Alternate Explanations
The myth that children don't die from short falls is incorrect on its face. We know from published medical data that perfectly healthy children die of short falls (1-4ft.). Furthermore, the myth that children don't die of short falls, assumes that those children do not possess any intervening factors that would make them more fragile to a head injury. As a metaphor, it would generally be assumed, and supported by medical literature, that children do not die of paper cuts or minor external head wounds. This would however be defied by cases involving hemophiliacs. One would be in great error to assume that a child was abused simply because it was disparate from the norm, without paying careful attention to intervening factors. In SBS cases doctors generally are unable (because the baby is deceased) or uninterested in pursuing other explanations for the injuries, once a diagnosis of SBS has been reached.
It needs to be made clear from the outset that we believe that short falls can and do kill healthy children. However, there are also several underlying medical conditions that can lessen the degree of force necessary to cause the injuries found in "SBS" cases:
· "Chronic" or "old" subdural hematomas an infant with an old or chronic subdural hematoma may suffer "re-bleeds" with little or no impact at all. Witnesses for the State will generally argue that chronic subdural hematomas do not bleed or re-bleed without force equal to or greater than that incurred in a 2-3 story fall. This testimony however is not supported by the literature on re-bleeds.
Most of the literature available on chronic subdural hematomas is on hematomas in adults. However, for adults it is generally assumed that chronic subdural hematomas by their very nature evolve and can re-bleed over time. Though little has been punished specifically about re-bleeding subdurals in infants but there is an extensive literature on chronic subdural hematomas in infancy, it is assumed by most experts in the treatment field that the processes involved in production of a chronic subdural hematoma is the same, regardless of age . Studies have showed that the disruption in the organization of membranes created by the (resolving) subdural hematoma can often cause new hematomas to form. Most experts will agree, if pressed, that chronic subdural hematomas are likely to re-bleed with little to no impact at all.
Case Note
BB was an 8-week-old infant that arrested 11 days after his second well baby checkup. The child had been lethargic and refusing food for several days. The parents reported that he cried more when he was laid flat and that his cry was more nasal and whining than normal. He had what could be interpreted as seizures and had been brought to the doctor with "raccoon eyes" the week before. The raccoon eyes (periorbital echymosis) were diagnosed as a vitamin K deficiency and treated with a shot of vitamin K. On the day the baby arrested the child had been taken to the emergency in the morning for projectile vomiting in the church daycare. Later that day, the baby arrested while in the care of the father (the mother was taking a bath). The paramedics arrived and took the child to the local hospital. They diagnosed him with reflux and told the parents he would have to stay over night. Later that night when the baby started having seizures he was taken to a trauma hospital in a nearby town. The CAT scans performed at this hospital revealed an acute subdural hematoma, evidence of an old subdural hematoma dating several weeks old, and a unilateral retinal hemorrhage. The infant was sedated for several weeks and had regular cat scans performed until his release. The CAT scans and MRIs showed the subdural hematoma spontaneously rebleed at periodic intervals throughout the six weeks the infant stayed in the hospital and his intracranial pressure fluctuated over time. The case was tried by Michael Moore in Warner Robbin's Georgia. The jury acquitted in less than a half an hour.
· Hydrocephalus:Hydrocephalus, literally water on the brain, is a generic term that covers several conditions:
External hydrocephalus: (excessive cerebrospinal fluid-CSD over the brain with normal or relatively normal ventricle size.
Internal hydrocephalus: (excessive CSF inside the ventricles of the brain). Clinical symptoms are similar to other closed head trauma; unsteady broad based gait, history of falling, apathy/lethargy, inattentiveness etc.
Hydrocephalus can be caused by several phenomena as embodied in their names.
Obstructive or non-communicating hydrocephalus involves impedance to flow of CSF from or between the ventricular chambers in the brain and the brain's surface. This can be due to prior viral or other infection with scarring of the exiting foramina at the base of the cerebellum, obliteration by scar, tumor, or some other process of the narrow connecting passages (foramina of Munro, aqueduct of Sylvius) between the ventricles within the brain.
