Vaccination Liberation - Information
Legal: Science: Misc: Searches:

Package Inserts
Ingredients of Vaccines
Artificially Sweetened Times
Books Videos Tapes
100+ Anti-Vax links
Breaking News
Smallpox Alert!

Shaken Baby/Impact Syndrome: Flawed Concepts and Misdiagnoses
Disclaimer: Dr. Buttram wanted this information to be shared widely. However, some formating on this web page does not reproduce the authors' original formating.

Topical Index

B E G I N    R E A D I N G Link to earlier version of this article, Dr. Buttram's Home page, and WhoIsDrButtram, on his site:

Shaken Baby/Impact Syndrome: Flawed Concepts and Misdiagnoses

(Based on a Review of Twenty-Eight Cases)


Harold E Buttram, M.D.

February 5, 2003

The following article represents a review of twenty-eight cases of shaken baby syndrome (SBS) accusations and/or convictions over a period of approximately three and a half years. Its primary purpose is to offer a composite of information gained from study of these cases to parents or caretakers who have been accused and/or convicted of child abuse in the form of SBS, information which may be of value in their defense. Although effort has been made to maintain simplicity and clarity in the organization of the material, there is unavoidably some technical complexity due to the nature of the material. Each section is designed to be complete in itself, and for this reason some portions may be repetitious.

Among the many adversities and difficulties facing the American family today, there is a relatively new and growing hazard in which a parent or caretaker may be falsely accused of murdering or injuring an infant by the shaken baby syndrome, when the true cause of death or injury arises from other sources. Very 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. I know of an attorney, an anesthesiologist, a Mormon mother, an Amish mother, and others accused and/or imprisoned (many believe falsely) on charges of injuring or murdering an infant by SBS. It could happen to anyone regardless of race, sex, educational, financial, or social status. It has happened and is happening to more than a few.

Medical-Legal Facets of Shaken Baby Syndrome:
By the inherent nature of SBS cases, where a caretaker or parent is alone with an infant at the time of collapse or accidental injury of the infant, it is rarely if ever possible to prove the innocence of parent or caretaker, there being no witnesses to corroborate the stories of the accused person in maintenance of his or her innocence. Defense of these cases, therefore, must be based on evidence showing a likelihood that death or injury of the infant arose from causes other than child abuse. This is done by a careful analysis of the clinical history and findings supported by scientific and medical literature, together with bringing to light the fallibility of current concepts surrounding SBS. It is also done by finding (as one often does) unreserved and vehement support of the innocence of the accused by family or friends.

One of the main reasons for my opinion as to the their innocence of many accused parents or caretakers is a rather strange pattern that often takes place in hospital emergency rooms, where once a suspicion of SBS or non-accidental injury arises, in many instances all thought of further diagnostic investigation ceases. I know of no other situation in medicine where the usual diagnostic thoroughness one finds in such centers is abandoned. For this and other reasons, I have not seen a single case where, in my opinion, the prosecution has met the standards of "proof beyond a reasonable doubt," standards which are supposed to apply in criminal cases.

Current Concepts and Assumptions in Diagnosis of SBS — Shaky Foundations:

SBS, sometimes classified as nonaccidental injury (NAI) commonly describes a combination of subdural hematoma (brain hemorrhage), retinal hemorrhage, and diffuse axonal injury (diffuse injury of nerve cells in brain and/or spinal cord) as the triad of diagnostic criteria. In some, the presence of rib or other fractures is also taken as sign of child abuse (1-4) These basic concepts, which originated approximately 30 years ago, remain a basis for most SBS accusations and convictions today in spite of newer scientific publications which promise to revolutionize these older concepts.

At the present time the following assumptions concerning SBS/NAI usually prevail in both hospitals and the courts:

  • - That the severity of shaking force required to produce injuries (retinal and subdural hemorrhages, etc) is such that it cannot occur in any normal activity but is of such violence that untrained observers would immediately recognize it as dangerous and intentional; (5)

  • - that such central nervous system (brain) injury on an accidental basis can only be associated with a massive force equivalent to a motor vehicle accident or a fall from a second story building;

  • - that such injury is immediately symptomatic and cannot be followed by a lucid interval, so that from this reasoning, the last caretaker with the injured child is automatically considered guilty of abusive injury, especially if the incident is unwitnessed; (1, 6-8)

  • - that changing symptoms in a child with prior head injury is due to newly inflicted injury and not just a rebleed; (9-13)

  • - that the presence of retinal/subdural hemorrhages in the absence of known disease or accident (as described) above are exclusively diagnostic of SBS.
In the case of retinal hemorrhages, as an example, the present conventional doctrine is that findings of both intraretinal hemorrhage (hemorrhage with the substance of the retina) and preretinal hemorrhage (on the surface of the retina) are exclusively diagnostic of shaken baby syndrome. (96-101) This is based largely on studies of Buys and Duhaime, (100, 101) which reported on a total of 148 children under three years of age, 28 with suspected child abuse, the remainder with accidental injury, who were specifically examined for retinal hemorrhage. As interpreted by a professor of ophthalmology, testifying as a prosecution witness in one of the cases I have reviewed, retinal hemorrhage was found in only one case among accidental injuries, a high speed car accident. In contrast, retinal hemorrhages were found in 12 of 28 cases of suspected child abuse.

The professor went on to say, "it has been assumed that the shaking has to be fairly vigorous" (to bring sufficient shearing forces to cause retinal hemorrhage). Parenthetically, the professor's use of the term, "it has been assumed," is interesting in that it infers that current concepts of SBS may be based more on assumption than on basic science. A recently published review of this controversy by Patrick D Barnes, MD (see next page) brings strong evidence that this is the case.

As will be reviewed in the remainder of this paper, the conventional view that diagnostic criteria for SBS are exclusively diagnostic, miss a key point: that the accidental cases reported by Buys and Duhaime were presumably among healthy children, whereas the large majority of infants and children suffering death or injury and subsequently diagnosed as SBS either came from problem pregnancies, or had been ill before death or injury, or perhaps most important of all, had recently had routine childhood immunizations from which they were suffering reactions. In other words they differed from the accident cases in being largely a sick population. Consequently these children could have had smoldering hemorrhagic vasculitis from vaccines, poor connective tissue formation with fragile blood vessels, or multiple nutrient deficiencies, one example being subclinical scurvy. I have yet to see a case in which these possibilities were taken into consideration.

In a comprehensive review of ethical issues in radiological diagnosis of child abuse, Patrick D Barnes, MD, with the radiology department of Stanford University Medical Center, Palo Alto, California, wrote the following concerning difficulties of diagnosing NAI/SBS in the absence of witnessed or admitted violent shaking:

"This problem is magnified further by the lack of consistent and reliable criteria for the diagnosis of NAI/SBS, and that the vast body of literature on child abuse is composed of anecdotal care series, case reports, reviews, opinion, and position papers... From an evidence-based medicine perspective, quality of evidence ratings for diagnostic criteria regarding the literature on SBS reveal that few published reports merit a rating above class IV (any design where the test is not applied in blinded evaluation, where evidence is provided by expert opinion alone, or in descriptive case series without controls). Such quality of evidence hardly earns a diagnostic criteria recommendation level of "optional," much less as a "guideline" or a "standard." (14)

Continuing next into the main body of discussion, the remainder of this article will review major problem areas showing that not only can there be other causes of the findings now thought to be exclusively diagnostic of SBS, but that these other causes may well comprise a majority of cases now being diagnosed as SBS. These categories include residual effects of birth trauma, vaccine reactions, respiratory paralysis from accidental (nonviolent) whiplash of the infant's neck, Barlow's Disease (rediscovered subclinical scurvy), and a variety of old and newly recognized metabolic disorders:

Residual Effects of Birth Trauma:

One of the cases that I recently reviewed typifies this type of problem in which a probable residual subdural or brain hemorrhage from birth trauma was later misdiagnosed as SBS or child abuse. The mother was known to have uterine fibroids from ultra sound exams taken during her pregnancy. Her labor started following spontaneous rupture of the membranes, but after several hours with limited progression, she was started on pitocin drip. In spite of hard labor which went on for several hours there was still little progression, and a Cesarian section was performed. Under these circumstances it can be assumed that the increased force of uterine contractions generated by the pitocin drip, together with outlet obstruction within the uterine cavity, would have generated much greater mechanical pressure on the fetal head than would have taken place during normal labor. This is indicated by a survey of retinal hemorrhages conducted at Tel Aviv University Center of 100 newborns following labor induced by intravenous pitocin or oral dinoprostone, following which retinal hemorrhages were found in 40% of the neonates in the dinoprosone group and 28% of the pitocin group. (16) Almost by definition this could have been considered a traumatic birth for the fetus with significant risk for brain hemorrhage,

As it turned out, it is highly probable that this is what did happen. The baby died two months later from a massive acute subdural hematoma, but at autopsy an older or chronic subdural hematoma was also found, in my opinion almost certainly the result of birth trauma. Instead of considering the possibility of a rebleed from a birth-related chronic subdural hematoma, the father, who was attending the baby at time of his collapse, was accused and convicted of child abuse and is now serving a prolonged prison sentence. (Refer to next page for additional information on chronic subdural hematomas as a risk factor for rebleeds).

