ILLUSTRATIVE CASE

Roller Coaster–Induced Subdural Hematoma in a Previously
Healthy Teenager
Peggy Tseng, MD, Yvette Liza Kearl, MD, and Ashkon Ansari, MD
Abstract: Of the multitude of neurologic injuries related to roller-coaster
rides, a majority of them are reported about adults. In this case, we present a
patient who presented to the pediatric emergency department with new-onset
seizure and hemiplegia 2 days after a roller-coaster ride. She was ultimately
diagnosed with a subdural hematoma. The acceleration and G forces of roller
coasters are hypothesized to cause enough stress and shearing forces that are
thought to directly cause subdural hemorrhage.
Advances in roller-coaster technology may surpass the passenger's
physical capacity for acceleration and rotary forces, and we may see an increased number of medical complications after these rides. We recommend
that emergency and pediatric health care providers consider amusement park
thrill rides as a possible cause of subdural hematomas in previously healthy
patients with new neurologic complaints.
Key Words: neuroimaging, neurologic injury, roller coaster, seizure,
subdural hematoma, traumatic brain injury
(Pediatr Emer Care 2019;35: e76–e78)

T

he US Consumer Product Safety Commission and the International Association of Amusement Parks and Attractions estimate that almost 300 million people visit amusement parks every
year in the United States,1,2 and in 2004 the US Consumer Product
Safety Commission examined retrospective data from 100 emergency departments (EDs) and found that 5900 nonoccupational injuries related to amusement parks resulted in hospital presentations.
In a retrospective study of adult ED and pediatric ED (PED) patients who came from local amusement parks in Pennsylvania, head
injuries were the second most common type of injury (14%) after
soft tissue lacerations.3 Ultimately 89% of all the patients were
discharged to home with benign diagnoses. Estimates of roller
coaster–related injuries range from 17% to 26%,1,3 and although
unknown, the national number of national roller coaster–related
catastrophic injury or death is rare. Yet traditionally these few reports have always garnered headline news attention.
The earliest report in medical literature of clinically significant
head injury from a roller coaster dates back to 1979, and since then,
a total of 22 cases of neurologic injuries associated with roller
coasters have been described. The injuries range from vertebral or
carotid artery dissections with or without concomitant cerebral
stroke, carotid thrombosis, intraparenchymal cerebral hemorrhage,
cerebrospinal fluid leak, subdural and subarachnoid hemorrhage,
subdural hygroma, and even spinal cord injuries.4–8 Most of these
cases were in adult patients, and only 2 were in pediatric patients
younger than 18 years. The most recent was a 2006 report of a

From the Department of Emergency Medicine, Los Angeles County–University
of Southern California, Los Angeles, CA.
Disclosure: The authors declare no conflict of interest.
Reprints: Ashkon Ansari, MD, Los Angeles County–University of Southern
California Medical Center, 1200 N State St, Los Angeles, CA 90033
(e‐mail: ashkon88@gmail.com).
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ISSN: 0749-5161

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healthy 13–year-old who presented 14 days after a roller-coaster
ride in Mexico with headache and right-sided paresis, and she
was found to have a subdural hematoma requiring neurosurgical
evacuation.9 We present another case of subdural hematoma associated with roller-coaster ride in a previously healthy pediatric patient.

