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

  1. A critical look at Shaken Baby Syndrome (review) by Dr. Waney Squier
  2. Dr. Waney Squier's Curriculum Vitae (credentials, publications, lectures, positions, accomplishments)

by Waney Squier


The diagnosis “shaken baby syndrome” (SBS) has been widely accepted for over 30 years, but recent
evidence from biomechanical and clinical observational studies questions the validity of the syndrome.


The diagnosis of SBS is based on the clinical triad of encephalopathy, retinal hemorrhage (RH), and
subdural hemorrhage (SDH) in infants, usually under six months of age, who may die unexpectedly or
survive with greater or lesser degrees of neurological damage [1]. The term non-accidental head injury
(NAHI) has been preferred as it has no implications for mechanism of injury. Other features often
associated include a sole carer at the time of collapse and a clinical history that is incompatible with the
severity of the injuries. The diagnosis of inflicted injury becomes less problematic if there is objective
evidence of violence, such as bruises, fractures, or burns, but objective evidence of trauma has not
always been necessary in making the diagnosis.

Central to the assessment of these cases is whether the triad of findings can be regarded as diagnostic
of abuse with any degree of certainty. This review examines the evidence base for each element of
the triad and the current biomechanical evidence regarding mechanisms of infant head injury and its
pathological investigation.


SDH has been associated with child abuse since the mid-19th century [2]. Kempe described SDH with
multiple skeletal injuries and bruises as the battered child syndrome and Caffey described long bone
fractures and SDH [3–5], but it is Guthkelch [6] who developed the hypothesis that the whiplash–like
movements during shaking cause the characteristic bilateral thin film SDH of the syndrome. He based
his hypothesis, that shaking causes tearing of the cerebral bridging veins leading to SDH, on the
biomechanical studies of Ommaya [7] who was researching adult head injury in road traffic accidents.
Following Guthkelch’s paper, the “shaken baby syndrome” has become widely accepted as a form of
child abuse [1].
The Triad of Injuries

The three elements of the triad are encephalopathy, RH, and SDH.

Retinal Hemorrhages (RHs)

RHs have been regarded as an important indicator of inflicted injury, but many other causes of retinal
bleeding are recognized in infants, for example after normal birth, raised intracranial pressure, blood
dyscrasias, hemoglobinopathies, extracorporeal membrane oxygenation, cataract surgery, and accidental
trauma [8]. Postmortem indirect ophthalmoscopy has shown RHs to be more common after natural disease
and accidental injury than after inflicted injury [9]. These authors also noted that infants suspected
to have been abused were more likely to have ophthalmological examination in life than infants with
accidental injuries or natural diseases. This bias readily distorts the true incidence of RH in non-accidental
injury. Indeed Vinchon [10] noted in his study of infant head injury that “In the construct of our study
we could not obviate the circularity bias, and the evaluation of the incidence of RH in child abuse remains a
self-fulfilling prophecy”. These authors did, however, suggest that the extent and nature of retinal bleeds
may be more important as indicators of inflicted head injury than their existence per se [10]. The main
hypotheses for genesis of RH are that it is the result of venous obstruction, which in turn may
result from compression of the optic nerve by raised intracranial or intravascular pressure, even
transiently, or that the tissues of the retina are torn during the act of shaking. This latter hypothesis does
not withstand biomechanical scrutiny [11].


This term may be widely interpreted to include a range of clinical manifestations from feeding difficulties,
vomiting, and sleepiness to seizures and fulminating cerebral edema.

The specific neuropathological features of traumatic brain injury are contusions and traumaticaxonal injury. Hypoxic-ischemic injury and brain swelling are frequently seen but are not specific for trauma. Contusions
are very uncommon in infant brain trauma in the absence of skull fractures. Identification of axonal injury now depends on the immunocytochemical demonstration of beta amyloid precursor protein (BAPP). This is a
very sensitive marker of interruption of normal axonal flow but may be upregulated after hypoxic–ischemic
injury and metabolic disruption as well as trauma.









(Figure 1).  (a) Acute axonal injury. Bands of BAPP expression in an infarcted area of brain in acute hypoxic-ischemic injury. (b) Axonal swellings expressing BAPP restricted to the pontine cortico-spinal tracts, considered to indicate traumatic damage

Distinction of traumatic axonal expression of BAPP from other causes is fraught with difficulty, and depends in part on its distribution [12], [13], [14]. Neuropathological studies have shown that in babies who die following
NAHI, the underlying brain pathology is widespread hypoxic-ischemic injury and not diffuse traumatic axonal injury as previously believed [12, 13]. In this series axonal injury was seen in a limited distribution in the lower brainstem and in only a minority of cases. Radiological studies have confirmed these pathological observations [15].