As stated in Nelson Textbook of Pediatrics, 16th Edition:

"Traumatic epidural, subdural, or subarachnoid hemorrhage is especially likely when the fetal head is large in proportion to the size of the mother"s pelvic outlet; when for other reasons the labor is prolonged as in malposition....." (17)

In an article published in Archives of Neurology in 1994, Fenichel and colleagues identified 22 term newborns with intracranial hemorrhage by computerized tomography in an intensive care unit for newborns. Primary subarachnoid hemorrhage was the most common type of hemorrhage, caused either by traumatic deliver or severe hypoxic-ischemic encephalopathy...(18) In a three-year survey at the Southwestern medical Center, Dallas, Texas, 26 near-term and term nonasphyxiated infants were found to have small subdural hematomas on computed tomography. It was concluded that the presence of subdural hematoma is not necessarily always indicative of birth trauma and may occur as sequelae of an otherwise uncomplicated delivery. (19) In 1989 Demir reported on an atraumatic antepartum subdural hematoma causing fetal death. (105) In addition, prenatal ultrasound examinations have revealed the existence of unexplained subdural hemorrhages in utero. (106) Patrick D Barnes also commented that "birth trauma may persist beyond the neonatal period and mimic abuse." (14)

Acute Brain Hemorrhage (Rebleeding) from Pre-Existing Chronic Subdural Hematoma or Malformations such as Hydrocephalus:
In rebuttal to the current SBS doctrine that changing symptoms in a child with head injury is due to newly inflicted injury and not to a rebleed, as outlined on page 3, Joseph Piatt reported on a case of retinal hemorrhages and bilateral subdural hematomas in a child with external hydrocephalus following a minor fall. In discussion of the case he wrote:

"The presence of craniocerebral disproportion that develops from any cause — external hydrocephalus, internal hydrocephalus, arachnoid cyst, or chronic subdural hematoma " makes the patient exceptionally susceptible to subdural hemorrhage after what would otherwise be inconsequential trauma... as a result of the vulnerability of the bridging veins." (20)

Other authors have also reported on similar findings, including the proneness of a chronic hematoma to rebleed with minimal trauma. (21-23, 73) In an article by Hymel et al published in November, 2002, the authors reviewed the pathophysiology of subdural hematomas and the mechanisms by which chronic subdural hematomas may brebleed spontaneously or with minimal trauma. (112) In addition, in a table extending nearly four pages the authors provided a list of possible differential diagnoses for subdural hematomas. In my opinion, even this list was incomplete, as it did not include scurvy or childhood vaccines.

Once established, chronic subdural hematomas may take on lives of their own. 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 in turn tends to thin the clot converting it into a consistency similar to "crankcase oil." Also, after a period of two weeks or so, a thin healing membrane begins to form around the clot. However, because of the fragility of this membrane, it is very prone to have off and on capillary oozing of blood into the clot area. Because of these and other variables, subdural clots may sometimes resolve spontaneously, they may continue active but stable for months, or even in one documented case for years, or they may slowly grow and potentially end in catastrophe. (112) The bridging veins, which are located in the subdural space, may play a key role in this, as experiments have shown that they tend to rupture when stretched more than 40%. In such instances acute, massive rebleeds may take place with minimal or no trauma. (113)

The propensity of chronic subdural hematomas/hygromas for secondary rebleeding is further supported by study by Kawakami et al in which 19 patients with chronic subdural hematomas had venous blood taken at the time of surgical aspiration from the chronic subdural hematomas. Both the venous blood and surgical aspirate were then tested and compared for various coagulation factors with the following results:

"Compared with coagulation results for venous blood the hematoma contents demonstrated marked prolongation of the recalcification time, prothrombin time, and activated partial thromboplastin time, and marked reduction of clotting factor V, the hepaplastin test, prothrombin, and fibrinogen" These finding indicate excessive activation of the clotting system, thrombin generation, and increased fibrinolytic activity occurring in the hematomas... fibrin and fibrinogen degradation products were increased in the hematomas... From these results, excessive activation of both the clotting and fibrinolytic systems is emphasized to be the possible etiological factor for the origin and development of chronic subdural hematoma. (114) (And for the proneness for rebleeding). (Editorial comment).

The Controversy of the Lucid Interval:
In rebuttal to another of the standard SBS doctrines, that an ultimately fatal head injury cannot be followed by a lucid interval (an interval between trauma and onset of symptoms), a retrospective study of 76 children who died from head injuries was done by M.G.F. Gilliland. The children were divided into those who died from shaking, those who died from impact, and those who died from combined of the two. It was found that 20 % of the shaken children and 25% of the impact children had lucid intervals over 24 hours. In the latter groups there were four children for whom the interval was over 72 hours. (56) Similarly in a retrospective report by J Plunkett of 18 fall-related head injury fatalities from distances of 2 to 10 feet, 12 of the 18 children had a lucid interval.(57)

The Vaccine Issue:
Since 1999 there have been ongoing hearings in the U.S. Congress concerning growing concerns about vaccine safety. Primarily these hearings have dealt with concerns about a possible link between the MMR vaccine and the growing epidemic of childhood autism in the U.S.A. Out of these hearings there is now an emerging background pattern of deficiencies in basic science in vaccine testing. As a result of these deficiencies, large numbers of unrecognized vaccine reactions may be taking place, especially reactions of a delayed nature.

Based on these hearings, as a general statement scientific evidence does not support the safety of immunizations in that safety studies on vaccinations are limited to short periods only: several days to several weeks. 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 immune parameters and brain function of babies, studies which should be considered indispensable information of a basic science for the vaccines. Inadequate consideration has been given to the additive or synergistic adverse effects of multiple simultaneous vaccines, although in cases of toxic chemicals, two chemicals together may be 10 times more toxic than either separately, or 3 chemicals 100 times more toxic. (24-25)

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 of the safety of the hepatitis B vaccine. When the committee, which carried the responsibility for determining the safety of vaccines by Congressional Mandate, investigated five possible and plausible adverse effects, they were unable to come to conclusion for four of them, because they found that relevant safety research had not been done. Furthermore, they found that serious "gaps and limitations" exist in both the knowledge and infrastructure needed to study vaccine adverse events. Among the 76 types of vaccine adverse events reviewed by the 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." (26)

Several examples of before-and-after studies from older medical literature will be cited as examples of these deficiencies.

Vaccines and Immune Paralysis:

The first example involves a study reported in 1984 in the New England Journal of Medicine (27) which involved the testing of T-lymphocyte subpopulations (white blood cells which help govern the immune system) in 11 healthy adults 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 immune systems. And yet, as far as I am aware, this test has never been repeated.

Comment: In my mind, until this study is repeated and disproved, it would be both folly and insupportable to claim that vaccines are not having an effect in contributing to the increasing patterns of sickness now seen as a matter of common observation in today's children. In point of fact, reports are now appearing from widely separated geographic areas in which vaccinated children were found to have more allergic disorders (and patterns of sickness) than children with limited or no vaccines. (28-31) (Also see Appendix entitled, "Vaccines and Allergy Citations")

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. (32) In two of the children he found that the EEGs turned 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."

Careful search of the literature has disclosed only one similar before-and-after immunization study, one from Japan in which it was found that 61 children with epilepsy or a history of febrile seizures showed significant increases in "epileptic spikes" on EEGs following DTP, DT, or BCG vaccines. (33)

Comment: Both of these studies, the only studies of their kind as far as I am aware, show strong evidence that subclinical brain damage may be taking place on a far larger scale than has been officially recognized.

The Controversy of the Latent Period:

Several leading authorities who formerly held positions in the regulation and licensing of medicines in the United Kingdom have published statements that pre-licensing observation periods for vaccines (in this instance referring to the MMR vaccine) have been too short to include the onset of delayed neurological (emphasis mine) or other adverse events, (34) one of the former health officers stating that pre-licensing observation periods should have been extended to a year rather than several weeks, as was the case with the MMR vaccine.

In my opinion the fundamental flaw in current medical legal standards in the U.S.A. for the latent period, and probably also in other English-speaking countries, is that their time limitations allow only for immediate or anaphylactic-type of reactions, by inference denying the possibility or even the existence of delayed-type reactions. This is clearly unrealistic, as delayed-type hypersensitivity directed against the nervous system has been demonstrated by BCG vaccine in the laboratory. (35)

In this regard, two of the vaccines routinely given to children, the Pertussis and Haemophilus influenza vaccines, are known to be potent in causing hypersensitivity reactions. (36,37)

Vaccine Reactions Mimicking the Diagnostic Criteria of Shaken Baby Syndrome:

As previously reviewed, (1-4) shaken baby syndrome commonly describes a combination of subdural hematoma (brain hemorrhages), retinal hemorrhages, and diffuse axonal injury (diffuse injury of nerve cells in brain and spinal cord) as a sign of child abuse. In the absence of known accidental or disease causes, these findings in a child are considered as diagnostic of non-accidental injury or SBS. The following information, however, will show that there may be other causes, among which may be unrecognized vaccine reactions.

In medical research it is standard procedure to develop an animal model of a disease for experimentation before proceeding into human studies. In the case of shaken baby syndrome, these animal models already exist in publications involving pertussis toxin reactions mimicking the diagnostic criteria of SBS.

Studies by Iwasa stressed the finding of brain edema as a feature of pertussis-induced encephalopathy. (38) It is also of interest to point out that there are anecdotal human reports of infants which developed increased intracranial pressure with bulging fontanelles following DTP immunization which tend to support these animal findings. (39-41) In addition, in 1972 Galazka reviewed a series of autopsies on children whose deaths followed the pertussis vaccine. Although autopsies were limited in number, findings included brain edema, hyperemia, and soft meninges. (42) As will be reviewed in the next section, studies of J Geddes have shown that brain edema in and of itself may result in retinal and brain hemorrhages.

Munoz in turn conducted mice studies with pertussigen, an endotoxin derivative of the pertussis bacteria, in which he found (inflammatory) infiltrates of lymphocytes surrounding blood vessels in the brain and spinal cord, findings compatible with an autoimmune encephalitis. (43)

It is noteworthy that vaccines such as pertussis have been used to induce allergic encephalomyelitis in laboratory animals since 1973, (44) characterized by brain swelling and hemorrhages similar to those caused by mechanical injuries. As another example, in 1982 Steinman and coworkers described mice studies following pertussis immunization as follows:

"Post-mortem examination of the brain (in experimental mice) after immunization revealed diffuse vascular congestion and parenchymal haemorrhage in both the cortex and white matter. Cortical neurons showed ischaemic changes. Occasional areas of hypercellularity were evident in the meninges"B pertussis has a wide range of physiological effects including increased IgE production, increased sensitivity to anaphylactic shock, lymphocytosis, and hyperinsulinaemia. Its ability to induce increased vascular permeability may account for the tendency to produce haemorrhage. (45)

In terms of human studies, I have available a list of 109 references involving reports of adverse reactions from hepatitis B vaccine, a vaccine which appears to be especially prone to be followed by hemorrhagic complications. Among these reactions various forms of vasculitis (inflammation of blood vessels) appear with special frequency, which may contribute to hemorrhagic complications because of greater fragility and friability of blood vessels and consequently may mimic both cutaneous and cerebral hemorrhagic findings now considered to be diagnostic of SBS. In addition, Burton Waisbren has reported on 3 cases of severe meningoencephalitis following hepatitis B vaccine, as well as 58 cases of acquired autoimmunity following this vaccine. (87)

In regard to the issue of retinal hemorrhages, in the text Ocular Differential Diagnosis by Frederick Hampton Roy, M.D., papilledema (swelling in the retinal area) and increased intracranial pressure (from any cause) are listed as possible causes of retinal hemorrhages. (46) DPT vaccine is also listed as a possible cause, along with other routine childhood immunizations (OPV, MMR).

