Taken from the Huffington Post which is found HERE.
When my cancer-stricken, elderly father passed away at home with family by his side, I grieved and wept, but my grief was gentle because my dad had lived a very full and rich life. I can tell you the experience of losing my 27-year-old son on April 5, 2013 to suicide was not at all the same.
Matthew – an incredibly kind, funny and compassionate young man whose sweet spirit was encouragement and comfort to many – suffered from severe mental illness.
For more than two decades he struggled. He took his life to end his pain, and he did it in a violent way.
Our family is scarred.
We were left with – not gentle grief – but traumatic grief. Guilt. Regret. Unanswered questions. Horror.
• Half of all adults will suffer from mental illness in their lifetime.
• Half of all chronic mental illness begins by the age of 14.
• One in five children will have a mental illness by age 18.
• Ninety percent of people who die by suicide also had mental illness.
Sixty million Americans – that’s one in five adults – will experience a mental illness in the coming year. That means every one of us knows someone who is living with a mental illness – depression, anxiety, schizophrenia, an eating disorder, bipolar disorder, borderline personality disorder and some additionally have a substance abuse.
The sad fact is the mental health system is broken in the United States. I can’t say that strongly enough. It is not that people aren’t trying and not that there aren’t some really wonderful, compassionate people in the field of mental health, but the problem is complicated, and most of the attempts to help don’t always help.
But there is hope for mental illness, and I believe the Church can lead the way.
When you realize that a large portion of people suffering with mental illness go to either their priest, pastor or rabbi before they even go to a healthcare professional, it makes equipping faith leaders more urgent than ever. Most are not well equipped, yet clergy are dealing with people with mental health issues every day.
We have witnessed this firsthand in our own church. At Saddleback Church there is a higher-than-average awareness of mental illness and the devastation it can cause. Our Pastoral Care Team reports that 23 percent of their ministry is to people living with mental illness or their families.
Most people understand that mental illness is just that – an illness – and as such, often requires medication and treatment by mental health professionals for management and improved health. But the flip side of that realization can lead us to believe that there is nothing significant the faith community can offer to a person with a illness. This is a misperception. In reality, the Church is tasked with caring for the whole person – body, mind and soul – and that means we must recognize and care for the person who is affected by an illness. The Church can speak into the soul and personhood of the individual in ways that medical professionals cannot.
The Church’s central commitment is to be the hands and feet of Jesus. This should include intentionally coming alongside people living with mental illness and supporting their families. If the Church lives out its calling in this area, its compassionate voice will rise within the community, the nation and the world – extending an unwavering message of hope and acceptance for those affected by mental illness.
I believe every church can be a solution by developing a mental health ministry. That is why we are hosting Saddleback Church’s Gathering on Mental Health and The Church October 7-9, 2015. The event will be three days packed with practical help and hope for individuals affected by mental illness, their loved ones, church leaders, and mental health professionals.
It’s time to join together and create a pathway to hope.
It’s time for the Church to offer a place of refuge, love, and compassion for those who need it most. It’s a time to acknowledge the facts and embrace the millions of people suffering everyday from mental illness.
As someone who was diagnosed with a third mental illness last year, I can be overly sensitive to what people say or do around me. It got me thinking… How many times do kind, well-meaning people slip up and say something that causes more pain and harm than good?
Here’s a list of things not to say to someone with a mental illness or who is struggling with their mental health.
1. Do not refer to the individual by their illness. I am not the depressed girl or the bipolar chick. I am Nichole. A young woman who happens to struggle with a mental illness.
2. If an individual tries to commit suicide, that does not forever make them suicidal.
3. Someone who has struggled with self-harm should not be referred to as an emo, goth or cutter.
4. Do not tell individuals who struggle with self-harm, depression or anxiety they are doing it for attention or drama. These struggles are real and should be taken seriously.
5. Although I may have a mental illness, don’t call me fragile, broken or weak. I’m a strong, independent, successful woman who happens to be diagnosed with a mental illness.
