Introduction

The shaken baby syndrome theory, as it stands today, assumes that findings of brain and/or retinal hemorrhages in the absence of known major accidental trauma are diagnostic of shaken baby syndrome (SBS), sometimes also referred to as non-accidental injury. For reasons that will be reviewed in this article, this theory is being increasingly challenged in the scientific literature.

Although there are many variations of SBS, in our experiences a common pattern is emerging in which there is an abrupt and unexpected onset of apnea (respiratory collapse) in a delayed onset following immunizations. A parent or caretaker may understandably panic in such a situation. Most being untrained in resuscitation techniques, they may slap or shake the infant as an emergency measure. Later admitting this to the police, they may then be accused of child abuse or, upon death of the infant, murder. We believe this line of thinking is superficial. The real question is what caused the apnea that preceded the shaking.

A counter-science to SBS is developing and has now advanced to the point where there are grounds for claiming that many SBS accusations and convictions are the result of misdiagnosis for the following reasons:

1. The current theory of shaken baby syndrome—that shaking alone without impact can cause brain hemorrhages—is an assumption not supported by scientific evidence. In addition, in court cases where brain damage was assumed to be the result of impact, it has been very unusual in our experiences to find significant bruises or other marks of trauma upon the infant’s first arrival at a hospital emergency room—marks one would expect to find if there had been impacts severe enough to cause brain hemorrhage.

2. Due to gross deficiencies in scientific infrastructure in safety testing of childhood immunizations, it is a near certainty that many adverse vaccine reactions are taking place unrecognized as such. Some of these reactions may mimic findings now thought to be diagnostic of SBS.

3. Many or most cases of SBS involve medically fragile infants from a variety of causes (to be reviewed below).

4. Based on the limited science we do have on vaccine reactions, it is probable that immunizations in fragile infants may at times provoke a smoldering inflammatory encephalopathy with initiation of brain edema (swelling), which often culminates in apnea. Brain hypoxia (lack of oxygen) following the collapse then causes an acceleration of the brain edema. Locked into the skull as it is, the swelling brain may reach a point where it acts as its own tourniquet, cutting off venous outflow. Brain and/or retinal hemorrhages may then take place secondary to a very rapid increase in central venous pressure.

The rationale for these conclusions will be reviewed in the following:

Controversies Surrounding Shaken Baby Syndrome (SBS)

Shaken baby syndrome, as reviewed in the Journal of the Royal Society of Medicine and other journals [1-3], describes a combination of subdural hematoma, retinal hemorrhage, and diffuse axonal (nerve) injury (DAI) as the complex of diagnostic criteria. In some cases, the presence of rib or other fractures is also taken as a sign of abuse. The basic issue is whether or not in some instances in which a father, mother, or caretaker has been accused of causing the death or injury of an infant by SBS, the true cause was a catastrophic vaccine reaction.

Of special interest in this regard is an unpublished series of dozens of cases of accusations or convictions of SBS, largely collected by jury counselor Toni Blake of San Diego, California (private communication, 2002). Also pertinent are many cases in our personal experiences. All these cases have the following suggestive features:

• All occurred in fragile infants born from complicated pregnancies. Problems included prematurity, low birth weight, drug/alcohol problems, diabetic mother, or other maternal complications.
• All were 6 months age or less.
• In each instance there was a pattern of timing at 2, 4, or 6 months, with onset of signs/symptoms of deterioration in most instances following within 12 or 13 days of vaccines, although in some instances this time period (referred to as a “latent period”) was more prolonged.
• All had subdural hematomas.
• Some had multiple fractures.

When Toni Blake was first contacted, in the year 2000, she reported that she had 25 of these cases, but in a communication in 2002, she said that the series had become much larger.

As will be reviewed in a later section, gross deficiencies in the scientific safety infrastructure of vaccines have been revealed in the past several years, so that, as a matter of opinion, it is a virtual certainty that many unrecognized vaccine reactions are taking place. Among these may be complications now being (mis)diagnosed as shaken baby syndrome.

