Posts Tagged CBT

[Infographic] COGNITIVE BEHAVIORAL THERAPY Facts

Cognitive behavioral therapy facts - Dr. Axe

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[WEB SITE] Quiz: What Type of Therapy is Best for You?

Quiz: What Type of Therapy May Be Best for You?

Medically reviewed by psychologist Sarah Schewitz, Psy.D.

Walking into therapy for the first time can feel a little like walking into “The Twilight Zone.” It’s hard to know what to expect and intimidating to think you’ll be sharing so much information with a stranger. Not to mention, each type of therapy has its own guidelines and perspective. And, while the relationship you have with your clinician is perhaps the most important indicator of how well therapy will work for you, not every type of therapy will be a good fit.

Before booking your first therapy session or enrolling in a program, it’s a good idea to find out how your new therapist might meet your needs. After all, you don’t want to be stuck in a room with a counselor whose thoughts on what’s going on for you just don’t jive at all with your experience. Plus, doing a little legwork ahead of time to match the type or types of therapy a counselor uses can help you determine who you might have the best relationship with.

Although some professionals and programs strictly adhere to one type of therapy, many now use several different types of therapy to work with clients. This lets them borrow important skills from each type to better serve your needs. These therapists consider themselves integrative or even eclectic. Keep this in mind as you’re looking for therapist — and taking the following quiz.

This quiz is not professional or medical advice, but simply a way to introduce you to some of the more common types of therapy out there — these are only four of dozens of options. Your results from this quiz will help guide you to what type of therapy may be a good fit for you.

Don’t be worried about answering the questions perfectly. There are no wrong answers. When you are finished with the quiz you will receive your match. For more information on each type of therapy, check below the quiz for more information and where you can find counselors who use those skills in their practice.

Without further ado, visit WEB SITE to TAKE the QUIZ

Cognitive Behavioral Therapy (CBT)

It’s been said what you think is who you are. Just ask Ralph Waldo Emerson, Mahatma Gandhi — or even the Bible. Cognitive behavioral therapy (CBT) borrows a little from this concept: By changing your thoughts, you can also change your emotions and behaviors for a more satisfying life.

In the CBT world, your current thoughts, emotions and behaviors interact with each other. By addressing thoughts that don’t help you, CBT therapists believe you’ll start to experience more well-being. Typically, CBT doesn’t delve way back into your childhood and it’s a format that might include homework, like keeping a log of unhelpful thoughts that might pop into your head that make you feel depressed. It’s skills-based and action-oriented, so this is a good fit if you like to get things done efficiently and in a shorter amount of time — CBT therapy is usually completed in less than 20 sessions.

Because CBT is generally very structured and focuses on concrete, in-the-moment skills, it’s especially helpful if you’re dealing with an anxiety or panic disorder, a specific phobia or obsessive-compulsive disorder (OCD). Many people with depression, suicidal ideation or self-harm, substance use disorders and eating disorders also find CBT helpful. If you live with chronic pain, your treatment team may recommend CBT because it can help you accept the pain you can’t change and learn new coping skills.

You can find CBT therapists through the Association for Behavioral and Cognitive Therapies (ABCT) or Academy of Cognitive Therapy websites.

Dialectical Behavioral Therapy (DBT)

If things feel out of control and super intense — your emotions, relationships, even sometimes your behaviors — dialectical behavior therapy (DBT) is designed with exactly that in mind. This form of therapy focuses on four main areas to help you master your well-being, including mindfulness, distress tolerance, emotion regulation and interpersonal relationships.

DBT was created to treat borderline personality disorder (BPD) and those who struggle with persistent suicidal thoughts or self-harm. One of DBT’s strengths is it gives you a toolbox full of useful life skills so you feel more in control, especially when you didn’t learn those basic emotion regulation or relationship skills earlier in life. DBT is also useful if you’re dealing with other mental health conditions like post-traumatic stress disorder (PTSD), substance use disorders and eating disorders, among others.

There are a couple ways you can do DBT. The traditional, full program includes individual sessions with a DBT therapist, a weekly group skills class and phone coaching between sessions. This can get expensive, so you can also look for a therapist with training to incorporate DBT skills into your regular sessions or participate in just a group skills class.

In whatever context you try DBT, be prepared to work. Studies show DBT can be incredibly effective but you’ll have homework, be expected to track your progress and practice your skills regularly. And know DBT is full of acronyms that might seem overwhelming at first, but soon you’ll be PLEASE-skilling and DEAR MAN-ing like a pro.

To find a DBT therapist near you, search the directories on Behavioral Tech or DBT-Linehan Board of Certification.

Psychodynamic

The premise of psychodynamic therapy is very much based in exploring how the current issues you are dealing with and who you are today originated from your early experiences. By talking through the free associations that come to mind from your past, present, future and dreams, you work with a therapist to find meaning and understanding from your history. These therapists especially focus on their relationship with you, and, traditionally, they use their reactions to you and relationship with you as another tool to help you understand yourself. Relationship is key in psychodynamic formats.

If you’re not a fan of a strict format or homework, are drawn to almost exclusively talk therapy and want to focus on how your past affected you, the more free-flowing nature of psychodynamic therapy may be a good fit for you. Over the years research has shown psychodynamic therapies can help with a variety of mental health conditions, particularly if you’ve experienced trauma.

However, because of the more open format of psychodynamic therapy, if you’re struggling with suicidal thoughts or an active substance use or eating disorder, traditional psychodynamic therapy might not be a good idea. A more structured, skills-based therapy might be needed to make sure you’re safe first. If you still want to work with a psychodynamic therapist in these instances, be sure to ask if they also have training in skills designed to keep you safe during higher-risk times in your life.

Find a psychodynamic therapist near you on Psychology Today.

Interpersonal Psychotherapy (IPT)

If you want to approach your mental health from a well-rounded perspective that takes into account your physical, social, emotional and spiritual health, you might be drawn to interpersonal psychotherapy (IPT). Its major tenant suggests struggles in your interpersonal relationships are directly connected to your mental health symptoms. IPT also believes in the medical model of mental illness, so if you often find yourself comparing dealing with a mental illness to a physical illness, IPT might suit you.

This type of therapy focuses mostly on the present and not on therapy itself, but your life in the real world. IPT is very structured and lasts a set amount of time, usually 12 to 16 sessions. It’s based on attachment — the idea your connections with others is one of the most important aspects of your emotional health. By examining and exploring issues in your current relationships, an IPT therapist works to help you develop stronger connections to reduce your mental health symptoms. This work is done using techniques like role-playing and analyzing how you communicate.

IPT was originally created to treat major depressive disorder and studies also found it’s effective for conditions like anxiety and eating disorders. It’s also helpful when you’re moving through transitions in your life, like a divorce, a move to a new city or a new job. This form of therapy can be used in group therapy settings as well.