6. Talking about it doesn’t make it happen again. Talking about depression won’t make me depressed. Talking to others about self-harm won’t make them hurt themselves. Don’t think avoiding the topic is for our own good.
7. Do not blame every emotion or action on my mental illness. I still make my decisions. I (usually) have control of my actions.
8. Things like “Try harder,” “You must not want to get better,” or“It’s your decision to get better,” do not help someone with a mental illness. We are not feeling sorry for ourselves. Many of these illnesses are actually chemical imbalances or neurological disorders.
9. Saying things like “You’re not alone,” can be helpful, but saying something like, “There’s someone worse off than you,” is not.
10. Do not assume you know how the individual feels. Even if you’ve gone through the same situations, or have the same disorder, everyone is different and handles these things differently.
11. “Have you tried drinking tea?” Or, “Have you been taking this supplement or herb?” In some instances this might be OK, but for most it’s like saying, “Have you tried waving a wand and making it all disappear?” It’s just not that simple.
12. “Just get out of bed! Have you tried keeping busy? It will distract you.” Or not. Sometimes getting out of bed can be a huge obstacle and “keeping busy” can seem impossible.
13. “You need to change your attitude or your way of thinking. Just focus on the good things.” Although this can help at times, it’s not an end all solution and should not be meant as such.
14. “You’re just lazy.” No. No, I’m not. The fact that I got out of bed today is a miracle. It was a struggle you probably don’t understand.
15. “You’re not praying hard enough.” As someone who grew up in the church, I have heard this many times. Not only is it unhelpful, it makes the individual feel even worse about themselves. As stated before, many disorders are a chemical imbalance and although I do believe prayer can help and even heal, sometimes we need to use medication or therapy as well. Although this always seems to be a huge controversy, I’d like to say this: If you have a cold you can pray and ask for healing. But if it doesn’t go away immediately, you might look for cough or sinus medication to help ease the discomfort. Mental illness should be treated with the same sort of mindset as any other illness.
The untimely death of Sandra Bland in a rural Texas jail last month has led to many unanswered questions.
Texas prison authorities say Bland hanged herself with a plastic garbage bag in her cell, a claim her family has questioned. Many suspect that Bland was murdered by corrupt law enforcement officials or correctional officers.
Lost in the emotion of yet another tragic death of a young African American in police custody is the real possibility that untreated mental illness led to Sandra Bland’s death.
Regardless of what happened in that Texas jail, Centers for Disease Control data tell us that rates of suicide have seen a steady increase each year since 2000. Suicide is now the 10th leading cause of deathamong all Americans.
And, while African Americans have lower suicide rates relative to whites, the rate of suicide among African-American males and femaleshas also been climbing each year since 2009.
As a mental health services researcher, I’ve spent years examining factors that prevent vulnerable youth from getting mental health services. My work as a psychotherapist has involved treating folks suffering from depression – folks like Sandra Bland who told police she had tried to commit suicide last year.
The importance of the social network
Sociologist Bernice Pescosolidosuggests that mentally ill individuals don’t decide about getting treatment in a vacuum. Those closest to the individual are critical to facilitating entree into care, providing care or doing nothing.
Through my work, I have seen how serious mental illness such as chronic depression or bipolarity can wreak havoc on not just the ill individual, but also on their families and friends. In a sick individual’s social networks, accusations fly. Loved ones duck for cover or they hold back for fear of offending. At this unstable and vulnerable juncture, finding a way to treatment is difficult and staying in treatment is even tougher.
Depression is one of the most debilitating health issues anyone can experience. It is a leading cause of engagement in suicidal behaviors – aprecursor, of sorts, to suicide.
The problem is that not enough people with depression actually receive treatment. The numbers vary widely by age and race. Approximatelyone third of youth with depression receive treatment. That number increases slightly – to about one half – for 20-somethings like Sandra Bland. The lack of care is even more disproportionate in ethnic minority communities relative to white communities. African Americans, Latino Americans and Asian Americans all have lower treatment rates.
