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Published in: Current Neurology and Neuroscience Reports 1/2013

01-01-2013 | Nerve and Muscle (M Hirano and LH Weimer, Section Editors)

Inclusion Body Myositis

Authors: Mazen M. Dimachkie, Richard J. Barohn

Published in: Current Neurology and Neuroscience Reports | Issue 1/2013

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Abstract

Sporadic inclusion body myositis (IBM) is the most common idiopathic inflammatory myopathy (IIM) after age 50 years. It presents with chronic insidious proximal leg and distal arm asymmetric muscle weakness. Despite similarities with polymyositis (PM), it is likely that IBM is primarily a degenerative disorder rather than inflammatory muscle disease. IBM is associated with a modest degree of creatine kinase (CK) elevation and an electromyogram (EMG) demonstrates a chronic irritative myopathy. Muscle histopathology demonstrates endomysial inflammatory exudates surrounding and invading non-necrotic muscle fibers often times accompanied by rimmed vacuoles. We review IBM with emphasis on recent developments in the field and discuss ongoing clinical trials.
Literature
1.
go back to reference Phillips BA, Zilko PJ, Mastaglia FL. Prevalence of sporadic inclusion body myositis in Western Australia. Muscle Nerve. 2000;23(6):970–2.PubMedCrossRef Phillips BA, Zilko PJ, Mastaglia FL. Prevalence of sporadic inclusion body myositis in Western Australia. Muscle Nerve. 2000;23(6):970–2.PubMedCrossRef
2.
go back to reference Lotz BP, Engel AG, Nishino H, Stevens JC, Litch WJ. Inclusion body myositis. Observations in 40 patients. Brain. 1989;112(Pt 3):727–47.PubMedCrossRef Lotz BP, Engel AG, Nishino H, Stevens JC, Litch WJ. Inclusion body myositis. Observations in 40 patients. Brain. 1989;112(Pt 3):727–47.PubMedCrossRef
3.
go back to reference Badrising UA, Maat-Schieman ML, van Houwelingen JC, et al. Inclusion body myositis. Clinical features and clinical course of the disease in 64 patients. Neurology. 2005;252(12):1448–54.CrossRef Badrising UA, Maat-Schieman ML, van Houwelingen JC, et al. Inclusion body myositis. Clinical features and clinical course of the disease in 64 patients. Neurology. 2005;252(12):1448–54.CrossRef
4.
go back to reference Wilson FC, Ytterberg SR, St Sauver JL, et al. Epidemiology of sporadic inclusion body myositis and polymyositis in Olmsted County, Minnesota. J Rheumatol. 2008;35(3):445–7.PubMed Wilson FC, Ytterberg SR, St Sauver JL, et al. Epidemiology of sporadic inclusion body myositis and polymyositis in Olmsted County, Minnesota. J Rheumatol. 2008;35(3):445–7.PubMed
5.
go back to reference Amato AA, Gronseth GS, Jackson, et al. Inclusion body myositis: clinical and pathological boundaries. Ann Neurol. 1995;40:581–6.CrossRef Amato AA, Gronseth GS, Jackson, et al. Inclusion body myositis: clinical and pathological boundaries. Ann Neurol. 1995;40:581–6.CrossRef
7.
go back to reference Badrising UA, Maat-Schieman M, van Duinen SG, et al. Epidemiology of inclusion body myositis in The Netherlands: a nationwide study. Neurology. 2000;55:1385–7.PubMedCrossRef Badrising UA, Maat-Schieman M, van Duinen SG, et al. Epidemiology of inclusion body myositis in The Netherlands: a nationwide study. Neurology. 2000;55:1385–7.PubMedCrossRef
8.
go back to reference Lindberg C, Persson LI, Bjorkander J, Oldfors A. Inclusion body myositis: clinical, morphological, physiological, and laboratory findings in 18 cases. Acta Neurol Scand. 1994;89:123–31.PubMedCrossRef Lindberg C, Persson LI, Bjorkander J, Oldfors A. Inclusion body myositis: clinical, morphological, physiological, and laboratory findings in 18 cases. Acta Neurol Scand. 1994;89:123–31.PubMedCrossRef
9.
