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S E C T I O N V I   Pediatric Critical Care: Neurologic

Intracranial Hemorrhage and Vascular
Malformations

aneurysms, and generally will be required before surgical or endovascular intervention. In the appropriate clinical setting, however,
such as a spontaneous SAH without etiology, a negative MRI,
MRA, or CTA should not exclude a catheter angiogram. Arterial
aneurysms are much less common in children than in adults, with
many of those seen likely being congenital or due to infection in
contrast to the typical acquired berry aneurysms seen in adults. As
in adults, all but the smallest aneurysms can be seen on MRA or
CTA, with CTA sensitivity for berry aneurysms in adult series
reported in the range of 80% to 97%.18 These studies, though,
need to be of optimum resolution, are generally targeted to the
high-risk locations for aneurysms in adults, and may not include
less common aneurysm locations, which are seen with greater
frequency in children. Angiographically occult lesions—including
capillary telangiectasia, cavernous malformation, and developmental venous anomalies—are seen on MRI but usually are not
of consequence except in cases of the occasional large cavernous
malformation.
A vein of Galen aneurysmal malformation (VGAM) is a misnomer because it is not the vein of Galen but rather is a persistent
embryonic vein that is dilated in association with a large fistula.42

Intracranial hemorrhage can be readily detected using noncontrast CT or MRI with SWI and GRE sequences. The presence of
nontraumatic intracranial hemorrhage could indicate hemorrhagic conversion of an ischemic stroke, underlying coagulopathy,
hemorrhagic neoplasm, or vascular malformation. A large study
found an incidence of hemorrhagic stroke of 1.4 per 100,000
person years in those younger than 20 years of age. An underlying

aneurysm was found in 13%, including 57% of those with pure
SAH, 2% of those with a pure parenchymal hemorrhage, and 5%
of those with a mixed hemorrhage.41 Etiologic workup of hemorrhagic stroke in children includes a broad differential. In the setting of hemorrhagic stroke of unknown obvious cause, MRA and
CTA are important imaging tests.
Most arteriovenous malformations and aneurysms can be detected with a combination of MRI and MRA or CTA, although
small lesions can be missed (Fig. 61.14). Catheter angiogram
remains the gold standard for arteriovenous malformation diagnosis, confirming flow dynamics and the presence of intranidal
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•  Fig. 61.14  ​A

14-year-old child with a left occipital arteriovenous malformation (AVM). (A) Axial T2weighted magnetic resonance imaging shows multiple flow voids in the left occipital lobe (arrow). (B) Lateral
view from catheter angiogram confirms the presence of an AVM (arrow) and early draining veins (curved
arrow). (C) Lateral maximum-intensity projection image from a magnetic resonance angiogram shows an
enlarged posterior cerebral artery branch (arrows), which feeds the tangle of abnormal vessels.


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•  Fig. 61.15  ​Vein of Galen aneurysmal malformation. (A) Axial noncontrast computed tomography scan
shows the dilated embryonic vein (arrows). Axial T2 (B) and sagittal T1 (C) magnetic resonance imaging
demonstrates the dilated embryonic vein (arrows) and the draining vein (arrowheads).

VGAMs presenting in the newborn period can manifest with
cardiac symptoms resulting from the large shunt and high-output
congestive cardiac failure. VGAM can be identified on cranial
ultrasound and head CT (Fig. 61.15). In the presence of a
VGAM, MRI with MR angiography will give an overall vascular
road map for planning endovascular intervention, because the
limited amount of iodinated contrast that can be used in a neonate necessitates directed intervention.

