I have been kicking these observations around for the past year, and have been unable to find a big fish willing to ‘bite’.  I truly believe that the observations below have the potential to dramatically change the approach to opioid treatment of chronic pain.  Since I have a blog, I have a soapbox– so I’ll share the idea, and welcome comments in return.  I do ask that proper attribution be provided if this article is shared.

Introduction:

Long-term opioid analgesia without tolerance, respiratory depression, or euphoria?  Introducing the Holy Grail for chronic pain treatment!

Premise:

The miracle of opioid pain relief is fatally limited by tolerance, addiction and respiratory depression. Buprenorphine, when combined with a mu agonist, results in game-changing effects. Patients experience potent, dose-related analgesia from the agonist, but have NO euphoria. The therapeutic window is widened. Patients unable to control their use of a mu agonist alone gain that control when on buprenorphine. And most exciting, buprenorphine indefinitely anchors tolerance, maintaining analgesia WITHOUT DOSE ESCALATION. This finding offers huge implications for pain management.

Discussion:

Use of opioids for chronic pain has severe limitations. Tolerance removes the benefits of opioid analgesics over time. Worse, tolerance is associated with dependence and withdrawal. Many patients use additional doses of their prescription early in the month, then suffer through withdrawal while awaiting refills. Others find opioids through less-reliable, non-clinical sources.

At the same time, addiction to mu opioids is a nationwide epidemic. Reformulation Oxycontin has pushed many opioid users toward diacetylmorphine—brand name Heroin. Some physicians recommend avoiding mu opioids altogether for chronic pain (e.g. Physicians for Responsible Opioid Prescribing), while pain treatment advocates argue to ease narcotic restrictions.

Over the past six years I have treated over 500 patients using buprenorphine, mostly for opioid dependence. Buprenorphine, a partial mu agonist, is the active ingredient in Suboxone, a medication used for treating opioid dependence. The majority of my patients began their addictions with narcotics prescribed by doctors for back pain, knee pain, shoulder pain, fibromyalgia, chronic headaches, and other conditions.

Many of my patients found their pain reduced or gone after stopping mu agonists and substituting buprenorphine. Buprenorphine has the mu activity of 40 mg of daily methadone, but this activity is unlikely responsible for significant analgesia, since patients rapidly become tolerant to the agonist actions of buprenorphine. Instead, their pain while on mu agonists was likely maintained by psychological forces.

Patients on buprenorphine occasionally need opioid analgesia, just like other patients. My patients have had knees replaced, gallbladders removed, hysterectomies and c-sections, rotator cuff repairs, and in two cases, cardiac surgery. In all cases, sufficient analgesia was provided by maintaining daily buprenorphine at 4-8 mg per day, and using potent mu agonists, usually oxycodone, in doses ranging from 15-45 mg every 4-6 hours as needed.

Several patients have severe chronic pain from avulsion of the brachial plexus, failed spinal fusion, or other conditions, where prior opioid use resulted in rapid tolerance that prevented effective analgesia. These patients are now successfully maintained on combinations of buprenorphine plus mu agonists.

The combination of buprenorphine plus mu agonists has provided perioperative analgesia for patients on buprenorphine. Patients universally describe adequate pain relief, even after major surgeries. They also described the absence of euphoria, and to their surprise, the ability to control their use of pain medication—something impossible before taking buprenorphine.

But it is the effects on chronic pain that suggest a ‘game-changer’ for pain treatment. Even after over a year on combination buprenorphine/oxycodone, my patients 1. have no euphoria; 2. are often able to manage their own narcotic medication; and most important, 3. describe stable analgesia WITHOUT agonist dose escalation.

The ability to treat pain long-term without tolerance or dose-escalation is as exciting a development as was the initial discovery of opioids for pain relief!

Properties of a combination agent

Buprenorphine is administered sublingually, and could be prescribed as a separate medication, and use verified through urine monitoring. But greater safety benefits would come through regulations requiring buprenorphine (or a similar partial agonist) to be an inseparable part of every opioid prescription. Such a policy would dramatically lower the addictiveness and reduce the respiratory depression of mu agonists WITHOUT removing efficacy. The most obvious formulation would be a transdermal system that delivers buprenorphine and fentanyl, since both are already available in separate transdermal systems.

