A Introduction
Among the many adversities facing the American family today, there is a relatively new and growing hazard to parent or caretaker: being falsely accused of injuring or murdering an infant by the Shaken Baby Syndrome (SBS), when the true case of death or injury arises from other sources. Tragically, child abuse does occur and deserves appropriate punishment. However, it is equally tragic when a family, already grieving from the death of their infant, finds a father or mother unjustly accused, convicted, and imprisoned for murder of the infant, a murder of which he or she is innocent. Only those who have observed these events can appreciate their devastating effects upon on these families.

The following material represents over 6 years of experience in reviewing many SBS cases. Its primary purpose is to offer a composite of information gained from study of these cases, information which may be of value in defense of parents or caretakers who have been falsely accused and/or convicted of inflicted child abuse in the form of SBS. Although much of the material involves technical complexities, every effort has been made to present it in a clear and simple manner.

Shaken Baby Syndrome, a Phantom Diagnosis without Scientific Basis
In 1971 Guthkelch hypothesized that subdural hematomas could be caused by manually shaking an infant, without the head impacting any surface. (1) One year later, Caffey alluded, in a paper describing “parent-infant traumatic stress syndrome”, to manual shaking causing intracranial injury in the form of subdural hematoma and cerebral contusions in infants. (2) Two further papers by Caffey over the next two years emphasized shaking as a means of inflicting intracranial bleeding in children. (3-4)

After publication of these papers, SBS became widely accepted as a clinical diagnosis for inflicted head injury in infants, in which the findings of subdural (brain) hemorrhages and/or retinal hemorrhages became accepted as exclusively diagnostic of SBS in the absence of known major accidental injury. However, in 1987 and again in 2003, careful laboratory investigations based on the known biomechanics of head injuries showed that human beings cannot achieve the necessary accelerations for causing intracranial injury in infants by manual shaking alone, but that impact is required. (5,6) Moreover, after more than 33 years, despite numerous reports of series of case studies, an actual witnessed incident in which an infant sustained an intracranial injury as a result of shaking alone has yet to be documented. (7) .

A Biomechanical Considerations
Our understanding of trauma to living tissue is derived from both clinical observation and laboratory experimentation. While there is a physiologic response to trauma, the initiating event of necessity must involve mechanical disruption of living tissue. In the physical universe, as described by classical Newtonian physics, force is the product of mass and acceleration. Insofar as living tissue has mass and undergoes motion, these same laws are equally applicable to living tissue as they are to motion of the planets. The application of these laws to a study of living tissue is referred to as biomechanics, and an understanding of trauma to the nervous system necessitates some understanding of this discipline. .

It is significant that in all four previously cited original papers regarding the hypotheses of shaking, both Guthkelch and Caffey refer to a single paper by Ommaya published in 1968 (8) as a justification for this concept, but apparently misinterpreting the contents of the paper, which never demonstrated quantitatively that human beings could generate the required rotational acceleration by manual shaking to cause brain injury. Therefore, it is important to understand what was attempted and accomplished by Ommaya. As Ommaya and other clinical neurosurgeons observed, people who sustained whiplash injuries to the neck in motor vehicle accidents sometimes also exhibited symptoms referable to altered brain function such as altered sensorium, diplopia, and even occasional intracranial bleeding.

Threshold of Injury
Working with the US Department of Transportation, Ommaya devised an experiment to measure more precisely the amount of rotational acceleration necessary to reach the threshold of brain injury. A contoured fiberglass chair was built, mounted on wheels, and placed on tracks with a piston behind it. Rhesus monkeys were strapped into the chair with their heads free to rotate. The piston then impacted the chair, simulating a rear-end motor vehicle collision.

