The Dual Reuptake Wars

The Dual Reuptake Wars

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I know what you’re thinking, “This is going to be a Cymbalta vs. Effexor article, and Cymbalta will get another TCR drubbing as it did last year.”

Not quite. In fact, there are two major battles to be reviewed: Effexor vs. Cymbalta, but probably more relevant, Effexor vs. Lexapro.

First, a quick review. With the initial approval of Prozac in 1988, the 1990s were the age of the SSRIs. The first SNRI, Effexor (venlafaxine), made its debut in 1995, but this immediate release form bombed, largely because no patient could take a dose without nausea, insomnia, and fatigue, earning the product the early nickname of “side effexor.” But in 1998, Effexor XR came to the rescue, as an extended release version that was remarkably well tolerated. In 2001, a Wyeth guardian angel named Michael Thase published the famous “pooled analysis,” combining the results of eight Effexor vs. SSRI trials, and reporting a 45% remission rate for Effexor vs. 35% for SSRIs and 25% for placebo (Br J Psychiatry 2001;178:234-241).

Then, along came Lexapro, gaining FDA approval in 2002. TCR did a brief review of Lexapro in 2003 (TCR, January 2003). We reviewed studies comparing it with Celexa, showing that 10 mg of Lexapro proved as effective as 40 mg of Celexa, and was better tolerated. Forest ran with the data, and mounted an ingenious marketing campaign that basically convinced most physicians that Lexapro is the most tolerable SSRI on the market, and that you don’t have to sacrifice efficacy for tolerability.

The campaign was so good that the trade journal Medical Marketing & Media gave Forest’s Lexapro crew its “marketing team of the year award” for 2003. This reward didn’t come cheap. The most recent drug advertising survey reported that Lexapro was the most lavish spender on glossy ads in medical journals, outspending all other drugs in America, whether “psychiatric” or “medical.”

Chances are that you, dear reader, have bought into the Lexapro message of high tolerability, since most psychiatrists I talk to seem to believe it. But the data to support this is surprisingly weak. Your local Forest reps have certainly circulated two Forest-funded studies comparing Lexapro with Effexor, which is not the right comparison, since most of us already believe that Effexor less tolerable than SSRIs but we use it because of putatively better efficacy. Nonetheless, one study compared Lexapro 10-20 mg with Effexor XR 75-225 mg, and reported a discontinuation rate of 16% on Effexor vs. 4.1% on Lexapro (J Clin Psychiatry 2004; 65:1190-1196).

The hitch was that the design forced investigators to rapidly titrate Effexor up to 225 by day nine, a nausea- inducing schedule that we community psychiatrists only use when we’re desperate to decrease our patient load. So you can throw out those numbers as being irrelevant to usual practice.

The other, saner, study, started patients at 75 mg of Effexor, and allowed investigators to double the dose in two weeks if clinically indicated. The mean doses at week 8 were 12.1 mg for Lexapro and 95.2 mg for Effexor. The dropout rates were 11% for Effexor and 8% for Lexapro–not statistically different. However, the specific side effects of nausea, constipation, and increased sweating were all significantly more common among Effexor patients (Neuropsychobiology 2004; 50:57-64). The bottom line is that Effexor is somewhat less tolerable than Lexapro in typical clinical practice circumstances–but not dramatically less.

More to the point, of course, would be a comparison between Lexapro and an SSRI in terms of side effects. But the only such comparison published is between Lexapro and Celexa. Studies that found that a tiny 10 mg of Lexapro was better tolerated than a hefty 40 mg of Celexa–no big surprise there. These studies were apparently crafted to show up Celexa as it was on the verge of going generic.

What about Effexor’s famous efficacy gap? The two head-to-heads between Lexapro and Effexor showed similar efficacy, calling this into question. A larger pooled analysis of Effexor vs. SSRI studies, called the COMPARE study, is nearing publication (preliminary data available from Wyeth Medical Affairs). Instead of only 8 studies, this one includes data from 32 studies, and the Effexor efficacy gap has narrowed to a 41% to 35% advantage (vs. 45% to 35% in the smaller analysis). As with the original study, the most damning critique is that many patients in the SSRI arm may have tried and failed SSRIs in the past. Such patients were not excluded from these studies, and if there were many of them, it would stack the odds in favor of Effexor.

And Cymbalta? It got a nice shot in the arm with a recent FDA approval for treating diabetic neuropathy. How does this relate to depression? It doesn’t, although it does put a little more face validity on Lilly’s journal-saturating ads encouraging us to ask patients “Where does it hurt?”

In terms of response and remission rates, Cymbalta posts similar numbers to all the existing antidepressants, with reported response rates in the range of 45-50% and remission rates of 31-43% (see TCR Jan 2004 for a full review of this data). The only head-to-head involving Cymbalta compared it with Prozac (fluoxetine), but the study design was stacked in Cymbaltas favor, since a robust 60 mg a day of Cymbalta was compared with a paltry 20 mg of Prozac (J Clin Psychiatry 2002, 63:225- 231). With regard to side effects, it’s probably a little bit better tolerated than Effexor, a little worse than the SSRIs.

Cymbalta is taking a mild hit because of safety data showing that 1% of Cymbalta-treated patients develop elevated liver function tests (LFTs), vs. only 0.2% of patients on placebo (see its package insert for details). Lilly reps have taken to discouraging Cymbalta prescribing in the hard-drinking population for this reason, and TCR recommends occasional monitoring of LFTs in any patient on Cymbalta.

TCR VERDICT: The antidepressant horse race continues!

Psychotherapy and Pharmacotherapy for Patients with Dissociative Identity Disorder

There is a wide variety of what have been called 𠇍issociative disorders,” including dissociative amnesia, dissociative fugue, depersonalization disorder, dissociative identity disorder, and forms of dissociative disorder not otherwise specified. Some of these diagnoses, particularly dissociative identity disorder, are controversial and have been questioned by many clinicians over the years. The disorders may be under-diagnosed or misdiagnosed, but many persons who have experienced trauma report 𠇍issociative” symptoms. Prevalence of dissociative disorders is unknown, but current estimates are higher than previously thought. This paper reviews clinical, phenomenological, and epidemiological data regarding diagnosis in general, and illustrates possible treatment interventions for dissociative identity disorder, with a focus on psychotherapy interventions and a review of current psychopharmacology recommendations as part of a comprehensive multidisciplinary treatment plan.


Symptoms of PTSD generally begin within the first three months after the inciting traumatic event, but may not begin until years later. [1] [3] In the typical case, the individual with PTSD persistently avoids either trauma-related thoughts and emotions or discussion of the traumatic event, and may even have amnesia of the event. [1] However, the event is commonly relived by the individual through intrusive, recurrent recollections, dissociative episodes of reliving the trauma ("flashbacks"), and nightmares (50 to 70% [19] ). [20] While it is common to have symptoms after any traumatic event, these must persist to a sufficient degree (i.e., causing dysfunction in life or clinical levels of distress) for longer than one month after the trauma to be classified as PTSD (clinically significant dysfunction or distress for less than one month after the trauma may be acute stress disorder). [1] [21] [22] [23] Some following a traumatic event experience post-traumatic growth. [24]

Associated medical conditions

Trauma survivors often develop depression, anxiety disorders, and mood disorders in addition to PTSD. [25]

Substance use disorder, such as alcohol use disorder, commonly co-occur with PTSD. [26] Recovery from post-traumatic stress disorder or other anxiety disorders may be hindered, or the condition worsened, when substance use disorders are comorbid with PTSD. Resolving these problems can bring about improvement in an individual's mental health status and anxiety levels. [27] [28]

In children and adolescents, there is a strong association between emotional regulation difficulties (e.g. mood swings, anger outbursts, temper tantrums) and post-traumatic stress symptoms, independent of age, gender, or type of trauma. [29]

Persons considered at risk include combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk. [31] Other occupations that are at higher risk include police officers, firefighters, ambulance personnel, health care professionals, train drivers, divers, journalists, and sailors, in addition to people who work at banks, post offices or in stores. [32]


PTSD has been associated with a wide range of traumatic events. The risk of developing PTSD after a traumatic event varies by trauma type [33] [34] and is highest following exposure to sexual violence (11.4%), particularly rape (19.0%). [35] Men are more likely to experience a traumatic event (of any type), but women are more likely to experience the kind of high-impact traumatic event that can lead to PTSD, such as interpersonal violence and sexual assault. [36]

Motor vehicle collision survivors, both children and adults, are at an increased risk of PTSD. [37] [38] Globally, about 2.6% of adults are diagnosed with PTSD following a non-life threatening traffic accident, and a similar proportion of children develop PTSD. [35] Risk of PTSD almost doubles to 4.6% for life-threatening auto accidents. [35] Females were more likely to be diagnosed with PTSD following a road traffic accident, whether the accident occurred during childhood or adulthood. [37] [38]

