J. Paediatr.

Child Health (2000) 36, 139–144

Magnetic resonance imaging findings in cerebral palsy

R YIN,1 DS REDDIHOUGH,2 MR DITCHFIELD3 and KJ COLLINS4
1,2,4Department of Child Development and Rehabilitation, 3Department of Medical Imaging,
Royal Children’s Hospital, Melbourne, Australia.

Objective: To review all cases of cerebral palsy (CP) that had magnetic resonance imaging (MRI) over a defined period
of time.
Methodology: The MRI brain scans of 42 children (12 premature, 30 full-term) with CP were studied. The scans were
performed at the Royal Children’s Hospital, Melbourne, between January 1995 and June 1996.
Results: Abnormalities were found in 39 of the 42 scans. Five children had cortical malformations and three children
had white matter hypoplasia, indicating insults during the second trimester of pregnancy. Twenty-one children had
hypoxic–ischaemic lesions (eight premature, 13 full-term) with patterns of periventricular leucomalacia, subcortical lesions
or cortical infarction indicating insults perinatally or in the third trimester. Only 10 children had scans that could not be
categorized into these groups.
Conclusions: In this study sample of children with CP, MRI was useful in revealing underlying brain abnormalities, most
of which were due to events in the third trimester or the perinatal period.

Key words: cerebral palsy; magnetic resonance imaging brain scan.

There have been radical changes in our understanding of the There have been a number of reports of MRI studies in
aetiology of cerebral palsy (CP) over the past decade. In 1863, patients with CP. Truwit et al. studied 40 cases and found that CP
Little reported that spastic CP was caused by abnormal circum- in 29 term infants was often the result of prenatal factors, and less
stances at birth.1 From that time it was widely accepted that commonly related to the perinatal period.7 Steinlin et al. analysed
most cases of CP were due to birth asphyxia. This assumption the MRI findings of 33 children with congenital hemiplegia and
was called into question by recent epidemiological research. their data suggested a prenatal origin in 20 to 40% of cases.8
Nelson reported that CP attributable to birth asphyxia was in Krageloh-Mann et al. studied a series of 56 cases with bilateral
the range of 3 to 13% and did not exceed 21%.2 Blair and spastic CP, and found a predominantly prenatal aetiology in term
Stanley in a matched control study estimated that in only 15 of children. Periventricular leucomalacia (PVL) was found in 53%
183 children with spastic CP (8%) was intrapartum asphyxia of term children without clinical evidence of a perinatal or neo-
the possible cause of their brain damage.3 natal aetiology and it was thus deduced to be prenatal in origin.8
In their series of term singleton births, Yudkin et al. reported Many questions remain regarding the aetiology of CP. The
that 10% of all cases of CP were associated with birth objective of this study was to review all cases of CP that had
asphyxia.4 Other studies of term infants suggested that prenatal MRI over a defined period at the Royal Children’s Hospital,
factors may be the cause of 20–25% of cases, with perinatal Melbourne, to determine the spectrum of MRI abnormalities,
and neonatal factors responsible for 21 to 34% of cases.5,6 the timing of the insults, and whether this investigation had
Despite advances both in the care of mothers and babies and furthered our knowledge of this important condition.
the development of new methods of investigation, the cause of
CP is unclassifiable or unknown in 41–58% of full-term
children.5,6 In premature infants, the contribution of perinatal METHODS
and neonatal factors is likely to be higher than in full-term
infants but the causes of prematurity are still generally elusive. A consecutive group of 42 children with the clinical diagnosis
Magnetic resonance imgaing (MRI) is a relatively new tech- of CP (24 boys and 18 girls), aged 3 months to 18 years (mean
nology which can provide information about the nature and age 5.4 years) were gathered from the MRI Register at the
timing of brain lesions. It is increasingly used in the investiga- Royal Children’s Hospital, Melbourne. Their scans had been
tion of CP but it is important to determine how much it can performed between January 1995 and June 1996. Information
assist in understanding the aetiology of this condition because concerning their birth details was obtained from the Victorian
it is still an expensive procedure and a general anaesthetic may Cerebral Palsy Register. Patients with postnatally acquired CP
be required in young children. were excluded from the study.
The MRI scans were performed on a GE Sigma 1.5 Scanner
(GE Medical Systems, Milwaukee, WI, USA). Routinely, the
scans obtained were transverse and coronal fast spin echo
Correspondence: Dr DS Reddihough, Department of Child Develop-
ment and Rehabilitation, Royal Children’s Hospital, Flemington Road,
(TR 4400, TE 102, echotrain 14), axial fast spin echo FLAIR
Parkville, Victoria 3052, Australia. Fax: (03) 9345 5871. (TR 10 000, TE 220, inversion 2200), 3D fast spoiled GRASS
R Yin, Honorary Fellow. DS Reddihough FRACP, Director. MR IR prep. FSPGR (TR 22 TE 3.2 Flip 25).
Ditchfield, FRACR, Radiologist. KJ Collins, FRACP, Neurologist. Magnetic resonance imaging scans were reviewed by one
Accepted for publication 13 September 1999. paediatric radiologist who was aware of the diagnosis of CP
140 R Yin et al.

