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Chronic Traumatic Encephalopathy

Chronic Traumatic Encephalopathy. Barry D. Jordan M.D., M.P.H. Assistant Medical Director Burke Rehabilitation Hospital Associate Professor of Clinical Neurology Weill Cornell Medical College of Cornell University Chief Medical Officer New York State Athletic Commission

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Chronic Traumatic Encephalopathy

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  1. Chronic Traumatic Encephalopathy Barry D. Jordan M.D., M.P.H. Assistant Medical Director Burke Rehabilitation Hospital Associate Professor of Clinical Neurology Weill Cornell Medical College of Cornell University Chief Medical Officer New York State Athletic Commission NFL Players Association Mackey-White Traumatic Brain Injury (TBI) Committee National Collegiate Athletic Association (NCAA) Concussion Task Force

  2. Chronic Traumatic Brain Injury • Long term consequences of traumatic brain injury • Chronic traumatic encephalopathy (CTE) • Dementia pugilistica • Chronic postconcussion syndrome (CPCS) • Posttraumatic dementia • Posttraumatic cognitive impairment • Posttraumatic parkinsonism

  3. Epidemiology • Estimated that 17% of boxers will exhibit CTE • Frequency in other sports is unknown

  4. Putative Risk Factors • Increased Exposure • Late age of retirement • Long duration of career • Increasing number of bouts • Poor performance • Sluggers and non-scientific boxers • Difficult to knockout • Multiple concussions • Subconcussive impacts • Apolipoprotein E (APOE) ε4

  5. CLINICAL PRESENTATION • COGNITIVE • MOTOR • BEHAVIORAL or PSYCHIATRIC • NEUROENDOCRINE

  6. Cognitive • Early • Decreased complex attention • Middle • Mild deficits in memory, attention, and executive function • Late • Dementia, prominent slowness of thought, amnesia, andexecutive dysfunction

  7. Motor • Dysarthria, scanning speech • Incoordination, ataxia • Spasticity • Tremors, parkinsonism • Motor neuron disease

  8. CTBI/Motor Neuron Disease • McKee et al. 2010 • Reported on 12 cases of CTE and noted that 3 cases also had a progressive motor neuron disease • 2 football players who played 27 and 16 years • 1 boxer who boxed 10 years • Signs and symptoms include progressive muscle atrophy, weakness, spasticity, diffuse fasciculations, hyperreflexia, and speech impairment

  9. Behavioral/Psychiatric • Emotional lability • Irritability • Inappropriate violent outbursts • Disinhibited/poor impulse control

  10. Behavioral/Psychiatric • Substance abuse • Euphoria/hypomania • Risk taking behavior • Psychotic, paranoid • Impaired insight • Depression • Suicidal

  11. Neuroendocrine • Tanriverdi et al (2008) • Assessed pituitary function in 61 active and 17 retired male boxers of the Turkish National Team • 9/61 (15%) growth hormone deficiency • 5/61 (8%) ACTH • 8/ 17 (47%) retired boxers had GH deficiency

  12. Diagnostic Evaluation • Clinical history • Neurological examination • Neuropsychological testing • Laboratory testing • Electrophysiological testing • Neuroimaging

  13. Neuroimaging • Traditional structural neuroimaging • CT • MRI • Newer structural neuroimaging • DTI • Functional and metabolic scanning • SPECT • PET • MRS • fMRI

  14. Neuroimaging Cavum septum pellucidum (CSP) Diffuse atrophy Ventricular dilitation ? White matter changes

  15. FDDNP-PET • Small et al. 2013 • 5 retired NFL players with mood and cognitive symptoms c/w 5 controls • FDDNP-PET to measure tau and amyloid • Higher signals were located in the amygdala and subcortical regions • Caudate • Putamen • Thalamus • Subthalamus • Midbrain • Cerebellar white matter

  16. Pathology • Cerebellar atrophy/scarring • Degeneration of the substantia nigra • Diffuse atrophy and ventricular dilitation • Atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies and brainstem • CSP • Thinning of the hypothalamic floor

  17. Histopathology • Although it appears to be a distinct entity it shares common histopathological features with Alzheimer’s Disease (AD) and Frontotemporal Dementia (FTD) • Tau • Amyloid • TDP-43

  18. Management of CTE • Cognitive • Behavioral • Motor • ? Headache • ? Neuroendocrine

  19. Conclusions Cumulative effects of concussion represents a serious concern in sports True prevalence is unknown Increased exposure is an important risk factor for CTE However the exposure threshold is unknown (How many concussions are too many?) Genetics may play a role

  20. Conclusions • CTE is a distinct clinical entity that shares characteristics with other neurodegenerative disorders such as AD, FTD +/- MND

  21. Conclusions Definitive diagnosis can only be made postmortem and the antemortem diagnosis can be difficult (can’t attribute all neurological conditions in an athlete exposed to repetitive concussion to CTE) Newer diagnostic technologies may provide supportive evidence

  22. THANK YOU QUESTIONS?

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