Patrick Barnes, MD
Abstract Because of the widely acknowledged controversy involving the determination of nonaccidental injury (NAI), the radiologist must be familiar with the issues, the literature, and the principles of evidence-based medicine in order to properly understand the role of imaging. Children with suspected NAI must not only receive protective evaluation, but also require a timely and complete clinical and imaging workup, to include strong consideration for the mimics of abuse. The imaging findings cannot stand alone and must be correlated with clinical findings (including current and past history), adequate laboratory testing, and proper pathologic and forensic examinations. In the context of evidence-based medicine, along with recent legal challenges, the medical and imaging evidence cannot reliably diagnose "intentional" injury. Only the child protection investigation may provide the basis for "inflicted" injury in the context of supportive medical, imaging, biomechanical, or pathology findings.
Nonaccidental, inflicted, or intentional, trauma is said to be the most frequent cause of traumatic injury in infants with peak incidence at about 6 months of age, and accounting for about 80% of the deaths from traumatic brain injury in children under the age of two years [1-9]. Nonaccidental injury (NAI), or nonaccidental trauma (NAT), is the more recent terminology applied to the traditional labels “child abuse”, “battered child syndrome”, and “shaken baby syndrome” (SBS). A more recent restatement of the traditional definition of SBS is that it represents a form of physical NAI to infants characterized by the triad of (1) subdural hemorrhage - SDH, (2) retinal hemorrhage - RH, and (3) encephalopathy (i.e. diffuse axonal injury - DAI) occurring in the context of inappropriate or inconsistent history (particularly when unwitnessed), and commonly accompanied by other apparently inflicted injuries (e.g. skeletal)  . This empirical formula is under challenge by evidence-based medical and legal principles [10-23].
Traumatic Central Nervous System Injury
The spectrum of traumatic central nervous system (CNS) injury has been categorized in a number of ways [7,22]. Clinically and pathologically, primary injury (e.g. contusion, shear injury) directly results from the initial traumatic force and is immediate and irreversible. Secondary injury arises from, or is associated with, the primary injury and is potentially reversible (e.g. swelling, hypoxia-ischemia, seizures, herniation). Traditional biomechanics teaches that impact loading is associated with linear forces and produces localized cranial deformation and “focal” injury (e.g. fracture, contusion, epidural hematoma - EDH). Accidental injury (AI) is said to be typically associated with impact and, with the exception of EDH, is usually not life threatening. Impulsive loading refers to angular acceleration / deceleration forces resulting from sudden non-impact motion of the head on the neck (i.e. whiplash) and produces “diffuse” injury, i.e. shear strain deformation and disruption at tissue interfaces (i.e. SBS including bridging vein rupture with SDH and white matter shear injury – DAI ). The young infant is said to be particularly vulnerable to the latter mechanism (i.e. SBS) because of weak neck muscles, a relatively large head, and an immature brain. SBS is traditionally postulated to result in the triad of primary traumatic injury (i.e. SDH, RH, and DAI) which has been reportedly associated with the most severe and fatal CNS injuries.
Stated assault mechanisms in NAI have include battering, shaking, impact, shaking-impact, strangulation, suffocation, and combined assaults (shake-bang-choke) [1-9,22]. The spectrum of CNS injury occurring with NAI overlaps that due to AI. However, certain patterns have been reported to be characteristic of, or highly suspicious for, NAI [7,9,22]. These include multiple or complex cranial fractures, acute interhemispheric SDH, acute-hyperacute SDH, DAI, chronic SDH, and the combination of chronic and acute SDH. The latter is said to be indicative of more than one abusive event. Imaging evidence of CNS injury may occur with, or without, other clinical findings of trauma (e.g. bruising) or with other traditionally “higher specificity” imaging findings of abuse (e.g. metaphyseal or rib fractures) [7,9]. Therefore, clinical and imaging findings of injury out of proportion to the history of trauma, and injuries of different ages, are two traditional criteria used by medical professionals, including radiologists, to make a medical diagnosis and offer expert testimony that such “forensic” findings are “proof” of NAI / SBS, particularly when encountered in the premobile, young infant.
