Imaging of Traumatic Intracranial Hemorrhage
Imaging of Traumatic Intracranial Hemorrhage
Christian Koegel, M.D., Raluca McCallum, M.D., Mark Greenhill, B.S., Diana López García, M.D.,
Ajay Kohli, M.D., Mea Mallon, M.D.,* Robert Koenigsberg, D.O., Khuram S. Kazmi, M.D.
Departments of Radiology, Hahnemann University Hospital and St. Christopher Children’s Hospital,* Drexel University, Philadelphia, PA
I ntracranial hemorrhage (ICH) is
a common entity encountered in
clinical emergency medicine. Imag-
ing is the cornerstone in the diagnosis
of traumatic ICH. In a large study of
patients with a head injury and a de-
creased Glasgow Coma Scale (GCS),
46% of patients demonstrated intracra-
nial hemorrhage. Of these, 30% were
subdural hematomas (SDH), 22% were
epidural hematomas (EDH), 22% were
intraparenchymal hemorrhages (IPH),
and 14% were subarachnoid hemor-
rhages (SAH).1 Current literature re-
ports up to 72% incidence of diffuse
axonal injury (DAI) in moderate to se-
vere head injury.2 Timely and accurate
diagnoses of ICH is key to successful
patient management given the emer-
gent nature of ICH.
CT is the initial modality of choice
due to its accuracy, short study time,
low cost, and robustness against arti-
facts. MR is also used given its increased
sensitivity in detecting DAI, as well
as subacute and chronic hemorrhage.3
Although lumbar punctures were pre-
viously more common in the diagnostic
workup of SAH, there has been a para-
digm shift away from performing this
procedure, as nonenhanced CT (NECT)
has been shown to be highly accurate in
J Am Osteopath Coll Radiol 2018; Vol. 8, Issue 3
detecting SAH when performed within 6
hours of symptom onset.4
This article will review the key
vascular anatomy associated with ICH
followed by a strategy for imaging eval-
uation and reporting. This is followed
by a detailed review of the different
types of traumatic ICH with an empha-
sis on imaging findings.
Meningeal Vascular Anatomy
The three meningeal layers (dura,
arachnoid and pia mater) are perfused by
the anterior, middle and posterior menin-
geal arteries. The anterior and posterior
meningeal arteries originate from the an-
terior ethmoidal and ascending pharyn-
geal arteries, respectively, and perfuse
dura of the anterior and posterior cranial
fossa.5 The middle meningeal artery, a
maxillary artery branch, enters the skull
at the foramen spinosum.5 Trauma to the
parietotemporal skull can lacerate these
vessels resulting in hemorrhage.6
The meningeal venous drainage oc-
curs via dural sinuses, located between
the periosteum of the skull and the dura
mater, mainly via the superior sagittal,
transverse and sigmoid sinuses. Cen-
tral brain regions drain via the inferior
sagittal sinus and great vein of Galen
into the straight sinus. Relatively small
venous blood volumes exit the skull
through the cavernous sinus and oph-
thalmic veins.7 Injury to bridging veins
leads to SDH; injury to the cerebral
veins/arteries leads to SAH. Skull-base
fractures can injure a dural sinus, which
bears the probability of massive blood
loss into an extra-axial hematoma.
Imaging Evaluation and Reporting
Given the critical nature of ICH,
the interpreting physician must take
necessary steps to prevent overlook-
ing ICH on imaging. Although axial
imaging is the standard for evaluating
head CT, using additional reconstruc-
tions should be considered in routine
clinical practice. ICH detection rate
increases when axial and coronal
images are viewed. 9 Among missed
acute intracranial hemorrhages, SDH
accounts for 39%, followed by SAH
with 33%. 10 A customized checklist
approach (Table 1) may be beneficial
to the radiologist, particularly to en-
sure classic areas for subtle findings
are evaluated (Figure 1). CT windows
should also be considered when inter-
preting studies as subtle findings may
be obscured due to windowing. In addi-
tion to standard CT head windows, the
authors’ institution has found a width
Page 13
 Imaging of Traumatic Intracranial Hemorrhage

