(
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Three areas of the brain in which function may be altered in PTSD have been identified: the
prefrontal cortex,
amygdala, and
hippocampus.
Much of this research has utilised PTSD victims from the Vietnam War.
For example, a prospective study using the Vietnam Head Injury Study
showed that damage to the prefrontal cortex may actually be protective
against later development of PTSD.
[70] In a study by Gurvits et al., combat veterans of the
Vietnam War with PTSD showed a 20% reduction in the volume of their
hippocampus compared with veterans having suffered no such symptoms.
[71] This finding could not be replicated in chronic PTSD patients traumatized at an
air show plane crash in 1988 (Ramstein, Germany).
[72]
In human studies, the amygdala has been shown to be strongly involved
in the formation of emotional memories, especially fear-related
memories.
Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD.
[73] However, during high stress times the
hippocampus,
which is associated with the ability to place memories in the correct
context of space and time, and with the ability to recall the memory, is
suppressed. This suppression is hypothesized to be the cause of the
flashbacks that often plague PTSD patients. When someone with PTSD undergoes
stimuli
similar to the traumatic event, the body perceives the event as
occurring again because the memory was never properly recorded in the
patients memory.
[28]
Regions of the brain associated with stress and posttraumatic stress disorder[6
The amygdalocentric model of PTSD proposes that it is associated with
hyperarousal of the amygdala and insufficient top-down control by the
medial
prefrontal cortex and the
hippocampus in particular during extinction.
[74] This is consistent with an interpretation of PTSD as a syndrome of deficient
extinction ability.
[74][75] A study at the European Neuroscience Institute-Goettingen (Germany) found that fear extinction-induced
IGF2/
IGFBP7
signalling promotes the survival of 17–19-day-old newborn hippocampal
neurons. This suggests that therapeutic strategies that enhance IGF2
signalling and adult
neurogenesis might be suitable to treat diseases linked to excessive fear memory such as
PTSD.
[76] Further animal and clinical research into the amygdala and
fear conditioning may suggest additional treatments for the condition.
The maintenance of the fear involved with PTSD has been shown to include the HPA axis, the
locus coeruleus-
noradrenergic systems, and the connections between the
limbic system and
frontal cortex. The HPA axis that coordinates the hormonal response to stress,
[77]
which activates the LC-noradrenergic system, is implicated in the
over-consolidation of memories that occurs in the aftermath of trauma.
[78] This over-consolidation increases the likelihood of one's developing PTSD. The
amygdala
is responsible for threat detection and the conditioned and
unconditioned fear responses that are carried out as a response to a
threat.
[28]
The
LC-
noradrenergic system has been hypothesized to mediate the over-consolidation of fear memory in PTSD. High levels of
cortisol
reduce noradrenergic activity, and because patients with PTSD tend to
have reduced levels of cortisol, it is proposed that individuals with
PTSD fail to regulate the increased noradrenergic response to traumatic
stress.
[79] It is thought that the intrusive memories and conditioned fear responses to associated triggers is a result of this response.
Neuropeptide Y has been reported to reduce the release of
norepinephrine and has been demonstrated to have
anxiolytic
properties in animal models. Studies have shown people with PTSD
demonstrate reduced levels of NPY, possibly indicating their increased
anxiety levels.
[28]
The
basolateral
nucleus (BLA) of the amygdala is responsible for the comparison and
development of associations between unconditioned and conditioned
responses to stimuli, which results in the fear conditioning present in
PTSD. The BLA activates the
central nucleus
(CeA) of the amygdala, which elaborates the fear response, (including
behavioral response to threat and elevated startle response). Descending
inhibitory inputs from the
medial prefrontal cortex
(mPFC) regulate the transmission from the BLA to the CeA, which is
hypothesized to play a role in the extinction of conditioned fear
responses.