Venous Infarct
Dural venous sinus thrombosis and venous infarct can produce

a range of clinical presentations ranging from headache due to
intracranial hypertension to herniation syndromes, such as those
related to intraparenchymal hemorrhage. Intraparenchymal
hemorrhage or imaging evidence of edema in a nonarterial distribution raises suspicion of a venous stroke. In the setting of
suspected dural venous sinus thrombosis or venous stroke,
evaluation of the cerebral venous system should be undertaken.
Ultrasound has limited utility in this setting, although evaluation of superior sagittal sinus flow can be undertaken in the
young infant with an open fontanelle. CT evidence of a venous
clot can be detected as hyperdense venous sinuses acutely on
noncontrast scans and as the empty delta sign (lower density in
area of clot surrounded by enhancing blood) in the superior
sagittal sinus on contrast-enhanced scans. This assessment can
be problematic in the newborn in whom the normal low-density
unmyelinated brain and typically higher hematocrit make the
venous sinuses appear dense normally on CT. Classically, the
venous phase of a catheter angiogram has been used to look for
venous sinus thrombosis. Catheter evaluation of the venous sinuses, however, has been effectively replaced with MRV techniques. MRV uses flow-sensitive sequences that can delineate
the major venous sinuses quite effectively without the need for
IV contrast (see Fig. 61.5). A subacute clot in a venous sinus also
can be evident on standard T1- and T2-weighted MRI as bright
areas in the venous sinuses, although an acute clot can be more
difficult to appreciate. On MRI, GRE and SWI sequences may
demonstrate low signal, and T1 contrast-enhanced sequences
may demonstrate areas of nonenhancement of thrombosed
venous sinuses.

•  Fig. 61.16  ​Posterior

reversible encephalopathy syndrome. Axial fluidattenuated inversion recovery magnetic resonance imaging showing
subcortical foci of hyperintensity (arrows) associated with cyclosporin

toxicity. Note that abnormalities may have a variable distribution and are
frequently, but not always, posterior in location.

Posterior Reversible Encephalopathy Syndrome
Posterior reversible encephalopathy syndrome (PRES) results
from a loss of autoregulation in the older infant and child as seen
in hypertensive encephalopathy, cytotoxic and immunosuppressive drug neurotoxicity, and thrombotic thrombocytopenia purpura. Typically, PRES preferentially involves a posterior and
parasagittal distribution of the brain with T2 and FLAIR hyperintensities and, less frequently, can involve the frontal lobes and
brainstem.43,44 Lesions often are relatively symmetric, confluent,
centered in the subcortical white matter, and, rarely, demonstrate
patchy enhancement (Fig. 61.16). Frequently, because the underlying pathology causes only vasogenic edema, these lesions will
not be restricted on DWI. However, ischemia can be triggered by


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• Fig. 61.17  ​Obstructive hydrocephalus. Axial (A) and midline sagittal (B) T2 magnetic resonance imaging

(MRI) shows dilated lateral (asterisks) and third (III) ventricles that result from aqueductal obstruction (arrow).
(C) Chiari II malformation with hydrocephalus. Image demonstrates utility of heavily T2-weighted, halfFourier acquisition, single-shot, turbo spin-echo MRI in evaluation of ventricles. Sequence can be​
obtained rapidly without the need for sedation; this avoids the radiation associated with repeated computed tomography scans.

a severe increase in blood pressure, resulting in superimposed
cytotoxic edema and therefore diffusion-restricted lesions that
usually result in infarctions, the severity of which often correlates
with prognosis. In children, PRES can have less typical imaging
patterns than those observed in adults.

Central Nervous System Infection
Imaging findings and the role of imaging in cerebral infection will
depend on the organism and location of the infection.45,46 The
appearance will also depend on the cell type infected and the host
immune response. Infection can involve the subarachnoid spaces
and meninges, parameningeal spaces, or the brain parenchyma
itself, either primarily or secondarily. With bacterial meningitis
the appearance on CT and MRI may range from normal to diffuse swelling with loss of gray-white differentiation and obliteration of ventricular and cisternal CSF spaces. Coxsackievirus,
echovirus, and mumps infect the meninges more than the neurons, whereas poliovirus infects the neurons, particularly the motor neurons. Herpes simplex virus type 1 has a predilection for the
limbic system, most commonly affects the temporal lobes, and is
the most common sporadic viral encephalitis.47 Herpes simplex
virus type 2 encephalitis is most commonly acquired at birth and
does not display a predilection for the temporal lobes. Although
MRI is more sensitive than CT, a normal MRI still does not entirely exclude viral encephalitis. In the clinical setting of suspected
meningeal infection, CT may be indicated prior to lumbar puncture to exclude hydrocephalus or swelling that potentially would
preclude lumbar puncture without neurosurgical consultation.
Imaging alone should not be used to exclude meningeal infection, however. Particularly early in the setting of meningitis,
contrast-enhanced CT is often normal. Although MRI with
gadolinium is more sensitive, only 55% to 70% of persons with
proved meningitis have abnormal CT or MRI scans.8 Some investigators believe that CSF hyperintensity on the FLAIR sequence

