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Problems? I Have a NAC for That

1/30/2014

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SOURCE: Psychology Today
January 22, 2012 | Emily Deans, M.D

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In the chemical soup that comprises our bodies and biochemistry, oxidants and antioxidants are at constant war.  A supplement called N-acetylcysteine (we'll shorten that to NAC) has the potential to make a huge difference in how we process toxins.  I'd heard of NAC before, of course, as the punishment/savior for people who show up in the ER having overdosed on that most disgusting of things to overdose on, acetaminophen (Tylenol, or paracetamol). If you decide to down a whole bottle (or far, far less with alcohol - even the upper limits of a normal daily dose can damage your liver when combined with alcohol), you might feel sick immediately, but then perhaps recover and think nothing of it - until a few days later, when the accumulated killing of hepatocytes and rotten liver make you very very ill, and nothing short of a liver transplant will save you. Failing that, you die a rather horrible death. Livers are vital, we have no substitutes, no bypass machines, mechanical livers, or liver-like dialysis machines. Apparently there are 56,000 ER visits a year from tylenol overdoses in the US, and 100 deaths.

Well, if someone shows up with a tylenol OD to the ER, you get a level four or more hours post-ingestion, and plot the level and hours post-ingestion on a handy graph. Above the dark line on the graph? Welcome to the world of N-acetylcysteine, a disgusting compound typically administered with fruit juice, but still makes some people vomit. You give a loading dose of 150mg/kg followed by 70 mg/kg for 17 more doses. If you can't keep down the dose, it has to be repeated. During this time is when the psychiatrist is typically called to the ER to figure out whether it is safe to let the person go, or if it was a serious suicide attempt in need of further intervention. It is surprisingly easy to overdose on tylenol accidently, as acetaminophen is in a zillion over the counter medicines, plus perscription painkillers percocet and vicodin, etc. 4000 mg a day is the upper limit of "safe" (without alcohol) - you can get acute liver failure with as little as 7800 mg if you are unlucky.

The treatment is as simple as it is magical - possible fuliminant liver failure on one side, skipping out of the hospital doing just fine on the other. And the treatment has everything to do with the body's master antioxidant, glutathione. Seems that a metabolite of tylenol, NAPQI, kills liver cells like gangbusters. Glutathione can bind to it and render it harmless, but once you run out of glutathione, the leftover NAPQI does its nasty job. That's where N-acetylcysteine (NAC) comes in - it is a ready precursor to glutathione, so your liver can have a bountiful supply to fight off the NAPQI.

Well, have a look at the Wikipedia article. NAC is not only the treatment for mucus build-up in cystic fibrosis, but also acetaminophen overdose, perhaps to reduce the kidney toxicity of contrast dye (though that doesn't seem to be holding up), in interstitial lung disease, and investigationally in reduction of noise-induced hearing loss, lessening the destruction of pancreatic beta cells, curing a hangover, and decreasing symptoms of the flu. But of course I don't care about all that. As a specialist I am required by medical convention to stick to the brain and keep my little nose out of other parts of the body... but NAC has some interesting properties in the noggin as well.

As usual it all goes back to glutamate, the excitatory neurotransmitter of doom. In short, having too much glutamate around is to your neurons rather like whipping your horse to go and go and go until you kill it. Horses and brains need time at pasture, chilling out and eating appropriate foods, and sometimes a nice rubdown and brushing. Well, NAC seems to be able to get into some tricky areas of the brain and do some amazing management of glutamate. Over the past few years, a number of intriguing studies have come out using NAC alone or as adjunct treatment for some difficult psychiatric conditions. Some of these were decent multicenter randomized controlled trials. The real deal.

