363
Loperamide poisoning
in children
are indiscriminately used in countries. The World Health Organisation recommends that no anti-diarrhoeal agent should be used in ordinary acute watery diarrhoea because most such preparations are either useless or even dangerous for children. One such drug is loperamide (’Imodium’), a powerful anti-motility agent that is available in Pakistan as capsules, syrup, and drops. Drops (2 mg/ml) are often used in infants. The package states that the drug should not be used in children less than one year of age. In practice this warning is useless in a country where drugs are freely available over the counter, where 99% of patients cannot read, and where unqualified people (quacks and Hakim) use drugs without knowing the side-effects. During November and December, 1989, our department saw 19 infants with severe abdominal distension and paralytic ileus as a result of being given imodium drops. 18 children (4 girls, 14 boys) were aged between I and 612 months; the other girl was 2 years old. Of these 19 children 6 died, 4 left the ward seriously ill because the parents wanted the child to be at home before he or she died, and 9 recovered fully. No other cause of abdominal distension could be established and electrolytes were normal (sodium 114-138 and potassium 27-61mmol/1). The dose given varied from 2 to 15 drops every time the child passed a stool and from 6 to 30 drops per
SiR,-Anti-diarrhoeal agents
developing
Ultrathin section of muscle from a patient on cyclosporin after renal transplant, showing abnormally large vacuoles and enlarged mitochondria, some with ruptured cristae.
.
atrophy. Muscle strength was grade IV - /V proximal and V/V distal. Serum muscle enzymes were normal. Electromyography suggested mild peripheral sensory-motor neuropathy without signs of myopathy. An open left deltoid muscle biopsy specimen showed type-2 fibre atrophy, the presence of internal nuclei affecting about 10% of the fibres, and some nuclear clumps. One sample showed cytoplasmic small size vacuoles in most fibres. Abundant lipidic vacuoles pushing the myofibres (figure), abnormal large-size mitochondria with cristae loss, and membranous whorls were seen in ultrathin sections. Cyclosporin dose was reduced to 4 mg/kg daily. The patient’s clinical condition gradually improved. Muscle pain disappeared in two weeks and he slowly recovered his strength. Two months after biopsy, serum cyclosporin concentration was 80 ng/ml. The patient was symptom-free. A second muscle biopsy (Bergstrom needle) was normal, apart from the presence of some nuclear clumps, suggesting a long-standing neuropathy, probably related to his previous uraemia. These findings strongly suggest type B cyclosporin toxicity.4.5 The histological muscle abnormalities, although not specific, are highly suggestive of toxic myopathy, and no other obvious causes of myopathy were present. The pathogenesis of cyclosporin myopathy is probably related to a direct toxic effect on muscle cells, as occurs in other organs.’ Such toxicity is very unusual at low serum concentrations. Since reductions in cyclosporin dose were rapidly followed by the disappearance of clinical and histological features we believe that cyclosporin is myotoxic, and its toxicity is dose-dependent. Serum cyclosporin concentrations should be monitored to avoid this adverse effect. Muscle biopsy, although not specific, would confirm such myotoxicity. Muscle Research Group,
Department of Internal Medicine and Kidney Transplant Unit, Hospital Clinic, University of Barcelona, 08036 Barcelona, Spain
1. Noppen
J. FERNANDEZ-SOLA J. CAMPISTOL J. CASADEMONT J. M. GRAU A. URBANO-MARQUEZ
M, Velkeners B, Dierckx R, Bruyland M, Vanhaelst L. Cyclosporine and myopathy. Ann Intern Med 1987; 107: 945-46. 2. Goy JJ, Stauffer JC, Deruaz JP, et al. Myopathy as a possible side-effect of cyclosporin. Lancet 1989; i: 1446-47. 3. Chassagne P, Mejjad O, Moore N, Leloet X, Deshayes P. Myopathy as possible side-effect of cyclosporin. Lancet 1989; ii: 1104. 4. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probabilty of adverse drug reactions. Clin Pharmacol Ther 1981; 30: 239-45. 5. Bateman DN, Chaplin S. New drugs: adverse reactions I. Br Med J 1988; 296: 761-64. 6 Victor M. Toxic and nutritional myopathies. In: Engel AG, Banker BQ, eds.Myology, basic and clinical. New York: McGraw Hill, 1986: 1807-12. 7. Hunsiker LG. Impact of cyclosporine on cadaveric renal transplantation: a summary. Am J Kidney Dis 1985, 5: 335-40.
