The Shaken Baby Syndrome Myth
renamed "Abusive Head Trauma" or "Non-Accidental Injury"



* SBS began as an unproven theory and medical opinions, now discredited by biomechanical engineering studies
* No DIFFERENTIAL DIAGNOSIS done to eliminate other causes, abuse assumed without evidence
* Shaken Baby diagnostic symptoms not caused by shaking
* Child protective agencies snatch children, destroy families based on medical accusations without proof of wrong-doing
*Poor or deceptive police investigations, falsified reports, perjured testimony threaten legal rights, due process
* Prosecutors seek "victory", over justice; defense attorneys guilty of ineffective counsel, ignorance, lack of effort
* Care-takers threatened, manipulated, in order to force plea bargains, false confessions
* A fractured criminal justice system--a big piece for the rich, a small piece for the poor, and none for alleged SBS cases.



Related websites/ important people and projects ShakenBabySyndrome/Vaccines/YurkoProject
"Shaken Baby Syndrome or Vaccine Induced Encephalitis-- Are Parents Being Falsely Accused?" by Dr Harold Buttram, with Christina England (WEBSITE)
Evidence Based Medicine and Social Investigation:
EBMSI conferences, resources and information Articles and Reports
VacTruth: Jeffry Aufderheide; The SBS conection and other dangerous or deadly side effects of vaccination true, suppressed history of the smallpox vaccine fraud and other books:
Patrick Jordan
Sue Luttner, must-read articles and information on Shaken Baby Syndrome: her resources link
The Amanda Truth Project: Amanda's mother speaks out at symposium
Tonya Sadowsky


(SBS/AHT) DAI--Articles that include the potential misdiagnosis of a condition that has causes other than non-accidental violent injury in infants.

  1.   In an article by Jennian F Geddes, a neuropathologist at Royal London Hospital, and colleagues, Geddes's team studied the brains of 53 children suspected of dying from deliberate injury. (5) 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 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 point where the brain meets the spinal cord, where a (non-violent) rocking motion can damage the vital part of the spinal cord that controls breathing. 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.

    Diffuse injury:  A 2001 study reported that the predominant histological abnormality in cases of inflicted head injury in the very young is diffuse hypoxic brain damage, not diffuse axonal injury (DAI), and suggested two possible explanations: either the unmyelinated axon of the immature cerebral hemispheres is relatively resistant to traumatic damage, or in shaking-type injuries the brain is not exposed to the forces necessary to produce DAI
    ^ Geddes JF, Hackshaw AK, Vowles GH, Nickols CD, Whitwell HL (July 2001). "Neuropathology of inflicted head injury in children. I. Patterns of brain damage". Brain 124 (7): 1290–8. doi:10.1093/brain/124.7.1290. PMID 11408324.
    DIFFUSE AXONAL ‘INJURY’ --The use of italics for the word ‘injury’ is deliberate because the pathology involved is not always caused by an ‘inflicted injury’. Kaur et al, J Clin Pathol. 1999;52::203-209, state:
    " Conclusions – Axonal bulbs staining positively for _APP may occur in the presence of hypoxia and in the absence of head injury. The role of hypoxia, raised intracranial pressure, oedema, shift effects, and ventilatory support in the formation of axonal bulbs is discussed. The presence of axonal bulbs cannot necessarily be attributed to shearing forces alone."

    Rosomoff et al, Crit Care Med, 1996, Feb;24(2 Suppl):S48-56, state:
    "Severe traumatic brain injuries are extremely heterogenous. At least seven of the secondary derangements in that have been identified as occurring after most traumatic brain injuries also occur after cardiac arrest."

    Geddes et al, Neuropathol Appl Neurobiol 2000 Apr:26(2):105-16, state:
    "The lack of correlation between well-documented histories and neuropathological findings means that in the interpretation of assault cases at least, a diagnosis of traumatic axonal injury or diffuse axonal injury is likely to be of limited use for medicolegal purposes."

    Little more needs to be said about this except to state that, in many cases, diffuse axonal injury is presented as clear evidence of shaking. The animated video showing how the brain is supposed to move inside the skull when a baby is shaken, and ‘tear’ the axons apart, certainly impresses the judge and the jury. The effect of that video is, indeed, dramatic. Attempting to counter that, even with extensive references from the best medical literature, is difficult—particularly when the video is presented by authorities with impeccable qualifications.