is more sensitive than gadolinium-enhanced T1-weighted sequence for meningitis. However, CSF hyperintensity on FLAIR

associated with supplemental oxygen and anesthesia as well as
noninfectious meningeal irritation and leptomeningeal tumor
render this finding less specific.48,49
Complications associated with meningeal infection include
compromise of the BBB leading to vasogenic edema, arterial
spasm that can cause ischemia with cytotoxic edema and eventual
infarction, and hydrocephalus potentially with the development
of transependymal CSF flow/interstitial edema. Hydrocephalus
can be obstructive, typically at the level of the cerebral aqueduct
(Fig. 61.17) or outlet of the fourth ventricle, or more commonly
communicating because of impaired CSF resorption from arachnoid granulation obstruction with exudates. This impairment of
CSF resorption can become permanent because of leptomeningealependymal fibrosis and require shunting. Ultrasound can be used
in very young patients; otherwise, CT and more recently half
Fourier acquisition single-shot turbo spin echo (HASTE) or other
rapid, heavily T2-weighted MRI sequences usually are used to
follow ventricular dilation. A primary role for imaging in meningitis is to evaluate for these complications. Two patterns of abnormal meningeal enhancement are seen on MRI with meningitis. A
pachymeningeal pattern appears as diffuse linear thickening of the
normal dural lining. However, this appearance is not specific because the same pattern can be seen in other settings, including
after surgery and occasionally following shunt revision, in some
cases because of intracranial hypotension. The other pattern is a
leptomeningeal enhancement in which enhancement is seen
along the pia-arachnoid membranes following the sulcal grooves.
This pattern also is not specific, with a similar appearance being
seen at times with leptomeningeal spread of tumor.
Extraaxial collections can develop in association with meningitis, including subdural effusions and, less commonly, subdural
abscesses or empyema. Effusions are crescentic collections that
typically are isodense to CSF on CT and isointense to CSF on
most MRI sequences, although because the protein level may be

increased, the collections may be hyperintense on T1 and FLAIR
(Fig. 61.18). Subdural abscesses can be crescentic or lentiform
when larger and typically slightly denser than CSF on CT. A rim


CHAPTER 61  Neuroimaging

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•  Fig. 61.18  ​Chronic

subdural effusions following meningitis. Axial T2weighted magnetic resonance imaging shows mass effect with sulcal
compression associated with bifrontal subdural collections (arrows). Note
that these subdural collections can be differentiated from enlarged subarachnoid spaces because the latter would have bridging vessels crossing
the cerebrospinal fluid in the subarachnoid spaces.

of enhancement of variable thickness is generally better detected
on MRI (Fig. 61.19). DWI can demonstrate restricted diffusion
in subdural empyemas due to the relatively restricted movement
of water molecules in purulent material. Subdural (and brain)
abscess also can occur as a direct extension of paranasal sinus or
mastoid infection.
Infection of the brain parenchyma can take the form of an
abscess or a more diffuse encephalitis. Encephalitis in isolation or
associated with meningitis generally will produce nonspecific cerebral parenchymal changes or cerebritis that appear bright on T2
and FLAIR sequences. Differentiation by imaging of cerebritis
from ischemic changes associated with meningoencephalitis is
problematic, especially because cerebritis also can demonstrate
restricted diffusion. Areas of cerebritis evolve into focal abscesses
that will generally demonstrate a central focus of low density on

