NEUROIMAGING IN CEREBRAL PALSY

JENNIFER ACCARDO, MD, HEATHER KAMMANN, BA, LLB, AND ALEXANDER H. HOON JR, MD
Parents and clinicians concerned about high-risk infants and children with motor delay or cerebral palsy seek information on
cause, treatment, prognosis, and recurrence risk. Used in combination with history and examination, neuroimaging studies can
improve diagnosis and management. In premature infants, cranial ultrasound is a reliable, noninvasive diagnostic modality.
Nuclear magnetic resonance techniques including magnetic resonance imaging and diffusion weighted imaging can be used
effectively in neonatal encephalopathies. In children with motor delay and cerebral palsy syndromes including spastic diplegia,
quadriplegia, hemiplegia, and extrapyramidal movement disorders, conventional magnetic resonance imaging has become an
important determinant of diagnosis and management. The aim of this article is to help clinicians select and interpret imaging
studies of benet in clinical care. (J Pediatr 2004;145:S19-S27)
D
espite a wide range of accepted medical and rehabilitative interventions for high-risk infants and children with cerebral
palsy, there is often imprecise understanding of cause, variability in determination of treatment, and inconsistency in
outcome.
1-4
Over the period of the past decade, magnetic resonance imaging (MRI) and other neuroimaging modalities
have begun to provide a foundation to address these problems, translating into real
5
and anticipated
6
benets in care.
Considering that pneumoencephalography (injected air with x-ray visualization) was the state-of-the-art method to image
the brain only 50 years ago,
7
current techniques are remarkable.
8,9
Clinicians have a powerful array of tools to assess brain structure
and function: ultrasound, computed tomography (CT), and multiple nuclear magnetic resonance techniques including MRI,
magnetic resonance spectroscopy (MRS), diffusion weighted imaging (DWI), diffusion tensor imaging (DTI), and functional
MRI (fMRI).
10
Structural neuroimaging studies clearly demonstrate disorder-specic ndings in children with a wide range of
developmental impairments prenatally
11
and postnatally,
12
and functional modalities are being used to map regional cognitive
processing
13,14
and to examine cortical plasticity.
15
Seventy to ninety percent of children with cerebral palsy have abnormalities on brain MRI.
16,17
When combined with
history and neurological examination, imaging can provide insights into cause and pathogenesis, including patterns of selective
vulnerability specic to acquired or genetic disorders; improve treatment options; rene prognosis; and address recurrence
risks.
18,19
This article reviews specic imaging techniques, developmental brain vulnerability, and the utility of imaging in high-
risk infants and children with cerebral palsy.
IMAGING TECHNIQUES
Selection of the appropriate neuroimaging modality is optimally determined with an
understanding of principles, indications, limitations, and side effects of each technique
(Table I). Currently, the most commonly used clinical modalities are ultrasound and MRI,
with CT of benet in specic situations. DWI, MRS, DTI, and fMRI are emerging
nuclear magnetic techniques used in clinical care and research. Positron emission
tomography and single photon emission computed tomography are radionuclide studies
used in management of epilepsy and brain tumors.
20
Cranial Ultrasound
Ultrasound uses high-frequency sound waves to produce images with good clarity.
Both the anterior and posterior fontanel can be used as acoustic windows. Cranial
From the Johns Hopkins University
School of Medicine, and the Kennedy
Krieger Institute.
Division of Neurology and Develop-
mental Medicine, Baltimore,
Maryland.
Submitted for publication Mar 2, 2004;
accepted May 11, 2004.
Reprint requests: Alexander H. Hoon,
MD, Kennedy Krieger Institute, Johns
Hopkins University School of Medi-
cine, 707 N Broadway, Baltimore, MD
21205. E-mail: hoon@kennedykrieger.
org.
0022-3476/$ - see front matter
Copyright 2004 Elsevier Inc. All rights
reserved.