day. We wrote a letter to Johnson & Johnson Pakistan Pvt Ltd, which distributes imodium under licence from Janssen Pharmaceutica telling them about the deaths and asking for the drug to be withdrawn. We have had no response, so we are turning to The Lancet to ask the manufacturers to withdraw imodium from Pakistan before it kills any more children. Department of Paediatric Medicine, and Diarrhoea Training Unit, Nishtar Medical College and Hospital, Multan, Pakistan
TARIQ IQBAL BHUTTA KHALID IQBAL TAHIR
1. Editorial. Misuse of anti-diarrhoeal medicines. Lancet
1989; ii: 995.
in infantile spasms SiR,—The anti-epileptic efficacy of vigabatrin (gamma-vinyl GABA) is especially high in patients with partial complex seizures.! We have recently completed a single-blind study of vigabatrin in 61 children with refractory epilepsy.2 Infantile spasms (IS) is a unique epileptic syndrome affecting infants during the first year of life. It is one of the most refractory types of epilepsy and carries a poor prognosis. The most effective treatment is steroids, but side-effects are common, efficacy is often transient, and whether there are long-term benefits is controversial.4 Results vary but a recent prospective series showed that 48% of children had a long-term response.’ Efficacy of other anti-epileptic drugs such as the benzodiazepines or valproate is less striking though they are better
Vigabatrin
tolerated.6 We have
opportunity to observe the efficacy of aged 2 months to 10 years (mean 26 with months) drug-resistant IS. According to Glaze et al,s 27 of these children could be classified as having cryptogenic IS; the remaining 18 had symptomatic IS, including 8 children with tuberous sclerosis. All were resistant to previous treatment, including corticosteroids (hydrocortisone) (28 patients) and benzodiazepines or valproate (45). Before the start of vigabatrin vigabatrin
now
on
had the
45 children
therapy spasms had been present for between 0-5 and 145 months (mean 22). The mean frequency of spasms was about 130 per month. 14 patients also had partial seizures. Concomitant medication ranged from 1 to 3 other drugs (mean 1-8). We could not evaluate the efficacy of vigabatrin in 3 patients since the drug was discontinued because of hypotonia in 1, hypertonia in 1, and hyperexcitability in 1 soon after the start of treatment. The remaining 42 children have now been treated with vigabatrin 50-200 mg/kg daily for 4-24 months (mean 9-5). A greater than 50% reduction in spasms
was
obtained in 30 onset of
patients (71 %) and complete suppression from the
364
16 (38%). Concomitant anti-epileptic drugs were reduced in 15, and 7 are now on vigabatrin monotherapy. Better results were seen when vigabatrin treatment had been started earlier in the course of the disease-where spasms had been present for less than a year, 13 of 25 patients responded, compared with only 3 of the 17 who had had spasms for over a year. Perhaps the most striking finding was the response to vigabatrin in relation to the aetiology of IS. Amuch better effect was seen in symptomatic IS, with 11 (69%) of 16 showing complete control compared with only 5 (19%) of 26 with cryptogenic IS. This response was further confirmed in the children who also had tuberous sclerosis-7 of 8 had complete suppression of their spasms. Control seemed to be transient in 6 of the cryptogenic cases following an initial seizure-free period of 3-12 months, whereas seizure control has been maintained so far in all
vigabatrin in
symptomatic cases (mean follow-up 15 months). Apart from the 3 children from whom vigabatrin was withdrawn, most patients tolerated the drug well, with only mild and transient adverse events being reported in 9 (hyperkinesia, weight gain, drowsiness). These preliminary findings suggest that vigabatrin is potentially very valuable in the management of intractable IS, especially when they are associated with tuberous sclerosis, since this condition is known to have a very poor prognosis.’ INSERM U 29 and Neuropaediatric Department, Hôpital Saint Vincent de Paul, 75674 Pans Cedex, France Merrell Dow Research Institute, Winnersh Research Centre, Winnersh, Berkshire RG11 5HQ
C. CHIRON O. DULAC
phenolsulphotransferase activity could explain her sudden intolerance for red wine after marrow transplantation, and that the enzyme defect was transferred by bone-marrow transplantation. Departments of Internal Medicine, Clinical Immunology, and Transplantation Surgery, Karolinska Institute,
Huddinge Hospital, Huddinge, Sweden
S-141 86
B. LÖNNQVIST O. RINGDÉN
1. Littlewood J, Glover V, Sandler M, Petty R, Peatfield R, Rose FC. Platelet phenolsulphotransferase deficiency in dietary migraine. Lancet 1982; i: 983-86. 2. Littlewood JT, Bigg C, Glover V, Sandler M, Davies PTG, Rose FC. Red wine as a cause of migraine. Lancet 1988; i: 558-59. 3. Singleton VL, Noble AC. Wine flavour and phenolic substances. In: Charalambous G, Katz I, eds. Phenolic, sulfur and nitrogen compounds in food flavours. Am Chem Soc Symp 1976; 26: 47-70.