Communicating hydrocephalus assumes that CSF can exit the brain but there may be impedance due to scarring of the subarachnoid space, or scarring or other dysfunction of the arachnoid granulations where CSF is absorbed (possibly due to recent or remote subarachnoid hemorrhage). Combinations of all of the above may result in impaired transport or absorption of CSF relative to the amount produced by the brain. This may lead to increased intracranial pressure and complications from this.
· Coagulopathies
The blood constantly exists in an equilibrium of clotting on the one hand and anti-coagulation on the other. Disruption of this equilibrium leads to the condition of coagulopathy. Coagulopathy can have two faces, clotting in various locations or everywhere within the vessels leading to deposition in a worst case of intravascular clots in brain, lungs, kidney and other organs (disseminated intravascular coagulation-DIC). Once clotting factors have been consumed or otherwise inactivated, spontaneous bleeding may occur anywhere in the body but is most likely where some form of injury of any kind exists. There are many conditions, circumstantial, acquired, and inherited that can cause a dysfunction in clotting manifested in many ways. These conditions may not be all or none in their expressions.
An apparently uncommon, but probably under appreciated complication of coagulopathy is thrombosis of the superior sagittal sinus (and/or other intradural venous sinuses) as well as cortical veins. In its most virulent form affected individuals may suddenly decompensate with rapid rise in intracranial pressure, subarachnoid and subdural hemorrhage, venous infarction and bleeding within the brain. Such individuals usually die. There may be lesser more subtle forms of this process that may not be immediately or ever recognized for they are clinically. This may include intermittent or partial thrombosis of a major cortical draining vein with or without venous sinus thrombosis. The consequences of this can be headache, lethargy, seizures, irritability, or prostration. There may be cerebral edema, subarachnoid hemorrhage, subdural hemorrhage and sometimes bleeding in the brain as well. Such individuals may also show retinal hemorrhages. These conditions may be caused, especially in young infants by dehydration (secondary to persistent vomiting, diarrhea, insufficient fluid intake), fever, infections and sepsis, brain trauma, and a host of other conditions. Sagittal sinus and venous thrombosis may occur in conjunction with the "respirator" brain phenomenon and have nothing to do with any prior condition. A careful post mortem examination can often differentiate whether the process is premortem or intramortem.
· Disseminated Intravascular Coagulopathies are a group of disorders that affect clotting or thrombosis. These disorders come in both genetic and acquired forms and are not easily diagnosed. Coagulation Disorders produce increased vascular permeability and a decreased ability to clot after suffering a subdural hematoma. Unfortunately, because most of the clotting and complement disorders can only be tested on circulating blood, it is nearly impossible to determine retrospectively, during autopsy, whether a child had a clotting disorder that exacerbated or caused a subdural hematoma.
Thrombocytopenia (TCP) is a coagulopathy defined by platelet counts less than 100,000/mm of blood. Platelet counts of less than 50,000 have been associated with bleeds from minor trauma whereas platelet counts between 10,000-15,000 results in spontaneous hemorrhages. TCP can travel with other congenital conditions, such as TCP with Absent Radii (TAR) syndrome, May Hegglin Syndrome, Wiskott-Aldrich Syndrome, and Autosomal Recessive TCP. TCP can also be idiopathic. Ideopathic or immune TCP is caused by an autoimmune process which destroys platelets. It is found in 1 in 10,000 people. Ideopathic TCP is generally diagnosed from bruises or petichae on the body or mucosa sinuses, bleeding gums, epistaxis hematuria, menorrhagia, weight loss, fever, and headache. Treatment includes prednisone or splenectomy. TCP has three major causes:
1. Decreased bone marrow production: Can be tested by bone marrow biopsy. Generally affects hemopoeisis so may be accompanied by varying degrees of anemia or luekopenia.
2. Splenic Sequestration Abnormalities: Check for enlarged spleen. Most common cause is portal hypertension secondary to liver disease.