This observation is important as traumatic axonal injury will lead to immediate loss of function causing clinical symptoms from the time of trauma. In contrast, hypoxic-ischemic injury and ensuing brain swelling take variable periods of time to develop and a baby so damaged may not show immediate symptoms. Even fatal brain trauma may present with a lucid interval between injury and clinical collapse [16, 17]. Lucid intervals are more frequently seen in infants less than two years of age [18], reflecting the very different responses of the infant brain to
injury due to the specific intracranial pathophysiology before the skull bones fuse [19].

Damage to the cervical nerve roots has been documented as part of the pathology of shaking injury [14]. It has not been established that this is the result of shaking, as cervical cord displacement resulting from brain swelling may also cause traction on nerve roots in the region. Autopsy studies in man and primates have shown that the spinal cord is displaced during extension and flexion of the neck [20, 21] and it remains a possibility that hyperextension and flexion could cause traction damage to nerve roots throughout the length of the spinal cord, but this has
not been documented in living infants.

Subdural Hemorrhage (SDH)

SDH is perhaps the most important and consistent component of the triad. In the acutely sick infant, it
is frequently the first clinical sign, identified on brain scan, to raise the question of abuse. There are no
specific imaging patterns that can distinguish inflicted from accidental intracranial injury [22, 23]. Autopsy and imaging studies show that infant SDH is usually a thin bilateral film and not a thick, unilateral space occupying
clot as seen in traumatic SDH in older children and adults [12, 13, 24]. This raises the question of whether the
two forms have the same etiology and anatomical source.

Causes of Subdural Hemorrhage. The commonest cause of SDH in infants is said to be trauma [25] although
a recent study has shown a significant incidence (26%) of birth-related SDH [26]. Other causes in infants include benign enlargement of the extracerebral spaces (BEECS), clotting disorders, hemorrhagic disease of the newborn, rare metabolic diseases, vascular malformations, and neurosurgical procedures [25, 27].

Traumatic SDH
Proposed traumatic causes of infant SDH are inflicted injury such as shaking and/or impact and accidental
injuries such as falls. Impact includes blunt impact of an object on the head and that resulting from a fall
or striking the moving head on a rigid surface. The biomechanical aspects of these injuries are discussed
below. The vast majority of cases described as SBS have evidence of impact [28]. While the pathologist
may be able to determine features indicative of impact, it is not, of course, possible to distinguish
accidental from non-accidental injuries by pathology.

Low-Level Falls
Low-level falls have the potential, albeit only rarely, to cause SDH in infants and young children. Absolute
height is not as important a criterion for injury as the exact nature of the fall for a particular infant, in a particular circumstance [29]. The effects of twisting, rotation, or crushing of the structures of the neck are crucial in terms of outcome. Biomechanical studies show that falls even from low levels of 3–4 ft can generate far greater forces in the head than shaking [11]. There are a number of case series demonstrating that infants and children may suffer
intracranial damage including retinal and intracranial hemorrhage after falls from levels as low as 3 ft [10,
17, 30–33]. While most babies may suffer little from an apparently trivial fall, this is clearly not always
the case.

Birth-Related SDH
Three studies, using magnetic resonance imaging (MRI), have shown a surprisingly high incidence of SDH after birth in asymptomatic infants. Whitby identified SDH in the first two days of life in 9% [32], while SDH was seen in up to 46% of otherwise normal neonates using higher resolution MRI scanning [26, 34]. With regard to method of delivery, ventouse or instrumental deliveries have been associated with a higher incidence of intracranial injury
[35, 36]. Towner [37] found an increased incidence of intracranial hemorrhage after instrumental delivery
with ventouse or forceps and emergency caesarean section, but the incidence was lower after caesarean
section before labor had begun. However, it should be noted that all of Looney’s cases followed normal
vaginal delivery [26]. While neonates with SDH may be asymptomatic [26, 35] they may also have signs in the neonatal period including unexplained apnoea, dusky episodes, hypotonia, seizures, and lethargy [38].

Sources of SDH. Traditional belief is that in SBS the SDH results from tearing of the superficial bridging
veins as they cross from the brain to the dural sinuses [6] (Figure 2) This has never been proved. 