[28]
Diagnostic and Statistical Manual
The diagnostic criteria for PTSD, stipulated in the
Diagnostic and Statistical Manual of Mental Disorders IV (Text Revision) (DSM-IV-TR), may be summarized as:
[4][80]
A:
Exposure to a traumatic event. This must have involved
both
(a) loss of "physical integrity", or risk of serious injury or death,
to self or others, and (b) a response to the event that involved intense
fear, horror, or helplessness (or in children, the response must
involve disorganized or agitated behavior). (The
DSM-IV-TR
criterion differs substantially from the previous DSM-III-R stressor
criterion, which specified the traumatic event should be of a type that
would cause "significant symptoms of distress in almost anyone," and
that the event was "outside the range of usual human experience."
[81])
B:
Persistent re-experiencing. One or more of these must be present in the victim:
flashback
memories, recurring distressing dreams, subjective re-experiencing of
the traumatic event(s), or intense negative psychological or
physiological response to any objective or subjective reminder of the
traumatic event(s).
C:
Persistent avoidance and emotional numbing. This involves a sufficient level of:
- avoidance of stimuli associated with the trauma, such as certain thoughts or feelings, or talking about the event(s)
- avoidance of behaviors, places, or people that might lead to
distressing memories as well as the disturbing memories, dreams,
flashbacks, and intense psychological or physiological distress[18]
- inability to recall major parts of the trauma(s), or decreased involvement in significant life activities
- decreased capacity (down to complete inability) to feel certain feelings
- an expectation that one's future will be somehow constrained in ways not normal to other people.
D:
Persistent symptoms of increased arousal not present before.
These are all physiological response issues, such as difficulty falling
or staying asleep, or problems with anger, concentration, or
hypervigilance. Additional symptoms include irritability, angry outbursts, increased startle response, and concentration or sleep problems.
[18]
E:
Duration of symptoms for more than 1 month. If all other criteria are present, but 30 days have not elapsed, the individual is diagnosed with
Acute stress disorder.
[18]
F:
Significant impairment. The symptoms reported must lead to
"clinically significant distress or impairment" of major domains of life
activity, such as social relations, occupational activities, or other
"important areas of functioning".
[82]
Assessment
Since the introduction of
DSM-IV,
the number of possible events that might be used to diagnose PTSD has
increased; one study suggests that the increase is around 50%.
[83] Various scales to measure the severity and frequency of PTSD symptoms exist.
[84][85] Standardized screening tools such as
Trauma Screening Questionnaire[86] and
PTSD Symptom Scale[87]
can be used to detect possible symptoms of posttraumatic stress
disorder and suggest the need for a formal diagnostic assessment.
DSM-5
In
DSM-5, published in May, 2013, PTSD is classified as a trauma- and stress-related disorder.
[1]
- Criterion A: (applicable to adults, adolescents and children over 6.
There is a separate Posttraumatic stress disorder for children 6 years
and younger.) Exposure to real or threatened death, injury, or sexual
violence.
- Several items in Criterion B (intrusion symptoms) are rewritten to add or augment certain distinctions now considered important.
- Special consideration is given to developmentally appropriate
criteria for use with children and adolescents. This is especially
evident in the restated Criterion B—intrusion symptoms. Development of
age-specific criteria for diagnosis of PTSD is ongoing at this time.
- Criterion C (avoidance and numbing) has been split into "C" and "D":
- Criterion C (new version) now focuses solely on avoidance of
behaviors or physical or temporal reminders of the traumatic
experience(s). What were formerly two symptoms are now three, due to
slight changes in descriptions.
- New Criterion D focuses on negative alterations in cognition and
mood associated with the traumatic event(s) and contains two new
symptoms, one expanded symptom, and four largely unchanged symptoms
specified in the previous criteria.
- Criterion E (formerly "D"), which focuses on increased arousal and
reactivity, contains one modestly revised, one entirely new, and four
unchanged symptoms.
- Criterion F (formerly "E") still requires duration of symptoms to have been at least one month.
- Criterion G (formerly "F") stipulates symptom impact ("disturbance") in the same way as before.
- Criterion H stipulated the disturbance is not due to the effects of a substance or another medical condition.
- Specify whether:
- With dissociative symptoms: (not due to effects of a substance or another medical condition)
- In addition, meets the criteria of Depersonalization
- In addition, meets the criteria of Derealization
- Specify if:
- With delayed expression Full criteria not met until more than 6 months after the event
Research-based groups
Emerging
factor analytic research
[88] suggests that PTSD symptoms group empirically into four clusters, not the three currently described in the
Diagnostic and Statistical Manual of Mental Disorders.