The experiment was photographed with a high-speed camera, enabling calculations of generated rotation accelerations. Measuring the arc of the head rotating and accelerating around the neck, Ommaya was able to demonstrate that a rotational acceleration of 40,000 radians/second squared was sufficient to cause concussion in the animal subjects. Ommaya was able to produce intracranial injury to 19 of the animals, with 11 of them also demonstrating neck injury. (8) Then, using the scaling parameters, he estimated that less rotational acceleration would be required to produce concussion in the larger human brain, perhaps on the order of 6,000 to 7,000 radians/second squared. (9)

After a laps of 19 years the next study of historical note involved biomechanician Lawrence Thibault and team members Duhaime and Gennarelli (1987) who, devising a surrogate doll with a accelerometer attached to its neck, employed young athletes to shake the model as hard as they could. The most force they were able to generate was a mean of 1,138 radians per second squared, (5) far below the 6,000 to 7,000 established by Ommaya as required for brain injury.

In a more recent study by Ommaya, Goldsmith, and Thibault (2002) it was found that impact creates 50-100 time the Gravity (G) force created by shaking, and that shaking alone in an otherwise healthy infant did not create enough force to cause subdural hematomas and retinal hemorrhages. (10) In 2003 Prange, Coats, Duhaime, Margulies used the anthropomorphic surrogate doll (of a 1.5 month-old human infant) to simulate falls from 1 ft, 3 ft, and 5 ft, as well as vigorous shakes and inflicted head impact. Once again, there was no evidence supporting the concept that shaking alone could produce brain damage. (6)

It is also important to point out that, in the Ommaya studies on the Rhesus monkeys, 11 of the 19 monkeys sustaining brain injury also sustained neck injuries. In my personal experience of reviewing 76 cases of SBS over a period of 6 or so years, I have never come across a case in which neck injury was described, nor have I read of such in the literature. This fact alone should raise suspicions as to the validity of the SBS as a diagnosis.

Based on the above, the Shaken Baby Syndrome, though widely taught and held in the USA, fails the Frye legal standard because it has been discredited and dismissed as lacking in evidence by those who have conducted the only research in the field to date.

Birth Trauma, Premature Birth, Very Low Birth Weight, and Other Alternative Causes of Brain Hemorrhage (Other than Physical Child Abuse)
As noted above, when infants are brought into hospital emergency rooms and found to have subdural (brain) hemorrhages and retinal hemorrhages, these findings are usually considered exclusively diagnostic of SBS in absence of known accidental injury. The following references show that these findings may and commonly do arise from other sources.

As reviewed in Nelson Textbook of Pediatrics, 16th Edition, intracranial hemorrhage in the newborn may result from birth trauma or asphyxia. This is especially likely when the fetal head is large in proportion to the size of the mother’s pelvic outlet; when for other reasons labor is prolonged; in breech or precipitate deliveries; or as a result of mechanical assistance with delivery. (11)

Also as stated in Maternal-Fetal Medicine, (12) intracerebral hemorrhage occurs in up to 50% of very low-birth-weight infants and is thought to represent a substantial cause of morbidity and mortality in these patients. If hemorrhage were to take place in the ventricles, it could lead to hydrocephalus at a later time.

From Neonatal-Perinatal Medicine, Fifth Edition, 1992, subdural hemorrhage over the cerebral hemisphere occurring at time of birth may be clinically silent, clinically apparent in the first few days after birth, or not apparent until as late as the sixth week of life….when an infant shows evidence of a convex subdural hematoma, there is usually an increasing head circumference, poor feeding, or vomiting. (13) From Neonatology –Pathology and Management of the Newborn, (1999) “The data must be interpreted with the recognition that mild subdural hemorrhage may have few associated clinical abnormalities and may remain undiagnosed.” (82)

In 2003 MK Tauscher et al reported on brain hemorrhages in preterm infants associated with histologic chorioamnionitis (inflammation of the placenta), thus reporting on a newly recognized risk factor for fetal or neonatal brain hemorrhages. (14) Patrick Barnes has commented that “birth trauma may persist beyond the neonatal period and mimic abuse.” (15)

According to GN Rutty et al (1999), late-form hemorrhagic disease of the newborn is a bleeding disorder which may arise 4 to 6 weeks or even longer following birth in which intracranial bleeding may occur in up to 100% of cases. Retinal hemorrhages may also take place. (77) Predisposing factors include antibiotic therapy in the neonatal period, gastroenteritis with vomiting and/or diarrhea, malabsorption, and liver disease.

