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BARBITURATE COMA AND BLISTERS
904 What is not clear from the studies carried out so far on nocturnal angina is whether the relation with dreaming sleep is due to a possible increase in the work of the heart occasioned by surges of tachycardia and rises in pressure during dreams, or whether there is general sympathetic discharge at this time causing alterations in the coronary circulation itself or in the metabolic processes in the myocardium. Dr. Turner is quite right in drawing attention to the implication for hypnotic therapy and its cessation on leaving hospital. Although some of the P-blockers seem to be associated with increased dreaming (or at least awareness of dreams), it seems probable that by mitigating the cardiovascular effects of dreaming they might be beneficial during nocturnal angina. This may not always be so, however, for in some patients nocturnal angina is clearly associated with episodes of left ventricular failure at night, and -blockade in this situation would, of course, be harmful unless digitalis had been given beforehand. Radcliffe Infirmary, Oxford OX2 6HE.
PETER SLEIGHT
CLINICS FOR THE TREATMENT OF EPILEPSY AND CONVULSIONS SIR,-In a debate in the House of Lords,l Lord Aberdare stated in reply to a question concerning the Reid report on people with epilepsy that professional opinion was by no means unanimous over the question of providing special epilepsy clinics. There seem to be certain misunderstandings about such clinics, especially about whether they should be diagnostic or follow-up, and anxiety has been expressed to me over the referral to such clinics of patients who have had their first fit, it being felt that such patients are better seen at the general outpatient clinics of physicians, neurologists, and pxdiatricians. Doubts are also expressed about the feasibility of multidisciplinary clinics as envisaged in the Reid report. I think it is important that the protagonists in the discussion on special epilepsy clinics should publish their views before the impending discussions about implementation of the Reid report, and that some figures should be provided in support of these views. I have been in charge of an epilepsy clinic, mainly for " adults, for about 18 years, and I have held a convulsions clinic " in a children’s hospital for some years, though I am not a pxdiatrician. This latter clinic has recently become multidisciplinary, my colleagues being a consultant poediatrician particularly interested in neurology, a consultant in developmental medicine, and a consultant in subnormality. This arrangement has advantages to all concerned. A survey of patients seen at my adult clinic in 1965 showed that only 15% of 117 consecutive patients were referred by their general practitioner because of a first attack, and nearly half of them did not have epilepsy. Of the remaining cases 27% were referred by another consultant, and 39% of the cases referred by general practitioners had already seen another consultant at some time. Thus 66% of all cases had already seen another consultant because of their epilepsy. Review of the current situation at the two clinics is as follows:
It is, of course, most important to avoid attaching an incorrect label of epilepsy because of the social and psychological difficulties which face all who receive this label. It 1. Hansard
(Lords), Jan. 27, 1972, col.
485.
is of interest that a fifth of the patients referred to thetwo clinics did not appear to be suffering from epilepsy. Both clinics are " open ", and this seems essential since it is important to see some new patients. I consider that a special epilepsy clinic should be both diagnostic and
follow-up. I think that the best service to the patient with epilepsy will be provided by any doctor who is particularly interested in epilepsy, whether he be (in alphabetical order) a clinical
neurophysiologist, neurologist, neurosurgeon, paediatrician. physician, or psychiatrist, as is at present the case. 42 Westfield
Road, Edgbaston, Birmingham B15 3QG.
P.
M. JEAVONS.
BARBITURATE COMA AND BLISTERS SIR,-Another type of blister not mentioned in your editorial (April 1, p. 733) is that seen in diabetes mellitus. Clinically, they are the same as the blisters associated with barbiturates and other drugs, though they are often more serious because of an associated ischsemic limb.l Histological examination2 showed intraepidermal splitting without acantholysis, and, as in the barbiturate blister, dermal
change was slight. Although the presence of peripheral neuropathy in diabetes has been thought to be associated with these blisterswe suggested that an intraepidermal metabolic change, with associated hypoxia, might be the underlying cause, related to poor control of hyperglycxmia. The clinical similarity to the barbiturate blisters may indicate that
hypoxia is
common to
both types of blister.
Belfast City Hospital, Belfast BT9.
G. E. ALLEN.
Royal Victoria Hospital, Belfast BT12.
D. R. HADDEN.
DIARRHŒA INDUCED IN HUMANS BY GLUCAGON PLUS GASTRIN SiR,—Both glucagon and pentagastrin have been shown to stimulate intestinal secretion in dogs.44 Glucagon and pentagastrin given simultaneously by constant intravenous infusion produced an explosive cholera-like diarrhoea in
dogs. Neither glucagon nor pentagastrin had such an effect on their own.5 We have extended the study of the effect of these hormones
to human patients. Glucagon (Eli Lilly & Co.) (45 {1.g. per kg. per hr.) and pentagastrin (I.C.I.) (6 {1.g. per kg. per hr.) were given simultaneously to 3 fasting human volunteers by continu-
intravenous infusion for four hours. In the 1 patient was usually constipated) the test had to be stopped when he passed a very large loose stool. The other 2 patients passed loose, or watery, stools immediately after a meal eaten at the end of the four-hour hormone infusion. The role played by the meal is uncertain. Neither patient had diarrhaea before the test. 2 of these 3 patients were given glucagon alone in the same dose; neither had diarrhoea. Another patient with histologically proven ZollingerEllison syndrome, and known to have high blood-gastrin levels, was given an infusion of glucagon alone. This induced a profuse watery diarrhoea which was different in character and severity from his usual loose stool. Glucagon and pentagastrin may be implicated in the pathogenesis of diarrhoeas characterised by excessive intestinal secretion in man, and more particularly with certain
ous
(who
1. Allen, G. E. Practitioner, 1969, 203, 189. 2. Allen, G. E., Hadden, D. R. Br. J. Derm. 1970, 82, 216. 3. Rocca, F. F., Pereyra, E. Diabetes, 1963, 12, 220. 4. Barbezat, G. O., Grossman, M. I. Science, N.Y. 1971, 174, 422. 5. Barbezat, G. O., Grossman, M. I. Lancet, 1971, i, 1025.
