外傷後ストレス障害, post-traumatic stress disorder, posttraumatic stress disorder
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/12/21 11:21:43」(JST)
心的外傷後ストレス障害 | |
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分類及び外部参照情報 | |
ICD-10 | F43.1 |
ICD-9 | 309.81 |
DiseasesDB | 33846 |
MedlinePlus | 000925 |
eMedicine | med/1900 |
Patient UK | 心的外傷後ストレス障害 |
MeSH | D013313 |
心的外傷後ストレス障害(しんてきがいしょうごストレスしょうがい、Posttraumatic stress disorder、PTSD)は、命の安全が脅かされるような出来事、天災、事故、犯罪、虐待などによって強い精神的衝撃を受けることが原因で、著しい苦痛や、生活機能の障害をもたらしているストレス障害である[1]。
心の傷は、心的外傷またはトラウマ(本来は単に「外傷」の意で、日本でも救命や外傷外科ではその意味で使われ、特に致命的外傷の意味で使われることが多いが、一般には心的外傷として使用される場合がほとんどである)と呼ばれる。トラウマには事故・災害時の急性トラウマと、児童虐待など繰り返し加害される慢性の心理的外傷がある。
心的外傷後ストレス障害は地震、洪水、火事のような災害、または事故、戦争といった人災、あるいはいじめ、テロ、監禁、虐待、パワハラ、モラハラ、ドメスティックバイオレンス、強姦、体罰などの犯罪、つまり、生命が脅かされたり、人としての尊厳が損なわれるような多様な原因によって生じうる。
以下の3つの症状が、PTSDと診断するための基本的症状であり、これらの症状が、強い恐怖、無力感または戦慄を伴う出来事の後、1ヶ月以上持続している場合にはPTSD、1ヶ月未満の場合にはASD(急性ストレス障害)と診断する(DSM-IV-TR)[1]。
患者が強い衝撃を受けると、精神機能はショック状態に陥り、パニックを起こす場合がある。そのため、その機能の一部を麻痺させることで一時的に現状に適応させようとする。そのため、事件前後の記憶の想起の回避・忘却する傾向、幸福感の喪失、感情鈍麻、物事に対する興味・関心の減退、建設的な未来像の喪失、身体性障害、身体運動性障害などが見られる。特に被虐待児には感情の麻痺などの症状が多く見られる。
精神の一部が麻痺したままでいると、精神統合性の問題から身体的、心理的に異常信号が発せられる。そのため、不安や頭痛・不眠・悪夢などの症状を引き起こす場合がある。とくに子供の場合は客観的な知識がないため、映像や感覚が取り込まれ、はっきり原因の分からない腹痛、頭痛、吐き気、悪夢が繰り返される。
診断の前提として、災害、戦闘体験、犯罪被害など強い恐怖感を伴う体験が存在することが必要である[1]。 主に以下のような症状の有無により、診断がなされる。
これらの症状が1か月以上持続し、社会的、精神的機能障害を起こしている状態を指す。症状が3か月未満であれば急性、3か月以上であれば慢性と診断する。大半のケースはストレス因子になる重大なショックを受けてから6か月以内に発症するが、6か月以上遅れて発症する「遅延型」も存在する。
現在から過去にさかのぼる「出来事」に対する記憶が、診断に重要である。しかしながら、 1)重大な「出来事」の記憶 2)それほど重大でなかったが事後的に記憶が再構成される 3)もともとなかった「出来事」が、あたかもあったかのように出来事の記憶となる このような3つの分類ができる点に留意する必要があろう。
なお、PTSDを発症した人の半数以上がうつ病、不安障害などを合併している。
PTSDを持つ人はしばしばアルコール依存症や薬物依存症といった嗜癖行動を抱えるが、それらの状態は異常事態に対する心理的外傷の反応、もしくは無自覚なまま施していた自己治療的な試みであると考えられている。しかし、嗜癖行動を放置するわけにはいかないので、治療はたいがい、まずその嗜癖行動を止めることから始まる。
PTSDに関するエビデンスは集約されつつあり、精神療法においては認知行動療法やEMDR、ストレス管理法である[2]。成人のPTSDにおける薬物療法はSSRI系の抗うつ薬であるが、中等度以上のうつ病が併存しているか、精神療法が成果を上げないあるいは利用できない場合の選択肢である[3]。
SSRIの種類としては、フルオキセチンとパロキセチンなどのSSRIである。
おそらく効果がないとされているものは、薬物療法においてはVenlafaxineであり、精神療法においてはデブリーフィングと指示的カウンセリングである。
持続エクスポージャー療法は、トラウマに焦点を当てた認知行動療法であり、セラピストとの会話を通じて心的外傷に慣れていく心理療法である。国際的に推奨されている。しかし、一方で有効性に限界がある。技法に精通していなければストレス症状を強めるため注意が必要である。
EMDR(眼球運動による脱感作および再処理法)は、睡眠における眼球が動くレム睡眠の際に、記憶が消去されていることに着目した技法である。
認知行動療法は、認知のクセを修正することを目的とした心理療法である。読書を通じて、認知のクセを修正する手順を自助的に行うための書籍も販売されている。
また、認知行動療法のほうが効果的であるが、ストレス管理法は広く利用することのできる選択肢である[3]。
PTSDの予防法として心理的デブリーフィング(緊急事態ストレスマネジメント)が一時期提唱された。これは災害などの2~3日後から1週間までに行われるグループ療法であり、2~3時間かけて出来事を再構成したり、感情の発散、トラウマ反応の心理教育などがなされるものである。
しかし、日本トラウマティック・ストレス学会によれば、1990年代後半からデブリーフィングの有効性の疑問視する報告が相次ぎ、現在では苦痛の緩和やPTSDのとはならないため、強制的なデブリーフィングはやめるべきであるとされている[4]。 2003年の日本の厚生科学研究による『災害時地域精神保健医療活動ガイドライン』でも、災害直後に体験を聞き出すようなカウンセリングは古い考えに基づいていて有害であり、国際学会やアメリカ国立PTSDセンターのガイドラインでも非推奨とされているため、「行ってはならない」と記されている[5]。
日本のPTSDに関する2006年のガイドラインでは、パロキセチンやセルトラリンといったSSRIが推奨され、ベンゾジアゼピン系の薬剤は推奨できないとされる[6]。2008年の国際トラウマティック・ストレス学会のガイドラインでも、成人、児童共に同様にベンゾジアゼピン系の薬物が有効であるという根拠は乏しい[7]。
2013年の世界保健機関によるガイドラインは以下のとおりである。PTSDに対しては、SSRIの投与は、トラウマに焦点を当てた認知行動療法やEMDRが失敗した時や、そうしたリソースを利用できない場合、あるいは、中等度以上のうつ病がみられる場合に考慮されるべきであり、最初の選択ではないとしている[3]。また、児童や青年のPTSDにおいては抗うつ薬は使用されるべきではない[8]。成人および児童に対する、急性外傷性ストレスに対して、ベンゾジアゼピンおよび抗うつ薬は投与してはいけないとしている[9]。成人および児童に対して、ストレスの強い出来事のあった最初の1ヶ月に、不眠症に対してベンゾジアゼピンは投与されるべきではない[10]。
2012年のアメリカの不安障害協会の年次会議では、ベンゾジアゼピン系の抗不安薬の使用は、心的外傷後ストレス障害(PTSD)に対し視床下部-下垂体-副腎系(HPA)軸を抑制するためストレス症状を増大させ、また、恐怖反応はGABA作動性の扁桃体機能を介して消失されるが、このような学習や記憶を無効にするため心理療法の結果を否定的にすることが報告された[11][12]。アメリカにおける戦争帰還兵におけるPTSDで、非定型抗精神病薬が推奨できないことが強調されている[13]。