A B
Table 1: Example Checklist
for a Systematic Search Pattern
for Subtle Intracranial
Hemorrhage
Axial images
•C
 heck the posterior tip of occip-
ital horns and interpeduncular
cistern
•C
 heck for asymmetric increased
gyrus to inner table distance
•C
 heck for asymmetrically effaced
Sylvian fissure

FIGURE 1. Two patients with subtle intracranial hemorrhage. (A) Axial unenhanced CT demon-
Coronal images
strates high-density blood (arrow) in the posterior horn of the left lateral ventricle following a fall.
• E valuate for falcine/tentorial (B) Axial unenhanced CT in a second patient with small amount of high-density blood in the inter-
hemorrhage peduncular fossa (arrow).

A B
Axial and coronal images
•C
 heck for extra-axial fluid
collection of the anterior and
middle cranial fossa floor
• Check for vertex bleed
•C
 heck for skull fracture and,
if present, evaluate for
contralateral injury

of 99 Hounsfield units, level of 93 HU

images can make hemorrhage optically
more conspicuous (Figure 2).
Additionally, it is important to have
a general understanding of imaging
findings and information that referring
physicians need to guide management.
In particular, findings that help deter-
mine a need for surgical decompres-
sion/evacuation should be reported,
although the decision for surgery is
based on clinical information in addi-
tion to imaging. When encountering
ICH on CT or MR several items should
be routinely reported including midline
shift (particularly if > 5 mm), hema-
toma thickness/volume, mass effect,
effacement of ventricles and/or cisterns,
evidence of herniation, evidence of
hydrocephalus, and coexistent injuries
such as skull fractures and intracranial
foreign bodies.11
FIGURE 2. Subdural hematoma detection aided by windowing. (A) Axial unenhanced CT demon-
strates a small subdural hematoma (yellow arrow) along posterior falx and superior sagittal sinus.
Asymmetric effacement of left Sylvian fissure and extra-axial fluid collection (blue arrow) lateral
to anterior left temporal lobe appears similar in brightness to overlying skull. Its biconvex shape
mimics an epidural hematoma. (B) Axial unenhanced CT with a more optimally windowed (width
of 99 HU, level of 93 HU) improves conspicuity and reveals subdural blood, indicated by wavy
crescent-shaped contour of the collection (red arrow).
Imaging Features of more severe cases, additional sites of in-
Intracranial Hemorrhage jury occur in the brainstem. Within hours,
Diffuse Axonal Injury axonal deformation damages its cytoskel-
Unequal rotational and accelera- eton, resulting in arrest of axoplasmic
tion-deceleration forces cause the brain flow on a microscopic level, followed by
to pivot around the brainstem, causing axonal swelling and subsequently axon
stretching and shearing of axons and re- rupture.13 Mechanisms of injury vary, but
sulting in the clinical diagnosis of DAI. include high-impact falls and motor vehi-
Shear forces peak at the grey-white mat- cle accidents.
ter interface, due to its peripheral location Foci of axonal edema with or with-
and differences in tissue density; hence, out hemorrhage are imaging findings
67% of DAI lesions are in this region.12 In of DAI and these foci may vary in size

Page 14 J Am Osteopath Coll Radiol 2019; Vol. 8, Issue 3

 Imaging of Traumatic Intracranial Hemorrhage

A B C D

FIGURE 3. Typical CT appearance of diffuse axonal injury. (A-D). Axial unenhanced CT images in a young male patient in a motor vehicle accident
demonstrates numerous punctate hyperdensities indicating hemorrhage (yellow arrows) at junctions of the grey and white matter. Additional micro-
hemorrhage in corpus callosum (blue arrow) and intraventricular hemorrhage (red arrow) are noted.

may be multiple and bilateral. Cerebral

A B edema may be relatively mild acutely;
however, progression of cerebral edema
is common and can result in midline shift
and herniation syndromes. IPH can be
complicated by continued enlargement
and/or re-hemorrhage. Likewise, new
lesions can be detected on follow-up
imaging. MRI is useful to identify trau-
matic intraparenchymal damage without
blood products, termed nonhemorrhagic
cerebral contusion (Figure 6). Sequelae
after resolution are common and include
gliosis, encephalomalacia and associated
volume loss.

