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Innocent Till Proven Guilty


Medical evidence grossly neglected during a court case and conviction of a father for allegedly murdering his four month old infant, Amanda, is presented. A reasonable forensic investigation evidenced multiple risk factors for fetal brain hemorrhage from birth trauma. These factors could have sourced the material finding of hemosiderin-laden macrophages found in brain stroma at autopsy. These risk factors included a primiparous mother with slight body frame, pitocin-assisted labor that likely prolonged labor contractions, and an unusually large fetal head of 95 percentile resulting in fetal-pelvic dysproportion and likely cranial stress and strain during birth.

Both father and his sister had Moyamoya disease, a poorly understood occlusive disease involving large intracranial arteries occurring mainly in Asian children and young adults. The father probably was experiencing transient ischemic attacks (TIAs) on the day of Amanda’s fatal injury. The father testified that he accidentally dropped Amanda approximately four and a half feet with her hitting head-first onto a thinly carpeted concrete floor; with a lethal minor fall (LMF) being the cause of death rather than inflicted child abuse.

The “healing rib fractures” demonstrated on X-rays during terminal hospitalization probably occurred from birth trauma. The mother had virtually no sunshine exposure during her pregnancy, her consumption of vitamin D-containing foods was negligible, and prenatal vitamins were taken irregularly. Consequently the fetus was likely born with congenital rickets as a contributory source of the fractures.

Reflux problems almost certainly perpetuated multiple nutrient deficiencies, including vitamin D. Skull fractures may have originated at birth but also extended by the fatal fall.
This study is provided in the hope that future cases of this nature may be more thoroughly examined in service of justice.

“Innocent till proven guilty”?


Harold E. Buttram and Alan Yurko


This is a case study in which “shaken infant syndrome” (SIS) (more commonly referred to as “shaken baby syndrome,” (SBS), was designated the primary diagnosis and alleged cause of death at the University of Cleveland Hospitals. Alternatively, the autopsy report cited “blunt impact to the head – homicide” as cause of death. Thus, in advancing a legal defense, it is first necessary to dismiss the diagnosis of SBS, while at the same time show the potential lethality of accidental minor falls, (LMF).

Background: Origin of “Shaken Baby Syndrome” (SBS)

Working with the U.S. Department of Transportation, an Oxford-trained neurosurgeon, AK Ommaya devised an experiment to measure the amount of rotational acceleration required to reach the threshold of brain injury with adult Rhesus monkeys as subjects. As reviewed by R Uscinski:

“A contoured fiberglass chair was built, mounted on wheels, and placed on tracks with a piston behind it. The monkeys were strapped into the chair with their heads free to rotate in such a way that there would be no impact. The piston then impacted the chair, simulating a rear-end motor vehicle collision. The experiment was photographed with a high-speed camera, allowing calculations of generated rotational accelerations. Ommaya was able to demonstrate that a rotational acceleration of 40,000 radians/second (squared) was sufficient to produce intracranial injury in 19 of the animals, with 11 of them also demonstrating neck injuries. Then, using the scaling parameters, he estimated that less rotational acceleration would be required to produce concussion in the larger human brain, perhaps on the order of 6,000 to 7,000 radians/second (squared),”(1)

Calculations were based on the same laws as described in classical Newtonian physics, as applied to movements of planetary bodies, that force is the product of mass and acceleration.
Ommaya’s experiments were published in the Journal of the American Medical Association in 1968.(2) In 1971 Guthkelch reported on the first diagnosed case of SBS in which he hypothesized that subdural hematomas could be caused by manually shaking an infant without the head impacting on any surface.(3) One year later Caffey alluded to the parent-infant stress syndrome, with manual shaking causing intracranial injury in the form of subdural hematoma and cerebral contusion of infants.(4) Two additional papers published by Caffey over the next two years emphasized shaking as a means of inflicting intracranial bleeding in children.(5,6) It is important to note that each of these four papers referred to Ommaya’s publication of 1968 as justification for this concept.
After publication of these four papers, the term Shaken Baby Syndrome became widely accepted as a clinical diagnosis for inflicted (nonaccidental) head injury in infants in which findings of subdural (brain) hemorrhages and/or retinal hemorrhages became accepted as exclusively diagnostic of SBS in the absence of known major accidental injury and remains so today in hospital emergency rooms.

SBS Theory: Irreconcilable with the Weakness of the Human Infant’s Neck

From its origins, the SBS has been based on the assumption that a parent or caretaker, becoming irritated over a baby’s prolonged fussiness and crying, loses self-control and, grasping the infant by the chest or heels, shakes the infant with such violence that any onlooker would recognize it as excessive and dangerous.
It is true that shaking does sometimes take place, and an infant can collapse and stop breathing as a result, which is a common presentation in these cases.
In cases wherein infants collapse, panicked parents, usually untrained in resuscitation, pick up the infant and (not knowing what else to do) mildly shakes the infant that has just gone into respiratory arrest. However, these instances do not in any sense constitute SBS.
As pointed out in the Uscinski report,(1) the brain and head of an infant is nearly seven times larger and heavier than that of a monkey. In addition, monkeys are known to be incredibly strong, approximately four times stronger than humans. There would be no comparison, therefore, between the neck muscle strength of an adult monkey and that of an infant, barely able to hold up his or her head by age six months. With these facts in mind, these considerations follow:

‘ Most SBS cases in the USA take place during the first six months of life, when there are negligible infant neck muscles. As will be shown further on, the major impact of violent shaking would fall at the junction between the base of the skull and brainstem area and upper cervical spinal cord. In most if not all instances this would result in instant death or cervical spinal cord paralysis (paraplegia).
‘ 11 of the 19 monkeys (over 50 percent) in the Ommaya experiments had neck as well as brain injuries.
‘ Although human brain injuries may occur in rear-end vehicle collisions, whiplash injuries to the neck comprise an overwhelming majority of adult injuries, in which ligaments and muscles are torn, resulting in destabilization of the cervical (neck) vertebral column. Since infants have only rudimentary neck muscles and connective tissues as cushions, the full impact of shaking would fall on the highly vulnerable cervical spinal cord near the base of the brain, which almost certainly would be fatal.
In view of these considerations, one would expect a far greater incidence as well as severity of neck and cervical spinal cord injuries in infants than took place in the monkeys, and yet this type of injury has not been documented in any SBS case to date.