10.1016/j.jpeds.2004.05.018
ADC Apparent diffusion coefficient
CT Computed tomography
DTI Diffusion tensor imaging
DWI Diffusion-weighted imaging
FLAIR Fluid attenuation inversion recovery
fMRI Functional magnetic resonance imaging
HIE Hypoxic-ischemic encephalopathy
IVH Intraventricular hemorrhage
MRI Magnetic resonance imaging
MRS Magnetic resonance spectroscopy
PHI Periventricular hemorrhagic infarction
PVL Periventricular leukomalacia
S19
ultrasonography can be serially performed with minimal
perturbation of the neonate, making it the study of choice in
high-risk preterm infants.
21
Although ultrasound is not as
sensitive to subtle white matter changes and hemorrhagic
lesions as MRI, it readily identies periventricular white
matter lesions associated with later neurologic morbidity as
well as hemorrhage or malformation in the posterior fossa.
22
Recently, prenatal cerebral sonography has been used to
identify fetal white matter injury in women with
uteroplacental insufciency.
23
Computed Tomography
The x-ray acquired images of CT depend on tissue
atomic number and electron density, with the images produced
by a map of the local x-ray absorption coefcient.
24
By using
computer-applied algorithms, new scanners produce high-
resolution images in a matter of minutes. CT scans can there-
fore often be obtained without sedation. Calcication, which
may not be visualized on MRI, is readily seen on CT. CTscans
are less costly than MRI and often can be obtained after a
shorter waiting period. However, x-ray exposure may be of con-
cern to parents and clinicians, especially with repeated studies.
Magnetic Resonance Imaging
Magnetic resonance imaging has become the most
widely used imaging modality in clinical pediatrics. It uses
nuclear magnetic resonance, the intrinsic magnetic properties
of protons, to produce gray-scale images in multiple
planes.
25,26
The signal generated and the resulting images
are based on proton density in tissues, and T1 and T2
relaxation times, which describe recovery and delay of nuclear
magnetism after perturbations with an oscillating radio-
frequency magnetic eld. Gadolinium, an inert contrast
material, may be infused intravenously to identify vascular
structures and regions of breakdown in the bloodbrain
barrier.
Images are produced on the basis of T1 and T2
relaxation characteristics. T1 weighting refers to longitudinal
relaxation time. Mature white matter, which has a short T1, is
bright on T1 weighted sequences. Gray matter appears gray
and cerebrospinal uid dark. T1 images, which are commonly
viewed in sagittal and axial planes, are useful for the
determination of normal anatomy as well as structural abnor-
malities. T2 weighting refers to transverse relaxation time.
Cerebrospinal uid is bright on T2 weighted images, and
Table I. Neuroimaging modalities
Modality Sedation Advantages Disadvantages
US Not necessary Non-invasive Operator-dependent
No radiation Acoustic window needed
Portable bedside assessment
US Doppler Not necessary Same as above As above
Quantitative cerebral ow
parameters (velocity, resistive index)
Assessment of major vessels only
CT May be required Fast scanning Radiation exposure
Readily available Iodinated contrast may be needed
MR imaging Frequently required High imaging resolution Relatively long imaging time
No exposure to radiation Motion sensitive
Contrast agent very safe Environment (noise, monitoring)
MR compatible monitoring devices
MRS Frequently required No exposure to radiation See MR imaging above
Biochemical, metabolite information Need for age-matched normal controls
May be done in addition to routine MRI
MR-DWI Frequently required MR sequence evaluating water diffusion See MR imaging above
Aids diagnosis in ischemic setting
fMRI Not used, can affect results No exposure to radiation Only preliminary data available
Task performance cooperation required
PET Not routinely used Functional metabolic imaging Not readily available
High sensitivity Radiation exposure
Low spatial resolution
Arterial sampling for quantication
Control data not available
SPECT Not routinely used Functional metabolic imaging Lower sensitivity compared with PET
Relatively high sensitivity Radiation exposure
Low spatial resolution
Control data may not be available
Data taken from reference 9.