大麻は、PTSDによる不安やフラッシュバックの影響を弱め、PTSDの症状を減少させるという証拠は蓄積されてきている[14]。合成カンナビノイドのナビロンを用いた小規模な試験では、悪夢の治療に用い、47人中34人(72%)が悪夢の頻度や強さを減少させ、28人(59%)で悪夢が完全に休止した[15]。
PTSDの研究には、大きく分けて三つの流れがある。「ヒステリー研究」「戦闘ストレス反応」「性的・家庭内暴力」の三つである。
第一の流れは、19世紀後半から始まったヒステリー研究、女性の心的外傷の原型である。19世紀後半、フランスの神経学者ジャン=マルタン・シャルコーによってヒステリー研究がされる。シャルコーは患者の運動麻痺、感覚麻痺、痙攣、健忘に注目した。シャルコーはヒステリーを大神経症と呼び、患者を解説のために臨床講義で大衆の前に展示した。ヒステリー患者は、絶え間ない暴力やレイプを逃れてきた若い女性たちであった。
症状に着目したシャルコーに対して、後にこの分野の研究者は原因に着目した。中でもピエール・ジャネとジークムント・フロイトのライバル意識は強く、彼等は患者との「対話」によって新しい発見者になろうとした。この「対話」という研究法は大きな成果をもたらし、それぞれ近い結論に辿り着いた。外傷的な出来事に関する、耐え難い情動反応が一種の変成意識をひきおこし、この変成意識がヒステリー症状を生んでいるという結論である。ジャネはこれを「解離」と呼び、フロイトと共同研究者のヨーゼフ・ブロイアーは「二重意識」と呼んだ。
現代において有効性が確立されている持続エクスポージャー療法は、認知行動療法の一種である。安全な環境で、体験を認識しなおす手順を踏み、熟練されたカウンセラーによらなければ、ストレス反応が強めてしまう可能性がある。
第二の流れは、砲弾神経症(シェルショックともいう)、戦闘ストレス反応である。この研究は、第一次世界大戦における塹壕戦の経験を踏まえ、戦後米国と英国から始まった。ベトナム戦争後には、その戦争自体への懐疑からのストレス症状が起きた。戦闘ストレス反応は、戦争において精神的に崩壊する兵士が驚くべき多数に上ったことから認知されはじめた。そして、アメリカでは戦争から帰還した兵士のPTSDの多さに、軍による治療ガイドラインなども作成されている。
友人たちの手足が一瞬にして吹き千切れるのを見、捕虜になり閉じ込められるなどして孤立無援状態におかれたり、一瞬にして吹き飛ばされ殺されるという恐怖から気を緩める暇もないという状況が、驚くべき現象を生み出したのである。兵士たちはヒステリー患者と同じ行動をし始めた。身体的には金縛りで動けなくなる、震えが止まらない等が現れ、精神的には金切り声ですすり泣く者や、逆に感情が麻痺し、無言、無反応になる等が現れたり、健忘が激しくなる者もいた。
軍の伝統的な立場のものは、この現象を臆病者であるからだと結論し、処罰と脅迫による電気ショック治療を提唱した。進歩的なものは、これを士気の高い兵士にも起こりうるれっきとした精神障害であると人道的治療を進めた。その後の調査の過程で、これらの一部の状態に対してASDやPTSDという名称がつけられたのである。
近年認知され始めた例として無人航空機の操縦者にPTSDを発症する率が高いというものがある。無人機は機体そのものに人間が搭乗しないため撃墜されたり事故をおこしても操縦員に危険はなく、また衛星経由でアメリカから遠隔操作が可能であるため、操縦員は長い期間戦地に派遣されることもなく、任務を終えればそのまま自宅に帰ることも可能である。このような無人機の運用は操縦者が人間を殺傷したという実感を持ちにくいという意見がある[16][17]が、「いつミサイルを発射してもおかしくない状況から、次には子どものサッカーの試合に行く」という平和な日常と戦場を行き来する、従来の軍事作戦では有り得ない生活を送ることや、敵を殺傷する瞬間をカラーTVカメラや赤外線カメラで鮮明に見ることが無人機の操縦員に大きな精神的ストレスを与えているという意見もある[18]。国際政治学者のP・W・シンガーによると、無人機のパイロットは実際にイラクに展開している兵士よりも高い割合でPTSDを発症している[19]。
第三の流れは、ごく最近認知されてきた性的暴力と家庭内暴力、家庭外暴力の外傷である。19世紀後半のヒステリー研究は、性的暴力の研究でつまづいてしまった。当時は、家庭内に性的暴力が多く存在するといった概念がなかったため、フロイトがその研究を退けたのである。
『PTSDの医療人類学』[20]は、その疾病概念がいかに構成され現実化してきたのかを批判的に問うている。
PTSDに関する多くの研究や発展は戦闘帰還兵を対象にしたものであった。最も頻度の多いPTSDは、戦争における極限状態が生み出す外傷より、市民生活の中での性的暴力や家庭内暴力であるといった認識がなかったのである[21]。
家族という密室を隠れ蓑にして、幼少時から長期にわたり、親をはじめとした大人たちから受けるさまざまな形の児童虐待が、はるか後年、成人してから多様な症状を生じさせることが発見され、PTSDの一種として検討されるようになった。ジュディス・ハーマンは「複雑性トラウマ(complex trauma)」[21]、ヴァン・デル・コルクは「複合型トラウマ」(combined-type trauma)[22]という概念を提示している。
前帯状皮質が小さいと発症しやすいことを東北大学加齢医学研究所のグループが解明した。発症後眼窩前頭皮質が萎縮することも判明[23]。
犯罪の被害者や交通事故、自然災害の被災者などにも同様の診断が示されることとなり、PTSDの診断名は広く一般的に使用されるに至った。
日本では阪神・淡路大震災、地下鉄サリン事件、新潟少女監禁事件、JR福知山線脱線事故の時に広く病名が知られるようになった。
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It has been suggested that Trauma trigger be merged into this article. (Discuss) Proposed since December 2013. |
Posttraumatic stress disorder | |
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Art therapy project created by a U.S. Marine with posttraumatic stress disorder
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Classification and external resources | |
Specialty | Psychiatry |
ICD-10 | F43.1 |
ICD-9-CM | 309.81 |
DiseasesDB | 33846 |
MedlinePlus | 000925 |
eMedicine | med/1900 |
Patient UK | Posttraumatic stress disorder |
MeSH | D013313 |
Posttraumatic stress disorder[note 1] (PTSD) is an anxiety disorder that can develop after a person is exposed to one or more traumatic events, such as sexual assault, warfare, traffic collisions, terrorism or other threats on a person's life.[1] Symptoms include disturbing recurring flashbacks, avoidance or numbing of memories of the event, and hyperarousal, continue for more than a month after the occurrence of a traumatic event.[1]
