Auditory M50 Sensory Gating Deficit and Superior Temporal Gyrus Pathology in Post-Traumatic Stress Disorder

Neurocognitive dysfunction has been well established in post-traumatic stress disorder (PTSD), but the neurobiological underpinnings of this dysfunction are not well understood. A rich line of PTSD research has investigated changes in auditory information processing of non-traumatic (neutral) stimuli through analysis of evoked responses. A number of previous electroencephalography (EEG) studies in PTSD have found impaired sensory gating of the P50 auditory potential using a paired click (500 ms) paradigm. However, since the P50 signal is best measured in the midline (electrode Cz), the hemispheric and neuronal (source space) etiologies of this deficit in PTSD are not well understood. We utilized magnetoencephalography to measure gating of the 50 ms evoked field (M50), which is equivalent to P50, in a group of seven Vietnam veterans with PTSD with combat-related PTSD and ten normal controls. Using MEG and magnetic source imaging, we found that M50 is localized to the superior temporal gyrus (STG). Furthermore, M50 gating was impaired in PTSD patients, but only in the right hemisphere and right M50 amplitude correlated with PTSD symptomatology. Using a regression model, we also found that thinner right hemisphere STG cortical thickness predicted sensory gating deficits. Our work suggests that abnormalities in early abnormal information processing in PTSD, particularly filtering of redundant stimuli, are explained by structural changes in the right temporal lobe (STG). There is growing literature documenting cortical thinning in PTSD patients involving mainly the frontal and temporal lobes; other groups have found specific changes in the STG. We discuss our findings in light of other evidence of abnormal hemispheric lateralization and temporal lobe dysfunction in PTSD.