These tricky conditions? Trichotillomania (compulsive hair-pulling, which is both common and exceptionally difficult to treat - several decades of research has come up with nothing as effective as the NAC trial!). Schizophrenia. Bipolar Depression (another very difficult and disabling condition that doesn't respond particularly well to therapy or medicine, and the condition I've seen respond most favorably to NAC in my own practice). There is an ongoing study on OCD. The studies vary between 2000-4800mg daily of the capsules (these are better tolerated than the emergency room drink, which is a much higher overall dose), and in most of the studies, there were more adverse events and side effects in the placebo arm than in the treatment arm. Many of the studies were as long as 6 months, which is a lifetime for randomized controlled clinical trials, and all of the studies had positive effects. That is pretty astounding, considering how pharmaceutical companies have no doubt spent millions and millions chasing down bipolar depression, for example, without much to show for it (there's quetiapine, fluoxetine, and olanzapine+fluoxetine with modest effects and plenty of side effects). Another cute little study used NAC to reduce cocaine cravings - again, something for which there is really no effective FDA-approved medical treatment.

Why would a precursor for the master antioxidant have anything to do with glutamate in the brain? The mechanism is sort of hysterically complicated, so I'll quote the trichotillomania paper:

[NAC] is a hepatoprotective antioxidant that is converted to cysteine, a substrate for the glutamate-cysteine antiporter. This antiporter allows for the uptake of cysteine, which causes the reverse transport of glutamate into the extracellular space, which stimulates inhibitory metabotropic glutamate receptors and, thereby, reduces synaptic release of glutamate. The restoration of the extracellular glutamate concentration in the nucleus accumbens seems to block reinstitution of compulsive behaviors.

Translating the sciencespeak: NAC helps excess (and toxic) glutamate stop being at the wrong place at the wrong time. It helps us put that brain out to pasture for some rest and recovery.

What are the downsides of NAC? I can think of two problems that might be biggies - first off, NAC is a mucolytic that thins mucus by cutting disulfide bonds. I suspect that might raise risks - one wouldn't want too little mucus. Mucus is important. Paul Jaminet mentions this issue and links a study here. Also, cutting disulfide bridges within the body is what that inflammatory baddie homocysteine is supposed to do, leading to crispy collagen and inelastic elastin in the arteries (which would possibly first show up as high blood pressure).

Of course, no hunter gatherer was chugging 2 grams of NAC daily. It's not evolutionary psychiatry. But it does seem to have the potential to replicate, perhaps with some downsides, the natural brain glutamate situation of a lower-stress life with plenty of appropriate minerals and micronutrients. Hey, maybe even absence of tons of carbs on top of an inflammatory rodent diet. Or some ketosis. We live a modern life - some brains are already tracking in the wrong direction. It would certainly be worth studying NAC further so we have more information, and, in my view, in intractable or otherwise untreatable conditions that significantly impair functioning, giving it a try.


Some Studies....
  • The efficacy of N-acetylcysteine as an adjunctive treatment in bipolar depression: an open label trial
  • N-acetyl cysteine for depressive symptoms in bipolar disorder—a double-blind randomized placebo-controlled trial
  • N-acetylcysteine for major depressive episodes in bipolar disorder
  • N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action
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A Visual Guide to Opioid Receptors

1/30/2014

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A video on Mu, Delta, Kappa and ORL1 receptors on Pharmacology Corner
This lecture discusses the following topics:
  • General classification
  • Cellular actions of opioid receptors
  • Anatomical distribution and physiologic effects of mu, delta and kappa receptors
  • Agonists and antagonists
  • ORL-1 receptors

Part 1: Classification and Cellular Actions
Provides an introduction to the classification of  opioid receptors,  it also discusses the cellular effects of  opioid receptor activation (presynaptic inhibition of neurotransmitter release).

Part 2: Mu, Kappa and Delta receptors 
Lists the most relevant agonists and antagonists for the different subtypes of opioid receptor, then effects upon activation (opioid physiology) are reviewed.

Part 3: ORL1, Nociceptin or Orphanin FQ receptor
An overview on the recently discovered ORL1 receptor.