Evidence-based Medicine & the Law Evidence-based medicine (EBM) is now the guiding principle in establishing standards and guidelines as medicine has moved from an authoritarian to an authoritativeera in order to overcome bias [23-27]. EBM quality of evidence (QOE) ratings of the literature are based upon levels of accepted scientific methodology and biostatistical significance (e.g. p values) and applies to every aspect of medicine including diagnostics, therapeutics, and forensics. EBM analysis reveals that few published reports in the traditional NAI / SBS literature merit a QOE rating above class IV (e.g. expert opinion alone) . Such low ratings do not meet EBM recommendations for standards (e.g. class I) or for guidelines (e.g. class II). Difficulties exist in the rational formulation of a “medical” diagnosis or “forensic” determination of NAI / SBS based on an alleged event (e.g. shaking) that is inferred from clinical, imaging, or pathologic findings in the subjective context of (a) an “unwitnessed” event, (b) a “noncredible” history, or (c) an admission or confession under dubious circumstances . This problem is further confounded by the lack of consistent and reliable criteria for the diagnosis of NAI / SBS, and that much of the traditional literature on child abuse consists of anecdotal case series, case reports, reviews, opinions, and position papers [10,11,28,29]. Many reports include cases having impact injury which undermines the SBS hypothesis by imposing a “shaking-impact” syndrome. Also, the inclusion criteria provided in many reports are criticized as arbitrary. Examples include “suspected abuse”, “presumed abuse”, “likely abuse”, and “indeterminate” [28,29]. Furthermore, the diagnostic criteria often appear to follow “circular logic” such that the inclusion criteria (e.g. the triad) becomes the conclusion (i.e. the triad equals SBS/NAI).
Regarding the rules of evidence within the justice system, there are established standards for the admissibility of expert testimony [12,13,30]. The Frye standard requires only that the testimony be generally accepted in the relevant scientific community. The Daubert (and Kumho) standard requires assessment of the scientific reliability of the testimony. A criticism of the justice system is that the application of these standards vary with the jurisdiction (e.g. according to state v. federal law). Additional legal standards regarding proof are also applied in order for the triar of fact (e.g. judge or jury) to make the determination of civil liability or criminal guilt. In a civil action (e.g. medical malpractice lawsuit), money is primarily at risk for the defendant health care provider, and proof of liability is based upon a preponderance of the evidence (i.e. at least 51% scientific or medical certainty).
In a criminal action, life or liberty is at stake for the defendant, including the permanent loss of child custody [12,13,30]. In such cases, the defendant has the constitutional protection of due process that requires a higher level of proof. This includes the principle of innocent until proven guilty beyond a reasonable doubt with the burden of proof on the prosecution and based upon clear and convincing evidence. However, no percentage of level of certainty is provided for these standards of proof in most jurisdictions. Furthermore, only a preponderance of the medical evidence (i.e. minimum of 51 % certainty) is required to support proof of guilt whether the medical expert testimony complies with the Frye standard (i.e. general acceptance without the requirement of scientific reliability) or the Daubert standard (i.e. scientific reliability requirement). A further criticism of the criminal justice process is that in NAI cases, medical experts have defined SBS / NAI as “the presence of injury (e.g. the triad) without a sufficient historical explanation”, and that this definition unduly shifts the burden to the defendant to establish innocence by proving the expert theory wrong.
