중증근육무력증의 역사
The History of Myasthenia Gravis
1
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Since Willis described ‘fatigable weakness’ in 1672, most physicians consider it as a kind of hysteria due to the inconsistent fluctuation of symptoms. Erb presented three cases of ‘bulbal palsy’ in the 1870s, and Oppenheim and Hopper considered myasthenia gravis as a disease similar to curare poisoning and as a disease induced by attack of the motor centers by intrinsic toxins, respectively. In 1903, Elliot suggested that a ‘chemical substance’ mediates the nerve impulses at synapse. However, it was not until 1921 that this was demonstrated by Loewi, who provided evidence from the famous two-frog-hearts experiment. Dale later revealed the substance to be acetylcholine, and he also suggested that myasthenia gravis is due to a problem with the motor end plate. In 1934, Walker was prompted by the resemblance between myasthenia gravis and curare poisoning to apply physostigmine, a curare-poisoning antidote, to a patient, which produced a dramatic result. Since then the use of anticholinesterase inhibitors has been adopted for standard therapeutic modality. Some prominent surgeons have also applied thymectomy as a surgical modality. The most recent focus of myasthenia gravis has been immunological. In 1960, Simpson proposed the autoimmune hypothesis, and Chang et al. showed that snake venom contained a selective antagonist of the nicotinic acetylcholine receptor, α-bungarotoxin. The immunization of rabbits with acetylcholine receptor purified from the electrical organs of electric eels by Patrick et al. induced myasthenic symptoms and signs, and these were reversed by acetylcholinesterase inhibitors. The role of the autoimmune system has led to the introduction of an immunosuppressive modality and plasma exchange to the field of clinical neurology.
Abstract
Since Willis described ‘fatigable weakness’ in 1672, most physicians consider it as a kind of hysteria due to the inconsistent fluctuation of symptoms. Erb presented three cases of ‘bulbal palsy’ in the 1870s, and Oppenheim and Hopper considered myasthenia gravis as a disease similar to curare poisoning and as a disease induced by attack of the motor centers by intrinsic toxins, respectively. In 1903, Elliot suggested that a ‘chemical substance’ mediates the nerve impulses at synapse. However, it was not until 1921 that this was demonstrated by Loewi, who provided evidence from the famous two-frog-hearts experiment. Dale later revealed the substance to be acetylcholine, and he also suggested that myasthenia gravis is due to a problem with the motor end plate. In 1934, Walker was prompted by the resemblance between myasthenia gravis and curare poisoning to apply physostigmine, a curare-poisoning antidote, to a patient, which produced a dramatic result. Since then the use of anticholinesterase inhibitors has been adopted for standard therapeutic modality. Some prominent surgeons have also applied thymectomy as a surgical modality. The most recent focus of myasthenia gravis has been immunological. In 1960, Simpson proposed the autoimmune hypothesis, and Chang et al. showed that snake venom contained a selective antagonist of the nicotinic acetylcholine receptor, α-bungarotoxin. The immunization of rabbits with acetylcholine receptor purified from the electrical organs of electric eels by Patrick et al. induced myasthenic symptoms and signs, and these were reversed by acetylcholinesterase inhibitors. The role of the autoimmune system has led to the introduction of an immunosuppressive modality and plasma exchange to the field of clinical neurology.