but blinded to clinical details such as the timing of the potential seen in T2 weighted images. The three cases born between 30
insults. In each case, the images were assessed for abnormal and 33 weeks gestation had PVL only but the other five children
volume and signal within the white and cortical gray matter, had additional lesions. Three children born at 36 weeks had
the basal ganglia, thalami and cerebellum. The degree of subcortical lesions (SCL) (Fig. 2) in addition to PVL (cases
myelination and ventricular size were routinely assessed. Any 6–8). In addition to the changes of SCL and PVL, one child
other abnormalities such as cysts or migrational abnormalities with a clinical diagnosis of neurofibromatosis had MRI lesions
were documented. consistent with neurofibromatosis type I (increased signal
Periventricular leucomalacia was diagnosed when the within the left globus pallidus and within the cerebellar
periventricular white matter demonstrated increased signal peduncles bilaterally) and the other child had a large left
intensity on FLAIR or T2 weighted sequences in conjunction temporo-occipital porencephalic cyst.
with reduced white matter volume and associated lateral Four children did not demonstrate PVL or SCL. Case 9 had
ventricular enlargement (Fig. 1). hydranencephaly due to extensive infarction of the left cerebral
The 42 cases were separated into two groups according to hemisphere and infarction of a portion of the right frontal lobe,
their gestation. Group 1 was a group of children who were born with consequent porencephaly. Case 10 had bilateral temporal
prematurely at less than 37 weeks and consisted of 12 cases. arachnoid cysts with a left temporal and a left ventricular cyst.
Group 2 was a group of children who were born at term Case 11 with a clinical diagnosis of neurofibromatosis had
(37–42 weeks) and consisted of 30 cases. multiple MRI lesions typical of neurofibromatosis. The final
child in the group (case 41) had a normal MRI.

RESULTS
Group 2
Details of all cases are summarized in Table 1.
Group 2 included 30 children who were born between 37 and
42 weeks gestation. The MRI findings demonstrated three main
Group 1 patterns, hypoxic-ischaemic lesions (13), cortical migrational
malformations (five), and disorders of white matter develop-
Group 1 consisted of 12 cases who were born at less than ment (three). Seven children had miscellaneous lesions which
37 weeks gestation. Periventricular leucomalacia was found in did not fit specifically into any group and two children had
eight of 12 cases (cases 1–8). White matter hyperintensity was normal MRI scans.

