Hannah Kinney, MD
Professor of Pathology (Neuropathology)
Harvard Medical School/
Children's Hospita l
Department of Neuroscience

MRRC Project(s)

P01 NS38475-01
Periventricular Leukomalacia in the Premature Infant - PI, Prj 2: Cellular Basis of PVL in Autopsied Human Brain

R01 HD20991-14
Brainstem Maturation in the Sudden Infant Death Syndrome

P01 HD36379-03
The Ventral Medulla and the Sudden Infant Death Syndrome- Program Director and PI, Prj 5: Protective Responses and Brainstem Analysis in SIDS

Brainstem Research in the Sudden Infant Death Syndrome

Despite a dramatic 38% fall in the incidence of the sudden death syndrome (SIDS) in the United States following the 1994 national recommendation for the supine sleeping position, SIDS remains the leading cause of postneonatal infant mortality. Its incidence is 0.8/1000 live births. SIDS is defined as the sudden death of an infant under one year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history. The syndrome is temporally associated with sleep periods, leading to the premise that SIDS occurs during sleep or transitions between sleep and waking, and may be a failure of arousal to a life-threatening challenge in the prone position. The cause(s) of SIDS remain(s) unknown.

Oligodendrocyte Maturation in the Developing Human Brain

Periventricular leukomalacia (PVL) is the leading cause of cerebral palsy in premature infants who survive the neonatal period, and results, at least in part, from disrupted cerebral myelination. The greatest period of risk (24-32 weeks gestation) occurs when cerebral white matter is immature, i.e., when oligodendrocyte precursors are proliferating and differentiating, and before myelin sheaths are actively synthesized. Although the pathogenesis of PVL likely involves multiple factors, e.g., ischemia, infection, cytokines, and oxidative stress, the correlation of the timing of the lesion with the possible dominance of developing oligodendrocytes in cerebral white matter suggests that intrinsic factors related to developing oligodendrocytes may be critical. While much is known about the regional and biochemical sequences of human myelination, little is known about the cellular sequences, nor about the definition of the nature and timing of the successive stages in human oligodendrocyte (OL) lineage. The following studies addressed these issues in relationship to the clinical problem of PVL.