Cot Death

The causes of cot death
By Ken Norman (June 2000)

(The science is so abstruse, and so many claims and counter-claims have been made over the years, that almost anything, and its opposite, is believable. - John Lichfield, journalist, on conflicting views concerning BSE).

If a baby is a victim of a rare genetic defect which kills only one in a million persons, that is misfortune, not criminality. If that child's parents give birth to a second child, the risk of genetic defect is already there. And it is already there for a third, fourth, fifth, sixth and seventh child.

It is fatuous beyond belief to argue that the odds against these children dying in infancy are 1:1 million for the first baby, 1:1 billion for the second, 1:1 billion billion for the third, 1:1 billion billion billion billion for the fourth, and so on.

According to a report in the British Medical Journal (July 10, 1999) a panel, Confidential Enquiry into Stillbirths and Deaths in Infancy, looked into 573 deaths, randomly-selected as a one-in-ten sample of all stillbirth and neonatal deaths reported to the inquiry in 1996-7. Selected cases were reviewed by a multidisciplinary panel of at least six specialists. They judged that in 28% a different approach "might have made a difference to the outcome," and a further 22% of cases "could reasonably have been expected to make a difference to the outcome."

The association between death and suboptimal care was strongest for neonatal deaths [the newborn], the link being identified in 61% of cases, and 73% of intrapartum [about-to-be-born] cases. The main cause of death was unidentified in 81% of stillbirths. These deaths were often thought to be unavoidable "but a review of these cases has shown that this is often not the case." [A similar link between suboptimal care and cot death probably applies, but in this case the blame does not devolve upon hospitals and doctors, for a parent or carer can become scapegoat - and this may or may not be fair. The percentage of unidentifiable deaths may also be very similar, except that 'unidentifiable' can be made to equate with abuse or murder.]

The authors suggested that the most common shortfall was in foetal surveillance, particularly in the interpretation of cardiotocograms. Poor record-keeping had occurred in one-third of the deaths.

"Suboptimal care" was defined as "failure to act appropriately, failure to recognise problems, failure of communication, shortfall in foetal surveillance, poor record-keeping.

It is also a scenario for misdiagnosis of VKDB [Vitamin K Deficiency Bleeding], according to John Heptonstall, director of the Morley Acupuncture Clinic and Complementary Therapy Centre, near Leeds.

"Do some staff merely go through the motions," he asks, "either injecting or providing orally Vitamin K and then fail to follow-up the neonate whose Vit K status drops dramatically at about eight to twelve weeks for intramuscular injection, and three to four weeks for oral administration? Are all SIDS cases checked for Vit K levels, and are mothers assessed for having had e.g. anti-coagulant, anti-epileptic or antibiotic therapy during gestation, which are contributing factors to neonatal VKDB?

"It has a maximum occurrence in children aged one to three months and involves intra-cranial haemorrhage in a large proportion of neonates; Vitamin K is involved in the lungs, kidney, nervous system, glucose metabolism, cell differentiation aspects and affects coagulation, so bleeding may occur elsewhere - perhaps in the lungs.

"Vit K is also involved in calcium metabolism and therefore bone metabolism; fractures in neonates are not uncommon. Could some alleged abuse be due to deficiency of Vit K? If a baby has liver problems this may preclude proper use of supplemented Vit K according to recent research, and even if supplementation is given the deficiency could continue. Anti-coagulants, anti-epileptics, antibiotics taken by the mother during gestation all predispose a child to VKDB."

Some of this knowledge is very new; fears that Vit K injections may cause leukaemia and tumours may have increased oral Vit K supplementation and reduced the more protective intra-muscular injections, leaving particular children at risk of VKDB.

"Are these some of the SIDS cases we are seeing?" asks Mr Heptonstall. "Would a predisposition to VKDB be familial and therefore likely to affect more than one child in any family? Is VKDB initially ruled out at autopsy? Would medical strategies adopted in SIDS cases identify and admit to failing to maintain needy neonates' Vit K levels during the 'dangerous' first few months of life? Do vaccination schedules pose dangers to such children? If these questions cannot be answered one must question medical knowledge, opinion, and surveillance strategies in SIDS cases. And allegations of child abuse or murder must also be questioned."

A US Food and Drug Administration study of Lyme Disease vaccinations publicised on March 9, 2000, referred to 298 reports of adverse reactions in the first year that the vaccine was on the market. "A very small number of the 600,000 people who took the vaccine," said the manufacturers. But law suits have been filed alleging that the drug-maker failed to warn doctors and the public that LYMErix exposes people of a certain genetic type - 20 to 30 percent of the population - 'to the risk of a chronic, degenerative and incurable autoimmune disease which is much greater than the risk posed to these individuals by an ordinary Lyme-carrier tick bite'." [Lyme Disease, more common in the US than in Britain, is carried by ticks on deer.]

The significance, for this article, is that for the first time it provides solid, test-tube evidence for there being a genetic factor explaining why some infants may be more susceptible to vaccine reaction than others. Most evidence of this reaction is hopelessly vague and contentious; now it is shown to be down to the suspect protein itself. There is no reason on earth why similar factors might not apply to other vaccines. The genetics versus environment argument may be irrelevant for the two could interact. In other words an infant might have a genetic predisposition to react badly to vaccines, so that some parents lose all their children while others may lose just one (particularly over a few years as the vaccine content is changed).

As an example of the sometimes blurred dividing line between natural death and murder, a pathologist in Dornsife, Pennsylvania, saw blood in the brain and haemorrhaging in one retina of a dead Amish girl, Sarah Lynn Glick, aged four months. She had been vomiting for days, then was found unconscious and died two days later. The coroner ruled that this was homicide, stunning the scattered ultra-conservative religious community which claims that the modern world has a corrupting influence on family values, and shuns cars, telephones and electric lighting.
For generations their church banned marriage outside the community, and as a consequence, one-in-ten Amish carry glutaric aciduria (a metabolic deficiency that strikes soon after birth and can cause bleeding in the brain and cerebral palsy). Only eight cases have been reported in the rest of the world; it may be that there are far more but the cause is unrecognised and deaths are recorded as murder.

Days after the Dornsife inquest, Dr Holmes Morton, of the Clinic for Special Children in Strasburg, challenged the coroner's ruling. He had made a study of the Amish sect and their close cousins, the Mennonites, almost all descended from a small group of German and Swiss immigrants who reached America three centuries ago.