(Comment: In medical schools doctors are taught to measure and record height, weight, and head circumference at all well-baby visits. In many SBS cases the head circumference measurements could be pivotal, showing that abnormal head enlargements from brain hemorrhage and/or hydrocephalus had commenced long before the alleged act of physical child abuse by parent or caretaker. More often than not in my experience these measurements have been deficient in the medical records, thus depriving the accused person of crucial evidence that might have exonerated him or her.)

Atrophy-of-Disuse as Applied to Fetal Bone Development: Spontaneous Fractures Taking Place during Childbirth or the Neonatal Period, Mistakenly Attributed to Child Abuse
Atrophy-of-disuse is a universal principle as applied to human organs, tissues, and physiology. Bone is no exception. Common examples include bone weakening and rapid decalcification that takes place during prolonged bed confinement, thereby predisposing to spontaneous fractures or fractures with minimal trauma. As reported by Brayev et al, eight children with clubfeet experienced metaphyseal fractures during physical therapy when their legs were passively manipulated, their legs having been immobilized for prolonged periods by corrective casts. (78-79) In a study of the long bones in eleven newborn infants with congenital muscular dystrophy (with marked weakening of muscles), the bones were found to be thin, hyopmineralized, and elongated. In most of the bones there were multiple diaphyseal or metaphyseal fractures or both. (80) A study of rat fetuses that were curarized (paralyzed) during the later phases of pregnancy revealed marked thinning and delay in ossification of bone. (81)

Conversely, it is well recognized that exercise, especially weight lifting, strengthens bone as well as muscle.

As reviewed by Marvin Miller (2003), (16) it is well known that premature infants are at increased risk to develop temporary brittle bone state. It has traditionally been thought that the primary cause was insufficient calcium and phosphate in the diet of the premature infant. However, there is emerging evidence that the bone disease of prematurity may be more of a biomechanical issue than one of nutritional mineral deficiency. (17) It has been found that there is increased bone resorption in the bone disease of prematurity which would indicate some other explanation for this condition, other than lack of mineral availability. (18,19) Miller suggested that this increased bone resorption in the premature infant compared to the term infant is secondary to decreased bone loading. During the last trimester of a full-term pregnancy the fetus is actively kicking and bouncing against the mother’s uterus. This fetal activity with associated muscle development is the primary determinant of fetal bone formation. Fetal movement also promotes muscle growth which contributes to bone loading. In a premature infant, muscles are as yet insufficiently developed to produce necessary level of bone loading (stimulation), leaving the bone weak and poorly ossified.

It has been shown that preterm infants who receive 5-10 minutes of daily physical activity realize a 76% greater gain in bone density by one month of life compared to control premature infants who receive no physical activity. (20) This finding explains the observation that very sick premature infants who are on ventilators and require parenteral nutrition have a much greater frequency of bone fractures compared to premature infants who can take oral feeds and are not on ventilators. (21-22)

Miller and Hangartner have observed a comparable clinical situation referred to as “temporary brittle bone disease” associated with lack of fetal movement during the last trimester of pregnancy, in which the baby is susceptible to spontaneous fractures or fractures with minimal trauma for 6 or more months following birth. This may be looked upon as another form of atrophy-of-disuse, a universal principle as applied to human organs and tissues. (73)

Finally, still another potential cause of spontaneous fractures in infants is a re-emergence of vitamin D-deficient rickets and an alarming prevalence of low circulating levels of vitamin D in the United States population, according to a National Institute of Health (NIH) conference on Vitamin D, October 9-10, 2003. (http://www.nichd.nih.gov/prip/)

Causes of this re-emergence include general reduction in milk intake (milk allergies, lactose intolerance); reduction in vitamin D-fortified fats (concerns about fats); reduced intake of calcium-rich foods, including milk, in teenagers and young women of reproductive age; an increase in use of sun screens and decreased exposure to sunlight because of skin cancer concerns; current prevalence of exclusive breast feeding by US women (breast milk is a poor source of vitamin D unless supplemented), and other causes.