D. LUNA L. PALACIOS S. MONDRAGON D. BEAUMONT J. P. MUMFORD
1. Editorial. Vigabatrin. Lancet 1989; i: 532-33. 2. Luna D, Dulac O, Pajot N, Beaumont D. Vigabatrin in the treatment of childhood
3.
enzyme which inactivates a wide range of phenols. Furthermore, red wine provoked a migraine attack in most of these patients, but diluted vodka did not.2 The major chemical difference between red and white wine lies in the content of phenolic flavanoids.3 It has been reported that red wine may contain more than 20 times the amount of these complex phenols than white wine. Unfortunately, our patient relapsed and died, and the amount of the relevant enzyme in her donor-derived platelets was not investigated. However, it seems reasonable to suggest that low
activity-an
epilepsies: a single-blind placebo-controlled study. Epilepsia 1989; 30: 430-37. Jeavons PM, Bower BD. Infantile spasms: a review of the literature and a study of 112
cases. London: Heinemann Medical, 1964. 4. Jeavons PM, Bower BD, Dimitrakoudi M. Long term prognosis of 150 cases of "West syndrome". Epilepsia 1973; 14: 153-64. 5. Glaze DG, Hrachovy RA, Frost JD, Kellaway P, Zion TE. Prospective study of outcome of infants with infantile spasms treated during controlled studies of ACTH and prednisone. J Pediatr 1988; 112: 389-96. 6. Siemes H, Spohr HL, Michael TH, Nau H. Therapy of infantile spasms with valproate: results of a prospective study. Epilepsia 1988; 29: 553-60. 7. Yamamoto N, Yatanabe K, Negoro T, et al. Long-term prognosis of tuberous sclerosis with epilepsy in children. Brain Dev 1987; 9: 292-95.
Migraine precipitated by red wine after bone-marrow transplantation SIR,-Professor Williams and Dr Franklin report (Nov 25, p 1286) the case of a young man who had severe migraine after receiving a bone-marrow graft from his phenotypically HLA-matched mother, who had had migraine since childhood. We have also seen such a case. Our patient was a 44-year-old woman with a 5-year history of multiple myeloma of IgA-type. In September, 1986, she underwent bone-marrow transplantation, with her 38-year-old HLA-identical and MLC-non-reactive brother as the donor. The donor and the patient’s mother and daughter had classic migraine. The patient had grade I acute graft-versus-host disease of the skin which responded well to steroids. Two months after transplantation, during a period of cytomegalovirus reactivation with fever and pancytopenia, bacterial sinusitis developed. She had no other transplantation related complications. During the episode of sinusitis, she had her first classic migraine attack. When she recovered and was discharged she discovered that she could no longer drink more than a small glass of red wine without bringing on right-sided migraine attacks. The same amount of alcohol taken as white wine or spirits was tolerated. Infections could also precipitate migraine. Neurological examination was normal except for a mild diminution in sensation of the ring and little fingers of the right hand. Littlewood et all drew attention to the fact that patients with migraine induced by dietary factors had, compared with controls, significantly lower mean levels of platelet phenolsulphotransferase
Poliomyelitis
in the UK