The “Medical” Prosecution of NAI and its EBM Challenges Traditionally, the prosecution of NAI has been based upon the presence of one, or all, of the injury components of the triad as supported by the premises that (a) shaking alone in an otherwise healthy child can cause SDH leading to death, (b) that such injury can never occur on an accidental basis (e.g. short fall) because it requires a massive force equivalent to a motor vehicle accident or a fall from a two-story building, (c) that such injury is immediately symptomatic and cannot be followed by a lucid interval, and (d) that changing symptoms in a child with prior head injury indicates newly inflicted injury and not a spontaneous rebleed [12,13,23]. Using this reasoning, the last caretaker is automatically guilty of abusive injury, especially if not witnessed by an independent observer. Also, it has been asserted that RHs of a particular pattern are diagnostic of SBS / NAI.
Reports from clinical, biomechanical, pathology, forensic, and legal disciplines, within and outside of the child maltreatment literature, have challenged the evidence base for NAI / SBS as the only cause for the triad [10-23]. Such reports indicate that the triad may also be seen with accidental injury (including witnessed short falls, lucid intervals, and rehemorrhage), as well as in medical conditions. These are the “mimics” of NAI and often present as acute life threatening events (ALTE) [31-34]. The mimics include hypoxia-ischemia (e.g. apnea, choking, respiratory or cardiac arrest), ischemic injury (arterial vs. venous occlusive disease), seizures, infectious or post-infectious conditions, coagulopathy, fluid-electrolyte derangement, and metabolic or connective tissue disorders including vitamin deficiencies and depletions (e.g. C,D,K).
Many ALTE appear to be multifactorial and involve a combination, sequence, or cascade of predisposing and complicating events or conditions [23,31]. As an example, an infant may suffer a head impact, or choking spell, followed by a seizure or apnea, and then undergoes a series of interventions including prolonged or difficult resuscitation and problematic airway management with subsequent hypoxia-ischemia and coagulopathy. Another example is a young infant with a predisposing condition such as infectious illness, fluid-electrolyte imbalance, or a coagulopathy, who then suffers seizures, respiratory arrest, and resuscitation with hypoxia-ischemia. In many cases of alleged SBS/NAI it is often assumed that nonspecific premorbid symptoms (e.g. irritability, lethargy, poor feeding) in an “otherwise healthy” infant is an indicator of ongoing abuse or that such symptoms become the inciting factor for the abuse. A thorough and complete medical investigation in such cases may reveal that the child is “not” otherwise healthy and, in fact, is suffering from a medical condition that progresses to an ALTE [10-23].
The “mechanical” basis for SBS as originally hypothesized by Guthkelch (1971) and Caffey (1972, 1974), and then subsequent authors, was extrapolated from a single scientific source [5,6,35]. The biomechanical and neuropathological experiment conducted by Ommaya (1968) used a whiplash model comprised of adult rhesus monkeys mounted on a piston-driven sled to determine the angular acceleration threshold (i.e. 40g) for head injury (i.e. concussion, SDH, shear injury) as well as neck injury . From this experiment, it was assumed by Gutkelch and Caffey that manual shaking of an infant could generate these same forces and produce the triad [37-39]. Caffey stated “current evidence, though manifestly incomplete and largely circumstantial, warrants a nationwide educational campaign on the potential pathogenicity of habitual shaking of infants [6,35].” As a result, centers for child abuse (e.g. Kempe, Chadwick) were established all across the country, along with mandated reporting laws, with the anticipation of further research into these issues.
Probably the first and most widely reported biomechanical test of the SBS hypothesis was conducted by Duhaime et al (1987) who measured the angular accelerations associated with adult manual shaking (11g) and impact (52g) in a 1-month old infant anthropormorphic test device (ATD) . Only accelerations associated with impact (4-5 times that associated with shakes), on an unpadded or padded surface, exceeded the injury thresholds determined by Ommaya. Furthermore, in the same study, the authors reported a series of 13 fatal cases of NAI / SBS in which all had evidence of blunt head impact (more than half noted only at autopsy) . The authors concluded that CNS injury in SBS / NAI in its most severe form is usually not caused by shaking alone. Their results contradicted many of the original reports that had relied upon the “whiplash” mechanism as causative of “the triad.” These authors also concluded that fatal cases of SBS / NAI, unless in children with predisposing factors (e.g. subdural hygroma, atrophy, etc.), are not likely to result from shaking during play, feeding, swinging, or from more vigorous shaking by a caretaker for discipline. They suggested the use of the new term “shaken-impact syndrome .”