References and Further Reading
  • Katzung, B. Basic and Clinical Pharmacology. 11th ed. McGraw Hill Medical, 2009
  • Koneru A, Sreemantula S, Rizwan. Endogenous Opioids: Their Physiological Role and Receptors. Global J. Pharmacol., 3 (3): 149-153, 2009
  • McDonald J, Lambert DJ. Opioid Receptors. Continuing Education in Anaesthesia, Critical Care & Pain 2005 5:1
  • Trescot A, Sukdeb D. Opioid Pharmacology. Pain Physician 2008; 11:S133-S153

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The FDA has approved Fetzima for the treatment of major depressive disorder

1/25/2014

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SOURCE: Pharmacy Times
January 15, 2014 | Monica Holmberg, PharmD, BCPS
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The FDA has approved Fetzima (levomilnacipran extended-release capsules) for the treatment of major depressive disorder (MDD) in adult patients. Fetzima carries a boxed warning regarding the potential for an increased risk of suicidal thoughts and behaviors in children, adolescents, and young adults and the need for close monitoring in this population. Fetzima is not approved for use in pediatric patients. The approval of Fetzima also carries the limitation that it is not approved for the management of fibromyalgia.

MDD is a leading cause of disability in the United States, with approximately 16 million Americans—7.3% of the adult population—affected by it. The World Health Organization expects MDD to become the second-leading cause of disability by the year 2020. Fetzima was discovered by Pierre Fabre Laboratories and codeveloped by Forest Laboratories, Inc. 

Pharmacology and Pharmacokinetics 
Fetzima is a serotonin and norepinephrine reuptake inhibitor (SNRI). Fetzima has a terminal elimination half-life of approximately 12 hours and a median time to peak concentration of 6 to 8 hours after oral administration. The elimination of Fetzima is primarily renal. The pharmacokinetics of Fetzima are not affected by age, gender, or race.  

Dosage and Administration 
The recommended dose of Fetzima is 40 to 120 mg once daily. It should be initiated as 20 mg once daily for 2 days and then increased to 40 mg once daily, with subsequent increases in 40-mg increments every 2 days or more based on efficacy and tolerability. The capsule may be taken with or without food, and it should never be opened, chewed, or crushed. The maximum dose of Fetzima for patients with moderate renal impairment (creatinine clearance of 30 to 59 mL/min) is 80 mg per day. The maximum dose of Fetzima for patients with severe renal impairment (creatinine clearance of 15 to 29 mL/min) is 40 mg per day. Fetzima should not be used in patients with end-stage renal disease. Whenever possible, the dose of Fetzima should be gradually reduced before discontinuing therapy and patients should be monitored closely.

Clinical Trials 
The efficacy of Fetzima was established in three 8-week randomized, double-blind, placebo-controlled studies in a total of over 1600 patients. Studies 1 and 2 were fixed dose; study 3 was flexible dose. In each study, the primary end point evaluated the overall improvement in depressive symptoms through the change from baseline to end point in the Montgomery-Åsberg Depression Rating Scale total score. The secondary end point evaluated the improvement in functional impairment through change from baseline to end point in the Sheehan Disability Scale. A statistically significant difference was found for both end points in each study.

Contraindications, Warnings, and Precautions 
Fetzima is contraindicated in patients with hypersensitivity to any of its components, uncontrolled narrow-angle glaucoma, concurrent or recent use of monoamine oxidase inhibitors, or concurrent use of linezolid or intravenous methylene blue. 
As stated in the boxed warning, patients should be monitored for increased suicidal thoughts and behaviors. Fetzima is not approved for use in pediatric patients. Serotonin syndrome has been reported in patients using serotonin reuptake inhibitors and SNRIs, especially when used in combination with other serotonergic substances, such as triptans, tricyclics, fentanyl, lithium, tramadol, tryptophan, buspirone, and St. John’s Wort. Blood pressure and heart rate should be monitored throughout treatment with Fetzima; preexisting hypertension should be controlled prior to initiation of therapy. Fetzima may increase the risk of bleeding. Patients at risk for or with elevated intraocular pressure should be monitored carefully. Urinary hesitation or retention may occur. Fetzima may activate mania or hypomania in bipolar patients. Fetzima should be used cautiously in patients with seizure disorder. Hyponatremia may occur during treatment with Fetzima. 
Do not exceed 80 mg daily when Fetzima is used in combination with strong CYP3A4 inhibitors, such as ketoconazole. Fetzima is Pregnancy Category C. The most common adverse reactions (≥5%) are nausea, constipation, hyperhidrosis, increased heart rate, erectile dysfunction, tachycardia, vomiting, and palpitations.

