 50% of the patients, LEMS is a paraneoplastic manifestation and caused by a small cell lung carcinoma (SCLC). Both LEMS patients with SCLC and those without this tumour have in 85% of cases pathogenetic antibodies of very high LEMS specificity against voltage-gated calcium channels (VGCCs) in the cell membrane of the presynaptic motor nerve terminal. Better understanding of LEMS pathogenesis has lead to targeted symptomatic therapy aimed at the neuromuscular junction and to semispecific immuno-suppression. For SCLC LEMS, tumour therapy is essential.
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Radioligand-binding assay reveals distinct autoantibody preferences for type I interferons in APS I and myasthenia gravis subgroups.
J. Clin. Immunol.
PUBLISHED: 05-24-2011
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Patients with autoimmune polyendocrine syndrome type I (APS I) or acquired thymoma-associated myasthenia gravis (MG) surprisingly share several common features, including defective expression of the transcription factor AIRE and autoantibodies against type I interferons. Here, we have adapted and validated the radioligand-binding assay we recently developed against (35)S-Met-interferon-?, for rapid and specific screening for autoantibodies against interferons-?2 and -?8. We then investigated their potential for diagnosis and for predicting clinical manifestations in patients with APS I and different subgroups of MG. Autoantibodies against interferons-?, -?2, and -?8 occurred more often in patients with APS I (100%) and MG with thymoma (73%) than in late-onset MG (39%) and early-onset MG (5%). These autoantibodies showed preferences for interferon-? in APS I and for the interferon-?s in MG, hinting at thymic aberrations in both groups. The exact profile of type I interferon antibodies may indicate MG subtype and may hint at thymoma recurrence.
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Myasthenia gravis: a review of available treatment approaches.
Autoimmune Dis
PUBLISHED: 04-14-2011
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Patients with autoimmune myasthenia gravis (MG) should be further classified before initiating therapy, as treatment response varies for ocular versus generalised, early onset versus late onset, and acetylcholine receptor antibody positive versus MuSK antibody positive disease. Most patients need immunosuppression in addition to symptomatic therapy. Prednisolone and azathioprine represent first choice drugs, whereas several second choice options are recommended and should be considered. Thymectomy should be undertaken in MG with thymoma and in generalised, early-onset MG. For MG crises and other acute exacerbations, intravenous immunoglobulin (IvIg) and plasma exchange are equally effective and safe treatments. Children and females in child bearing age need special attention regarding potential side effects of immunosuppressive therapy. MG pathogenesis is known in detail, but the immune therapy is still surprisingly unspecific, without a pin-pointed attack on the defined disease-inducing antigen-antibody reaction being available.
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Matrix metalloproteinase-3 in myasthenia gravis compared to other neurological disorders and healthy controls.
Autoimmune Dis
PUBLISHED: 04-10-2011
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MMP-3 is capable of degrading a variety of proteins, including agrin, which plays a critical role in neuromuscular signaling by controlling acetylcholine receptor clustering. High MMP-3 levels in a proportion of myasthenia gravis (MG) patients have been reported. A pathogenic role of MMP-3 in other neurological disorders has been suggested but not proven. We have therefore examined the levels of MMP-3 in 124 MG patients and compared them to 59 multiple sclerosis (MS) patients, 74 epilepsy patients, 33 acute stroke patients, and 90 healthy controls. 15.3% of the patients in the MG group were MMP-3-positive (defined as higher than cutoff value 48?ng/mL) with very high mean MMP-3 concentration (79.9?ng/mL), whereas the proportion of MMP-3 positive patients in the MS (3.4%), epilepsy (6.7%), stroke (0%), and the control group (4.4%) was significantly lower. Mean MMP-3 concentration in the total MG group (25.5?ng/mL) was significantly higher than in the MS (16.6?ng/mL) and stroke (11.7?ng/mL) groups, but did not differ significantly from the epilepsy (19.4?ng/mL) and the control group (23.4?ng/mL). MMP-3 may have a specific pathogenic effect in MG in addition to being associated with autoimmune diseases in general.
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Treatment for postpolio syndrome.
Cochrane Database Syst Rev
PUBLISHED: 02-18-2011
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Postpolio syndrome (PPS) may affect survivors of paralytic poliomyelitis and is characterised by a complex of neuromuscular symptoms leading to a decline in physical functioning. The effectiveness of pharmacological treatment and rehabilitation management in PPS is not yet established.
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Heat-shock proteins in clinical neurology.
Eur. Neurol.
