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