Learning that many of their children died of genetic disorders that went untreated he opened a local clinic which has saved dozens of lives and won him the Albert Schweizer Prize for Humanitarianism in 1993.

He believes that Vitamin K deficiency or a genetic liver disorder related to glutaric aciduria were responsible. "Both could give the appearance of a beating," he said. The disease mimics the bruising, bleeding or fractures of shaken baby syndrome.

"When you see a child that has blood in the brain you must think child abuse, because unfortunately that happens in our culture, but you must also think of other disorders that mimic it." Earlier last century, he said, doctors frequently saw babies with haemorrhaging caused by Vitamin K deficiencies; today infants get Vitamin K in shots and baby formulae, but Sarah, delivered by a midwife and then breast-fed, got neither. As a result her blood did not clot properly. Compounding this problem was a genetic liver defect, and even if she had been given the vitamin her body would not have been able to break it down. "The data was in the file on the day she died, and was never read or understood by the people that pressed this investigation. We haven't discovered anything that supports a diagnosis of abuse in this child."

Two months later, the authorities were still trying to decide, with the parents remaining under suspicion of murder. Their seven other children had been put into foster care (four of them with non-Amish families, which shocked the community). All were eventually allowed to return, although Mrs Glick was ordered to have another adult with her at all times.

"You're going to err on the side of protecting the child," said Susan Gaertner, a prosecutor in Minnesota. "Would people want us to do it any other way, when a child's safety is at risk?"

A fair question. But doctors, pathologists, police, prosecutors, judge, jury, the public and the media all want to err on the side of protecting the child, or other children if there has been a fatality - and the consequence is gross injustice and false conviction for murder.

Reports of similar cases involving Vitamin K deficiency have appeared in several medical journals.

Other diseases that can mimic child abuse include hypophosphatasia, juvenile osteoporosic [brittle, fragile bones caused by loss of bony tissue, especially as a result of hormonal changes or deficiency of calcium or Vitamin D]; Alagille's Syndrome, a liver disease that can cause clotting problems and a thin skull that cracks easily; Byler's Disease, one of three kinds of liver disease particularly common among the Amish; Glutaric Aciduria (GA-1), which can lead to a dangerous build-up of acid in newborn children, causing brain damage, paralysis and retinal bleeding; Mongolian Spots, birthmarks that may be confused with bruising.

In 1999 a Minnesota infant, one-year-old Wyatt Hines, was taken from home for three months because fractured bones indicated abuse. His parents insisted that Wyatt was suffering "brittle bone disease," Osteogenesis Imperfecta, hard to diagnose but said by the Osteogenesis Imperfecta Foundation to affect 20,000 to 50,000 people in the USA.

A newborn girl was taken from her parents in 1991 and sent to a foster home in Denver before a liver disorder, glutaris aciduria type 1, was diagnosed.

Two years later a Nashville infant was briefly sent to a foster home before the liver disease Alagille's Syndrome was diagnosed.

Three Newcastle medical students, Thomas Beckingsale, Nicholas Ohly and Stephen Land, with their tutor Richard Edwards have pointed out that not enough is known about post-infective subdural haemorrhages, and infection may be a provoking factor more often than is realised.

An article in the British Medical Journal advised that a clotting screen should be done in all cases.

Writing from Germany to the BMJ in response to a paper, Johannes Zchocke, Georg Hoffman and Ania Muntau said: "We were surprised that neither the authors nor the accompanying editorial considered the possibility of metabolic disorders in their differential diagnosis. It is now well established that subdural haematomata after minor head trauma may be caused by disorders such as glutaric aciduria type I (GA1).

"We personally experienced four children with GA1 who after mild head trauma suffered intracranial bleeds, in one case even retinal haemorrhages. One child had had apparently normal development in the first months of life but during the episode suffered an acute encephalopathic crisis. . . . The patients were accused of child abuse, and the correct diagnosis was only made four years after the event. Several other children with GA1 and subdural haematomata have been reported in the literature.

"Careful evaluation of neuroradiological findings and a good metabolic work-up including the analysis of urinary organic acids should be part of routine investigations in children with subdural haemorrhages."

Any or all of the allegedly murdered infants could have suffered an acute encephalopathic crisis due to a metabolic disorder. This would cause a deterioration in level of consciousness, probably accompanied by a fit, which might not have been noticed. Haemorrhage in the brain and retinae could follow, and then there would have been rapid deterioration in general condition; there could have been breathing difficulties and probable vomiting, even inhalation of vomit.

An article on glutaric aciduria appeared in the Archives of Disease in Childhood, 1999;80:404-405 (May). It says that features similar to non-accidental injury are occasionally found in patients with GA1, and have led to misdiagnosis of abuse. Subdural haematomas have been found in symptomatic and asymptomatic patients, even in the immediate postnatal period. They can occur with minimal trauma, sometimes repeatedly, presumably because the bridging veins are elongated in the presence of cerebral atrophy and are easily ruptured. Retinal haemorrhages have also been reported. Investigation for GA1 is not entirely straightforward and the usual symptoms and abnormalities are not always present, particularly when the child is clinically stable.

(For data on GA1, see the British Medical Journal and electronic responses, eBMJ 11, December 1998. This research was not available for consideration at Helen Stacey's trial, and therefore constitutes new evidence, as required for an appeal. The symptoms are those which Helen herself described, indicating that her evidence was truthful. And this also applies to Louise Woodward and the trial of Mrs Manjit Basuta, where the jury ignored evidence of vomiting that would have supported the defence.)

The co-existence of subdural haematoma and retinal haemorrhage in an infant is considered by some pathologists to be virtual proof of abuse. But Dr Joseph Piatt, of the Departments of Neurosurgery and Pediatrics, Oregon Health Services University, Portland, reports the case of an infant with external hydrocephalus [an abnormal amount of fluid within the brain, usually associated with large heads but also found in children with normal or even small head circumferences] who developed retinal as well as subdural haemorrhages after sustaining a minor head injury. He advocates a more cautious interpretation of allegations of abuse.

One of the clinical hallmarks of child abuse, he says, is a discrepancy between the injury and the explanation offered by the child's carer. The child, for example may be reported to have caused a self-injury in a manner which is inconsistent with age or development; or the severity of the injury is out of proportion with the forces said to have caused it.

In the latter case, says Dr Piatt, the physician must take care to rule out pre-existing diseases, such as platelet disorders, deficiencies of coagulation factors and Osteogenesis Imperfecta [brittle bones] which might make the child exceptionally susceptible to injury.