In view of these facts, the Shaken Baby Syndrome theory defies both reason and common observation. It is physiologically impossible. ( Most of the relevant scientific references on this subject can be accessed at www.sbsreferences.com. )
Reflecting these considerations, F.A. Bandak, Ph.D., (a biomechanical research scientist and research professor in the Department of Neurology with the Uniformed Services University of the Health Sciences, U.S.A., and a former director of head injury research at the National Highway Traffic Safety Administration, U.S.A.) wrote in a paper published in 2005:

“Forceful shaking can severely injure or kill an infant. This is because the cervical spine would be severely injured and not because subdural hematomas would be caused by high head rotational accelerations. We have determined that an infant head subjected to the rotational velocity and acceleration called for in the SBS literature, would experience forces on the infant neck far exceeding the limits for structural failure of the cervical spine. Furthermore, shaking cervical spine injury can occur at much lower levels of head velocity and acceleration than those reported for the SBS.(8)

Perhaps the most definitive statements on this issue come from three bioengineers, Chris Van Ee, PhD,(9) Kenneth L Monson, PhD,(10) and Kirk L Thibault, PhD,(11) each of whom offered “Accepted Findings Will Assist Court” documents in defense of a specific Arizona SBS case. As these reports are now within the public domain, they are offered here for educational purposes. Sections are chosen from the Chris Van Ee report as generally consistent with the conclusions of the other two doctors. (These can be found as exhibits 14A, (9) 14B, (10 )and 14C, (11) on www.sbsreferences.com.)

Chris Van Ee, PhD, Subject: Dynamic Biomechanical Findings on Shaken Baby Syndrome (SBS) and Lethal Minor Falls (LMF)

“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 intracerebral trauma.

“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 intracerebral trauma (if SBS were valid, which it is not).

“If a 0- to 2-year-old child accidentally falls from a height of six feet and impacts head-first on a hard surface such as carpeted cement, the sudden impact has the potential to generate sufficient head acceleration to cause fatal intracerebral 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.

“ 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.

“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……” (9)

(Comment: Members of the one and only scientific specialty who, by reasons of their many years of background with the U.S. Highway Department, can be considered experts in the biomechanics of head and neck whiplash injuries, universally reject the shaken baby syndrome. In contrast, their work does confirm the potential lethality of minor falls to infants and children.
The abstracts provided in APPENDIX B provide examples showing that the shaken baby syndrome (SBS) has been discredited, while lethal minor falls (LMF) have been confirmed.)


As noted in the clinical history detailed in APPENDIX A, Amanda’s head injury occurred when the father tripped on a blanket which had dropped to the floor in a bedroom, at which time he was holding Amanda outstretched in his hands, resulting in her being dropped and landing head-first onto a thinly carpeted concrete floor in their home.
As described in some detail by the mother, the father was accustomed to carrying Amanda in this way (holding her outstretched with the palms of his hands). The father being 6 ft and 5 inches in height, and commonly holding Amanda at his mid-chest level, the fall would have been 4 ½ to 4 ¾ feet. For these reasons, it is likely that this unfortunate accident was the source of Amanda’s head injuries as well as the external bruises described clinically following hospitalizations as well as at autopsy.
Also, considering the father’s 2:00 pm phone call to the mother on June 29th, that he had fallen over and destroyed a coffee table, this is an indication that, on the afternoon of June 29th, he was experiencing transient ischemic attacks (TIAs) from Moyamoya disease, resulting in impaired neuromuscular control of which he may not have been aware, and which may have been a major factor in his dropping Amanda later that afternoon.

Clinical Discussion: Moyamoya Disease

As reviewed in Harrison’s Principles of Internal Medicine, 16th Edition, page 2379, under a section entitled “LESS COMMON CAUSES OF STROKE,” Moyamoya disease is discussed as follows:

“Moyamoya disease is a poorly understood occlusive disease involving large intracranial arteries, especially the distal internal carotid artery and the stem of the middle and anterior cerebral arteries. Vascular inflammation is absent. The lenticulostriate arteries develop a rich collateral circulation around the occlusive lesion, which gives the impression of a “puff of smoke” (Moyamoya in Japanese) on conventional x-ray angiography. Other collaterals include transdural anastomoses between the cortical surface branches of the meningeal and scalp arteries. The disease occurs mainly in Asian children or young adults, but the appearance may be identical in adults who have atherosclerosis. The etiology of the childhood form is unkown. Because of the occurrence of intracranial hemorrhage from rupture of the transdural and pial anastomotic channels, anticoagulaton is risky. Breakdown of dilated lenticulostriate arteries may produce parenchymal hemorrhage, and progressive occlusion of large surface arteries can occur, producing large-artery distrubition strokes. Bypass of extracranial carotid arteries to the dura or MCAs may prevent stroke and hemorrhage.”

(COMMENT: Both Amanda’s father and his sister, who are half Japanese, have been diagnosed with Moyamoya disease and therefore susceptible to brain hemorrhage as well transient ischemic attacks, which includes the possibility of transient loss of muscle control. This is corroborated by the father’s medical history of recurrent bouts of ataxia and losses of mental stability. It is plausible that, during the afternoon of June 29th, when the father accidentally stumbled over and destroyed a coffee table around 2:00 pm and a little later dropped Amanda, that he was experiencing transient ischemic attacks from Moyamoya disease.)

