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Review

Imaging in children presenting with acute neurological
deficit: stroke
Darshana D Rasalkar, Winnie C W Chu
Department of Imaging and
Interventional Radiology, The
Chinese University of Hong
Kong, Prince of Wales Hospital,
Shatin, New Territories, Hong
Kong, China
Correspondence to
Professor Winnie C W Chu,
Department of Imaging and
Interventional Radiology, The
Chinese University of Hong
Kong, Prince of Wales Hospital,
Ngan Shing Street, Shatin, New
Territories, Hong Kong, China;
winnie@med.cuhk.edu.hk
Received 6 April 2011
Accepted 10 March 2012
Published Online First
13 April 2012

ABSTRACT
Neurological deficits in the paediatric age group are
much rarer than in adults; however, it is an urgent
condition that relies heavily on imaging for a prompt
accurate diagnosis. Neurological deficits caused by
cerebrovascular diseases are defined as stroke, whereas
conditions manifesting with neurological deficits without
underlying cerebrovascular diseases are referred to as
stroke mimics. To the best of the authors’ knowledge,
there is a lack of systematic pictorial review that
collectively describes the imaging of neurological deficit
in children. The purpose of the present series is to
discuss the causes and imaging appearance of
neurological deficits in childhood, based on the
experience of a tertiary paediatric referral centre These
are broadly categorised into stroke, infection,
inflammation, metabolic disorder, cerebral neoplasms
and drug poisoning. Different entities of stroke and their
respective imaging findings are discussed. Paediatric
stroke can further be divided into arterial ischaemic
stroke, sino-venous stroke, haemorrhagic stroke and
hypoxiceischaemic encephalopathy.

Paediatric stroke is a relatively rare condition
resulting in acute neurological deficits. The reported
incidence of paediatric stroke is 2.1 to 13.1 per
100 000 children per year.1e5 Nearly 50% of paediatric stroke are ischaemic in nature, while the other
half are haemorrhagic or idiopathic in origin.6
Another classification of paediatric stroke is based
on the age of onset, divided into perinatal stroke
(between 28 weeks of gestation and 28 weeks after
birth) and childhood stroke.7
There is a significant overlap in clinical history,
presentation and neurological examination in
paediatric stroke despite various underlying causes.
This often poses a diagnostic challenge8 to physicians. Furthermore, clinical evaluation is often
difficult in paediatric patients of very young age.
Early identification of the stroke versus other causes
of neurological deficit is crucial in guiding appropriate treatment, thus preventing lifelong debility
and achieving a better prognosis.9

IMAGING CONSIDERATIONS IN PAEDIATRIC
STROKE
Neurosonography is the preferred imaging
modality for evaluating hypoxic brain injury in
neonates.10 11 The sensitivity of transcranial ultrasound is, however, low particularly in the first week
of life and thus a negative study should not be
interpreted as normal.11e13 The sensitivity
increases when transcranial ultrasound is
performed after 7 days. The advantage of ultraPostgrad Med J 2012;88:649–660. doi:10.1136/postgradmedj-2011-130087

sound, however, is that it can be performed at the
bedside, which can minimise the risk of transportation or sedation. MRI remains the imaging of
choice in highly suspected cases of stroke whenever
the neonate can be transported to the radiology
department. MRI has a higher sensitivity for the
detection of white matter infarction and is capable
of detecting underlying causes.14 Diffusionweighted imaging (DWI) enables the early detection of brain injury within hours after the hypoxic
event,15 and is useful in predicting the extent of
infarct and outcome of deficit.16 17 On magnetic
resonance spectroscopy (MRS), stroke is characterised by reduced N-acetyl aspartate and increased
lactate. The presence of a high lactate peak suggests
a poor prognosis, with development of encephalomalacia in the affected region. For older infants and
children with stroke, cranial MRI including
magnetic resonance angiography (MRA) is considered the first imaging modality. Although catheter
angiography is more sensitive in detecting medium
and small vessel disease, it is only reserved for
difficult cases in which endovascular surgical
intervention is anticipated.18

