CT for acute stage of closed head injury.
ABSTRACT Brain damage after head injury can be classified by its time course. Primary damage that includes acute subdural hematoma (SDH), acute epidural hematoma (EDH), and intraaxial lesions that include contusions, diffuse axonal injury (DAI), and intracranial hemorrhage (ICH), occurs at the moment of impact and is thought to be irreversible. Secondary damage that includes herniations, diffuse cerebral swelling, and secondary infarction and hemorrhage, evolves hours or days after injury as a consequence of systemic or intracranial complications. The duration and severity of secondary damage influence outcome. Head injury management is focused on preventing, detecting, and correcting such secondary damage. CT has been widely used for the neuromonitoring of head trauma. CT is the gold standard for the detection of intracranial abnormalities and is a safe method for survey. While MRI is more sensitive and accurate in diagnosing cerebral pathology, CT is considered the most critical imaging technique for the management of closed head-injured patients in the acute stage. In this article, we review the imaging findings and literature of various lesions of closed head injury in the acute stage.
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ABSTRACT: It is now well accepted that traumatic white matter injury constitutes a critical determinant of post-traumatic functional impairment. However, the contribution of preexisting white matter rarefaction on outcome following traumatic brain injury (TBI) is unknown. Hence, we sought to determine whether the burden of preexisting leukoaraiosis of presumed ischemic origin is independently associated with outcome after TBI. We retrospectively analyzed consecutive, prospectively enrolled patients of ≥50 years (n = 136) who were admitted to a single neurological/trauma intensive care unit. Supratentorial white matter hypoattenuation on head CT was graded on a 5-point scale (range 0-4) reflecting increasing severity of leukoaraiosis. Outcome was ascertained according to the modified Rankin Scale (mRS) and Glasgow outcome scale (GOS) at 3 and 12 months, respectively. After adjustment for other factors, leukoaraiosis severity was significantly associated with a poor outcome at 3 and 12 months defined as mRS 3-6 and GOS 1-3, respectively. The independent association between leukoaraiosis and poor outcome remained when the analysis was restricted to patients who survived up to 3 months, had moderate-to-severe TBI [enrollment Glasgow Coma Scale (GCS) ≤12; p = 0.001], or had mild TBI (GCS 13-15; p = 0.002), respectively. We provide first evidence that preexisting cerebral small vessel disease independently predicts a poor functional outcome after closed head TBI. This association is independent of other established outcome predictors such as age, comorbid state as well as intensive care unit complications and interventions. This knowledge may help improve prognostic accuracy, clinical management, and resource utilization.Neurocritical Care 04/2014; · 3.04 Impact Factor
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ABSTRACT: A significant portion of previously deployed combat Veterans from Operation Enduring Freedom and Operation Iraqi Freedom/Operation New Dawn (OEF/OIF/OND) are affected by comorbid posttraumatic stress disorder (PTSD) and mild traumatic brain injury (mTBI). Despite this fact, neuroimaging studies investigating the neural correlates of cognitive dysfunction within this population are almost nonexistent, with the exception of research examining the neural correlates of diagnostic PTSD or TBI. The current study used both voxel-based and surface-based morphometry to determine whether comorbid PTSD/mTBI is characterized by altered brain structure in the same regions as observed in singular diagnostic PTSD or TBI. Furthermore, we assessed whether alterations in brain structures in these regions were associated with behavioral measures related to inhibitory control, as assessed by the Go/No-go task, self-reports of impulsivity, and/or PTSD or mTBI symptoms. Results indicate volumetric reductions in the bilateral anterior amygdala in our comorbid PTSD/mTBI sample as compared to a control sample of OEF/OIF Veterans with no history of mTBI and/or PTSD. Moreover, increased volume reduction in the amygdala predicted poorer inhibitory control as measured by performance on the Go/No-go task, increased self-reported impulsivity, and greater symptoms associated with PTSD. These findings suggest that alterations in brain anatomy in OEF/OIF/OND Veterans with comorbid PTSD/mTBI are associated with both cognitive deficits and trauma symptoms related to PTSD.BioMed research international. 01/2014; 2014:691505.
