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EDUCATION AND DEBATE: A W Craft and D M B Hall Munchausen syndrome by proxy and sudden infant death BMJ 2004; 328: 1309-1312 [Full text]

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Medicalisation

C Johnson   (29 May 2004)

Recurrent SIDS is not synonymous with homicide.

James A. Morris   (29 May 2004)

The SBS Myth

Michael Innis   (30 May 2004)

Differentiating MSbP from Infanticide

John J Plunkett   (31 May 2004)

Shot at dawn as an example to others

Mark Struthers   (31 May 2004)

Muddled terms cause further confusion

Richard Braithwaite   (1 June 2004)

Re: Differentiating MSbP from Infanticide

Penny Mellor   (1 June 2004)

Protecting children from the Child Protection system

Charles Pragnell   (3 June 2004)

Munchausen Syndrome by Proxy Can Inflame Needless Fears

Loren Pankratz   (6 June 2004)

Sudden unexpected death and covert homicide in infancy

Christopher J Bacon, Sara Levene   (8 June 2004)

SIDS family clusters: the neglected role of infection

Paul N. Goldwater, Karl A. Bettelheim   (17 June 2004)

Re: SIDS family clusters: the neglected role of infection

Hilary Butler   (18 June 2004)

The mathematics of multiple sudden infant deaths

Ray Hill   (27 June 2004)

Study first, judge later

Viera Scheibner   (29 June 2004)

Re: Study first, judge later

Clive Davies   (29 June 2004)

Re: Study first, judge later

Michael D Innis   (30 June 2004)

Re: Re: Study first, judge later

Lisa C Blakemore-Brown   (30 June 2004)

Comparative Child Mortality of Munchausen's By Proxy

Colin Pritchard   (2 July 2004)

Some Questions for Clive Davies or Anyone

L. Travis Haws   (3 July 2004)

Re: Study first, judge later

Viera Scheibner   (3 July 2004)

Mortality in Munchausen's By Proxy exaggerated.

Brian Morgan   (3 July 2004)

Re: Comparative Child Mortality of Munchausen's By Proxy

Michael D Innis   (3 July 2004)

Concerns about MSBP

Helen P Hayward-Brown PhD   (4 July 2004)

Re: Comparative Child Mortality of Munchausen's By Proxy

Charles Pragnell   (7 July 2004)

Re: Some Questions for Clive Davies or Anyone

Viera Scheibner   (23 July 2004)

Getting the facts right

Penny Mellor   (27 July 2004)

MSbP and sudden infant death: authors' reply

David M Hall, Alan Craft   (11 October 2004)

Re: MSbP and sudden infant death: authors' reply

C Johnson   (11 November 2004)

Re: Re: MSbP and sudden infant death: authors' reply

Dr John Rumbold   (12 November 2004)

Re: Re: Re: MSbP and sudden infant death: authors' reply

Penny Mellor   (13 November 2004)

Re: Re: Re: Re: MSbP and sudden infant death: authors' reply

Ed Cooper   (14 November 2004)

What is MSbP?

Brian Morgan   (14 November 2004)

Re: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply

Penny Mellor   (16 November 2004)

Re: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply

C Johnson   (16 November 2004)

Defining FII

Ed Cooper   (18 November 2004)

MSBP/FII - science and facts are needed, not mythology.

Charles Pragnell   (21 November 2004)

Re: Defining FII

C Johnson   (23 November 2004)

Re: Munchausen syndrome‚ MSBP, and FII

Graeme Johnston   (23 November 2004)

Re: Defining FII

Ed Cooper   (23 November 2004)

FII - give us the science and not the mythology

Charles Pragnell   (26 November 2004)

Re: Re: Munchausen syndrome‚ MSBP, and FII

Michael O'Donnell   (26 November 2004)

Defining FII - WINDSCALE NOW SELLAFIELD - MSbP NOW FII

Clifford G. Miller   (26 November 2004)

Re: Defining FII

Michael D Innis   (27 November 2004)

Cauliflowers/cabbages

Mark Struthers   (27 November 2004)

Re: Re: Defining FII

Penny Mellor   (27 November 2004)

SIDS – Joining The Dots

Michael D Innis   (5 May 2007)

Sudden Infant Death - Revisited

Michael D Innis   (19 June 2007)

