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Periventricular Leukomalacia: Relationship between Lateral Ventricular Volume on Brain MR Images and Severity of Cognitive and Motor Impairment¹

¹ From the Departments of Radiology (E.R.M., J.T.F., C.B.Q.), Neurology (M.V.J.), and Pediatrics (A.H.H., M.V.J.); the Departments of Neurology and Developmental Medicine (A.H.H., M.V.J.) and Nursing (E.M.R., S.W.D.), Kennedy Krieger Institute; and the School of Medicine (B.M.F.), Johns Hopkins Medical Institutions, 600 N Wolfe St, Houck Bldg B100G, Baltimore, MD 21287-2182. Received January 8, 1999; revision requested March 9; revision received March 22; accepted July 1. A.H.H. and M.V.J. supported in part by the United Cerebral Palsy Research and Education Foundation grant no. R-706-96. Address reprint requests to E.R.M. (e-mail: emelhem@rad.jhu.edu).

	Abstract

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
PURPOSE: To evaluate the utility of lateral ventricular volume measurements in predicting motor and cognitive impairment severity in children with periventricular leukomalacia (PVL), with or without seizures.

MATERIALS AND METHODS: The charts of children with spastic cerebral palsy and PVL documented on brain magnetic resonance (MR) images were reviewed. Affected children were grouped by motor and cognitive impairment severity and seizure disorder. An age-matched control group was established. Lateral ventricular volumes were measured on two-dimensional T2-weighted spin-echo MR images. Analysis of variance was used to identify significant differences in mean lateral ventricular volume between groups. Paired analyses of differences were performed with the Bonferroni t method.

RESULTS: Thirty-six children (24 boys, 12 girls) with spastic cerebral palsy and PVL and 21 age-matched control subjects (14 boys, seven girls) were identified. Mean lateral ventricular volumes of the moderate and marked motor deficit groups were significantly larger than those of the control and mild motor deficit groups (F = 29.24; = .01). Mean lateral ventricular volumes of all cognitive impairment groups were significantly larger than those of the control and no-cognitive-impairment groups (F = 21.10; = .01). There was no difference in mean lateral ventricular volume between children with PVL with or without seizures.

CONCLUSION: Lateral ventricular volume measurements can be used as quantitative markers of clinical impairment severity and as clinical outcome predictors before formal testing is possible.

Index terms: Brain, injuries, 161.5911, 161.829, 161.8729 • Cerebral palsy, 161.5911, 161.829, 161.8729 • Children, central nervous system, 161.4371, 161.829 • Fetus, abnormalities, 161.4371, 161.829 • Fetus, injuries, 161.829, 161.4371 • Leukomalacia, 161.4371, 161.829 • Magnetic resonance (MR) imaging, in infants and children, 161.121411

	Introduction

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
The term "cerebral palsy," originally used by Sir William Osler, describes a group of nonprogressive yet often changing motor impairment syndromes that result from disorders of early brain development (1–4). On the basis of the predominant clinical features, cerebral palsy is classified as spastic, extrapyramidal, or mixed (4,5).

Distinct magnetic resonance (MR) imaging findings are seen in the different types of cerebral palsy. In particular, MR imaging features of periventricular leukomalacia (PVL), which results from selective vulnerability of the periventricular white matter in the preterm neonate to ischemic, infectious, or metabolic insults, are strongly related to spastic cerebral palsy (spastic diplegia or quadriplegia) (6,7).

On MR images, findings of PVL are related to injury to developing periventricular white matter during the late second and early third trimesters of pregnancy, with resultant T1 and/or T2 prolongation, thinning of the posterior body of the corpus callosum, enlargement of the lateral ventricles, and irregularity of the lateral ventricular walls (6,8–10).

A correlation between late MR imaging findings of PVL with severity of motor deficit and cognitive impairment can be used to predict the level of neuropsychologic dysfunction before formal testing is feasible and to institute early rehabilitative programs (11–14).

We performed this study to indirectly quantify periventricular white matter loss in PVL by measuring lateral ventricular volume with a semiautomated, computer-based algorithm and to evaluate whether lateral ventricular volume measurements can help predict the severity of motor deficit and cognitive impairment and the presence of seizures.

Our null hypotheses were as follows: (a) There is no difference in lateral ventricular volumes between children in the control group and children with spastic cerebral palsy secondary to PVL. (b) There is no change in lateral ventricular volumes with differences in severity of motor deficit and cognitive impairment. (c) There is no difference between lateral ventricular volumes in affected children with seizures and in those without.

