Childhood Head Injury

A Short Bibliography of Must Read

Articles

What follows is a short bibliography of the articles that anyone intrested in the field of childhood head trauma must read. There are literally hundreds of articles written on the subject, but these are some of the essentials.

Accident vs. Abuse

American Academy of Pediatrics. American Academy of Pediatrics: Shaken Baby Syndrome: Rotational Cranial Injuries - Technical Report. Pediatrics 2001; 108(1)
This is the Prosecutor's Tutorial on "Shaken Baby Syndrome" (SBS). It gives a brief description of the current dogma surrounding childhood head injuries. The article also gives a list of symptoms/signs to look for in a purported case of "shaken baby syndrome" or non-accidental head trauma. Also included are some legal citations and tips for prosecutors on how to try these cases.

Donohoe M. Shaken baby syndrome and non-accidental injuries. A review 1999.
Excellent article reviewing the medical theories around the "shaken baby syndrome." Author takes a thorough look at the five axioms of controversy in SBS cases and the lack of literature and scientific data on the subject. Good tutorial on Shaken Baby Syndrome and the evolution of the theory over the years. A must read for defense attorneys.

Plunkett. Fatal pediatric head injuries caused by short distance falls. American Journal of Forensic Medicine and Pathology 2001; 22:1-12.
This study analyzed the Consumer Product Safety Commission's database on playground equipment falls, between Jan. 1988 and June 1999. In this study there were 18 deaths from falls of less than 10 feet. There were four falls from horizontal ladders; three falls from stationary platforms; and seven from swings. One child fell from a retaining wall; one from a seesaw; one from a slide; and one form a ladder attached to a slide. In that data set thirteen children had subdural hematomas, and twelve had lucid intervals ranging from five minutes to forty-eight hours. Four of the six that had fundoscope examinations had retinal hemorrhages. The study proves that short falls can kill children and retinal hemorrhages are not pathonemonic for non-accidental trauma. The study also calls into question our ability to time injuries and contradicts the theory that decomposition begins immediately after the SDH is formed.

Reiber G. Fatal falls in childhood. The American Journal of Forensic Medicine and Pathology 2001; 14(3):201-7.
Article documents 3 cases of deaths from corroborated, witnessed, short falls (10-20 feet). Author says all three children had SDH and fractures. Documents 2 of 3 children had lucid intervals and all 3 children died after a delayed period following the fall. 2 of 3 children showed periorbital echymosis. One child suffered a SDH and severe brain swelling from a 6-foot fall onto a carpeted floor. 1 child fell 2-3 feet from a rocking chair. Article suggests that soft surfaces can still cause fatal injuries. Includes a lengthy literature review on shortfall debate.

Root, I. Head injuries from short falls. The American Journal of Forensic Medicine and Pathology 1992; 13(1): 85-7.
The late biomechanics expert Irving Root walks us through the physics of decelerational injuries. He shows how shortfalls can equate to the same g-forces as long falls with rotational forces.

 

Biomechanics

Caffey J. On the Theory and Practice of Shaking Infants. American Journal of Diseases in Childhood 1972; 124:161-9.
This is the original article discussing what is now called Shaken Baby Syndrome. Caffey says the constellation of injuries found in "shaken-whiplash syndrome" is generally found in conjunction with fractures of the long bones and/or bilateral symmetrical fractures of the arms and legs. Caffey discusses fractures of the bones and joints from whiplash injuries. The article sites cases of whiplash injury from a father swinging an infant over his head. Caffey says injuries can be caused by coughing, overly vigorous burping, "riding the horse" tossing the baby up in the air, rough roads and flipping a toddler head over heels to his or her feet. Caffey says that CPR can lead to an increase in venous pressure that causes these types of injuries.

