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PRESENTED BY
BIPUL JYOTI DAS
M.Sc BIOTECHNOLOGY
DIBRUGARH UNIVERSITY
 Myasthenia gravis was first described by Thomas Willis in 1672.
 An uncommon chronic autoimmune disorder, literally meaning
‘muscle weakness’.
 Prevalence of MG is about 20 per 100,000 population in U.S
(Department of Neurology, University of Virginia, Charlottesville,
Virginia 22908, USA. lhp3n@virginia.edu)
 A neuromuscular disease, defect in the transmission of nerve
impulse.
 Women are affected more than men.
 Pediatric myasthenia gravis
 Neonatal group
 Juvenile group
 Adult myasthenia gravis
 Group1: Ocular
 Group2A: Mild generalized disease
 Group2B: Moderately similar generalized disease
 Group3: Acute fulminating disease
 Group4: Late severe disease
 Pediatric myasthenia gravis
 Neonatal
 Infants born of myasthenic mothers.
 Self limited
 Transplacental transfer of AchR
 antibodies
 Juvenile
 Non-myasthenic mother
 Tends to be permanent
 Onset anytime from birth to puberty.
 Adult myasthenia gravis
 Group1: Ocular
 limited to ocular muscles
 Group2A: Mild generalized disease
 Cranial, limbs and truncal muscle
 Low mortality
 Group2B: Moderately severe generalized disease
 exercise intolerance
 Bulbar muscles affected
 Limb weakness
 Group3: Acute fulminating disease
• Severe symptoms
• Thymoma relatively frequent
• High mortality
 Group4: Late severe disease
• High incidence of thymoma
• Poor response to anticholinesterase
 Autoantibodies block the receptors of acetylcholine in
neuromuscular junction.
 Autoantibodies against MuSK protein- tyrosine kinase receptor
which helps in neuromuscular junction formation.
 Thymoma- enlargement of thymus.
 Rare hereditary form of myasthenia gravis.
MYASTHENIA GRAVIS
 Eye muscles
 Drooping of one or both eyelids (ptosis).
 Double vision (diplopia)
 Face and throat muscles
 Altered speaking(dyasarthria)
 Difficulty swallowing(dysphagia)
 Problems chewing
 Limited facial expressions
 Neck and limb muscles
 Weakness in arms, legs, neck, fingers etc.
 Weakness in the chest muscles sometimes
 occurs. If this is severe, myasthenic crisis
 may result .
 Multiple sclerosis (MS)- MS effects central nervous system while
MG effect peripheral nervous system. Symptoms- problem in speech,
swallowing, visual problems etc.
 Hyperthyroidism- Symptoms include bulging eyes, weight loss, rapid
heart rate, weakness in arms and thighs, muscle fatigue.
 Myalgic encephalomyelitis (ME)- 'chronic fatigue syndrome’.
Symptoms- muscle weakness, joint pain, sore throat, cardiac and
respiratory problem.
 Lambert-Eaton myasthenic syndrome- Symptoms are similar.
Double vision is less common. Symptoms also include impaired
sweating, difficulties in urination etc.
 Ice Pack Test
 Blood Test
 Serology is performed to identify antibodies against
 Achr and MuSK protein.
 Single fibre electromyography
 EMG measures the electrical activity travelling between
 brain and muscles.
 Endrophonium Test
 Intravenous administration of endrophonium chloride.
 Imaging
MRI and CT scan of chest is performed.
 Pathological finding
Muscle biopsy is performed if the diagnosis remains in doubt and
clinical suspicion of MG persists.
Medications
 Acetylcholinesterase inhibitors: Neostigmine and pyridostigmine
 Corticosteroids: prednisone
 Immunosuppressive drugs: azathioprine, cyclosporin,
mycophenolate mofetil, tacrolimus.
Therapy
 Plasmapheresis can be used to remove the putative antibodies
from the circulation.
 Intravenous immunoglobulins (IVIGs) can be used to bind the
circulating antibodies.
Surgery
 Thymectomy
Pathophysiology of myasthenia gravis with antibodies to the acetylcholine
receptor, muscle-specific kinase and low-density lipoprotein receptor-related
protein 4.
Verschuuren JJ, Huijbers MG, Plomp JJ, Niks EH, Molenaar PC, Martinez-
Martinez P, Gomez AM, De Baets MH,Losen M,
DOI: 10.1016/j.autrev.2013.03.001
Abstract
Myasthenia gravis is caused by antibodies to the acetylcholine receptor, muscle-
specific kinase, low-density lipoprotein receptor-related protein 4, or possibly yet
unidentified antibodies. The mechanisms by which these antibodies interfere with
the function of postsynaptic proteins include complement activation, antigenic
modulation by crosslinking of the target proteins, competition with ligand binding
sites, or steric hindrance which inhibits conformational changes or binding to
associated proteins. Screening for auto-antibodies to different postsynaptic targets,
and also for low-affinity antibodies, is contributing to a more accurate diagnosis
of MG patients. Further studies into the specific pathophysiological pathways of
the several MG subforms might help to develop new, more antigen specific,
therapies.
