• Brian T Andrews, Anna Lydick, Scott Barbay, Peter Reisz, and Randolph J Nudo.
• *Department of Plastic Surgery †Department of Rehabilitation Medicine, University of Kansas Medical Center, Kansas City, KS.
• J Craniofac Surg. 2016 Oct 1; 27 (7): 1875-1878.

BackgroundHemi-craniectomy is a common surgical procedure which allows the brain to swell and herniate and is often utilized to treat traumatic brain injury. When left untreated the scalp skin typically sinks on the side of the craniectomy creating a phenotype termed "sinking skin flap syndrome." In addition, these same patients often develop long-term neurocognitive deficits termed "syndrome of the trephined" as a result of their craniectomy which reverse when the cranial skull is replaced. The authors hypothesize that a mouse animal model can be developed demonstrating long-term neurologic deficits attributed to hemi-craniectomy skull defects similar to humans with syndrome of the trephined.MethodsThirty C57 mice were randomized among 3 groups: Group 1 = control group (sham surgery), Group 2 = hemi-craniectomy only, and Group 3 = hemi-craniectomy with immediate cranioplasty. Motor deficits were studied using a beam walk test. Statistical comparison of differences among the 3 groups was performed.ResultsBeam walk test results demonstrated the craniectomy group had a statistically higher contralateral footfault slip/step ratio when compared with the control group (P <0.05). Comparison of the control group and the cranioplasty group demonstrated contralateral footfault slip/step ratio that was statistically different for 7 days postoperative but no statistical differences thereafter. Comparison of the craniectomy group and the cranioplasty group demonstrated statistically significant differences for 14 days; however, motor deficits were not statistically different than baseline thereafter. No ipsilateral footfault deficits were detected in this study.ConclusionMotor deficits that are attributed to hemi-craniectomy bone defects alone are demonstrated in a mouse animal model. These motor deficits resemble some symptoms associated with human syndrome of the trephined.

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