Most people who have experienced a traumatizing event will not develop PTSD.[2] People who experience assault-based trauma are more likely to develop PTSD, as opposed to people who experience non-assault based trauma such as witnessing trauma, accidents, and fire events.[3] Children are less likely to experience PTSD after trauma than adults, especially if they are under ten years of age.[2] War veterans are commonly at risk for PTSD.
Medications including fluoxetine and paroxetine may improve symptoms a small amount.[4] Most medications do not have enough evidence to support their use.[4] It is unclear as of 2010 if medication and therapy together are better than either alone.[5]
The term "posttraumatic stress disorder" was coined in the late 1970s in large part due to diagnoses of US military veterans of the Vietnam War.[6] The concept of stress-induced mental disorder was already known since at least the 19th century, and had been referred to previously under various terms including "soldier's heart", "shell shock" and "battle fatigue".[citation needed]
Posttraumatic stress disorder is classified as an anxiety disorder in the DSM IV; the characteristic symptoms are not present before exposure to the violently traumatic event. In the typical case, the individual with PTSD persistently avoids all thoughts and emotions, and discussion of the stressor event and may experience amnesia for it. However, the event is commonly relived by the individual through intrusive, recurrent recollections, flashbacks, and nightmares.[7] The characteristic symptoms are considered acute if lasting less than three months, and chronic if persisting three months or more, and with delayed onset if the symptoms first occur after six months or some years later. PTSD is distinct from the briefer acute stress disorder, and can cause clinical impairment in significant areas of functioning.[8][9][10]
PTSD is believed to be caused by the experience of a wide range of traumatic events and, in particular if the trauma is extreme, can occur in persons with no predisposing conditions.[12][13]
Persons considered at risk include, for example, combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Individuals frequently experience "survivor's guilt" for remaining alive while others died. Causes of the symptoms of PTSD are the experiencing or witnessing of a stressor event involving death, serious injury or such threat to the self or others in a situation in which the individual felt intense fear, horror, or powerlessness.[14] Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk.[14]
Children or adults may develop PTSD symptoms by experiencing bullying.[15]
Several biological indicators have been identified that are related to later PTSD development. Heightened startle responses and a smaller hippocampal volume have been identified as biomarkers for the risk of developing PTSD.[16] Additionally, one study found that soldiers whose leukocytes had greater numbers of glucocorticoid receptors were more prone to developing PTSD after experiencing trauma.[16]
There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone. 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).[17] There is evidence that those with a genetically smaller hippocampus are more likely to develop PTSD following a traumatic event. 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.[18]
Most people will experience at least one traumatizing event in their lifetime.[19] Men are more likely to experience a traumatic event, 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.[2]