CLASSIFICATION/CAUSES OF PAEDIATRIC
STROKES
Arterial ischaemic stroke
The incidence of ischaemic stroke in childhood
exceeds 3.3 per 100 000 a year.5 The most common
presentation of arterial ischaemic stroke (AIS) in
childhood is hemiparesis attributable to the relatively frequent involvement of the middle cerebral
artery (MCA). Other less common presenting
features include altered mental status and focal
neurological signs, such as aphasia and visual
disturbance.19 Stroke in the posterior circulation is
rare and when it occurs it is usually associated with
vertebral artery dissection,20 presenting with
ataxia, vertigo, or vomiting.21 A focal pattern of
infarction occurs in non-progressive arteriopathies
and thromboembolic disease,10 whereas a more
diffuse pattern of infarction involving the deep
watershed area is seen in the progressive occlusive
vasculopathies. Braun et al22 alternatively has classified AIS causes into arteriopathy (moyamoya,
dissection,
vasculitis,
non-specific
stenosis,
systemic vasculitis with cerebral involvement or
infarction after tentorial herniation); cardioembolic
stroke (after congenital cardiac disease or cardiac
surgery, after the exclusion of arteriopathy by
vascular imaging); metabolic stroke accompanying
metabolic diseases; and those with prothrombotic
risk factors with or without associated arteriopathy. Out of these, moyamoya and metabolic
stroke have been described in detail separately.
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Figure 1 A 17-year-old patient
presented with sudden onset of leftsided weakness and facial palsy. MRI
brain: (A) diffusion-weighted imaging
(DWI) and (B) apparent diffusion
coefficient (ADC) map. Hyperintensity
on DWI (black arrow) and
corresponding hypointense signal on
ADC map (white arrow) are compatible
with restricted diffusion over the right
parietal region. Features are suggestive
of an acute infarct. (C) MRI angiogram
of the circle of Willis using the time of
flight technique reveals short segments
of severe stenosis in the proximal M1
segment of the right middle cerebral
artery (white arrow) and distal A1
segment of the right anterior cerebral
artery (white arrowhead).

Figure 2 A 2-month-old boy was
brought to an emergency department
after observation of decreased left limb
movement by the parents. MRI brain:
(A) T1-weighted and (B) T2-weighted
images. There is increased T2-weighted
and decreased T1-weighted signal,
which is nearly identical to the
unmyelinated white matter, resulting in
a ‘missing cortex’ appearance in the left
parietal region (white arrows).

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Figure 3 MRI and CT brain showing
chronic/old left middle cerebral infarcts
in two different adolescent patients with
right hemiparesis since early childhood.
The patient presented with a history of
recent onset of seizures. (A) MRI, fluidattenuated inversion recovery and (B)
CT axial images showing cystic
encephalomalacia in the left cerebral
hemisphere involving the left
frontoparietal lobe and left basal ganglia
(white arrow). Note the ipsilateral
cerebral atrophy and ex-vacuo dilatation
of the left lateral ventricle (black arrow).

DWI is the mainstay of diagnosis in acute AIS. In practice,
a high signal in DWI and low values on apparent diffusion
coefficient (ADC) maps represent restricted diffusion due to
cytotoxic oedema, which can be detected within minutes of
onset allowing quick and reliable detection of ischaemic/
infarcted areas (figure 1A,B). ADC maps usually normalise after
approximately 5e7 days. Non-atherosclerotic cerebral arteriopathy constitutes a leading cause and is reported in up to 80% of
children presenting with acute AIS;4 20 21 23 24 the detection of
which is important for secondary risk prevention. Time of flight
(TOF) MRA is equally sensitive to conventional angiography for
the detection of vasculopathy involving the internal carotid
artery (ICA), proximal segments of the MCA and the anterior
cerebral artery25e27 (figure 1C). TOFeMRA might, however,
overestimate the severity and length of a stenosis, whenever
there is dephasing secondary to turbulence, slow flow or in-plane
flow.28 The above pitfalls can be overcome by contrast-enhanced
MRA; however, the spatial resolution of MRA still limits an

accurate assessment in medium and small-calibre intracranial
arteries.29 30
In neonates with acute stroke, the ischaemic/oedematous
cortex reveals an increased T2-weighted and decreased T1weighted signal, which is nearly identical to the unmyelinated
white matter, resulting in a ‘missing cortex’ appearance10
(figure 2). The salvageable penumbra often reverses with an
early thrombolysis or neurointerventions while the acute
infarcted tissues probably evolve into a chronic infarct,
resulting in cystic encephalomalacia, associated with brain
volume loss and ex-vacuo dilatation of the ipsilateral ventricular system (figure 3).