More recently, Prange et al (2003) using a 1.5 month-old ATD showed that (a) peak angular accelerations and maximum change in angular velocity increased with increasing fall height and surface hardness, (b) that inflicted impacts against hard surfaces were more likely to be associated with brain injury than falls from less than 1.5m or from vigorous shaking, and (c) there are no data to show that such measured parameters during shaking or inflicted impacts against unencased foam is sufficient to cause SDH or TAI in an infant . Their results along with other animal, cadaver, and clinical case studies also indicate that SDH and death from minor falls in infants are more likely to occur with falls > 1.5 m (4-5 ft.) and on to a hard surface . With further improvements in ATDs, more recent experiments indicate that maximum head accelerations may exceed injury reference values (IRV) at lower fall heights than previously determined [Table 1; 41a]. Subsequent studies with varying QOE ratings and using biomechanical (ATD), animal, or computer models have either supported, or failed to invalidate, the Duhaime study [42-50]. Some critics of the Duhaime and Prange studies (Cory & Jones 2003, Roth et al 2006, Pierce & Bertocci 2008) also contend that there is no adequate human infant surrogate yet designed to properly test “shaking vs. impact [44,49,50].” Even more recently, Coats and Margulies (2008) used an innovative 3D biomechanical technique to provide preliminary verification of prior cadaver drop results that infant linear skull fractures may occur with head-first fall heights 0.9 m (3 feet) onto carpet and 0.6-0.9 m (2-3 feet) onto concrete [44a].
Other reports (Ommaya et al 2002, Bandak 2005, etc.) also show that shaking alone cannot result in brain injury (i.e. the triad) unless there is concomitant structural failure with injury to the neck, cervical spinal column, or cervical spinal cord, since these are the “weak links” between the body and head of the infant [42,45]. Although Bandak’s results were criticized by Margulis et al [45a], to whom Bandak subsequently responded [45b], Margulis et al acknowledged the possibility for neck injury during severe shaking without impact. Spinal cord injury without radiographic abnormality (SCIWORA), whether AI or NAI, is an important form of primary neck and spinal cord injury with secondary brain injury . For example, a falling infant experiences a head-first impact with subsequent neck hyperextension or hyperflexion from the force of the trailing body mass. There is resultant upper spinal cord injury without detectable spinal column injury on plain films or CT. Compromise of the respiratory center at the cervico- medullary junction results in hypoxic brain injury including the “thin” SDH. CT often shows the brain injury, but only MRI may show the additional neck or spinal cord injury.
The minimal force required to produce one or more of the elements of the triad has yet to be established. However, from the current evidence base in biomechanical science, one may reasonably conclude that (1) shaking may not produce direct brain injury, but may cause indirect brain injury if associated with neck and cervical spinal cord injury, (2) angular acceleration / deceleration injury forces clearly occur with impact trauma, (3) that such injury on an accidental basis does not require a force that can only be associated with a two-story fall or a motor vehicle accident, (4) that household (i.e. short-distance falls) may produce direct or indirect brain injury, (5) that in addition to fall height, impact surface and type of landing are important factors, and (6) that head-first impacts in young infants not having developed a defensive reflex (e.g. extension of a limb to break the fall) are the most dangerous and may result in direct or indirect brain injury (e.g. SCIWORA).
