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Trauma and Stressor-Related Disorders 1: Acute Stress Disorder,

Posttraumatic Stress Disorder

Article · November 2015

DOI: 10.1007/978-3-319-11005-9_16

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 Trauma and Stressor-Related
Disorders 1: Acute Stress Disorder, 16
Posttraumatic Stress Disorder

Hoyle Leigh

Contents 16.1 Vignettes

16.1 Vignettes .................................................... 237
1. An 18-year-old man was admitted to the
16.2 Introduction: Stress, Trauma,
Reactions, and Results ............................. 238 intensive care unit following an automobile
accident. He was a passenger in the car whose
16.3 Posttraumatic Stress Disorder (PTSD)
and Acute Stress Disorder (ASD)............ 238
driver was killed in the crash. The patient had
suffered 30 % second degree burn. On the
16.4 Pathophysiology ........................................ 239
fourth day of admission, a psychiatric consul-
16.5 Treatment .................................................. 240 tation was requested for suspected depression.
16.5.1 Psychotherapy ............................................ 240 The patient admitted to some feelings of
16.5.2 Pharmacotherapy ........................................ 241
sadness, flashbacks, and interrupted sleep due
References ............................................................... 241 to nightmares in spite of significant opiate
analgesics. An acute stress disorder was diag-
nosed, and a regimen of Olanzapine 2.5 mg
p.o. at bedtime for 2 weeks was initiated. The
patient’s nightmares and flashbacks subsided
within 24 h. He was subsequently discharged
without any psychotropic medications.
2. A 32-year-old woman with a history of
repeated suicide attempts was referred to the
Psychiatric Consultation Service following
another acetaminophen overdose for evalua-
tion of “suicidal gesture.” On interview, the
patient admitted to feeling depressed, para-
noid, and abusing methamphetamines. History
revealed that the patient had repeated trau-
H. Leigh, MD, DLFAPA, FACP, FAPM (*) matic rapes when she was involved with a
Professor of Psychiatry, Department of Psychiatry, motorcycle gang in her teens, and she had
University of California, San Francisco, CA, USA
severe flashbacks, startle reactions, and almost
Director, Psychosomatic Medicine Program daily nightmares. The patient was diagnosed
& Psychiatric Consultation-Liaison Service,
with major depression, posttraumatic stress
UCSF-Fresno, 155N. Fresno St., Fresno,
CA 93701, USA disorder, and methamphetamine abuse.
e-mail: [email protected] Prazosin 1 mg h.s. was prescribed for the

H. Leigh and J. Streltzer (eds.), Handbook of Consultation-Liaison Psychiatry, 237

DOI 10.1007/978-3-319-11005-9_16, © Hoyle Leigh & Jon Streltzer 2015
238 H. Leigh

nightmare as well as sertraline 50 mg per day are discussed in this chapter. The disorders that
for depression and PTSD once the liver func- are not exclusively seen in children are:
tion returned to normal, and she was referred Posttraumatic Stress Disorder (PTSD), Acute
for outpatient treatment. Stress Disorder (ASD), Adjustment Disorders
(AD), Other Specified Trauma- and Stressor-
Related Disorders, and Unspecified Trauma- and
16.2 Introduction: Stress, Trauma, Stressor-Related disorders. The latter three disor-
Reactions, and Results ders are discussed in Chap. 17.