Diffuse Axonal Injury (DAI)

Diffuse Axonal Injury is one of the triad of symptoms claimed to be diagnostic of Shaken Baby Syndrome (SBS). This is the kind of injury seen in vehicle accidents when there is head impact, causing diffuse brain injury which is the most frequent cause of permanent brain damage leading to chronic vegetative states. The unproven SBS hypothesis which only surfaced in 1972 following the first of two related articles by a Dr. John Caffey, who believed that injuries he was seeing without external signs of trauma were caused by shaking. It remained unproven because Caffey failed to take the most basic steps--eliminating other causes of the same symptoms. Basically, it was "junk science" which by-passed the usual safeguards in science and medicine which require supporting science, to become accepted medical theory as selectively applied to Shaken Baby Syndrome as a diagnostic symptom.

Shaking Brain Impact Is False Diagnosis Lacking Scientific Basis

In a letter written to a court in 2008, expert Injury Biomechanics Researcher: Chris Van Ee, PhD explains that "...while many in the medico-legal communities have debated these injury causation mechanisms, the Court is advised that most medical doctors are not trained in our scientific discipline and do not access our databases nor study our peer-reviewed research." He   goes on to assure the court that biomechanics tackles "Inconvenient Truths" that "some have ignored or distorted" head on.

The findings are as follows:

(A) Scientific testing has shown that head acceleration levels from anterior/posterior human shaking of a normal 0- to 2-year-old child in the sagittal plane results in head acceleration and force levels that are much lower than those which are associated with traumatic head injury. Repeated testing of this hypothetical has shown that the head accelerations associated with shaking are far below the level associated with injury and there is no quality data to support the SBS brain injury mechanism. Thus shaking, even if done in a fit of anger, is not expected to result in head dynamics sufficient to cause direct intra cerebral trauma.

(B) Human shaking (id.) may cause lethal brain stem and cervical spine injuries in a 0-to 2-year-old child, as the forces necessary for these injuries are well below the level needed for fatal brain injuries and are consistent with the forces that can be produced in shaking. Put another way, these neck injuries would be expected in any hypothetical-superhuman-strength case of SBS where superhuman dynamics resulted in head accelerations leading to inter cerebral trauma (if SBS were valid, which it is not).

(C) If a 0- to 2-year-old child accidentally falls from a height of six feet and impacts head- first on a hard surface face such as carpeted cement, the sudden impact has the potential to generate sufficient head accelerations to cause fatal intra cerebral injuries. Whether any given fall is fatal depends on a host of variables and the fall mechanics which are different in each accident, but the potential head dynamics that result from a 6 foot high fall could far exceed the tolerance associated with fatal head injury.

(D) Intentionally impacting a 0- to 2-year-old child’s head against a hard surface could easily cause fatal brain injuries that would mimic those of a fall and today’s science cannot distinguish accidental from non-accidental impacts of falls of similar magnitude, barring extraordinary signs, e.g., grip marks or eye-witness accounts.

(E) The foregoing findings are based on principles universally accepted within my field and concern scientific subject matters that I am willing to testify on in this case. The findings are overwhelmingly supported by the following reference list of biomechanical tests and studies.

Full text and references: 

They Can't Tell The Difference Between DAI Caused By Head Impact and Non-Traumatic Brain Swelling (Hypoxic-Ischemic Brain Injury)

Int J Legal Med. 1999;112(4):261-7.
Pontine axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain damage.

Oehmichen M, Meissner C, Schmidt V, Pedal I, König HG.

Department of Legal Medicine, Medical University of Lübeck, Germany.

