1033
single contact with an A.T.C. prolonged treatment there.
was
only marginally
inferior
When Dr Glatt can demonstrate with double-blind randomised controlled trials that alcoholics leaving the St Pancras A.T.C. have a significantly better chance of not returning to excessive consumption than if they had not entered the centre, I for one will believe that the radical recasting of the alcoholism services called for in your editorial of Sept. 3 (p. 488) is not reauired.
Northgate Hospital, Morpeth Northumberland NE61
H. KINNELL
3BP
PROLACTIN IN HYPERTENSION
SIR,-Dr Stumpe and his colleagues (July 30, p. 211) suggest that raised plasma-prolactin concentrations in men with normal-renin essential hypertension may reflect reduced central dopaminergic activity, a factor postulated in the aetiology of the hypertension. We have also measured plasma-prolactin by radioimmunoassay in male and female hypertensive patients with renin status categorised by the intravenous frusemide test.’ All patients had been off antihypertensive drugs for at least 3 weeks. Plasma-prolactin was determined in ambulatory, non-stressed hypertensive patients and controls between 8 and 10 A.M. hours, shortly before the intravenous frusemide test. The results analysed by Student’s t test (unpaired), are shown in the table. PLASMA-PROLACTIN IN CONTROLS AND HYPERTENSIVE PATIENTS
There was no significant difference in plasma-prolactin between low and normal renin hypertensive patients, though both means were lower than control means. However, since plasma-prolactin falls with age in womenand since our predominantly female control population was younger, we hesitate to conclude that plasma-prolactin is decreased in essential hypertension. The normal range (mean+2 s.D.) for this population is 2.3-33.9ng/ml. Plasma-prolactin in hypertensive patients with uncategorised renin status has previously been reported to be normal. Furthermore, in tableI of the paper by Stumpe et al. there was essentially no difference in recumbent P.R.A. between low and normal renin patients. Stumpe et al. refer to subnormal P.R.A. responsiveness as defined by other investigators,’ but they do not define their own normal ranges to these stimuli. There might have been overlap in the categorisation of the low and normal renin subgroups. The limited age range (21-27) of the hypertensive patients of Stumpe et al. and the failure to study female hypertensives indicate the need for additional studies to place this interesting and provocative paper in perspective. We did not measure plasma-prolactin on early-morning blood-samples, and it is possible that only by sampling at this time can a difference be distinguished.
Radioimmunoassay
agents
were
supplied by
Department of Internal Medicine, University of Texas Health Science Center, Dallas, Texas 75235, U.S.A. 1
LEVODOPA IN SUBACUTE SCLEROSING PANENCEPHALITIS
to
N.I.A.M.D.D.
O.BRYAN HOLLAND CELSO E. GOMEZ-SANCHEZ
Kaplan, N. M., Kem, D. C., Holland, O. B., Kramer, N. J., Higgins, J., Gomez-Sanchez, C. Ann. intern. Med. 1976, 84, 639. 2. Vekemans, M., Robyn, C. Br. med. J. 1975, iv, 738. 3. Horrobin, D. F., Nowaczynski, W., Messerli, F. H., Kuchel, O., Genest, J. New Engl. J. Med. 1975, 292, 318. 4 Crane, M. G., Harris, J. J., Johns, V. J., Jr. Am. J. Med. 1972, 52, 457.
SIR,—Among patients seen at neurological units in univerpaediatric departments, the proportion of children with s.s.P.E. (subacute sclerosing panencephalitis) seems to be increasing. In 1961-70 only 3 cases were diagnosed in about 1142 children (0-002%) admitted to the neurological unit of pasdiatric department n at the Institute of Paediatrics in Krakow; but 9 cases among approximately 660 neurological patients (0-012%) were seen in 1971-75 and 13 cases in the academic year 1976/77 in about 230 children with neurological disease (5.6%) among admissions to the corresponding unit in Szczecin. The same trend has been recorded by others.1-4 All cases since 1971 have been strictly verified clinically and electroencephalographically and by c.s.F. electrophoresis and raised measles-antibody titres in serum and in c.s.F. Some
sity
also confirmed at necropsy. had an inexorable deteriorating course, with the typical, phasic pattern of the disease. In 1975 we tried levodopa to control the continuous, previously untreatable myoclonic movements in one patient. The dose was raised to 500 mg/day. The involuntary movements improved, and the progress of the disease itself slowed down in this 3t-year-old boy. The disease progress is still in a state of arrest after 2 years. At first we used levodopa alone in subsequent patients but later we tried ’Sinemet’ (levodopa 250-375 mg/day, carbidopa 12.5-18.75 mg, in two or three divided doses). Some of them were diagnosed at the initial phase of the disease, characterised by slowing and perseveration in mental activities, speech disorders and ataxic gait, behaviour and mood alterations, as well as hypokinesis, connected with sparse, slight myoclonic jerks. The E.E.G. pattern differs from that seen later; a diffuse disorganisation pattern relating to the dominant hemisphere was the prominent E.E.G. feature. Ten children were treated with levodopa alone or with carbidopa ; three were given a monoamine-oxidase inhibitor (nialamide) as well. Four children with stageI S.S.P.E. (speech disorders, tremor, cases were
All
s.s.P.E.