Post-traumatic stress reactions have been studied in children and adolescents. [39] The rate of PTSD might be lower in children than adults, but in the absence of therapy, symptoms may continue for decades. [40] One estimate suggests that the proportion of children and adolescents having PTSD in a non-wartorn population in a developed country may be 1% compared to 1.5% to 3% of adults. [40] On average, 16% of children exposed to a traumatic event develop PTSD, varying according to type of exposure and gender. [41] Similar to the adult population, risk factors for PTSD in children include: female gender, exposure to disasters (natural or manmade), negative coping behaviours, and/or lacking proper social support systems. [42]

Predictor models have consistently found that childhood trauma, chronic adversity, neurobiological differences, and familial stressors are associated with risk for PTSD after a traumatic event in adulthood. [43] [44] [45] It has been difficult to find consistently aspects of the events that predict, but peritraumatic dissociation has been a fairly consistent predictive indicator of the development of PTSD. [46] Proximity to, duration of, and severity of the trauma make an impact. It has been speculated that interpersonal traumas cause more problems than impersonal ones, [47] but this is controversial. [48] The risk of developing PTSD is increased in individuals who are exposed to physical abuse, physical assault, or kidnapping. [49] [50] Women who experience physical violence are more likely to develop PTSD than men. [49]

Intimate partner violence

An individual that has been exposed to domestic violence is predisposed to the development of PTSD. However, being exposed to a traumatic experience does not automatically indicate that an individual will develop PTSD. [51] There is a strong association between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy. [52]

Those who have experienced sexual assault or rape may develop symptoms of PTSD. [53] [54] PTSD symptoms include re-experiencing the assault, avoiding things associated with the assault, numbness, and increased anxiety and an increased startle response. The likelihood of sustained symptoms of PTSD is higher if the rapist confined or restrained the person, if the person being raped believed the rapist would kill them, the person who was raped was very young or very old, and if the rapist was someone they knew. The likelihood of sustained severe symptoms is also higher if people around the survivor ignore (or are ignorant of) the rape or blame the rape survivor. [55]

War-related trauma

Military service is a risk factor for developing PTSD. [56] Around 78% of people exposed to combat do not develop PTSD in about 25% of military personnel who develop PTSD, its appearance is delayed. [56]

Refugees are also at an increased risk for PTSD due to their exposure to war, hardships, and traumatic events. The rates for PTSD within refugee populations range from 4% to 86%. [57] While the stresses of war affect everyone involved, displaced persons have been shown to be more so than others. [58]

Challenges related to the overall psychosocial well-being of refugees are complex and individually nuanced. Refugees have reduced levels of well-being and a high rates of mental distress due to past and ongoing trauma. Groups that are particularly affected and whose needs often remain unmet are women, older people and unaccompanied minors. [59] Post-traumatic stress and depression in refugee populations also tend to affect their educational success. [59]

Unexpected death of a loved one

Sudden, unexpected death of a loved one is the most common traumatic event type reported in cross-national studies. [35] [60] However, the majority of people who experience this type of event will not develop PTSD. An analysis from the WHO World Mental Health Surveys found a 5.2% risk of developing PTSD after learning of the unexpected death of a loved one. [60] Because of the high prevalence of this type of traumatic event, unexpected death of a loved one accounts for approximately 20% of PTSD cases worldwide. [35]

Life-threatening illness

Medical conditions associated with an increased risk of PTSD include cancer, [61] [62] [63] heart attack, [64] and stroke. [65] 22% of cancer survivors present with lifelong PTSD like symptoms. [66] Intensive-care unit (ICU) hospitalization is also a risk factor for PTSD. [67] Some women experience PTSD from their experiences related to breast cancer and mastectomy. [68] [69] [61] Loved ones of those who experience life-threatening illnesses are also at risk for developing PTSD, such as parents of child with chronic illnesses. [70]

Pregnancy-related trauma

Women who experience miscarriage are at risk of PTSD. [71] [72] [73] Those who experience subsequent miscarriages have an increased risk of PTSD compared to those experiencing only one. [71] PTSD can also occur after childbirth and the risk increases if a woman has experienced trauma prior to the pregnancy. [74] [75] Prevalence of PTSD following normal childbirth (that is, excluding stillbirth or major complications) is estimated to be between 2.8 and 5.6% at 6 weeks postpartum, [76] with rates dropping to 1.5% at 6 months postpartum. [76] [77] Symptoms of PTSD are common following childbirth, with prevalence of 24-30.1% [76] at 6 weeks, dropping to 13.6% at 6 months. [78] Emergency childbirth is also associated with PTSD. [79]


There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone. [46] For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twin's having PTSD compared to twins that were dizygotic (non-identical twins). [80] Women with a smaller hippocampus might be more likely to develop PTSD following a traumatic event based on preliminary findings. [81] Research has also found that PTSD shares many genetic influences common to other psychiatric disorders. Panic and generalized anxiety disorders and PTSD share 60% of the same genetic variance. Alcohol, nicotine, and drug dependence share greater than 40% genetic similarities. [46]

Several biological indicators have been identified that are related to later PTSD development. Heightened startle responses and, with only preliminary results, a smaller hippocampal volume have been identified as possible biomarkers for heightened risk of developing PTSD. [82] Additionally, one study found that soldiers whose leukocytes had greater numbers of glucocorticoid receptors were more prone to developing PTSD after experiencing trauma. [83]


PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, which creates deep neurological patterns in the brain. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations. [21] [84] During traumatic experiences, the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD. [85]

PTSD causes biochemical changes in the brain and body, that differ from other psychiatric disorders such as major depression. Individuals diagnosed with PTSD respond more strongly to a dexamethasone suppression test than individuals diagnosed with clinical depression. [86] [87]

Most people with PTSD show a low secretion of cortisol and high secretion of catecholamines in urine, [88] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals. [89] This is in contrast to the normative fight-or-flight response, in which both catecholamine and cortisol levels are elevated after exposure to a stressor. [90]

Brain catecholamine levels are high, [91] and corticotropin-releasing factor (CRF) concentrations are high. [92] [93] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.

The maintenance of fear 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, [94] which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma. [95] 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. [46]

The HPA axis is responsible for coordinating the hormonal response to stress. [46] Given the strong cortisol suppression to dexamethasone in PTSD, HPA axis abnormalities are likely predicated on strong negative feedback inhibition of cortisol, itself likely due to an increased sensitivity of glucocorticoid receptors. [96] PTSD has been hypothesized to be a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis. [97]

Low cortisol levels may predispose individuals to PTSD: Following war trauma, Swedish soldiers serving in Bosnia and Herzegovina with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms, following war trauma, than soldiers with normal pre-service levels. [98] Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained—that is, longer and more distressing—response, setting the stage for PTSD.

It is thought that the locus coeruleus-noradrenergic system mediates the over-consolidation of fear memory. High levels of cortisol reduce noradrenergic activity, and because people with PTSD tend to have reduced levels of cortisol, it has been proposed that individuals with PTSD cannot regulate the increased noradrenergic response to traumatic stress. [85] Intrusive memories and conditioned fear responses are thought to be a result of the response to associated triggers. 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. [46]

Other studies indicate that people that suffer from PTSD have chronically low levels of serotonin, which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity. [99] Serotonin also contributes to the stabilization of glucocorticoid production.

Dopamine levels in a person with PTSD can contribute to symptoms: low levels can contribute to anhedonia, apathy, impaired attention, and motor deficits high levels can contribute to psychosis, agitation, and restlessness. [99]

Several studies described elevated concentrations of the thyroid hormone triiodothyronine in PTSD. [100] This kind of type 2 allostatic adaptation may contribute to increased sensitivity to catecholamines and other stress mediators.

Hyperresponsiveness in the norepinephrine system can also be caused by continued exposure to high stress. Overactivation of norepinephrine receptors in the prefrontal cortex can be connected to the flashbacks and nightmares frequently experienced by those with PTSD. A decrease in other norepinephrine functions (awareness of the current environment) prevents the memory mechanisms in the brain from processing the experience, and emotions the person is experiencing during a flashback are not associated with the current environment. [99]

There is considerable controversy within the medical community regarding the neurobiology of PTSD. A 2012 review showed no clear relationship between cortisol levels and PTSD. The majority of reports indicate people with PTSD have elevated levels of corticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone. [46] [101]


A meta-analysis of structural MRI studies found an association with reduced total brain volume, intracranial volume, and volumes of the hippocampus, insula cortex, and anterior cingulate. [103] Much of this research stems from PTSD in those exposed to the Vietnam War. [104] [105]

People with PTSD have decreased brain activity in the dorsal and rostral anterior cingulate cortices and the ventromedial prefrontal cortex, areas linked to the experience and regulation of emotion. [106]

The amygdala is strongly involved in forming emotional memories, especially fear-related memories. During high stress, the hippocampus, which is associated with placing memories in the correct context of space and time and memory recall, is suppressed. According to one theory this suppression may be the cause of the flashbacks that can affect people with PTSD. 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 person's memory. [46] [107]

The amygdalocentric model of PTSD proposes that the amygdala is very much aroused and insufficiently controlled by the medial prefrontal cortex and the hippocampus, in particular during extinction. [108] This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability. [108] [109]

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. [46] While as a whole, amygdala hyperactivity is reported by meta analysis of functional neuroimaging in PTSD, there is a large degree of heterogeniety, more so than in social anxiety disorder or phobic disorder. Comparing dorsal (roughly the CeA) and ventral(roughly the BLA) clusters, hyperactivity is more robust in the ventral cluster, while hypoactivity is evident in the dorsal cluster. The distinction may explain the blunted emotions in PTSD (via desensitization in the CeA) as well as the fear related component. [110]

In a 2007 study Vietnam War combat veterans with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans having suffered no such symptoms. [111] This finding was not replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany). [112]

Evidence suggests that endogenous cannabinoid levels are reduced in PTSD, particularly anandamide, and that cannabinoid receptors (CB1) are increased in order to compensate. [113] There appears to be a link between increased CB1 receptor availability in the amygdala and abnormal threat processing and hyperarousal, but not dysphoria, in trauma survivors.