You can search for an interpersonal psychotherapist near you on Psychology Today.

If there’s a specific type of therapy you want to try, it may be hard to find a professional in your area that’s affordable and available. If you’re having a hard time finding a local therapist, you’re not alone. You can call the National Alliance on Mental Illness (NAMI) Helpline for assistance finding mental health treatment resources in your area, including therapy and group support. Mental Health America also provides a resource list for other ways you can find referrals and mental health resources.

via Quiz: What Type of Therapy is Best for You? | The Mighty

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[ARTICLE] Pharmacological management of long-term aggression secondary to traumatic brain injuries

Abstract
Aggression is common after traumatic brain injuries (TBI) in acute and chronic settings. However, there is limited guidance regarding its assessment and effective management. Whilst a number of pharmacological options are available for long term treatment, the evidence base is not of an adequate strength to support a unified practice. This article will explore the currently available guidelines and recommendations for treating chronic aggression after TBIs and evaluate the evidence for its pharmacological management.


Introduction

Aggression is a long term neurobehavioural sequelae of TBIs with incidences quoted from 11.5-33.7%.1 In TBI patients, aggressive behaviour tends to be impulsive rather than premeditated and can manifest as episodic dyscontrol syndrome, disinhibition or exacerbated premorbid antisocial traits.2 The underlying mechanisms of aggression are complex allowing numerous and diverse interventions targeting various pathways.

In acute settings, Lombard and Zafonte (2005) describe non-pharmacological measures to manage aggression including environmental alterations and ensuring minimal or non-contact restraints. Screening for systemic causes, optimising pain control and patients’ sleep-wake cycle are also advocated. In the event of failed non-pharmacological treatment, Lombard and Zafonte (2005) recommend that medication choice should be tailored to individuals; with side effect profiles taken into consideration.3

For chronic aggression, psychological therapies are used as a first line with pharmacological interventions trialled in later stages.4 Psychological therapy options include cognitive behavioural therapy (CBT), behavioural management utilising operant learning theory and contingency management. However, a review by Alderman (2013) concluded that further evidence using scientific methods is needed to analyse these approaches.5  Comparatively, there is a diverse body of literature addressing long term pharmacological treatment although quality among studies are varied. This article will focus on the aetiology for chronic post TBI aggression, current management guidelines and the evidence for long term pharmacological interventions.

Aetiology

Post TBI aggression has been associated with lesions affecting the prefrontal cortex – particularly the orbitofrontal and ventromedial areas – causing a loss of behavioural regulation. Disruption to inhibitory pathways between the prefrontal cortex and limbic system also results in limbic kindling and inappropriate emotional responses to negative stimuli thus facilitating aggressive behaviour.2 Associated neurotransmitter abnormalities include low cortical serotonin and impaired gamma amino-butyric acid (GABA)/ glutamate levels.6 Altered catecholamine and cholinergic levels are associated with cognitive impairment2 thus distorting information processing and predisposing patients to aggression.6 In TBI patients, underlying anxiety, affective disorders, seizures and frontal lobe dysfunction also increase susceptibility.10

Differentials for aggression

When identifying a cause for chronic aggressive behaviour, a patient’s previous experiences, comorbid psychiatric conditions and alcohol and/or substance abuse must be established with a collateral history.2,7  McAllister (2008) highlights the importance of determining pre-injury behaviour in order to exclude the possibility of symptoms being an exaggeration of pre-injury personality traits.8 Additionally, psychosocial factors must be deduced to identify possible triggers.2,7

Clinicians must be aware that aggression can be a presenting feature of other psychiatric disorders. Depression has a prevalence of 18.5% to 61% in post-TBI patients  and is linked with aggression due to their shared association with frontal lobe lesions and serotonin level imbalance.9 Other differentials include manic disorders (which can involve a more marked aggressive component if secondary to TBIs), anxiety disorders and alcohol and/or substance abuse. Personality and behavioural disorders such as affective lability, behavioural disinhibition and acquired antisocial behaviour should also be considered.8

Management guidelines

The National Institute for Health and Care Excellence (NICE) refers to the Scottish Intercollegiate Guidelines Network (SIGN) for rehabilitating patients with acquired brain injuries (ABIs). Psychological treatments advocated by SIGN include CBT, contingency management procedures, music therapy and comprehensive neurobehavioural rehabilitation (CNR).10 Family involvement appears to be associated with better outcomes2 and is also recommended.10

Of the studies quoted by SIGN, CNR was found to cause a positive effect in ABI patients in one systematic review although inconsistent results were obtained for the other three methods. Regarding pharmacological treatment, SIGN advises propranolol and pindolol as first line options.10

Pharmacological treatment

The aberrant neurotransmitter changes in the cortex and limbic areas as a result of TBIs2 provide targets for pharmacological therapy (as summarised in Table 1). Theoretically, cortical behavioural regulation can be enhanced by serotonergic agents and antagonists of dopaminergic and noradrenergic neurotransmission. Limbic hyperactivity can be dampened by the use of gamma aminobutyric acid (GABA) agonists, glutamatergic antagonists and anticholinergics.6

Impaired behavioural regulation

Antidepressants

Selective serotonin reuptake inhibitors (SSRIs) are indicated for their increase in dopamine and serotonin availability and the treatment of depression contributing to aggressive behaviour. In a trial conducted by Kant et al (1998), sertraline reduced aggression within one week of treatment although TBI severities were variable within the population.11 These results are mirrored in other trials presenting sertraline as a viable treatment option.12 Citalopram used in conjunction with carbamazepine successfully treated behavioural symptoms in a clinical trial of 22 patients conducted by Perino et al (2001)13 although the separate effects of both drugs are impossible to differentiate. A case study by Sloan et al (1992) found that fluoxetine improved emotional lability in one patient within a week.13

Tricyclic antidepressants have been shown to be useful for managing both post-traumatic and chronic aggression. Amitriptyline has reduced aggression with good tolerability despite its strong anticholinergic side effects in several studies and is suggested as the best option for treating behavioural disorders secondary to frontal lobe injuries without impairing cognition.13

Antipsychotics

There is a wide body of literature advocating antipsychotics for managing aggression due to their sedative effects.13 Nevertheless, the cognitive and extrapyramidal side effects of typical antipsychotics limit their value for chronic use. Comparatively, atypical antipsychotics have a milder side effect profile and are preferred although their cognitive impact in TBI patients is unclear.2 Furthermore, unlike older generations, atypical antipsychotics antagonise 5HT2 receptors and are therefore implicated in reduced aggression.9

Of the typical antipsychotics, chlorpromazine reduced explosiveness in one case study conducted by Sandel et al (1993). Various case studies also report haloperidol improving chronic agitation in TBI patients although significant side effects were encountered.13 Of the atypical antipsychotics the level of evidence is low. Quetiapine reduced aggression and irritability in seven patients in a trial conducted by Kim and Bijlani (2006).11 Olanzapine significantly reduced aggression within six months in a case study conducted by Umansky and Geller (2000). Clozapine was associated with varying levels of improvement in six case studies conducted by Michals et al (1993) however seizures were experienced in two patients.13