go back to reference Sayers ME, Chou SM, Calabrese LH. Inclusion body myositis: analysis of 32 cases. J Rheumatol. 1992;19:1385–9.PubMed Sayers ME, Chou SM, Calabrese LH. Inclusion body myositis: analysis of 32 cases. J Rheumatol. 1992;19:1385–9.PubMed
10.
go back to reference Needham M, James I, Corbett A, et al. Sporadic inclusion body myositis: phenotypic variability, and influence of HLA-DR3 in a cohort of 57 Australian cases. J Neurol Neurosurg Psychiatry. 2008;79(9):1056–60.PubMedCrossRef Needham M, James I, Corbett A, et al. Sporadic inclusion body myositis: phenotypic variability, and influence of HLA-DR3 in a cohort of 57 Australian cases. J Neurol Neurosurg Psychiatry. 2008;79(9):1056–60.PubMedCrossRef
11.
go back to reference Barohn RJ, Amato AA, Sahenk Z, Kissel JT, Mendell JR. Inclusion body myositis: explanation for poor response to immunosuppressive therapy. Neurology. 1995;45(7):1302–4.PubMedCrossRef Barohn RJ, Amato AA, Sahenk Z, Kissel JT, Mendell JR. Inclusion body myositis: explanation for poor response to immunosuppressive therapy. Neurology. 1995;45(7):1302–4.PubMedCrossRef
12.
go back to reference Estephan B, Barohn RJ, Dimachkie MM, et al. Sporadic IBM: a case cohort. J Clin Neuromuscul Dis. 2011;12(3):18–9. Estephan B, Barohn RJ, Dimachkie MM, et al. Sporadic IBM: a case cohort. J Clin Neuromuscul Dis. 2011;12(3):18–9.
13.
go back to reference •• Griggs RC, Askanas V, DiMauro S, et al. Inclusion body myositis and myopathies. Ann Neurol. 1995;38(5):705–13. Authors of this article propose diagnostic criteria for definite and possible sporadic inclusion body myositis based on a combination of clinical features and laboratory findings including serum creatine kinase, electromyography, and muscle histopathology. This is the first major effort to define diagnostic criteria for IBM. These criteria have withstood the test of time with some additions as in reference 14.PubMedCrossRef •• Griggs RC, Askanas V, DiMauro S, et al. Inclusion body myositis and myopathies. Ann Neurol. 1995;38(5):705–13. Authors of this article propose diagnostic criteria for definite and possible sporadic inclusion body myositis based on a combination of clinical features and laboratory findings including serum creatine kinase, electromyography, and muscle histopathology. This is the first major effort to define diagnostic criteria for IBM. These criteria have withstood the test of time with some additions as in reference 14.PubMedCrossRef
14.
go back to reference •• Hilton-Jones D, Miller A, Parton M, et al. Inclusion body myositis: MRC Centre for Neuromuscular Diseases, IBM workshop, London, 13 June, 2008. Neuromuscul Disord. 2010;20(2):142–7. In addition to the Griggs categories of pathologically defined IBM and possible IBM, participants of the 2008 European Neuromuscular Center workshop introduced clinically defined IBM to include IBM cases with weakness involving finger flexion more than shoulder abduction as well as knee extension more than hip flexion. The pathologic criteria for possible IBM and clinically defined IBM are invasion of non-necrotic fibers by mononuclear cells, or rimmed vacuoles, or increased MHC-1 expression on the surface of muscle fibers. This facilitates the diagnosis of patients who fulfill clinical criteria for IBM but do not have the pathologic features set forth by Griggs et al.PubMedCrossRef •• Hilton-Jones D, Miller A, Parton M, et al. Inclusion body myositis: MRC Centre for Neuromuscular Diseases, IBM workshop, London, 13 June, 2008. Neuromuscul Disord. 2010;20(2):142–7. In addition to the Griggs categories of pathologically defined IBM and possible IBM, participants of the 2008 European Neuromuscular Center workshop introduced clinically defined IBM to include IBM cases with weakness involving finger flexion more than shoulder abduction as well as knee extension more than hip flexion. The pathologic criteria for possible IBM and clinically defined IBM are invasion of non-necrotic fibers by mononuclear cells, or rimmed vacuoles, or increased MHC-1 expression on the surface of muscle fibers. This facilitates the diagnosis of patients who fulfill clinical criteria for IBM but do not have the pathologic features set forth by Griggs et al.PubMedCrossRef
15.