[dated info]
One model supported by this research divides the traditional avoidance
symptoms into a cluster of numbing symptoms (such as loss of interest
and feeling emotionally numb) and a cluster of behavioral avoidance
symptoms (such as avoiding reminders of the trauma).
[89]
An alternative model adds a fourth cluster of dysphoric symptoms. These
include symptoms of emotional numbing, as well as anger, sleep
disturbance, and difficulty concentrating (traditionally grouped under
the hyperarousal cluster).
[90][91] A literature review
[92] and meta-analysis
[93] did not find strong support across the literature for one of these models over the other.
International Classification of Diseases
The diagnostic criteria for PTSD, stipulated in the
International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10), may be summarized as:
[94]
- Exposure to a stressful event or situation (either short or long
lasting) of exceptionally threatening or catastrophic nature, which is
likely to cause pervasive distress in almost anyone.
- Persistent remembering or "reliving" the stressor by intrusive flash
backs, vivid memories, recurring dreams, or by experiencing distress
when exposed to circumstances resembling or associated with the
stressor.
- Actual or preferred avoidance of circumstances resembling or
associated with the stressor (not present before exposure to the
stressor).
- Either (1) or (2):
- Inability to recall, either partially or completely, some important aspects of the period of exposure to the stressor
- Persistent symptoms of increased psychological sensitivity and
arousal (not present before exposure to the stressor) shown by any two
of the following:
- difficulty in falling or staying asleep
- irritability or outbursts of anger
- difficulty in concentrating
- hyper-vigilance
- exaggerated startle response.
The
International Statistical Classification of Diseases and Related Health Problems 10 diagnostic guidelines state:
[94]
In general, this disorder should not be diagnosed unless there is
evidence that it arose within 6 months of a traumatic event of
exceptional severity. A "probable" diagnosis might still be possible if
the delay between the event and the onset was longer than 6 months,
provided that the clinical manifestations are typical and no alternative
identification of the disorder (e.g., as an anxiety or
obsessive-compulsive disorder or depressive episode) is plausible. In
addition to evidence of trauma, there must be a repetitive, intrusive
recollection or re-enactment of the event in memories, daytime imagery,
or dreams. Conspicuous emotional detachment, numbing of feeling, and
avoidance of stimuli that might arouse recollection of the trauma are
often present but are not essential for the diagnosis. The autonomic
disturbances, mood disorder, and behavioural abnormalities all
contribute to the diagnosis but are not of prime importance. The late
chronic sequelae of devastating stress, i.e. those manifest decades
after the stressful experience, should be classified under
F62.0.
Differential diagnosis
A diagnosis of PTSD requires exposure to an extreme stressor such as
one that is life-threatening. Any stressor can result in a diagnosis of
adjustment disorder
and it is an appropriate diagnosis for a stressor and a symptom pattern
that does not meet the criteria for PTSD, for example a stressor like a
partner being fired, or a spouse leaving. If any of the symptom pattern
is present before the stressor, another diagnosis is required, such as
brief psychotic disorder or
major depressive disorder. Other differential diagnoses are
schizophrenia or other disorders with psychotic features such as Psychotic disorders due to a general medical condition.
Drug-induced psychotic disorders can be considered if substance abuse is involved.
[4]
The symptom pattern for
acute stress disorder
must occur and be resolved within four weeks of the trauma. If it lasts
longer, and the symptom pattern fits that characteristic of PTSD, the
diagnosis may be changed.
[4]
Obsessive compulsive disorder may be diagnosed for intrusive thoughts that are recurring but not related to a specific traumatic event.
[4]
Malingering should be considered if a financial and/or legal advantage is a possibility.
Prevention
Modest benefits have been seen from early access to
cognitive behavioral therapy, as well as from some medications such as
propranolol.
[95] Critical incident stress management has been suggested as a means of preventing PTSD, but subsequent studies suggest the likelihood of its producing
iatrogenic outcomes.
[96][97] A
review
"...did not find any evidence to support the use of an intervention
offered to everyone", and that "...multiple session interventions may
result in worse outcome than no intervention for some individuals.