A 2020 study found no evidence for conclusions from prior research that suggested low IQ is a risk factor for developing PTSD. [114]

PTSD can be difficult to diagnose, because of:

  • the subjective nature of most of the diagnostic criteria (although this is true for many mental disorders)
  • the potential for over-reporting, e.g., while seeking disability benefits, or when PTSD could be a mitigating factor at criminal sentencing [citation needed]
  • the potential for under-reporting, e.g., stigma, pride, fear that a PTSD diagnosis might preclude certain employment opportunities
  • symptom overlap with other mental disorders such as obsessive compulsive disorder and generalized anxiety disorder [115]
  • association with other mental disorders such as major depressive disorder and generalized anxiety disorder
  • substance use disorders, which often produce some of the same signs and symptoms as PTSD and
  • substance use disorders can increase vulnerability to PTSD or exacerbate PTSD symptoms or both and
  • PTSD increases the risk for developing substance use disorders.
  • the differential expression of symptoms culturally (specifically with respect to avoidance and numbing symptoms, distressing dreams, and somatic symptoms) [116]


There are a number of PTSD screening instruments for adults, such as the PTSD Checklist for DSM-5 (PCL-5) [117] [118] and the Primary Care PTSD Screen for DSM-5 (PC-PTSD-5). [119]

There are also several screening and assessment instruments for use with children and adolescents. These include the Child PTSD Symptom Scale (CPSS), [120] [121] Child Trauma Screening Questionnaire, [122] [123] and UCLA Post-traumatic Stress Disorder Reaction Index for DSM-IV. [124] [125]

In addition, there are also screening and assessment instruments for caregivers of very young children (six years of age and younger). These include the Young Child PTSD Screen, [126] the Young Child PTSD Checklist, [126] and the Diagnostic Infant and Preschool Assessment. [127]


Evidence-based assessment principles, including a multimethod assessment approach, form the foundation of PTSD assessment. [128] [129] [130]

Diagnostic and statistical manual

PTSD was classified as an anxiety disorder in the DSM-IV, but has since been reclassified as a "trauma- and stressor-related disorder" in the DSM-5. [1] The DSM-5 diagnostic criteria for PTSD include four symptom clusters: re-experiencing, avoidance, negative alterations in cognition/mood, and alterations in arousal and reactivity. [1] [3]

International classification of diseases

The International Classification of Diseases and Related Health Problems 10 (ICD-10) classifies PTSD under "Reaction to severe stress, and adjustment disorders." [131] The ICD-10 criteria for PTSD include re-experiencing, avoidance, and either increased reactivity or inability to recall certain details related to the event. [131]

The ICD-11 diagnostic description for PTSD contains three components or symptom groups (1) re-experiencing, (2) avoidance, and (3) heightened sense of threat. [132] [133] ICD-11 no longer includes verbal thoughts about the traumatic event as a symptom. [133] There is a predicted lower rate of diagnosed PTSD using ICD-11 compared to ICD10 or DSM-5. [133] ICD-11 also proposes identifying a distinct group with complex post-traumatic stress disorder (CPTSD), who have more often experienced several or sustained traumas and have greater functional impairment than those with PTSD. [133]

Differential diagnosis

A diagnosis of PTSD requires that the person has been exposed to an extreme stressor. 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.

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. [20]

Obsessive compulsive disorder may be diagnosed for intrusive thoughts that are recurring but not related to a specific traumatic event. [20]

In extreme cases of prolonged, repeated traumatization where there is no viable chance of escape, survivors may develop complex post-traumatic stress disorder. [134] This occurs as a result of layers of trauma rather than a single traumatic event, and includes additional symptomatology, such as the loss of a coherent sense of self. [135]

Modest benefits have been seen from early access to cognitive behavioral therapy. Critical incident stress management has been suggested as a means of preventing PTSD, but subsequent studies suggest the likelihood of its producing negative outcomes. [136] [137] A 2019 Cochrane 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." [138] The World Health Organization recommends against the use of benzodiazepines and antidepressants in for acute stress (symptoms lasting less than one month). [139] Some evidence supports the use of hydrocortisone for prevention in adults, although there is limited or no evidence supporting propranolol, escitalopram, temazepam, or gabapentin. [140]

Psychological debriefing

Trauma-exposed individuals often receive treatment called psychological debriefing in an effort to prevent PTSD, which 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. [141] However, several meta-analyses find that psychological debriefing is unhelpful and is potentially harmful. [141] [142] [143] This is true for both single-session debriefing and multiple session interventions. [138] As of 2017 The American Psychological Association assessed psychological debriefing as No Research Support/Treatment is Potentially Harmful. [144]

Risk-targeted interventions

Risk-targeted interventions are those that attempt to mitigate specific formative information or events. It can target modeling normal behaviors, instruction on a task, or giving information on the event. [145] [146]

Reviews of studies have found that combination therapy (psychological and pharmacotherapy) is no more effective than psychological therapy alone. [12]


The approaches with the strongest evidence include behavioral and cognitive-behavioral therapies such as prolonged exposure therapy, [147] cognitive processing therapy, and eye movement desensitization and reprocessing (EMDR). [148] [149] [150] There is some evidence for brief eclectic psychotherapy (BEP), narrative exposure therapy (NET), and written narrative exposure therapy. [151]

A 2019 Cochrane review evaluated couples and family therapies compared to no care and individual and group therapies for the treatment of PTSD. [152] There were too few studies on couples therapies to determine if substantive benefits were derived but preliminary RCTs suggested that couples therapies may be beneficial for reducing PTSD symptoms. [152]

A meta-analytic comparison of EMDR and cognitive behavioral therapy (CBT) 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. [153] A meta-analysis in children and adolescents also found that EMDR was as efficacious as cognitive behavioral therapy. [154]

Children with PTSD are far more likely to pursue treatment at school (because of its proximity and ease) than at a free clinic. [155]

Cognitive behavioral therapy

CBT seeks to change the way a person feels and acts by changing the patterns of thinking or behavior, or both, responsible for negative emotions. Results from a 2018 systematic review found high strength of evidence that supports CBT-exposure therapy efficacious for a reduction in PTSD and depression symptoms, as well as the loss of PTSD diagnosis. [156] 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. [157] [158] 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. [159] [160] The provision of CBT in an Internet-based format has also been studied in a 2018 Cochrane review. This review did find similar beneficial effects for Internet-based settings as in face-to-face but the quality of the evidence was low due to the small number of trials reviewed. [161]

Exposure therapy is a type of cognitive behavioral therapy [162] 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. [ citation needed ] The success of exposure-based therapies has raised the question of whether exposure is a necessary ingredient in the treatment of PTSD. [163] Some organizations [ which? ] have endorsed the need for exposure. [164] [165] The U.S. Department of Veterans Affairs has been actively training mental health treatment staff in prolonged exposure therapy [166] and Cognitive Processing Therapy [167] in an effort to better treat U.S. veterans with PTSD.

Recent research on contextually based third-generation behavior therapies suggests that they may produce results comparable to some of the better validated therapies. [168] Many of these therapy methods have a significant element of exposure [169] and have demonstrated success in treating the primary problems of PTSD and co-occurring depressive symptoms. [170]

Eye movement desensitization and reprocessing

Eye movement desensitization and reprocessing (EMDR) is a form of psychotherapy developed and studied by Francine Shapiro. [171] 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. [171]

In 2002, Shapiro and Maxfield published a theory of why this might work, called adaptive information processing. [172] 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. [173] The therapist initiates voluntary rapid eye movements while the person focuses on memories, feelings or thoughts about a particular trauma. [40] [174] 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. [40] EMDR closely resembles cognitive behavior therapy as it combines exposure (re-visiting the traumatic event), working on cognitive processes and relaxation/self-monitoring. [40] 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. [175]

There have been several small controlled trials of four to eight weeks of EMDR in adults [176] as well as children and adolescents. [174] There is moderate strength of evidence to support the efficacy of EMDR "for reduction in PTSD symptoms, loss of diagnosis, and reduction in depressive symptoms" according to a 2018 systematic review update. [156] 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 and thus results should be interpreted with caution pending further research. [176] There was not enough evidence to know whether or not EMDR could eliminate PTSD in adults. [176] In children and adolescents, a recent meta-analysis of randomized controlled trials using MetaNSUE to avoid biases related to missing information found that EMDR was at least as efficacious as CBT, and superior to waitlist or placebo. [154] There was some evidence that EMDR might prevent depression. [176] There were no studies comparing EMDR to other psychological treatments or to medication. [176] Adverse effects were largely unstudied. [176] 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. [174]