Subdural Hematoma
FIGURE 4. Improved sensitivity of MR over CT to detect DAI in an adolescent in a motorcycle Acute SDH is characterized by an
accident. (A) Axial unenhanced CT demonstrates a subtle solitary punctate hyperdensity (arrow) extra-axial crescent-shaped hemor-
suggestive of DAI. (B) Susceptibility-weighted MR image of the same patient later the same day
at a similar level demonstrates considerably more extensive DAI involving bifrontal lobes (yellow
rhage in a potential space between the
arrows) and basal ganglia (red arrows) as demonstrated by small areas of susceptibility artifact. dura and arachnoid. A direct blow to
the head is not necessary to incur an
(Figure 3). Despite DAI being present lesions detected within 4 weeks after in- SDH. Instead, an SDH may be related
in up to 72% of patients with moderate jury improve functional status and long- to acceleration-deceleration forces
to severe head injuries, 50% to 80% term outcome due to changes in patient secondary to the impact from a fall or
of initial CT and MRI studies are neg- management.15 Therefore, MRI is rec- shaking of an infant.17 Regardless of
ative.2 MRI is more sensitive than CT ommended within 4 weeks of traumatic the mechanism, shear forces on the
in detecting lesions (Figure 4). 12-14 brain injury (TBI).16 bridging veins or cortical arteries can
Gradient echo (GRE) and susceptibil- lead to injury and rupture.18-20 Elderly
ity-weighted imaging (SWI) are the Intraparenchymal Hemorrhage are predisposed to develop SDH due to
most sensitive sequence, revealing the Traumatic acute IPH, commonly cortical atrophy. Additionally, antico-
highest number of lesions at the highest referred to as a cerebral contusion, agulants and antiplatelet agents (Figure
number of locations compared to other usually occurs after a significant di- 7) raise concern for increased risk of
MR sequences. The classic triad seen in rect head injury. It commonly involves hemorrhage. Contrary to epidural he-
DAI is diffuse damage to axons, a focal brain parenchyma adjacent to bony matomas, classic SDH are limited by
lesion in the corpus callosum, and a protuberance/dural fold.5 CT displays dural duplications, but can cross suture
focal lesion in the dorsolateral quadrant a patchy, irregular, hyperdense area lines and, therefore, can extend over an
of the rostral brainstem adjacent to the of acute hemorrhage on an edematous entire hemisphere. The vast majority
superior cerebellar peduncles.12 DAI background (Figure 5). Hemorrhages of small, atypically shaped, extra-axial

