Anatomical characterization of athetotic and spastic cerebral palsy using an atlas-based analysis.

PURPOSE: To analyze diffusion tensor imaging (DTI) in two types of cerebral palsy (CP): the athetotic-type and the spastic-type, using an atlas-based anatomical analysis of the entire brain, and to investigate whether these images have unique anatomical characteristics that can support functional diagnoses. MATERIALS AND METHODS: We retrospectively analyzed the DTI of seven children with athetotic-type, 11 children with spastic-type, and 20 healthy control children, all age-matched. The severity of motor dysfunction was evaluated with the Gross Motor Function Classification System (GMFCS). The images were normalized using a linear transformation, followed by large deformation diffeomorphic metric mapping. For 205 parcellated brain areas, the volume, fractional anisotropy, and mean diffusivity were measured. Principal component analysis (PCA) was performed for the Z-scores of these parameters. RESULTS: The GMFCS scores in athetotic-type were significantly higher than those in spastic-type (P < 0.001). PCA extracted anatomical components that comprised the two types of CP, as well as the severity of motor dysfunction. In the athetotic group, the abnormalities were more severe than in the spastic group. In the spastic group, significant changes were concentrated in the lateral ventricle and periventricular structures. CONCLUSION: Our results quantitatively delineated anatomical characteristics that reflected the functional findings in two types of CP.

Athetotic and spastic cerebral palsy: anatomic characterization based on diffusion-tensor imaging.

PURPOSE: To evaluate the anatomy of deep gray and white matter structures in children with athetotic cerebral palsy (CP) and those with spastic CP by using diffusion-tensor (DT) imaging and to investigate whether these types of CP have unique anatomic correlates that can support their diagnosis and prognosis. MATERIALS AND METHODS: This study was approved by the institutional review board of each participating institution, and written informed consent was obtained from the parents of each patient. DT imaging was used to retrospectively evaluate 19 children with clinically diagnosed athetotic CP (mean age, 3.4 years ± 3.3 [standard deviation]), 26 children with spastic CP (mean age, 3.3 years ± 3.2), and 31 healthy control subjects (mean age, 3.2 years ± 3.0). Fractional anisotropy (FA) and mean diffusivity (MD) were measured with a region of interest (ROI) method. The ROIs were drawn on bilateral deep gray and white matter structures, including projection fibers, association fibers, and commissural fibers. Statistical analysis was performed by using the Kruskal-Wallis test with Bonferroni correction. P < .05 indicated a significant difference. RESULTS: FA values in the athetotic CP group were significantly lower than those in the control and spastic CP groups for multiple structures, including deep gray and white matter (P < .05 and P = .0001, respectively); these differences were also associated with increasing MD (P < .05 and P < .001, respectively). On the other hand, in the spastic CP group, the significantly decreased FA values, compared with those of the normal group, were limited to several white matter structures (P < .05 and P = .0001). CONCLUSION: In children with athetotic CP, the extent of change on DT images due to early brain damage tends to be more diffuse, including multiple brain structures, compared with the changes in children with spastic CP.

Morphologic study of neuronal death, glial activation, and progenitor cell division in the hippocampus of rat models of epilepsy.

PURPOSE: To clarify the relationship of neuronal death to cellular responses, we studied neuronal death as well as reactions of glia and progenitor cells in the hippocampus of two rat models of epilepsy. METHODS: Seizures were induced by either kainic acid (KA) administration or electrical kindling. Neuronal degeneration was assessed by in situ DNA fragmentation analysis. Reactions of glial cells were studied by immunohistochemistry. Progenitor cell division was evaluated using the bromodeoxyuridine (BrdU) labeling method. RESULTS: DNA fragmentation and reactive microglia were observed in the CA1, CA3, and hilus region for 24 h to 4 weeks after KA injection, but not detected in the kindling model. Reactive astrocytes and enhancement of progenitor cell division were seen in both animal models. The number of BrdU-positive cells began to increase on day 3 after KA injection, peaked on day 5, and returned to baseline on day 10. After kindling, the number of BrdU-positive cells began to increase after five consecutive experience of stage I seizures. CONCLUSIONS: These observations show that neuronal degeneration is not necessary for triggering the upregulation. Microglial activation is closely related to the neuronal death process induced by KA.