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SEASONAL AFFECTIVE DISORDER

 

Now that the days are getting shorter, the air is getting cooler, Virginians have had the first glimpse of cold for the season, some of us begin to feel the winter blues. These feelings of low energy and sleepiness may actually be Seasonal Affective Disorder, or SAD.

SAD is a form of depression related to the changing seasons. It usually starts in the late fall, especially in our northern climes. The decreasing hours of sunlight, along with the cold and snow, cause our bodies to retreat into the warmth and coziness of our homes. We tend to crave carbohydrates, eat comfort foods, and socially KWC_SADwithdraw as we sleep more, and move less; much like we are hibernating!

Those most at risk for SAD are people already suffering from major depression or bipolar disorder. Risk factors include being female, family history, young age, and the further you live from the equator, the higher your risk.   However, there are ways to decrease your risk, and increase your mood.

What can you do to improve your mood? Soak up the sun! When the weather allows, go for a walk on those bright, crisp sunny days. If the temperature or the ice and snow don’t allow you to venture outside, open the curtains and let the sun shine in. Exercise and eating healthy are both options to make you feel better. Vitamins, especially vitamin D, the sunshine vitamin can help with mood. Be social, visit with friends. A phone call, visit, or even a vacation to visit your “snowbird” friends will keep you socially involved.

So, if these options aren’t working or you just need something more to improve your mood, your healthcare provider may recommend seeking help from a psychotherapist. They may offer medications, light box therapy, or talk therapy.

 

Ketamine therapy is an option to help make it through dark times when nothing else seems to work. Contact 703-844-0184 for a consultation.

 

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Seasonal Affective Disorder

Overview

Seasonal Affective Disorder (SAD) is a type of depression that comes and goes with the seasons, typically starting in the late fall and early winter and going away during the spring and summer. Depressive episodes linked to the summer can occur, but are much less common than winter episodes of SAD.

Signs and Symptoms

Seasonal Affective Disorder (SAD) is not considered as a separate disorder. It is a type of depression displaying a recurring seasonal pattern. To be diagnosed with SAD, people must meet full criteria for major depression coinciding with specific seasons (appearing in the winter or summer months) for at least 2 years. Seasonal depressions must be much more frequent than any non-seasonal depressions.

Symptoms of Major Depression

  • Feeling depressed most of the day, nearly every day
  • Feeling hopeless or worthless
  • Having low energy
  • Losing interest in activities you once enjoyed
  • Having problems with sleep
  • Experiencing changes in your appetite or weight
  • Feeling sluggish or agitated
  • Having difficulty concentrating
  • Having frequent thoughts of death or suicide.

Symptoms of the Winter Pattern of SAD include:

  • Having low energy
  • Hypersomnia
  • Overeating
  • Weight gain
  • Craving for carbohydrates
  • Social withdrawal (feel like “hibernating”)

Symptoms of the less frequently occurring summer seasonal affective disorder include:

  • Poor appetite with associated weight loss
  • Insomnia
  • Agitation
  • Restlessness
  • Anxiety
  • Episodes of violent behavior

Risk Factors

Attributes that may increase your risk of SAD include:

  • Being female. SAD is diagnosed four times more often in women than men.
  • Living far from the equator. SAD is more frequent in people who live far north or south of the equator. For example, 1 percent of those who live in Florida and 9 percent of those who live in New England or Alaska suffer from SAD.
  • Family history. People with a family history of other types of depression are more likely to develop SAD than people who do not have a family history of depression.
  • Having depression or bipolar disorder. The symptoms of depression may worsen with the seasons if you have one of these conditions (but SAD is diagnosed only if seasonal depressions are the most common).
  • Younger Age. Younger adults have a higher risk of SAD than older adults. SAD has been reported even in children and teens.

The causes of SAD are unknown, but research has found some biological clues:

  • People with SAD may have trouble regulating one of the key neurotransmitters involved in mood, serotonin. One study found that people with SAD have 5 percent more serotonin transporter protein in winter months than summer months. Higher serotonin transporter protein leaves less serotonin available at the synapse because the function of the transporter is to recycle neurotransmitter back into the pre-synaptic neuron.
  • People with SAD may overproduce the hormone melatonin.Darkness increases production of melatonin, which regulates sleep. As winter days become shorter, melatonin production increases, leaving people with SAD to feel sleepier and more lethargic, often with delayed circadian rhythms.
  • People with SAD also may produce less Vitamin D. Vitamin D is believed to play a role in serotonin activity. Vitamin D insufficiency may be associated with clinically significant depression symptoms.

Treatments and Therapies

There are four major types of treatment for SAD:

  • Medication
  • Light therapy
  • Psychotherapy
  • Vitamin D

These may be used alone or in combination.

Medication

Selective Serotonin Reuptake Inhibitors (SSRIs) are used to treat SAD. The FDA has also approved the use of bupropion, another type of antidepressant, for treating SAD.

As with other medications, there are side effects to SSRIs. Talk to your doctor about the possible risks of using this medication for your condition. You may need to try several different antidepressant medications before finding the one that improves your symptoms without causing problematic side effects. For basic information about SSRIs and other mental health medications, visit NIMH’s Medications webpage. Check the FDA’s website for the latest information on warnings, patient medication guides, or newly approved medications.

Light Therapy

Light therapy has been a mainstay of treatment for SAD since the 1980s. The idea behind light therapy is to replace the diminished sunshine of the fall and winter months using daily exposure to bright, artificial light. Symptoms of SAD may be relieved by sitting in front of a light box first thing in the morning, on a daily basis from the early fall until spring. Most typically, light boxes filter out the ultraviolet rays and require 20-60 minutes of exposure to 10,000 lux of cool-white fluorescent light, an amount that is about 20 times greater than ordinary indoor lighting.

Psychotherapy

Cognitive behavioral therapy (CBT) is type of psychotherapy that is effective for SAD. Traditional cognitive behavioral therapy has been adapted for use with SAD (CBT-SAD). CBT-SAD relies on basic techniques of CBT such as identifying negative thoughts and replacing them with more positive thoughts along with a technique called behavioral activation. Behavioral activation seeks to help the person identify activities that are engaging and pleasurable, whether indoors or outdoors, to improve coping with winter.

Vitamin D

At present, vitamin D supplementation by itself is not regarded as an effective SAD treatment. The reason behind its use is that low blood levels of vitamin D were found in people with SAD. The low levels are usually due to insufficient dietary intake or insufficient exposure to sunshine. However, the evidence for its use has been mixed. While some studies suggest vitamin D supplementation may be as effective as light therapy, others found vitamin D had no effect.

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Ketamine for Depression

Everyone occasionally feels blue or sad. But these feelings are usually short-lived and pass within a couple of days. When you have depression, it interferes with daily life and causes pain for both you and those who care about you. Depression is a common but serious illness.

Many people with a depressive illness never seek treatment. But the majority, even those with the most severe depression, can get better with treatment. Medications, psychotherapies, and other methods can effectively treat people with depression.

There are several forms of depressive disorders.

Major depression,—severe symptoms that interfere with your ability to work, sleep, study, eat, and enjoy life. An episode can occur only once in a person’s lifetime, but more often, a person has several episodes.

