Publications by authors named "Johan A Aarli"

28 Publications

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Author response.

Neurology 2014 Feb;82(8):734

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February 2014

Myasthenia gravis.

Autoimmune Dis 2011 24;2011:697575. Epub 2012 Jan 24.

Department of Neurology, University of Bergen, Bergen, Norway.

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http://dx.doi.org/10.4061/2011/697575DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270513PMC
August 2012

Myasthenia gravis: a review of available treatment approaches.

Autoimmune Dis 2011 5;2011:847393. Epub 2011 Oct 5.

Department of Clinical Medicine, University of Bergen, 5020 Bergen, Norway.

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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http://dx.doi.org/10.4061/2011/847393DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189457PMC
November 2011

Global perspectives.

Neurology 2011 Oct;77(16):1565-7

Damascus Hospital/Department of Neurology, Kafer Sosseh 69, Damascus 965, Syrian Arab Republic.

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http://dx.doi.org/10.1212/WNL.0b013e318236856cDOI Listing
October 2011

Neurological effects of deep diving.

J Neurol Sci 2011 May 4;304(1-2):17-21. Epub 2011 Mar 4.

National Centre for Hyperbaric and Diving Medicine, Department of Occupational Medicine, Haukeland University Hospital, N-5021 Bergen, Norway.

Deep diving is defined as diving to depths more than 50 m of seawater (msw), and is mainly used for occupational and military purposes. A deep dive is characterized by the compression phase, the bottom time and the decompression phase. Neurological and neurophysiologic effects are demonstrated in divers during the compression phase and the bottom time. Immediate and transient neurological effects after deep dives have been shown in some divers. However, the results from the epidemiological studies regarding long term neurological effects from deep diving are conflicting and still not conclusive. Prospective clinical studies with sufficient power and sensitivity are needed to solve this very important issue.
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http://dx.doi.org/10.1016/j.jns.2011.01.021DOI Listing
May 2011

Neurological perspectives on person-centered medicine.

Authors:
Johan A Aarli

Int J Integr Care 2010 Jan 29;10 Suppl:e006. Epub 2010 Jan 29.

University of Bergen, Norway, President, World Federation of Neurology.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834897PMC
http://dx.doi.org/10.5334/ijic.476DOI Listing
January 2010

Herzmyasthenie: myasthenia of the heart.

Authors:
Johan A Aarli

Arch Neurol 2009 Nov;66(11):1322-3

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http://dx.doi.org/10.1001/archneurol.2009.231DOI Listing
November 2009

Chapter 41: the history of neurology in Scandinavia.

Handb Clin Neurol 2010 ;95:657-66

Department of Neurology, Haukeland University Hospital, Bergen, Norway.

Neurology is well developed in Scandinavia (Denmark, Finland, Iceland, Norway, and Sweden) with a large number of clinical departments and specialists. The care for neurological patients is fairly equally organized even if neurology has evolved from different sources, from psychiatry in Denmark and Finland, internal medicine in Sweden and electrotherapy in Norway. Evidence of diagnostic activity and treatment of neurological diseases can be found in Scandinavia for more than 5000 years. The oldest are trepanned skulls. Written documentation exists from the Viking era, describing treatment of seizures and possibly also the effect of ergotamine. The methods were in concordance with medical practice in the rest of Europe. Scandinavian neurobiologists have produced important contributions to neuroscience during the last 300 or 400 years. Their names can be recognized as eponyms and Nobel prize laureates. Examples are Niels Stensen (Nicolaus Stenoni), the Bartholin family and Knud Krabbe of Denmark, Ragnar Granit of Finland, Bjørn Sigurdsson (the concept of slow virus infections) of Iceland, Asbjørn Følling and Sigvald Refsum of Norway and Gunnar Wohlfart, Eric Kugelberg, Lisa Welander and Arvid Carlsson of Sweden. In addition, well known neurological diseases were described in Scandinavia long before those neuroscientists that today have their names attached to them: Otto Christian Stengel, Norway (1826: Batten-Spielmayer-Vogt's disease), Johan Christian Lund, Norway (1860: Huntington's chorea) and Ernst Alexander Homén, Finland (1889: Wilson's disease).
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http://dx.doi.org/10.1016/S0072-9752(08)02141-6DOI Listing
December 2010

Neurology and psychiatry: "Oh, East is East and West is West ...".

