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CEREBRAL ATROPHY IN YOUNG CANNABIS SMOKERS
1314 it is not fully developed till much later. This is a efficient mechanism than the infant’s fluid swallow, and would greatly reduce the risk of choking or inhaling saliva. The emergence of this swallow at four months and its progressive development could help to determine the upper age-limit of S.I.D.S. It is accepted that in premature infants the rate of S.I.D.S. is greater than in full-term babies.44 This could be associated with the poor neuromuscular coordination often seen in prematures. The condition occurs later in prematures than in full-term infants. This would be consistent with the later onset of salivation in premature infants because of their younger
though
Letters
to
the Editor
CEREBRAL ATROPHY IN YOUNG CANNABIS SMOKERS SIR,-The paper by Dr. Campbell and his colleagues (Dec. 4, p. 1219) is of great importance, and there are other reasons for expecting that gross irreversible brain damage may occur in young drug-addicts. It is both astonishing and I think reprehensible that we are still quite unable to spell-out either the temporary or the irrecoverable damage to the brain that results from drugaddiction. Dr. Campbell refers to other causes of brain decay in young people. Here it may be relevant to add that gross brain damage may result not only from obvious cerebral anoxia, but also in exceptional types of " battle exhaustion ". It seems possible that the taking of drugs during a period of severe physiological fatigue might be particularly harmful, and it would certainly be of interest to know if drug-addicts are liable to develop a variety of parkinsonism, such as occasionally follows battle exhaustion. It may also be worth noting that I think that the outbreak of " encephalitis lethargica " in the 1920s, which had similar after-effects, was never proved to be due to an infection. The need for a vigorous research programme is painfully obvious. W. RITCHIE RUSSELL. Oxford.
SIR,ņYour leader (Dec. 4, p. 1240) is excessively cautious. Dr. Campbell and his colleagues (p. 1219) do not claim proof, but their evidence is amply sufficient to justify the continuation and strengthening of every possible measure to suppress cannabis. You, Sir, may .agree with this, but, regrettably, you do not say so. Little Cocklands, F. J. NATTRASS. Burford, Oxford. POSSIBLE ROLE OF SALIVA IN THE SUDDEN INFANT-DEATH SYNDROME SIR,-All observers of the sudden infant-death syndrome (S.I.D.s.) are agreed that it occurs between one and ten months of age. 90% of cases occur between one and five months, and the peak incidence is between two and four months. It is practically absent in the first month. My hypothesis is that the infant’s inability to cope with excess saliva by swallowing and drooling may cause 3 conditions - (1) choking, (2) laryngospasm, either alone or in association with other factors, and (3) initiation of the diving reflex-any of which could produce the S.l.D.S. Babies in the first two months secrete little saliva. After this time the amount increases, the quantity (and possibly the viscosity) varying greatly. The baby has not learned to swallow all his saliva, and so dribbling (drooling) occurs. The age of major onset of the incidence of S.l.D.S. thus correlates with the time of onset of salivation. If it is assumed that the onset of salivation is a factor in determining the time of onset of S.l.D.S., one should look for some factor relative to salivation in similarly determining the age at which S.l.D.S. becomes infrequent. This could well be associated with the increasing efficiency of the swallowing mechanism. The infant has a fluid swallow which is different from that of the adult.At about four months of age he begins to develop the mature swallow,3 1. Froggatt, P. L. in Sudden Infant Death Syndrome (edited by A. B. Bergman, J. B. Beckwith, and C. G. Ray); p. 77. Seattle, 1970. 2. Lewis, J. A., Counihan, R. S. J. Speech Hear. Disorders, 1965, 30, 280. 3. Hoffman, L. A., Hoffman, R. L. ibid. p. 105.
