Dr. Hannah C. Kinney—In Memoriam: End of an Era?

August 2026

Introduction

Our field of neonatal neurology recently lost a truly extraordinary individual, in many ways a unique, foundational pillar, who, I fear, may be irreplaceable in the current era. Additionally, she was a cherished friend and a close and trusted colleague. I write here of Dr. Hannah Chase Kinney, esteemed neuropathologist and investigator, who died after a prolonged and difficult illness at her beloved home on the Chesapeake Bay on June 6 of this year. During my final conversation with her, a couple of days earlier, she asked me to remember our great interactions while working together. I responded that I couldn’t possibly ever forget.

In the following I will describe briefly her early years and the teachers who influenced her development as a distinguished neuropathologist. Then, within the limitations of space in these Volpe’s Views, I will outline only briefly her work on the sudden infant death syndrome (SIDS) and more extensively, her pioneering studies on neonatal neuropathology.

Early Years

Hannah grew up in the 1960s and she enjoyed emphasizing that she was a “child of the sixties,” an idealist and humanist, with a yearning for discovery. She was influenced greatly by her father, Dr. Thomas Kinney, who was Chair of Pathology at Duke University and introduced her to the power of microscopic pathology.¹

The stimulation for Hannah to study the human brain began during her first year of medical school at Case Western School of Medicine in Cleveland, where she was taught and greatly stimulated by the brilliant neuropathologist, Dr. Betty Banker. (Dr. Banker, with the esteemed neuropathologist Dr. Jeanne-Claudie Larroche, had described the characteristics of periventricular leukomalacia, a disorder that Hannah would describe in great detail decades later.) During her neuropathology training at Harvard she was stimulated by another well-known neuropathologist, Dr. Floyd Gilles. Additionally, she studied the intricacies of brainstem anatomy and function with the legendary Harvard anatomist, Dr. Richard Sidman. The latter work proved seminal for her later groundbreaking studies SIDS.

Major Contributions

Hannah’s major contributions are many, but best loosely characterized as those related to SIDS and those related to neonatal neuropathology. I will note the SIDS work only briefly here (see Hannah’s own recent review of this work in Annual Review of Pathology’s Mechanisms of Diseases¹).

SIDS

Hannah’s overall “triple risk” hypothesis was that the infant vulnerable for SIDS had (1) an intrinsic defect in brainstem sites which (2) mediate cardiopulmonary resuscitative reflexes during sleep during (3) a critical developmental window of the first year of life. Her work included a wonderful series of discoveries, based on detailed immunocytochemical studies of brainstem cellular anatomy and pathology. The gist of her work elucidated the likely brainstem deficit as a disorder of serotonin receptors. Subsequent epidemiologic studies showing the relation of SIDS risk to prone sleeping position and the decline in SIDS incidence with the back-to-sleep movement showed the importance of her work in a dramatic and gratifying manner.

Neonatal Neuropathology

Of particular importance for neonatal neurology, Hannah contributed enormously to the understanding of normal human brain development and of brain disorders of early life, especially those affecting the premature infant. Concerning normal developmental features, her work on the regional development of myelin stands as a reference point for neurobiologists worldwide.^2,3 Her later work addressed myelin development at the cellular level, including the details of oligodendroglial differentiation and its relation to the onset and progression of myelination.^4,5 Her landmark study of cerebral axonal development had major implications for elucidation of the dysmaturational cerebral cortical disturbances, so critical for the neurocognitive deficits in survivors of very preterm birth.⁶

Her studies of the principal brain injury in premature infants, cerebral white matter injury, greatly broadened the understanding of this common disorder. (As noted earlier, the initial neuropathological description of this disorder was by the esteemed neuropathologist, Dr. Betty Banker, whom Hannah always mentioned as the first individual who inspired her, in medical school, to study neuropathology.) In collaboration with our research group, Hannah delineated the particular phase of the oligodendroglial lineage that is the principal cellular target in white matter injury of the premature infant.^7-9 This observation set the stage for research into agents that could protect this particular oligodendroglial phase. Then, in a major advance utilizing state-of-the-art methods, she and her coworkers identified the association of axonal injury in cerebral white matter injury¹⁰ and then, as a potential consequence, accompanying deficits in cortex, thalamus and elsewhere,^11-14 deficits likely critical in the genesis of the later neurocognitive deficits in surviving infants.⁸