Persistent depressive disorder—depressed mood that lasts for at least 2 years. A person diagnosed with persistent depressive disorder may have episodes of major depression along with periods of less severe symptoms, but symptoms must last for 2 years.

Some forms of depression are slightly different, or they may develop under unique circumstances. They include:

  • Psychotic depression, which occurs when a person has severe depression plus some form of psychosis, such as having disturbing false beliefs or a break with reality (delusions), or hearing or seeing upsetting things that others cannot hear or see (hallucinations).
  • Postpartum depression, which is much more serious than the “baby blues” that many women experience after giving birth, when hormonal and physical changes and the new responsibility of caring for a newborn can be overwhelming. It is estimated that 10 to 15 percent of women experience postpartum depression after giving birth.
  • Seasonal affective disorder (SAD), which is characterized by the onset of depression during the winter months, when there is less natural sunlight. The depression generally lifts during spring and summer. SAD may be effectively treated with light therapy, but nearly half of those with SAD do not get better with light therapy alone. Antidepressant medication and psychotherapy can reduce SAD symptoms, either alone or in combination with light therapy.

Bipolar depression, also called manic-depressive illness, is not as common as major depression or persistent depressive disorder. Bipolar disorder is characterized by cycling mood changes—from extreme highs (e.g., mania) to extreme lows (e.g., depression).

Causes

Most likely, depression is caused by a combination of genetic, biological, environmental, and psychological factors.

Depressive illnesses are disorders of the brain. Brain-imaging technologies, such as magnetic resonance imaging (MRI), have shown that the brains of people who have depression look different than those of people without depression. The parts of the brain involved in mood, thinking, sleep, appetite, and behavior appear different. But these images do not reveal why the depression has occurred. They also cannot be used to diagnose depression.

Some types of depression tend to run in families. However, depression can occur in people without family histories of depression too. Scientists are studying certain genes that may make some people more prone to depression. Some genetics research indicates that risk for depression results from the influence of several genes acting together with environmental or other factors. In addition, trauma, loss of a loved one, a difficult relationship, or any stressful situation may trigger a depressive episode. Other depressive episodes may occur with or without an obvious trigger.

Signs & Symptoms

“It was really hard to get out of bed in the morning. I just wanted to hide under the covers and not talk to anyone. I didn’t feel much like eating and I lost a lot of weight. Nothing seemed fun anymore. I was tired all the time, and I wasn’t sleeping well at night. But I knew I had to keep going because I’ve got kids and a job. It just felt so impossible, like nothing was going to change or get better.”

People with depressive illnesses do not all experience the same symptoms. The severity, frequency, and duration of symptoms vary depending on the individual and his or her particular illness.

Signs and symptoms include:

  • Persistent sad, anxious, or “empty” feelings
  • Feelings of hopelessness or pessimism
  • Feelings of guilt, worthlessness, or helplessness
  • Irritability, restlessness
  • Loss of interest in activities or hobbies once pleasurable, including sex
  • Fatigue and decreased energy
  • Difficulty concentrating, remembering details, and making decisions
  • Insomnia, early-morning wakefulness, or excessive sleeping
  • Overeating, or appetite loss
  • Thoughts of suicide, suicide attempts
  • Aches or pains, headaches, cramps, or digestive problems that do not ease even with treatment.

Who Is At Risk?

Major depressive disorder is one of the most common mental disorders in the United States. Each year about 6.7% of U.S adults experience major depressive disorder. Women are 70 % more likely than men to experience depression during their lifetime.  Non-Hispanic blacks are 40% less likely than non-Hispanic whites to experience depression during their lifetime.  The average age of onset is 32 years old. Additionally, 3.3% of 13 to 18 year olds have experienced a seriously debilitating depressive disorder.

Diagnosis

“I started missing days from work, and a friend noticed that something wasn’t right. She talked to me about the time she had been really depressed and had gotten help from her doctor.”

Depression, even the most severe cases, can be effectively treated. The earlier that treatment can begin, the more effective it is.

The first step to getting appropriate treatment is to visit a doctor or mental health specialist. Certain medications, and some medical conditions such as viruses or a thyroid disorder, can cause the same symptoms as depression. A doctor can rule out these possibilities by doing a physical exam, interview, and lab tests. If the doctor can find no medical condition that may be causing the depression, the next step is a psychological evaluation.

The doctor may refer you to a mental health professional, who should discuss with you any family history of depression or other mental disorder, and get a complete history of your symptoms. You should discuss when your symptoms started, how long they have lasted, how severe they are, and whether they have occurred before and if so, how they were treated. The mental health professional may also ask if you are using alcohol or drugs, and if you are thinking about death or suicide.

Other illnesses may come on before depression, cause it, or be a consequence of it. But depression and other illnesses interact differently in different people. In any case, co-occurring illnesses need to be diagnosed and treated.

Anxiety disorders, such as post-traumatic stress disorder (PTSD), obsessive-compulsive disorder, panic disorder, social phobia, and generalized anxiety disorder, often accompany depression. PTSD can occur after a person experiences a terrifying event or ordeal, such as a violent assault, a natural disaster, an accident, terrorism or military combat. People experiencing PTSD are especially prone to having co-existing depression.

Alcohol and other substance abuse or dependence may also co-exist with depression. Research shows that mood disorders and substance abuse commonly occur together.

Depression also may occur with other serious medical illnesses such as heart disease, stroke, cancer, HIV/AIDS, diabetes, and Parkinson’s disease. People who have depression along with another medical illness tend to have more severe symptoms of both depression and the medical illness, more difficulty adapting to their medical condition, and more medical costs than those who do not have co-existing depression. Treating the depression can also help improve the outcome of treating the co-occurring illness.

Treatments

Once diagnosed, a person with depression can be treated in several ways. The most common treatments are medication and psychotherapy.

Medication

Antidepressants primarily work on brain chemicals called neurotransmitters, especially serotonin and norepinephrine. Other antidepressants work on the neurotransmitter dopamine. Scientists have found that these particular chemicals are involved in regulating mood, but they are unsure of the exact ways that they work. The latest information on medications for treating depression is available on the U.S. Food and Drug Administration (FDA) website .

Popular newer antidepressants

Some of the newest and most popular antidepressants are called selective serotonin reuptake inhibitors (SSRIs). Fluoxetine (Prozac), sertraline (Zoloft), escitalopram (Lexapro), paroxetine (Paxil), and citalopram (Celexa) are some of the most commonly prescribed SSRIs for depression. Most are available in generic versions. Serotonin and norepinephrine reuptake inhibitors (SNRIs) are similar to SSRIs and include venlafaxine (Effexor) and duloxetine (Cymbalta).

SSRIs and SNRIs tend to have fewer side effects than older antidepressants, but they sometimes produce headaches, nausea, jitters, or insomnia when people first start to take them. These symptoms tend to fade with time. Some people also experience sexual problems with SSRIs or SNRIs, which may be helped by adjusting the dosage or switching to another medication.