Comment: As stated previously, animal models for vaccine reactions mimicking the diagnostic features of SBS exist for each of the major criteria of SBS. In my opinion, it is only from the lack of basic science in the vaccine field that these reactions very frequently are not being recognized for their true nature and therefore misdiagnosed as SBS.

New Findings that May Change the Diagnostic Criteria of SBS:
As reported in the medical journal, Brain, in a study which may 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. (47) Of the 53 children, 37 were less than a year old.

In the past, brain damage in such circumstances has been blamed on the brain banging against the skull as a baby is violently shaken or struck. It has been thought that this direct assault causes a characteristic kind of damage to the axons of the nerves known as diffuse axonal injury (DAI). However, the researchers found evidence of DAI in only two of the 37 babies. Instead they found that three-quarters of the 37 babies had 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 cord. When babies stop breathing as a result of this injury, subsequent lack of oxygen causes the brain to swell dramatically, which in turn causes hemorrhagic complications and brain damage formerly attributed to violent shaking or blows.

The cranio-cervical junction is uniquely vulnerable in very young babies, the authors explained, because their neck muscles are weak and their heads relatively large and heavy.

The researchers found subdural hemorrhages in 72% of the 53 cases, although most were too superficial to cause death. Also, retinal hemorrhages were found in 71% of the 38 cases in which the eyes were examined, but the authors felt that these resulted from a lack of oxygen to the brain (and the brain edema or swelling) rather than trauma.

There are scenarios in which such nonviolent, unintentional injuries might take place, as in an accidental fall of a parent or caretaker while holding an infant, the infant in turn receiving a whiplash of the neck and secondary injury to the respiratory center at the base of the brain, or a parent awakening in the night to sooth a crying infant, and the parent still not being fully awake, rocking the baby without adequate head support.

Although vaccines were not mentioned in the Geddes study, it would be very interesting to know how many of these adverse events occurred in a time-related fashion following vaccines.

The Issue of Retinal Hemorrhages:
Based on my own review of medical records involving SBS accusations and convictions, ophthalmologists are always called to examine infants for retinal hemorrhages following hospitalization where there is suspected non-accidental trauma or SBS. Without exception in each of the cases I have seen, the finding of retinal hemorrhage has been considered diagnostic of non-accidental trauma from violent shaking or impact, the basis of which has been previously reviewed. (96-101)However, it would appear from the medical literature that others disagree as to the diagnostic specificity of retinal findings. John Plunkett in the American Journal of Forensic Medicine and Pathology made the following statements concerning this issue:

"I do not understand the "retinal hemorrhage" litmus test for shaken infant. No one knows what causes retinal hemorrhage, although it is highly correlated with rotational deceleration injury/subdural hemorrhage in children, but retinal hemorrhage indistinguishable from that found in rotational deceleration may be found in association with ruptured vascular malformations , arachnoid cysts, and CNS (central nervous system) infections. (48)

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 retinal vein occlusion, high altitude retinopathy, and subarachnoid hemorrhage secondary to ruptured intracranial aneurysms." (49) Also there is a report of retinal hemorrhages after near drowning (50) and three reports following CPR resuscitation. (51-53) Retinal hemorrhage may be caused by ligating the central retinal vein or its tributaries, or by suddenly increasing intracranial venous pressure. (88,89) In reality, any sudden increase in intracranial pressure may cause a retinal hemorrhage. (90,91) Furthermore, retinal and optic nerve sheath hemorrhages associated with a ruptured vascular malformation are due to an increase in venous pressure, not extension of blood along extravascular spaces. (88,89,92,93) Patrick Barnes reported that retinal hemorrhages may be seen with a variety of conditions including accidental trauma, resuscitation, increased intracranial pressure, increased venous pressure, subarachnoid hemorrhage, sepsis, coagulopathy, certain metabolic disorders, and systemic hypertension. (14)

Vaccines, Disseminated Intravascular Coagulation, and Brain Hemorrhages

In an unpublished series of cases involving accusations or convictions of inflicted trauma in the form of "shaken/impact baby syndrome," largely collected by attorney and jury counselor Toni Blake of San Diego, California (personal communication, 2000), the cases had the following features in common: 1) All occurred in fragile infants born from complicated pregnancies; problems included prematurity, low birth weights, drug/alcohol problems, maternal toxemia, diabetic mothers, or other maternal complications; 2) all infants were 6 months age or less; 3) onset of signs and symptoms occurred at about 2, 4, or 6 months of age, within 12 days of vaccines; 4) all infants had subdural hematomas; 5) some infants had multiple fractures. In the year 2000 the series included 25 cases, but I understand that it is now much larger.

Common experience has shown an unmistakable time-related onset of many types of health complications in infants following immunizations. Brain hemorrhages are among these complications, as demonstrated by the above-series. As already stated, animal models for vaccine reactions exist for each of the diagnostic criteria now considered exclusively diagnostic of SBS. The large area still remaining virtually untouched and unknown in the safety testing and basic science of vaccines is two-fold: 1) lack of long-term surveillance following vaccines and 2) systematic before-and-after human tests on the effects of childhood vaccines on the neurologic, immunologic, hematologic, and other systems of the body. Because of these lacks it is predictable that unknown numbers of vaccine reactions are taking place, unrecognized as to their true nature, as previously reviewed.

In the case of brain hemorrhages, we know that they happen following vaccines because we see them, but we do not know the mechanism. Not knowing the mechanism, we are unable to prove a causal relationship between vaccines and brain hemorrhages so that, in my opinion, many parents and caretakers are being falsely accused and/or convicted of violent child abuse. This is the heart of the problem. We have no positive means of diagnosing vaccine reactions other than observation, which is usually discounted in the courts and dismissed as coincidental.

Turning now to the subject of disseminated intravascular coagulation (DIC) as a plausible common denominator for brain hemorrhages following vaccines, in Williams Hematology, Sixth Edition,(115) DIC is described as a condition brought about by the introduction of procoagulants (clotting factors) into the blood circulation which overcome the normal anticoagulant (teflon-like) endothelial lining of blood vessels and cause widespread thrombin (clotting-factor) generation with microthrombi (clots) involving multiple organ systems. Bleeding manifestations are caused by consumption of platelets, fibrinogen, coagulation factors V and VIII, as well as secondary fibrinolysis. Major clinical causes of DIC include two major categories. The first takes place when blood is exposed to "tissue factor," a clot-inducing substance present in the cell membranes of most body tissues, as may occur with trauma, burns, malignant metastasis, or amniotic fluid embolism. The second category, more germane to our purposes here, can result from systemic viral, fungal, bacterial infections, or bacterial toxins in which the invading organisms (or toxins) activate tissue factors from monocytes and endothelial cells, which may then activate a pro-coagulant cascade.

The Williams text did cite experiments in which tissue factor was activated in primates (monkeys) by injection of live E coli bacteria, and in humans by injection of low-dose bacterial endotoxin. Hemorrhagic encephalopathy (hemorrhagic brain inflammation) with DIC has also been described clinically in 6 patients suffering from Gram-negative septicemia. (116) If the cascade of DIC can be initiated by a common bacterial endotoxin, why not expect the same result from injections of potentially virulent diphtheria and pertussis endotoxins? Unfortunately for a generation of children and for many parents now embattled with accusations of violent child abuse, this is where human research and surveillance has stopped. We know little or nothing about the potential activity of endotoxin-bearing vaccines or viral vaccines in bringing about harmful procoagulant reactions and hemorrhagic complications simply because this area has been largely neglected (some believe purposely avoided) in research circles. If this cannot be proven at this time due to deficiencies in research, by the same taken it cannot be disproved. Proof of safety of vaccines should rest on the prosecutors in cases in cases such as these and not on the parent, as often occurs in our courts; on the contrary, should not the burden of proof should rest on prosecutors to provide scientific reasons why vaccine-related coagulopathy and DIC should be not be considered as a valid possibility in the differential diagnosis of brain hemorrhages?

As a practical note relating to initial screening tests in cases of suspected child abuse, it is of utmost importance to perform most or all of the standard coagulation tests including prothrombin time (PT), activated partial prothrombin time (apt), fibrinogen, d-dimer, fibrinogen degradation products, and the examination of a red blood film to check for fragmented red cells. The purpose is to differentiate between acute and chronic DIC. ACUTE DIC: low PT, low aPTT, and low or falling platelets. The fibrinogen may be normal but falls with time. D-dimer levels and fibrinogen degradation products may be elevated. CHRONIC DIC: Pt AND APTT may be normal, while fibrinogen degradation products, and d-dimer are usually elevated. Fragmented red blood cells are commonly but not universally present. (115)

Comment: The differentiation between acute and chronic DIC is of utmost importance in the courts, as it places the initial events causing brain hemorrhage in entirely different time frameworks. Acute DIC of course reflects a recent event, on which basis most shaken/impact baby accusations are made, but chronic DIC would tend to implicate other causes of earlier origin.

In an unpublished paper by Frank Hartman entitled, "Vaccination Toxicity, Infection and Science," which will be submitted with this report, Hartman proposed a very plausible theory implicating aluminum toxicity as one of the prime agents in vaccines leading to intravascular coagulation. There are over 7000 references to the toxicity of aluminum, he noted. In regards to its procoagulant effects, he quoted a simple experiment of making a mixture of flour and water (in which the flour readily goes into solution). When one drop of an antiperspirant (contains aluminum) is added, the flour immediately clumps and settles to the bottom. Touching on areas of physics, Hartman went on to explain:

"All trace minerals, metals, inorganic materials, proteins and amino acids are held in suspension in liquids as microscopic and > sub microscopic particles like dust particles in the air. The very small particles are called colloids... Colloids are held in suspension via a very slight electro-negative charge on the surface of each particle. This charge is called a zeta > Potential. The ability of a liquid to carry material in suspension is a function of these minute electrical charges. As the electro-negative > charge increases, more material can be carried in suspension. As the charge decreases, the particles move closer to each other and the liquid is unable to carry the same amount of materials. Calcium and heavy metals drop out first adhering to the vessel wall or organ surface.