Moyamoya disease/syndrome
Moyamoya disease is a progressive occlusive vasculopathy. On
angiography, the characteristic appearance of dilated lenticulostriate perforating vessels is described as a puff of cigarette smoke
or moyamoya in Japanese. Moyamoya can either be primary or

Figure 4 A 13-year-old boy presented with recurrent headache and repeated episodes of bilateral lower limb weakness. (A) Fluid-attenuated
inversion recovery image shows hyperintensities in the bilateral frontal periventricular white matter (white arrows). (B) T2-weighted axial image shows
prominent serpiginous collaterals in the parasagittal region (white arrow). (C) Magnetic resonance arteriography confirms absent bilateral internal
carotid arteries associated and severe middle cerebral artery (MCA) stenosis (arrowhead). Note multiple serpiginous collaterals arising from the
bilateral MCA (white arrows). Overall features are consistent with moyamoya disease.
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Figure 5 A 4-year-old girl presented
with left-sided weakness. The cause of
infarcts was not apparent at
presentation but she was subsequently
diagnosed to have mitochondrial
myopathy, encephalopathy, lactic
acidosi, and stroke syndrome by
biochemical tests. No basal ganglia
lesions were detected in this case.
Cranial MRI (A and B). Fluid-attenuated
inversion recovery coronal images show
multiple T2 hyperintensities in the
bilateral cerebral hemispheres involving
the bilateral insular cortices, left
hippocampus and bilateral corona
radiata (black arrows).

idiopathic (in which case it is referred to as moyamoya disease),
or secondary related to underlying disorders such as Down’s
syndrome, sickle cell disease, neurofibromatosis type 1 or cranial
radiotherapy (in which it is referred to as moyamoya syndrome).
The clinical symptoms include headaches, transient ischaemic
attacks, AIS, intracranial haemorrhage or silent cerebral infarctions (figure 4A).31 Initially, the steno-occlusive changes typi-

cally involve the distal intracranial ICA at the level of its
bifurcation. Later, the stenosis progresses to involve the proximal anterior cerebral artery and MCA. Involvement of posterior
circulation is rare, only occurring in the later stage and is
reported in 25% of affected individuals.32 33 The secondary
collateral formation in response to the progressive stenosis and
chronic cerebral hypoperfusion subsequently lead to multiple

Figure 6 An 8-month-old girl was
found to have rapidly increasing head
circumference and gross developmental
delay with repeated episodes of
decreased left limb power and
hypotonia. MRI scan of brain: (A, B and
C) T2-weighted axial images show
symmetric widening of the sylvian
fissures (white arrows) with poor
operculisation giving rise to ‘bat wings
appearance’. This is accompanied by an
expansion of external cerebrospinal fluid
spaces anterior to the temporal lobes
(black arrows) resulting in
frontotemporal volume loss. Chronic
subdural collections (arrowheads) are
present. Overall features are typical of
‘glutaric aciduria type I’.

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Figure 7 A preterm baby was born at
home. She was found to have
bradycardia, hypotonia and fixed pupils
after 1 h of birth requiring active
resuscitation for more than 45 min
before arriving at the intensive care unit.
Urgent CT brain (A) shows diffuse
hypodensity in bilateral basal ganglia
(arrows). This involvement of the deep
nuclei is typically seen in of ‘profound’
hypoxiaeischaemia and (B) the
presence of acute left posterior parietal
epidural haematoma (arrow). (C) and
(D) Follow-up MRI after 1 week shows
T1-weighted hyper and T2 mixed signal
intensities in the bilateral basal ganglia
and thalami (white arrows) compatible
with hypoxiceischaemic brain injury.
(E) T1-weighted and (F) T2-weighted
axial MRI show T1-weighted hyper and
T2-weighted hyperintense blood
products compatible with the presence
of methaemoglobin in subacute
extradural haematoma (arrows).