Medical-Legal Issues

As reviewed in an amicus brief filed in several court cases and signed by dozens of experts around the world, provided through the courtesy of Toni Blake [4], the following beliefs have become prevalent in courts dealing with SBS: (1) shaking alone in an otherwise healthy child can cause a subdural hematoma; (2) non-traumatic new bleeding in an existing subdural hematoma will always present only minor symptoms; (3) a child suffering from an ultimately fatal brain injury will not experience any lucid interval; (4) short-distance falls by children are never fatal; and (5) retinal hemorrhage occurs only in shaken babies. For the sake of brevity, only beliefs (1), (2), and (5) will be considered here.

Belief #1: Shaking alone in an otherwise healthy child can cause a subdural hematoma. Dr. Buttram has a number of publications which have led us to the opinion that shaken baby syndrome is based on assumptions unsupported by scientific evidence. Foremost among these is an article by Mark Donohoe (2003, American Journal of Forensic Medicine and Pathology) in which he stated that half of the articles about SBS were published before 1999, and half after 1999. Given that 1998/1999 is regarded as a turning point in acceptance of the tenets and practice of evidence-based medicine, it seemed reasonable to the author to assess the quality of evidence before 1999 and to compare it with the quality of evidence on the same subject since that time.

Quality of evidence was placed in four broad categories, with level I or level II indicating compelling evidence from consistent findings in two or more well-constructed, controlled trials or population-based epidemiologic studies. In contrast, level IV evidence represented consensus statements of the expert panel according to clinical experience and limited scientific data. Following a review of articles on SBS published before 1999, Donohoe found that the majority of evidence showed a level of IV, “opinions that shed no new light upon SBS and did not add to knowledge about SBS.” None were found that exceeded a level III.[5]

In the fall issue of The Warrior, Journal of the Trial Lawyers College, 2003, Attorney Elaine Whitfield Sharp wrote a comprehensive article reviewing the history of SBS.[6] Beginning in 1966 and 1968 Ayub K. Ommaya, MD, a Pakistani-born and Oxford-educated neurosurgeon, set out to determine the amount of force it takes to cause certain types of brain injuries and hemorrhages from rear-end car crashes. In experiments with rhesus monkeys (experiments now mercifully prohibited), Ommaya used the monkeys to mimic car accidents by accelerating them on chairs fixed to a track and decelerating them without impact to their heads. Ommaya’s experiments showed that it took between 35,000 to 40,000 radians per second (squared) of angular or rotational acceleration to cause brain hemorrhages in the monkeys.

Transposing the size of monkey brains to that of human brains, Ommaya calculated that the amount of force required to cause brain hemorrhages in humans would be 6,000 to 7,000 radians. According to the review by Sharp, other notable names in the field of SBS transposed Ommaya’s findings to the field of SBS.

It was not until 1987 that a specialist in biomechanics and a group of neurosurgeons set out to prove that subdural hemorrhages in babies were not caused by shaking but by impact. The biomechanics specialist was Lawrence E. Thibault who, with team members made a surrogate baby model and attached an accelerometer to its neck. First they asked some burly football players to shake the model as hard as they could. The most force they were able to generate was a mean of 1,138 radians, far below the 6,000 to 7,000 radians required to cause human brain hemorrhages.[7]

Other publications since that time tend to confirm rather than contradict these findings, one example being a report by Prange, Coats, Duhaime, and Margulies which concluded that “there are no data showing that the maximum change in angular velocity….during shaking and inflicted impact against unencased foam is sufficient to cause subdural hemorrhages or primary traumatic axonal (nerve) injury in an infant.”[8]

Belief #2: Nontraumatic new bleeding in an existing subdural hematoma will always present only minor symptoms. There are a number of publications reporting on instances in which rebleeding took place in chronic hematomas with minimal trauma.[9-12] In an article by Hymel et al, (2002) the authors reviewed the pathophysiology of subdural hematomas and the mechanisms by which chronic subdural hematomas may rebleed spontaneously or with minimal trauma.[13] In addition, the authors provided a table extending nearly four pages of possible differential diagnosis for subdural hematomas.

Perhaps the most convincing evidence that brain hematomas, whatever their location, may lead to spontaneous and significant rebleeding comes from the work of Kawakami et al in which 19 patients with chronic subdural hematomas had venous blood taken at the same time as surgical aspiration from subdural hematomas. Both the blood and surgical aspirates were then tested for coagulation factors. The venous blood tests were found to be normal, but blood from the chronic hematomas was found to have markedly prolonged coagulation markers (prothrombin and partial thromboplastin times), marked reduction of clotting factors (prothrombin, fibrinogen, and clotting factor V), and increased indications of clot disintegration (increased fibrin and fibrinogen degradation products).[14] In other words, each brain hemorrhage was generating its own coagulation process, thus consuming clotting factors. As clotting factors were depleted, conditions for potential spread of the bleeding were created.