Medicalisation 29 May 2004
C Johnson, Parent LA9 Send response to journal: Re: Medicalisation	Is not MSbP/FII the medicalisation of deception simply because it occurs in a medical context? Here are four historical examples: 1 - is it a case of MSbP/FII if a mother falsely tells doctors her child is ill in order to get her husband released from jail on compassionate grounds? 2 - is it a case of MSbP/FII if CVS records a mother taking out her frustration at being stuck in hospital on her infant, then explains away the broken arm as accidental? 3 - is it a case of MSbP/FII if a mother, already convicted of cheque and credit fraud, falsely tells her neighbours her child has cancer in order to raise financial donations? 4 - is it a case of MSbP/FII if a father falsely tells his employer his child is sick in order to get time off work? Cases one, two and three involved the mother; case four involved the father. Cases one, two and three have all been identified as MSbP/FII by one expert or another. Case four has not. In cases one and four the parent perpetrated no physical acts upon the child; in cases two and three the parent did (violently in case two, not in case three). In cases three and four the parent did not approach healthcare workers; in cases one and two the parent did. Would it not be better to identify an act of abuse by its name - e.g. smothering, poisoning - and require evidence of the act before accusation, and proof in prosecution? Would it not be better to identify an act of deception by its name - e.g. fraud - and also prosecute it accordingly? Competing interests: None declared
Recurrent SIDS is not synonymous with homicide. 29 May 2004
James A. Morris, Consultant Pathologist Department of Pathology, Royal Lancaster Infirmary, Lancaster LA1 4RP. Send response to journal: Re: Recurrent SIDS is not synonymous with homicide.	Professors Craft and Hall state "we are concerned that everything we have learnt over the past 40 years about sudden infant death syndrome and the spectrum of child abuse seems to have been forgotten". This is a response to the intense media interest and comment following three recent high profile cases in which mothers were accused of murdering their infants. One problem is that much that is written about sudden infant death syndrome (SIDS) and child abuse is based on insecure foundations. For instance Craft and Hall state "Bleeding from the nose and mouth suggests deliberate suffocation, and the presence of haemosiderin laden macrophages in the lungs might signify previous episodes of suffocation". But there is no reliable information on the sensitivity nor on the specificity of either marker. Thus it is not possible to calculate positive and negative predictive values and use the results in a sensible and scientific manner. This would not be good enough for any other branch of medicine and should not be acceptable in a Court of Law. The authors go on to state "In a single case neither the autopsy findings nor other background information are likely to provide unequivocal evidence". With that I agree. My main concern, however, is their section on recurrent sudden infant death symdrome; in my opinion it is misleading. The risk of SIDS was close to 2 per 1000 live births in the mid 1980s but then gradually fell to approximately 0.5 per 1000 following the "back to sleep" campaign. The risk in a subsequent sibling of an index case was approximately 1 per 100 in the 1980s and is of the same order at the present time. Any study attempting to measure recurrent risk inevitably deals with low numbers and has wide confidence intervals but the several different estimates give similar results [1 - 4]. It is generally accepted that most cases diagnosed as SIDS are due to natural disease (90% or over) but a minority (10% or less) are a consequence of gentle smothering that leaves no marks of injury. All natural disease is a consequence of the environment interacting with genetic constitution and chance. The environment and genetics together set a level of risk that could be 1 in 10, 1 in 100, 1 in 1000, 1 in 10,000 and so on. Since our environments vary and our genetic constitutions vary then so will the risk between infants and between families. Let us assume, to simplify presentation and calculation, that the risk of SIDS is 1 per 1000 for the general population (midway between the 1985 and 1995 figures). If SIDS were due entirely to chance, with no environmental or genetic influence, and the risk was exactly the same in all infants then the risk of two deaths in a mother who had given birth to two infants would be 1 per million. The risk of two deaths in a mother who had had three infants would be 3 per million, and the risk of two deaths in a mother with four infants would be 6 per million. There are approximately 700,000 live births per annum in England and Wales; thus each year at least one mother would have a second case of SIDS. She would risk being accused of homicide and might be found guilty but she would be innocent. The risk of SIDS, however, is not constant. It varies because there are environmental influences that vary such as sleeoing position and exposure to tobacco smoke amongst others [3]. The CESDI SUDI study found that the average risk in families with no recognised environmental risk factors was 1 in 8543; in those with one factor it was 1 in 1616; in those with two factors it was 1 in 596; and in those with three it was 1 in 214. A consequence of this is that if the risk varies then the number of families with two deaths will rise. To illustrate this point consider a population in which the overall risk is 1 per 1000, but 90% have a very low risk and 10% have a risk of 1 per 100. This would in fact give a recurrence rate in siblings of 1 per 100. Mothers at risk in this population would have a 1 in 10,000 chance of two deaths if they had two infants and a 3 per 10,000 chance of two deaths if they had three infants. In a population the size of England and Wales there would be approximately 7 to 10 new cases each year in which a mother had a second case of SIDS. This is higher than the number actually observed (extrapolated from the CESDI study). Thus if risk varied to this degree all second deaths could be explained as natural disease. The CESDI study showed that the average risk in families with no recognised environmental risk factors was 1 in 8500. This does not mean that the actual risk in all those families is the same; some will have a lower risk and some a higher risk. This is because they will vary in hitherto unrecognised environmental risk factors and in genetic risk factors. If one of the families has a cot death then that family is more likely to be in the higher rather than the lower risk groups. The best estimate we have of the risk prior to the first death is 1 in 8500, but the best estimate after the first death is 1 per 100 i.e. the risk of death in a subsequent sibling. If a mother in this group has two infants following a first death then the risk of a second death is 1 in 50. Craft and Hall state "Chance has no memory, so a low risk family would have a 1 in 8500 risk of a second death". The first part of the sentence is correct, chance has no memory, but the second part is simply wrong. The prior risk is 1 in 8500 but the subsequent risk is much higher for reasons given above. This is a serious error in view of all the discussion that has followed the notorious quotation of "a one in 73 million chance" and indicates a major failure of the peer review process of the British Medical Journal. Craft and Hall go on to state, "There is little evidence of familial clustering of SIDS". This is misleading. All natural disease is influenced to some degree by genetics and the environment, as noted above. Siblings share a similar environment and have genes in common so that the risk of SIDS must be increased in families compared with the general population, and studies indicate that it is [1 - 4]; the risk rising from around 1 per 1000 to 1 per 100. If there are two deaths in a family then homicide is a possibility as is inherited disease. But if investigation of inherited disease draws a blank that does not mean that homicide is the most likely. At least one eminent paediatrician has argued that two deaths indicate homicide or some gentic disease unknown to medical science; a statement that is superficially plausible but deeply flawed. There are 30,000 genes in the genome and myriad ways in which deleterious mutations and neutral mutations could influence the risk of death. A failure to name the genes responsible is not a reason for doubting their influence. It is possible to do a similar analysis for three deaths in one family. If the risk is 1 per 1000 for all infants then the chance of a mother with three infants experiencing three deaths is 1 per billion. There haven't been a billion births in England since the Norman Conquest and that remote possibility can be ignored. But if 90% of the population have a low risk and 10% have a risk of 1 per 100 then a new family with three deaths would appear in England and Wales every ten years. If we then allow for the fact that the mother might have four or more children with just three deaths then the situation would occur every four years (approximate). A one per 100 risk is a low genetic risk and it is likely that there are a few families in which the risk is closer to 1 in 10. If that were the case then families with three deaths would arise at a rate of one per year or one every other year. That is approximately the rate at which they do occur and thus even three deaths don't indicate homicide. A mother should not be convicted of murder unless there is evidence, beyond reasonable doubt, that a crime has been committed. The medical evidence for smothering, in the absence of significant injury, is rarely enough. A conviction should not be based soley on the occurrence of two or three infant deaths in one family as natural disease is a more likely explanation. I agree with the authors that more research is required, particularly into the pathogenesis of SIDS. The sciences of genomics and proteomics can provide answers if the investment is made. References 1. Peterson DR, Chinn NM, Fisher LD. The sudden infant death syndrome. J Paediatr. 1980; 97: 265 - 270. 2. Irgens LM, Skjaerven R, Peterson DR. Prospective assessment of recurrence risk in sudden infant death syndrome siblings. J Paediatr. 1984; 104: 349 - 351. 3. Fleming PJ, Bacon CJ, Blair PS, Berry PJ. Sudden unexpected deaths in infancy - the CESDI SUDI studies 1993 - 1996. London: The Stationery Office, 2000. 4. Irgens LM. Recurrent death from natural causes : SIDS and non SIDS. Proceedings of 7th SIDS International Conference, Florence, 2002; 26 - 27. Competing interests: I was an expert witness, introduced by the defence,in two of the three cases mentioned in the above article. i am also involved in a further case in which the issues are similar.
The SBS Myth 30 May 2004
Michael Innis, Director Medisets International Home 4575 Send response to journal: Re: The SBS Myth	Editor, Professors Craft and Hall state, “Caffey described what was undoubtedly child abuse in 1946 but was reluctant to draw the obvious conclusions.” The constellation of subdural haematoma, brain injury and retinal haemorrhages in a child is what they are referring to. However, child abuse is not necessarily the way in which these lesions can be induced. From an analysis of 22 cases of alleged child abuse sent to me from the United Kingdom, United States of America, Australia and Iceland I conclude 1.Vaccines administered within 21 days of the onset of symptoms 2.Disorders of Haemostasis and 3.Nutritional disorders are the main causes of the condition commonly known as Shaken Baby Syndrome. Can Professor Craft or Professor Hall, or anyone of the 106 signatories [1] to the letter responding to the Editorial of Drs Geddes and Plunkett, document a SINGLE case in which the three causes mentioned above could be excluded? No they cannot. As Drs Geddes and Plunkett wisely conclude in their Editorial on the subject “We need to reconsider the diagnostic criteria, if not the existence, of shaken baby syndrome.” [2] I can only add the Shaken Baby Syndrome is a myth invented to hide ignorance and inadequate or improper investigation. Michael D Innis MBBS; DTM&H; FRCPA; FRCPath Reference: 1.Reece RM The evidence base for shaken baby syndrome BMJ 2004;328:1326-1317 2.Geddes JF, Plunkett J. The evidence base for shaken baby syndrome Editorial BMJ 2004; 328; 718 –720 Competing interests: Previously declared paid Court appearances
Differentiating MSbP from Infanticide 31 May 2004
John J Plunkett, Laboratory and Medical Education Director Regina Medical Center, Hastings, MN 55033 Send response to journal: Re: Differentiating MSbP from Infanticide	Infanticide: The intentional killing of an infant or child. It may be "serial". It is murder. I don't know the psychopathology. However, it is NOT MSbP. It does NOT present as an ALTE. It presents as a dead child. It may be impossible to detect or prove. MSbP: Factitious or induced illness in an infant or child with the intent to make oneself appear as the "savior". This MAY present itself as an ALTE. There is NO intent to kill. I, too, have seen the videos. When MSbP and infanticide are "lumped", both lose their meaning. Competing interests: As previously disclosed
Shot at dawn as an example to others 31 May 2004
Mark Struthers, GP Bedfordshire Send response to journal: Re: Shot at dawn as an example to others	This defensive paper by professors Craft and Hall is a sad reflection on paediatrics and child protection and the state they’re in. Amidst widespread confusion, threat and denial they’ve got it wrong again. The protagonists, both medical and legal, in this sorry saga should admit mistake, apologise and accept fair punishment for doing wrong. Then will come ‘closure’. Only then can we move forward to begin the process of restoring public faith in a child protection system that should befit a civilised society. There is no other way. Competing interests: None declared
Muddled terms cause further confusion 1 June 2004
Richard Braithwaite, Staff Grade Psychiatrist West Wight Community Mental Health Team, Chantry House, Pyle St, Newport, Isle of Wight, PO30 1JW Send response to journal: Re: Muddled terms cause further confusion	Editor, Professors Craft and Hall [1] add confusion to an already complex area by muddling various medical and legal terms surrounding the issue of homicide and sudden infant death syndrome (SIDS). Infanticide is a legal term, defined in the UK by the Infanticide Act of 1938. It specifically refers to death caused by a mentally unbalanced mother within the first year of life, the mental imbalance caused by the effects of childbirth or lactation [2]. Thus it does not include every homicide by a parent upon his or her infant. The other two legal categories of homicide are murder and manslaughter. With the exception of manslaughter, Craft and Hall appear to use all these terms interchangeably. Munchausen syndrome by proxy, as first described by Meadow, involves parents fabricating or faking symptoms in their children, thus seeking medical investigations and needless treatment [3]. It is classified in the tenth revision of the International Classification of Diseases (ICD-10) as a form of child abuse, rather than as a medical diagnosis. This is in contrast to the unrelated Munchausen syndrome, which is classified in ICD- 10 as a personality disorder [4]. The 10% of SIDS cases that may be due to foul play are not related to Munchausen syndrome by proxy. The parent is not seeking unnecessary investigations or treatment for the child; he or she has purely and simply killed the child. Craft and Hall are unable to provide any evidence that those who exhibit Munchausen syndrome by proxy behaviour during the first few months of parenthood go on to kill their babies, subsequently claiming “cot death”. They point out, in a section entitled “Is Munchausen’s the best label?” that “many UK paediatricians feel that the term [Munchausen syndrome by proxy] should be abandoned” [1]. They back up this view robustly with no counter-argument, yet use this very label in the title of their paper. There is ample research, cited in the paper, to suggest that a minority of child abusers do fit Meadow’s description of Munchausen syndrome by proxy; the term need not be abandoned in those circumstances. But it cannot be used when describing parents who kill their babies. The public outcry over this issue has been caused by misinformation about the frequency and causes of SIDS. Let us not continue this process by confusing sudden infant death, of whatever cause, with an unrelated form of child abuse that is serious but rarely lethal. References: 1. Craft AW, Hall DMB. Munchausen syndrome by proxy and sudden infant death. BMJ 2004;328:1309-1312. 2. Gelder M, Gath D, Mayou R, Cowen, P. Oxford Textbook of Psychiatry (3rd Edition) Oxford: Oxford University Press, 1996. 3. Meadow R. Management of Munchausen syndrome by proxy. Arch Dis Child 1985;60:385-93. Cited in [2] 4. World Health Organisation. The ICD-10 International Classification of Mental and Behavioural Disorders. Clinical Descriptions and Diagnostic Guidelines. Geneva: WHO, 1992. Competing interests: None declared
Re: Differentiating MSbP from Infanticide 1 June 2004
Penny Mellor, Advocate Home WV9 5HX Send response to journal: Re: Re: Differentiating MSbP from Infanticide	Craft and Hall go on to state, "There is little evidence of familial clustering of SIDS". Does that mean that the jury in the Patel trial were wrong? Does it also mean that Lord Deputy Chief Justice Judge is wrong when the court of appeal in Cannings stated in paragraph 177 "We recognise that the occurrence of three sudden and unexpected infant deaths in the same family is very rare, or very rare indeed, and therefore demands an investigation into their causes. Nevertheless the fact that such deaths have occurred does not identify, let alone prescribe, the deliberate infliction of harm as the cause of death. Throughout the process great care must be taken not to allow the rarity of these sad events, standing on their own, to be subsumed into an assumption or virtual assumption that the dead infants were deliberately killed, or consciously or unconsciously to regard the inability of the defendant to produce some convincing explanation for these deaths as providing a measure of support for the Prosecution's case. If on examination of all the evidence every possible known cause has been excluded, the cause remains unknown." (1) It is interesting that Dr Plunkett makes the comment that he has seen CVS tapes and states for the record that there was no intention to kill, unlike the paper by Sudden unexpected death and covert homicide in infancy S Levene, C J Bacon. (2) in which they assert "Suffocation may leave no external signs and noclear postmortem evidence.10 The significance of intra-alveolar haemorrhage and siderophages is still subject to debate.11 We know that mothers do sometimes suffocate their babies because a number have made very credible confessions,12 13 while others have been witnessed by video surveillance.14" The implication being that because in the UK parents/carers have been caught on camera, that this in turn would lead to death "covert homicides". Of course the reality is quite different. Intervention at 20 seconds (3) occurred and therefore there is no way of knowing whether or not the "smothering" would have continued. It is a presumption only that it would ultimately have led to death and furthermore there is no reference to a control group for this particular research, we have no idea how many parents/carers were filmed that did not harm their child in any way. We can't work out what percentage of parents may harm their child if we only have the one set of figures to study and in particular this research was not random the suspicion of abuse was already there which invalidates the whole thing as a scientific study to be relied upon. As to credible confessions, I question this ascertation, mothers who have had children die for no apparent reason feel incredibly guilty and further to that, if they have surviving infants and there is a prospect of their permanant removal if they don't "admit", there is a very strong motive to "confess" to something you haven't done and within the criminal arena even more so as a confessed infanticide does not lead to imprisonment. Far more research into how the confessions were obtained and under what circumstances needs to be done before such claims can be made. Or even references to research so that we can study this particular statement. I hope that forensic psychiatrists and psychologists contribute to this particular aspect of the debate. When all is said and done, this whole area has been confused by a label that does not look at evidence, just a cluster of events, which may or may not be sinister. The research into this area is at best inadequate, confusing and based mainly on suposition and anecdotal stories. That is not robust enough to remove children and incarcerate mothers. I maintain my stance that until we have a full public inquiry into this entire area, children can not and will not be adequately protected, because in pursuing a negative false allegation, resource is being drained from a child that really does need protecting and to falsley accuse a parent with surviving children is an abuse in itself. 1 http://www.bailii.org/ew/cases/EWCA/Crim/2004/1.html 2 http://press.psprings.co.uk/adc/may/443_ac36202.pdf. 3 http://medicine.ucsd.edu/peds/Pediatric%20Links/Links/General%20Pediatrics%20Inpatient/Covert%20Video%20Recordings%20of%20Life%20Threatening%20Child%20Abuse%20Pediatrics%20Nov%201997.htm. Competing interests: Campaigner against false allegations of child abuse