Caffey J. The parent-infant traumatic stress syndrome: (Caffey-Kempe Syndrome), (Battered Babe Syndrome). Amer J Radiol 1972; 114:218-29.
The article was published later the same year altering Caffey's theory of SBS- Article looked at 12 cases of "SBS" from other articles. Caffey uses anecdotal data from a nurse who confessed to shaking several children in her care. Some of those children showed Caffey's signs of Shaken Baby Syndrome; some didn't. Author goes through the literature on SBS and reviews babies used in other studies to prove his point. Study defines SBS triad as: 1) Retinal hemorrhage 2) Subdural hemorrhage, and 3) Lack of external signs of abuse. Some of the cases Caffey discusses show lucid intervals. Caffey cites 14% of newborns show signs of retinal hemorrhage.

Caffey J. The whiplash shaken infant syndrome: manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation. Pediat 1974; 54:396-403.
In this article, Caffey comes up with yet another rendition of his theory. The author posits that it is the whip lashing of the head onto the thorax that causes traction-stretching stresses and causes SBS. Now Caffey believes Shaken Whiplash Syndrome is characterized by: 1) Bilateral SDH, 2) Bilateral RH and 3) external signs of trauma to the head and neck.

Duhaime A.C, Gennarelli T, Tibualt L.E, Bruce D.A, Margulies S.S, and Wiser R. The Shaken Baby Syndrome: A clinical, pathological, and biomechanical study. Journal of Neurosurgery 1987; 66:409-15.
This article makes a biomechanical model with the parameters of an infant's head. The accelerometer is placed in the model and they experiment with shaking vs. impact injuries. The study determines that angular decelerations for shaking were less than that for impact by a factor of 50. They found that shaking alone, of an otherwise normal infant, could not cause the degree of injuries generally associated with shaken baby syndrome.

Duhaime A.C, Alario AJ, Lewander J et al. Head injury in very young children: mechanisms, injury types, and ophthalmologic findings in 100 hospitalized patients younger than 2 years of age. Pediatrics 1992; 90:179-85.
Authors looked at one hundred children under two years of age with head injuries. Authors conclude (with a circular argument/classification system) that nine children out of ten with retinal hemorrhages were victims of inflicted trauma. The tenth one was a victim of an MVA. Seven of the nine patients with inflicted head trauma experienced seizures as part of their course. Four of the infants from this study died; one from accidental causes (had subdural hemorrhage and retinal hemorrhage) and three from non-accidental causes.

Duhaime AC, Christian CW, Rorke LB, Zimmerman RA. Non-accidental head injury in infants - the "shaken-baby syndrome". New Engl J Med 1998; 338:1822-9.
Authors discuss translational vs. rotational forces with regards to non-accidental head trauma. They analyze the significance of retinal hemorrhages and subdural hemotomas and the degree of force needed to inflict the injuries seen in SBS cases. Authors look at the timing of head injuries through radiological studies and autopsies.

Subdural Hematomas

 

Howard M, Bell B.A, and Uttley D. The pathophysiology of infant subdural haematomas. British Journal of Neurosurgery 1993; 7: 355-6.
Authors did a retrospective review of 28 babies with SDH over a 20-year period (>18 months; N=18 boys and 10 girls). Study sample included 17 white, 10 non-white babies and 1 mixed race baby. Non-Caucasians with a head injury were more likely to have SDH than whites (67% v. 21%). Short falls (including high chairs) were often the cause of injury. 11 infants went unconscious immediately following the traumatic head injury and 10 infants were observed having breathing difficulties. Babies were observed experiencing vomiting (50%) and irritability (25%). Seizures were more common in non-whites (90%) than whites (41%). Article discusses 3 infants with chronic SDH that were not thought to be abused. All three had minor impact more than a week prior to their hospital admission. One other case presented with a CSDH and questionable circumstances. There was an absence of impact site in 29% of Caucasians and 80% of non-whites. 11/20 of the infants that had funduscope examinations had retinal hemorrhages, 9 were normal, 6 (33%) of white infants had evidence of extra cranial injuries; none of the non-whites had those signs. Great article for cases involving babies of color.

