Disruption of Cerebellar Development: Potential Complication of Extreme Prematurity

Overview

Journal AJNR Am J Neuroradiol

Specialty Neurology

Date 2005 Aug 11

PMID 16091510

Citations 52

Authors

Agnes Messerschmidt

Peter C Brugger

Eugen Boltshauser

Gerlinde Zoder

Walter Sterniste

Robert Birnbacher

Daniela Prayer

Affiliations

Soon will be listed here.

Abstract

Background And Purpose: Infants with very low birth weight are at high risk for cerebral lesions. Although supratentorial brain damage is a common radiologic finding, posterior fossa pathologies are rare. We studied the morphology of cerebellar involvement in a large series of 28 premature infants born before the 30th week of gestation to define typical patterns and identify possible risk factors for this pathology.

Methods: Cranial sonograms were obtained in the early neonatal period. MR imaging was performed between the 2nd month and the 6th year of life. Morphologic patterns of cerebellar involvement were evaluated.

Results: Three morphologic patterns of cerebellar involvement were recognized: (1) symmetric volume reduction of the cerebellar hemispheres, which were floating immediately beneath the tentorium, and a small vermis with preserved shape; (2) symmetrical reduction in hemispheric volume with an enlarged, balloon-shaped fourth ventricle and a small, deformed vermis; and (3) normal overall cerebellar shape with extensive reduction of its dimensions. A small brain stem with flattened anterior curvature of the pons and loss of supratentorial white matter was present in all patients.

Conclusion: Symmetric cerebellar volume reduction was found as a consequence of extreme prematurity. Selective vulnerability of the developing cerebellum in the window of 24-30 weeks of gestation, combined with several additive perinatal risk factors (eg, hemosiderin deposits) seems to lead to destruction of immature structures and developmental arrest. Therefore, the resulting condition is the consequence of disrupted cerebellar development.

Citing Articles

Extremely Preterm Infants with a Near-total Absence of Cerebellum: Usefulness of Quantitative Magnetic Resonance in Predicting the Motor Outcome.

Calandrelli R, Tuzza L, Romeo D, Arpaia C, Colosimo C, Pilato F Cerebellum. 2023; 23(3):981-992.

PMID: 37603264 DOI: 10.1007/s12311-023-01593-7.

Pharmacological pain and sedation interventions for the prevention of intraventricular hemorrhage in preterm infants on assisted ventilation - an overview of systematic reviews.

Strozyk A, Paraskevas T, Romantsik O, Calevo M, Banzi R, Ley D Cochrane Database Syst Rev. 2023; 8:CD012706.

PMID: 37565681 PMC: 10421735. DOI: 10.1002/14651858.CD012706.pub2.

Classic "PCH" Genes are a Rare Cause of Radiologic Pontocerebellar Hypoplasia.

Zakaria R, Malta M, Pelletier F, Addour-Boudrahem N, Pinchefsky E, Martin C Cerebellum. 2023; 23(2):418-430.

PMID: 36971923 DOI: 10.1007/s12311-023-01544-2.

Brain Biometry Reveals Impaired Brain Growth in Preterm Neonates with Intraventricular Hemorrhage.

Steiner M, Schwarz H, Kasprian G, Rittenschober-Boehm J, Schmidbauer V, Fuiko R Neonatology. 2023; 120(2):225-234.

PMID: 36805535 PMC: 10906469. DOI: 10.1159/000528981.

Stem cell-based interventions for the prevention and treatment of intraventricular haemorrhage and encephalopathy of prematurity in preterm infants.

Romantsik O, Moreira A, Thebaud B, Aden U, Ley D, Bruschettini M Cochrane Database Syst Rev. 2023; 2:CD013201.

PMID: 36790019 PMC: 9932000. DOI: 10.1002/14651858.CD013201.pub3.

References

DeSouza N, Chaudhuri R, Bingham J, Cox T . MRI in cerebellar hypoplasia. Neuroradiology. 1994; 36(2):148-51. DOI: 10.1007/BF00588085. View

Bhutta A, Anand K . Vulnerability of the developing brain. Neuronal mechanisms. Clin Perinatol. 2002; 29(3):357-72. DOI: 10.1016/s0095-5108(02)00011-8. View

Muntoni F, Goodwin F, Sewry C, Cox P, Cowan F, Airaksinen E . Clinical spectrum and diagnostic difficulties of infantile ponto-cerebellar hypoplasia type 1. Neuropediatrics. 1999; 30(5):243-8. DOI: 10.1055/s-2007-973498. View