Protecting children from the Child Protection system 3 June 2004
Charles Pragnell, Expert Defence Witness - Child Protection U.K./Australasia Send response to journal: Re: Protecting children from the Child Protection system	Drs Craft and Hall are suggesting moving forward by preserving the status quo with only a few minor modifications to what has been exposed on many occasions as a child protection system which is deeply, flawed, erratic, and grossly dysfunctional that has been contributed to in large measure by the shortcomings and inadequacies of medical research and opinion. Craft and Hall “are concerned that everything we have learnt over the last 40 years about sudden infant death syndrome and the spectrum of child abuse seems to have been forgotten.” What the public and many professionals have not forgotten are the child protection scandals of the last 40 years of which recent events are just the latest episode. These child protection scandals have caused incalculable harm to many thousands of children and their families and to many care workers, teachers, and others, from false and wrongful accusations of child abuse. Many thousands of children have been wrongfully removed into state care and adoption and many hundreds of parents have been imprisoned. Yet on the other hand, many children have been killed or been horribly abused while agencies failed to act on the signs of abuse and abysmally failed “to communicate with each other”. After every one of these scandals the child protection agencies have made claims that lessons have been learned and procedures have been changed to prevent similar recurrences only for another scandal to occur within a few years if not months when another child has died or another family has been destroyed by false accusations. It is clear that lessons have not been learnt from any of these scandals, or at least only how better to protect agencies and individuals from the legal and financial consequences of their malpractices and misdeeds. Many of these scandals have involved the use of medical and other theories of child abuse which lacked scientific integrity and authenticity but have been zealously grasped by the child protection industry under a perverse pretext of protecting children whilst inflicting immense harm on children and families by their unnecessary and unwarranted interventions and with little thought or compassion for the innocents who suffer as a consequence of their ill-considered decision making based on those flawed theories. Even in those instances where only minor abuse of a child has occurred, the punishment far outweighs the offence and often results in children being separated for the rest of their lives from their genetic family and kinship groups. Those who administer and implement the child protection system seem not to know nor understand the devastating effects on children and families from false accusations of abuse. Of children who live in constant fear of being removed and extreme anxiety that they will be torn from their familiar world, never to return. Of parents who are stigmatized and persecuted in the communities in which they live, who are rejected by their extended families, neighbours and friends and are .paralysed with dread that every knock on the door may lead to their imprisonment and the destruction of their family. Research by Wexler (1991) and others has shown that, “the War against child abuse has become a War against Children” and that the incidence of false and wrongful accusations of child abuse has reached unconscionable levels. It is this research which appears to have been forgotten. The child protection industry now operates Craft and Hall are correct when they state that there is a desperate need to “restore the faith of the public and the professions in the child protection system that are vital for a civilized society”. But such faith, trust, and confidence will not be obtained by continuing to go into denial that there are very serious defects in the present child protection system which are leading to immense suffering by children and families from overzealous and unnecessary interventions and failures to intervene. Nor will it be achieved by paediatricians who are claiming victim status or that there is some kind of orchestrated campaign to discredit them. Such claims are as fanciful as the unproven theories on which they have based their assertions of child abuse. Such a campaign would be welcome if it eventually led to a root and branch reform of the present child protection system. I agree with Dr Mark Struthers that the child protection industry can only move forward when those responsible are able to admit their wrongdoings, apologies are given to those who have been harmed by the child protection system, and the wrongdoers are able to accept fair and just punishment for their misdeeds. The lessons which must now be learned are that a rigorous procedure of investigation and authentication must be introduced to prevent the introduction of medical theories of child abuse which have no basis in scientifically-conducted research and are no more than conjecture, speculation, and supposition. In the future children and families must be protected from a system which is terrorising and harming children and parents under a perverse pretext of protecting those children. Yet at the same time is ignoring those children where the signs of abuse are obvious and the children are dying as a consequence. And smug defensive comments of “damned if we do and damned if we don’t”, are no longer a valid excuse for incompetence and inaction. Competing interests: Concern to reform of the U.K. Child Protection system
Munchausen Syndrome by Proxy Can Inflame Needless Fears 6 June 2004
Loren Pankratz, Clinical Professor, Oregon Health & Sciences University 1525 SW Palatine St.. Portland, OR 97219 Send response to journal: Re: Munchausen Syndrome by Proxy Can Inflame Needless Fears	Craft and Hall(1) suggest that we must not forget everything we have learned over the past 40 years about child abuse. But do not forget that we fall off both sides of the horse. To his surprise, Roy Meadow(2) admitted in 1995 that Munchausen syndrome by proxy had become so popular that it was being overused and misunderstood by some social workers and legal professionals. Since then, many have tried to define the disorder in a way that avoids over-inclusion and diagnostic error. However, the medical literature does not convey the prevalence of these misunderstandings or the devastating consequences, especially as they unfold in juvenile courts across the country. In my experience, most of these mothers have problems that should have been solved clinically, but instead they became entangled in a confrontational legal system. I have written 22 reports on mothers accused of Munchausen syndrome by proxy, and I offer them to any institutionally approved committee investigating this disorder. Although some describe tragic child abuse, the majority illustrate how quickly this diagnosis can enflame needless fears. 1. Craft AW, Hall MB. Munchausen syndrome by proxy and sudden infant death syndrome. BMJ 328:1309-1312. 2. Meadow R. What is, and what is not, "Munchausen syndrome by proxy?" Arch Dis Child 1995;72:534-538. Competing interests: I provide consultations on MSbP.
Sudden unexpected death and covert homicide in infancy 8 June 2004
Christopher J Bacon, Medical adviser, Foundation for the Study of Infant Deaths Foundation for the Study of Infant Deaths, Artillery House, Artillery Row, London SW1P 1RT., Sara Levene Send response to journal: Re: Sudden unexpected death and covert homicide in infancy	We welcome this timely discussion of a very difficult subject, and particularly the recommendations for better procedures when parents are suspected of harming their children. However we should like to comment on two points of detail. First, the authors say it is estimated that around 10% of otherwise unexplained infant deaths may be caused by deliberate suffocation, citing our recent paper [1] as a reference. In fact in our paper we make it plain that the figure of 10%, which was derived from the CESDI SUDI studies [2], referred not just to deliberate suffocation, but to deaths arising from all kinds of maltreatment, ranging from deliberate smothering to negligence and poor care. Deaths due to deliberate suffocation were not separately identified, but they comprise only a proportion of the 10% in question. Second, we agree with Professor Morris [3] that the risk of a second case of SIDS in a family is not the same as the risk for the first death. Calculation of the risk of repeat SIDS from observational studies is complicated by the difficulty in identifying and excluding cases of familial disease and covert homicide. On theoretical grounds, however, SIDS, like most other conditions, arises from a combination of genetic and environmental factors, and if these stay constant, a family who has lost one baby by SIDS must have an increased risk of losing another. References 1. Levene S, Bacon C. Sudden unexpected death and covert homicide in infancy. Arch Dis Child 2004; 89: 443-7. 2. Fleming P, Bacon C, Blair P, Berry PJ. Sudden unexpected deaths in infancy: the CESDI SUDI studioes 1993-1996. London, Stationery Office 2000. 3. Morris JA. Recurrent SIDS is not synonymous with homicide. bmj.com 29 May 2004. Competing interests: Both the authors are or have been medical advisers to the Foundation for the Study of Infant Deaths
SIDS family clusters: the neglected role of infection 17 June 2004
Paul N. Goldwater, senior consultant clinical micr Women's & Children's Hospital, North Adelaide, South Australia 5006, Karl A. Bettelheim Send response to journal: Re: SIDS family clusters: the neglected role of infection	In the very interesting article by Craft & Hall (BMJ 328:1309- 1312), the authors discuss the argument that multiple deaths of infants in one family may indicate the possibility of infanticide, and point to "little evidence of familial clustering of sudden infant death syndrome". In cases where this clustering occurs they suggest two possibilities: homicide or inherited conditions. We would like to draw readers' attention to a third possibility, which has been neglected by many investigators of this condition, namely infection. Indeed, the non-random socioepidemiological factors listed by the authors apply even more to risk of infection than to risk of infanticide. In our researches on a possible infective agent responsible for sudden infant death syndrome, especially the possible role of Escherichia coli, we have noted cases where siblings who died of sudden infant death syndrome some time apart carried the same E. coli serotype, indicating infection from a common source. Karl A Bettelheim Paul N. Goldwater Competing interests: None declared
Re: SIDS family clusters: the neglected role of infection 18 June 2004
Hilary Butler, freelance journalist home 1892 NZ Send response to journal: Re: Re: SIDS family clusters: the neglected role of infection	Dear Sir, Paul Goldwater and Karl Bettelheim, indeed raise a very important point about endotoxemia and SIDS. I have followed all the literature on e -coli endotoxemia and endotoxemia in general as far back as I could trace. I would like the above authors to expand for the readers, on their comments. Drs Goldwater and Bettelheim mention one serotype of E.coli. However, I believe that this is misleading for the following reasons. It is clear from the medical literature from way back, that all serotypes of E.coli (and other bacteria) are capable of endotoxemia. This is not a function of ONE type of e.coli, but seems to be, rather, a function of a fragment of lipopolysaccharide which (for the lack of a better description) floats free off each bacteria, when it multiplies in the gut. The toxicity of the lipopolysaccharide doesn't appear to be dependant on the type. It appears to be a function of the reproductive nature of the bacteria itself. So how might this impact on babies? We all know that endotoxemia causes dysfunction in both the cardiac and respiratory system, that bradycardia is not uncommon..That bacterial endotoxins not detoxified by the liver injure blood platelets which then release large amounts of serotonin (as much as 100-fold). What is the result of this? The Bezold- Jarish reflex, leading to profound bradycardia, hypotension and vascular collapse. If rather less sudden, you would expect to see oedema and haemorrhage by diapedesis.. and after six hours of more, if the process is slower, you would expect to see fibrin platelet clots present as disseminated intravascular coagulation in lungs, kidneys and other organs and tissues. But DIC is not necessary for death by endotoxemia. It all depends on the baby, the health of the baby, feeding methods, medical interventions which have been "imposed" on the baby. So what might doctors be able to test to show the effects of endotoxemia? I have a letter on file from a Professor L. Joe Barry, in which he discusses the fact that Dr Henry Lardy reported finding low levels of the enzyme Phosphoenolypyruvate carboxykinase (PEPCK) in livers of human infants who died of SIDS. (I have this paper) In this letter Professor Barry then describes that he has in brief, proven that endotoxin blocks synthesis of PEPCK and since it has a half life of about two hours, results in changes soon after endotoxin is present. I notice also that a paper in Epidemiol Infect. 1993, 110, 507-617 discussed the role of toxigenic Staphylococcus aureaus likewise causing a potential form of endotoxemia in SIDS children. Having read all of Goldwater and Bettelheims’ papers, I am struck how little notice the rest of the medical world has taken of their vital work. In particular, it seems to me to be a relatively simple matter to test for endotoxemia, and perhaps for that reason, should be part of routine testing on all near SIDS and SIDS babies, yet who else does it, but Drs Bettelheim and Goldwater? In other letters such as Archives of disease in childhood, 1994; 70:252 (" Sudden infant death syndome" by JCK Wells, and PSW Davies), the point is made that heat production has been identified as a risk factor in SIDs. Yet no-one in the endotoxin field has made the point that bacteria such as E.coli literally go berserk when in the presence of heat, either heat by fever/infection, or overclothing.... Furthermore, anyone familiar with the various clinical scenarios and autopsies following SIDs can at times clearly see tell-tale signs of endotoxemia, yet, because it is not understood by clinicians not versed in its vast metabolic effects, these "signs" are considered to be “of unknown origin.” One of the earliest references that would have alerted doctors wanting to understand the role of endotoxin, was an article in Amer J. Dis Child 89:701-716, 1955 ("Hepatitis in Infants and Small Children by Richard Capps, et al) , which showed that inoculation of DPT and infection with other viral agents, caused liver dyfunction changes of shorter duration, which could be confused with hepatitis virus infection. This was later confirmed in mice ( as opposed to humans), in an abstract from the Sixth International Symposium on Pertussis (Dept of Health and Human Services, USPHS, FDA, 1990) on page 124 called "Alternations in Hepatic Drug Metabolism following Vaccine Administration to Mice", by Sherry Ansher and William Habig, who worked for the Center for Biologics Evaluation and Research, Bethesda Maryland. This abstract stated: "There have been several reports of inhibition of drug metabolism following administration of vaccines .... the relationship of these observations to the mechanism for the inhibition of drug metabolism is not known..." They then go on to describe what happened on the administration of DTP...; "DPT vaccine increased hexobarbital-induced sleep time in mice injected with a single human dose of vaccine. Measurement of barbiturate- induced sleep time (the time from injection of hexobarbital to return of the redressment or righting reflex) is a sensitive indicator of specific cytochrome P-450 enzyme function. A minimum of one single human dose was required to induce significant increases in hexobarbital-induced sleep time. Sleep time increased significantly 12 hours after DTP vaccine administration and reached a maximum increase of 2.2 - 2.4 fold above controls 7 - 10 days after a single injection. The effect declined rapidly to levels not significantly different from the controls by day 14. DPT vaccine caused dose and time dependent alterations in hexobarbital- induced sleep time and drug-metabolizing enzyme actitivies. Microsomal cytochrome P-450 and other microsomal and cytosolic enzyme activities were altered in a time dependent manner in mice injected with DTP vaccine. Spectrally assayed cytochrome P-450 was decreased by 50% for 7 days, and similar effects were observed in benzpyrene monooxygenase, benzphetamine demethylase, and ethylmorphine demethylase activity. Cytosolic glutathione transferases and quinone reductase activities were altered, but the time course was different than that observed with the microsomal enzyme activities." "the increased hexobarbital-induced sleep times were not limited to DTP vaccine. Other vaccines with Bordetella pertussis components caused alterations in drug metabolism. One common component of many vaccines is endotoxin, and its presence could enhance, or be responsible for, the observed effects on hepatic drug metabolism." Since this time, there has been little done in children. Though there is one study ( http://www.pediatrics.org/cgi/content/full/101/3/e3 ) Interleukin-6, C-Reactive Protein, and Abnormal Cardiorespiratory Responses to Immunization in Premature Infants”by Massroor Pourcyrous* et al, Clearly, for anyone with any clinical understanding of endotoxemia this study shows this phenomenon very clearly. Yet it appears the authors were stumped. E-coli and endotoxemia in general, in babies, is a grossly neglected, but blatantly obvious area, which has been disregarded, ….. and had it not been so neglected, parents would be better off today. So lets consider endotoxemia briefly in a broader context. A key article to understand this in a fuller context is "Role of the Intestinal Flora in Major Trauma" by P.W.H. Woodruff et al. in The Journal of infectious diseases, Vol 128, Supplement, July 1973. (The whole supplement is on endotoxemia, and is very good. Just because it is "early work", doesn't mean anyone should turn their nose up at it...) They took patients with septic and nonseptic dosorders in whom circulating endotoxin was demonstrated. Tthey also encountered additional patients who had clinical features suggesting persisting endotoxemia, but in whom the test was negative. This study looks at these patients in detail. This article clearly shows "Data indicated that the finding of endotoxin in the livers of these patients signified an endotoxemia consequent on a failure of the endotoxin-detoxifying mechanisms."