In many instances there is a family history of this condition and in most cases the abnormal amount of fluid has gone by the time school age is reached.

He concludes that the development of subdural haematoma after a minor bump to the head, in an infant with craniocerebral disproportion, might lead to incorrect accusations of child abuse.

An inherited enzyme (MCAD) deficiency has been found in about seven percent of cot-death babies, in whom death may have been triggered by infection. There are thousands of enzymes in the body, each with a different chemical structure, many needing a coenzyme, an additional component, perhaps derived from a vitamin or a mineral.

Research taking place at Edinburgh University is intended to prove that Sudden Infant Death Syndrome (in certain forms) can run in families. The belief is that some victims may have had an abnormal reaction to bacteria, which causes the body's natural defences to over-react.

"Blood samples will be taken from families who have had cot death and from those who haven't, to see how their white blood cells react to bacteria implicated in cot death," said the research team chief, Dr Caroline Blackwell.

"If we can demonstrate a good reason for cot death this will help parents to understand their babies didn't die because of something they did wrong." It might also show the courts that Maxine Robinson, Donna Anthony, Sally Clark, Marie Noe and many others did nothing wrong, and were falsely convicted. The possibility is that if each of these women had twenty babies, all might die in infancy for no other reason than inherited genetic flaws, without a degree of medical treatment which may not yet be possible.

But there is a problem with an investigation like this. Perhaps only one in several hundred SIDS victims suffers these particular flaws (for the term is applied to any sudden death of an infant when there is no known cause). And the Edinburgh researchers may have difficulty in finding the appropriate subjects.

Mrs Robinson, Mrs Anthony, Mrs Noe and Mrs Clark, and their husbands, would be ideal for this purpose, but because these mothers have been selected for prosecution, and four have been convicted, would the tests be permitted?

This is a Catch 22 situation carrying extreme risk of miscarriage of justice. Juries convict with no knowledge of the medical arguments, and may thereby exclude these women from testing which could demonstrate that a dogmatic assertion of odds of 73 million-to-one against natural death is 72,999,990 wide of the mark.

Writing in 1982, Professor Bernard Knight referred to eight known instances of twins dying from SIDS on the same day.

A report, Recurrence incidence of SIDS (Archives of Disease in Childhood, 1988, 63, 924-930) states: "Families in which two or more siblings died from SIDS differed from families in which only one infant died from SIDS in several ways. More infants were over 12 months old, and the mothers had an increased incidence of previous miscarriages and threatened miscarriage. In one family both infants had broncomalacia. We have identified a small subgroup (8%) with a significantly increased risk of recurrence."

The author Catherine Cookson had five miscarriages. If she had persisted and two infants were born alive, would they have suffered cot deaths and brought life sentences upon their mother?

Mrs Noe suffered a miscarriage and another infant died in hospital at six hours old, in addition to a series of cot deaths; Mrs Rioch Edwards-Brown had five miscarriages before the birth of a child who nearly died from subdural haemorrhage; perhaps there are genetic, inheritable flaws which bring risk to foetus and/or infant.

Accusations of shaking can rest upon "possible white matter tear," a fantasy once confined to the wilder fringes of America, says a medical researcher. "It is possible that such a tear could be caused by shaking, but there are so many other reasons for it - especially during the post-mortem itself - that this diagnosis becomes nothing more than guesswork.

"It was on this basis that a Medical Examiner in the USA assessed a series of cases as shaking when previous examiners had regarded the deaths as natural. The life/death sentences which resulted have only recently been discredited, and new trials/abandoned trials/acquittals are now going on. I'm shocked to see this happening in British courts.

"It's my belief that the moment this word 'shaking' is used, all reason flies out of the window. They don't need to show it makes any sense (for instance there exists not a shred of evidence that Louise Woodward ever resented the child she was accused of murdering, or even resented anyone else, but the motive for murder was 'resentment.' In Sally Clark's case the motive seems to be 'tiredness.' OK, babies are very tiring, but where is the evidence that, at the time she was alleged to have done this, (a) she was tired, (b) the baby was playing up?

"It doesn't make any difference. First diagnose murder then work back to motive, and if there is no motive invent one.

"Shaken Baby Syndrome was really a sub-set of Battered Child Syndrome; as such it was violent assault with characteristic signs which included violent acceleration of the head.

"Because it's perfectly possible to shake a baby (though a small one) hard enough to injure it without leaving much evidence of the traditional kind, it has gradually become the situation that any damage that 'might' be caused by shaking is diagnosed as Shaken Baby Syndrome, regardless of the impossibility of proving this. People always did have to prove they were innocent if accused of battering a child, but it was once possible to do that. It is not so with the present cases. Sally Clark cannot possibly prove that her children died of natural causes, but that is what she was asked to do."

Blindly and without reason
Sudden Infant Death Syndrome (SIDS) by its very nature always strikes blindly and without apparent reason. It was first defined as recently as 1968 as "the sudden death of an infant or young child which is unexpected by history and in which a thorough post-mortem examination fails to demonstrate an adequate cause for the death."

The consequence is that the origin of any such death can be difficult or impossible to trace. In half the cases post-mortems detect nothing wrong; the others were not so well internally.

Professor Bernard Knight, in his book `Sudden death in infancy' (Faber and Faber), says the condition of SIDS must be distinguished from a true disease. "It is called the sudden infant death syndrome which means that it is a recognisable set of circumstances, though without evidence of a single, constant cause, such as is found in smallpox or tuberculosis.

"One must not assume either that the number of factors necessary for SIDS is the same in every case or that the nature of the factors is constant. SIDS is a final common pathway, almost certainly via respiratory failure leading to heart failure and this pathway can be reached by a number of different routes. (Note that respiratory failure may appear very similar to deliberate suffocation.)

"It seems clear now that different cases of cot death have arrived at the common pathway via different initial routes and some of the theories may fit some cases but not others," says Professor Knight. "The number of speculative ideas is vast. Every month a new idea is sprung upon the medical world."

This is the factor with which the prosecutor tricks juries - by requiring that pathologists under cross-examination should give specific alternatives to suffocation as cause of death, fully aware that as responsible professionals they are unable to be specific and cannot speculate, and from their reluctance the jury draws false conclusions.