Authors:
Johan A Aarli

Neuropsychiatr Dis Treat 2005 Dec;1(4):285-6

University of Bergen Norway.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2424115PMC
December 2005

Myasthenia gravis in the elderly: Is it different?

Authors:
Johan A Aarli

Ann N Y Acad Sci 2008 ;1132:238-43

Department of Neurology, University of Bergen, Bergen, Norway.

We have defined myasthenia gravis (MG) in the elderly as onset after the age of 50 years. MG is diagnosed more often today than previously. The increase is mainly found in patients over the age of 50 years. Neurologists therefore see more old patients with MG now than before. Prevalence of the early-onset form of MG seems to be unchanged. Recent data indicate that MG may still be substantially underdiagnosed in very old people. Ptosis, diplopia, weakness of the facial muscles, and problems of articulation are important clinical signs in MG and are easier to detect in a youthful appearance. Since ageing causes a decrease in the total eyelid area with sagging of the lower eyelids, a ptosis may be more difficult to diagnose in the elderly. In addition, diplopia may not be detected because of reduced vision due to macular degeneration or cataract formation. Ocular symptoms of MG are therefore more easily missed in the elderly. Thymomatous MG is more common among older patients than it is in younger onset. The mean age at onset of MG for thymoma cases is 50-60 years. Approximately 10-15% of all MG patients have a thymoma, and around 40% of all thymoma cases are associated with MG. During normal aging, the thymus tissue becomes atrophic and replaced with fat. Recent data on MG thymus pathology suggest that lymphocyte accumulation indicating residual thymus may also be found in the elderly, and that there is little qualitative difference between the young and the old thymus from MG patients. The mean concentration of antibodies to acetylcholine receptor (AChR) is lower in MG in the elderly than in early-onset or thymoma-associated MG. Seronegative MG is less common among older patients. Approximately 30% of patients with late-onset, nonthymoma MG have antibodies to titin, while such antibodies are extremely scarce in early-onset MG. Titin antibodies in MG patients seem to be associated with a higher frequency of DR7 antigen and a decrease of DR3 antigen. The antibody response in MG may therefore be influenced by the genetic background.
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http://dx.doi.org/10.1196/annals.1405.040DOI Listing
September 2008

The wind of change.

Authors:
Johan A Aarli

Arch Neurol 2007 Dec;64(12):1694-5

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http://dx.doi.org/10.1001/archneur.64.12.1694DOI Listing
December 2007

Neurology in sub-Saharan Africa: a challenge for World Federation of Neurology.

Neurology 2007 Oct;69(17):1715-8

University of Bergen, Institutt for nevrologi, Haukeland sykehus, Bergen, Norway.

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http://dx.doi.org/10.1212/01.wnl.0000285102.47543.02DOI Listing
October 2007

WHO/WFN Survey of neurological services: a worldwide perspective.

J Neurol Sci 2006 Aug 19;247(1):29-34. Epub 2006 Apr 19.

School of Psychiatry and Clinical Neurosciences, University of Western Australia, Perth, Australia.

According to the findings obtained in the context of a Global Initiative on Neurology and Public Health carried out by the World Health Organization (WHO), there has been a lack of reliable and comparative data on services and other resources for neurological disorders in many parts of the world. In view of these findings and in collaboration with the World Federation of Neurology (WFN), WHO has recently organized an international Survey of Country Resources for Neurological Disorders, which involved 109 countries and covered over 90% of the world's population. This large WHO/WFN collaborative endeavour collected expert information on a number of aspects of neurological care provision around the world including availability of neurological services in primary care; human resources for neurological disorders; sub-specialized neurological services; primary method of financing of neurological care; and disability benefits for patients with neurological disorders. The WHO/WFN Survey results clearly demonstrate that there are inadequate resources for patients with neurological disorders in most parts of the world, and highlight inequalities in the access to neurological care across different populations, and in particular in those living in low-income countries and in developing regions of the world. The key findings of the WHO/WFN Survey including their impact on delivery of neurological care around the world are presented and discussed in this paper. The entire set of WHO/WFN Survey results including numerous tables, graphs and accompanying commentaries can be found in the WHO/WFN Atlas of Country Resources for Neurological Disorders, which is available on request from WHO or at http://www.who.int/mental_health/neurology/ .
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http://dx.doi.org/10.1016/j.jns.2006.03.003DOI Listing
August 2006

The role of complement in myasthenia gravis: serological evidence of complement consumption in vivo.