go back to reference Amato AA, Barohn RJ. Inclusion body myositis: old and new concepts. J Neurol Neurosurg Psychiatry. 2009;80(11):1186–93.PubMedCrossRef Amato AA, Barohn RJ. Inclusion body myositis: old and new concepts. J Neurol Neurosurg Psychiatry. 2009;80(11):1186–93.PubMedCrossRef
16.
go back to reference Garlepp MJ, Laing B, Zilko PJ, et al. HLA associations with inclusion body myositis. Clin Exp Immunol. 1994;98:40–5.PubMedCrossRef Garlepp MJ, Laing B, Zilko PJ, et al. HLA associations with inclusion body myositis. Clin Exp Immunol. 1994;98:40–5.PubMedCrossRef
17.
go back to reference Degardin A, Morillon D, Lacour A, Cotten A, Vermersch P, Stojkovic T. Morphologic imaging in muscular dystrophies and inflammatory myopathies. Skeletal Radiol. 2010;39(12):1219–27.PubMedCrossRef Degardin A, Morillon D, Lacour A, Cotten A, Vermersch P, Stojkovic T. Morphologic imaging in muscular dystrophies and inflammatory myopathies. Skeletal Radiol. 2010;39(12):1219–27.PubMedCrossRef
18.
go back to reference Cox FM, Reijnierse M, van Rijswijk CS, Wintzen AR, Verschuuren JJ, Badrising UA. Magnetic resonance imaging of skeletal muscles in sporadic inclusion body myositis. Rheumatology. 2011;50(6):1153–61.PubMedCrossRef Cox FM, Reijnierse M, van Rijswijk CS, Wintzen AR, Verschuuren JJ, Badrising UA. Magnetic resonance imaging of skeletal muscles in sporadic inclusion body myositis. Rheumatology. 2011;50(6):1153–61.PubMedCrossRef
19.
go back to reference Maetzler W, Reimold M, Schittenhelm J, et al. Increased [11C]PIB-PET levels in inclusion body myositis are indicative of amyloid beta deposition. J Neurol Neurosurg Psychiatry. 2011;82(9):1060–2.PubMedCrossRef Maetzler W, Reimold M, Schittenhelm J, et al. Increased [11C]PIB-PET levels in inclusion body myositis are indicative of amyloid beta deposition. J Neurol Neurosurg Psychiatry. 2011;82(9):1060–2.PubMedCrossRef
20.
go back to reference Chahin N, Engel AG. Correlation of muscle biopsy, clinical course, and outcome in PM and sporadic IBM. Neurology. 2008;70(6):418–24.PubMedCrossRef Chahin N, Engel AG. Correlation of muscle biopsy, clinical course, and outcome in PM and sporadic IBM. Neurology. 2008;70(6):418–24.PubMedCrossRef
21.
go back to reference Van der Meulen MF, Hoogendijk JE, Moons KG, Veldman H, Badrising UA, Wokke JH. Rimmed vacuoles and the added value of SMI-31 staining in diagnosing sporadic inclusion body myositis. Neuromuscul Disord. 2001;11:447–51.PubMedCrossRef Van der Meulen MF, Hoogendijk JE, Moons KG, Veldman H, Badrising UA, Wokke JH. Rimmed vacuoles and the added value of SMI-31 staining in diagnosing sporadic inclusion body myositis. Neuromuscul Disord. 2001;11:447–51.PubMedCrossRef
22.
go back to reference Greenberg SA, Pinkus GS, Amato AA, Pinkus JL. Myeloid dendritic cells in inclusion-body myositis and polymyositis. Muscle Nerve. 2007;35(1):17–23.PubMedCrossRef Greenberg SA, Pinkus GS, Amato AA, Pinkus JL. Myeloid dendritic cells in inclusion-body myositis and polymyositis. Muscle Nerve. 2007;35(1):17–23.PubMedCrossRef
24.
