3.

3
NEUROIMAGING OF THE BRAIN
Beverly Wical

Neuroimaging adds significantly to our understanding of the pathogenesis and patho-

physiology of the heterogeneous group of disorders responsible for cerebral palsy
(Korzeniewski et al. 2008). In the newborn and postnatal period, imaging is directed towards
identifying conditions or acute injury that may require treatment, as well as those that may
be antecedents of cerebral palsy. In the older child, imaging often shows structural changes
in the brain associated with motor impairment. Cranial ultrasonography, computed
tomography (CT) and magnetic resonance imaging (MRI) are the main modalities utilized.
Cranial ultrasonography of the preterm and newborn brain is a clinical mainstay in
identifying injury (Hintz and O’Shea 2008). It is safe, portable, and widely available. It is
less sensitive than CT or MRI, however; abnormalities of the brainstem, cerebellum or
cerebral convexities are not well visualized. Cranial ultrasound’s predictive value may be
hampered by interpreter reliability, particularly for less severe lesions (De Vries et al. 2004,
Hintz et al. 2007).
CT is acutely sensitive for fresh hemorrhage, and is best for bone and scalp lesions. It
is widely available, and the acquisition of images of newborn infants is not as dependent
on the specialized skills of technologists as is cranial ultrasonography. Only axial images
are typically acquired, limiting views of intracranial contents. Exposure to ionizing radiation
occurs, causing concern regarding the amount received by young infants. As few as two or
three CT procedures in infants may increase the risk of subsequent malignancy (Brenner
and Hall 2007). Definitive long-term risks are still emerging, but we avoid CT in young
infants whenever possible.
MRI provides the most detailed structural analysis of the developing brain. It adds to our
understanding of the timing of injury, as well as the structural correlates of developmental
and acquired disorders causing cerebral palsy. Additional techniques permit visualization of
the venous structures and arterial tree. Diffusion weighted MRI, now in wide clinical use,
allows the best timing of certain types of brain injury – particularly hypoxic–ischemic
encephalopathy, and cerebral infarction. Emerging techniques such as diffusion tensor
magnetic imaging allow exquisite delineation of white-matter tracts not previously possible.
No ionizing radiation exposure occurs and no harm to humans has yet been identified from
exposure to magnetic fields at the strengths used to produce medical images.

Neuroimaging of the fetus at risk for cerebral palsy

In utero ultrasonography is able to identify potential nervous system lesions associated with
cerebral palsy. Ventriculomegaly on ultrasound is the most common cause for referral for

222
fetal MRI. From 18 weeks of gestation onward, MRI images can be obtained successfully
from about 95% of fetuses (Zimmerman and Bilaniuk 2006). Despite this, early MRI may
not correlate well with postnatal studies. The most common findings associated with fetal
ventriculomegaly detected by ultrasonography are hydrocephalus, cortical malformations,
or evidence of cerebral destruction due to infarction or hemorrhage. These are typically
associated with cerebral palsy.

Neuroimaging of the preterm infant at risk for cerebral palsy

Routine screening cranial ultrasound is recommended between days 7 and 14 of life for
infants born <30 weeks gestation; 65%–90% of intraventricular hemorrhage (IVH) occurs
by the 7th day of life. Infants of 30–33 weeks gestation remain at risk for IVH, but at a
substantially lower rate than children born earlier (Harris et al. 2007). Severe degrees of IVH
(Fig. 3.3.1) are more reliably ascertained on ultrasound than mild IVH or white-matter
lesions. Subtle abnormalities may be missed (Hintz et al. 2007).

Fig. 3.3.1
Ultrasound of a
child born at
24 weeks
gestation; now
3 weeks of age
(27 weeks). Head
ultrasound shows
parenchymal
injury (arrows)
consistent with
grade IV IVH.