[98] The
World Health Organization recommends against the use of
benzodiazepines and
antidepressants in those having experienced trauma.
[99]
Early detection
The ability to prescreen individuals would be of great help in
getting treatment to those at risk of PTSD prior to development of the
syndrome. Several biological indicators have been identified that are
related to later PTSD development. First, Delhanty
[100] found that higher response times and a smaller
hippocampal
volume were identified as linked to later PTSD development. However,
both of these indicators are relatively difficult to test for and need
specialized tests or equipment, or both, to identify. A blood biomarker
is much easier to test for. Van Zuiden et al.
[101]
found a biomarker when testing U.S. Army soldiers prior to deployment.
They found that soldiers with more glucocorticoid receptors (GR) were
more likely to be diagnosed with PTSD six months after deployment.
However, higher GR levels have not been identified as a cause of PTSD,
and may instead be an intermediator, or even an indicator that the
individual has previously experienced traumatic events. There is a great
deal of overlap between high GR levels and those later diagnosed with
and without PTSD. Thus, the identification of high GR is simply a
vulnerability indicator at this time.
Delhanty
[100]
found that biological precursors existed directly following traumatic
exposure in those that later developed chronic PTSD and were
significantly different from those who did not. Directly following the
traumatic event, later sufferers often have significantly lower levels
of
hypothalamic
pituitary-adrenal activity and a corresponding decrease in Cortisol.
Other methods of early detection include the identification of specific
risk factors associated with later PTSD symptoms. Resnick, Acierno,
Holmes, Kilpatrick, and Jager,
[102]
for example, were able to identify that the forensic exam given to
victims after a rape was associated with PTSD. Finally, global
treatments attempt to avoid the problems of early detection by simply
treating everyone involved. However, many studies
[100]
have found this to be often ineffective and for global treatments to at
times increase prevalence rates of PTSD. Stepped collaborative care is
where individuals who are at risk are monitored for symptoms.
[95] As symptoms of PTSD appear the level of care is increased to treat those symptoms.
Psychological debriefing
Trauma-exposed individuals often receive a purported preventive treatment called
psychological debriefing.
[95]
Psychological debriefing is the most often used preventive measure,
partly because of the relative ease with which this treatment can be
given to individuals directly following an event. It consists of
interviews that are meant to allow individuals to directly confront the
event and share their feelings with the counselor and to help structure
their memories of the event. However, research has revealed that
psychological debriefing does not help trauma survivors, and it might
even hurt them.
[95]
Although from the outset, early psychological debriefing research
yielded mixed results, some initial research suggested that
psychological debriefings helped ameliorate peritraumatic symptoms and
prevent post-traumatic symptom development.
[77] But as research progressed, several
meta-analyses made it clear that psychological debriefing is unhelpful and potentially harmful.
[103][104]
The first Cochrane meta-analysis concerned single-session debriefing.
More recently a Cochrane review on multiple session interventions was
conducted and also found negative results.
[105] The
American Psychological Association judges the status of psychological debriefing as
No Research Support/Treatment is Potentially Harmful.
[106]
Medications
Some medications have shown benefit in preventing PTSD or reducing
its incidence, when given in close proximity to a traumatic event. These
medications include:
Alpha-adrenergic agonists: Anecdotal report of success in using
clonidine ("Catapres") to reduce traumatic stress symptoms
[107] suggests that it may have benefit in preventing PTSD.
Beta blockers:
Propranolol
("Inderal"), similar to clonidine, may be useful if there are
significant symptoms of "over-arousal". These may inhibit the formation
of traumatic memories by blocking adrenaline's effects on the
amygdala.
[108]
Glucocorticoids: There is some evidence suggesting that administering
glucocorticoids
immediately after a traumatic experience may help prevent PTSD. Several
studies have shown that individuals who receive high doses of
hydrocortisone for treatment of
septic shock, or following surgery, have a lower incidence and fewer symptoms of PTSD.
[109][110][111]
Psychobiological treatments have also found success, especially with cortisol.