(Comment: Although radiologists are trained to look for classic findings of rickets, it is important to emphasize that there are no visible changes in whiteness on plain radiographs until calcium loss is greater than 30%, a level associated with marked increase in fracture risk. (83-84) Blood testing for 25-hydroxy Vitamin D, therefore, is the definitive test in medical-legal cases involving rib and/or long bone fractures, and yet I personally have not seen a single instance in which vitamin D was tested in these cases.)

Recurrence of Brain Hemorrhage from Pre-Existing Chronic Subdural Hematoma and/or Hydrocephalus
Old subdural hematomas and/or hydrocephalus pose increased risks for recurrent, fresh brain hemorrhages, which may at times be massive, as indicated by the following body of medical literature:

As described by Parent, (23) Hymel, (24) and Piatt, (25) once acute subdural hemorrhages take place they tend to take on lives of their own. Initially acute hemorrhages have a high density due to the iron content in the red blood cells, which show up as white on brain CT scans or MRIs. Very often, as a result of tears in the tissue-paper thin subarachnoid membrane which separates the subdural space from the brain, there is a leakage of cerebrospinal fluid into the subdural hematoma. This tends to thin the clot. Also, the red blood cells soon begin lysing (breaking up) and releasing their iron, which is picked up by scavenging white blood cells and carried out of the area in the form of hemosiderin. This process starts in about 4 days after the initial hemorrhage. Thus over a period of about 3 weeks the former clot is changed into a consistency similar to “crankcase oil” with a density slightly above that of water, referred to as a “hygroma.” This turns up as black on CT scans and MRIs. Generally speaking the “acute phase” with high density lasts up to a week, followed by a “subacute phase” with gradually reducing density for another two weeks, followed in turn by the “chronic” (hygroma) phase with low density. Radiologists can estimate the age of acute and subacute phases of hemorrhages with some accuracy. However, once in the chronic phase, it is very difficult if not impossible to determine their age, which may be a few weeks or many months.

Chronic subdurals may be resorbed, or they may persist with gradual expansion. In the latter case they are susceptible to rebleeding for the following reasons:

After a period of two weeks or so, a thin healing membrane begins to form around the subdural clot (as a general rule, all injuries heal by forming a healing membrane). Based on electron microscopy studies, one of the characteristics of these membranes (macrocapillaries) is the frequent formation of gap junctions between adjacent endothelial cells, these gaps being large enough to spill blood cells into the subdural clot area. (26) Based on studies by Ito et al (27-29) it has been demonstrated that mean daily hemorrhage (from healing membranes) into subdural hematomas amounted to 6.7% of their volumes, indicating continuous or intermittent hemorrhage into the subdural cavity. These hemorrhages were partly activated by a process of fibrinolysis in the outer membranes of the subdural clots, this fibrinolysis not only tending to liquefy but also enlarge the clot by continuous hemorrhage from the healing neomembranes.

Therefore it would appear that subdural clots not only can enlarge and expand but do so with some degree of frequency. This expansion may cause a stretching of the bridging veins traversing the subdural space, and once stretched beyond a certain point (some estimate this to be beyond 40%), these veins may rupture spontaneously or with minimal trauma and cause acute, sometimes massive rebleeding.

Turning next to hydrocephalus (again for general information) most cerebral spinal fluid (CSF) is formed in the ventricular system by the choroids plexus, which is situated in the bilateral 3rd ventricles and the 4th ventricle, although approximately 25% originates from extrachoroidal sources, including capillary endothelium within the brain parenchyma. Normally CSF travels through the narrow aqueduct of Sylvius into the 4th ventricle and from there into the cisterns at base of the brain. CSF is absorbed primarily by the arachnoid villi through tight junctions of their endothelium by the pressure forces. Internal hydrocephalus (obstructive or non-communicating) occurs when there is blockage of communicating channels (aqueducts) between the ventricles. External hydrocephalus (non-obstructive or communicating) hydrocephalus occurs when there is obliteration of the subarachnoid cisterns or malfunction of the arachnoid villi external to the brain. In premature infants this usually comes from clotted blood from brain hemorrhages. Blood in the subarachnoid spaces (extermal to the brain) may cause obliteration of the cisterns or arachnoid villi and obstruction of CSF pathways. (30)

New Concepts with Alternate Explanations for Brain and Retinal Hemorrhages in Infants Now Being Diagnosed with Shaken Baby Syndrome
As reported in the medical journal, Brain, in a study which promises to revolutionize current concepts of SBS, Jennian F Geddes, a neuropathologist at Royal London Hospital and colleagues, examined the brains of 53 children suspected of dying from deliberate injury. (54-55) Of the 53 children, 37 were less than a year old.