Overall, there is no reliable evidence advocating antipsychotic use for managing chronic post-TBI aggression. If antipsychotics are commenced for this purpose, it is suggested that their use is restricted to patients with psychosis.13

Beta blockers

Beta blockers are useful for cases where aggression is caused by underlying anxiety13 due to its inhibition of noradrenergic levels.9 A Cochrane review of four RCTs found that pindolol and propranolol reduced aggression within two to six weeks of starting treatment in ABI patients however no recommendations were made due to heterogeneity between samples, a small number of trials and small sample sizes.  The authors acknowledge that the trials involved high doses and so recommend caution when prescribing beta blockers for aggression.4

Methylphenidate

Methylphenidate is a psychostimulant indicated for its enhancement of dopamine and noradrenaline in the frontal lobe improving arousal and alertness.13 Mooney (1993) found in a single RCT that methylphenidate significantly improved anger scores in TBI patients.4 However other studies have yielded mixed results12,13 and no firm conclusion can be made.

Amantadine

Amantadine increases dopamine availability and acts on glutamatergic pathways. An advantage of its use is its non-sedating qualities however there is contradicting evidence for its efficacy.13 An RCT conducted by Schneider (1999) found no significant improvement4 however the trial was limited by a small sample size and large heterogeneity. Interestingly, studies of a lower level of evidence demonstrate favourable results.13 Due to this variability, its efficacy is still in question.

Buspirone

Buspirone – a serotonergic agonist licensed for treating anxiety13 – has also reduced aggression in several case studies2,12,14 warranting further research. Its side effects are amenable for use in TBIs although one disadvantage is its delayed onset.13

Hyperactive limbic drive

Anticonvulsants

The mood stabilising effects of anticonvulsants are mediated through their enhancement of GABA transmission.2 Carbamazepine has been demonstrated in studies to be effective for managing acute and chronic post- TBI aggression.12,13 Its side effects include impaired balance, sedation13 and cognitive impairment particularly in brain injured patients2 due to their heightened sensitivity. In a trial conducted by Mattes (2005), Oxcarbazepine reduced impulsive aggression however the number of TBI participants in the sample was unclear. Nine of the 48 participants also dropped out due to adverse effects11 suggesting more research is needed into its tolerability in TBI patients. Valproate has also been demonstrated to effectively manage behavioural and affective disorders13 with a milder cognitive impact compared to carbamazepine.2 Regarding other anticonvulsants, the evidence is of a lower standard. Pachet et al (2003) found that lamotrigine reduced aggression with good tolerability in one case study.11 Topiramate has been demonstrated to effectively treat manic symptoms but due to its side effects of psychosis and cognitive impairment,2 may be inappropriate for TBI patients. Case reports reference lithium to reduce post – TBI agitation however it may be unsuitable as a first line option due to its neurotoxicity.13

Benzodiazepines

Benzodiazepines are indicated for their anticonvulsive, anti-anxiety and sedative qualities facilitated by stimulation of the GABA receptor.13 There is limited literature on their chronic use in TBI patients due to their side effects of agitation, cognitive impairment and tolerance2 thus they are recommended to be more appropriate for cases of acute agitation or anxiety.11

Conclusion

There are many challenges in assessing and managing chronic aggression due to its complex aetiology. Previous literature presents a selection of pharmacological options however, their effect on TBI patients has not been confirmed resulting in limited guidance. The heterogeneity between samples also renders it impossible to predict treatment outcomes in the TBI population warranting the need for low doses, slow titration and frequent monitoring.13 A six-week trial period is advised by Fleminger et al (2006) to ascertain effects of treatment before trialling a new medication.4 Patient and family education regarding realistic treatment outcomes and side effects of treatments is also necessary to ensure treatment compliance.2 In future, a clarification of the underlying neurochemical changes is needed to identify further treatment targets. Additional larger scale RCTs are also needed to guide decision making and predict treatment outcomes. Table 2 offers a practical guide on medication choice in relation to aggressive behaviour in ABI.

References

  1. Tateno A, Jorge RE, Robinson RG. Clinical correlates of aggressive behaviour after traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(2):155-60.
  2. Kim E. Agitation, aggression and disinhibition syndromes after traumatic brain injury. NeuroRehabilitation 2002;17:297-310.
  3. Lombard LA, Zafonte RD. Agitation after traumatic brain injury: considerations and treatment options. Am J Phys Med Rehabil. 2005;84(10):797-812.
  4. Fleminger S, Greenwood RJ, Oliver DL. Pharmacological management for agitation and aggression in people with acquired brain injury. Cochrane Database Syst Rev. 2006;18(4):CD003299.
  5. Alderman N, Knight C, Brooks J. Rehabilitation Approaches to the Management of Aggressive Behaviour Disorders after Acquired Brain Injury. Brain Impairment. 2013;14(1):5-20.
  6. Siever LJ. Neurobiology of Aggression and Violence. Am J Psychiatry. 2008;165(4):429-42.
  7. McAllister TW. Neurobehavioral sequelae of traumatic brain injury: evaluation and management. World Psychiatry. 2008;7(1):3-10.
  8. Schwarzbold M, Diaz A, Martins ET, Rufino A, Amante LN, Thais ME et al. Psychiatric disorders and traumatic brain injury. Neuropsychiatr Dis Treat. 2008;4(4):797-816.
  9. Coccaro EF, Siever LJ. Pathophysiology and treatment of aggression. In: Davis KL, Charney D, Coyle JT, Nemeroff C, editors. Neuropsychopharmacology: The Fifth Generation of Progress. 5th ed. Pennsylvania: Lipincott, Williams & Wilkins; 2002:1709-23.
  10. Scottish Intercollegiate Guidelines Network. Brain injury rehabilitation in adults. Edinburgh: SIGN; 2013. 68 p. Report no.:130.
  11. Luauté J, Plantier D, Wiart L, Tell L, the SOFMER group. Care management of the agitation or aggressiveness crisis in patients with TBI. Systematic review of the literature and practice recommendations. Ann Phys Rehabil Med 2016;59(1):58-67.
  12. Warden DL, Gordon B, McAllister TW, Silver JM, Barth JT, Bruns J, et al. Guidelines for the Pharmacological Treatment of Neurobehavioral Sequelae of Traumatic Brain Injury. J Neurotrauma 2006;23(10):1468-501.
  13. Levy M, Berson A, Cook T, Bollegala N, Seto E, Tursanski S, et al. Treatment of agitation following traumatic brain injury: A review of the literature. NeuroRehabilitation 2005;20(4):279-306.
  14. Chew E, Zafonte RD. Pharmacological management of neurobehavioral disorders following traumatic brain injury – a state-of-the-art review. J Rehabil Res Dev 2009;46(6):851-79.

