Journal of Forensic and Legal Medicine 74 (2020) 102024

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Journal of Forensic and Legal Medicine
journal homepage: http://www.elsevier.com/locate/yjflm

A verified period of normal neurologic status in a young victim of abusive
head trauma
Rene Romig, Angela Doswell, Danielle Horton, Cree Kachelski, Jim Anderst *
Children’s Mercy Hospital, Kansas City, MO, United States

A R T I C L E I N F O

A B S T R A C T

Keywords:
Abusive head trauma
Injury timing
Child physical abuse
Child protection

Abusive head trauma (AHT) is the leading cause of child physical abuse fatalities, and survivors frequently face
life-long consequences. Victims of AHT are typically infants, and many are subjected to repeat AHT if not
accurately identified and protected. Identifying the timing of AHT is often a medical-forensic process, and
investigative personnel use the determination of timing of AHT to guide safety decisions for the child victim. If
the medical-forensic timing of AHT is incorrect, a child could be inappropriately placed and/or an innocent
caregiver could be subject to prosecution. Victims of AHT who suffer severe/permanent injury are felt to
demonstrate symptoms immediately after the trauma, and AHT victims with milder injury are thought to
generally have persistent or recurrent clinical signs shortly after the trauma. Periods of normal neurologic
appearance, in which a victim of AHT is completely asymptomatic for an extended time after the trauma, are felt
to be rare and have not been well characterized in the literature. This case involves a 2-month-old infant victim
of AHT who presented to medical care with mild neurologic symptoms that resolved without intervention from
medical personnel. While hospitalized, the infant had an asymptomatic period of approximately 38 hours prior to
more severe neurologic decompensation, then later returned to neurologic baseline. This case highlights the
challenges in accurately timing AHT in very young victims who return to neurologic baseline by characterizing a
verifiable prolonged period of normal neurologic appearance and function after AHT.

1. Introduction

infants who eventually return to neurologic baseline. Most studies
examining neurologic status after head trauma involve children older
than most AHT victims or children who suffer permanent neurologic
damage or death.10–16 Studies examining neurologic status in relation to
timing of trauma in infants who survive AHT typically rely on a single
witness account, often the alleged perpetrator, with minimal details
regarding the infant’s neurologic state and/or progression of
symptoms.11,17
We present the case of a 2-month-old male victim of AHT and a
verifiable extended period of normal neurologic status after the abusive
trauma. The infant then suffered neurological decompensation but
subsequently returned to neurologic baseline. This case uniquely dem­
onstrates the challenges in accurately timing non-fatal AHT in very
young infants, specifically when the infant returns to neurologic
baseline.

Abusive head trauma (AHT) is the leading cause of child physical
abuse fatalities. Survivors frequently face life-long consequences.1 In the
past two decades, clear links have been established between the specifics
of the clinical history of presentation, physical findings, radiological
findings and AHT, facilitating increased confidence in diagnosis.2–5
However, at times, identifying the timing of AHT remains challenging.
As timing based on neuroimaging is imprecise,6 clinical symptoms are
often the most useful tool.7,8 Consensus has been reached that children
with fatal head trauma generally have altered mental status immediately
subsequent to the injury and do not experience prolonged periods of
normal behavior/neurologic status occurring after head injury, prior to
later decompensation.9 In non-fatal victims of AHT who demonstrate
neurologic compromise, the moment of onset of clear and persistent
neurologic symptoms may provide the best estimate of timing of AHT;
however, prolonged periods of normal neurologic function may occur
due to a few clinical scenarios.7,8 Cases with a detailed, verifiable delay
in symptoms in infants after head trauma are lacking, particularly for

2. Case report
A previously well 2-month-old male infant born at 38 weeks via

* Corresponding author. Division of Child Adversity and Resilience, Children’s Mercy Hospital, 2401 Gillham Road, Kansas City, MO, 64108, United States.
E-mail address: jdanderst@cmh.edu (J. Anderst).
https://doi.org/10.1016/j.jflm.2020.102024
Received 27 February 2020; Received in revised form 9 July 2020; Accepted 13 July 2020
Available online 18 July 2020
1752-928X/© 2020 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.