go back to reference Greenberg SA, Sanoudou D, Haslett JN, et al. Molecular profiles of inflammatory myopathies. Neurology. 2002;59(8):1170–82.PubMedCrossRef Greenberg SA, Sanoudou D, Haslett JN, et al. Molecular profiles of inflammatory myopathies. Neurology. 2002;59(8):1170–82.PubMedCrossRef
25.
go back to reference Greenberg SA, Bradshaw EM, Pinkus JL, et al. Plasma cells in muscle in inclusion body myositis and polymyositis. Neurology. 2005;65(11):1782–7.PubMedCrossRef Greenberg SA, Bradshaw EM, Pinkus JL, et al. Plasma cells in muscle in inclusion body myositis and polymyositis. Neurology. 2005;65(11):1782–7.PubMedCrossRef
26.
go back to reference • Salajegheh M, Lam T, Greenberg SA. Autoantibodies against a 43 kDa muscle protein in inclusion body myositis. PLoS One. 2011;6:e20266. Since microarray studies reported abundant immunoglobulin gene transcripts in IBM muscle derived from local abundant plasma cells, this provided a rationale for searching for circulating autoantibodies. Imunoblots against normal human muscle demonstrate that 52 % of IBM patient samples recognized a 43 kDa muscle protein. None of those with other diseases or healthy volunteers had this protein.PubMedCrossRef • Salajegheh M, Lam T, Greenberg SA. Autoantibodies against a 43 kDa muscle protein in inclusion body myositis. PLoS One. 2011;6:e20266. Since microarray studies reported abundant immunoglobulin gene transcripts in IBM muscle derived from local abundant plasma cells, this provided a rationale for searching for circulating autoantibodies. Imunoblots against normal human muscle demonstrate that 52 % of IBM patient samples recognized a 43 kDa muscle protein. None of those with other diseases or healthy volunteers had this protein.PubMedCrossRef
27.
go back to reference Askanas V, Engel WK. Inclusion-body myositis: a myodegenerative conformational disorder associated with Abeta, protein misfolding, and proteasome inhibition. Neurology. 2006;66(2 Suppl 1):S39–48.PubMedCrossRef Askanas V, Engel WK. Inclusion-body myositis: a myodegenerative conformational disorder associated with Abeta, protein misfolding, and proteasome inhibition. Neurology. 2006;66(2 Suppl 1):S39–48.PubMedCrossRef
28.
go back to reference Wojcik S, Engel WK, McFerrin J, Paciello O, Askanas V. AbetaPP-overexpression and proteasome inhibition increase alpha B-crystallin in cultured human muscle: relevance to inclusion-body myositis. Neuromuscul Disord. 2006;16(12):839–44.PubMedCrossRef Wojcik S, Engel WK, McFerrin J, Paciello O, Askanas V. AbetaPP-overexpression and proteasome inhibition increase alpha B-crystallin in cultured human muscle: relevance to inclusion-body myositis. Neuromuscul Disord. 2006;16(12):839–44.PubMedCrossRef
29.
go back to reference Askanas V, Engel WK. Sporadic inclusion-body myositis: conformational multifactorial ageing-related degenerative muscle disease associated with proteasomal and lysosomal inhibition, endoplasmic reticulum stress, and accumulation of amyloid-β42 oligomers and phosphorylated tau. Presse Med. 2011;40(4 Pt 2):e219–35.PubMedCrossRef Askanas V, Engel WK. Sporadic inclusion-body myositis: conformational multifactorial ageing-related degenerative muscle disease associated with proteasomal and lysosomal inhibition, endoplasmic reticulum stress, and accumulation of amyloid-β42 oligomers and phosphorylated tau. Presse Med. 2011;40(4 Pt 2):e219–35.PubMedCrossRef
30.
go back to reference Salajegheh M, Pinkus JL, Nazareno R, et al. Nature of “Tau” immunoreactivity in normal myonuclei and inclusion body myositis. Muscle Nerve. 2009;40(4):520–8.PubMedCrossRef Salajegheh M, Pinkus JL, Nazareno R, et al. Nature of “Tau” immunoreactivity in normal myonuclei and inclusion body myositis. Muscle Nerve. 2009;40(4):520–8.PubMedCrossRef
31.