My own research indicates these groups are also likely to have greater connections to their families and friends, who pray with them about their condition or offer advice. This might help explain their overall lower rates of suicide relative to whites.
Responsibility of law enforcement
While it is critical for social network members to both see and do something to help their loved ones get connected to treatment, it is equally critical for law enforcement to be trained on how to successfully address interactions with the mentally ill.
Imagine for a moment what would have happened if Sandra Bland had been pulled over by a police officer who was trained to recognize if she was suffering from a mental illness that required immediate attention. Imagine a police officer having the skills to engage Bland – or many others much like her – in a process of recovery.
That novel notion is being carried out by Dr Michael Compton and others who implement the Crisis Intervention Training, a program that trains law enforcement officials on the signs and symptoms of mental illness and how to address these matters in a health-oriented rather than enforcement manner. This program has helped police redirect countless individuals into mental health treatment instead of jails. Indeed, successful CIT programs have emerged all over the country, including in Memphis and Chicago.
The circumstances surrounding Sandra Bland’s death remain unclear. But many who are struggling with a mental illness surround us. Paying attention to the signs and having true engagement with the presenting behaviors can save lives.
God, in olden time suffered man to be kept in ward by the law that he might learn the more excellent way of faith. For by the law he would see God’s holy standard and by the law he would see his own utter helplessness; then he would be glad to learn God’s way of faith.
God still shuts us up to faith. Our natures, our circumstances, trials, disappointments, all serve to shut us up and keep us in ward till we see that the only way out is God’s way of faith. Moses tried by self-effort, by personal influence, even by violence, to bring about the deliverance of his people. God had to shut him up forty years in the wilderness before he was prepared for God’s work.
Paul and Silas were bidden of God to preach the Gospel in Europe. They landed and proceeded to Philippi. They were flogged, they were shut up in prison, their feet were put fast in the stocks. They were shut up to faith. They trusted God. They sang praises to Him in the darkest hour, and God wrought deliverance and salvation.
John was banished to the Isle of Patmos. He was shut up to faith. Had he not been so shut up, he would never have seen such glorious visions of God.
Dear reader, are you in some great trouble? Have you had some great disappointment, have you met some sorrow, some unspeakable loss? Are you in a hard place? Cheer up! You are shut up to faith. Take your trouble the right way. Commit it to God. Praise Him that He maketh “all things work together for good,” and that “God worketh for him that waiteth for him.” There will be blessings, help and revelations of God that will come to you that never could otherwise have come; and many besides yourself will receive great light and blessing because you were shut up to faith. –C. H. P
Great things are done when men and mountains meet,
These are not done by jostling in the street.
Taken from the National Institute On Aging which is found HERE.
Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear in their mid-60s. Estimates vary, but experts suggest that more than 5 million Americans may have Alzheimer’s.
Alzheimer’s disease is currently ranked as the sixth leading cause of death in the United States, butrecent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people.
Alzheimer’s is the most common cause of dementia among older adults. Dementia is the loss of cognitive functioning—thinking, remembering, and reasoning—and behavioral abilities to such an extent that it interferes with a person’s daily life and activities. Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person’s functioning, to the most severe stage, when the person must depend completely on others for basic activities of daily living.
The causes of dementia can vary, depending on the types of brain changes that may be taking place.Other dementias include Lewy body dementia, frontotemporal disorders, and vascular dementia. It is common for people to have mixed dementia—a combination of two or more disorders, at least one of which is dementia. For example, some people have both Alzheimer’s disease and vascular dementia.
Alzheimer’s disease is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems, and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary, or tau, tangles).
These plaques and tangles in the brain are still considered some of the main features of Alzheimer’s disease. Another feature is the loss of connections between nerve cells (neurons) in the brain. Neurons transmit messages between different parts of the brain, and from the brain to muscles and organs in the body.