Anum Bhatti is currently in her final year of training for her MBchB at Keele University. She is interested in pursuing psychiatry as a career choice.

 

Dr George El-Nimr, MBChB, MSc (Neuropsych), MRCPsych, MSc (Psych), MMedEd, is a Consultant Neuropsychiatrist and Academic Secretary of the Faculty of Neuropsychiatry at the Royal College of Psychiatrists.

 

Correspondence to: Dr El-Nimr, Consultant Neuropsychiatrist, Neuropsychiatry Services, Bennett Centre, Richmond Terrace, Shelton, Stoke-on-Trent ST1 4ND. Tel: 01782 441614
Conflict of interest statement: None declared
Provenance and peer review: Submitted and externally reviewed
Date first submitted: 18/4/18
Date submitted after peer review: 21/9/18
Acceptance date: 15/5/19
To cite: Bhatti A, El-Nimr G. 
ACNR 2019;18(4);15-17
Published online: 1/8/19

via Pharmacological management of long-term aggression secondary to traumatic brain injuries | ACNR | Online Neurology Journal

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[WEB SITE] VRHealth unveils VR software for hot flashes

The new technology will provide users with an AI guide that will lead them through CBT.

By Laura Lovett, December 12, 2018

Photo credit: VRHealth

 

VRHealth has exclusively unveiled to MobiHealthNews a virtual reality product called Luna that was designed to help patients manage hot flashes.

The new VR product, which can be used by patients going through menopause or chemotherapy treatment, employs cognitive behavioral therapy (CBT). It also gives users a data analysis of their treatment.

When a user puts on the VR headset, they are greeted by an AI trainer called Luna who guides users through CBT and other coping mechanisms. The technology also lets users virtually travel to another environment.

“That trainer you can take to different places. One part of the app is called practice breathing in an environment. It [let’s you] see how you breath,” Eran Orr, CEO of VRHealth, told MobiHealthNews. “Users can actually see the environment and go into a lake or waterfall.”

While the technology will first be given to patients in a hospital setting, Orr said that the idea is for the system to go home with the patients.

“Patients will be introduced to it during chemotherapy or treatment in the hospital and will take [the] headset back home,” he said. “It is an AI that is basically a trainer that follows improvement and can be adjusted automatically.”

The idea for Luna came out of a personal connection. One of the members of the VRHealth team developed the idea for the technology after undergoing chemotherapy for breast cancer and experiencing hot flashes as a side effect.

Orr said that Luna will officially launch in January of 2019 at CES.

Why it matters

Hot flashes, which are often triggered by a hormone drop, are associated with breast cancer chemotherapy and surgery to remove the ovaries as well as menopause, according to the Cancer Treatment Centers of America (CTCA). While women are most likely to experience hot flashes, the CTCA said that men can also experience the condition.

Common treatment options include hormone therapy, antidepressants and other prescription medications, according to the Mayo Clinic. Alternative medicine including meditation, acupuncture and CBT are also used.

VRHealth is pitching this technology as another avenue to treat the condition, and Orr hinted that in yet-to-be-released clinical trials Luna outperformed medications for hot flash treatment.

What’s the trend

VRHealth was in the news in September when it teamed up with Facebook’s Oculus, which makes VR hardware and other related products, on a range of healthcare-focused VR applications to be delivered on the latter’s hardware.

VR as a whole is growing. Many in healthcare are looking to the technology to help with pain, discomfort and anxiety. Clinicians are deploying it in a wide range of settings including obstetricspediatrics and rehabilitation.

On the record 

“We believe VR can be an amazing replacement for opiates or any kind of nonnatural hormone and the most common treatments that have a lot of side effects,” Orr said. “We believe VR could be a good solution.”

via VRHealth unveils VR software for hot flashes | MobiHealthNews

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[WEB SITE] OCD: Brain mechanism explains symptoms

A large review of existing neuroscientific studies unravels the brain circuits and mechanisms that underpin obsessive-compulsive disorder. The researchers hope that the new findings will make existing therapies more effective, “or guide new treatments.”
doctors looking at brain scans

New research analyzes the brain scans of almost 500 people to unravel the brain mechanisms in OCD.

Obsessive-compulsive disorder (OCD) is a mental health condition that affects more than 2 million adults in the United States.

People with OCD often experience recurring, anxiety-inducing thoughts or urges — known as obsessions — or compulsive behaviors that they cannot control.

Whether it is repeatedly checking if the door is locked or switching lights on and off, OCD symptoms are uncontrollable and can severely interfere with a person’s quality of life.

Treatments for OCD include medication, psychotherapy, and deep brain stimulation. However, not everyone responds to treatment.

In fact, reference studies have found that only 50 percent of people with OCD get better with treatment, and just 10 percent recover fully.

This treatment ineffectiveness is partly down to the fact that medical professionals still do not fully understand the neurological roots of the condition. A new study, however, aims to fill this gap in research.

Scientists led by Luke Norman, Ph.D., a postdoctoral research fellow in the Department of Psychiatry at the University of Michigan (U-M) in Ann Arbor, corroborated and analyzed large amounts of data from existing studies on the neurological underpinnings of OCD.

The scientists published their meta-analysis in the journal Biological Psychiatry.

Studying the brain circuitry in OCD

Norman and colleagues analyzed studies that scanned the brains of hundreds of people with OCD, as well as examining the brain images of people without the condition.

“By combining data from 10 studies, and nearly 500 patients and healthy volunteers, we could see how brain circuits long hypothesized to be crucial to OCD are indeed involved in the disorder,” explains the study’s lead author.

Specifically, the researchers zeroed in on a brain circuit called the “cingulo-opercular network.” This network involves several brain regions that are interconnected by neuronal pathways in the center of the brain.

Studies have previously associated the cingulo-opercular network with “tonic alertness” or “vigilance.” In other words, areas in this brain circuit are “on the lookout” for potential errors and can call off an action to avoid an undesirable outcome.

Most of the functional MRI studies included by Norman and colleagues in their review had volunteers respond to errors while inside the brain scanner.

An analysis of data from the various studies revealed a salient pattern: Compared with people who did not have OCD, those with the condition displayed significantly more activity in brain areas associated with recognizing an error, but less activity in the brain regions that could stop an action.

Study co-author Dr. Kate Fitzgerald of U-M’s Department of Psychiatry explains the findings, saying “We know that [people with OCD] often have insight into their behaviors, and can detect that they’re doing something that doesn’t need to be done.”

She adds, “But these results show that the error signal probably isn’t reaching the brain network that needs to be engaged in order for them to stop doing it.”

The researcher continues using an analogy.

It’s like their foot is on the brake telling them to stop, but the brake isn’t attached to the part of the wheel that can actually stop them.”