S20 Accardo, Kammann, and Hoon The Journal of Pediatrics

August 2004
mature white matter dark. T2 weighted images, including fast
spin echo and uid attenuation inversion recovery (FLAIR)
images, are useful in visualizing brain pathology, which
frequently appears bright.
Magnetic resonance imaging has several advantages over
CT, including better tissue contrast resolution, image
generation in multiple planes, and lack of ionizing radiation
and bone artifact. However, MRI costs more than CT and
more frequently requires sedation or previous behavioral
modication of young children. Furthermore, with the recent
trend toward anesthesia coverage when sedation is required, it
may be more difcult to schedule in a timely fashion.
SEDATION
Sedation should be considered carefully when required
for any study.
27
Adequate sedation is critical to obtaining
studies not degraded by motion artifact. Chloral hydrate is
usually used for infants and young children, intravenous
Nembutal for older children, and general anesthesia for
children who cannot remain still on their own or who fail to
respond to other forms of sedation. Experienced personnel
with knowledge of good airway management, 1:1 patient
assignment, continuous monitoring, and sufcient periods for
observation after the study is completed are required to provide
sedation safely. Children with developmental disorders may
have atypical reactions to sedation, which should be explained
to parents before the children are sedated, and may require
longer periods of observation once the study is completed.
IMAGE INTERPRETATION
Image interpretation requires knowledge of normal
brain anatomy and development,
28
recognition of ndings in
specic disorders
29
(Table II), and an awareness of potential
study artifacts. Although clinicians can readily interpret
imaging studies, neuroradiologists are more familiar with
imaging techniques
30,31
and potential artifacts including
chemical shift, motion, susceptibility, and truncation,
32
and should determine study sequences and be the gold
standard for image interpretation. For example, an aware-
ness of artifacts sharpens image interpretation, as seen in
Figure 1.
Dialogue with a neuroradiologist is helpful, with
discussion of history and examination focusing interpretation.
For example, white matter abnormalities in the context of
prematurity are most likely periventricular leukomalacia
(PVL), but without that history might be interpreted as
adrenoleukodystrophy or metachromatic leukodystrophy.
Neurological ndings of extrapyramidal cerebral palsy should
prompt a careful assessment of the basal ganglia and thalamus
for abnormal signal intensity or atrophy.
Imaging studies, like clinical evaluations, represent only
a single point in time and should be interpreted with this in
mind. Serial studies, analogous to repeated neurological
examinations, can provide new diagnostic insights, especially
in progressive neurological disorders,
33,34
as well as in ongoing
medical or surgical management in situations including
ventriculomegaly and hydrocephalus.
Table II. Conventional MRI ndings in selected childhood motor impairment syndromes
Disorder Primary ndings Other abnormalities
Angelman syndrome Normal
Ataxia-telangiectasia Cerebellar atrophy
Carbon monoxide Globus pallidus
Dopa responsive dystonia Normal
Glutaric aciduria, type 1 Caudate, putamen
GM1 Type 3 Putamen
Hypoxic-ischemic Putamen, thalamus, Cortical white matter, encephalomalacia
encephalopathy peri-rolandic
Juvenile Huntington Caudate, putamen
Kernicterus Globus pallidus
Leighs disease Caudate, putamen,
brainstem, white matter
Methylmalonic academia Globus pallidus Internal capsule
Mitochondrial encephalo-myopathies Caudate, putamen Cortical white matter
Pantothenate kinase-associated
neurodegeneration Globus pallidus
Proprionic academia Globus pallidus, 1/ putamen
Periventricular leukomalacia Cortical white matter Thalamus
Pyruvate dehydrogenase deciency Globus pallidus Caudate, putamen
Rett syndrome Normal
Wilsons disease Putamen, pons, atrophy Midbrain, thalamus, caudate
Data taken from reference 9.