[95]
Psychobiological treatments target biological changes that occur after a
traumatic event. They also attempt to chemically alter learning or
memory formation. Cortisol treatments after a traumatic event have found
success in mitigating later diagnosis of PTSD. As discussed earlier,
cortisol is often lower in individuals at risk of PTSD after a traumatic
event than their counterparts. By increasing cortisol levels to normal
levels this has been shown to reduce arousal post event as well prevent
GR upregulation.
Management
Psychological
Many forms of psychotherapy have been advocated for trauma-related
problems such as PTSD. Basic counseling practices common to many
treatment responses for PTSD include education about the condition and
provision of safety and support.
[5][87]
The psychotherapy programs with the strongest demonstrated efficacy include cognitive behavioral programs, variants of
exposure therapy, stress inoculation training (SIT), variants of cognitive therapy (CT),
eye movement desensitization and reprocessing (EMDR),
[73] and many combinations of these procedures.
[112][113]
A 2010 review disagrees that these treatments have proven efficacy and
points out methodological flaws in the studies and previous
meta-analyses.
[114]
EMDR and trauma-focused
cognitive behavioral therapy
(TFCBT) were recommended as first-line treatments for trauma victims in
a 2007 review; however, "the evidence base [for EMDR] was not as strong
as that for TFCBT ... Furthermore, there was limited evidence that
TFCBT and EMDR were superior to supportive/non-directive treatments,
hence it is highly unlikely that their effectiveness is due to
non-specific factors such as attention."
[115] A
meta-analytic comparison of EMDR and
cognitive behavioral therapy
found both protocols indistinguishable in terms of effectiveness in
treating PTSD; however, "the contribution of the eye movement component
in EMDR to treatment outcome" is unclear.
[116]
Cognitive behavioral therapy
Cognitive behavioral therapy
(CBT) seeks to change the way a trauma victim feels and acts by
changing the patterns of thinking or behavior, or both, responsible for
negative emotions. CBT has been proven to be an effective treatment for
PTSD and is currently considered the standard of care for PTSD by the
United States Department of Defense.
[117]
In CBT, individuals learn to identify thoughts that make them feel
afraid or upset and replace them with less distressing thoughts. The
goal is to understand how certain thoughts about events cause
PTSD-related stress.
Recent research on contextually based third-generation
behavior therapies suggests that they may produce results comparable to some of the better validated therapies.
[118] Many of these therapy methods have a significant element of exposure
[117] and have demonstrated success in treating the primary problems of PTSD and co-occurring depressive symptoms.
[119]
Exposure therapy is a type of cognitive behavioral therapy
[120]
that involves assisting trauma survivors to re-experience distressing
trauma-related memories and reminders in order to facilitate habituation
and successful emotional processing of the trauma memory. Most exposure
therapy programs include both imaginal confrontation with the traumatic
memories and real-life exposure to trauma reminders; this therapy
modality is well supported by clinical evidence. The success of
exposure-based therapies has raised the question of whether exposure is a
necessary ingredient in the treatment of PTSD.
[121] Some organizations
[which?] have endorsed the need for exposure.
[122][123] The US Department of Veterans Affairs has been actively training mental health treatment staff in
prolonged exposure therapy[124] and
Cognitive Processing Therapy[125] in an effort to better treat US Veterans with PTSD.
Eye movement desensitization and reprocessing
Eye movement desensitization and reprocessing (EMDR) is a form of psychotherapy developed and studied by
Francine Shapiro.
[126]
She had noticed that, when she was thinking about disturbing memories
herself, her eyes were moving rapidly. When she brought her eye
movements under control while thinking, the thoughts were less
distressing.
[126]
In 2002, Shapiro and Maxfield published a theory of why this might work, called adaptive information processing.
[127]
This theory proposes that eye movement can be used to facilitate
emotional processing of memories, changing the person's memory to attend
to more adaptive information.
[128]
The therapist initiates voluntary rapid eye movements while the person
focuses on memories, feelings or thoughts about a particular trauma.
[2][129]
The therapists uses hand movements to get the person to move their eyes
backward and forward, but hand-tapping or tones can also be used.
[2] EMDR closely resembles
cognitive behavior therapy as it combines exposure (re-visiting the traumatic event), working on cognitive processes and relaxation/self-monitoring.