>> Check the article out HERE


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Click HERE to see MPR's Slideshow reviewing medication details

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Antidepressant Brintellix (vortioxetine) Approved by FDA

1/25/2014

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SOURCE: PsychCentral
October 1, 2013 | John M. Grohol, Psy.D. 
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The U.S. Food and Drug Administration (FDA) approved a new medication Monday to treat clinical depression called Brintellix (vortioxetine). It has been approved for use in adults only.

“Major depressive disorder can be disabling and can keep a person from functioning normally,” said Mitchell Mathis, M.D., acting director of the Division of Psychiatry Products in the FDA’s Center for Drug Evaluation and Research.

“Since medications affect everyone differently, it is important to have a variety of treatment options available for patients who suffer from depression.”

A total of six clinical studies were conducted to garner FDA’s drug approval. The trials compared Brintellix with a placebo in people with clinical depression. An additional study showed Brintellix decreased the likelihood of participants becoming depressed again after treatment of their depressive episode. These studies were conducted in the United States and other countries.

The most common side effects reported by participants taking Brintellix in clinical trials included nausea, constipation and vomiting. Overall, 5 to 8 percent of the patients who received Brintellix 5 to 20 mg/day in short-term trials discontinued treatment due to an adverse reaction, the most common being nausea, compared with 4 percent of placebo-treated patients in these studies.

According to the manufacturers of Brintellix, Takeda Pharmaceutical & H. Lundbeck, the mechanism of the antidepressant effect of Brintellix is not fully understood.

What is known is that the new drug is an inhibitor of serotonin (5-HT) reuptake, and also acts as an agonist at 5-HT1A receptors, a partial agonist at 5-HT1B receptors and an antagonist at 5-HT3, 5-HT1D and 5-HT7 receptors. The contribution of each of these activities to Brintellix’s antidepressant effect has not been established, but it is considered to be the first and only compound with this combination of pharmacodynamic activity.

“There are very few new antidepressant drugs currently in development even though so many patients still struggle with depression. We are excited about the approval of Brintellix and being able to offer a new option for patients,” said Anders Gersel Pedersen, executive vice president and head of research and development for Lundbeck.

Major depressive disorder (MDD), commonly referred to as depression or clinical depression, is an often serious mental disorder characterized by mood changes and other symptoms that interfere with a person’s ability to work, sleep, study, eat and enjoy once-pleasurable activities.

Other signs and symptoms of MDD include loss of interest in usual activities, significant change in weight or appetite, insomnia or excessive sleeping (hypersomnia), restlessness/pacing (psychomotor agitation), increased fatigue, feelings of guilt or worthlessness, slowed thinking or impaired concentration, and suicide attempts or thoughts of suicide. Not all people with MDD experience the same symptoms.

Brintellix will be available in 5 mg, 10 mg, 15 mg and 20 mg tablets.
Brintellix was discovered by Lundbeck researchers in Copenhagen, Denmark. The clinical trial program in the U.S. was conducted jointly by Lundbeck and Takeda, and Takeda holds the new drug application for the U.S. market.

Brintellix and other antidepressant drugs have a Boxed Warning and a Medication Guide alerting patients and healthcare professionals that antidepressants can increase the risk of suicidal thoughts and behavior in children, adolescents and young adults ages 18 to 24 during initial treatment.

Studies show adults older than 24 years of age do not appear to have an increased risk of suicidal thoughts and behavior, while adults ages 65 and older appear to have a reduced risk. Patients starting antidepressant therapy should be closely monitored for worsening of their depression and the emergence of suicidal thoughts and behavior.