The Enigma of the Brain, Cerebellar, and Dural Hemosiderin

Pathology slides from the autopsy revealed hemosiderin-laden macrophages in the lepto meninges of both brain and cerebellum, as well as dural stroma. As reviewed in Forensic Pathology, by Vincent J and Dominick DiMaio, 2001, CRC Press, page 167, brain hemorrhages are divided into acute, subacute, and chronic phases. The acute phases manifest themselves clinically within 72 hours of injury, subacute phase between 3 days and 2-3 weeks, and the chronic phase within 3-4 weeks following the acute hemorrhage. About 3 days following an acute hemorrhage, the red blood cells begin lysing or breaking up, gradually releasing their iron, (which marks the beginning of the subacute phase). The iron in turn is gradually scavenged by macrophage cells and carried out of the clot area in the form of hemosiderin, a process taking place over a period of approximately three weeks, ending in the chronic phase which may persist for prolonged periods of time. What then was the source of the hemosiderin in the present case? For answers, we must return to the prenatal and birth records.
Since the accidental dropping of Amanda had occurred on June 29, 2007 and her being declared dead the next day (June 30), the time was too short for the appearance of hemosiderin-laden cells, which, by definition, would not begin to appear until the commencement of the subacute phase 72 hours following injury. What then was the source?
It will be recalled that the mother’s weight was 118 lbs in an early stage of pregnancy, so that her frame was relatively slight. It was her first pregnancy with an
unstretched uterus, and she was 31 years old. However, an additional risk factor for fetal brain hemorrhage from birth trauma occurred at birth with a “nuchal hand and arm,” which presented with the neck and which likely would have obstructed the head at an earlier state as the head moved down the birth canal. In addition, the head was excessively enlarged with circumference of 36 cm (95 percentile). The combination of the arm presentation with an unusually enlarged (95 percentile) head may well have posed a significant fetal head/maternal pelvic disproportion and a major risk factor for fetal brain hemorrhage, according to standard pediatric texts. For this reason it is a near certainty that birth trauma was the source of original brain hemorrhages, which in turn left residues of hemosiderin demonstrated on pathology slides.

The Rib Fractures

The autopsy report cited healing callus fractures of lateral ribs 3 to 6 on the right and healing callus fractures of lateral ribs 3 to 4 on the left, the timing of which would also be in perfect accord with birth trauma in a 4-month-old baby. (As reviewed in the Forensic Pathology text by Vincent DiMaio and Dominick DiMaio, second edition, 2001, page 115, a callus is usually visible in two weeks following fracture in children. The bone is consolidated in 4 to 6 weeks, though it usually takes 2 to 3 months to heal solidly.)
Following the now-discredited theory of shaken baby syndrome (SBS), the second major area involving charges of inflicted child abuse is that of multiple fractures in infants, while in the view of this observer, findings attributed to inflicted trauma are almost always due to metabolic bone disease. This opinion is based on two highly definable differences between the two. First, with metabolic bone disease bone fractures are rarely separated, misplaced, or misaligned, nor are there internal chest injuries when rib fractures are involved.
This was entirely the case with 30 cases of infants with multiple fractures reviewed previously by the first author, with the exception of one infant with a pleural effusion. With traumatic fractures, in contrast, whether accidental or from inflicted abuse, there is a high percentage of severed, misplaced, and/or misaligned bone fragments. This is especially true for traumatic rib fractures in children which are accompanied by a high percentage of internal chest injuries and significant rate of fatalities. This is reflected in a 1990 study by Garcia who reported on a series of 33 children brought into a trauma treatment center with rib fractures, all brought about by blunt trauma. Nearly 70 percent were from auto accidents, 21.2 from child abuse, and 9.1 percent from falls. 72 percent of the children with three rib fractures had internal chest injuries such as lung punctures or tears and/or injuries to other internal chest organs. With four or more rib fractures there were 100 percent internal chest injuries. Mortality was 42 percent.(12)
A second differential sign is the relative absence of pain in fractures from metabolic bone disease, while traumatic fractures are usually very painful. This difference is explained because metabolic fractures usually involve only the bone which has no pain fibers, while traumatic fractures will almost always involve surrounding connective tissues, which are abundantly supplied with pain fibers. In a majority of cases that I have reviewed, as was true in the present case, there were seldom any office notes indicating signs of discomfort or distress when examined during routine pediatric visits, fractures not being recognized until later when swelling or lack of movement was noted in an arm or leg or from incidental X-rays, as in the present case.
In 2006 a publication appeared in Pediatrics by C. Jenny, Committee on Child Abuse and Neglect, setting standards for evaluating children with multiple fractures. The guidelines listed the following differential diagnosis:(13)

1. Child abuse.
2. Osteogenesis imperfecta.
3. Preterm birth.
4. Rickets (vitamin D deficiency).
5. Osteomyelitis.
6. Copper deficiency.
7. Fractures secondary to demineralization from paralysis.
8. Other rare conditions that mimic child-abuse fractures (including prolonged administration of glucocorticoids, cancer medications, or prostaglandins.)
9. Hypothesized conditions presented in multiple cases referring to the “temporary brittle bone disease.”


Based on a phone consultation with the mother inquiring into her diet and supplements during her pregnancy, with special reference to the nutritional sources of vitamin D as well as exposures to sunshine, she replied that she had very little sunshine exposure during her first trimester due to intractable nausea and vomiting, nor during the second and third trimesters which took place during fall and winter seasons in a northern state. She further that she had taken flintstone vitamins irregularly during her pregnancy and that she drank only skim milk, which would have lacked vitamin D. (Being fat soluble, vitamin D is found only in the cream portion of milk.) She did eat some eggs, but she avoided seafood because of concern about mercury.
For these reasons vitamin D-deficient rickets stands as a the probable source of the multiple fractures, with birth trauma playing a secondary role. This conculsion is further supported by a two-day conference held by the National Institute of Health (14)(October 9-10, 2003) when it was announced that there is a reemergence of vitamin-D deficient rickets and an alarming prevalence of low circulating levels of vitamin D in the USA, leading to an increased incidence of infant fractures, especially when premature.
In a study conducted at the Pittsburgh Graduate School of Public Health, (15)(2007) serum 25-hydroxy vitamin D was measured at 4-21 week gestation and predelivery in 200 white and 200 black pregnant women and in cord blood of their neonates. Over 90 percent of women used prenatal vitamins. Results showed that black and white pregnant women and neonates residing in the northern US are at high risk of vitamin D insufficiency, even when mothers are compliant with prenatal vitamins. Causes of the reemergence include reduction in milk intake, (milk allergies, lactose intolerance, reduction in vitamin D-containing fats, and increased use of sun screens, which prevent sun rays from generating vitamin D precursors from skin oils).
A nutritional rickets has also been described with normal circulating 25-hydroxy vitamin D attributed to dietary calcium deficiency in infants. Elevated parathormone (PTH) levels are generally found in these cases. (16) Amanda’s intractable reflux problems almost certainly would have contributed to calcium deficiency as well of deficiencies in other minerals and vitamins.

