Jose G. Merino, MD, MPhil

Disclosures

June 11, 2014

In This Article

Hot Topics at the Podium

Every year, one of the most interesting sessions at the meeting of the American Academy of Neurology is the "Hot Topics" plenary. For this session, the Science Committee selects 4 researchers whose work bridges the laboratory, clinical, and public health spheres, and has a major impact on how we study, diagnose, conceptualize, or treat neurologic conditions. The variety of topics discussed by the speakers only highlights the richness of the field of neurology.

Chronic Traumatic Encephalopathy

Traumatic brain injury is among the major contributors to the global neurologic burden of disease. Some patients with mild to moderate brain injury recover, others develop chronic stable symptoms (postconcussion syndrome), and still others have the progressive behavioral and cognitive changes of chronic traumatic encephalopathy (CTE) that lead to dementia. Recent research has shed some light on the pathologic substrate of these phenotypic manifestations, but as Dennis Dickson, MD, Professor of Laboratory Medicine & Pathology at the Mayo Clinic in Jacksonville, Florida, reminded us in his talk,[1] this field of research is still in its infancy.

The prevalence of CTE is unknown, but according to data from the Mayo brain bank, Dr. Dickson estimates that it could be as high as 20% in male athletes involved in contact sports. CTE is a chronic and progressive disorder characterized neuropathologically by the accumulation of hyperphosphorylated tau. In the earliest stages of the disease, tau deposits are found in the deep layers of the sulci of the frontal neocortex, but as clinical and pathologic severity increase, neurofibrillary tangles involve other brain areas, including the insula, temporal lobe, amygdala, hippocampus, and subcortical structures.[2]

The clinical manifestations of CTE are variable, but Ann McKee and her group at Boston University have identified 2 phenotypes: The first is characterized by early behavioral and mood changes, and the second by prominent cognitive impairment that progresses to dementia. It is unclear what factors determine the phenotype in each individual.[3]

The lack of definitive neuropsychological, clinical, and neuropathologic criteria hampers developments in the field. Several groups are working to develop serum, cerebrospinal fluid, and imaging biomarkers to study CTE in vivo. Techniques under study include diffusion tensor imaging to evaluate changes in the white matter, functional MRI to assess changes in neuronal networks, and tau PET to identify molecular markers that will allow localization and identification of the spread of the pathology and differentiation of CTE from other tauopathies.[4]

In 2010, researchers at Boston University reported an intriguing association between CTE and amyotrophic lateral sclerosis (ALS).[5] Using samples from the Mayo brain bank, Dr. Dickson found that 5 of 61 patients with ALS also had changes suggestive of stage II CTE in the brain. This is an intriguing association and could represent more than a coincidental link. Could trauma precipitate the pathologic changes in some patients with clinical ALS? Prospective studies to explore this possibility are ongoing.

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