Parent A.D. Pediatric chronic subdural hematoma: a retrospective comparative analysis. Pediatric Neurosurgery 1992; 18:266-71.
Author reviewed the literature on chronic subdural hematomas. Study looked at 28 children less that 18 months old, over two decades. Most of the children in the data set were less than 4 months old. Males were overly represented in both the first (78%) and second (60%) decade of study. Kids in both sample tended to present with macrocephaly, lethargy, failure to feed, apnea and seizures. Some children in the more recent sample, presented with headaches only, or no symptoms at all. Fractures were rarely seen with subdural hematomas in either sample. Mortality rates in the 70s study were around 50% where as in the 80s they were closer to 10%; Seizures increased from 40% to 46%, but psychomotor retardation reduced from 33% to 28%. Authors attribute 40% of subdurals in infants to child abuse. Birth Traumas and rebleeds comprised a small percentage of the subdural bleeds. Parent discusses the evolution of a SDH and the tendency of those with them to develop hydrocephalus over time. The author also discusses eschemia secondary to chronic subdural hematoma because of impaired cerebral blood flow. The study found that craniotomies were rare as a course of treatment in modern times but were very popular in the 80s. He sites the increased tendency in infants to bleed or to develop new subdurals after a membranectomy or crainiotomy. Modern courses of treatment generally involve subdural taps or subdural peritoneal shunts. Author indicates that the histopathology of CSDH in children is the same as that in adults in that they tend to wax and wane and rebleed. He says that capillary fragility was the major cause of repeated hemorrhage in CSDH.

Piatt J. A pitfall in the Diagnosis of Child Abuse: External Hydrocephalus, Subdural Hematoma & Retinal Hemorrhages. Neurosurgical Focus 1999; 7(4)(4):1-9.
http://www.aans.org/journals/online j/oct99/7-4-4.html
Author describes a child who developed SDH and retinal hemorrhage from external hydrocephalus (previously referred to as benign subdural effusions of infancy). Author discusses how conditions such as external hydrocephalus, internal hydrocephalus, arachnoid cyst or a chronic subdural hematoma, can cause subdural hematomas from minor head injuries. Author says that development of a subdural hematoma after minor head trauma in an infant with craniocerebral disproportion might be the occasion for unjustified accusations of abuse. Article calls into question many of the myths on SBS. Author describes retinal hemorrhages and discusses the mechanisms behind re-bleeding SDH. The existence of retinal hemorrhages in this case adds to the literature supporting the argument that retinal hemorrhages are caused by a sudden increase in ICP rather than abuse. Great article for re-bleeds, hydrocephalus, retinal hemorrhages etc.

Sherwood D. Chronic subdural hematoma in infants. Am J Dis Child 1930; 39:980.
This is a remarkable article that clearly shows that infants do get chronic subdurals that do "re-bleed"…quotes articles from 1890's and early 1900' about chronic subdural patients WITH retinal hemorrhages. Raises issues of abuse in some of them. This is first mention I have found of this "new" phenomenon.

