Problems and Challenges with Inflicted Trauma at the Extremes of Life
Moderators: Gregory G. Davis and Roger W. Byard
Section 2 -
Shaken Baby Syndrome - Evidence For and Against
Henry F. Krous
Children's Hospital-San Diego
University of California, San Diego School of Medicine
San Diego SIDS/SUDC Research Project
Despite this abundance of observational and experimental evidence about shaken baby syndrome (SBS),
unresolved controversies, both in the scientific literature as well as in the prosecution of alleged
perpetrators, persist and have been the subject of several reviews.
the term "whiplash shaken baby syndrome" to describe a constellation of findings in infants that included
subdural and subarachnoid hemorrhages, metaphsyeal fractures, and retinal hemorrhages; further he
proposed that consequences to survivors might include cerebral palsy, developmental delay, and epilepsy.
Based on research of Ommaya and colleagues,
Guthkelch suggested that
repeated acceleration and deceleration rather than direct impact was the cause of the intracranial
hemorrhages.  To date, greater than 280 citations about SBS appear in PubMed searches.
Controversies addressed herein are:
- Is SBS better referred to as inflicted traumatic head
injury (ITHI) or abusive head trauma (AHT)?
- Is SBS a diagnosable entity?
- Can violent shaking without impact cause the pathology
associated with SBS?
Is SBS Better Identified As Inflicted Traumatic Head Injury or Abusive Head Trauma?
There is increasingly widespread agreement that SBS is better referred to as "inflicted traumatic
head injury" (ITHI) or "abusive head trauma" (AHT) since it moves the focus towards the cause and manner
of death, and away from controversies, that although scientifically relevant, obfuscate criminal
prosecutions.  Paradigms supporting this approach can facilitate appropriate analyses of
individual cases. 
Presently, there is widespread consensus that the following injuries are associated with rotational
acceleration and deceleration: concussion, tearing of bridging veins with subdural and subarachnoid
hemorrhage, interhemispheric subdural hemorrhage, gliding contusions and lacerations at the gray-white
interface, traumatic axonal injury, corpus callosum and cerebellar peduncle white matter tearing,
craniocervical injury, and diffuse retinal hemorrhages. Hypoxic-ischemia and reperfusion produces
secondary cerebral edema progressing to herniation, hypotension, and seizures.
Is SBS A Diagnosable Entity?
Similar to Caffey's original description,
SBS continues to be generally recognized by
the presence of intracranial and retinal hemorrhages and acute encephalopathy that
are not explained by the history.  Other injuries commonly associated with SBS,
including to the neck, spinal cord, skeleton, and soft tissues, may also be seen. Infants are the most
common victims of SBS. Given the repetition of the injuries and supportive data, the answer is yes.
Can Violent Shaking Alone Cause The Pathology Associated With SBS?
Confessions by perpetrators are the first line of evidence suggesting that shaking without impact can
cause the intracranial injuries associated with SBS.
Skull or scalp injuries were
identified in only 12% (4/32) of cases with perpetrators admitting to only shaking. 
Symptoms appeared immediately after the abuse in 91% of the cases. Minns reported a 4-month-old infant
who presented with clinical features of SBS.  Shortly after admission, the perpetrator
admitted shaking the infant angrily "in the air". MRI imaging studies of infants with SBS provide
evidence that shaking only can produce SDH, cerebral contusion, lacerations, and gray-white interface
The second line of evidence rests upon the head and neck anatomy unique to the infant. The large
head accounts for 10% of infant body weight compared to 2% in the adult. The weak neck muscles give the
infant little control over its head movement thereby allowing it to whiplash with each shake. The large
extracerebral space is up to 1 cm in depth perhaps predisposing the bridging veins to tearing and
subsequent SDH. The laxity of the falx and tentorium of the infant suggests less tethering of the brain
allowing it greater movement within the skull. And, the differences in the specific gravity of the gray
and white are larger as a result of less myelin, more water, and a cortex fully populated with neurons.
Thus greater differences between inertia and tangential accelerations at different radial positions in
the gray and white matter predispose to shearing injuries.