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ABSTRACT: O trauma é a principal causa de morte em pessoas entre 1 e 44 anos de idade. O traumatismo crânio-encefálico é o principal fator determinante da mortalidade e da morbidade decorrentes do trauma. A predição do prognóstico é um dos principais problemas associados ao traumatismo crânio-encefálico grave, já que o valor preditivo variável da avaliação clínica complica a identificação de pacientes com maior risco para desenvolvimento de lesões secundárias e desfecho fatal. Devido a estas questões, há considerável interesse no desenvolvimento de biomarcadores que reflitam a gravidade do dano cerebral e que se correlacionem com mortalidade e prognóstico funcional em longo prazo. As proteínas S100B e enolase neuronal específica estão entre os marcadores mais estudados para este fim, mas há também estudos com a proteína glial fibrilar ácida, a creatinino quinase cerebral, a proteína mielina básica, o ácido desoxirribonucléico plasmático, a proteína de choque quente 70, o fator von Willebrand, as metaloproteinases, o fator neurotrófico derivado do cérebro, dentre outros. Evidências sugerem que a inflamação, o estresse oxidativo, a excitotoxicidade, as respostas neuroendócrinas e a apoptose têm um importante papel no desenvolvimento de lesões secundárias. Marcadores envolvidos nestes processos também estão sendo estudados no traumatismo crânio-encefálico. Revisamos estes marcadores, muitos dos quais apresentam resultados promissores para uma futura aplicação clínica.Revista Brasileira de Terapia Intensiva 12/2008; 20(4):411-421.
Volume 23, Number 5
Radiation Medicine: Vol. 23 No. 5, 309–316 p.p., 2005
Yoshihiro Toyama,* Takuya Kobayashi,** Yoshihiro Nishiyama,**
Katashi Satoh,* Motoomi Ohkawa,** and Keisuke Seki***
Brain damage after head injury can be classified by its time course. Primary damage that
includes acute subdural hematoma (SDH), acute epidural hematoma (EDH), and intraaxial
lesions that include contusions, diffuse axonal injury (DAI), and intracranial hemorrhage (ICH),
occurs at the moment of impact and is thought to be irreversible. Secondary damage that
includes herniations, diffuse cerebral swelling, and secondary infarction and hemorrhage,
evolves hours or days after injury as a consequence of systemic or intracranial complications.
The duration and severity of secondary damage influence outcome. Head injury management
is focused on preventing, detecting, and correcting such secondary damage.
CT has been widely used for the neuromonitoring of head trauma. CT is the gold standard for
the detection of intracranial abnormalities and is a safe method for survey. While MRI is more
sensitive and accurate in diagnosing cerebral pathology, CT is considered the most critical
imaging technique for the management of closed head-injured patients in the acute stage.
In this article, we review the imaging findings and literature of various lesions of closed head
injury in the acute stage.
Key words: head trauma, closed head injury, brain damage, diagnostic imaging, CT
the major cause of neurological disability. Several
clinical guidelines and protocols have been published
and proposed.1-5 The major topics of these guidelines
are trauma care systems, prehospital care, and ICU man-
agement. In almost all of the guidelines, the outcomes
of patients with a Glasgow Coma Scale (GCS) score of
8 or less in adults have been discussed.6 The GCS is one
of the most common tools used by trauma care providers
RAUMATIC BRAIN INJURY IS A SIGNIFICANT PUBLIC
health problem. Sequelae to these injuries represent
as it enables the gradation of head injury severity using
simple observations rather than invasive or specialist
techniques. However, many patients arrive at the hospital
already intubated, and, therefore, the GCS is often
difficult to obtain.7
According to a multicenter survey in Japan, CT has
been widely used for the neuromonitoring of head
trauma.8 CT is the gold standard for the detection of
intracranial abnormalities and is a safe method for sur-
vey. CT provides a rapid assessment of structural brain
injuries, is readily available in most medical institutions,
and is relatively cheap.