In the words of the Countess of Limerick, of the Institute of Cot Death, SIDS is the most common but least understood kind of death among babies aged between one week and two years. (Note that all the infants considered on this site were well within this range). The number, she says, is substantially larger than that of all children aged under 15 who are killed on the roads. And, she says, cot deaths are important not only for numerical reasons but also because of the profound psychological impact upon the bereaved parents by the sudden death of an apparently normal infant, whose symptoms of illness, if any, appeared trivial. (Try to imagine the psychological impact upon Marie Noe, MaxineRobinson and Donna Anthony, bereaved of all their children and falsely imprisoned).

Concerning cot deaths of children over a year old, Sarah Murphy, author of `Coping with cot death', tells of the "dearest memory of `Jill,' whose son `Duncan' died at one-and-a-half years" (about Christine Robinson's age). "How Duncan would sit in the baby-seat behind her in the car, how she would smile at him in her rear-view mirror and how much, after his death, she missed his smiley face beaming back at her, to the extent that, for a while, she could still see him. With an older child there has been more time to discover personality and to watch it blossom. Parents who lose a toddler suddenly find that they do not know what to do with their hands when out walking because there is no pushchair to push and no small hand to hold in theirs. Sometimes these parents receive less help and understanding than parents whose babies die when they are very young."

Professor Knight, an authority on SIDS, has stated that at the age of three months, more deaths arise from SIDS than all other causes combined. (In other words, unknown causes outnumber those which can be fully identified.) In his book, `Sudden death in infancy' , he says the child may have been put to bed in apparently good health The mother may have noticed nothing wrong during the previous days, or there were symptoms of a cold, a snuffly nose or loose bowel motions. In most cases the child is found lying face-up, with bedclothes and blankets well away from the face.

Infanticide, according to Sarah Murphy's `Coping with Cot Death,' is very infrequent, and believed to be responsible for only one percent of all unexplained baby deaths. (This, of course, is anyone's guess.)

She lists 28 main areas in which research has taken place: breathing patterns and reflexes, heart rates and rhythms, heart conduction defects, sleep apnoea (temporary cessation of breathing), allergy to cows' milk, allergy to house mites, viral infection, bacterial infection, botulism, failure of the immune system, hyperthermia (over-heating), hypothermia (low temperature), malignant hyperpyrexia (excessive degree of fever), carbon-dioxide pooling (the child breathes out carbon dioxide then breathes it in again because it has not dispersed), stress, carbon-monoxide poisoning, errors of metabolism (chemical processes within the body), internal mechanical obstruction to breathing, external mechanical obstruction to breathing, abnormal lung surfactant (a substance which reduces surface tension), low calcium levels/laryngeal spasm, hypernatraemia (high level of sodium in the blood), hypoglycaemia (low blood sugar), thyroid-hormone imbalances, deficiency of trace elements, vitamin deficiency, biotin deficiency, thiamine deficiency.

"An inherited enzyme (MCAD) deficiency has been found in about seven percent of cot-death babies, in whom death may have been triggered by infection. MCAD stands for Medium Chain Acyl CoA Dehydrogenase," she says.

[There are thousands of enzymes in the body, each with a different chemical structure, many needing a coenzyme, an additional component, perhaps derived from a vitamin or a mineral. Here we have reference to an inherited deficiency causing seven times as many deaths as infanticide (or murder), and triggered by infection.

For example, Vicki, Christine and Anthony Robinson may have inherited susceptibility to an infection picked up during their hours of paddling, making them at high risk of cot death . . . . [I wonder whether the police bothered to investigate this possibility before or since bringing charges?]

"There has been the suggestion," says Mrs Murphy, "that some deaths can be caused by whooping cough" [almost impossible to diagnose even after death in its early but highly contagious stage: a cough or sneeze in the general direction of any other child can pass it on. It can affect both babies and toddlers].

A study in which Professor Knight collaborated showed a strong link with Influenza A infections in the community, but not with Influenza B. Other studies have concerned magnesium deficiency, Vitamin E deficiency, selenium deficiency and spinal haemorrhages.

"Controversy concerning heart conduction defects has continued for a number of years," says Professor Knight. "There is no doubt that near-miss infants, who narrowly escape dying from SIDS, tend to have a high incidence of cardiac abnormalities in terms of physiological testing. Pathologists working on minute details of the heart structure recovered at post-mortem examination have found frequent abnormalities, though their significance is disputed.

"The functional abnormalities which are now beyond doubt are hard to evaluate in terms of cause or effect. Heart changes can occur from oxygen deficiency. So are the heart changes primary and a cause of SIDS, or are they secondary to diffuse damage caused by oxygen lack from respiratory defects?" [Which came first, the chicken or the egg?]

An Australian study discovered a significantly higher level of immunoglobulin (antibody) in the lungs of cot death infants, suggesting that they had an abnormal response to minor infections.

Some deaths are the result of a lung infection, usually due to a virus. These children could have an innate tendency to poor control of their breathing, which may cease even from a mild infection such as a cold.

Signs of a cold in the head when put to bed are another factor.

Here are extracts from `Cot Deaths,' by Jacquelynn Luben (Thorsons Publishing Group).

Sometimes an explanation for the death is found at the post-mortem examination. The baby may be shown to have had a virus, for example, not recognised by those people who saw the baby before its death. This may still be regarded as a cot death. More often a thorough post-mortem examination fails to demonstrate an adequate cause of death.

A study of the deaths from all causes of nearly one thousand babies, commissioned by the Department of Health, which announced its findings in January 1985, showed that only nine cases were officially recorded as infanticide and only a further fifteen aroused doubts or unproven suspicions * a maximum of 2.5 percent.

It seems that a number of cot death victims have experienced a common cold, days or hours previously; but is there any significance in this? Jacquelynn Luben asked a doctor how he would feel if a cot death occurred to a baby he had previously seen with a cold. His answer was:

Once the post-mortem has established that it was a cot death, there's nothing the mother could have done that would have prevented it, because we don't know what causes it. This is a very difficult concept for people to understand, because it is assumed that doctors know everything about all diseases, and in fact there are many illnesses, including those causing deaths, which we do not understand.

Research on the sudden infant death syndrome lacks integration due to absent aetiological direction, says Dr Michael Simpson, a consultant anaesthetist working in Portugal. [In other words, nobody knows where to begin looking for the study of its causes.]

His belief is that there are many causes that lead to similar deaths, even for babies which are well cared for. The human upper airway is controlled by 24 paired muscles that need to work in rhythm or breathing will be obstructed. During normal sleep, with eye movement which is not rapid, this `tone' is much reduced, and when there is rapid eye movement during sleep it is almost nil. When there is sufficient sleep deprivation the airway `tone' can become zero.