Disturbed B cell subpopulations and increased plasma cells in
myasthenia gravis patients
Siegfried Kohler, Thomas Oskar Philipp Keil, Marc Swierzy, Sarah
Hoffmann DOI: 10.1016/j.jneuroim.2013.09.006.
Abstract
 Whether there is a general perturbation of B and plasma cell subsets in
myasthenia gravis (MG) has not been investigated so far. Here we
performed a detailed flow cytometric analysis of blood and if available
thymic tissue in order to detect MG-specific and therapy-induced changes.
We observed significant differences in the distribution of B cell subsets in
MG patients, yet these were mainly attributable to medical treatment.
Furthermore MG is associated with significantly increased frequencies of
plasma cells that were especially activated in purely ocular disease
manifestation. In contrast to thymoma, B cell subset distribution in
hyperplastic thymus could be distinguished from peripheral blood,
however both tissues were not significantly enriched with plasma cells.
Thus B cell differentiation in general is not defective in MG, but modified
by therapy and enhanced frequencies of plasma cells can be detected in
MG patients.
 An autoimmune neuromuscular disorder caused by auto
antibodies against AchR .
 Myasthenia gravis is an immune-mediated post-synaptic
disorder of neuromuscular transmission, most commonly
presenting as oculobulbar and proximal muscle weakness
associated with easy fatigability.
 The typical main symptom is weakness of muscles that gets
worse with activity and improves with rest.
 Once diagnosed, proper treatment is necessary for living a
normal life.
 BOOKS
 Owen J.A, Punt J, Stranford S.A (Seventh edition,2013) Kuby
Immunology
 Kenneth S. Saladin (Third edition) Anatomy & Physiology :The
unit of form and function
 LINKS
 http://www.medicinenet.com/myasthenia_gravis/article.htm
 http://www.nlm.nih.gov/medlineplus/myastheniagravis.html
 http://www.healthline.com/health/myasthenia-gravis
 http://www.niams.nih.gov/Health_Info/myasthenia_gravis/
 http://www.medicalnewstoday.com/info/myasthenia-gravis/
MYASTHENIA GRAVIS

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MYASTHENIA GRAVIS

  • 1. PRESENTED BY BIPUL JYOTI DAS M.Sc BIOTECHNOLOGY DIBRUGARH UNIVERSITY
  • 2.  Myasthenia gravis was first described by Thomas Willis in 1672.  An uncommon chronic autoimmune disorder, literally meaning ‘muscle weakness’.  Prevalence of MG is about 20 per 100,000 population in U.S (Department of Neurology, University of Virginia, Charlottesville, Virginia 22908, USA. lhp3n@virginia.edu)  A neuromuscular disease, defect in the transmission of nerve impulse.  Women are affected more than men.
  • 3.  Pediatric myasthenia gravis  Neonatal group  Juvenile group  Adult myasthenia gravis  Group1: Ocular  Group2A: Mild generalized disease  Group2B: Moderately similar generalized disease  Group3: Acute fulminating disease  Group4: Late severe disease
  • 4.  Pediatric myasthenia gravis  Neonatal  Infants born of myasthenic mothers.  Self limited  Transplacental transfer of AchR  antibodies  Juvenile  Non-myasthenic mother  Tends to be permanent  Onset anytime from birth to puberty.
  • 5.  Adult myasthenia gravis  Group1: Ocular  limited to ocular muscles  Group2A: Mild generalized disease  Cranial, limbs and truncal muscle  Low mortality  Group2B: Moderately severe generalized disease  exercise intolerance  Bulbar muscles affected  Limb weakness
  • 6.  Group3: Acute fulminating disease • Severe symptoms • Thymoma relatively frequent • High mortality  Group4: Late severe disease • High incidence of thymoma • Poor response to anticholinesterase
  • 7.  Autoantibodies block the receptors of acetylcholine in neuromuscular junction.  Autoantibodies against MuSK protein- tyrosine kinase receptor which helps in neuromuscular junction formation.  Thymoma- enlargement of thymus.  Rare hereditary form of myasthenia gravis.
  • 9.  Eye muscles  Drooping of one or both eyelids (ptosis).  Double vision (diplopia)  Face and throat muscles  Altered speaking(dyasarthria)  Difficulty swallowing(dysphagia)  Problems chewing  Limited facial expressions  Neck and limb muscles  Weakness in arms, legs, neck, fingers etc.  Weakness in the chest muscles sometimes  occurs. If this is severe, myasthenic crisis  may result .