Experimental studies have shown that diffuse axonal injury is usually induced by positive or negative acceleration mechanisms. In order to determine the reliability of axonal injury (AI) as a marker of this type of traumatic insult, we compared cases of trauma-induced focal cortical hemorrhage without dural involvement (n = 67) with cases of trauma-induced subdural bleeding without cortical hemorrhage (n = 26). Both groups exhibited a wide range of post-traumatic survival times. The injuries in the first group were caused mainly by direct impact to the head, those in the second by acceleration/deceleration mechanisms. The investigations were based primarily on immunohistochemical demonstration of antibodies targeted to beta-amyloid precursor protein (beta-APP) in the pons as a marker of AI and the results were assessed semiquantitatively. No significant differences were found between the two groups. In both groups AI was detected in 80-100% of cases with survival times of more than 3 h and two thirds of all positive cases showed pronounced positivity. Additional comparison of cases of brain death due to mechanical trauma (n = 14) with cases of brain death due to non-mechanical trauma (n = 18) also disclosed no significant inter group differences. Finally, investigations of the pons in cases of non-traumatic death due to cerebral hypoxia/ischemia (n = 51) demonstrated AI with the same frequency as in the other groups, although the expression tended to be less pronounced. Our results confirm that beta-APP expression in the pons is a reliable indicator of AI but does not discriminate between injuries caused by traumatic strain or shearing mechanisms and secondary damage due to cerebral hypoxia/ischemia or edema. In the large majority of cases with prolonged post-traumatic survival, it can therefore be assumed that AI in the pons is the consequence of primary and/or secondary events or a combination of both, as is common in non-missile head injury survived for more than 90-120 min. Therefore, positive differentiation of the type of biomechanical event based on this criterion alone is not possible.

"Shaken Babies" by Archie Kalokerinos, MD          (*hypoxia--low oxygen levels)


The use of italics for the word ‘injury’ is deliberate because the pathology involved is not always caused by an ‘inflicted injury’.--Kalokerinos

Kaur et al, J Clin Pathol. 1999;52::203-209, state:
" Conclusions – Axonal bulbs staining positively for _APP may occur in the presence of hypoxia and in the absence of head injury. The role of hypoxia, raised intracranial pressure, oedema, shift effects, and ventilatory support in the formation of axonal bulbs is discussed. The presence of axonal bulbs cannot necessarily be attributed to shearing forces alone."

Rosomoff et al, Crit Care Med, 1996, Feb;24(2 Suppl):S48-56, state:
"Severe traumatic brain injuries are extremely heterogenous. At least seven of the secondary derangements in that have been identified as occurring after most traumatic brain injuries also occur after cardiac arrest."

Geddes et al, Neuropathol Appl Neurobiol 2000 Apr:26(2):105-16, state:
"The lack of correlation between well-documented histories and neuropathological findings means that in the interpretation of assault cases at least, a diagnosis of traumatic axonal injury or diffuse axonal injury is likely to be of limited use for medicolegal purposes."

Injections of Brain "Excitotoxins" Causes Inflammation and DAI
Excitotoxins produced by the brain are triggered by components of vaccines among other causes, particularly from mercury and aluminum additives.

Inflammation. 2008 Feb;31(1):24-35. Epub 2007 Sep 25.
Diffuse axonal damage, myelin impairment, astrocytosis and inflammatory response following microinjections of NMDA into the rat striatum.

Lima RR, Guimaraes-Silva J, Oliveira JL, Costa AM, Souza-Rodrigues RD, Dos Santos CD, Picanço-Diniz CW, Gomes-Leal W.

Laboratory of Experimental Neuroprotection and Neuroregeneration, Department of Morphology, Biological Sciences Center, Federal University of Pará, Belém-Pará, Brazil.

White matter damage and inflammatory response are important secondary outcomes after acute neural disorders. Nevertheless, a few studies addressed the temporal outcomes of these pathological events using non-traumatic models of acute brain injury. In the present study, we describe acute inflammatory response and white matter neuropathology between 1 and 7 days after acute excitotoxic striatal damage. Twenty micrometer sections were stained by hematoxylin and eosin technique for gross histopathological analysis and immunolabed for neutrophils (anti-mbs-1), activated macrophages/microglia (anti-ed1), astrocytes (anti-gfap), damaged axons (anti-betaapp) and myelin basic protein (MBP). Recruitment peak of neutrophils and macrophages occurred at 1 and 7 days post-nmda injection, respectively. Diffuse damaged axons (beta-app + end-bulbs) were apparent at 7 days, concomitant with progressive myelin impairment and astrocytosis. Further studies using electron microscopy and blockers of inflammatory response and glutamatergic receptors should be performed to confirm and address the mechanisms of white matter damage following an excitotoxic lesion. --Vaccination connection to excitotoxin production -- The role of excitotoxins in autistic behavior