J Neuroimmunol 2005 Jan;158(1-2):191-4

Department of Neurology, Haukeland University Hospital, Bergen N-5021, Norway.

Background: Antibodies to the acetylcholine receptor (AChR) titin and the ryanodine receptor (RyR) occur in myasthenia gravis (MG). These antibodies are capable of complement activation in vitro. The involvement of the complement system should cause consumption of complement components such as C3 and C4 in vivo.

Materials And Methods: Complement components C3 and C4 were assayed in sera from 78 AChR antibody-positive MG patients and 52 healthy controls. Forty-eight of the patient sera contained titin antibodies as well, and 20 were also RyR antibody-positive.

Results: MG patients with AChR antibody concentrations above the median (11.2 nmol/l) had significantly lower mean C3 and C4 concentrations in serum compared to those with AChR antibody concentrations below the median. Titin antibody-positive MG patients, titin antibody-negative early-onset MG patients, titin antibody-negative late-onset MG patients, and controls had similar C3 and C4 concentrations. Nor did mean C3 and C4 concentrations differ in MG patients with RyR antibodies. Patients with severe MG (grades 4 and 5) had similar C3 and similar C4 levels compared to those with mild MG (grades 1 and 2).

Conclusion: An increased in vivo complement consumption was detected in MG patients with high AChR antibody concentrations, unrelated to MG severity and non-AChR muscle antibodies.
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http://dx.doi.org/10.1016/j.jneuroim.2004.08.002DOI Listing
January 2005

[Intravenous immunoglobulin in postpolio syndrome].

Tidsskr Nor Laegeforen 2004 Sep;124(18):2357-8

Nevrologisk avdeling, Haukeland Universitetssykehus 5021 Bergen.

Background: Postpolio syndrome is characterised by new muscular weakness, pain, and fatigue several decades after the acute polio, and affects approximately 1/4 of patients with previous paralytic polio.

Material And Methods: A 47-year-old woman with a previous history of acute poliomyelitis developed progressive muscular weakness in her left arm and right leg with muscular pain and fatigue. Clinical examination, MRI, and electromyography gave no other explanation to her progressive muscular weakness and fatigue than postpolio syndrome. She was treated with 400 mg/kg immunoglobulin intravenously for five consecutive days.

Results: At follow-up two and three months later, she had a considerable increase in isokinetic muscle strength in knee extension and flexion on the right side, and experienced less fatigue.

Interpretation: This case suggests that stabilisation of an autoimmune dysfunction may be a therapeutic option in postpolio syndrome.
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September 2004

[Thymectomy and muscle antibodies in myasthenia gravis].

Tidsskr Nor Laegeforen 2004 Mar;124(5):629-31

Nevrologisk avdeling, Haukeland Universitetssykehus, 5021 Bergen.

Background: Thymectomy as a treatment for myasthenia gravis (MG) is widely carried out as there is good clinical evidence for post-thymectomy improvement in younger MG patients.

Material And Methods: We examined the relationship between thymectomy, MG severity, the occurrence of muscle autoantibodies against acetylcholine receptor (AChR), titin, and ryanodine receptor (RyR), and pharmacological treatment in 52 early and 43 late-onset MG patients.

Results And Interpretation: Thymectomy in early-onset MG gave a rapid, highly significant, and long-lasting improvement during the first one to two years after surgery. Several patients had a remission. In late-onset MG, thymectomy did not provide the same improvement, but these patients responded well to immunosuppressive drug treatment, which was necessary in 75% of late-onset MG patients compared to only 25% of early-onset patients. The concentration of AChR, titin, and RyR antibodies did not predict the outcome of thymectomy. The occurrence of titin/RyR antibodies in late-onset MG indicated a less favorable prognosis.
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March 2004

[Skeletons in the cupboard--treatment of Arne Torkildsen].

