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MILK-DRINKING MOTHERS WITH COLICKY BABIES
261 evident. Coordination of extremities on the left side was also affected, and computerised axial tomography revealed atrophy of cerebellum after 24 days. After a critical period, with fever and impaired respiration, during the fourth to sixth weeks of her illness she slowly improved. On discharge from hospital in late June, 1979, cerebral nerve involvement was much improved; her temperature was normal and, with help, she could walk, though she still had low grade mental reduction. On July 17, 1980, she had a second attack with paresis of the leg, loss of vision (finger counting only at 1 m), and an increased mental reduction. At follow-up in April, 1981, there had been no further attacks, but many of the symptoms she had had in 1980 persisted (notably, the mental changes), and an
electroencephalogram showed generalised arrhythmic activity. The ratio between antibody titres for RSV in blood and CSF was 28 at day 12 and 20 two years later. These antibody ratios were, respectively, 270 and 453 for HSV and 113 and 226 for varicellazoster. In our system, a ratio below 80 is abnormal and, since the HSV and varicella-zoster antibody ratios were normal, the only explanation for the abnormal RSV ratio is CNS production of antibodies against RSV. The ratio between HSV ratio and RSV ratio was 9-5 5 in the acute phase and 22-6 6 two years later. This ratio is below 2’ 5. normally The immunological findings have been reproduced several times, so the abnormalities cannot be due to methodological error. The only explanation compatible with no association between RSV infection and her neurological disease is cerebral illness due to this virus before 1979. However, she had never been ill before symptoms appeared, so this explanation is unlikely. We conclude that RSV can affect the CNS in adults and cause severe neurological disorders. Since RSV is not usually thought of in the context of CNS infection it is not routinely sought in such cases: systematic search might reveal a more frequent association of RSV with CNS disease. Virological Department, National Institute of Public Oslo 1, Norway
(10-26%).’
sometimes be absent I do not agree with Swart et al. that the prognosis has not changed substantially in twenty years, although it seems to be worse in Asians. Our mortality over a wide age spectrum was 15% and currently it is similar for children. 3-5 Truly remarkable recoveries may be observed and pessimistic forecasts have often proved misplaced. This probably relates to the cerebral pressure problems and oedema so characteristic of tuberculous meningitis and here neurosurgery can play a vital role and shold be considered early. The ideal drug combination has yet to be determined, and a large controlled trial (in India?) is desirable. My personal choice is isoniazid, rifampicin, and ethambutol. With patients in stage 11 or III, I would also add initially ethionamide and (more controversially) steroids. The direst complication is vasculitis which is untreatable and, with our current drugs, possibly unpreventable. Department of Infectious Diseases, Ruchill Hospital, Glasgow G20 9NB
E.A.L. TJØTTA B.
BERG-JENSEN
DERMOT H. KENNEDY
MILK-DRINKING MOTHERS WITH COLICKY BABIES
SIR,-It is difficult to admit that one man’s successful treatment is another’s
Health,
Neurological Department, Telemark Central Hospital
tubercle bacilli can be demonstrated in CSF after chemotherapy has
begun (in 43% of our series). Substantive clues to the diagnosis can be obtained from a history of exposure (40-69%)1,3,5 or from a positive chest X-ray (4488%),1,3-6 and, particularly, from the clinical presentation. Tuberculous meningitis is a subacute meningitis (perhaps termed more appropriately an encephalomeningitis) where neurological features may superimpose insidiously on symptoms of tuberculous toxaemia. Distinctive findings include papilloedema (9-33%)’’ and cranial nerve palsies (12-13%)’’" whilst nuchal rigidity may
placebo.
I
am
in this difficult situation.