Neuroimaging in Cerebral Palsy S21
Brain Development and Vulnerability
The elegant and genetically determined choreography of
brain development leads to precise temporal and spatial
structural organization.
35,36
Neural tube closure at one month
of gestational age is followed by forebrain cleavage. During
the second to fth months of gestation, there are bursts of
neuronal proliferation, followed by waves of cortical neuronal
migration, leading to the normal six-layered cortex. This is
followed by proliferative organizational events including
elaboration of synapses and myelination
37
as well as elimina-
tion of cells
38
(apoptotic cell death) and synapses
39
(synaptic
pruning), leading to motor, cognitive, and behavioral
capabilities characteristic of children.
Selective vulnerability refers to the susceptibility of
specic cell types and brain regions to injury during times of
active development.
29
Early insults or genetic abnormalities
affecting fetal brain development often affect the brain
globally and result in midline abnormalities including
holoprosencephaly
40
and agenesis of the corpus callosum,
microcephaly,
41
and migrational abnormalities including
heterotopias and lissencephaly.
42
During the late second to early third trimester, the
primary vulnerability is in the cortical and subcortical white
matter, where developing oligodendroglia are susceptible to
injury.
43,44
Recognized antecedents include hypoxia-ischemia,
infection, and maternal metabolic abnormalities involving
thyroid function and glucose homeostasis.
45
Under the general
heading of white matter damage, the spectrum of terminology
for lesions seen on ultrasound and sustained during this period
of development includes periventricular hemorrhagic infarction
(PHI), PVL, periventricular echodensities and echolucencies, and
hyperechoic or hypoechoic lesions. The MRI correlates are PVLor
PHI.
46-48
As the fetus approaches term, primary vulnerability to
hypoxia-ischemia shifts from white matter to neurons in the
cerebral cortex, basal ganglia, and thalamus, related to
disruption of glutamate synapses, excitotoxic injury, and cell
death from necrosis and apoptosis.
49
Characteristic patterns of
selective vulnerability seen on MRI include hyperintense signal
in the putamen and ventrolateral thalamus from acute, total
asphyxial events, as seen in three children in Figure 2; parasa-
gittal cortical infarction; and multicystic encephalomalacia.
50-52
Postnatally, there is wide variability in vulnerability in
supratentorial and infratentorial structures. This is often
related to the type of genetic disorder or acquired insult.
Clinical Syndromes
Although there are several clinical situations in which
imaging is of benet, pediatricians and other clinicians
commonly consider utility in high-risk premature infants, in
neonatal encephalopathies, and in infants and young children
with motor delay or cerebral palsy. Appropriate timing and
selection will often improve the clinical utility of imaging
studies.
High-risk Premature Infants
Infants may be born prematurely in association with
anomalies in early brain development, including hydroceph-
alus, neuronal migration disorders, and absence of the corpus
callosum. However, the most common antecedent of the
motor, cognitive, and behavioral disorders seen in children
born prematurely is PVL or PHI,
53,54
as seen in Figure 3.
Ultrasound has been recommended for infants less than 30
weeks between 7 and 14 days of age and near term-corrected
age to identify intraventricular hemorrhage (IVH), PVL, and
low-pressure ventriculomegaly.
21
Twenty to twenty-ve
percent will have one or more of these lesions, with
signicantly increased risks of later major developmental
impairments.
55
Premature infants may also sustain posterior
fossa hemorrhages
22,56
and decreased cortical gray matter
volumes associated with white matter injury.
57
Reduced
cerebellar volumes in children have been associated with
decits in cognition, but not motor neurological signs.
58
The childhood motor spectrum of children with white
matter injury, primarily PVL, ranges from mild neurological
dysfunction to quadriplegic cerebral palsy. A common pre-
sentation is often spastic diplegia, with lower extremity
spasticity, truncal hypotonia, and upper extremity athetosis
or dystonia. MRI ndings include thinning of the corpus
callosum, ventricular dilatation with scalloping at the margins,
gliotic response in white matter, and white matter volume
loss.