extrapyramidal dyskinesia, gait disturbances, myoclonic jerks) became clinically normal after 1-4 weeks of treatment. So did a child in stage 11, with predominant, generalised myoclonic movements. In a child with generalised myoclonia, pyramidaltract symptoms and mental confusion (stage II/III) the only improvement was an alleviation of the myoclonia. Four children in stage iv did not respond to levodopa or sinemet. The six children with proven
stageI are free of 2-3 months. Treatment began 3-6 weeks after the first symptoms were noticed. The age of the children was 32months to 11 years. M.A.O. inhibitor in low doses (25-50 mg daily) was subsequently added to levodopa/carbidopa treatment, and some additional benefit seems possible. The concept of immunological brain enzyme inhibition and immune neurone lesion’6 has been advanced; in S.S.P.E. this may affect noradrenergic or dopaminergic nerve terminals.6 Levodopa treatment might thus be overcoming some metabolic block on the way to neurotransmitter synthesis. In any case, symptoms
over
a
s.s.P.E.
period of follow-up lasting
in early-diagnosed S.S.P.E. (stage I and worth a more extended clinical trial. Child Neurology Unit, Paediatric Institute Pommeranian Medical Academy, Szczecin, Poland
ii) levodopa seems
to
be
B. HALIKOWSKI M. PIOTROPAWLOWSKA-WEINERT
1. Baguley, D. M., Glasgow, S. L. Lancet, 1973, ii, 763. 2. Lerman, P. ibid. 1974, i, 1289. 3. Kolar, O. ibid. 1973, ii, 1082. 4. Kipps, A., MacKenzie, D. J. M., Navdé, W. du T.,
McDonald,
R. ibid. p.
1388. 5. 6.
Hökfelt, T., Fuxe, K., Goldstein, M. Brain Res. 1973, 62, 461. Blessing, W. W., Costa, M., Geffen, L. B., Rush, R. A., Fink, 1977, 267, 368.
G. Nature,
single contact with an A.T.C. prolonged treatment there.
was
only marginally
inferior
When Dr Glatt can demonstrate with double-blind randomised controlled trials that alcoholics leaving the St Pancras A.T.C. have a significantly better chance of not returning to excessive consumption than if they had not entered the centre, I for one will believe that the radical recasting of the alcoholism services called for in your editorial of Sept. 3 (p. 488) is not reauired.
Northgate Hospital, Morpeth Northumberland NE61
H. KINNELL
3BP
PROLACTIN IN HYPERTENSION
SIR,-Dr Stumpe and his colleagues (July 30, p. 211) suggest that raised plasma-prolactin concentrations in men with normal-renin essential hypertension may reflect reduced central dopaminergic activity, a factor postulated in the aetiology of the hypertension. We have also measured plasma-prolactin by radioimmunoassay in male and female hypertensive patients with renin status categorised by the intravenous frusemide test.’ All patients had been off antihypertensive drugs for at least 3 weeks. Plasma-prolactin was determined in ambulatory, non-stressed hypertensive patients and controls between 8 and 10 A.M. hours, shortly before the intravenous frusemide test. The results analysed by Student’s t test (unpaired), are shown in the table. PLASMA-PROLACTIN IN CONTROLS AND HYPERTENSIVE PATIENTS
There was no significant difference in plasma-prolactin between low and normal renin hypertensive patients, though both means were lower than control means. However, since plasma-prolactin falls with age in womenand since our predominantly female control population was younger, we hesitate to conclude that plasma-prolactin is decreased in essential hypertension. The normal range (mean+2 s.D.) for this population is 2.3-33.9ng/ml. Plasma-prolactin in hypertensive patients with uncategorised renin status has previously been reported to be normal. Furthermore, in tableI of the paper by Stumpe et al. there was essentially no difference in recumbent P.R.A. between low and normal renin patients. Stumpe et al. refer to subnormal P.R.A. responsiveness as defined by other investigators,’ but they do not define their own normal ranges to these stimuli. There might have been overlap in the categorisation of the low and normal renin subgroups. The limited age range (21-27) of the hypertensive patients of Stumpe et al. and the failure to study female hypertensives indicate the need for additional studies to place this interesting and provocative paper in perspective. We did not measure plasma-prolactin on early-morning blood-samples, and it is possible that only by sampling at this time can a difference be distinguished.