A “Yeasty” Baby and Gastroesophageal Reflux

The mother did attempt breast-feedings supplemented with formula but ultimately abandoned breast feedings, primarily because of the infant’s difficulty in sucking. Under normal circumstances, breast-feeding establishes a prevalence of highly beneficial and protective Lactobacillus bifidis in the infant’s intestinal flora, but the mother was administered 2 grams of ampicillin intravenously during her labor with Amanda, which would have largely eliminated the L. bifidis. This in turn would have opened the way for yeast infestations, later manifesting as cradle cap, “yeasty” neck folds, and intestinal yeast overgrowth, the true source of the intractable colic and reflux problems. These in turn in all likelihood would have led to unrecognized nutrient mineral and vitamin deficiencies including calcium, magnesium, zinc, and vitamins A, C, and D.

The Bruising Issues

As noted in the clinical history, there was no record of prophylactic vitamin K administration in Amanda’s hospital newborn records either by mouth or by injection, which is recommended for prevention of Hemorrhagic Disease of the Newborn. Furthermore, Amanda’s intractable reflux problems along with routine vaccines administered on June 19th, known to cause oxidative stresses on the body,(17) might well have brought about an unrecognized terminal clinical scurvy as a contributory source of the bruising noted on the autopsy report.
As reviewed in the clinical history, the examining doctor at the emergency department of Fairview Hospital described only two bruises, an obvious left parietal hematoma and a mild contusion to the right chest. Consequently, the additional bruises on thigh and abdomen described on subsequent admission to University Hospital and at autopsy must have come about at a later time, most likely from CPR attempts.

Summary and Conclusions

As reviewed in some detail above, there are plausible alternate explanations for each and every pathologic autopsy finding in the case of Amanda Sadowsky, other than the hospital and autopsy conclusions of inflicted child abuse. Almost certainly the fatal brain damage resulted from an accidental lethal minor fall. Almost certainly the rib fractures and residual brain, cerebellar, and dural hemosiderin were the results of birth trauma in combination with congenital rickets from vitamin D deficiency. The skull fractures could have also originated from birth trauma and reinjured or expanded from the accidental fall. None of these possibilities were mentioned in the hospital records nor in the autopsy report.
If there is still any validity in the time-honored principle of “considered innocent until proven guilty,” the gross deficiencies in establishing a differential diagnosis of other possible sources for the findings, as listed above, in both the hospital and autopsy reports, should more than vindicate the father of intentionally injuring his daughter.


(1) Uscinski R. The Shaken Baby Syndrome. J Amer Phys Surg, Fall, 2004; 9(3):76-77.
(2) Ommaya AK. Whiplash injury and brain damage. JAMA, 1968; 204:75-79.
(3) Guthkelch A. Infantile subdural haematoma and its relationship to whiplash injuries. BMJ, 19712(759):430-431.
(4) Caffey J. The parent-infant traumatic stress syndrome. Am J Roentgen, 1972;114:217-228.
(5) Caffey J. On the theory and practice of shaking infants. Am J Dis Child, 1972; 24:161-169.
(6) Caffey J. The whiplash shaken infant syndrome: Manual shaking by the extremities with whiplash-induced intracranial and intraocular pleadings, link with residual permanent brain damage and mental retardation. Pediatrics, 1974; 54:396-403.
(7) As “Shepardized” from 3001131 via Lexus and Westlaw.
(8) Bandak FA. Shaken Baby Syndrome: A biomechanics analysis of injury mechanisms, Forensic Science Intern, June 30, 2005; 151(1):71-79.
(9) See Exhibit 14A, accessible on www.sbsreferences.com
(10) See Exhibit 14B, accessible on www.sbsreferences.com.
(11) See Exhibit 14C, accessible on www.sbsreferences.com.
. Bone, 2003; 33:466-474.
(12) Garcia, V., Gotschall, C., Eichelberger, M., Bowman, L. Rib fractures in children: a marker of severe trauma, Journal of Trauma. 1990; 30(6):695-700.
(13) Jenny, C, Committee on Child Abuse and Neglect, Evaaluating infants and young children with multiple fractures, Pediatrics, 2006; 118(3): 1299-1303.
(14) National Institute of Health (NIH) conference on vitamin D, October 9-10,2003. http://www.nichd.nih.gov/about/meetings/2003/prip_vitd.cfm
(15) Bodnar, LM, Simhan, HN, Powers, RW et al, High prevalence of vitamin D insufficiency in black and white pregnant women residing in the Northern United States and their neonates. Journal of Nutrition, 2007; 137: 447-452.
(16) DeLucia, M.C., Mitnick, M.E., and Thomas O Carpenter. Journal of Clinical Endocrinology and Metabolism. Nutritional rickets with normal circulating 25-hydroxyvitamin D: A call for reexamining the role of dietary calcium intake in North American infants. Journal of Clinical Endocrinology and Metabolism; 2003; 88(8):3539-3545.
Blaylock, R.L., The danger of excessive vaccination during brain development:
The case for a link to autism spectrum disorder, Medical Veritas, 2008; 5(1): 1727-1741.


Summary Review of Maternal Prenatal Timeline of Events and Observations

6-19-06: Pregnancy confirmed.
6-26-06: 1st OB/GYN – certified midwife appt.
7-18-06 to 8-03-06: recurrent vomiting, requiring IV fluids on 8-03-06.
9-11-06: Weight 118 lbs.
9-26-06: Doubled over with pain in right lower abdomen.
10-07-06: Another cold, which she had been fighting for 4 weeks.
11-06-06: Weight 130 lbs.
11-08-06: Called off work: sick.
11-17-06: Sharp pains in right abdomen.
1-02-07: Weight 145 lbs.
2-12-07: Membranes stripped; felt feverish afterwards.
2-15-07: Membranes ruptured spontaneously.

By phone consultation the mother reported that she had intractable nausea and vomiting during her first trimester, losing 10 pounds, but subsequently gaining 40 pounds.

Hospital Labor, Delivery, and Newborn Records, Southwest General Hospital.

