Head Trauma by Brianna Kramer

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 repeatedlyâ&#x20AC;&#x201D;but not consistentlyâ&#x20AC;&#x201D;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

Head Trauma

Edited and designed by Kramer Press. This book was produced for Katherine Hughesâ&#x20AC;&#x2122;s Type III class at the Massachusetts College of Art and Design, Spring 2017. No portion of this publication may be reproduced by any means (electronic, mechanical, recording, photocopying or otherwise) without the explicit written permission of the author.

Head Trauma AN ORIGINAL LETTER BY KURT VONNEGUT WITH RESEARCH FROM THE NATIONAL CENTER FOR PTSD

Bre (1995) provided the first evidence of decreased

pal volume in PTSD, a brain region related to memory and fear extinct

studies, but not all, have replicated this finding in PTSD, depression, and va

psychiatric disorders. Gray matter reductions in PTSD have also been dem

other brain regions (e.g. anterior cingulate). These findings are consistent with cal model in which stress dysregulates hypothalamic-pituitary-adrenal (HPA)

function, leading to increased glutamate excitotoxicity, and subsequent gray mat

Supporting this model, pilot studies have shown normalization of hippocampal

function following treatment (Levy-Gigi et al., 2013; reviewed by Thomaes et al. 2014

elegant twin study by Gilbertson et al. (2002) has provided strong evidence for small hip

as a predisposing factor for PTSD, rather than a consequence. More recent work has pr

complex picture wherein altered brain structures constitute both vulnerabilities to a

posttraumatic stress (Sekiguchi et al. 2013). Reduced prefrontal cortex, but increased amygd

response to emotional processing (see Phan et al., 2002), has been repeatedlyâ&#x20AC;&#x201D;but not consistentl

in PTSD. Etkin et al. (2007) therefore undertook a meta-analysis and confirmed these abnormalities

the prefrontal impairment to PTSD was also demonstrated, supporting a PTSD model of reduced

combined with increased bottom-up emotional sensitization. In contrast, in the dissociative subtype of

(2012) found an increase in limbic inhibition by the midline prefrontal cortex. Shin et al. (2011) used the Vie

to confirm previous work suggesting that enhanced resting metabolic activity in the dorsal anterior and m

(dACC/MCC) constitutes a familial risk factor, rather than state marker for PTSD. In this study, Shin et al. demon

Veterans with PTSD and their unexposed co-twins had significantly greater activation in the dorsal anterior cin

difference scores on the Multi-Source Interference Task, as compared to combat Veterans without PTSD and their co

by Bryant et al. (2008) demonstrated the possible utility of imaging biomarkers in predicting treatment response. Oth

abnormalities predict poor response to cognitive behavior therapy (CBT) and eye movement desensitization and

emner et al Bremner et al (1995) provided the first evidence of decreased hippocampal volume in PTSD, a brain region related to memory and fear extinction. S

hippocamstudies, but not all, have replicated this finding in PTSD, depression, and various other psychiatric disorders. Gray matter reductions in PTSD have a

tion. Several demonstrated in other brain regions (e.g. anterior cingulate). These findings are consistent with a hypothetical model in which stress dysregulates

FROM: arious other ic-pituitary-adrenal (HPA) axis and glial function, leading to increased glutamate excitotoxicity, and subsequent gray matter reduction. Supporting PFO. K. VONNEGUT, JR.,

monstrated in U.S. ARMY. pilot studies have 12102964 shown normalization of hippocampal structure and function following treatment (Levy-Gigi et al., 2013; reviewed by Thomaes e

h a hypothetisubsequent elegant twin study by Gilbertson et al. (2002) has provided strong evidence for small hippocampus size as a predisposing factor for PT

axis and glial a consequence. More recent work has presented a more complex picture wherein altered brain structures constitute both vulnerabilities to and ou

tter reduction. posttraumatic stress (Sekiguchi et al. 2013). Reduced prefrontal cortex, but increased amygdala, activation in response to emotional processing (se

l structure and 2002), has been repeatedly—but not consistently—demonstrated in PTSD. Etkin et al. (2007) therefore undertook a meta-analysis and confirmed th

4). A subsequent ties. The specificity of the prefrontal impairment to PTSD was also demonstrated, supporting a PTSD model of reduced top-down control combined

ppocampus size bottom-up emotional sensitization. In contrast, in the dissociative subtype of PTSD, Lanius et al. (2012) found an increase in limbic inhibition by th

resented a more TO: prefrontal cortex. Shin et al. (2011) used the Vietnam Twin Registry to confirm previous work suggesting that enhanced resting metabolic activity i