In this article, we review the CT findings and literature
of various lesions of head injury.
Initial patient management
According to the Japan Advanced Trauma Evaluation
and Care (JATEC) guidelines, the primary survey
includes assessing the airways, breathing, and circula-
tion, dysfunction of central nervous system, exposure,
and environmental control, this being the so called
ABCDEs method. If the patient has central nervous
system dysfunction, a secondary survey including diag-
nostic imaging is needed. The desire to rush patients for
CT examination before optimal stabilization has been
*Department of Clinical Radiology, Faculty of Medicine, Kagawa
**Department of Radiology, Faculty of Medicine, Kagawa
***Department of Emergency Medicine, Faculty of Medicine,
Reprint requests to Yoshihiro Toyama, M.D., Department of
Clinical Radiology, Faculty of Medicine, Kagawa University, 1750-
1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, JAPAN.
Part of this work was presented at the 39th autumn meeting of the
Japan Radiological Society in April 2004, and is published in
Radiation Medicine at the request of the Japan Radiological Society.
CT for Acute Stage of Closed Head Injury
TOYAMA ET AL
shock or may worsen brain function, to produce seizures
or encephalopathy. If a small hyperdense hematoma
is located adjacent to the bone, it may be difficult to
differentiate from overlying bone by using brain paren-
chyma windows (WW 70-80, WL 25-30). CT with soft
tissue windows (WW 150-200 HU, WL 10-30 HU) and
bone windows (1,600-4,000 HU, WL 250-400 HU) is
necessary to rule out small hematoma and skull fracture,
respectively (Fig. 1).
If the initial CT findings are normal, and the patient’s
status has not changed within 24 hours after trauma, the
patient can be discharged. A repeat CT should be
considered if the initial CT findings were abnormal or if
the patient’s status has changed within 24 hours after
trauma (Fig. 2). Follow-up CT examination is important
because lesions may increase or new lesions develop,
mainly within 12 to 24 hours of trauma. It should be
noted that an initially negative CT scan does not rule
out the delayed development of an intracranial hemor-
rhage (ICH) after injury. For this reason routine follow-
achieved must be resisted. Only in the presence of rapid
neurological deterioration or signs of developing herni-
ation is urgent CT examination required, but only after
resuscitation. Optimal monitoring and supervision
should be available during intra-hospital transport and
CT is recommended for patients with severe (GCS<8)
and moderately severe (GCS=9-12) head injury, and is
also recommended for patients with mild (GCS>12) head
injury who have the following risk factors: (1) loss of
consciousness, (2) amnesia, (3) over 60 years of age,
(4) skull fracture, (5) seizure, (6) previous neurosurgery,
(7) drinker, (8) bleeder, (9) drug abuse.10-12
Method of CT and follow-up
Axial non-contrast CT scanning is the gold standard
technique. In patients with acute craniocerebral trauma,
contrast enhanced CT adds minimal diagnostic
information. If patients have suffered multiple traumatic
injuries, contrast material may cause renal failure or
Fig. 1. Axial non-contrast CT scans with
A: CT with brain parenchyma windows
(WW 70, WL 25) shows a subtle SDH along
the falx cerebri.
B: CT with soft tissue windows (WW 200
HU, WL 10 HU) shows a small SDH
(arrows) that is difficult to see on the brain
parenchyma windows because of the high
density overlying the calvarial vault.
Fig. 2. Axial non-enhanced CT scans in a
patient with closed head injury and GCS
A: Initial CT scan shows a small left
temporal SDH and bilateral SAH. There is
a small mass effect of SDH.
B: Clinical deterioration and mydriasis are
present 3 hours later. Repeat CT scan shows
large SDH and subfalcine herniation of the
lateral ventricles. Decompression surgery
was performed and SDH was evacuated.