Belief #5: Retinal hemorrhages occur only in shaken babies. Proponents of the SBS theory have been allowed to testify that retinal hemorrhages are pathognomic (diagnostic) of SBS in spite of foundational objections. To the contrary, relevant scientific literature reveals that retinal hemorrhages are found with a myriad of pathologies, including cardio-pulmonary resuscitation, scurvy, pre-existing brain hemorrhages, strangulation (drowning) cases, Hepatitis B vaccine, cerebral edema (swelling) from any cause, any situation associated with a sudden increase in intracranial pressure, and in persons with coagulation disorders.[15-19, 59-62] The amicus brief for SBS provides 36 references in support of this contention, only a representative few of which are given here—others will be provided on request.

Deficiencies in Scientific Safety Infrastructure in Childhood Vaccines

ASince 1999 there have been ongoing hearings in the U.S. Congress concerning growing concerns about vaccine safety. These hearings have dealt primarily with a possible link between the MMR vaccine and the growing epidemic of childhood autism in the USA. From these hearings there is now an emerging a background pattern of deficiencies in basic science in vaccine testing. Autoimmune reactions, for example, may be delayed for months or even years, and simply go unrecognized.

Since misdiagnosed SBS is merely one phase of potential vaccine reactions, it is a virtual certainty that many adverse vaccine reactions are taking place unrecognized due to this pattern of deficiencies in safety testing and scientific infrastructure of vaccines.

In cases of misdiagnosed SBS, Dr. Buttram has seen two reactions that occurred within the same day, most within 12 to 13 days, but also some delayed for 2 or 3 months. The causal relation was apparent in that the families noticed subtle but distinct and persistent changes in behavior of the infants (such as fussiness, fever, and high-pitched screaming) which persisted until sudden and unexpected respiratory collapse.

Based on these hearings, scientific evidence does not support the safety of immunizations. Particularly unfortunate is that there are no long-term (months or years) safety studies on any childhood vaccine in use today. In addition there have been no systematic before-and-after studies on the effects of vaccines on the immune, hematologic, brain, and neurologic systems of babies—studies which should be considered indispensable for any ongoing medical intervention. Nor has adequate consideration been given to the additive or synergistic adverse effects of multiple simultaneous vaccines, even though in cases of chemical toxicity 2 chemicals together may be 10 times as toxic than either separately, or 3 chemicals 100 times more toxic.[20-21]

As one example of the deficiencies in basic science among the vaccines, in 1994 the Institute of Medicine, a federal government advisory board, published a comprehensive review addressing the safety (or lack of it) of the Hepatitis B vaccine. When the committee investigated five possible and plausible adverse effects, they were unable to come to a conclusion on four of them, because they found that relevant safety research had not been done. Furthermore, they found that serious “gaps and limitations” existed in both the knowledge and infrastructure needed to study vaccine adverse events.

Among the 76 types of potential adverse reactions reviewed by IOM, the basic science evidence was inadequate to assess definitive vaccine causality for 50 (66%). The IOM also noted that “if research…(is) not improved, future reviews of vaccine safety will be similarly handicapped.”[22]

Following are three examples of before-and-after studies provided as examples of studies that are not being done in a systematic fashion, but should be:

Vaccines and Immune Paralysis
As reported in the New England Journal of Medicine in 1984 [23], 11 healthy adults had tests involving subpopulations of T-lymphocytes (white blood cells which mediate immune function) before and after routine tetanus booster immunizations. The results showed a significant though temporary drop in T-helper lymphocytes. Special concern rests in the fact that in 4 of the subjects the T-helper lymphocytes dropped to levels found in active AIDS patients. If this was the result of a single vaccine in healthy adults, it is sobering to think of the immune consequences of the multiple vaccines given to infants with their immature and vulnerable immunity. This study should have served as a pilot for ongoing vaccine safety studies, but as far as can be determined from surveys of the medical literature, it has never been repeated.

