YOUNG VISITORS

YOUNG VISITORS

222 TREATMENT OF RETROBULBAR NEURITIS WITH CORTICOTROPHIN have shown1 that when patients with retroSIR,-We bulbar neuritis are treated with a 30-day c...

141KB Sizes 2 Downloads 65 Views

222 TREATMENT OF RETROBULBAR NEURITIS WITH CORTICOTROPHIN have shown1 that when patients with retroSIR,-We bulbar neuritis are treated with a 30-day course of corticotrophin (40 units daily intramuscularly) their initial recovery is quicker and more complete than that of untreated controls. The study only covered the first 30 days, but we did notice that in the second half of the treatment period the control group was closing the gap. We now have the results for each treated and control patient, 12 months from the beginning of the study. Table I shows the visual acuity (Jaeger scale) of the treated and control groups on entry into the double-blind trial (day 1), on day 30, and at 12 months. There were 25 patients in each group. Table II shows the proportion of

TABLE II-PROPORTIONS OF PATIENTS IN TREATED AND CONTROL GROUPS WITH NORMAL VISION

D

TABLE

=

Difference.

S.B.D.

=

Standard

error

of difference.

OF VISUAL ACUITIES IN TREATED AND CONTROL GROUPS

I-FREQUENCY DISTRIBUTION

tical significance, we have been impressed by the fact that 4 patients in the control group remain virtually blind in the affected eye, and 3 of these have severe optic atrophy. Clinical empiricism suggests to us that this is a significant fact. Until further evidence accumulates to the contrary, it will certainly be our policy to give corticotrophin for acute relapses in multiple sclerosis-and for acute retrobulbar neuritis particularly, if the presenting visual acuity is J16 or worse. It only remains to be added that treatment should be given as early as possible after the affection

begins.

F/c finger-counting. p/1 = perception of light.

We are indebted to Dr. J. T. Boyd of the M.R.C. Statistical Research Unit for his help. University Department of Neurology, M. D. RAWSON Royal Infirmary,

L. A. LIVERSEDGE.

Manchester M13 9WL.

patients in the treated and control groups with normal vision on day 1 and on days 8, 15, 21, and 30, and at 12 months. In the treated group 24 of the 25 patients had visual acuities of J1 or J2 12 months after the onset. The remaining patient has always been difficult to assess, and has given rather variable results, with curious changes of visual acuity ranging between Jland J16. In the control group 20 patients had achieved Jl or J2 12 months after the onset. Of the remaining 5, 3 had severe optic atrophy and were only able to perceive light, or at most count firigers. The other 2 had visual acuities of J16 and J12. All the patients with a persistent visual defect at the end of 12 months had had visual acuities of J16 or worse on entry to the trial. As in our paper,1 we submitted our results to Dr. J. T. Boyd, of the M.R.C. Statistical Research Unit, who made

thefollowing

comments:

"

At the end of twelve months the percentage difference between control and treated groups does not reach a level of technical significance. This also applies when the patients who entered the trial with a visual acuity of J. 16 or worse are considered separately. These analyses do not mean that the 16-20% difference between the groups at 12 months has to be automatically dismissed as a chance effect. They do, however, show that present data cannot exclude the latter possibility, and hence call for caution in their interpretation. The alternative explanation, that these findings could reflect a real difference and that failure to establish’significance’ is largely due to small numbers, may seem attractive, but again cannot be established on present data."

Our results after a 12-month period do not alter our previous opinion that corticotrophin exerts a favourable effect on the acute demyelinating episode. Its effect in the long term remains, of course, uncertain. Corticotrophin certainly seems to have no value in preventing relapses in multiple sclerosis.2 Despite the lack of statis1.

Rawson,

M.

D., Liversedge,

L. A.,

Goldfarb, G. Lancet, 1966, ii,

1044. 2.

Millar, J. H. D., Vas, C. J., Noronha, Rawson, M. D. Lancet, 1967 ii, 429.

M. I.,

Liversedge, L. A.,

YOUNG VISITORS battle for free visiting of children in hospital SiR,ņThe to have been won. May I suggest that next appears largely we should press for fewer restrictions on the visiting of adults in hospital by their children ? R. B. WOODD-WALKER. London W.2.

CARDIAC TRANSPLANTATION

SIR,-Your leading article (May 10, p. 973) poses the question of the benefit of heart transplantations and requests a period of sombre reflection. May I offer some comments from the field of technology ? The thrombosis seen after the implantation of circulatory-assistance devices can be prevented. Unfortunately, the impression prevails within the medical community that all materials, with the possible exception of amber vessels, are thrombogenic. However, in the light of experiments recently reported to the Electrochemical Society and of new electrophysiology concepts, we physicians may have to change our mind about the obligatory thrombogenecity of surgical prostheses. It seems that high voltage technologists have found a procedure by which intravascular thrombosis

can

be avoided.

High-voltage technology affects biological tissues: " If we calculate the potential gradient across the membrane [biological transmembrane potential 50 mV; membrane thickness 50A] we find that it is of the order of 100,000 volts per cm, which can readily be appreciated as involving considerable electrostatic forces ".1 From technology" it is known that virtually any organic material " holds electric charges and inhibits their migration once the material has been " pre-stressed 1.

Suckling,

E. E.

Bioelectricity;

"

with voltages of the

p. 122. New

York, 1961.