	MATERIALS AND METHODS

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
Subjects
The charts of 65 children who were currently patients at our institutions' Center for Cerebral Palsy and Motor Disorders were reviewed for sex, gestational age at birth, availability of MR images, severity and type of motor and cognitive impairments, and presence of a seizure disorder.

Clinical inclusion criteria were the presence of spastic diplegia or quadriplegia and the availability of a brain MR imaging study obtained at one of our institutions. Children with mixed (pyramidal and extrapyramidal) cerebral palsy and spastic hemiparesis were excluded.

The children were stratified into (a) three groups on the basis of the severity of motor impairment: mild (clumsiness with spasticity), moderate (diplegia), or marked (quadriplegia); (b) four groups of different cognitive impairment levels on the basis of established score ranges for the Bayley Scales of Infant Development and the Stanford-Binet Intelligence Scale: no cognitive impairment, mild cognitive impairment, moderate cognitive impairment, and marked cognitive impairment; and (c) two groups on the basis of the presence of a seizure disorder.

The control group consisted of healthy siblings of patients with Rett syndrome or Turner syndrome who were imaged as part of an ongoing study, for which both institutional review board approval and informed consent from parents or guardians had been obtained, and of children who underwent brain MR imaging for symptoms referable to the orbits, base of the skull, or posterior fossa.

MR Imaging
All children included in the study underwent a standard pediatric brain MR imaging examination performed with a 1.5-T superconducting magnet (Signa; GE Medical Systems, Milwaukee, Wis), with the following parameters: sagittal and transverse T1-weighted spin-echo (SE) (550/20 [repetition time msec/echo time msec]) and transverse T2-weighted double-echo SE (3,000/20, 80) imaging. Complete brain coverage with the transverse double-echo SE sequence was obtained with 23 5-mm-thick interleaved sections (no gap). The MR images were reviewed by a neuroradiologist (E.R.M.).

For the children with spastic cerebral palsy, MR imaging findings limited to PVL (T1 and/or T2 prolongation in the periventricular white matter; reduction in the periventricular white matter, especially in the regions of the atria; thinning of the posterior body of the corpus callosum; and irregularities of the lateral ventricular walls) were used to include children in the study.

Other MR imaging findings associated with congenital or other perinatal brain damage (ie, schizencephaly, deep gray matter abnormalities, hemispheric gray matter damage, germinal matrix hemorrhage, and hydrocephalus) were used to exclude children from the study. In particular, children with hydrocephalus were excluded on the basis of the relative sparing of the temporal horns, the configuration of the frontal horns, and the lack of effacement of the cortical sulci and basal cisterns.

For the control group, the MR images were evaluated for any supratentorial abnormalities that might have affected the size or shape of the lateral ventricles.

Image Processing
The T2-weighted SE MR images of the children who met the clinical and MR imaging inclusion criteria were transferred to an offline workstation (Allegro; ISG Technologies, Ontario, Canada). Volumes of the lateral ventricles were generated by using software written at our institution. Window width and level were adjusted to best display the anatomy of the lateral ventricles. Upper and lower pixel intensity thresholds were set such that the lateral ventricles were included in this region.

Subsequently, a seed was dropped in the atrium of the left lateral ventricle. In an automated fashion, the seed grew into adjacent pixels with signal intensity that was within the range set by the thresholds. This search process was repeated for each new included pixel until the generated region of interest reached the boundaries of the range set by the thresholds.

Occasionally, the signal intensity values of the region of interest could not be sufficiently differentiated from adjoining areas on the basis of setting range boundaries alone. In such instances, boundary recognition and morphologic algorithms helped to prevent the region from leaking into extraneous areas. Manual checking and editing were used to remove unwanted additions (ie, third ventricle).

Once the region was considered complete, the process was repeated for the next image in the section stack. A three-dimensional reconstruction algorithm created at our institution was used to stack the regions of interest (the lateral ventricles) from each section and to generate the lateral ventricular volume.

Statistical Analysis
Multiple range tests (modified least significant difference test, Bonferroni adjustment) were used to compare the age composition of the control group with that of the nine subject groups. The Spearman rank correlation was used to examine the correlation between gestational age at time of birth and the lateral ventricular volumes of the affected subjects. Analysis of variance was used to determine the existence of significant differences in the mean lateral ventricular volume between the three motor-deficit groups and the control group, between the four cognitive-impairment groups and the control group, and between the two seizure-disorder groups and the control group. When differences were found, paired analyses of differences were performed with the Bonferroni t method.

	RESULTS

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Thirty-six children (24 boys, 12 girls; mean age at time of MR imaging, 4.5 years; age range, 1.5–12.5 years) with spastic cerebral palsy and MR imaging findings limited to PVL fulfilled the clinical and MR imaging inclusion criteria (Fig 1).