Fig. 1 Periventricular leukomalacia. The periventricular white matter Fig. 2 Subcortical lesions. An axial FLAIR sequence demonstrates
is thin and shows increased signal in association with lateral ventricular increased signal within the periventricular white matter, which are
enlargement. This most markedly affects the parietal and occipital predominantly subcortical.
white matter.
Cerebral MRI in cerebral palsy 141

1. Hypoxic–ischaemic lesions (ii) Main artery infarct – four cases (15–18): A pattern of
cerebral artery infarction was demonstrated in four children
Hypoxic–ischaemic lesions were found in 13 cases. The group
(cases 15–18), of which three had hemiplegia and one had asym-
included PVL and SCL in nine cases and cerebral artery
metric quadriplegia. The middle cerebral artery was involved in
infarcts in four cases.
three cases; the posterior cerebral artery was involved in one
(i) PVL and SCL – nine cases (12, 14, 19–25): Seven chil-
case. All of these cases demonstrated T2 intensity signal (well
dren had SCL in addition to PVL (cases 19–25). Perinatal risk
seen in FLAIR sequences) which was present bilaterally as
factors included fetal distress, breech presentation, hypo-
well as an abnormal MR angiogram (MRA) in the involved
thermia, twin pregnancy and two children had evidence of birth
arteries (attenuated or hypoplastic) which supplied the infarcted
asphyxia. It is not possible to be certain of the role of these
area.
factors in the resulting lesions. One child had an uncomplicated
perinatal history. The two cases with only PVL (cases 12, 14)
2. Cortical malformations
were born at 40 and 42 weeks gestation, respectively. There
were problems immediately before birth (persistent occipito– Neuronal migration anomalies were present in five cases. Clin-
posterior position and deep transverse arrest in one case, ically, all children had spastic quadriplegia with severe intellec-
obstructed labour in the other). tual disability. Three cases had lissencephaly (cases 30–32)

Table 1 Details of 42 children, including magnetic resonance imaging findings

Birth-
Case Sex weight Gestation Age at CP type Severity MRI findings
(g) MRI

1 F 1370 30 11 y Diplegia Mild PVL

2 M 2150 33 20 m Diplegia Mild PVL
3 M 1620 33 9y Quadriplegia Severe PVL
4 M 2220 35 8y Diplegia Mild PVL, porencephalic cyst
5 M 1950 35 14 y Diplegia Moderate PVL, neurofibromatosis
6 F 1655 36 17 y Hemiplegia Mild SCL, PVL
7 F 2472 36 18 y Quadriplegia Mild SCL, PVL
8 F 2350 36 16 y Diplegia Mild SCL, PVL
9 F NA. 36 9y Hemiplegia Mild Infarction, porencephaly
10 M 3040 36 5y Quadriplegia Moderate Arachnoid cysts
11 M 3476 36 8y Diplegia Mild Neurofibromatosis
12 F 3346 42 17 m Hemiplegia Mild PVL
13 M 3049 40 5y Hemiplegia Mild Miscellaneous
14 M 4800 40 16 y Diplegia Mild PVL
15 F 2960 37 10 m Hemiplegia Mild Infarction
16 M 2890 40 1y Hemiplegia Mild Infarction
17 M NA 40 13 m Hemiplegia Mild Infarction
18 M 3744 40 33 m Quadriplegia Mild Infarction
19 M 3490 39 3y Quadriplegia Severe PVL, SCL
20 M 3065 40 5m Quadriplegia Severe PVL, SCL
21 M 2195 38 13 m Hemiplegia Mild PVL, SCL
22 M 2225 38 1y Quadriplegia NA PVL, SCL
23 F 2230 38 26 m Hemiplegia Mild PVL, SCL
24 F 2350 38 4y Quadriplegia Moderate PVL, SCL
25 F 2560 38 1y Quadriplegia NA PVL, SCL
26 M NA 40 4y Diplegia Severe Miscellaneous
27 F 3051 40 20 m Hemiplegia Mild Miscellaneous
28 M 2930 38 28 m Quadriplegia Severe Miscellaneous
29 F 2780 37 11 y Ataxia Mild Miscellaneous
30 F 3500 40 4y Quadriplegia Severe Lissencephaly
31 F 3345 40 6y Quadriplegia Severe Lissencephaly
32 F 3400 40 11 y Quadriplegia Severe Lissencephaly
33 M 3940 41 4y Quadriplegia Severe Polymicrogyria
34 M 4190 40 3m Quadriplegia Severe Polymicrogyria
35 F 2650 41 5y Quadriplegia Severe Dis. white matter dev.
36 M 3300 40 14 m Quadriplegia Severe Dis. white matter dev.
37 M 2925 41 8m Quadriplegia Mild Dis. white matter dev.
38 M 3856 41 3y Quadriplegia Mild Miscellaneous
39 F 2710 41 4y Quadriplegia Severe Miscellaneous
40 M 2900 40 3y Quadriplegia Severe Normal
41 M 2450 35 7y Ataxia Mild Normal
42 F 3660 40 3y Ataxia Mild Normal