dilated vascular channels, which often involve the lenticulostriate, thalamostriate perforators and the cortico-leptomeningeal
vessels.34 As these collaterals only have weak intimal walls
intrinsically, they are prone to haemorrhage or small aneurysm
formation.35 36 Conventional MRI sequences demonstrate loss
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of flow voids of the terminal ICA and its proximal branches
secondary to arterial stenosis. Dilated perforator vessels can be
seen as flow voids within the basal ganglia, thalamus and basal
cisterns on T2-weighted imaging (figure 4B). TOFeMRA (figure
4C) confirms the findings and together with structural imaging
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Figure 8 An 8-month-old girl was
found to have acute onset stretching
and tightness of all four limbs. On
examination there was generalised
hypertonia and hyperreflexia with
decerebrate posture. (A) Emergency CT
brain demonstrating profound loss of
grey white matter differentiation
bilaterally suggestive of global
ischaemia (black arrows) with sparing
of the cerebellum seen as reversal of
cerebellum sign (white arrow) (B).
Follow-up MRI after 3 months (C) T1weighted and (D) T2-weighted images
show T1-weighted hyperintense signal
along the bilateral gyri (white arrow)
and multiple T1-hypo and T2hyperintense signal in the subcortical
white matter; features suggestive of
cortical laminar necrosis and
established infarcts in the bilateral
cerebral hemispheres.

has a sensitivity and specificity approaching 100%37 38 for the
diagnosis of moyamoya disease/syndrome.

Metabolic stroke
Inborn metabolic disorders are generally caused by spontaneous
mutations or hereditary gene defects resulting in biochemical
alterations involving one or more metabolic pathways. The
clinical features are non-specific, variable and may at times
mimic stroke.

A. Mitochondrial encephalopathy with lactic acidosis and
stroke-like episodes
Patients with mitochondrial encephalopathy with lactic acidosis
and stroke-like episodes (MELAS) syndrome are usually healthy
at birth. Later, the affected children exhibit delayed growth,
episodic vomiting, seizures, and recurrent cerebral injuries
resembling stroke. These stroke-like events, probably as the
result of proliferation of dysfunctional mitochondria in the
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smooth muscle cells of small arteries, may give rise to
either permanent or reversible deficits. The disease course is
progressive with periodic acute exacerbation.39e41 Serum and
cerebrospinal fluid lactate levels are usually elevated. MRI
demonstrates multiple cortical and subcortical infarct-like
lesions that cross vascular boundaries (figure 5), along with
varying degrees of generalised cerebral and cerebellar atrophy.
The parietal and occipital lobes and the basal ganglia are
frequently involved. Follow-up MRI may show resolution
and then subsequent reappearance of the abnormal areas. MRS
may reveal the presence of lactate even when the conventional
MRI findings are unremarkable. MRS can be regarded as
a screening tool in patients with suspected mitochondrial
cytopathy.42

B. Glutaric acidurea
Glutaric aciduria is a genetic disorder in which mutations in
certain genes cause a deficiency or reduce the efficiency of
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Figure 9 A 3-year-old boy with
developmental delay and spastic
diplegia. He was an ex-preterm baby
delivered at 29 weeks of gestation with
a history of asphyxia at birth. MRI brain:
(A) T1-weighted; (B) T2-weighted and
(C) fluid-attenuated inversion recovery
(FLAIR) axial images showing T1weighted iso to hypo and T2
hyperintensities in the bilateral
periventricular white matter (white
arrowhead) and ventricular enlargement
(black arrowhead). Note there are cystic
changes in bilateral trigonal regions,
best appreciated in FLAIR images (black
arrow). Features are suggestive of
‘white matter injury of prematurity’,
a pattern of established
hypoxiceischaemic encephalopathy,
typically seen in preterm injury.