go back to reference • Nogalska A, D’Agostino C, Engel WK, Klein WL, Askanas V. Novel demonstration of amyloid-β oligomers in sporadic inclusion-body myositis muscle fibers. Acta Neuropathol. 2010;120(5):661–6. Askanas’ group reported for the first time in 2010 that IBM muscle samples had accumulation of toxic low-molecular weight amyloid β oligomers on dot-immunoblots with a variety of molecular weights and intensity but none of the control muscle biopsies had amyloid β oligomers. Nonfibrillar cytotoxic “Aβ-Derived Diffusible Ligands” originally derived from Aβ42 are prominently increased on dot-immunoblots, being consistent with the concept that intracellular toxicity of Ab42 oligomers is likely an important aspect of IBM pathogenesis. Finally, they demonstrated in cultured human muscle fibers that inhibition of autophagy is a novel cause of Aβ oligomerization.PubMedCrossRef • Nogalska A, D’Agostino C, Engel WK, Klein WL, Askanas V. Novel demonstration of amyloid-β oligomers in sporadic inclusion-body myositis muscle fibers. Acta Neuropathol. 2010;120(5):661–6. Askanas’ group reported for the first time in 2010 that IBM muscle samples had accumulation of toxic low-molecular weight amyloid β oligomers on dot-immunoblots with a variety of molecular weights and intensity but none of the control muscle biopsies had amyloid β oligomers. Nonfibrillar cytotoxic “Aβ-Derived Diffusible Ligands” originally derived from Aβ42 are prominently increased on dot-immunoblots, being consistent with the concept that intracellular toxicity of Ab42 oligomers is likely an important aspect of IBM pathogenesis. Finally, they demonstrated in cultured human muscle fibers that inhibition of autophagy is a novel cause of Aβ oligomerization.PubMedCrossRef
32.
go back to reference Salajegheh M, Pinkus JL, Taylor JP, et al. Sarcoplasmic redistribution of nuclear TDP-43 in inclusion body myositis. Muscle Nerve. 2009;40:19–31.PubMedCrossRef Salajegheh M, Pinkus JL, Taylor JP, et al. Sarcoplasmic redistribution of nuclear TDP-43 in inclusion body myositis. Muscle Nerve. 2009;40:19–31.PubMedCrossRef
33.
go back to reference Verma A, Bradley WG, Ringel SP. Treatment-responsive polymyositis transforming into inclusion body myositis. Neurology. 2008;P060.19. Verma A, Bradley WG, Ringel SP. Treatment-responsive polymyositis transforming into inclusion body myositis. Neurology. 2008;P060.19.
34.
go back to reference Benveniste O, Guiguet M, Freebody J, et al. Long-term observational study of sporadic inclusion body myositis. Brain. 2011;134(Pt 11):3176–84.PubMedCrossRef Benveniste O, Guiguet M, Freebody J, et al. Long-term observational study of sporadic inclusion body myositis. Brain. 2011;134(Pt 11):3176–84.PubMedCrossRef
35.
go back to reference Amato AA, Barohn RJ, Jackson CE, Pappert EJ, Sahenk Z, Kissel JT. Inclusion body myositis: treatment with intravenous immunoglobulin. Neurology. 1994;44(8):1516–8.PubMedCrossRef Amato AA, Barohn RJ, Jackson CE, Pappert EJ, Sahenk Z, Kissel JT. Inclusion body myositis: treatment with intravenous immunoglobulin. Neurology. 1994;44(8):1516–8.PubMedCrossRef
36.
go back to reference Dalakas MC, Sonies B, Dambrosia J, Sekul E, Cupler E, Sivakumar K. Treatment of inclusion-body myositis with IVIg: a double-blind, placebo-controlled study. Neurology. 1997;48:712–6.PubMedCrossRef Dalakas MC, Sonies B, Dambrosia J, Sekul E, Cupler E, Sivakumar K. Treatment of inclusion-body myositis with IVIg: a double-blind, placebo-controlled study. Neurology. 1997;48:712–6.PubMedCrossRef
37.