There may be situations, for example hospice care, where euphoria would be a desirable part of opioid treatment. But for other cases, analgesia without euphoria has obvious benefits.

I have written to several pharmaceutical companies with this idea, and have heard back that while the idea is interesting and scientifically sound, the generic nature of the component medications reduce the potential for profit that would motivate development. But given the potential value of this approach for multiple problems– addiction and chronic pain among them—I have to think that there is money to be made—not to mention the advances in treatment that the approach offers.

Reference:

Some supporting background information can be found in: Alford, D., P Compton, and J Samet, Acute Pain Management for Patients Receiving Maintenance Methadone or Buprenorphine Therapy. Ann Intern Med. 2006 January 17; 144(2): 127–134.

I also discuss this approach to pain treatment in my ‘Users Guide to Suboxone’, sold on Amazon and at bupeguide.com

Jeffrey T Junig MD PhD

Please do not reproduce without attribution.

The other day I met a new patient who described a long history of anxiety and depression that recently became severe.  She had been to two other psychiatrists in the past year, and was seeing me because she was not getting any better; in fact if anything she was getting worse.  She described symptoms that changed from anxiety and mild depression to severe panic attacks and social withdrawal; symptoms that were almost certainly the consequence of her being prescribed large doses of alprazolam (Xanax).  She described a pattern that I have seen very often;  a person has relatively mild, manageable anxiety, and is prescribed a benzodiazepine.  After a few weeks the ‘benzo’ is no longer effective because of a process called ‘tolerance,’ and worse, if the person misses a dose, the discontinuation symptoms FEEL like severe anxiety and panic– leading the person to take more of the benzo.  The dose must be increased to get a response, and then the discontinuation symptoms become even greater… leading to a spiral of increasing anxiety and medication use.  This is a difficult pattern to break, because the patient must reduce and taper off the medication that once was providing relief– all the while tolerating a certain amount of anxiety and insomnia. 

I feel bad for patients in this situation, because they would be better off had they never gone to a doctor for their anxiety in the first place.  But the situation in my new patient was even worse– and what had happened to her was not uncommon.  As her ‘anxiety’ worsened, the psychiatrist treating her piled on more and more medications.  She was prescribed Depakote without relief.  Then whe was prescribed risperidone.  Then lamotrigine.  These medications are all somewhat sedating, and when she complained of being too drowsy she  was prescribed the stimulant Adderall, and then modafanil.  The stimulants made her shaky, and so the original benzo was increased.

Medications like Depakote, lamotrigine, and risperidone have a place in psychiatry;  all three are mood stabilizers, and are used to treat bipolar disorder among a few other conditions.  In order to qualify for a diagnosis of bipolar I (the more serious form of bipolar disorder) a person must have a history of ‘mania’– a period of 7 days (shorter if the person is hospitalized) when the person is ‘revved up,’ with less need for sleep, increased risk-taking, racing thoughts, and other specific criteria.  There is some credible evidence that the diagnosis of bipolar has been overdone in recent years, particularly in children.  Over-diagnosis of depression would not be a horrible thing, given that the medications primarily used to  treat depression, a class of medication called ‘SSRIs’, are relatively benign.  But the same cannot be said of over-diagnosis of bipolar disorder; medications used to treat bipolar have a number of significant side effects ranging from sedation and tremor to weight gain and diabetes!

When I asked the patient about her diagnosis, she was confused.  She was not told that she had bipolar disorder, and so she was not certain why she was taking so many medications.  She had no idea that some of the medications were prescribed only to treat side effects from other medications.  And she had no idea that the medications had the potential to cause a wide range of systemic illnesses and conditions.

I don’t know what to make of THAT kind of psychiatry.  I talk often on my radio show about the need for patients and psychiatrists to spend TIME with each other;  time to get the diagnosis right, or in this case to at least come to SOME diagnosis!  Too often, medications seem to be prescribed out of desperation; an overly-busy, short-on-time prescriber adding medication not according to a sound treatment plan for a careful diagnosis, but rather using medications to blunt symptoms like firefighters in a helicopter dropping water on a fire.

Not all psychiatric conditions require medications, but sometimes, medications are useful and even necessary.  When medications ARE used, I encourage all patients to demand to know the diagnosis that is being treated, the options in medication and non-medication treatments, and the effects and side effects of anything that is prescribed.  That understanding will probably take some time– but that time should be a basic part of every psychiatric relationship.