"The quantity of positive and negative charges from chemical elements in suspension as colloids has a major effect on carrying capacity. Electropositive ions decrease carrying capacity while electronegative ions increase it. Elements with only one excess positive or one excess negative ion have little effect on suspensions. Elements with two positive or two negative ions (divalent) such as magnesium and beryllium (+2) and selenium (-2) have 3,000 times more effect on coagulation or dispersion than elements with single ions. Elements with a valence of 3, such as aluminum (+3) and nitrogen and phosphorus (-3) have 6,000 times more effect on carrying capability due to the three extra positive charges. Vaccines contain aluminum salts which greatly exacerbate coagulation."

Older medical literature does include vaccines as a potential cause of "Haemorrhagic and perivenous encephalitis." (117) Louis Reik Jr (1980) outlined a hypothetical mechanism for post-vaccine brain hemorrhages in the following statements:

"Common to all the postinfectious and postvaccinal complications affecting the nervous system is the initial introduction of a foreign antigen, through either invasion or inoculation, followed by a variable free of nervous system symptoms and then clinical nervous system involvement. During this asymptomatic period, antibodies could form and combine with the foreign antigen to form circulating immune complexes. If such complexes are of appropriate size and contain the correct proportion of antigen to antibody, they can cause systemic liberation of vasoactive substances. An increase in vascular permeability results, complexes are trapped in vessel walls in a focal fashion, complement is activated, and inflammatory cells accumulate and release proteolytic enzymes, causing tissue injury. (118)

As a further observation on this subject, in an article entitled "Activation of the Coagulation System in the Gulf War Illness: a Potential Pathophysiologic Link with Chronic Fatigue Syndrome; a laboratory approach to diagnosis," by KL Hannon et al (2000), the authors reported on a controlled study of 33 veterans with the Gulf War Illness which confirmed hypercoagulability states in the veterans as compared with controls. (119) In discussing these findings the authors pointed out that there appears to be significant overlap in the symptoms of Gulf War Illness, chronic fatigue, and fibromyalgia, each having in common an activation of the clotting cascade with fibrin deposition in the circulatory system and reduced flow of oxygen and nutrients to the nerves and muscles of the body. The authors listed live virus vaccines such as smallpox or polio, vaccine adjuvants (additives), vaccine toxins and contaminants among various possible causes of the syndrome. Current laboratory tests available for hypercoagulatility ``include fibrinogen, fibrin monomer, prothrombin fragment, and thrombin-antithrombin complex.

Comment: The only missing link in this chain of evidence that vaccines may be causing brain edema, retinal hemorrhages, and brain hemorrhages in large numbers of children now being misdiagnosed as shaken baby syndrome is the final mechanism provoking brain hemorrhages. As a scientist Reik stopped short of stating this, this being an area with very limited research. However, it is easily imagined how hemorrhagic complications may follow the vascular injuries from immune-complexes with increased local release of vasoactive substances and proteolytic enzymes, these in turn acting destructively on the blood vessels of the brain.

Diffuse Axonal Injury (DAI), the Third Diagnostic Criteria for SBS:

There is no doubt that diffuse axonal (nerve injury) may take place in head trauma. The question is whether or not the pathologic findings with widespread B-amyloid precursor protein deposits and axonal spheroids, are specific for non-accidental injury or whether these findings are also present in other, non-head injured conditions, including vaccine injury.

Based on the work of F.E. Sherriff and associates, this question can be answered, (54) as described in the following:

"Severe non-missile head injury commonly results in a form of brain damage known as diffuse axonal injury (DAI). The histological diagnosis of DAI is made by silver staining for the presence of axonal retraction balls... We have used immunocytochemistry for the B-amyloid precursor protein (BAPP) as a marker for axonal injury in formalin-fixed, paraffin-imbedded sections of human brain. Axonal BAPP was present in all (23 cases of head injury) that survived for 3 hours or more... BAPP immunoreactivity was also found in some (5 of 13) non-head injury cases and so cannot to considered to be a specific marker for trauma." (Emphasis mine)

In a survey conducted at the department of forensic medicine, University of Sheffield, UK, GN Rutty and associates studied sections from a series of brains comprised of four groups: those showing evidence of hypoxia with no history of head trauma, those with head trauma but no evidence of hypoxic change, those with history of head trauma and hypoxic change, and four controls originally described as "diffuse axonal injury." Using the same staining technique as described above in the Sherriff study, it was found that axonal bulbs may occur from hypoxia in the absence of head injury. It was concluded that "the presence of axon bulbs cannot necessarily be attributed to shearing forces alone." (55)

Barlow's Disease (Subclinical Scurvy) Rediscovered:

Physicians and the lay-public alike generally think of scurvy as an historical disease of the days of wooden sailing ships, which was eliminated by the introduction of limes or other citrus fruit into the diet. However, as the younger generations in industrialized nations turn increasingly to commercially processed "fast foods" as a major part of their diets, subtle forms of scurvy may be returning and contributing to the hemorrhagic complications now thought to be exclusively diagnostic of SBS.

In contrast to classical scurvy of earlier times which was characterized by a total lack of vitamin C in the diet, "subclinical scurvy" describes a condition with marginal dietary deficiencies of vitamin C (apparently very common today) where an additional stress, such as a viral infection, further drains away the already lowered levels of vitamin C, thus predisposing to serious or catastrophic consequences should additional stresses be placed on the body. The credit for clinical recognition of sublinical scurvy probably should be attributed to Dr. Archivedes Kalokerinos of Australia.

In the early 1970s Dr. Kalokerinos, then stationed as a medical officer among the Australian aborigines, was troubled by a very high child mortality rate, in some areas approaching 50%. Having observed signs of scurvy in some of the children, and noticing that they 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, oral vitamin C supplements, avoidance of vaccines during minor illnesses, and injectable vitamin C during crises, infant mortality was virtually abolished. (58) As a result of this work he was awarded the Australian Medal of Merit in 1978.

One of the primary roles of vitamin C in the body being that of producing and maintaining connective tissue, Dr. Kalokerinos hypothesized that with minor viral infections further depleting an already marginal store of vitamin C, the administration of toxin-bearing vaccines would sweep away the small residual traces of vitamin C, somewhat like a flash-fire, provoking fulminating scurvy with hemorrhagic complications from the weakening of blood vessels. Does such a theory have a foundation in the scientific literature? Based on the following, I believe that it does.

Basic Facts about Vitamin C:

  • - Vitamin C deficiency still does occur in the Western World. The plasma vitamin C status was found to be depleted, between 0.2 and 0.5 mg/100 ml (or 11 to 28 micromol/L) in 30 %, and to be deficient, below 0.2 mg/100 ml in 6% of people attending a Health Maintenance Organization (HMO clinic) in Tempe, Arizona in 1998. (59)

  • - The blood leukocyte ascorbic acid concentration is further reduced by infection. Even the common cold causes a fifty per cent reduction of the leukocyte ascorbic acid concentration within 24 hours. (60) Moreover, E coli endotoxin has been shown to inhibit the uptake of vitamin C by mouse fibroblasts in tissue culture. (61)

  • - When the human plasma ascorbic acid level falls below 0.2 mg/100 ml, the whole blood histamine level is doubled or quadrupled. (62) Ascorbic acid is needed for the conversion of histamine to hydantoin-5-acetic acid and on to aspartic acid in vivo. (63)

  • - The whole blood histamine level is also increased by vaccines or toxoids, by stresses such as heat or cold, and by various drugs in guinea pigs. (63) Sleep-lack more than doubles the blood histamine levels of resident physicians. (64) Ascorbic acid supplementation rapidly reduces the blood histamine levels of ascorbate-depleted subjects. (62)

  • - Blood histamine concentration begins to rise when the plasma ascorbic acid level falls below the normal level of 1 mg/100 ml and rises exponentially when it falls below 0.7 mg/100 ml. (62)

  • - Vitamin C impairs the hydroxylation of proline and lysine, which are essential building blocks for the synthesis of collagen, which forms the foundation for fibrous tissue, cartilage, bone and teeth. (65)

  • - It is the increased blood histamine, or histaminemia, that causes separation of the endothelial cells from one another in scurvy, (66) which causes the capillary fragility and bleeding of scurvy.

  • - Humans are vulnerable to vitamin C deficiency as we lack the enzyme, L-gulono-gamma-lactone oxidase, needed to synthesize this essential substance, making us totally dependent on dietary vitamin C from our diet. This is in contrast to most other mammals which are able to manufacture their own vitamin C from simple sugars in the liver.

  • - Vitamin C protects against diphtheria toxin, (67-68), tetanus toxin, (69) and typhoid endotoxin. (70)

  • - A 1932 report on the hemorrhagic complications of scurvy stated that these occurred most commonly beneath the periosteum of the long bones and into joint spaces, but frequently also involved the skin, mucous membranes (gums), orbits (eyes), and serous cavities of the body. (71) One of the most characteristic signs of adult scurvy was swollen bleeding gums, but this is never seen in edentulous infants. It is the bacteria in the crevice between the tooth and the gum that cause local infection and bleeding gums.