Emergency room doctors are now being taught that the findings of brain and retinal hemorrhages in infants should be considered diagnostic of SBS and/or violent head impact in the absence of a known major accident. However, in examining the brains of the 37 infants, Geddes et al found signs of diffuse axial (brain) injury (one of the original diagnostic criteria for SBS) in only 2 of the 37 babies. Instead they found that three-quarters of the 37 babies died because they stopped breathing as a result of previously unseen and undescribed pathology that was focused on the cranio-cervical junction, the area which controls breathing, where the brain meets the spinal cold. They also found subdural hemorrhages in 72% of the 53 cases, although most were too superficial to cause death, and retinal hemorrhages in 71% of the 38 cases in which eyes were examined. However, the authors felt that these resulted from a lack of oxygen to the brain and subsequent brain edema (swelling) rather than trauma. (Emphasis mine)

Because stretch injury to the craniocervical junction “need not involve either violence or impact,” according to the authors, the following hypothesis was offered regarding the intradural (brain) hemorrhages:

“Our observations in the present series indicate that, in the immature brain, hypoxia both alone (from respiratory arrest following craniocervical junction injuries) and in combination with infection is sufficient to activate the pathophysiological cascade which culminates in altered vascular permeability and extravasation of blood with and under the dura. In the presence of brain swelling and raised intracranial pressure, vascular fragility and bleeding would be exacerbated by additional haemodynamic forces, such as venous hypertension, and the effects of both sustained systemic arterial hypertension and episodic surges in blood pressure…Cerebral venous hypertension occurs when there is an obstruction to flow, which is the situation where there is cerebral swelling…Similarly, retinal haemorrhages can be explained by rises in intracranial and central venous pressure, with and without hypoxia.(55)

In other words, brain swelling of more than slight degree will meet with solid resistance of the skull. At the same time the eyes will be pushed in varying degrees into eye sockets of the skull. In both instances the venous outflow from both the brain and eyes will become obstructed much in the same manner as an arm tourniquet will obstruct venous outflow from the arm. This combination of factors will produce a precipitous rise in intracranial pressure, the true cause of brain and retinal hemorrhages in these situations. (32-36)

Retinal Hemorrhages: Not Diagnostic of Child Abuse
AC Tongue mentions that “hemorrhages in all layers of the retina occur in a number of nontraumatic disorders associated with changes in cerebrovascular dynamics such as central vein retinal occlusion, high altitude retinopathy, and subarachnoid hemorrhage secondary to ruptured intracranial aneurysms. (31) In reality, any sudden increase in intracranial pressure may cause retinal hemorrhages. (32-36) Furthermore, retinal and optic nerve sheath hemorrhages associated with a ruptured vascular malformation are due to an increase in central cranial venous pressure. (37-38) Patrick Barnes reported that retinal hemorrhages may be seen with a variety of conditions including accidental trauma, resuscitation, increased intracranial pressure, increased (intracranial) venous pressure, subarachnoid hemorrhage, coagulopathy, and certain metabolic disorders. (15) In 1999 GN Rutty et al listed the following possible causes of retinal hemorrhages other than child abuse: natural and assisted birth, prematurity, raised intracranial venous pressure, abnormal intracranial blood vessels, and vitamin deficiencies. (39)

