title: Pathology of the Superior Colliculus in Chronic Traumatic Encephalopathy.
abstract: To investigate neuropathological changes in the superior colliculus in chronic traumatic encephalopathy.
  
  
  
  The densities of the tau-immunoreactive neurofibrillary tangles, neuropil threads, dot-like grains, astrocytic tangles, and neuritic plaques, together with abnormally enlarged neurons, typical neurons, vacuolation, and frequency of contacts with blood vessels, were studied across the superior colliculus from pia mater to the periaqueductal gray in eight chronic traumatic encephalopathy and six control cases.
  
  
  
  Tau-immunoreactive pathology was absent in the superior colliculus of controls but present in varying degrees in all chronic traumatic encephalopathy cases, significant densities of tau-immunoreactive neurofibrillary tangles, NT, or dot-like grains being present in three cases. No significant differences in overall density of the tau-immunoreactive neurofibrillary tangles, neuropil threads, dot-like grains, enlarged neurons, vacuoles, or contacts with blood vessels were observed in control and chronic traumatic encephalopathy cases, but chronic traumatic encephalopathy cases had significantly lower mean densities of neurons. The distribution of surviving neurons across the superior colliculus suggested greater neuronal loss in intermediate and lower laminae in chronic traumatic encephalopathy. Changes in density of the tau-immunoreactive pathology across the laminae were variable, but in six chronic traumatic encephalopathy cases, densities of tau-immunoreactive neurofibrillary tangles, neuropil threads, or dot-like grains were significantly greater in intermediate and lower laminae. Pathological changes were not correlated with the distribution of blood vessels.
  
  
  
  The data suggest significant pathology affecting the superior colliculus in a proportion of chronic traumatic encephalopathy cases with a laminar distribution which could compromise motor function rather than sensory analysis.
authors.affiliation: *DPhil †MD ‡PhD Vision Sciences, Aston University, Birmingham, United Kingdom (RAA); Department of Pathology and Laboratory Medicine, VA Boston Healthcare System, Boston, Massachusetts (ACMc); Departments of Neurology and Pathology, Boston University School of Medicine, Boston, Massachusetts (ACMc); and Departments of Neurology and Pathology & Immunology, Washington University School of Medicine, St. Louis, Missouri (NJC).
authors.forename: Richard A
authors.initials: RA
authors.lastname: Armstrong
authors.forename: Ann C
authors.initials: AC
authors.lastname: McKee
authors.forename: Nigel J
authors.initials: NJ
authors.lastname: Cairns
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000070627:Chronic Traumatic Encephalopathy / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D016874:Neurofibrillary Tangles / Q000378:metabolism; D009474:Neurons / Q000473:pathology; D013477:Superior Colliculi / Q000378:metabolism / Q000473:pathology*; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016875:tau Proteins