Dr. Kate Fitzgerald

“This analysis sets the stage for therapy targets in OCD because it shows that error processing and inhibitory control are both important processes that are altered in people with the condition,” says Fitzgerald.

Findings may boost existing treatments

The researcher also explains how the findings may enhance current treatments for OCD, such as cognitive behavioral therapy (CBT).

“In [CBT] sessions for OCD, we work to help patients identify, confront, and resist their compulsions, to increase communication between the ‘brake’ and the wheels, until the wheels actually stop. But it only works in about half of patients.”

“Through findings like these, we hope we can make CBT more effective, or guide new treatments,” Dr. Fitzgerald adds. The team is currently recruiting participants for a clinical trial of CBT for OCD.

In addition to CBT, Dr. Fitzgerald also hopes that the results will enhance a therapy known as “repetitive transcranial magnetic stimulation” (rTMS).

“If we know how brain regions interact together to start and stop OCD symptoms, then we know where to target rTMS,” she says. “This is not some deep dark problem of behavior,” Dr. Fitzgerald continues.

OCD is a medical problem, and not anyone’s fault. With brain imaging, we can study it just like heart specialists study EKGs of their patients — and we can use that information to improve care and the lives of people with OCD.”

Dr. Kate Fitzgerald

via OCD: Brain mechanism explains symptoms

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[WEB SITE] Is There a Science to Psychotherapy?

Neuroscience findings suggest that psychotherapy alters the brain.

Since the decade of the brain, 1990-1999, neuroscience has captured enormous amounts of attention from both the scientific community and the general public. Many books and media reports describe the brain’s basic anatomy and function. There has been a proliferation of neuroscience institutes at universities. In laboratories all over the world, neuroscience has become one of the most exciting and productive branches of inquiry.

Yet not everyone is completely pleased with what neuroscience has to tell us. In particular, some decry neuroscience for trying to delegitimize the “mind.” Going back to the original Cartesian mind-body duality, these critics insist that neuroscience can only go so far by describing the function of neurons and neurotransmitters. What cannot be reached by science, they say, is that ineffable “mind” that constitutes the human spirit. For them, neuroscience is purely an attempt to reduce the complexities and wonders of human experience to brain scan images and electrical recordings from axons and dendrites.

In a new book, Neuroscience at the Intersection of Mind and Brain (Oxford University Press, 2018), one of us (Jack) attempts to allay fears that neuroscience will somehow reduce human experience and creativity to the “mere” workings of the physical brain. There is, in fact, nothing “reductive” about the physical brain. Rather, the brain is a gloriously complex, fascinating, and well-organized structure that constitutes, as neuroscientist Eric Kandel so eloquently put it, “the organ of the mind.”

Biologists versus Psychologists

As a resident in psychiatry in the late 1970s, Jack witnessed the emergence of psychopharmacology as the dominant discipline for academic psychiatry and lived through the often bitter battles between “biologists” and “psychologists.” This may be, in part, where the mistrust of neuroscience began. The biologists believed that their method of treating psychiatric illness—medication—was based on solid science and rejected psychotherapy as unscientific.  They also believed that neuroscience explained why the new psychiatric drugs worked and therefore promoted brain science as the basis for their discipline. Every lecture about depression or schizophrenia in those days began with a picture of a pre- and postsynaptic neuron forming a synapse across which neurotransmitters like serotonin, noradrenaline, and dopamine carried information. The new medications interact with receptors for these neurotransmitters and, it was taught at the time, this explains how they work to treat depression, anxiety, and psychosis.

 Andrew Rybalko/Shutterstock

Source: Andrew Rybalko/Shutterstock

It turns out that the picture of neurons everyone used back then was a vast oversimplification of what a synapse really looks like and that almost nothing we know about neurotransmitters and their receptors actually explains how psychiatric drugs work. But what really bothered the psychologists was the complete dismissal of psychotherapy by the biologists. Years of studying various types of psychotherapy convinced them that indeed they had science on their side. Furthermore, they objected to the biologists’ emphasis on inherited abnormalities as the sole basis for psychiatric illness. Psychologists had always been more interested in the ways that human experience, from birth onwards, shaped personality and behavior.

Over time, many (but thankfully not all) psychologists came to see neuroscience as the branch of science devoted to promoting pharmacology as the only treatment for psychiatric illness and to trying to prove that those illnesses were entirely due to inherited brain abnormalities. Biologists stood with nature; psychologists with nurture.

This fear of neuroscience’s aims is entirely misplaced. Over the last several decades, neuroscience has, in fact, focused a great deal of attention on the biology of experience, elucidating the ways in which what happens to us in life affects the structure and function of the brain. Every time we see, hear, smell, or touch something, learn a new fact, or have a new experience, genes are activated in the brain, new proteins are synthesized, and neural pathways communicate the new information to multiple brain regions.

Neuroscience is not, therefore, synonymous with psychopharmacology, nor does it invalidate the complexities of human experience. It has shown, for example, that early life interactions between a parent and child shape how the brain will function for the rest of a person’s life.

This has tremendous implications for understanding the mechanism of action of psychotherapy if we accept the idea that psychotherapy itself is a form of life experience and therefore capable of changing brain function at molecular, cellular, and structural levels. Here are two examples that illustrate ways in which neuroscience informs psychotherapy.

CBT and the Prefrontal to Amygdala Connection

It is now clear that the expression of conditioned fear is dependent upon an intact, functioning amygdala. Scientists have shown that the amygdala, located in a primitive part of the brain often referred to as the limbic cortex, reciprocally inhibits and is inhibited by a more evolutionarily advanced part of the brain, the medial prefrontal cortex (mPFC). Thus, under circumstances of heightened fear, the amygdala shuts down the ability of the mPFC to exert reason over emotion and initiates a cascade of fearful responses that include increased heart rate and blood pressure and freezing in place. When the mPFC is able to reassert its capacity for logic and reason, it can, in turn, inhibit the amygdala and reduce and extinguish fear.

Cognitive behavioral therapy (CBT) is an evidence-based intervention that is the first-line treatment for most anxiety disorders and for mild, moderate, and in many cases even severe depression. Because the automatic, irrational fears and avoidance behaviors manifested by patients with anxiety disorders and depression resemble the behavior of rodents in Pavlovian fear conditioning experiments, scientists have wondered if CBT works, at least in part, by strengthening the prefrontal cortex to amygdala pathway, thereby reducing amygdala activity. Indeed, many studies have shown that anxious and depressed patients have reduced activity in this pathway and exaggerated amygdala responses to fearful stimuli. Studies have also shown that successful CBT for social anxiety disorder decreases amygdala activation.