mitochondrial enzymes. The majority of untreated children
present with an acute stroke-like neurological crisis when the
introduction of a high protein diet starts at approximately
6e18 months of age. Classically these children present with
spasms, jerking, rigidity, weakness and a tendency for seizures
with loss of sucking and swallow reflexes. Abnormal bleeding
commonly occurs and may raise the suspicion of non-accidental
injury due to the presence of subdural haematoma (SDH).
However, there are characteristic neuroimaging features on MRI,

which help to suggest the correct diagnosis (figure 6).43 Elevated
glutaric acid levels in either blood or urine are diagnostic. The
mainstay of treatment is dietary manipulation aimed at
reducing the production of glutaric acid and other intermediate
metabolites by diet modifications.

Hypoxiceischaemic brain injury
Hypoxiceischaemic brain injury (HIE) is more common
in preterm neonates than in term neonates.11 Overall,

Figure 10 Ultrasound appearance of
periventricular leucomalacia in
a premature (32 weeks) twin male baby
who presented with respiratory distress
and hypotonia at birth. Note the multiple
cysts occupying the frontal, parietal and
occipital horn of the cerebral
hemisphere (white arrows). They are
not communicating with the ventricular
system. Feature is suggestive of cystic
encephalomalacia.

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Figure 11 Neurosonographic appearance of intraventricular haemorrhage of different grades. (A) Grade I germinal matrix haemorrhage (GMH). Note
the increased echogenecity of the subependymal tissue in the right caudothalamic groove (white arrows). (B) Grade II GMH. Clinically the baby
presented with a rapid increase in head circumference with widened sutures. There is extension of echogenic blood clot in the frontal horn of the left
lateral ventricle (white arrows). There is no intraparenchymal haemorrhage or hydrocephalus. (C) Grade III GMH. There is residual blood clot adhered to
the choroid plexus (white arrows) with associate post-haemorrhagic hydrocephalus (black arrows). No intraparenchymal haemorrhage. (D) Grade III
GMH with periventricular haemorrhagic infarction. The entire ventricular system is filled with echogenic blood, resulting in obstructive hydrocephalus.
On the left, there is also intraparenchymal haemorrhage consistent with periventricular haemorrhagic infarction (white arrows). There is mild rightward
midline shift with flattening of the sulci/gyri pattern.
approximately 50% of cases of cerebral palsy occur in individuals
born prematurely.44 Cerebral palsy occurs in up to 5% of infants
born before 32 weeks and up to 19% of infants born before
28 weeks gestational age.11 In term patients, the prevalence of
HIE is estimated to be between two and four per 1000 live
births,45 of these 15% and 20% of infants die during the neonatal
period, and an additional 25% develop permanent neurological
disabilities.46
Childhood hypoxic brain injuries can present with different
distributional patterns depending on various factors. These

include the maturity of the brain, child’s age at the time of the
insult, severity of hypotension and duration of the injury.
During severe hypotension, preterm and term neonates are
vulnerable to hypoxic injury to the thalami, basal ganglia (figure
7) and brainstem. In addition, the dorsal brainstem and perirolandic cortex are typically involved in term neonates, whereas
these findings are unusual in preterm neonates.10 47 In older
children, diffuse cortical injury (figure 8A) and basal ganglia
lesions dominate. Characteristically the cerebellum, being less
susceptible to the hypoxic ischaemic change, remains higher in

Figure 12 A 15-year-old boy
presented with sudden onset of
disorientation and right-sided
weakness. CT brain: unenhanced
images (A) showing right frontal lobe
haemorrhage and perilesional white
marrow oedema (black arrow) and (B)
showing right epidural haematoma
(white arrow). The boy later was found
to have haemophilia A.