Several studies have shown that a state of chronic hypoxia (low level of oxygen) can be detected in many SIDS cases if methods of investigation are sufficiently refined, and a research team led by Professor John Emery at Sheffield detected fatty replacement on a microscopic scale in parts of the brain-stem, concluding that this might be due to chronic hypoxia.

In the first six months, writes Dr Simpson in `Hospital Doctor' (October 1996), a baby's respiratory system is immature; the tongue is large and can obstruct breathing, so that serious obstruction of breathing as a result of sleep deprivation becomes even more possible.

A more physically mature child has greater ability to struggle to open a collapsed airway. Normally, in cot deaths, there has been no effort by the child to resume breathing; where strong effort has been made to suck in air before death, pathology can confirm this.

[This means that when a child has been suffocated (as with a pillow) a pathologist could expect to have considerable evidence that death was unnatural. This would be especially evident in the case of a 19-month-old infant whose efforts to breathe would be much greater than those of a four-month sibling. But, as Professor Berry and Professor Knight have stated, there was no pathological evidence indicative of suffocation when they examined Christine and Anthony Robinson.]

Children who die, or nearly die, of SIDS usually demonstrate abnormal sleep patterns, hyperactivity and chronic sleep deprivation. This includes failure to arouse normally from sleep, which greatly increases the risk of airway obstruction.

Winter is a risk factor because infection is more common, causing nasal obstruction; the child should be frequently aroused to maintain a clear airway, even at the expense of sleep, says Dr Simpson. [But it is highly possible that playing in a paddling pool on unusually hot days could also bring on a cold and nasal obstruction.]

`Mosby's Medical and Nursing Dictionary' has yet another list of possible origins for cot deaths, which it defines as apparently normal, healthy infants dying during sleep, with no physical or autopsic evidence of disease. The suggested multiple causes include lack of biotin (one of the Vitamin B's found in egg yolk, liver and yeast, and involved in the metabolism of carbohydrates, fats and proteins), abnormality of the endogenous-opioid system, mechanical suffocation, a defect in respiratory mucosal defence (mucose not clearing from the airway), prolonged apnoea (temporary cessation of breathing), an unknown virus, anatomical abnormality of the larynx, and immunoglobulin abnormalities (faults in and of the group of structurally-related proteins which function as antibodies).

Cot death, says `Mosby's,' is not contagious or hereditary, although there is a greater than average risk of its occurrence within the same family, which may indicate the influence of polygenic factors (polygene: each of a group of independent genes which collectively affect a characteristic).

[To a layman the list is bewildering. Cot death is not contagious or hereditary, says one expert, immediately going on to the apparent contradiction that there is greater than average risk of cot death occurring within one family. This contradicts some research which indicates that children are put at risk of cot death by hereditary characteristics. And of course, if there are multiple causes, some of them can be hereditary or contagious.]

Dr Tonkin, an Australian specialist, believes that the airway may be blocked at the back of the throat during sleep. A large tongue, or the act of sucking, may collapse the back of the throat, or its sides may come together when taking in air, just as a straw can collapse in on itself when wet and being sucked hard.

The belief is that these things may occur several times, perhaps frequently during the first few months of life, resulting in hypoxia (a deficiency of oxygen reaching the tissues), periods of slow heart-beat, and eventually to an unstable heart condition.

This may create a situation colourfully known as Ondine's Curse, a descending spiral of hypoxia, temporary cessation of breathing, slow heart-beat, producing further hypoxia and heart-failure. In normal rhythms of sleep, children (and adults) slow their breathing; for a few seconds no breaths are taken, then the normal pattern is rapidly regained. However, some infants cease to breathe for periods of more than 15 seconds - prolonged sleep apnoea (PSA). During these periods a deficiency of oxygen is being taken into the bloodstream, and if sleep apnoea is unduly prolonged, hypoxia (oxygen deficiency) takes effect.

If there is a deliberate attempt to hold the breath, the brain becomes aware of carbon dioxide build-up and decrease of oxygen, and over-rides the effort. But in some infants the brain does not respond quickly enough or strongly enough during sleep, and the crisis situation can occur. Unless this cycle is interrupted the child will die. But many infants can break out of the cycle or there is some external intervention (both are termed `near-misses'). The parents may be unaware that anything has happened and the child is in the majority of cases back to normal next morning.

For this prolonged sleep apnoea theory to have any foundation there must first be a baby with an inborn tendency to PSA, says Professor Knight [meaning that it can be hereditary]. "Secondly there is very frequently some kind of virus infection in these infants." There may also be some other factors such as abnormality and insensitivity of the chemical receptors for oxygen or carbon dioxide (and there is a considerable amount of direct pathological and physiological evidence that these factors do exist in some SID infants). "If all these factors are present in one infant, then there would appear to be a substantial risk of SIDS occurring."

There are other forms of airway obstruction under suspicion of producing cot death. They concern nasal narrowing, closure of the glottis (the space between the voicebox and the vocal cords), and the possibility of obstruction near the larynx (Adam's apple). If the vocal cords are shut, as in the beginnings of a cold, little or no air can pass to or from the lungs. This is known as a laryngeal spasm and it can also be linked with tetany (intermittent muscular spasms caused by malfunction of the parathyroid glands and a consequent deficiency of calcium). This makes the airway muscles very irritable and prone to spasms.

In an infant the voicebox is scarcely as wide as a pencil. It can very easily become blocked.

In his book, `An A - Z of a Child's Health,' Dr David Delvin tells of an incident when his own son "suddenly started to crow. Moments later, as the degree of obstruction increased, he began to turn an ominous shade of dark blue."

He tried the standard first aid treatment, holding the baby upside down by his ankles and smacking between the shoulder blades. Although the chest was heaving, no air was going in or out.

"There's no doubt that the baby could have been dead within a minute or two. Fortunately, by running my forefinger back over his tongue I was just able to hook my nail round the object that was jammed in his throat * a piece of toy roof tile." With its removal there was a rush of air into the lungs and within seconds the child's colour had changed back to pink.

However, inflammation is the commonest cause of croup. The child usually (although not always) has had a slight head cold for a day or two, suddenly becomes hoarse, and within minutes is making a croupy noise. Urgent medical attention may be needed.

Another theory is that children at risk of SIDS may be allergic to house mites, which are found in large numbers in the cleanest of homes. They are known to cause various allergies including a form of asthma and skin rashes but it is not generally accepted that there is a direct link with SIDS. On the other hand, according to Professor Knight, they may be a precipitating factor or a trigger * one part of a lethal cocktail.

