Jeffrey S. Kuerbitz, MD, PhD

Dr. Kuerbitz is a board-certified Child Neurologist and Physician-Scientist with subspecialty training in clinical neurophysiology and pediatric electroencephalography (EEG). His clinical interests encompass pediatric epilepsy, developmental and epileptic

encephalopathies and quantitative EEG interpretation. He is a Child Neurology Career Development Program (CNCDP) K12 Scholar supported by the National Institute of Neurological Disorders and Stroke, with research dedicated to understanding the genetic and transcriptional mechanisms underlying neurodevelopmental disorders. His research program investigates transcriptional regulation of cerebellar inhibitory neuron development in EBF3-related Hypotonia, Ataxia, and Delayed Development (HADDS) syndrome and identifies electrographic biomarkers in KCNQ2-related developmental and epileptic encephalopathy.

Dr. Kuerbitz has been associated with Baylor College of Medicine and Texas Children's Hospital since completed his child neurology residency through the Basic Neuroscience Pathway, during which he joined the laboratory of Hsiao-Tuan Chao, MD, PhD. Under Dr. Chao's mentorship, he characterized the anatomical and behavioral consequences of Ebf3 loss in cerebellar inhibitory neurons and conducted transcriptomic analysis of patient fibroblasts to identify molecular mechanisms underlying HADDS syndrome. He then completed a subspecialty fellowship training here in clinical neurophysiology with a pediatric EEG emphasis.

Personal Statement

I am a physician-scientist dedicated to caring for children with epilepsy and neurodevelopmental disorders. I believe that meaningful clinical care is built on a foundation of trust, careful listening and honest communication. Families navigating complex neurological diagnoses face profound challenges, and I am committed to partnering with them closely, understanding their individual goals and circumstances, and providing evidence-based, personalized care that supports each child in reaching their full potential.

My research program is located at the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital. As a researcher, I am driven by the conviction that understanding the genetic and molecular mechanisms of disease is essential to improving outcomes for the patients I treat. My research and my clinical practice are deeply intertwined: the questions I encounter in clinic motivate my scientific work and the insights I gain in the laboratory inform how I approach diagnosis and treatment. My long-term goal is to translate emerging discoveries in neurodevelopmental neuroscience into meaningful advances for the children and families I serve.

Clinical Interests

Pediatric epilepsy; neurogenetics; clinical neurophysiology and electroencephalography (EEG); EBF3-related Hypotonia, Ataxia, and Delayed Development(HADDS) syndrome

Education

Organizations

Board Certification

Honors and awards

2026

K12 Scholar Child Neurology Career Development Program

2026

Epilepsy Exchange Young Researcher Award, Texas Medical Center

2026

Trainee Travel Scholarship, American Clinical Neurophysiology Society

2025

Taeun Chang Outstanding Junior Member Award, Child Neurology Society 

2024

Futures in Neurologic Research Scholarship Recipient, American Academy of Neurology

* Texas Children’s Hospital physicians’ licenses and credentials are reviewed prior to practicing at any of our facilities. Sections titled From the Doctor, Professional Organizations and Publications were provided by the physician’s office and were not verified by Texas Children’s Hospital.

Research interests

My work spans two complementary areas.

· First, I investigate the transcriptional mechanisms governing cerebellar inhibitory neuron development, with a particular focus onEBF3-related Hypotonia, Ataxia, and Delayed Development (HADDS) syndrome. Using mouse genetic models and transcriptomic analysis of patient-derived cell lines, I aim to identify the cellular pathways disrupted by pathogenic EBF3 variants and define targets for future therapeutic intervention.

· I study electrographic biomarkers in genetic epilepsies, with the goal of improving early diagnosis and informing prognosis.

Kuerbitz J., Madhavan M., Ehrman L.A., Kohli V., Waclaw R.R., Campbell K. Temporally Distinct Roles for the Zinc Finger Transcription Factor Sp8 in the Generation and Migration of Dorsal Lateral Ganglionic Eminence (dLGE)-Derived Neuronal Subtypes in the Mouse. Cerebral Cortex, 31(3):1744-17622021

Kuerbitz J., Arnett M., Ehrman S., Williams M.T., Vorhees C.V., Fisher S.E., Garratt A.N., Muglia L.J., Waclaw R.R., Campbell K. Loss of Intercalated Cells (ITCs) in the Mouse Amygdala of Tshz1 Mutants Correlates with Fear, Depression, and Social Interaction Phenotypes. Journal of Neuroscience, 38(5):1160-1177, 2018

Schmid C.M., Ruiz A., Bazus C.M., Herman I., Ammouri F., Kotzaeridou U., McNiven V., Dupuis L., Steindl K., Begemann A., Rauch A., Suter A.A., Isidor B., Mercier S., Nizon M., Cogné B., Deb W., Besnard T., Haack T.B., Falb R.J., Müller A.J., Linden T., Haldeman-Englert C.R., Ockeloen C.W., Mattioli F., Reymond A., Ibrahim N., Naz S., Lacaze E., Bassetti J.A., Hoefele J., Brunet T., Riedhammer K.M., Elloumi H.Z., Person R., Zou F., Kahle J., Cremer K., Schmidt A., Delrue M.A., Almeida P.M., Ramos F., Srivastava S., Quinlan A., Robertson S., Manka E., Küchler A., Spranger S., Nowaczyk M.J.M., Elshafie R.M., Alsharhan H., Hillman P.R., Dunnington L.A., Braakman H.M.H., McKee S., Moresco A., Ignat A.D., Newbury-Ecob R., Banneau G., Patat O., Kuerbitz J., Rzucidlo S., Sell S.S., Gordon P., Schuhmann S., Reis A., Halleb Y., Stoeva R., Keren B., Al Masseri Z., Tümer Z., Hammer-Hansen S., Sølyst S.K., Steigerwald C.G., Abreu N.J., Faust H., Müller-Nedebock A., Mau-Them F.T., Sticht H., Zweier C. A. Further delineation of the SCAF4-associated neurodevelopmental disorder. Eur. J. Hum. Genet. 33, 588–594 (2025).Saeed H., Sinha S., Mella C., Kuerbitz J., Cales M., Steele M., Stanke J., Damron D., Safadi F., Kuerbitz S. Aberrant epigenetic silencing of neuronatin is a frequent event in human osteosarcoma. Oncotarget, 11(20): 1876-1893, 2020