Swift, Dale M. Chronic Subdural Hematomas in Children. Journal of Chronic Subdural Hematomas 2000; July 11(3).
Author reviews the data on intracranial fluid collections. Says there is three ways to generate subdural fluid collections. 1) recurrent bleeding of the chronic subdural hematoma in the subdural space. 2) An opening in the subarachnoid allows the CSF to enter the subdural space. (This can occur after shunt placement in hydrocephalic or macrocephelic babies. The CSF then mixes with blood and results in a thin xanthochromic fluid, sometimes called subdural hygromas), and 3) Response to an infection or process. Subdural empyemas can result from sinitis or otitis media, into the epidural space and then into the subdural space. Purulent subdural collections are sometimes seen after bacterial meningitis. Especially those due to hemophilia influenza. Cultures may or may not show organisms because the patient is usually started on antibiotics before the tests are done. Fluid can also accumulate around the brain after destructive disease processes such as hypoxia. These rarely cause symptoms. The most common cause of subdural hematomas is trauma, but underlying tissue may predispose a baby to subdural bleeding with minor trauma. Author says that frequently the symptoms go unnoticed and without medical attention. Causes can be accidental or non-accidental, non-accidental is the most common for children less then two years of age. Author says coagulopathy can underlie subdural bleeding or abnormalities in intracranial structure. Also discusses relationship between arachnoid cysts in the middle fosa and chronic subdural hematomas. Author indicates that the degree of trauma needed to produce injury in children with fluid collections in their brain is less then the normal infant population, and that childbirth can cause chronic subdural hematomas. Author indicates that age of infants is correlated with presentation of subdural hematomas. Infants can present acutely with apnea or seizures, or more protracted with a history of lethargy, vomiting, and a failure to feed. Older children present usually two weeks after trauma with symptoms of headaches and advanced intracranial pressure. Hemiparesis or reflux asymmetry are also common in older children. Chronic subdural hematomas tend to occur unilaterally in older children and bilaterally in younger children. Author indicates treatment has moved away form craniotomes and membranectomies to subdural shunts and bur holes. About 50% of this data set had the central nervous system problems and developmental delay.

Yamashima T. The inner membrane of subdural hematomas. Neurosurgery Clinic of North America 2000; 11(3): 413-23.
A very good paper by a careful worker who has been involved in basics of subdurals for a long time. Author makes the point that sometimes chronic subdurals (surgical specimens) can have proliferated arachnoid elements rather than dural neomembrane elements in them. This indicates chronicity. Useful to establish chronicity.

Lucid Intervals

Barnes Patrick D. Ethical Issues in Imaging Nonaccidental Injury: Child Abuse Topics in Magnetic Resonance Imaging 2002. 13(2): 85-94.
Well respected Pediatric Radiologist Patrick Barnes questioning the effectiveness of dating and timing subdural hematomas by CT and MRIs. The author calls into question some of the historical assumptions surrounding the theory of shaken baby syndrome and dispels some of the radiological myths. He concludes that Subdural hematomas and retinal hemorrhages come from rotational decelerational injuries both accidental and non-accidental and that current radiological findings alone, cannot tell you the nature or mechanism of injury. The author reviews articles showing that retinal hemorrhages come from a myriad of different conditions. The article mentions coagulopathies, metabolic disorders and vaccines as conditions that could contribute to or be misdiagnosed as shaken baby syndrome. Barnes says that MRI (T1 and T2 SE) is the most effective way to identify and date injuries and that CTs are often inadequate to determine the nature or age of fluid collections on the brain, particularly in the presence of an anemia or coagulopathy. The author also spells out the job of an expert witness and the windows for dating subdural hematomas with an MRI.

Dacey R.G, Alves W, Rimel R, Winn R, and Jane J. Neurosurgical complications after apparently minor head injury. Neurosurgery 1986; 65:203-10.
Authors studied 610 patients at a Washington trauma center. Of 66 patients with skull fractures, 5 had intracranial hematomas, 13 had some type of Neurosurgical complications. Neurological complications and lucid intervals were more likely to be found in boys than girls and are more likely to occur in a fall rather than by some other mechanism. The increased ICP is found after about 50% of severe head injuries. Skull fractures increase likelihood of Neurosurgical procedures. Article documents the existence of lucid intervals. Authors found that 3% of minor head injury cases will deteriorate after experiencing a lucid interval.

Greenes D, Schultzman S.A. Occult intracranial injury in infants. Annals of Emergency Medicine 1998; 32(6):680-6.
The study looked at infants admitted to the emergency room of Children's Hospital Harvard (over a 6.5 year period). Occult (hidden) injuries (i.e. lucid intervals) were seen in fourteen of the 52 infants (27%) under the age of 6 months, 5 of 34 babies (15%) 6 months to a year and none of the infants over a year. 95% of the children had scalp contusions or hematomas and 95% had fractures. None of the infants with occult injuries required medical assistance such as surgery etc. to manage increased innercranial pressure.