223
 Identification of IVH is clinically important for assessing comorbidities and extent
of injury (Hintz et al. 2005). Infants with documented IVH need serial ultrasonography
because lesions may enlarge or new hemorrhage may occur. A repeat scan at conceptual
age of 36–40 weeks may allow identification of infants with low-pressure ventriculomegaly
(associated with white-matter injury) or lesions that increase risk for cerebral palsy but were
not identifiable on early scans. Cystic lesions or ventriculomegaly may be found in infants
near term with previously normal cranial ultrasounds (Goetz et al. 1995, Ito et al. 1997,
Hayakawa et al. 1999).
Although most preterm infants with subsequent cerebral palsy have white-matter lesions
on imaging, it is important to note that the majority of children with such abnormalities do
not develop cerebral palsy. Of 344 children with ultrasounds documenting white-matter
injury, only 24.4% were subsequently diagnosed with cerebral palsy. Of 76 with cystic
periventricular leukomalacia, 57% had cerebral palsy. Of 164 children in the cohort
diagnosed with cerebral palsy by the age of 2 years, over 30% had normal ultrasounds in
the neonatal period (Ancel et al. 2006). Normal early and late cranial ultrasounds were
found in 1473 infants with birthweights <1000 g and mean gestational ages of 26 weeks.
Cerebral palsy occurred in 9.4% of the infants, and a Bayley Mental Development Index of
<70 was found in 25.3% (Laptook et al. 2005).
The use of CT in those born preterm is limited. It may be used to verify findings
identified on ultrasound, evaluate extent of hemorrhage, or assess position of intraventricular
shunts or drains (Fig. 3.3.2).

Fig. 3.3.2
CT demonstrating severe
hydrocephalus due to
meningitis in a child born
at 34 weeks gestation.
The child died. Arrows
indicate fluid filled spaces
replacing destroyed brain.

224
 MRI best evaluates white-matter damage, hypoxic–ischemic encephalopathy, or other
cerebral injury in the preterm infant. As in all other ages, MRI best delineates cerebral
dysgenesis and other malformative processes. Atlases of the fetal and preterm infant brain
are available and delineate the ontogenesis of development (Barkovitch 1990, Levine 2005).
In early survivors of preterm birth with white-matter injury, MRI yields much more detailed
information than screening ultrasounds. Abnormal signal change in the posterior limb of
the internal capsule is a marker for significant risk of hemiplegia after grade III or IV IVH.
In one study of preterm infants with such signal change on early MRI, all had hemiplegia
by 12–24 months of age (De Vries et al. 1999). If the posterior limb of the internal capsule
signal was symmetrical bilaterally, all had normal neuromotor outcome. If no abnormal
signal is identified near the corona radiata white-matter tract on early MRI, essentially all
infants will have a normal motor outcome. Similar findings occur in infants with
periventricular leukomalacia. Lesions in the corona radiata above the posterior limb of the
internal capsule are highly predictive of adverse motor outcome (Nanba et al. 2007). Early
MRI assessment for white-matter injury correlates well with studies done at 18 months of
age; this suggests that a second MRI may not be of much value in infants who had an early
study (Sie et al. 2005). Moderate to severe white-matter injury on MRI in 167 preterm
infants born at <30 weeks gestational age strongly correlated with a subsequent diagnosis
of cerebral palsy (Woodward et al. 2006). Figures 3.3.3–6 demonstrate such injuries.

Fig. 3.3.3 MRI of a child with

diplegia demonstrates the late
sequelae of periventricular
leukomalacia. Fluid in
ventricles appears white.
Ventricles are enlarged due to
white-matter loss. Gray areas
projecting into ventricles
represent normal basal ganglia
structure.

225
Moderate or severe injury was found in 21% of patients but nearly half of them did not have
neurodevelopmental impairments when examined at 2 years of age.
Although strongly associated, abnormal imaging studies do not necessarily predict
cerebral palsy. The degree and distribution of abnormalities must be must be considered
(Dyet et al. 2006). A cohort of adolescents 15 years of age who had been very low-
birthweight infants and survived without obvious neurologic impairment underwent MRI.
Mild white-matter abnormalities were found in 13/56, yet there was no difference in the
neurological examination between those with MRI changes and those without (Gaddlin et
al. 2008).
Injury to the cerebellum in very preterm infants is now recognized as a cause of cerebral
palsy, as well as ataxia or dystonia. It may be identified in up to a third of these infants. It
is readily seen on MRI and images should be examined for this finding (Bodensteiner and
Johnsen 2005, 2006, Limperopoulos et al. 2005, Kułak et al. 2007).

Fig. 3.3.4
MRI of a child
with quadriplegia
due to severe
periventricular
leukomalacia.
Ventricles are
enlarged. Arrows
show areas of
gliosis/scarring.

226
 Fig. 3.3.5 MRI of a child
with quadriplegia and
greater involvement of
legs demonstrates
moderately severe
periventricular
leukomalacia and thinning
of the corpus callosum as
indicated by arrow.