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conceptional age. Choking.-In the course of a follow-up of babies I have observed a syndrome in infants 4--11 weeks old which " near-miss " of s.i.D.s. The usual story appears to be a was that the infant had been placed on his back after the bath, or put down to have the napkin changed. He choked, struggled for breath, became suffused, stiffened, then stopped breathing and became limp and ashen pale. The mother often thought he was dead. At this point she usually picked him up and applied some form of cutaneous stimulation. As the infant recovered, saliva in a large quantity-sometimes described as thick and often as frothy-issued from the mouth. In no instance was there food or vomitus in the saliva. The description of the attack was quite different from that of a convulsion, the initial
symptom always being that of choking. Apparently the saliva had pooled and been inhaled. Had these episodes occurred when the infants were unattended and unhelped they could have ended in death. Laryngospasm.-It has been thought for many years that this might be the mechanism of death in S.I.D.s. Excess saliva could play a part in triggering laryngospasm. Autonomic imbalance is common in infancy, and evidence of parasympathetic overactivity in the larynx is encountered. Some infants may exhibit croupy breathing if emotionally upset and crying, and others may develop this if exposed to cold air-both indicating a tendency to laryngospasm. Because the parasympathetic nerves are motor to the salivary glands it is possible that such infants could have a good flow of saliva. If saliva entered the larynx it could produce a reflex laryngospasm, particularly if the larynx had been rendered irritable by the presence of upperrespiratory-tract infection or cold air. The presence of viral infection in S.I.D.S. has been substantiated by many investigators,b though the infection has not been of sufficient severity to produce death by itself. S.I.D.S. tends to occur in clusters and is commoner in cold weather, when respiratory infection is more rife. Observers6 have also noted that deaths tended to occur on the same day, suggesting common environmental factors such as a very cold day or high winds. I would therefore hypothesise that, while the presence of saliva in the larynx, of itself, could excite laryngospasm in a predisposed infant, it is more likely to do so in association with other factors such as upper-respiratory-tract infection or cold air, and that such laryngospasm could be a cause of s.i.D.s. The diving reflex.-This reflex can be produced in man by immersion of the nares in fluid. This could occur if the infant lay prone with his nares in a pool of saliva. With this reflex there occur apnoea, bradycardia, and at times cardiac arrhythmias. Jameshas demonstrated physiological resorptive degeneration of the left bundle of His in the first year of life, and suggests that impulse formation and 4. Bergman, F. T. in Sudden Infant Death Syndrome (edited by A. B. Bergman, J. B. Beckwith, and C. G. Ray); p. 49. Seattle, 1970. 5. Ray, G. D. ibid. p. 155. 6. Steele, R. ibid. p. 66. 7. James, T. N. ibid. p. 119.
though
Letters
to
the Editor
CEREBRAL ATROPHY IN YOUNG CANNABIS SMOKERS SIR,-The paper by Dr. Campbell and his colleagues (Dec. 4, p. 1219) is of great importance, and there are other reasons for expecting that gross irreversible brain damage may occur in young drug-addicts. It is both astonishing and I think reprehensible that we are still quite unable to spell-out either the temporary or the irrecoverable damage to the brain that results from drugaddiction. Dr. Campbell refers to other causes of brain decay in young people. Here it may be relevant to add that gross brain damage may result not only from obvious cerebral anoxia, but also in exceptional types of " battle exhaustion ". It seems possible that the taking of drugs during a period of severe physiological fatigue might be particularly harmful, and it would certainly be of interest to know if drug-addicts are liable to develop a variety of parkinsonism, such as occasionally follows battle exhaustion. It may also be worth noting that I think that the outbreak of " encephalitis lethargica " in the 1920s, which had similar after-effects, was never proved to be due to an infection. The need for a vigorous research programme is painfully obvious. W. RITCHIE RUSSELL. Oxford.
