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Comment & Response
November 27, 2017

Sensitivity to the Deficits Associated With Traumatic Brain Injury or Chronic Traumatic Encephalopathy

Author Affiliations
  • 1University of Central Florida, Orlando Veterans’ Affairs Medical Center, Lake Nona, Orlando
JAMA Neurol. Published online November 27, 2017. doi:10.1001/jamaneurol.2017.3569

To the Editor The cognitive and depression outcomes observed between football players and nonplaying counterparts by Deshpande et al1 are not surprising. Traumatic brain injury (TBI) has a predilection of the frontotemporal lobes and associated circuitry that are relatively “blind” to standard neuropsychological testing (NPT) and often neuropsychiatric assessments, including depression. Several influential neurological cases published during the last century have repeatedly alerted clinicians to the dramatic cognitive and behavioral dissociation after frontal lobe lesions. The Boston Crow Bar case and several frontal lobe patients emphasized the profound behavioral impairments in the context of otherwise normal NPT. Arnold Pick’s frontotemporal (FT) dementia variant description noted primarily disinhibition and abulia, not cognitive impairment. Single TBI, repetitive TBI, and chronic traumatic encephalopathy, have been shown to directly cause FT dementia and TAR DNA binding protein 43 proteolysis.2 The neuropathological data were discerning, with chronic traumatic encephalopathy diagnosed in 99% of National Football League players.3

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