This was the mother’s first pregnancy, with birth at 40.2 weeks gestation. She was 31 years old. Her blood type was O positive. Duration of labor was recorded as 9 hours and 5 minutes.
According to hospital records, an uncomplicated delivery was accomplished with pitocin-drip-augmentation and epidural anesthesia. The mother was also given 2 grams of intravenous ampicillin. Birth took place with nuchal arm presentation (arm came out with the neck). By phone consultation, the mother reported that she had a peritoneal “ripping” as the baby’s head was delivered in spite of preceding episiotomy.
The baby’s weight was 7 lbs and 10 ozs (75 percentile), length 51.0 cm (75 percentile), head circumference 36.0 cm (95 percentile). APGARS were 9/9. Newborn P.E. was normal.
Hepatitis B vaccine was administered on day-of-birth. (NOTE: On the next day, Feb. 17th, according to mother’s notes, Amanda was brought in to her from the nursery screaming, as “she was bothering the other babies in the nursery,” suggestive of an encephalalitic reaction to the hepatitis B vaccine, something rarely recognized for its true nature. There was no note of vitamin K administration in the records.)
Routine newborn screening blood tests were acceptable, as were CBCs. Bilirubin levels reached a peak of 13.95 on February 18th and dropped to 12.18 on the 19th. On
2-18-07 Amanda was placed under a “heat lamp” according to mother’s notes (This was likely phototherapy).
Hearing test was “nonpass” for the right ear on initial testing but was “pass” with repeat testing.
The baby was placed on combination of breast and formula feedings. At times mother had to pump her milk, as the baby was having difficulty in sucking, (a problem which continued following hospital discharge).
Amanda was discharged with her mother on 02-19-07.

Pediatric Outpatient Visits, Westshore Primary Care Associates

2-21-07: Wt 7 lbs and ½ oz. Follow up appointment for jaundice. Baby described as active and alert. Bilirubin 11.2 with direct of 2.0.
2-28-07: Jaundice had cleared.
3-2-07: (Two weeks well-baby visit.):Weight 7 lbs, 13 ozs, length 20.5 inches, head circumference 14.5 inches (85 to 90 percentile). Notes describe “loud breathing at night.” Exam unremarkable.
3-14-07: Amanda threw up several times during the night.
3-15-07: Amanda seen by pediatrician, Dr. Sanderson. Wt 9 lbs. Exam negative. Throwing up attributed to reflux (GERD). Pepcid RX ordered.
3-19-07: Mother described “cradle cap.”
3-20-07: Stopped breast feeding.
3-23-07: Cradle cap treated with topical hydrocortisone.
3-26-07: Seen by Dr. Sanderson for constipation. Wt 9 lbs and 15 oz. Small anal lesion noted from previous hard stool. Amanda had been 3 days without a stool. Per advice of pediatrician, formula was mixed with pear juice.
3-30-07: Coconut oil applied to head for cradle cap.
4-17-07: Two-month well baby check. Weight 10 lbs 6.5 oz, length 22.5 inches, head circumference 39 cm (< 85 percentile). Pepcid prescription DCd.
4-17-07: 8-wk/4d well baby visit: Wt 10 lb, 6.5 oz, length 22 ½ in., head circumf. 39 cm. Office note mentioned much less reflux but still occurring 1-2 times a day. Pepcid therapy was resumed. The following vaccines were administered:
DTaP, Aventis Pasteur, lot # C2554AA.
Comvax, Merck, lot # 1415F (Hib and Hep B).
IPV, Aventis Pasteur, lot # 20547.
Rotateq, Merck, lot # 1238F.
PCV7 1, Wyeth/Lederle, lot # B056532 (pneumoccoal vaccine)
4-18-07: According to mother’s notes, baby had fever that night – also developed gas pains with diarrhea.
4-19-07: Amanda had screaming and crying fits with gassiness and diarrhea, the screaming recurred over the next several days.
5-10-07: Yeasty neck folds described by mother.
5-14-07: placed on Benadryl for facial rash.
5-25-07: Seen by Dr. Sanderson. Wt 12 lbs, 6 oz. Screaming fits attributed to reflux. Pepcid increased to 0.4 cc twice daily.
6-19-07: 17 wk/4d well baby appt: Wt 13 lbs, 13 oz, length 24 in., H.C. 40.5 cm.
the following vaccines were administered:

DTaP, Aventis Pasteur, lot # C2605AA.
Comvax, Merck, lot # 1244F, (Hib and Hep B).
IPV, Aventis Pasteur, lot # 20872.
Rotateq, Merck, lot # 0031?
PCV7 1, Wyeth/Lederle, lot # B086548.

Per my phone call with mother on May 19th, 2009, both father and his sister had been previously diagnosed with Moya Moya disease. (The father and his sister are half Japanese). On the morning of June 29th, 2007, Amanda’s mother and father routinely dressed the baby. She had no bruises or skin blemishes at that time with exception of pre-existing birth mark on top of left shoulder. At 2:00 p.m. the father called with mother, who was at work, saying that he had fallen and broken a coffee table. At 3:15 pm the father called again saying that he had tripped on a blanket that had slid off of the bed in the bedroom and dropped Amanda , that her head was swelling and that she was having trouble breathing. He said that he immediately called 911. On later information, the baby fell head first onto a thin and worn carpet covering a cement floor of the bedroom, which is on the first floor of the building. (The father’s height is 6 ft and 5 inches. He had been holding Amanda with outstretched hands at about lower chest level, an estimated 4 or more foot elevation from the floor.)

(NOTE: As reviewed in the clinical discussion below, Moyamoya disease is a poorly understood occlusive disease involving large intracranial arteries, especially the distal internal carotid artery and the stem of the middle and anterior cerebral arteries. Vascular inflammation is absent. The lenticulostriate arteries develop a rich collateral circulation around the occlusive lesion, which gives the impression of a “puff of smoke” (Moyamoya in Japenese) on conventional x-ray angiography. The disease occurs mainly in Asian children or young adults, but the appearance may be identical in adults who have atherosclerosis. Breakdown of dilated lenticulostriate arteries may produce parenchymal hemorrhage, and progressive occlusion of large surface arteries can occur, producing large-artery distribution strokes.
Based on these descriptions of Moyamoya disease, Amanda’s father may have been experiencing transient ischemic attacks (TIAs) during the series of mishaps that occurred on June 29th, with his stumbling over and destroying a coffee table at 2:00 pm and dropping Amanda a little later (3:15 pm).

