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Levy Place, New York, NY 10029 USA. Levy Place, New York, NY 10029 USA. Currently, the diagnosis of CTE can only be definitively established postmortem. Here we report a 39 year old retired National Football League player who suffered 22 concussions and manifested progressive neuropsychiatric symptoms. Emotional lability and irritability were the chief complaints. Serial neuropsychological exams revealed a decline in executive functioning, processing speed and fine motor skills. Naming was below average but other cognitive functions were preserved. Structural analysis of longitudinally acquired magenetic resonance imaging scans revealed cortical thinning in the left frontal and lateral temporal areas, as well as volume loss in the basal ganglia. CTE is characterized neuropathologically by progressive deposition of neurofibrillary tangles of hyperphosphorylated tau.4 Amyloidosis is a less consistent feature, present in only half of the cases of CTE examined at postmortem. The tauopathy shows a particular perivascular, sulcal, and neocortical distribution, distinguishing CTE from AD and other tauopathies.4, 7, 8 CTE also involves widespread axonal disruption, with eventual degeneration of the neocortex, hippocampus and other limbic structures, and basal forebrain.7, 9 Clinically, individuals with CTE can display symptoms that overlap with those seen in AD, such as impairments in memory and executive function, but, in contrast to AD, CTE is more frequently characterized by irritability, emotional lability, aggression, impulsivity, suicidality and substance abuse.7, 10, 11 Changes in mood and behavior typically precede cognitive decline in CTE, although clinical presentation is highly variable.7, 11Although individuals with CTE are at risk for severe functional impairment as well as disabling and life threatening behavioral disturbances; currently, the oakley prescription glasses expensive disease can only be definitively diagnosed at postmortem.11 Because of this limitation, the discovery of reliable and valid body fluid and neuroimaging biomarkers is crucial to developing diagnostic specificity and identifying the underlying pathology in order to track and treat these individuals during life. Current estimates of prevalence based solely on neuropsychological exams or solely on neuropathology are each inherently susceptible to certain biases that could be mitigated with a reliable molecular biomarker. Currently, little is known about the progression of CTE pathology in vivo. Attempts to detect CTE in living individuals have been challenging. Clinical symptoms are often based on the retrospective reports of family members after the loss of a loved one with suspected pathology, and common signs overlap with those seen in other neurodegenerative disorders.7, 12 Standard neuroimaging often reveals no gross lesions.13 However, neuropsychological testing can detect subtle changes in cognition, and recent studies of retired athletes with a history of concussions have revealed focal impairments in episodic memory,14, 15, 16 executive function,14 naming15 and semantic fluency.16 In addition, the identification of biomarkers, such as levels of serum and cerebrospinal fluid (CSF) tau17, 18 and CSF neurofilament proteins,18 have shown promise in detecting peripheral changes that may appear when CTE or other tauopathy is present. Although studies examining blood and CSF levels of tau and other neuronal injury markers after acute TBI have been mixed (for reviews see refs 19, 20), a recent study of professional hockey players showed that total serum level of tau increased after concussion and was correlated with clinical outcome.17 Structural imaging can also aid in the diagnosis of CTE. Studies using diffuse tensor imaging have shown that diffusion abnormalities, representing microstructural white matter damage, may be associated with repetitive TBI (reviewed in ref. 13). In addition, a handful of cross sectional magnetic resonance imaging (MRI) studies showing ventricular enlargement and cortical thinning after mild TBI,21 including in childhood athletes,22 retired professional athletes16 and military veterans,23, 24 appear to support postmortem findings. However, we are unaware of any longitudinal studies that have examined structural changes in MRI in individuals with a history of repetitive mild TBI. Molecular imaging is also a promising tool in detecting CTE pathology in vivo. In addition, in vivo detection of brain deposits of tau, the hallmark of CTE, is now possible through the use of novel positron emission tomography (PET) radiotracers. In particular, the presence of perivascular tauopathy at the depths of the cerebral cortical sulci has been determined to be pathognomonic for CTE by a recent National Institute on Neurological Diseases and Stroke (NINDS) neuropathology.4 We also present longitudinal neuropsychological and structural MRI data revealing patterns that may aid in understanding disease progression and further inform the development of diagnostic criteria. Top of pageMaterials and methodsClinical and experimental structural brain imagingThe 2011 MRI was obtained on a 3 Tesla Siemens Verio MR system (Siemens Medical Solutions, Erlangen, Germany) at a Quest Imaging Center. Processing of individual time points included removal of non brain tissue, automated Talairach transformation and intensity normalization, and