  • - Lund and Kimble of Madison, Wisconsin in 1943 reported that "Hyperemesis Gravidarum may lead to dangerously low levels of vitamin C. Clinical scurvy may appear. The retinal hemorrhages of severe hyperemesis gravidarum are a manifestation of vitamin C deficiency and are similar to petechial hemorrhages seen elsewhere. The hemorrhages cease after adequate therapy with vitamin C; henceforth they are not necessarily an indication for the use of therapeutic abortion. (107)

  • - Sanford et al (1942) drew attention to the low blood vitamin C values obtained in 6 neonatal infants with cerebral hemorrhage (0.03 to 0.25 mg/100 ml) and emphasized the need for vitamin C. (122) {Comment: Histamine is removed by vitamin C-activated conversion to hydantoin-5-acetic acid and on to aspartic acid in the body. When the rate of accumulation of histamine in the blood exceeds the rate of its removal by vitamin C, the blood histamine level rises, causing capillary and venular fragility, leading to bleeding. The blood escaping from the blood vessels slowly undergoes hemolysis, and this causes further vitamin C depletion.}

With the foregoing information as a background, it may now be timely to cite a personal communication (2000) with Toni Blake, Attorney and Jury Counselor of San Diego, who told of a series of 25 cases in which a parent had been accused of shaken baby syndrome in which the babies had the following features in common:
1) All came from problem pregnancies including prematurity, low birth weight, maternal drug/alcohol problems, maternal toxemia of pregnancy, or other prenatal risk factors;
2) All were 6 months or less of age;
3)All had subdural hemorrhages;
4) complications interpreted as shaken baby syndrome occurred at 2, 4, or 6 months of age, within 11 or 12 days of vaccines.
5) Many also had fractures. A recent communication from Attorney Blake informed me that this series is now much larger.

It is probably in situations of fragile infants, as described above, that one finds a final common pathway for most major risk factors for vaccine reactions with
1) sub-optimal nutrition, including marginal vitamin C deficiency;
2) immature liver and kidneys, where most body detoxification takes place;
3) ongoing minor viral infections, which further deplete vitamin C levels (pediatricians commonly ignore the presence of viral infections in administrations of vaccines);
4) formula feeding rather than breast feeding (breast milk has four times the level of vitamin C as the mother's blood level of vitamin C). In such situations, the toxins from diphtheria, tetanus, and pertusis vaccines may overwhelm the liver's marginal detoxification system, sweep away the small vitamin C reserve, and potentially lead to catastrophic vaccine reactions. In my view this is probably a common scenario in which parents are being blamed and accused of death or injury from SBS, when the true causes arose from vaccine reactions. This series of reactions, in which disseminated intravascular coagulapthy (DIC) may also be involved, might be thought of as a variant of classical scurvy, or Barlow's Disease.

Acute Autoimmune Hemolytic Anemia from DTP Vaccine:
In 2001 KA Downes and colleagues reported on a 4-month old child admitted to the hospital with fever and increasing lethargy a few days following the second series of routine immunizations, which included the DTP vaccine. By the third hospital day the hemoglobin had dropped to 2.3 grams%. The child subsequently died, but careful evaluation before death identified an acute autoimmune hemolytic anemia from the DTP vaccine. (74) In a review of the literature the authors found 7 other reports of autoimmune hemolytic anemia following DTP vaccines. (If this reaction were routinely sought in hospitals, as it was in this case report, probably the numbers would be much greater).

In my own case reviews there were several admitted to hospitals with hemoglobin levels in the 6s and 7s. One child was admitted with a hematocrit of 6% and a hemoglobin of 2 grams %, dying within hours of admission. In none of these cases was there mention or investigation in the medical records of a possible hemolytic process, at least none that I could find.

Bleeding Diatheses from Coagulopathy
In his medical review of the death of Baby Alan Yurko, Dr. Michael D Innis, MBBS, DTM&H, FRCPath, Honorary Consultant Haematologist, Princess Alexandra Hospital, Brisbane, Australia, diagnosed death from intracranial hemorrhage and a bleeding diathesis following a coagulopathy resulting from failure of the liver to synthesize clotting factors in adequate amounts.

Liver failure was diagnosed by significant elevations of liver enzymes and significant lowering of serum albumen, cholesterol, and creatinine, from which it was concluded that there was inadequate liver production of coagulation factors II, VII, IX, and X. (74)

The presence of a coagulopathy, in turn was reflected by an elevated prothrombin time, high D Dimer test, and high fibrin spit products. (Fibrinogen not done) Marked platelet elevation ruled out disseminated intravascular coagulopathy. (75)

In my opinion, bleeding studies of the types described above should be done in all infants or children with retinal/brain hemorrhages before entertaining a diagnosis of SBS. According to Dr. Innis's report, coagulopathies can result in subdural bleeding, intracerebral bleeding, retinal hemorrhages, bleeding into the spinal cord and into the skin in the form of bruising. (76)

Skeletal Fractures:

In cases of suspected child abuse where skull, rib, or long bone fractures are found in addition to brain and retinal hemorrhages, medical-legal difficulties are greatly increased for the accused parent or caretaker and defenders. It is therefore important to point out a variety of known conditions in which fractures can take place spontaneously or with minimal trauma. When fractures are found from any of these conditions in infants, birth trauma should be considered as a possible source.

Skull fractures:

In a postmortem study of infant skulls reported by S Margulies and K Thibault with ages ranging up to 6 months at time of death, skull thicknesses were reported as 3 to 5 mm, (94) so that from this it can be assumed that a normal skull thickness for a 7-month-old child would have been greater than 5 mm. On this basis we have a standard for measurement of excessive thinness of the skull, which can carry increased risk of fracture with minimal trauma, as indicated by the following study from Germany:

  • - In the German scientific journal Z Rechtsmed, 1990: 103(4):311-313, W Weber performed postmortem biomechanical fragility tests on infant skulls. As reported in the article abstract, "skulls were dropped from 82-centimeter heights onto (A) stone, (B) carpet, and (c) foam-backed linoleum. 35 further falling tests were carried out onto softly cushioned ground. In 10 cases (D) a 2-cm thick foam rubber mat was chosen and in 25 further cases (E) a double-folded (8-cm-thick) camel hairblanket. Hence the results of altogether 50 tests could be evaluated. In test groups A-C on a relatively hard surface, skull fractures of the parietals were observed in every case; in test group D this fracture was seen in one case and in test group E in four cases. Measurements along the fracture fissures showed bone thickness of 0.1-0.4 mm. The fracture injuries originated in paper-thin single-layerbone areas without diploe, which can also be considered the preferred regions for skull fractures of older infants following falls from low heights. These results indicate that it is no longer possible to assume that the skull of infants is not damaged after falls from table height."

  • - As noted above on page 2, common doctrine on which shaken/impact baby syndrome charges are based holds that injuries, such as skull fractures, can only be caused by forces equivalent to a fall from a second story building. However, it would appear that this doctrine is based more on supposition than fact, as indicated by the following representative articles: In a report entitled, "Fatal Head Injuries from Short Distance Falls," J Plunkett reported on 18 fall-related fatalities taken from the U.S Consumer Product Safety Commission database for head injury associated with playground equipment. The youngest child was 12-months old, the oldest 13 years. The falls were from 2 to 10 feet. (78) In an article entitled "The Mortality of Childhood Falls," JR Hall et all reported on a survey of pediatric deaths due to falls of the Cook County Medical Examiner's office (Chicago) from January, 1983 through December, 1986, in which it was found that falls were the third leading cause of death in children less than 4 years of age (mean age 2.3 years); and among these falls forty-one percent of deaths occurred from minor falls such as falls from furniture or while playing. (120) Also there is the report of a freak accident in which an eight-month old boy received a parietal skull fracture when his sister dropped or tossed a toy airplane (480 gms) which landed on the boy's head. (121)

  • - Metabolic conditions subject to spontaneous fractures, or to fractures with minimal trauma include scurvy, (vitamin C deficiency), rickets (vitamin D deficiency), osteogenesis imperfecta (79-80), and temporary brittle bone disease (TBBD). (81-82) In regard to the latter, Miller and Hangartner described the condition characterized by transient bone weakness and presenting as multiple unexplained fractures during the first year of life. For this reason it has often been confused with child abuse. In a study involving 26 infants with TBBD it was found that 25 had a history of decreased fetal movement or confinement in limited uterine space during the mother's pregnancies. Plain X-ray films were normal in all cases, but osteopenia was confirmed by bone densitometry studies. (82)

  • - In a report by Kirschner in 1985 entitled, "The Mistaken Diagnosis of Child Abuse," a number of cases were presented in which mistaken diagnosis of child abuse was confirmed. (83) One of these was a case with pseudo fractures from atypical parietal suture lines. An attempted search of the literature on the subject revealed one reference on parietal pseudosutures. (95)

Spontaneous Rib Fractures; Alternate Explanations other than Child Abuse:

There is a general consensus in the medical community that spontaneous fractures can occur where there is:
(1) Brittle bone disease;
(2) scurvy with imperfect connective tissue formation in fetal or infant skeletal tissue;
(3) osteomalacia;
(4) traumatic birth situations;
(5) during cardiopulmonary resuscitation;
(6) rickets;
(7) and osteogenesis imperfecta.

Rib Fractures and Other Long Bone Skeletal Fractures; Due to Epiphyseal Slippages and Not Due to Trauma:

According to a study by V.F. Garcia et al (1990) published in Journal of Trauma titled, "Rib fractures in children: a marker for severe trauma," (104) of the 2080 children studied in trauma centers in Australia, 33 had multiple rib fractures. Among these 33, the injuries were accompanied by severe (emphasis mine) internal thoracic injuries in 85% of the cases. (It will be recalled that no thoracic injuries were reported in the present case).

Comment: {If severe internal chest injuries took place in 85% of cases with multiple traumatic rib fractures, this represents a 15% margin for error for a single occasion of trauma sufficiently severe to cause rib fractures. In cases with multiple rib fractures (or apparent rib fractures), which appear to be in different phases of healing, the parents often became subject to charges of repeated acts of violent squeezing or trauma. However, if one thinks about it, this scenario would be virtually impossible without causing severe internal chest injuries, in that the partially healed fractures from the first act of violence, scarcely beginning to heal, would become easily dislodged and act as shards or spears pointing and plunging into the thoracic cavity with a second or third incident of violent squeezing or battering. The odds that this could happen repeatedly without causing severe injuries in the thoracic cavity are extremely unlikely, quickly reaching the vanishing point.