Fig. 3.3.6 MRI of a child with severe

quadriplegia who experienced severe
prenatal ischemia at 30 weeks
gestation. Most of the brain has been
destroyed and replaced with fluid-
filled cysts (white areas).

227
Neuroimaging of the term newborn infant at risk for cerebral palsy
CT best identifies intraparenchymal, subdural, subarachnoid and intraventricular blood. It
is indicated when an encephalopathic infant has a history of birth trauma, coagulopathy, or
low hematocrit, as did the infant in Figure 3.3.7 – suggesting intracranial hemorrhage (Ment
et al. 2002). If an infant is too unstable to undergo MRI, CT may be useful.
MRI is the study of choice for term newborn infants with encephalopathy, seizures, or
features suggestive of cerebral malformation. Moderate to severe hypoxic–ischemic injury
in the term infant (sustained either acutely or subacutely) is associated with the development
of cerebral palsy. Early identification of those infants severely affected allows more accurate
outcome predictions. Acute processes affecting blood flow or perfusion require diffusion-
weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps for optimal
evaluation. Cytotoxic and vasogenic edema in areas most vulnerable to hypoxic injury cause
signal change due to restricted diffusion of water (Zimmerman and Bilaniuk 2006). When
hypoxic–ischemic injury is suspected, DWI should be performed between 48 and 120 hours
of life. Images are likely to be most definitive at 72 hours post-injury, corresponding to the
maximal edema and clinical encephalopathy. Newborn infants with significant asphyxia
may have normal or near normal MRI/DWI in the first 24 hours post-injury, only to
have significant signal change emerge after 48 hours. We have found the studies more
reliable in the 48 hour–5 day window. Timing of scanning is crucial in obtaining accurate

Fig. 3.3.7 CT from the

first day after birth in a
term infant demonstrates
a large chronic
hemorrhage that
occurred in utero
(see arrows).

228
information to aid in clinical decision-making and outcome predictions. If magnetic
resonance spectroscopy is available in the same time frame, it may give additional
information regarding extent of injury (Ment et al. 2002).
Certain MRI findings are associated with the most common patterns of asphyxia
seen in the newborn (Zimmerman and Bilaniuk 2006, Okereafor et al. 2008). Findings
reflect our knowledge of the pathophysiology of hypoxic brain injury in the full-term
newborn infant. Profound acute asphyxia typically due to a catastrophic event just before
delivery (uterine rupture, placenta abruptio) causes lesions in the putamen, ventrolateral
thalamic nuclei, cortex and white matter along the central sulcus and the internal capsule
(particularly the posterior limb). Findings on DWI imaging (such as in Fig. 3.3.8), although
subtle in appearance, correlate strongly with this type of injury. A very young infant
who suffers severe acute asphyxia from another cause (such as life-threatening apnea)
may demonstrate a pattern of injury identical to the newborn infant. Infants with this
constellation of imaging findings have a significant risk of death or disability (Fig. 3.3.9).
Partial prolonged asphyxia (often occurring in utero, but also identifi
ed in the perinatal and
postnatal periods) is associated with bilateral watershed infarctions both anteriorly
and posteriorly as in Figure 3.3.10. Although the insult is global, the infarctions may be
asymmetric. Severe partial prolonged asphyxia causes signal changes that are bihemi-
spheric, large, and involve both gray and white matter. Diffusion imaging is most sensitive

Fig. 3.3.8 MRI

demonstrates late
sequelae of severe acute
hypoxic–ischemic
encephalopathy. Faint
signal changes (arrows)
in the basal ganglia are
the main abnormality.
The child has severe
spastic quadriplegia and
microcephaly.

229
Fig. 3.3.9
MRI demonstrates late
sequelae of severe acute
hypoxic–ischemic
encephalopathy.
Faint signal changes
(arrows) in the basal
ganglia are the main
abnormality; he also
has microcephaly.
The child has severe
spastic quadriplegia.

Fig. 3.3.10
Diffusion MRI
demonstrates
moderate to severe
partial prolonged
hypoxic–ischemic
encephalopathy in a
term infant. White
areas indicated by
arrows show a
watershed pattern
of injury.

