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Transl Psychiatry. 2014 Sep 16;4:e441. doi: 10.1038/tp.2014.91.

Tauopathy PET and amyloid PET in the diagnosis of chronic traumatic encephalopathies: studies of a retired NFL player and of a man with FTD and a severe head injury.

Author information

1
1] Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA [2] Mount Sinai's Alzheimer's Disease Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA [3] James J. Peters VA Medical Center, Bronx, NY, USA.
2
1] Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA [2] James J. Peters VA Medical Center, Bronx, NY, USA [3] Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA [4] The NFL Neurological Program, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
3
Department of Nuclear Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
4
1] Mount Sinai's Alzheimer's Disease Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA [2] Fishberg Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
5
Department of Radiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
6
Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
7
Institute for Neurodegenerative Disorders, Yale University, New Haven, CT, USA.
8
Department of Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
9
Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
10
Department of Neurology, University of Virginia, Charlottesville, VA, USA.
11
1] Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA [2] James J. Peters VA Medical Center, Bronx, NY, USA [3] Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
12
1] The NFL Neurological Program, Icahn School of Medicine at Mount Sinai, New York, NY, USA [2] Department of Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
13
1] Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA [2] Mount Sinai's Alzheimer's Disease Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA [3] James J. Peters VA Medical Center, Bronx, NY, USA [4] Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA [5] The NFL Neurological Program, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Abstract

Single, severe traumatic brain injury (TBI) which elevates CNS amyloid, increases the risk of Alzheimer's disease (AD); while repetitive concussive and subconcussive events as observed in athletes and military personnel, may increase the risk of chronic traumatic encephalopathy (CTE). We describe two clinical cases, one with a history of multiple concussions during a career in the National Football League (NFL) and the second with frontotemporal dementia and a single, severe TBI. Both patients presented with cognitive decline and underwent [(18)F]-Florbetapir positron emission tomography (PET) imaging for amyloid plaques; the retired NFL player also underwent [(18)F]-T807 PET imaging, a new ligand binding to tau, the main constituent of neurofibrillary tangles (NFT). Case 1, the former NFL player, was 71 years old when he presented with memory impairment and a clinical profile highly similar to AD. [(18)F]-Florbetapir PET imaging was negative, essentially excluding AD as a diagnosis. CTE was suspected clinically, and [(18)F]-T807 PET imaging revealed striatal and nigral [(18)F]-T807 retention consistent with the presence of tauopathy. Case 2 was a 56-year-old man with personality changes and cognitive decline who had sustained a fall complicated by a subdural hematoma. At 1 year post injury, [(18)F]-Florbetapir PET imaging was negative for an AD pattern of amyloid accumulation in this subject. Focal [(18)F]-Florbetapir retention was noted at the site of impact. In case 1, amyloid imaging provided improved diagnostic accuracy where standard clinical and laboratory criteria were inadequate. In that same case, tau imaging with [(18)F]-T807 revealed a subcortical tauopathy that we interpret as a novel form of CTE with a distribution of tauopathy that mimics, to some extent, that of progressive supranuclear palsy (PSP), despite a clinical presentation of amnesia without any movement disorder complaints or signs. A key distinguishing feature is that our patient presented with hippocampal involvement, which is more frequently seen in CTE than in PSP. In case 2, focal [(18)F]-Florbetapir retention at the site of injury in an otherwise negative scan suggests focal amyloid aggregation. In each of these complex cases, a combination of [(18)F]-fluorodeoxyglucose, [(18)F]-Florbetapir and/or [(18)F]-T807 PET molecular imaging improved the accuracy of diagnosis and prevented inappropriate interventions.

PMID:
25226550
PMCID:
PMC4203018
DOI:
10.1038/tp.2014.91
[Indexed for MEDLINE]
Free PMC Article

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