Nahelsky M, and Dix J. The time interval between lethal infant shaking and onset of symptoms: A review of the Shaken Baby Syndrome Literature. The American Journal of Forensic Medicine and Pathology 1995; 16(2):154-157.
Good article. Agrees with Bruce and Zimmerman and Duhaime's theory that you must have impact to create the damages like those seen in SBS. Article comments on the paucity of studies done discussing the onset of symptoms for SBS. Looks at time between "shaking" and symptoms. Article discusses three cases of "shaking" injury where children experienced lucid intervals of 3 hours, 3 days and 4 days. The last child had bilateral retinal hemorrhages. The article concludes that there is very little data available to suggest the actual time limits between fatal head injuries and death. Shows that lucid intervals do exist and that perpetrators cannot be narrowed down to the last person holding the baby.

Usinski Ron. Shaken Baby Syndrome: Fundamental Question. British Journal of Neurosurgery 2002;16(3): 217-219.
Great article by well known Neurosurgeon Ronald Usinski. The author reviews a history of the "shaken baby syndrome" and highlights the fact that the theory is greatly disputed by medical and biomechanical evidence. The author does a quick tutorial in Newtonian physics and shows that the G Forces required to cause a subdural hematoma, cannot be caused by human shaking alone without impact. The author indicates that prior to 1972 retinal hemorrhages used to be used in diagnosing increased intracranial pressure or head injury, now it is somehow said to be diagnostic of SBS. He says that there is little dispute that chronic subdurals rebleed in adults during the normal healing process during membrane formation and we do not look for abuse in adults who suffer rebleeding subdurals. He argues that there is no data to suggest that children's brains react any different than adult brains.

Retinal Hemorrhages

Goetting MG, Sowa B. Retinal hemorrhage after cardiopulmonary resuscitation in children: an etiologic reevaluation. Pediatrics 85:585-588, 1990.
2 of 20 children given CPR showed retinal hemorrhages with no history of trauma or abuse. The cases and mechanism of hemorrhages is discussed.

Greenwald MJ, Weiss A, Oestlerle CS, Friendly DS. Traumatic retinoschisis in battered babies. Ophth 1986; 93:618-25.
Retinal hemorrhages are found in cases with a sudden increase in cranial pressure. Article cites cases of retinal hemorrhages from CPR, swinging the child by the feet or vaginal delivery. Authors say fundus hemorrhages are found in battered babies. Necrosis of the inner layer of blood is said to be responsible for "late" RH. Authors document one case of RH with no SDH but elevated ICP. They theorize that mechanical forces involved in the shaking (lens shifting in vitreous humor) cause retinal hemorrhages. The forces applied to the eyes in shaking make the lens move back and forth within the ocular fluids. Force translates through the lens, vitreous gel and retina to create tugging on the retina and tearing the blood vessels in the subdural space of the retina, (referred to as vitreous traction of the retina). Editorial comment by Torch says it's not retinoschisis it is retinal hemorrhage secondary to increased venous pressure changes. Other processes related to increased ICP include, Central Retinal Vein occlusion, high altitude retinopathy, and subarachnoid hemorrhages secondary to aneurysm.

Gutman, F. Evaluation of a Patient with Central Vein Occlusion. American Academy of Ophthalmology 1983; 90(5) 481-3.
Article says central retinal vein occlusion can cause retinal hemorrhages. Documents all the reasons for central retinal vein occlusions. Says blood-clotting disorders, alterations in viscosity of blood and abnormalities in the vein wall can cause increased intracranial pressure which then results in retinal hemorrhages.