CT and low T1, high T2, and FLAIR signal on MRI, with a ring
of enhancement and variable surrounding edema (Fig. 61.20).
More commonly in adults with a ring-enhancing lesion, there
can be uncertainty in differentiating between a brain abscess and
necrotic tumor. The brain abscess generally will have a thinner
rim of enhancement, and on DWI a pyogenic abscess will demonstrate restricted diffusion. The necrotic tumor often shows a
thick, irregular rim with increased diffusion or T2 shine-through.
In differentiating pyogenic, tubercular, and fungal abscesses,
some studies have described a greater likelihood of homogeneous
diffusion restriction with pyogenic and tubercular abscesses but a
variable pattern with fungal abscesses.50,51 Exclusion of a meningeal or parameningeal abscess in the head can be accomplished
largely with contrast-enhanced CT, looking for a fluid collection

•  Fig. 61.19  ​Subdural abscess or subdural empyema. Axial T1-weighted
magnetic resonance imaging with gadolinium demonstrates a small rimenhancing right frontal paramedian subdural abscess (arrows). This area
was restricted on diffusion-weighted imaging (not shown).

with a surrounding enhancing rim, although occasionally a small
collection may be missed on CT but detected by MRI. Evaluation for meningeal or parameningeal abscess in the spine should
be approached with MRI.

Demyelinating Disease
Multiple sclerosis (MS) is much less common in children than in
adults, whereas ADEM primarily occurs in children. ADEM can
manifest with symmetric involvement of central gray matter at
times (Fig. 61.21), with an imaging picture that overlaps with
some metabolic diseases. In other cases of ADEM, lesions, typically in the cerebral white matter, can be scattered with a picture
similar to vasculitis or embolic infarction. The appearance of MS
and ADEM can be similar, though some features, such as the
perivenule orientation (Dawson fingers) of lesions, are more characteristic of MS. The presence of lesions of multiple ages would

be consistent with MS (Fig. 61.22) rather than ADEM. Demyelinating lesions are seen most commonly in white matter but appear in gray matter as well. Acute demyelinating lesions demonstrate enhancement. Acute lesions also can demonstrate restricted
diffusion, with an appearance on DWI that mimics an acute ischemic lesion. Often, however, the pattern of involvement is useful
in distinguishing demyelinating disease from ischemic disease.
The spinal cord can be involved with MS or ADEM (Fig. 61.23),
although relatively rarely in isolation. Hence, imaging the brain to
look for additional involvement can be useful in some cases to
distinguish between a cord demyelinating process and infarct,
which can have a similar imaging appearance.


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S E C T I O N V I   Pediatric Critical Care: Neurologic

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•  Fig. 61.20  ​Frontal brain abscesses. (A) Axial T2-weighted magnetic resonance imaging (MRI) demonstrates a right frontal ring-enhancing lesion with a T2 hypointense capsule that has considerable surrounding vasogenic edema and leftward midline shift. The lesion is bright on diffusion (B) and dark on the apparent diffusion coefficient map (C), suggesting that it is diffusion restricted. (D) In another patient, axial
postcontrast T1-weighted MRI demonstrates a right frontal periventricular ring-enhancing lesion with T1
hypointense vasogenic edema surrounding it.

Trauma
CT remains the primary imaging modality in persons with acute
traumatic brain injury (TBI) and has the advantage of relative
ease of scanning compared with MRI, including speed of scanning and allowing non-MRI-compatible monitoring and life support equipment to be used during imaging. CT is usually sufficient for evaluation of most TBI requiring intervention, including

assessment of swelling and acute hemorrhage within the intraaxial
and extraaxial compartments. CT is generally more sensitive than
MRI in detecting acute SAH and in the evaluation of bony injury
(Fig. 61.24). CT is generally sufficient to detect cerebral swelling
associated with herniation syndromes and therefore can identify
the potential need for neurosurgical intervention (Fig. 61.25).

MRI is more sensitive for the detection of parenchymal injury
and for more subtle extraaxial collections, including more
chronic subdural hematomas, a hallmark of abusive head trauma
associated with child abuse. MRI is indicated when there is
doubt as to the presence of a subdural blood collection in the
setting of suspected trauma. Also, in the setting of abusive head
trauma, MRI can detect evidence of old parenchymal or extraaxial hemorrhage not seen with CT using the GRE sequence (see
Fig. 61.8D). In particular, gradient sequences and susceptibilityweighted imaging can reveal evidence of old parenchymal
hemorrhages. Bony injury of the spine is better evaluated with
CT, although cord compression and injury are better assessed
with MRI.