Tidsskr Nor Laegeforen 2003 Dec;123(24):3588-91

Nevro-urologisk laboratorium, Nevrologisk avdeling, Ullevål universitetssykehus, 0407 Oslo.

Arne Torkildsen (1899-1968) developed Torkildsen's operation, the first successful shunt operation treating increased intraventricular pressure in the brain. He defended his doctoral thesis "Ventriculo-cisternostomy" in the University of Copenhagen in 1950, a thesis that had been rejected by the University of Oslo in his home country Norway. He was not found qualified for the post of associate professor in neurosurgery in spite of being recommended by two international adjudicating committees on four occasions. Torkildsen was accused of having misled the university by omitting one third of the operated patients from his thesis. No-one actually called him a cheat, but tales of cheating and infighting between colleagues aspiring to the same academic posts leave a confusing picture. This paper sums up the story and the possible motives different actors might have had for trying to promote or stop Torkildsen's academic career.
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December 2003

Detection of viral sequences in archival spinal cords from fatal cases of poliomyelitis in 1951-1952.

J Virol Methods 2003 Dec;114(1):91-6

Department of Neurology, Haukeland University Hospital, N-5020 Bergen, Norway.

Poliovirus (PV) subjected to genetic characterization is often isolated from faecal carriage. Such virus is not necessarily identical to the virus causing paralytic disease since genetic modifications may occur during replication outside the nervous system. We have searched for poliovirus genomes in the 14 fatal cases occurring during the last epidemics in Norway in 1951-1952. A method was developed for isolation and analysis of poliovirus RNA from formalin-fixed and paraffin-embedded archival tissue. RNA was purified by incubation with Chelex-100 and heating followed by treatment with the proteinase K and chloroform extraction. Viral sequences were amplified by a reverse transcriptase-polymerase chain reaction (RT-PCR), the products subjected to TA cloning and sequenced. RNA from the beta-actin gene, as a control, was identified in 13 cases, while sequences specific for poliovirus were achieved in 11 cases. The sequences from the 2C region of poliovirus were rather conserved while those in the 5'-untranslated region were variable. The developed method should be suitable also for other genetic studies of old archival material.
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http://dx.doi.org/10.1016/j.jviromet.2003.08.013DOI Listing
December 2003

Thymectomy and antimuscle antibodies in nonthymomatous myasthenia gravis.

Ann N Y Acad Sci 2003 Sep;998:481-90

Department of Neurology, Haukeland University Hospital, N-5021 Bergen, Norway.

The clinical effect of thymectomy in early- and late-onset myasthenia gravis (MG) and the correlation to MG severity, pharmacological treatment, and antimuscle antibodies were examined in two series of consecutive acetylcholine receptor (AChR) antibody-positive nonthymoma MG patients. The results indicate a benefit of thymectomy in early-onset MG, but no obvious clinical benefit in late-onset MG. The presence of muscle autoantibodies did not influence the outcome of thymectomy in early-onset MG. In late-onset MG, improvement is least likely in patients with titin and/or RyR antibodies. Thymectomy should always be considered shortly after MG onset in early-onset MG patients and might only be considered in late-onset patients who have early-onset-like immunological characteristics.
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http://dx.doi.org/10.1196/annals.1254.062DOI Listing
September 2003

Myasthenia gravis in individuals over 40.

Ann N Y Acad Sci 2003 Sep;998:424-31

Department of Neurology, University of Bergen, Bergen, Norway.

Myasthenia gravis (MG) in individuals over 40 years of age comprises three groups: early-onset MG with prolonged disease duration, late-onset MG with thymoma, and late-onset of nonthymomatous MG. The clinical features do not differ between the three groups, except that early-onset patients with prolonged disease duration usually have a less severe disease. More than 60% of our MG patients are now more than 50 years of age, often with disease onset after age 40. Although 2 out of the 3 patients in Erb's original description had onset of myasthenic symptoms after age 40, this was apparently infrequent in 1879, when the disease was first identified. Onset of MG after age 40 is now common. For example, in our material, 88/184 (47.8%) had onset of MG after age 40. Eighteen (20.5%) had a thymoma. The female:male ratio in the early-onset group was 2.4:1, whereas it was 1:1.1 among those with onset after age 40. There was no human leukocyte antigen association for MG with thymoma. Antibodies to the acetylcholine receptor were detected in 88% of sera from nonthymomatous MG and in 100% of those with late-onset MG with thymoma. Antibodies to titin were found in sera from 85.7% of MG patients with thymoma (all age groups) and in 58% of nonthymomatous MG with late onset and acetylcholine receptor antibodies. Late-onset, nonthymomatous MG comprises two subgroups, one corresponding to delayed early onset and one immunologically similar to that seen in patients with MG and thymoma.
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http://dx.doi.org/10.1196/annals.1254.055DOI Listing
September 2003