>> Click HERE to read the article


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Click HERE to see MPR's Slideshow reviewing medication details

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ABSTRACT: Bupropion as an Add-on Therapy in Depressed Bipolar Disorder Type I Patients With Comorbid Cocaine Dependence

1/25/2014

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SOURCE: Clinical Neuropharmacology
January/February 2014 - Volume 37 Issue 1
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Objectives: The treatment of bipolar disorder type I (BD-I) with a comorbid cocaine dependence disorder (CDD) is a challenge in current psychiatric practice. Drugs with proven efficacy in manic/mixed episodes, such as atypical antipsychotics and mood stabilizers, sometimes do not prevent depressive relapses; on the other hand, the use of antidepressants during acute depressive episodes may increase the risk of a manic switch. The aim of the present study was to investigate the short-term efficacy of bupropion augmentation in acutely depressed BD-I patients with co-occurring CDD.

Methods: Twelve depressed BD-I patients, with a comorbid CDD, treated with valproate 1000 to 1500 mg/d and aripiprazole 10 mg/d, were randomly assigned to receive bupropion 150 mg/d as an open-label add-on therapy (n = 5) or to continue their previous treatment (n = 7).

Results: After 4 weeks of observation, patients receiving add-on therapy with bupropion have improved in terms of Hamilton Depression Rating Scale scores and Drug Abuse Screening Test scores, with respect to those of the comparison group, whereas no significant increase of Young Mania Rating Scale scores over time was observed.

Conclusions: Our preliminary findings suggest that combining bupropion with mood stabilizers and atypical antipsychotics may be a good therapeutic option in short-term treatment of depressed BD-I patients with comorbid CDD.


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No Need for Blood: Nine Alternatives to the Antidepressant Debate

1/25/2014

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SOURCE: Psychiatric Times
January 23, 2014 | James Phelps, MD
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At the recent International Society for Bipolar Disorders (ISBD) meeting, 2 experts debated the role of antidepressants in the treatment of bipolar disorder. Both sides of the debate presented rational interpretations of existing literature (thus the jest about more blood). Both speakers agreed there is very little evidence for the efficacy of antidepressants in the treatment of bipolar disorder, particularly for longer-term use. They disagreed regarding evidence for the capacity of antidepressants to exacerbate bipolar disorder. The risk of inducing manic symptoms was their main focus, although one should also consider risk of inducing mixed states and the risk of “mood destabilization,” ie, inducing cycling such that more mood-stabilizing medications are required than would be needed without the antidepressant. For all of these risks, there remains room for debate.

Yet such debate may be moot. Look closely at the benefit to risk ratio for treatment of manic episodes in bipolar depression. Imagine a competition, based on this ratio, between antidepressant modalities. In this competition, any treatment that can leap over the bar of efficacy can be compared on the basis of its potential to exacerbate bipolar disorder. If the efficacy bar is set close to zero, which both speakers agreed appears to be the case for antidepressants, then virtually any treatment with evidence of antidepressant effects in some form of depression can be considered for the treatment of bipolar depression. The competition comes down to evidence of exacerbation and other adverse effects and risks—not efficacy.

>> Read the rest of the article HERE


Summary

This antidepressant debate, however rational, was moot before it began. Clinicians have at least 9 alternatives to antidepressants, all of which have as much evidence for efficacy in bipolar depression as antidepressants do. All 9 alternatives have less risk of inducing hypomania/mania, and at least 5 have very little risk at all—and most of them have additional benefits. The pharmacotherapies have significant risks and warrant careful discussion with patients and individualized decision making. But for the benefit to risk ratio for mania, there is no need for further debate—or blood.
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Mistimed Sleep Disrupts Circadian Regulation of Gene Expression

1/25/2014

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SOURCE: MPR - HealthDay News
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Delaying sleep by just a few hours for several days reduces circadian gene expression in the blood six-fold without affecting centrally-driven melatonin circadian rhythms, according to a study published online Jan. 20 in the Proceedings of the National Academy of Sciences.

Simon N. Archer, PhD, from the University of Surrey in Guildford, UK, and colleagues analyzed changes in gene expression in the blood of 22 healthy volunteers who were placed on a mistimed sleep cycle, where sleep was delayed by four hours for three consecutive days.

The researchers found that mistimed sleep led to a reduction in circadian transcripts in the blood, from 6.4% to 1%, without affecting the centrally-driven circadian rhythm of melatonin. The genes affected included those associated with chromatin modification, transcription, translation, temperature-regulated transcription, and core clock genes.

