Original article

European Journal of Nuclear Medicine and Molecular Imaging

, 33:817

First online:

Loss of neuronal integrity: a cause of hypometabolism in patients with traumatic brain injury without MRI abnormality in the chronic stage

  • Tohru ShigaAffiliated withDepartment of Nuclear Medicine, Hokkaido University School of Medicine Email author 
  • , Katsunori IkomaAffiliated withDepartment of Rehabilitation, Hokkaido University,
  • , Chietsugu KatohAffiliated withDepartment of Tracer kinetics, Hokkaido University,
  • , Hirotaka IsoyamaAffiliated withDepartment of Rehabilitation, Hokkaido University,
  • , Tetsuaki MatsuyamaAffiliated withDepartment of Nuclear Medicine, Hokkaido University School of Medicine
  • , Yuji KugeAffiliated withDepartment of Tracer kinetics, Hokkaido University,
  • , Hiroyuki KageyamaAffiliated withDepartment of Nuclear Medicine, Hokkaido University School of Medicine
  • , Tomoya KohnoAffiliated withDepartment of Nuclear Medicine, Hokkaido University School of Medicine
  • , Satoshi TeraeAffiliated withDepartment of Radiology, Hokkaido University,
    • , Nagara TamakiAffiliated withDepartment of Nuclear Medicine, Hokkaido University School of Medicine

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Abstract

Purpose

Traumatic brain injury (TBI) causes brain dysfunction in many patients. However, some patients have severe brain dysfunction but display no abnormalities on magnetic resonance imaging (MRI). There have been some reports of hypometabolism even in such patients. The purpose of this study was to investigate the relationship between metabolic abnormality and loss of neuronal integrity in TBI patients with some symptoms but without MRI abnormalities.

Methods

The study population comprised ten patients with TBI and ten normal volunteers. All of the patients were examined at least 1 year after the injury. 15O-labelled gas PET and [11C]flumazenil (FMZ) positron emission tomography (PET) were carried out. The cerebral metabolic rate of oxygen (CMRO2) and binding potential (BP) images of FMZ were calculated. Axial T2WI, T2*WI and FLAIR images were obtained. Coronal images were added in some cases.

Results

All of the patients had normal MRI findings, and all showed areas with abnormally low CMRO2. Low uptake on BP images was observed in six patients (60%). No lesions that showed low uptake on BP images were without low CMRO2. On the other hand, there were 14 lesions with low CMRO2 but without BP abnormalities.

Conclusion

These results indicate that there are metabolic abnormalities in TBI patients with some symptoms after brain injury but without abnormalities on MRI. Some of the hypometabolic lesions showed low BP, indicating a loss of neuronal integrity. Thus, FMZ PET may have potential to distinguish hypometabolism caused by neuronal loss from that caused by other factors.

Keywords

Brain imaging PET MRI Flumazenil Traumatic brain injury