KURT VONNEGUT, and outcomes of anterior and medial cingulate cortices (dACC/MCC) constitutes a familial risk factor, rather than state marker for PTSD. In this study, Shin et al. dem WILLIAMS CREEK,

dala, activation in INDIANAPOLIS, INDIANA. combat-exposed Veterans with PTSD and their unexposed co-twins had significantly greater activation in the dorsal anterior cingulate and a large

ly—demonstrated difference scores on the Multi-Source Interference Task, as compared to combat Veterans without PTSD and their co-twins. Finally, a proof-of-conce

s. The specificity of et al. (2008) demonstrated the possible utility of imaging biomarkers in predicting treatment response. Other PTSD studies have shown that gray m

d top-down control predict poor response to cognitive behavior therapy (CBT) and eye movement desensitization and reprocessing (EMDR) therapy. In depression, brai

f PTSD, Lanius et al. have been related to poor response to serotonergic drugs, but enhanced response to glutamatergic antidepressants, suggesting the presence of a

etnam Twin Registry patients with possible glutamate-based abnormalities leading to structural deficits and treatment resistance to serotonergic drugs (Abdallah et a

medial cingulate cortices (1995) provided the first evidence of decreased hippocampal volume in PTSD, a brain region related to memory and fear extinction. Several studies

nstrated that combat-exposed replicated this finding in PTSD, depression, and various other psychiatric disorders. Bremner et al (1995) provided the first evidence of decreased h

ngulate and a larger response time brain region related to memory and fear extinction. Several studies, but not all, have replicated this finding in PTSD, depression, and various other

o-twins. Finally, a proof-of-concept study reductions in PTSD have also been demonstrated in other brain regions (e.g. anterior cingulate). These findings are consistent with a hypothetical

her PTSD studies have shown that gray matter 5 hypothalamic-pituitary-adrenal (HPA) axis and glial function, leading to increased glutamate excitotoxicity, and subsequent gray matter reduction

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et al. (2008) demonstrated the possible utility of imaging biomarkers in predicting treatment response. Other PTSD studies have shown that gray m

predict poor response to cognitive behavior therapy (CBT) and eye movement desensitization and reprocessing (EMDR) therapy. In depression, brai

have been related to poor response to serotonergic drugs, but enhanced response to glutamatergic antidepressants, suggesting the presence of a

patients with possible glutamate-based abnormalities leading to structural deficits and treatment resistance to serotonergic drugs (Abdallah et al

(1995) provided the first evidence of decreased hippocampal volume in PTSD, a brain region related to memory and fear extinction. Several studies

replicated this finding in PTSD, depression, and various other psychiatric disorders. Bremner et al (1995) provided the first evidence of decreased hi brain region related to memory and fear extinction. Several studies, but not all, have replicated this finding in PTSD, depression, and various other reductions in PTSD have also been demonstrated in other brain regions (e.g. anterior cingulate). These findings are consistent with a hypothetical

hypothalamic-pituitary-adrenal (HPA) axis and glial function, leading to increased glutamate excitotoxicity, and subsequent gray matter reduction

shown normalization of hippocampal structure and function following treatment (Levy-Gigi et al., 2013; reviewed by Thomaes et al. 2014). A subseq

has provided strong evidence for small hippocampus size as a predisposing factor for PTSD, rather than a consequence. More recent work has prese

structures constitute both vulnerabilities to and outcomes of posttraumatic stress (Sekiguchi et al. 2013). Reduced prefrontal cortex, but increased 11 Gray matter reductions in PTSD have ... been demonstrated in other brain regions.

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ysregulates hypothalamic-pituitary-adrenal (HPA) axis and glial function, leading to increased glutamate excitotoxicity, and subsequent gray matte

et al., 2013; reviewed by Thomaes et al. 2014). A subsequent elegant twin study by Gilbertson et al. (2002) has provided strong evidence for small hip

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also been demonstrated in other brain regions (e.g. anterior cingulate). These findings are consistent with a hypothetical model in which stress dys

everal studies, but not all, have replicated this finding in PTSD, depression, and various other psychiatric disorders. Gray matter reductions in PTSD

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everal studies, but not all, have replicated this finding in PTSD, depression, and various other psychiatric disorders. Gray matter reductions in PTSD

sregulates hypothalamic-pituitary-adrenal (HPA) axis and glial function, leading to increased glutamate excitotoxicity, and subsequent gray matter

In contrast, in the dissociative subtype of PTSD, Lanius et al. (2012) found an increase in limbic inhibition by the midline prefrontal cortex.