Kaur B, & Taylor D. Current Topic: Retinal Hemorrhages. Arch. Dis. Child 1990; 65:1369-72.
Article describes the different types and causes of retinal hemorrhages. Authors say that neonatal retinal hemorrhages are generally Dot and Blot or flame shaped and located at the posterior or periphery. Article indicates that 1/3 of babies born with occipital presentation have retinal hemorrhages. Incidence increased with prolonged labor or obstetric procedures, and decreased with c-sections and breech presentations. Retinal hemorrhages are also more common in mothers with Toxemia. With subarachnoid bleeding there may be an increase in intra-cranial pressure, optic nerve sheath hemorrhage, and an increase in the pressure within the optic nerve sheath because of raised central retinal venous pressure. Retinal hemorrhages occur 20-32% of the time with SAH: they occur simultaneously or within a few days. Streak and preretinal hemorrhages occur mainly around the optic disc. Preretinal hemorrhages may leak into the vitreous (Tersons Syndrome). Retinal and preretinal hemorrhages are consistently seen in infants with SDH. Superficial retinal hemorrhages can occur from sneezing, crying, or squeezing of the chest (valsalva's hemorrhagic retinopathy). Hemorrhages into all layers of the retina may be more common in non-accidental trauma. Also sites vomiting, epileptic seizures, crying, chest compressions, and coughing spells as causes of retinal hemorrhages.

Kirschner R H, and Stein R J. The Mistaken Diagnosis of Child Abuse. American Journal of Diseases in Childhood 1985; 139:873-5.
Article reports a case of retinal hemorrhages after vigorous chest compressions on a 3-month-old infant. Article looks at differentiating diagnosis of abuse from coagulopathies, CPR, TCP, SIDS, meningitis, etc. Author says mistaken diagnosis often occur when a child dies with no explanation for his/her injuries and those injuries are consequently cited as indicators of abuse. Author lists other disease processes that mimic abuse but doesn't go into them in depth.

Lantz, P E; Sinal, S H; Stanton, C A; Weaver, R G Jr. Perimacular retinal folds from childhood head trauma. British Medical Journal 2004; 328(27)
Evidence based case report gives an account of a child who presented with extensive head injuries caused by a television falling on his head. The child deteriorated and died within 18 hours. Because the child had retinal hemorrhaging and retinal folds, CPS removed the other child from the home. Lantz et al. explain that "An evidence based analysis of indexed medical publications on shaken baby syndrome from 1966-1998 uncovered a weak scientific evidence base." Lantz et al. conclude in saying that "Until good evidence is available, we urge caution in interpreting eye findings out of context."


Rosenberg N with discussants Singer J, Bolte R, Cristian C, and Selbst S.M. Retinal Hemorrhage. Pediatric Emergency Care 1994; 10(5) 303-5.
Great piece. Ophthalmologist Norman Rosenberg creates a fact pattern, which includes a subdural hematoma, and retinal hemorrhages. Each of the four discussants is asked to give a diagnosis on the case. Some call it abuse some don't. The article demonstrates the amount of variability in the opinions on retinal hemorrhages.

Tongue Andrea. The Opthalmologists Role in Diagnosing Child Abuse. Ophthalmology 1991; 98(7): 1009-10.
Author indicates that retinal hemorrhages predominantly occur in children with central nervous system injuries. She says that although it is possible that certain types of hemorrhages are signs of shaken baby syndrome, there was no evidence to date that establishes that any type of retinal hemorrhage was pathenomonic for non-accidental trauma. Tongue recognizes that retinal hemorrhages are found in scenarios that do not include child abuse. They are seen in newborns, in infants after cataract surgery, in infants undergoing extra corporeal membrane oxygenation therapy, or infants with subdural or subarachnoid hemorrhages secondary to accidental trauma, and with bleeding byforasias and hemoglobinopathies. Author says non-accidental trauma associated with retinal hemorrhage is most often found in children under the age of two, but there is no research out there to back up the pathology. Author says there is no proof that retinal folds are indicative of vitreous traction mechanisms or child abuse.

