Contribution to the Pathologic Physiology of Botulism

Abstract

4. Pain of Coronary Thrombosis.-Rapid blocking of a large coronary vessel, almost always thrombosis of a sclerosed artery, is accompanied usually by long continued heart pain of very severe nature, not relieved by rest, digitalis or the nitrites, and requiring repeated doses of morphin. The seat of the pain is generally precordial or substernal, but now and then it is abdominal, particularly epigastric, or right or left hypochondrial, and in such instances it is likely to be confused with acute abdominal conditions, such as gallstone colic or perforation of a peptic ulcer. Recov¬ ery may .occur in spite of the extreme severity of the pain and the gravity of the condition.5. Aortic Pain.-In aortic disease of syphilitic ori¬ gin-that is, syphilitic aortitis and aneurysm-there is a fairly characteristic dull high substernal ache, some¬ times increased to a sharper pain and even radiating, but not paroxysmal. This does not respond to digitalis, rest or nitroglycerin, but tends to melt away under antisyphilitic treatment. It is likely that potassium iodid has gained some of its great reputation through its action in this type of case. It must be remembered that in syphilitic aortitis, in addition to the aortic pain, involvement of the coronary arteries may give rise apparently to the typical paroxysmal pain of coronary disease.6. Pains of Pericarditis (and of hepatic engorge¬ ment).-Finally, there are also the transient pains of acute fibrinous pericarditis (and the epigastric and right hypochondrial distress of engorgement of the liver due to congestive cardiac failure) which are generally easily recognized.Mention should be made of the probable coexistence in various cases of pains of different type ; for exam¬ ple, the fatigue pain of mitral stenosis and the pain of the nervous heart in a neurotic woman with advanced mitral stenosis, or the aortic pain of syphilitic aortitis and the fatigue pain of aortic régurgitation, perhaps also the paroxysmal pain of angina pectoris in a middle-aged man with cardiovascular syphilis. (In syphilitic aortitis there is frequent involvement of the mouths of the coronary arteries.) In such cases the analysis of the pain is difficult but interesting. SUMMARY Heart pain may be thus classified: 1. Simple fatigue pain : (a) Chronic hypertension. (b) Aortic stenosis or régurgitation. (c) Mitral stenosis. (d) Pulmonic stenosis-congenital heart dis¬ ease. (e) Adherent pericarditis. (/) Paroxysmal tachycardia or paroxysmal auricular fibrillation or flutter.(g) Permanent auricular fibrillation or flutter with high ventricular rate. (h) Permanent coronary narrowing due to arteriosclerosis.2. Nervous heart pain, including effort syndrome. 3. Paroxysmal heart pain (probably of coronary disease or irritability), the so-called true angina pectoris.4. Pain of coronary thrombosis. 5. Aortic pain, of syphilitic aortitis and aneurysm. 6. Pain of pericarditis. Frequently, combinations of these factors occur.

Properties and use of botulinum toxin and other microbial neurotoxins in medicine.

“…Botulinum toxin is toxic to all vertebrates through weakening of skeletal muscle, and death may come about through paralysis of the muscles of respiration. Van Ermengen (226) considered that the toxin acted on the central nervous system, but it was later shown that the action is peripheral rather than central (50,60). Most early studies on the mechanism of action of botulinum toxin were carried out with type A crystalline toxin (29,33,79).…”

The botulinal, tetanal, and enterostaphylococcal toxins: A review

“…50. 01, 59 The details of this early work have been reviewed. 177 By 1955 certain salient features of the mechanism and site of action of botulinal toxin had been established.…”

Protein Structure and Clinical Problems

“…The pharmacology of the toxin has been investigated by many workers (for example, Edmunds and Long, 1923;Dickson and Shevky, 1923;Bishop and Bronfenbrenner, 1936;Guyton and MacDonald, 1947), and ithasbeenestablished that the site of action is at the neuromuscular junction. In an investigation of the various factors involved in the paralysis, Burgen, Dickens, and Zatman (1948) utilized the isolated rat phrenic nerve diaphragm preparation of Bulbring (1946).…”