Not content with identifying the morphological aspects of premature brain injury and cellular dysmaturation, Hannah collaborated with basic scientists in our group to address the molecular mechanisms leading to these deleterious effects. Her work showed the role of reactive oxygen and nitrogen species in the genesis of injury to the developing oligodendrocyte.^15,16 Microglia were identified as key cellular mediators,¹⁷ and delayed development of anti-oxidant defenses in premature brain was shown to underlie the vulnerability of cerebral white matter of the premature infant.^16,18,19 She and others in our group showed that the sources of reactive oxygen and nitrogen species particularly included specific cytokines and altered glutamate homeostasis.^20,21

Thus, Hannah’s work has been of enormous importance for our understanding of normal human brain development at the cellular and molecular levels and the widespread effects of brain injury and dysmaturation in the premature infant. Her work has set the stage for subsequent studies, currently underway, to prevent or ameliorate the deleterious effects of this common and devastating impairment.

Personal Reflections

Hannah was a cherished personal friend and a trusted colleague. She was, in many ways, one of the most authentic individuals I have had the privilege to know in medicine. Her pursuit for the truth was relentless, and she abhorred “jumping to conclusions.” I remember vividly in our research team gatherings, when a junior (or senior!) member of the group seemed to jump to a conclusion, perhaps prematurely, Hannah’s gentle question, with a twinkle in her eyes, “How do you really know that?”

She was a truly genuine and caring person who could critique work in such a way as to leave the author gratified but eager to exert maximum effort to correct course when necessary. Moreover, she never hesitated to do more than her part to help directly when needed.

She was a master teacher of neuropathology. Some of my most gratifying experiences with Hannah were sitting with her as we gazed at microscopic specimens through a two-head microscope. As she described cytologic features and answered my queries, I learned more each time, despite my career-long interest and experience in neuropathology. She was masterful.

A Final Concern

My final concern is that, with Hannah’s passing, we may have lost not only the most gifted neonatal neuropathologist in our field, but perhaps also our recognition of neuropathology as the crucial, definitive modality to understand the disorders that we address now and in the future. My hope, one shared by Hannah, is that microscopic neuropathology, buttressed by modern methodologies, including advanced immunocytochemistry, molecular genetics, “omics” of all sorts, etc., will continue to be the cornerstone of our study of the newborn brain.

