Accession Number : ADA599905


Title :   Parallel Human and Animal Models of Blast- and Concussion-Induced Tinnitus and Related Traumatic Brain Injury (TBI)


Descriptive Note : Annual rept. 1 Jan-31 Dec 2013


Corporate Author : WAYNE STATE UNIV DETROIT MI


Personal Author(s) : Zhang, Jinsheng ; Cacace, Anthony ; Haacke, E M ; Berkowitz, Bruce ; Hu, Jiani ; Benson, Randall ; Woodward, John


Full Text : https://apps.dtic.mil/dtic/tr/fulltext/u2/a599905.pdf


Report Date : Jan 2014


Pagination or Media Count : 201


Abstract : Blast trauma causes onset and chronic tinnitus and hearing impairment in rats. The induced chronic tinnitus latter shifts to the high-frequency region. Blast also induces onset hyperactivity in the auditory brainstem, which later shifts to the auditory cortex. The induced tinnitus is accompanied by increased neuronal activity in limbic structures such as the amygdala and anterior cinculate cortex and by increased anxiety. Compared to concussion, blast exposure induces significant TBI as revealed by sustained astrogliosis and axonal injury in auditory brain centers. In patients with blast induced hearing loss and tinnitus, we show significant relations among hearing, psychometric, neuropsychological variables and neuroimaging related parameters; most notably metabolites and neurotransmitters and white matter tracks vis-a-vis the FA metric. Patients with blast-induced hearing loss and tinnitus had slowed reaction time, increased reaction time variability, and lower accuracy that may be associated with difficulty inhibiting attention to distracting tinnitus signals. Several aspects of processing speed and delayed incidental are associated with tinnitus severity.


Descriptors :   *AUDITORY DEFECTS , *DEAFNESS , *NERVE CELLS , *NEUROLOGY , *TRAUMATIC BRAIN INJURIES , AUDITORY NERVE , BLAST , METABOLITES , NERVE FIBERS , NEUROPHYSIOLOGY , NEUROTRANSMITTERS , NOISE , PATIENTS , TRAUMA , WOUNDS AND INJURIES


Subject Categories : Medicine and Medical Research
      Stress Physiology


Distribution Statement : APPROVED FOR PUBLIC RELEASE