SIR,-We highlight the continuing dangers of poliomyelitis infection in the British population. On Dec 14, 1988, we admitted a 65-year-old man who had been on a 1-week holiday in Morocco without taking medical advice about vaccinations or prophylactic drug treatments. While there he had a bout of diarrhoea which settled, but within 10 days of his return he had a dry cough, headache, and a raised temperature with myalgia. Paralysis of his limbs and respiratory muscles ensued. Cerebrospinal fluid showed 28 mononuclear cells and 1150 mg/1 protein, and stool culture revealed poliomyelitis virus, identified at the Public Health Laboratory Service, Colindale, as being of wild type 1. The rising serum type 1 antibody further confirmed the diagnosis of poliomyelitis infection. He needed continuous and then intermittent ventilation for 33 days, and is slowly recovering without such support. He has a profound, symmetrical lower limb weakness, and is wheelchair-bound. A review of paralytic poliomyelitis from 1970 to 19841 revealed 70 cases in England and Wales, of which 11 were contracted abroad, 17 (mainly infants) after vaccination (1 in a million chance), 12 from a vaccine contact, and 30 from an unknown source. A previous report from this unit2 emphasised the need to ensure that all nonimmunised relatives and household contacts are immunised before or at the same time as their children; this should reduce the number of contact cases.’1 Particular care should be taken to provide oral immunisation to adults travelling abroad, even if just on short sun-seeking breaks to Mediterranean countries. Immunodeficient patients should receive the inactivated and not the live vaccine (British National Formulary, September, 1989). Since only 95 % of British adults have antibodies to poliomyelitis,3 doctors should be aware of the need for continual education of patients and vigilance. Further, it is not always appreciated that wild poliomyelitis is still present in Britain, and of the nineteen wild strains obtained in Begg and colleagues’ series1 14 were contracted in England and Wales. Wessex
Neurological Centre, Southampton General Hospital, Southampton SO9 4XY, UK
C. J. ELLIS P. TELFER N. F. LAWTON
1. Begg NT, Chamberlain R, Roebuck M. Paralytic poliomyelitis in England and Wales, 1970-84. Epidemiol Infect 1987; 99: 97-106. 2. Bateman DE, Elrington G, Kennedy P, et al. Vaccine related poliomyelitis in non-immunised relatives and household contacts. Br Med J 1987; 294: 170-71. 3. Roebuck M, Chamberlain B. Prevalence of antibodies to poliovirus in 1978 among subjects aged 0-88. Br Med J 1982; 284: 697-700.
Loperamide poisoning
in children
are indiscriminately used in countries. The World Health Organisation recommends that no anti-diarrhoeal agent should be used in ordinary acute watery diarrhoea because most such preparations are either useless or even dangerous for children. One such drug is loperamide (’Imodium’), a powerful anti-motility agent that is available in Pakistan as capsules, syrup, and drops. Drops (2 mg/ml) are often used in infants. The package states that the drug should not be used in children less than one year of age. In practice this warning is useless in a country where drugs are freely available over the counter, where 99% of patients cannot read, and where unqualified people (quacks and Hakim) use drugs without knowing the side-effects. During November and December, 1989, our department saw 19 infants with severe abdominal distension and paralytic ileus as a result of being given imodium drops. 18 children (4 girls, 14 boys) were aged between I and 612 months; the other girl was 2 years old. Of these 19 children 6 died, 4 left the ward seriously ill because the parents wanted the child to be at home before he or she died, and 9 recovered fully. No other cause of abdominal distension could be established and electrolytes were normal (sodium 114-138 and potassium 27-61mmol/1). The dose given varied from 2 to 15 drops every time the child passed a stool and from 6 to 30 drops per
SiR,-Anti-diarrhoeal agents
developing
Ultrathin section of muscle from a patient on cyclosporin after renal transplant, showing abnormally large vacuoles and enlarged mitochondria, some with ruptured cristae.
.