The eye movement component of the therapy may not be critical for benefit. [40] [173] 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. [175] Authors of a meta-analysis published in 2013 stated, "We found that people treated with eye movement therapy had greater improvement in their symptoms of post-traumatic stress disorder than people given therapy without eye movements. Secondly we found that that in laboratory studies the evidence concludes that thinking of upsetting memories and simultaneously doing a task that facilitates eye movements reduces the vividness and distress associated with the upsetting memories." [149]

Interpersonal psychotherapy

Other approaches, in particular involving social supports, [177] [178] may also be important. An open trial of interpersonal psychotherapy [179] reported high rates of remission from PTSD symptoms without using exposure. [180] A current, NIMH-funded trial in New York City is now (and into 2013) comparing interpersonal psychotherapy, prolonged exposure therapy, and relaxation therapy. [181] [ full citation needed ] [182] [183]


While many medications do not have enough evidence to support their use, four (sertraline, fluoxetine, paroxetine, and venlafaxine) have been shown to have a small to modest benefit over placebo. [14] With many medications, residual PTSD symptoms following treatment is the rule rather than the exception. [184]


Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) may have some benefit for PTSD symptoms. [14] [185] [186] Tricyclic antidepressants are equally effective but are less well tolerated. [187] Evidence provides support for a small or modest improvement with sertraline, fluoxetine, paroxetine, and venlafaxine. [14] [188] Thus, these four medications are considered to be first-line medications for PTSD. [185] [4]


Benzodiazepines are not recommended for the treatment of PTSD due to a lack of evidence of benefit and risk of worsening PTSD symptoms. [189] Some authors believe that the use of benzodiazepines is contraindicated for acute stress, as this group of drugs can cause dissociation. [190] Nevertheless, some use benzodiazepines with caution for short-term anxiety and insomnia. [191] [192] [193] While benzodiazepines can alleviate acute anxiety, there is no consistent evidence that they can stop the development of PTSD and may actually increase the risk of developing PTSD 2–5 times. [13] 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. For those who already have PTSD, benzodiazepines may worsen and prolong the course of illness, by worsening psychotherapy outcomes, and causing or exacerbating aggression, depression (including suicidality), and substance use. [13] Drawbacks include the risk of developing a benzodiazepine dependence, tolerance (i.e., short-term benefits wearing off with time), and withdrawal syndrome additionally, individuals with PTSD (even those without a history of alcohol or drug misuse) are at an increased risk of abusing benzodiazepines. [4] [194] Due to a number of other treatments with greater efficacy for PTSD and less risks (e.g., prolonged exposure, cognitive processing therapy, eye movement desensitization and reprocessing, cognitive restructuring therapy, trauma-focused cognitive behavioral therapy, brief eclectic psychotherapy, narrative therapy, stress inoculation training, serotonergic antidepressants, adrenergic inhibitors, antipsychotics, and even anticonvulsants), benzodiazepines should be considered relatively contraindicated until all other treatment options are exhausted. [11] [195] For those who argue that benzodiazepines should be used sooner in the most severe cases, the adverse risk of disinhibition (associated with suicidality, aggression and crimes) and clinical risks of delaying or inhibiting definitive efficacious treatments, make other alternative treatments preferable (e.g., inpatient, residential, partial hospitalization, intensive outpatient, dialectic behavior therapy and other fast-acting sedating medications such as trazodone, mirtazapine, amitripytline, doxepin, prazosin, propranolol, guanfacine, clonidine, quetiapine, olanzapine, valproate, gabapentin). [4] [195] [196]


Prazosin, an alpha-1 adrenergic antagonist, has been used in veterans with PTSD to reduce nightmares. Studies show variability in the symptom improvement, appropriate dosages, and efficacy in this population. [197] [198] [19]


Glucocorticoids may be useful for short-term therapy to protect against neurodegeneration caused by the extended stress response that characterizes PTSD, but long-term use may actually promote neurodegeneration. [199]


As of 2019 cannabis is specifically not recommended as a treatment. [200] [201] However, use of cannabis or derived products is widespread among U.S. veterans with PTSD. [202]

The cannabinoid nabilone is sometimes used for nightmares in PTSD. Although some short-term benefit was shown, adverse effects are common and it has not been adequately studied to determine efficacy. [203] Currently, a handful of states permit the use of medical cannabis for the treatment of PTSD. [204]


Exercise, sport and physical activity

Physical activity can influence people's psychological [205] and physical health. [206] 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. [207]

Play therapy for children

Play is thought to help children link their inner thoughts with their outer world, connecting real experiences with abstract thought. [208] Repetitive play can also be one way a child relives traumatic events, and that can be a symptom of trauma in a child or young person. [209] 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. [40] [208]

Military programs

Many veterans of the wars in Iraq and Afghanistan have faced significant physical, emotional, and relational disruptions. In response, the United States Marine Corps has instituted programs to assist them in re-adjusting to civilian life, especially in their relationships with spouses and loved ones, to help them communicate better and understand what the other has gone through. [210] Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist service members avoid or ameliorate PTSD and related problems. Wounded Warrior Project partnered with the US Department of Veterans Affairs to create Warrior Care Network, a national health system of PTSD treatment centers. [211] [212]


In 2020, the United States Food and Drug Administration granted marketing approval for an Apple Watch app call NightWare. The app aims to improve sleep for people suffering from PTSD-related nightmares, by vibrating when it detects a nightmare in progress based on monitoring heart rate and body movement. [213]

There is debate over the rates of PTSD found in populations, but, despite changes in diagnosis and the criteria used to define PTSD between 1997 and 2013, epidemiological rates have not changed significantly. [215] [216] Most of the current reliable data regarding the epidemiology of PTSD is based on DSM-IV criteria, as the DSM-5 was not introduced until 2013.

The United Nations' World Health Organization publishes estimates of PTSD impact for each of its member states the latest data available are for 2004. Considering only the 25 most populated countries ranked by overall age-standardized Disability-Adjusted Life Year (DALY) rate, the top half of the ranked list is dominated by Asian/Pacific countries, the US, and Egypt. [217] Ranking the countries by the male-only or female-only rates produces much the same result, but with less meaningfulness, as the score range in the single-sex rankings is much-reduced (4 for women, 3 for men, as compared with 14 for the overall score range), suggesting that the differences between female and male rates, within each country, is what drives the distinctions between the countries. [218] [219]

As of 2017, the cross-national lifetime prevalence of PTSD was 3.9%, based on a survey were 5.6% had been exposed to trauma. [220] The primary factor impacting treatment-seeking behavior, which can help to mitigate PTSD development after trauma was income, while being younger, female, and having less social status (less education, lower individual income, and being unemployed) were all factors associated with less treatment-seeking behaviour. [220]

Age-standardized Disability-adjusted life year (DALY) rates for PTSD, per 100,000 inhabitants, in 25 most populous countries, ranked by overall rate (2004)
Region Country PTSD DALY rate,
overall [217]
females [218]
males [219]
Asia / Pacific Thailand 59 86 30
Asia / Pacific Indonesia 58 86 30
Asia / Pacific Philippines 58 86 30
Americas USA 58 86 30
Asia / Pacific Bangladesh 57 85 29
Africa Egypt 56 83 30
Asia / Pacific India 56 85 29
Asia / Pacific Iran 56 83 30
Asia / Pacific Pakistan 56 85 29
Asia / Pacific Japan 55 80 31
Asia / Pacific Myanmar 55 81 30
Europe Turkey 55 81 30
Asia / Pacific Vietnam 55 80 30
Europe France 54 80 28
Europe Germany 54 80 28
Europe Italy 54 80 28
Asia / Pacific Russian Federation 54 78 30
Europe United Kingdom 54 80 28
Africa Nigeria 53 76 29
Africa Dem. Republ. of Congo 52 76 28
Africa Ethiopia 52 76 28
Africa South Africa 52 76 28
Asia / Pacific China 51 76 28
Americas Mexico 46 60 30
Americas Brazil 45 60 30

United States

The National Comorbidity Survey Replication has estimated that the lifetime prevalence of PTSD among adult Americans is 6.8%, with women (9.7%) more than twice as likely as men [99] (3.6%) to have PTSD at some point in their lives. [49] More than 60% of men and more than 60% of women experience at least one traumatic event in their life. The most frequently reported traumatic events by men are rape, combat, and childhood neglect or physical abuse. Women most frequently report instances of rape, sexual molestation, physical attack, being threatened with a weapon and childhood physical abuse. [99] 88% of men and 79% of women with lifetime PTSD have at least one comorbid psychiatric disorder. Major depressive disorder, 48% of men and 49% of women, and lifetime alcohol use disorder or dependence, 51.9% of men and 27.9% of women, are the most common comorbid disorders. [221]