One popular antidepressant that works on dopamine is bupropion (Wellbutrin). Bupropion tends to have similar side effects as SSRIs and SNRIs, but it is less likely to cause sexual side effects. However, it can increase a person’s risk for seizures.

Tricyclics

Tricyclics are older antidepressants. Tricyclics are powerful, but they are not used as much today because their potential side effects are more serious. They may affect the heart in people with heart conditions. They sometimes cause dizziness, especially in older adults. They also may cause drowsiness, dry mouth, and weight gain. These side effects can usually be corrected by changing the dosage or switching to another medication. However, tricyclics may be especially dangerous if taken in overdose. Tricyclics include imipramine and nortriptyline.

MAOIs

Monoamine oxidase inhibitors (MAOIs) are the oldest class of antidepressant medications. They can be especially effective in cases of “atypical” depression, such as when a person experiences increased appetite and the need for more sleep rather than decreased appetite and sleep. They also may help with anxious feelings or panic and other specific symptoms.

However, people who take MAOIs must avoid certain foods and beverages (including cheese and red wine) that contain a substance called tyramine. Certain medications, including some types of birth control pills, prescription pain relievers, cold and allergy medications, and herbal supplements, also should be avoided while taking an MAOI. These substances can interact with MAOIs to cause dangerous increases in blood pressure. The development of a new MAOI skin patch may help reduce these risks. If you are taking an MAOI, your doctor should give you a complete list of foods, medicines, and substances to avoid.

MAOIs can also react with SSRIs to produce a serious condition called “serotonin syndrome,” which can cause confusion, hallucinations, increased sweating, muscle stiffness, seizures, changes in blood pressure or heart rhythm, and other potentially life-threatening conditions. MAOIs should not be taken with SSRIs.

How should I take medication?

All antidepressants must be taken for at least 4 to 6 weeks before they have a full effect. You should continue to take the medication, even if you are feeling better, to prevent the depression from returning.

Medication should be stopped only under a doctor’s supervision. Some medications need to be gradually stopped to give the body time to adjust. Although antidepressants are not habit-forming or addictive, suddenly ending an antidepressant can cause withdrawal symptoms or lead to a relapse of the depression. Some individuals, such as those with chronic or recurrent depression, may need to stay on the medication indefinitely.

In addition, if one medication does not work, you should consider trying another. NIMH-funded research has shown that people who did not get well after taking a first medication increased their chances of beating the depression after they switched to a different medication or added another medication to their existing one.

Sometimes stimulants, anti-anxiety medications, or other medications are used together with an antidepressant, especially if a person has a co-existing illness. However, neither anti-anxiety medications nor stimulants are effective against depression when taken alone, and both should be taken only under a doctor’s close supervision.

Report any unusual side effects to a doctor immediately.

 

 

 

 

IV Ketamine Therapy

One of the most exciting new treatment options for depression is with a long known drug, ketamine. Ketamine has been used historically as an anesthetic. Recently, it has emerged as an effective treatment option for severe depression (citations below). The mechanism of action for ketamine’s antidepressant effects is not fully understood and hotly debated. However, studies of the neurobiology of depressed patients have revealed possible abnormalities that may have a causal link to depression such as increased inflammatory cytokines, decreased BDNF, and reduced hippocampal volume. Interestingly, there is much overlap in the neurobiology of depression and known consequences of ketamine treatment. Ketamine has been found to reduce neuroinflammation, increase BDNF production and hippocampal volume. Thus, it is highly likely that ketamine possesses a robust pharmacological profile that works collectively to correct abnormalities common to severe depression. Although only FDA-approved as an anesthetic, ketamine is used off-label by many physicians in cases of severe, treatment-resistant depression.

Resources for Ketamine and Depression:

Schwartzman, R. J., G. M. Alexander, J. R. Grothusen, T. Paylor, E. Reichenberger and M. Perreault (2009). “Outpatient intravenous ketamine for the treatment of complex regional pain syndrome: a double-blind placebo controlled study.” Pain 147(1-3): 107-115.

Best, S. R. and B. Griffin (2015). “Combination therapy utilizing ketamine and transcranial magnetic stimulation for treatment-resistant depression: a case report.” Int J Neurosci125(3): 232-234.

Clark, P. (2014). “Treatment-refractory depression: a case of successful treatment with intranasal ketamine 10%.” Ann Clin Psychiatry 26(2): 145.

Galvez, V., E. O’Keefe, L. Cotiga, J. Leyden, S. Harper, P. Glue, P. B. Mitchell, A. A. Somogyi, A. DeLory and C. K. Loo (2014). “Long-lasting effects of a single subcutaneous dose of ketamine for treating melancholic depression: a case report.” Biol Psychiatry 76(3): e1-2.

Hu, Y. D., Y. T. Xiang, J. X. Fang, S. Zu, S. Sha, H. Shi, G. S. Ungvari, C. U. Correll, H. F. Chiu, Y. Xue, T. F. Tian, A. S. Wu, X. Ma and G. Wang (2016). “Single i.v. ketamine augmentation of newly initiated escitalopram for major depression: results from a randomized, placebo-controlled 4-week study.” Psychol Med 46(3): 623-635.

Li, C. T., M. H. Chen, W. C. Lin, C. J. Hong, B. H. Yang, R. S. Liu, P. C. Tu and T. P. Su (2016). “The effects of low-dose ketamine on the prefrontal cortex and amygdala in treatment-resistant depression: A randomized controlled study.” Hum Brain Mapp 37(3): 1080-1090.

Murrough, J. W., K. E. Burdick, C. F. Levitch, A. M. Perez, J. W. Brallier, L. C. Chang, A. Foulkes, D. S. Charney, S. J. Mathew and D. V. Iosifescu (2015). “Neurocognitive effects of ketamine and association with antidepressant response in individuals with treatment-resistant depression: a randomized controlled trial.” Neuropsychopharmacology 40(5): 1084-1090.

Murrough, J. W., D. V. Iosifescu, L. C. Chang, R. K. Al Jurdi, C. E. Green, A. M. Perez, S. Iqbal, S. Pillemer, A. Foulkes, A. Shah, D. S. Charney and S. J. Mathew (2013). “Antidepressant efficacy of ketamine in treatment-resistant major depression: a two-site randomized controlled trial.” Am J Psychiatry 170(10): 1134-1142.

Murrough, J. W., A. M. Perez, S. J. Mathew and D. S. Charney (2011). “A case of sustained remission following an acute course of ketamine in treatment-resistant depression.” J Clin Psychiatry 72(3): 414-415.

Price, R. B., D. V. Iosifescu, J. W. Murrough, L. C. Chang, R. K. Al Jurdi, S. Z. Iqbal, L. Soleimani, D. S. Charney, A. L. Foulkes and S. J. Mathew (2014). “Effects of ketamine on explicit and implicit suicidal cognition: a randomized controlled trial in treatment-resistant depression.” Depress Anxiety 31(4): 335-343.

Singh, J. B., M. Fedgchin, E. J. Daly, P. De Boer, K. Cooper, P. Lim, C. Pinter, J. W. Murrough, G. Sanacora, R. C. Shelton, B. Kurian, A. Winokur, M. Fava, H. Manji, W. C. Drevets and L. Van Nueten (2016). “A Double-Blind, Randomized, Placebo-Controlled, Dose-Frequency Study of Intravenous Ketamine in Patients With Treatment-Resistant Depression.” Am J Psychiatry: appiajp201616010037.