(Figure 2) Infant bridging veins may be visualized by opening the skull very carefully, but they are readily torn in normal autopsy procedures. (Picture courtesy of Dr P. Lantz)

Indeed it is very difficult to find documented evidence of torn bridging veins at surgery or at autopsy. Cushing,
who operated on neonates with SDH and subsequently performed the autopsies wrote “In two of the cases I have examined I have satisfied myself that such ruptures were present. A positive statement, however, cannot be given even for these cases, since the dissection and exposure, difficult enough under any circumstances, owing to the delicacy of the vessels is the more so when they are obscured by extravasated blood” [39]. More recently Maxeiner [40] addressed the problem by injecting radio-opaque dye into the veins at autopsy to assess their integrity after removing the top of the head in one piece, hard-boiled egg style. This approach is not widely used as it destroys much of the brain and injection pressures need to be carefully monitored if the veins are not to be ruptured artifactually.

Volpe [41] said that SDH was by no means always traumatic and suggested that in neonates without tentorial tears the bleeding may arise from the tributary veins of the dural sinuses. Autopsy studies from the older literature show bridging vein rupture is uncommon, Craig described 62 neonatal SDH, of which only 3 had torn bridging veins, all of those with overriding sutures [42]. Larroche described 700 autopsies 18% with SDH. [43] She noted an association with hypoxic-ischemic injury (Figure 3)

(Figure 3) Fresh subdural blood seen after birth asphyxia. (Picture courtesy of Dr I. Scheimberg)

She did not identify torn veins. If SDH does not arise from torn bridging veins, what other sources may there be? Two obvious alternative sites of origin exist, the dura itself and the old subdural membranes (Figure 4).

(Figure 4) Diagram representing a coronal slice through the brain and dura indicating the intradural sinuses and their
relationship to cortical surface veins, arachnoid granulations, and intradural fluid channels

Dural Hemorrhage
The dura is composed of two leaflets, the periosteal and the meningeal dura, separated by a thin vascular channel, which widens to form the large dural sinuses [44]. There are particularly extensive venous sinuses in the posterior falx, [45] a frequent site of high signal on brain scans in asphyxiated infants. Bleeding into the falx is well recognized in asphyxiated infants [46]. It has long been acknowledged that optic nerve sheath hemorrhage arises from the dura [47] and more recently the dura was proposed as the source of intracranial SDH in infants [48] (Figure 5)


(Figure 5) (a) The dura is thickened and congested and there is patchy subarachnoid and subdural blood. Autopsy 44 h
after collapse following choking episode. (Courtesy of Dr I. Sheimberg.) (b) H & E stained section of falx showing it to
be destroyed by massive acute bleeding

Careful microscopic examination of the dura confirms that intradural bleeding is common in asphyxiated infants, particularly in the dural folds of the falx and tentorium close to the large venous sinuses [49]. In some cases intradural bleeding leaks out on to the subdural surface leading to macroscopically evident subdural haematoma [50]
Healing Subdural Membranes
Healing of SDH is by formation of a thin, vascular membrane consisting of fibroblasts, macrophages, which often contain altered blood products, and wide thin-walled capillaries with a potential to rebleed [51] (Figure 6).

Figure 6 (a) Dural surface showing a very thin yellow-brown
membrane, which has partly lifted during removal of the
brain. Head injury four weeks prior to death. (b) H & E
stained section of acute bleed overlying a chronic membrane,
which consists of some six layers of fibroblasts between
which are macrophages and new capillaries (three days after
collapse with acute SDH) (c) Same section stained with CD34
to show endothelial cells. Note capillaries growing into the
fresh clot


It is uncommon in infants to see a double layered membrane around a localized mass f resolving clot, as seen in the elderly, probably because the infant SDH usually forms as a thin film rather than as a mass lesion. Contrast injection is required to identify the membranes radiologically [52]. In some cases, acute SDH leads to accumulation of fluid in the subdural space. The reasons for this are unknown. Fluid collections may result from immaturity of the arachnoid granulations and impaired cerebrospinal fluid (CSF) absorption [22],
and be influenced by the method of treatment of the acute hematoma. Surgical evacuation or tapping may prevent later reaccumulation of fluid [53, 54]. The period of time for redevelopment of subdural fluid collections may be long, between 15 and 111 days [55]. It is likely that an important contribution to chronic subdural fluid accumulation is repeated rebleeding and oozing from a chronic subdural membrane [56, 57]. There is little information regarding the potential for birth-related SDH to evolve into chronic fluid collections. Whitby followed nine cases with a repeat scan at one month; none had developed a chronic collection [35]. Rooks followed 18 cases for up to 3 months, one developed a further subdural bleed [34]. However these studies could not identify membranes as contrast was not used. Chronic membranes have been seen at autopsy in up to 31% of infants dying unexpectedly without previous clinical evidence of chronic SDH [58]. In view of the potential for acute accidental SDH to evolve into a chronic collection several months later [55], it would appear likely that the same pattern would follow birth-related SDH. At this time, we simply have insufficient information