Pathogenesis of myositis and myasthenia associated with titin and ryanodine receptor antibodies.

Ann N Y Acad Sci 2003 Sep;998:343-50

Department of Neurology, University of Bergen, Bergen, Norway.

Some myasthenia gravis (MG) patients have antibodies against skeletal muscle antigens in addition to the acetylcholine receptor (AChR). Two major antigens for these antibodies are the Ca(2+) release channel of the sarcoplasmic reticulum, the ryanodine receptor (RyR), and titin, a gigantic filamentous muscle protein essential for muscle structure, function, and development. RyR and titin antibodies are found in MG patients with a thymoma and in a proportion of late-onset MG, and they correlate with severe MG disease. The RyR antibodies recognize a region near the N-terminus important for channel regulation. They inhibit Ca(2+) release from sarcoplasmic reticulum in vitro. There is electrophysiological evidence for a disordered excitation-contraction coupling in MG patients. The presence of titin antibodies, which bind to key regions near the A/I junction and in the central I-band, correlates with myopathy in MG patients. However, so far, there is no direct evidence that antibodies against the intracellular antigens RyR and titin are pathogenic in vivo.
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http://dx.doi.org/10.1196/annals.1254.039DOI Listing
September 2003

Role of cytokines in neurological disorders.

Authors:
Johan A Aarli

Curr Med Chem 2003 Oct;10(19):1931-7

Department of Neurology, University of Bergen, Norway.

The balance between cytokines with pro- and anti-inflammatory effects contributes to the course of the Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy. TNFalpha seems to be an important factor in the cascade of events leading to demyelination and even axonal damage. During the acute phase, the serum concentrations of TNFalpha and IL-6 are elevated while anti-inflammatory cytokines are up-regulated in the recovery phase. Cytokines also have a key role in the pathogenesis of multiple sclerosis and most data suggest that this effect is mediated by myelin-specific CD4 T lymphocytes secreting Th type 1 cytokines. However, several different immune cells including B lymphocytes, CD8 T lymphocytes and NK T lymphocytes are also involved in the pathogenesis. Both Th1 and Th2 lymphocytes and cytokines probably participate in the development of myasthenia gravis (MG). The IFNalpha production is probably related to the severity of the disease, with clinical improvement associated with decreased production. The serum levels of IL-18 are significantly elevated in MG, with highest concentrations in patients with generalized disease. The immune system may be involved in the pathogenesis of AD by the effect of microglia, which can induce microglial activation with subsequent release of pro-inflammatory cytokines. In parkinsonism, there is evidence of chronic inflammation in the substantia nigra and striatum. Activated microglia, producing proinflammatory cytokines, surround the degenerating dopaminergic neurons and may contribute to the dopaminergic neuron loss. Studies of patients with epilepsy and animals with experimentally induced seizures indicate that cytokines may also influence the electrophysiological properties of neurons.
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http://dx.doi.org/10.2174/0929867033456918DOI Listing
October 2003

[When can the diagnosis of multiple sclerosis be confirmed?].

Authors:
Johan A Aarli

Tidsskr Nor Laegeforen 2003 May;123(10):1316

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May 2003

Fcgamma receptor IIIA polymorphism as a risk factor for acute poliomyelitis.

J Infect Dis 2002 Dec 19;186(12):1840-3. Epub 2002 Nov 19.

Department of Neurology, Haukeland University Hospital, N-5021 Bergen, Norway.