go back to reference Dalakas MC, Koffman B, Fujii M, Spector S, Sivakumar K, Cupler E. A controlled study of intravenous immunoglobulin combined with prednisone in the treatment of IBM. Neurology. 2001;56:323–7.PubMedCrossRef Dalakas MC, Koffman B, Fujii M, Spector S, Sivakumar K, Cupler E. A controlled study of intravenous immunoglobulin combined with prednisone in the treatment of IBM. Neurology. 2001;56:323–7.PubMedCrossRef
38.
go back to reference Muscle Study Group. Randomized pilot trial of betaINF1a (Avonex) in patients with inclusion body myositis. Neurology. 2001;57:1566–70.CrossRef Muscle Study Group. Randomized pilot trial of betaINF1a (Avonex) in patients with inclusion body myositis. Neurology. 2001;57:1566–70.CrossRef
39.
go back to reference Muscle Study Group. Randomized pilot trial of high-dose betaINF-1a in patients with inclusion body myositis. Neurology. 2004;63:718–20.CrossRef Muscle Study Group. Randomized pilot trial of high-dose betaINF-1a in patients with inclusion body myositis. Neurology. 2004;63:718–20.CrossRef
40.
go back to reference Badrising UA, Maat-Schieman ML, Ferrari, et al. Comparison of weakness progression in inclusion body myositis during treatment with methotrexate or placebo. Ann Neurol. 2002;51:369–72.PubMedCrossRef Badrising UA, Maat-Schieman ML, Ferrari, et al. Comparison of weakness progression in inclusion body myositis during treatment with methotrexate or placebo. Ann Neurol. 2002;51:369–72.PubMedCrossRef
41.
go back to reference Lindberg C, Trysberg E, Tarkowski A, Oldfors A. Anti-T-lymphocyte globulin treatment in inclusion body myositis: a randomized pilot study. Neurology. 2003;61:260–2.PubMedCrossRef Lindberg C, Trysberg E, Tarkowski A, Oldfors A. Anti-T-lymphocyte globulin treatment in inclusion body myositis: a randomized pilot study. Neurology. 2003;61:260–2.PubMedCrossRef
42.
go back to reference Rutkove SB, Parker RA, Nardin RA, Connolly CE, Felic KJ, Raynor EM. A pilot randomized trial of oxandrolone in inclusion body myositis. Neurology. 2002;58(7):1081–7.PubMedCrossRef Rutkove SB, Parker RA, Nardin RA, Connolly CE, Felic KJ, Raynor EM. A pilot randomized trial of oxandrolone in inclusion body myositis. Neurology. 2002;58(7):1081–7.PubMedCrossRef
43.
go back to reference Barohn RJ, Herbelin L, Kissel JT, et al. Pilot trial of etanercept in the treatment of inclusion-body myositis. Neurology. 2006;66(2 Suppl 1):S123–4.PubMedCrossRef Barohn RJ, Herbelin L, Kissel JT, et al. Pilot trial of etanercept in the treatment of inclusion-body myositis. Neurology. 2006;66(2 Suppl 1):S123–4.PubMedCrossRef
44.
go back to reference Dalakas MC, Rakocevic G, Schmidt J, et al. Effect of Alemtuzumab (CAMPATH 1-H) in patients with inclusion-body myositis. Brain. 2009;132(Pt 6):1536–44.PubMedCrossRef Dalakas MC, Rakocevic G, Schmidt J, et al. Effect of Alemtuzumab (CAMPATH 1-H) in patients with inclusion-body myositis. Brain. 2009;132(Pt 6):1536–44.PubMedCrossRef
45.
go back to reference Sancricca C, Mora M, Ricci E, Tonali PA, Mantegazza R, Mirabella M. Pilot trial of simvastatin in the treatment of sporadic inclusion-body myositis. Neurol Sci. 2011;32(5):841–7.PubMedCrossRef Sancricca C, Mora M, Ricci E, Tonali PA, Mantegazza R, Mirabella M. Pilot trial of simvastatin in the treatment of sporadic inclusion-body myositis. Neurol Sci. 2011;32(5):841–7.PubMedCrossRef
46.
go back to reference Saperstein DS, Levine T, Hank N, Kitazawa M, Bowser R, LaFerla F. Pilot Trial of lithium treatment in inclusion body myositis. Neurology. 2011;76 Suppl 4:A106. Saperstein DS, Levine T, Hank N, Kitazawa M, Bowser R, LaFerla F. Pilot Trial of lithium treatment in inclusion body myositis. Neurology. 2011;76 Suppl 4:A106.