PETER SLEIGHT
CLINICS FOR THE TREATMENT OF EPILEPSY AND CONVULSIONS SIR,-In a debate in the House of Lords,l Lord Aberdare stated in reply to a question concerning the Reid report on people with epilepsy that professional opinion was by no means unanimous over the question of providing special epilepsy clinics. There seem to be certain misunderstandings about such clinics, especially about whether they should be diagnostic or follow-up, and anxiety has been expressed to me over the referral to such clinics of patients who have had their first fit, it being felt that such patients are better seen at the general outpatient clinics of physicians, neurologists, and pxdiatricians. Doubts are also expressed about the feasibility of multidisciplinary clinics as envisaged in the Reid report. I think it is important that the protagonists in the discussion on special epilepsy clinics should publish their views before the impending discussions about implementation of the Reid report, and that some figures should be provided in support of these views. I have been in charge of an epilepsy clinic, mainly for " adults, for about 18 years, and I have held a convulsions clinic " in a children’s hospital for some years, though I am not a pxdiatrician. This latter clinic has recently become multidisciplinary, my colleagues being a consultant poediatrician particularly interested in neurology, a consultant in developmental medicine, and a consultant in subnormality. This arrangement has advantages to all concerned. A survey of patients seen at my adult clinic in 1965 showed that only 15% of 117 consecutive patients were referred by their general practitioner because of a first attack, and nearly half of them did not have epilepsy. Of the remaining cases 27% were referred by another consultant, and 39% of the cases referred by general practitioners had already seen another consultant at some time. Thus 66% of all cases had already seen another consultant because of their epilepsy. Review of the current situation at the two clinics is as follows:
It is, of course, most important to avoid attaching an incorrect label of epilepsy because of the social and psychological difficulties which face all who receive this label. It 1. Hansard
(Lords), Jan. 27, 1972, col.
485.
is of interest that a fifth of the patients referred to thetwo clinics did not appear to be suffering from epilepsy. Both clinics are " open ", and this seems essential since it is important to see some new patients. I consider that a special epilepsy clinic should be both diagnostic and
follow-up. I think that the best service to the patient with epilepsy will be provided by any doctor who is particularly interested in epilepsy, whether he be (in alphabetical order) a clinical
neurophysiologist, neurologist, neurosurgeon, paediatrician. physician, or psychiatrist, as is at present the case. 42 Westfield
Road, Edgbaston, Birmingham B15 3QG.
P.
M. JEAVONS.
BARBITURATE COMA AND BLISTERS SIR,-Another type of blister not mentioned in your editorial (April 1, p. 733) is that seen in diabetes mellitus. Clinically, they are the same as the blisters associated with barbiturates and other drugs, though they are often more serious because of an associated ischsemic limb.l Histological examination2 showed intraepidermal splitting without acantholysis, and, as in the barbiturate blister, dermal
change was slight. Although the presence of peripheral neuropathy in diabetes has been thought to be associated with these blisterswe suggested that an intraepidermal metabolic change, with associated hypoxia, might be the underlying cause, related to poor control of hyperglycxmia. The clinical similarity to the barbiturate blisters may indicate that
hypoxia is
common to
both types of blister.
Belfast City Hospital, Belfast BT9.
G. E. ALLEN.
Royal Victoria Hospital, Belfast BT12.
D. R. HADDEN.
DIARRHŒA INDUCED IN HUMANS BY GLUCAGON PLUS GASTRIN SiR,—Both glucagon and pentagastrin have been shown to stimulate intestinal secretion in dogs.44 Glucagon and pentagastrin given simultaneously by constant intravenous infusion produced an explosive cholera-like diarrhoea in
dogs. Neither glucagon nor pentagastrin had such an effect on their own.5 We have extended the study of the effect of these hormones
to human patients. Glucagon (Eli Lilly & Co.) (45 {1.g. per kg. per hr.) and pentagastrin (I.C.I.) (6 {1.g. per kg. per hr.) were given simultaneously to 3 fasting human volunteers by continu-
intravenous infusion for four hours. In the 1 patient was usually constipated) the test had to be stopped when he passed a very large loose stool. The other 2 patients passed loose, or watery, stools immediately after a meal eaten at the end of the four-hour hormone infusion. The role played by the meal is uncertain. Neither patient had diarrhaea before the test. 2 of these 3 patients were given glucagon alone in the same dose; neither had diarrhoea. Another patient with histologically proven ZollingerEllison syndrome, and known to have high blood-gastrin levels, was given an infusion of glucagon alone. This induced a profuse watery diarrhoea which was different in character and severity from his usual loose stool. Glucagon and pentagastrin may be implicated in the pathogenesis of diarrhoeas characterised by excessive intestinal secretion in man, and more particularly with certain
ous
(who
1. Allen, G. E. Practitioner, 1969, 203, 189. 2. Allen, G. E., Hadden, D. R. Br. J. Derm. 1970, 82, 216. 3. Rocca, F. F., Pereyra, E. Diabetes, 1963, 12, 220. 4. Barbezat, G. O., Grossman, M. I. Science, N.Y. 1971, 174, 422. 5. Barbezat, G. O., Grossman, M. I. Lancet, 1971, i, 1025.