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P4‐141: Clinical and pathologic phenotype of dementia after traumatic brain injury (TBI)
Author(s) -
Sayed Nasreen,
DiazArrastia Ramon
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.2163
Subject(s) - dementia , traumatic brain injury , chronic traumatic encephalopathy , irritability , medicine , depression (economics) , mood , psychiatry , psychology , disease , concussion , poison control , injury prevention , anxiety , environmental health , economics , macroeconomics
athy, inertia, emotional blunting, dietary changes and self neglect. The two others, aged 52 and 60 at onset, rapidly developed severe behavioral troubles with disinhibition and compulsive behavior at foreground. They died 3 and 5 years later respectively. Although patients had various combinations of vascular risk factors their brain MRI only showed mild vascular modifications. There was neither significant frontotemporal atrophy nor hypometabolism. Pathological examination showed isolated chronic ischemic changes: severe arteriolosclerosis, perivascular spaces dilatations and microinfarcts in the frontal white matter and basal ganglia, and moderate myelin loss. Conclusions: These three cases illustrate that isolated subcortical microvascular pathology may underlie atypical presentation of bvFTD including the long lasting, slowly progressive variant. These observations also support the revised diagnosis criteria for bvFTD (international bvFTD criteria consortium, 2010) which require both functional decline and imaging results consistent with bvFTD to meet criteria for a probable diagnosis.