Bacterial infection is not considered to be a cause of SIDS, since evidence of it could, by definition, distinguish the death from those having no known causes. On the other hand, some bacteria die before they can be grown in cultures for forensic examination; they would therefore be undetectable by post-mortem

Snoring linked with SIDS
Adults who suffer from heavy snoring and sleep deprivation because of a breathing problem may pass this on to their children, putting them at risk of cot death, according to researchers Rajar Mathur and Dr Neil Douglas, from the respiratory medicine unit at Edinburgh University, in a 1997 article in The Lancet.

They suggest that sleep apnoea [when a person stops breathing for short periods during sleep] and Sudden Infant Death Syndrome may be manifestations of the same condition, resulting from a facial structure which narrows the upper airways.

Infant death victims, they say, have small upper airways and studies have shown that a slow heartbeat can precede sudden death. This corresponds with sleep apnoea/hypopnea syndrome in adults who snore heavily.

They carried out a survey of 29 sleep-affected families and 35 normal families. There were eight unexpected and unexplained infant deaths among the sleep-affected families and none in the other families. Two of the sleep-affected families had lost two children to SIDS, including twins.

"Obstructive apnoea would produce the associated bradycardiac [slow heartbeat] observed in the sudden infant death syndrome," they say.

Both of Maxine Robinson's parents snore heavily; so does she. So, I am told, does Peter Robinson. Donna Anthony and her parents are said to be heavy snorers. It would be very interesting to hear whether Marie Noe, Sally Clark and their husbands are also victims.

These convictions are not safe
I believe it to be a disgrace to the law that mothers who are grieving at the inexplicable death of their babies can find themselves convicted of murder by jurors lacking all ability to evaluate what they have been told.

Opening the trial of Mrs Sally Clark at Chester Crown Court the prosecution said evidence would be presented showing that the odds were 73 million-to-one against two cot deaths to one mother. This claim was later repeated by Professor Roy Meadow.

At Bristol Crown Court in the successful prosecution of Mrs Donna Anthony for the deaths of two infants, Professor Meadow said that a single cot death was a thousand-to-one misfortune, therefore two deaths in one family were a million-to-one chance and indicated murder.

In the US, at the trial of Mrs Marie Noe, the claim was that one cot death is a tragedy, two is a mystery, three is murder."

In a case in New York the medical examiner originally concluded that three infants in one family had died from natural causes (SIDS). A fourth baby was taken to hospital with what was later diagnosed as reflux syndrome. The paediatrician became suspicious when she heard of the family's history and this child was not returned. A neglect and abuse hearing began, and the attending physician testified that the likelihood of three cot deaths in a family was one in a billion. One cot death took place in every 1,000 births, it was claimed, therefore three would be ten to the ninth power.

Are these figures anything other than wild guesses?

If a fortune teller tried to predict blindly that a specific couple would suffer three cot deaths, the odds against this happening would be astronomic; but if the prediction had been made by a medical researcher in full knowledge of the genetic flaws, there could be a 1:256 chance of accuracy - better than this if there were surviving children too. If a couple - whatever their affluence - unknowingly carry genetic flaws, the death of their first child, at odds of 1:4, would be inexplicable; grief would bring longing for a second child (and they would be reassured by Professor Meadow's certainty that risk was almost non-existent). But survival odds would again be 1:4, and a third child would have this same chance. It is very, very far removed from 1:73 million for just two cot deaths.

Here is an article from "Health":

Cot death rates have fallen in recent years. The Sally Clark case highlights the difficulties faced by doctors trying to judge between genuine cot death cases, and those in which a parent played a part. Solicitor Mrs Clark was convicted of murdering her two babies Christopher and Harry within 14 months of each other.

She and her husband said that sudden infant death syndrome (SIDS) was to blame for both. Much of the available evidence on cot death is contradictory. The court was told by one expert witness that the chances of both children suffering cot deaths were one in 73 million. However, cot death support and research groups point to strong evidence that families which suffer the trauma of a genuine cot death are at higher risk of suffering a second such tragedy.

The verdict will reawaken the controversy over whether doctors, and the statistical analysis they produce, are able to distinguish between genuine tragedy and foul play. And parents who have suffered the trauma of cot death will be distressed that suspicions could be aroused, regardless of the presence or absence of clear physical evidence.

The term "sudden infant death syndrome", as with many other medical syndromes, is a catch-all term, used in this case to describe any death of a baby which remains unexplained even after a full post mortem has been carried out. However, research suggests that some form of maltreatment, either deliberate harm, or simply cases of poor care or neglect, is probably to blame in a small percentage of cot death cases. A government study, known as the confidential enquiry into sudden deaths of infants, looked at deaths in the UK between 1993 and 1996, and put the figure at six percent. Another University of Sheffield-based study suggested that only a total of 2.5 per cent of deaths were either infanticide, or suspicious.

The fall in cot death rates over recent years means that cases are subject to more scrutiny than before. There are few telltale signs for the pathologist to spot. The presence of bleeding in the lungs has been taken by some as a clear result of smothering of the child, but many commentators say that this is an unreliable method of diagnosis. So, are some parents still getting away with murder?

Sir Roy Meadow, head of the Department of Paediatric and Child Health at St James' Hospital, Leeds, looked at 81 cases of children in which the courts had found the parents guilty of killing them. He found 49 of these had originally been certified as cot deaths following post mortem. [My own comment: Sir Roy advocates "thinking dirty," and believes that 40% of SIDS are falsely diagnosed. It may be that some of the original diagnoses were correct.]

He wrote in the journal Archives of Childhood: "SIDS has been used, at times, as a pathological diagnosis to evade awkward truths."

Certainly, in the Clark case, the two deaths were originally treated as SIDS.

A recent investigative guideline sent to Canadian pathologists urged them to "think dirty" when confronted with a possible SIDS case, just to be sure to exclude all possibility of foul play. The Foundation for the Study of Infant Deaths is at pains to stress that the vast majority of cot deaths are natural - in fact, it says it has evidence that one family every year in the UK loses a second child to the syndrome.

A spokesman said: "If a couple have a child who dies suddenly and unexpectedly the risk of it happening again does increase. The reasons for this are varied and range from metabolic disorders, to maltreatment and environmental and social factors.

"Certainly second cot deaths can be true cot deaths, where all other causes have been excluded." The problem facing doctors confronted with an apparent case of cot death is that medical science simply does not conclusively know what causes it. It is virtually impossible for them, in the absence of unequivocal signs of physical abuse, to rule it out entirely."