....."Because of the extreme sensitivity of man to endotoxin, we suspected that clinical endotoxemia.... we undertook postmortem studies on a random series of patients having observed that in animals dying of endotoxic shock, the liver and spleen immediately after death contain considerably higher concentrations of endotoxin that the blood or other tissue..." Without quoting more, they found that some patients lost the ability to detoxify endotoxin, and that because postmortems showed that a septic process was absent, they assumed that the endotoxin was derived from the intestine. So why is this not looked at in babies? It is plain that not only CAN vaccines stop the liver detoxifying endotoxin in SOME babies, the risk to that particular baby is greatly increased if their gut flora have large amounts of E.coli as a result of bottlefeeding, or stress. But the fact is, that if the vaccine was NOT given, these baby’s livers would at least have a better chance to deal with both endogenous and vaccine endotoxin. In essence, in some babies, vaccines could be the equivalent of pulling a trigger, releasing a bullet. The key to survival for these babies, is a well functioning liver, and also nutritional adequacy. There is enough work now to show that adequate vitamin C is crucial in all the endotoxin pathways. I notice that from the very start of Dr Bettelheim and Goldwater's interest in endotoxin, they do not quote key historical information relating to either the overall clinical problem or the actual process. Perhaps that is because some of it, like J. Bendig and H Haenel's landmark paper, called "Gastrointestinal microecology in sudden unexpected death of infants" in "Proceedings of the Eighth International congress of Butrition, Prague, September 1969 is a bit old??? Or take one of the best papers around "The role of Endotoxin in Liver injury" by James P. Nolan in "Gastroenterology 69: 1346-1356 1975. Yes old. But sets it all in its proper context. To study a topic requires a foundation. Gut flora and endotoxemia is such a crucial topic, which even benefits from the studying of the 1905 - 8 works by M. Henry Tissier, and also the studies on the Intestinal Flora of Infants by Erik Olsen, 1949. Considered into this whole equation must ALSO be the blase way doctors prescribe antibiotics to babies without any thought as to its destructive effects on the beneficial gut flora needed to keep toxin producing gram negative bacteria at bay. There is also enough literature on this to suggest that antibiotics have a major down side for many babies. Now, we have these studies they are doing in this country to try to reduce allergies by giving babies a probiotic mix for the first two years of their life, to replace that which babies appear now, to be missing??? Why is that? Wouldn't it be better if the babies guts weren't messed up in the first place? The reality is that, as Dr Catherina Svanborg from Lund University has shown, the intestinal tract/gut flora, is really the seat of the immune system. Whatever is done, to mess that up, be it bottle feeding, or the overuse and abuse of antibiotics, vaccine which shut down the liver,…will all have far-reaching consequences. Naturally, breastfeeding is a must in this regard. Why? It has long since been proven that bottle-fed babies have far higher concentrations of e-coli in their gut. That can be found in the work of Dr Robert Reisinger (and others as well) , who also did extensive studies in other mammals, and proved the crucial protective nature of the right sort of gut flora. If you put this together with the fact that it has LONG BEEN KNOWN, both in humans and animals that vaccines can down-regulate key liver functions which process and eliminate the particles of the bacteria envelope which are the toxin,... and if you put that along side the fact that endotoxemia itself, causes disseminated vascular coagulation which in many cases, will result in haemorrhaging.... yes, perhaps even into the brain ... we start to see a more complete more complex picture. As Dr Michael Innis has stated repeatedly on this forum, there are other very specific haemotological markers which COULD be used in order to get correct diagnoses for parents who currently innocent, but who are in jail for SBS by spurious assertions by people who know nothing about the topic of endotoxemia, or those field in which Dr Innis is an “expert”. There are also other tests, which Dr Bettelheim and Goldwater know only too well, which should also be mandatory for any autopsy following any death of any baby. Where haemorrhaging and other related conditions are implicated, there is a lot more that could be done, than is being done right now. The shame is that prosecution "experts" don't appear to wish to look at anyone else's work. They appear to feel that their own, is the only valid expertise, and that no-one else has anything to offer. There is now enough work on the topic of E-coli to sink a ship. BUT.... most of it is not concerned with clinical practicalities. It is surrounding such topics like genetic typing, looking at the minutae of X factors, until the cows come home. It is time for this situation to be brought into balance. It is time for medical people to openly share expertise with people like Dr Goldwater, Bettelheim,...Dr Michael Innis - to work out exactly what blood tests will show what, and start to "own up" to the real meaning of science, and get their heads around the fact that SBS is not a valid diagnosis on present case histories. It is time for some decent medical studies to be done on the etiology of endotoxemias and related problems. I think here of Professor Clemetson.s CRC Press 3 volume text on Vitamin C in which he details why Vitamin C is so important when looking at infection and endotoxemia. The problem is that in order to do such a study, the researchers have to have a very broad and more complete understanding of all aspects of endotoxemia, haemorrhagic Diseases, Malabsorption or malnutrition, and infections. A broader understanding of the function of the liver in these disorders, particularly relating to endotoxin detoxification is crucial. But there is a problem. The minute the word "vaccine" comes into it, its almost as if any topic is dirty by association. We have this "lets talk about anything but vaccines" syndrome. Don't want to ruin our reputations, or our funding, by challenging the status quo. Why is the issue of vaccines crucial? Because the trend is towards combo vaccines with much larger numbers of vaccines in them. Already this month a bulletin was released showing that combo vaccine plans used in three injections instead of four, are resulting in more fevers, more antibiotic use. Why is that? Could it be that there is an endotoxin trigger here? Well, oops. No-one is either looking at, or thinking about that.... www2.epediatricnews.com/scripts/om.dll/serve?action=searchDB&searchDBfor=art&artType=full&id=aqp04038601d It is interesting that the vaccines concerned include pertussis, haemophilus and the 7 prevnar types. All bacteria capable of creating forms of endotoxemia, which of course, does not even factor in endogenous endotoxemia sources which might add as a co-factor. I can see nothing which studies just WHAT administering these vaccines does to either the PEPCK/liver, or resultant immunological parameters other than the Pourcyrous study above. But even then, while they state the "results", they plainly miss the "why".... When the medical profession starts to grapple with the clinical realities of the role of endotoxemia in SIDS, SBS and other childhood conditions, then maybe parents will have half a fair shot at justice. Until then, parents continue to be at the mercy of the arrogance of ignorance. Hilary Butler. Competing interests: None declared
The mathematics of multiple sudden infant deaths 27 June 2004
Ray Hill, Professor of Mathematics School of Computing, Science and Engineering, Newton Building, University of Salford, Salford M5 4WT Send response to journal: Re: The mathematics of multiple sudden infant deaths	Professors Craft and Hall state that “there is little evidence of familial clustering of SIDS”. To see three examples, they need look no further than the cases of Sally Clark, Angela Cannings and Trupti Patel (assuming that the authors now accept the innocence of these parents). Of course, to prove that two SIDS in a particular family are associated with a familial link is asking the impossible. To establish the link would necessitate establishing the causes of death, in which case the deaths would cease to be classified as SIDS. However, it would be astonishing if there were no familial clustering and, as Professor Morris [1] points out, there is plenty of statistical evidence that SIDS is significantly more likely to occur in a family which has had a previous SIDS. For example, in the CESDI study [2], among the 323 SIDS families studied there were 5 previous SIDS, while among the 1288 control families there were only 2 previous SIDS. This suggests that SIDS is about 10 times more likely in a family which has had a previous SIDS than in one which has not. Other studies, both in the UK and overseas, suggest an increased risk factor of at least 5. So Craft and Hall’s assertion that, in a low-risk family for which the chances of SIDS are 1 in 8,500, the chances of second SIDS (given a first) are also 1 in 8,500, is plainly wrong. Their preceding remark that “chance has no memory” should be reserved for truly random events such as the Lotto draw and the ineffectiveness of playing “hot” or “cold” numbers. As the authors themselves had earlier stated, “sudden infant deaths do not follow a random pattern”. Incidentally, the use of the figure of 1 in 8,500 for a first SIDS in a low-risk family has the potential to be misleading. It compares with a figure of 1 in 1,300 for an average-risk family and so it might be inferred (say, by a prosecution witness or a juror) that when a sudden death has occurred in a low-risk family, the chances of foul play are 6 times greater than would have been the case in an average-risk family. This would be a fallacy. The figures simply show that SIDS will come along in low-risk families rather less often than in high-risk families. When a case does come along, the very factors which make SIDS less likely (e.g. affluent parents in a stable relationship) also make murder less likely, and so there is no justification for any significant increase in suspicion. A more worrying feature of Craft and Hall’s article is that it appears to perpetuate the myth that a second or third sudden death in a family should be viewed with considerably more suspicion than a first. They quote a United States Court judgement that “there might be insufficient evidence in any one child death to prove murder or infanticide, but evidence of repeated incidents was admissible as evidence of non-accidental deaths”. So what are the relevant figures here? What is of no direct relevance is a figure such as 1 in 73 million (obtained by the invalid squaring of 8,543) or even a corrected figure for the chances of two SIDS in the same family. What is relevant is an estimate of the relative chances of double SIDS or double murder in cases where two or more sudden deaths have occurred. Obtaining reliable estimates, based on limited data, is fraught with difficulty. However, my own calculations [3] give the following rough estimates. Single cot deaths outweigh single murders by about 17 to 1, double cot deaths outweigh double murders by about 9 to 1, and triple cot deaths outweigh triple murders by about 2 to 1. So each successive death does give rise to some slightly increased suspicion, but to nothing like the extent that a dictum such as the so- called “Meadow’s Law” would imply. In particular, when multiple sudden infant deaths have occurred in a family, there is no initial reason to suppose that they are more likely to be homicide than natural. In the cases of Clark, Cannings and Patel, it seemed that the second or third death served in itself as the trigger for a criminal investigation and subsequent prosecution. Surely, if these cases are to teach us anything, it is that simplistic rules of thumb should have no place in our thinking, and that all sudden deaths, whether first, second or subsequent, should be thoroughly, but sympathetically, investigated. References Morris JA. Recurrent SIDS is not synonymous with homicide. bmj.com 29 May 2004. Fleming P, Bacon C, Blair P and Berry PJ. Sudden unexpected deaths in infancy: the CESDI studies 1993-1996. London, The Stationery Office, 2000. Hill R. Multiple cot deaths: coincidence or beyond coincidence? Paediatric and Perinatal Epidemiology, to appear. Competing interests: I wrote reports for the defence in two of the three cases mentioned above.
Study first, judge later 29 June 2004
Viera Scheibner, Principle Research Scientist (Retired) Blackheath, NSW 2785 Australia Send response to journal: Re: Study first, judge later	I would like to refer Craft and Hall to my Rapid Response dated 2 April 2004 (http://bmj.bmjjournals.com/cgi/eletters/328/7442/766#55368) which pointed out that Caffey was not a formally trained radiologist and made a real mess of the radiology of what are typical scurvy fractures, misinterpreting them as fractures caused by physical trauma inflicted by parents and other carers. One has to have studied in depth a great deal of medical research to correctly analyse and understand many medical issues. I urge Craft and Hall to do a great deal more study before they enter this foray and muddy the picture with many pieces of incorrect information, such as their claim that multiple cot deaths in one family are rare: quite to the contrary, the risk of another cot death in the same family is increased (2 per 100 of such families)(Gunteroth 1990. J Pediatrics; 116: 520-524) The accusations of parents causing what are typical vaccine injuries is not only reprehensible, it is an indictment of the ignorance of medical doctors about published facts. Medical doctors have a vitally important social, and indeed legal, responsibility to find the correct facts before cluttering medical literature with incorrect information which results in victimisation of innocent carers. Competing interests: None declared
Re: Study first, judge later 29 June 2004
Clive Davies, GP Wimpole Street, London W1 Send response to journal: Re: Re: Study first, judge later	Sheibner mentions Caffey in her rapid response from 26th March, not her one from 2nd April. Agreed, Caffey was not a formally trained radiologist -- but what would radiology training have consisted of in those days? Remember that Caffey was born in 1895 (the same year that Roentgen discovered x-rays). Caffey became professor of radiology at Columbia University, and University of Pittsburgh. Though he described the association between subdurals and limb fractures in 1946 ("Multiple Fractures in the Long Bones of Infants Suffering From Chronic Subdural Hematoma") he didn't jump to the conclusion that these were inflicted. This dawned on him years later. Competing interests: None declared
Re: Study first, judge later 30 June 2004
Michael D Innis, Director Medisets International Home 4575 Send response to journal: Re: Re: Study first, judge later	Editor, Accusing parents of ”causing what are typical vaccine injuries is not only reprehensible, it is an indictment of the ignorance of medical doctors about published facts” –Viera Scheibner. I agree entirely. “…but we are concerned that everything we have learnt over the past 40 years about sudden infant death syndrome and the spectrum of child abuse seems to have been forgotten” say Craft and Hall. I say ‘so much the better’. It’s time to learn the signs and symptoms of Infantile Scurvy (Barlow's Disease), induced by vaccines, and not further abuse children and their parents by perpetuating ignorance. Forget Caffey [1] he was mistaken, and get up to date with Kalokerinos [2] and Clemetson.[3] Michael Innis References: 1.Caffey J. Multiple fractures in long bones of infants suffering from subdural hematoma. Am J Roentgenol, 1946, 56: 163-73 2.Kalokeinos A. Every Second Child. Foreword by Linus Pauling.Keats Publishing, Inc. New Canaan Connecticut 3.Clemetson CAB. Barlow’s Disease. Medical Hypotheses (2002) 59(1).52 -56 Competing interests: I have declared SBS a myth.
Re: Re: Study first, judge later 30 June 2004
Lisa C Blakemore-Brown, Psychologist UK based Send response to journal: Re: Re: Re: Study first, judge later	Drs Innis and Kalokerinos restored my faith in the medical profession when we all spoke at a recent conference in Sydney, Australia. These caring, insightful and brilliant men personified how medics should behave. Stories about how a careful audit trail led them to very different conclusions in many cases of suspected child abuse, mapped onto my own experiences. Their highly detailed, careful work, including interweaving others' intelligent research into their own perceptions, led, for instance, to clear evidence of system failure in vulnerable infants and young children following multiple vaccinations. Dr Innis has outlined his findings on these pages in many Rapid Responses. Whilst prevention is the ideal, from this position of fully understanding what had happened to the children's systems, it was possible for some fortunate children to be given appropriate interventions. It was a joy to see `after` pictures of some children up and laughing after appropriate treatment - given the right diagnosis - but who looked as if they had cigarette burns all over them in the 'before' pictures and who had been at high risk of not surviving. Their form of Kawasaki Syndrome was triggered post vaccine. It should not be the case, in our so called advanced society, that the caring attitudes, highly detailed research and logical observations of these Doctors stand out as unusual. But they do. One day, what they know, what they do and what they say will be heard and appreciated. For the sake of all the children damaged, or likely to be, by vaccinations and experimental drugs, and all the parents falsely accused of causing that damage, or likely to be, given the current climate, may that day come very soon. Competing interests: Specialist and Expert in ASD and ADHD spectrum disorders
Comparative Child Mortality of Munchausen's By Proxy 2 July 2004
Colin Pritchard, Research Professor in Psychiatric Social Work Bournemouth University BH1 3 UH Send response to journal: Re: Comparative Child Mortality of Munchausen's By Proxy	Dear Editor, The over-simplistic media response to Muchausen's By Proxy [MBP] leads me to share new data which suggests that MBP people have a substantially higher child mortality rate than child homicide assailants [1] Based upon a decade of child homicides in a 5% sample of the General Population of England it was found that in terms of acutal numbers Mentally-Ill-Mothers were resonsible for 30% of deaths, Mothers on the `At Risk of Abuse Register' 22%, 15% respectively for Mentally-Ill-Fathers and Non-Blood Fathers with prior conviction for violence and the 19% `Extra Family' assailants were all `Multi-Criminal Violent-Child Sex-Abusers [MCVCSA]. However in epidemiological terms the Mentally-Ill-Mothers rate was 10 per 100,000 but the MCVCSA rate was 869 per 100,000.[2] These rates were juxtaposed [1] against a two-year cohort of 128 parents referred to a `paediatric survelleince unit', who included a substantial number thought to be possible MBP parents [3]. They had an annual child mortality of 6%, an epidemiological rate of 6,250 per 100,000, i.e. seven times the rate of the most dangerous MCVCSA. MBP is an imprecise condition and may well include atypical psychotics but it has been found in over 20 Western countries [4]. British Child Protection [social work, health visitors, general practitioners, police and paeditrics}, despite the media image, in terms of reducing child homicide over the past 25 years, is amongst the best in the world [5]. We must resist an ill-informed and scapegoating media, and rely upon the best evidenced based practice, otherwise the complaint that we are too active will swing if paediatrics are over cautious, and we shall be castigated for being too passive. We must avoid being driven by an irresponsible media to the detriment of the children we are charged to protect Yours truly Colin Pritchard Research Professor in Psychiatric Social Work [1] Pritchard C. The Child Abusers: Research & Controversy, Open University Press. 2004 [2] Pritchard C & Bagley C. Suicide and murder in child murdereres and child sex abusers Journal Forensic Psychiatry. 2001: 12: 269-286 [3] McClure R, Davies P, Meadows R & Sibert J. Epidemiology of Munchausen's Syndrome By Proxy: Non-accidental poisonings & suffocating. Archives Childhood Disease. 1996: 75: 57-61 [4] Feldman M & Brown R. Muchuasen's By Proxy in an interantional context. Child ABuse Neglect.2002: 26:509-524 [5] Pritchard C & Butler A . A comparative study of children's and adult homicide in the USA and the 2003: 18: 341-350major Western countries 1974-1999. Journal Family Violence Competing interests: None declared