Probable Role of Vaccines in Many Cases Attributed to SBS
As disclosed by a series of US Congressional Hearings on issues of vaccine safety (1999-2004), sponsored by the Congressional Committee for Government Reform, there have been many and serious deficiencies in safety testing of current childhood vaccines. (40) Among these are:
(a) Pre-licensing surveillance periods have been limited to short periods only: several days to several to several weeks. There are no long-term (months or years) safety studies on any childhood vaccine in use today. Consequently there are legitimate concerns that many delayed-type (autoimmune) reactions may be taking place unrecognized. (For the Hepatitis B vaccine, as one example, Physicians’ Desk References list surveillance periods from 4 to 6 days).
(b) Vaccines are the only biologicals that the FDA does not require animal studies on before licensure.
(c) Perhaps the most glaring deficiency in vaccine safety testing is in the form of before-and-after vaccine studies specifically designed to test for adverse effects of vaccines on the brain, nervous system, and the immune system, and in finding adverse effects to seek safer methods. The very few before-and-after safety tests that are in the scientific literature are far from reassuring. To the contrary, they indicate that many more vaccine reactions may be taking place than currently recognized. (41-43,85)
(d) Animal models of vaccine-induced hemorrhagic encephalitis exist for clinical features now thought to be exclusively diagnostic of Shaken Baby Syndrome. (44-46).
(e) A significant number of anecdotal reports are found in the medical literature on adverse reactions from the medical literature on adverse reactions from the Hepatitis B vaccine. As outlined in the book, The Hepatitis B Vaccination Program in the United States – Lessons for the Future, by Burton A Waisbren, Sr, MD, (47) there have been 26,760 reports of adverse reactions from Hepatitis B vaccine as reported in the Vaccine Adverse Event Reporting System (VAERS) including 79 reports of Guillain-Barre Syndrome, 96 of multiple sclerosis, 63 of myelitis, and 70 of encephalomyelitis. It is universally recognized that the VAERS system of passive medical reporting is a poor system with less than 10% of adverse drug reactions being reported, so that the true incidence of adverse vaccine reactions can be assumed to be far greater.
(f) In studies from the United Kingdom, (48) Texas, (49) and Australia, (50-51) preterm infants in hospital settings were administered DPT (diphtheria-pertussis-tetanus) and/or Hib (Hemophilus influenzae) vaccines and monitored for episodes of apnea and bradycardia. In each study the results were compared with unimmunized infants serving as controls. Each study showed significant increases in apnea and bradycardia following immunizations. In some instances oxygen desaturation required supplemental oxygen. A report from the United Kingdom in 1999 cited four infants with apnea severe enough to warrant full resuscitation measures following DPT and Hib vaccines. (52) Similar studies from Switzerland using the acellular DTaP vaccine, Hib, inactivated polio virus (IPV), and Hepatitis B vaccine showed comparable incidence of apnea and bradycardia. (53)

It is sobering to reflect that if similar instances of prolonged apnea with oxygen desaturation were to take place unwitnessed in a home, many infants might have progressed into full respiratory arrest. The resultant brain hypoxia would set in motion fulminating brain edema. As described by Geddes and coworkers, the combination of hypoxia with sudden increase in intracranial pressure from the brain edema would be the true source of brain and retinal hemorrhages.(54-55) With this scenario, the person last in attendance of the infant at time of collapse would likely be accused of child abuse, or in case of death of the infant, of murder.

Does Free Iron in the Brain Interact with Vaccines to Trigger Lipid Peroxidation and Hemorrhagic Encephalopathy? (56)
Subdural Hematomas in Infants

Subdural hematomas are not uncommon in asymptomatic term newborns. Based on magnetic resonance imaging (MRI), Whitby et al reported small subdurals in 9 out of 111 infants in 2004. (57) Similar findings had been reported in 2002 by Chamnanvanakij and coworkers, (58) but the Whitby study repeated the positive MRIs in four weeks and found that the hematomas had completely resolved. Largely unaddressed is the fate and possible adverse effects of the residual iron from the hematomas.

