Lesions such as cerebellar hemorrhage (CBH), infarction, and cerebellar atrophy have been increasingly diagnosed in preterm and term infants using improved neuroimaging techniques [4
]. The incidence of these lesions is strikingly dependent on the degree of prematurity. Thus, in the study of Limperopoulos et al. [17
], the incidence of lesions in infants <750
g birth weight was 15%, and 2% were seen in those >750
g to 1499
g. The topography of the CBH is primarily focal, unilateral, and within the peripheral parenchyma of the cerebellar hemisphere. Subpial germinal matrix bleeding within the external granular layer may account for some intrahemispheric CBH. The vermis is involved in slightly less than one-third of patients [17
]. Cases of vermian hemorrhage represent hemorrhage within the germinal matrix located in the subependymal layer of the roof of the fourth ventricle [33
CBH may occur concomitantly with cerebral lesions such as hemorrhagic parenchymal infarction, intraventricular hemorrhage with dilatation, and periventricular leukomalacia. In these last cases, premature infants at term-equivalent age have reduced cerebellar volume. This reduction may be due to a primary cerebellar injury that is not detectable by MR imaging at term-equivalent age or due to Wallerian degeneration secondary to cerebral lesions. Cerebellar atrophy is usually focal in the unilateral supratentorial lesions and often generalized in the bilateral cerebral lesions [3
]. These data suggest important insights into the highly integrated anatomic and functional integrations between the cerebrum and the cerebellum during development, such as trophic transsynaptic effects along the corticopontocerebellar pathway.
The neuropathological basis of the decreased cerebellar volume remains to be elucidated. In preterm of 32 gestational week (gw), neuronal loss and gliosis were detected in dentate nucleus, cerebellar cortex, or the brain stem cerebellar relay nuclei, basis pontis, and inferior olive, in only 5% to 15% of infants, in particularly in presence of leukomalacia [6
The possibility that cerebellum atrophy in premature infants may be related to adverse blood product as hemosiderin deposit following hemorrhage has been suggested by Messerschmidt and colleagues [5
]. Tam et al. [4
] found that more severe supratentorial intraventricular hemorrhage (IVH) was associated with slower growth of cerebellar volumes. No changes in volumes were found with IVH at 30 weeks postmenstrual age (95% CI 26–33 weeks), but volumes by 40 weeks were 1.4
lower in premature infants with grade 1-2 IVH and 5.4
lower with grade 3-4 IVH. The same magnitude of decreased volume was found whether the IVH was ipsilateral or contralateral. No association was found with severity of white matter injury (P
Whether these blood products are crucial or not in the onset of the cerebellar lesion remain unclear (see [33
]). Early effects of decreased cerebellar volume associated with supratentorial IVH in either hemisphere may be a result of concurrent cerebellar injury or direct effects of subarachnoid blood on cerebellar development.
Preterm delivery associated to other adverse insults could disrupt the developmental program of the cerebellum. A recent postmortem study on premature infants who had survived in an exutero environment reports cerebellar abnormalities in the development of granular cells which parallel a decrease of Sonic hedgehog in the Purkinje cell layer [35
In fact the pathogenesis of lesions of the cerebellum is multifactorial. Univariate analyses identified maternal, intrapartum, and early postnatal hemodynamic risk factors; multivariate regressions indicate that emergent caesarian section, patent ductus arteriosus, and lower 5-day minimum pH independently increased the odds of cerebellar hemorrhage [17
]. Different mechanisms appear plausible to explain the disturbance of cerebellar development after premature birth. The correlation of lesions of the cerebellum in preterm with animal models can highlight the precise pathophysiology of these lesions.