Military combat

The United States Department of Veterans Affairs estimates that 830,000 Vietnam War veterans suffered symptoms of PTSD. [222] The National Vietnam Veterans' Readjustment Study (NVVRS) found 15% of male and 9% of female Vietnam veterans had PTSD at the time of the study. Life-time prevalence of PTSD was 31% for males and 27% for females. In a reanalysis of the NVVRS data, along with analysis of the data from the Matsunaga Vietnam Veterans Project, Schnurr, Lunney, Sengupta, and Waelde found that, contrary to the initial analysis of the NVVRS data, a large majority of Vietnam veterans suffered from PTSD symptoms (but not the disorder itself). Four out of five reported recent symptoms when interviewed 20–25 years after Vietnam. [223]

A 2011 study from Georgia State University and San Diego State University found that rates of PTSD diagnosis increased significantly when troops were stationed in combat zones, had tours of longer than a year, experienced combat, or were injured. Military personnel serving in combat zones were 12.1 percentage points more likely to receive a PTSD diagnosis than their active-duty counterparts in non-combat zones. Those serving more than 12 months in a combat zone were 14.3 percentage points more likely to be diagnosed with PTSD than those having served less than one year. Experiencing an enemy firefight was associated with an 18.3 percentage point increase in the probability of PTSD, while being wounded or injured in combat was associated with a 23.9 percentage point increase in the likelihood of a PTSD diagnosis. For the 2.16 million U.S. troops deployed in combat zones between 2001 and 2010, the total estimated two-year costs of treatment for combat-related PTSD are between $1.54 billion and $2.69 billion. [224]

As of 2013, rates of PTSD have been estimated at up to 20% for veterans returning from Iraq and Afghanistan. [225] As of 2013 13% of veterans returning from Iraq were unemployed. [226]

Man-made disasters

The September 11 attacks took the lives of nearly 3,000 people, leaving 6,000 injured. [227] First responders (police and firefighters), emergency medical services, sanitation workers, and volunteers were all involved in the recovery efforts. The prevalence of probable PTSD in these highly exposed populations was estimated across several studies using in-person, telephone, and online interviews and questionnaires. [227] [228] [229] Overall prevalence of PTSD was highest immediately following the attacks and decreased over time. However, disparities were found among the different types of recovery workers. [227] [228] The rate of probable PTSD for first responders was lowest directly after the attacks and increased from ranges of 4.8-7.8% to 7.4-16.5% between the 5-6 year follow-up and a later assessment. [227] When comparing traditional responders to non-traditional responders (volunteers), the probable PTSD prevalence 2.5 years after the initial visit was greater in volunteers with estimates of 11.7% and 17.2% respectively. [227] Volunteer participation in tasks atypical to the defined occupational role was a significant risk factor for PTSD. [228] Other risk factors included exposure intensity, earlier start date, duration of time spent on site, and constant, negative reminders of the trauma. [227] [228] Additional research has been performed to understand the social consequences of the September 11 attacks. Alcohol consumption was assessed in a cohort of World Trade Center workers using the cut-annoyed-guilty-eye (CAGE) questionnaire for alcohol use disorder. Almost 50% of World Trade Center workers who self-identified as alcohol users reported drinking more during the rescue efforts. [229] Nearly a quarter of these individuals reported drinking more following the recovery. [229] If determined to have probable PTSD status, the risk of developing an alcohol problem was double compared to those without psychological morbidity. [229] Social disability was also studied in this cohort as a social consequence of the September 11 attacks. Defined by the disruption of family, work, and social life, the risk of developing social disability increased 17-fold when categorized as having probable PTSD. [229]

United States

The United States provides a range of benefits for veterans that the VA has determined have PTSD, which developed during, or as a result of, their military service. These benefits may include tax-free cash payments, [230] free or low-cost mental health treatment and other healthcare, [231] vocational rehabilitation services, [232] employment assistance, [233] and independent living support. [234] [235]

Young Iraqis have high rates of post-traumatic stress disorder due to the 2003 invasion of Iraq. [236]

United Kingdom

In the UK, there are various charities and service organisations dedicated to aiding veterans in readjusting to civilian life. The Royal British Legion and the more recently established Help for Heroes are two of Britain's more high-profile veterans' organisations which have actively advocated for veterans over the years. There has been some controversy that the NHS has not done enough in tackling mental health issues and is instead "dumping" veterans on charities such as Combat Stress. [237] [238]


Veterans Affairs Canada offers a new program that includes rehabilitation, financial benefits, job placement, health benefits program, disability awards, peer support [239] [240] [241] and family support. [242]

The 1952 edition of the DSM-I includes a diagnosis of "gross stress reaction", which has similarities to the modern definition and understanding of PTSD. [243] Gross stress reaction is defined as a normal personality using established patterns of reaction to deal with overwhelming fear as a response to conditions of great stress. [244] The diagnosis includes language which relates the condition to combat as well as to "civilian catastrophe". [244]

A USAF study carried out in 1979 focused on individuals (civilian and military) who had worked to recover or identify the remains of those who died in Jonestown. The bodies had been dead for several days, and a third of them had been children. The study used the term "dysphoria" to describe PTSD-like symptoms. [245]

Early in 1978, the diagnosis term "post-traumatic stress disorder" was first recommended in a working group finding presented to the Committee of Reactive Disorders. [246] The condition was described in the DSM-III (1980) as posttraumatic stress disorder. [243] [246] In the DSM-IV, the spelling "posttraumatic stress disorder" is used, while in the ICD-10, the spelling is "post-traumatic stress disorder". [247]

The addition of the term to the DSM-III was greatly influenced by the experiences and conditions of U.S. military veterans of the Vietnam War. [248] Owing to its association with the war in Vietnam, PTSD has become synonymous with many historical war-time diagnoses such as railway spine, stress syndrome, nostalgia, soldier's heart, shell shock, battle fatigue, combat stress reaction, or traumatic war neurosis. [249] [250] Some of these terms date back to the 19th century, which is indicative of the universal nature of the condition. In a similar vein, psychiatrist Jonathan Shay has proposed that Lady Percy's soliloquy in the William Shakespeare play Henry IV, Part 1 (act 2, scene 3, lines 40–62 [251] ), written around 1597, represents an unusually accurate description of the symptom constellation of PTSD. [252]

The correlations between combat and PTSD are undeniable according to Stéphane Audoin-Rouzeau and Annette Becker, "One-tenth of mobilized American men were hospitalized for mental disturbances between 1942 and 1945, and, after thirty-five days of uninterrupted combat, 98% of them manifested psychiatric disturbances in varying degrees." [253] In fact, much of the available published research regarding PTSD is based on studies done on veterans of the war in Vietnam. A study based on personal letters from soldiers of the 18th-century Prussian Army concludes that combatants may have had PTSD. [254] Aspects of PTSD in soldiers of ancient Assyria have been identified using written sources from 1300–600 BCE. These Assyrian soldiers would undergo a three-year rotation of combat before being allowed to return home, and were reported to have faced immense challenges in reconciling their past actions in war with their civilian lives. [255] Connections between the actions of Viking berserkers and the hyperarousal of post-traumatic stress disorder have also been drawn. [256]

The researchers from the Grady Trauma Project highlight the tendency people have to focus on the combat side of PTSD: "less public awareness has focused on civilian PTSD, which results from trauma exposure that is not combat related. " and "much of the research on civilian PTSD has focused on the sequelae of a single, disastrous event, such as the Oklahoma City bombing, September 11th attacks, and Hurricane Katrina". [257] Disparity in the focus of PTSD research affects the already popular perception of the exclusive interconnectedness of combat and PTSD. This is misleading when it comes to understanding the implications and extent of PTSD as a neurological disorder. Dating back to the definition of Gross stress reaction in the DSM-I, civilian experience of catastrophic or high stress events is included as a cause of PTSD in medical literature. The 2014 National Comorbidity Survey reports that "the traumas most commonly associated with PTSD are combat exposure and witnessing among men and rape and sexual molestation among women." [49] Because of the initial overt focus on PTSD as a combat related disorder when it was first fleshed out in the years following the war in Vietnam, in 1975 Ann Wolbert Burgess and Lynda Lytle Holmstrom defined Rape trauma syndrome, RTS, in order to draw attention to the striking similarities between the experiences of soldiers returning from war and of rape victims. [258] This paved the way for a more comprehensive understanding of causes of PTSD.