detection of gray matter matter and gray matter fluid boundaries. Cortical thickness was calculated as the distance between these tissue boundaries (white matter and pial surfaces). Reconstruction was performed with a 400 matrix utilizing iterative reconstruction, with 24 subsets and 4 iterations. The z axis filter was standard, summed images 5.0 full width maximum Gaussian filter was used. The field of view was 50 in diameter, with 74 total slices. In addition, mean PET intensity values were derived from subcortical region of interests defined by the Harvard subcortical structural atlas and the Talairach atlas. In accordance with the standard practice of tauopathy PET, regional SUVrs were calculated using the cerebellar cortex as a reference region.27, 37 Top of pageResultsClinical presentationA 39 year old retired professional football player sustained 22 concussions, four of which resulted in loss of consciousness, during an 11 year career as an NFL player (Figure 1). He presented with complaints of irritability, emotional lability and cognitive decline. Following an informed consent process approved by the local institutional review board, he was evaluated at ISMMS in 2015 as part of a larger study comparing individuals with a history of multiple concussions to healthy controls and individuals with mild cognitive impairment with no concussion history. He also released to ISMMS investigators the medical records from his 2010 evaluation at the Boston University Center for Traumatic Encephalopathy. 1989 high school football. 1995 college football. 1999 National Football League. The last concussion from the 2009 season was incurred in 2010. Full figure and legend (36K) Concussion history was determined based on an in depth interview performed in 2010 by a neurologist specializing in TBI and CTE. An abbreviated version of the Brain Injury Screening Questionnaire38 was administered in 2015 and corroborated the 2010 report. Detailed information was obtained about reported concussions, including their approximate date, descriptions of the events, and the nature and duration of immediate post concussion symptoms (for example, confusion, disorientation, retrograde and anterograde amnesia, loss of consciousness). Total number of games played was also recorded, as this information may reflect history of exposure to subconcussive impacts (Figure 1). Concussions were classified according to guidelines developed by the American Academy of Neurology.39On the basis of these criteria, the evaluators determined that the patient experienced 22 concussive events, 20 of which were Grade II, one Grade I, and one Grade III. Four of the concussive events resulted in loss of consciousness. The last recorded concussion occurred 9 months before the 2010 neuropsychological testing. Detailed neurological examinations were conducted in 2010 and 2015 and were normal. In addition to memory complaints, the subject also reported numerous behavioral and functional symptoms such as increased agitation, irritability, impulsivity, migraine headaches, sleep disturbances, and increased sensitivity to noise. At the time of the 2010 evaluation, he reported experiencing feelings of being slowed cognition, headache irritability, poor concentration, and sensitivity to light. In the 2015 evaluation in clinical interview, the most prominent symptom was irritability. He also reported depression oakley prescription glasses edinburgh that occurred within the last 2 years and anxiety. The Beck Depression Inventory from 2015 was 24, indicating moderate depression. The Neuropsychiatric Inventory was completed in 2015 by his wife who endorsed severe irritability, moderate agitation depression disinhibition and sleep disturbance and mild delusional beliefs, anxiety and elation. His Clinical Dementia Rating (CDR) from 2015 was 0.5 and mild problems with memory, judgment and problem solving, community affairs and home and hobbies were endorsed. Premorbid intelligence, assessed by the Wide Range Achievement Test, was estimated to be in the superior range. Using available norms, neuropsychological tests, both from current assessment and previous testing identified in the medical records, were reported as z scores. Using this method, comparison of scores from 2010 to 2015 showed a decline in executive functioning, processing speed and fine motor function (Table 1). Additional tests given only in 2015 showed below average performance only in lexical retrieval. Performance was average or above average for long and short term verbal memory, working memory and semantic fluency, despite self reported severe impairment with working memory and distractibility. Both the 2011 and the 2015 MRI were evaluated by a neuroradiologist and were read clinically as within normal limits with no obvious atrophy or lesions. Comparison of 2011 and 2015 MRI scans also showed a negative trend with respect to volume of deep gray matter structures, with the largest decreases seen in the basal ganglia (globus pallidus, putamen and nucleus accumbens). Increases in volume were found in bilateral lateral ventricles and in summed left hemisphere Virchow spaces (Figure 3). Map of cortical thinning across the brain hemispheres are presented with dark gray regions representing sulci and light gray regions representing gyri. The top panel displays changes in thickness from 0 to 5 with no cutoff.

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