Most recently, a group of scientists from Oxford, Harvard, and Berkeley showed clearly that stimulation of the prefrontal cortex in human volunteers both reduced amygdala activation and fear. Maria Ironside and colleagues selected 18 women with high levels of trait anxiety and randomized them to receive either transcranial direct current stimulation (tDCS) to the prefrontal cortex or sham tDCS. The subjects underwent functional magnetic resonance imaging (fMRI) of the brain and performed an attentional load task that tests vigilance to threat. Real, but not sham, tDCS increased activity in the prefrontal cortex, decreased activity in the amygdala, and decreased threat responses.

This study is one example of preclinical and clinical neuroscience coming together to suggest a biological mechanism for the efficacy of a psychosocial intervention. We know that the cognitive portion of CBT strengthens a patient’s ability to assert reason over irrational thoughts and fears and that this decreases amygdala activity in some studies. We know clearly from animal studies that stimulating the prefrontal cortex reduces amygdala activation and potentiates fear extinction. Now we also know that in a group of anxious people, direct stimulation of the prefrontal cortex does exactly the same thing as it does in animal studies and, in addition, reduces anxiety. With this plausible hypothesis for how CBT works, scientists can now push further to see if brain imaging can ultimately help select patients with particularly weak prefrontal to amygdala pathway strength who might be prime candidates for CBT and then to track how they are doing in therapy objectively by repeating the brain imaging studies to see if and when that pathway is strengthened.

Psychoanalysis and Reconsolidation

CBT has been proven effective by many high-quality clinical trials and therefore is a prime candidate for biological studies, but can the same be said for such widely used but not empirically-validated treatments as psychoanalysis and psychoanalytic psychotherapy? In 2011, Jack and his colleague, Columbia psychiatrist and psychoanalyst Steven Roose, proposed that another aspect of fear conditioning—reconsolidation of fear memories—may explain one biological mechanism of action for how psychoanalysis works. In rats, when a conditioned fear memory is reactivated, it temporarily becomes labile and can be completely erased by blocking the biological mechanisms that permit reconsolidation of the memory. Could it be that in psychoanalytic therapies, the patient undergoes a process of reactivating distressing early memories that, once made conscious through the psychoanalytic process, can be manipulated by the therapist’s interpretations? According to this hypothesis, those now altered memories can then be reconsolidated into permanent memory in a less disturbing format.

The theory has been considered since then by many scientists and psychoanalytic theorists and a number of experiments show that the phenomena of labile reactivated memories and blockade of reconsolidation do indeed occur in humans. Blocking reconsolidation of reactivated memories has been shown to be effective in experiments attempting to help addicts overcome the powerful tendency to succumb to subtle cues and resume taking drugs even after successful rehabilitation. Here again, information gained from the basic neuroscience laboratory and from clinical neuroscience studies may help us understand how one aspect of psychoanalysis works to change the brain in ways that are helpful to people suffering with mental illness.

It is not necessary to invoke an ineffable “mind” to explain our unique human characteristics. Understanding the complexity of the human brain is sufficient to reveal how we are able to take what we experience and transform it into scientific theories, poetry, and philosophical ideas. Neuroscience is not superficial or reductionistic and it is not at all in the sole service of psychopharmacology and the genetic explanation for mental disorders. This becomes clear as we recognize the tremendous contributions neuroscientists have made to elucidating basic mechanisms that allow experiences to change the physical structure and function of the brain on a second-by-second basis. Everything we experience during life is translated into events that occur in the brain.

Psychotherapy is a form of life experience that changes the way the brain works, often ameliorating abnormalities caused by adverse experience and stressful life events. So yes, there is a science to psychotherapy, one that can be readily understood by learning about some of the fundamental and fascinating ways our brains work. Neuroscience at the Intersection of Mind and Brain tries to do just that.

via Is There a Science to Psychotherapy? | Psychology Today UK

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[WEB SITE] Cognitive Behavioral Therapy (CBT) and Transcranial Magnetic Stimulation (TMS): What Are These Therapies and How Are They Used?

Published 7 Feb 2018  – Reviewed 7 Feb 2018 – Author Melissa Galinato  – Source BrainFacts/SfN

When you have a cold, you might have a runny nose, a headache, and a cough. You may take different medications to treat each symptom to soothe your throat or ease your sneezing. Like treating a cold with multiple symptoms, there are different types of therapies to treat the multiple symptoms of depressive disorder, widely known as depression. Cognitive Behavioral Therapy (CBT) and Transcranial Magnetic Stimulation (TMS) are two therapy types that address specific symptoms of depression.

More than 300 million people around the world have depression, which is a common mental illness with multiple symptoms such as persistent sadness, irritability, a feeling of worthlessness, and loss of interest in activities—especially in things that previously brought joy or excitement.

With Cognitive Behavioral Therapy (CBT), a therapist helps a patient with depression to focus on understanding how three things – thoughts, feelings, and behavior – affect each other. “The goal of CBT for depression is to start targeting problematic thoughts and actions that are occurring in the present – as opposed to looking back in the past for a cause – teaching patients skills that they can use to become more aware of their negative thoughts, evaluate their validity and, when not accurate, replace them with more realistic/balanced ways of thinking,” says Simon Rego, Chief Psychologist at Montefiore Medical Center/Albert Einstein College of Medicine in New York.

“At the same time, the other goal of CBT is to help patients change maladaptive patterns of behavior, gradually increasing activities of pleasure and accomplishment, which are known to enhance mood. Taken together, changing how you think and what you do can have a powerful positive impact on your mood.”

Imagine setting a goal – like running a marathon for the first time. A running coach could help you reach that goal by giving you tips and developing a training to slowly build up your strength. In CBT, the therapist acts like a coach and helps people identify goals such as driving a car or giving a speech. Then the therapist helps to figure out actions to reach those goals such as practicing thinking strategies, writing in journals, and doing homework assignments between appointments. Doing these activities in CBT can help people learn coping skills, build self-confidence, and have a sense of control, and a growing number of studies show that CBT works very well for treating depression and several other mental health conditions.

“CBT is an effective treatment for depression because it targets the two main areas where people with depression struggle: negative thoughts and unhelpful behaviors,” said Rego. “The main theory in CBT is that how we feel is directly influenced by how we think and what we do (or don’t do). In the case of depression, we know that people tend to have many negative thoughts about themselves, the world, and the future (e.g., I am a failure, I’ll never get better, no one cares about me, I don’t have the energy to do anything, etc.) which only serve to perpetuate their negative mood.”

Another therapy called Transcranial Magnetic Stimulation (TMS) can be used for some patients with depression who do not get better with antidepressant medications or other treatments. “In our experience, TMS is an appropriate treatment for major depressive disorder, moderate in severity and who are still functioning in the home, community, and who have failed multiple antidepressant medications,” said Ananda Pandurangi, medical director and chair of inpatient psychiatry in the Department of Psychiatry at Virginia Commonwealth University School of Medicine. “It is not appropriate for patients with either “mild” depression or those with severe depression including those with psychosis or catatonia,” said Pandurangi, noting that psychotherapy and medications may be more appropriate for patients with mild to severe depression.