"The data show that mistimed sleep affects molecular processes at the core of circadian rhythm generation and imply that appropriate timing of sleep contributes significantly to the overall temporal organization of the human transcriptome," Archer and colleagues conclude.

>> Get the Full Text HERE
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Act Now to Prevent Restrictions on Psychiatric Medications in Medicare!

1/23/2014

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>> Click HERE to help now!
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The Federal Center for Medicare and Medicaid Services (CMS) has proposed a rule to restrict access to anti-depressant and anti-psychotic medications in the Medicare Part D program. 

Historically, Medicare Part D Plans have been required to include on their preferred drug lists all or substantially all psychiatric medications in recognition that personal choice and clinical judgment are critically important in decisions about these medications.   The proposed rule would restrict the availability of anti-depressant medications in 2015 and restrict the availability of anti-psychotic medications in 2016.

NAMI has long supported preserving open access to all Food and Drug Administration (FDA) approved medications in the Medicare Part D program. Restricting access to psychiatric medications can be extremely harmful for individuals living with serious mental illness, including increased hospitalizations and other negative consequences.  At a time when national attention is focused on improving mental health care, a rule restricting access to psychiatric medications does not make sense.

Final comments on the proposed rule are due to CMS by March 7, 2014.   NAMI will circulate sample comments prior to that date. 


>> Go HERE to send a letter to your U.S. Representative and Senators      
>> Go HERE to learn more about the proposed rule
>> Go HERE to see the proposed rule
Thank you for your advocacy!
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Updated Affordable Prescription Guide

1/23/2014

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Fresh off the press... a new prescription guide. I've gone through each of the stores posted medication lists and updated what needed updating. Additionally, I added RxOutreach to the list because I've found them quite helpful for several hard to get medications, such as Effexor XR. 
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btb_pharmacy-discount-list_20140123.pdf
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Kids With ADHD, Aggression May Benefit From 2nd Med

1/23/2014

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SOURCE: OrderConnect
Jan. 2, 2014 (HealthDay News) -- Children with attention-deficit/hyperactivity disorder (ADHD) who also are extremely aggressive might benefit from taking an antipsychotic drug along with their stimulant medication, a new study suggests.

Prescribing powerful antipsychotic medications to children with behavioral problems is controversial. Little is known about the long-term safety of these medications, which are approved by the U.S. Food and Drug Administration to treat severe mental illnesses such as schizophrenia and bipolar disorder. And previous studies have provided little evidence to support the idea that they help quell youngsters' violent outbursts.

But the new study, which was published online in the January issue of the Journal of the American Academy of Child and Adolescent Psychiatry, suggests there might be some merit to the idea, at least for severely troubled kids.

The study looked at a subset of children with ADHD who also are physically violent, meaning they're either destructive or aggressive toward themselves or others, the researchers said.

"The children who participated in this trial had far more significant behavioral issues than the typical child with ADHD alone," said study author Michael Aman, director of clinical trials at Ohio State University's Nisonger Center.

"These are children who are really in conflict with their communities and their families," Aman said. "They seem to be in a spiral they can't get out of."

The 168 children in the study were between 6 and 12 years old with a diagnosis of ADHD and oppositional-defiant disorder or conduct disorder. All had displayed recent episodes of serious physical aggression in which they destroyed property or, at a minimum, left bruises on themselves or others.

All were started on a stimulant medication -- typically long-acting methylphenidate (sold under the brand name Concerta), which is a common treatment for ADHD. Their parents got special training in how to manage impulsive behaviors.

After three weeks, those who had not been helped enough by the basic measures were allowed to start a second medication, which was assigned at the start of the study. Sixty-one kids who started the second medication took the antipsychotic risperidone (Risperdal) for six more weeks, while 69 children continued basic treatment and got an added placebo pill.

After nine weeks, children who took Risperdal in addition to their stimulant medication saw modest but significant improvements in behavior compared to those who continued on the stimulant by itself.

"I don't think it's a grand slam, but I do think it indicates that there is some justification for what doctors have begun to do, which is to combine treatment," Aman said.