Living With Depression

How do women experience depression?

Depression is more common among women than among men. Biological, life cycle, hormonal, and psychosocial factors that women experience may be linked to women’s higher depression rate. Researchers have shown that hormones directly affect the brain chemistry that controls emotions and mood. For example, women are especially vulnerable to developing postpartum depression after giving birth, when hormonal and physical changes and the new responsibility of caring for a newborn can be overwhelming.

Some women may also have a severe form of premenstrual syndrome (PMS) called premenstrual dysphoric disorder (PMDD). PMDD is associated with the hormonal changes that typically occur around ovulation and before menstruation begins.

During the transition into menopause, some women experience an increased risk for depression. In addition, osteoporosis—bone thinning or loss—may be associated with depression. Scientists are exploring all of these potential connections and how the cyclical rise and fall of estrogen and other hormones may affect a woman’s brain chemistry.

Finally, many women face the additional stresses of work and home responsibilities, caring for children and aging parents, abuse, poverty, and relationship strains. It is still unclear, though, why some women faced with enormous challenges develop depression, while others with similar challenges do not.

How do men experience depression?

Men often experience depression differently than women. While women with depression are more likely to have feelings of sadness, worthlessness, and excessive guilt, men are more likely to be very tired, irritable, lose interest in once-pleasurable activities, and have difficulty sleeping.

Men may be more likely than women to turn to alcohol or drugs when they are depressed. They also may become frustrated, discouraged, irritable, angry, and sometimes abusive. Some men throw themselves into their work to avoid talking about their depression with family or friends, or behave recklessly. And although more women attempt suicide, many more men die by suicide in the United States.

How do older adults experience depression?

Depression is not a normal part of aging. Studies show that most seniors feel satisfied with their lives, despite having more illnesses or physical problems. However, when older adults do have depression, it may be overlooked because seniors may show different, less obvious symptoms. They may be less likely to experience or admit to feelings of sadness or grief.

Sometimes it can be difficult to distinguish grief from major depression. Grief after loss of a loved one is a normal reaction to the loss and generally does not require professional mental health treatment. However, grief that is complicated and lasts for a very long time following a loss may require treatment. Researchers continue to study the relationship between complicated grief and major depression.

Older adults also may have more medical conditions such as heart disease, stroke, or cancer, which may cause depressive symptoms. Or they may be taking medications with side effects that contribute to depression. Some older adults may experience what doctors call vascular depression, also called arteriosclerotic depression or subcortical ischemic depression. Vascular depression may result when blood vessels become less flexible and harden over time, becoming constricted. Such hardening of vessels prevents normal blood flow to the body’s organs, including the brain. Those with vascular depression may have, or be at risk for, co-existing heart disease or stroke.

Although many people assume that the highest rates of suicide are among young people, older white males age 85 and older actually have the highest suicide rate in the United States. Many have a depressive illness that their doctors are not aware of, even though many of these suicide victims visit their doctors within 1 month of their deaths.

Most older adults with depression improve when they receive treatment with an antidepressant, psychotherapy, or a combination of both. Research has shown that medication alone and combination treatment are both effective in reducing depression in older adults. Psychotherapy alone also can be effective in helping older adults stay free of depression, especially among those with minor depression. Psychotherapy is particularly useful for those who are unable or unwilling to take antidepressant medication.

How do children and teens experience depression?

Children who develop depression often continue to have episodes as they enter adulthood. Children who have depression also are more likely to have other more severe illnesses in adulthood.

A child with depression may pretend to be sick, refuse to go to school, cling to a parent, or worry that a parent may die. Older children may sulk, get into trouble at school, be negative and irritable, and feel misunderstood. Because these signs may be viewed as normal mood swings typical of children as they move through developmental stages, it may be difficult to accurately diagnose a young person with depression.

Before puberty, boys and girls are equally likely to develop depression. By age 15, however, girls are twice as likely as boys to have had a major depressive episode.

Depression during the teen years comes at a time of great personal change—when boys and girls are forming an identity apart from their parents, grappling with gender issues and emerging sexuality, and making independent decisions for the first time in their lives. Depression in adolescence frequently co-occurs with other disorders such as anxiety, eating disorders, or substance abuse. It can also lead to increased risk for suicide.

An NIMH-funded clinical trial of 439 adolescents with major depression found that a combination of medication and psychotherapy was the most effective treatment option. Other NIMH-funded researchers are developing and testing ways to prevent suicide in children and adolescents.

Childhood depression often persists, recurs, and continues into adulthood, especially if left untreated.

How can I help a loved one who is depressed?

If you know someone who is depressed, it affects you too. The most important thing you can do is help your friend or relative get a diagnosis and treatment. You may need to make an appointment and go with him or her to see the doctor. Encourage your loved one to stay in treatment, or to seek different treatment if no improvement occurs after 6 to 8 weeks.

To help your friend or relative

  • Offer emotional support, understanding, patience, and encouragement.
  • Talk to him or her, and listen carefully.
  • Never dismiss feelings, but point out realities and offer hope.
  • Never ignore comments about suicide, and report them to your loved one’s therapist or doctor.
  • Invite your loved one out for walks, outings and other activities. Keep trying if he or she declines, but don’t push him or her to take on too much too soon.
  • Provide assistance in getting to the doctor’s appointments.
  • Remind your loved one that with time and treatment, the depression will lift.

How can I help myself if I am depressed?

If you have depression, you may feel exhausted, helpless, and hopeless. It may be extremely difficult to take any action to help yourself. But as you begin to recognize your depression and begin treatment, you will start to feel better.

To Help Yourself

  • Do not wait too long to get evaluated or treated. There is research showing the longer one waits, the greater the impairment can be down the road. Try to see a professional as soon as possible.
  • Try to be active and exercise. Go to a movie, a ballgame, or another event or activity that you once enjoyed.
  • Set realistic goals for yourself.
  • Break up large tasks into small ones, set some priorities and do what you can as you can.
  • Try to spend time with other people and confide in a trusted friend or relative. Try not to isolate yourself, and let others help you.
  • Expect your mood to improve gradually, not immediately. Do not expect to suddenly “snap out of” your depression. Often during treatment for depression, sleep and appetite will begin to improve before your depressed mood lifts.
  • Postpone important decisions, such as getting married or divorced or changing jobs, until you feel better. Discuss decisions with others who know you well and have a more objective view of your situation.
  • Remember that positive thinking will replace negative thoughts as your depression responds to treatment.
  • Continue to educate yourself about depression.

Information adapted from the National Institute of Mental Health (NIMH).

Article Links:

The National Institute of Mental Health Highlights Ketamine for Depression

IV Ketamine Shows Promise in Clinical Trial with Depressed Teens

Researchers from the University of Minnesota and The Mayo Clinic found that ketamine caused an average decrease of 42% on the Children’s Depression Rating Scale(CDRS)—the most widely used rating scale in research trials for assessing the severity of depression and change in depressive symptoms among adolescents. The study recruited adolescents, 12-18 years of age, with treatment-resistant depression (TRD; failure to respond to two previous antidepressant trials). The teens were administered intravenous ketamine (0.5 mg/kg) by infusion six times over two weeks.