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Figure 13 A 16-year-old boy presented with progressive visual loss on left side. There was a history of gradual progressive right upper and lower
limb weakness. (A) Proton density image and (B) T2-weighted axial images showing left occipital infarct with bunch of serpiginous structures with
flow voids (black arrow). (C) Magnetic resonance cerebral angiogram time of flight technique showing tufts of vessels arising from the left middle
cerebral artery compatible with cerebral arteriovenous malformation (white arrow).

attenuation than the hypodense infarcted cerebral hemispheres
on CT, producing the ‘reversal sign’ (figure 8B).
Cortical grey matter is more vulnerable to ischeamia when
compared with white matter. The ischaemic injury to cortical
neurons is known as ‘cortical laminar necrosis’. Cortical laminar
hyperintensity on T2-weighted and fluid-attenuated inversion
recovery images is invariably seen as early as day 1 after injury,
whereas hyperintensity on T1-weighted images usually occurs at
least 14 days after the injury48 (figure 8C,D). DWI may be able
to detect abnormal hyperintensity in grey matter as early as less
than 24 h at the early subacute phase with an adjusted window
level depending on the magnetic resonance manufactures. The
above imaging finding has been correlated with a poor outcome,
either a permanent vegetative state or brain death.49 Unlike
profound hypotension, mild and moderate hypotension allows
shunting of blood flow into the brainstem, cerebellum and basal
ganglia. In preterm neonates, periventricular white matter injury
prevails (figures 9 and 10), whereas term neonates and older
children have parasagittal watershed injuries.10

Table 1

Temporal changes of haematoma on MR imaging

Stage and time
from haematoma

Haemoglobin
(Hb) stage

Signal intensity
on T1W

Signal intensity
on T2W

Hyperacute (<6 h)
Acute (<6e3 days)
Early subacute
(3e7 days)
Late subacute
(1e4 weeks)
Early chronic
(>4 weeks)
Late chronic
(months to years)

Oxy-Hb
Deoxy-Hb
Intracellular meth-Hb

Grey
Grey
White

White
Black
Black

Extracellular meth-Hb

White

White

Extracellular meth-Hb
with hemosiderin rim
Hemosiderin

White

White with
black rim
Black

Black

Mild to moderate asphyxia in preterm neonates can lead to
intraventricular haemorrhage (IVH), the overall prevalence of
which is inversely related to gestational age and weight at
birth. Preterm neonates weighing less than 2000 g are
approximately 25%, and in the majority of cases this bleeding

Figure 14 A 17-year-old boy presented with recurrent headache and left-sided weakness. Cranial MRI: (A) Axial T2-weighted image shows
hyperintensities in the right frontal lobe (black arrow) predominantly involving the white matter. (B) Post-contrast axial image shows the empty delta
sign (white arrowhead). (C) Magnetic resonance venogram using time of flight technique showing absent anterior sagittal sinus (white arrow).
Features are compatible with cerebral sinovenous thrombosis.
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Figure 15 Day 1 child noticed to have
fever soon after birth. He presented with
mild respiratory distress, grunting and
mild in-sucking. Neurological
examination showed increasing tones
over four limbs. Urgent CT: (A)
Unenhanced axial CT shows left
occipital infarct (white arrow) and
intraventricular haemorrhages (black
arrows). (B) Post-contrast image shows
absent/thrombosed left transverse sinus
(white arrowhead).

occurs within the first 24 h of life.11 50 51 The majority of IVH
are in turn associated with germinal matrix haemorrhages.
IVH can be divided into grades IeIII and grade III with periventricular haemorrhagic infarction (equivalent to the previous
‘IVH grade IV’).47 The classification is based on radiological
appearance rather than pathophysiological description of
events leading to periventricular haemorrhageeIVH. In grade 1
haemorrhage, blood is limited to the subependymal region and/
or germinal matrix (figure 11A). In grade II, there is subependymal haemorrhage with extension into the lateral
ventricles without ventricular enlargement (figure 11B). In
grade III, subependymal haemorrhage extends into the lateral
ventricles with ventricular enlargement (figure 11C). Previously known as grade IV haemorrhage, recently termed grade
III with periventricular haemorrhagic infarction (figure 11D),
this condition is probably related to increased venous pressure
within the terminal veins and feeders leading to periventricular
haemorrhage.

