Late-onset neurocognitive deficits following traumatic brain injury: chronic traumatic encephalopathy (CTE) and psychotic disorder following TBI (PDF TBI)

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  • Takahata Keisuke
    Department of Molecular Neuroimaging Program, Molecular Imaging Center, National Institute of Radiological Sciences. Department of Neuropsychiatry, Keio University School of Medicine
  • Kato Motoichiro
    Department of Neuropsychiatry, Keio University School of Medicine
  • Mimura Masaru
    Department of Neuropsychiatry, Keio University School of Medicine
  • Shimada Hitoshi
    Department of Molecular Neuroimaging Program, Molecular Imaging Center, National Institute of Radiological Sciences.
  • Higuchi Makoto
    Department of Molecular Neuroimaging Program, Molecular Imaging Center, National Institute of Radiological Sciences.
  • Suhara Tetsuya
    Department of Molecular Neuroimaging Program, Molecular Imaging Center, National Institute of Radiological Sciences.

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  • 頭部外傷の分子イメージング: 慢性外傷性脳症 (CTE) と 頭部外傷後精神病 (PDFTBI) を中心に

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  Traumatic brain injury (TBI) can cause delayed-onset neurocognitive dysfunctions including such as chronic traumatic encephalopathy (CTE) and psychotic disorder following TBI (PDFTBI) . Initially, CTE was called punch-drunk syndrome since only athletes exposed to recurrent concussions in high-impact sports such as boxing were believed to develop such symptoms. However, it has been revealed that CTE can occur in the wider population including American football players, wrestlers, ice-hockey players and military persons. Pathologically, CTE is characterized by abnormal accumulations of tau proteins and less apparent amyloid-beta proteins, and definitive diagnosis of CTE can be made only at autopsy and no reli able biomarkers of CTE are available. PDFTBI is schizophrenia-like psychosis, which typically occurs several years after single severe TBI. About 3.4-8.9% of single-severe TBI patients develop PDFTBI in later life, and mean onset time after TBI is about 5 years. This temporal interval between onset of psychosis and time of head injury indicates that a neurodegeneration is involved in development of PDFTBI. Al though clinical subtypes associated these post-TBI syndromes are different, evidence suggest that single-severe and mild-repetitive TBI share similar neuropathological features. In this review, we discuss clinical characteristics of CTE and PDFTBI. Next, we describe how novel neuroimaging methods to detect tau and amyloid pathology improve diagnosis and prevention of post-TBI syndromes. Recent development of tau-selective radioligand such as［11C］PBB3 may be a powerful tool to detect tau pathology in the living brain of TBI patients.

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