Impairment in active navigation from trauma and Post-Traumatic Stress Disorder

Abstract

The study investigated the impact of trauma exposure and of Post-Traumatic Stress Disorder (PTSD) on spatial processing and active navigation in a sample (n=138) comprising civilians (n=91), police officers (n=22) and veterans (n=27). Individuals with previous trauma exposure exhibited significantly poorer hippocampal-dependent (allocentric) navigation performance on active navigation in a virtual environment (the Alternative Route task) regardless of whether or not they had PTSD (scoring above 20 on the PTSD Diagnostic Scale). No effect of trauma exposure was found in static perspective taking (the Four Mountains task). Moreover, an associative information processing bias in those with PTSD interfered with ability to use hippocampal-dependent processing in active navigation. This study provides new evidence of impaired active navigation in individuals with trauma exposure and highlights the importance of considering the relationship between trauma and spatial processing in clinical and occupational settings.

Memory and Forgetting

“…Consistent with this model, PTSD patients appear to have a selective deficit in allocentric spatial memory, implicating weaker hippocampal functioning [ 36 ]. In this study and in a separate study of navigation [ 37 ], exposure to previous trauma was associated with a greater impairment in specific aspects of spatial processing.…”

Impaired Spatial Memory and Enhanced Habit Memory in a Rat Model of Post-traumatic Stress Disorder

“…Several investigators have suggested that findings pertaining to the emotional modulation of memory are relevant to understanding a variety of human psychopathologies, in particular those involving high levels of stress and anxiety (e.g., McGaugh, 2004 ; Schwabe et al, 2011 ; Goodman et al, 2014 ; Goodman and Packard, 2016a , b ). For instance, subjects with post-traumatic stress disorder (PTSD) demonstrate impairments in spatial memory function ( Tempesta et al, 2012 ; Smith et al, 2015 ; Miller et al, 2017 ), as well as heightened avoidance responses to trauma-related stimuli (e.g., running away from a loud noise), which may be viewed as an exemplar of enhanced stimulus-response (S-R)/habit memory (for review, see Goodman et al, 2012 ). Some researchers have proposed that these PTSD symptoms may be partially attributed to the effects of emotional arousal, i.e., stress stemming from the traumatic event, on the hippocampus and dorsolateral striatum ( Packard, 2009 ; Schwabe et al, 2010b ; Goodman et al, 2012 ).…”

Noradrenergic gating of long-lasting synaptic potentiation in the hippocampus: from neurobiology to translational biomedicine

“…Noradrenergic hyperactivity is a key element of PTSD pathophysiology, as patients with PTSD have elevated levels of NE in cerebrospinal fluid (Geracioti et al, 2001), and animal models of PTSD reveal increased NE in several brain regions, including the hippocampus (Wilson, Ebenezer, McLaughlin, & Francis, 2014). However, PTSD is also associated with impairments of general hippocampusdependent memory (Miller, McDougall, Thomas, & Wiener, 2017;Tempesta, Mazza, Iaria, De Gennaro, & Ferrara, 2012) and altered threshold for induction of synaptic plasticity (Li et al, 2005). For instance, rats that undergo an extreme fear conditioning protocol exhibit increased freezing in response to the conditioned context, but impaired LTP induction for the subsequent 24 h (Li et al, 2005).…”