3. Accelerated Distraction: Abnormal vessels, fibrin thrombi or intravascular prostheses can all shorten the life span of a platelet and cause non-immunologic TCP.
a) Drug Induced TCP:
Most patients recover within 7-10 days. Some more
severely affected patients require platelet transfusions or temporary support with glucocorticoids or plasmapheresis. Patients are warned to avoid the offending drug in the future because even "minute" amounts of the drug are needed to set up subsequent immune reactions. Heparin is highly suspect to cause TCP and is more common in Heparin derived from beef lung. Vaccines have been shown to produce such results
b) Idiopathic TCP:
90% of the pediatric cases of immunologic TCP are seen following a recovery from upper respiratory illness or from a "viral exanthem." Acute idiopathic TCP generally recovers in 4-6 weeks though some cases take 3-6 months
Thrombocythemia (i.e. Thrombocytosis) is a coagulopathy characterized by platelet counts greater than 400,000. Both forms of TCC can cause hemorrhages in the veins of the skin, stomach, eyes, brain and vital organs
1. Primary Throbocythemia(TCC) is a condition where platelets are produced in greater number than usual.
2. Secondary Thrombocytopenia is more rare and more difficult to diagnose. It follows splenic atrophy, malignancy of the lungs etc. or chronic blood loss.
C. Von Willebrands Disease (VWD) is the most common inherited bleeding disorder. This disorder is characterized by a decreased production of Von Willebrand factor, (VWF) does two things.
1. Facilitates platelet adhesion under conditions of high shear stress by linking platelet membrane receptors to vascular subendothelium. Normal VWF levels are 10mg/L. "A modest reduction in VWF concentration or selective loss of high-molecule weight multimeters, decreases platelet adhesion and causes clinical bleeding."
2. Serves as a plasma carrier for factor VIII the antihemophilic factor that facilitates coagulation.
· Metabolic and Inflammatory Disorders - There are a number of metabolic or inflammatory disorders that may mimic SBS or that may play a roll in reducing the bodies ability to properly autoregulate after a head injury.
A. Disorders such as Waldenstrom's Macroglobulinemia, Multiple Mylomas, and Cryoglobulinemia increase a patients vulnerability to a head trauma by increasing blood viscosity which impairs blood flow through the capillaries. These disorders have also been known to cause retinal hemorrhages, CNS dysfunction, and skin necrosis.
B. GA-1- Is a metabolic disorder which mimics Shaken Baby Syndrome by thinning vein walls and causing spontaneous intracranial or retinal hemorrhages.
C. Sepsis or Endotoxic Shock Endotoxins are a gram negative bacteria produced when our immune system is put under stress. Illness, stress, antibiotics, and vaccines all increase the production of endotoxins in our system. Endotoxins create and/or exacerbate clotting disorders and coagulopathies by binding to the protein walls of the cell and breaking down the endothelium.
· Vaccines are counter-indicated for people with coagulation disorders, people with current illnesses and people with fragile immune systems. They are also contraindicated for people with seizures and for premature babies. The research thus far seems to indicate the mechanisms are not so sinister or complicated. The vaccines seem to cause inflammation in the brain in some of the more fragile babies. This in turn produces increased vascular permeability. With a short fall (or none at all) the child's brain starts to bleed at a fairly slow rate. The vaccines can also produce clotting disorders like TCP. . For some days and/or weeks prior to their death/arrest, they can bleed at a slow rate. This is evidenced by the varying ages of blood found in so many of these babies. It is also supported by caretakers, that infants exhibited the five precursor (ICP) symptoms seen on almost all of these babies prior to their alleged "shaking" (lethargy, vomiting, failure to feed, respiratory arrest, inconsolable/neurological cat cry, positional discomfort and/or seizures). Then at some point, a short fall (or none at all) exacerbates the subdural and causes arrest or death.
When doctors or experts are questioned as to whether a supposed SBS case could be the result of a vaccine injury, they generally indicate that the most common and most severe reaction to vaccines is redness at the site of injection. In fact, studies done by the vaccine companies themselves admit that it is relatively rare to see redness at the site of injection, but far more common to see systemic reactions to vaccines. Be aware that prosecutors will argue that even if the vaccines increases the amount of systemic reactions in children; this fact precipitates and instigates shaking events rather than serves as an alternative explanation for the subdural hematomas.
A. Studies done on Hepatitis B RECOMBIVAX HB indicates out of 432 doses administered to 147 infants only 0.2% of the infants showed redness at the site of injection whereas 10.4% had systemic reactions including irritability, fever, diarrhea, fatigue/weakness, diminished appetite, rhinitis (Product insert RECOMBIVAX HB) Merck and Co).
