Botulism
2000; Wiley; Volume: 23; Issue: 7 Linguagem: Inglês
10.1002/1097-4598(200007)23
ISSN1097-4598
AutoresRicardo A. Maselli, Nandini Bakshi,
Tópico(s)Parkinson's Disease Mechanisms and Treatments
ResumoMuscle & NerveVolume 23, Issue 7 p. 1137-1144 Case Report Botulism Ricardo A. Maselli MD, Ricardo A. Maselli MD Department of Neurology, University of California Davis, 1515 Newton Court, Room 502, Davis, California 95616-4859, USASearch for more papers by this authorNandini Bakshi MD, Nandini Bakshi MD Department of Neurology, University of California Davis, 1515 Newton Court, Room 502, Davis, California 95616-4859, USASearch for more papers by this author Ricardo A. Maselli MD, Ricardo A. Maselli MD Department of Neurology, University of California Davis, 1515 Newton Court, Room 502, Davis, California 95616-4859, USASearch for more papers by this authorNandini Bakshi MD, Nandini Bakshi MD Department of Neurology, University of California Davis, 1515 Newton Court, Room 502, Davis, California 95616-4859, USASearch for more papers by this author First published: 30 June 2000 https://doi.org/10.1002/1097-4598(200007)23:7 3.0.CO;2-7Citations: 41AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Abstract Early diagnosis of botulism is essential for effective treatment. Electrophysiologic testing can be of major help to establish a prompt diagnosis, but the classic electrodiagnostic features of botulism are often elusive. Decrement or increment of compound muscle action potential (CMAP) amplitudes to slow or fast rates of nerve stimulation are often unimpressive or totally absent. Reduction of CMAP amplitudes, denervation activity, or myopathic-like motor unit potentials in affected muscles are found more frequently but they are less specific. In general, the electrophysiologic findings taken together suggest involvement of the motor nerve terminal, which should raise the possibility of botulism. The case reported here illustrates a common clinical presentation of botulism. This study emphasizes realistic expectations of the electrodiagnostic testing, the differential diagnosis, and the potential pitfalls often encountered in the interpretation of the electrophysiologic data. © 2000 American Association of Electrodiagnostic Medicine. Muscle Nerve 23: 1137–1144, 2000 REFERENCES 1Arnon SS. Infant botulism. In: RD Feigin, JD Cherry, editors. Textbook of pediatric infectious diseases, 3rd ed. Philadelphia: Saunders; 1992. 2Bark IC, Wilson MC. Regulated vesicular fusion in neurons: snapping together the details. Proc Natl Acad Sci USA 1994; 91: 4621– 4624. 3Barohn RJ, Jacson CE, Rogers SJ, Ridings LW, McVey AL. Prolonged paralysis due to nondepolarizing neuromuscular blocking agents and corticosteroids. Muscle Nerve 1994; 17: 647– 654. 4Bird SJ, Macking GA, Schotland DL, Raps EC. Acute myopathic quadriplegia: a unique syndrome associated with vecuronium and steroid treatment. Muscle Nerve 1992; 15: 1208. 5Carsons S. The association of malignancy with rheumatic and connective tissue diseases. Semin Oncol 1997; 24: 360– 372. 6Cherington M. Electrophysiologic methods as an aid in the diagnosis of botulism: a review. Muscle Nerve 1982; 5(suppl): S28– S29. 7Cornblath DR, Sladky JT, Sumner AJ. Clinical electrophysiology of infantile botulism. Muscle Nerve 1983; 6: 448– 452. 8Danon MJ, Carpenter S. Myopathy with thick filament (myosin) loss following paralysis with vecuronium during steroid treatment. Muscle Nerve 1991; 14: 1131– 1139. 9Davis JB, Mattman LH, Wiley M. Clostridium botulinum in a fatal wound infection. JAMA 1951; 146: 646– 648. 10Davis LE. Botulinum toxin—from poison to medicine. West J Med 1993; 158: 25– 29. 11Dodds KL. Worldwide incidence and ecology of infant botulism. In: AHW Hauschild, KL Dodds, editors. Clostridium botulinum: ecology and control in foods. New York: Marcel Dekker; 1992. 12Dyck PJ, Johnson WJ, Lambert EH, O'Brien PC. Segmental demyelination secondary to axonal degeneration in uremic neuropathy. Mayo Clin Proc 1971; 46: 400– 431. 13Fakadej AV, Gutmann L. Prolongation of post-tetanic facilitation in infant botulism. Muscle Nerve 1982; 5: 727– 729. 14Fross RD, Daube JR. Neuropathy in the Miller Fisher syndrome: clinical and electrophysiologic findings. Neurology 1987; 37: 1493– 1498. 15Gansel M, Penner R, Dreyer F. Distinct sites of action of clostridial neurotoxins revealed by double-poisoning of mouse nerve terminals. Pflugers Arch 1987; 409: 533– 539. 16Guttman L, Pratt L. Pathophysiologic aspects of human botulism. Arch Neurol 1976; 33: 175– 179. 