After PTSD became an official psychiatric diagnosis with the publication of DSM-III (1980), the number of personal injury lawsuits (tort claims) asserting the plaintiff suffered from PTSD increased rapidly. However, triers of fact (judges and juries) often regarded the PTSD diagnostic criteria as imprecise, a view shared by legal scholars, trauma specialists, forensic psychologists, and forensic psychiatrists. Professional discussions and debates in academic journals, at conferences, and between thought leaders, led to a more clearly-defined set of diagnostic criteria in DSM-IV, particularly the definition of a "traumatic event". [259]

The DSM-IV classified PTSD under anxiety disorders, but the DSM-5 created a new category called "trauma and stressor-related disorders," in which PTSD is now classified. [1]

The Diagnostic and Statistical Manual of Mental Disorders does not hyphenate 'post' and 'traumatic', thus, the DSM-5 lists the disorder as posttraumatic stress disorder. However, many scientific journal articles and other scholarly publications do hyphenate the name of the disorder, viz., post-traumatic stress disorder. [260] Dictionaries also differ with regard to the preferred spelling of the disorder with the Collins English Dictionary – Complete and Unabridged using the hyphenated spelling, and the American Heritage Dictionary of the English Language, Fifth Edition and the Random House Kernerman Webster's College Dictionary giving the non-hyphenated spelling. [261]

Some, particularly current or former U.S. Department of Defense officials, have used the terminology "PTSS" (syndrome instead of disorder, to avoid connotation of stigma), or just "PTS". [262]

The comedian George Carlin criticized the euphemism treadmill which led to progressive change of the way PTSD was referred to over the course of the 20th century, from "shell shock" in the First World War to the "battle fatigue" in the Second World War, to "operational exhaustion" in the Korean War, to the current "post-traumatic stress disorder", coined during the Vietnam War, which "added a hyphen" and which, he commented, "completely burie[s] [the pain] under jargon". He also stated that the name given to the condition has had a direct effect on the way veteran soldiers with PTSD were treated and perceived by civilian populations over time. [263]

Most knowledge regarding PTSD comes from studies in high-income countries. [264]

To recapitulate some of the neurological and neurobehavioral symptoms experienced by the veteran population of recent conflicts in Iraq and Afghanistan, researchers at the Roskamp Institute and the James A Haley Veteran's Hospital (Tampa) have developed an animal model to study the consequences of mild traumatic brain injury (mTBI) and PTSD. [265] In the laboratory, the researchers exposed mice to a repeated session of unpredictable stressor (i.e. predator odor while restrained), and physical trauma in the form of inescapable foot-shock, and this was also combined with a mTBI. In this study, PTSD animals demonstrated recall of traumatic memories, anxiety, and an impaired social behavior, while animals subject to both mTBI and PTSD had a pattern of disinhibitory-like behavior. mTBI abrogated both contextual fear and impairments in social behavior seen in PTSD animals. In comparison with other animal studies, [265] [266] examination of neuroendocrine and neuroimmune responses in plasma revealed a trend toward increase in corticosterone in PTSD and combination groups.

Stellate ganglion block is an experimental procedure for the treatment of PTSD. [267]

Researchers are investigating a number of experimental FAAH and MAGL-inhibiting drugs of hopes of finding a better treatment for anxiety and stress-related illnesses. [268] In 2016, the FAAH-inhibitor drug BIA 10-2474 was withdrawn from human trials in France due to adverse effects. [269]

MDMA-assisted psychotherapy has been shown to significantly reduce symptoms of PTSD compared to psychotherapy alone. [270]


Trauma-focused psychotherapies for PTSD (also known as "exposure-based" or "exposure" psychotherapies), such as prolonged exposure therapy (PE), eye movement desensitization and reprocessing (EMDR), and cognitive-reprocessing therapy (CPT) have the most evidence for efficacy and are recommended as first-line treatment for PTSD by almost all clinical practice guidelines. [271] [272] [273] Exposure-based psychotherapies demonstrate efficacy for PTSD caused by different trauma "types", such as combat, sexual-assault, or natural disasters. [271] At the same time, many trauma-focused psychotherapies evince high drop-out rates. [274]

Most systematic reviews and clinical guidelines indicate that psychotherapies for PTSD, most of which are trauma-focused therapies, are more effective than pharmacotherapy (medication), [275] although there are reviews that suggest exposure-based psychotherapies for PTSD and pharmacotherapy are equally effective. [276] Interpersonal psychotherapy shows preliminary evidence of probable efficacy, but more research is needed to reach definitive conclusions. [277]

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Interactions between transcranial direct current stimulation (tDCS) and pharmacological interventions in the Major Depressive Episode: findings from a naturalistic study

Background: Transcranial direct current stimulation (tDCS) is a non-invasive, neuromodulatory technique with an emerging role for treating major depression.

Objective: To investigate the interactions between tDCS and drug therapy in unipolar and bipolar depressed patients who were refractory for at least one pharmacological treatment.

Methods: This was a naturalistic study using data from 54 female and 28 male patients (mean age of 54 years) that consecutively visited our psychiatric unit. They received active tDCS (five consecutive days, 2mA, anodal stimulation over the left and cathodal over the right dorsolateral prefrontal cortex, twice a day, 20minutes). The outcome variable (mood) was evaluated using the Beck Depression Inventory (BDI) and the Hamilton Depression Rating Scale (HDRS). Predictor variables were age, gender, disorder and pharmacological treatment (seven dummy variables). We performed univariate and multivariate analyses as to identify predictors associated to the outcome.

Results: After 5 days of treatment, BDI and HDRS scores decreased significantly (29%±36%, 18%±9%, respectively, P<0.01 for both). Benzodiazepine use was independently associated with a worse outcome in both univariate (β=4.92, P<0.01) and multivariate (β=5.8, P<0.01) analyses whereas use of dual-reuptake inhibitors positively changed tDCS effects in the multivariate model (β=-4.7, P=0.02). A similar trend was observed for tricyclics (β=-4, P=0.06) but not for antipsychotics, non-benzodiazepine anticonvulsants and other drugs.

Conclusion: tDCS over the DLPFC acutely improved depressive symptoms. Besides the inherent limitations of our naturalistic design, our results suggest that tDCS effects might vary according to prior pharmacological treatment, notably benzodiazepines and some antidepressant classes. This issue should be further explored in controlled studies.

Keywords: Benzodiazepines Bipolar disorder Major depressive disorder Serotonin uptake inhibitors Transcranial direct current stimulation.

Jonathan Pollard to Israeli spies: “go the fuck home”

Jonathan Pollard, the man who has been called “one of the worst traitors of the 20th century,”[1] has a message for Israeli spies like him. Pollard agrees that Israelis in the US will always have “dual loyalty.” In other words, they will always be traitors, spies, liars, deceivers, extortionists, con artists, and double agents.

Pollard said to those who have accused him and Jews of having dual royalties: “If you don’t like the accusation of double loyalty, then go the fuck home.”[2] Pollard continued to say:

“It’s as simple as that. If you live in a country where you are constantly under that charge, then you don’t belong there. You go home. You come home. If you[‘re] outside Israel, then you live in a society in which you are basically considered unreliable. The bottom line on this charge of dual loyalty is, I’m sorry, we’re Jews, and if we’re Jews, we will always have dual loyalty.”[3]

What would Pollard say to a young US Jew working in the American security?

“I’d tell him, not doing anything is unacceptable. So simply going home [to Israel] is not acceptable. Making aliyah is not acceptable,” Pollard said. “You have to make a decision whether your concern for Israel and loyalty to Israel and loyalty to your fellow Jews is more important than your life.

“If you do nothing, and you turn your back, or simply make aliyah, and go on with your life, you’ll be no better than those Jews who before and after the destruction of the Temple said, ‘It’s not my responsibility.”[4]

Why would he even bring the destruction of the Temple to this question? Doesn’t that imply that people like Pollard are aware of the two-thousand-year struggle between Logos and anti-Logos?

One should also be asked: where is the Zionist media, the very powerful superstructure that seeks to literally demonize and de-platform anyone who would even dare to repeat what Pollard said? Is Pollard an anti-Semite? If not, then why wouldn’t the media apply the same rule everywhere? Isn’t that bias in itself?

[2] “Pollard claims Jews ‘will always have dual loyalty,’ whether they know it or not,” Times of Israel, March 21, 2021.

Monday Methods: On why ɽid Ancient Warriors Get PTSD?' isn't such a simple question.

It's one of the most commonly asked questions on AskHistorians: did soldiers in the ancient world get PTSD?

It's a simple question, one that could potentially have a one word answer ('yes' or 'no'). It's one with at least some empathy - we understand that the ancients lived in a harsh, brutal world, and people these days who live through harsh, brutal events often get diagnosed by psychiatrists or psychologists with post-traumatic stress disorder (usually called by the acronym PTSD). It's a reasonable question to ask. As would be the far less common question about whether ancient women got PTSD after experiencing the horrors of war that women experience.

It's also not a simple question at all, in any way, shape, or form, and clinicians and historians differ fundamentally on how to answer the question. This is because the question can't be resolved without first resolving some fairly fundamental questions about human nature, and why we are the way we are, that inevitably end up tipping over into broader philosophical stances.

Put it this way in 2014, an academic book titled Combat Trauma And The Ancient Greeks was edited by Peter Meineck and David Konstan. Lawrence A. Tritle's Chapter Four argued that the idea that PTSD is a modern phenomenon, the product of the Vietnam War, is "an assertion preposterous if it was not so tragic." Jason Crowley's Chapter Five argues the opposing position: "the soldier [with PTSD] is not, and indeed, can never be, universal."

I am perhaps unusual amongst flairs on r/AskHistorians in that I teach psychology (and the history thereof) at a tertiary level. and so I have things to say about all of this. There's probably going to be more psychology in this post than the usual r/AskHistorians post but this is still fundamentally a question about history - the psychology is just setting the scene for how to go about the history.

So what is PTSD?

It's a psychiatric disorder listed in the American Psychiatric Association's Diagnostic and Statistical Manuals since 1980.

Okay then, what is a psychiatric disorder?