Stress is an adaptational demand on an entity, be

it an organism, an organ, a tissue, or a molecule, 16.3 Posttraumatic Stress
and conversely, a family, a nation, or a planet. Disorder (PTSD) and Acute
It may be in the form of matter-energy, as in Stress Disorder (ASD)
excessive or insufficient ambient heat, environ-
mental toxins, or in the form of information, as in Though classified as a primary psychiatric disor-
an unwelcome (or welcome) news, an approach- der, this syndrome is secondary to or the sequelae
ing exam, or an inundation by internet connec- of major identifiable stresses. In fact, until the
tion demands. term, PTSD, was introduced in 1970s and for-
Stress is obviously necessary for any change malized in DSM III in 1980, combat neurosis,
to take place, and optimal physical, intellectual, combat fatigue, and shell shock were the terms
and emotional development is contingent on a used to denote the psychiatric sequelae of expo-
steady dose of optimal stress. sure to the extreme stress of combat (1916; Crocq
When an organism encounters an excessive and Crocq 2000; Earlam 1998; Hayman 1946;
amount of stress, then homeostasis may fail, and Milligan 1916; Wadsworth et al. 1946).
the initial distortion exerted by the stress on the Now it is recognized that posttraumatic stress
organism, called strain, may remain as the new disorder is not confined to combats or wars, but
baseline and the organism may have to carry on any major trauma, either directly experienced or
further adaptation with the preexisting load (allo- witnessing such trauma to others, as well as
static load). This results in a distorted develop- learning about trauma to family or close friend,
mental path, which, if combined with a or experiencing repeated or extreme exposure to
constitutional/genetic vulnerability, may lead to details of traumatic events, may cause PTSD
the development of disease. (For further discus- (DSM-5).
sion on this topic, see Chap. 7.) About 8–9 % of the general population will have
What constitutes excessive stress? The answer PTSD during their lifetime (Hidalgo and Davidson
must always be an equation of the interaction: 2000; Yule 2001). In the CL setting, PTSD is often
gene × meme × stressor × environment as dis- found in trauma, burn, and rape victims. Patients
cussed in Chap. 7. Thus, the same stress (e.g., with acute coronary syndrome, and patients admit-
rape) may have different outcome just as the ted to the intensive care unit, often develop PTSD-
same genes (i.e., monozygous twins) may fare like symptoms (see Chap. 26.)
very differently depending on experience (of Others may have an existing posttraumatic
trauma or nurturance). stress disorder diagnosis from combat experience
In Trauma and Stressor-Related Disorders, and may be hospitalized for an unrelated medical
there is a presumption that a person experiences a condition. The prevalence of PTSD in combat
very strong stressor, and the outcome is classified veterans is considered to be about 25 %, and in
in DSM-5 on the basis of age of the individual and other traumatized groups, 3–60 %.
the type and severity of symptoms. The disorders PTSD is characterized by three classes of
in children are Reactive Attachment Disorder and symptoms and signs: (1) intrusion symptoms,
Disinhibited Social Engagement Disorder, which including intrusive thoughts, nightmares, and
16 Trauma and Stressor-Related Disorders 1: Acute Stress Disorder, Posttraumatic Stress Disorder 239

dissociative symptoms such as flashbacks; (2) experimental extinction, and behavioral