Primate Study Shows That Only Extreme Lateral (Sideways) Shaking Produces DAI
The full length article must be purchased, only the following abstract was available. It doesn't say how much force was used, but the primates were probably strapped into mechanical shaking devices which produced more force than can be applied by hand, and were instead replicating forces consistent with vehicle impacts. Sideways shaking by a caretaker would be unnatural and unlikely. All of the assumptions and SBS videos demonstrate up and down shaking.

Ann Neurol. 1982 Dec;12(6):564-74.
Diffuse axonal injury and traumatic coma in the primate.

Gennarelli TA, Thibault LE, Adams JH, Graham DI, Thompson CJ, Marcincin RP.

Traumatic coma was produced in 45 monkeys by accelerating the head without impact in one of three directions. The duration of coma, degree of neurological impairment, and amount of diffuse axonal injury (DAI) in the brain were directly related to the amount of coronal head motion used. Coma of less than 15 minutes (concussion) occurred in 11 of 13 animals subjected to sagittal head motion, in 2 of 6 animals with oblique head motion, and in 2 of 26 animals with full lateral head motion. All 15 concussioned animals had good recovery, and none had DAI. Conversely, coma lasting more than 6 hours occurred in one of the sagittal or oblique injury groups but was present in 20 of the laterally injured animals, all of which were severely disabled afterward. All laterally injured animals had a degree of DAI similar to that found in severe human head injury. Coma lasting 16 minutes to 6 hours occurred in 2 of 13 of the sagittal group, 4 of 6 in the oblique group, and 4 of 26 in the lateral group, these animals had less neurological disability and less DAI than when coma lasted longer than 6 hours. These experimental findings duplicate the spectrum of traumatic coma seen in human beings and include axonal damage identical to that seen in severe head injury in humans. Since the amount of DAI was directly proportional to the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae.

DAI Coma Caused By Brainstem Injury
Brainstem injury means a neck injury. There are no reports in known SBS convictions where neck injuries have been found.

J Neurosurg. 2000 Aug;93(2):315-22.
Immediate coma following inertial brain injury dependent on axonal damage in the brainstem. In this experiment, the head was mechanically rolled around, not shaken up and down.

Smith DH, Nonaka M, Miller R, Leoni M, Chen XH, Alsop D, Meaney DF.

Department of Neurosurgery, University of Pennsylvania, Philadelphia 19104, USA.

OBJECT: Immediate and prolonged coma following brain trauma has been shown to result from diffuse axonal injury (DAI). However, the relationship between the distribution of axonal damage and posttraumatic coma has not been examined. In the present study, the authors examine that relationship. METHODS: To explore potential anatomical origins of posttraumatic coma, the authors used a model of inertial brain injury in the pig. Anesthetized miniature swine were subjected to a nonimpact-induced head rotational acceleration along either the coronal or axial plane (six pigs in each group). Immediate prolonged coma was consistently produced by head axial* plane rotation, but not by head coronal plane rotation. Immunohistochemical examination of the injured brains revealed that DAI was produced by head rotation along both planes in all animals. However, extensive axonal damage in the brainstem was found in the pigs injured via head axial plane rotation. In these animals, the severity of coma was found to correlate with both the extent of axonal damage in the brainstem (p < 0.01) and the applied kinetic loading conditions (p < 0.001). No relationship was found between coma and the extent of axonal damage in other brain regions. CONCLUSIONS: These results suggest that injury to axons in the brainstem plays a major role in induction of immediate posttraumatic coma and that DAI can occur without coma.


Mechanical Rotation of Piglet Heads Causes DAI and Bleeding
Again, it required mechanical rolling around of the head, not forward and backward shaking to cause injuries, and there was substantial injury to the neck area noted, unlike in diagnosed SBS cases. No neck injury, no violent shaking.