R. Romig et al.

Journal of Forensic and Legal Medicine 74 (2020) 102024

vaginal delivery with an uncomplicated neonatal course was brought to
a hospital by emergency medical services (EMS). The infant’s mother
last saw him at 0300 after she fed him a bottle. At that time, he was
behaving normally, smiling and cooing, with no abnormal symptoms.
From that point on, the infant was in the sole care of his biological father
who reported that the infant remained normal until shortly after noon
when he experienced an episode of choking/emesis and limpness
without color change. The father denied any trauma or other abnormal
events prior to this episode. The father performed 1 minute of CPR and
subsequently noted spontaneous movement. He then called 911 at 1249.
On arrival at 1258, EMS noted that the infant was spontaneously
breathing, although respirations were labored and irregular, and he had
a fixed gaze without tracking. Despite normal pulse oximetry readings,
he was placed on 15 L of oxygen via non-rebreather mask. At 1310, the
patient was noted to develop recurrent 10–15 second episodes of
decorticate posturing followed by decerebrate posturing every 2 mi­
nutes. These episodes spontaneously resolved by the time of arrival at
the emergency department (ED) at 1327. At that time, the infant was
noted by EMS personnel to be “pink” and “breathing on his own very
well”.
Initial vitals taken at 1331 in the ED were normal for age. On the
initial physician assessment, the infant was alert without signs of res­
piratory distress or neurological compromise. Flexion of left extremities
was documented in multiple resident physician (physicians in training)
notes, with one indicating concern for seizure. The attending pediatric
emergency medicine physician noted that the flexion slowly relaxed
with consoling and did not document any concern for active seizing in
the emergency department. The infant was given 40 mg/kg of levetir­
acetam at 1354 and 0.1 mg/kg of IV midazolam at 1356 as a “precaution
for seizures due to the EMS report of prior posturing.” Radiology im­
aging obtained at that time included: CT head without contrast, CT spine
without contrast, skeletal survey, and CT abdomen/pelvis with contrast.
Imaging demonstrated no evidence of fracture or intrabdominal trauma,
but CT head revealed a thin left convexity SDH with greatest thickness in
right parasagittal area near the vertex (5mm in maximal thickness)
without midline shift (Fig. 1). The infant was then admitted to the pe­
diatric intensive care unit (PICU) at approximately 1450 on room air
with normal vitals. The initial exam in the PICU revealed spontaneous
eye opening and equal limb movements without evidence of focal
defects.
While in the PICU, ophthalmology was consulted and detected
bilateral “diffuse retinal hemorrhages, involving all layers, too
numerous to count, many with white centers extending from posterior

pole to ora serrata”. A brain MRI revealed “small left frontotemporal
hemorrhagic cerebral contusions as well as additional multifocal tiny
nonhemorrhagic left temporal parenchymal contusions” and “bilateral
supratentorial and infratentorial convexity subdural hemorrhages”
(Figs. 2 and 3). Brain MRA and MRV were normal, as was spine MRI.
The PICU stay constituted the majority of a 38-h period of normal
neurological status as documented by 11 normal nursing neurological
checks, each of which included an assessment of pupil appearance and
reactivity, response to verbal and tactile stimulation, muscle tone and
strength and spontaneous movements, and physical exams by 7 different
medical services. The infant did not receive any medications during this
time. He had no emesis or other symptoms of head trauma, but he was
not provided with oral feeds during the PICU stay. Due to his prolonged
normal neurologic status, he was transferred to the floor.
After transfer to the floor, the infant initially tolerated oral bottle
feeds provided by nursing staff, then subsequently had 2 episodes of
bradycardia to the mid-80s and 3 episodes of emesis. The infant then
exhibited seizure activity described as eyes rolling back and leg/hand
twitching and multiple self-resolving desaturations to the 70s and 80s.
He received 30 mg/kg levetiracetam and 0.1mg/kg lorazepam as
treatment. Approximately 35 minutes later, the infant was noted to be
apneic and unresponsive for 60 seconds with oxygen saturation to 47%;
bag-mask ventilation was initiated, and a code blue was called. He then
received 20 mg/kg fosphenytoin and was transferred to the PICU on 15
L/minute oxygen via face mask, after which the seizures stopped. Repeat
head CT (Fig. 4) again showed SDH, now measuring 7mm in maximal
thickness.
Within 24 hours of the transfer back to the PICU, the infant had
multiple seizures requiring 3 doses of fosphenytoin (each 10 mg/kg) and
two doses of lorazepam (each 0.1 mg/kg). He was then initiated on
oxcarbazepine maintenance. Levetiracetam was continued and enteral
feeds via nasojejunal tube were started. Four days after transfer to the
PICU, he had been seizure-free for 24 h. After six days in the hospital, he
had no neurologic abnormalities and was discharged to his maternal
great-grandmother. Three weeks after discharge, a repeat skeletal sur­
vey revealed no fractures. Children’s Protective Services substantiated
the allegation of abuse. The child remained in the care of his maternal
great-grandmother for the next 12 months. During that period, he
remained seizure free with no neurologic abnormalities.

Fig. 1. Coronal view of head CT on day of admission.

Fig. 2. T2 Coronal MRI of brain.
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Journal of Forensic and Legal Medicine 74 (2020) 102024