arousal symptoms, including hypervigilance, sensitization as well as the altered function of
hyperarousal, and startle reactions; (3) avoidance specific brain regions and neurochemical systems
of situations and stimuli that may remind the per- (Charney et al. 1993; Southwick et al. 1994).
son of the trauma, and (4) negative alterations in In addition to stress inducing the secretion of
cognitions and mood associated with the trau- norepinephrine, dopamine, and opioids, long
matic event, such as inability to remember aspects term potentiation through NMDA receptors in
of the trauma, persistent negative belief or expec- the amygdala may be involved in the encoding of
tations, persistent negative emotional state, traumatic memories vividly in PTSD (Ledoux
inability to experience positive emotions, mark- et al. 1989).
edly diminished interest, feelings of detachment An intriguing area of research is the role of the
and estrangement. In addition to these symptoms, protein, Stathmin, which is known to be involved
any number of psychiatric symptoms may be in fear memory formation. In one study, adult
associated with PTSD, including brief psychotic male rats were exposed to repetitive blast injury
episodes with hallucinations and delusions, while under anesthesia. Blast exposure induced a
depression, panic, substance abuse, and suicidal variety of PTSD-related behavioral traits that
behavior. Memory impairment and learning dis- were present many months after the blast expo-
ability may be prominent. In fact, PTSD may be sure, including increased anxiety, enhanced con-
called the SLE (systemic lupus erythematosus) of textual fear conditioning, and an altered response
psychiatry in the protean symptomatology. in a predator scent assay. The authors also found
A traumatic childhood may predispose an indi- elevation in the amygdala of the protein stathmin
vidual to adult stress disorders. 1. Because the blast overpressure injuries occurred
Therefore, PTSD should be included in the dif- while animals were under general anesthesia,
ferential diagnosis of any psychiatric symptom. their results suggest that a blast-related traumatic
brain exposure can, in the absence of any psycho-
logical stressor, induce PTSD-related traits that
16.4 Pathophysiology are chronic and persistent (Elder et al. 2012).
There is evidence that the balance between
The pathophysiology of PTSD involves the limbic neuronal activities of the amygdala and prefron-
system, particularly the amygdala, hippocampus, tal cortex defines an impairment or facilitation of
the locus ceruleus, and the prefrontal cortex. extinction to the cue while the hippocampus is
A reduced volume of the hippocampus has been involved in the context-specificity of extinction
consistently reported in PTSD (Bremner et al. (Martel et al. 2012).
1995; Karl et al. 2006). Hypercortisolemia associ- In memetic terms, PTSD results from an over-
ated with acute stress has been postulated to under- whelming infusion or activation of stress memes
lie the learning disability and memory impairment that take over the function of the brain (Leigh
associated with PTSD (Munhoz et al. 2010; 2010, 2012). The stress reaction involves the
Rodrigues et al. 2009; Sapolsky 1996). In addition activation of the hypothalamo-pituitary-
to dysfunctions of the limbic system and hippo- adrenocortical axis and massive production of
campus, there is dysfunction of contextualization glucocorticoids which are neurotoxic to the hip-
by medial prefrontal cortex in PTSD (Liberzon pocampus, and may result in a smaller volume
and Sripada 2008; Zovkic and Sweatt 2013). and difficulty in processing memory. With PTSD,
Charney and colleagues postulated that the there may be a permanent damage to the meme-
primary symptoms of PTSD, the persistent reex- processing ability of the brain, setting the stage
periencing of the traumatic event, avoidance of for a labile equilibrium among conflicting memes
stimuli associated with the trauma, and the symp- and susceptibility to be overwhelmed with new
toms of increased arousal, are related to the neu- incoming memes or an inability to process
ral mechanisms involved in fear conditioning, new and useful memes. The stress memes that
240 H. Leigh

