Evaluation of the resting cerebellum in blast induced mild traumatic brain injury: differences between perfusion and metabolic findings. of the resting cerebellum in blast induced mild traumatic brain injury: differences between perfusion and metabolic findings.

Objectives: Blast induced traumatic brain injury has been shown to uniquely induce cerebellar pathology. There are perfusion/metabolic differences in the normal human cerebellum during resting conditions. Specifically, there is much greater perfusion with relatively lower glucose extraction rates. The objective is to compare the ability of F18-FDG-PET versus Tc99m-HMPAO perfusion SPECT to detect cerebellar abnormalities in a blast induced mild traumatic brain injury patients.

Methods: As part of a core neuroimaging protocol of traumatic brain injury, 12 patients with subacute traumatic brain injury (mean time since injury 40.75 +/- 28.27 days, range 17-89 days) were evaluated with F-18 FDG PET, Tc99m -HMPAO perfusion SPECT and MRI imaging (1.5T; minimum sequences: T1, T2, DWI, FLAIR and GRE). Functional imaging was performed at rest with minimization of external stimuli. Of these patients, four had a normal brain MRI study determined visually by a board certified Neuroradiologist. The SPECT and PET images were evaluated visually by a board certified Nuclear Medicine Physician. Additionally, activity in the patient PET and SPECT studies was compared voxel by voxel with the activity in normal templates after count value normalization by the ratio of the total counts over the whole VOI set, focusing on detectable abnormalities in the cerebellar hemispheres.

Results: Four male, right handed patients, age ranging 21-36 years of age study patients had a normal brain MRI. Three of the four patients demonstrated cerebellar abnormalities on F18 FDG PET visually and had cerebellar regional activity at least two standard deviations under the normal. One patient did not demonstrate cerebellar abnormalities by visual analysis; however did have region activity one standard deviation under the normal. There were no corresponding cerebral cortical findings to indicated crossed cerebellar diaschesis as the etiology of cerebellar hypometabolism. Additionally, the findings were of sufficient volume to discount special resolution as the etiology of the imaging discrepancies. None of the four patients demonstrated detectable abnormalities in the cerebellum on SPECT perfusion imaging either visually or statistically when compared to a normal database.

Conclusion: Imaging findings within this limited cohort suggest F18 FDG-PET imaging is more sensitive for detecting cerebellar abnormalities following blast induced traumatic brain injury, potentially secondary to normal differences in cerebellar perfusion and glucose metabolism. Research Support: Peskind ER et al; Cerebrocerebellar hypometabolism associated with repetitive blast exposure mild traumatic brain injury in 12 Iraq war Veterans with persistent post-concussive symptoms. Neuroimage: 2011 Jan; 54 Suppl 1:S76-82. Meabon et al; Repetitive blast exposure in mice and combat veterans causes persistent cerebellar dysfunction. Sci Transl Med: 2016 Jan; Vol 8 Issue 321:1-15. Mac Donald et al; Cerebellar White Matter Abnormalitites following Primary Blast Injury in US Military Personnel. PLOS ONE: 2013 Feb; Vol 8 Issue2: 1-8. Sakamoto S, Ishii K; Low cerebral glucose extraction rates in the human medial temporal cortex and cerebellum. J Neurol Sci 172 (2000) 41 - 48. Holman et al; Biodistribution, Dosimetry, and Clinical Evaluation of Technetium-99m Ethyl Cysteinate Dimer in Normal Subjects and in Patients with Chronic Cerebral Infarction. J Nucl Med 20:1018-1024, 1989. Vallabhajosula et al; Technetium-99m ECD: A New Brain Imaging Agent: In Vivo Kinetics and Biodistribution Studies in Normal Human Subjects. J Nucl Med 30:599-604, 1989.