Volume 23, Number 5
up CT examination within 24 hours of trauma is
recommended, but should be performed earlier if the
clinical situation so dictates.
Mechanism and classification of head injury
Traumatic brain injury is usually the consequence of
impact to the head, which undergoes sudden acceler-
ation, deceleration, or rotation. Brain damage after head
injury can be classified by its time course.13 Primary
damage occurs at the moment of impact and is thought
to be irreversible. The major primary lesions are extra-
cerebral hemorrhage, which includes acute subdural
hematoma (SDH), acute epidural hematoma (EDH), and
intraaxial lesions that include contusions, diffuse axonal
injury (DAI), and ICH. Secondary brain damage evolves
hours or days after injury as a consequence of systemic
or intracranial complications. Secondary lesions include
herniations, diffuse cerebral swelling, and secondary
infarctions and hemorrhages. The duration and severity
of secondary damage influence outcome. Head injury
management is focused on preventing, detecting, and
correcting such secondary damage.
Primary brain damage
1. Acute epidural hematoma
EDH represents a collection of blood located between
the inner skull table and dura. This may result from
laceration of the middle or posterior meningeal artery,
whereas other EDH results from damage to the menin-
geal emissary veins or venous sinus. Skull fractures
adjacent to the hematoma are present in over 90% of
cases. The most common locations are the temporal,
frontal, and occipital regions. EDH also occurs in the
posterior fossa. There is an initial period of unconscious-
ness followed by a lucid interval, after which rapid
neurological deterioration develops. The lucid interval
is a delay between the trauma and the moment the EDH
enlarges and becomes symptomatic. A classic lucid
interval is seen in only 40% of patients with acute EDH.
Skull x-ray usually shows a linear fracture, most often
traversing the middle meningeal artery groove. CT
shows a well-localized, hyperdense, extracerebral lesion
(Fig. 3). The hematoma has a biconvex or lenticular
shape with sharp margination as a result of the fact that
the dura remains adherent at both edges. A lower atten-
uation swirl may be present within the clot, reflecting
active bleeding mixed with serum from clotted blood.
EDH tends not to cross cranial sutures, where the dura
is tightly adherent. Because they lie outside the dura,
EDH may cross the falx or displace the dural venous
sinuses from the inner table (Fig. 4). Surgical treatment
is required for nearly all acute EDH.
Fig. 3. Acute epidural
Axial non-enhanced CT
shows a well-localized,
hematoma in the left
frontal region. Alter-
nating areas of higher
and lower density repre-
sent a mixture of clotted
and unclotted blood.
Fig. 4. Differentiation of extension between EDH and SDH.
A: EDH tends not to cross cranial sutures, where the dura is tightly adherent. Because they lie outside the dura,
EDH may cross the falx or displace the dural venous sinuses from the inner table.
B: SDH tends to cross cranial sutures, and not to cross the falx or displace the dural venous sinuses from the
inner table. SDH may be more extensive than EDH. Blood spreads over the hemisphere.
TOYAMA ET AL
The prognosis of acute EDH is good, especially when
it is detected early in fully conscious patients and surgery
is performed as soon as possible.14 The overall mortality
rate with acute EDH is approximately 5%.
2. Acute subdural hematoma
SDH represents a collection of blood located between
the dura and arachnoid membrane. Acute SDH may be
caused by bleeding from the superficial veins or venous
sinus or by bleeding from cerebral contusions. Under-
lying cerebral injuries are more frequent with acute SDH
than acute EDH. Associated contusions are present in
50%. Swelling of the underlying hemisphere is common,
so that the mass effect is greater than expected based on
the size of the clot alone. One-third of patients with acute
SDH experience an initial lucid interval with subsequent
neurological deterioration. Forty percent of patients with
acute SDH were not initially unconscious after injury.