overwhelmed the brain are likely to reside in the sufficiently, and the association between the
brain and proliferate at every opportunity. Note memory of the event and a message of danger has
that strong emotions may enhance long-term not been extinguished even when the danger has
potentiation and thus memory formation through passed. The main components of PE, imaginal
dopaminergic and serotonergic mechanisms exposure and in vivo exposure, entail the revisit-
(“flashbulb memory”). Persons who have no ing of trauma memories and triggers to extin-
memory of a traumatic event in 24 h were shown guish this response, by facilitating habituation to
to be less likely to develop PTSD in 6 months the memory, decreasing avoidance, and eliminat-
than those who had memories of the trauma (Gil ing associations with danger by providing correc-
et al. 2005). This finding supports the notion that tive information about safety (Foa et al. 2007).
the ability to inhibit the traumatic meme prolif- During imaginal exposure, patients are instructed
eration (memory) prevents PTSD. to relate their trauma experience in detail with
Once PTSD has been established, reservoirs their eyes closed, while trying to engage emo-
of traumatic memes may proliferate unpredict- tionally in the memory. The patient retells his/her
ably and uncontrollably as in flashbacks and trauma experience repeatedly over the course of a
nightmares. number of sessions, thereby allowing the pro-
cessing of the trauma experience. In vivo expo-
sure entails approaching activities, people, and/or
16.5 Treatment places the patient may have been avoiding to
allow habituation to the environment, and the
16.5.1 Psychotherapy assimilation of the corrective information regarding
safety.
Remembering the traumatic event within 24 h Within CBT for PTSD, prolonged imaginal
after it occurred has been shown to be a predictor exposure may be used as a specific therapeutic
of future PTSD, whereas amnesia concerning the technique in various populations including sex-
event is a predictor of not developing PTSD (Gil ual assault and motor vehicle accidents (Cukor
et al. 2006). Thus, when a patient who suffered an et al. 2010).
acute stress, such as a motor vehicle accident or Cognitive processing therapy (CPT) is another
assault, has no memory of the incident, it is pru- exposure-based protocol with a strong emphasis
dent for the medical staff not to encourage the on increasing the cognitive components and
patient to remember it. Psychological debriefing decreasing the amount of exposure necessary for
and critical incident debriefing, in which the indi- treatment, which some believe will be more pal-
vidual relives in detail the traumatic experience in atable to individuals with PTSD. CPT consists of
a group situation, have been shown to be ineffec- a 12-session protocol comprising of two inte-
tive or even detrimental and more likely to result grated elements. The cognitive therapy compo-
in PTSD (Mayor 2005). In contrast to this type of nent focuses on deconstructing assimilated
acute reliving of trauma in group situations, indi- distorted beliefs, such as guilt, and more global
vidualized, planned psychotherapy seems to be beliefs about the world and self, and generating
the most effective treatment for PTSD. more balanced statements. The exposure compo-
Among the various modalities of psychother- nent entails having the patient write the trauma
apy, Cognitive behavioral therapy (CBT) and memory and read it to their therapist and to them-
Prolonged exposure therapy (PE) have strongest selves and then examine the writing for “stuck
evidence base for PTSD, and are probably far points”(Resick et al. 2002; Rizvi et al. 2009).
more effective than extant pharmacotherapy Initial case studies and clinical trials were
(Cukor et al. 2010). promising and led to a randomized controlled
PE is based on the learning theory model, and trial comparing CPT to PE and a minimal atten-
views PTSD as a disorder of extinction, whereby tion waitlist control for the treatment of PTSD in
the individual’s response to crisis does not diminish a sample of chronically distressed rape victims.
16 Trauma and Stressor-Related Disorders 1: Acute Stress Disorder, Posttraumatic Stress Disorder 241