M, male; F, female; m, month; y, year; NA, not available; PVL, periventricular leucomalacia; SCL, subcortical lesions; dis. white matter dev.,
disorder of white matter development; MRI, magnetic reonance imaging; CP, cerebral palsy.
142 R Yin et al.

(Fig. 3) and two of these children also had dysgenesis of the two cases (13,27) and diplegia in the case 26. Case 13 had
corpus callosum and abnormal signal in the white matter (cases congenital cataracts, and the MRI showed heterotopic grey
30, 31). Polymicrogyria was present in two cases (cases 33, 34). matter in the right parietal region with loss of the right sided
Both mothers had sustained trauma during the fifth month of basal ganglia and white matter suggesting previous infarction,
gestation although the role of this injury remains uncertain. as well as a right cerebellar abnormality suggesting infarction
There were no known perinatal insults clinically and no in the right posterior and inferior cerebral artery territories.
evidence of underlying tissue loss or gliosis to suggest ulegyria. There was abnormal high signal in the adjacent white matter.
Case 33, with congenital microcephaly, had a neuronal The findings were suggestive of multiple ischaemic episodes.
migration disorder associated with pachygyria or polymicro- Case 26 had severe spastic diplegia with global developmental
gyria. The white matter was grossly thinned corresponding to delay and microcephaly. The MRI showed a diffusely small
gross thinning of the body of the corpus callosum and the right cerebral hemisphere with reduced myelination. The right
ventricles were moderately dilated and irregular in shape with hippocampus was small with increased signal compatible with
minimal gliosis above the bodies of the lateral ventricles. Case mesial temporal sclerosis. Case 27 had hemiplegia and an
34 had diffuse polymicrogyria confirmed at autopsy. isolated cyst in the anterior tip of the right frontal horn of the
lateral ventricle. Cytomegalovirus infection early in pregnancy
3. Disorders of white matter development was suggested.
(ii) Lesions not involving cerebral hemisphere white matter
Disorders of white matter development were found in three
– four cases (28–39): Such lesions were present in three cases.
cases. Spastic quadriplegia with athetosis and severe intellec-
Gross cerebellar cortical and vermian atrophy was present in
tual disability with vision and speech impairment was present
case 28, small focal infarcts in the right thalamus were found in
in two of these cases (cases 35, 36). Case 35 demonstrated a
case 29, and case 38 showed symmetrical bilateral signal
decrease in the amount of myelinated white matter in the
abnormality in close association with or in both claustra. Case
centrum semiovale bilaterally and diminished arborization of
39 had marked and generalized dilatation of the third and
white matter in the subcortical regions with marked thinning of
lateral ventricles of uncertain significance.
corpus callosum. There was a history of bleeding during the
pregnancy. The MRI in case 36 was diffusely abnormal with
marked delay in myelination and vermian hypoplasia. Diffuse
DISCUSSION
white matter change was found in a case with quadriplegia
(case 37). A karyotype demonstrated extra material on the long
In this series of 42 patients, there was a high rate of positive
arm of chromosome 11. This MRI showed diffuse symmetrical
findings (39 out of 42 patients studied). This is similar to the
supratentorial white matter signal abnormality with mild lateral
yield of positive MRI scans in other series.8–11 For parents
ventricular dilatation.
seeking a cause for their child’s disability, a radiological
diagnosis is now possible in the majority of cases. However,
4. Miscellaneous lesions
this radiological diagnosis may not necessarily provide infor-
Seven children had miscellaneous lesions. (i) Unilateral mation as to why the brain lesion occurred. Important evidence
lesions – three cases (13,26,27): Hemiplegia was present in for the timing of the brain lesion may be provided which can be
useful not only for individuals but for directing research efforts
in the future.
The pattern of brain injury of patients with CP is closely
related to the gestational age of occurrence. Typical preterm
brain injuries include PVL and post-haemorrhagic poren-
cephaly. Periventricular leucomalacia usually occurs between
28 and 34 weeks of gestation8 and is caused by an ischaemic
process in the watershed zone that exists in the periventricular
white matter of the immature brain.12 The MRI features of
PVL include a reduction in the quantity of periventricular
white matter (late infancy and childhood), periventricular
gliosis and ventriculomegaly with irregular outline of the
lateral ventricles.12,13
After about 34 weeks of gestation, subcortical and cortical
areas are the most vulnerable regions of the brain for hypoxic-
ischaemic insult8,9 and the resulting lesions include subcortical
leucomalacia, multicystic encephalamalacia and gliosis.14,15 In
our study, the patients with CP who were born between 30 and
33 weeks gestation (there were no children born earlier than
30 weeks gestation) had typical PVL with obvious gliosis,
while the cortex and subcortical white matter remained spared.
Subcortical lesions and cortical atrophy, with or without
thalamic, brain stem and cerebellar lesions, were seen in
Fig. 3 Lissencephaly. A coronal T1W sequence demonstrating a infants who were born at or after 35–36 weeks gestation. Thus
diffuse smooth thickened cortex with a few broad flat gyri indicating we can conclude that for eight out of the 12 premature children
pachygyria (incomplete lissencephaly). There is a shallow sylvian in our series, the lesion occurred either in the third trimester or
fissure. in the perinatal period.
Cerebral MRI in cerebral palsy 143