The study reported that the average decrease in CDRS-R was 42.5% (p = 0.0004). Five (38%) adolescents met criteria for clinical response (defined as >50% reduction in CDRS-R). Three responders showed sustained remission at 6-week follow-up; relapse occurred within 2 weeks for the other two responders. The ketamine infusions were generally well tolerated; dissociative symptoms and hemodynamic symptoms were transient. Interestingly, higher dose was a significant predictor of treatment response.

“Adolescence is a key time period for emergence of depression and represents an opportune and critical developmental window for intervention to prevent negative outcomes,” the authors wrote in the study.

“Unfortunately, about 40% of adolescents do not respond to their first intervention and only half of non-responders respond to the second treatment,” they said. “Because standard interventions require prolonged periods (e.g., weeks to months) to assess efficacy, serial treatment failures allow illness progression, which in turn worsens the outcome. Hence, novel treatment strategies to address treatment-resistant depression in adolescents are urgently needed.”

The authors concluded that their results demonstrate the potential role for ketamine in treating adolescents with TRD. Additionally, evidence suggested a dose–response relationship; future studies are needed to optimize dose

 

Yale study found no safety issues with long-term ketamine treatment

 August 08, 2018
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Researchers at Yale published a new study titled “Acute and Longer-Term Outcomes Using Ketamine as a Clinical Treatment at the Yale Psychiatric Hospital” in Clinical Psychiatry.  In late 2014, Yale began providing ketamine as an off-label therapy on a case-by-case basis for patients who could not participate in research protocols.  The authors observed 54 patients that received IV ketamine infusion for the treatment of severe and treatment-resistant mood disorders such as depression.

“Ketamine is being used as an off-label treatment for depression by an increasing number of providers, yet there is very little long-term data on patients who have received ketamine for more than just a few weeks,” Samuel T. Wilkinson, MD,from the department of psychiatry, Yale School of Medicine and Yale Psychiatric Hospital, told Healio Psychiatry.

The Yale researchers studied the acute and longer-term outcomes in this patient population. Importantly, a subset of patients (n=14) received ketamine on a long-term basis, ranging from 12 to 45 total treatments, over a course of 14 to 126 weeks.  The researchers found no evidence of cognitive decline, increased proclivity to delusions, or emergence of symptoms consistent with cystitis in this subset of long-term ketamine patients.  They also reported that the infusions were generally well-tolerated.

Although this study population was relatively small, limiting the conclusions that can be drawn, this is still an important first step in establishing the long-term safety of ketamine for the treatment of a myriad of diseases that it’s being used to treat

CNN Reports ‘Ketamine offers lifeline for suicidal thoughts’

CNN featured a segment on the use of ketamine for treating suicidal ideation–a novel, off-label use for ketamine that is currently being explored in human clinical trials.  The segment featured Dr. Sanjay Gupta sharing the story of Alan Ferguson.  Mr. Ferguson discussed his experience with suicidal ideation, stating that he had planned his own suicide prior to a psychiatrist suggesting the off-label use of ketamine.  Fortunately, ketamine worked for him as it has for many others, completely eliminating all thoughts of suicide and depression.

While ketamine is a long-known, FDA-approved anesthetic, new uses for this old drug have recently been discovered.  The new indication that is probably the farthest along is for the treatment of depression.  It’s even undergoing phase III clinical trials for the treatment of depression, which are expected to be completed next year.  In depression, ketamine’s mechanism of action is still being explored. Scientists know that ketamine antagonizes the NMDA receptor, which causes a number of downstream cascades that may be relevant to it’s antidepressant effects. Ketamine also increases important neuronal growth factors that can create new synaptic connections.

While there are numerous anti-depressants that are already FDA-approved, they don’t always work and–even when they do–it takes weeks to see the effect.  This is what’s special about ketamine.  The anti-depressant effects of ketamine are instantaneous.  In the case of Alan Ferguson, his depression went from severe to mild after the first infusion, and was gone after the second. In cases of depression that involve suicidality, this rapid improvement can be the difference between life and death.  Even though ketamine is not yet approved for the treatment of depression or suicidal ideation, there is an abundance of data showing that it works and it’s already being used off-label in the clinic.

First study shows ketamine is safe and effective for depression in elderly patients

 

Australian researchers completed the world’s first randomized control trial (RCT), assessing the efficacy and safety of ketamine as a treatment for depression in elderly patients.

In this double-blind, controlled, multiple-crossover study with a 6-month follow-up, 16 participants (≥60 years) with treatment-resistant depression who relapsed after remission or did not remit in the RCT were administered an open-label phase. Up to five subcutaneous doses of ketamine (0.1, 0.2, 0.3, 0.4, and 0.5 mg/kg) were administered in separate sessions (≥1 week apart), with one active control (midazolam) randomly inserted. Twelve ketamine treatments were given in the open-label phase. Mood, hemodynamic, and psychotomimetic outcomes were assessed by blinded raters. Remitters in each phase were followed for 6 months.

The results, published in the latest American Journal of Geriatric Psychiatry, provide preliminary evidence that ketamine is effective as an antidepressant – when delivered in repeated intravenous doses.

Pilot Randomized Controlled Trial of Titrated Subcutaneous Ketamine in Older Patients with Treatment-Resistant Depression

“What we noticed was that ketamine worked incredibly quickly and incredibly effectively,” Professor Colleen Loo, who led the pilot program told ABC News. “By incredibly effective, we mean going rapidly from severely depressed to being completely well in one day.”

“Some people think, ‘oh maybe it was just a drug induced temporary high’ — and it wasn’t,” she said. “You had the woozy effects in the first hour or so, but the antidepressant effects kicked in later.”

None of the participants experienced problematic side effects, according to the research team who administered the drug through a small injection under the skin.

“Our results indicate a dose-titration method may be particularly useful for older patients, as the best dose was selected for each individual person to maximize ketamine’s benefits while minimizing its adverse side effects,” she said.

The authors noted that further study is needed, however, to understand the risks of ketamine use and possible side effects, such as its impact on liver function in the elderly.

IV Ketamine “most important breakthrough in antidepressant treatment in decades”

PTSD Treatment – Ketamine is a novel treatment for several psychiatric disorders including: Major Depressive Disorder, Bipolar Depression, Postpartum Depression, Obsessive-Compulsive Disorder (OCD), and Posttraumatic Stress Disorder or PTSD.  It was originally FDA approved for anesthesia but is now frequently used off-label due to its positive effects on the various disorders listed above.  PTSD is an devastating disorder that has become more and more common but medical treatments overall are still lacking.

What is PTSD?