Neuropathological Challenges Probably the first and largest systematic neuropathological study in alleged SBS / NAI (53 cases) was recently reported by Geddes et al (2001) [52,53]. The findings in their 37 infant cases ( age < 9 months) indicate (a) only 8 infants had no evidence of impact with only one case of admitted shaking, (b) that the cerebral swelling in young infants is more often due to “diffuse” axonal injury of hypoxic-ischemic encephalopathy (HIE) rather than traumatic axonal, or shear, injury (TAI); (c) that although fracture, “thin” SDH (e.g. dural vascular plexus origin), and RH are commonly present, the usual cause of death was increased intracranial pressure from brain swelling associated with HIE; and, (d) that cervical epidural hemorrhage and focal axonal brain stem, cervical cord, and spinal nerve root injuries were characteristically seen in these infants (most with impact). Such upper cervical cord / brainstem injury may result in apnea / respiratory arrest and be responsible for the HIE. In the older infant and child case group (16 victims: ages 13 months to 8 years), the pathologic findings were primarily those of the “battered child or adult trauma syndrome” including extracranial injuries (e.g. abdominal), large SDH (i.e. bridging vein rupture), and TAI.
Additional neuropathologic series by Geddes et al (2003, 2004) have shown that SDH are also seen in non-traumatic fetal, neonatal, and infant brain injury cases and that such SDH are actually of intradural vascular plexus origin rather than bridging cortical vein origin [54,55]. The common denominator in these cases is likely a combination of cerebral venous hypertension and congestion, arterial hypertension, brain swelling, immaturity with vascular fragility further compromised by HIE or infection. This “unified hypothesis” of Geddes et al has received criticism in nonscientific reviews and surveys (Punt et al 2004, Minns 2005, Byard et al 2007, David 2008, Jaspan 2008) [21,22,56-58].However, their findings and conclusions have been validated by the research of Cohen et al (2007), as well as others [59-62]. In their post-mortem series, Cohen et al described 25 fetuses (gestational age range 26-41 weeks) and 30 neonates (postnatal age range 1 hour – 19 days) with HIE who also had macroscopic intradural hemorrhage (IDH), including frank parietal SDH in two-thirds. The IDH component was most prominent along the posterior falcine and tentorial vascular plexuses (i.e. interhemispheric fissure). They concluded from their work, along with the findings of other cited researchers, that IDH and SDH are commonly associated with HIE (including the targeting of claudin-5, a key neurovascular tight-junction molecule), and particularly when associated with increases in central venous pressure  . This also explains the frequency of RH associated with perinatal events .
From the evidence base in forensic pathology, one may conclude that (1) shaking may not cause direct brain injury, but may cause indirect brain injury (i.e. HIE) if associated with cervical spinal cord injury, (2) that impact may produce direct or indirect brain injury (e.g. SCIWORA), (3) that the pattern of brain edema with thin SDH (dural vascular plexus origin) may reflect HIE whether due to AI or NAI, and (4) that the same pattern of injury may result from non-traumatic or medical causes (e.g. HIE from any cause of ALTE). Furthermore, since the observed edema does not represent TAI (which results in immediate neurologic dysfunction), a lucid interval is possible particularly in the infant whose sutured skull and dural vascular plexus have the distensibility to tolerate early increases in intracranial pressure. Also, the lucid interval invalidates the premise that the last caretaker is always responsible in alleged NAI.
Doubt has been raised in the literature that NAI / SBS is the cause in all traumatic cases manifesting the triad. In the prosecution of NAI, as previously mentioned, it is often stipulated that short falls cannot be associated with serious (e.g. fatal) head injury or a lucid interval. Additonally, it has been stipulated that non-intentional new bleeding in an existing SDH is always minor, that SDH does not occur in benign extracerebral collections, and that symptomatic or fatal new bleeding in SDH requires newly inflicted trauma [12,13,23]. A number of past and current reports refute the significance of low level falls in children, including in-hospital and outpatient clinic series [65-72]. However, there are other reports, including emergency medicine, trauma center, neurosurgical, and medical examiner series, that indicate a heightened need for concern regarding the potential for serious intracranial injury associated with “minor” or “trivial” trauma scenarios, particularly in infants [72-93]. This includes reports of skull fracture or acute SDH from accidental simple falls in infants, SDH in infants with predisposing wide extracerebral spaces (e.g. benign extracerebral collections of infancy, chronic subdural hygromas, arachnoid cyst, etc.), and fatal pediatric head injuries due to witnessed, accidental short-distance falls, including those with a lucid interval, SDH, RH, and malignant cerebral edema. Also included are infants with chronic SDH from prior trauma (e.g. at birth) who then develop rehemorrhage.