SIR,ņYour leader (Dec. 4, p. 1240) is excessively cautious. Dr. Campbell and his colleagues (p. 1219) do not claim proof, but their evidence is amply sufficient to justify the continuation and strengthening of every possible measure to suppress cannabis. You, Sir, may .agree with this, but, regrettably, you do not say so. Little Cocklands, F. J. NATTRASS. Burford, Oxford. POSSIBLE ROLE OF SALIVA IN THE SUDDEN INFANT-DEATH SYNDROME SIR,-All observers of the sudden infant-death syndrome (S.I.D.s.) are agreed that it occurs between one and ten months of age. 90% of cases occur between one and five months, and the peak incidence is between two and four months. It is practically absent in the first month. My hypothesis is that the infant’s inability to cope with excess saliva by swallowing and drooling may cause 3 conditions - (1) choking, (2) laryngospasm, either alone or in association with other factors, and (3) initiation of the diving reflex-any of which could produce the S.l.D.S. Babies in the first two months secrete little saliva. After this time the amount increases, the quantity (and possibly the viscosity) varying greatly. The baby has not learned to swallow all his saliva, and so dribbling (drooling) occurs. The age of major onset of the incidence of S.l.D.S. thus correlates with the time of onset of salivation. If it is assumed that the onset of salivation is a factor in determining the time of onset of S.l.D.S., one should look for some factor relative to salivation in similarly determining the age at which S.l.D.S. becomes infrequent. This could well be associated with the increasing efficiency of the swallowing mechanism. The infant has a fluid swallow which is different from that of the adult.At about four months of age he begins to develop the mature swallow,3 1. Froggatt, P. L. in Sudden Infant Death Syndrome (edited by A. B. Bergman, J. B. Beckwith, and C. G. Ray); p. 77. Seattle, 1970. 2. Lewis, J. A., Counihan, R. S. J. Speech Hear. Disorders, 1965, 30, 280. 3. Hoffman, L. A., Hoffman, R. L. ibid. p. 105.
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conceptional age. Choking.-In the course of a follow-up of babies I have observed a syndrome in infants 4--11 weeks old which " near-miss " of s.i.D.s. The usual story appears to be a was that the infant had been placed on his back after the bath, or put down to have the napkin changed. He choked, struggled for breath, became suffused, stiffened, then stopped breathing and became limp and ashen pale. The mother often thought he was dead. At this point she usually picked him up and applied some form of cutaneous stimulation. As the infant recovered, saliva in a large quantity-sometimes described as thick and often as frothy-issued from the mouth. In no instance was there food or vomitus in the saliva. The description of the attack was quite different from that of a convulsion, the initial
symptom always being that of choking. Apparently the saliva had pooled and been inhaled. Had these episodes occurred when the infants were unattended and unhelped they could have ended in death. Laryngospasm.-It has been thought for many years that this might be the mechanism of death in S.I.D.s. Excess saliva could play a part in triggering laryngospasm. Autonomic imbalance is common in infancy, and evidence of parasympathetic overactivity in the larynx is encountered. Some infants may exhibit croupy breathing if emotionally upset and crying, and others may develop this if exposed to cold air-both indicating a tendency to laryngospasm. Because the parasympathetic nerves are motor to the salivary glands it is possible that such infants could have a good flow of saliva. If saliva entered the larynx it could produce a reflex laryngospasm, particularly if the larynx had been rendered irritable by the presence of upperrespiratory-tract infection or cold air. The presence of viral infection in S.I.D.S. has been substantiated by many investigators,b though the infection has not been of sufficient severity to produce death by itself. S.I.D.S. tends to occur in clusters and is commoner in cold weather, when respiratory infection is more rife. Observers6 have also noted that deaths tended to occur on the same day, suggesting common environmental factors such as a very cold day or high winds. I would therefore hypothesise that, while the presence of saliva in the larynx, of itself, could excite laryngospasm in a predisposed infant, it is more likely to do so in association with other factors such as upper-respiratory-tract infection or cold air, and that such laryngospasm could be a cause of s.i.D.s. The diving reflex.-This reflex can be produced in man by immersion of the nares in fluid. This could occur if the infant lay prone with his nares in a pool of saliva. With this reflex there occur apnoea, bradycardia, and at times cardiac arrhythmias. Jameshas demonstrated physiological resorptive degeneration of the left bundle of His in the first year of life, and suggests that impulse formation and 4. Bergman, F. T. in Sudden Infant Death Syndrome (edited by A. B. Bergman, J. B. Beckwith, and C. G. Ray); p. 49. Seattle, 1970. 5. Ray, G. D. ibid. p. 155. 6. Steele, R. ibid. p. 66. 7. James, T. N. ibid. p. 119.