{Also considering the matter of pain, in the cases I have reviewed, if there had been fresh rib fractures at various times, unmistakable pain would have been observed such as when picking up the baby or changing diapers, and lasting up to a week or more following each fresh incident of fractures, and reported by family members. I have never seen this happen in a single instance in babies with multiple rib fractures.}

We now come to an anomaly in many instances if not a majority of rib fractures, in that they occur near or within the anterior or posterior costochondral junctions between ribs and cartilage attached to the sternum (breast bone), at the junction of ribs and spine if posterior, or in the epiphyseal plates of the long bone. These are unusual locations for traumatic fractures, as reviewed in a study by HG Hiller entitled, "Battered or Not — a Reappraisal of Metaphyseal Fragility." (111) In this study a group of 145 children admitted to a pediatric trauma center for traumatic fractures were reviewed. Not one case of metaphyseal plate (costochondral junction) type was found. The study also looked at five cases of metaphyseal plate fractures from another hospital, where in all five cases the bones had a chalky appearance on X-rays. Of the two cases available for microscopic evaluation and bone scan, both revealed abnormal bone formation and were ruled non-traumatic. In his discussion the author observed that this type of trauma is common in scurvy (emphasis mine) without undue trauma to the child, and that green stick fractures are equally common in rickets. Hiller interpreted these findings as causing doubt on the advisability of accepting multiple epiphyseal plate fractures as definite roentgenologic evidence of battering, and that they are in need of close reappraisal. Additional reports have pointed out that rib fractures may occur with traumatic births and may be mistaken for child abuse. (108-110)

In addition to scurvy, there is another situation in which spontaneous fractures are prone to take place: temporary brittle bone disease as described by Marvin Miller, M.D., Ph.D. In his publications he showed that unusually close uterine confinement with reduction of fetal movement resulted in increased fetal bone fragility and vulnerability to spontaneous fracture. As outlined by C.R. Paterson and cited by Miller, reduced movement in such instances delays fetal neo-ossification, which is controlled by a bone "mechanostat" mechanism. Dr. Miller stressed that TBBD could not be diagnosed by plain X-rays but required bone densitometry for diagnostic confirmation. (81,82)

Merck Manual, Seventeenth Edition, states that both rib fractures and costochondral separations can take place with cardiopulmonary resuscitation (CPR) (Page 1748)

Returning to the subject of bone changes in scurvy, in a book by AF Hess entitled, "Scurvy, Past and Present," published in 1920, one finds the following quotations: (85)

  • - As described by Hess, scurvy disrupts these areas, (epiphyseal plates) the bone breaks down, and the ribs may over-ride, forming in typical cases "beads." Then healing commences with new bone formation (looking just like true healing fractures). Furthermore, not all the ribs may be involved in this process, and the changes will not all occur at the same time " giving the appearance of multiple fractures of different ages. (Pages 94-95)

  • - Several illustrations provided in the Hess text showed separations of the epiphyses of the head of the humerus, and both partial and complete separation of the lower ends of the femora. Hess commented that this was a frequent lesion of fully-developed scurvy in infants, children, and even in young adults, being most frequent at the lower end of the femur, the upper end of the tibia, the head of the humerus, and the costochondral junctions. Very significantly as applied to the present case Hess stated, "it is to these epiphyseal separations that the term fracture or infraction usually refers," (Page 198)

  • - In perusing the literature but one study as been noted on the effect of a scorbutic diet on the foetus. This investigation was carried out on a large series of guinea-pigs by Ingier (1915)... In these experiments intra-uterine fractures, premature births and still-born litters are frequently mentioned. (Page 126)

  • - The most typical site of hemorrhage is beneath the periostium, a lesion widely known because of its clinical significance. (Subperiosteal hemorrhages occur under the periostium; that is, the "skin" of the bone). The blood is quickly ossified, and the appearance on X-ray is similar to what is seen when ribs are broken. (Pages 95, 108)

  • - Speaking of the classical X-ray finding seen in scurvy bones, the "white line" sometimes seen near the ends of long bones, Hess states: It is best seen at the lower end of the radius and femur, and appears as a white, transverse, somewhat irregular band. Its diagnostic value has been greatly exaggerated, as it is frequently not present when the disease is advanced. (page 199)

  • - These changes (subperiosteal hemorrhage, costochondral changes) are not found in every specimen, so that in order to exclude scurvy definitely, it is necessary to examine a considerable number of ribs, several may be normal, only one or two showing the characteristic microscopic changes. (page 91)

As another source of references on bone changes in scurvy, the 5th chapter, volume II of Dr. Clemeton's books on vitamin C, a chapter entitled "Bone Changes," (64) begins with the following introduction:

"One of the most basic defects in scurvy is the inability of connective tissue cells to form mature extracellular materials; the fibroblasts, the chondroblasts, the odontoblasts, and the cementoblasts are all connective which are related to one another and are responsible for the secretion of collagen fibers which are the foundation of fibrous tissue, bone, cartilage, dentin, and tooth cement respectively. In scurvy, it seems that they continue to secrete a semiliquid protocollagen, but the ability to form mature collagen fibers is lacking... Consequently the extracellular tissues lack the framework of collagen on which to grow."

Clemetson went on to comment that retarded growth, multiple fractures, and severe pain due to periosteal hematomas may lead to a suspicion of child abuse, especially if there are accompanying bruises and ecchymoses. Bruises of the thighs and even spontaneous fractures of both femurs have been recorded from the gentle act of raising the legs of an infant to change diapers.

Clemetson concluded the chapter with the following comments:

"The bone pathology of acute scurvy was described in detail by Wolbach (1937) and by Dalldorf (1938), but the changes observed in protracted moderate scurvy, as produced in guinea pigs by Ham and Elliott (1938) are much more relevant to the human condition than is total ascorbate deficiency. Not only did these workers observe osteoporosis, profound changes at the epiphyseal plates, slipped epiphyses, and the fractures which are so well documented in acute scurvy, they also observed a marked diminution in the amount of epiphyseal bone, resulting in loss of support for the articular cartilage."

Prematurity, a Risk Factor for Vaccines

Before concluding, I wish to place special emphasis on what I believe to have been ill-advised vaccines in a premature infant. If this had not been evident with the first series November 17, 2001, it certainly should have been on December 17 when the second series was administered to an ill child. In the New Complete Medical and Health Encyclopedia, (25) prematurity has been listed as a contraindication to vaccines during early infancy because of the relative immaturity of kidneys, liver, and other detoxification systems of the body, necessary for buffering and detoxification of the bacterial endotoxins and other toxic substances in the vaccines, these in turn bringing greater risk of vaccine reactions.

As an addendum to this report I am enclosing a series of selected published studies showing increased hazards of vaccine reactions in premature infants.

Thimerosal, the Mercury Issue:

As result of a US Congressional mandate, in June, 1999 the Food & Drug Administration (FDA) revealed the mercury content in childhood vaccines. Formerly generally unknown, it then came to be realized that children had been receiving far greater amounts of mercury in their vaccines in the form of the additive, thimerosal, than were considered safe. Up until that time many or most brands of DTP, DTaP, hepatitis B, and Hib vaccines contained mercury so that, depending on the combinations of vaccines used, children were receiving as much as 25 or 50 or even a 100-fold the amounts of mercury in a single day than were considered safe according to US Environmental Protection Agency standards. (102)

For over 200 years mercury has been known as a potent neural (brain) toxin and one of the most toxic of the heavy metals. Recent animal studies have shown that exposures to mercury vapors produce retrograde degeneration of neuronal (brain) membranes producing molecular lesions similar to those seen in the brains of patients dying with Alzheimer's disease. (103 Apparently as an offshoot of the Congressional hearings on vaccine safety, the Institute of Medicine (IOM) issued a report on October 1, 2001 entitled, "Thimerosal-Containing Vaccines and Neuro-developmental Outcomes." The IOM report states:

Page 10: "The committee concludes that although the hypothesis that exposure to thimerosal-containing vaccines could be associated with neuro-developmental disorders is not established and rests on indirect and incomplete information, primarily from analogies with methylmercury and levels of maximum mercury exposures from vaccines given in children, the hypothesis is biologically plausible." (emphasis mine)

It is true that thimerosal is now being withdrawn from childhood vaccines, a process which reportedly should be complete by the year 2003. However, considering that mercury has been used in vaccines since the 1930s, it is both possible and plausible that vaccine reactions, which result in part from mercury toxicity, have gone largely unrecognized for well over half a century by medical authorities. As a result, many conditions, including misdiagnosed cases of shaken baby syndrome, are not being traced to their true origins: vaccine reactions.

Are There Lessons To Be Learned?

In my opinion, unless doctors become more thoughtful and objective in evaluation of these cases as they come into hospital emergency rooms, the casual diagnostic evaluations commonly seen until now may become grounds for malpractice.

At a very minimum, the following should be added to the usual hospital procedures as routine screening tests when there is suspicion of SBS:

  • - With findings of retinal and subdural hemorrhages, check plasma ascorbate and serum histamine, to rule out subclinical scurvy; check prothrombin and partial prothrombin times, fibrinogen level, fibrin split products, D Dimer test, and blood smears to check for fragmented red blood cells to rule out coagulopathy, and if DIC presence is indicated, to differentiate between acute and chronic DIC.

  • - In cases of skeletal fractures, test plasma ascorbate and serum histamine along with appropriate textbook tests for rickets; bone densitometry should be done to rule out temporary brittle bone disease. If there are skull fractures and the baby comes to autopsy, specific measurements of skull thickness should be required.

  • - When there is significant lowering of hemoglobin, hematology consult should be requested and the patient evaluated for hemolysis.

  • - At the present time there are no officially recognized laboratory tests for diagnosis of vaccine reactions. In my opinion this is largely or entirely due to historical deficiencies in safety testing and scientific infrastructure in the vaccine field. Very sadly, there does not appear to be any official inclination to remedy these deficiencies at time of this writing. We can only hope that new and wiser heads will realize these needs and act upon them.

The same standards as those listed above should also apply in the courtroom in that:

  • - Prosecution attorneys and their witnesses should be held to standards of "proof of guilt beyond a reasonable doubt" in shaken/impact baby (SBS) cases, a standard which is or should be applied in all criminal cases. Since SBS is a diagnosis of exclusion, this proof should include the exclusion of alternate diagnostic possibilities.