These patterns were similar to those reported by Bardovich pregnancy. In case 35, the myelinated white matter was sparse
and Truwit15 who reviewed the MRI scans of 25 patients with in comparison with the gray matter structures, suggesting that
asphyxia documented at various gestational ages. They found the brain injury occurring early in utero before the glial cells
that infants of 24 and 26 weeks gestation had irregularly had developed sufficiently to produce gliosis. Brain injury
enlarged ventricular trigones with minimal periventricular occurring during the second trimester of pregnancy, prior to the
gliosis, patients at 28–34 weeks had variably dilated ventricles time of astrocyte generation, results in liquefaction necrosis
and periventricular gliosis, the 36 week infant had mild cortical without any glial response.18 There is an association between
and subcortical gliosis superimposed on deep white matter and maternal bleeding during pregnancy and congenital anomalies
periventricular gliosis and term infants had significant cortical of the central nervous system. Perfusion failure of the fetal
and subcortical gliosis and atrophy in the parasagittal brain or fetal malnutrition may be the outcome.23 These factors
watershed areas. may have been responsible for the pathology in case 35. Whilst
For infants born at term, we found a similar predominance of the cause of the diffusely abnormal scan with marked delay in
third trimester lesions. Thirteen of the 30 cases had hypoxic– myelination and vermian hypoplasia in case 36 is uncertain,
ischaemic lesions, presumed to have occurred in the third familial white matter hypoplasia has been reported, in some
trimester or perinatal period. All of the 13 cases with hypoxic– cases associated with agenesis of the corpus callosum and
ischaemic lesions also had PVL. It has been suggested that PVL growth deficiency.24,25
found in infants born at term may indicate that the lesion Partial distal deletion of chromosome 11 is associated with
occurred early in the third trimester14 but that the pregnancy psychomotor delay.26,27 Since the first case was described by
progressed. In a group of 152 cases with spastic CP, one-third of Jacobsen et al.,28 over 40 patients with terminal deletion of 11
full-term infants demonstrated preterm patterns of brain injury long arm (Jacobsen syndrome) have been reported. Variations
and PVL was present in 10% of term cases.14 The MRI findings in the deleted parts of 11q result in different clinical features.
of PVL in term infants was milder than those in patients born Our patient (case 37) had similar MRI findings to those
around 30 weeks gestation, indicating that the brain insult reported by Ono et al. with evidence of delayed myelination
responsible for PVL in term infants was less severe, and rather than demyelination.27
therefore did not result in preterm birth.15 One child (case 27) had evidence of possible congenital
Four children had evidence of cortical infarction which is cytomegalovirus infection. Congenital cytomegalovirus infection
less common in the premature than the term infant.16 The can cause a variety of lesions including neuronal migration
lesion is typically found in term babies born after an uneventful disorders.29 The contribution of congenital infection to the total
pregnancy and routine delivery.17 Most commonly, the infarct number of children with CP remains uncertain. In a series of 489
is in the distribution of the middle cerebral artery. It has been cases with spastic CP, in only 3.3% was congenital infection