[2]
However, exposure by way of being asked to think about the experience
rather than talk about it has been highlighted as one of the more
important distinguishing elements of EMDR.
[130]
There have been multiple small controlled trials of four to eight weeks of EMDR in adults
[131] as well as children and adolescents.
[129]
EMDR reduced PTSD symptoms enough in the short term that one in two
adults no longer met the criteria for PTSD, but the number of people
involved in these trials was small.
[131] There was not enough evidence to know whether or not EMDR could eliminate PTSD.
[131] There was some evidence that EMDR might prevent depression.
[131] There were no studies comparing EMDR to other psychological treatments or to medication.
[131] Adverse effects were largely unstudied.
[131]
The benefits were greater for women with a history of sexual assault
compared with people who had experienced other types of traumatizing
events (such as accidents, physical assaults and war). There is a small
amount of evidence that EMDR may improve re-experiencing symptoms in
children and adolescents, but EMDR has not been shown to improve other
PTSD symptoms, anxiety, or depression.
[129]
The eye movement component of the therapy may not be critical for benefit.
[2][128]
As there has been no major, high quality randomized trial of EMDR with
eye movements versus EMDR without eye movements, the controversy over
effectiveness is likely to continue.
[130]
Interpersonal psychotherapy
Other approaches, in particular involving social supports,
[46][47] may also be important. An open trial of interpersonal psychotherapy
[132] reported high rates of remission from PTSD symptoms without using exposure.
[133] A current, NIMH-funded trial in New York City is now (and into 2013) comparing interpersonal psychotherapy,
prolonged exposure therapy, and relaxation therapy.
[134][broken citation][135][136]
Medication
A variety of medications has shown adjunctive benefit in reducing PTSD symptoms,
[137] but "there is no clear drug treatment for PTSD".
[138]
In general, positive symptoms (re-experiencing, hypervigilance,
increased arousal) respond better to medication than negative symptoms
(avoidance, withdrawal), and it is recommended that any drug trial last
for at least 6–8 weeks.
[138]
With many medications, residual symptoms following treatment is the
rule rather than the exception, which has led to increased research in
the aggressive treatment of PTSD symptoms.
[139]
Some studies have shown that treatment with
hydrocortisone
shortly after a traumatic event, in comparison to a placebo, decreases
the likelihood that the patient will suffer from PTSD. Other studies
have indicated that
propranolol
administered within 6 hours of a traumatic event decreases the
physiological reactivity to a reminder of the traumatic event. However
propranolol had no effect on the rate of PTSD. Despite these studies,
there is not significant evidence that medication can prevent PTSD,
therefore none is routinely administered.
[140]
Symptom management
SSRIs (
selective serotonin reuptake inhibitors). SSRIs are considered to be a
first-line drug treatment.
[141][142] SSRIs for which there are data to support use include:
citalopram,
escitalopram,
[143] fluoxetine,
[144] fluvoxamine,
[145] paroxetine,
[146] and
sertraline.
[144][147]
Among the anti-depressants described in this section, bupropion and
venlafaxine have the lowest patient drop-out rates. Sertraline,
fluoxetine, and
nefazodone have a modestly higher drop-out rate (~15%), and the heterocyclics and paroxetine have the highest rates (~20%+).
[148]
Where drop-out is caused or feared because of medication side-effects,
it should be remembered that most patients do not experience such
side-effects.
[149]
Tricyclic antidepressants:
Amitriptyline has shown benefit for positive distress symptoms and for avoidance, and
imipramine has shown benefit for intrusive symptoms.
[144]
Alpha-adrenergic antagonists:
Prazosin, in a small study of combat veterans, has shown substantial benefit in relieving or reducing nightmares.
[49] Clonidine can be helpful with startle, hyperarousal, and general autonomic hyperexcitability.
[150]
Anti-convulsants,
mood stabilizers, anti-aggression agents:
Carbamazepine has likely benefit in reducing arousal symptoms involving noxious affect,
[144] as well as mood or aggression.
[151] Topiramate[49] has been effective in achieving major reductions in flashbacks and nightmares, and no reduction of effect was seen over time.