Poliomyelitis is a viral infection that causes flaccid paralysis in approximately 1% of cases. The Fc receptors for immunoglobulin G (FcgammaR) are associated with modifying effects of several infectious and autoimmune diseases. To assess the influence of FcgammaR polymorphisms on the acute and late course of poliomyelitis, 110 Norwegian patients with well-defined histories of acute poliomyelitis were genotyped, of whom 50 suffered from the postpolio syndrome (PPS). In comparison with healthy control subjects without a history of poliomyelitis, significantly fewer patients had the FcgammaRIIIA genotype V/V (P<.01). However, this genotype was not an independent risk factor for PPS. The FcgammaRIIA and IIIB genotypes and allele frequencies did not differ between the patients and control subjects. The FcgammaRIIIA V/V genotype may lower the risk for contracting acute poliomyelitis through better clearance of poliovirus.
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http://dx.doi.org/10.1086/345769DOI Listing
December 2002

Titin and ryanodine receptor epitopes are expressed in cortical thymoma along with costimulatory molecules.

J Neuroimmunol 2002 Jul;128(1-2):82-9

Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.

Cortical-type thymomas are associated with myasthenia gravis (MG) in 50% of the cases. MG is caused by antibodies against the acetylcholine receptors (AChR), but additional non-AChR muscle autoantibodies such as those against titin and ryanodine receptor (RyR) are found in up to 95% of MG patients with thymoma. To elucidate the induction of non-AChR autoantibodies in thymoma-associated MG, we studied cortical-type thymomas from seven thymoma MG patients, and sera from six of them. All six had titin antibodies, and four had RyR antibodies. Titin and RyR epitopes were co-expressed along with LFA3 and B7 (BB1) costimulatory molecules on thymoma antigen-presenting cells (APC) in all thymomas. In normal thymus, the staining by anti-titin, anti-RyR, anti-LFA3, and anti-BB1 antibodies was weak and occurred exclusively in the medulla and perivascularly. Our results indicate a primary autosensitization against titin and RyR antigens inside the thymoma. In MG-associated thymoma, the mechanisms involved in the initial autosensitization against titin and RyR are probably similar to those implicated in the autosensitization against AChR. In all cases, there is an overexpression of muscle-like epitopes and costimulatory molecules indicating that the T-cell autoimmunization is actively promoted by the pathogenic microenvironment inside the thymoma.
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http://dx.doi.org/10.1016/s0165-5728(02)00145-5DOI Listing
July 2002

Long-term follow-up of patients with nonparalytic poliomyelitis.

Arch Phys Med Rehabil 2002 Apr;83(4):533-7

Department of Neurology, Unit of Clinical Neurophysiology, Haukeland University Hospital, N-5021 Bergen, Norway.

Objective: To examine patients with previous nonparalytic poliomyelitis in search of muscle atrophy, weakness, and other late symptoms of poliomyelitis.

Design: A mailed questionnaire followed up with neurologic and neurophysiologic examinations of respondents who reported symptoms possibly related to the late sequelae of polio.

Setting: Neurology department at a university hospital.

Participants: Thirty-nine of 47 patients diagnosed with nonparalytic poliomyelitis and hospitalized at a Norwegian hospital between 1950 and 1954, during the Norwegian polio epidemic.

Interventions: Not applicable.

Main Outcome Measures: Electromyography to determine function of the anterior tibialis, vastus lateralis, and biceps brachii muscles; nerve conduction studies of the sural, peroneal, and tibial nerves; motor and sensory nerve conduction velocity, and compound muscle and sensory nerve action potentials, and distal latencies.

Results: Twenty-five of 47 patients (53.2%) reported symptoms possibly related to the late sequelae of poliomyelitis. Eight of 20 examined symptomatic patients had normal neurologic and neurophysiologic findings, whereas 9 others had other medical conditions that could explain the symptoms. Three patients (6.7%) had neurologic and neurophysiologic findings and development of symptoms consistent with motoneuron damage.

Conclusion: Some nonparalytic patients may have subclinical acute motoneuron damage with subsequent development and manifestation of motor weakness and neuromuscular symptoms many years later. These symptoms should be considered a differential diagnosis in patients who have a history of nonparalytic poliomyelitis.
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http://dx.doi.org/10.1053/apmr.2002.30936DOI Listing
April 2002
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