PUBLISHED: 02-17-2011
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Heat-shock proteins (HSPs) are antigen-presenting protein-aggregation-preventing chaperones, induced by cellular stress in eukaryotic cells. In this review, we focus on recent HSP advances in neurological disorders. In myasthenia gravis, patients responding to immunosuppressive therapy have reduced serum HSP-71 antibodies. Generalized and ocular myasthenia gravis patients have elevated serum HSP-70 antibodies, indicating common pathogenic mechanisms. In Guillain-Barré syndrome, HSP-70 antibodies are elevated in serum and cerebrospinal fluid, and serum levels are higher than in myasthenia gravis and multiple sclerosis. In multiple sclerosis, serum HSP-27 antibodies are elevated during relapses providing disease activation marker, while ?,?-crystallin expression in brain lesions indicates remission phase initiation. In acute stroke, serum HSP-27 antibodies are elevated irrespective of stroke type and duration. In epilepsy, HSP-27 is induced in patients astrocytes and cerebral blood vessel walls, and ?,?-crystallin is expressed in epileptic foci. In neurodegenerative disorders such as Alzheimer dementia and Parkinsons disease, HSPs are upregulated in brain tissue, and ?,?-crystallin modulates superoxide dismutase-1 (SOD-1) tissue accumulation in familial amyotrophic lateral sclerosis. HSPs play an important role in antigen-presentation and tolerance development. Antibody-mediated interference with their function alters immune responses causing neuropathology. The role of HSPs in clinical neurology should be the subject of future investigation.
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Propofol treatment in adult refractory status epilepticus. Mortality risk and outcome.
Epilepsy Res.
PUBLISHED: 01-07-2011
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To retrospectively study effect and safety of propofol treatment in adult refractory generalised tonic clonic status epilepticus.
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Matrix metalloproteinases in myasthenia gravis.
Eur. Neurol.
PUBLISHED: 01-06-2011
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Myasthenia gravis (MG) is an autoimmune disease with weakness in striated musculature due to anti-acetylcholine receptor (AChR) antibodies or muscle specific kinase at the neuromuscular junction. A subgroup of patients has periocular symptoms only; ocular MG (OMG). Matrix metalloproteinases (MMP) are increased in several autoimmune diseases, including generalized MG (GMG), and have been suggested to play a role in immune cell infiltration, basement membrane breakdown and autoimmune pathogenesis.
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Are MRI high-signal changes of alar and transverse ligaments in acute whiplash injury related to outcome?
BMC Musculoskelet Disord
PUBLISHED: 09-06-2010
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Upper neck ligament high-signal changes on magnetic resonance imaging (MRI) have been found in patients with whiplash-associated disorders (WAD) but also in non-injured controls. The clinical relevance of such changes is controversial. Their prognostic role has never been evaluated. The purpose of this study was to examine if alar and transverse ligament high-signal changes on MRI immediately following the car accident are related to outcome after 12 months for patients with acute WAD grades 1-2.
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Clinical aspects of myasthenia explained.
Autoimmunity
PUBLISHED: 04-13-2010
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Myasthenia gravis and myasthenic syndromes are diseases of the neuromuscular junction. Autoantibodies and toxins to or mutations in one of the synaptic proteins are the main causes of dysfunction. Myasthenic phenotypes can be classified according to the basic aetiological mechanisms or divided depending on the clinical phenotype.
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Anti-Heat Shock Protein 70 antibody levels are increased in myasthenia gravis and Guillain-Barré syndrome.
J. Neuroimmunol.
PUBLISHED: 02-17-2010
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Myasthenia gravis (MG) is an autoimmune disorder where patients develop autoantibodies towards skeletal muscle proteins (e.g. acetylcholine receptor and muscle specific kinase), causing weakness in striated muscles. Ocular MG (OMG) represents a subtype of (MG) affecting only the periocular muscles. The pathogenesis of this phenotype remains unclear. Heat Shock Protein 70 (Hsp70) plays a role in immune regulation. Antibodies against this protein are associated with several autoimmune diseases, and its biological significance has been shown in vivo. We have therefore examined the concentration of anti-Hsp70 antibodies in sera from 35 OMG patients and 94 patients with generalized MG (GMG) using ELISA assays. The antibody concentrations were compared to those in patients with multiple sclerosis (MS), Guillain-Barré syndrome (GBS) and to healthy controls. MG patients had significantly higher anti-Hsp70 antibody concentrations than both MS patients and healthy controls. GBS patients had higher antibody levels than all other groups. No difference in antibody levels was found when comparing OMG and GMG. Our results suggest that patients with MG and GBS have a previous or current increased exposure to Hsp70 antigens. The similarity between GMG and OMG strengthens the hypothesis that OMG represents a systemic disease, similar to GMG.