Posttraumatic stress reactions have not been studied as well in children and adolescents as adults.[2] The rate of PTSD may be lower in children than adults, but in the absence of therapy, symptoms may continue for decades.[2] 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, and much lower below the age of 10 years.[2]
Predictor models have consistently found that childhood trauma, chronic adversity, and familial stressors increase risk for PTSD as well as risk for biological markers of risk for PTSD after a traumatic event in adulthood.[20][21][22] Peritraumatic dissociation in children is a predictive indicator of the development of PTSD later in life.[18] This effect of childhood trauma, which is not well-understood, may be a marker for both traumatic experiences and attachment problems.[23][24] Proximity to, duration of, and severity of the trauma make an impact, and interpersonal traumas cause more problems than impersonal ones.[25]
Quasi-experimental studies have demonstrated a relationship between intrusive thoughts and intentional control responses such that suppression increases the frequency of unwanted intrusive thoughts. These results suggest that suppression of intrusive thoughts may be important in the development and maintenance of PTSD.[26]
Adults who were in foster care as children have a higher rate of PTSD.[medical citation needed]
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.[8] There is a strong association between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy.[27]
Early intervention appears to be a critical preventive measure.[28] Studies have shown that soldiers prepared for the potential of a traumatic experience are more prepared to deal with the stress of a traumatic experience and therefore less likely to develop PTSD.[8]
Among American troops in Vietnam a greater portion of women experienced high levels of war-zone stress compared to theater men—39.9 percent versus 23.5 percent. The key to this fact is that the vast majority (6,250 or 83.3%) of the women who served in the war zone were nurses who dealt almost daily with death. Black veterans had nearly 2.5 fold the risk of developing war zone-related PTSD as compared to white/other veterans. Hispanics had more than three times the risk. But the most revealing fact, theater veterans injured or wounded in combat had nearly four times the risk of developing PTSD compared to those not injured/wounded according to two key studies—the August 2014 National Vietnam Veterans Longitudinal Study (NVVLS). Paired with the late 1980s National Vietnam Veterans Readjustment Study (NVVRS).[29]
The long-term medical consequence of PTSD among male veterans who served in the Vietnam War was that they were almost twice as likely to die in the quarter of a century between the two key studies than those who did not have PTSD. It was also found those with PTSD were more likely to die of chronic conditions such as cancer, nervous system disorders, and musculoskeletal problems. The etiology of this relationship is not certain other than lingering stress from combat such as nightmares, intrusive memories, and hyper-vigilance are aggravating factors contributing to psychological and physiological illnesses.[29]
The racial similarity between Hispanic and Vietnamese soldiers, and the discrimination Hispanic soldiers faced from their own military, made it difficult for Hispanic soldiers to dehumanize their enemy. Hispanic veterans who reported experiencing racial discrimination during their service displayed more symptoms of PTSD than Hispanic veterans who did not.[30]