Vaccines and Seizure Disorders
For the second example, in 1955 AL Low of Chicago published a study in which he performed electroencephalograms (EEGs) on 83 children before and after pertussis immunization.[24] In two of the children he found that the EEGs became abnormal following the immunizations without other signs or symptoms of abnormal reactions. In his report he commented:

“This study suggests that mild but possibly significant cerebral reactions may occur in addition to the reported very severe neurological changes.”

Vaccines Provoking Patterns of Sickness
As reported in Mediators of Inflammation (2003), a study was undertaken to analyze the immune responses of live attenuated rubella vaccine in eighteen school girls ages 11 to 13 years by collecting blood before immunization and again at 7 and at 30 days after immunization to test whether or not there would be immune suppression.[25] Subclasses of lymphocytes (a class of white blood cells that mediates immune function) were tested before and after vaccine. Also, plasma samples were tested for cytokines (cellular messengers) including interleukins (IL). IL 4 and 10, tumor necrosis factor, and gamma-interferon (all pro-inflammatory) were measured. It was found that certain lymphocyte subsets were decreased and that IL 10 and tumor necrosis factor were markedly increased following vaccines. The study concluded: “Our data indicate that the vaccination with live attenuated rubella vaccine results in moderate but sustained immune disturbance. The signs of immunosuppresion, including defective lymphocyte response to mitogens and cytokine production, may persist for at least one month after vaccination.”

Increased Hazards of Vaccines in Premature Infants [26]

The authors of many well-documented studies have concluded that the risk and benefit of vaccination in preterm infants should be evaluated prior to administering the vaccines. They also emphasized that preterm infants who have received vaccines should be monitored. The following are descriptions of several selected studies conducted in the USA and other countries to illustrate these points.

• Case histories of 45 preterm babies who were vaccinated with DPT/Hib (diphtheria, tetanus toxoids, and pertussis (Haemophilus influenzae type B conjugate) in the neonatal intensive care unit of the Royal Gwent Hospital, Newport, UK between January 1993 and December 1998 were studied retrospectively (2001).[27] Apparent adverse events were noted in 17 of 45 (37.8%) babies; 9 (20%) had major events, i.e. apnea, bradycardia or desaturations, and 8 (17.8% had minor events; i.e. increased oxygen requirements, temperature instability, poor handling and feed intolerance. Age at 70 days or less was significantly associated with increased risk (p<0.01). Of 27 babies vaccinated at 70 days or less, 9 (33.3%) developed major events compared with none when vaccinated over 70 days. The authors concluded that vaccine-related cardiorespiratory events are relatively common in preterm babies. Problems were much more common if vaccine is administered at or before 70 days. Babies should therefore be monitored post-vaccination.

• After observing the occurrence of apnea (a respiratory pause of 20 seconds or longer, usually associated with bradycardia, heart rate less than 80 beats/min) in two preterm infants following immunization with DTP and HibC, Sanchez et al (1997) conducted a prospective surveillance of 97 preterm infants (50 girls and 47 boys) younger than 37 weeks of gestation who were immunized with DTP (94 also received HibC at the same time) in the neonatal intensive care unit in Texas USA [sic - in article] to assess the frequency of adverse reactions, and in particular the occurrence of apnea. For each infant data were recorded for a 3-day period before and after receipt of the immunizations.[28]

Their study showed that apneic episodes occurred in 34 infants (34%) after immunizations. Twelve infants (12%) experienced a recurrence of apnea, and 11 (11%) had at least a 50% increase in the number of apneic and bradycardia episodes in the 72 hours after immunization. This occurred primarily among smaller preterm infants who were immunized at a lower weight (p=0.01, who had experienced more severe apnea of prematurity (p=0.01), and who had chronic lung disease (p=0.03). Some of these infants required new medical intervention for the increased apneic/bradycardiac episodes.[23]

• Bothan et al (1997) conducted a prospective study of 98 preterm infants (53 males and 45 females) of gestational age 24-31 weeks who were immunizated at approximately 2 months postnatal age with diphtheria-tetanus whole-cell pertussis vaccine (DTPw) in the neonatal intensive care unit (NICU) at King George V Hospital in Sydney, Australia.[29] Half the infants also received Haemophilus influenzae type b conjugate vaccine (Hib) simultaneously. All infants were monitored for apnea and bradycardia in the 24 hour periods pre- and postimmunization.