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MRI of the transverse and alar ligaments in rheumatoid arthritis: feasibility and relations to atlantoaxial subluxation and disease activity.
Neuroradiology
PUBLISHED: 01-08-2010
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Dysfunctional transverse and alar craniovertebral ligaments can cause instability and osseous destruction in rheumatoid arthritis (RA). This study examined (1) the feasibility of high-resolution magnetic resonance imaging (MRI) of these ligaments in RA and (2) the relation between ligament high-signal changes and atlantoaxial subluxation and RA duration/severity.
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Mortality after traumatic spinal cord injury: 50 years of follow-up.
J. Neurol. Neurosurg. Psychiatr.
PUBLISHED: 09-02-2009
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To study mortality and causes of death in an unselected geographically defined cohort of patients with traumatic spinal cord injury (TSCI), 1952-2001.
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MRI of the alar and transverse ligaments in whiplash-associated disorders (WAD) grades 1-2: high-signal changes by age, gender, event and time since trauma.
Neuroradiology
PUBLISHED: 07-23-2009
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This study describes the prevalence of high-signal changes at magnetic resonance imaging (MRI) of the alar and transverse ligaments in whiplash-associated disorders (WAD) grades 1-2 in relation to age, gender, spinal degeneration, type of trauma event and time since trauma.
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Pregnancy, delivery, and outcome for the child in maternal epilepsy.
Epilepsia
PUBLISHED: 06-01-2009
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To investigate pregnancy, delivery, and child outcome in an unselected population of women with both treated and untreated epilepsy.
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Neurofilament ELISA validation.
J. Immunol. Methods
PUBLISHED: 05-03-2009
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Neurofilament proteins (Nf) are highly specific biomarkers for neuronal death and axonal degeneration. As these markers become more widely used, an inter-laboratory validation study is required to identify assay criteria for high quality performance.
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Autoimmune myasthenia gravis.
Expert Rev Neurother
PUBLISHED: 03-11-2009
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Myasthenia gravis (MG) is an autoimmune neuromuscular transmission disorder where well-defined autoantibodies against muscle and muscle cell membrane molecules are directly pathogenetic. All MG patients should be defined for subtype, as such a subclassification has treatment consequences. Ocular MG, early-onset MG, late-onset MG, MG with thymoma, MG with anti-muscle-specific tyrosine kinase antibodies and MG with no defined antibodies constitute the six MG categories. The MG diagnostic process includes neurophysiology, neuroimmunology, neuropharmacology and imaging. In addition to symptomatic therapy with acetylcholine esterase inhibitors, most patients need thymectomy and/or immunosuppressive drugs. Todays treatment is not immunospecific and far from antigen-specific, even if the pathogenesis is known in detail. Strategies for acetylcholine receptor tolerance induction, manipulating acetylcholine receptor antigen presentation or suppressing acetylcholine receptor-specific B-cells or plasma cells work in experimental MG, but have not yet been attempted properly for the human disease, or they do not work. Apart from the 10-15% of patients with paraneoplastic MG, the cause of the disease is not known. Until curative or antigen-specific therapy become available, the well-established treatment gives good-to-excellent results in most patients, with acceptable quality of life and no increased mortality. Acute and intensive care treatment during MG exacerbation is a cornerstone in the treatment.
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Interleukin-10 promoter polymorphisms in myasthenia gravis.
J. Neuroimmunol.
PUBLISHED: 02-06-2009
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Interleukin 10 (IL-10) is secreted by several hemopoietic cells and suppresses the Th1 mediated immune response, while stimulating B cell differentiation and the humoral immune response. IL-10 expression in Con A-stimulated peripheral blood mononuclear cells is related to three polymorphisms in the promoter region of the IL-10 gene; G/A at position -1082, T/C at position -819 and A/C at position -592. We analyzed the distribution of these IL-10 polymorphisms in 64 MG patients and 87 healthy blood donors to determine any influence on MG susceptibility. MG patients had a significantly higher frequency of the ACC/ACC haplotype (12.5% vs 3.4% in controls), as had the subgroups with late onset MG and thymomatous MG (20.0% and 21.4%, respectively). Early onset MG patients had a high frequency of the ATA/ATA haplotype (19.2% vs 3.4% in controls). Titin Ab-positive MG patients had high ACC/ACC (20.0%). This study indicates a direct link between IL-10 and MG pathogenesis, although the complex role of this multi-faceted cytokine in vivo is as yet not fully elucidated.