Fairview Hospital Emergency Dept, 6-29-07

The following notes were dictated by Emory Patrick, MD:

HISTORY OF PRESENT ILLNESS: This is a 4 month old brought in by EMS after unclear head trauma. The patient was found unresponsive and not breathing. EMS intubated the patient with a 4 ET tube. On arrival, the patient was being bagged by EMS. Good breath sounds were noted bilaterally. Initially it was thought there was no heart rate, but the patient did, in fact, have a heart rate of approx. 130…Subsequent to this, there were decreased breath sounds on the left. It was suspected that the ET tube was in the right main stem bronchus, which was verified on chest film, and the ET tube was immediately pulled back 2 cm with good breath sounds. Pulse oximetry was noted to be 92 and then increasing to 100%.

PHYSICAL EXAMINATION: Significant for an obvious left parietal (scalp) hematoma as well as diffuse right head swelling and a full anterior fontanelle. The rest of the HEENT exam was essentially normal. Pupils were noted to be 8 mm bilaterally and unresponsive. Breath sounds were clear. Normal S1, S2. No murmur. There was a mild contusion noted on the right chest. There were no marks noted on the abdomen, which was soft. There were no obvious injuries to any of the extremities. (NOTE: Physical Examination report at the Emergency Department of Fairfield Hospital described only a left partietal hematoma and mild contusion of the right chest. Additional bruises on thigh and abdomen described on admission to University Hospital and in the autopsy report must have come about at a later time, most likely from subsequent CPR attempts.)

(Repeated) attempts were made to get blood but were unsuccessful. After the patient was stabilized, the patient was brought to head CT, which showed diffuse edema but no focal neurological lesion. Specifically, there was no epidural or subdural hematoma noted on review with the trauma surgeon. The baby was then brought back to the Emergency Dept. Transport was arranged with Rainbow Babies and Children. The neck was stabilized with a collar, and the baby was transported to Rainbow for definitive care.

CT Brain WO Contrast, June 29, 4:27 PM

Bone window images show a fracture line in the calvarium on the left extending from the middle cranial fossa on the left to the parietal region. There is associated soft tissue swelling over the fracture line. An additional fracture is seen extending laterally on the right from the sagittal suture to the parietal region. The fractures do not appear to be depressed. Soft tissue swelling is also noted over the fractures on the right.

There is a low density area in the left posterior parietal region measuring 1.7 X 1.4 cm. There is no evidence of mass effect. This may represent an area of remote infarct.

There is linear increased density adjacent to the falx anteriorly, and there is increased density in the posterior aspect of the occipital horns. In addition, there is an area of subtle increased density in the left parietal lobe. The findings indicate both extra axial bleeding anteriorly, as well as interventricular blood and an area of parenchymal hemorrhage. There is no epidural or subdural hematoma adjacent to the bilateral skull fracture lines.


1. Bilateral temporoparietal and right occipital skull fractures.
2. Hemorrhage is seen adjacent to the falx, in the dependent portions of the occipital horns, and in a subtle area of parenchymal hemorrhage in the left parietal lobe.
3. There is an area of decreased attenuation in the left posterior parietal region compatible with a remote injury and focal encephalomalacia.

University Hospitals of Cleveland, Admission June 29 to 30, 2007 (expired)

Discharge summary dictated by Paul G. Smith, D.O:

Date of death, June 30, 2007.
FINAL DIAGNOSIS: Full arrest, non-accidental head trauma.
This is a 4-month-old infant who was brought in by helicopter from Fairview Hospital where she presented in full arrest. There she was resuscitated with mechanical intubation and started on a dopamine drip. She had a CT at that time that showed intracranial pathology. She was also thought to have a fracture of the fifth and sixth vertebral column by that report. Upon arrival to Rainbow Hospital she had a very poor perfusion and low heart rate despite being maintained on dopamine drip. Her pupils were fixed and dilated bilaterally, and she had negative signs of any cranial nerve activity throughout the several hours that she was in the pediatric intensive care unit. She had continued deterioration. She had an ophthalmologic examination that showed bilateral retinal hemorrhages and obvious bruising of the frontal chest. The fellow that was on that night discussed these findings with the mother and expressed concern that she would not survive through the night when she continued to have deterioration of her vital signs. The mother opted for “do not resuscitation status,” with which the intensive care unit physicians agreed. The patient expired on the above date (June 30).”

CT scan of abdomen and pelvis showed no abnormalities.

CT of cervical spine with reconstructions:

“Showed transverse lucencies on the right knee. Antero-lateral mass of c (cervical) 5, and on the left in the anteromedial mass of c (cervical) 6 suggests possible minimally displaced acute fractures. No subluxation is evident.”

Head CT:

“Scalp hematomas are evident and the largest is in the right apex.
Right frontal and bilateral parietal fractures are present. The right frontal parietal fracture is depressed by less than 5 mm. There are scattered parenchymal hyperdensities in bifrontal apex. There is a larger area of hyperdensity in the left parietal region. There is interventricular hemorrhage in the atria bilaterally. Extra axial hyperdensity is seen in a thin layer in the right frontal distribution. Hperdensity is also demonstrated in the anterior interhemispheric fissure.
There is diffuse loss of gray-white differentiation, and there is diffuse sulcal effacement. Basal cisterns are not evident. The third and fourth ventricles are not well demonstrated.
Multiple skull fractures. Bilateral cephalhematoma. intraparenchymal, subdural, subarachnoid, and intraventricular hemorrhage.
Diffuse loss of sulci and cisterns as well as gray-white differentiation consistent with global edema. Downward herniation cannot be excluded.”

Portable AP chest: interpreted as normal with normal-appearing bones.

Portable AP abdomen: normal.

“Admitting Diagnosis: SHAKEN INFANT SYNDROME
Other diagnosis: FX C5 VERTEBRA, CLOSED
Other Diag. OTHER FALL

Heart Donor Resection, 7-1-07.

Heart: 38 gram heart with vascular congestion and biventricular mural thrombi, atrial septal defect.