CASE
A previously healthy 17-year-old girl presented to her primary care doctor with a 2-day history of headache and 1 episode
of right leg weakness that morning and developed a witnessed
tonic-clonic seizure after riding roller coasters at a local amusement park. The patient was in good health until 2 days prior to presentation; she went to a local amusement park and rode 3 different
roller coasters. She recalled bumping her head on the seats during
the roller-coaster rides, and after the third roller coaster, she experienced brief dizziness, mild difficulty walking, and a posterior
headache that persisted but decreased in intensity over the subsequent days. On the morning of presentation, she presented to her
primary care clinic for the headache and body weakness and
was noted to have involuntary right-sided arm and leg movements,
which developed into a witnessed generalized tonic-clonic seizure
lasting for 2 minutes followed by 5 minutes of a postictal state, after which she returned to baseline mental status. She was brought
to the PED by ambulance. She had no prior seizure history, fevers,
drug use, alcohol use, and other head trauma, and otherwise review of systems was negative.
The patient's medical history included a normal birth history
and a benign ovarian teratoma removal 8 months prior to this presentation. She was not taking any medications.
On examination in the PED, the patient had a temperature of
36.7°C, blood pressure of 119/83 mm Hg, heart rate of 96 beats/
min, and respiratory rate of 20 breaths/min. She was alert and oriented to person, place, time, and events. Her head was atraumatic,
and ear, nose, throat were without lesions/erythema or exudates.
The neck was supple without meningismus. The patient's lungs
were clear to auscultation bilaterally, and her cardiovascular examination revealed a regular rhythm without murmurs. The abdomen
was soft, nondistended, and nontender on examination. She had
2+ pulses in all extremities with warm and dry skin without any rash.
However, the patient's neurologic examination was notable for 4/5
weakness to the right upper and right lower extremity compared with
5/5 strength on the left. She had symmetrically intact sensation to
light touch, normal reflexes, no clonus, no dysdiadochokinesia, or
dysmetria, and her gait was ataxic. Her Romberg examination
was negative.
The patient's initial glucose was 118 mg/dL and then
114 mg/dL. The rest of her basic metabolic panel and hemoglobin/
hematocrit were all within normal limits. Her urine pregnancy test
was negative. An unenhanced computed tomography (CT) scan of
the head revealed a small- to moderate-sized left frontal subdural
hematoma with local mass effect and 2 mm of left-to-right midline
shift (Figs. 1, 2). The patient's examination remained unchanged
and nontoxic, with no altered mental status or seizure activity. Immediately after she returned from radiology, the patient's head of
Pediatric Emergency Care • Volume 35, Number 4, April 2019

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Pediatric Emergency Care • Volume 35, Number 4, April 2019

FIGURE 1. Subdural hematoma, CT image 1.

bed was elevated to 45 degrees, and she received 1000 mg of levetiracetam intravenously. The neurosurgery team was consulted
because of the intracranial finding with midline shift. Prior to
transfer to the pediatric intensive care unit (PICU), a second CT
head was completed 6 hours after the first CT head, and it showed
a grossly stable size in appearance of the known left frontoparietal
hemorrhage (Figs. 3, 4). The neurosurgery team decided to manage the subdural hematoma conservatively without surgery and to
follow with serial neurological examinations in the PICU.
On hospital admission days 1 and 2, the patient continued
with levetiracetam 500 mg orally every 12 hours and acetaminophen orally as needed for headache. During her stay in the PICU,
the patient's headache and hemiparesis slowly improved, and there
were no new or worsening neurologic symptoms. Neurology was
consulted with a question of whether a magnetic resonance venogram
was needed to evaluate for increased susceptibility of the cerebral
veins for subdural hematoma; however, it was deemed unnecessary.
With a normal complete blood count, platelets, prothrombin time,
and partial thromboplastin time and no systemic signs or symptoms
of bleeding dysfunction or collagen vascular disease, the pediatric hematology team determined that no further hematologic workup was
indicated. The patient was transferred to the pediatric inpatient ward
for the third night of observation. The next day, the patient's only remaining neurological abnormality was 4/5 weakness in the right arm,
and she had complete strength resolution in the right leg. She was
discharged to home to continue with outpatient medication levetiracetam and folic acid, and she had a neurology clinic appointment in 1 week. She has not returned to the PED or clinic at the
time of our review 2 months after her initial presentation.

DISCUSSION
Pediatric neurologic injuries from roller coasters are scarce,
and luckily pediatric fatalities from neurologic complications are rarer. Pelletier and Gilchrist10 chronicled all the roller

FIGURE 2. Subdural hematoma, CT image 2.

Roller Coaster–Induced Subdural Hematoma

FIGURE 3. Subdural hematoma, CT image 3.

coaster–associated deaths in the United States between 1994
and 2004, and of the 40 people described, 8 deaths were the result
of intracranial hemorrhage. None of these 8 fatalities were younger than 20 years, and they had histories ranging from elderly on
anticoagulants, young with cerebral aneurysms, to no previous
medical history.10 Alternatively, a retrospective 10-year study examined data on pediatric injuries related to amusement parks from
the National Electronic Injury Surveillance System. Fatalities
were not included, but of the 92,885 children reported from
1990 to 2010, 7.3% were blunt or closed head injuries, and only
1.5% of all total injuries resulted in hospitalization.11 There are
no reports in the literature of pediatric deaths from intracerebral
hemorrhage associated with amusement park rides, and the only
2 cases of pediatric neurologic morbidity after roller-coaster ride
that have been reported were published in 1979 and 2006.4,9
The mechanism of formation of a subdural hematoma has
been well studied many decades ago. The meningeal layers of
the dura mater, arachnoid membrane, and pia mater are closely attached, but subdural hematomas occur when traumatic forces split
the bridging veins or the small cortical arterial vessels in the inherently weak dural border cell plane between the dura mater and
arachnoid membrane.12 Either direct or indirect, these disruptive
forces very frequently involve acceleration-type mechanisms such
as a vehicle crash or fall that produce short-duration, high-strain
loading on the brain. The bridging veins are at an increased risk
of rupture due to their anatomy and positioning, and this risk of
rupture has been related to the magnitude, rate of onset, and duration of acceleration.13 Although the mechanism for subdural hematoma formation is relatively well understood, there are only a
few theories on how the forces applied from a roller-coaster ride
can be directly related to an intracranial bleed.