참고문헌 (40)
- Penn AS, "Myasthenia gravis. In Merritt’s textbook of neurology 9th ed", pp.754~ (1995), Williams & Wilkins
- Amato AA, "Neuromuscular junction disorders and myopathies. In: Manual of neurologic therapeutics. 7th ed", pp.260~ (2004), Lippincott Williams & Wilkins
- 칼 지머, "영혼의 해부. 초판", pp.19~ (2007), 북하우스
- Pascuzzi RM. V, "The history of myasthenia gravis. In: Myasthenia gravis and myasthenic syndromes. In. Neurologic clinics", pp.231~232 (1994), WB Saunders Company
- Wilks S, "On cerebritis, hysteria, and bulbar paralysis, as illustrative of arrest function of the cerebrospinal centers", Guy’s Hospital Report, 22, pp.7~55 (1877)
- Pearce JM, "Mary Broadfoot Walker (1988-1974): a historic discovery in myasthenia gravis", Eur Neurol, 53, pp.51~53 (2005)
- Elliott TR, "The innervation of the bladder and urethra", J Physiol, 35, pp.367~445 (1907)
- "Nobel Foundation.Available from:URL:"[URL]
- "The Plants Database. National Plant Data Center, Baton Rouge, LA 70874-4490 USA"[URL]
- "The Nobel prize in physiology or medicine"[URL]
- "The Nobel prize in physiology or medicine"[URL]
- Fatt P, "An analysis of the end-plate potential recorded with intracellular electrode", J Physiol, 115, pp.320~370 (1951)
- Nicholls JG, "How acetylcholine gives rise to current at the motor end-plate", J Physiol, 578, pp.621~622 (2007)
- Fatt P, "Spontaneous subthreshold activity at motor nerve endings", J Physiol, 117, pp.109~128 (1952)
- Augustine GJ, "Quantal transmitter release and the foundations of presynaptic physiology", J Physiol, 578, pp.623~625 (2007)
- "The Nobel prize in physiology or medicine"[URL]
- Pascuzzi RM. V, "The history of mysthenia gravis. In Myasthenia gravis and myasthenic syndromes. In. Neurologic clinics", pp.236~ (1994), WB Saunders Company
- Edgeworth HI, "A report of progress on the use of ephedrine in a case of myasthenia gravis", JAMA, 94, pp.1136~ (1930)
- Pearce JM, "Mary Broadfoot Walker (1888-1974): a historic discovery in myasthenia gravis", Eur Neurol, 53, pp.51~53 (2005)
- 강건일, "이야기 현대약발견사", pp.216~ (1997), 까치
- Pearce JM, "Mary Broadfoot Walker (1888-1974): a historic discovery in myasthenia gravis", Eur Neurol, 53, pp.51~53 (2005)
- Keesey JC, "Contemporary opinion about Mary Walker: a shy pioneer of therapeutic neurology", Neurology, 51, pp.1433~1439 (1998)
- "Pathologisch-anatomischer Beitrag zur Erb’schen Krankheit (Myasthenia gravis)", Neurologisches Centralblatt, 20, pp.597~601 (1901)
- Kirschner PA, "Alfred Blalock and thymectomy for myasthenia gravis", Ann Thorac Surg, 43, pp.348~349 (1987)
- Pascuzzi RM. V, "The history of mysthenia gravis. In. Myasthenia gravis and myasthenic syndromes. In. Neurologic clinics", pp.235~ (1994), WB Saunders Company
- Simpson JA, "Myasthenia gravis. a new hypothesis", Scot Med J, 4, pp.419~436 (1960)
- Riggs AJ, "“Guess it right,” John A. Simpson, and myasthenia gravis. the role of analogy in science", Neurology, 62, pp.465~467 (2004)
- Lindstrom J, "Experimental autoimmune myasthenia gravis", J Neurol Neurosurg Psychiatry, 43, pp.568~576 (1980)
- Strauss AJ, "Immunofluorescence demonstration of muscle binding complement-fixing serum globulin fraction in myasthenia gravis", Proc Soc Exp Biol Med, 105, pp.184~191 (1960)
- Chang CC, "Isolation of neurotoxins from the venom of Bungarus multicintus and their modes of neuromuscular blocking action", Arch Int Pharmacodyn Ther, 144, pp.241~257 (1963)
- Fambrough DM, "Neuromuscular junction in myasthenia gravis: decreased acetylcholine receptors", Science, 182, pp.293~295 (1973)
- Patrick J, "Autoimmune response to acetylcholine receptor", Science, 180, pp.871~872 (1973)
- Lennon VA, "Experimental autoimmune myasthenia; a model of myasthenia gravis in rats and guinea pigs", J Exp Med, 141, pp.1365~1375 (1975)
- Engel AG, "Immune complexes (IgG and C3) at the motor end platein myasthenia gravis: ultrastructural and light microscopic localization and electrophysiological correlations", Mayo Clin Proc, 52, pp.267~280 (1977)
- Toyka KV, "Myasthenia gravis: passive transfer from man to mouse", Science, 190, pp.397~399 (1975)
- Simon HE, "Myasthenia gravis. Effect of treatment with anterior pituitary extract", JAMA, 104, pp.2065~2066 (1935)
- Bergström K, "The effect of thoracic duct lymph drainage in myasthenia gravis", Eur Neurol, 9, pp.157~167 (1973)
- "Plasmapheresis", BMJ, 1, pp.1011~1012 (1978)
- Pinching AJ, "Remission of myasthenia gravis following plasma-exchange", Lancet, 2, pp.1373~1376 (1976)