Aman said the average improvement on Risperdal was moderate. "Buried in that moderate are kids who did much better, kids who did somewhat better and some kids who didn't do better at all," he said.

Aman said scientists really need to look more closely to understand why some children had big improvements with the addition of Risperdal while others got no further help.

In some cases, Risperdal seemed to cancel some of the most bothersome side effects of the stimulants, including loss of appetite and trouble falling asleep.

But Aman cautioned that antipsychotics must always be prescribed with great care since they cause weight gain and increase the risk for type 2 diabetes.

The study was sponsored by a grant from the U.S. National Institute of Mental Health.

About half of children with ADHD who are referred for psychiatric help have behavioral disorders as well as ADHD, according to the U.S. Centers for Disease Control and Prevention.

An expert who was not involved in the research praised the study and said it would help doctors sort out what is often a tricky treatment decision.

In kids with ADHD and aggressive behavior, "recent guidelines say you should try to treat the ADHD first," said Joseph Blader, an associate professor at the University of Texas Health Science Center at San Antonio. "Then the issue is, how long do you spend doing that if the child is having these explosions, these meltdowns, potentially hurting people, on the threshold of getting kicked out of school? Two weeks? Three weeks?"

Blader said that, because so many of the kids in the study's placebo group continued to improve on the stimulant medication alone, doctors might be justified in waiting a few more weeks to see if the aggression improves along with the ADHD.

"I think this study shows that you get a lot of bang for your buck with stimulants and parent training," he said. "Unless it's a very extreme situation, it's optimal to let those play out [before trying a second medication]."
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Neurological side effects of antipsychotics

1/22/2014

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SOURCE: Psychopharmacology Institute
AKATHESIA & DYSTONIA
  • A classification of neurological side effects
  • Akathisia ( Clinical features, a clinical video, medications that can cause akathisia and management)
  • Acute dystonia (Clinical features, pathophysiology, management)
PARKINSONISM
  • Clinical features
  • Mechanism of EPS
  • Differences between antipsychotic induced parkinsonism and Parkinson’s disease
  • Management of antipsychotic induced parkinsonism
  • Risk of EPS and D2 occupancy
REFERENCES
  • Brunton LB, Lazo JS, Parker KL, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill; 2010.
  • Janicak, P G., S R. Marder, and M N. Pavuluri. Principles and Practice of Psychopharmacotherapy. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2010.
  • Stahl, S M. Stahl’s Essential Psychopharmacology: Neuroscientific Basis and Practical Applications. 3rd ed. New York: Cambrigde University Press; 2008
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Treatment Considerations for HIV-Infected Individuals with Severe Mental Illness

1/22/2014

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SOURCE: DocGuide
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There has been a general recognition of a syndemic that includes HIV/AIDS and severe mental illnesses including schizophrenia, major depression, bipolar disorder, post-traumatic stress disorder, and others. The pathophysiology and direction of effects between severe mental illness and HIV infection is less clear however, and relatively little work has been done on prevention and treatment for people with these complex, co-occurring conditions. Here we present the most recent work that has been published on HIV and mental illness. 

Further, we describe the need for better treatments for'triply diagnosed persons'; those with HIV, mental illness, and substance abuse and dependence. Finally, we describe the potential drug-drug interactions between psychotropic medications and anti-retrovirals, and the need for better treatment guidelines in this area. We describe one example of an individually tailored intervention for persons with serious mental illness and HIV (PATH+) that shows that integrated community-based treatments using advanced practice nurses (APNs) as health navigators can be successful in improving health-related quality of life and reducing the burden of disease in these persons.

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Medication for alcohol use disorder: Which agents work best?

1/21/2014

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SOURCE: Current Psychiatry
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In this article, we review FDA-approved medications and off-label agents and provide recommendations for treating patients with AUD.

BOTTOM LINE:
FDA-approved (acamprosate, naltrexone, and disulfiram) and off-label (baclofen, gabapentin, ondansetron, and topiramate) agents can help patients with alcohol use disorder achieve abstinence, reduce heavy drinking days, prevent relapse, and maintain sobriety. Research supports the use of pharmacotherapy combined with psychosocial modalities, such as 12-step programs, motivational interviewing, and cognitive-behavioral therapy.