PTSD Treatment

PTSD is a disorder that develops after a traumatic experience.  Such trauma sometimes involves combat, car accidents, natural disasters or sexual assaults.  Up to 80% of individuals in their life will experience at least one traumatic event but, fortunately, most people do not go on to develop PTSD.  The lifetime prevalence of developing PTSD is about 10% and women are twice as likely as men to develop PTSD.  Those who do go on to develop PTSD typically will have one or more of the following symptoms:

• traumatic nightmares
• flashbacks taking them back to the event
• distress after exposure to traumatic reminders or stimuli
• hypervigilance/hyperarousal
• avoidance of certain thoughts and situations
• negative thoughts and mood including shame, despair and depression.

A constellation of these symptoms must persist for at least a month for a diagnosis of PTSD to be made.
Most PTSD Treatment are ineffective for some patients and their all generally slow acting—meaning that the patient must wait weeks to have a meaningful impact on the patient’s wellness. Ketamine has now been shown to be effective at managing PTSD in several clinical studies. Moreover, physicians are beginning to present case reports where ketamine has helped their patients. One of the largest benefits of using Ketamine off label for the treatment of depression is that it is generally very fast-acting. Patients typically report feeling better after the first infusion or two. Sometimes, they report feeling 100% better after 5 days of IV ketamine therapy.

 

 

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The Psychopharmacology of Depression: Strategies, Formulations, and Future Implications

 

With well over two dozen traditional antidepressants available in the US, and an ever-growing list of other psychotropic compounds with apparent antidepressant properties, pharmacological options for treating clinical depression today are broad and vast. However, recent findings suggest that the magnitude of efficacy for most antidepressants compared with placebo may be more modest than previously thought.1Most depressed patients do not respond fully to a first antidepressant trial, and with each consequent trial, there is less chance of symptom remission.2 About one-third of patients receiving long-term treatment report persistent moderate-to-severe depression.3 Hence, there remains more than a little room for improvement.

Since the late 1950s, the traditional view of treating depression has focused on the role of monoamines (serotonin, norepinephrine, and dopamine) as the main targets for medications. Newer treatments are looking beyond effects on monoamines as potential strategies to leverage depressive symptoms.

A major challenge for progress in novel pharmacotherapies has been our lack of a full understanding about the causes of depression. Advances in functional neuroimaging and genetic markers have begun to shed new light on brain regions and pathways associated with aberrant neural functioning in depression, but not in ways that have led to treatments aimed at remedying its pathogenesis. This makes it hard to think of antidepressant medications as “treating” the pathophysiology of depression (as when antibiotics eliminate the cause of an infection); rather, antidepressant relieve symptoms by counteracting or compensating for depression’s consequences (as when diuretics alleviate peripheral edema regardless of its etiology).

Gone are the days of oversimplified theories that depression is caused by a “chemical imbalance.” More likely, depression involves changes in brain architecture and the interplay of complex circuits in which chemicals, or neurotransmitters, are the messengers of information, rather than the causes of faulty functioning. Table 1 summarizes some of the major conceptual shifts that have occurred in thinking about the probable causes of depression (or at least its neurobiological context), which sets the stage for new ways to consider innovative treatment strategies. Looking beyond the role of monoamines as treatment targets in depression, a number of novel therapeutic strategies have begun to receive growing interest in preclinical and clinical trials. Key points about emerging novel depression pharmacotherapies are summarized in Table 2, and described more fully below.

Subanesthetically dosed intravenous (IV) ketamine currently represents perhaps the most dramatic and innovative antidepressant pharmacotherapy to emerge in decades.4,5 It is pharmacodynamically unique in its rapid onset (hours rather than days to weeks) and its potential ability to reduce suicidal ideation after a single dose, independent of its antidepressant properties.6 (While both lithium and clozapine have been shown to reduce suicidal behaviors, neither has been shown to reduce ideation, much less in the same day after a single dose.) Meta-analyses suggest that 0.5 mg/kg IV ketamine produces nearly a 10-fold greater likelihood of response than placebo at day 1 and a 4- to 5-fold likelihood of sustained response after one week.7

The exact psychotropic mechanism of action of ketamine remains elusive. Initial work focused on blockade of ionotropic N-methyl-D-aspartate (NMDA) receptors as accounting broadly for its antidepressant effects. However, subsequent negative randomized trials with other NMDA receptor antagonists (such as riluzole8) redirected interest toward ketamine’s other, non-NMDA receptor-related mechanisms, such as sigma receptor agonism, mu opioid receptor antagonism, or midbrain monoaminergic inhibition. Other authors have suggested that at low doses, ketamine’s antidepressant effects may derive from an increase in glutamate transmission with increased α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor expression, leading to increased release of brain-derived neurotrophic factor (BDNF).9Murrough and colleagues10 recently observed the necessity of AMPA receptor activation for the antidepressant effects of ketamine. They reported that “directly targeting the NMDA [receptor] may not be required.” As noted by the American Psychiatric Association Council on Research Task Force on Novel Biomarkers and Treatments,11 future advances will depend on a better understanding of the many mechanisms of action relative to the antidepressant properties of ketamine.

Ketamine is currently not approved by the FDA as a treatment for depression. Uncertainty remains as to whether repeated dosing is safe, effective, and necessary to avoid relapse and, if so, when, at what frequency, and for how long. The aforementioned APA Council on Research Consensus Statement on ketamine treatment for depression11 stated that while some clinics already offer 2- to 3-week courses of ketamine delivered 2 to 3 times per week, “there remain no published data that clearly supports this practice, and . . . the relative benefit of each ketamine infusion [should] be considered in light of the potential risks associated with longer term exposure to ketamine and the lack of published evidence for prolonged efficacy with ongoing administration.” 11 Thus far, studies of other pharmacotherapies to sustain an initial ketamine response (such as riluzole or lithium) have proven no better than placebo.

Enantiomeric esketamine remains investigational as a possible easier-to-administer intranasal (IN) antidepressant, although IN bioavailability is only about half that of IV ketamine’s 100%. Two randomized multi-site trials of IN esketamine added to antidepressants showed dose-related better efficacy than placebo: Daly and colleagues12 found that 28 mg to 84 mg of IN ketamine twice weekly over two weeks produced significant improvement in depressive symptoms as compared to placebo beginning after 1 week and continuing through week 9 for the majority of responders. A study by Canuso and colleagues13 demonstrated a significant reduction in depressive symptoms within 4 hours of administration (56 mg to 84 mg insufflated over 15 minutes) and a medium to large effect size, sustained after 25 days; suicidal ideation reduced significantly at 4 hours but not beyond that time. Another recent randomized pilot trial of IN racemic ketamine (the mixture of S- and R-ketamine) was prematurely discontinued due to poor tolerability (including cardiovascular and neurological adverse effects) and highly variable absorption across subjects.14

Modulation of the endogenous opioid system has long been a target of interest in the treatment of mood disorders, but it is limited by safety risks, tolerance, and addiction potential. Recent work has focused on a proprietary combination of the μ-opioid partial agonist/kappa antagonist buprenorphine plus the μ-opioid receptor antagonist samidorphan (ALKS 5461). The potent blockade of μ-opioid receptors in samidorphan, which prevents buprenorphine access to these receptors, effectively renders buprenorphine a selective kappa opiate receptor (KOR) antagonist, which is its putative antidepressant mechanism. After initial favorable Phase II trials, in 2013 the FDA granted ALKS 5461 fast track status for accelerated regulatory review as an antidepressant adjunct. Subsequent randomized trials in treatment-resistant major depression revealed statistically significant differences from placebo on some, but not all, depressive symptom outcome measures and at some, but not all, doses studied.15,16 The FDA initially refused to review the new drug application for ALKS 5461 as an adjunctive therapy for depression because of concerns about bioavailability and lack of evidence, but then reversed its position. ALKS 5461 is currently under regulatory review and a decision regarding its possible approval is expected by early 2019.