230
early on; imaging after resolution of acute injury reveals varying degrees of cortical
necrosis, cystic encephalomalacia, or cerebral atrophy. These MRI findings are very highly
correlated with significant cerebral palsy. If partial prolonged asphyxia is then combined
with additional profound acute asphyxial injury, the imaging finding will show a com-
bination of the deep gray matter and internal capsule lesions and extensive watershed
infarctions. Cystic encephalomalacia, persistent deep gray-matter signal changes, and
profound cerebral atrophy are sequelae found on follow-up MRI (Fig. 3.3.11). Outcomes
associated with these findings include death or quadriparetic and dystonic cerebral palsy.
Other infants with less severe hypoxic–ischemic injury demonstrate moderate white-
matter injury and diplegic cerebral palsy patterns predominate. Isolated thalamic injury and
mild white-matter changes or normal patterns are not typically associated with cerebral
palsy outcomes. The role of early MRI changes in those infants who have undergone
hypothermic treatment for acute hypoxic–ischemic encephalopathy awaits further research
for accurate outcome prediction.
Perinatal arterial ischemic stroke may occur in as many as 1:4000 term infants (Kirton
and deVeber 2006). This was the single largest etiology (22%) in a series of 273 children
born at term with a subsequent diagnosis of cerebral palsy (Wu et al. 2006a). Typically, no
motor asymmetry is detected in the newborn infant but focal clonic seizures may occur. In
the absence of a specifi c clinical presentation, diagnosis is dependent on neuroimaging.
Cerebral infarction is easily identified by DWI within 24 hours or less of injury. The
restricted diffusion is in an arterial distribution (Krishnamoorthy et al. 2000, Kuker et al.

Fig. 3.3.11 MRI

demonstrates late sequelae
of severe acute and
prolonged hypoxic–ischemic
injury. Cortical atrophy is
present (arrows).

231
2004). Figures 3.3.12–14 demonstrate the exquisite sensitivity of DWI and MR angiography
techniques.
Approximately one-third of children with arterial stroke diagnosed in the newborn
period will have cerebral palsy emerge later. Those with a later diagnosis have cerebral
palsy 80% of the time. Most of these children have hemiplegia (Lee et al. 2005). In one study
of 76 children with perinatal stroke, 68% developed cerebral palsy with 87% of those
individuals manifesting a hemiplegic pattern (Golomb et al. 2008). Occlusion of the middle
cerebral artery is the most common etiology, occurring two-thirds of the time on the left.
Multiple infarctions can lead to triplegic or quadriplegic cerebral palsy. Cerebral venous
infarctions, often associated with dural sinus venous thromboses, may be the cause of up
to 30% of perinatal infarction. If located in a watershed distribution they may lead to diplegic
cerebral palsy (Kirton and deVeber 2006). DWI is the best method to image ischemic white-
matter change. Magnetic resonance venography (MRV) helps identify underlying venous
sinus thrombosis.
If arteriovenous malformation, venous angioma, or tumor is suspected, additional
studies with magnetic resonance angiography (MRA) or venography are indicated.
Cerebral dysgenesis is best identified by MRI. Severe malformative lesions such
as lissencephaly, a form of severely abnormal cortical development (Fig. 3.3.15), or
holoprosencephaly, the failure of the forebrain to divide (Fig. 3.3.16), occur in the fi rst
trimester of pregnancy. These are now frequently identified in the prenatal or newborn

Fig. 3.3.12
MRI demonstrates acute
infarction, focal edema,
and gray-matter changes
in the distribution of the
right middle cerebral
artery in a term infant
15 hours after birth.
Arrows indicate
blurring of gray- and
white-matter junction.

232
 Fig. 3.3.13 Diffusion
MRI of a term infant
15 hours after birth
demonstrating acute
infarction in the
distribution of the
middle cerebral artery.
The infarcted area
appears white in the
illustration.

Fig. 3.3.14
MR angiogram of
a term infant
15 hours after birth
demonstrating
complete occlusion
of the right middle
cerebral artery as
indicated by arrow.

233
Fig. 3.3.15
MRI demonstrates
lissencephaly in a child
with quadriplegia. Note
absence of gyri and
resultant smooth
cortex.

Fig. 3.3.16
MRI demonstrates
holoprosencephaly in a
child with quadriplegia.
Black area denotes
fluid-filled cyst behind
fused cortical remnant.

