TSD, a brain region related to memory and
sion, and various other psychiatric disorders.
g. anterior cingulate). These findings are
ary-adrenal (HPA) axis and glial function, leading to
this model, pilot studies have shown normalization of
d by Thomaes et al. 2014). A subsequent elegant twin
ze as a predisposing factor for PTSD, rather than a conse-
Bremner et al (1995) provided the first evidence of decreased hippocampal volume in PTSD, a brain region related to memory and fear extinc studies, but not all, have replicated this finding in PTSD, depression, and various other psychiatric disorders. Gray matter reductions in PTSD demonstrated in other brain regions (e.g. anterior cingulate). These findings are consistent with a hypothetical model in which stress dysreg ic-pituitary-adrenal (HPA) axis and glial function, leading to increased glutamate excitotoxicity, and subsequent gray matter reduction. Supp pilot studies have shown normalization of hippocampal structure and function following treatment (Levy-Gigi et al., 2013; reviewed by Thom subsequent elegant twin study by Gilbertson et al. (2002) has provided strong evidence for small hippocampus size as a predisposing factor consequence. More recent work has presented a more complex picture wherein altered brain structures constitute both vulnerabilities to an posttraumatic stress (Sekiguchi et al. 2013). Reduced prefrontal cortex, but increased amygdala, activation in response to emotional process 2002), has been repeatedly—but not consistently—demonstrated in PTSD. Etkin et al. (2007) therefore undertook a meta-analysis and confirm The specificity of the prefrontal impairment to PTSD was also demonstrated, supporting a PTSD model of reduced top-down control combine bottom-up emotional sensitization. In contrast, in the dissociative subtype of PTSD, Lanius et al. (2012) found an increase in limbic inhibitio prefrontal cortex. Shin et al. (2011) used the Vietnam Twin Registry to confirm previous work suggesting that enhanced resting metabolic act and medial cingulate cortices (dACC/MCC) constitutes a familial risk factor, rather than state marker for PTSD. In this study, Shin et al. demon posed Veterans with PTSD and their unexposed co-twins had significantly greater activation in the dorsal anterior cingulate and a larger res scores on the Multi-Source Interference Task, as compared to combat Veterans without PTSD and their co-twins. Finally, a proof-of-concept s demonstrated the possible utility of imaging biomarkers in predicting treatment response. Other PTSD studies have shown that gray matter cognitive behavior therapy (CBT) and eye movement desensitization and reprocessing (EMDR) therapy. In depression, brain structural deficits serotonergic drugs, but enhanced response to glutamatergic antidepressants, suggesting the presence of a subpopulation of patients with p structural deficits and treatment resistance to serotonergic drugs (Abdallah et al. 2014). Bremner et al (1995) provided the first evidence of d
Head Trauma
structures constitute both vulnerabilities to and outcomes of
mygdala, activation in response to emotional processing (see Phan et
. (2007) therefore undertook a meta-analysis and confirmed these
ated, supporting a PTSD model of reduced top-down control combined with
f PTSD, Lanius et al. (2012) found an increase in limbic inhibition by the
ous workmo suggesting that enhanced resting metabolic activity in the dorsal ry and ed to me
state marker for PTSD. ers. In this study, Shin et al. demonstrated that combat-exposed psychiatric disord
anterior cingulate and a larger response time difference scores on the Multi-Source hese findings are
-concept study on by, Bryant leadingettoal. (2008) demonstrated the possible utility of imaging and glial functi of es predict poorno response toncognitive behavior therapy (CBT) and eye movement desensitizarmalizatio es have shown
By Brie Kramer
Brie Kramer
twin nse to serotonergic drugs, enhanced response to glutamatergic antidepressants, suggesting gantbut nt ele 014). A subseque a conse-to serotonergic drugs (Abdallah et al. 2014). Bremner et al al deficits PT and treatment resistance rather than actor for SD, s ofnot all, have replicated this finding in PTSD, depression, and tcomebut and fearlne extinction. studies, to and ou rabilitiesSeveral both vu e Phan et ssing (seto procerelated olume in PTSD, a ot brain memory and fear extinction. Several studies, but not all, have ionalregion n response to em ese th ed rm D have also been in other brain regions (e.g. anterior cingulate). These findings are alysis and confi andemonstrated dertook a metad with rol combine down contglutamate glial function, leading top-increased excitotoxicity, and subsequent gray matter reduction. uced to red of l de mo SD n by the inhibitio limbic eatment (Levy-Gigi et al., 2013; reviewed by Thomaes et al. 2014). A subsequent elegant twin study by se in increa (2012) found an l ity in the dorsa c activwork tabolirecent ather than a consequence. has presented a more complex picture wherein altered brain resting meMore g that enhanced posed that combat-ex nstratedactivation refrontal cortex, increased amygdala, in response to emotional processing (see Phan et al., 2002), et al. demo Shin ,but SD. In this study -Source res on the Multi difference scoThe lysis and confirmed specificity of the prefrontal impairment to PTSD was also demone timeabnormalities. nsthese po res r ge lar a and imaging ssible utility of trated the po zation. In contrast, inmo thensdissociative subtype of PTSD, Lanius et al. (2012) found an increase in limbic inhibition by de ) 08 (20 al. zaBryant et ment desensiti T) and eye move erapy (CB vior thactivity at enhanced resting metabolic in the dorsal anterior and medial cingulate cortices (dACC/MCC) constitutes a ha be ve iti gn sponse to co s, suggesting c antidepressant rgi ate tam glu ponse to co-twins had significantly greater activation in the dorsal anterior cingulate and a ns with PTSD and their unexposed ed res hanc et al c drugs, but en
An original letter by Kurt Vonnegut with research from the National Center for PTSD