For concussion sufferers, a brain scan may warn it’s time to call it quits
To date, no living person has gotten a definitive diagnosis of chronic traumatic encephalopathy - the constellation of cognitive and psychiatric symptoms that appears to result from repeated blows to the head. The definition of the disease itself remains a work in progress, and its key physical hallmark - abnormal protein tangles scattered throughout the brain - has been seen only postmortem, in the autopsied brains of oft-concussed former athletes who died in various states of dementia, or by suicide.
New research may allow CTE to be diagnosed in the living. The new findings still need to be borne out by larger studies. But they raise the prospect that a simple brain scan could provide athletes and others who risk further brain injury early warning that damage with long-term consequences has already been done.
With early detection, patients might take steps to protect their brains from further injury, or get help to anticipate or head off CTE’s worst symptoms. As treatments are proposed, the authors added, such scans might also be used to help measure their effectiveness.
The new research, published Monday in the journal PNAS, sheds further light on the progression of a disease that is presumed to be degenerative. The study’s authors - neuroscientists and radiologists from UCLA, UC Davis and the University of Chicago - describe in former athletes with presumed CTE a pattern of abnormal protein deposits in the brain that is distinct from those seen in Alzheimer’s disease and motor neuron disease. While the behavioral symptoms of these disorders overlap with those of CTE, the new study suggests that they are very different afflictions.
In the new study, Positron Emission Tomography, or PET, scans of 14 former football players reveal patterns of tau protein deposits and neurofibrillary tangles in the brain that ranged from localized to extensive. The locations and extent of these abnormalities are seen to track with the severity of those retired athletes’ symptoms of depression, anxiety and intellectual impairment.
The retired football players ranged in age from 40 to 86, and all but one - a 64-year-old former quarterback - had some combination of cognitive impairment and anxiety or depression. While a quarterback, running back and wide receiver were among the 14 subjects, most had played positions on football’s offensive and defensive lines, where, in addition to blows that caused concussions, they would have been subject to regular, less-forceful impacts.
Those former athletes’ PET scans were compared with those of 28 control subjects with no evidence of neuropsychiatric problems and of 24 subjects with Alzheimer’s disease.
Compared with normal control subjects, all of the former athletes showed abnormal deposits of tau protein in their brains. Those who protein clumps were found only in the brainstem and the amygdala - a walnut-shaped structure deep in the brain that is key in processing strong emotions - generally had the mildest neuropsychiatric symptoms. Subjects who had tau deposits throughout a greater range of the brain’s innermost structures (the amygdala and medial temporal lobe, the hippocampus, key to memory, the entorhinal cortex and parahippocampal gyrus) had more pronounced symptoms.
Subjects who had more, and more extensive, tau protein deposits in those areas and in “gray matter” areas like the parietal lobes were found to have more sever symptoms of cognitive impairments, depression or anxiety. And those with the most extreme symptoms were found to have tau protein bundles throughout their brain’s deep structures, their gray matter, and the white matter that forms highways between the brain’s two hemisphere and among regions that perform different functions.
In a few of the former football players, the researchers saw some evidence of Alzheimer’s disease’s hallmark beta-amyloid plaques. But the researchers noted that those distinctive abnormalities tended to be most notable in the oldest subjects, suggesting either that their brains had come under separate attack from Alzheimer’s, or that the accumulation of beta-amyloid plaques represented a final stage of CTE.
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