59
MRI is of benet both to exclude other abnormalities,
some of which have genetic implications, and to assess the
extent of white matter loss and gliosis. Volumetric MRI has
shown a relationship between increasing ventricular size (as
Fig 1. Pulsation artifact (arrow) in a coronal FLAIR MRI, which
might be misinterpreted as a choroid plexus tumor in the left
ventricle.
S22 Accardo, Kammann, and Hoon The Journal of Pediatrics

August 2004
a measure of brain volume loss) and subsequent motor and
cognitive impairments.
60
Neonatal Encephalopathy
Neonatal encephalopathy describes term infants with
abnormal neurological function involving tone, reexes,
consciousness, feeding, respiration, and seizures.
61
Although it
is often assumed that the most common cause is obstetric error,
more than 100 years ago Freud
62
recognized that problems in
prenatal development might lead to perinatal distress.
Recent research has shown that there is an extensive
differential diagnosis for neonatal encephalopathy including
brain malformations, genetic or metabolic disorders, indirect
and direct infections, kernicterus, hypoxic-ischemic en-
cephalopathy (HIE), maternal thyroid disorders, severe
pre-eclampsia, thrombophilic disorders, and placental vas-
culopathy, and that the percentage varies widely in different
countries.
63
Furthermore, two distinct subgroups exist: one
with encephalopathic signs with or without seizures, and
a second with isolated seizures.
64
Infants in the latter group
have an increased likelihood of arterial strokes associated with
thrombophilic disorders. Neonatal MRI, CT, and DWI may
be of benet in diagnosis, with potential implications for
treatment, prognosis, and recurrence risk.
Hypoxic-ischemic encephalopathy is a recognized cause
of neonatal encephalopathy, as initially categorized by Sarnat
Fig 2. Axial T2 and FLAIR images from three children who developed extrapyramidal cerebral palsy after acute asphyxial insults at term
leading to neonatal encephalopathy. The ndings of hyperintense lesions in the posterior putamen and ventrolateral thalamus are characteristic
of this syndrome and are a commonly seen example of the selective vulnerability of deep gray nuclei to acute asphyxial insults.
Fig 3. This imaging sequence is from a child with triplegic cerebral palsy (involvement of both legs and one arm). A, Coronal ultrasound
showing hyperechoic lesion in right periventricular region (arrows) consistent with periventricular hemorrhagic infarction (grade 4 IVH); and
hyperechoic lesion in left ventricle (arrowhead) consistent with grade 3 IVH in a 28-week preterm infant on the third day of life. B, Clot
resolution (arrows) on the right and hyperechoic periventricular signal on the left in the same infant at 6 weeks of age. C, Coronal T2 MRI at 18
months of age showing porencephalic cyst (arrows), ventricular dilatation, and thinning of the corpus callosum. Reprinted with permission.
10
Neuroimaging in Cerebral Palsy S23
and Sarnat.
65
It is now determined by four ndings: fetal
distress, neonatal encephalopathy, subsequent development of
cerebral palsy, and absence of other cause.
66
It may result from
acute, total insults, or from partial, prolonged insults.
67
Imaging with acute, total insults often shows basal ganglia
injury in the putamen and ventrolateral thalamus associated
with developing glutaminergic circuits, whereas partial, pro-
longed insults may be associated with multicystic en-
cephalomalacia/diffuse atrophy. Watershed injury may also
be seen, especially after acute fall in blood pressure.
40
Early
identication of infants with HIE is the subject of much
interest now because of research in neuroprotective in-
terventions.
68,69
MRS and DWI have also been proposed as
methods to identify children who would benet from these
interventions.
Kernicterus, which may lead to choreoathetoid cerebral
palsy in childhood, can cause a newborn encephalopathy
similar to HIE.
70
Bilirubin is a toxin that targets the globus
pallidus,
71
rather than the putamen-thalamus, as in HIE.