Changes in the Brain
Scientists continue to unravel the complex brain changes involved in the onset and progression of Alzheimer’s disease. It seems likely that damage to the brain starts a decade or more before memory and other cognitive problems appear. During this preclinical stage of Alzheimer’s disease, people seem to be symptom-free, but toxic changes are taking place in the brain. Abnormal deposits of proteins form amyloid plaques and tau tangles throughout the brain, and once-healthy neurons stop functioning, lose connections with other neurons, and die.
The damage initially appears to take place in the hippocampus, the part of the brain essential in forming memories. As more neurons die, additional parts of the brain are affected, and they begin to shrink. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly.
Signs and Symptoms
Memory problems are typically one of the first signs of cognitive impairment related to Alzheimer’s disease. Some people with memory problems have a condition called mild cognitive impairment(MCI). In MCI, people have more memory problems than normal for their age, but their symptoms do not interfere with their everyday lives. Movement difficulties and problems with the sense of smell have also been linked to MCI. Older people with MCI are at greater risk for developing Alzheimer’s, but not all of them do. Some may even go back to normal cognition.
The first symptoms of Alzheimer’s vary from person to person. For many, decline in non-memory aspects of cognition, such as word-finding, vision/spatial issues, and impaired reasoning or judgment, may signal the very early stages of Alzheimer’s disease. Researchers are studying biomarkers(biological signs of disease found in brain images, cerebrospinal fluid, and blood) to see if they can detect early changes in the brains of people with MCI and in cognitively normal people who may be at greater risk for Alzheimer’s. Studies indicate that such early detection may be possible, but more research is needed before these techniques can be relied upon to diagnose Alzheimer’s disease in everyday medical practice.
Mild Alzheimer’s Disease
As Alzheimer’s disease progresses, people experience greater memory loss and other cognitive difficulties. Problems can include wandering and getting lost, trouble handling money and paying bills(PDF, 159K), repeating questions, taking longer to complete normal daily tasks, and personality and behavior changes. People are often diagnosed in this stage.
Moderate Alzheimer’s Disease
In this stage, damage occurs in areas of the brain that control language, reasoning, sensory processing, and conscious thought. Memory loss and confusion grow worse, and people begin to have problems recognizing family and friends. They may be unable to learn new things, carry out multistep tasks such as getting dressed, or cope with new situations. In addition, people at this stage may havehallucinations, delusions, and paranoia and may behave impulsively.
Severe Alzheimer’s Disease
Ultimately, plaques and tangles spread throughout the brain, and brain tissue shrinks significantly. People with severe Alzheimer’s cannot communicate and are completely dependent on others for their care. Near the end, the person may be in bed most or all of the time as the body shuts down.
What Causes Alzheimer’s
Scientists don’t yet fully understand what causes Alzheimer’s disease in most people. In people with early-onset Alzheimer’s, a genetic mutation is usually the cause. Late-onset Alzheimer’s arises from a complex series of brain changes that occur over decades. The causes probably include a combination of genetic, environmental, and lifestyle factors. The importance of any one of these factors in increasing or decreasing the risk of developing Alzheimer’s may differ from person to person.
The Basics of Alzheimer’s
Scientists are conducting studies to learn more about plaques, tangles, and other biological features of Alzheimer’s disease. Advances in brain imaging techniques allow researchers to see the development and spread of abnormal amyloid and tau proteins in the living brain, as well as changes in brain structure and function. Scientists are also exploring the very earliest steps in the disease process by studying changes in the brain and body fluids that can be detected years before Alzheimer’s symptoms appear. Findings from these studies will help in understanding the causes of Alzheimer’s and make diagnosis easier.
One of the great mysteries of Alzheimer’s disease is why it largely strikes older adults. Research on normal brain aging is shedding light on this question. For example, scientists are learning how age-related changes in the brain may harm neurons and contribute to Alzheimer’s damage. These age-related changes include atrophy (shrinking) of certain parts of the brain, inflammation, production of unstable molecules called free radicals, and mitochondrial dysfunction (a breakdown of energy production within a cell).