Haemorrhagic stroke
Haemorrhagic stroke is rare in children. The reported
incidence is approximately 1.2 per 1 000 000 children per year.1
Traumatic head injury, non-accidental injury, bleeding
disorders (haemophilia) (figure 12), arteriovenous malformations
(figure 13), haemorrhagic neoplasms are some of the leading
causes of haemorrhagic stroke in children.52 As a result of faster
acquisitions, CT is considered the preferred imaging investigation in these unstable patients. Depending on the stage of
haematoma, MRI can detect various blood products and
predict the time of onset of intracranial bleeding (table 1).53
These stages are, however, well studied in the adult population
and need some caution about the interpretation of absolute
time values based on imaging appearances in the paediatric
population.
In the paediatric population, the presence of SDH, particularly
in the absence of a history of significant accidental trauma,
should alert clinicians to the possibility of a non-accidental head
injury (NAHI). SDH at multiple sites, the presence of subdural
blood in the posterior interhemispheric fissure or the posterior
fossa are some of the features that favour the diagnosis of NAHI
over accident trauma.46 NAHI-associated skull fractures are
usually multiple, bilateral, diastatic and often cross suture
lines.44 Various types of other parenchymal injuries can be seen
following NAHI, in which the most common type is generalised
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Main messages
< Significant overlap is present in clinical history, presentation

and neurological examination in paediatric stroke and stroke
mimics posing a diagnostic challenge to physicians.
< Imaging plays an important role in the clinical decision thus
tremendously affecting the outcome of patients in paediatric
stroke.
< Neurosonography is the preferred imaging modality for
evaluating hypoxic brain injury in neonates; however, its
sensitivity is low particularly in the first week of life and thus
a negative study should not be interpreted as normal.
< DWI is the mainstay of diagnosis in acute AIS detecting
restricted diffusion due to cytotoxic oedema, which can be
detected within minutes of onset allowing quick and reliable
detection of ischaemic/infarcted areas.
< Abnormal bleeding commonly occurs in glutaric aciduria type
1 and may raise the suspicion of non-accidental injury due to
the presence of SDH. However, symmetric widening of the
sylvian fissures with poor operculisation giving rise to ‘bat
wings appearance’ accompanied by an expansion of external
cerebrospinal fluid spaces, frontotemporal volume loss and
chronic subdural collections are classically present in glutaric
aciduria type 1 and are helpful in differentiating these two
conditions.
< The distribution of hypoxic brain injuries depends on the
maturity of the brain, child’s age at the time of the insult,
severity of hypotension and duration of the injury. The
changes in preterm and term ‘profound’ hypoxic ischaemic
injury are very similar, and are centred on the basal ganglia
and thalami. The difference is that at term, the periorolandic
cortex and brainstem cortex can also be seen, whereas these
findings are unusual preterm.
< Forty per cent of paediatric patients with venous thrombosis
have venous infarction; 70% of venous infarctions are
haemorrhagic.
< The presence of haemorrhagic infarct should alert the clinician
to the possibility of venous stroke/thrombosis and warrants
contrast-enhanced venography rather than less reliable
contrast images.

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Current research questions
< Is the MRI interpretation of absolute time values of intracranial

haematoma based on imaging appearances applicable to the
paediatric population?
< What is the best imaging protocol for paediatric stroke?

parenchymal changes caused by hypoxiceischaemic change.
Less commonly, focal lesions including axonal shearing injuries
do not usually contribute to death in child abuse when
compared with hypoxiceischaemic changes.54 55

Venous stroke/thrombosis
Cerebral sinovenous thrombosis (CSVT) occurs in 0.41 per
100 000 live-born infants,56 and 40% of paediatric patients with
venous thrombosis have venous infarction. Seventy per cent of
venous infarctions are haemorrhagic.57 Clinically, infants most
commonly present with seizures and diffuse neurological
symptoms. Focal neurological signs, headache and alteration of
consciousness are typical symptoms in older children. Venous
infarctions involve non-arterial territories and tend to be
multiple, bilateral and occur over the convexities. The presence
of haemorrhagic infarct should alert the clinician to the possibility of CSVT10 (figure 14A). The ‘delta sign’, a hyperdensity
within the triangular superior sagittal sinus on the unenhanced
study suggests the diagnosis of CVST. The ‘empty delta sign’ of
CSVT wherein thrombus is seen as a filling defect within the
posterior portion of the superior sagittal sinus (figure 14B)
requires the presence of intravenous contrast, which is not
always given in routine protocols for intracranial haemorrhage,
or in the emergency department. A dedicated venogram instead
of less focused contrast-enhanced CT is recommended in a high
index of clinical suspicion58 (figure 14C). CSVT should be
suspected in infants who present with IVH (figure 15), especially when associated with unilateral thalamic haemorrhage.59
Thirty-one per cent of term infants diagnosed with CSVT were
shown to be associated with IVH.59 The location of the
secondary infarction depends on which draining veins are
occluded. Superior sagittal and lateral sinuses are most
frequently involved, followed by straight sinus.56 57 Deep cere-