J Am Osteopath Coll Radiol 2019; Vol. 8, Issue 3 Page 15

 Imaging of Traumatic Intracranial Hemorrhage

A B C

FIGURE 5. Delayed intraparenchymal hemorrhage. (A) Initial unenhanced axial CT demonstrates a nondisplaced longitudinal right temporal bone
fracture (arrow). (B) Initial unenhanced axial CT demonstrates an equivocal left posterior frontal/temporal hemorrhage (arrow) raising the possibility
of a coup-contrecoup mechanism. (C) Follow-up axial unenhanced CT one day later, demonstrates marked worsening with more typical appearing
intraparenchymal hemorrhage (yellow arrow) and new intraventricular hemorrhage (white arrow) with associated midline shift.
hemorrhages are due to a low-pressure
A B venous injury causing an SDH with
continued CT follow-up suggested if
clinical doubt remains as to whether an
extra-axial blood collection reflects an
EDH or SDH.
It is valuable for the radiologist to
be generally aware of the appearance of
blood products on CT based on the acu-
ity. Although imaging may not occur
this early, in the first few hours (hyper-
acute phase), SDH might be isodense to
the underlying cortex, as it is still liquid
(40-50 HU), and may not be detectable.
Hemorrhage becomes increasingly
FIGURE 6. Nonhemorrhagic cerebral contusions in a pedestrian struck by a car. (A,B) FLAIR (A)
and GRE (B) MR axial images demonstrate bilateral frontal lobe FLAIR hyperintensities (arrows)
dense as it coagulates and condenses
without associated susceptibility artifact on GRE (B) most suggestive of a nonhemorrhagic cere- during the acute phase (0-3 days) due
bral injury. to clot retraction by a decreased fluid
component and relative increase in iron
A B content in the red blood cells. Those
clots measure between 80-100 HU and
show the typical hyperattenuation. The
attenuation decreases in the subacute
phase as the blood products degrade and
eventually becomes similar to CSF den-
sity in the chronic phase (Figure 8).21
SDH requires heightened vigi-
lance and follow-up imaging to ensure
early detection of complications, such
as continued bleeding, rebleeding
(8% of cases), midline shift, or her-
niation.22 Mixed attenuation blood in
FIGURE 7. Right subdural hematoma with mass effect in an elderly patient on anticoagulant who which isodense areas are intermixed
fell. (A) Axial unenhanced CT demonstrates an acute subdural hematoma (yellow arrow) with mid-
line shift (blue arrow). (B) Improved midline shift after decompression craniotomy. A residual layer
by hyperdense areas suggest active (re)
of acute residual blood products is present (blue arrow) as is an adjacent low-density fluid collec- bleeding, which is termed the “swirl
tion (yellow arrow) in a surgical bed reflecting diluted blood products. sign” on NECT. Cerebral spinal fluid

Page 16 J Am Osteopath Coll Radiol 2019; Vol. 8, Issue 3

 Imaging of Traumatic Intracranial Hemorrhage

A B C D E

FIGURE 8. Evolution of subdural hematoma. (A-E) Multiple time-sequential unenhanced CTs of the head in an elderly patient on an anticoagulant
who fell. (A) Day of the head injury. Bilateral parietal-occipital loculated acute subdural hematomas (yellow arrows) with a mixed-density subacute
center (red arrow). (B) Day 2 with interval rebleeding with increasing density of the subdural hematomas (yellow arrows). (C) Day 3 with continued
high-density blood products (yellow arrows). (D) Day 14 with decreasing density reflects degradation of blood products (yellow arrows). (E) Day 39
with chronic subdural hematomas demonstrating density similar to CSF (CSF = 3HU).

in the subdural space (subdural hygro-

A B mas) is thought to be related to subdural
hematomas. An arachnoid membrane
tear with a “flap-valve” mechanism re-
sults in CSF leakage into the subdural
space.23,24

Epidural Hematoma
Hemorrhage into a potential space
between the inner table of the skull and
the dura mater occurs in 1% of minor
head injury and 10% following head
injury in patients who present in a co-
matose state.25,26 A provided history
of head injury days-to-months prior to
imaging should not eradicate the possi-
bility of an EDH, as 20% to 50% of pa-
FIGURE 9. Classic appearance of epidural hematoma. (A) Axial and (B) coronal unenhanced CT of
tients experience a symptom-free lucid
acute right temporal epidural hematoma (yellow arrows) confined by the squamous suture.
interval.27 Of patients with an EDH,
91% suffer from an associated skull
A B fracture.28 Typically supratentorially
located, EDH frequently involves injury
to the middle meningeal artery or ante-
rior ethmoidal artery. Rapid hematoma
expansion is common due to the rela-
tively high pressure of arterial blood.29
Classic CT findings are a high-density
convex or biconvex shaped extra-axial
fluid collection that does not cross the
sutures (Figure 9).
Venous epidural hemorrhage ac-
counts for 5% to 10% of all EDH and
FIGURE 10. Venous epidural hemorrhage. (A) Lateral skull radiograph of a 2-month-old after fall
occurs at specific locations including
showing acute skull fracture at the vertex (arrow). (B) Coronal T2 MR image showing biconvex
high-intensity midline collection, layering symmetrically between vertex skull fracture and superior the vertex (superior sagittal sinus in-
sagittal sinus, consistent with a venous EDH (arrow). In contrast to arterial EDH, venous EDH may jury), anterior middle cranial fossa
cross the midline, as seen with this case, as the bleeding origin is centered underneath the suture. (sphenoparietal sinus injury), and