B. Product inserts from Prevnar, the new adjuvant vaccine made to replace the older and more dangerous form of DPT, lists adverse side effects to the vaccine that run an uncanny resemblance to those seen in the in the medical histories given hours or days prior to the deaths of many of the supposed "shaken babies".
· Antibiotics: Certain Antibiotics have been known to increase endotoxins or inhibit coagulation .
· Tyelenol: The effects of Tylenol and other analgesics have not been thoroughly explored. But, any drug that alters blood viscosity, should be used sparingly when a child has signs of increased intracranial pressure.
References
1 .Plunkett (2001). Fatal pediatric head injuries caused by short distance falls. American Journal of Forensic Medicine and Pathology 22, No. 1-12.
2. Reiber, G. (1993). Fatal falls in childhood. The American Journal of Forensic Medicine and Pathology 14(3): 201-207.
3. Root, I. (1992). Head injuries from short falls. The American Journal of Forensic Medicine and Pathology 13(1): 85-87.
4. Howard, M., Bell, B.A. and Uttley, D., (1993). The pathophysiology of infant subdural haematomas. British Journal of Neurosurgery, 7, 355-356.
5. Nelson (1996) Nelson Textbook of Pediatrics. 15th ed.
6. Piatt (1999) A Pitfall in the Diagnosis of Child Abuse: External Hydrocephalis, subdural hemotomas, and retinal hemorrhages. Neurosurgical Focus 7(4).
7. Lindberg, R. Mechanisms of injury of death: Medicological investigations of death. Spitz and Fisher (1998) 590-636
8. Piatt J., (1999). A pitfall in the Diagnosis of Child Abuse: External Hydrocephalus, Subdural Hematoma & Retinal Hemorrhages. Neurosurgical Focus 7(4)(4):1-9
9. Miller, E. et al (2001). Idiopathic thrombocytopenic purpura and MMR vaccine, Archives of Disease In Children 84:227-229.
10. Harrison (1991) Principles of Internal Medicine. Chapter by Robert Handlin on Disseminated Intravascular Coagulation. 1508-1509.
11. Miller, E. et al (2001). Idiopathic thrombocytopenic purpura and MMR vaccine, Archives of Disease In Children
Childhood Head Injury
A Short Bibliography of Must Read Articles
What follows is a short bibliography of the articles that anyone interested 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.
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)
Glossary
Abrasion: a scraping injury that carries away a surface of skin and causes bleeding.
Acute Subdural Hematoma: an arbitrarily assigned age of a subdural hematoma: usually Zero to 3-4 days. There are clinical, gross, radiological and pathological characteristics for these.
Blow: force inflicted against a body generally by another individual.
Bridging Veins: small veins that channel blood from the brain surface to the superior sagittal and other intradural venous channels that cross the subarachnoid space. Breakage or injury of these vessels causes subdural hemorrhages.
Bruise: an injury that involves some degree (usually capillary) bleeding into a tissue (usually the skin).
CAT Scan: an image made by computed tomography.
Cause of Death: the medical cause(s) bringing about the death of an individual.
Cerebrospinal Fluid (CSF): the watery, clear fluid secreted by the choroids plexus, and probably the brain itself, that collects in the ventricles of the brain and surrounds the brain. It is produced at a constant rate at all times and must be correspondingly absorbed to maintain normal intracranial pressures.
Chronic Subdural Hematoma: an arbitrarily assigned age of a subdural hematoma: > 10 days old (usually when a neomembrane encloses or nearly encloses a hematoma). There are clinical, gross, radiological and pathological characteristics to these.
Clinician: a physician who treats patients (internist, surgeon, pediatrician, etc.).
Coagulopathy: an abnormality of blood coagulation (either too much or too little). Can be assessed by platelet count, levels of clotting factors and other measures of blood clotting in the laboratory.
Conjunctiva: the outer covering the eyeball (the white of the eye).
Contusion: a bruise.
Cutaneous: of, relating to, or affecting the skin.
Diffuse Axonal Injuries: Axonal injury that is widespread over the brain. Should have multiple samples, from different locations, to document.