View larger version (116K): [in this window] [in a new window] [Download PPT slide]   Figure 1a. (a) PVL in a 6-year-old boy with mild clumsiness and spasticity, no cognitive impairment, and no seizure disorder. (b) PVL in a 16-month-old boy with spastic quadriplegia, moderate cognitive impairment, and no seizure disorder. In both children, T2-weighted transverse brain MR images (3,000/80) at the level of the lateral ventricles demonstrate confluent hyperintensity in the periventricular white matter (solid arrows) and irregularities of the lateral ventricular walls (open arrows). However, the lateral ventricles were larger in the more severely affected child (b).

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   Figure 1b. (a) PVL in a 6-year-old boy with mild clumsiness and spasticity, no cognitive impairment, and no seizure disorder. (b) PVL in a 16-month-old boy with spastic quadriplegia, moderate cognitive impairment, and no seizure disorder. In both children, T2-weighted transverse brain MR images (3,000/80) at the level of the lateral ventricles demonstrate confluent hyperintensity in the periventricular white matter (solid arrows) and irregularities of the lateral ventricular walls (open arrows). However, the lateral ventricles were larger in the more severely affected child (b).

There was no correlation (r = -0.10) between gestational age at the time of birth and the lateral ventricular volumes of the affected children (Fig 2).

View larger version (9K): [in this window] [in a new window] [Download PPT slide]   Figure 2. Scatterplot of gestational age at the time of birth versus lateral ventricular volume (in cubic millimeters) for the children with spastic cerebral palsy shows no correlation between gestational age at the time of birth and lateral ventricular volumes.

View larger version (8K): [in this window] [in a new window] [Download PPT slide]   Figure 3. Bar graph of the mean lateral ventricular volumes (in cubic millimeters) from the control group and the spastic cerebral palsy groups, which are stratified according to the severity of motor deficit, shows a significant difference in the lateral ventricular volumes between (a) the control group and the mild group versus (b) the moderate group and the marked group.

A significant difference in the mean lateral ventricular volumes existed between the control group and the four cognitive impairment groups (F = 21.10, = .01, df = 52). Paired analyses demonstrated a significant difference between the mild group and the control group, the moderate group and the control group, the marked group and the control group, the mild group and the no-cognitive-impairment group, the moderate group and the no-cognitive-impairment group, the marked group and the no-cognitive-impairment group, the mild group and the marked group, and the moderate group and the marked group. There was no difference between the no-cognitive-impairment group and the control group or between the mild group and the moderate group (Fig 4).

View larger version (8K): [in this window] [in a new window] [Download PPT slide]   Figure 4. Bar graph of the mean lateral ventricular volumes (in cubic millimeters) from the control group and the spastic cerebral palsy groups, which are stratified according to the severity of cognitive impairment, shows a significant difference in lateral ventricular volumes between the control group and the mild, moderate, and marked cognitive impairment groups.

A significant difference in the mean lateral ventricular volumes existed between the control group and the two seizure-disorder groups (F = 28.35, = .01, df = 54). Paired analyses demonstrated a significant difference between the no-seizure-disorder group and the control group and between the seizure-disorder group and the control group. There was no significant difference between the two seizure-disorder groups (Fig 5).

View larger version (8K): [in this window] [in a new window] [Download PPT slide]   Figure 5. Bar graph of the mean lateral ventricular volumes (in cubic millimeters) from the control group and spastic cerebral palsy groups, which are stratified on the basis of the presence of seizure disorder, shows no significant difference in lateral ventricular volumes between the two seizure-disorder groups. + = present, - = not present.

	DISCUSSION

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

On MR images, late findings of PVL are the result of white matter cavitation, loss, and gliosis, with relative sparing of the overlying cortical mantle. Lateral ventricular enlargement and irregularities and corpus callosal thinning are secondary manifestations (8,9).

In this study, we used lateral ventricular volumes as an indirect measurement of periventricular white matter loss. The reasons that we determined lateral ventricular volumes and not white matter volumes are related to anatomic and image postprocessing issues. The relative sparing of cortical gray matter and subcortical white matter and the often poor contrast between gray and white matter and between affected and unaffected white matter on the available MR images render most segmentation algorithms tedious (because they require more manual editing), unreliable, and inaccurate (19).

Setting boundary ranges and segmenting the lateral ventricles by using semiautomated algorithms are easy and reproducible. Large differences in signal intensity ranges and well-defined boundaries between cerebrospinal fluid and surrounding brain parenchyma reduce the extension of the iterative process beyond the lateral ventricles (19–21).