J Am Osteopath Coll Radiol 2019; Vol. 8, Issue 3 Page 17

 Imaging of Traumatic Intracranial Hemorrhage

Traumatic Subarachnoid Hemorrhage

A B Traumatic SAH (tSAH) results
from disruption of pial vessels with
bleeding into the subarachnoid space.
It is often coexistent with other pathol-
ogies in the setting of trauma. Vessel
injury more commonly arises in the
cerebral convexities/sulci following
a high-impact mechanical force to the
head. Of patients with severe TBI,
40% develop tSAH.34 Be cautious with
SAH in the setting of acute trauma as
differential diagnosis includes tSAH
as well as nontraumatic SAH (eg, rup-
tured aneurysm) that may have pre-
C D ceded (and perhaps led to) the reported
trauma (Figure 11). Differentiating
traumatic from nontraumatic SAH by
imaging is not always possible. How-
ever, SAH identified around the cere-
bral convexities with relative sparing
of the basilar cisterns around the circle
of Willis would favor trauma.35 Simi-
larly, SAH associated with other signs
of trauma on CT such as a countercoup
pattern associated with a parenchymal
contusion may also favor a traumatic
etiology. When doubt exists, the CT
or traditional angiography may be
performed for further evaluation to ex-
clude an aneurysm.
FIGURE 11. Subarachnoid hemorrhage in three trauma patients with different etiologies. (A) Imaging characteristics that por-
Axial unenhanced CT demonstrates isolated, focal tSAH in asymptomatic elderly with suprathera- tend a worse prognosis include other
peutic INR (10.4) following minor ground level fall without external head injury with high-density
evidence of brain trauma including
blood in the subarachnoid space on the right (arrow). (B) Axial unenhanced CT demonstrates a
left tSAH (arrow) in a young patient after a blow to the right temple demonstrating a coup-con- brain contusions, especially if enlarg-
trecoup pattern. (C, D) Axial unenhanced CT (C) and right carotid approach cerebral angiogram ing.36 Complications of tSAH include
(D) in a young patient who fell off a chair and minor facial trauma to the nose following a sei- hydrocephalus and cerebral vaso-
zure. CT shows symmetric, midline SAH (arrow in C) is typical for aneurysmal SAH. Subsequent spasm. 35,37 Table 2 summarizes dif-
angiography confirmed nontraumatic etiology, a ruptured anterior communicating artery aneu-
ferentiating key features of EDH, SDH
rysm (arrow in D). This case is a reminder to always consider aneurysmal etiology in SAH patients
regardless of the history of trauma. and SAH.

posterior occipital region (transverse/
sigmoid sinus injury). The latter can
rapidly cause tonsillar herniation.
However, the majority of venous EDH
are unlikely to expand because venous
pressure is insufficient to further strip
off the dura from the skull.30 Similar to
arterial EDH, an associated fracture/
diastasis is common. Venous EDH typ-
ically displaces the sinus away from the
fracture and, in contrast to arterial EDH,
can occasionally cross suture lines (Fig-
ure 10). One should suspect a venous
EDH if a skull fracture runs through the
expected location of a dural sinus.
Rarely, direct bleeding from a skull
fracture causes EDH.5 Similar to the
other causes of ICH, co-existent and/or
complicating findings may be encoun-
tered including mass effect, rebleeding,
herniation, brain edema, and/or intra-
parenchymal hemorrhage.31-32 Similar
to SDH, the appearance of the blood
on CT and MR depends on its age, as
hemoglobin is progressively degraded
over time.33
Conclusion
Traumatic intracranial hemorrhage
is an urgent finding requiring prompt
and accurate evaluation by the inter-
preting radiologist with excellent com-
munication and documentation of key
findings that may affect patient man-
agement. Given the trauma and further
complicating patient management, ad-
ditional critical coexistent injuries may
also be present and require urgent treat-
ment. Thus, at many medical centers a
multidisciplinary neurotrauma team