In 1980 that the American Psychiatric Association published their third edition of the Diagnostic and Statistical Manual - the DSM-III - which was the first to include a disorder much like PTSD. The DSM-III was a radical and controversial change, in general, from previous DSMs, and it reflected a movement in psychiatry away from a post-Freudian framework, with its talk of neuroses and conversion disorders, to a more medical framework. From the 1950s to the 1970s, the psychiatric world had been revolutionised by the gradual introduction of a whole suite of psychiatric drugs which seemed to help people with neuroses. The DSM-III reflected psychiatry's interest in the medical, and its renewed interest in using medicine (as opposed to talking while on couches) to treat psychiatric disorders. The DSM-III was notably also agnostic towards the causes of psychiatric disorders - it was based on statistical studies which attempted to tease apart clusters of symptoms in order to put different clusters in different boxes.

There are some important ramifications of this. So, with a disease like diabetes, we know the cause(s) of the disease - a chemical in our body called insulin isn't doing what it should. As a result of knowing the cause, we also know the treatment: help the body regulate insulin more properly (NB: it may be slightly more complicated than this, but you get the gist).

However, with a diagnosis like depression (or PTSD), psychiatrists and psychologists fundamentally do not know what causes it. Sure, there are news articles every so often identifying such an such a brain chemical as a factor in depression, or such and such a gene as a factor. However, it's basically agreed by all sides that while these things may play a role, it's a complex stew. When it comes down to it, we're not entirely sure why antidepressants work (a type of antidepressant called a selective serotonin reuptake inhibitor inhibits the reuptake of a neurochemical called serotonin, and this seems to help depressed people feel a bit better - but it's also clear from voluminous neuroscience research that serotonin's role in 'not being depressed' is way more complicated than being the factor). Some researchers, recently, have argued that depression is in fact several different disorders with a variety of different causes despite basically similar symptoms. PTSD may well be a lot like depression in this sense. It might be that there are several different PTSD-like disorders which all get lumped into PTSD.

But at a deeper level, the way that psychiatrists put together the DSM-III and its successors lay this out into the open: PTSD, or any other psychiatric disorder in the DSM, is a construct. In its original form, it doesn't pretend to be anything other than a convenient lumping together of symptoms, for the specific purpose of a) giving health insurance some kind of basis for believing that the patient has a real disorder and b) giving the psychiatrist or psychologist some kind of guide as to how to treat the symptoms in the absence of a clear cause (e.g., unlike diabetes).

Additionally, psychologists and psychiatrists typically don't diagnose PTSD from afar - a psych only really diagnoses someone after talking to them extensively and seeing how their symptoms manifest. Despite the official designations seeming quite clear, too, often psychiatric disorders are difficult to diagnose - there's more grey area than youɽ think from the crisp diagnostic criteria in the DSM or the ICD. The most recent version of the DSM, the DSM-5, has begun to move away from pigeonholes and discuss disorders in terms of spectra (e.g., that Asperger's disorder is now just part of an autistic spectrum).

Okay then, what's the current diagnostic criteria for PTSD?

Well, the full criteria in the DSM-5 are copyrighted, and so I can't print them here, but the VA in the US has a convenient summary which I can copy-paste for your reference:

Criterion A (one required): The person was exposed to: death, threatened death, actual or threatened serious injury, or actual or threatened sexual violence, in the following way(s):

*Learning that a relative or close friend was exposed to a trauma

*Indirect exposure to aversive details of the trauma, usually in the course of professional duties (e.g., first responders, medics)

Criterion B (one required): The traumatic event is persistently re-experienced, in the following way(s):

Unwanted upsetting memories

Emotional distress after exposure to traumatic reminders

Physical reactivity after exposure to traumatic reminders

Criterion C (one required): Avoidance of trauma-related stimuli after the trauma, in the following way(s):

*Trauma-related thoughts or feelings

Criterion D (two required): Negative thoughts or feelings that began or worsened after the trauma, in the following way(s):

*Inability to recall key features of the trauma

*Overly negative thoughts and assumptions about oneself or the world

*Exaggerated blame of self or others for causing the trauma

*Decreased interest in activities

*Difficulty experiencing positive affect

Criterion E (two required): Trauma-related arousal and reactivity that began or worsened after the trauma, in the following way(s):

*Irritability or aggression

*Risky or destructive behavior

*Heightened startle reaction

Criterion F (required): Symptoms last for more than 1 month.

Criterion G (required): Symptoms create distress or functional impairment (e.g., social, occupational).

Criterion H (required): Symptoms are not due to medication, substance use, or other illness.

What do psychiatrists and psychologists think cause PTSD?

With the proviso that the research in this area is very much unfinished, it's important to note that not every modern person who goes to war - or experiences other traumatic events - gets PTSD. Research does seem to suggest that some people are more prone to developing PTSD than others. There might be some genetic basis to it after all, in a very real way, PTSD is a disorder which manifests both psychologically and physiologically, and is a disorder which is clearly related to the body's infrastructure for dealing with stress (some of which is biochemical).

So, did ancient soldiers fit these criteria?

One important problem here is that they're no longer around to ask. We almost certainly do not have certain evidence that anyone from antiquity meets all of these criteria. There are certainly some suggestive tales which look familiar to people familiar with PTSD, but Homer and Herodotus and the various other historians simply weren't modern psychiatrists. They didn't do an interview session with the person in question, asking questions designed to see whether they fit all of these criteria, because, like I said - not modern psychs. It's also difficult to know whether symptoms were due to other illness after all, the ancient Greeks did not have our ability to diagnose other illnesses either.

To reiterate: diagnosis is usually done in privacy, with psychs who know what they're looking for asking detailed questions about it. It's partially for this reason that psychiatrists and psychologists are reluctant to diagnose people in public (and that there was a big controversy in 2016 about whether psychiatrists and psychologists were allowed to publicly diagnose a certain American political candidate with a certain manifestation of a personality disorder, despite having never met him.) But, well, unless psychs suddenly find a TARDIS, no Ancient Greek soldier has ever been diagnosed with PTSD.

Additionally, it's clear from the history of psychiatry that disorders are at the very least culturally situated to some extent. In Freud's Introductory Lectures On Psychoanalysis, he discusses cases of a psychiatric disorder called hysteria at length, essentially assuming of his readers that they already know what hysteria looks like, in the same way that a psychologist today might start discussing depression without first defining it. Hysteria was common, one of the disorders that a general psychiatric theory like Freud's would have to cover to be taken seriously. Hysteria is still in the DSM-5, under the name of ɿunctional neurological symptom disorder', but was until recently also called ɼonversion disorder'. However, you've probably never had a friend diagnosed with conversion disorder it's not anywhere as common a diagnosis as it used to be a century ago.

So why did hysteria more or less disappear? Well - hysteria was famously something that, predominantly, women experienced. And there are perhaps obvious reasons why women today might experience less hysteria we live in a post-feminist world, where women have a great deal more freedom within society to follow their desires (whether they be social, career, emotional, sexual) than they had cooped up in Vienna, where their lives were dominated by the family, and within the family, dominated by a patriarch. But maybe, also, the fact that everybody knew what hysteria was played a role in the way that their symptoms were interpreted, and perhaps even in the symptoms they had, given that we're talking about disorders of the mind here, and that the mind with the disorder is the same mind that knows what hysteria is. It might be that hysteria was the socially recognised way of dealing with particular mental and social problems, or that doctors saw hysteria everywhere, even where it wasn't actually present. There was certainly a movement in the 1960s - writers like Foucault, Szasz and Laing - who argued that society plays a much bigger role in mental illness than previously appreciated. Some of their arguments, at the philosophical level, are hard to argue against.

PTSD may be similar to hysteria in this way. It might be that there is a feedback loop between knowledge of PTSD and the experience of PTSD, that people who have experienced traumatic events in a society that recognises PTSD can express their minds as such.

What do psychologists see as the aetiology of PTSD?

Aetiology is simply the study of causes. Broadly speaking, there is no clear agreed-upon single cause for PTSD, judging by recent research. Sripada, Rauch & Liberzon (2016) argue that four key factors play a role in the occurence and maintenance of PTSD after a traumatic event: a) an avoidance of emotional engagement with the event, b) a failure of fear extinction, meaning that fear responses related to the event are not inhibited as well, c) poorer ability to define the narrower context in which a stress response is justified in civilian life vs a military situation, d) less ability to tolerate the feeling of distress - perhaps something like being a bit less resilient, and e) 'negative posttraumatic cognitions' - not exactly being sunny in disposition or how you interpret events. Kline et al., (2018) found that with sexual assault survivors, the levels of self-blame immediately after the assault seemed to correlate with the extent to which PTSD was experienced. Zuj et al. (2016) focus on fear extinction as a specific mechanism by which genetic and biochemical factors which correlate with fear extinction might be expressed. There's also a body of research suggesting that concussion, and the way that it disorients and causes cognitive deficits, plays a larger role in PTSD than previously suspected.