atrophy. Muscle strength was grade IV - /V proximal and V/V distal. Serum muscle enzymes were normal. Electromyography suggested mild peripheral sensory-motor neuropathy without signs of myopathy. An open left deltoid muscle biopsy specimen showed type-2 fibre atrophy, the presence of internal nuclei affecting about 10% of the fibres, and some nuclear clumps. One sample showed cytoplasmic small size vacuoles in most fibres. Abundant lipidic vacuoles pushing the myofibres (figure), abnormal large-size mitochondria with cristae loss, and membranous whorls were seen in ultrathin sections. Cyclosporin dose was reduced to 4 mg/kg daily. The patient’s clinical condition gradually improved. Muscle pain disappeared in two weeks and he slowly recovered his strength. Two months after biopsy, serum cyclosporin concentration was 80 ng/ml. The patient was symptom-free. A second muscle biopsy (Bergstrom needle) was normal, apart from the presence of some nuclear clumps, suggesting a long-standing neuropathy, probably related to his previous uraemia. These findings strongly suggest type B cyclosporin toxicity.4.5 The histological muscle abnormalities, although not specific, are highly suggestive of toxic myopathy, and no other obvious causes of myopathy were present. The pathogenesis of cyclosporin myopathy is probably related to a direct toxic effect on muscle cells, as occurs in other organs.’ Such toxicity is very unusual at low serum concentrations. Since reductions in cyclosporin dose were rapidly followed by the disappearance of clinical and histological features we believe that cyclosporin is myotoxic, and its toxicity is dose-dependent. Serum cyclosporin concentrations should be monitored to avoid this adverse effect. Muscle biopsy, although not specific, would confirm such myotoxicity. Muscle Research Group,
Department of Internal Medicine and Kidney Transplant Unit, Hospital Clinic, University of Barcelona, 08036 Barcelona, Spain
1. Noppen
J. FERNANDEZ-SOLA J. CAMPISTOL J. CASADEMONT J. M. GRAU A. URBANO-MARQUEZ
M, Velkeners B, Dierckx R, Bruyland M, Vanhaelst L. Cyclosporine and myopathy. Ann Intern Med 1987; 107: 945-46. 2. Goy JJ, Stauffer JC, Deruaz JP, et al. Myopathy as a possible side-effect of cyclosporin. Lancet 1989; i: 1446-47. 3. Chassagne P, Mejjad O, Moore N, Leloet X, Deshayes P. Myopathy as possible side-effect of cyclosporin. Lancet 1989; ii: 1104. 4. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probabilty of adverse drug reactions. Clin Pharmacol Ther 1981; 30: 239-45. 5. Bateman DN, Chaplin S. New drugs: adverse reactions I. Br Med J 1988; 296: 761-64. 6 Victor M. Toxic and nutritional myopathies. In: Engel AG, Banker BQ, eds.Myology, basic and clinical. New York: McGraw Hill, 1986: 1807-12. 7. Hunsiker LG. Impact of cyclosporine on cadaveric renal transplantation: a summary. Am J Kidney Dis 1985, 5: 335-40.
day. We wrote a letter to Johnson & Johnson Pakistan Pvt Ltd, which distributes imodium under licence from Janssen Pharmaceutica telling them about the deaths and asking for the drug to be withdrawn. We have had no response, so we are turning to The Lancet to ask the manufacturers to withdraw imodium from Pakistan before it kills any more children. Department of Paediatric Medicine, and Diarrhoea Training Unit, Nishtar Medical College and Hospital, Multan, Pakistan
TARIQ IQBAL BHUTTA KHALID IQBAL TAHIR
1. Editorial. Misuse of anti-diarrhoeal medicines. Lancet
1989; ii: 995.
in infantile spasms SiR,—The anti-epileptic efficacy of vigabatrin (gamma-vinyl GABA) is especially high in patients with partial complex seizures.! We have recently completed a single-blind study of vigabatrin in 61 children with refractory epilepsy.2 Infantile spasms (IS) is a unique epileptic syndrome affecting infants during the first year of life. It is one of the most refractory types of epilepsy and carries a poor prognosis. The most effective treatment is steroids, but side-effects are common, efficacy is often transient, and whether there are long-term benefits is controversial.4 Results vary but a recent prospective series showed that 48% of children had a long-term response.’ Efficacy of other anti-epileptic drugs such as the benzodiazepines or valproate is less striking though they are better
Vigabatrin
tolerated.6 We have
opportunity to observe the efficacy of aged 2 months to 10 years (mean 26 with months) drug-resistant IS. According to Glaze et al,s 27 of these children could be classified as having cryptogenic IS; the remaining 18 had symptomatic IS, including 8 children with tuberous sclerosis. All were resistant to previous treatment, including corticosteroids (hydrocortisone) (28 patients) and benzodiazepines or valproate (45). Before the start of vigabatrin vigabatrin