This is another example of the concept of selective
vulnerability, and supports the importance of imaging to
determine lesion location. Although RhoGAM and WinRho
administration has greatly decreased Rh incompatibility as
a cause, other causes are hemolysis, neonatal meningitis, and,
rarely, breast feeding.
72,73
Cerebral Palsy
Cerebral palsy describes a group of motor impairment
syndromes secondary to genetic and acquired disorders of the
developing brain.
74
Spastic, extrapyramidal, and mixed forms
are generally recognized. Spasticity is dened by hypertonicity
that increases with increased velocity of movement. Bilateral
spastic cerebral syndromes such as spastic diplegia and spastic
quadriplegia have greater involvement of legs than arms,
whereas unilateral spastic hemiplegia may be either arm-
dominant or leg-dominant. Extrapyramidal cerebral palsy
syndromes are characterized by rigidity, elicited clinically by
passive stretch independent of velocity or dystonia, which is
often action-induced twisting or xed postures. Arm use is
typically more affected than leg function.
Although neurological ndings may be similar in
various cerebral palsy syndromes, etiological underpinnings
may be diverse. As a generality, children with spastic
syndromes often show white matter injury, whereas extrapy-
ramidal syndromes frequently have basal ganglia abnormalities
on imaging. However, in these syndromes, differential
diagnosis is often broad, including a number of recognizable
genetic and acquired disorders, as seen in Tables III and IV.
Imaging can be very important in distinguishing these
disorders, with important implications for treatment, prognosis,
and recurrence risk. For example, extrapyramidal cerebral palsy
may result from genetic metabolic disorders such as glutaric
aciduria type 1 (caudate/putamen),
75
mitochondrial disorders
such as Leigh syndrome (globus pallidus/caudate/putamen),
76
kernicterus (globus pallidus), or HIE (putamen/thalamus).
77
Likewise, although spastic diplegia is most closely linked
to PVL, it may also be secondary to congenital HIV;
dopa-responsive dystonia; hereditary spastic paraplegia; or
spinal pathology, arginase deciency, and Sjogren-Larsson
syndrome, with characteristic appearances on imaging.
However, although there is often a relationship between
the type and severity of imaging abnormalities and degree of
clinical impairment, exceptions exist, as seen in Figure 4.
Telling parents that treatment is directed toward their
Table III. Differential diagnosis of syndromes with spasticity
Spastic diplegia Spastic quadriplegia Spastic hemiplegia
Periventricular leukomalacia (PVL) PVL (severe) Prenatal stroke
Dopa responsive dystonia (DRD, Segawa disease) Brain malformations Schizencephaly
HIV TORCH Perinatal stroke
Hydrocephalus HIE
*
Grade 4 IVH
y
Arginase deciency Hydrocephalus Postnatal stroke
Sjogren-Larsson syndrome Non-accidental trauma
Other bacterial/viral
*Partial, prolonged insult
y
Periventricular-intraventricular hemorrhage.
Table IV. Differential diagnosis of extrapyramidal
movement disorders
Dystonia/Athetoid Choreic
Hypotonic/
Ataxic
Hypoxic-ischemic
encephalopathy
*
Kernicterus Genetic
disorders
Glutaric aciduria, type 1 Post-pump
syndrome
Mitochondrial
Propionic acidemia Propionic acidemia
Methylmalonic acidemia
Wilson disease
Juvenile Parkinson
Lesch-Nyhan
Juvenile Huntington
Progressive disorders (other)
*Acute, total insult.
S24 Accardo, Kammann, and Hoon The Journal of Pediatrics

August 2004
children and not the scan abnormalities can often be reassuring
to them, especially when they appreciate that brain structure is
distinctly different from normal.
IMAGING DEVELOPMENT
Advanced imaging modalities are continually being
developed and rened, including MRS, DWI, DTI, and
fMRI.
78
These techniques have the potential to show
connections between neuronal activity and brain function,
map white matter development, and facilitate early identi-
cation and treatment of high-risk infants.