  • - Juries should be made aware of the gross deficiencies in safety testing of vaccines, and of the likelihood that large-scale adverse reactions are taking place unrecognized as to their true nature. Among these, in many instances, may be vaccine reactions mimicking the current diagnostic criteria of SBS and a being source of many misdiagnoses. Deficiencies in safety testing of vaccines include: 1) a total lack of long-term surveillance of any vaccine in use today, and 2) gross deficiencies in systematic before-and-after testing of vaccines for possible adverse effects on the brain, the nervous and immune systems, as well as other systems of the body; and in finding adverse reactions, to seek for safer methods.


(1) David TJ, Shaken baby (shaken impact) syndrome: non-accidental head injury in infancy, Royal Soc Med, Nov.,1999; 99:556-561

(2) Weston IT, The pathology of child abuse, in: Heifer RE, Kempe CH Eds, The Battered Child, University of Chicago Press, 1968, Pp 77-100.

(3) Caffey J, On the theory and practice of shakng infants: its potential residual effects of permanent brain damage and mental retardation, Am J Dis child, 1972; 124:161-169.

(4) Guthkelch AN, Infantile subdural hematoma and its relationship to whiplash injury, Brit Med J, 1971; 11:430-431.

(5) Joint Statement on Shaken Baby Syndrome, Minister of Public Works and Government Services, Ottawa, 2001.

(6) Brown J, Minns R, Non-accidental head injury, with particular reference to whiplash shaking injury and medical legal aspects, Dev Med Child Neurol, 1993; 35:849-869.

(7) Plunkett J, Shaken baby syndrome and the death of Matthew Eapen: A forensic pathologist's response, Am J Forensic med Pathol,1999; 20:17-21.

(8) Wilkin B, Head injury — abuse or accident? Arch Dis child, 1997; 76:393-397.

(9) Kemp AM, Investigating subdural hemorrhage in infants, Arch Dis Child, 2002; 86:98-102.

(10) Kleinman PK, Barnes, PD, Head Trauma in, Kleinman PK, ed, Diagnostic Imaging of Child Abuse, 2nd edition, St Louis, MosbyYearbook, 1998:285-342.

(11) Jenny C, Hymnel KP, Ritzen A et al, Analysis of missed cases of abusive head trauma, JAMA, 1999; 281:621-626.

(12) Levitt CJ, Smith, WL, Alexander RC, Abusive head trauma, In Reece RM, ed: Child Abuse; Medical Diagnosis and Management, Philadelphia, Lea & Febiger, 1994: 1-22.

(13) Shannon P, Becker L, Mechanisms of brain injury in infantile child abuse, (commentary), Lancet, 2001; 358:686-687.

(14) Chester AC, Levine PH, Concurrent sick-building syndrome and chronic fatigue syndrome: epidemic neuromyasthenia revisited, Clin Infect dis, (Suppl 1), 1996;18:S43-S48.

(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) Schoenfeld A, Buckman G, Cohen S et al, Retinal hemorrhages in the newborn following labor induced by oxytocin or dinoprostone, Arch Ophthalmol, July, 1985; 103:932-934.

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

(18) Fenichel GM, Webster DL, Wong WKT, Intracranial hemorrhage in the term newborn, Arch Neurol, Jan., 1984; 41:30-34.

(19) Chamnanvanakij S, Rollins N, Perlman JM, Subdural hematoma in term infants, Pediatr Neurol, 2002; 26:301-304.

(20) Piatt, JH, A pitfall in the diagnosis of child abuse: external hydrocephalus, subdural hematoma, and retinal hemorrhages, Neurosurg Focus, 1999; 7(4): Article 4

(21) Parent Ad, Pediatric chronic subdural hematoma: A retrospective comparative analysis, Pediatr Neurosurg, 1992; 18: 266-271.

(22) Hwang SK, Kim SL, Infantile head injury with special reference to the development of chronic subdural hematoma, Child Nerv Syst, 2000; 16:590-594.

(23) Kim KA, Wang MYGriffith PM, et al, Analysis of pediatric head injury from falls, Neurosurg Focus, 2000; 8:1-8.

(24) Arnold SF et al, Synergistic activation of estrogen receptor with combinations of environmental chemicals, Science, 1996; 272:1489-1492.

(25) Abou-Donia AB et al, Neurotoxicity resulting from exposure to Pyridostigmine bromide, DEET, and permitrin; implications of Gulf War chemical exposures, J Tox & Environ Health, 1996; 48:35-36.

(26) Stratton KR, CJ Howe, and RB Johnston, Jr, Editors, Adverse events associated with childhood vaccines; evidence bearing on causality, Institute of Medicine, National Academy Press, Washington DC;, 1994: 211-236.

(27) Eibl M et al, Abnormal T-lymphocyte subpopulations in healthy subjects after tetanus booster immunization, (letter) NEJM, 1984; 310(3): 198-199.

(28) Shaneen SO et al, Measles and atopy in Guinea-Bissau, Lancet, June 19, 1996: 347:1792-1796.

(29) Odent MR, Pertussis vaccination and asthma; is there a link? JAMA, 1994; 271:229-231.

(30) Alm JS et al, Atopy in children of families with anthroposophic lifestyle, Lancet, 1 May, 1999; 353:1485-1488.

(31) Kemp T et al, Is infant immunization a risk factor for childhood asthma or allergy? Epidemiology; November, 1997; 8(6): 678-680.

(32) Low AL, Electroencephalographic studies following Pertussis immunization, J Pediatrics, 1955; 47:35-39.

(33) Nouno S et al, Adverse effects on EEG and clnical condition after immunizing children with convulsive disorder, Acta Paediatr Japan, Aug., 1990; 32(4):357-360.

(34) Hurley DR, Vere DW, Fletcher AP, Referee 1, 2, 3 & 4, Adverse Drug React Toxicol Review, 2001; 19(4): 1-2.

(35) Newman TA, Wooley ST, Hughes PM et al, T-cell and macrophage-mediated axon damage in the absence of a CNS-specific immune response: involvement of metalloproteinases, Brain, 2001; 124: 2203-2214.

(36) Kosecka U et al, Pertussis adjuvant prolongs intestinal hypersensitivity, Int Arch Allergy Immunol, July, 1999, 119(3):205-211.

(37) Terpstra GK, Comparison of vaccination of mice and rats with Haemophilus influenzae and Bordetella pertussis as models of atopy, Clin Exp Pharmacol Physiol, March-April, 1979; 6(2): 139-149.

(38) Iwasa S, Ishida S, Akama K, Swelling of the brain caused by pertussis vaccine: its quantitative determination and the responsible factors in the vaccine, Japan Med J Sci Biol, April, 1985; 38(2):53-65.

(39) Jacob J, Manning F, Increased intracranial pressure after diphtheria, tetanus, pertussis immunization, J Dis Child, Feb.., 1979; 133:217-218.

(40) Gross TP et al, Bulging fontanel after immunization with diphtheria-tetanus-pertussis vaccine and diphtheria-tetanus vaccine, J Pediatr, March, 1989; 114(3):423-425.

(41) Mathur R, Kamuri S, Bulging fontanel following DPT, Indian Pediatr, June, 1981; 18(6):417-418.

(42) Galazka A, Kardymowiez BA, Complications and reactions after vaccination with pertussis, Epidemiol Rev, 1972; 26:411-424.

(43) Munoz JJ et al, Elicitation of experimental encephalomyelitis in mice with the aid of pertussigen, Cellular Immunology, 1984; 83(1): 92-100.

(44) Levine S, Lowinski R, Hyperacute encephalomyelitis, Am J Pathol, 1973; 37:247-250.

(45) Steinman L, Sriram S, Adelman NE, et al, "Murine model for pertussis vaccine encephalopathy: Linkage to H-2," Nature, 21 October, 1982, 2

(46) Ocular Differential Diagnosis, Sixth Edition, Frederick Hampton Roy, Williams & Wilkins Publ., Philad., 1997:527-532.

(47) Geddes JF, Hackshaw AK, Vowles GH et al, Neuropathology of inflicted head injury in children, 1. Patterns of brain damage, Brain, July, 2001, 124(7):1290-1298.

(48) Plunkett J, Shaken baby syndrome and other mysteries, Am J Forens Med Path, Letter submitted spring, 1998.

(49) Tongue AC, Discussion, Ophthalmology, 1986; 93:624-625.

(50) Goetting MG, Sowa B, Retinal hemorrhage after cardiopulmonary resuscitation in children: an etiologic reevaluation, Pediatrics, 1990; 85:585-588.

(51) Weeden VW et al, Retinal hemorrhage following CPR, Am J Forens Med Path, 1990; 11:79-82.

(52) Kirschner RH, Stein RJ, The mistaken diagnosis of child abuse, Am J Dis Child, 1985; 139:873-875.

(53) Kramer K, Goldstein B, Retinal hemorrhage following CPR, Clin Pediatr, 1993; 32:366-368.

(54) Sherriff FE, Bridges LR, Sivaloganathan S, Acta Neuropathol, 1994; 87:55-62.

(55) Kaur B, Rutty GN, Timberley WR, The possible role of hypoxia in the formation of axonal bulbs, V Clin Pathol, March, 1999; 52(3):302-209.

(56) Gilliland, MGF, Interval duration between injury and severe symptoms in nonaccidental head trauma in infants and young children, J Forensic Science, 1998; 43(3):723-725.

(57) Plunkett J, Fatal pediatric head injuries caused by short-distance falls, Am J Forens Med Pathol, 2001; 22(1):1-12.

(58) Kalokerinos A, Every Second Child, Thomas Nelson, Australia, 1974.

(59) Johnston CS, Thompson MS, Vitamin C status of an out-patient population, J Amer Col Nutr, 1998; 17:366-370.

(60) Hume R, Weyers E, changes in the leucocyte ascorbic acid concentration during the common cold, Scot Med J, 1973; 18:3.

(61) Aleo JJ, Padh H, Inhibition of ascorbic acid uptake by endotoxin, Proc Soc Exper Biol Med, 1985; 179:128-131.

(62) Clemetson CAB, Histamine and ascorbic acid in human blood, J Nutr, 1980; 110:662-668.

