POSTTRAUMATIC SYNDROME

POSTTRAUMATIC SYNDROME

36 after extraction of A substance, and the smaller then appear similar to the fine filaments of the I-Z region. If fibrils previously treated with tr...

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36 after extraction of A substance, and the smaller then appear similar to the fine filaments of the I-Z region. If fibrils previously treated with trypsin are extracted in this way, " ghost fibrils are left which easily pass into solution ; or if the extraction of A substance is followed by the removal of actin, the organised fibril structure disappears. Hanson and Huxley, then, present a picture of discontinuous distribution of myosin filaments along the length of the myofibril. These filaments are aranged in hexagonal arrays across the fibril, with the actin filaments lying between them and forming the continuous element of each sarcomere. This conception of the structure of the muscle seems consistent with established biochemical knowledge. If it can be related to the contraction mechanism, it will be an important advance. "

PREPARATIONS OF DEOXYCORTONE

ONE of the chief aims in treating Addison’s disease must be to prevent the depletion of salt from the body which results from the lack of the salt-retaining fraction of the adrenal cortical secretion. This is sometimes achieved simply by giving extra salt. Usually, however, the patient needs also to have a hormonal preparation which enables him to retain the salt ; and cortisone, although a valuable adjunct to the treatment of Addison’s disease, is not a potent salt retainer. This function is covered by the synthetic steroid, deoxycortone, which, since it was introduced in 1938,1 has been put out in several forms. The acetate in oily solution has to be injected each day or on alternate days ; dissolved in propylene glycol it can be taken sublingually, but this is a rather extravagant way of giving the drug. Pellets of the acetate can be implanted ; and a single implant usually lasts six months or longer. The glucoside of deoxycortone is water-soluble ; this form is useful in meeting the occasional need for rapid action. New esters may now supersede the others in the maintenance treatment of Addison’s disease.23 These are aqueous suspensions of microcrystals of the trimethylA acetate or of the phenylacetate of deoxycortone. single injection of the trimethylacetate lasts five to six weeks and releases about a fortieth of its dose daily. Of 45 patients followed for six months, most required an injection of 60 mg. monthly ; the range of doses was 15-90 mg. monthly.3 The effects were similar to those of the acetate, but obviously the long-acting microcrystalline preparation is very much more convenient. At least those patients who are having daily injections of deoxycortone acetate will be glad to change to the new preparation if they can be maintained with it. In regulating the dose it is worth recalling that the effect of a given dose of deoxycortone probably depends on the amount of salt the patient is receiving.4 POSTTRAUMATIC SYNDROME MOST of those familiar with the methods commonly used for reabling patients who have had a head injury would agree that the posttraumatic syndrome with headache, giddiness, and various psychological symptoms has become less common, and that, in the absence of serious brain damage, it generally indicates inadequate supervision and reablement before the patient has resumed work. Professor McConnell,5 however, takes a different view. For many years it has been his practice to operate on patients who are not getting on well after a head injury, whatever their symptoms. Of 75 such cases " 20 complained of headache, 7 of headache and Simpson, S. L. Lancet, 1938, ii, 557. Sorkin, S. Z., Soffer, L. J. Metabolism, 1953, 2, 404. Thorn, G. W., Jenkins, D., Arons, W. L., Frawley, T. F. J. clin. Endocrin. 1953, 13, 957. 4. Relman, A. S., Schwartz, W. B. Yale J. Biol. Med. 1952, 24, 540. 5. McConnell, A. A. Brain, 1953, 76, 473. 1. 2. 3.

and 38 of headache, giddiness and some of mental disability ... many were depressed 10 were compensation cases with litigation out-a standing." In 65 of these 75 cases he found at operation =an accumulation of fluid in the subdural space, and where this was found " the results of its removal were‘= uniformly good even when the symptoms had persisted for years." At operation the brain was often tight and bulged into the trephine opening. In such cases the subdural " fluid was not at first obvious ; but if a " raspatory was slipped under the dura in several directions the fluid would well up and the brain would relax. = Professor McConnell thinks that the fluid he finds originates in a cerebrospinal-fluid leak into the subdural space ; and in support of this view he has demonstrated air in the subdural space twenty-four hours after air encephalography. He now dispenses, however, with air encephalography in these cases and makes burr-holes in them all. Professor McConnell put forward these opinions in 1941 6 ; but they have not been widely accepted, and this latest account contains little fresh evidence. Thus there is no detailed comparison of the frequency of subdural air after encephalography in traumatic and in non-traumatic cases. A puzzling feature is the almost constant finding of a tight brain, which is at variance with the experience of other surgeons ; and one wonders what anaesthesia was used. The dramatic cure which McConnell reports in 9 out of 10 compensation cases might testify more to his personality than to his operation, especially as the wounds were reopened as often as necessary if the symptoms recurred. The nature and volume of the fluid is unfortunately reported for only a few cases in which the protein content was very high, and it is not clear whether these cystic collections were found in the early or in the late cases. There are many doubts about the mechanism of some of the postconcussional symptoms ; and evidently, when they have been allowed to develop, they can be cured in many different ways. In this type of case the assessment of separate remedies is extremely difficult.

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PROLONGED GENERALISED VACCINIA

GENERALISED vaccinia is a rare complication of primary vaccination. In England and Wales in 1952, it apparently arose in 1 in 20,000 primary vaccinations.’ Its incidence is much greater in people with skin disease, especially eczema, than in those with healthy skins. In the latter the secondary lesions of generalised vaccinia mature in the same way as the primary lesion, but rather more rapidly owing to increasing formation of antibody; thus all the lesions tend to regress simultaneously. This is " typical generalised vaccinia." The secondary lesions are undoubtedly viræmic metastases, which become established as a result of unusually poor capacity for antibody formation. Hall, Cunliffe, and Dudgeon 8 now present the pathological findings of an extreme case, already reported by Laurance et awl. in which there was virtually complete failure of specific antibody formation. The result was numerous scattered secondary vaccinal lesions on the skin which did not heal, became ulcerated, and spread to become large deep sores. Ultimately the patient died; and numerous necrotic foci up to 2 mm. in diameter were found in the lungs, liver, kidneys, adrenals, and pancreas, but not in the spleen. Although no inclusion bodies were found in these foci, there was every reason to regard them 6. J. Neurol. Psychiat. 1941, 4, 237. 7. Report of the Ministry of Health, 1952. Part II : On the State of the Public Health. H.M. Stationery Office, 1953. 8. Hall, G. F. M., Cunliffe, A. C., Dudgeon, J. A. J. Path. Bact. 1953, 66, 25. 9. Laurance, B., Cunliffe, A. C., Dudgeon, J. A. Arch. Dis. Childh. 1952 27, 482