Their study showed only one infant had apnea and/or bradycardia pre-immunization compared with 17 post-immunization. For 12 infants these events were brief, self-limiting and not associated with desaturations (oxygen saturation <90%). However, for five infants (30%) these events were associated with oxygen desaturation, and two of these infants required supplemental oxygen. When considering immunization for preterm infants, the benefits of early immunization must be balanced against the risk of apnea and bradycardia.

• Slack et al, (1999) from the United Kingdom stated that four premature infants developed apneas severe enough to warrant resuscitation after immunization with diptheria-tetanus-pertussis (DTP) and Haemophilus influenzae B (Hib).[30] One required intubation and ventilation. They also reported that, although apneas after immunization are recognized, they are not well documented. They concluded that it is time for further research to elucidate the best time to immunize such infants.

• Botham et al (1994) conducted a prospective study to document respiratory and cardiac events in 97 preterm infants who were immunized with DTP.[31] The mean gestational age at birth was 28.1 weeks (range 24 to 34) and the mean age at immunization was 80.6 days (range 44-257). They found that nineteen (20%) infants developed apnea or bradycardia within 24 hours of immunization. The infants who developed apnea and/or bradycardia had a younger gestational age at birth than those who did not (p=0.03), were artificially ventilated for longer (p=0.01), and were more likely to have a diagnosis of chronic lung disease (p=0.006). Two infants who developed concurrent upper respiratory tract infections required additional oxygen, and one of them was treated with oral theophylline. The researchers stated that cardiorespiratory function should be monitored after immunization in very preterm infants who had prolonged ventilatory support and/or chronic lung disease.

In Nelson Textbook of Pediatrics, 16th Edition, there are precautions in the use of potentially toxic medications in premature infants because of diminished renal clearances for almost all substances excreted in the urine.[32] The text also cautions about drugs that are detoxified in or conjugated by the liver in premature infants.

As will be found in current editions of the Physicians’ Desk Reference, potentially toxic and/or sensitizing substances routinely found in childhood vaccines include aluminum phosphate, mercury (still present in some vaccines), formaldehyde, phenols, alcohols, mineral oils, antibiotics, animal serums, animal DNA, and aborted fetal tissue. In addition, the Hepatitis B vaccine, which is cloned in yeast cells, runs the risk of causing sensitivity reactions in children who may be sensitive to yeast.

Diphtheria-Pertussis-Tetanus (DPT) Vaccines and Infant Apnea in Sudden Infant Death Syndrome (SIDS)

RAccording to a report by WC Torch of Reno, Nevada in 1986, over 150 DPT-postvaccinal deaths had been reported in the literature by 37 authors in 12 countries.[66] The report is not particularly well written, but we include it here because of its historical importance. Although the technical details are ambiguous in some places, it is one of the very few published articles in the literature which dares to say that vaccines can and do kill babies:

Although 90% of the deaths occurred within one week of DPT, the remainder occurred as long as 20 months, following protracted reactions. About one-half were sudden-infant-death-like (SIDS) or anaphylactic; about one-half followed neurotoxic or systemic symptoms (dyspnea, seizures, shock, irritability, lethargy, apathy, coma, decerebrate-decorticate rigidity, spasticity, hypotonia, paralysis, or apnea). In deaths within 3 hours of DPT, the brain was normal; in deaths between 6 and 72 hours, varying degrees of brain edema, vascular congestion, petechiae or (brain) hemorrhage, monocytic infiltrates, and neuronal degeneration were seen. In some later deaths, demyelination, gliosis, or atrophy were seen. The author and others maintained a causal relationship between DPT vaccine and yet-to-be determined SIDS fraction.

Vaccines, Vitamin C Depletion and Shaken Baby Syndrome [33]

TIn the next 25 years or so, when there is greater knowledge about the adverse reactions and aftermath from current childhood vaccine programs, physicians and scientists, as well as the lay public, may look back on these programs with embarrassment if not worse. This is not to say that vaccines do not have a proper role in preventive health, which they do, but not with neglect in safety considerations.

The rationale for these statements is based largely on the work of Dr. Archivedes Kalokerinos, who worked as a medical officer among the Australian aborigines in the “outback” in the 1960s and 1970s. Troubled by very high infant mortality, in some areas approaching 50%, he began to investigate possible causes. Having noticed signs of scurvy in some of the infants, and observing that the children often died following immunizations, especially if they had colds or minor respiratory infections, the thought occurred to him that there might be a connection between vitamin C deficiency and deaths following vaccines.