Short falls, lucid intervals, and malignant edema. Hall et al (1989) reported that 41% of childhood deaths (mean age 2.4 yr.) from head injuries associated with AI were from low level falls (3 feet or less), while running, or down stairs . Chadwick et al (1991) reported fatal falls of less than 4 feet in 7 infants, but considered the histories unreliable . Plunkett (2001) reported witnessed fatal falls of 2-10 feet in 18 infants and children, including those with SDH, RH, and lucid intervals . Greenes and Schutzman (1998) reported intracranial injuries, including SDH, in 18 asymptomatic infants with falls of 2 feet to 9 stairs . Christian et al (1999) reported 3 infants with unilateral RH and SDH / SAH due to witnessed accidental household trauma .
Denton and Mileusic (2003) reported a witnessed, accidental 30-inch fall in a 9 month old infant with a 3 day lucid interval before death . Murray et al (2000) reported more intracranial injuries in young children (49% < age 4 yr.; 21% < age 1 yr.) with reported low level falls (< 15 feet), both AI and NAI . Kim et al (2000) reported a high incidence of intracranial injury in children (ages 3 mo. – 15 yr.; 52% < age 2yr.) accidentally falling from low heights (3-15 feet; 80% < 6 feet; including 4 deaths) . Because of the “lucid” intervals in some patients, including initially favorable Glascow Coma scores (GCS) with subsequent deterioration, both Murray and Kim expressed concern regarding caretaker delays and medical transfer delays contributing to the morbidity and mortality in these patients [74-76,78-81].
Bruce et al (1981) reported one of the largest pediatric series of head trauma (63 patients, ages 6 months to 18 years), both AI and NAI, associated with “malignant brain edema” and SAH / SDH . In the higher GCS (>8) subgroup, there were 8 with a lucid interval and all 14 had complete recovery. In the lower GCS (= 8) subgroup, there were 34 with immediate and continuous coma, 15 with a lucid interval, 6 deaths, and 11 with moderate to severe disability. More recently, Steinbok et al (2006) reported 5 children (4 < age 2yr.; 3 falls) with witnessed AI, including SDH and cerebral edema detected by CT 1-5 hours post-event . All experienced immediate coma and rapid progression to death.
Benign extracerebral collections (BECC). BECC of infancy (aka benign external hydrocephalus - BEH, benign extracerebral subarachnoid spaces – BESS) is a common and well-known condition characterized by diffuse enlargement of the subarachnoid spaces [85-94]. A transient disorder of cerebrospinal fluid circulation, probably due to delayed development of the arachnoid granulations, is widely accepted as the cause and develops from birth. BECC is typically associated with macrocephaly, but may also occur in infants with normal or small head circumferences, including premature infants. As with any cause of craniocerebral disproportion (e.g. BECC, hydrocephalus, chronic SDH or hygroma, arachnoid cyst, underdevelopment or atrophy), there is a susceptibility to SDH that may be spontaneous or associated with “trivial” trauma. A recent large series report and review by Hellbusch (2007) emphasizes the importance of this predisposition and cites other confirmatory series and case reports (30 references) . Papasian and Frim (2003) designed a theoretical model that predicts the predisposition of BEH to SDH with minor head trauma . Piatt’s case report (1999) of BECC with SDH (27 references), including RH, along with McNeely et al case series (2006) are further warnings that this combination is far from specific for SBS / NAI [86,92].