Autopsy, performed on July 1, 2007 by Coroner of Cuyahoga Country, Elizabeth K. Balraj, MD:

“The following is the report of autopsy to the best of my knowledge and belief. This person was a female, single, aged 4 months 14 days of the Causasian race with medium complexion, had brown eyes, brown hair, absent teeth, was 25 inches in height, weighing 17 pounds, a native of Middleburg Heights, Ohio with an occupation of infant.

“Marks and Wounds:

“Contusions of face, right thorax, left shoulder, and left arm.
Contusions of right thorax
Abrasions of abdomen.
Evidence of recent therapy.

Anatomic Diagnoses

1. Blunt impacts to head
A. Contusion of right submandibular face.
B. Contusions (two) of right and left scalp.
C. Fractures (three) of parietal bones and occipital bone.
D. Epidural and subdural hematomas with extensions along cervical and thoracic spinal cord.
E. Cerebral and cerebellar subarachnoid hemorrhages.
F. Intraventricular hemorrhages.
G. Lacerated contusion of the left parieto-occipital cerebrum, right occipital cerebrum, and right cerebellum.
H. Diffuse cerebral edema.
I. Bilateral retinal hemorrhages.
II. Remote blunt impact to head.
A. Remote subdural hemorrhage.
B. Remote left parietal and left occipital cerebral contusion.
III. Blunt impact to neck, trunk, and left upper extremity.
A. Abrasions of anterolateral left abdomen.
B. Cutaneous contusions of right thorax, left shoulder, and left upper arm.
C. Subcutaneous contusions of cervical and thoracic paraspinal soft tissues.
D. Healing fracture calluses of lateral right third through sixth ribs. and lateral left third and fourth ribs.
E. Pulmonary hemosiderosis.
IV. Therapeutic procedures.
A. Indwelling nasogastric catheter, endotracheal tube, intravascular catheter, and intraosseous catheter.
B. Puncture wounds of extremities.
C. Patient identification bracelet.
D. Postmortem organ donation of heart.

(NOTE: Brain weight was 770 grams, markedly elevated in comparison with normal weight of 595 grams for a 4-month-old-girl. This extreme brain swelling can be attributed to the accidental fall described in the medical history and does not in any way selectively imply inflicted abuse.)

Cause of death: Blunt impacts to head with skull and brain injuries.

(Signed by pathologist, Joseph A. Felo, D.O., and coroner Elizabeth K. Balraj, M.D.)

Toxicology Report: Assays from liver, urine, and vitreous humor were negative for prescription drugs, opiates, cocaine, salicylates, acetaminophen, glucose, ketones, and volatile chemicals.

Laboratory at Bonfils Reports (Denver, Colorado): Hepatitis Bc Ab NONREACTIVE, HIV-1 NONREACTIVE; the remainder of tests were negative for Hepatitis B surface antigen, Hepatitis C, HIV-1/HIV2 antibody, RPR syphilis serology, and


“38 gram heart with vascular congestion and biventricular mural throbi, atrial septal defect..”

Relevant Pathology (Microscopic) Reports

“MUSCULOSKELETAL: Nodular fracture calluses are in the lateral right 3rd through 6th ribs and the lateral left 3rd and 4th ribs. No other fractures or abnormalities are noted.

“HEAD/BRAIN: The frontal scalp shows no evidence of contusions or galeal hemorrhages. The frontal bone is intact and no fractures are palpable with the facial skeleton. The sutures are open and the anterior fontanelle is soft and flat. The dura is smooth and glistening. There is faint golden brown staining of the subdural surface of the left cerebral convexity and the bilateral posterior cranial fossa. A 3 cm X 2.5 cm X 2.5 cm dark brown-dark red concavity is in the parasagittal convexity surface of the left parietal and left occipital cerebrum. The leptomeninges are thin and transparent. The frontal and temporal cerebral hemisphere subarachnoid space does not contain any hemorrhage. The cerebrum presents normal convolutions with diffuse flattening of the gyri and narrowing of the sulci. There is no evidence of subfalcial, uncal, or cerebellar tonsillar herniation present. The major cerebral arteries are normally developed and show no congenital anomalies. The roots of the cranial nerves are unremarkable. No hemorrhages are along the optic nerve sheaths. The brain is fixed in formalin prior to further sectioning. After two days of formalin fixation, serial coronal sections through the cerebral hemispheres show a mostly normal cortical ribbon and underlying white matter. The concave lesion within the left parietal and left occipital cerebrum focally extends to the posterior horn of the left lateral ventricle. The cerebral tissue adjacent to the cerebral hemisphere show a grossly normal cortical ribbon and underlying white matter. The basal ganglia and diencephalons show no gross abnormalities. Serial coronal sections through the brainstem and sagittal sections through the cerebellum show mostly normal cerebral structures. There are focal punctate hemorrhages through the left anterior mid brain. The ventricular system is symmetrical with hemorrhages in the third and fourth ventricles. Serial cross sections through the spinal cord with attached dura show epidural and subdural hemorrhages with no focal lesions within the spinal cord parenchyma.

“DURA: Acute extravasation of blood within dural stroma. Hemosiderin-laden macrophages within dural stroma and within thin fibroblastic subdural membrane.

“BRAIN: Acute extravasation of blood with mild hemosiderin-laden macrophages with cerebral and cerebellar leptomeninges. Irregular cerebral defect with acute hemorrhages on irregular margins and with adjacent neuropil. Organizing cerebral infarction with destruction of cerebral gyrus, acute and organizing hemorrhage with fibrocapillary proliferation and prominent hemosiderin-laden macrophages, and marginal reactive gliosis.

“SPINAL CORD: Acute and early organizing epidural hemorrhage. Acute subdural hemorrhage.”

Eyes: There are no microscopic eye reports.


The Shaken Baby Syndrome: A Clinical, Pathological, and Biomechanical Study.
Duhaime, AC, Gennarelli, TA, Thibault, LE, Margulies, SS et al, Journal of Neurology, 1987; 66:409-415.