Radioimmunoassay
agents
were
supplied by
Department of Internal Medicine, University of Texas Health Science Center, Dallas, Texas 75235, U.S.A. 1
LEVODOPA IN SUBACUTE SCLEROSING PANENCEPHALITIS
to
N.I.A.M.D.D.
O.BRYAN HOLLAND CELSO E. GOMEZ-SANCHEZ
Kaplan, N. M., Kem, D. C., Holland, O. B., Kramer, N. J., Higgins, J., Gomez-Sanchez, C. Ann. intern. Med. 1976, 84, 639. 2. Vekemans, M., Robyn, C. Br. med. J. 1975, iv, 738. 3. Horrobin, D. F., Nowaczynski, W., Messerli, F. H., Kuchel, O., Genest, J. New Engl. J. Med. 1975, 292, 318. 4 Crane, M. G., Harris, J. J., Johns, V. J., Jr. Am. J. Med. 1972, 52, 457.
SIR,—Among patients seen at neurological units in univerpaediatric departments, the proportion of children with s.s.P.E. (subacute sclerosing panencephalitis) seems to be increasing. In 1961-70 only 3 cases were diagnosed in about 1142 children (0-002%) admitted to the neurological unit of pasdiatric department n at the Institute of Paediatrics in Krakow; but 9 cases among approximately 660 neurological patients (0-012%) were seen in 1971-75 and 13 cases in the academic year 1976/77 in about 230 children with neurological disease (5.6%) among admissions to the corresponding unit in Szczecin. The same trend has been recorded by others.1-4 All cases since 1971 have been strictly verified clinically and electroencephalographically and by c.s.F. electrophoresis and raised measles-antibody titres in serum and in c.s.F. Some
sity
also confirmed at necropsy. had an inexorable deteriorating course, with the typical, phasic pattern of the disease. In 1975 we tried levodopa to control the continuous, previously untreatable myoclonic movements in one patient. The dose was raised to 500 mg/day. The involuntary movements improved, and the progress of the disease itself slowed down in this 3t-year-old boy. The disease progress is still in a state of arrest after 2 years. At first we used levodopa alone in subsequent patients but later we tried ’Sinemet’ (levodopa 250-375 mg/day, carbidopa 12.5-18.75 mg, in two or three divided doses). Some of them were diagnosed at the initial phase of the disease, characterised by slowing and perseveration in mental activities, speech disorders and ataxic gait, behaviour and mood alterations, as well as hypokinesis, connected with sparse, slight myoclonic jerks. The E.E.G. pattern differs from that seen later; a diffuse disorganisation pattern relating to the dominant hemisphere was the prominent E.E.G. feature. Ten children were treated with levodopa alone or with carbidopa ; three were given a monoamine-oxidase inhibitor (nialamide) as well. Four children with stageI S.S.P.E. (speech disorders, tremor, cases were
All
s.s.P.E.
extrapyramidal dyskinesia, gait disturbances, myoclonic jerks) became clinically normal after 1-4 weeks of treatment. So did a child in stage 11, with predominant, generalised myoclonic movements. In a child with generalised myoclonia, pyramidaltract symptoms and mental confusion (stage II/III) the only improvement was an alleviation of the myoclonia. Four children in stage iv did not respond to levodopa or sinemet. The six children with proven
stageI are free of 2-3 months. Treatment began 3-6 weeks after the first symptoms were noticed. The age of the children was 32months to 11 years. M.A.O. inhibitor in low doses (25-50 mg daily) was subsequently added to levodopa/carbidopa treatment, and some additional benefit seems possible. The concept of immunological brain enzyme inhibition and immune neurone lesion’6 has been advanced; in S.S.P.E. this may affect noradrenergic or dopaminergic nerve terminals.6 Levodopa treatment might thus be overcoming some metabolic block on the way to neurotransmitter synthesis. In any case, symptoms
over
a
s.s.P.E.
period of follow-up lasting
in early-diagnosed S.S.P.E. (stage I and worth a more extended clinical trial. Child Neurology Unit, Paediatric Institute Pommeranian Medical Academy, Szczecin, Poland
ii) levodopa seems
to
be
B. HALIKOWSKI M. PIOTROPAWLOWSKA-WEINERT
1. Baguley, D. M., Glasgow, S. L. Lancet, 1973, ii, 763. 2. Lerman, P. ibid. 1974, i, 1289. 3. Kolar, O. ibid. 1973, ii, 1082. 4. Kipps, A., MacKenzie, D. J. M., Navdé, W. du T.,
McDonald,
R. ibid. p.
1388. 5. 6.
Hökfelt, T., Fuxe, K., Goldstein, M. Brain Res. 1973, 62, 461. Blessing, W. W., Costa, M., Geffen, L. B., Rush, R. A., Fink, 1977, 267, 368.
G. Nature,