Distribution. In the first few days after bleeding, subdural blood sediments under the influence of gravity and undergoes secondary redistribution to the most dependent part, the posterior falx and tentorium [59]. Radiological studies show that subdural blood tracks down around the spinal cord [60] and, if the spine of babies with intracranial SDH is examined at autopsy, blood is regularly seen in the subdural space and around sacral nerve roots in the most dependent parts of the dural sac (Figure 7).























(Figure 7) (a) A collection of fresh subdural blood at the dorsal aspect of the sacral spinal cord. Baby died within hours of inflicted abdominal injury with acute and chronic subdural hemorrhage. (b) Microscope section showing an elliptical collection of fresh blood dorsal to the spinal cord. The blood is within a chronic subdural membrane indicated by the iron pigment, stained here by Perl’s stain. Baby died three weeks after traumatic subdural hemorrhage

Differential Diagnosis of SBS

The most common causes of the triad are impact, birth-related SDH, BEECS, coagulopathies, apnoea, asphyxia and choking, acute life-threatening events  (ALTEs), osteogenesis imperfecta, osteopenia of prematurity, and metabolic diseases [14, 28, 61, 62, 63].


In a considerable number of cases, vomiting and/or reflux are described at the time of collapse, and in some there is a history of feeding difficulties, gastroesophageal reflux, and choking or apnoeic episodes [14, 62]. SBS is commonly diagnosed in the first three months of life, the age of peak incidence of sudden infant death syndrome. Inhalation of feed or vomit may play a part in sudden infant death [64] and awake apnoea is associated with gastroesophageal reflux [65]. The physiological response to aspiration may be dramatic; foreign material on the larynx causes laryngospasm, which is associated with startle, cessation of respiration, hypoxaemia, bradycardia,
and a doubling of blood flow to the brain [66].

These circumstances, with or even without vigorous resuscitation, may cause reperfusion injury and a preexisting healing subdural membrane may bleed. The dura itself may become hemorrhagic and ooze blood into the subdural space (Figure 8).

(Figure 8) (a) Cortical vein thrombosis. Infant died 10 days after collapse following two choking episodes. Several surface veins are thrombosed (arrows). (b) Section of thrombosed vein shows a network of new capillaries growing into the periphery of the thrombus (CD31)









As long ago as 1905,Cushing suggested that coughing, choking, and venous congestion may explain some forms of infant SDH [39], a hypothesis recently revived by Geddes, [48, 67] 


Biomechanics is the application of principles of physics to biological systems and has been the mainstay of research into motor vehicle safety for six
decades. It was just such research into noncontact head injury from rear-end shunts that stimulated Guthkelch to formulate his hypothesis for SBS in
1971 [6]. Ommaya [7] had caused concussion, SDH, and white matter shearing injury (diffuse axonal injury) in primates by whiplash. Guthkelch suggested
that the rotational forces of shaking would cause tearing of bridging veins and bilateral subdural bleeding, although Ommaya himself warned that “It is
improbable that the high speed and severity of the single whiplash produced in our animal model could be achieved by a single manual shake or even a short series of manual shaking of an infant in one episode” More recent studies using “crash test dummies” indicate that impact generates far more force than shaking (Figure 9)

(Figure 9) Comparative forces generated by dropping or shaking and slamming a dummy representing a six-month-old infant (C Van Ee, personal communication 2007)

and that impact is required to produce SDH [68]. Cory and Jones [69] generated forces that exceeded the injury threshold for concussion, but not for SDH or axonal injury. Their adult shaker volunteers fatigued after 10 seconds. While they concluded that “It cannot be categorically stated, from a biomechanical perspective, that pure shaking cannot cause fatal head injuries in an infant ”, they noted that in their experiments there were chin and occipital contacts at the extremes of the shaking motion that could have caused impact. These authors expressed their concerns regarding the difficulties in extrapolating to human infants the findings in both dummy and animal models. Biomechanical studies have shown that falls and impact to the head produce significant rotational forces when the impacting forces are not aligned through the center of gravity of the head, due to hinging of the head on the neck. Shaking is not necessary to cause rotational acceleration.