The Effect of Iron Released from Subdurals
Free iron released from subdural hematomas and taken up by nearby tissues in the form of hemosiderin is another consideration. Iron overload is known to be destructive in cases of hemochromatosis, resulting in liver, pancreatic and renal failure as well as coagulopathies. (59) The effect of free iron as a potent free-radical generator in or surrounding the brain is as yet unknown. However, in other tissues, hydroxyl and superoxide radicals are formed. The superoxide is converted by superoxide dismutase to hydrogen peroxide, which may injure cells by peroxidation of lipids of the membranes of the microsomes, mitochondria, or other cell membrane structures. (60) Although we do not know how long the hemosiderin remains in or around the brain, it probably persists and remains hazardous for a time after resolution of the hematoma.

The brain is unique among the organs. It is highly fatty, with membrane lipid constituting 60 percent of the solid matter. (61) Although constituting about 6 percent of body weight in an infant, (62) it receives about 15 percent of normal cardiac output and accounts for nearly 25 percent of the body’s oxygen consumption. (63) In addition, both brain and retina contain a relatively high percentage of the omega-3 fatty acid docosahexaenoic acid (DHA), (64-68) which serves as the primary building block of the membranes of these structures. As it is highly unsaturated, DHA is far more unstable and prone to damaging peroxidation (rancidity) than other classes of fats. Reason indicates the probable danger of free iron in a highly oxygenated area combined with fats unusually susceptible to oxidative damage. The addition of other metabolic stresses and/or toxins, such as vaccines, may trigger a firestorm of free-radical pathology in the brain.

The firelock musket of earlier times might serve as an analogy, the brain being compared with potentially explosive gun powder, the iron with the flint lock, and vaccines as the spark.

The respiratory center at the base of the brain appears to be unduly susceptible to this process, as many cases now being (mistakenly) diagnosed with Shaken Baby Syndrome present with abrupt and unexpected onset of apnea (respiratory collapse) in varying time intervals following vaccines (69-70)

Vaccines and Vitamin C Depletion
In the 1960s and 1970s, Kalokerinos, while working as a health officer among the Australian aborigines, became appalled by nearly 50% infant mortality. Observing signs of scurvy in some infants, and noting that the infants commonly died following immunizations, especially if ill with common viral infections, Kalokerinos began administering regular vitamin C supplements and avoiding vaccines when a child was ill, even if just a runny nose. Thereafter, pediatric death rates dropped nearly to zero in his health district. (71) Since that time, Kalokerinos’s clinical observations have been supported academically by Clemetson. (74) Unfortunately, the importance of these clinical observations has not yet been recognized, and meaningful scientific investigation into a possible connection between vitamin C deficiency and vaccine reactions remains unexplored.

While the recommended 30 mgs of vitamin C per day is generally adequate for a healthy infant, it may be rapidly consumed when the infant is stressed, as by the presence of free-iron in or around the brain, the injection of vaccine components, or viral infection, especially when in combination. The common cold, for instance, has been shown to reduce vitamin C levels in the blood by 50%. (72) Vaccines contain numerous toxins and free-radical generators, including formaldehyde, mercury, aluminum, phenols, alcohols, mineral oil, antibiotics, bacterial endotoxins, and foreign viral DNA. All of these are pro-oxidants which will tend to drain the body’s supply of vitamin C. (75-76)

Returning to the analogy of the flintlock musket, vitamin C would play the role of a fire-retardant in the explosive mixture of a highly inflammable brain, free iron, and free- radical inducing vaccines. This was “proven” as much as anything can be proven by the work of Kalokerinos in reducing an appalling infant death rate to nearly zero among the Australian aborigines by introducing a number of precautionary measures surrounding vaccines, including preventive administration of oral vitamin C and injections during crises.

Summary and Conclusions
Based on personal observation over a number of years, when an infant is taken to a hospital emergency room and found to have unexplained brain hemorrhages, retinal hemorrhages, and/or skeletal fractures, almost always there are charges of inflicted child abuse against parent or caretaker, usually in the form of Shaken Baby Syndrome. Once SBS has been diagnosed, there is seldom any serious pursuit in search of other possible causes of these findings.

Other possible causes include previously undetected brain hemorrhages with sudden and unexpected rebleeding, previously undetected hydrocephalus, and unrecognized scurvy with vascular fragility (I have yet to see a single case in which vitamin C level was tested in hospital emergency rooms). In instances of unexplained fractures of ribs or long bones, there is rarely any recognition that they may be due to “atrophy of disuse,” as commonly found in prematurity and other clinic settings, all of which are described in the medical literature.