Having
read
Jacobson and Lindberg’s paperl in 1978 on cow’s milk as a cause of infantile colic in breast fed infants, our entire paediatric care team (myself, clinical medical officer, health visitors, and nurses) sought
colicky breast-fed babies and advised their mothers to stop drinking cow’s milk to see if their baby’s behaviour improved. If the colic did not disappear we then advised the mothers to cut out other dairy products as well. Within 24 hours most mothers reported a welcome improvement in their baby’s behaviour. The babies became less factious, less jittery, and more amenable, and the agonising colic which had caused screaming and feeding problems disappeared. A further challenge that we advised to confirm the diagnosis nearly always reproduced the original behaviour. It then became important to advise the mothers on how to eat a diet with out
TUBERCULOUS MENINGITIS and colleagues (July 4, p. 15) have done the service by reminding us of the diverse and sometimes profession of cerebral tuberculosis, especially in manifestations "atypical" Asian patients. The lesson of tuberculous meningitis,’ to be repeatedly taught, is that treatment should be started as swiftly as possible on clinical grounds. Delay through bewilderment or procrastination through uncertainty is dangerous and often leads to a worse prognosis.2 The mortality in stage ill disease (marked neurosurgical and sensorial changes) ranges from 25 to 50%,1,3-5 yet patients can be allowed to deteriorate into this stage whilst all due deliberation is given to alternative (and largely untreatable) aetiologies. Unfortunately, and CSF picture can occur in tuburculous meningitis including a polymorph cell preponderance (14-27%)’- and a normal glucose level (13-22%).1,3, ,6 Whilst the cornerstone of diagnosis is the microscopic demonstration of tubercle bacilli in CSF, this is often achieved only with difficulty and determination. Nevertheless in our recent series of 52 cases,positive CSF smears were eventually obtained in 87%. Exhaustive searches of CSF will yield dividends if the physician, alerted by clinical and epidemiological suspicions, exhorts his laboratory colleagues to do them. It is further reassuring that
SiR,-Dr Swart a
1. Kennedy DH, Fallon RJ. Tuberculous meningitis. JAMA 1979; 241: 264-68. 2 Fallon RJ, Kennedy DH. Treatment and prognosis in tuberculous meningitis. J 3 4 5
Infect
1981, 3 (suppl 1): 39-44. Sumaya CV, Simek M, Smith MHD, Seidemann MF, Ferriss GS, Rubin W. Tuberculous meningitis in children during the isoniazid era. J Pediat 1975; 87: 43-49. Smith AL Tuberculous meningitis in childhood. Med J Aust 1975; 1: 57-60. Idriss ZH, Smno AA, Kronfol NM. Tuberculous meningitis in childhood. Am J Dis Child 1976, 130: 364-67.
6 Hinman AR. Tuberculous
1959 to 1963. Am Rev
meningitis at Cleveland Metropolitan General Hospital Resp Dis 1967; 95: 670-73.
sufficient food value to make up for the absent milk. We often find mothers consuming three, four, or even five pints of milk in a day, in the belief, often fostered by advisers else-where, that cow’s milk helps the breast milk supply. Usually by the time the baby was six months old the cow’s milk in the maternal diet produced no symptoms, and we invited our mothers to reintroduce cow’s milk to see if the child still became colicky. Very occasionally a baby continued to be unduly sensitive to cow’s milk in the maternal diet and, in the baby’s or the mother’s
diet, and a soya based preparation was necessary. What do I do now having read Dr Evans and his colleagues’ paper (June 20, p. 1340) who seems to show that avoidance of cow’s milk by mothers who were breast feeding did not reduce the rate of
infantile colic? What do I say to all those mothers who appeared to have carried out a perfectly adequate confirmatory test before stopping cow’s milk in their own diet?-that what they had observed and what we had observed had been merely a placebo response? I think the truth is that there is something wrong with the experiment reported by your columns. Could it be that 600 ml of cow’s milk a day is not enough. Most of our mothers drank more and many a lot mnrp
50 Church Road, Ashford, Middx. TW 15 2TV
1. Jacobson I, Lindberg T. Cows milk Lancet 1978; ii: 437-39.
G. H. CURTIS as a cause
of infantile colic
in
JENKINS
breast fed infants.
electroencephalogram showed generalised arrhythmic activity. The ratio between antibody titres for RSV in blood and CSF was 28 at day 12 and 20 two years later. These antibody ratios were, respectively, 270 and 453 for HSV and 113 and 226 for varicellazoster. In our system, a ratio below 80 is abnormal and, since the HSV and varicella-zoster antibody ratios were normal, the only explanation for the abnormal RSV ratio is CNS production of antibodies against RSV. The ratio between HSV ratio and RSV ratio was 9-5 5 in the acute phase and 22-6 6 two years later. This ratio is below 2’ 5. normally The immunological findings have been reproduced several times, so the abnormalities cannot be due to methodological error. The only explanation compatible with no association between RSV infection and her neurological disease is cerebral illness due to this virus before 1979. However, she had never been ill before symptoms appeared, so this explanation is unlikely. We conclude that RSV can affect the CNS in adults and cause severe neurological disorders. Since RSV is not usually thought of in the context of CNS infection it is not routinely sought in such cases: systematic search might reveal a more frequent association of RSV with CNS disease. Virological Department, National Institute of Public Oslo 1, Norway
(10-26%).’
sometimes be absent I do not agree with Swart et al. that the prognosis has not changed substantially in twenty years, although it seems to be worse in Asians. Our mortality over a wide age spectrum was 15% and currently it is similar for children. 3-5 Truly remarkable recoveries may be observed and pessimistic forecasts have often proved misplaced. This probably relates to the cerebral pressure problems and oedema so characteristic of tuberculous meningitis and here neurosurgery can play a vital role and shold be considered early. The ideal drug combination has yet to be determined, and a large controlled trial (in India?) is desirable. My personal choice is isoniazid, rifampicin, and ethambutol. With patients in stage 11 or III, I would also add initially ethionamide and (more controversially) steroids. The direst complication is vasculitis which is untreatable and, with our current drugs, possibly unpreventable. Department of Infectious Diseases, Ruchill Hospital, Glasgow G20 9NB
E.A.L. TJØTTA B.