These factors are likely not to be the be-all and end-all, it should be said - it's a complicated issue and research is still in its infancy. But nonetheless, you can see many ways in which culture and environment might effect these factors, including the genetic ones. Broadly speaking, some societies are more inclined towards emotional engagement with war events than others - Ancient Greece was heavily militarised in ways that most Anglophone countries in 2018 are not. Some upbringings probably lead to more resilience than others, and depending on the norms of a society, those upbringings might be more concentrated in those societies. The way that people around you interpret your 'negative posttraumatic cognitions' is going to be different depending on the culture you grow up in. Some societies may be structured in such a way that fear extinction is more likely to occur.

So in this context, what do Crowley and Tritle actually argue?

Broadly speaking, what I argued in the last paragraph is the kind of thing that Crowley's paper in Combat Trauma and the Ancient Greeks argues. There are much more severe injunctions against killing in modern American society than Ancient Greek society, which was not Christian and thus didn't have Christianity's ideals of the sacredness of life - instead, in many Ancient Greek societies, war was considered something that was fucking glorious, and societies were fundamentally structured around the likelihood of war in ways that modern America very much is not.

Additionally, in Ancient Greek society, war was a communal effort, done next to people you knew before the war in civilian life and continued to know after the war in contrast, in modern war situations, where recruits are found within a diverse population of millions, there is a constantly rotating group of people in a combat division who may not have strong ties. Additionally, with the rise of combat that revolves around explosive devices and guns, fighting has changed, and Crowley argued, made people more susceptible to PTSD these days, if soldiers are in a tense, traumatic situation, it is better for them to be spread out so as to limit the damage when under attack. This, Crowley argues, leads to many more feelings of self-blame and helplessness - the kind of thing that might lead to negative posttraumatic cognitions - because blame for events is not spread out amongst a group in quite the same way.

In contrast, Tritle points to a lot of evidence from ancient sources of people seeming to be traumatised in various ways after battles, ways which do strike veterans with PTSD as being of a piece with their experiences:

. Young’s claim that there is no such thing as “traumatic memory” might well astound readers of Homer’s Odyssey. On hearing the “Song of Troy” sung by the bard Demodocus at the Phaeacian court, Odysseus dissolves into tears and covers his head so others do not notice (8. 322). 11 Such a response to a memory should seem to qualify as a “traumatic” one, but Young would evidently reject Odysseus’ tears as “traumatic” and other critics are no less coldly analytic.

Tritle - a veteran himself - clearly wishes to see his experiences as being contiguous with those of ancient soldiers. And there is actually something of an industry in putting together reading groups where veterans with PTSD read accounts of warriors from the classics. The books Achilles In Vietnam and Odysseus In America by the psychiatrist Jonathan Shay explicitly make this link, and it does seem to be useful for many veterans to make this comparison, to view a society where war and warriors are more of a integral part of society than they are in modern America (notwithstanding the fad for saying something about 'respecting your service'). For Tritle, there's something offensive in the way that critics like Crowley dismiss the idea that there was PTSD in Ancient Greece because of their being too ɼoldly analytic'. Tritle also emphasises the physical structure and pathways of the brain:

A vast body of ongoing medical and scientific research demonstrates that traumatic stressors —especially the biochemical reactions of adrenaline and other hormones (called catecholamines that include epinephrine, norephinephrine, and dopamine)—hyperstimulate the brain’s hippocampus, amygdala, and frontal lobes and obstruct bodily homeostasis, producing symptoms consistent with combat-stress reactions. In association with these, the glucocorticoids further enhance the impact of adrenaline and the catecholamines.

But while I'm happy as a psychologist for veterans to learn about ancient warriors if evidence suggests that it helps them contextualise their experiences, as a historian I am personally more on Crowley's side than Tritle's here. The mind is fundamentally an interaction between the brain and the environment around us - we can't be conscious without being conscious of stuff, and all the chemicals and structures in the brain fundamentally serve that purpose of helping us get around in the environment. And history does tell us that, as much as people are people, the world around us, and the societies we make in that world, can vary very considerably. It may well be that PTSD is to some extent a result of modernity and the way we interact with modern environments. This is not to say that people in the past didn't have (to use Tritle's impressive neurojargon) adrenaline and other hormones that hyperstimulate the brain's hippocampus, amygdala, and frontal lobes. Human neuroanatomy and biochemistry doesn't change that much, however modern our context. But so many of the things that lead to these brain chemistry changes, that trigger PTSD as an ongoing disorder beyond the heat of battle - or even those which increase the trauma of the heat of battle - seem to be contextual, situational.

Edit for a new bit at the end for clarity and conclusiveness

I am in no way saying that the people with PTSD have something that's not really real. PTSD as a set of symptoms - whatever its cause, however socially bound it is - causes a whole lot of genuine suffering in people who have already been through a lot. Those people are not faking, or unduly influenced by society. They are simply normal people dealing with a set of circumstances that might not have existed in the same way before the 20th century. I am also not saying that people in the ancient world didn't experience psychological trauma of various sorts after traumatic events - clearly they did I'm just saying that the specific symptomology of PTSD is enough of a product of its times that we should distinguish between it and the very small amount that we know of the trauma experienced by ancient warriors (or others). And finally, PTSD can be treated successfully by psychologists - if you are suffering from it and you have the means to do so, I do encourage you to make steps in that treatment.

Other related r/AskHistorians answers of mine you might find interesting:


1) Which of the following is not an antidepressant drug?

2) Anxiolytic drugs are used to treat:

3) What is a major side effect of Prozac?

4) antipsychotics do which of the following?

5) Beck's Cognitive therapy for depression requires the individual to:

6) Behaviour analysis is based upon the principles of:

7) Behaviour modification is a type of:

8) Drugs called Benzodiazepines are used to treat:

9) Client centred therapy is a type of:

10) Which of the following might be considered as the central tenets of Client-Centred Therapy:

11) It is generally considered that Cognitive behavioural therapy changes:

12) Cognitive Behavioural Therapy is generally perceived as:

13) Which of the following is not a Behaviour Therapy technique?

14) The principle of extinction assumes that emotional problems can be:

15) Counterconditioning is an exposure therapy technique which involves:

16) Contininual professional development (CPD) demonstrates that a therapist:

17) Counselling is a profession that aims to:

18) According to the psychodynamic view dream analysis is one of the central tenets of:

21) Group therapy can be advantageous when an individual:

22) Which of the following possibilities makes email a useful adjunct to face to face sessions?

23) Family therapy is generally used to:

24) Systems theory involves:

25) Faulty learning involves:

26) Functional analysis is a therapy based on:

27) Token Economy is an influential intervention based upon:

28) When determining whether a treatment works because of the principles it contains it is known as:

29) Meta-analysis is often used to compare the effectiveness of studies that have used:

30) Monoamine oxidase inhibitors (MAOIs) are effective for the treatment of:

Drugs That Influence Neurotransmitters

Perhaps the greatest practical application for the discovery and detailed understanding of how neurotransmitters function has been the development of drugs that impact chemical transmission. These drugs are capable of changing the effects of neurotransmitters, which can alleviate the symptoms of some diseases.

  • Agonists vs Antagonists: Some drugs are known as agonists and function by increasing the effects of specific neurotransmitters. Other drugs and referred to as antagonists and act to block the effects of neurotransmission.  
  • Direct vs Indirect Effects: These neuro-acting drugs can be further broken down based on whether they have a direct or indirect effect. Those that have a direct effect work by mimicking the neurotransmitters because they are very similar in chemical structure. Those that have an indirect impact work by acting on the synaptic receptors.

Drugs that can influence neurotransmission include medications used to treat illness including depression and anxiety, such as SSRIs, tricyclic antidepressants, and benzodiazepines.

Illicit drugs such as heroin, cocaine, and marijuana also have an effect on neurotransmission. Heroin acts as a direct-acting agonist, mimicking the brain's natural opioids enough to stimulate their associated receptors. Cocaine is an example of an indirect-acting drug that influences the transmission of dopamine.  

How to blow up the Death Star

Not only has the Death Star fascinated economists and policy analysts, who have found it to be a wasteful boondoggle of galactic proportions the complexity and destructive force of the Empire's "ultimate weapon" also darkly fascinates scientists and engineers.

“What would students prefer: formulas, or the soundtrack of the Imperial March?” says Guy Walker, a civil engineering professor at Scotland’s Heriot-Watt University.

Walker applied real-world techniques to the notoriously explosion-prone Death Star as an example for his civil engineering students of analyzing flaws in big engineering projects. After obtaining its plans from an official technical manual, he and his colleagues gave themselves the equivalent of four days—the amount of time the Rebel Alliance had with the plans—to test two different flaw-finding techniques.

Diversity, Equity and Inclusion Committee's Statement and Report on DEI-related activities in our Department over the past year

The tragic murder of George Floyd happened one year ago this week. His death followed and was preceded by the deaths of countless other black men and women at the hands of police. In the wake of this tragedy last year, members of the Columbia University Psychology Department sent a letter asking, “what can we do now – as individuals, a department, a university, an academic discipline – to contribute to making Black Lives Matter in reality rather than simply in rhetoric.” To begin the conversation, they highlighted areas of focus for meaningful change, which we reference throughout this do

Watch the video: How To UNLOCK The New CHARACTER Richie! - Dude Theft Wars! (August 2022).