With improved nutrition; routine oral vitamin C supplementation; avoidance of immunizations during illnesses, even minor ones, such as a runny nose; and large doses of injectable vitamin C during crises, infant mortality was virtually abolished. Although Kalokerinos and his research partner, Glen Dettman, PhD, who was originally sent to prove Kalokerinos wrong, were awarded the Australian Medal of Merit in 1978 for their work, it has never been acknowledged by mainstream medicine. What is worse, it has never been subjected to systematic, meaningful scientific studies.

In contrast to classical scurvy of earlier times in the days of wooden sailing ships, when scurvy was characterized by a total lack of vitamin C, what we may be seeing today is something quite different. As described by Dr. Kalokerinos [34] and C. Alan Clemetson, MD [35], subclinical scurvy is a condition in which apparently healthy infants with marginally low but adequate levels of vitamin C in unstressed conditions may be suddenly thrown into states of critical vitamin C depletion by combinations of stresses from common infections and toxins, including the toxins found in vaccines.

As one example of marginal vitamin C deficiency on the modern scene, in a study of people attending an HMO (Health Maintenance Organization clinic) in Tempe, Arizona in 1998, 30% were found to be depleted, with plasma vitamin C levels between 0.2 and 0.5 mgs/100 ml; and 6% to be deficient, with levels below 0.2%.[36] In regards to infants, it is true that infant formulas have been mandated to include vitamin C at levels providing the required 30 mgs per day. However, this is a maintenance level and makes no allowances for additional stresses which may bring about manifold increases in need for vitamin C. Common colds, for instance, have been shown to reduce vitamin C levels up to 50%.[37]

No one knows the effects of vaccines on vitamin C levels in infants, because before-and-after studies of this type have never been done, but vitamin C is known to neutralize the toxins of diphtheria, [38-41] tetanus, [42] typhoid endotoxin, [43] and four varieties of gas gangrene.[44] As will be described below, in the process of neutralizing these toxins, vitamin C is necessarily depleted.

If the reader will consult with these references, which were extracted from an article by Clemetson [45], it will be found that most of these studies are quite old and some published in foreign languages. To us that is the pity of it, as our own scientific & medical system has never recognized their importance or followed through with further investigations.

Returning to the importance of vitamin C in relation to vaccines, one of the prime roles of vitamin C in the body is its action as an antioxidant in donating electrons to quench free-radical and inflammatory damage from toxins and/or infections, with our consideration here being vaccine toxins. In the process of donating electrons, vitamin C necessarily becomes depleted. Once the level is reduced to the point that it can no longer protect the brain, which is unduly susceptible to toxic and infectious damage, it (the brain) may become subject to free-radical damage.

By definition, a free radical consists of a molecular fragment with one or more unpaired electrons in its outer orbital ring, causing it to be highly oxidative, unstable, and to react instantaneously with other substances in its vicinity. Within a few millionths of a second, free radicals can react with and damage nearby molecules and cell membranes with a chain reaction effect.[46-47] When uncontrolled, such as may occur during exposure to harmful ionizing radiation, these reactions can be very destructive to the body.

Vitamin C is critically important in protecting against free-radical proliferation because, in donating electrons, it neutralizes the unpaired electrons in the free-radical molecular fragments. Of all the organs of the body, the brain appears to be most vulnerable to this type of damage because of its relatively high fat content. For these reasons, the combination of ill-advised vaccines given to fragile infants with highly immature detoxification organs (liver and kidneys) and immature immune function, or, as often takes place, in the presence of viral or bacterial infections, may be an invitation to disaster, with the brain being potentially subjected to a firestorm of free-radical damage and inflammation.

Once this pattern has been set in motion, there may be a variable latent period with gradual progression of inflammatory brain edema (swelling). The breathing center, located at the base of the brain, appears to be uniquely vulnerable to the process, resulting in respiratory paralysis and collapse. In other instances there may be seizures. Among the cases of SBS that we have reviewed, this pattern has occurred too frequently to be coincidental.