The adult primate experiments of Ommaya et al
and Gennarelli and Thibault
 documented that rotational acceleration/deceleration alone can cause concussion, and brain
and upper cord hemorrhage and contusions. Raghupathi, et al subjected 3-5-day-old piglet to rapid,
inertial (nonimpact) rotation of the head about its axial plane sustained immediate coma, and postmortem
findings of SAH and traumatic axonal injury in central and peripheral white matter tracts in the frontal
and temporal lobes and in the midbrain.  Subsequently, Raghupathi et al demonstrated graded
traumatic axonal injury responses of the brain of 3-5-day-old piglets subjected to a single or double,
rapid, non-impact, axial head rotations. 
Using the biomechanical model of a one-month old baby designed and tested by Duhaime and co-workers
in 1987, Cory et al found that combining changes in certain parameters that would lead to increased
angular head acceleration with maximal physical shaking could cause angular head acceleration spanning
two scaled tolerance limits for concussion.  These changes exceeded the original 1987
results suggesting those earlier measured tolerance limits may not be reliable; they therefore concluded
"there must now be sufficient doubt in the reliability of the Duhaime et al. (1987) biomechanical study
to warrant the exclusion of such testimony in cases of suspected shaken baby syndrome.
In Gennarelli and Thibault's study,  single acceleration/deceleration pulses were applied to
securely-fitted Rhesus monkey heads which rotated through a 600 arc for times varying from 5
to 25 msec with G forces ranging between 100 and 3000. Bilateral acute subdural hemorrhage from torn
parasaggital bridging veins caused death in 37 of 128 animals.
In his PhD thesis, Morison, the first to use a three dimensional model that accurately represented CSF
(protective against translation brain acceleration but lubricates rotation), demonstrated that the
combined effect of buoyancy and acceleration resulted in a reduction in the relative translational brain
acceleration to only 0.22% of that applied to the skull, 
(cited by Minns )
thereby accounting for the low likelihood of severe brain injury following translational and inertial
acceleration impacts. The rotational component of shaking accounts for approximately 93% of the bridging
vein strain. This model also demonstrated that the maximum bridging vein stretch ratio is very sensitive
to shaking frequency, especially at frequencies between 2-5 Hz; small increases in shaking
frequency will result in a disproportionate increase in this ratio increasing the likelihood
of tearing and SDH. The ultimate stretch ratio of the bridging veins is 1.5 although some veins may tear
at ratios as little as 1.15. Since shaking at a frequency of 4 Hz and amplitude of ± 600 can
produce a stretch ratio of approximately 1.26, this model shows that manual shaking places an infant at
high risk for SDH.
Evidence Against SBS
In his report of 54 cases in which someone admitted to have shaken an injured infant, Leestma
concluded that valid statistical analyses were not possible and many of the commonly stated aspects of
SBS could not be supported.  However, it should be noted that his manner of case selection
artificially limited the sample size thereby limiting the power for statistics.  Detailed
case studies are generally published early after recognition of a new disease or pattern of injury in
contrast to subsequent papers that present case series, with analysis of case characteristics.
Therefore, by restricting his review to published case histories, Leestma eliminated from consideration
two published studies in which perpetrators admitted that they inflicted head trauma.
In the more recent of these two articles,  69 perpetrators gave enough information to discern
reported mechanism of injury; 32 admitted shaking alone.  Of these 32 cases, 28 (88%)
showed neither skull fracture nor scalp injury. These 28 cases would have markedly increased the
statistical power of Leestma's sample, and led to a very different conclusion. Importantly, among the
cases which Leestma did review, 18 were fatalities with presentation of both clinical and pathological
findings. Analysis of these 18 cases in which data was provided, abnormal mental status (17/17),
seizures (6/7), SDH (16/16), retinal hemorrhages (14/14), subarachnoid hemorrhage (9/9), cerebral edema
(7/7), and respiratory status (8/8) were reported.  Thus, his series actually supports
"many of the commonly stated aspects" of SBS.
Bandak compared results of head rotational velocity and acceleration derived from his biomechanical
experiments on the structural failure limits of the cervical spines of human neonatal cadavers and
several animals with those reported in the SBS literature.  In contrast to levels of head
velocity and acceleration reported in SBS, he calculated that 1. The cervical spine of an infant would
experience forces well beyond its structural failure limits, 2. Shaking should cause injury to the
cervical spine at considerably lower levels, and 3. The magnitude of his calculated forces are
incompatible with the reported rarity of cervical spine injury in SBS.  Margulies and
Prange subsequently repeated his calculations and found that Bandak's results for neck forces for every
single value in his Tables 3 and 4 were actually more than 10 times lower
than stated; therefore, they concluded that severe shaking can cause neck injury. 
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