FIGURE 4. Subdural hematoma, CT image 4.

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Pediatric Emergency Care • Volume 35, Number 4, April 2019

Tseng et al

A G force is defined as a unitless measure of acceleration
(change of velocity divided by time) divided by the constant of acceleration caused by gravity. Assuming no air resistance, Earth's
gravity changes free-falling objects' speeds by a constant of
9.81 m/s2 (32 ft/s2). The US Air Force Flight Surgeon's manual
describes G-LOC as the threshold of sustained G forces where human subjects lose consciousness.14 Sustained G forces cause a hydrostatic drop in blood pressures, which decrease cerebral blood
flow, and venous pooling in the extremities causes a delayed effect
of reduced cardiac output. These changes are believed to lead to decreased perfusion of the retina, causing visual color and perception
changes briefly before progressing to a lapse of consciousness.
G-LOC has been associated with confusion, amnesia, and seizures.14 While the most comprehensive of G-force studies are
from space and aviation research, they focus on more sustained
periods of exposure to G forces in centrifuges rather than the short
intermittent exposure that are associated with roller coasters. Extrapolating information from these studies to the forces of amusement park rides may not be accurate.
However, there are few studies in the medical literature that
have directly investigated the physiologic effects of roller-coaster
rides on the human body. The most notable is a group of researchers
who examined 13 subjects and discovered that roller coasters cause
tachycardia that reaches maximum rate within 8 seconds.15 They
warned that the rapid onset of tachycardia and thus myocardial oxygen demand from a roller coaster may be comparable to a cardiac
stress test, putting individuals with underlying ischemic heart disease at risk of a cardiac event.15
Currently, there is a debate between legislators and industry
experts about the levels of Gs for the physiological threshold for
human safety. Some scientists have used mathematical models
with G force data from roller coasters to estimate the peak head rotational accelerations and indirectly concluded that they do not believe the current amusement park rides produce high-enough
forces to mechanically deform and injure the brain.16 Yet even
these authors agree that theoretically brain injury from significant
acceleration can occur because of rapid deformations of the brain
and the rotation acceleration can initiate severe injury as well.
The authors of published case reports of neurologic morbidity after roller-coaster rides have proposed theories to explain how G
forces and rotational acceleration of roller coasters can cause both
neuroparenchymal and neurovascular injury. Bo-Abbas and Bolton17 theorize that up-and-down, to-and-fro, and rotary acceleration
of a roller-coaster ride impact a deformable brain moving within a
fixed and rigid skull. These tensile and shearing forces in some
cases may be severe enough to rupture cortical veins leading to subdural hematomas, and the authors liken this to the pathophysiology
of “shaken baby syndrome.”17 In another report, Fernandes and
Daya18 also hypothesize that in the absence of other predisposing
factors the acceleration forces of roller coasters can tear bridging
veins, which cause subdural hematomas. Finally, the acceleration
and abrupt changes of direction in a roller coaster have been likened
to the uncontrolled rotation of the head, which is seen in acute deceleration of a motor vehicle collision.19 The resulting stretching
of the cervical vessels and aorta may explain the case reports of
roller coaster–induced vascular dissections. To date, no research
has been completed to find the human G force threshold for cerebral injuries.
The advances of roller-coaster technology and industry competition for thrill-seeking patrons may ultimately improve acceleration and performance beyond the passenger's physical ability to
tolerate them. We may see the point where the G forces of these attractions have surpassed the human body's threshold for acceleration

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and shearing forces, causing an increase in head, neck, and back
trauma that presents to the PED. Hopefully, medical researchers
and roller-coaster engineers will work together to study the physiologic capacity and response of healthy riders in order to maximize
the acceptable margin of safety. It is very possible that medical
cases similar to ours will present to the ED more frequently in the
future. We suggest that ED health care providers and pediatricians
consider amusement park thrill rides as a potential cause of neurologic complaints in the absence of other inciting events or predisposing factors in otherwise healthy patients.
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