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if it was worth it.

ave also been demonstrated in other brain regions (e.g. anterior cingulate). These findings are consistent with a hypothetical model in which stress

atter reduction. Supporting this model, pilot studies have shown normalization of hippocampal structure and function following treatment (Levy-G

mall hippocampus size as a predisposing factor for PTSD, rather than a consequence. More recent work has presented a more complex picture wher

ortex, but increased amygdala, activation in response to emotional processing (see Phan et al., 2002), has been repeatedly—but not consistently—d

mpairment to PTSD was also demonstrated, supporting a PTSD model of reduced top-down control combined with increased bottom-up emotional

ortex. Shin et al. (2011) used the Vietnam Twin Registry to confirm previous work suggesting that enhanced resting metabolic activity in the dorsal a

emonstrated that combat-exposed Veterans with PTSD and their unexposed co-twins had significantly greater activation in the dorsal anterior cing

o-twins. Finally, a proof-of-concept study by Bryant et al. (2008) demonstrated the possible utility of imaging biomarkers in predicting treatment res

ovement desensitization and reprocessing (EMDR) therapy. In depression, brain structural deficits have been related to poor response to serotoner

utamate-based abnormalities leading to structural deficits and treatment resistance to serotonergic drugs (Abdallah et al. 2014). Bremner et al (19

ut not all, have replicated this finding in PTSD, depression, and various other psychiatric disorders. Bremner et al (1995) provided the first evidence

nding in PTSD, depression, and various other psychiatric disorders. Gray matter reductions in PTSD have also been demonstrated in other brain regi

HPA) axis and glial function, leading to increased glutamate excitotoxicity, and subsequent gray matter reduction. Supporting this model, pilot stud

subsequent elegant twin study by Gilbertson et al. (2002) has provided strong evidence for small hippocampus size as a predisposing factor for PTS

The Germans herded us through scalding de-

lities to and outcomes of posttraumatic stress (Sekiguchi et al. 2013). Reduced prefrontal cortex, but increased amygdala, activation in response to

lousing showers. Many men died from shock

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in the showers after ten days of starva-

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tion, thirst and exposure.

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onstitutes a familial risk factor, rather than state marker for PTSD. In this study, Shin et al. demonstrated that combat-exposed Veterans with PTSD a

he Multi-Source Interference Task, as compared to combat Veterans without PTSD and their co-twins. Finally, a proof-of-concept study by Bryant et a

atter abnormalities predict poor response to cognitive behavior therapy (CBT) and eye movement desensitization and reprocessing (EMDR) therapy

ntidepressants, suggesting the presence of a subpopulation of patients with possible glutamate-based abnormalities leading to structural deficits

olume in PTSD, a brain region related to memory and fear extinction. Several studies, but not all, have replicated this finding in PTSD, depression, an

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ith a hypothetical model in which stress dysregulates hypothalamic-pituitary-adrenal (HPA) axis and glial function, leading to increased glutamate

nd function following treatment (Levy-Gigi et al., 2013; reviewed by Thomaes et al. 2014). A subsequent elegant twin study by Gilbertson et al. (2002

resented a more complex picture wherein altered brain structures constitute both vulnerabilities to and outcomes of posttraumatic stress (Sekiguc

epeatedly—but not consistently—demonstrated in PTSD. Etkin et al. (2007) therefore undertook a meta-analysis and confirmed these abnormalities.

ith increased bottom-up emotional sensitization. In contrast, in the dissociative subtype of PTSD, Lanius et al. (2012) found an increase in limbic in

esting metabolic activity in the dorsal anterior and medial cingulate cortices (dACC/MCC) constitutes a familial risk factor, rather than state marker f

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rein altered brain structures constitute both vulnerabilities to and outcomes of posttraumatic stress (Sekiguchi et al. 2013). Reduced prefrontal

demonstrated in PTSD. Etkin et al. (2007) therefore undertook a meta-analysis and confirmed these abnormalities. The specificity of the prefrontal sensitization. In contrast, in the dissociative subtype of PTSD, Lanius et al. (2012) found an increase in limbic inhibition by the midline prefrontal

anterior and medial cingulate cortices (dACC/MCC) constitutes a familial risk factor, rather than state marker for PTSD. In this study, Shin et al.

gulate and a larger response time difference scores on the Multi-Source Interference Task, as compared to combat Veterans without PTSD and their

sponse. Other PTSD studies have shown that gray matter abnormalities predict poor response to cognitive behavior therapy (CBT) and eye

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ions (e.g. anterior cingulate). These findings are consistent with a hypothetical model in which stress dysregulates hypothalamic-pituitary-adrenal

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al. (2008) demonstrated the possible utility of imaging biomarkers in predicting treatment response. Other PTSD studies have shown that gray

y. In depression, brain structural deficits have been related to poor response to serotonergic drugs, but enhanced response to glutamatergic

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nd various other psychiatric disorders. Bremner et al (1995) provided the first evidence of decreased hippocampal volume in PTSD, a brain region

orders. Gray matter reductions in PTSD have also been demonstrated in other brain regions (e.g. anterior cingulate). These findings are consistent

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chi et al. 2013). Reduced prefrontal cortex, but increased amygdala, activation in response to emotional processing (see Phan et al., 2002), has been

. The specificity of the prefrontal impairment to PTSD was also demonstrated, supporting a PTSD model of reduced top-down control combined

nhibition by the midline prefrontal cortex. Shin et al. (2011) used the Vietnam Twin Registry to confirm previous work suggesting that enhanced

for PTSD. In this study, Shin et al. demonstrated that combat-exposed Veterans with PTSD and their unexposed co-twins had significantly greater

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