The classic CT appearance of an acute SDH is a crescent-
shaped homogeneously hyperdense extraaxial collec-
tion that spreads diffusely over the affected hemisphere
(Fig. 5). However, in up to 40% of acute SDH, the atten-
uation of the clot may be lower than expected due to
unclotted blood, low hematocrit value, or admixture with
cerebrospinal fluid. With bilateral SDH, there may be
no midline shift, and the cortical sulcal spaces are sym-
metrically effaced. An interhemispheric SDH is caused
by laceration of veins between the parietal-occipital
cortex and superior sagittal sinus. CT shows a band of
increased attenuation along the falx (Fig. 1) and remote
from the sagittal sinus. The usual management of acute
SDH is surgical. The use of early surgery, however, has
not always improved the outcome. The mortality rate is
from 37-57%.15-18 Most cases of acute SDH with low
GCS score had poor outcomes, and one of the reasons
was the frequent association of diffuse cerebral swelling.
3. Subarachnoid hemorrhage
Traumatic subarachnoid hemorrhage (T-SAH) usually
arises from hemorrhagic contusion with bleeding into
the subarachnoid space. T-SAH is a frequent occurrence
in severe head injury (26-53%).1 The most frequent
location is over the convexity, followed by the fissures
and basal cisterns. CT shows increased attenuation in
the cortical fissures and sulci or basal cisterns (Fig. 6).
T-SAH is seen more often in the cortical sulci near the
surface than in the basal cisterns as with aneurysmal
rupture. A larger extent of T-SAH is related to a poorer
outcome.19 A twofold increase in the risk of dying was
noted in the group with T-SAH. However, in patients
with mild and moderate head injury the adverse influence
of T-SAH on outcome was much less pronounced.
Contusions are a focal injury of the brain surface due to
direct impact with the calvarium. Contusions are most
common at sites of bony protuberances of the skull base
and therefore are seen in the frontal poles, orbital surface
of the frontal lobes, temporal poles, and inferior surface
of the temporal lobes and adjoining the anterior sylvian
fissure near the lesser sphenoid wing. They are multiple
in approximately 30% and are commonly associated with
extracerebral hematomas. Predominant pathological
lesions are subpial hemorrhage, necrosis, and edema.
Fig. 5. Acute subdural hematoma.
Axial non-enhanced CT in a head-injured patient with rapid
clinical deterioration. The high-density crescent-shaped fluid
collection spreads diffusely over the underlying right hemi-
sphere. The midline is deviated to the left. A herniated uncus
down to the suprasellar cistern and dilatation of the contralateral
inferior horn due to hydrocephalus are demonstrated. De-
compression surgery was performed, and SDH was evacuated.
Fig. 6. Traumatic subarachnoid hemorrhage.
Axial non-enhanced CT shows high-density hematoma
in the superficial sulci at the right side.
Volume 23, Number 5
On plain CT, hemorrhagic contusions appear as
heterogeneous, hyperdense lesions surrounded by an
irregularly marginated hypodense component. A hyper-
dense portion represents hemorrhage; a hypodense
component reflects edema and necrosis. This mixture
creates a mottled or salt-and-pepper pattern (Fig. 7).
Edema and mass effect typically increase in the first few
days after the traumatic insult, then gradually diminish
over time. Hyperdense lesion and mass effect resolve
within 10 to 14 days. Hypodense lesion may persist for
as long as 1 month after injury. Nonhemorrhagic con-
tusions are hypodense and often difficult to visualize.
CT performed 24 to 48 hours after injury commonly
shows previously undetected contusions, more extensive
hemorrhage, and increased edema. MRI is much more
sensitive than CT in the detection of nonhemorrhagic
contusions after the first 24 hours. However, some pa-
tients who talk after head trauma unexpectedly deterio-
rate and die. This is a case of “talk and die” head injury.