234
periods. Severe spastic quadriparesis is the outcome. More subtle malformations may be
identified in infants with moderate encephalopathy without identifi able perinatal cause,
those with multiple congenital anomalies, or those with seizures (Fig. 3.3.17). Along with
infarction, cerebral malformations constitute a significant etiology for cerebral palsy in the
term infant (Wu et al. 2006a, b).
Cerebral infection, particularly toxoplasmosis, rubella, cytomegalovirus, herpes
simplex, syphilis, human immunodeficiency virus (HIV), varicella-zoster, and lymphocytic
choriomeningitic viruses may account for 5%–10% of cases of cerebral palsy (Stanley et
al. 2000). MRI is most useful to detect meningeal enhancement, cerebritis, abcess formation,
focal ischemia and hemorrhage. Contrast enhancement after administration of gadolinium
may provide increased sensitivity to cerebral and meningeal inflammation. CT is indicated
to identify intracerebral calcifications; Figures 3.3.18 and 19 show classic imaging findings
in a child affected by congenital cytomegalovirus.

Fig. 3.3.17 MRI demonstrates fused diencephalon (arrow) in a child with

quadriplegia. There is large a fluid-filled cyst in temporal area.

235
Fig. 3.3.18 CT of a
child with congenital
cytomegalovirus
infection demonstrating
periventricular
calcifications
(see arrows).

Fig. 3.3.19 MRI of a

child with congenital
cytomegalovirus infection
demonstrating neuronal
migration disorder. The
arrows point to a dysplastic
cortex.

236
Neuroimaging in the child diagnosed with cerebral palsy
Although cerebral palsy is a clinical diagnosis the location and type of structural brain injury
correlates with cerebral palsy of differing types. CT scanning has demonstrated usefulness
in identifying causation of cerebral palsy. Pooled studies of CT in 782 children with cerebral
palsy showed abnormalities on 77% of scans (Ashwal et al. 2004). When just Class I studies
were evaluated, 88% of children had abnormalities. The yield of abnormal studies varied
with type of cerebral palsy: 89% in hemiplegic cerebral palsy and 36% in dyskinetic cerebral
palsy. Despite these data, CT should not be a routine part of the evaluation of the child
newly diagnosed with cerebral palsy.
MRI eclipses all other modalities in sensitivity and specificity for identifying associated
conditions. Unless imaging results from the neonatal period are available for review and
reveal clear structural changes consistent with the child’s clinical condition, MRI is
recommended for a child with the clinical signs of cerebral palsy. Lesions acquired in the
prenatal or neonatal period may be clinically silent until later in the infancy or early
childhood when motor impairment and spasticity emerge.
Data from 10 studies with a total of 644 children with cerebral palsy who underwent
MRI scanning showed imaging abnormalities in 89% (range 68%–100%) (Ashwal et al.
2004). Injuries to white matter, basal ganglia, thalami or cerebellum were readily detected
on MRI. Lesions were identified in 98% of children with quadriplegia, 96% with hemiplegia,
and 70% with dyskinetic cerebral palsy. MRI is useful in determining when brain injury
occurs. In studies of 345 children with various types of cerebral palsy, prenatal onset
occurred in 37%, perinatal in 35%, and postnatal in 4%.
MRI gives neuroanatomic correlation with clinical types of cerebral palsy. Systematic
review of studies utilizing MRI to evaluate 388 children with cerebral palsy found abnormal
scans in 334 (86%) (Krägeloh-Mann and Horber 2007). Findings were related to the pattern
of cerebral palsy in 83% of individuals. Periventricular white-matter lesions were the
most common abnormalities found overall (56%). White-matter lesions were found in
90% of the preterm infants with cerebral palsy but only 20% of full-term infants with
cerebral palsy showed similar pathology. As anticipated, spastic diplegic cerebral palsy
occurred in 84% of the preterm infants. Gray-matter lesions (cortical or deep gray) were
found in 18% (69/388) of infants. These affected term infants far more than pre-
term infants (33% versus 3.5%), reflecting the pathophysiology of hypoxic–ischemic
encephalopathy and white-matter injury in infants of different stages of maturation. Severe
forms of quadriplegia and athetoid cerebral palsy were most common in children with
gray-matter lesions. Again, this correlates with our understanding of the particular
vulnerability of the deep gray-matter structures to hypoxic injury. Children with gray-
matter lesions and unilateral MRI findings typically had hemiplegia most commonly
associated with cerebral infarction; focal brain malformations were also frequently
identified.
Identification of abnormalities on MRI is also related to preterm, term, or postnatally
acquired injury (Figs 3.3.20, 21). Of 620 children with cerebral palsy, MRI showed
abnormalities in 99% of preterm infants, 92% of term infants, and 79% of infants over
1 month of age (Ashwal et al. 2004).