Finally, as to the possible role of vaccines in these cases, the US Congressional hearings on vaccine safety (1999-2004) disclosed major deficiencies in scientific infrastructure of childhood vaccines in areas of safety testing. Because of these deficiencies we have no means of proving adverse effects of vaccines when they do take place. By the same token it is impossible to rule out that large-scale vaccine reactions are taking place unrecognized, and there is much circumstantial evidence that this is precisely what is happening. Among these may be vaccine reactions (mis)diagnosed as Shaken Baby Syndrome, especially those instances involving sudden and unexpected onset of apnea (respiratory collapse) of infants, a large majority of which in my opinion are from vaccine reactions rather than physically inflicted child abuse.

References

(1) Guthkelch AN, Infantile subdural haemtoma and its relationship to whiplash injuries, BMJ, 1971; 2(759):430-431.

(2) Caffey J, The parent-infant traumatic stress syndrome, Am J Roentgen, 1972; 114:217-228.

(3) Caffey J, On the theory and practice of shaking infants, Am J Dis Child, 1972; 24:161-169.

(4) Caffey J, The whiplash shaken infant syndrome: Manual shaking by the extremities with whiplash-induced intracranial and intraocular pleadings, link with residual permanent brain damage and mental retardation, Pediatrics, 1974; 54: 396-403.

(5) Duhaime A, Gennarelli, T, Thibault L et al, The shaken baby syndrome – a clinical, pathological, and biomechanical study, J Neurosurg, 1987; 86:409-415.

(6) Prange M, Coats B, Duhaime A, Margulies S, Anthropomorphic simulations of falls, shakes, and inflicted impacts in infants, J Neurosurg, 2003; 99:143-150.

(7) Uscinski R, the shaken baby syndrome, J Am Phys Surg, Fall, 2004; 9(3):76-77.

(8) Ommaya AK, whiplash injury and brain damage, JAMA, 1968; 204:75-79.

(9) Ommaya AK, Hirsch AE, Harris E et al, Scaling of experimental data on cerebral concussion in subhuman primates to concussive thresholds in man, In: Procedings of the 11th Stapp car crash conference of automotive engineers, New York, 1967.

(10) Ommaya AK, Goldsmith, thibault, Biomechanics and neuropathology of adult and pediatric head injury, Brit J Neurosurg, 2002; 16(3):220-242.

(11) Nelson Textbook of Pediatrics, 16th Edition, Behrman RE, Kliegman RM, Jenson HB, Editors, WB Saunders Co, 2000, Page 489.

(12) Ibid, Page 1169

(13) Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant, Fifth Edition, (2-volume set), AA Fanaroff, Mosby Books, WB Saunders, Philadelphia, 192, page 715.

(14) Tauscher MK, Berg D, Brockman M et al, Association of histologic chorioamnionitis, increased levels of cord blood cytokines, and intracerebral hemorrhage in preterm neonates, Biolog Neonate, 2003; 83:166-170.

(15) Barnes PD, Ethical issues in imaging nonaccidental injury: child abuse. Topics in Magnetic Resonance Imaging, 2002; 13(2):85-94. (Lippincott, Williams, & Wilkins Inc , Philadelphia).

(16) Miller ME, The lesson of temporary brittle bone disease: all bones are not created equal, Bone, 2003; 33:466-474.

(17) Miller ME, The bone disease of prematurity: a biomechanical perspective, Pediatr Res, 2003; 53:10-15.

(18) Beyers N, Alheit B, Taljaard JF et al, High turnover osteopenia in preterm infants, Bone, 1994; 15:5-13.

(19) Mora S, Weber G, Bellini A et al, Bone modeling alteration in premature infants, Arch Pediatr Adolesc Med, 1994; 148:1215-1217.

(20) Moyer-Mileur LJ, Brunstetter V, McNaught TP et al, Daily physical activity program increases bone mineralization and growth in preterm very low birth weight infants, Pediatrics, 2000; 106:1088-1092.

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