Antiinflammatories and immunomodulators

There has been growing recognition of complex interrelationships between depression and inflammation. Some but not all patients with clinically significant depression appear to have elevated serum markers of systemic inflammation, such as high sensitivity C-reactive protein (hs-CRP) and inflammatory cytokines. While causal relationships between depression and inflammation are poorly understood and questions remain whether depression causes inflammation or vice versa, randomized trial data suggest potential antidepressant value of nonsteroidal anti-inflammatory drugs (NSAIDs), particularly the COX-2 inhibitor celecoxib. A pooled meta-analysis of 5447 participants from 10 NSAID trials and 4 cytokine inhibitors (as mono- or add-on therapy for depression) revealed statistically significant advantages over placebo, with small to medium effect sizes, for response (odds ratio = 6.6; 95% confidence interval=2.2-19.4) or remission (odds ratio = 7.9; 95% confidence interval=2.9-21.1)17It has not been established whether adding celecoxib or other NSAIDs to an antidepressant may be more useful only in the setting of elevated serum markers of inflammation. Elsewhere, preliminary studies reveal that inflammatory depressive subtypes (ie, high baseline hs-CRP) may respond better to a tricyclic than SSRI,18 adjunctive L-methylfolate,19 or the tumor necrosis factor (TNF) antagonist infliximab (admnistered IV at 5 mg/kg over 3 doses).20

The antimicrobial minocycline exerts anti-inflammatory and anti-oxidative properties and has been preliminarily studied mostly in small or open/nonrandomized trials. A meta-analysis of 3 randomized controlled trials found an overall significantly greater effect than placebo with a medium to large effect size and good tolerability, although the small number of well-designed studies and samples sizes (total N = 158) limits their generalizability.21

Anticholinergic muscarinic agents

Harkening back to the 1970s hypothesis that depression could reflect cholinergic-adrenergic dysregulation, interest has turned to the possible antidepressant effects of the muscarinic cholinergic antagonist scopolamine. Preliminary studies of intravenous scopolamine dosed at 4 µg/kg in both unipolar and bipolar depression have produced remission rates from 45% to 56% (Cohen’s d ranged from 1.2-3.4) typically within several days of administration, with persistence for 10 to 14 days.22Antimuscarinic adverse effects such as sedation, dry mouth, and blurry vision are common but transient. Neurocognitive measures reaction time during selective attention tasks reveal no significant delays following IV scopolamine infusion.23 Analogous to IV ketamine, questions remain about the optimal number of infusions to minimize relapse as well as the use of nonparenteral formulations.

Brexanolone (SAGE-547), also known as allopregnanolone, is a positive allosteric modulator of GABA-A receptors. It is a progesterone metabolite that exerts neuroprotective, pro-cognitive, and possible antidepressant/anxiolytic properties. Precipitous drops in progesterone and allopregnanolone after childbirth prompted interest in the use of allopregnanolone specifically in postpartum depression. A small (N = 21) initial trial of brexanolone (administered intravenously because of its short half-life and poor oral bioavailability) or placebo for severe postpartum depression yielded a substantial reduction in depressive symptom severity within 60 hours (effect size = 1.2).24 Further data remain pending. SAGE-217 is reformulated brexanolone that has good oral bioavailability, allowing for oral administration, as well as a longer half-life allowing once-a-day dosing. It is currently being studied as an adjunctive agent for treatment resistant depression.

PPAR-γ agonists and incretins

Thiazolidinediones are insulin sensitizers that also demonstrate antidepressant properties in animal studies and appear to possess anti-inflammatory, neuroprotective, antioxidant and anti-excitatory properties. Pioglitazone, a PPAR-γ agonist thiazolidinedione, has been studied versus placebo or metformin in major depression, both as monotherapy and in combination with antidepressants or lithium. A meta-analysis of 4 trials revealed significantly higher remission rates than controls (27% versus 10%, respectively; odds ratio of remission in major depression = 5.9 (95% confidence interval=1.6-22.4), p = .009), with an NNT = 6.25 Even though PPAR-γ agonists can decrease insulin resistance, weight gain can be an undesired adverse effect that is possibly a result of a combination of fat cell proliferation, fluid retention, and increased appetite. Pioglitazone also carries serious adverse risks for congestive heart failure and bladder cancer.

Glucagon-like peptide 1

Another class of antidiabetic drugs known as glucagon-like peptide 1 (GLP-1) agonists mimic the action of insulin (so-called incretins) and are of interest as a potential target for depression. GLP-1 agonists such as liraglutide possess neuroprotective and antiapoptotic properties, and animal studies suggest it has antidepressant and pro-cognitive effects, particularly involving reward and motivation. Human studies have thus far focused more on weight-reducing and possible cognitive benefits of liraglutide more than its potential antidepressant efficacy, but its mechanism represents a promising direction for further study.

Future directions

This brief overview has focused on emerging novel pharmacotherapies for depression. While the provisional nature of proof-of-concept studies may be encouraging, they are far from definitive. The aforementioned findings are largely preliminary and meant more to prompt larger randomized trials to establish efficacy, safety, and generalizability rather than inspire premature immediate uptake into clinical practice.

Given the focus on neuroprotection and enhanced neuroplasticity as proposed targets of treatment, it would seem remiss not to at least mention the neurobiological impact of depression-specific psychotherapies, mindfulness meditation, and related psychosocial interventions. Psychotherapy is, among other things, a behavioral learning paradigm, presumably rendering alterations in cognitive functions (memory, attention, and decision-making), fear extinction, and emotional processing. Evidence-based psychotherapies for depression have been shown to produce changes in brain network connectivity26 (recapitulating the idea of Hebbian synapses, where “neurons that fire together wire together”) and upregulation of intracellular transcription factors involved in neuronal plasticity.27Enhanced neuroplasticity may represent a common denominator target for effective biological or psychosocial treatments for depression.

Increasingly, drugs we call antidepressants are diversifying to include broader classes of molecules. A more neuroscience-based nomenclature for psychotropic drugs has already been proposed28 and will no doubt invoke more novel drug mechanisms, supplanting older concepts about depression as a chemical imbalance as perspectives continue to evolve about how antidepressants impact neuronal viability and brain microarchitecture.

References:

1. Cipriani A, Furukawa TA, Salanti G,et al.Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis. Lancet 2018; S0140-6736:32802-7. [Epub ahead of print]

2. Trivedi MH, Rush AJ, Wisniewski SR, et al. Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. Am J Psychiatry. 2006;163:28-40.