J Neurotrauma. 2002 Jul;19(7):843-53.
Traumatic axonal injury after closed head injury in the neonatal pig.

Raghupathi R, Margulies SS.

Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

Closed head injury is the leading cause of morbidity and mortality in infants and children, and results in pathologies such as diffuse axonal injury (DAI) and subarachnoid hematoma (SAH). To better understand the mechanical environment associated with closed head injury in the pediatric population, animal models that include salient features of human infant brain must be utilized. Based on detailed information regarding the parallels between brain development in the pig and the human, the 3-5-day-old piglet was used to represent the infant at less than 3 months of age. Anesthetized piglets (n = 7) were subjected to rapid, inertial (nonimpact) rotation of the head about its axial plane and sacrificed at 6 h postinjury. Immediately following injury, five of seven piglets were apneic, with an absence of pupillary and pain reflexes. All piglets exhibited severe coma immediately postinjury, but recovered by sacrifice time. Blood was present on the surface of the frontal lobes, cerebellum, and brainstem, and subarachnoid hemorrhage was evident in the frontal cortex. In six of seven brain-injured piglets, accumulation of the 68-kDa neurofilament protein was evident in contiguous axons (swollen) and occasionally in disconnected axons (axonal bulbs), suggestive of traumatic axonal injury (TAI). Mapping of the regional pattern of TAI revealed injured axons predominantly in central and peripheral white matter tracts in the frontal and temporal lobes and in the midbrain. The number of injured axons was equivalent in both hemispheres, and did not correlate to the load applied to the head. Together, these data demonstrate that rapid rotation of the piglet head without impact results in SAH and TAI, similar to that observed in children following severe brain trauma.

They Had To Hit Baby Rats On The Head Three Times To Cause DAI
In order to fit their findings to the SBS hypothesis, they interpret this to mean that caretakers have Shaken/Impacted infants several times over a period of time to cause DAI, which will be hard to explain in cases where first-time caretakers have been accused.

J Neurotrauma. 2007 Jan;24(1):15-27.
Basic science; repetitive mild non-contusive brain trauma in immature rats exacerbates traumatic axonal injury and axonal calpain activation: a preliminary report.

Huh JW, Widing AG, Raghupathi R.

Department of Anesthesiology and Critical Care, Children's Hospital of Philadelphia, Philadelphia, PA, USA.

Infants who experience inflicted brain injury (shaken-impact syndrome) present with subdural hematoma, brain atrophy, and ventriculomegaly, pathologic features that are suggestive of multiple incidences of brain trauma. To develop a clinically relevant model of inflicted brain injury in infants, the skulls of anesthetized 11-day-old rat pups were subjected to one, two, or three successive mild impacts. While skull fractures were not observed, a single impact to the intact skull resulted in petechial hemorrhages in the subcortical white matter, and double or triple impacts led to hemorrhagic tissue tears at 1 day postinjury. Whereas the singly impacted brain did not exhibit overt damage at 7 days, two impacts resulted in an enlarged ventricle and white matter atrophy; three impacts to the brain led to similar pathology albeit at 3 days postinjury. By 7 days, cortical atrophy was observed following three impacts. Reactive astrocytes were visible in the deep cortical layers below the impact site after two impacts, and through all cortical layers after three impacts. Swellings were observed in intact axons in multiple white matter tracts at 1 day following single impact and progressed to axonal disconnections by 3 days. In contrast, double or triple impacts resulted in axonal disconnections by 1 day postinjury; in addition, three impacts led to extensive axonal injury in the dorsolateral thalamus by 3 days. Calpain activation was observed in axons in subcortical white matter tracts in all brain-injured animals at 1 day and increased with the number of impacts. Despite these pathologic alterations, neither one nor two impacts led to acquisition deficits on the Morris water maze. While indicative of the graded nature of the pathologic response, these data suggest that repetitive mild brain injury in the immature rat results in pathologic features similar to those following inflicted brain injuries in infants.

PMID: 17263667 [PubMed - indexed for MEDLINE]


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Dianne Jacobs Thompson  Est. 2007
Also (alternative medicine featuring drugless cancer treatments)
Author publication: NEXUS MAGAZINE "Seawater--A Safe Blood Plasma Substitute?"