Birth Issues. In addition to the examples cited above ( e.g. short falls, BECC), another important but often overlooked factor is birth-related trauma [7,23,95-109]. This includes “normal” as well as complicated labor and delivery events (e.g. pitocin augmentation, prolonged labor, vaginal delivery, instrumented delivery, c-section, etc.). It is well-known that acute SDH often occurs even with the normal birth process, and that this predisposes to chronic SDH, including in the presence of BECC. Intracranial hemorrhages, including SDH and RH, have been reported in a number of CT and MRI series of “normal” neonates including a frequency of 50% by Holden et al (1999), 8% by Whitby et al (2004), 26% by Looney et al (2007), and 46% by Rooks et al (2008) [95,97-99]. Chamnanvanakij et al (2002) reported 26 symptomatic term neonates with SDH over a 3-year period following uncomplicated deliveries . Long-term followup imaging has not been provided in many of these series, although Rooks et al did report one child in their series who developed SDH with rehemorrhage superimposed upon BECC .
Chronic SDH and re-hemorrhage. Chronic SDH is one of the most controversial topics in the NAI vs. AI debate [1-9,19,21-23,37-39]. The “unexplained” SDH is often ascribed to NAI. By definition, a newly discovered chronic SDH started as an acute SDH that, for whatever reason, may have been “subclinical.” There is likely more than one mechanism for SDH which has prompted a revisiting of the concept of the “subdural compartment” [19,55,62,110,111]. In some cases of infant trauma, dissection at the relatively weak dura-arachnoid borderzone (i.e. dural border cell layer - DBCL) may allow cerebrospinal fluid (CSF) to collect and enlarge over time as a dural interstitial (i.e. intradural) hygroma. In other cases, there is bridging vein rupture within the dural interstitium that results in an acute subdural or intradural hematoma that extends along the DBCL. Further yet, traumatic disruption of the dural vascular plexus (i.e. venous, capillary, lymphatic), which is particularly prominent in the young infant, may also produce an acute intradural hematoma. Some of these collections undergo resorption while others progress to become chronic SDH. Some progressive collections may represent mixed CSF-blood collections.
The pathology and pathophysiology of neomembrane formation in chronic SDH, including rebleeding, is well-established in adults and appears similar, if not identical, to that in infants [112-133] . While acute SDH is most often due to impact or deformational trauma, whether AI or NAI, it must be differentiated from chronic SDH with re-hemorrhage. Progression of chronic SDH and rehemorrhage is likely related to capillary leakage and intrinsic thrombolysis [112,113]. Other factors include dural vascular plexus hemorrhage associated with increases in intracranial or central venous pressures (e.g. birth trauma, venous thrombosis, dysphagic choking), or with increased meningeal arterial pressure (e.g. reperfusion following hypoxia-ischemia) with resultant acute hemorrhage (or re-hemorrhage) in “normal” infants or superimposed upon “predisposing” chronic BECC, hygromas, hematomas, or arachnoid cysts [19,31,55,62,85-94,110,111]. The phenomenon of acute infantile SDH, whether AI or NAI, evolving to chronic SDH and re-hemorrhage, including RH, is well-documented in several neurosurgical series reports including Aoki et al (1984, 1990), Ikeda et al (1987), Parent (1992), Howard et al (1993), Hwang et al (2000), Vinchon (2002,2004), and others [114,117-119,122-124].
From the clinical evidence base, in addition to the biomechanical science and forensic pathology data bases, one may conclude that
(1) significant head injury, including SDH and RH, may result from low fall levels, (2) such injury may be associated with a lucid interval, (3) in some, the injury may result in immediate deterioration with progression to death, (4) BECC predisposes to SDH, (5) SDH may date back to birth, and (6) rehemorrhage into an existing SDH occurs in childhood and may be serious.