Neck injuries may be underreported in babies dying after severe abuse [70]. In Ommaya’s study, 11 of 19 primates had neck injuries; these were adult animals with mature neck structure and musculature. It is likely that the forces required to cause intracranial injury will also damage the weak infant neck [71]. In road traffic accidents, infants who suffer single severe hyperextension forces have cervical fractures, dislocations, spinal cord injury, and torn nerve roots, not SDH [72–74].


Investigation of Shaken Baby Syndrome

SBS or NAHI is most likely to occur in an infant dying suddenly under the age of six months. Autopsy should be performed with careful consideration of
this diagnosis and appropriate steps taken to support or exclude it. The records of pregnancy and delivery must be carefully studied to look for any evidence of complications that could mimic NAHI. These include pregnancy disorders such as oligohydramnios, fetal hypokinesia, and prematurity, which lead to osteopenia and predispose to fractures. The birth history and method of delivery are important as SDH may arise at this time while being entirely asymptomatic in the neonatal period. Head circumference charts are important; head circumference measurements taken at birth and in the subsequent weeks may reflect abnormal head growth, which can indicate an accumulating subdural fluid collection and a propensity to rebleed.

The clinical history may give clues to other problems in the early weeks of life. Vomiting, feeding problems, and apnoeic episodes and ALTEs may
indicate difficulties with coordination of breathing, sucking and swallowing, and vulnerability to choking. Any event that threatens life may also potentially
end it. The history of the baby’s terminal collapse must also be carefully examined. Parents may describe events that reveal a cause for collapse. In any other field of medicine, the clinical history is regarded as the cornerstone of diagnosis and it should not be disregarded without serious critical evaluation.

The autopsy can reveal evidence of trauma such as deep bruises and fractures not seen in clinical examination. The examination of the intracranial
contents is paramount. The scalp and skull require careful examination for evidence of bruising and fractures. Suture separation due to raised intracranial
pressure and wormian bones can be mistaken for fractures. When the cranium is opened, the presence of any intracranial bleeding must be noted. Unclotted blood may escape from the subdural space as the skull is opened and be mistaken for bleeding from the dural sinuses. It is important to note the volume and nature of blood and the presence of xanthochromia, indicating older bleeding. As the cranium is opened, the bridging veins should be visualized and their integrity assessed. If there is a question of bridging vein rupture, histological examination may assist in establishing this. The dural sinuses and draining veins should be examined for evidence of thrombosis. The dura must be carefully examined for evidence of older bleeding. A chronic subdural membrane may be thin and patchy and represented only by patches of light brown discoloration. Multiple samples should be taken from the dura, including the falx and tentorium, for histological examination to look for evidence of intradural bleeding and rupture onto the subdural surface. This may be the source of significant subdural blood. The brain must be fixed for detailed histological examination.

In all of these cases, the time between collapse and death may play a significant part in the final pathology. A baby who has collapsed and becomes
apnoeic with subsequent cardiopulmonary rescuscitation (CPR) and ventilation will be shocked and suffer multiorgan failure with altered clotting, loss
of integrity of vessels and membranes, oozing of blood into intracranial compartments, including the subarachnoid and subdural spaces, and development
of the “respirator brain”. Review of the brain imaging in life is essential in assessing, as far as possible, just how much hemorrhage occurred at the time of collapse and how much may be the result of subsequent secondary changes. It is recognized that SDH may continue to bleed after initial onset [75] especially if a baby is very sick. Finding a large clot at autopsy may suggest traumatic rupture of a large vessel, but comparison with early brain scans may indicate that the bleed was only minor at the outset, indicating a slower oozing process with different implications for causation. It
is becoming increasingly obvious that not all SDH arises from traumatic rupture of blood vessels.


I would like to thank Dr Irene Scheimberg and Dr Pat Lantz for providing pictures and Dr Chris Van Ee for valuable discussion and for preparing
Figure 8.


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Dr. Waney Squier is a neuropathologist at the John Radcliffe Hospital and clinical lecturer for the University of Oxford. For over 25 years, she has studied the developing human brain and damage which may occur during pregnancy, birth and the first years of life. She believed in 'shaken baby syndrome' until 10 years ago, when new research led her to question the dogma.

2.) Dr. Waney Squier's Curriculum Vitae as follows--this information was taken from a legal case where Dr. Squier testified as an expert witness. It was put online as a scanned document, and most of the pages were scanned crooked, which couldn't be corrected:



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