Results found that both PE and CPT were highly in PTSD because of its potentially addictive
successful in treating PTSD and comorbid nature and the question of whether it may
depressive symptomatology. contribute to the development of PTSD, but in
Stress management and relaxation therapy, practice, it is frequently used to target more
may be effective. isolated symptoms such as insomnia and anxiety
Couples and family therapy may also be (Cukor et al. 2010).
helpful in treating PTSD patients. Prazosin is an alpha-1 adrenergic receptor
blocker which is efficacious in treating sleep-
related PTSD symptoms. These symptoms are
16.5.2 Pharmacotherapy believed to be moderated by increased central ner-
vous system adrenergic activity, resulting in greater
The SSRIs are considered to be the first line of release of norepinephrine and increased sensitivity
treatment. For many patients who experience to norepinephrine at receptor sites. Prazosin’s
insomnia, nightmares, flashbacks, and hypervigi- effectiveness for the treating nightmares has been
lance shortly after severe trauma, antipsychotic reported in various studies, with reports of 50 %
mood stabilizers such as olanzapine in small decrease in nightmares after 8 weeks of treatment
doses (e.g., 2.5–5 mg) hs for 2 weeks to 1 month at 1–6 mg h.s. dosing (Ipser and Stein 2012).
may be particularly helpful (Labbate and Douglas D-Cycloserine (DCS, Seromycin) is a cogni-
2000; Stein et al. 2002). For nightmares associ- tive enhancer that shows promise among pharma-
ated with PTSD, the α-adrenergic blocker prazo- cologic agents for PTSD for its potential to
sin (1 mg h.s. po gradually increased up to 6 mg) facilitate extinction learning. Originally devel-
has been shown to be useful. Benzodiazepines oped as an antituberculosis antibiotic, DCS is a
may also be used for reducing anxiety. For PTSD, partial agonist for the N-methyl-D-aspartate
the treatment is always symptomatic, as the (NMDA) glutamate receptor, which has a crucial
symptoms may range from depression, to impul- role in learning and memory functions. DCS has
sivity, to psychotic symptoms, to panic. Thus, in been shown to facilitate extinction learning in
addition to SSRIs and antipsychotics, mood sta- animal models of conditioned fear and in some
bilizers such as valproic acid and lithium may be human trials of other types of learning including
indicated. Beta-blockers such as propranolol and social phobia and shows a potential role of DCS
alpha-2 agonists like clonidine, as well as drugs in facilitating fear extinction and reducing post-
that act on NMDA and MDMA receptors may be treatment relapse (Cukor et al. 2010)
helpful in modifying the fear conditioning pro-
cess in PTSD (Kerbage and Richa 2013).
Only two pharmacologic agents are FDA References
approved for the treatment of PTSD: sertraline
and paroxetine. These selective serotonin reup- (1916). Sections of psychiatry and neurology: Special dis-
cussion on shell shock without visible signs of injury.
take inhibitors (SSRIs) have response rates rarely
Proceedings of Royal Society of Medicine, 9, i–xliv.
over 60 % with less than 30 % achieving full Berger, W., Mendlowicz, M. V., Marques-Portella, C.,
remission (Berger et al. 2009). Overall, less than Kinrys, G., Fontenelle, L. F., Marmar, C. R., et al.
50 % of PTSD patients improve on SSRIs. (2009). Pharmacologic alternatives to antidepressants
in posttraumatic stress disorder: A systematic review.
Nevertheless, practice guidelines endorse SSRIs
Progress in Neuro-Psychopharmacology & Biological
as first line pharmacotherapy for PTSD (Ipser Psychiatry, 33, 169–180.
and Stein 2012). Antipsychotics such as risperi- Bremner, J. D., Randall, P., Scott, T. M., Bronen, R. A.,
done or olanzapine may be useful for some Seibyl, J. P., Southwick, S. M., et al. (1995). MRI-
based measurement of hippocampal volume in patients
symptoms such as insomnia, and anticonvulsants
with combat-related posttraumatic stress disorder. The
seem helpful when used as an augmentation to American Journal of Psychiatry, 152, 973–981.
other therapeutic regimens (Berger et al. 2009). Charney, D. S., Deutch, A. Y., Krystal, J. H., Southwick,
Benzodiazepines are generally not recommended S. M., & Davis, M. (1993). Psychobiologic
242 H. Leigh