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Is it safe to use statins in patients with myasthenia gravis?
Nat Clin Pract Neurol
PUBLISHED: 01-31-2009
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This Practice Point commentary discusses a retrospective study by Oh et al. in which the consequences of using statins in patients with myasthenia gravis (MG) were examined. Out of 170 patients with MG seen at a single hospital center during a 2.5-year period, 54 used statins. Six of these patients reported a worsening of MG symptoms within 8 weeks after receiving statins; in two cases the worsening was associated with a confirmed increase in serum acetylcholine receptor antibody concentration. A further seven patients retrospectively reported temporary muscle aching during the first 8 weeks after statin treatment. This effect was less clearly attributable to the drugs. The effects of statins on MG symptoms were believed to be mediated by the immune system. Statins should be used for the same indications in patients with MG as in those without the condition. However, patients with MG should be informed about the possibility of MG exacerbation, and the statins should be withdrawn if this occurs.
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Myasthenia and the neuromuscular junction.
Curr. Opin. Neurol.
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Myasthenic syndromes are distinct disorders at the neuromuscular junction, most often with well characterized autoimmune or genetic pathology. New aspects of the dysfunctions give insight into the normal neuromuscular function in addition to giving therapeutic clues and tailoring the therapy to the pathophysiology in individual patients.
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Late onset myasthenia gravis is associated with HLA DRB1*15:01 in the Norwegian population.
PLoS ONE
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Acquired myasthenia gravis (MG) is a rare antibody-mediated autoimmune disease caused by impaired neuromuscular transmission, leading to abnormal muscle fatigability. The aetiology is complex, including genetic risk factors of the human leukocyte antigen (HLA) complex and unknown environmental factors. Although associations between the HLA complex and MG are well established, not all involved components of the HLA predisposition to this heterogeneous disease have been revealed. Well-powered and comprehensive HLA analyses of subgroups in MG are warranted, especially in late onset MG.
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Geographical distribution of a seropositive myasthenia gravis population.
Muscle Nerve
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To assess age- and sex-specific myasthenia gravis (MG) occurrence and incidence in the different geographical regions in Norway and thereby to identify factors that may contribute to the development of MG.
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Traumatic spinal cord injuries--incidence, mechanisms and course.
Tidsskr. Nor. Laegeforen.
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The primary purpose of this article is to provide an overview of demography, neurological level of injury, extent of lesion, incidence, prevalence, injury mechanisms as well as lethality and causes of death associated with traumatic spinal cord injuries.
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Pregnancy complications in patients with epilepsy.
Curr. Opin. Obstet. Gynecol.
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Epilepsy is a common neurological disorder affecting 0.4-0.8% of pregnant women. Preeclampsia, gestational hypertension, bleeding in pregnancy, induction of labour, caesarean delivery and major congenital malformations of the children occur more frequently in this group. The objective of this review is to evaluate the pregnancy and delivery complications including congenital abnormalities in women with epilepsy. This review comments on results of recently published studies including the Medical Birth Registry of Norway. A second aim of the review is to examine the effect of antiepileptic-drug treatment on pregnancy complications, and also their association with congenital abnormalities associated with these medications.
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Serum levels of matrix metalloproteinases: implications in clinical neurology.
Eur. Neurol.
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Matrix metalloproteinases (MMPs) are zinc-dependent enzymes involved in remodeling extracellular matrix and cell-matrix interactions. A pathogenic role of MMPs in neurological disorders is likely. This paper focuses on serological clinical aspects only. In multiple sclerosis, higher serum MMP-3 is seen during relapses. Lower serum MMP-8 and -9 levels correlate with fewer contrast-enhanced T(2)-weighted MRI lesions, and serum MMP-9 can be used in monitoring treatment. In myasthenia gravis, serum MMP-2, -3, and -9 levels are elevated in both generalized and ocular diseases. A proportion of the patients have markedly increased serum MMP-3. In acute stroke, higher serum MMP-9 correlates with larger infarct volume, stroke severity, and worse functional outcome, and serum MMP-3 is significantly lower than in several other neurological disorders and healthy controls. In amyotrophic lateral sclerosis, serum MMP-2 correlates with disease progression, and both serum MMP-1 and -2 are elevated. In Alzheimers disease, serum MMP-3, -9, and -10 are elevated. In migraine, serum MMP-2 is elevated, and also MMP-9 in those patients with migraine without aura. MMP-9 is implicated in the pathogenesis of experimental epilepsy. A pathogenic role of MMPs in these conditions could be related to their ability to degrade extracellular matrix. MMPs may also facilitate autoimmunity.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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