Magnetic resonance spectroscopy uses software
modications to existing MRI hardware to provide an
assessment of brain biochemistry.
79
When the water signal is
suppressed, metabolites present in tissue in lower con-
centrations become detectable as spectra. Some of the
metabolites that can be detected include N-acetyl aspartate
(a neuronal marker), creatine (a bioenergetic marker), choline-
containing compounds (which may be released when cell
membranes are disrupted), lactate (associated with increased
anaerobic tissue metabolism), and neurotransmitters including
gamma aminobutyric acid. MRS can be used to identify
changes associated with HIE
80
as well as mitochondrial
disorders such as mitochondrial encephalopathy, lactic
acidosis, and stroke-like episodes.
81
Diffusion weighted imaging uses the diffusion, or slow,
random movement of water molecules (Brownian motion)
that occurs normally in the central nervous system, and is
routinely used to identify ischemic brain injury in infants,
children, and adults.
82,83
The apparent diffusion coefcient
(ADC) characterizes the movement of multiple water
molecules over a single small image region, called a voxel.
The ADC is inuenced by the type of tissue present in the
voxel (CSF, gray matter, or white matter), the myelination and
orientation of white matter tracts, and the presence of
ischemic change. In acute ischemia, the ADC is diminished,
with the region appearing bright on DWI images. DWI shows
promise for the early identication of brain injury in
infants with neonatal encephalopathy secondary to HIE,
who might potentially benet from early neuroprotective
interventions.
21
Diffusion tensor imaging is a nuclear magnetic reso-
nance modality using anisotropy, which is the variability in
water diffusion in different directions based on structural
tissue organization, to map white matter pathways.
84
Although this is primarily a research modality at this time,
85
it will nd increasing clinical applicability.
86
It has been used
to identify white matter injury in the neonatal period
87
as well
as later in childhood in children with cerebral palsy.
Preliminary data in a small number of children have suggested
that the primary mechanism of spasticity is injury in sensory
pathways connecting parietal and occipital cortex rather than
the corticospinal tracts.
88
If validated in future studies, DTI
may alter our understanding of pathogenesis in cerebral palsy
and other developmental disorders and potentially lead to
improved treatment for affected infants and children.
Functional MRI is a technique used to study brain
organization during cognitive and motor activities.
89,90
Taking advantage of the paramagnetic effect of de-
oxyhemoglobin, fMRI provides high-resolution images with-
out radiation or contrast. Blood oxygen leveldependent
imaging, a commonly used technique, produces images as
a result of changes in the local vascular deoxyhemoglobin
concentration. In children with hemiplegic cerebral palsy, the
technique has demonstrated cortical reorganization.
91
It is
anticipated that alone and in combination with other imaging
modalities, fMRI will improve the understanding of the neural
pathways in movement.
CONCLUSIONS
Clinicians may wonder whether the adage when all else
fails, examine the patient remains valid, with the wide range
of genetic testing and imaging techniques now readily
available. Although history and examination remain the
foundation of clinical care, imaging has emerged as an
Fig 4. Coronal T1 weighted MRI from a child with normal
intelligence and left hemiplegia shows moderate-severe bilateral
colpocephaly, absence of the septum pellucidum, and white matter
loss. If viewed without relevant clinical information, the prediction
from this image might be of a child with moderate-severe motor and
cognitive impairments.
Neuroimaging in Cerebral Palsy S25
important modality to further diagnosis and treatment.
Ongoing dialogue with colleagues in radiology, neuroradiol-
ogy, and anesthesia when necessary will facilitate appropriate
sedation, technique selection, and image interpretation,
leading to improved care. Whenever possible, parents should
be involved in the study and discussion of their childs imaging
and appreciate when lms are explained to them with clarity.
We acknowledge Michael Johnston, MD, for his review of
the manuscript, and Doris Lin, MD, for her comments on the
images.
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