PTSD is under-diagnosed in female veterans.[31] Sexual assault in the military is a leading cause for female soldiers developing PTSD; a female soldier who is sexually assaulted while serving in the military is nine times more likely to develop PTSD than a female soldier who is not assaulted. A soldier's assailant may be her colleague or superior officer, making it difficult for her to both report the crime and to avoid interacting with her assailant again.[32] Until the Tailhook scandal drew attention to the problem, the role that sexual assault in the military plays in female veterans developing PTSD went largely unstudied.[33]
Protective effects include social support, which also helps with recovery if PTSD develops.[34][35] For more aggravating factors to recovery once home, see social alienation among returning war veterans.
Drug abuse and alcohol abuse commonly co-occur with PTSD.[36] Recovery from posttraumatic stress disorder or other anxiety disorders may be hindered, or the condition worsened, by medication or substance overuse, abuse, or dependence; resolving these problems can bring about a marked improvement in an individual's mental health status and anxiety levels.[37][38]
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.[8][39] During traumatic experiences the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD.[40]
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.[41][42]
In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine,[43] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[44] 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.[45]
Brain catecholamine levels are high,[46] and corticotropin-releasing factor (CRF) concentrations are high.[47][48] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.
The HPA axis is responsible for coordinating the hormonal response to stress.[18] 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.[49]
Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis.[50]
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.[51] 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.
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.[52] Serotonin also contributes to the stabilization of glucocorticoid production.
Dopamine levels in a person with PTSD can help contribute to the symptoms associated. Low levels of dopamine can contribute to anhedonia, apathy, impaired attention, and motor deficits. Increased levels of dopamine can cause psychosis, agitation, and restlessness.[52]
Hyperresponsiveness in the norepinephrine system can 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 that the experience, and emotions the person is experiencing during a flashback are not associated with the current environment.[52]
However, there is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relationship between cortisol levels and PTSD. However, 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.[18][53]
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Three areas of the brain in which function may be altered in PTSD have been identified: the prefrontal cortex, amygdala, and hippocampus. Much of this research has utilised PTSD victims from the Vietnam War. For example, a prospective study using the Vietnam Head Injury Study showed that damage to the prefrontal cortex may actually be protective against later development of PTSD.[55] 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.[56] This finding could not be replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).[57]
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.[58] 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 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.[18][59][unreliable medical source?]