Diffuse Axonal Injuries

Geddes J.F. The diagnosis of diffuse axonal injury: implications for forensic practice. Neuropathology and Applied Neurobiology 1997; 23: 339-47.
This article shows that diffuse axonal injuries occur in varying degrees and can't be standardized across people or across incidents. Article says in order to diagnose DAI the Pathologist should take 6-12 blocks from the brain. Authors theorize that DAI is diagnostic of trauma whereas focal or multi-focal axonal injury is more indicative of a hypoxic-eschemic event (infarction).

Geddes J.F.Traumatic axonal injury: practical issues for diagnosis in medico legal cases. Neuropathology and Applied Neurobiology 2000; 26: 105-16.
Author compares traumatic axonal injury (TAI) with diffuse axonal injuries (DAI) and says the latter occupies only the most severe end of the spectrum of diffuse trauma induced brain injury. It has been traditionally thought that DAI was the most common indicator of a patient who had become immediately unconscious after a head injury then lapsed into prolonged coma, in the absence of a focal mass lesion with severe disability or a persistent vegetative state. Early experimental work showed that DAI was primarily a non impact phenomenon resulting from angular or rotational acceleration as found in motor vehicle accidents or falls from appreciable heights. Author indicates that it is difficult to distinguish between axonal swelling (a large intact bulb) and an axon or retraction bulb, which is no longer in continuity with the rest of the axon because axotomy has occurred. Furthermore, axotamy may not take place at the same time in all parts of the brain. Axons of different sizes react differently and secondary axotomy may continue for some time after injury. Axonal degeneration has been reported in rats as far out as a year after brain trauma. Geddes distinguishes features of TAI and DAI. If the brain was swollen or herniating at least some of the axon damage will be vascular in nature and will be found in areas affected by the herniation. Geddes suggests the importance of where and how many blocks of tissues are taken to determine whether the axonal damage is diffuse of multifocal. Linear or geographic patterns of BAPP accumulation were more likely representative of axonal damage at the edge of a focus of early ischemia while scattered groups of damaged axons, particularly those involving single white matter bundles, were more likely traumatic in nature. Multiple areas of BAPP reactivity are common with a swollen brain particularly in cases of mass affect. Authors suggest that the term DAI should not to be used as a neuropathological diagnosis in medicolegal cases unless preceded by the qualifiers traumatic or hypoxic.

Geddes J.F. Neuropathology of Inflicted head injury in children. Brain 2001; 124(7): 1299-1306.
Reports the findings of 37 infants less then nine months of age, all who died of inflicted head trauma, and fourteen controls that died of other causes. In 76% of the cases the presenting symptom was respiratory arrest. They used beta amylase precursor protein to look for diffuse axonal injuries. BAPP was positive in 25 out of the 37 cases, including 11 of the 14 cases that were said to be found dead. In 13 of 25 cases axonal pathology seemed to be vascular in nature, and associated with brain swelling and a raise in intercranial pressure. Five brains showed minimal traumatic axonal damage only in the corpus collosum or central white matter. DAI was present in 2. Authors said it was not always easy to distinguish between escemic and traumatic damage to the axon, but in a few cases, pathologies were present for both. In eight cases axon bulbs were found on the brain stem and cortical spinal bundle, on both sides of the pons and medulla. In seven of the eight cases this is the only axonal damage found. In the control group there were two cases of vascular axonal damage in the white and to the lesser extent, gray matter. One was a child who died of gastroenteritis, the other was a child that was born at thirty-six weeks had perinatal hypoxia/eschemia and who only lived for two days. There was no BAPP in cortical spinal tracks or axons in the cervical cord of any of the controls, and no axonal damage or rebleeds that could be interpreted as traumatic. The non-accidental trauma group had wide spread hypoxia in 29 of the 37 cases, which had no documented survivors. The control group only had one case, a severally premature child, who showed severe hypoxic changes. Two other non-accidental trauma cases had a milder degree of hypoxia throughout the brain. Article shows that axonal damage occurs in the brains of both head injured subjects and controls in much the same distribution, and with similar appearances as those that are described in previous literature by Shannon and Gleckman. She says it is not DAI but diffuse vascular or hypoxic eschemic injury attributable to brain swelling and a raise in intercranial pressure. She says that severe traumatic axonal damage is rare in infants with non-accidental injuries, unless there is a considerable impact and diffuse damage responsible for loss of consciousness. Geddes says, in the majority of cases it is due to hypoxia and not trauma and we should not dismiss the apnea reported by most of the cases, hypoxic damage due to apnea could lead to severe brain swelling and death. The control cases with respiratory problems did not show as severe as hypoxic changes as non-accidental injuries.