mechanisms of posttraumatic stress disorder. Archives Leigh, H. (2010). Genes, memes, culture, and mental illness:
of General Psychiatry, 50, 295–305. Toward an integrative model. New York, NY: Springer.
Crocq, M. A., & Crocq, L. (2000). From shell shock and Leigh, H. (2012). Memory, memes, cognition, and mental
war neurosis to posttraumatic stress disorder: A his- illness—Toward a new synthesis. Journal of Cognitive
tory of psychotraumatology. Dialogues in Clinical Science, 13, 329–354.
Neuroscience, 2, 47–55. Liberzon, I., & Sripada, C. S. (2008). The functional neu-
Cukor, J., Olden, M., Lee, F., & Difede, J. (2010). roanatomy of PTSD: A critical review. Progress in
Evidence-based treatments for PTSD, new directions, Brain Research, 167, 151–169.
and special challenges. The Annals of the New York Martel, G., Hevi, C., Wong, A., Zushida, K., Uchida, S., &
Academy of Sciences, 1208, 82–89. Shumyatsky, G. P. (2012). Murine GRPR and stathmin
Earlam, R. (1998). Shell-shock: A history of the changing control in opposite directions both cued fear extinction
attitude to war neurosis. British Medical Journal, 316, and neural activities of the amygdala and prefrontal
1683A. cortex. PLoS One, 7, e30942.
Elder, G. A., Dorr, N. P., De Gasperi, R., Gama Sosa, Mayor, S. (2005). Psychological therapy is better than
M. A., Shaughness, M. C., Maudlin-Jeronimo, E., debriefing for PTSD. BMJ, 330, 689.
et al. (2012). Blast exposure induces post-traumatic Milligan, E. T. (1916). A method of treatment of “Shell
stress disorder-related traits in a rat model of mild Shock.”. British Medical Journal, 2, 73–74.
traumatic brain injury. Journal of Neurotrauma, 29, Munhoz, C. D., Sorrells, S. F., Caso, J. R., Scavone, C., &
2564–2575. Sapolsky, R. M. (2010). Glucocorticoids exacerbate
Foa, E. B., Hembree, E. A., & Rothbaum, B. O. (2007). lipopolysaccharide-induced signaling in the frontal
Prolonged exposure therapy for PTSD: Emotional cortex and hippocampus in a dose-dependent manner.
processing of traumatic experiences : Therapist guide. The Journal of Neuroscience, 30, 13690–13698.
New York, NY: Oxford University Press, Oxford. PTSD.http://www.nimh.nih.gov/health/topics/post-traumatic-
Gil, S., Caspi, Y., Ben-Ari, I. Z., Koren, D., & Klein, E. stress-disorder-ptsd/index.shtml
(2005). Does memory of a traumatic event increase the Resick, P. A., Nishith, P., Weaver, T. L., Astin, M. C., &
risk for posttraumatic stress disorder in patients with Feuer, C. A. (2002). A comparison of cognitive-
traumatic brain injury? A prospective study. The processing therapy with prolonged exposure and a wait-
American Journal of Psychiatry, 162, 963–969. ing condition for the treatment of chronic posttraumatic
Gil, S., Caspi, Y., Ben-Ari, I., & Klein, E. (2006). Memory stress disorder in female rape victims. Journal of
of the traumatic event as a risk factor for the develop- Consulting and Clinical Psychology, 70, 867–879.
ment of PTSD: Lessons from the study of traumatic Rizvi, S. L., Vogt, D. S., & Resick, P. A. (2009). Cognitive
brain injury. CNS Spectrums, 11, 603–607. and affective predictors of treatment outcome in cog-
Hayman, M. (1946). The administrative aspect of combat nitive processing therapy and prolonged exposure for
neurosis. Bulletin of the U.S. Army Medical posttraumatic stress disorder. Behaviour Research and
Department. United States. Army Medical Department, Therapy, 47, 737–743.
6, 160–166. Rodrigues, S. M., LeDoux, J. E., & Sapolsky, R. M.
Hidalgo, R. B., & Davidson, J. R. (2000). Posttraumatic (2009). The influence of stress hormones on fear cir-
stress disorder: Epidemiology and health-related con- cuitry. Annual Review of Neuroscience, 32, 289–313.
siderations. The Journal of Clinical Psychiatry, Sapolsky, R. M. (1996). Stress, glucocorticoids, and dam-
61(Suppl 7), 5–13. age to the nervous system: The current state of confu-
Ipser, J. C., & Stein, D. J. (2012). Evidence-based phar- sion. Stress, 1, 1–19.
macotherapy of post-traumatic stress disorder Southwick, S. M., Bremner, D., Krystal, J. H., & Charney,
(PTSD). The International Journal of D. S. (1994). Psychobiologic research in post-
Neuropsychopharmacology, 15, 825–840. traumatic stress disorder. The Psychiatric Clinics of
Karl, A., Schaefer, M., Malta, L. S., Dorfel, D., Rohleder, North America, 17, 251–264.
N., & Werner, A. (2006). A meta-analysis of structural Stein, M. B., Kline, N. A., & Matloff, J. L. (2002). Adjunctive
brain abnormalities in PTSD. Neuroscience & olanzapine for SSRI-resistant combat-related PTSD: A
Biobehavioral Reviews, 30, 1004–1031. double-blind, placebo-controlled study. The American
Kerbage, H., Richa, S. (2013). Non-Antidepressant Long- Journal of Psychiatry, 159, 1777–1779.
Term Treatment in Post-Traumatic Stress Disorder Wadsworth, G. L., Lacy, T., & Pomeranz, A. A. (1946).
(PTSD). Current clinical pharmacology. Feb 4. Reconditioning program for combat neurosis in for-
Labbate, L. A., & Douglas, S. (2000). Olanzapine for ward combat zones. Military Surgeon, 98, 146–155.
nightmares and sleep disturbance in posttraumatic Yule, W. (2001). Posttraumatic stress disorder in the gen-
stress disorder (PTSD). Canadian Journal of eral population and in children. The Journal of Clinical
Psychiatry, 45, 667–668. Psychiatry, 62(Suppl 17), 23–28.
Ledoux, J. E., Romanski, L., & Xagoraris, A. (1989). Zovkic, I. B., & Sweatt, J. D. (2013). Epigenetic mecha-
Indelibility of subcortical emotional memories. nisms in learned fear: Implications for PTSD.
Journal of Cognitive Neuroscience, 1, 238–243. Neuropsychopharmacology, 38, 77–93.

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