Page 18 J Am Osteopath Coll Radiol 2019; Vol. 8, Issue 3

 Imaging of Traumatic Intracranial Hemorrhage

A B C

FIGURE 12. Epidural hematoma with evacuation. (A) Axial unenhanced CT in an elderly patient with right parietal depressed skull fracture (arrow)
following a ground-level fall. (B) On the same CT, an acute, right epidural hematoma is present as a largely high-attenuating biconvex extra-axial fluid
collection with a central hypoattenuating component representing active bleeding (arrow). Note that the blood extends but does not cross the coro-
nal suture anteriorly and lambdoid suture posteriorly. The patient was taken to surgery for evacuation. (C) Follow-up CT 6 weeks post-trauma demon-
strates significant improvement with minimal residual blood products/dural thickening (arrow).

Table 2. Classic Mechanisms and Imaging Feature of Intracranial Hemorrhage

Classic Trauma Mechanism Imaging Features
Epidural hematoma High-impact blow to head Biconvex fluid collection
Crosses dural duplication
Confined by sutures
Subdural hematoma Fall, low-impact trauma Crescent-shaped
Crosses sutures but not dural duplications
Subarachnoid hemorrhage High-impact blow to head Blood products in subarachnoid spaces including sulci
and basal cisterns

guides management and determines the
need for surgical decompression/evacu-
ation (Figure 12).
Furthermore, the radiologist must
be vigilant about new and/or worsening
edema, midline shift, signs of hydro-
cephalus, worsening hemorrhage (re-
bleeding), or other complicating factors
on follow-up studies that may alter pa-
tient management. Medical and surgical
management in these patients is com-
plex and multifactorial requiring timely
and accurate imaging information, thus
solidifying the radiologists’ key role in
the management of traumatic ICH.
References
1. Perel P, Roberts I, Bouamra O, Woodford M,
Mooney J, Lecky F. Intracranial bleeding in patients
with traumatic brain injury: a prognostic study. BMC
Emerg Med 2009;9:15.
2. Skandsen T, Kvistad KA, Solheim O, Strand IH,
Folvik M, Vik A. Prevalence and impact of diffuse
axonal injury in patients with moderate and severe
head injury: a cohort study of early magnetic reso-
nance imaging findings and 1-year outcome. J Neu-
rosurg 2010;113(3):556-563.
3. Kidwell CS, Chalela JA, Saver JL, et al. Compari-
son of MRI and CT for detection of acute intracere-
bral hemorrhage. JAMA 2004;292(15):1823-1830.
4. Carpenter CR, Hussain AM, Ward MJ, et al. Spon-
taneous subarachnoid hemorrhage: a systematic
review and meta-analysis describing the diagnostic
accuracy of history, physical examination, imaging,
and lumbar puncture with an exploration of test
thresholds. Acad Emerg Med 2016;23(9):963-1003.
5. Yousem, D, Zimmerman R, Grossman R. In Nad-
gir R, ed. Neuroradiology: The Requisites. 3rd Edition.
Philadelphia, PA: Mosby/Elsevier. 2010. https://www.
elsevier.com/books/neuroradiology-the-requisites/
yousem/978-0-323-04521-6. Accessed April 14, 2019.
6. Aurangzeb A, Ahmed E, Afridi EA, et al. Fre-
quency of extradural haematoma in patients with
linear skull fracture. J Ayub Med Coll Abbottabad
2015;27(2):314-317.
7. Mancall EL, Brock, DG. Gray’s Clinical Neuro-
anatomy. Philadelphia, PA: Elsevier/Saunders;
2011. https://www.us.elsevierhealth.com/grays-
clinical-neuroanatomy-9781416047056.html.
Accessed April 14, 2019.
8. Cranial Vault & Skull Base - Diagnosis - Skull
base, Anterior skull base fractures - AO Surgery
Reference. https://www2.aofoundation.org/wps/
portal/!ut/p/a0/04_Sj9CPykssy0xPLMnMz0vMAf-
GjzOKN_A0M3D2DDbz9_UMMDRyDXQ3dw9w-
MDAzMjfULsh0VAbWjLW0!/?bone=CMF&classi-
fication=93-Skull%20base%2C%20Anterior%20
skull%20base%20fractures&segment=Crani-
um&showPage=diagnosis&teaserTitle=&conten-
tUrl=srg/93/01-Diagnosis/skull_base-skull_base.jsp.
Accessed April 14, 2019.
9. Wei SC, Ulmer S, Lev MH, Pomerantz SR,
González RG, Henson JW. Value of coronal reforma-
tions in the CT evaluation of acute head trauma. Am
J Neuroradiol 2010;31(2):334-339.
10. Strub WM, Leach JL, Tomsick T, Vagal A. Over-
night preliminary head CT interpretations provided
by residents: locations of misidentified intracranial
hemorrhage. Am J Neuroradiol 2007;28(9)1679-
1682. http://www.ajnr.org/content/28/9/1679.
Accessed April 14, 2019.
11. Escobedo LVS, Habboushe J, Kaafarani H,
Velmahos G, Shah K, Lee J. Traumatic brain
injury: a case-based review. World J Emerg Med
2013;4(4):252-259.

