689 treated meningococcal or pneumococcal meningitis. It is, howessential that high titre precipitating antisera are used in the c.).E. test if the small amounts of antigen present in the c,s.F. of these patients are to be detected. ever,

Facultyof Medicine, Ahmadu Bello University, Zaria, Nigeria

B. M. GREENWOOD H. C. WHITTLE

PARAQUAT POISONING RISK S)R,—I was interested in Dr Barraclough’s letter about paraquat toxicity,’ but I think it is better to argue on the basis of permanent risk rather in terms of numbers of deaths. Poisoning by paraquat is not common, few people being exposed to it. Farmers do not necessarily handle pesticides themselves, and paraquat is not used by all spraymen. However, if we consider the small number of people exposed to paraquat and the real number of poisoning cases, the accident risk might be very

high. Clinique Toxicologique, Hôpital Fernand Widal, 75010 Pans, France

S. DALLY

ABNORMAL POLYGRAPHIC FINDINGS IN NEAR-MISS SUDDEN INFANT DEATH

SIR,-The description, by Dr Guilleminault and his colleagues,’ of autonomic dysfunction in cases of near-miss sudden infant death prompts me to record my observations of the sudden unexpected death of a 5-month-old girl in my consulting-rooms in January, 1974. The baby had been brought to me because of problems with weaning. The apparently well baby was seen being bottle-fed, when pallor suddenly developed, and prescience of impending disaster led to hurried examination. The body-temperature was 38’C, the respiration became increasingly irregular without initial apnoea or observed respiratory obstruction, the pupils dilated unequally, the abdomen became distended, and bradycardia preceded worsening collapse. There had been no sleep disturbance, and previous development had been normal. Intensive resuscitation failed, and within 5 min of the first signs of distress the heart stopped beating. Post-mortem studies, including full microbiological investigation, were negative; there was no histological evidence for metabolic disease, although such may have been undetected. The parents had been more annoyed by what they interpreted as the child’s stubbornness on the previous day than worried by the possibility of acute disease. The infant’s problem might not have attracted attention but for the family historv, which included the stillbirth of the first full-term pregnancv and the death of the second child with proven respiratory-distress syndrome after elective term caesarean section-a relatively uncommon situation and, for the mother, a source of continuing anxiety (rightly in the event) with caring for this latest baby. Certainly, in the case described there was evidence of Autonomic-nervous-system dysfunction. The family history rams questions of high-risk association of sudden-infant-death - ndrome with a family history of unusual neonatal respira:m disorders. Perhaps others may be able to report similar :’.?cnences.

Royal Children’sHospital, Flemin

gton Road,

le 3052,

Parkvil

Australia

1 Barraclough, B 2 Guille

JOHN MCNAMARA

M. Lancet, 1976, i, 1353. minault, C , Anagno, R , Souquet, M , Dement, W. C Lancet, 1976,

i, 1326.

GLUTEN AND SCHIZOPHRENIA SIR,-We would like to comment on your editorial’ which discussed our work.2 Our report did briefly address the issue of whether wheatgluten effects could have been due to interference with the absorption or pharmacological activity of the concurrently given neuroleptics. Three observations spoke against this possibility-the adverse gluten effect predominated in the patients with less favourable response to neuroleptic treatment; the undesirable pharmacological effects of medication were as prevalent in the gluten-challenge period as in the gluten-free periods; and the gluten-sensitive psychiatric characteristics of the patients with coeliac disease tend to resemble those in schizophrenia and no neuroleptics are involved here. Wheat-gluten effects contrast with the effects of anticholinergic agents which we have also found, using a similar research design, to be countertherapeutic in schizophrenics.34 The therapeutic reversal with anticholinergics was predominantly seen in the more treatment-responsive patients,S suggesting that anticholinergics directly antagonised neuroleptic actions, whereas wheat-gluten effects probably appeared by accentuation of the components of schizophrenia not controlled by the medication. Consider the opposite issue-i.e., the attenuation of possible pathogenic effects of wheat gluten by the neuroleptics. Since wheat gluten is an abundant constituent of the diet the patients ordinarily eat, the neuroleptics must be effective in the presence of wheat gluten. At the same time, the need for continuous long-term medication to maintain symptomatic improvement in schizophrenia and the high probability of exacerbation after medication is withdrawn, would suggest that neuroleptics may be acting to block, if only partially, the pathogenic manifestations of a factor or factors that continue to act. This means that in our experiment, any pathogenic effects of wheat gluten may have been less evident than if the wheat gluten had been given to unmedicated recovered schi-

zophrenics. Your reference to the work of Curry et al.6 was not pertinent to the question of gluten effects in our study. Their work suggested that the chlorpromazine levels in plasma were sometimes lower when medication was given on a full stomach (with breakfast) than when given on an empty stomach. In our study, the relationship of medication intake to meals as well as to the "special drinks" was the same in the wheat-gluten challenge period as in the control periods, in which soy flour was substituted for wheat gluten in the drinks. Estimation of plasma levels of the medication, which you recommend, may not resolve the issue. There may be considerable intra-patient variations in plasma levels,6 and concentrations of chlorpromazine have been found to decrease merely as a function of time without a concomitant deterioration in the clinical state.’ The addition of barbiturates may further lower the plasma level of chlorpromazine without change in the clinical state.7 We believe, therefore, that for a more definitive answer, the next step should be to test the effect of wheat gluten in unmedicated recovered schizophrenics. You confuse the purely speculative issue of mechanism(s) of pathogenesis with the empirical finding that wheat gluten9 seems to worsen the schizophrenic process. Neither Dohan’s8 work nor ours was a test of any allergic mechanisms or immunological abnormalities in schizophrenia. Mechanisms that do not involve these processes (e.g., the absorption of some psy1. Lancet, 1976, 1, 844. 2. Singh, M. M., Kay, S. R. Science, 1976, 191, 401. 3. Singh, M. M., Smith, J. M. J. nerv. ment. Dis. 1973, 157, 50. 4. Singh, M. M., Kay, S. R. ibid. 1975, 160, 258. 5. Singh, M. M., Kay, S. R. unpublished. 6. Curry, S. H., Davis, J. M., Janowsky, D. S., Marshall, J. H. L. Archs. gen. Psychiat. 1970, 22, 209. 7. Loga, S., Curry, S., Lader, M. Br. J. clin. Pharm. 1975, 2, 197. 8. Dohan, F. C., Grasberger, J. C., Lowell, F. M., Johnston Jr., H. T., Arbegast, A. Br. J. Psychiat. 1969, 115, 595. 9. Dohan, F. C. Am. J. Psychiat. 1973, 130, 1400.

Letter: Abnormal polygraphic findings in near-miss sudden infant death.

689 treated meningococcal or pneumococcal meningitis. It is, howessential that high titre precipitating antisera are used in the c.).E. test if the sm...
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