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Understanding Syndrome of the Trephined: Development of a Novel Mouse Model
Jude Kluemper, BS
Bilan Yakoub, BS
Sabrina Almashni, BS
Abdulaziz Elemosho, MD
Taborah Z Zaramo, BS
Kerry-Ann S Mitchell, MD PhD
The Ohio State University College of Medicine
2024-01-15
Presenter: Jude Kluemper
Affidavit:
I certify that the work presented here is the original work of Jude Kluemper and members of the Mitchell lab. This work has not been presented at another major meeting.
Director Name: Gregory Pearson
Author Category: Medical Student
Presentation Category: Basic Science Research
Abstract Category: Craniomaxillofacial
Introduction: Syndrome of the Trephined (SoT) is a disorder characterized by neurological deterioration after a segment of the skull is removed. SoT lacks well-defined diagnostic criteria, with the main feature being neurologic improvement after the skull is repaired in a cranioplasty surgery. The aim of this study is to elucidate the underlying pathophysiology of SoT by evaluating neurologic dysfunction in a novel mouse model of decompressive craniectomy and cranioplasty after traumatic brain injury (TBI).
Methods: This study utilized a controlled cortical impact model of TBI. Cohorts of adult C57/BL6 mice underwent right-sided craniectomy with or without a TBI. In certain groups, the removed calvarial bone was cryopreserved and replaced in a cranioplasty surgery several weeks later. Behavioral testing was performed at various timepoints after craniectomy and cranioplasty to evaluate neurological function.
Results: Preliminary results indicate that prior to cranioplasty, mice who received a TBI had significantly more neurologic dysfunction compared to the control mice (p=0.004). After cranioplasty was performed, there was a trend toward improvement in neurologic functioning, although this was not significant. Notably, after cranioplasty, there was no longer a significant difference in neurologic function between the TBI mice and control mice (p = 0.08).
Conclusion: To our knowledge, this is the first report of an animal model of SoT following a neurologic insult. It is anticipated that these studies will lead to an increased understanding of the pathophysiology underlying SoT.