Some Questions for Clive Davies or Anyone 3 July 2004
L. Travis Haws, Dentist Lakewood CO 80228 Send response to journal: Re: Some Questions for Clive Davies or Anyone	Editor: Clive Davies states that Caffey concludes the so called long bone fractures were inflicted. Here are some questions regarding; the so called proof of battering, inflicted abuse...? Let's take a journey back some 30 years to some of the original SBS research by Caffey. (1) This article is quoted frequently by SBS proponents as the ground-breaking "proof" of what we now know as SBS, non- accidental injury, inflicted trauma... In the paper, Caffey is describing what he calls injury evidence of whiplash shaking deaths. It appears Caffey's suspicions were confirmed when an infant nurse confessed to shaking, heavy handed burping... Caffey spends some time describing necropsies of two babies--babies H and K. To quote from the 1974 article: "Baby H, 12 days of age, premature girl was well until tonight, when she awakened crying as if in pain. There were no external signs of trauma. Nutrition good, respirations deep and gasping, anterior fontanel bulged slightly, diffuse hemorrhages in the ocular fundi...no history of trauma, no fracture of calvaria. Necropsy findings: skin normal, thymus large microscopic focal hemorrhages in the myocardium: pinkish cellular exudates in the pulmonary alveoli: small subcapsular laceration of the liver filled with fresh blood, liver capsule intact. Brain and head: bulging anterior fontanel, bilateral subdural hematomas, bilateral subarachnoid bleedings, subpial bleeding, lacerations of the cerebral parenchyma, pyknosis and death of ganglion cells and large perivascular bleedings...” "Baby K, girl 11 weeks of age. Chief complaint: bulging of anterior fontanel. Fell asleep well but awakened crying and lethargic; semicomatose on arrival, tachypneic, fontanel bulging, reflexes hyperactive, ocular fundi invisible (bleeding?), moderate generalized cyanosis. Cerebrospinal fluid was bloody, gross fresh blood. Infant turned greyish and died 2 hours after admission. No external signs of trauma on the face or head...No evidence of fractures. Several small foci of atelectasis in the lungs. Brain: no external signs of trauma to the head; bilateral subdural hematomas with subarachnoid hemorrhages...extensive bleedings at the sites of attachment of the bridging cerebral veins to the superior sagittal sinus...eyes not examined." It is important to note that Caffey, in his prior paper, discusses at length, traumatic "involucra" at the ends of long bones as eluded to by Dr. Davies. (2) Caffey concludes from these necropsies that "the findings in these two necropsies demonstrate that the manual whiplash shaking by an adult assailant was pathogenic, especially to the brains and eyes." A few more "supportive" examples discussed by Caffey: 1)--"An infant 2 months of age was treated for "sunken fontanelle" by his Mexican grandmother. Two days before admission to the hospital, she had attempted to raise the sunken fontanel by...holding the infant topsy- turvy by its ankles, and then shaking the infant up and down while an assistant slapped and pounded on the soles of its feet. The sunken fontanel did rise and had become bulgy...subhyaloid hemorrhages were found in the ocular fundi...clonic seizures developed and the cerebrospinal fluid from the cranial subdural space and the lumbar subarachnoidal space contained fresh blood." 2)--"the father at first attempted to "strangle the infant with a blanket," but when the infant convulsed during this assault and became stuporous, the father apparently repented, and then with the mother spent the rest of the night manually shaking the comatose infant in a belated effort to revive it...the infant was admitted to the hospital with extensive bruising of the skin and bilateral intraocular bleedings...necropsy findings included bilateral large subdural hematomas and widely scattered intraocular hemorrhages in the retinas." Caffey concludes at the end of the article that "the essential elements in the infantile whiplash shaking syndrome present an extraordinary diagnostic contradiction. They include intracranial and intraocular hemorrhages, in the absence of signs of external trauma to the head or fractures of the calvaria, and are associated with traction lesions of the periosteums of the long bones in the absence of fractures and traumatic changes in the overlying skin of the extremities." Questions: 1) In the description of Baby H, are "the hemorrhages in the myocardium: pinkish cellular exudates in the pulmonary alveoli: small subcapsular laceration of the liver filled with fresh blood" of significance? And how do they relate to whiplash shaking? What would be your list of differentials considering the above? What additional testing should have been done to eliminate or confirm differential diagnosis? 2) What of Baby H's going to bed well, but awakening as if in pain...and then proceeding to her demise? Did the nurse sneak in and shake the baby while it was sleeping/not crying? Don't the SBS "experts" tell us, depending on the day and case, that the "trauma" immediately precedes the ill infant? 3) In the description of Baby K: semi-comatose with hyperactive reflexes, several areas of atelectasis, no fractures, eyes not visible and/or not examined (?). Again, how does baby K relate to Caffey's whiplash shaking conclusions and the trio of proposed signs? I only see one of the signs. What of the atelectasis? What is your list of differentials? What further testing...could have been done according to the list of differentials? What of Baby K falling asleep well, but awakening crying and lethargic? Again, did the nurse sneak in and violently shake the well sleeping infant? Don't the SBS "experts" tell us, depending on the day and case, that the "trauma" immediately supercedes the ill infant? 4) Does the example of the Mexican grandmother support whiplash shaking? Or does it sound more like cervical compression/extension? Do you agree or disagree that increased intracranial blood pressure from topsy-turvy up and down shaking...may have played a significant role in the hemorrhages and edema as compared to acceleration/deceleration? Where are the accompanying long bone traumatic involucra? One certainly would think this case would show periosteal traction? 5) Does the strangling example support SBS or whiplash? Did the subsequent shaking/revival attempts have anything to do with the hemorrhages? Or does this case more adequately support hypoxic induced hemorrhages from the strangle attempt? Or, along the same lines, does this case also support increased intracranial blood pressure (strangling blocking cerebral venous return...) induced hemorrhages? In this case, how would one go about differentiating between these etiologies? 6) In general, what happened to the long bone lesions? The traumatic involucra? I thought that was part of the triad? Would you agree, or disagree, that bones grow at the epiphysis? Would you agree, or disagree, that such newly forming bone tissues/periosteum may stretch rather easily as compared to mature developed tissue? Perhaps during play, swinging a baby, picking one up by the legs or arms? Or does it require violent abusive forces? Would bone fractures from inflicted abuse/trauma commonly result in changes in the overlying skin...i.e. bruising, edema...? 7) This is a little off of Caffey's discussions, but do you agree or disagree that rib fractures, caused from inflicted non-accidental trauma/abuse, would result in significant pain upon respiration/expiration, physical palpation from a pediatric office visit, laughing, crying...? Or would the infant generally not have pain from the trauma? Would spontaneous fractures from poor nutrition, TBBD be more or less likely to exhibit pain than traumatic fractures? 8) Considering all the above, what do you think the internal validity of Caffey's paper is? Are the conclusions made from the available data valid or potentially mis-leading? 9) Considering all the above, what is the external validity of Caffey's paper? Can the conclusions be generalized to all infants with subdural hematoma and intraocular hemorrhage as pathognomonic of SBS or does thorough testing or history taking need to be carried out to eliminate other causes? Without thorough testing, what is the confidence of diagnosing SBS from Caffey's paper? 10) Do you think much more research should have been done, especially regarding tissue properties, tissue injurability thresholds, biomechanics...before drawing such bold conclusions? Especially in regards to the few, more recent biomechanical studies, that conflict with Caffey's conclusions? (3,4) 11) What are your feelings on the reliability of confessions? How might such confessions effect internal or external validity? How would coercion, threats, promises of leniency, the "immunity or right to keep your kids if you name your partner game"...effect the reliability of a confession, and thus, the reliability of such data? Believe me, there are many more similar questions regarding the rest of the "supportive" SBS literature. L. Travis Haws 1) Caffey J. The whiplash shaken infant syndrome: manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation. Pediat 1974; 54:396-403. 2) Caffey J. On the Theory and Practice of Shaking Infants. American Journal of Diseases in Childhood 1972; 124:161-9. 3) Duhaime A. et al., The Shaken baby syndrome. A clinical, pathological, and biomechanical study. J Neurosurg 1987; 66:409-415. 4) Prange M. et al. Anthropomorphic simulations of falls, shakes, and inflicted impacts in infants. Journal of Neurosurgery 2003 99: 143-150. Competing interests: As previously disclosed
Re: Study first, judge later 3 July 2004
Viera Scheibner, Principle Research Scientist (Retired) Blackheath, NSW 2785 Australia Send response to journal: Re: Re: Study first, judge later	I will respond myself to the purported conflict of interest issue in a subsequent post, but in response to Clive Davies, the point of my response to the Craft and Hall article was that to this day medical doctors, radiologists and others dealing with child abuse are still influenced by Caffey (1946, 1965a,b, 1970, 1972a,b) papers which (yes) were based on ignorance and misinterpretations of the observed x-rays of the babies whose carers are still being accused of inflicted trauma. By saying: “…but what would radiology training have consisted of in those days? Remember that Caffey was born in 1985 (the same year that Roentgen discovered x-rays)” Dr Davies is actually supporting my argument that Caffey was not well qualified to make such judgments, as opposed to demonstrating that he was. The sad part is that even these days the formally trained radiologists still follow Caffey’s misinterpretations, or is Dr Davies going to tell us that their training also leaves much to desire? If so, he would appear to be right. Why otherwise would they still continue interpreting clear and typical scurvy fractures as traumatic? I juxtapose Caffey’s and his followers misinterpretations with the contemporary interpretation of Hiller (1972), a formally trained Australian radiologist who correctly pointed out already in Caffey’s time that what Caffey considers traumatic fractures are in fact scurvy-type structural changes to the trabecular pattern of the bone tissue resulting in typical and bizarre fractures of such affected bones. Our discussion is not only academic in its nature. The consequences of Caffey’s and others’ misinterpretations of x-rays of the children whose carers still continue being accused of inflicted trauma are horrendous injustices of medieval proportions, destroying children and their carers and whole families. Caffey and his followers do not deserve our sympathy and consideration for their ignorance: Hess (1920) in his ahead of its time almost 300 page volume on “Scurvy past and present” elegantly demonstrated the effect of scurvy on many organs of the human body and devoted a number of pages specifically to the scurvic changes to the bone structure resulting in bizarre fractures. There was no excuse for Caffey and his followers misinterpretations or ignorance since Hess’ work was well-known in their times. Just as Roy Meadow’s (and others’) flawed statistics and the Munchausen per proxy ‘diagnosis’ which caused injustices and unspeakable suffering to innocent carers deserve resounding rejection, so does Caffey and his followers‘ ignorant and incorrect interpretations of x-rays. There are further major problems with the diagnosis of shaken baby syndrome and Munchausen per proxy, such as devaluation of the rule evidence in law and in science (and medicine. Please note my distinction between science and medicine as mutually exclusive entities) by the proponents of NAI (non- accidental injury): there is no eye-witness evidence that anybody injured their babies by shaking. In many cases, the accused carers have been persuaded to illogically believe themselves that they injured or killed the babies in their care even though they shook them AFTER they found them unconscious or dead, in their effort to resuscitate them. This applies to the bulk of the SBS cases: there is no eye-witness account of such harmful activity. As one judge in the USA pointed out, such accusations represent a factitious diagnosis carefully fabricated by medical profession. This leads us to the real cause of this factitious diagnosis: vaccination. I urge medical doctors to study more of medical literature which has demonstrated that vaccines are capable and do cause symptoms such as brain and retinal haemorrhages and bizarre fractures which are automatically and incorrectly considered pathognomic of non-accidental indicted trauma. How come thousands of carers from all walks of life, all educational, cultural and religious backgrounds know how to exactly shake a child to get exactly the same injuries and (with very few exceptions such as birth injury) always after, and never before vaccination? There has been no research addressing the issue of why shaking would only cause these specific injuries and no others. Unless this vital issue is properly addressed, the cases of vaccine damage will continue to be diagnosed as NAIT (non-accidental inflicted trauma) and the innocent carers will be dragged through the courts and thrown in jail. Let’s not forget that some magistrates in the US are calling for the death penalty for SBS. This is more than just an academic debate. It is the innocent victims of Caffey’s errors who deserve our consideration and sympathy. Competing interests: None declared
Mortality in Munchausen's By Proxy exaggerated. 3 July 2004
Brian Morgan, Freelance Journalist Cardiff CF11 6LF Send response to journal: Re: Mortality in Munchausen's By Proxy exaggerated.	Exaggeration of mortality from MSBP abuse has already been discussed in the BMJ, as a search would have disclosed. "Death from Munchausen syndrome by proxy is overestimated" Letters, BMJ 1999;318:462 (13 February). The 128 cases referred to in Professor Pritchard's response were not all suspected MSBP cases, as he correctly suggests. Only one of the eight deaths mentioned in the epidemiology study cited might have been from MSBP, and from my own experience of investigating such cases I strongly suspected this death might have been from a case I know well. My substantive point in the letter has never been challenged, though sadly exaggerations of mortality based on unclear reporting in the study continue to appear. An understanding of the process leading to inclusion on the child protection register (children's names only by the way, never the carers) led me to question with one of the epidemiology study authors whether so many deaths could have resulted from MSBP abuse if any at all. Once a referral has been made to social services in which MSBP was suspected, then at the time data for the epidemiology were being gathered registration of the child and siblings was certain to happen. I was aware of only one case at around that time where the local authority rejected the referral because of already known controversy surrounding the diagnosis - a rare assessment by an unusually enlightened social worker. Children were in most cases taken into care by Emergency Protection Order and therefore no death after that time is likely from what was defined as MSBP abuse - other reasons possibly. Thus the one death that might allegedly have been due to MSBP abuse was very likely to have been of a deceased previously born sibling prior to the referral and registration of a later one. Such a case is known from that period (1992 to 1994) and this will be subject to appeal under procedures already under way following the successful Cannings appeal. Knowing as I do who the experts were whose evidence led to the mother's conviction, the appeal is most certain in my opinion to be successful and at that point there will not even be one death that can be attributed even remotely to MSBP during that study period. It's hard to see how Professor Pritchard's reasoning can be sustained, even with one suggested death, not in respect of MSBP anyway - yes, for the other deaths by poisoning and suffocation possibly. But bear in mind that two of the deaths were the result of a suicide and murder combined (by carbon monoxide poisoning in a motor car), where the dynamics are likely to be complex and very different from the context of Professor Pritchard's letter. Competing interests: I wrote the letter to the BMJ referred to by myself in this response.
Re: Comparative Child Mortality of Munchausen's By Proxy 3 July 2004
Michael D Innis, Director Medisets International Home 4575 Send response to journal: Re: Re: Comparative Child Mortality of Munchausen's By Proxy	Editor, Professor Prichard says his new data suggests that Muchausen's By Proxy people have a child mortality rate seven times the rate of child homicide assailants. However, one has to ask how many of the 128 parents he refers to are now having their cases reviewed? Perhaps he should wait till after the Review, which I understand is to take place following some wrongful convictions, before he is led “to share new data.” He may then have a different set of data showing the “over-simplistic media response to Muchausen's By Proxy” is justified Michael Innis Competing interests: I have evidence of mothers accused of MSBP who were innocent.
Concerns about MSBP 4 July 2004
Helen P Hayward-Brown PhD, Research Fellow Social Justice and Social Change Research Centre, University of Western Sydney, Australia, 1797 Send response to journal: Re: Concerns about MSBP	Dear Sir, Having completed my doctorate in the area of false and highly questionable accusations of Munchausen Syndrome by Proxy (MSBP), I would draw Craft and Hall’s (BMJ Vol 328 May 29, 2004) attention to the following issues: 1. Serious concerns raised by parents, academics, the media and other medical professionals are not occurring in any other area of medicine. There is a simple reason for outcries against the discourse of MSBP. A civilised society will accept many deficiencies, but it will not accept repeated harm by professionals of innocent families. 2. The credentials of experts need to be closely examined. This article relied heavily upon the expertise of Professor Southall. What are Professor Southall’s credentials in the specialty of respiratory illness and cot death? In the courts of South Australia, in relation to MSBP, Professor Southall’s evidence was regarded only as an informed lay person’s opinion. 3. The statement that there is little evidence of familial clustering of sudden infant death syndrome needs further consideration. I would refer the authors to the work of Professor Carl Hunt, who states ‘subsequent siblings appear to be at increased risk for the same natural cause of infant mortality as the first sibling’ - explained or unexplained. 4. Changing the label from MSBP to fabricated or induced illness is simply semantics – changing a label does not change outcomes. 5. In the U.K. in October 2003 Dr Umapati Biswas was found guilty of serious professional misconduct and was struck off the medical register for making a false allegation of child abuse. Competing interests: Completion of doctorate on false and highly questionable allegations of Munchausen Syndrome by Proxy (MSBP). Currently completing research fellowship on concerns and issues in relation to MSBP and other 'syndromes'.
Re: Comparative Child Mortality of Munchausen's By Proxy 7 July 2004