Abstract: Because a history of shaking is often lacking in the so-called “shaken baby syndrome,” the diagnosis is usually based on a constellation of clinical and radiographic findings. Forty-eight cases of infants and young children with this diagnosis between 1978 and 1985 at the Children’s Hospital of Philadelphia were reviewed. All patients had a presenting history thought to be suspicious of child abuse, and either retinal hemorrhages with subdural or subarachnoid hemorrhages or a computerized tomography scan showing subdural or subarachnoid hemorrhages with interhemispheric blood. The physical examination and presence of associated trauma were analyzed; autopsy findings for the 13 fatalities were reviewed. All fatal cases had signs of blunt impact to the head, although in more than half of them these findings were noted only at autopsy. All deaths were associated with uncontrollably increased intracranial pressure.
Models of 1-month-old infants with various neck and skull parameters were instrumented with accelerometers and shaken and impacted against padded or unpadded surfaces. Angular accelerations for shakes were smaller than those for impacts by a factor of 50. All shakes fell below injury thresholds established for subhuman primates scaled for the same brain mass, while impacts spanned concussion, subdural hematoma, and diffuse axonal injury ranges. It was concluded that severe head injuries commonly diagnosed as shaking injuries require impact to occur and that shaking alone in an otherwise normal baby is unlikely to cause the shaken baby syndrome.

Anthropomorphic simulations of falls, shakes, and inflicted impacts in infants.
Prange, MT, Coats, B, Duhaime, AC, Margulies, SS. Journal of Neurology, 2003; 99:143-150:

Abstract: Object: Rotational loading conditions have been shown to produce subdural hemorrhage and diffuse axonal injury. No experimental data are available to compare the rotational response of the head of any infant during accidental and inflicted head injuries. The authors sought to compare rotational deceleration sustained by the head among free falls, from different heights onto different surfaces with those sustained during shaking and inflicted impact. Methods: An anthropomorphic surrogate of a 1.5 month-old human infant was constructed and used to simulate falls from 0.3 meter (1 feet), 0.9 m (3 ft), and 1.5 m (5 ft), as well as vigorous shaking and inflicted head impact. During falls, the surrogate experienced occipital contact against a concrete surface, carpet pad, or foam mattress. For shakes, investigators repeatedly shook the surrogate in an anteroposterior plane; inflicted impact was defined as the terminal portion of a vigorous shake, in which the surrogate’s occiput made contact with a rigid or padded surface. Rotational velocity was recorded directly and the maximum (peak-peak) change in angular velocity…and peak angular acceleration…were calculated…….. Conclusions: Vigorous shakes of this infant model produced rotational responses similar to those resulting from minor falls, but inflicted impacts produced responses that were significantly higher than even a 1.5-m fall onto concrete. Because larger accelerations are associated with an increasing likelihood of injury, the findings indicate tht inflicted impacts against hard surfaces are more likely to be associated with inertial brain injuries than falls from a height of less than 1.5 m or from shaking.

Plunkett, John, Fatal pediatric head injuries caused by short-distance falls, American Journal of Forensic Medicine and Pathology, 2001; 22(1):1-12.

Abstract: Physicians disagree on several issues regarding head injury in infants and children, including the potential lethality of a short-distance fall, a lucid interval in an ultimately fatal head injury, and the specificity of retinal hemorrhage for inflicted trauma.
There is scant objective evidence to resolve these questions, and more
information is needed. The objective of this study was to determine whether there are witnessed or investigated short-distance fall that were concluded to be accidental. The author reviewed the January 1, 1988 through June 30, 1999 United States Consumer Product Safety Commission database for head injury associated with use of playground equipment. The author obtained and reviewed the primary source data, hospital and emergency medical services’ records, law enforcement reports, and coroner or medical examiner records) for all fatalities involving a fall.
The results revealed 18 fall-related injury fatalities in the database. The youngest child was 12 months old, the oldest 13 years. The falls were from 0.6 to 3 meters (2-10 feet). A noncaretaker witnessed 12 of the 18, and 12 had a lucid interval. Four of the six children whom funduscopic examination was documented in the medical record had bilateral retinal hemorrhage. The author concludes that an infant or child may suffer a fatal head injury from a fall of less than 3 meters (10 feet). The injury may be associated with a lucid interval and bilateral retinal hemorrhage.

Denton, S, and Mileusnic, D, Delayed sudden death in an infant following an accidental fall; A case report with review of the literature, American Journal of Forensic Medicine and Pathology, 2003; 24(4):371-376.

Abstract: Several controversies exist regarding ultimately lethal head injuries in small children. Death from short falls, timing of head injury, lucid intervals, presence of diffuse axonal injury (DAI), and subdural hematoma (SDH) as marker of DAI are the most recent controversial topics of debate in this evolving field of study. aIn this area of debate we present a case of delayed death from a witnessed fall backwards off a bed in a 9-month-old black child who struck his head on a concrete floor and was independently witnessed as “healthy” for 72 hours postfall until he was discovered dead in bed. Grandmother, babysitter, and mother all independently corroborated under police investigation that the child “acted and behaved normally” after the fall until death. Autopsy showed a linear nondisplaced parietal skull fracture, diastasis of adjacent occipital suture, subgaleal hemorrhage with evidence of aging, small posterior clotting, subdural hemorrhage, marked cerebral edema, and a small tear of the midsuperior body of the corpus callosum consistent with focal axonal injury. No DAI was seen, and there were no retinal hemorrhages. All other causes of death were excluded upon thorough police and medical examiner investigation..…..

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

Abstract: Falls accounted for 5.9% of the childhood deaths due to trauma in a review of the medical examiner’s files in a large urban county. Falls represented the seventh leading cause of traumatic death in all children 15 years or younger, but the third leading cause of death in children 1 to 4 years old. The mean age of those with accidental falls was 2.3 years, which is markedly younger than that seen in hospital admission series, suggesting that infants are much more likely to die from a fall than older children. Forty one percent of the deaths occurred from “minor” falls such as falls from furniture or while playing; 50% were falls from one story or greater; the remainder were falls down stairs…..…

Gardner, Horace, A witnessed short fall mimicking presumed shaken baby syndrome (inflicted neurotrauma), Pediatric Neurosurgery, 2007; 43:433-435.

An 11-month old infant was witnessed to fall backwards from a sitting position, the head striking a carpeted floor. The infant immediately cried, vomited and exhibited some seizure-like activity including tongue-biting and curling of the right hand. Three hours later a large acute left frontal subdural hematoma was removed surgically


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