Most people with Alzheimer’s have the late-onset form of the disease, in which symptoms become apparent in their mid-60s. The apolipoprotein E (APOE) gene is involved in late-onset Alzheimer’s. This gene has several forms. One of them, APOE ε4, increases a person’s risk of developing the disease and is also associated with an earlier age of disease onset. However, carrying the APOE ε4 form of the gene does not mean that a person will definitely develop Alzheimer’s disease, and some people with no APOE ε4 may also develop the disease.
Also, scientists have identified a number of regions of interest in the genome (an organism’s complete set of DNA) that may increase a person’s risk for late-onset Alzheimer’s to varying degrees.
Early-onset Alzheimer’s occurs in people age 30 to 60 and represents less than 5 percent of all people with Alzheimer’s. Most cases are caused by an inherited change in one of three genes, resulting in a type known as early-onset familial Alzheimer’s disease, or FAD. For others, the disease appears to develop without any specific, known cause, much as it does for people with late-onset disease.
Most people with Down syndrome develop Alzheimer’s. This may be because people with Down syndrome have an extra copy of chromosome 21, which contains the gene that generates harmful amyloid.
Research suggests that a host of factors beyond genetics may play a role in the development and course of Alzheimer’s disease. There is a great deal of interest, for example, in the relationship between cognitive decline and vascular conditions such as heart disease, stroke, and high blood pressure, as well as metabolic conditions such as diabetes and obesity. Ongoing research will help us understand whether and how reducing risk factors for these conditions may also reduce the risk of Alzheimer’s.
Doctors use several methods and tools to help determine whether a person who is having memory problems has “possible Alzheimer’s dementia” (dementia may be due to another cause) or “probable Alzheimer’s dementia” (no other cause for dementia can be found).
To diagnose Alzheimer’s, doctors may:
Ask the person and a family member or friend questions about overall health, past medical problems, ability to carry out daily activities, and changes in behavior and personality
Conduct tests of memory, problem solving, attention, counting, and language
Carry out standard medical tests, such as blood and urine tests, to identify other possible causes of the problem
Perform brain scans, such as computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET), to rule out other possible causes for symptoms.
These tests may be repeated to give doctors information about how the person’s memory and other cognitive functions are changing over time.
Alzheimer’s disease can be definitely diagnosed only after death, by linking clinical measures with an examination of brain tissue in an autopsy.
People with memory and thinking concerns should talk to their doctor to find out whether their symptoms are due to Alzheimer’s or another cause, such as stroke, tumor, Parkinson’s disease, sleep disturbances, side effects of medication, an infection, or a non-Alzheimer’s dementia. Some of these conditions may be treatable and possibly reversible.
If the diagnosis is Alzheimer’s, beginning treatment early in the disease process may help preserve daily functioning for some time, even though the underlying disease process cannot be stopped or reversed. An early diagnosis also helps families plan for the future. They can take care of financial and legal matters, address potential safety issues, learn about living arrangements, and develop support networks.
In addition, an early diagnosis gives people greater opportunities to participate in clinical trials that are testing possible new treatments for Alzheimer’s disease or other research studies.
Treatment of Alzheimer’s Disease
Alzheimer’s disease is complex, and it is unlikely that any one drug or other intervention can successfully treat it. Current approaches focus on helping people maintain mental function, manage behavioral symptoms, and slow or delay the symptoms of disease. Researchers hope to develop therapies targeting specific genetic, molecular, and cellular mechanisms so that the actual underlying cause of the disease can be stopped or prevented.
Maintaining Mental Function
Several medications are approved by the U.S. Food and Drug Administration to treat symptoms of Alzheimer’s. Donepezil (Aricept®), rivastigmine (Exelon®), and galantamine (Razadyne®) are used to treat mild to moderate Alzheimer’s (donepezil can be used for severe Alzheimer’s as well). Memantine (Namenda®) is used to treat moderate to severe Alzheimer’s. These drugs work by regulating neurotransmitters, the chemicals that transmit messages between neurons. They may help maintain thinking, memory, and communication skills, and help with certain behavioral problems. However, these drugs don’t change the underlying disease process. They are effective for some but not all people, and may help only for a limited time.