Kaur B, Rutty G.N, Timperley W.R. The possible role of hypoxia in the formation of axonal bulbs. Clin Pathol. 1999; 52: 203-9.
Authors look at 28 brains with cerebral hypoxia and no head trauma; four brains with head trauma and no hypoxia; 8 brains with head trauma and hypoxia; and four control brains originally described as having diffuse axonal injuries. BAPP staining was positive in all four controls; in all four cases of head injury only; in seven of the eight cases of head injury and hypoxia: and in 12 of the 28 cases of hypoxia with no trauma. 22 of the 25 cases that had been ventilated, showed positive for BAPP staining. Axonal bulbs often stain positive for BAPP with hypoxia and without a head injury. Author concludes that the presence of axonal bulbs is not an indicator of shearing forces.

Oehmichen M, Meibner C, Schmidt V, Pedal I, Konig H.G, Saternus K. Axonal injury- a diagnostic tool in forensic neuropathology? A Review 1998.
Authors study diffuse axonal injury in 252 deaths. From non-missile closed head injuries (119), gunshot injury (30), fatal cerebral eschemia/hypoxia (51), brain death caused by mechanical trauma (14), or non-mechanical trauma (18), an acute hemorrhagic shock (20). Axonal injury was observed in 65 to 100% of the cases of closed head injuries, fatal cerebral eschemia/hypoxia and brain deaths with survival time of more then three hours. AI could not be detected in cases with acute hemorrhagic shock. There was no statistically significant difference between traumatic and non-traumatic induced AI. There was also no correlation between AI and different types of external force. (i.e.. acceleration/deceleration injuries and trauma). Authors conclude that AI is not a good indicator of manner of death but it might be a good indicator of time of death. The cases under 180 minutes did not show BAPP staining.

Alternate Theories

Vaccines

Devin F, Roques G, Disdier P, Rodor F, Weiller P.J. Occlusion of central retinal vein after hepatitis B vaccination. The Lancet 1996; 147: 1626.
Author reviews the case of a twenty-seven year old man with no risk factors for central retinal vein occlusion or hepatitis B, who reported blurred vision eight days after his first injection of the hepatitis B vaccine. Fluorescein Angiography showed prethrombotic conditions of the central retinal vein in the right eye, with papillary edema and retinal hemorrhages. One month later a second vaccine was given, six days after which the patient developed total retinal vein occlusion of the right eye. The arithrimite sedimentation rate and coagulation studies were all normal. There was no lupus anti coagulant and no resistance to activated protein C. All the tests were negative and showed normal, except immune complexes were found 6-6 ug's per liter. Author concludes that this could be indicative of a vaccine reaction.

Miller E. et al. Idiopathic thrombocytopenic purpura and MMR vaccine. Archives of Disease In Children 2001; 84:227-229.
Article investigates 21 children with TCP and shows a significant causal link between it and the MMR vaccine. Authors cited a six-week post immunization risk period. Authors cited an article by Cohn that found over 70% of the cases of ITP follow virus infections. Nine of thirteen cases were attributable to MMR and the relative risk for contracting ITP is one in 22,300 doses. The highest incidents occurred between 15-28 days. Two of every three cases of ITP were vaccine related but infants who already had ITCP were not at an increased risk of incidents after MMR. The study found that vaccine related incidents tended to be milder and not as likely to reoccur. See also: Devin (1996)