237
Fig. 3.3.20
MRI demonstrating acute
edema in a 4-month-old
child who sustained non-
accidental trauma. The
arrows point to areas of
cortical edema.

Fig. 3.3.21
MRI demonstrating late
outcome of severe
encephalomalacia and
subdural hematomas (white
areas). This MRI, taken 3
weeks later, is of the same
child portrayed in Figure
3.3.20. Arrows point to areas
of severe cortical injury,
which will eventually be
replaced by cysts.

238
 If children with brain malformations suffer motor symptoms that are consistent with the
definition of cerebral palsy, they are now considered to have the disorder (Rosenbaum
2006). Data from scans of 1426 children with cerebral palsy identified major brain
malformation on 12% of MRIs. Malformations of cortical development in the first tri-
mester are typically most severe. If the lesion is unilateral (as a schizencephalic cleft or
porencephalic cyst may be), hemiplegia is the usual result (Figs 3.3.22, 23).
MRI abnormalities thought to correlate with causation of cerebral palsy are very high
in children with spastic types. In one study they were found in 123/129 (95%) children,
including 45/45 with quadriplegia, 37/40 with diplegia, and 42/45 with hemiplegia (Kułak
et al. 2007). However, depending on patient selection criteria and methodology, up to 15%
of MRI studies are considered normal. Athetotic or dyskinetic cerebral palsy has a much
lower incidence of MRI abnormality than the spastic subtypes; at least 30% of scans are
unrevealing. A normal MRI of the brain does not preclude a diagnosis of cerebral palsy
(Ashwal et al. 2004). In such children, careful re-evaluation of historical information and
clinical monitoring over time for signs of slow neurologic deterioration are warranted.
Imaging of the spinal cord should be considered in any child who has apparently normal
bulbar function and intellect, yet has significant spastic quadriparesis.
Neuroimaging may need to be repeated in the child with cerebral palsy. New onset
seizures with an abnormal EEG may be an indication for re-imaging. Alteration in a child’s
clinical history or examination suggestive of progressive symptoms, or new-onset
neurological signs/symptoms superimposed on pre-existing cerebral palsy are indications
for re-imaging, as well as diagnostic re-evaluation.

Fig. 3.3.22
MRI demonstrating a
unilateral schizencephalic
cleft in a child with
hemiplegia.

239
Fig. 3.3.23 MRI demonstrating
neuronal migration disorder in a
child with hemiplegia. The
arrows point to thickened cortex.

TABLE 3.3.1
Grades of intraventricular hemorrhage (from Papile et al. 1978, Dammann and Leviton 1997)

Grade I: Hemorrhage in the subependymal germinal matrix

Grade II: Hemorrhage into the ventricle, does not distend it
Grade III: Hemorrhage into ventricle with associated ventricular enlargement
Grade IV: Hemorrhage in the parenchyma; may not be expansion of IVH, but may be parenchymal
hemorrhage due to venous infarction.

TABLE 3.3.2
MRI findings associated with certain patterns of cerebral palsy

Diplegia:
Periventricular leukomalacia
Hemiplegia:
Unilateral cortical encephalomalacia (cerebral infarction, trauma)
Cystic encephalomalacia (intraparenchymal hemorrhage or venous infarction)
Focal cerebral dysgenesis
Unilateral schizencephaly
Focal polymicrogyria/pachymicrogyria
Quadriplegia:
Bilateral encephalomalacia (hypoxia–ischemia, bilateral trauma)
Cerebral dysgenesis (lissencephaly, bilateral schizencephaly)
Athetoid:
Abnormal signal change in basal ganglia, thalamus (hypoxia–ischemia in term infant, cerebellar infarction)

240
 TABLE 3.3.3
Etiologies of cerebral palsy identified on MRI

Preterm brain injury

Periventricular leukomalacia
Ventriculomegaly (due to white-matter loss)
Cystic lesions in white matter
Hypoxic–ischemic injury
Basal ganglia and thalamic injury
Encephalomalacia
White-matter loss
Cortical atrophy (elegyria)
Cerebral atrophy
Cerebral infarction
Prenatal: porencephalic cysts
Perinatal: focal cortical encephalomalacia
Malformations
Lissencephaly
Schizencephaly
Polymicrogyria/pachygyria
Holoprosencephaly
Cerebellar hypoplasia/malformation
Residuals of congenital infection
Porencephalic cyst
Schizencephaly
Cystic encephalomalacia (focal/bilateral)
Intracranial calcifications (best seen on CT)

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