now
on
had the
45 children
therapy spasms had been present for between 0-5 and 145 months (mean 22). The mean frequency of spasms was about 130 per month. 14 patients also had partial seizures. Concomitant medication ranged from 1 to 3 other drugs (mean 1-8). We could not evaluate the efficacy of vigabatrin in 3 patients since the drug was discontinued because of hypotonia in 1, hypertonia in 1, and hyperexcitability in 1 soon after the start of treatment. The remaining 42 children have now been treated with vigabatrin 50-200 mg/kg daily for 4-24 months (mean 9-5). A greater than 50% reduction in spasms
was
obtained in 30 onset of
patients (71 %) and complete suppression from the
364
16 (38%). Concomitant anti-epileptic drugs were reduced in 15, and 7 are now on vigabatrin monotherapy. Better results were seen when vigabatrin treatment had been started earlier in the course of the disease-where spasms had been present for less than a year, 13 of 25 patients responded, compared with only 3 of the 17 who had had spasms for over a year. Perhaps the most striking finding was the response to vigabatrin in relation to the aetiology of IS. Amuch better effect was seen in symptomatic IS, with 11 (69%) of 16 showing complete control compared with only 5 (19%) of 26 with cryptogenic IS. This response was further confirmed in the children who also had tuberous sclerosis-7 of 8 had complete suppression of their spasms. Control seemed to be transient in 6 of the cryptogenic cases following an initial seizure-free period of 3-12 months, whereas seizure control has been maintained so far in all
vigabatrin in
symptomatic cases (mean follow-up 15 months). Apart from the 3 children from whom vigabatrin was withdrawn, most patients tolerated the drug well, with only mild and transient adverse events being reported in 9 (hyperkinesia, weight gain, drowsiness). These preliminary findings suggest that vigabatrin is potentially very valuable in the management of intractable IS, especially when they are associated with tuberous sclerosis, since this condition is known to have a very poor prognosis.’ INSERM U 29 and Neuropaediatric Department, Hôpital Saint Vincent de Paul, 75674 Pans Cedex, France Merrell Dow Research Institute, Winnersh Research Centre, Winnersh, Berkshire RG11 5HQ
C. CHIRON O. DULAC
phenolsulphotransferase activity could explain her sudden intolerance for red wine after marrow transplantation, and that the enzyme defect was transferred by bone-marrow transplantation. Departments of Internal Medicine, Clinical Immunology, and Transplantation Surgery, Karolinska Institute,
Huddinge Hospital, Huddinge, Sweden
S-141 86
B. LÖNNQVIST O. RINGDÉN
1. Littlewood J, Glover V, Sandler M, Petty R, Peatfield R, Rose FC. Platelet phenolsulphotransferase deficiency in dietary migraine. Lancet 1982; i: 983-86. 2. Littlewood JT, Bigg C, Glover V, Sandler M, Davies PTG, Rose FC. Red wine as a cause of migraine. Lancet 1988; i: 558-59. 3. Singleton VL, Noble AC. Wine flavour and phenolic substances. In: Charalambous G, Katz I, eds. Phenolic, sulfur and nitrogen compounds in food flavours. Am Chem Soc Symp 1976; 26: 47-70.
D. LUNA L. PALACIOS S. MONDRAGON D. BEAUMONT J. P. MUMFORD
1. Editorial. Vigabatrin. Lancet 1989; i: 532-33. 2. Luna D, Dulac O, Pajot N, Beaumont D. Vigabatrin in the treatment of childhood
3.
enzyme which inactivates a wide range of phenols. Furthermore, red wine provoked a migraine attack in most of these patients, but diluted vodka did not.2 The major chemical difference between red and white wine lies in the content of phenolic flavanoids.3 It has been reported that red wine may contain more than 20 times the amount of these complex phenols than white wine. Unfortunately, our patient relapsed and died, and the amount of the relevant enzyme in her donor-derived platelets was not investigated. However, it seems reasonable to suggest that low
activity-an
epilepsies: a single-blind placebo-controlled study. Epilepsia 1989; 30: 430-37. Jeavons PM, Bower BD. Infantile spasms: a review of the literature and a study of 112
cases. London: Heinemann Medical, 1964. 4. Jeavons PM, Bower BD, Dimitrakoudi M. Long term prognosis of 150 cases of "West syndrome". Epilepsia 1973; 14: 153-64. 5. Glaze DG, Hrachovy RA, Frost JD, Kellaway P, Zion TE. Prospective study of outcome of infants with infantile spasms treated during controlled studies of ACTH and prednisone. J Pediatr 1988; 112: 389-96. 6. Siemes H, Spohr HL, Michael TH, Nau H. Therapy of infantile spasms with valproate: results of a prospective study. Epilepsia 1988; 29: 553-60. 7. Yamamoto N, Yatanabe K, Negoro T, et al. Long-term prognosis of tuberous sclerosis with epilepsy in children. Brain Dev 1987; 9: 292-95.