3. Cartwright C, Gibson K, Read J, et al. Long-term antidepressant use: patient perspectives of benefits and adverse effects. Patient Prefer Adher. 2016;10:1401-1407.

4. Zarate CA Jr., Singh JB, Carlson PJ, et al. A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Arch Gen Psychiatry. 2006;63:856-864.

5. Murrough JW, Iosifescu DV, Chang LC, et al. Antidepressant efficacy of ketamine in treatment-resistant major depression: a two-site randomized controlled trial. Am J Psychiatry. 2013;170:1134-1142.

6. Wilkinson ST, Ballard ED, Bloch MH, et al. The effect of a single dose of intravenous ketamine on suicidal ideation: a systematic review and individual participant data meta-analysis. Am J Psychiatry. 2018;175:150-158.

7. Newport DJ, Carpenter LL, McDonald WM, et al. Ketamine and other NMDA antagonists: early clinical trials and possible mechanisms in depression. Am J Psychiatry. 2015;172:950-966.

8. Mathew SJ, Gueorguieva R, Brandt C, et al. A randomized, double-blind, placebo-controlled, sequential parallel comparison design trial of adjunctive riluzole for treatment-resistant major depressive disorder. Neuropsychopharmacol 2017;42: 2567-2574.

9. Duman RS, Li N, Liu RJ, et al. Signaling pathways underlying the rapid antidepressant actions of ketamine. Neuropharmacol. 2012;62:35-41.

10. Murrough JW, Abdallah CG, Mathew SJ. Targeting glutamate signalling in depression: progress and prospects. Nat Rev Drug Discov. 2017;16:472-486.

11. Sanacora G, Frye MA, McDonald W, et al. A consensus statement on the use of ketamine in the treatment of mood disorders. JAMA Psychiatry. 2017;74:399-405.

12. Daly EJ, Singh JB, Fedgchin M, et al. Efficacy and safety of intranasal esketamine adjunctive to oral antidepressant therapy in treatment-resistant depression: a randomized clinical trial. JAMA Psychiatry. 2018;75:139-148.

13. Canuso CM, Singh JB, Fedgchin M, et al. Efficacy and safety of intranasal esketamine for the rapid reduction of symptoms of depression and suicidality in patients at imminent risk for suicide: results of a double-blind, randomized, placebo-controlled study. Am J Psychiatry. April 2018; Epub ahead of print.

14. Gálvez V, Li A, Huggins C, et al. Repeated intranasal ketamine for treatment-resistant depression – the way to go? Results from a pilot randomised controlled trial. J Clin Psychopharmacol. 2018;32:397-407.

15. Ehrich E, Turncliff R, Du Y, et al. Evaluation of opioid modulation in major depressive disorder. Neuropsychopharmacol. 2015;40:1448-1455.

16. Fava M, Memisoglu A, Thase ME, et al. Opioid modulation with buprenorphine/samidorphan as adjunctive treatment for inadequate response to antidepressants: a randomized double-blind placebo-controlled trial. Am J Psychiatry. 2016;173:499-508.

17. Köhler O, Benros ME, Nordentoft M, et al. Effect of anti-inflammatory treatment on depression, depressive symptoms, and adverse effects: a systematic review and meta-analysis of randomized clinical trials. JAMA Psychiatry. 2014;71:1381-1391.

18. Uher R, Tansey KE, Dew T, et al. An inflammatory biomarker as a differential predictor of outcome of depression treatment with escitalopram and nortriptyline. Am J Psychiatry. 2014;171:1278-1286.

19. Papakostas GI, Shelton RC, Zajecka JM, et al. Effect of adjunctive L-methylfolate 15 mg among inadequate responders to SSRIs in depressed patients who were stratified by biomarker levels and genotype: results from a randomized clinical trial. J Clin Psychiatry. 2014;75:855-863.

20. Raison CL, Rutheford RE, Woolwine BJ, et al. A randomized controlled trial of the tumor necrosis factor antagonist infliximab for treatment-resistant depression: the role of baseline inflammatory biomarkers. JAMA Psychiatry. 2013;70:31-41.

21. Rosenblat JD, McIntyre RS. Efficacy and tolerability of minocycline for depression: a systematic review and meta-analysis of clinical trials. J Affect Disord. 2018;227:219-225.

22. Drevets WC, Zarate CA Jr, Furey ML. Antidepressant effects of the muscarinic cholinergic antagonist scopolamine: a review. Biol Psychiatry. 2013;73:1156-1163.

23. Furey ML Pietrini P, Haxby JV, et al. Selective effects of cholinergic modulation on task performance during selective attention. Neuropsychopharmacol 2008; 33:913-923.

24. Kanes S, Colquohoun H, Grunduz-Bruce H, et al. Brexanolone (SAGE-547 injection) in post-partum depression: a randomised controlled trial. Lancet. 2017;390:480-489.

25. Colle R, de Larminat D, Rotenberg S, et al. Pioglitazone could induce remission in major depression: a meta-analysis. Neuropsychiatr Dis Treat 2016;13: 9-16.

26.Yang CC, Barrós-Loscertales A, Pinazo D, et al. State and training effects of mindfulness meditation on brain networks reflect neuronal mechanisms of its antidepressant effect. Neural Plast. 2016;2016:9504642.

27. Koch JM, Hinze-Selch D, Stingele K, et al. Changes in CREB phosphorylation and BDNF plasma levels during psychotherapy of depression. Psychother Psychosom. 2009;78:187-192.

28. ECNP Neuroscience Applied. Neuroscience-based Nomenclature. https://www.ecnp.eu/research-innovation/nomenclature.aspx. Accessed June 6, 2018.

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Ketamine for Chronic Pain & Depression

Intravenous Ketamine is proving to be a tremendous treatment for intractable depression as well as chronic pain.  About half the patients treated respond positively with results lasting up to a week in most of the responders.

It has emerged as a treatment option for a variety of chronic pain conditions including fibromyalgia, small fiber neuropathy, Complex Regional Pain Syndrome (CRPS), Reflex Sympathetic Dystrophy (RSD) and psychiatric conditions including depression, Post Traumatic Stress Disorder (PTSD), suicidal ideation, and Obsessive-Compulsive Disorder (OCD).

Ketamine in the News

Remarkable secrets of ketamine’s antidepressant effect unlocked by scientists

Could Party Drug Ketamine Be a Treatment for Depression?

‘The fog is gone’: How ketamine could help lift hard-to-treat depression

Ketamine Research

Ketamine for Depression, 1: Clinical Summary of Issues Related to Efficacy, Adverse Effects, and Mechanism of Action.

Ketamine safety and tolerability in clinical trials for treatment-resistant depression.

Low-dose ketamine for treatment resistant depression in an academic clinical practice setting.

Symptomatology and predictors of antidepressant efficacy in extended responders to a single ketamine infusion.

How does ketamine elicit a rapid antidepressant response?

The use of ketamine as an antidepressant: a systematic review and meta-analysis.

Ketamine for rapid reduction of suicidal ideation: a randomized controlled trial.

Do the dissociative side effects of ketamine mediate its antidepressant effects?

Rapid and longer-term antidepressant effects of repeated ketamine infusions in treatment-resistant major depression.