Miyata M, Miyata H, Mikoshiba K, Ohama E . Development of Purkinje cells in humans: an immunohistochemical study using a monoclonal antibody against the inositol 1,4,5-triphosphate type 1 receptor (IP3R1). Acta Neuropathol. 1999; 98(3):226-32. DOI: 10.1007/s004010051073. View

Huang C, Liu C . The differences in growth of cerebellar vermis between appropriate-for-gestational-age and small-for-gestational-age newborns. Early Hum Dev. 1993; 33(1):9-19. DOI: 10.1016/0378-3782(93)90169-u. View

Sarnat H, Alcala H . Human cerebellar hypoplasia: a syndrome of diverse causes. Arch Neurol. 1980; 37(5):300-5. DOI: 10.1001/archneur.1980.00500540078012. View

Soto-Ares G, Vinchon M, Delmaire C, Abecidan E, Dhellemes P, Pruvo J . Cerebellar atrophy after severe traumatic head injury in children. Childs Nerv Syst. 2001; 17(4-5):263-9. DOI: 10.1007/s003810000411. View

Johnston M . Excitotoxicity in neonatal hypoxia. Ment Retard Dev Disabil Res Rev. 2002; 7(4):229-34. DOI: 10.1002/mrdd.1032. View

Anand K, Scalzo F . Can adverse neonatal experiences alter brain development and subsequent behavior?. Biol Neonate. 2000; 77(2):69-82. DOI: 10.1159/000014197. View

10.

Fukumizu M, Takashima S, Becker L . Neonatal posthemorrhagic hydrocephalus: neuropathologic and immunohistochemical studies. Pediatr Neurol. 1995; 13(3):230-4. DOI: 10.1016/0887-8994(95)00183-g. View

11.

Squier W, Hope P, Lindenbaum R . Neocerebellar hypoplasia in a neonate following intra-uterine exposure to anticonvulsants. Dev Med Child Neurol. 1990; 32(8):737-42. DOI: 10.1111/j.1469-8749.1990.tb08436.x. View

12.

Ramaekers V, Heimann G, Reul J, Thron A, Jaeken J . Genetic disorders and cerebellar structural abnormalities in childhood. Brain. 1997; 120 ( Pt 10):1739-51. DOI: 10.1093/brain/120.10.1739. View

13.

Ten Donkelaar H, Lammens M, Wesseling P, Thijssen H, Renier W . Development and developmental disorders of the human cerebellum. J Neurol. 2003; 250(9):1025-36. DOI: 10.1007/s00415-003-0199-9. View

14.

Lafarga M, Andres M, Calle E, Berciano M . Reactive gliosis of immature Bergmann glia and microglial cell activation in response to cell death of granule cell precursors induced by methylazoxymethanol treatment in developing rat cerebellum. Anat Embryol (Berl). 1998; 198(2):111-22. DOI: 10.1007/s004290050169. View

15.

Fukumizu M, Takashima S, Becker L . Glial reaction in periventricular areas of the brainstem in fetal and neonatal posthemorrhagic hydrocephalus and congenital hydrocephalus. Brain Dev. 1996; 18(1):40-5. DOI: 10.1016/0387-7604(95)00103-4. View

16.

Mercuri E, He J, Curati W, DUBOWITZ L, Cowan F, Bydder G . Cerebellar infarction and atrophy in infants and children with a history of premature birth. Pediatr Radiol. 1997; 27(2):139-43. DOI: 10.1007/s002470050085. View

17.

Miall L, Cornette L, Tanner S, Arthur R, Levene M . Posterior fossa abnormalities seen on magnetic resonance brain imaging in a cohort of newborn infants. J Perinatol. 2003; 23(5):396-403. DOI: 10.1038/sj.jp.7210941. View

18.

Johnston M . Neurotransmitters and vulnerability of the developing brain. Brain Dev. 1995; 17(5):301-6. DOI: 10.1016/0387-7604(95)00079-q. View

19.

Bourgouin P, Tampieri D, Melancon D, del Carpio R, Ethier R . Superficial siderosis of the brain following unexplained subarachnoid hemorrhage: MRI diagnosis and clinical significance. Neuroradiology. 1992; 34(5):407-10. DOI: 10.1007/BF00596502. View

20.

Salman M, Blaser S, Buncic J, Westall C, Heon E, Becker L . Pontocerebellar hypoplasia type 1: new leads for an earlier diagnosis. J Child Neurol. 2003; 18(3):220-5. DOI: 10.1177/08830738030180031201. View