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.[60] This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.[60][61] 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.[62] 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,[63] which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma.[64] 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.[18]
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 people 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.[65] 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.[18]
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.[18]
Studies have also shown that PTSD patients show hypoactiviation or 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.[66]
A number of screening instruments, including the UCLA PTSD Index for DSM-IV, which have good reliability and validity, are used for the screening of PTSD for children and young adults.[67] Primary Care PTSD Screen and PTSD Checklist are other screening tools.[68]
The American Academy of Child and Adolescent Psychiatry practice parameters is a guidelines for the assessment and treatment of PTSD.[69]
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%.[70] Various scales to measure the severity and frequency of PTSD symptoms exist.[71][72] Standardized screening tools such as Trauma Screening Questionnaire[73] and PTSD Symptom Scale[74] can be used to detect possible symptoms of posttraumatic stress disorder and suggest the need for a formal diagnostic assessment.
In DSM-5, published in May, 2013, PTSD is classified as a trauma- and stress-related disorder.[1]
The diagnostic criteria for PTSD, stipulated in the International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10), may be summarized as:[75]
The International Statistical Classification of Diseases and Related Health Problems 10 diagnostic guidelines state:[75] In general, this disorder should not be diagnosed unless there is evidence that it arose within 6 months of a traumatic event of exceptional severity. A "probable" diagnosis might still be possible if the delay between the event and the onset was longer than 6 months, provided that the clinical manifestations are typical and no alternative identification of the disorder (e.g., as an anxiety or obsessive-compulsive disorder or depressive episode) is plausible. In addition to evidence of trauma, there must be a repetitive, intrusive recollection or re-enactment of the event in memories, daytime imagery, or dreams. Conspicuous emotional detachment, numbing of feeling, and avoidance of stimuli that might arouse recollection of the trauma are often present but are not essential for the diagnosis. The autonomic disturbances, mood disorder, and behavioural abnormalities all contribute to the diagnosis but are not of prime importance. The late chronic sequelae of devastating stress, i.e. those manifest decades after the stressful experience, should be classified under F62.0.
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.[7]
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.[7]
Obsessive compulsive disorder may be diagnosed for intrusive thoughts that are recurring but not related to a specific traumatic event.[7]
Malingering should be considered if a financial and/or legal advantage is a possibility.
Modest benefits have been seen from early access to cognitive behavioral therapy.[76] Critical incident stress management has been suggested as a means of preventing PTSD, but subsequent studies suggest the likelihood of its producing negative outcomes.[77][78] 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."[79] The World Health Organization recommends against the use of benzodiazepines and antidepressants in those having experienced trauma.[80] Some evidence supports the use of hydrocortisone for prevention in adults, however no evidence supports propranolol, escitalopram, temazepam, or gabapentin.[81]
Trauma-exposed individuals often receive treatment called psychological debriefing in an effort to prevent PTSD.[76] Several meta-analyses; however, find that psychological debriefing is unhelpful and is potentially harmful.[76][82][83] This is true for both single-session debriefing and multiple session interventions.[79] The American Psychological Association judges the status of psychological debriefing as No Research Support/Treatment is Potentially Harmful.[84]
Psychological debriefing was; however, 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.[76]
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.[85][86]
This section needs more medical references for verification or relies too heavily on primary sources. Please review the contents of the section and add the appropriate references if you can. Unsourced or poorly sourced material may be removed. (October 2015) |
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.[8][74]
The psychotherapy programs with the strongest demonstrated efficacy include cognitive behavioral programs, variants of exposure therapy[citation needed], stress inoculation training (SIT), variants of cognitive therapy (CT), eye movement desensitization and reprocessing (EMDR),[87] mindfulness-based meditation[88] and many combinations of these procedures.[89]
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."[90] 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.[91]
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.[92] 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.[93] Many of these therapy methods have a significant element of exposure[92] and have demonstrated success in treating the primary problems of PTSD and co-occurring depressive symptoms.[94]
Exposure therapy is a type of cognitive behavioral therapy[95] 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.[96] Some organizations[which?] have endorsed the need for exposure.[97][98] The US Department of Veterans Affairs has been actively training mental health treatment staff in prolonged exposure therapy[99] and Cognitive Processing Therapy[100] in an effort to better treat US veteranswith PTSD.