suggested that such cerebral infarcts may occur prior to considered to be the major aetiological factor.5
delivery17 or within the early days of life.16 In conclusion, we have described the findings in a consecu-
The four cases of cerebral infarction in our study all tive series of MRI scans performed to determine the cause of
demonstrated abnormal intensity T2 signal on the contra- CP. Brain lesions occurring in the third trimester or perinatal
lateral side. This may indicate that the pathology of these full period accounted for 50% of children with CP and 43% of full-
term infarcts was based on diffuse hypoxic–ischaemic brain term children. It was possible to provide an indication of the
lesions, similar to PVL and SCL. When the ischaemic lesion timing of events in 29 of the 42 cases. Twenty-one cases were
is more severe, it is partially due to local artery damage. third trimester or perinatal, three were second trimester, and
There is lack of direct evidence that the attenuated cerebral five were the result of events around the end of the first
artery in the involved area shown on MRA is the cause or the trimester or early second trimester. Hence in only 10 cases was
result of infarction. the timing uncertain.
Five out of 42 cases had cortical malformations indicating Our findings are consistent with other studies in suggesting
insults during the second trimester of pregnancy. The that insults occurring during the third trimester or the perinatal
neuronal migration anomalies demonstrated in our study were period account for a large proportion of cases of CP.9 There
lissencephaly (three cases) and polymicrogyria (two cases). was a wide age range in our series, including several older
Lissencephaly or complete agyria, signifies complete absence children. While it seems likely that there would be similar
of sulci. It has been suggested that the insult occurs before the findings in a younger, more recent cohort of children, further
end of the third month of gestation or between the 12th and studies would be useful to confirm this. Since there is
15th week of gestation.18,19 The corpus callosum forms during evidence that perinatal insults are implicated in only a small
the same period20 and it was of note that two of our cases had proportion of children with CP, we believe that events in the
dysgenesis of the corpus callosum. third trimester should be closely examined to further identify
The two basic varieties of polymicrogyria, layered and the causes of CP.
non-layered, appear to have differing times of onset. The non-
layered type represents a disorder of neuronal migration and
the time of onset of this variety of polymicrogyria appears to
be generally no later than the fourth to fifth month of gestation. ACKNOWLEDGEMENTS
The layered variety of polymicrogyria includes those cases
with evidence of laminar neuronal necrosis in the cortex after The authors wish to acknowledge the contribution of Ms J
the end of neuronal migration, that is, between 20 and Walstab and Ms L Robert, who are responsible for the
30 weeks of gestation.21,22 In our study, there were two cases of Victorian Cerebral Palsy Register. We also thank the Victorian
polymicrogyria (cases 33, 34). Perinatal Data Collection Unit who assisted us in providing
Three cases demonstrated varieties of cerebral white matter data. This project was also supported by the Royal Children’s
hypoplasia, suggesting insults during the second trimester of Hospital Research Institute.
144 R Yin et al.

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