Tinnitus and hearing loss and changes in hippocampus

Approximately 12 to 14% of adults experience tinnitus and prevalence estimates for tinnitus in children range from 12 to 37% in those with normal hearing and up to 66% with those with hearing loss. Approximately 1% of patients suffer from debilitating tinnitus that requires clinical treatment or intervention. The neural mechanisms responsible for tinnitus, however, remain elusive. Because tinnitus is often associated with cochlear hearing loss, the phantom sound of tinnitus was traditionally believed to originate in the cochlea. More recently, modern brain imaging methods employing positron emission tomography have identified regions in the central auditory pathway (auditory cortex, medial geniculate body) and limbic system (hippocampus) that are activated when patients with somatic tinnitus voluntarily change the loudness of the phantom sound by moving the face, jaw, or upper torso. Somatic tinnitus appears to develop as a function of somatosensory system invasion of the deafferented (deafened) regions of the auditory cortex. Additionally, the involvement of the hippocampus in tinnitus gains further credence from structural imaging studies that reveal a significant decrease in hippocampal gray matter in tinnitus patients. The hippocampus, a structure involved with memory, mood, and spatial navigation, is a major site of neurogenesis in the adult brain. New data suggest that unilateral noise exposure resulting in deafness significantly suppresses the birth of newborn neurons in the hippocampus and leads to memory impairment in noise-exposed animals.