Charles Pragnell, Expert Defence Witness-Child Protection and Child/Family Advocate U.K./Australasia Send response to journal: Re: Re: Comparative Child Mortality of Munchausen's By Proxy	Colin Pritchard’s rallying call to British Child Protection workers is typical of the head-in-the-sand denials which have followed every child protection scandal in Britain over the last three decades. In case Colin Pritchard hadn’t noticed, the current scandal was not caused by the media but by the actions of at least two paediatricians who have been prominent in child protection but whose opinions and actions have been respectively described by Courts and a national disciplinary body as “manifestly wrong’, “grossly misleading”, inappropriate”, irresponsible”, and an abuse of professional position”. After every previous scandal we have heard the well-worn cliché of “Damned if we do, and damned if we don’t”, and the totally meaningless, “Lessons have been learnt!.”. No social worker will be damned if they intervene appropriately when there is clear evidence of abuse, and nor will they be damned if they do not intervene when the accusation is completely without foundation. No lessons have been learnt by the British child protection industry from previous scandals or there would not have been so many repeated incidents of children dying while under the care or supervision of British child protection workers or wrongfully accusing innocent parents of child abuse based on research theories which are totally lacking in scientific integrity. Lessons have clearly not been learnt by the child protection industry although massive resources and new powers have been given to the industry following these scandals. Such additional resources and powers have been used to drag even more children and their families into unwarranted and unnecessary investigations and a child protection process which creates severe emotional trauma for the children and parents and stigmatises them for life. “We must …… rely upon the best evidence-based practice”, states Colin Pritchard and who could disagree with such a statement, however his letter relies on little more than junk science and flawed research as has been shown by Brian Morgan and in Pritchard’s own statement that the cohort of 128 parents were “THOUGHT TO BE POSSIBLE MBP PARENTS”. What part does “thought to be” play in `evidence-based’ practice?. How many of the cases included in the `research’ used by Colin Pritchard had been thoroughly and exhaustively tested to establish whether the children’s illnesses were caused by genetic factors, birth injuries, vaccine damage, surgical injury, prescribed medications, severe allergic reactions, or were in fact commonly known diseases. Research into MBP/FII, or whatever the currently fashionable title and definition (an “imprecise condition” according to Pritchard) is, relies solely on the `opinions’ and `suspicions’ of paediatricians and social workers and nothing more. How then can such research be described as `evidence-based’?. It is claimed by Colin Pritchard that British child protection workers have been responsible for “reducing child homicides” and “is amongst the best in the world”. He gives no evidence in support of this opinion and there are strong arguments that the credit for the reduction in child homicides lies in other directions. Far from being the “Best (child protection system) in the world”, the most recent scandal amply demonstrates that the British Child Protection system is deeply-flawed, erratic, and dysfunctional and the evidence from Public Inquiries, Appeal Court Hearings and other authentic sources clearly shows that the child protection system is causing far more harm to children than any parent may have done. What are British child protection workers “best” at?. Creating unnecessary fear in thousands of British children that they may be removed on the basis of false accusations of abuse?. Permanently removing them from their immediate families and kinship groups and placing them with strangers. Providing little or no support for families with disabled children suffering Autism/ ADHD/ Cystic Fibrosis/ Chronic Fatigue Syndrome and then blaming parents for causing such illnesses (FII) and subjecting them to the traumas of child protection processes?. Approaching child protection investigations, not in an open-minded, impartial, or objective way, but with the belief that the abuse has occurred and their job is solely to gather the evidence to prove it?. Culpability and responsibility for these child protection scandals is shared by the British Universities who have taught child protection theories based on this junk science and flawed research to generations of child protection social workers and by the national training and inspection bodies who have permitted and colluded in this continuing brainwashing of child protection workers with these unscientific theories. Clearly Colin Pritchard is stuck in the mindset of so many British child protection workers and expert medical witnesses that, “These are my suspicions/beliefs/opinions/fanciful speculations, therefore they must be fact!.” Far from supporting evidence-based practice he has shown that personal beliefs and opinions are of first and greatest importance. Competing interests: Concerns to reform the child prtoection system
Re: Some Questions for Clive Davies or Anyone 23 July 2004
Viera Scheibner, Principle Research Scientist (Retired) Blackheath, NSW 2785 Australia Send response to journal: Re: Re: Some Questions for Clive Davies or Anyone	Caffey: “The whiplash shaken baby syndrome: manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation”. Pediatrics 1974; 54: 396-403. Yes, this article is widely quoted by the proponents of SBS as providing some ground-breaking “proof” of what is now widely used “diagnosis” of SBS. The best way to respond to Caffey’s articles is to look at the photographs of his “fractures” and describe what they really show. In his article “Traumatic cupping of the metaphyses of growing bones” 1970 Am J Roentgenol Radium Therapy and nuclear Medicine: 108(3): 451-460, Caffey described as “traumatic” the cupping of the right and left distal metaphysis and distal end of femur (Figures 1, 2, 3, 4, 5, 6, & 8) which in fact is characteristic of scurvy as described by Hess (1920) and many others (Hiller 1972) as such. Kogutt et al. (1974) described clavicular, sternal, scapular and spine and spinal cord injuries (vertebral notching), rib fractures and skull fractures and spread of the cranial sutures either alone or in combination. Such fractures were also described by Hess (1920) as typical scurvy fractures. Especially characteristic is rib and vertebral beading. Hiller (1972) described the “typical” epiphyseal plate fractures usually involving a flake of metaphysis, with or without obvious displacement of the epiphysis. These fractures often produce periosteal stripping up of the shafts of the bones, with added subperiosteal haematoma formation which later shows extensive ossification. Silverman (1953) first suggested that all infants and children who demonstrated this type of fracture, without an obvious cause, might possibly be victims of battering. Only a few years later, all and sundry considered that the case had been proven and that these bizarre fractures should now be accepted generally as a strong evidence of battering. In other words, the suggestion changed into evidence without any detailed study, and without any evidence. A mess of gigantic proportions, especially since to this day radiologists who should know better, jump uncritically and blindly on the band wagon of shaken baby syndrome. Hiller (1972) also pointed out that such “bizarre fractures and also bones in no way involved with the fractures, show a chalky appearance on the rontgenogram which, at first glance, suggests a degree or Osteopetrosis but which is not as dense and white as in this condition. It is, however, noticeable enough to have been seen when viewing routine chest roentgenograms and to have initiated a search for fractures of the long bones. Silverman (1953) records this finding hut draws no conclusion from it “, writes Hiller (1972). Another interesting finding is the occurrence of epiphyseal plate fractures on both sides of a joint - often appearing at the same time on roentgenogram and therefore almost certainly being sustained at the same time (Fig 4). As confirmed by a number of orthopedic surgeons, they had never seen this occur in the presence of normal bone even with various manipulative procedures sometimes carried out on the infant to aid in a correction of deformities. It is conceivable that, with twisting or torsion strain such as have been suggested to cause such fractures, the fractures might occur at one side of a joint, but how could it possibly occur at both sides? writes Hiller. He further wrote: “In patients presenting with these unusual fractures, other fractures are often present - the commonest being multiple rib fractures and skull vault fractures. These, of course, could well be sustained as the result of direct trauma, but the occurrence on more than one occasion of a fracture of the acromion (Fig. 5), and of spinous processes (Fig. 6), causes some difficulty in explaining the trauma alone theory. Greenstick fractures of. a number of metatarsals in a 4 month old infant are also difficult to explain (Fig. 7, A and B) [by trauma]”. Hiller (1972) concluded that it is [equally] important not to cause unjust blame to fall on parents or guardians of children who have exhibited epiphyseal plate fractures. It is well known that this type of fractures is common in scurvy without undue trauma to the child, and that greenstick fractures are equally common in rickets. In both these conditions it is known that there is an underlying reason for the bone fragility... the presence of a dense chalky bone structure throughout skeleton is striking enough to alert the pediatric radiologist... Perhaps these infants and children suffer from a collagen disease of acute or subacute nature, affecting predominantly bone collagen. Finally, the inability of social workers to fault the social background of these parents in many cases is another not unimportant point against maltreatment of these children”. In reference to Caffey (1974) case histories, a glance at the ages of the affected children suggest strongly that they developed their problems after vaccination. This is especially relevant to Baby K, a girl aged 11 weeks; an infant 2 months of age (“’sunken fontanelle”). Caffey’s conclusion at the end of his article that “the essential elements in the infantile whiplash shaking syndrome present an extraordinary diagnostic contradiction. They include, intracranial and intraocular hemorrhages, in the absence of signs of external trauma to the head or the fractures of the calvaria… ” should be seen as a warning that the diagnosis of shaking is a red herring and should not be used in a parrot-like fashion by people who quite obviously have no knowledge of these issues. One also has to question their motivation which is quite obviously hostile towards parents and other carers as amply demonstrated in the case of the Clark parents’ baby boys (see BMJ 2004; 328: 1393). However, unless vaccination as the cause of such injuries is properly addressed, the accusations of innocent parents and other carers will continue. The medical profession.should have a good look at itself and reform their hostile ways fuelled by an alarming degree of ignorance about medicine. References Caffey J. 1910. Traumatic cupping of the metaphyses of growing bones. Am J Roentgenol Radium Therapy & Nuclear Med; 108(3): 451-460. Hess AF. 1920. Scurvy - past and present. JB Lippincott Company, Philadelphia and London. Hiller HG. 1972. Battered or not - a reappraisal of metaphyseal fragility. Am J Roentgenol Radium Therapy & Nuclear Med 114(2): 241- 246. Caffey J. 1972. On the theory and practice of shaking infants, its potential residual effects of permanent brain damage and mental retardation. Am J Dis Child; 124: 161-170. Caffey J. 1974. The whiplash shaken infant syndrome: manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation. Pediatrics; 54(4): 396-403. Kogutt MS et al. 1974. Patterns of injury and significance of uncommon fractures in the battered child syndrome. Am J Roentgenol Radium Therapy & Nuclear Med; 121(1): 143-149. Silverman FN, 1953. the roentgen manifestations of unrecognised skeletal trauma in infants. Am J Roentgenol Radium Therapy & Nuclear Med; 69(3): 413-427. Dyer 0. 2004. Doctor charged with misconduct over murder charge. BMJ; 328: 1393. Competing interests: None declared
Getting the facts right 27 July 2004
Penny Mellor, Advocate Home WV9 5HX Send response to journal: Re: Getting the facts right	Professors Craft and Hall state in their paper "There is little evidence of familial clustering of sudden infant death syndrome, and more than one unexplained infant death in the same family suggests two other possibilities, w20: homicide or inherited conditions such as metabolic disorders (for example, medium chain acyl coenzyme A dehydrogenase deficiency), cardiac arrhythmias (including prolonged QT syndrome), immune deficits predisposing to infection, and abnormalities of ventilatory control.2 These conditions probably account for a small fraction of cases,w21-23 but their existence and the possibility that some may remain to be discovered add a dimension of uncertainty in any death where autopsy findings are negative or equivocal." "In future this may sometimes need to include a search for genes that might be associated with conditions predisposing to sudden death. Parents have a right to expect that their baby's tragic unexplained death will be investigated as thoroughly as would be the case for any other citizen." Perhaps Alan Craft and David Hall would now like to rewrite this paper in light of the identification of a gene that causes the sudden deaths of infants, found in the Amish community in the USA from which 21 infants from two generations died. I shudder to think what would have happened if certain paediatricians had been involved in determining the causes of death in this case. The condition is called SIDDT and the babies appear normal at birth but rapidly develop malfunctioning organs. Death occurs before the age of one, caused by sudden heart and lung failure. [1] So maybe we should be genetically testing ALL new-born babies, think of the heartache that could be prevented and this is the only recent discovery either, only last week research also showed that some babies could be prevented from dying, researchers describe the specific group of neurons that are responsible for gasping and what happens to these cells when they are deprived of oxygen. Since gasping resets the normal breathing pattern for babies, the scientists suspect that a malfunction in these respiratory pacemakers is the cellular mechanism that leads to SIDS. [2] Don't take my word for it as a "lay campaigner" read the papers for yourselves. General paediatricians are trained to deal with live babies and children and their illnesses, they are neither paediatric pathologists nor are they geneticists and in my opinion shouldn't give evidence either to social services, police or to the courts on areas of medicine that they have not specialised in. I learn from what I read and regularly discuss aspects of SIDS with forensic paediatric pathologists, not in the UK though because we only have the one and he's retired now! (such is the value of a child's life in this country the government/NHS couldn't or wouldn't pay for the right expertise)! If a baby dies form Long QT Syndrome it leaves NO MARK at death, therefore it is essential that it is identified through genetic testing whilst a child is alive so that a parent can't be accused falsely and for the safety of any other family members who may carry the defective gene. This condition is not as rare as previously thought. This condition is believed to kill between one and two infants in every thousand and is very likely to happen in clusters given that it is genetic in it's origins (outside of drug induced arrhythmias). [3] Prevention is better than cure isn't it? [1] http://www.tgen.org/news/index.cfm?newsid=264 [2] http://www.news-medical.net/?id=3182 [3] http://www.qtsyndrome.ch/sidsp.html Competing interests: Campaigner against false allegations of MSbP etc. Pro bono researcher for law firms into the causes of sudden death in infancy.
MSbP and sudden infant death: authors' reply 11 October 2004
David M Hall, professor of community paediatrics Sheffield University S5 7AU, Alan Craft Send response to journal: Re: MSbP and sudden infant death: authors' reply	Editor: Re rapid responses to our article - EDUCATION AND DEBATE: A W Craft and D M B Hall Munchausen syndrome by proxy and sudden infant death BMJ 2004; 328: 1309-1312 We thank all the correspondents who in total contributed 26 rapid responses to our article on Munchausen syndrome by proxy and sudden infant death. Some clearly find it hard to accept the evidence that infants are sometimes harmed or killed by their parents, even when there is video evidence or a confession by the perpetrator. Several letters presented hypotheses about alternative causes of sudden infant death and how such cases might be wrongly assumed to be homicide, but we did not set out to discuss all the many possible causes of unexplained infant death and would refer these authors to the many expert reviews on the subject. Some respondents put forward what we would regard as extreme views about errors in child protection work and called for apology, punishment and even execution at dawn. Of course individual professionals make mistakes which in child protection work, as in most other areas of health care, can have disastrous consequences - and they should not hesitate to apologise when they get it wrong. But much of this correspondence castigates professionals because they did not know yesterday what we know today. Child protection like any other field of medicine or social care changes in the light of new knowledge and insights. Contrary to the image of professionals eager to snatch children away from their families, implied in terms like “the child protection industry”, we have almost certainly made more, and more deadly, errors by not acting decisively than by over-reacting (1) . Dr Braithwaite argued that we mis-used the term “infanticide”. As he says, this term acquired a specific meaning in English law in 1938. As a defence, it relies on a mother admitting that she killed her baby, but did so because of a mental state related to child birth. However, the concept that the killing of a baby may be different from other forms of homicide has been accepted for centuries (2) . We agree that “homicide” is the best and most inclusive term for all deaths that are not accidental. Dr Bacon pointed out that we mis-quoted his paper. The figure of 10% was a “best guess” for the proportion of infant deaths that may be covert homicide, but although smothering is the most obvious mechanism there are probably other forms of homicide included in this figure. Drs Morris, Bacon and Hill all commented on the difficult statistical issues to do with recurrent deaths and we thank them for their detailed analyses. If an event such as sudden infant death was truly random, a family that had lost one baby in this way would have the same risk with subsequent children. The existence of risk factors, established causes and genes that might predispose to infant death (3) does indeed mean that such deaths are not random and our article emphasised that this is why it is important to search for a cause, when there are two or more unexplained infant deaths in one family. Notwithstanding the tone of many of the responses to our article, we actually agree with much of what they said. Prosecutions and convictions solely on statistical grounds are probably unsafe. Health professionals, and the legal profession, must have the humility to acknowledge uncertainty. It is not doctors or social workers but the judiciary who have the burden of deciding what is in a child’s best interests, whenever there is doubt. The term “Munchausen syndrome by proxy” is imprecise and, although it may accurately describe a few cases, it is more helpful to focus on the fact that someone has fabricated or induced the child’s presenting symptoms and signs and then to consider the mental state and motivation that were responsible. This is why the preferred term is now Fabricated or Induced Illness. Child protection is not an exact science - we still have much to learn and more research is required. In order to have the best available information on which to base opinions and advice, we must ensure that every case is thoroughly investigated; in particular, we urgently need to establish a more scientific investigation and enquiry process into unexplained infant death, as recommended by Kennedy (4) . None of these things is likely to happen unless our society develops a more mature and less punitive attitude to these very distressing issues. 1 Ellaway BA, Payne EH, Rolfe K, Dunstan FD, Kemp AM, Butler I, Sibert JR. Are abused babies protected from further abuse? Arch Dis Child 2004, 89: 845-846. 2 Pitt SE, Bale EM. Neonaticide, infanticide, and filicide: a review of the literature. Bull Am Acad Psychiatry Law, 1995; 23: 375- 386. 3 Weese-Mayer DE, Berry-Kravis EM, Zhou L, Maher BS, Curran ME, Silvestri JM, Marazita ML. Sudden Infant Death Syndrome: Case- Control Frequency Differences at Genes Pertinent to Early Autonomic Nervous System Embryologic Development. Pediatric Research, 2004. 56:391- 395. 4 Royal College of Pathologists and Royal College of Paediatrics and Child Health, 2004. Sudden unexpected death in infancy – a multi-agency protocol for care and investigation. Report of a working group convened by the Royal College of Pathologists and Royal College of Paediatrics and Child Health. Chair: the Baroness Helena Kennedy QC. Available at www.rcpath.org and www.rcpch.ac.uk. AW Craft and D Hall a.w.craft@ncl.ac.uk d.hall@sheffield.ac.uk Competing interests: None declared