Eye movement desensitization and reprocessing (EMDR) is a form of psychotherapy developed and studied by Francine Shapiro.[101] 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.[101]
In 2002, Shapiro and Maxfield published a theory of why this might work, called adaptive information processing.[102] 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.[103] The therapist initiates voluntary rapid eye movements while the person focuses on memories, feelings or thoughts about a particular trauma.[2][104] 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.[105]
There have been multiple small controlled trials of four to eight weeks of EMDR in adults[106] as well as children and adolescents.[104] 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.[106] There was not enough evidence to know whether or not EMDR could eliminate PTSD.[106] There was some evidence that EMDR might prevent depression.[106] There were no studies comparing EMDR to other psychological treatments or to medication.[106] Adverse effects were largely unstudied.[106] 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.[104]
The eye movement component of the therapy may not be critical for benefit.[2][103] 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.[105] 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."[87]
Other approaches, in particular involving social supports,[34][35] may also be important. An open trial of interpersonal psychotherapy[107] reported high rates of remission from PTSD symptoms without using exposure.[108] A current, NIMH-funded trial in New York City is now (and into 2013) comparing interpersonal psychotherapy, prolonged exposure therapy, and relaxation therapy.[109][broken citation][110][111]
Most medications do not have enough evidence to support their use.[4] With many medications, residual symptoms following treatment is the rule rather than the exception.[112]
Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) may have some benefit for PTSD symptoms.[4][113] Tricyclic antidepressants are equally effective but are less well tolerated.[114] Evidence provides support for a small or modest improvement with sertraline, fluoxetine, paroxetine, and venlafaxine.[115][4]Thus, these four medications are considered to be first-line medications for PTSD.[116][113]
Benzodiazepines are not recommended for the treatment of PTSD due to a lack of evidence of benefit.[117] Nevertheless, some use benzodiazepines with caution for short-term anxiety relief,[118][119] hyperarousal, and sleep disturbance.[120] However, some authors believe that the use of benzodiazepines is contraindicated for acute stress, as this group of drugs promotes dissociation and ulterior revivals.[121] 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.[116][122]
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.[123]
The cannabinoid nabilone is sometimes used off-label for nightmares in PTSD. Although some short-term benefit was shown, adverse effects are common and it has not been adequately studied for long-term use.[124]
Physical activity can have an impact on people's psychological wellbeing[125] and physical health.[126] 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.[127]
Play is thought to help children link their inner thoughts with their outer world, connecting real experiences with abstract thought.[128] Repetitive play can also be one of the ways a child relives traumatic events, and that can be a symptom of traumatization in a child or young person.[129] 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][128]
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.[130] Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist service members avoid or ameliorate PTSD and related problems.
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 2007, epidemiological rates have not changed significantly.[132]
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.[133] 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.[134][135]
Region | Country | PTSD DALY rate, overall[133] |
PTSD DALY rate, females[134] |
PTSD DALY rate, males[135] |
---|---|---|---|---|
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 |
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[52] (3.6%) to have PTSD at some point in their lives.[136] 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.[52] 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 abuse or dependence, 51.9% of men and 27.9% of women, are the most common comorbid disorders.[137]
The United States Department of Veterans Affairs estimates that 830,000 Vietnam War veterans suffered symptoms of PTSD.[138] The National Vietnam Veterans' Readjustment Study (NVVRS) found 15.2% of male and 8.5% of female Vietnam veterans to suffer from current PTSD at the time of the study. Life-Time prevalence of PTSD was 30.9% for males and 26.9% 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.[139]
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 a 18.3 percentage point increase in the probability of PTSD, while being wounded or injured in combat was associated 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.[140]
As of 2013, rates of PTSD have been estimated at up to 20% for veterans returning from Iraq and Afghanistan.[19] As of 2013 13% of veterans returning from Iraq were unemployed.[141]
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.[142][143]
Veterans Affairs Canada offers a new program that includes rehabilitation, financial benefits, job placement, health benefits program, disability awards, peer support[144][145][146] and family support.[147]
The 1952 edition of the DSM-I includes a diagnosis of "gross stress reaction", which bears striking similarities to the modern definition and understanding of PTSD.[148] Gross stress reaction is defined as a “normal personality [utilizing] established patterns of reaction to deal with overwhelming fear” as a response to “conditions of great stress”.[149] The diagnosis includes language which relates the condition to combat as well as to “civilian catastrophe”.[149]
Early in 1978, the term was used in a working group finding presented to the Committee of Reactive Disorders.[150] The condition was added to the DSM-III, which was being developed in the 1980s, as posttraumatic stress disorder.[148][150] In the DSM-IV, the spelling "posttraumatic stress disorder" is used, while in the ICD-10, the spelling is "post-traumatic stress disorder".[151]
The addition of the term to the DSM-III was greatly influenced by the experiences and conditions of US military veterans of the Vietnam War.[6] Due 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.[152][153] 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[154]), written around 1597, represents an unusually accurate description of the symptom constellation of PTSD.[155]
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."[156] 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.[157]
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”.[158] 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.”[159] 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.[160] This paved the way for a more comprehensive understanding of causes of PTSD.