47.
go back to reference Pasquali L, Longone P, Isidoro C, Ruggieri S, Paparelli A, Fornai F. Autophagy, lithium, and amyotrophic lateral sclerosis. Muscle Nerve. 2009;40(2):173–94.PubMedCrossRef Pasquali L, Longone P, Isidoro C, Ruggieri S, Paparelli A, Fornai F. Autophagy, lithium, and amyotrophic lateral sclerosis. Muscle Nerve. 2009;40(2):173–94.PubMedCrossRef
48.
go back to reference Wang Y, He J, McVey AL, et al. Twelve-month change of IBMFRS in the arimocolomol inclusion body myositis pilot study. Poster 7.255 presented at the American Academy of Neurology. Annual Meeting. New Orleans, LA, USA; April 26 2012. Actual page etc from Dr. Baroh’s CV). Wang Y, He J, McVey AL, et al. Twelve-month change of IBMFRS in the arimocolomol inclusion body myositis pilot study. Poster 7.255 presented at the American Academy of Neurology. Annual Meeting. New Orleans, LA, USA; April 26 2012. Actual page etc from Dr. Baroh’s CV).
49.
50.
go back to reference Cox FM, Titulaer MJ, Sont JK, Wintzen AR, Verschuuren JJ, Badrising UA. A 12-year follow-up in sporadic inclusion body myositis: an end stage with major disabilities. Brain. 2011;134(Pt 11):3167–75.PubMedCrossRef Cox FM, Titulaer MJ, Sont JK, Wintzen AR, Verschuuren JJ, Badrising UA. A 12-year follow-up in sporadic inclusion body myositis: an end stage with major disabilities. Brain. 2011;134(Pt 11):3167–75.PubMedCrossRef
51.
go back to reference Arnardottir S, Alexanderson H, Lundberg IE, Borg K. Sporadic inclusion body myositis: pilot study on the effects of a home exercise program on muscle function, histopathology, and inflammatory reaction. J Rehabil Med. 2003;35(1):31–5.PubMedCrossRef Arnardottir S, Alexanderson H, Lundberg IE, Borg K. Sporadic inclusion body myositis: pilot study on the effects of a home exercise program on muscle function, histopathology, and inflammatory reaction. J Rehabil Med. 2003;35(1):31–5.PubMedCrossRef
52.
go back to reference Johnson GL, et al. The effectiveness of an individualized, home-based functional exercise program for patients with sporadic inclusion body myositis. J Clin Neuromuscul Dis. 2007;8:187–94.CrossRef Johnson GL, et al. The effectiveness of an individualized, home-based functional exercise program for patients with sporadic inclusion body myositis. J Clin Neuromuscul Dis. 2007;8:187–94.CrossRef
53.
go back to reference Johnson LG, Collier KE, Edwards DJ, et al. Improvement in aerobic capacity after an exercise program in sporadic inclusion body myositis. J Clin Neuromuscul Dis. 2009;10(4):178–84.PubMedCrossRef Johnson LG, Collier KE, Edwards DJ, et al. Improvement in aerobic capacity after an exercise program in sporadic inclusion body myositis. J Clin Neuromuscul Dis. 2009;10(4):178–84.PubMedCrossRef
Metadata
Title
Inclusion Body Myositis
Authors
Mazen M. Dimachkie
Richard J. Barohn
Publication date
01-01-2013
Publisher
Current Science Inc.
Published in
Current Neurology and Neuroscience Reports / Issue 1/2013
Print ISSN: 1528-4042
Electronic ISSN: 1534-6293
DOI
https://doi.org/10.1007/s11910-012-0321-4

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