Re: MSbP and sudden infant death: authors' reply 11 November 2004
C Johnson, parent LA9 Send response to journal: Re: Re: MSbP and sudden infant death: authors' reply	Sir Would Alan Craft and David M Hall explain the MSbP/FII distinction of the following cases already cited above (1) but which their author's reply has not addressed: 1 - is it a case of MSbP/FII if a mother falsely tells doctors her child is ill in order to get her husband released from jail on compassionate grounds? 2 - is it a case of MSbP/FII if CVS records a mother taking out her frustration at being stuck in hospital on her infant, then explains away the broken arm as accidental? 3 - is it a case of MSbP/FII if a mother, already convicted of cheque and credit fraud, falsely tells her neighbours her child has cancer in order to raise financial donations? 4 - is it a case of MSbP/FII if a father falsely tells his employer his child is sick in order to get time off work? Cases one, two and three involved the mother; case four involved the father. Cases one, two and three have all been identified as MSbP/FII by one expert or another. Case four has not. In cases one and four the parent perpetrated no physical acts upon the child; in cases two and three the parent did (violently in case two, not in case three). In cases three and four the parent did not approach healthcare workers; in cases one and two the parent did. I would be grateful for an explanation of the expertise needed to identify one from the other. http://bmj.bmjjournals.com/cgi/eletters/328/7451/1309#60779 Competing interests: None declared
Re: Re: MSbP and sudden infant death: authors' reply 12 November 2004
Dr John Rumbold, n/a West Midlands Send response to journal: Re: Re: Re: MSbP and sudden infant death: authors' reply	Ms Johnson, you do not need an expert on MSBP to tell you that case 4 is fundamentally different. That is the only case where the child is not being exposed to actual or potential (from unnecessary tests/treatment) harm. If your point is that MSBP is a method for persecuting mothers you have chosen the wrong cases. Competing interests: None declared
Re: Re: Re: MSbP and sudden infant death: authors' reply 13 November 2004
Penny Mellor, Advocate Home Send response to journal: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply	I am interested to know if Dr Rumbold is a medical doctor or an academic as his qualifications would be relevant to his response. As it happens under the guidelines of the RCPCH FII paper [1] none of the four cases Ms Johnson listed should fall into the category of MSbP/FII, all however have done! Case two is child abuse. Cases one, three and four are motivated for reasons other than to gain attention from the medical profession, proof in themselves that it can not be MSbP. The definition of MSbP/FII is very clear, a parent or a carer that induces or exagerates a child's illness in order to gain attention from doctors. Perhaps Dr Rumbold should read the literature before he comments and if he is a medical doctor he certainly needs to educate himself before he makes the same mistake. FII/MSbP is notoriously skewed by different versions of what it is or isn't, unlike other forms of child abuse. Hence the current problems relating to false allegations. Physical abuse is physical abuse. Neglect is neglect. Poisoning is poisoning Suffocation is suffocation Paedophilia, whether it be the physical touching and sexual abuse of a child or viewing it on child pornography sites, is paedophilia. MSbP/FII is a mish mash of a hundred and one things, the mongrel of child abuse and as such has no scientific validity. [1]http://www.rcpch.ac.uk/publications/recent_publications/FII.pdf Competing interests: Campaigner against false allegations of MSbP etc
Re: Re: Re: Re: MSbP and sudden infant death: authors' reply 14 November 2004
Ed Cooper, Locum Cons. Pediatrician London Send response to journal: Re: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply	It was helpful of Penny Mellor to include the reference to the Royal College of Paediatrics and Child Health document on Factitious or Induced Illness in children (http://www.rcpch.ac.uk/publications/recent_publications/FII.pdf). However, I cannot see that this supports her statement: "The definition of MSbP/FII is very clear, a parent or a carer that induces or exaggerates a child's illness in order to gain attention from doctors". The cited document calls for the removal of the MSbP, and then for FII it does not give this narrow definition at all. But don't take my word for this, or Mrs. Mellor's, or, for that matter, Dr. Rumbold's. Have a look. Competing interests: None declared
What is MSbP? 14 November 2004
Brian Morgan, Freelance Journalist Cardiff CF11 6LF Send response to journal: Re: What is MSbP?	It's important in my opinion to see aspects of the definition of Munchausen's Syndrome by Proxy returning to the agenda, as it were. The BMJ has readership and contributors in europe, both sides of the atlantic, australasia, the asian subcontinents and elsewhere. So what do they think of these definitions of MSBP, which come from news reports only a few days ago in the USA? Wednesday, November 10, 2004 http://www.post-gazette.com/pg/04315/409549.stm 'Munchausen's Syndrome by Proxy is a mental or personality disorder in which a parent, usually the mother, intentionally feigns or produces symptoms of illness in a child.' Thursday, November 11, 2004 http://www.clickondetroit.com/news/3912825/detail.html 'Local 4 spoke with Dr. Patricia Siegel, of Children's Hospital, an expert on Munchausen's Syndrome by Proxy (MSP). MSP is a parenting disorder where parents, usually the mother, fabricate symptoms in their children, thus subjecting them to unnecessary medical tests and/or surgical procedures, according to the SIDS Network Web site."We see it quite frequently," said Siegel. "They use illness in their child to demonstrate love."' MSBP is a mental or personality disorder, and a parenting disorder too, it seems. There must be experts in these specialities who can comment? Why have paediatricians been the front runners in what is clearly, from these definitions anyway, not part of their mainstream expertise? What exactly are the diagnostic tests needed to establish whether these parents suffer or do not suffer from this disorder? brianmorgan@ntlworld.com Competing interests: None declared
Re: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply 16 November 2004
Penny Mellor, Advocate Home WV9 5HX Send response to journal: Re: Re: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply	Thank you Dr Cooper, however I referenced the FII paper in respect of what isn't MSbP/FII. Not for the well known definition that can be referenced from just about any medical publication you care to think of. As to abandoning MSbP and changing it to FII, a rose is a rose by any other name. Competing interests: Campaigner against MSbP etc
Re: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply 16 November 2004
C Johnson, parent LA9 Send response to journal: Re: Re: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply	Ed Cooper has a point. The RCPCH's document on FII gives such a woolly definition that it is worse than useless. I'm particularly fond of the statement: "It... includes... those who fail to give needed treatment as well as those who treat unnesessarily." Hardly helpful. Reading the rest of the document, if one sought a definition that covers the limititations of modern medicine, or an individual paediatrician's inexperience, negligence or dishonesty, one could hardly come up with something more suitable. It is an exemplary work of arrogance-based medicine. I think, therefore, that Ms Mellor can't be blamed for believing that little has changed. In the absence of a better definition, a suspicious paediatrician is likely to fall back on the old one. While defining FII is like trying to nail down a blancmange, diagnosing it must be dangerous and foolish. If paeditricians were required to identify an act of abuse as the real thing, or an act of fraud as the real thing, they would better distinguish genuine cases of abuse and fraud from their own limitations. And if they can't do it, they should say so. Competing interests: None declared
Defining FII 18 November 2004
Ed Cooper, Locum Cons. Pediatrician London Send response to journal: Re: Defining FII	I do not see much to be woolly about in defining fabricated or induced illness, nor that much definition is needed. Fabricated illness is apparent illness in a child that is fabricated by an adult looking after that child, induced illness is illness in a child that is induced by an adult looking after that child. The focus is on the child and their apparent or real symptoms and signs. The motivation of the adult perpetrator does not enter the definition. Munchausen Syndrome by Proxy, in contrast, is difficult to define and is a disputed entity, because the focus is on the state of mind of the adult perpetrator. Munchausen Syndrome is a clinical phenomenon of very low prevalence where an adult invents or fakes symptoms and signs and thereby gains a great deal of medical attention. This was described as a phenomenon by Richard Asher. The patients often have numerous scars from unnecessary procedures and operations and the doctors who cared for them often look and feel foolish. It is a phenomenon within the direct experience of many doctors, because although the individuals are rare, they travel from one health facility to another and are seen by innumerable health workers. When unmasked, they discharge themselves and go to another facility. They do not engage in long disputes with the same medical carer, insisting that they have a physical illness. Patients who do the latter are much more common,and sometimes they are right, but they do not have Munchausen Syndrome. Roy Meadow observed some cases of factitious or induced illness in children and promoted the term Munchausen Syndrome by Proxy in describing them, thereby implying that the adult perpetrators had Munchausen Syndrome but gained medical attention through presenting their children to a doctor, rather than themselves. This concept has been fiercely attacked in a prolonged campaign, e.g. through the website M.A.M.A., Mothers Against Munchausen Allegations. Penny Mellor has been much associated with this and indeed describes herself as a campaigner. One of the points persistently made by the campaigners, frequently in BMJ rapid responses, is that paediatricians are ill-qualified to diagnose Munchausen Syndrome in the adult carer and therefore they are ill- qualified to diagnose it by proxy, the child being the proxy. And this is where I become quite bemused. For Penny Mellor, Brian Morgan et al won that point. Because they won it, the Royal College document on Fabricated and Induced Illness by Carers(www.rcpch.ac.uk/publications/recent_publications/FII.pdf) sought to drop the designation Munchausen Syndrome by Proxy. Craft and Hall, above, reiterate this. So now there is no such thing as MSbP/FII, and yet it is Penny Mellor who seems to wish to join two distinct labels by that "/", as if they were interchangeable. It is she who says a rose is a rose by any name, echoing Helen P Hayward-Brown who wrote "Changing the label from MSBP to fabricated or induced illness is simply semantics – changing a label does not change outcomes" in an earlier Response, above. But it is not just semantics, a rose is not a cauliflower; I believe I have made it quite clear above why they are different. Penny Mellor says "Poisoning is poisoning": yes, that's right, and it is also obviously induced illness. Poison a child and you will induce illness in it. Therefore it is FII. What on earth are we all arguing about? The poisoned child is not a case of "MSbP/FII" because, although it is certain that this is FII, it is highly uncertain that any MSbP is involved, a disputable entity in any case, a point conceded to M.A.M.A. As for Carol Johnson's attempt to make the document look woolly by citing ""It... includes... those who fail to give needed treatment as well as those who treat unnecessarily", surely it is easy to think of an example. Child does not have cancer, is given cancer drugs: induced illness. Child does have cancer, in remission, drugs withheld, relapses: induced illness. Competing interests: None declared
MSBP/FII - science and facts are needed, not mythology. 21 November 2004
Charles Pragnell, Expert Defence Witness-Child Protection and Child/Family Advocate UK/Australasia Send response to journal: Re: MSBP/FII - science and facts are needed, not mythology.	Dr. Cooper states, “Roy Meadow observed some cases of factitious or induced illness in children and promoted the term Munchausen Syndrome by Proxy in describing them …….”, and from such observations made conjectures and speculations regarding the existence of a `condition’ he termed Munchausen Syndrome By Proxy. The RCPCH drew heavily on such `observations’ in preparing its document on Fabricated and/or Induced Illness in Children and in fact largely re-gurgitated the contentions and suppositions of Professor Meadow and others as can be verified by an examination of the bibliography and references in the RCPCH document. In a letter to the British Medical Journal in October 2004 concerning child abuse research, Patrick E. Lantz, a forensic pathologist at Wake Forest University Health Sciences in North Carolina, U.S.A, and forty other physicians and scientists stated that, “Evidence based medicine is the conscientious, explicit, and judicious use of scientific evidence in making medical decisions and cautions against unsystematic, untested reasoning and institution-based clinical applications”. Where may I ask is the “conscientious, explicit, and judicious use of scientific evidence in making medical decisions” in the conjectures and speculations of Professor Meadow?. Or for that matter in the document produced by the RCPCH?. There are some anecdotal contentions as reiterated by Dr Cooper and largely based on the assertions of a minority group of paediatricians, probably less than 10% of the paediatric profession in the U.K., but there is a complete absence of any scientific evidence to support the existence or otherwise of MSBP/FII or any replication of whatever research may have been by Meadow or any others, undertaken to support such existence. Where are the statistics on false positives and false negatives in the application of MSBP/FII?. Where is the evidence of the incidence of its occurrence?. Alleged cases in the U.K. appear to be in clusters in certain geographical areas so is there some risk to certain sections of the population and that other sections of the population are risk-free?. Dr. Cooper asserts that, “Patients who do the latter are much more common, and sometimes they are right, but they do not have Munchausen Syndrome” implying that MSBP/FII is a medical condition that certain individuals suffer from. Where are the medical criteria for identifying such a condition, what are the symptoms of this condition, how is it unequivocally diagnosed, and what treatments are currently available to alleged “sufferers”. Professor Meadow has stated (1995) that no one `suffers’ from MSBP, neither a child nor an adult and Meadow has disputed claims that it is a psychiatric condition. Yet Dr. Cooper is now seeking to change the criteria set by Professor Meadow. Professor Meadow has also stated that it is a paediatric condition and can only be `diagnosed’ by paediatricians. Yet it has been diagnosed by individual within various professional and pseudo-professional groups such as psychotherapists, physiotherapists, social workers, child abuse professionals, anaesthetists, and even a veterinary surgeon. Not all use the terms MSBP/FII but it is clear from their descriptions of the behaviours of the individuals that this is their purpose and intent. Courts [e.g. Queensland Supreme Court 2004] have declared that MSBP/FII is not a psychiatric condition and that paediatricians should present facts of child abuse to Courts and not labels [i.e. MSBP/FII] describing behaviours which may or may not apply to the individuals concerned. Indeed Dr, Cooper, what are we arguing about?. Until the conscientious, explicit, and judicious use of scientific evidence is apparent in the assertions of a minority of physicians of the existence of MSBP/FII, then Courts and medical scientists and researchers will continue to refute its existence and to question its use in child protection matters. More rational professionals who are committed to evidence-based practices will also continue to be circumspect regarding a contention of a form of child abuse which has no scientific basis for its existence, has no commonly agreed and accepted definition, which can be applied by virtually any member of any profession or pseudo-profession, and which serves to obscure the absence of facts rather than to enlighten and inform inquiries into alleged child abuse. Competing interests: A concern to reform the child protections ystem
Re: Defining FII 23 November 2004
C Johnson, parent LA9 Send response to journal: Re: Re: Defining FII	Ed Cooper states: "Penny Mellor says "Poisoning is poisoning": yes, that's right, and it is also obviously induced illness. Poison a child and you will induce illness in it. Therefore it is FII. What on earth are we all arguing about?" What we appear to be arguing about, Dr Cooper, is that if you were to claim I'd poisoned an adult, you'd struggle to gain credence unless you could identify it as such. But as a paediatrician you might tell police, social workers, the courts or other medical professionals that my child has FII (or that you merely suspect it), and your expert 'diagnosis' need not identify any poison or evidence of it to destroy my family and even cost my child their life. That is what has been happening to children and their families to date. The same criteria by which victims of Cisapride were diagnosed as MSbP are the same criteria by which they would now be diagnosed as FII. By changing the name from MSbP to FII, you and the RCPCH have indeed ducked the thorny issue of motive which underpinned Meadow's theory; but in doing so you demonstrate that the term FII is rather pointless anyway. Are we to call a broken motor vehicle a case of 'Fabricated or Induced Mechanical Failure' if we suspect it was caused deliberately or faked? If a severed brake-fluid line is intended to kill the driver it's called attempted murder. If a false claim of damage is intended to rip off an insurance company it's called fraud. Do we need an expert to identify a new sabotage syndrome or label with which to dispense with having to produce the cut brake-line or dodgy documents that would prove our suspicions right or wrong? And doesn't the health and welfare of children and their families warrant at least as much attention to detail? The irony is that having created an unnecessary label on which to demonstrate their expertise, paediatricians have provided one which even those with no medical expertise can also claim to identify, as the recent American experience shows. Lawyers, social workers, estranged spouses - they're all having a go - because they don't need to describe an act of abuse or deception; they just say the words 'MSbP' or 'FII'. Competing interests: None declared