Migraine precipitated by red wine after bone-marrow transplantation SIR,-Professor Williams and Dr Franklin report (Nov 25, p 1286) the case of a young man who had severe migraine after receiving a bone-marrow graft from his phenotypically HLA-matched mother, who had had migraine since childhood. We have also seen such a case. Our patient was a 44-year-old woman with a 5-year history of multiple myeloma of IgA-type. In September, 1986, she underwent bone-marrow transplantation, with her 38-year-old HLA-identical and MLC-non-reactive brother as the donor. The donor and the patient’s mother and daughter had classic migraine. The patient had grade I acute graft-versus-host disease of the skin which responded well to steroids. Two months after transplantation, during a period of cytomegalovirus reactivation with fever and pancytopenia, bacterial sinusitis developed. She had no other transplantation related complications. During the episode of sinusitis, she had her first classic migraine attack. When she recovered and was discharged she discovered that she could no longer drink more than a small glass of red wine without bringing on right-sided migraine attacks. The same amount of alcohol taken as white wine or spirits was tolerated. Infections could also precipitate migraine. Neurological examination was normal except for a mild diminution in sensation of the ring and little fingers of the right hand. Littlewood et all drew attention to the fact that patients with migraine induced by dietary factors had, compared with controls, significantly lower mean levels of platelet phenolsulphotransferase
Poliomyelitis
in the UK
SIR,-We highlight the continuing dangers of poliomyelitis infection in the British population. On Dec 14, 1988, we admitted a 65-year-old man who had been on a 1-week holiday in Morocco without taking medical advice about vaccinations or prophylactic drug treatments. While there he had a bout of diarrhoea which settled, but within 10 days of his return he had a dry cough, headache, and a raised temperature with myalgia. Paralysis of his limbs and respiratory muscles ensued. Cerebrospinal fluid showed 28 mononuclear cells and 1150 mg/1 protein, and stool culture revealed poliomyelitis virus, identified at the Public Health Laboratory Service, Colindale, as being of wild type 1. The rising serum type 1 antibody further confirmed the diagnosis of poliomyelitis infection. He needed continuous and then intermittent ventilation for 33 days, and is slowly recovering without such support. He has a profound, symmetrical lower limb weakness, and is wheelchair-bound. A review of paralytic poliomyelitis from 1970 to 19841 revealed 70 cases in England and Wales, of which 11 were contracted abroad, 17 (mainly infants) after vaccination (1 in a million chance), 12 from a vaccine contact, and 30 from an unknown source. A previous report from this unit2 emphasised the need to ensure that all nonimmunised relatives and household contacts are immunised before or at the same time as their children; this should reduce the number of contact cases.’1 Particular care should be taken to provide oral immunisation to adults travelling abroad, even if just on short sun-seeking breaks to Mediterranean countries. Immunodeficient patients should receive the inactivated and not the live vaccine (British National Formulary, September, 1989). Since only 95 % of British adults have antibodies to poliomyelitis,3 doctors should be aware of the need for continual education of patients and vigilance. Further, it is not always appreciated that wild poliomyelitis is still present in Britain, and of the nineteen wild strains obtained in Begg and colleagues’ series1 14 were contracted in England and Wales. Wessex
Neurological Centre, Southampton General Hospital, Southampton SO9 4XY, UK
C. J. ELLIS P. TELFER N. F. LAWTON
1. Begg NT, Chamberlain R, Roebuck M. Paralytic poliomyelitis in England and Wales, 1970-84. Epidemiol Infect 1987; 99: 97-106. 2. Bateman DE, Elrington G, Kennedy P, et al. Vaccine related poliomyelitis in non-immunised relatives and household contacts. Br Med J 1987; 294: 170-71. 3. Roebuck M, Chamberlain B. Prevalence of antibodies to poliovirus in 1978 among subjects aged 0-88. Br Med J 1982; 284: 697-700.
