The relationship between motor pathway injury and motor impairment was investigated by voxelwise correlation analysis in 43 patients (median age 12 years) with periventricular leucomalacia and spastic diplegia at Yonsei University College of Medicine, Seoul, Korea. Functional connectivity of motor cortical and thalamocortical pathways was also evaluated in 11 patients using functional MRI, and results in patients with spastic diplegia CP were compared with normal controls. White matter volume reduction was not significantly correlated with motor dysfunction. Fractional anisotropy within the white matter tracts of patients was lower than controls, and that within the corticospinal tracts and corpus callosum was significantly correlated with motor dysfunction (P<0.03). A lesser correlation occurred with that in thalamocortical pathways (P<0.05). Cortical volume of pre- and post-central gyri and paracentral lobule tended to be negatively correlated with motor function. Motor cortical connectivity was diminished in the somatosensory cortex, paracentral lobule, cinglate motor area and visual cortex, whereas thalamovisual connectivity was spared, despite optic radiation injury. Neuronal g-aminobutyric acid receptor binding potential, measured with positron emission tomography scans (n=27) and compared with controls (n=20), was focally increased in the lower extremity homunculus, cingulate cortex, visual cortex and cerebellum (P<0.05), a compensatory plasticity response to injury. The mechanism of motor dysfunction in patients with periventricular leucomalacia involves injury to descending motor tracts and reduction in cortical volume and functional connectivity. [1]

COMMENT. Pathophysiological mechanisms of motor impairment in patients with periventricular leukomalacia and spastic cerebral palsy are controversial [2, 3] The above study demonstrates that descending motor pathway injury and reduction of overlying cortical volume are leading mechanisms.

Neuronal cell death in neonatal hypoxia-ischemia, reviewed by researchers at Johns Hopkins University School of Medicine [4], is manifested as a continuum of programmed cell death (PCD) from apoptosis (dismantling of cells, Type I PCD) to necrosis (lytic destruction of cells) and autophagy (degradation of cells by lysosomal system, Type II PCD), and not as distinct categories of neurocellular degeneration. Hypothermia in infants with HIE protects against necrosis and apoptosis.