more severe neurologic symptoms. Even if the infant had neurologic
decompensation at the moment of seizure prophylaxis in the ED, he
would have had at least an approximately 25 to 30-min period of normal
neurologic status after AHT. After the one-time seizure prophylaxis, he
had an approximately 38-h period of normal neurologic status after
AHT. Had the infant not presented to care after his initial, minor
symptoms of injury, it is possible that his more severe, later neurologic
compromise would have occurred under supervision of different care­
givers who had no knowledge of the prior symptoms. In such a case, if
the AHT was incorrectly timed to the onset of severe neurologic symp­
toms, investigation into the potential perpetrator would likely have been
limited to these caregivers, potentially missing a critical contact or
suspect. This case demonstrates the challenges of accurately timing AHT
in young infants who suffer no apparent long-term neurologic
complications.
There is generalized agreement that children who have severe, per­
manent brain injury have immediate or near immediate and persistent
symptoms after the head injury.7–9 Studies involving perpetrator ad­
missions demonstrate immediate and persistent symptoms in cases with
sufficient details.17,18 Other studies evaluating for possible delayed
neurologic decompensation typically involve subjects older than most
victims of AHT and/or subjects who suffer permanent neurologic dam­
age or death.10–16 However, there is also a degree of agreement that, in
some cases, particularly those in which the child eventually returns to
neurologic baseline, a period of normal neurologic appearance is pos­
sible.7–9 The potential for delayed decompensation is most often
attributed to gradually increasing intracranial pressure (from an
expanding extra-axial hematoma or brain swelling due to hypoxia, so­
dium imbalance, progressive injury, or other causes) or post-traumatic
seizures. Although the possibility for such situations is acknowledged,
published scientific support that includes verified behaviors during and
duration of the period of normal neurologic appearance in young infants
is lacking. This case demonstrates a verifiable, extended, asymptomatic
interval after AHT in a young victim who had delayed neurologic
decompensation but subsequently returned to neurologic baseline.
The infant involved in this case most likely suffered later neurologic
decompensation due to post-traumatic seizures, and, possibly, to
expansion of the SDH. Though post-traumatic seizures are a well-known
entity, they are not well described in relation to the timing of AHT or in
severity after AHT. In the case described here, the child’s neurologic
decompensation was severe and persistent for days. This type of
neurologic decompensation typically occurs immediately after severe
head trauma. Additionally, the infant rapidly transitioned from
asymptomatic to significantly symptomatic, as can be seen immediately
after head trauma. He did receive minor medical interventions at initial
presentation (1 dose each of 2 prophylactic anti-epileptic medications
and oxygen), despite having returned to neurologic baseline. It is
possible that the anti-epileptic medications contributed to the duration
of the normal neurologic appearance. The half-lives of the medications,
approximately 5 hours for levetiracetam and 1–3 hours for mid­
azolam,19,20 suggest that the medications were unlikely to be providing
clinically significant seizure suppression during much of the hospitali­
zation. Additionally, levetiracetam reaches maximal concentration 1
hour after dosing, and typically requires twice daily dosing for two days
to reach steady state levels.19 The effect of midazolam peaks at 15–30
minutes after dosage.20 As such, it seems unlikely that the single doses of
the two medications fully explain the lengthy period of apparent normal
neurologic function after the AHT.
Although the child’s presence in the hospital provides documented
evidence of his normal neurologic status after AHT, the hospital in­
terventions create a limitation. In addition to the potential contribution
of the anti-epileptic medications to the duration of the period of normal
neurologic status, the infant was not given oral feeds for a period in the
PICU as he awaited sedation for the MRI. He initially tolerated oral feeds
after transfer to the floor, but then began vomiting in the hours prior to
his neurologic decompensation. It is unknown if he would have tolerated

Fig. 3. Axial view of susceptibility weighted imaging sequence of brain MRI.
The arrow demonstrates the left fronto-temporal hemorrhagic contusion.

Fig. 4. Coronal view of head CT after 38 hours of normal neurologic status
followed by more severe neurologic decompensation.

Written authorization for this case report was obtained by the in­
fant’s legal guardian.
3. Discussion
This case describes a 2-month-old infant with findings most consis­
tent with AHT who had a symptom-free interval between minor and
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Journal of Forensic and Legal Medicine 74 (2020) 102024

oral feeds during the period when they were not allowed.
Cases such as this are rare in the literature likely because they are
rare in clinical presentation. Despite the rarity of such a presentation,
the existence of a well-documented, prolonged period of normal
neurologic function after AHT must be considered when attempting to
time the occurrence of AHT in very young infants who return to
neurologic baseline. Physicians involved in such cases should obtain a
detailed history regarding any prior symptoms or caregivers over the
days preceding initial presentation and acknowledge that timing such
cases is difficult in some situations. Information from this case should
not be applied to older infants or infants who die or suffer permanent
neurologic sequalae. Future studies are needed detailing the clinical
course of very young victims of head trauma to better inform medicalforensic decision-making.

they have no conflict of interest.
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Human and animal rights
This research was performed in accordance with the ethical stan­
dards as laid down in the 1964 Declaration of Helsinki and its later
amendments or comparable ethical standards. This article does not
contain any studies with animals performed by any of the authors.
Funding source
None.
Contributor’s statement page
Dr. Anderst conceptualized the case report and reviewed and revised
the manuscript.
Dr. Romig conceptualized the case report, drafted the initial manu­
script, and reviewed and revised the manuscript.
Drs. Kachelski, Horton, and Doswell critically analyzed and inter­
preted the information in the case report, reviewed the manuscript for
scientific accuracy and revised the manuscript.
All authors approved the final manuscript as submitted and agree to
the accountable for all aspects of the work.
Declaration of competing interest
Dr. Anderst has provided paid expert testimony and case consulta­
tion in cases of alleged child abuse. The remaining authors declare that

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