J Am Osteopath Coll Radiol 2019; Vol. 8, Issue 3 Page 19

 Imaging of Traumatic Intracranial Hemorrhage
12. Parizel PM, Ozsarlak, Van Goethem JW, et al.
Imaging findings in diffuse axonal injury after closed
head trauma. Eur Radiol. 1998;8(6):960-965.
13. Hill CS, Coleman MP, Menon DK. Traumatic axo-
nal injury: mechanisms and translational opportuni-
ties. Trends Neurosci 2016;39(5):311-324.
14. Kinoshita T, Moritani T, Hiwatashi A, et al.
Conspicuity of diffuse axonal injury lesions on
diffusion-weighted MR imaging. Eur J Radiol
2005;56(1):5-11.
15. Bansal M, Sinha VD, Bansal J. Diagnostic and
prognostic capability of newer magnetic resonance
imaging brain sequences in diffuse axonal injury
patient. Asian J Neurosurg 2018;13(2):348-356.
16. Moen KG, Brezova V, Skandsen T, Håberg AK,
Folvik M, Vik A. Traumatic axonal injury: the prog-
nostic value of lesion load in corpus callosum,
brain stem, and thalamus in different magnetic
resonance imaging sequences. J Neurotrauma
2014;31(17):1486-1496.
17. Gennarelli TA, Thibault LE. Biomechan-
ics of acute subdural hematoma. J Trauma
1982;22(8):680-686.
18. DeKosky ST, Ikonomovic MD, Gandy S. Trau-
matic brain injury--football, warfare, and long-term
effects. N Engl J Med 2010;363(14):1293-1296.
19. Maxeiner H, Wolff M. Pure subdural hema-
tomas: a postmortem analysis of their form
and bleeding points. Neurosurgery 2007;61(1
Suppl):267-272; discussion 272-273.
20. Haines DE, Harkey HL, al-Mefty O. The “subdu-
ral” space: a new look at an outdated concept. Neu-
rosurgery 1993;32(1):111-120.
Page 20
21. Berlin L. Avoiding errors in radiology: case-based
analysis of causes and preventive strategies. JAMA
2011;306(11):1267-1268.
22. Lee K-S, Shim J-J, Yoon S-M, Doh J-W, Yun I-G,
Bae H-G. Acute-on-Chronic subdural hematoma:
not uncommon events. J Korean Neurosurg Soc
2011;50(6):512-516.
23. Duy L, Badeeb A, Duy W, et al. CT Attenuation
of acute subdural hematomas in patients with ane-
mia. J Neuroimaging 2019, February 16.
24. McCluney KW, Yeakley JW, Fenstermacher MJ,
Baird SH, Bonmati CM. Subdural hygroma versus
atrophy on MR brain scans: “the cortical vein sign.”
AJNR Am J Neuroradiol 1992;13(5):1335-1339.
25. Baykaner K, Alp H, Ceviker N, Keskil S, Seçkin Z.
Observation of 95 patients with extradural hema-