[49] Zolpidem has also proven useful in treating sleep disturbances.
[150]
Lamotrigine may be useful in reducing reexperiencing symptoms, as well as avoidance and emotional numbing.
[49][152][153][154] Valproic acid and has shown reduction of symptoms of irritability, aggression, and impulsiveness, and in reducing flashbacks.
[150] Similarly,
lithium carbonate has worked to control mood and aggressions (but not anxiety) symptoms.
[151] Buspirone has an effect similar to that of lithium, with the additional benefit of working to reduce hyperarousal symptoms.
[150]
Antipsychotics such as
risperidone can be used to help with
dissociation, mood issues, and aggression.
[155]
Serotonin antagonists.
Cyproheptadine can be used to help with sleep disorders and nightmares.
[156]
Atypical
antidepressants:
[157] Nefazodone can be effective with sleep disturbance symptoms and with secondary depression,
anxiety, and
sexual dysfunction symptoms.
[144] Trazodone can also reduce or eliminate problems with anger, anxiety, and disturbed sleep.
[144]
Beta blockers:
Propranolol has demonstrated possibilities in reducing hyperarousal symptoms, including sleep disturbances.
[108][150]
Benzodiazepines: These drugs are not recommended by clinical guidelines for the treatment of PTSD due to a lack of evidence of benefit.
[158] Nevertheless some doctors use benzodiazepines with caution for short-term anxiety relief,
[155][159] hyperarousal, and sleep disturbance.
[150]
However, some authors believe that the use of benzodiazepines is
contraindicated for acute stress, as this group of drugs promotes
dissociation and ulterior revivals.
[160]
While benzodiazepines can alleviate acute anxiety, there is no
consistent evidence that they can stop the development of PTSD, or are
at all effective in the
treatment of posttraumatic stress
disorder. Additionally, benzodiazepines may reduce the effectiveness of
psychotherapeutic interventions, and there is some evidence that
benzodiazepines may actually contribute to the development and
chronification of PTSD. Other drawbacks include the risk of developing a
benzodiazepine dependence and
withdrawal syndrome; additionally, individuals with PTSD are at an increased risk of
abusing benzodiazepines.
[141][161]
Glucocorticoids: In addition, post-stress high-dose
corticosterone
administration was recently found to reduce "PTSD-like" behaviors in a
rat model of PTSD. In this study, corticosterone impaired memory
performance, suggesting that it may reduce risk for PTSD by interfering
with consolidation of traumatic memories.
[162] The neurodegenerative effects of the glucocorticoids, however, may prove this treatment counterproductive.
[163]
Monoamine-oxidase inhibitors (MAOIs):
Phenelzine has for some time
[when?] been observed to be effective with hyperarousal and depression and is especially effective with nightmares.
[144]
Other
- Exercise, sport and physical activity
Physical activity can have an impact on people's psychological wellbeing
[165] and physical health.
[166]
The U.S. National Center for PTSD recommends moderate exercise as a way
to distract from disturbing emotions, build self-esteem and increase
feelings of being in control again. They recommend a discussion with a
doctor before starting an exercise program.
[167]
Some uncontrolled studies have found benefits for people with PTSD from exercise programs.
[165]
A small trial studied adding a physical component to biofeedback-based
CBT with traumatized refugees. The authors concluded that physical
activity may lead to clinical improvement, but bigger trials are needed.
[168] More trials are underway.
[169][170][171]
- Play therapy for children
Play is thought to help children link their inner thoughts with their
outer world, connecting real experiences with abstract thought.
[172]
Repetitive play can also be one of the ways a child relives traumatic
events, and that can be a symptom of traumatization in a child or young
person.
[173]
Play is a familiar way for children and young people to indirectly
address what worries them, so it is often used as an element of
psychological treatment – for example, using play materials or drawing
to help a child focus on their feelings and events.
[2][172]
Play therapy means using games, drawings and play materials to express,
understand and control feelings rather than as a means of
communication.
[172][174]
Although it is commonly used, there have not been enough studies
comparing outcomes in groups of children receiving and not receiving
play therapy, so the effects of play therapy are not yet understood.
[2][172]