The Human Fertilisation and Embryology Authority, describing its work, has said: "This [is] about helping families avoid passing on serious genetic diseases to their children." For parents who had had repeated miscarriages or seen previous children die, screening offered hope but it had so far been used in only a handful of fatal disorders caused by single genes."

Sally Clark's children were said to have sustained rib fractures, one certainly post-mortem; the other, sustained around birth, had self-healed. Here, from the Miller ME. Institution Department of Pediatrics, Wright State University School of Medicine and the Children's Medical Center, Dayton, OH 45404, USA., is a report, "Temporary brittle bone disease: a true entity? Source: Seminars in Perinatology. 23(2):174-82, 1999 Apr. Local Messages. Held at BMA Library Abstract

Temporary brittle bone disease is a recently described phenotype of increased fracture susceptibility in the first year of life in which there are multiple unexplained fractures without evidence of other internal or external injury.

Most child abuse experts do not accept the existence of temporary brittle bone disease and presume these cases are child abuse. The author reviewed 26 cases of infants with multiple unexplained fractures that fit the criteria of temporary brittle bone disease and studied nine of them with either computed tomography or radiographic bone density measurements.

The results show a striking association between temporary brittle bone disease and decreased fetal movement, usually from intra-uterine confinement, and low bone density measurements in eight of the nine infants.

The association with decreased fetal movement and intrauterine confinement is in keeping with the mechanostat-mechanical load theory of bone formation.

The author feels that temporary brittle bone disease is a real entity and that historical information related to decreased fetal movement or intrauterine confinement and the use of bone density measurements can be helpful in making this diagnosis.

The British Medical Journal has published these notes by Heather Bacon:

Whether or not the term sudden infant death syndrome should be abandoned, the present system for categorising sudden deaths in infancy seems to be in a muddle.

Analysis of 450 autopsies in the recent study of sudden unexpected deaths in infancy (SUDI) shows that the extent of investigation varies widely with the specialism of the pathologist, paediatric pathologists doing the most tests and forensic the least. Furthermore pathologists may not always agree in their interpretation of the same findings, especially whether or not they constitute an adequate cause for the death, and so whether it should be classified as SIDS. The SUDI study, like the multicentre study 20 years ago, found frequent discrepancies between the opinions of the original pathologist and the expert assessor. Then the way in which pathologists report their conclusions may result in omissions from the totals given by the Office for National Statistics (ONS) both for SIDS and for sudden infant deaths in general. For example, if a pathologist thinks a death should be classified as SIDS but also finds bronchitis, and both terms appear on the death certificate, ONS will allocate the death to bronchitis rather than SIDS, international guide-lines requiring the selection of the more specific condition. Similarly, if a baby dies unexpectedly and a cause such as septicaemia is identified at autopsy, the death will not be included in the generic total of sudden infant deaths if there is no allusion to its suddenness on the certificate. In addition, pathologists and coroners vary in their willingness to accept SIDS as a designation for unexplained deaths.

In recent years, partly as a result of Green's advocacy, there has been an increasing tendency to categorise as unascertained deaths where there is any suspicion of maltreatment, infant deaths under the relevant code rising from 18 in 1996 to 26 in 1997 and 46 in 1998. Similarly about ten deaths a year that might otherwise be categorised as SIDS are coded under respiratory failure. Now that the total of sudden infant deaths has fallen these various anomalies have greater effect, distorting national and local figures and reducing the validity of comparisons. We need agreement on a standard system for post-mortem examination and certification that all coroners and pathologists will follow.

Responding to the "think dirty" campaign which is now advocated by some pathologists and paediatricians, Ms Sylvia Limerick, vice-chairman of the Foundation for the Study of Infant Deaths has asked, " Is the clock being turned back 30 years? The views of a few authors highlighting the small number of unnatural infant deaths that have been misclassified as sudden infant death syndrome have been widely publicised. Some views risk returning us to a time when there was no registrable nomenclature for identifying natural unexplained sudden infant deaths, no mechanism for supporting bereaved parents, and no research base for elucidating preventive measures."

She quotes the Brodrick report of 1971 as stating that "in the investigation of a 'cot death' a good clinical history is almost as important as a good post-mortem examination." It recommends that "a coroner should consider with the greatest care whom he should ask to visit the home and attempt to obtain from the parents relevant information about the history of events leading to the death." [In other words, post-mortem 'evidence' of murder is largely guesswork, and if the police or "Think dirty" pathologists are the first ones to question the parents there is high risk that, whatever their reaction, it will be interpreted as suspicious. There is need for a balanced team to make these vital assessments.]

Ms Limerick adds that a paediatric pathologist with special training, working with a forensic pathologist if necessary, should undertake histological, toxicological and bacteriological tests to an agreed national standard. This should ensure the utmost scrutiny in determining whether an inquest is necessary and, most importantly, identifying the more rare causes of sudden infant death.

[I would add that it is an urgent duty for the GMC to set an agreed national standard, and that the paediatric pathologist and forensic pathologist should each be duplicated. Just as the state employs professionals to represent the child in certain court cases, so there should be forensic specialists to represent the parents from the earliest stages, whenever there is concern that death may be unnatural.]

She concludes: "Sudden unexplained infant death is still the largest category of death in infants aged over one month. However heterogeneous the aetiology of these deaths, a collective term is still needed for identification, for explanation, and as a basis for expert study and sensitive support to bereaved families."

Mrs Donna Anthony received two life sentences after Professor Meadow had claimed that, having been given apnoea monitors after the first child was taken to hospital because of a breathing lapse, she had made five attempts to murder the children because in all there were five emergency visits to hospital, reporting breathing problems. Surely that is precisely what apnoea monitors are for, to allow quick resuscitation of children in this situation. The doctors who advised use of monitors must have believed there would be such incidents. If they did not, and the monitors were provided only for the entrapment of Donna, surely the hospital doctors were guilty of condoning the child murders for they should have taken steps to have the infants taken away from her before the deaths occurred

To my mind a gulf has developed between pathologists over the past five years and this is creating gross injustice. On the one side is a small clique of eminent pathologists, Meadow, Green and Southall prominent among them. They call for others to "think dirty" when carrying out autopsies on infants who might be SIDS victims. This is not the correct approach. The pathologist should act responsibly, as a professional, taking a neutral stance. It is the job of the police to "think dirty" with a view to securing convictions.