Common behavioral symptoms of Alzheimer’s include sleeplessness, wandering, agitation, anxiety, and aggression. Scientists are learning why these symptoms occur and are studying new treatments—drug and non-drug—to manage them. Research has shown that treating behavioral symptoms can make people with Alzheimer’s more comfortable and makes things easier for caregivers.
Looking for New Treatments
Alzheimer’s disease research has developed to a point where scientists can look beyond treating symptoms to think about addressing underlying disease processes. In ongoing clinical trials, scientists are developing and testing several possible interventions, including immunization therapy, drug therapies, cognitive training, physical activity, and treatments used for cardiovascular and diabetes.
Support for Families and Caregivers
Caring for a person with Alzheimer’s disease can have high physical, emotional, and financial costs. The demands of day-to-day care, changes in family roles, and decisions about placement in a care facility can be difficult. There are several evidence-based approaches and programs that can help, and researchers are continuing to look for new and better ways to support caregivers.
Becoming well-informed about the disease is one important long-term strategy. Programs that teach families about the various stages of Alzheimer’s and about ways to deal with difficult behaviors and other caregiving challenges can help.
Good coping skills, a strong support network, and respite care are other ways that help caregivers handle the stress of caring for a loved one with Alzheimer’s disease. For example, staying physically active provides physical and emotional benefits.
Some caregivers have found that joining a support group is a critical lifeline. These support groups allow caregivers to find respite, express concerns, share experiences, get tips, and receive emotional comfort. Many organizations sponsor in-person and online support groups, including groups for people with early-stage Alzheimer’s and their families.
The National Institute on Aging’s ADEAR Center offers information and publications for families, caregivers, and professionals on diagnosis, treatment, patient care, caregiver needs, long-term care, education and training, and research related to Alzheimer’s disease. Staff members answer telephone, email, and written requests and make referrals to local and national resources. Visit the ADEAR website to learn more about Alzheimer’s and other dementias, find clinical trials, and sign up for email updates.
Alzheimer’s Foundation of America
Taken from the National Institute Of Mental Health which is found HERE.
Post-traumatic stress disorder (PTSD) is an anxiety disorder that some people develop after seeing or living through an event that caused or threatened serious harm or death. Symptoms include flashbacks or bad dreams, emotional numbness, intense guilt or worry, angry outbursts, feeling “on edge,” or avoiding thoughts and situations that remind them of the trauma. In PTSD, these symptoms last at least one month.
To aid those who suffer with PTSD, the National Institute of Mental Health (NIMH) is supporting PTSD-focused research, and related studies on anxiety and fear, to find better ways of helping people cope with trauma, as well as better ways to treat and ultimately prevent the disorder. This research fact sheet will highlight several important areas that NIMH researchers have recently learned about:
possible risk factors,
treating the disorder, and
next steps for PTSD research.
For more information about PTSD, please see the NIMH Post-Traumatic Stress Disorder booklet. You can also find a list of places to find more information about PTSD and NIMH at the end of this fact sheet.
Research on Possible Risk Factors for PTSD
Currently, many scientists are focusing on genes that play a role in creating fear memories. Understanding how fear memories are created may help to refine or find new interventions for reducing the symptoms of PTSD. For example, PTSD researchers have pinpointed genes that make:
Stathmin, a protein needed to form fear memories. In one study, mice that did not make stathmin were less likely than normal mice to “freeze,” a natural, protective response to danger, after being exposed to a fearful experience. They also showed less innate fear by exploring open spaces more willingly than normal mice.1
GRP (gastrin-releasing peptide), a signaling chemical in the brain released during emotional events. In mice, GRP seems to help control the fear response, and lack of GRP may lead to the creation of greater and more lasting memories of fear.2
Researchers have also found a version of the 5-HTTLPR gene, which controls levels of serotonin — a brain chemical related to mood-that appears to fuel the fear response.3 Like other mental disorders, it is likely that many genes with small effects are at work in PTSD.