In his autobiography, Dr. Kalokerinos describes the mechanisms involved in the production of brain edema, with retinal and brain hemorrhages in much the same fashion:[34]

1. Endotoxin (endogenous and/or from vaccines) damages the endothelial linings of the brain’s blood vessels.
2. Endotoxin then ‘leaks’ through to the surrounding brain tissue. This includes the retina that is an extension of the brain.
3. The brain tissue is damaged.
4. The blood supply to the portions of the brain involved is reduced.
5. Insufficient oxygen, glucose, and vitamin C follows.
6. Parts of the brain are ‘rich’ in ‘bound’ (controlled) iron. This is released.
7. Violent free radical reactions result, and these cannot be controlled because of a lack of immediately available vitamin C and other antioxidants.
8. So further, and rapid, brain tissue damage results, with more free radical reactions.
9. Hemorrhages occur in the area/areas involved.
10. After a variable period (depending on a host of factors) some of the red blood cells in the hemorrhages break down and release their stores of iron and copper.
11. This results in a further cascade of free radical reactions and tissue destruction.
12. Cerebral edema (brain swelling) occurs.

By way of historical comparison, in Vienna in the 1840s, long before recognition of the importance of sanitation and the role of microbes in causing disease, a doctor named Ignaz Semmelweis was assigned to an obstetrical post at a birthing center which was notorious for its high maternal mortality rates. Based on simple observation, Semmelweis deduced that doctors and nurses were carrying infections from one patient to another and subsequently required that they wash their hands between patients. As a result, the mortality rate among maternity patients under his care was reduced from nearly 30% in other wings of the hospital to less than 2% for patients under his care or supervision.

Was Semmelweis honored at the time by his peers for this discovery? No, instead he was dismissed from the hospital staff because his procedures did not conform with the medical thinking of the time. In the cases of Drs. Archivedes Kalokerinos and C. Alan Clemetson, could history be repeating itself?

In reviewing many medical-legal cases involving accusations of SBS over the last four years, we have yet to see a case in which hospital emergency room doctors have included tests for vitamin C as part of the diagnostic evaluation. We know from references 38-44 that vitamin C detoxifies bacterial endotoxins and that it would inevitably be reduced in a baby’s system as a result, very likely to critically low levels. There are good reasons for believing that this is one of the primary missing links in many of these cases.

Plasma Vitamin C / Histamine Levels, and Capillary Fragility

In 1980, C. Alan Clemetson reported that the whole-blood histamine levels of human subjects are inversely proportional to their plasma vitamin C levels [48], in that 34 percent of people who had subnormal but not deficient ascorbic acid levels were found to have significantly increased blood histamine concentrations. The 2 percent of subjects who were markedly vitamin C depleted (<0.2 mg/100 ml) had a four-to-five-fold increase in their blood histamine concentrations. Frank scurvy does not occur until blood histamine is increased more than tenfold. Nevertheless, the blood histamine concentration returns to normal very rapidly following the oral administration of ascorbic acid.

Indications that elevated blood histamine is the true cause of capillary fragility in scurvy comes from electron-microscopic studies by Gore et al in guinea pigs with scurvy, in which widening of the intercellular junction gaps were demonstrated in the vascular endothelium.[49] Moreover, Majno and Palade have observed similar widening of the endothelial junction gaps and leakage of tracer particles through endothelial gaps in rats following the injection of histamine.[50] Consequently it seems that histaminemia is the crucial factor causing bleeding in scurvy and may be responsible for the fragility of the bridging veins and venules between the brain and the dura mater, as well as the retinal petechiae.

In our opinion, Clemetson’s work in elucidating the inverse relationship between vitamin C and blood histamine levels, with elevated histamine being the primary cause of capillary fragility, is of critical importance in shaken baby syndrome, such that there should be mandatory requirements for obtaining blood plasma levels of vitamin C and whole blood histamine in hospital emergency rooms before bringing charges of shaken baby syndrome.

Rib Fractures

Fairly often in SBS cases there are findings of multiple skeletal fractures along with brain and/or retinal hemorrhages. This is not surprising since a majority are “fragile” infants with immature, delayed, or impaired development organ and tissues systems. Attention here will be limited to rib fractures which appear to be the most common of the fractures.