(63) Chatterjee IB, Majumder AK, Nandi BK et al, Synthesis and some major functions of vitamin C in animals, Ann NY Acad Sci, 1975; 258:24-47.

(64) Clemetson CAB, Vitamin C, (Volume I of 3-volume set), CRC Press, 1998, Pp 215-221.

(65) Stone N, Meister A, function of ascorbic acid in the conversion of proline to collagen hydroxyproline, Nature, (London), 1962; 194:555.

(66) Gore I, Tanaka Y, Fujinamik T et al, Endothelial changes produced by ascorbic acid deficiency in guinea pigs, Arch Pathol, 1965; 80:371-376.

(67) King CG, Menten ML, The influence of vitamin C level upon resistance to diphtheria toxin, J Nutr, 1935; 10:129-140.

(68) Jungblut CW, Zwemer RL, Inactivation of diphtheria toxin in vivo and in vitro by crystalline vitamin C (ascorbic acid), Proc Soc Exper Biol Med, 1935; 32: 1229-1234.

(69) Dey PK, Efficiency of vitamin C in counteracting tetanus toxin toxicity, Naturwissenschaften, 1966; 53:310.

(70) Fukada T, Koyama T, Prevention by ascorbic acid of liver glycogen depletion in endotoxin intoxication, Nature (London), 1963; 200:1327.

(71) Gilman BB, Tanzer RC, Subdural hematoma in infantile scurvy, JAMA, September 17, 1932; 99(12): 989-991.

(72) Butler, H, Position Paper on the Role of Vaccines in SIDS (Draft Version), 25 Harrisville road, Tuakau 1982, New Zealand (a portion of this 33 page report reviews the importance of breast feeding, as reflected in the higher incidence of Sudden Infant Death Syndrome (SIDS) in bottle fed babies as compared with those that are breast-fed). Presumably the same relationship applies with vaccine reactions.

(73) Kawakami S, Chikama M, Tamiya T et al, Coagulation and fibrinolysis in chronic subdural hematoma, J Neurosurgery, 1989; 25:25-29.

(74) Downes KA, Domen RE, McCarron, KF, Bringelsen, KA, Acute autoimmune hemolytic anemia following DTP vaccination: report of a fatal case and review of the literature, Clin Pediatr, 2001; 40:355-358

(75) Williams Hematology, Sixth Edition, E Beutler, BS Coller, U Seligsohn, MA Lichtman, TJ Kpps, Ed., McGraw-Hill Medical Publ Division, New York, 2001, page 1673 (76) Ibid, page 1475

(77) The Innis report can be found on the Yurko website:

(78) Plunkett J, Fatal head injuries caused by short-distance falls, Am J Forens Med Path, 2001; 22(1):1-12.

(79) Pozzati E, Poppi M, Gaist G, Acute bilateral extradural hematomas in a case of osteogenesisi imperfecta congenital, Neurosurgery, 1983; 13:66-68.

(80) Tokoro K, Nakajima F, Yamataki A, Infantile chronic subdural hematoma with local protrusion of the skull in a case of osteogenesis imperfecta, Neurosurgery, 1988; 22:595-598.

(81) Miller ME, Temporary brittle bone disease: a true entity?, Seminars in Perinatology, April, 1999, 23(2):174-182.

(82) Miller ME, Hangartner, Temporary brittle bone disease: associated with decreased fetal movement and osteopenia, Calcif Tissue Int, 1999; 64:137-143.

(83) Kirschner RH, Stein RJ, the mistaken diagnosis of child abuse, AJDC, September, 1985; 139, 873-875.

(84) A Kalokerinos, Autobiography, publication pending,

(85) Scurvy, Past and Present, Alfred F Hess, M.D., J.B. Lippincott Co., Philadelphia, 1920.

(86) Hiller HG, Battered or not — a reappraisal of metaphyseal fragility, Am J Roent Rad Ther & Nucl Med, 1972; 114(2):241-246.

(87) The Hepatitis B Vaccination Program in the United States — Lessons for the Future, Burton A waisbren, Sr, M.D., Delzer Lithograph Company, PO Box 679, Waukesha, WI 53186-0679, Copyright Pending, pages 34-36. The 58 case reports of acquired autoimmunity following hepatitis B vaccine were provided in a supplemental report accompanying the book.

(88) Smith DC, Kearns TP, Sayre GP, Pre-retinal and optic nerve sheath hemorrhage: pathologic and experimental aspects in subarachnoid hemorrhage, Trans Am Acad Opthalmol Otolaryngol, 1957; 61:201-211.

(89) Lehman RAW, Krupin T, Podos SM, Experimental effect of intracranial hypertension upon intraocular pressure, J Neurosurgery, 1972; 36:60-66.

(90) David DB, Mears T, Quinlan MP, Ocular complications associated with bungee jumping, Brit J Ophthalmol, 1994; 78:234-235.

(91) Jain BK, Talbot EM, Bungee jumping and intraocular hemorrhage, Br J Opthalmol, 1994: 78:236-237.

(92) Vanderlinden RG, Chisolm LD, Vitreous hemorrhages and sudden increased intracranial pressure, J Neurosurg, 1974; 41:167-176.

(93) Edlow JA, Caplan LR, Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage, New Engl J Med, 2000; 342:29-36.

(94) Margulies SS, Infant skull and suture properties: measurements and implications for mechanisms of pediatric brain injury, Transactions of the ASME, August, 2000; 122:364-371.

(95) Fenton LZ, Sirotnak AP, Handler MH, Parietal pseudofracture and spontaneous intracranial hemorrhage suggesting nonaccidental trauma: report of 2 cases, Pediatric Neurosurgery, 2000; 33:318-322.

(96) Ophthalmology Child Abuse Working Party, Child abuse in the eye, Eye, 1999; 13:3-10.

(97) Green, Ocular and cerebral trauma in nonaccidental injury in infancy: underlying mechanisms and implications for pediatric practice. Brit J Ophthalmol, 1996; 80:282-287.

(98) Taylor D, Unnatural injuries, Eye, 2000; 14:123-150.

(99) Duhaime, AC, Nonaccidental head injury in infants — the shaken baby syndrome, New Eng J Med, 1998; 338:1822-1828.

(100) Duhaime AC, Alario AJ, Lewander WJ et al, Head injury in very young children: mechanisms, injury types, and ophthalmologic findings in 100 hoepitalized patients younger than 2 years of age, Pediatrics; 90(2):179-185.

(101) Buys, Retinal findings after head trauma in infants and young children, J ophthalmology, 1992; 99:1718-1723.

(102) Halsey NA, Limiting infant exposure to thimerosal in vaccines and other sources of mercury, JAMA, 1999; 282:1763-1766. (According to current Environmental Protection Agency (EPA) standards, the maximum safe mercury exposure in a single day should be 0.1 micrograms per kilogram of body weight).

(103) Leong CCW, Naweed IS, Lorscheiderae FL, Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury, NeuroReport, Accepted for publication Dec. 12, 2000; 12(4):0733-0737.

(104) Garcia VF, Gotschall CS, Martin MA et al, Rib fractures in children: a marker of severe trauma, J Trauma, 1990; 30(6):695-700.

(105) Demir RH, Gleicher N, Myers SA, Atraumatic antepartum subdural hematoma causing fetal death, Am J Obstet Gynecol, 1989; t160:619-620.

(106) Gunn TR, Subdural hemorrhage in utero, Pediatrics, Oct. 1985; 76(4):606-609.

(107) Lund CJ, Kimble MS, Some determinants of maternal and plasma vitamin C levels, Am J Obstet Gyn, 1943; 46:635.

(108) Hartmann RW Jr, Radiological case of the month; Rib fractures produced by birth trauma, Arch Pediatr Adolesc Med, 1997; 151(9):947-948.

(109) Rizzolo PJ, Coleman PR, Neonatal rib fracture; birth trauma or child abuse? J Fam Pract; 1989; 29(5):561-563.

(110) Cumming WA, Neonatal skeletal fractures, Birth trauma or child abuse? J Canad Asso Radiol, 1979; 30(1):30-33.

(111) Hiller HG, Battered or not: a reappraisal of metaphyseal fragility, Am J Roentgen Radiotherapy & Nucl Med, 1972; 114(2):241-246.

(112) Hymel KP, Jenny C, Block RW, Intracranial hemorrhage and rebleeding in suspected victims of abusive head trauma: addressing the forensic controversies, Child Maltreatment, November, 2002; 7(4):329-348.

(113) Personal communication, Jan E Leestma, MD, board certified in Neuropathology and Anatomic Pathology, 2002.

(114) Kawakami Y, Chikama M, Tamiya T, Shimamura Y, Coagulation and fibrinolysis in chronic subdural hematoma, Neurosurgery, 1989; 25:25-29.

(115) Williams Hematology, Sixth Edition, Beutler E, Coller BS, Seligsohn U, Lichtman MA, Kipps TJ, Editors; McGraw-Hill Publishing, New York, 2001, Pages 1677-1695.

(116) Graham DI, Behan PO, More AR, Brain damage complicating septic shock, J Neurol, Neurosurgery, Psychiatry, 1979; 42:19-28.

(117) Hart Mn, Earle KM, Haemorrhagic and perivenous encephalitis: a clinical-patholotical review of 38 cases, J Neurol Neurosurg Psychiatry, 1975; 38:585-591.

(118) Reik L, Disseminated vasculomyelinopathy: an immune complex disease, Ann Neurol, 1980; 7:291-296.

(119) Hannan KI, Berg DE, Baumzweiger W et al, Activation of the coagulation system in Gulf War Illness: A potential pathophysiologic link with the chronic fatigue syndrome; a laboratory approach to diagnosis, Blood Coagulation and Finbrinolysis, 2000; 11:673-678.

(120) Hall JR, Reyes HM, Horvat M, et al, The mortality of childhood falls, J Trauma, 1989; 29(9):1273-1275.

(121) Blumenthal I, Skull fracture — child abuse or an accident? Lancet, July 15, 2000; 356:258.

(122) Sanford HN et al, JAMA, 1942; 118:697.

SBS and SIDS Index of Articles on Vaclib site

A longer article on only the 'latent period' by Dr. Buttram:
The Controversy of the Latent Period Following Immunizations