Joseph J. Volpe, MD

Department of Neurology, Boston Children’s Hospital

Bronson Crothers Professor of Neurology, Emeritus, Harvard Medical School

Boston MA

References

1. Kinney HC. Reflections on a Career in Pediatric Neuropathology, with a Note of Gratitude. Annu Rev Pathol 20:1-11, 2025. DOI: 10.1146/annurev-pathmechdis-111523-023355
2. Brody BA, Kinney HC, Kloman AS, Gilles FH. Sequence of central nervous system myelination in human infancy. I. An autopsy study of myelination. J Neuropathol Exp Neurol 46:283-301, 1987. DOI: 10.1097/00005072-198705000-00005
3. Kinney HC, Brody BA, Kloman AS, Gilles FH. Sequence of central nervous system myelination in human infancy. II. Patterns of myelination in autopsied infants. J Neuropathol Exp Neurol 47:217-34, 1988. DOI: 10.1097/00005072-198805000-00003
4. Haynes RL, Sleeper LA, Volpe JJ, Kinney HC. Neuropathologic studies of the encephalopathy of prematurity in the late preterm infant. Clin Perinatol 40:707-22, 2013. DOI: 10.1016/j.clp.2013.07.003
5. Volpe JJ, Kinney HC, Jensen FE, Rosenberg PA. The developing oligodendrocyte: key cellular target in brain injury in the premature infant. Int J Dev Neurosci 29:423-40, 2011. DOI: 10.1016/j.ijdevneu.2011.02.012
6. Haynes RL, Borenstein NS, Desilva TM, Folkerth RD, Liu LG, Volpe JJ, Kinney HC. Axonal development in the cerebral white matter of the human fetus and infant. J Comp Neurol 484:156-67, 2005. DOI: 10.1002/cne.20453
7. Billiards SS, Haynes RL, Folkerth RD, Borenstein NS, Trachtenberg FL, Rowitch DH, Ligon KL, Volpe JJ, Kinney HC. Myelin abnormalities without oligodendrocyte loss in periventricular leukomalacia. Brain Pathol 18:153-63, 2008. DOI: 10.1111/j.1750-3639.2007.00107.x
8. Volpe JJ. Dysmaturation of Premature Brain: Importance, Cellular Mechanisms, and Potential Interventions. Pediatr Neurol 95:42-66, 2019. DOI: 10.1016/j.pediatrneurol.2019.02.016
9. Back SA, Luo NL, Borenstein NS, Volpe JJ, Kinney HC. Arrested oligodendrocyte lineage progression during human cerebral white matter development: dissociation between the timing of progenitor differentiation and myelinogenesis. J Neuropathol Exp Neurol 61:197-211, 2002. DOI: 10.1093/jnen/61.2.197
10. Haynes RL, Billiards SS, Borenstein NS, Volpe JJ, Kinney HC. Diffuse axonal injury in periventricular leukomalacia as determined by apoptotic marker fractin. Pediatr Res 63:656-61, 2008. DOI: 10.1203/PDR.0b013e31816c825c
11. Kinney HC, Haynes RL, Xu G, Andiman SE, Folkerth RD, Sleeper LA, Volpe JJ. Neuron deficit in the white matter and subplate in periventricular leukomalacia. Ann Neurol 71:397-406, 2012. DOI: 10.1002/ana.22612
12. Andiman SE, Haynes RL, Trachtenberg FL, Billiards SS, Folkerth RD, Volpe JJ, Kinney HC. The cerebral cortex overlying periventricular leukomalacia: analysis of pyramidal neurons. Brain Pathol 20:803-14, 2010. DOI: 10.1111/j.1750-3639.2010.00380.x
13. Pierson CR, Folkerth RD, Billiards SS, Trachtenberg FL, Drinkwater ME, Volpe JJ, Kinney HC. Gray matter injury associated with periventricular leukomalacia in the premature infant. Acta Neuropathol 114:619-31, 2007. DOI: 10.1007/s00401-007-0295-5
14. Ligam P, Haynes RL, Folkerth RD, Liu L, Yang M, Volpe JJ, Kinney HC. Thalamic damage in periventricular leukomalacia: novel pathologic observations relevant to cognitive deficits in survivors of prematurity. Pediatr Res 65:524-9, 2009. DOI: 10.1203/PDR.0b013e3181998baf
15. Haynes RL, Folkerth RD, Keefe RJ, Sung I, Swzeda LI, Rosenberg PA, Volpe JJ, Kinney HC. Nitrosative and oxidative injury to premyelinating oligodendrocytes in periventricular leukomalacia. J Neuropathol Exp Neurol 62:441-50, 2003. DOI: 10.1093/jnen/62.5.441
16. Haynes RL, Folkerth RD, Trachtenberg FL, Volpe JJ, Kinney HC. Nitrosative stress and inducible nitric oxide synthase expression in periventricular leukomalacia. Acta Neuropathol 118:391-9, 2009. DOI: 10.1007/s00401-009-0540-1
17. Billiards SS, Haynes RL, Folkerth RD, Trachtenberg FL, Liu LG, Volpe JJ, Kinney HC. Development of microglia in the cerebral white matter of the human fetus and infant. J Comp Neurol 497:199-208, 2006. DOI: 10.1002/cne.20991
18. Haynes RL, Folkerth RD, Szweda LI, Volpe JJ, Kinney HC. Lipid peroxidation during human cerebral myelination. J Neuropathol Exp Neurol 65:894-904, 2006. DOI: 10.1097/01.jnen.0000235858.56631.97
19. Folkerth RD, Haynes RL, Borenstein NS, Belliveau RA, Trachtenberg F, Rosenberg PA, Volpe JJ, Kinney HC. Developmental lag in superoxide dismutases relative to other antioxidant enzymes in premyelinated human telencephalic white matter. J Neuropathol Exp Neurol 63:990-9, 2004. DOI: 10.1093/jnen/63.9.990
20. Desilva TM, Kinney HC, Borenstein NS, Trachtenberg FL, Irwin N, Volpe JJ, Rosenberg PA. The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter. J Comp Neurol 501:879-90, 2007. DOI: 10.1002/cne.21289
21. DeSilva TM, Borenstein NS, Volpe JJ, Kinney HC, Rosenberg PA. Expression of EAAT2 in neurons and protoplasmic astrocytes during human cortical development. J Comp Neurol 520:3912-32, 2012. DOI: 10.1002/cne.23130