Brain contusion is the major cause of delayed deterio-
ration and death of patients with head trauma.20
5. Intracerebral hematoma
Traumatic intracerebral hematoma (T-ICH) results from
shearing or rapid deceleration injuries. Blood vessels
are torn, and blood is extravasated into brain paren-
chyma. The majority occur in the frontal and temporal
regions. They are usually superficial in location, rarely
occurring in deep structures. CT shows a large high atten-
uation intraaxial mass usually in the frontal or temporal
lobes or the basal ganglia (Fig. 8). Delayed ICH results
from damage to blood vessels in association with local
hypoxia and hypercapnia. This delayed ICH was found
after a time interval varying from 7 hours to 10 days
(Fig. 9). The major indication for surgical intervention
is evidence of diffuse edema with marked mass effect
and compartment shift, e.g., transtentorial herniation.
6. Diffuse axonal injury
A DAI is now widely accepted as one of the most
common types of primary brain lesions in patients with
severe head trauma. Patients with DAI usually present
with severe impairment of consciousness from the
moment of impact. The mechanism is one of widespread
tearing of axons due to shearing forces during accelera-
tion, deceleration, and rotation of the brain. The occur-
rence, localization, and severity of shearing injuries are
mainly determined by two factors: (1) The direction and
magnitude of rotational acceleration or deceleration
forces, and (2) the differences in density and rigidity
between two adjacent tissues, e.g., cerebral gray and
white matter. DAI lesions are commonly found in the
hemispheric subcortical lobar white matter, central
semiovale, corpus callosum, basal ganglia, brain stem,
and cerebellum (Fig. 10). Lesions range in size from 1
mm to 15 mm. They are usually ovoid in shape, with
their long axis parallel to the direction of the involved
axonal tracts. They tend to be multiple. In the acute phase
CT may show petechial foci of hemorrhage. Early
imaging evident for acute DAI may be subtle or non-
existent; only 20-50% of patients with DAI have
abnormalities on initial CT examination. DAI lesions
may be better visualized with MRI. Conversely, T2-
weighted images are more sensitive than T1-weighted
images (92.4% vs 72.3%) in detecting non-hemorrhagic
Fig. 7. Traumatic contusion.
Axial non-enhanced CT shows patchy hemorrhagic foci mixed
with low-density edema (salt-and-pepper appearance) in the left
frontal and temporal lobes. Small SDH and bilateral SAH were
also demonstrated. Perimesencephalic cistern closed bilaterally
due to bilateral subtentorial herniation.
Fig. 8. Traumatic intracerebral hematoma.
Axial non-enhanced CT scan shows a high-density
hematoma in a right frontal subcortical region.
TOYAMA ET AL
lesions.21 Recent data support the use of fluid attenuated
inversion recovery (FLAIR) sequences to show non-
hemorrhagic DAI.22 CT shows brain atrophy several
months later. DAI is the most common cause of vege-
tative state and severe disability after injury. The
incidence of vegetative state and severe disability is
significantly higher in patients with DAI than in patients
Secondary brain damage
The cranial cavity is functionally divided into compart-
ments by combinations of bony ridges and dural folds.
An elevation of the intracranial pressure will result in
displacement of contiguous cerebral structures into ad-
joining anatomic compartments. This causes pressure
effects on the adjacent brain and vascular structures.
The most important point is to control ICP with both
medical and surgical treatment, including decompressive
a) Subfalcine herniation
This type is herniation of the cingulated gyrus beneath
the free edge of the falx cerebri. CT findings in subfalcine
herniation include a shift of the midline structures to the
contralateral side (Fig. 2B, 5). The herniation results in
ipsilateral compression of the lateral ventricle and en-
largement of the contralateral ventricle due to obstruction
of the foramen Monro. The ipsilateral anterior cerebral
artery (ACA) and deep subependymal veins are shifted
across the midline. In severe cases, ACA occlusion may
result in secondary ischemia and infarction.