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Long-Term Benzodiazepines for Anxiety Linked to Adverse Events

1/21/2014

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SOURCE: Clinical Psychiatry News
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By: ELIZABETH MECHCATIE

ARLINGTON, VA. - Widespread long-term use of benzodiazepines for anxiety remains a reality, despite guidelines that recommend against the practice, according to speakers participating in a roundtable discussion at the annual conference of the Anxiety Disorders Association of America..

Benzodiazepines alleviate anxiety symptoms, but they do not help to resolve anxiety disorders in the long term, with posttreatment relapse rates reported as high as 63%. Learning impairment associated with benzodiazepines is the side effect that "significantly diminishes the effects" of cognitive-behavioral therapy (CBT), said Dominic A. Candido, Ph.D., a psychologist in the department of psychiatry at the Dartmouth Geisel School of Medicine, Hanover, N.H.

He cited a 2010 study that found benzodiazepine usage rates in the general population ranged from about 2% to almost 18%. In the study, about one-third of people who received an initial prescription stayed on the drug long term – despite the recommendation in treatment guidelines that suggests limited short-term use. Recently, the departments of Veterans Affairs and Defense guidelines recommended against the use of benzodiazepines for posttraumatic stress disorder – partly because benzodiazepines increase the likelihood of stress symptoms.

"When practitioners do not have alternatives, they tend to go to these agents that will give them short-term relief but often at long-term detriment to the patient," he said.

Shanna Treworgy, Psy.D., also of Geisel medical school, said the impact on procedural memory "perhaps is the worst side effect" of benzodiazepines in the treatment of anxiety. "Research that has successfully pulled apart explicit and implicit memory has demonstrated significant effects on procedural learning and memory" during treatment with benzodiazepines, she said. "This happens through impairing acquisition of new memories through reduced arousal or sedative effects."

The studies include a 1997 investigation of exposure therapy in women with flying phobia, which evaluated the acute and long-term effects of alprazolam. Women on alprazolam had significantly reduced levels of anxiety compared with those on placebo during the first flight. But during a second flight a week later, when the former group of women was not medicated, they had significantly increased feelings of anxiety, an increased heart rate, a desire to leave the plane, and panic, while those who had been on the placebo during both flights showed decreases in multiple measures of anxiety. "We’re wondering if this perhaps was preventing new learning," Dr. Treworgy said, adding that the authors suggested that exposure therapy to flying phobia was incompatible with benzodiazepine treatment.

Summing up the evidence, she said, "What seems to be happening is that the result is reduced anxiety in the moment but worse long-term anxiety reactions documented in both animal and human studies."

A psychiatrist at Geisel School of Medicine, Dr. Matthew S. Duncan said that in clinical practice, benzodiazepine prescribing can be tailored to CBT to help patients stop taking the medications and become more functional. He added that he has experienced a paradigm shift in the prescribing of benzodiazepines, which also entails explaining this approach to patients. "I have to be able to convince them and articulate that prescribing benzodiazepines for your anxiety may have short-term gains but keep you sicker longer," said Dr. Duncan.

Dr. Candido said he and his colleagues have developed a CBT protocol to treat patients with anxiety that involves starting patients with 3 days of a benzodiazepine administered at three doses a day (preferably one with a short half-life, such as lorazepam) and no beta-blockers, followed by 3 days with no benzodiazepine treatment, gradually increasing the drug-free period. Single as-needed doses are never taken, and the drug is never used before a coping skill session, he said.

An audience member pointed out that as CBT becomes less available, the use of benzodiazepines for anxiety increases, and another member of the audience commented that he would use this approach all the time if more CBT therapists were available.

Dr. Candido and Dr. Treworgy said they had no relevant financial disclosures. Dr. Duncan reported having no relationship with any entity or institution other than the Geisel School of Medicine.


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Deep Brain Stimulation & Depression: A Decade of Progress

1/20/2014

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A webinar and virtual Q&A on Deep Brain Stimulation & Depression presented  by Brain & Behavior Research Foundation on Tuesday, January 14, 2014.
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