It is well understood in the medical literature that there are a variety of conditions in which multiple fractures can take place spontaneously or with minimal trauma, including scurvy, rickets, osteogenesis imperfecta, and birth trauma. Standard texts point out that subperiosteal hemorrhages (bleeding beneath the fibrous covering of bone) is the most common type of hemorrhage in scurvy and may be indistinguishable from fractures in their healing phases. Three references are provided showing a coincidental relationship of posterior rib fractures with birth trauma.[51-53] In addition, temporary brittle bone disease (TBBD) is a condition wherein spontaneous fracture occurs during the neonatal period, as described by Miller and Hangartner, associated with decreased fetal movement.[54-55]

Based on personal experiences, it is unusual to find thorough evaluations of these infants to rule out alternate causes of fractures. But in most infants there are even more compelling reasons for excluding parental or caretaker trauma: (1) in a majority of cases there are no bruises or external marks of trauma in association with the fractures; (2) in instances of multiple rib fractures, there are no findings of internal thoracic trauma; (3) there are negligible indications of pain in these infants when handled or moved.

Taking each of these in turn:
The literature provides evidence that surface injury should be present if multiple fractures are from child abuse. First, when a child incurs a fracture caused by physical abuse, there is a probability that the traumatic event will also cause a bruise. Mathew et al determined the frequency of bruising in children with fractures.[56] The frequency was 8% at time of presentation and 28% during the first week of trauma. Using this information the probability of trauma to an infant who is followed by health care providers during the first few weeks of life during which there are no findings of bruises can be calculated. If there are multiple fractures, then each fracture is an independent event for showing bruising, and the likelihood that a series of fractures could have taken place without showing bruising is quite small.

Next, Garcia et al found that in infants who have normal-strength ribs and incurred multiple rib fractures from trauma (either from child abuse or motor vehicle accidents), there was always internal thoracic injury or other internal injury when 4 or more rib fractures were involved.[57]

In regards to the pain issue, traumatic rib fractures are very painful at any age. Multiple rib fractures from trauma should be quite painful to the infant and immediately apparent to the handler. This situation has rarely arisen in cases we have reviewed. Further insights into the nature of spontaneous fractures of metabolic origin, possibly explaining why they would be relatively pain-free, was provided in an article by Hiller, entitled “Battered or Not – a Reappraisal of Metaphyseal Fragility” [58], in which the author cited studies showing a proneness for epiphyseal slippages at the ends of long bones in rickets and scurvy.

Slippages would either be posterior at the vertebral-costal junctions (junctions of the ribs with the spine) or anterior at the costo-sternal junctions (junctions of ribs with the sternum). In long bones of arms and legs these “slippages” would take place at the proximal or distal ends. Although these slippages result in subsequent callus formations, which radiologists would read as healing fractures, they are not the same. This may be the reason they are usually less painful.

Summary and Conclusions

As previously reviewed, experience has shown that there is a common pattern in many shaken baby syndrome cases with sudden and unexpected onset of apnea (cessation of breathing) in a delayed fashion following immunizations. Untrained parents or caretakers may shake the baby in sheer panic to restore breathing and later be accused of child abuse or murder when, on the baby’s hospitalization, tests and exams show the presence of brain and/or retinal hemorrhages.

The hypothesis proposed here is that, in many cases, a smoldering hemorrhagic encephalitis with gradual development of brain edema is triggered by vaccines ultimately affecting and paralyzing the respiratory center at base of the brain, this in turn causing sudden onset of apnea. Once this takes place the resultant hypoxia (lack of oxygen) causes an acceleration of the brain edema. Since the brain has little room for expansion inside of the skull, the swelling may reach a point where the brain becomes its own tourniquet by cutting off the easily collapsible venous outflow from the brain. As a result there is a rapid increase in central venous pressure in the brain, which then becomes the source and cause of brain and retinal hemorrhages.[59-62]

This concept is supported by publications of Jennian Geddes, neuropathologist at Royal London Hospital, and colleagues who have shown that the abrupt onset of apnea in many supposed SBS cases is the result of injuries to the respiratory center not necessarily involving either violence or impact.[63-64] Although Geddes et al did not take into account a possible role of vaccines in the process, they did specify that brain swelling rapidly ensues as a result of hypoxia following respiratory collapse and that the brain and retinal hemorrhages were secondary to the brain edema.

A reasonably full spectrum of animal models already exists for vaccine-induced hemorrhagic encephalitis, which is reviewed elsewhere.[65] The time is long overdue for vaccine safety testing at a human level, establishing a valid and objective scientific infrastructure in this area. Let the chips fall where they may.

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