204
hoped that these results will be published as soon as possible so that transfusion centres and clinicians can know the risks involved and the precautions needed to prepare this very valuable blood component. Laboratory, Regional Transfusion Laboratory L A. A DERRICK DERRIC TOVEY I-.L. A. 1 OVEY Bridle Path, S. M. MANOHITHARAJAH. Leeds LS15 7TW.
FETAL/MATERNAL INCOMPATIBILITY SIR,-Mr. Sophian (Jan. 1, p. 36) seems to have misunderstood our suggestions on the interpretation of data relating to pre-eclamptic toxaemia in twin pregnancies and zygosity. Of course, as he states, there is direct evidence that toxaemia occurs in monozygous twin pregnancies. All that the data published suggested was that pre-eclampsia was more common in twin pregnancies when the twins were dizygous than when they were monozygous. In theory, the frequency of pre-eclamptic toxxmia should be the same in monozygous twin and in single-fetus pregnancies. We hope, at a later date, to provide supporting evidence for this from accumulating data from Ankara. A final point may be of interest. So far we have no evidence from Alexandria or Ankara that hydramnios is more common in women related to their husbands than in those unrelated. M.R.C. Population Genetics Unit, Old Road, Headington, Oxford OX3 7LE.
ALAN C. STEVENSON.
GLYCEROL IN ACUTE CEREBRAL INFARCTION
SIR,-We should like to thank Dr. Tarsy (Dec. 11, 1322) for his interest in our paper and respond with the following information. It seems that acute cerebral infarction is regularly associated with cerebral cedema, the degree of which is variable. Previously published experimental data from this centre support this view. 1. In addition, Garcia et awl.3 have shown swelling of perivascular astrocytic processes p.
within twenty minutes of experimental cerebral infarction induced by middle-cerebral-artery occlusion. It is probably true that only about a quarter of patients with acute cerebral infarction exhibit unequivocal clinical signs of expanding mass lesion due to cerebral oedema, such as Plum4 described, but we submit that it is not advisable to permit these signs to develop. Regional cerebral cedema is not necessarily reflected by measurement of cerebrospinalfluid pressure at the lumbar level. 5,6 Brock7 recently stressed the importance of regional oedema with localised increases in tissue perfusion pressure which may exist without any increase of the c.s.F. pressure. Reduction of these pressure gradients may be expected to greatly increase cerebral blood-flow in the zones of oedema. We emphasised the fact that it is logical to try to reduce the increased tissue perfusion and regional cerebral cedema by glycerol therapy, which has been shown to increase the regional blood-flow in the area of infarction in patients with recent stroke.a
appearing
Teraura, T., Meyer, J. S., Sakamoto, K., Hashi, K., Marx, P., Sterman-Marinchesu, C., Shinmaru, S. J. Neurosurg. 1971 (in the press). 2. Meyer, J. S., Fukuuchi, Y., Shimazu, K., Ohuchi, T., Ericcson, A. D. Stroke (in the press). 3. Garcia, J. H., Dodson, R. F., Hashi, K., da Cunha, B. F. Abstract of Scientific Communication presented at the Annual Meeting 1.
of the American Association of Neuropathologists, 1971. 4. Plum, F. Proc. Ass. Res. nerv. Dis. 1966, 41, 318. 5. Plum, F. in Cerebral Vascular Diseases: 7th Conference (edited by J. Moosy and R. Janeway); p. 52. New York, 1971. 6. Ng, L. K. Y., Nimmanitya, J. Stroke, 1970, 1, 158. 7. Brock, M. in Brain Hypoxia (edited by J. B. Brierley and B. S. Meldrum); p. 14. New York, 1971. 8. Mathew, N. T., Meyer, J. S., Bell, R. L., Johnson, P. C., Neblett, C. R. Unpublished.
Regarding the recommendation
of controlled trials bv
double-blind therapeutic trial of glycerol in patients with cerebral infarction is in progresss in our centre. In order to respond to his letter the code was broken for the first 28 patients (14 on glycerol, 14 on placebo) and the results were found to be near statistical significance in favour of the drug (p < 03). Additional patients are being admitted to this double-blind study.
Dr. Tarsy,
we
agree, and
a
Department of Neurology, Baylor College of Medicine, Texas Medical Center, Houston, Texas 77025, U.S.A.
NINAN T. MATHEW N1EYER JOHN JOHN SS. MEYER VICTOR M. RIVERA.
LEVODOPA AND PSORIASIS SIR,- The controversy 1-4 around the treatment of psoriasis with fusidic acid and the known difficulty in the management of this variable illness5 prompts us to report another possible approach which, in view of the preliminary results, warrants further evaluation. The association of seborrhoeic dermatitis with parkinsonism has long been known .6Levodopa is now recognised as the best available treatment for parkinsonism.’ The early investigation of this drug revealed a clear improvement in the seborrhoea as well as in the neurological symptoms. 7 ,8 Objective records of this finding were provided by many authors.9-11 Other skin effects of levodopa were also observed, such as the rare production of alopecia.12 Levodopa, however, was of no therapeutic value in acne vulgarise In 1970, we first reported 14 that levodopa used for neurological reasons produced a striking improvement in the accompanying psoriasis in two cases of parkinsonism. We have since confirmed this finding in a further 5 patients who have both diseases. For the past three years we have preferred to treat parkinsonian patients with a combination of levodopa and Ro 4-4602, a peripheral dopa-decarboxylase inhibitor. This combination has achieved significant reductions in the total daily dose of levodopa, in peripheral side-effects, and in the time necessary to obtain satisfactory results without loss of overall clinical e-,"Rcacy.15 Recently we had the occasion to treat with this combination a 65-year-old woman with parkinsonism who for the past six years had psoriatic eruptions on the face, elbows, knees, or ankles, The last episode affecting the dorsal and lateral aspects of both feet had been present continuously and without change for eight months when treatment began. Levodopa and Ro 4-4602 doses were gradually raised over two weeks to 600 mg. levodopa and 200 mg. Ro 4-4602 daily and then continued at the same doses without side-effects. During this whole period of observation in hospital, all previous topical treatments, stopped one month before, were prohibited. The patient was not informed that we were also observing the effect of levodopa on the psoriasis. Within sixteen days the psoriatic lesions on both feet and smaller lesions in the nasal area and on one elbow completell
12. 13.
Voetmann, E. Lancet, Aug. 21, 1971, p. 435. Hall-Smith, P. ibid. Sept. 4, 1971, p. 544. Levantine, A. V., Baker, H. ibid. Sept. 18, 1971, p. 661. Jackson, N. ibid. Sept. 25, 1971, p. 712. Dahl, M. G. C. Br. med. J. 1971, iii, 234. Pochi, P. S. S., Strauss, J. S., Mescon, H. J. invest. Derm. 1962, 38, 145. Barbeau, A. Can. med. Ass. J. 1969, 101, 791. Yahr, M. D. Trans. Am. Neurol. Ass. 1968, 93, 56. Burton, J. L., Shuster, S. Lancer, 1970, ii, 19. Harville, D. D., Appenzeller, O. Arch. Derm. 1971, 103, 492. Glick, A. W., Mones, R., Wilentz, J. M., Berger, B. Cutis, 1971 8, 26. Marshall, A., Williams, M. J. Br. med. J. 1971, ii, 47. Burton, J. L., Libman, L. J., Hall, R., Shuster, S. Lancet, 1971.
14.
Barbeau,
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
370. A. Can. med. Ass. J. 1970, 103, 824. 15. Barbeau, A., Gillo-Joffroy, L., Mars, H. Clin. Pharm. Ther. 1971
12, 353.