  • 10.  Multiple sclerosis (MS)- MS effects central nervous system while MG effect peripheral nervous system. Symptoms- problem in speech, swallowing, visual problems etc.  Hyperthyroidism- Symptoms include bulging eyes, weight loss, rapid heart rate, weakness in arms and thighs, muscle fatigue.  Myalgic encephalomyelitis (ME)- 'chronic fatigue syndrome’. Symptoms- muscle weakness, joint pain, sore throat, cardiac and respiratory problem.  Lambert-Eaton myasthenic syndrome- Symptoms are similar. Double vision is less common. Symptoms also include impaired sweating, difficulties in urination etc.
  • 11.  Ice Pack Test  Blood Test  Serology is performed to identify antibodies against  Achr and MuSK protein.  Single fibre electromyography  EMG measures the electrical activity travelling between  brain and muscles.  Endrophonium Test  Intravenous administration of endrophonium chloride.
  • 12.  Imaging MRI and CT scan of chest is performed.  Pathological finding Muscle biopsy is performed if the diagnosis remains in doubt and clinical suspicion of MG persists.
  • 13. Medications  Acetylcholinesterase inhibitors: Neostigmine and pyridostigmine  Corticosteroids: prednisone  Immunosuppressive drugs: azathioprine, cyclosporin, mycophenolate mofetil, tacrolimus. Therapy  Plasmapheresis can be used to remove the putative antibodies from the circulation.  Intravenous immunoglobulins (IVIGs) can be used to bind the circulating antibodies. Surgery  Thymectomy
  • 14. Pathophysiology of myasthenia gravis with antibodies to the acetylcholine receptor, muscle-specific kinase and low-density lipoprotein receptor-related protein 4. Verschuuren JJ, Huijbers MG, Plomp JJ, Niks EH, Molenaar PC, Martinez- Martinez P, Gomez AM, De Baets MH,Losen M, DOI: 10.1016/j.autrev.2013.03.001 Abstract Myasthenia gravis is caused by antibodies to the acetylcholine receptor, muscle- specific kinase, low-density lipoprotein receptor-related protein 4, or possibly yet unidentified antibodies. The mechanisms by which these antibodies interfere with the function of postsynaptic proteins include complement activation, antigenic modulation by crosslinking of the target proteins, competition with ligand binding sites, or steric hindrance which inhibits conformational changes or binding to associated proteins. Screening for auto-antibodies to different postsynaptic targets, and also for low-affinity antibodies, is contributing to a more accurate diagnosis of MG patients. Further studies into the specific pathophysiological pathways of the several MG subforms might help to develop new, more antigen specific, therapies.
  • 15. Disturbed B cell subpopulations and increased plasma cells in myasthenia gravis patients Siegfried Kohler, Thomas Oskar Philipp Keil, Marc Swierzy, Sarah Hoffmann DOI: 10.1016/j.jneuroim.2013.09.006. Abstract  Whether there is a general perturbation of B and plasma cell subsets in myasthenia gravis (MG) has not been investigated so far. Here we performed a detailed flow cytometric analysis of blood and if available thymic tissue in order to detect MG-specific and therapy-induced changes. We observed significant differences in the distribution of B cell subsets in MG patients, yet these were mainly attributable to medical treatment. Furthermore MG is associated with significantly increased frequencies of plasma cells that were especially activated in purely ocular disease manifestation. In contrast to thymoma, B cell subset distribution in hyperplastic thymus could be distinguished from peripheral blood, however both tissues were not significantly enriched with plasma cells. Thus B cell differentiation in general is not defective in MG, but modified by therapy and enhanced frequencies of plasma cells can be detected in MG patients.
  • 16.  An autoimmune neuromuscular disorder caused by auto antibodies against AchR .  Myasthenia gravis is an immune-mediated post-synaptic disorder of neuromuscular transmission, most commonly presenting as oculobulbar and proximal muscle weakness associated with easy fatigability.  The typical main symptom is weakness of muscles that gets worse with activity and improves with rest.  Once diagnosed, proper treatment is necessary for living a normal life.
  • 17.  BOOKS  Owen J.A, Punt J, Stranford S.A (Seventh edition,2013) Kuby Immunology  Kenneth S. Saladin (Third edition) Anatomy & Physiology :The unit of form and function  LINKS  http://www.medicinenet.com/myasthenia_gravis/article.htm  http://www.nlm.nih.gov/medlineplus/myastheniagravis.html  http://www.healthline.com/health/myasthenia-gravis  http://www.niams.nih.gov/Health_Info/myasthenia_gravis/  http://www.medicalnewstoday.com/info/myasthenia-gravis/