MR imaging-based and computer-based semiautomated segmentation algorithms provide reliable in vivo quantification of specific intracranial structures, which in turn may be used as a predictor of clinical outcome. This may improve parent counseling and promote timely implementation of intervention programs (14).

Our results show that the severity of the motor or cognitive impairment in children with PVL correlates with increased mean lateral ventricular volumes. The implication is that lateral ventricular volume quantification may help predict clinical outcome before formal testing is possible.

In children with PVL, spastic cerebral palsy is the result of injury to the corticospinal tract that traverses dorsally and laterally to the external angle of the lateral ventricle (6). There is preferential disruption of the corticospinal tract that innervates the lower extremities (spastic diplegia) in all but the most severe cases of PVL, in which extensive white matter loss results in both lower and upper extremity involvement (spastic quadriplegia). Our results demonstrate that lateral ventricular volume quantification reasonably reflects the severity of motor impairment and is a good marker for the degree of periventricular white matter loss.

The pattern of cognitive impairment in children with PVL is characterized by the greater involvement of visuomotor and perceptual abilities than of verbal abilities (12). Using qualitative scoring systems, Yokoshi et al (11) found no correlation between the severity of mental impairment, expressed in terms of full-scale IQ, and the degree of periventricular white matter loss.

On the other hand, other investigators, using a similar scoring system, found a significant correlation between the degree of periventricular white matter loss and the severity of mental impairment expressed in terms of full-scale IQ and performance IQ (12,14). These apparently contradictory results may be due partly to the qualitative nature of the scoring systems used. In our study, lateral ventricular volume quantification proved to be a good marker for the overall severity of cognitive impairment (Fig 4).

Seizure disorder in children with PVL is most likely secondary to concomitant subtle cortical malformations that result from disruption of neuronal migration and are often undetectable on MR images (22). The lack of difference in mean lateral ventricular volumes between affected children with or without seizure disorder is not unexpected, since subtle cortical abnormalities have no effect on the measured volumes (Fig 5).

The lack of correlation between the gestational age at the time of birth and lateral ventricular volume (Fig 2) supports the belief that some fetuses sustain periventricular white matter injury before 34 weeks gestational age and remain in utero until term (23). Because of the decreased vulnerability of periventricular white matter in late gestation, a perinatal insult in a fetus carried to term is expected to cause less white matter loss and result in smaller lateral ventricular volumes compared with a perinatal insult in the preterm neonate.

In this study, a reevaluation of the relationship between T2 prolongation in the affected periventricular white matter and the severity of neurologic and/or neuropsychologic deficits was not performed. This was in view of the well-documented lack of correlation (14).

For the purpose of defining a homogeneous cohort, children with MR imaging findings suggestive of previous intraventricular or subependymal hemorrhage or hydrocephalus were excluded. Children with spastic hemiplegia were also excluded because of a documented correlation with periventricular hemorrhagic infarction (24,25). These exclusion criteria were thought to be necessary to eliminate any influence on lateral ventricular volume quantification not related to PVL.

Potential limitations of this study were, in part, related to its retrospective nature. We were unable to directly quantify periventricular white matter volumes because of the nonavailability of MR images with high gray-to-white matter contrast.

Also, we were limited to the clinical information available in the patients' charts, especially with regard to the type and severity of cognitive impairment. Unfortunately, distinction between verbal and performance IQ and information regarding the different types of learning disabilities were not available.

Finally, this study was probably influenced by sampling bias, in that children with spastic cerebral palsy who undergo brain MR imaging are usually more severely affected and may not constitute a representative sample.

In conclusion, lateral ventricular volume measurements can be used as quantitative markers of the severity of clinical impairment and as predictors of clinical outcome in children with PVL before formal testing is possible.

	Footnotes

 
Abbreviations: PVL = periventricular leukomalacia SE = spin echo

Author contributions: Guarantor of integrity of entire study, E.R.M.; study concepts and design, E.R.M., A.H.H.; definition of intellectual content, E.R.M., A.H.H.; literature research, E.R.M., A.H.H.; clinical studies, B.M.F., S.W.D., J.T.F., C.B.Q., E.M.R.; data acquisition and analysis, B.M.F., S.W.D., J.T.F., C.B.Q., E.M.R.; statistical analysis, E.R.M.; manuscript preparation, E.R.M.; manuscript editing, A.H.H.; manuscript review, M.V.J.

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This Article Abstract Figures Only Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Melhem, E. R. Articles by Johnston, M. V. Search for Related Content PubMed PubMed Citation Articles by Melhem, E. R. Articles by Johnston, M. V.