Studying parts of the brain involved in dealing with fear and stress also helps researchers to better understand possible causes of PTSD. One such brain structure is the amygdala, known for its role in emotion, learning, and memory. The amygdala appears to be active in fear acquisition, or learning to fear an event (such as touching a hot stove), as well as in the early stages of fear extinction, or learning not to fear.4
Storing extinction memories and dampening the original fear response appears to involve the prefrontal cortex (PFC) area of the brain,4 involved in tasks such as decision-making, problem-solving, and judgment. Certain areas of the PFC play slightly different roles. For example, when it deems a source of stress controllable, the medial PFC suppresses the amygdala an alarm center deep in the brainstem and controls the stress response.5 The ventromedial PFC helps sustain long-term extinction of fearful memories, and the size of this brain area may affect its ability to do so.6
Individual differences in these genes or brain areas may only set the stage for PTSD without actually causing symptoms. Environmental factors, such as childhood trauma, head injury, or a history of mental illness, may further increase a person’s risk by affecting the early growth of the brain.7 Also, personality and cognitive factors, such as optimism and the tendency to view challenges in a positive or negative way, as well as social factors, such as the availability and use of social support, appear to influence how people adjust to trauma.8 More research may show what combinations of these or perhaps other factors could be used someday to predict who will develop PTSD following a traumatic event.
Research on Treating PTSD
Currently, people with PTSD may be treated with psychotherapy (“talk” therapy), medications, or a combination of the two.
Cognitive behavioral therapy (CBT) teaches different ways of thinking and reacting to the frightening events that trigger PTSD symptoms and can help bring those symptoms under control. There are several types of CBT, including
exposure therapy — uses mental imagery, writing, or visiting the scene of a trauma to help survivors face and gain control of overwhelming fear and distress
cognitive restructuring — encourages survivors to talk about upsetting (often incorrect) thoughts about the trauma, question those thoughts, and replace them with more balanced and correct ones.
stress inoculation training — teaches anxiety reduction techniques and coping skills to reduce PTSD symptoms, and helps correct inaccurate thoughts related to the trauma.
NIMH is currently studying how the brain responds to CBT compared to sertraline (Zoloft), one of the two medications recommended and approved by the U.S. Food and Drug Administration (FDA) for treating PTSD. This research may help clarify why some people respond well to medication and others to psychotherapy
In a small study, NIMH researchers recently found that for people already taking a bedtime dose of the medication prazosin (Minipress), adding a daytime dose helped to reduce overall PTSD symptom severity, as well as stressful responses to trauma reminders.9
Another medication of interest is D-cycloserine (Seromycin), which boosts the activity of a brain chemical called NMDA, which is needed for fear extinction. In a study of 28 people with a fear of heights, scientists found that those treated with D-cycloserine before exposure therapy showed reduced fear during the therapy sessions compared to those who did not receive the drug.10 Researchers are currently studying the effects of using D-cycloserine with therapy to treat PTSD.
Propranolol (Inderal), a type of medicine called a beta-blocker, is also being studied to see if it may help reduce stress following a traumatic event and interrupt the creation of fearful memories. Early studies have successfully reduced or seemingly prevented PTSD in small numbers of trauma victims.11
Treatment After Mass Trauma
NIMH researchers are testing creative approaches to making CBT widely available, such as with Internet-based self-help therapy and telephone-assisted therapy. Less formal treatments for those experiencing acute stress reactions are also being explored to reduce chances of developing full blown PTSD
For example, in one preliminary study, researchers created a self-help website using concepts of stress inoculation training. People with PTSD first met face-to-face with a therapist. After this meeting, participants could log onto the website to find more information about PTSD and ways to cope, and their therapists could also log on to give advice or coaching as needed. Overall, the scientists found delivering therapy this way to be a promising method for reaching a large number of people suffering with PTSD symptoms.12
Researchers are also working to improve methods of screening, providing early treatment, and tracking mass trauma survivors; and approaches for guiding survivors through self-evaluation/screening and prompting referral to mental health care providers based on need.