Ecchymosis: the escape of blood into the tissues from ruptured blood vessels. Also, a small hemorrhagic spot, larger than a petechia, in the skin or mucous membrane forming a nonelevated, rounded or irregular, blue or purplish patch.
Edema: abnormal amounts of water that has accumulated outside vessels into the spaces between cells in an organ.
Ependyma: the cellular covering (lining) of the brain's ventricular cavities. These are ciliated low cuboidal cells that facilitate movement of cerebrospinal fluid through the ventricles.
Forensic Pathology: the medical subspecialty within pathology devoted to the medical-legal aspects of pathology. Forensic pathologists usually function as a medical examiner's pathologist and have special statutory responsibilities.
G-force: the force of gravity. Acceleration of deceleration is often expressed in Gs… representing the added "gravity" force acting on a body. If someone weighed 100 lbs. At rest, and experienced a force of 3 G acceleration, they would experience the feeling of weight of 300 lbs. Tissues of the body have tolerance limits to G forces that are known.
Hematoidin: a yellow pigment not containing iron that is the product of blood degradation.
Hemosiderin: a brown-yellow pigment that contains iron and is a product of degradation of blood, usually found in scavenger cells called "sideophages".
Herniation: a breakthrough of a body organ or part of an organ through a tear or part of a membrane, muscle, or other tissue.
Hydrocephaly (Hydrocephalus): too much cerebrospinal fluid in and/or over the brain that is usually associated with increased intracranial pressure in children.
Hypoxic Ischemia: Injury from lack of blood and/or oxygen to the brain. Often mistaken for Diffuse Axonal Injury.
Hypoxia: not enough oxygen.
Impact: force directed against a body by any means (can include blow, falls, and other impacts).
Infaret: dead and dying tissue due to insufficient blood or nutrient supply.
Injury: any harmful effect on any tissue in the body by any means (not meant to imply willful force necessarily).
Ischemia: not enough blood supply.
Laceration: a cutting type injury to the skin or other organ.
Lucid Interval: In psychoses or delirium, a rational period appearing in the course of the mental disorder.
Manner of Death: a quasi-legal determination stipulated by statute of how the death occurred (homicide, suicide, accident, natural disease, undetermined or judicial-execution). The Medical Examiner is empowered and required by stature to determine manner of death. Hospital pathologists generally don't determine this.
Mass Effect: Damage to the brain due to the bulk of a tumor, the blockage of fluid or excess accumulation of fluid within the skull.
MRI: a noninvasive diagnostic technique that produces computerized images of internal body tissues and is based on nuclear magnetic resonance of atoms within the body induced by the application of radio waves.
Neomembrane: a membrane of inflammatory cells, reactive cells (fibroblasts), newly formed vessels and scar tissue (collagen) formed in the course of time after a subdural hemorrhage occurs. The age of this process can be estimated microscopically.
Neuropathology: the medical subspecialty of the pathology devoted to the diseases of the nervous system.
Parenchyma: Working tissue of an organ, as opposed to supporting or connective tissue
Pathology: the medical specialty devoted to understanding the mechanisms, causes and manifestations of disease processes (cancer, infection, traumatic injury, toxic injury, congenital anomalies, etc.). Pathologists do autopsies, examine tissues from surgery, and use a variety of laboratory technologies and research methods. Pathologists generally don't treat patients or admit them to hospital.
Platelets: microscopic cellular elements of the blood vital to clotting.
Retina: the light-sensing element inside the eye.
Subacute Subdural Hematoma: an arbitrarily assigned age of a subdrual hematoma: 5-10+ days. There are clinical, gross, radiological and pathological characteristics for these.
Subarachnoid Hemorrhage: bleeding in the subarachnoid space (space normally filled with cerebrospinal fluid, below the arachnoid membrane and above the brain.
Subcutaneous: being, living, used, or made under the skin.
Subdural Hemorrhage or Hematoma: bleeding beneath the dura and above the arachnoid and brain of whatever age.
Subgaleal Hemorrhage: bleeding in the deep tissues of the scalp just above the skull.
Tentorium: a fold of the dura mater which separates the cerebellum from the cerebrum and often encloses a process or plate of the skull called the bony tentorium.
Traumatic Axonal Injuries: Axonal injury due to trauma. Generally observed as focal injuries.
WBC: white blood cell count.
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