Re: Munchausen syndrome‚ MSBP, and FII 23 November 2004
Graeme Johnston, Student MK7 6AA Send response to journal: Re: Re: Munchausen syndrome‚ MSBP, and FII	Mr Pragnell seems to have ignored a crucial point made in Dr Cooper's rapid response: MSBP is not the same as FII. If they are lumped together, confusion is bound to occur. Is this what Mr Pragnell wants? Mr Pragnell also seems to have confused Munchausen Syndrome and Munchausen Syndrome by Proxy. He wrote: "Dr. Cooper asserts that 'Patients who do the latter are much more common, and sometimes they are right, but they do not have Munchausen Syndrome' implying that MSBP/FII is a medical condition that certain individuals suffer from". Actually, that section of Dr Cooper's letter was clearly referring to Munchausen syndrome. Competing interests: None declared
Re: Defining FII 23 November 2004
Ed Cooper, Locum Cons. Pediatrician London Send response to journal: Re: Re: Defining FII	I did not manage to understand Dr. Charles Pragnell's response, and he evidently could not understand mine: I notice that he did not understand my paragraph about Munchausen Syndrome (as described by Richard Asher) as being about Munchausen Syndrome, not about'Munchausen Syndrome by Proxy'. But I do see that he is intent on keeping 'MSbP/FII' alive since he uses the conjoined acronym 6 times. Perhaps it is difficult to let it go when it makes a target to attack and you are in the attacking game. But it should be let go. It is unproductive to attack a chimaera. I do not believe there is, or can be, any such thing as 'MSbP/FII'. To batter on with the point, how about trying some other conjoined acronyms? What about something absurd:'BPD/PCP'? BPD is Borderline Personality Disorder, an entity staunchly supported by some doctors but rejected as meaningless by others. So it is a disputed entity, difficult to define, difficult to use in predictive value calculations, etc. PCP is Pneumocystis carinii pneumonia, an entity disputed by nobody. BPD may or may not exist, PCP definitely physically exists, the difference is not semantic, the conditions are not related, the terms cannot be interchanged, there is no such thing as 'BPD/PCP', it is a complete absurdity. Try 'ME/CFS'. That's all right, the difference is semantic. Some strongly prefer Myalgic Encephalomyelitis as a label, others equally strongly Chronic Fatigue Syndrome, but they do agree that it is two names for more or less the same thing. Finally, 'ME/MS'. No, impossible again. ME and Multiple Sclerosis do have some features in common, they relate to the nervous system, but ME is clearly not a new label for MS, there are some very great biological differences. To me, for attackers and defenders alike, speaking of 'MSbP/FII' is like speaking of 'ME/MS'. Speak of one or the other, but do not conjoin them. Competing interests: None declared
FII - give us the science and not the mythology 26 November 2004
Charles Pragnell, Expert Defence Witness and Child/Family Advocate U.K./Australasia Send response to journal: Re: FII - give us the science and not the mythology	In response to Graeme Johnston, it is not I who is seeking to spread confusion, the confusion already exists and no more so than in the minds of the proponents of MSBP/FII and Dr. Ed Cooper has not established that FII is not the same as MSBP. Since the initial ascription of the label of MSBP by Professor Sir Roy Meadow in 1977 there have been a succession of variant labels such as Meadow’s Syndrome, Polle’s Syndrome, Factitious Disease (Disorder/Illness) By Proxy, Munchausen By Proxy, Paediatric Condition Falsification etc etc. Each has been but a slight variation on the preceding labels but having the same core definition. FII is therefore simply a continuation of the same theme. Secondly, the quotations of Dr. Cooper which I used were to illustrate his claims that Munchausen Syndrome and Munchausen Syndrome By Proxy were both medical conditions. They are not. At best they are labels given by a few doctors to describe their conjectures, suppositions, and fanciful speculations regarding the behaviours of some people. Behaviours which are quite commonplace, unsurprisingly even among members of the medical profession. If Dr, Cooper wishes to batter on with the point of acronyms, how about Rubella/German Measles i.e. R/GM, or Chicken Pox/Varicella i.e. CP/V. Notably Graeme Johnston and Dr. Ed Cooper studiously evade the central and most important issue in my letter that there is no scientific basis for FII as there was not for MSBP. Neither the RCPCH nor the Dept of Health undertook any scientifically based studies before producing their respective documents on FII having merely selectively trawled the literature by MSBP proponents. (At the time those documents were written, there was no literature on FII so the existing literature was regarding MSBP which further denigrates Dr. Ed Cooper’s claims). Leaving aside for the moment whether or not MSBP and FII are synonymous, and in order that Dr Ed Cooper clearly understands my points, I ask him to produce scientifically-based studies which support the existence of FII, the independently replicated studies which confirm those findings, and the peer reviews of these studies?. Where are the statistics of false positives and false negatives of the application of FII?. Until Dr. Cooper can produce such evidence then FII remains merely a label used by a minority of physicians to support their anecdotal stories and their conjectures, suppositions, and fanciful speculations. Competing interests: Concern to reform a dysfunbctional child protection system
Re: Re: Munchausen syndrome‚ MSBP, and FII 26 November 2004
Michael O'Donnell, FRCGP. Former GP turned journeyman writer Loxhill GU8 4BD Send response to journal: Re: Re: Re: Munchausen syndrome‚ MSBP, and FII	Richard Asher, who had an impish sense of irony, would have enjoyed this discussion. Those of us who sought out his lectures often heard him explain that one reason he described Munchausen Syndrome was to show that if you took a collection of symptoms, called it a syndrome and gave it a memorable name, doctors would start diagnosing it. Asher applied the Munhausen label to a tiny group of disparate individuals, who went from hospital to hospital telling dramatic and untruthful tales that deceived ingenuous doctors. Their tales were plausible enough for the tellers to be admitted and they sometimes ended up on the operating table, their abdomens becoming scoreboards on which the scars recorded the number of surgeons they had deceived. They nearly always discharged themselves against advice after quarrelling violently with doctors and nurses. Asher stressed, however that Munchausen Syndrome was a descriptive not a diagnostic label – and a description of behaviour, not of motive. Indeed he suspected that different individuals had different motives for embarking on their voyages of deception. The motives he suggested included: a desire to be the centre of interest and attention - a Walter Mitty fantasy in which, instead of playing the surgeon, they assumed the equally dramatic role of patient; a grudge against doctors and hospitals which could be satisfied by frustrating or deceiving them; a way to get drugs; the need to escape from the police – a need which led many to swallow objects like nails and chains, to try to enlarge or infect their wounds, or to warm up their thermometers; a desire to get free board and lodgings for the night. Asher suspected that these scanty motives were probably supplemented by some “strange twist of personality” but warned us against accepting a description as a diagnosis. He used to illustrate the perils of descriptive diagnosis with another example: "'What is this strange skin condition with red rings which expand from the centre in widening circles?' “‘That,” says the dermatologist, “is erythema annulare centrifugum.’ “He has spoken the words of power, and the dignity of the profession has been upheld.[1]” 1. Asher,R. Talking Sense. London: Pitman Medical, 1972 Competing interests: None declared
Defining FII - WINDSCALE NOW SELLAFIELD - MSbP NOW FII 26 November 2004
Clifford G. Miller, Lawyer, graduate physicist, former University examining lecturer in law BR3 3LA Send response to journal: Re: Defining FII - WINDSCALE NOW SELLAFIELD - MSbP NOW FII	Dear Sir, WINDSCALE NOW SELLAFIELD - MSbP NOW FII Redefinition and renaming is an old game, here played on a different pitch. The broad underlying problem is the same. As is the overlying problem, that this is an issue of power and control. When medical 'science' (that elusive beast) wants its own way against detractors, it claims there is no scientific evidence for such and such. When it wants its own way for its protagonists, it claims such and such exists, when there is no science to back it up, just conjecture and what it terms 'anecdotal' evidence. Let's face it, there is no such commonly occurring thing as MSbP and/or FII, even if once or twice some medical scientist claims to have witnessed behaviour that fitted such a pattern in wholly unusual and rare circumstances, unlikely to recur, if it ever occurred at all. What there is instead is open season on Moms for situations in which those who seek to retain power and control over medicine and the lives of others have no answers. So, it must be for MSbP and/or FII. All of these debates are part of a perennial pattern of struggle of right against wrong. If we lived in a society that espoused strong ethical and moral values, and if every one of our civic, religious and political leaders espoused and lived applying those values, and we had strong communities which did so also, there is little doubt greater openness and honesty would prevail. Instead we live in a very different world. We can see in so many ways the failure by all manner of leadership of social, political, civic, professional and other organisations to operate in accordance with strong ethical and moral values. This is all in the void left by the failure of mainstream organised religions to deliver and their old role in building strong communities with strong belief systems has been eradicated with the communities they used to nurture. In such a Society, how many trust the General Medical Council to do the right thing. This is exemplified by witchhunts, which seem to be so common of late, against those who express alternative views or failures to mete out strong and appropriate sanctions against those in the 'mainstream' who have practised 'medicine' lacking any proper basis and causing great harm and more often than not to the most vulnerable. That is the backdrop within which the small part this debate takes in the universal drama played out daily on the world stage. There are innumerable such struggles and those who fight the good fight must all recognise the overall problem and work for ways in which to overcome it, whether secularly or spiritually based. In doing so battles such as this could well be all but won before they start. Or they may never start; lacking an environment to sustain and nurture the ill provoking them. This is not to say all those who adopt and apply theories of the kind in question are or are not evil or immoral. I have seen so many times those who convince themselves they are doing the right thing, having justified it to themselves with reasons they cling to with quasi-religious fervour. Those reasons seem to be essential in maintaining self belief in their own actions being moral and ethical which, when seen in the proper light, are not. In doing so they seem to be suppressing the internal conflicts arising from holding mutually irreconcilable positions. Some medical professionals must surely be just as prone to this behaviour as other mortals. Should we give it a name? How about Mutually Self-contradictory Belief Personality (MSBP)? Competing interests: None declared
Re: Defining FII 27 November 2004
Michael D Innis, Director Medisets International Home 4575A Send response to journal: Re: Re: Defining FII	Editor, It is time paediatricians scrapped their bible [1] and realized it is not parents who “Fabricate Illness” but rather “some parents (who) continue to be at the mercy of the arrogance of ignorance ….in essence, in some babies, vaccines could be the equivalent of pulling a trigger, releasing a bullet,” as Hilary Butler says[2]. It is unlikely that a government that mandates vaccination, and doctors that pull “the trigger”, are going to acknowledge that ignorance voluntarily. The ballot box may be the answer. Michael Innis Reference: 1 Fabricated or Induced Illness Report . Report of the Working Party of Royal College of Paediatricians and Child Health November 2001. 2. Butler H. Rapid Response 18th June 2004. Competing interests: As previously declared
Cauliflowers/cabbages 27 November 2004
Mark Struthers, General Practitioner Bedfordshire. mark.struthers@which.net Send response to journal: Re: Cauliflowers/cabbages	For a mistaken diagnosis of either MSbP or FII the outcome is the same. For the falsely accused the two conditions are conjoined. When a paediatrician misdiagnoses MSbP/FII the result is a rancid soup. However, you won’t get your money back and the head chef won’t apologise for the mess he’s served up. There is no rose on the table in this restaurant. Competing interests: None declared
Re: Re: Defining FII 27 November 2004
Penny Mellor, Advocate Home WV9 5HX Send response to journal: Re: Re: Re: Defining FII	Dr Cooper Hall and Craft, in their original paper tie MSbP and FII together, in fact if they wanted to lose the term MSbP why did they use it as part of the title? [1] Point of clarification; The picture in Hall and Craft's piece seems to imply that parents wearing scarves around their faces is somehow sinister, they did this at the request of the media because they were involved in family court proceedings and could NOT be identified. Nothing more nothing less. I hardly think a banner saying "innocent until proven guilty" is threatening. Great propaganda for the paeds though. At the end of the peacefull protest outside the Royal Courts of Justice, the police officers present thanked us all for conducting ourselves with such dignity, given the very emotive subject. I guess I shouldn't expect anything else from people who see criminal activity where there is none. [1]http://bmj.bmjjournals.com/cgi/content/full/328/7451/1309 Competing interests: Campaigner against MSbP
SIDS – Joining The Dots 5 May 2007
Michael D Innis, Director Medisets International Home 4575 Send response to journal: Re: SIDS – Joining The Dots	Editor, With regard to Sudden Infant Deaths Hall and Craft ask, “how should we move forward “[1] while Nattie and Kinney observe the association between Nicotine, Serotonin, and Sudden Infant Death Syndrome (SIDS) and wonder how nicotine fits into this scenario[2]. Perhaps the answer lies in “joining the dots”. Serotonin (5-HT) in the nervous system is a major factor in facilitation of the brain centre for respiration[3]. Respiration and the prevention of anoxia is controlled by 5-HT neuron firing, synthesis, release, and clearance. If you have more serotonin neurons, as do infants with SIDS [4] “it may be because you have less serotonin and more neurons are recruited to produce and use serotonin to correct this deficiency”[5]. But what causes the deficiency of serotonin in infants with SIDS in the first place? The neurotransmitters, norepinephrine and serotonin require Vitamin C to catalyzes the conversion of dopamine to norepinephrine and the conversion of tryptophan to serotonin [6]. Hence, less Vitamin C means less serotonin. But why less Vitamin C in SIDS? Analysis of the National Health and Nutrition Examination Survey(NHANES II) data confirms that cigarette smoking, hence nicotine, is associated with decreased serum vitamin C levels[7]. That is how Nicotine, and mothers smoking, fit into the SIDS scenario. quod erat demonstrandum Michael Innis References: 1. Craft AW, Hall DMB Munchausen syndrome by proxy and sudden infant death Education and debate BMJ 2004;328:1309-1312 2. Nattie E. Kinney H. Nicotine, Serotonin, and Sudden Infant Death Syndrome American Journal of Respiratory and Critical Care Medicine 2002:Vol 166. pp. 1530-1531 3 Naoko Narita*, , Masaaki Narita , Sachio Takashima§, Masahiro Nakayama , Toshiro Nagai*, and Nobuo Okado. Serotonin Transporter Gene Variation Is a Risk Factor for Sudden Infant Death Syndrome in the Japanese Population. PEDIATRICS Vol. 107 No. 4 April 2001, pp. 690-692 4.Paterson DS, Trachtenberg FL, Thompson EG, Belliveau RA, Beggs AH, Darnall R, Chadwick AE, Krous HF, Kinney HC. Multiple serotonergic brainstem abnormalities in sudden infant death syndrome. JAMA 2006: 296 (17);2124-32 5.Bock R, Miller MG. SIDS Infants Show Abnormalities In Brain Area Controlling Breathing, Heart Rate NIH News October 31 2006. http://www.nih.gov/news/pr/oct2006/nichd-31.htm 6.http://www.springboard4health.com/notebook/v_c.html 7. Schectman G, Byrd JC, Gruchow HW. The influence of smoking on vitamin C status in adults. Am J Public Health. 1989 February; 79(2): 158–162. Competing interests: None declared
Sudden Infant Death - Revisited 19 June 2007
Michael D Innis, Director Medisets International Home Send response to journal: Re: Sudden Infant Death - Revisited	Editor, Professors Craft and Hall, in relation to the Sudden Infant Death Syndrome (SIDS), state “parents have a right to expect that their baby's tragic unexplained death will be investigated as thoroughly as would be the case for any other citizen.[1] Perhaps investigators could follow the example of Zinka et al; who, investigating unexplained cases of sudden infant death shortly after hexavalent vaccination, found mast cell Tryptase was elevated in three cases in which it was sought.[2] Tryptase and Histamine are markers of both mast cell antigenic stimulation and markers of anaphylaxis [3] suggesting some vaccines cause sudden infant death by anaphylactic shock. Fleming et al, investigating sudden unexpected deaths in infancy concluded “immunisation does not lead to sudden unexpected death in infancy, and the direction of the relation is towards protection rather than risk”[4]. However Fleming et al; had no record of the level of Tryptase or Histamine in the blood and it is especially interesting to note that the blood histamine level starts to rise when the plasma ascorbic acid level falls below 1 mg/100 ml in human beings[5]. While the “official” cause of most cases of SIDS is unknown Richard Follis Jr reported the sudden deaths of three infants with scurvy in 1942 [6] and in 1974 Archie Kalokerinos eliminated the SIDS from his practice by the administration of Vitamin C prior to immunization[7]. In summary the Sudden Infant Death Syndrome would appear to be provoked by two distinct mechanisms both mediated by Vitamin C deficiency: a.Mothers who smoke reduce the level of Vitamin C in their blood and deprive their new born infants of the means to convert Tryptophan to Serotonin. The result is a failure of “protective” reflexes to counteract the hypoxia and airways obstruction induced by sleeping prone. [8] b.Histamine and Tryptase induced Anaphylaxis following antigenic stimulation in the presence of reduced tissue Vitamin C. Michael Innis. FRCPA, FRCPath. References: 1. Craft AW, Hall DMB Munchausen syndrome by proxy and sudden infant death Education and debate BMJ 2004;328:1309-1312 2. Zinka B, Rauch E, Buettner A, Ruëff F, Penning R. Unexplained cases of sudden infant death shortly after hexavalent vaccination. Vaccine. 2006; Jul 26;24(31-32):5779-80. 3. Schwartz LB, Metcalfe DD, Miller JS, Earl H, Sullivan T. Tryptase levels as an indicator of mast-cell activation in systemic anaphylaxis and mastocytosis NEJM 1987; 316: 1622-1626 4. Fleming PJ, Blair PS, Platt MW, Tripp J, Smith IJ, Golding J, and the CESDI SUDI research group The UK accelerated immunisation programme and sudden unexpected death in infancy: case-control study BMJ, Apr 2001; 322: 822 ; doi:10.1136/bmj.322.7290.822 5. Clemetson CAB. Vitamin C Vol III p 11 CRC Press Inc Boca Raton Florida 6. Follis RH Sudden Death In Infants Scurvy. Journal of Pediatrics 1942; 20: 347-351 7. Kalokerinos A. Every Second Child Sydney Australia. Thomas Nelson 1974 8. Nattie E. Kinney H. Nicotine, Serotonin, and Sudden Infant Death Syndrome American Journal of Respiratory and Critical Care Medicine 2002:Vol 166. pp 1530-1531 Competing interests: I have given evidence for the Defense in cases of alleged child abuse.