b) Descending transtentorial herniation
In this type the temporal uncus is herniated into the
transverse fissure. The herniation results in ipsilateral
compression of the mesencephalic cistern and contra-
lateral displacement of the midbrain (Fig. 11). In the
early stage, the brainstem is rotated or displaced, and
the ipsilateral mesencephalic cistern is enlarged. At a
more advanced stage, the tentorial incisura is completely
plugged from displacement of the temporal lobe.25 The
midbrain is elongated anteroposteriorly, and brainstem
hemorrhage (Duret’s hemorrhage) causes stretching of
perforating arteries (Fig. 12). Injury of the contralat-
eral cerebral peduncle due to compression against the
edge of the tentorium is called Kernohan’s notch. The
posterior cerebral artery and anterior chroidal artery are
more easily crushed by the herniated uncus against the
free edge of the tentorium. This may produce infarction.
c) Central herniation
Bilateral lesions, particularly those located near the
convexity of the brain, compress the brainstem by
exerting on it a retro-caudal pressure. This results in a
downward displacement of the brainstem and in
herniation of both temporal unci. This double herniation
appears as a virtually symmetrical obliteration of the
lateral parts of the perimesencephalic cistern (Fig. 7).
The brainstem, being crushed transversally, appears to
be elongated on its antero-posterior axis.
d) Posterior herniation
This herniation is marked by the total or partial
disappearance of the quadrigeminal cistern with or
Fig. 9. Delayed intracerebral hematoma.
Axial non-enhanced CT scans in a patient with severe head injury sustained in a traffic accident. This
patient had liver cirrhosis.
A: Axial CT on admission shows a small volume of subdural blood in the posterior interhemispheric fissure.
B: Right-sided hemiplegia prompted a repeat scan. The repeat CT scan obtained 4 hours after the initial
CT shows a large hematoma of the corpus callosum. Surgical drainage was performed.
Volume 23, Number 5
without deformation of the tectum. At a more advanced
stage of herniation the culmen entirely occupies the
posterior part of the pacchionian foramen and displaces
the midbrain rostrally. Compression of the midbrain
results in stenosis of the aqueduct, which in turn results
8. Acute cerebral swelling
Acute cerebral swelling may be due to increased water
content of brain tissue. This results from brain edema
and increasing cerebral blood volume. The mass effect
raises intracranial pressure, and acute hemispheric
swelling is related to ischemic brain damage as a con-
sequence or a cause, all being related to poor outcome.
CT findings in diffuse cerebral swelling include the
following: homogeneous decreased density, non-
visualization of cortical sulcal spaces, loss of the gray-
white matter interface, relative hyperdensity of the
cerebellum (white cerebellum sign), effacement of the
basal cisterns, especially the perimesencephalic cis-
terns, and bilateral compression of ventricles (Fig. 13).
Cerebral swelling may sometimes be associated with
fatal outcome due to acute cerebral edema.26 The mor-
tality rate is 22-77%.
CT has been widely used for neuromonitoring of head
trauma. CT is the gold standard for the detection of
intracranial abnormalities and is a safe method for
survey. CT can be relatively easily performed while the
patient is maintained by life support equipment. While
MRI is more sensitive and accurate in diagnosing
cerebral pathology, CT is considered the most critical
Fig. 12. Duret’s hemorrhage.
The herniated uncus has resulted
in compression of the midbrain. A
large centrally located hemor-
rhage is present in the midbrain.
Fig. 11. Descending transtentorial herniation.
A right temporal large traumatic ICH is demonstrated.
CT shows enlargement of the ipsilateral ambient cistern
caused by contralateral brainstem displacement.
Fig. 10. Diffuse axonal injury.
Non-enhanced CT shows multiple punctuate hemor-
rhages in right hemispheric subcortical white matter
tracts and bilateral lenticular nuclei (arrows).
TOYAMA ET AL
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Fig. 13. Diffuse cerebral swelling.
Axial non-enhanced CT scan in a patient with severe head injury
and GCS of 6.
There is bilateral SDH, SAH, and diffuse cerebral swelling. CT
shows effacement of superficial sulci and perimesencephalic cis-
tern, loss of differentiation between gray and white matter, and
small ventricles. Decompression surgery was performed, but was
unsuccessful due to inability to control intracranial hypertension.