toma and review of the literature. Surg Neurol
1988;30(5):339-341.
26. Freytag E. Autopsy findings in head injuries from
blunt forces. Statistical evaluation of 1,367 cases.
Arch Pathol 1963;75:402-413.
27. Kushner D. Mild traumatic brain injury: toward
understanding manifestations and treatment. Arch
Intern Med 1998;158(15):1617-1624.
28. Zimmerman RA, Bilaniuk LT. Computed tomo-
graphic staging of traumatic epidural bleeding.
Radiology 1982;144(4):809-812.
29. de Andrade AF, Figueiredo EG, Caldas JG, et al.
Intracranial vascular lesions associated with small
epidural hematomas. Neurosurgery 2008;62(2):416-
420; discussion 420-421.
30. Gean AD, Fischbein NJ, Purcell DD, Aiken AH,
Manley GT, Stiver SI. Benign anterior temporal epi-
J Am Osteopath Coll Radiol 2019; Vol. 8, Issue 3
dural hematoma: indolent lesion with a characteris-
tic CT imaging appearance after blunt head trauma.
Radiology 2010;257(1):212-218.
31. Bullock MR, Chesnut R, Ghajar J, et al. Surgical
management of acute epidural hematomas. Neuro-
surgery 2006;58(3 Suppl):S7-15; discussion Si-iv.
32. Glastonbury CM, Gean AD. Current neuroimag-
ing of head injury. Semin Neurosurg 2003;14:79-88.
33. Hosoda K, Tamaki N, Masumura M, Matsumoto
S, Maeda F. Magnetic resonance images of chronic sub-
dural hematomas. J Neurosurg 1987;67(5):677-683.
34. Jaeger M, Meixensberger J. Traumatic subarach-
noid hemorrhage and its clinical relevance. Inten-
sivmed Notfallmedizin 2004;41(3):148-152.
35. Heit JJ, Iv M, Wintermark M. Imaging of intra-
cranial hemorrhage. J Stroke 2017 Jan;19(1):11-27.
36. Chieregato A, Fainardi E, Morselli-Labate AM,
Antonelli V, et al. Factors associated with neuro-
logical outcome and lesion progression in traumatic
subarachnoid hemorrhage patients. Neurosurgery
2005;56(4):671-680.
37. Biedert S, Wolfshörndl H. Extraventricular
obstructive hydrocephalus. Fortschr Neurol Psychi-
atr. 1994;62(11):405-408.
38. Verma RK, Kottke R, Andereggen L, et al.
Detecting subarachnoid hemorrhage: compari-
son of combined FLAIR/SWI versus CT. Eur J Radiol
2013;82(9):1539-1545.
39. Winn W. Youmans and Winn Neurological
Surgery, 4-Volume Set. 7th ed. Philadelphia, PA:
Elsevier; 2016. https://www.elsevier.com/books/you-
mans-and-winn-neurological-surgery-4-volume-set/
winn/978-0-323-28782-1. Accessed April 14, 2019.