The Next Steps for PTSD Research
In the last decade, rapid progress in research on the mental and biological foundations of PTSD has lead scientists to focus on prevention as a realistic and important goal.
For example, NIMH-funded researchers are exploring new and orphan medications thought to target underlying causes of PTSD in an effort to prevent the disorder. Other research is attempting to enhance cognitive, personality, and social protective factors and to minimize risk factors to ward off full-blown PTSD after trauma. Still other research is attempting to identify what factors determine whether someone with PTSD will respond well to one type of intervention or another, aiming to develop more personalized, effective and efficient treatments.
The examples described here are only a small sampling of the ongoing work at NIMH. To find more information about ongoing PTSD clinical studies, see NIMH’s PTSD clinical trials Web page. As gene research and brain imaging technologies continue to improve, scientists are more likely to be able to pinpoint when and where in the brain PTSD begins. This understanding may then lead to better targeted treatments to suit each person’s own needs or even prevent the disorder before it causes harm.
Information from NIMH is available online, in PDF, or as paper brochures sent through the mail. If you would like to have NIMH publications, you can order them at http://www.nimh.nih.gov or contact NIMH at the numbers listed below.
National Institute of Mental Health
Office of Science Policy, Planning, and Communications
6001 Executive Boulevard
Room 8184, MSC 9663
Bethesda, MD 20892-9663
Phone: 301-443- 4513, 1-866-615-NIMH (6464) toll-free
TTY: 1-866-415-8051 toll free
1. Shumyatsky GP, Malleret G, Shin RM, et al. stathmin, a Gene Enriched in the Amygdala, Controls Both Learned and Innate Fear.Cell. Nov 18 2005;123(4):697-709.
2. Shumyatsky GP, Tsvetkov E, Malleret G, et al. Identification of a signaling network in lateral nucleus of amygdala important for inhibiting memory specifically related to learned fear. Cell. Dec 13 2002;111(6):905-918.
3. Hariri AR, Mattay VS, Tessitore A, et al. Serotonin transporter genetic variation and the response of the human amygdala. Science. Jul 19 2002;297(5580):400-403.
4. Milad MR, Quirk GJ. Neurons in medial prefrontal cortex signal memory for fear extinction. Nature. Nov 7 2002;420(6911):70-74.
5. Amat J, Baratta MV, Paul E, Bland ST, Watkins LR, Maier SF. Medial prefrontal cortex determines how stressor controllability affects behavior and dorsal raphe nucleus. Nat Neurosci. Mar 2005;8(3):365-371.
6. Milad MR, Quinn BT, Pitman RK, Orr SP, Fischl B, Rauch SL. Thickness of ventromedial prefrontal cortex in humans is correlated with extinction memory. Proc Natl Acad Sci U S A. Jul 26 2005;102(30):10706-10711.
7. Gurvits TV, Gilbertson MW, Lasko NB, et al. Neurologic soft signs in chronic posttraumatic stress disorder. Arch Gen Psychiatry. Feb 2000;57(2):181-186.
8. Brewin CR. Risk factor effect sizes in PTSD: what this means for intervention. J Trauma Dissociation. 2005;6(2):123-130.
9. Taylor FB, Lowe K, Thompson C, et al. Daytime Prazosin Reduces Psychological Distress to Trauma Specific Cues in Civilian Trauma Posttraumatic Stress Disorder. Biol Psychiatry. Feb 3 2006.
10. Ressler KJ, Rothbaum BO, Tannenbaum L, et al. Cognitive enhancers as adjuncts to psychotherapy: use of D-cycloserine in phobic individuals to facilitate extinction of fear. Arch Gen Psychiatry. Nov 2004;61(11):1136-1144.
11. Pitman RK, Sanders KM, Zusman RM, et al. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biol Psychiatry. Jan 15 2002;51(2):189-192.
12. Litz BT WL, Wang J, Bryant R, Engel CC. A therapist-assisted Internet self-help program for traumatic stress. Prof Psychol Res Pr. December 2004;35(6):628-634.
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