BERG-JENSEN
DERMOT H. KENNEDY
MILK-DRINKING MOTHERS WITH COLICKY BABIES
SIR,-It is difficult to admit that one man’s successful treatment is another’s
Health,
Neurological Department, Telemark Central Hospital
tubercle bacilli can be demonstrated in CSF after chemotherapy has
begun (in 43% of our series). Substantive clues to the diagnosis can be obtained from a history of exposure (40-69%)1,3,5 or from a positive chest X-ray (4488%),1,3-6 and, particularly, from the clinical presentation. Tuberculous meningitis is a subacute meningitis (perhaps termed more appropriately an encephalomeningitis) where neurological features may superimpose insidiously on symptoms of tuberculous toxaemia. Distinctive findings include papilloedema (9-33%)’’ and cranial nerve palsies (12-13%)’’" whilst nuchal rigidity may
placebo.
I
am
in this difficult situation.
Having
read
Jacobson and Lindberg’s paperl in 1978 on cow’s milk as a cause of infantile colic in breast fed infants, our entire paediatric care team (myself, clinical medical officer, health visitors, and nurses) sought
colicky breast-fed babies and advised their mothers to stop drinking cow’s milk to see if their baby’s behaviour improved. If the colic did not disappear we then advised the mothers to cut out other dairy products as well. Within 24 hours most mothers reported a welcome improvement in their baby’s behaviour. The babies became less factious, less jittery, and more amenable, and the agonising colic which had caused screaming and feeding problems disappeared. A further challenge that we advised to confirm the diagnosis nearly always reproduced the original behaviour. It then became important to advise the mothers on how to eat a diet with out
TUBERCULOUS MENINGITIS and colleagues (July 4, p. 15) have done the service by reminding us of the diverse and sometimes profession of cerebral tuberculosis, especially in manifestations "atypical" Asian patients. The lesson of tuberculous meningitis,’ to be repeatedly taught, is that treatment should be started as swiftly as possible on clinical grounds. Delay through bewilderment or procrastination through uncertainty is dangerous and often leads to a worse prognosis.2 The mortality in stage ill disease (marked neurosurgical and sensorial changes) ranges from 25 to 50%,1,3-5 yet patients can be allowed to deteriorate into this stage whilst all due deliberation is given to alternative (and largely untreatable) aetiologies. Unfortunately, and CSF picture can occur in tuburculous meningitis including a polymorph cell preponderance (14-27%)’- and a normal glucose level (13-22%).1,3, ,6 Whilst the cornerstone of diagnosis is the microscopic demonstration of tubercle bacilli in CSF, this is often achieved only with difficulty and determination. Nevertheless in our recent series of 52 cases,positive CSF smears were eventually obtained in 87%. Exhaustive searches of CSF will yield dividends if the physician, alerted by clinical and epidemiological suspicions, exhorts his laboratory colleagues to do them. It is further reassuring that
SiR,-Dr Swart a
1. Kennedy DH, Fallon RJ. Tuberculous meningitis. JAMA 1979; 241: 264-68. 2 Fallon RJ, Kennedy DH. Treatment and prognosis in tuberculous meningitis. J 3 4 5
Infect
1981, 3 (suppl 1): 39-44. Sumaya CV, Simek M, Smith MHD, Seidemann MF, Ferriss GS, Rubin W. Tuberculous meningitis in children during the isoniazid era. J Pediat 1975; 87: 43-49. Smith AL Tuberculous meningitis in childhood. Med J Aust 1975; 1: 57-60. Idriss ZH, Smno AA, Kronfol NM. Tuberculous meningitis in childhood. Am J Dis Child 1976, 130: 364-67.
6 Hinman AR. Tuberculous
1959 to 1963. Am Rev
meningitis at Cleveland Metropolitan General Hospital Resp Dis 1967; 95: 670-73.
sufficient food value to make up for the absent milk. We often find mothers consuming three, four, or even five pints of milk in a day, in the belief, often fostered by advisers else-where, that cow’s milk helps the breast milk supply. Usually by the time the baby was six months old the cow’s milk in the maternal diet produced no symptoms, and we invited our mothers to reintroduce cow’s milk to see if the child still became colicky. Very occasionally a baby continued to be unduly sensitive to cow’s milk in the maternal diet and, in the baby’s or the mother’s
diet, and a soya based preparation was necessary. What do I do now having read Dr Evans and his colleagues’ paper (June 20, p. 1340) who seems to show that avoidance of cow’s milk by mothers who were breast feeding did not reduce the rate of
infantile colic? What do I say to all those mothers who appeared to have carried out a perfectly adequate confirmatory test before stopping cow’s milk in their own diet?-that what they had observed and what we had observed had been merely a placebo response? I think the truth is that there is something wrong with the experiment reported by your columns. Could it be that 600 ml of cow’s milk a day is not enough. Most of our mothers drank more and many a lot mnrp
50 Church Road, Ashford, Middx. TW 15 2TV
1. Jacobson I, Lindberg T. Cows milk Lancet 1978; ii: 437-39.
G. H. CURTIS as a cause
of infantile colic
in
JENKINS
breast fed infants.