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.[161] 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,[161][162] examination of neuroendocrine and neuroimmune responses in plasma revealed a trend toward increase in corticosterone in PTSD and combination groups.
MDMA was used for psychedelic therapy for a variety of indications before its criminalization in the US in 1985. In response to its criminalization, the Multidisciplinary Association for Psychedelic Studies was founded as a nonprofit drug-development organization to develop MDMA into a legal prescription drug for use as an adjunct in psychotherapy.[163] The drug is hypothesized to facilitate psychotherapy by reducing fear, thereby allowing patients to reprocess and accept their traumatic memories without becoming emotionally overwhelmed. In this treatment, patients participate in an extended psychotherapy session during the acute activity of the drug, and then spend the night at the treatment facility. In the sessions with the drug, therapists are not directive and support the patients in exploring their inner experiences. Patients participate in standard psychotherapy sessions before the drug-assisted sessions, as well as after the drug-assisted psychotherapy to help them integrate their experiences with the drug.[164] Preliminary results suggest MDMA-assisted psychotherapy might be effective for individuals who have not responded favorably to other treatments. Future research employing larger sample sizes and an appropriate placebo condition, i.e., one in which subjects cannot discern if they are in the experimental or control condition, will increase confidence in the results of initial research.[165][166]
Clinical research is also investigating using D-cycloserine, hydrocortisone, and propranolol as adjuncts to more conventional exposure therapy.[166]
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.[167] 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.[168]
Psychiatry portal |
Some drugs have a small positive impact on PTSD symptoms
While evidence-based, trauma-focused psychotherapy is the preferred treatment for PTSD, pharmacotherapy is also an important treatment option. First-line pharmacotherapy agents include selective serotonin reuptake inhibitors and the selective serotonin-norepinephrine reuptake inhibitor venlafaxine.
The cumulative evidence summarized in this review indicates that pharmacotherapy significantly reduces PTSD, anxiety, and depressive symptom severity among combat veterans with PTSD. The magnitude of the overall effects of pharmacotherapy on PTSD (Δ = 0.38), anxiety (Δ = 0.42), and depressive symptoms (Δ = 0.52) were moderate...
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国試過去問 | 「102A029」「105I024」「095B006」「095A007」「099D004」「112E015」「106C005」 |
リンク元 | 「外傷後ストレス障害」「post-traumatic stress disorder」「posttraumatic stress disorder」「過覚醒」 |
関連記事 | 「PT」「PTS」 |
E
※国試ナビ4※ [102A028]←[国試_102]→[102A030]
C
※国試ナビ4※ [105I023]←[国試_105]→[105I025]
E
※国試ナビ4※ [095B005]←[国試_095]→[095B007]
C
※国試ナビ4※ [095A006]←[国試_095]→[095A008]
E
※国試ナビ4※ [099D003]←[国試_099]→[099D005]
C
※国試ナビ4※ [112E014]←[国試_112]→[112E016]
E
※国試ナビ4※ [106C004]←[国試_106]→[106C006]
急性ストレス反応 | 外傷後ストレス障害 | 適応障害 | |
ストレス強度 | 大 | 大 | 小 |
個体要因 | 小 | 小 | 大 |
発現時間 | 1hr以内 | 遅発性 (数W~数M) |
1M以内 |
症状 | 幻覚、抑うつ、不安、激怒、絶望、葛藤、引きこもり | 再体験、回避、精神麻痺、過覚醒 | 抑うつ、不安、行為障害 |
経過 | 48hr以内に沈静化 | 慢性、動揺性の経過 1Y後に50%が回復 |
1M以内、遅くとも5M以内 |
.