Research should be carried out to allow a true picture of the bruising, retinal and subdural haemorrhaging and injuries to strap muscles, cartilages, neck, back and limbs, likely to be suffered by infants of varying weights and ages in "violent, prolonged shaking," falls on to concrete from a first-storey window, etc. This could take the form of collating medical data from all over the country when children are known to have suffered falls from upper floors or down stairs, or from beds or furniture on to various surfaces. Also there should be reasonably accurate assessment of the likelihood of multiple SIDS cases, the need for apnoea monitors and how to interpret them (indicative of attempted smothering or of "near miss" SIDS?), and a compilation of possible causes of child death: are "baby bouncers" dangerous?; how frequently does urgent attempted resuscitation in a speeding ambulance produce bruising and rib-fractures?, does retinal haemorrhage and blood in the lung rule out SIDS?, does subarachnoid bleeding at birth bring possible risk of subdural haemorrhage a few months later?

How can time of injury be accurately assessed? All too often (as in the conviction of Mrs Helen Stacey at Norwich Crown Court) the jury is called upon to decide whether injury had been caused in the specific period when one person was in charge of the child - say a carer who received the child at 7 a.m. on the day of death. Shaking sustained during that day must have been extremely violent to have fatal consequence. How accurately can medical evidence differentiate between quick and slow subdural haemorrhage? If the jury convicts has it done so by guesswork or by the toss of a coin, or by preferring the mannerisms of medical witnesses for the prosecution to those of the defence experts, or does the expert telling the greatest whopper sound most convincing?

There should be guidance notes issues to all pathologists concerning assessment of SIDS or child abuse, estimated time of injury, the possible causes of bruising or other injuries, and whether they were incurred at an earlier date, at time of death, or during attempted resuscitation or during post-mortems.

Prosecution witnesses such as Southall, Meadow and Green, giving opinions which are certainly not shared by other pathologists, may over the years mislead juries into inflicting life sentences upon hundreds of innocent women; their success rate will make it inevitable that in every trial for alleged child-murder they and others like them will be the specialists called to carry out autopsies and give evidence for the Crown. Yet their claims may be nothing more than grossly inflated guesstimates.

The cases detailed on this site demonstrate that murder convictions can be obtained without any definite knowledge as to what happened.

We need agreement on a standard system for post-mortem examination and certification that all coroners and pathologists will follow, as was suggested in the article in "Health."

A paediatric pathologist with special training, working with a forensic pathologist if necessary, should undertake histological, toxicological and bacteriological tests to an agreed national standard.

To obviate the likelihood that jurors will be unable to understand abstruse conflict of medical opinion, the defence should have the right to demand medical qualifications for every juror.

It can never be known whether, in ten years' time, a researcher will present proof that if one partner has genetic flaw category 542GG and the other chromosome deficiency X276, the combination makes it almost impossible for an offspring to survive infancy.

And then the trials of the present day will be held up to ridicule as being little better than the witch burnings of earlier centuries.

In the effort to bring conviction, truth plays a minor role or is written out of the script. "Like a 15-foot fall on to concrete" has become the standard claim by medical witnesses. The comment of one man is: "It's a long time since I did physics and I'm open to correction, but a rough calculation would be that the child was travelling at a speed of about 10 m.p.h. when he struck the ground. If these 'experts' think that would cause a hair-line fracture of the baby's skull, I suggest that as adults they try walking into a lamppost at 4 m.p.h., not forgetting that the severity of impact is four times as great for every doubling of the speed."

Professor David Southall believes that 95 percent of acute subdural haemorrhaging in babies, with retinal haemorrhages, result from child abuse. Professor Bernard Knight strongly disputes this.

The Times on September 10, 1999, quoted Michael Green, from Sheffield University's Department of Forensic Pathology, as claiming in the BMJ that up to 40 per cent of children registered as "cot deaths" may have been killed by their parents or other adults.

"'We can only hazard guesses,' he continues. [But on this basis of guesswork the courts convict for murder.]

This guesswork as to guilt might happen in hundreds of cases; it is NOT justice. I have argued for changes in the jury system in letters to MPs. The Prime Minister (with the signature of Private Secretary, Mr Angus Lapsley) replied blandly: "The Government believes that jury service is an important civic duty and that juries have a pivotal role in representing the collective judgement and sense of the community. Each individual juror must take an oath, or solemnly affirm, that he or she will faithfully try the defendant and give a true verdict according to evidence.

"It is one of the strengths of the system that the facts of the case are considered by the jury as a whole and not through individual verdicts. . . . The weight of numbers helps to form a more reliable view on, say, the credibility of an individual witness, and the case as a whole. It would place an unfair burden on jurors, who are unlikely to be skilled or experienced in the task, to require them to produce a detailed statement of their reasons for arriving at a particular verdict."

So it’s the "weight of numbers" that matter, not whether some jurors are under duress and constraint to force a conviction out of them, or are unskilled in matters of vital importance such as forensic science in a case of suspected child murder.

My reply was "boloney. In practice, jurors are forced to abandon their ‘individual experience’ and subordinate it to the will of the most forceful, opinionated and prejudiced. Failing this they must remain locked in futile argument for hours or days, encountering the wrath of their fellow jurors and the displeasure of the judge.

"This is not a system which produces reasoned verdict, but a recipe for quick and apparently unquestioned convictions - and for miscarriages of justice."

Juries should not be forced jointly to reach verdicts with which, individually, they disagree.

Each juror, having heard the evidence, should go in solitude for perhaps half-an-hour of reflection. If questions arise, all should return to court for the judge’s elucidation. Then back to ‘solitary’ for perhaps a further half-hour, before recording a statement of opinion, preferably with reasons (which can be vital in an appeal).

Meanwhile, the judge would hear evidence of previous convictions, mitigation pleas, social reports, etc., and record a provisional sentence - in the case of life imprisonment giving a tariff such as ‘at least 12 years.’

The (anonymous) individual opinions would be read out, each ‘Not guilty’ reducing the provisional sentence or tariff by, say, 25 percent. Four ‘Not guilty’ opinions would bring acquittal. Even one would give automatic grounds for appeal. Two or three would imply serious doubt. And with split decisions the media would not be free to use headlines such as "Child-killer jailed."

There would be fewer miscarriages of justice and shorter incarceration for the innocent, plus less contempt for the law. But the Powers-that-Be would hate this. The system has been used since hangings at Tyburn, so that’s how it’s got to be.
(Posted June 2000)

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