17Hatheway CL. Botulism: the present state of the disease. Curr Top Microbiol Immunol 1995; 195: 55– 75. 18Hauschild AHW. Epidemiology of human foodborne botulism. In: AHW Hauschild, KL Dodds, editors. Clostridium bolutinum: ecology and control in foods. New York: Marcel Dekker; 1992. 19Hirano M, Ott BR, Raps EC. Acute quadriplegic myopathy: a complication of treatment with steroids, nondepolarizing blocking agents or both. Neurology 1992; 42: 2082– 2087. 20Ismail MK, Midani HA. Post-exercise facilitation in myasthenia gravis [abstract]. Muscle Nerve 1998; 21: 1600. 21Lambert EH, Engel AG, Cherington M. End-plate potentials in human botulism [abstract]. Excerpta Medica 1974; 334: 65. 22Lucchinetti CF, Kimmel DW, Lennon VA. Paraneoplastic and oncologic profiles of patients seropositive for type 1 antineuronal nuclear autoantibodies. Neurology 1998; 50: 652– 657. 23MacDonald L, Rutherford GW, Friedman SM, Dietz JR, Kaye BR, McKinley GF, Tenney JH, Cohen ML. Botulism and botulism-like illness in chronic drug abusers. Ann Intern Med 1985; 102: 616– 618. 24Maddison P, Newsom-Davis J, Mills KR. Distribution of electrophysiological abnormality in Lambert–Eaton myasthenic syndrome. J Neurol Neurosurg Psychiatry 1998; 65: 213– 217. 25Mandler R, Maselli RA. Single fiber EMG in wound botulism. Muscle Nerve 1996; 19: 1171– 1173. 26Maselli RA. Pathogenesis of human botulism. Myasthenia gravis and related diseases. Ann NY Acad Sci 1998; 841: 122– 139. 27Maselli RA. Electrodiagnosis of disorders of neuromuscular transmission. Myasthenia gravis and related diseases. Ann NY Acad Sci 1998; 841: 696– 711. 28Maselli RA, Burnett ME, Tonsgard JH. In vitro microelectrode study of neuromuscular transmission in a case of botulism. Muscle Nerve 1992; 15: 273– 276. 29Maselli RA, Ellis W, Mandler RN, Sheikh F, Senton G, Knox S, Salari-Namin H, Agius M, Wollman RL, Richman DP. Cluster of wound botulism in California: clinical, electrophysiologic, and pathologic study. Muscle Nerve 1997; 20: 1284– 1295. 30Maselli RA, Wollman RL, Leung C, Distad B, Palombi S, Richman DP, Salazar-Grueso EF, Roos RP. Neuromuscular transmission in amyotrophic lateral sclerosis. Muscle Nerve 1993; 16: 1193– 1203. 31Midura TF, Arnon SS. Infant botulism: identification of Clostridium botulinum and its toxin in faeces. Lancet 1976; ii: 934– 936. 32Montecucco C, Schiavo G. Structure and function of tetanus and botulinum neurotoxins. Q Rev Biophys 1995; 28: 423– 472. 33Norris FH. Adult spinal neuron disease progressive muscular dystrophy (Aran's disease) in relation to amyotrophic lateral sclerosis. In: PJ Vinken, GW Bruyn, editors. Handbook of clinical neurology. Vol. 22. New York: Elsevier; 1975. p 1– 56. 34Pickett J, Berg B, Chaplin E, Brunstetter MA. Syndrome of botulism in infancy: clinical and electrophysiologic study. N Engl J Med 1976; 295: 770– 772. 35Rich MM, Teener JW, Raps EC, Schotland DL, Bird SJ. Muscle is electrically inexcitable in acute quadriplegic myopathy. Neurology 1996; 46: 731– 736. 36Rivner MH, Swift TR. Electrical testing in disorders of neuromuscular transmission. In: WF Brown, CF Bolton, editors. Clinical electromyography. Newton, MA: Butterworth-Heinemann; 1993. p 625– 651. 37Sauron B, Bouche P, Cathala HP, Chain F, Castaigne P. Miller Fisher syndrome: clinical and electrophysiologic findings. Neurology 1984; 34: 351– 364. 38Sharma SK, Singh BR. Hemagglutinin binding mediated protection of botulinum neurotoxin from proteolysis. J Nat Toxins 1998; 7: 239– 253. 39Singh BR, Li B, Read D. Botulinum versus tetanus neurotoxins: why is botulinum neurotoxin but not tetanus neurotoxin a food poison? Toxicon 1995; 33: 1541– 1547. 40Tim RW, Massey JM, Sanders DB. Lambert–Eaton myasthenic syndrome (LEMS) clinical and electrodiagnostic features and response to therapy in 59 patients. Myasthenia gravis and related diseases. Ann NY Acad Sci 1998; 841: 823– 826. 41Vincent A, Li Z, Hart A, Barrett-Jolley R, Yamamoto T, Burges J, Wray D, Byrne N, Molenaar P, Newsom-Davis J. Seronegative myasthenia gravis: evidence for plasma factor(s) interfering with acetylcholine receptor function. Ann NY Acad Sci 1993; 681: 529– 538. 42Weber JT, Goodpasture HC, Alexander H, Werner SB, Hatheway CL, Tauxe, RV. Wound botulism in a patient with a tooth abscess: case report and review. Clin Infect Dis 1993; 16: 635– 639. Citing Literature Volume23, Issue7July 2000Pages 1137-1144 ReferencesRelatedInformation
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