TMS aims to alter brain circuitry. Using an electromagnetic coil, called a stimulator, to affect brain activity and treat depression, TMS treatment involves a doctor placing the stimulator near the forehead against the scalp. This activates brain cells in an area of the brain that includes the prefrontal cortex and controls mood and depression.

Sessions typically use repetitive TMS (rTMS) where recurrent magnetic pulses stimulate the brain. In 2008, the FDA approved rTMS for depression treatment after several research studies showed this TMS treatment lowers signs of depression and improves mood in people with treatment-resistant depression.

REFERENCES

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-5). 5th ed. Washington, DC: American Psychiatric Publishing; 2013. 

Butler AC, Chapman JE, Forman EM, Beck AT. The empirical status of cognitive-behavioral therapy: a review of meta-analyses. Clinical Psychology Review. 26(1), 17-31 (2006).

Depression. National Alliance on Mental Illness. Accessed 2/7/2018.

Depression. World Health Organization. February 2017.

Dobson D, Dobson KS. Evidence-based practice of cognitive-behavioral therapy. Guilford Publications. 2016. 

Gaynes BN, Lloyd SW, Lux L, Gartlehner G, Hansen RA, et al. Repetitive transcranial magnetic stimulation for treatment-resistant depression: a systematic review and meta-analysis. The Journal of Clinical Psychiatry. 75(5), 477-89 (2014).

Huguet A, Rao S, McGrath PJ, Wozney L, Wheaton M, et al. A systematic review of cognitive behavioral therapy and behavioral activation apps for depression. PLoS One. 11(5), e0154248 (2016). 

Lefaucheur JP, André-Obadia N, Antal A, Ayache SS, et al. Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS). Clinical Neurophysiology. 125(11), 2150-2206 (2014). 

Levkovitz Y, Isserles M, Padberg F, Lisanby SH, Bystritsky A, et al. Efficacy and safety of deep transcranial magnetic stimulation for major depression: a prospective multicenter randomized controlled trial. World Psychiatry. 14(1), 64-73 (2015). 

Pascual-Leone A, Rubio B, Pallardó F, Catalá MD. Rapid-rate transcranial magnetic stimulation of left dorsolateral prefrontal cortex in drug-resistant depression. The Lancet. 348(9022), 233-237 (1996). 

Psychotherapy. National Alliance on Mental Illness. Accessed 2/7/2018.

Wassermann EM, Williams WA, Callahan A, Ketter TA, Basser P, et al. Daily repetitive transcranial magnetic stimulation (rTMS) improves mood in. Neuroreport. 6, 1853-1856 (1995). 

via Cognitive Behavioral Therapy Transcranial Magnetic Stimulation what are these therapies 020718

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[Abstract] Cognitive behavior therapy to treat sleep disturbance and fatigue after traumatic brain injury – CNS

OBJECTIVE: To evaluate the efficacy of adapted cognitive behavioral therapy (CBT)
for sleep disturbance and fatigue in individuals with traumatic brain injury
(TBI).
DESIGN: Parallel 2-group randomized controlled trial.
SETTING: Outpatient therapy.
PARTICIPANTS: Adults (N=24) with history of TBI and clinically significant sleep
and/or fatigue complaints were randomly allocated to an 8-session adapted CBT
intervention or a treatment as usual (TAU) condition.
INTERVENTIONS: Cognitive behavior therapy.
MAIN OUTCOME MEASURES: The primary outcome was the Pittsburgh Sleep Quality Index
(PSQI) posttreatment and at 2-month follow-up. Secondary measures included the
Insomnia Severity Index, Fatigue Severity Scale, Brief Fatigue Inventory (BFI),
Epworth Sleepiness Scale, and Hospital Anxiety and Depression Scale.
RESULTS: At follow-up, CBT recipients reported better sleep quality than those
receiving TAU (PSQI mean difference, 4.85; 95% confidence interval [CI],
2.56-7.14). Daily fatigue levels were significantly reduced in the CBT group (BFI
difference, 1.54; 95% CI, 0.66-2.42). Secondary improvements were significant for
depression. Large within-group effect sizes were evident across measures (Hedges
g=1.14-1.93), with maintenance of gains 2 months after therapy cessation.
CONCLUSIONS: Adapted CBT produced greater and sustained improvements in sleep,
daily fatigue levels, and depression compared with TAU. These pilot findings
suggest that CBT is a promising treatment for sleep disturbance and fatigue after
TBI.

via Traumatic Brain Injury Resource Guide – Research Reports – Cognitive behavior therapy to treat sleep disturbance and fatigue after traumatic brain injury

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[WEB SITE] OCD: Cognitive behavioral therapy improves brain connectivity

MRI scans show that people diagnosed with OCD who have undergone CBT have intensified connectivity between key brain networks.

Researchers have used brain scans to measure changes in the cerebral activity of people with obsessive-compulsive disorder after undergoing a type of cognitive behavioral therapy. They found that the connectivity of key brain networks is improved, suggesting new targets for therapy.

Obsessive-compulsive disorder (OCD) is a condition marked by inescapable, intrusive thoughts that cause anxiety (hence “obsessive”), and repetitive, ritualistic behaviors aimed at reducing that feeling (hence “compulsive”).

OCD can be a debilitating condition and can severely impair daily functioning. The National Institutes of Mental Health estimate that, in the United States, the yearly prevalence of OCD amounts to 1 percent of the total adult population. Around half of these cases are deemed “severe.”

Treatments for OCD include the administration of selective serotonin reuptake inhibitors and cognitive behavioral therapy (CBT), a type of therapy that aims to improve damaging mind associations.

Researchers from the University of California, Los Angeles – who were led by Dr. Jamie Feusner – have conducted a study aiming to find out whether and how CBT might change levels of activity and network connectivity in the brains of people diagnosed with OCD.

They explain that although the efficacy of CBT in treating OCD has been previously explored, this is likely the first study to use functional MRI (fMRI) to monitor what actually happens in the brains of people with OCD after exposure to this kind of therapy.

The researchers’ findings were recently published in the journal Translational Psychiatry.

Changes in key brain regions following CBT

The team specifically targeted the effects of exposure and response prevention (ERP)-based CBT, which entails exposure to triggering stimuli and encouraging the individual to wilfully resist responding to those stimuli in the way that they normally would.

For the study, 43 people with OCD and 24 people without it were recruited. The results for the two groups were later compared, at which point the 24 individuals without OCD were taken as the control group.

All the participants diagnosed with OCD received intensive ERP-based CBT on an individual basis in 90-minute sessions on 5 days per week, for a total of 4 weeks.

Participants from both groups underwent fMRI. Those diagnosed with OCD, who had received CBT, were scanned both before the treatment period and after the 4 weeks of treatment. Participants from the control group, who did not undergo CBT, also had fMRI scans after 4 weeks.