bral vein thrombosis is associated with bilateral thalamic
haemorrhages.
In conclusion, this pictorial essay discusses the imaging
appearances and imaging protocol in paediatric stroke. Imaging
plays an important role in the clinical decision, thus tremendously affecting the outcome of patients in paediatric stroke.

MULTIPLE CHOICE QUESTIONS
1. The first imaging technique of choice in neonates and young
infants to rule out intracranial abnormality is
A. CT scan.
B. MRI.
C. Ultrasound.
D. Plain x-ray of the skull.

2. The following are the important findings regarding cerebral
infarction, which should be included in imaging report except
A. Areas of haemorrhages.
B. Acute versus chronic.
C. Territory involved.
D. Mass effect.
E. Areas of calcifications.

3. The signal of an early subacute infarct on MRI would appear
as
A. Decreased on ADC and increased on DWI.
B. Decreased on ADC and DWI.
C. Increased on ADC and DWI.
D. Increased on ADC and decreased DWI.

4. All are correct regarding the appearance of intraparenchymal
blood on MRI except
A. Hyperacute blood (<6 h) is grey on T1-weighted and white
on T2-weighted MRI.
B. Late chronic blood (months to years) has black signal on
both T1-weighted and T2-weighted MRI as a resuslt of
haemosiderin.
C. MRI signal in the acute phase (6e72 h) is grey on T1weighted and black on T2-weighted MRI.
D. Late subacute blood (1e4 weeks) has black signal on
both T1-weighted and T2-weighted MRI as a result of
haemosiderin.

5. Regarding tuberculous meningitis, all the options are correct
except

Key references
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< Shellhaas RA, Smith SE, O’Tool E, et al. Mimics of childhood
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< Miyamoto O, Auer RN. Stroke in children: the coexistence of
multiple risk factors predicts poor outcome. Neurology
2000;54:362e78.
< Beitzke D, Simbrunner J, Riccabona M. MRI in paediatric
hypoxiceischaemic disease, metabolic disorders and
malformations e a review. Eur J Radiol 2008;68:199e213.
< Eichler F, Krishnamoorthy K, Grant PE. Magnetic resonance
imaging evaluation of possible neonatal sinovenous thrombosis. Pediatr Neurol 2007;37:317e23.
Postgrad Med J 2012;88:649–660. doi:10.1136/postgradmedj-2011-130087

A. Most common in developing country.
B. Complications include hydrocephalus, empyema and abscess.
C. Negative imaging virtually excludes the possibility of
meningitis.
D. Exudates are mainly located at basal cisterns.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.

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ANSWERS
1. Correct answer: (C). Ultrasound is radiation free, can be done at the bedside. It can
also be performed quickly without any need for sedation.
2. Correct answer: (E). Remaining four are the most important findings deciding plan
of management in practice.
3. Correct answer: (A).
4. Correct answer: (D). Late subacute blood (1e4 weeks) is mainly due to
extracellular meth-Hb, which signal appears white on both T1-weighted and T2weighted MRI.
5. Correct answer: (C). Imaging is mainly to look for complications and may be
entirely normal at early stages.

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Imaging in children presenting with acute
neurological deficit: stroke
Darshana D Rasalkar and Winnie C W Chu
Postgrad Med J 2012 88: 649-660 originally published online April 13,
2012

doi: 10.1136/postgradmedj-2011-130087

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