When the scans of participants with OCD were compared, the results from before exposure to CBT and after it were found to be largely contrasting.

The researchers noticed that the brains of people with OCD exhibited a significant increase in connectivity between eight different brain networks, including the cerebellum, the caudate nucleus and putamen, and the dorsolateral and ventrolateral prefrontal cortices.

 The cerebellum is involved with processing information and determining voluntary movements, while the caudate nucleus and putamen are key in learning processes and controlling involuntary impulses.

The dorsolateral and ventrolateral prefrontal cortices are involved with planning action and movement, as well as regulating certain cognitive processes.

Dr. Feusner and team point out that an increased level of connectivity between these cerebral regions suggests that the brains of the people who underwent CBT were “learning” new non-compulsive behaviors and activating different thought patterns.

He suggests that these changes may be novel ways of coping with the cognitive and behavioral idiosyncrasies of OCD.

The changes appeared to compensate for, rather than correct, underlying brain dysfunction. The findings open the door for future research, new treatment targets, and new approaches.”

Dr. Jamie Feusner

First study author Dr. Teena Moody adds that being able to show that there are quantifiable positive changes in the brain following CBT may give people diagnosed with OCD more confidence in following suitable treatments.

“The results could give hope and encouragement to OCD patients,” says Dr. Moody, “showing them that CBT results in measurable changes in the brain that correlate with reduced symptoms.”

Source: OCD: Cognitive behavioral therapy improves brain connectivity

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[WEB PAGE] What Is PTSD? – PTSD: National Center for PTSD

What Is PTSD?

PTSD (posttraumatic stress disorder) is a mental health problem that some people develop after experiencing or witnessing a life-threatening event, like combat, a natural disaster, a car accident, or sexual assault.

It’s normal to have upsetting memories, feel on edge, or have trouble sleeping after this type of event. At first, it may be hard to do normal daily activities, like go to work, go to school, or spend time with people you care about. But most people start to feel better after a few weeks or months.

If it’s been longer than a few months and you’re still having symptoms, you may have PTSD. For some people, PTSD symptoms may start later on, or they may come and go over time.

What factors affect who develops PTSD?

PTSD can happen to anyone. It is not a sign of weakness. A number of factors can increase the chance that someone will have PTSD, many of which are not under that person’s control. For example, having a very intense or long-lasting traumatic event or getting injured during the event can make it more likely that a person will develop PTSD. PTSD is also more common after certain types of trauma, like combat and sexual assault.

Personal factors, like previous traumatic exposure, age, and gender, can affect whether or not a person will develop PTSD. What happens after the traumatic event is also important. Stress can make PTSD more likely, while social support can make it less likely.

What are the symptoms of PTSD?

PTSD symptoms usually start soon after the traumatic event, but they may not appear until months or years later. They also may come and go over many years. If the symptoms last longer than four weeks, cause you great distress, or interfere with your work or home life, you might have PTSD.

There are four types of symptoms of PTSD (en Español), but they may not be exactly the same for everyone. Each person experiences symptoms in their own way.

  1. Reliving the event (also called re-experiencing symptoms). You may have bad memories or nightmares. You even may feel like you’re going through the event again. This is called a flashback.
  2. Avoiding situations that remind you of the event. You may try to avoid situations or people that trigger memories of the traumatic event. You may even avoid talking or thinking about the event.
  3. Having more negative beliefs and feelings. The way you think about yourself and others may change because of the trauma. You may feel guilt or shame. Or, you may not be interested in activities you used to enjoy. You may feel that the world is dangerous and you can’t trust anyone. You might be numb, or find it hard to feel happy.
  4. Feeling keyed up (also called hyperarousal). You may be jittery, or always alert and on the lookout for danger. Or, you may have trouble concentrating or sleeping. You might suddenly get angry or irritable, startle easily, or act in unhealthy ways (like smoking, using drugs and alcohol, or driving recklessly.

Can children have PTSD?

Children can have PTSD too. They may have symptoms described above or other symptoms depending on how old they are. As children get older, their symptoms are more like those of adults. Here are some examples of PTSD symptoms in children:

  • Children under 6 may get upset if their parents are not close by, have trouble sleeping, or act out the trauma through play.
  • Children age 7 to 11 may also act out the trauma through play, drawings, or stories. Some have nightmares or become more irritable or aggressive. They may also want to avoid school or have trouble with schoolwork or friends.
  • Children age 12 to 18 have symptoms more similar to adults: depression, anxiety, withdrawal, or reckless behavior like substance abuse or running away.

What other problems do people with PTSD experience?

People with PTSD may also have other problems. These include:

  • Feelings of hopelessness, shame, or despair
  • Depression or anxiety
  • Drinking or drug problems
  • Physical symptoms or chronic pain
  • Employment problems
  • Relationship problems, including divorce

In many cases, treatments for PTSD will also help these other problems, because they are often related. The coping skills you learn in treatment can work for PTSD and these related problems.

Will people with PTSD get better?

“Getting better” means different things for different people. There are many different treatment options for PTSD. For many people, these treatments can get rid of symptoms altogether. Others find they have fewer symptoms or feel that their symptoms are less intense. Your symptoms don’t have to interfere with your everyday activities, work, and relationships.

What treatments are available?

There are two main types of treatment, psychotherapy (sometimes called counseling or talk therapy) and medication. Sometimes people combine psychotherapy and medication.

Psychotherapy for PTSD

Psychotherapy, or counseling, involves meeting with a therapist. There are different types of psychotherapy:

  • Cognitive behavioral therapy (CBT) is the most effective treatment for PTSD. There are different types of CBT, such as cognitive therapy and exposure therapy.
    • One type is Cognitive Processing Therapy (CPT) where you learn skills to understand how trauma changed your thoughts and feelings. Changing how you think about the trauma can change how you feel.
    • Another type is Prolonged Exposure (PE) where you talk about your trauma repeatedly until memories are no longer upsetting. This will help you get more control over your thoughts and feelings about the trauma. You also go to places or do things that are safe, but that you have been staying away from because they remind you of the trauma.
  • A similar kind of therapy is called Eye Movement Desensitization and Reprocessing (EMDR), which involves focusing on sounds or hand movements while you talk about the trauma. This helps your brain work through the traumatic memories.

Medications for PTSD

Medications can be effective too. SSRIs (selective serotonin reuptake inhibitors) and SNRIs (serotonin-norepinephrine reuptake inhibitors), which are also used for depression, are effective for PTSD. Another medication called Prazosin has been found to be helpful in decreasing nightmares related to the trauma.

IMPORTANT: Benzodiazepines and atypical antipsychotics should generally be avoided for PTSD treatment because they do not treat the core PTSD symptoms and can be addictive.

Visit Site —> What Is PTSD? – PTSD: National Center for PTSD

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