Another installment of the radio program.  For newcomers, this is a program that I do each Monday morning.  You can subscribe to this content on i-tunes;  just search for ‘Junig’ or ‘shrink zone’ in the podcast section.  I will be posting past programs every time I think of it– hopefully at a pace of 2 or 3 per week until I am caught up to the present.  Thank you very much for listening, and I welcome your comments– which can be made through my home page at fdlpsychiatry.com.  I also provide telepsychiatry for patients in distant locations, as described here.

Another show from the archives.  I should mention that the other person on the show with me is Bob Hoffmaster, who does the morning show at KFIZ Fond du Lac every day.  As you can hear, he makes the show a breeze;  he has a curiosity about everything, and all I have to do is come in and chat with him.  It is always the high point of my week– too bad it has to happen on a Monday!!

I’ll TRY to keep this brief… People with mood or anxiety disorders are often treated with SSRI’s or SNRI’s. In fac, such meds are the appropriate treatment for anxiety disorders, not ‘benzos’– a topic that I have already discussed in a prior post.  The SSRIs are ‘selective serotonin reuptake inhibitors’ and SNRIs are ‘serotonin and norepinephrine reuptake inhibitors.’  In general, SNRIs are more potent;  psychiatrists often start with and SSRI or maybe try one and then if necessary a second SSRI, and THEN go on to an SNRI if the patient doesn’t find adequate symptom relief.  SNRIs are chosen as a second option because they tend to be, in general, more difficult to tolerate.  The difficulty usually consists of  short period of ‘activation’ when the medication is first started;  patients will complain of a couple days of irritability or insomnia for example.  Both SSRIs and SNRIs are very well tolerated after a few days or at most weeks have passed on the medication.

The few days of side effects to SSRIs and SNRIs comes from a nonspecific effect of an increase in brain serotonin– NOT from the therapeutic actions of the medication.  When people taking an SSRI or SNRI say ‘I don’t like how it makes me feel’, they are feeling something that is NOT going to be around when actual therapeutic actions occur, several weeks in the future.

I will use brand names for this post;  the brand name for citalopram is Celexa.  Lexapro is the brand name for ‘escitalopram.’  The brands of SSRIs include both of those medications, and also Zoloft, Paxil, Prozac, Luvox, and some names for products in other countries (and I feel like I am forgetting one).  The brand names for SNRI’s in the US are Cymbalta, Effexor, and Pristiq.  This talk, though, is primarily about Lexapro and Celexa.

Celexa was (is) a very good SSRI.  Some SSRIs cause weight gain (Paxil), sedation  (Paxil), weight loss (Prozac), activation or insomnia (Prozac), or nausea (Zoloft)… but Celexa does not cause significant amounts of any of those side effects.  Like all other SSRIs (except, perhaps, Lexapro), Celexa requires at least a few weeks to start working.  Eventually Celexa went ‘off patent’ and became an inexpensive generic– four bucks at WalMart, as a matter of fact.  Around the time Celexa went generic it was replaced by an antidepressant that is very similar, called Lexapro.  So now a frequent issue is whether Lexapro, at ‘brand prices’ of over $100 per month, is worth the money over Celexa, at $4 per month.  What does that extra money get you?  I am not going to be able to give a solid answer to that question, but I will show why the question is there, so that perhaps you can make a better decision yourself.

As I will show in a minute, the two drugs are more than ‘similar’– they are almost identical.  Both medications treat depression and anxiety– of that there is NO doubt.  There have been studies that show that Lexapro works faster than Celexa;  that Celexa takes about 4 weeks to work whereas Lexapro works in as fast as 2 weeks.  There are also those who believe that Celexa has more side effects– a bit more weight gain perhaps, or some sedative effects.  This issue is not absolutely ‘cut and dried’.  The studies favorable to Lexapro have usually been supported by the manufacturer of Lexapro.  On the other hand, I have no doubt that the people doing the studies were honest about the work they have done– my concern is that if you look for something long enough, you will find it by chance alone.  And I do not know how many studies have looked for a positive difference of Lexapro over other SSRIs in order to come up with studies that showed the desired finding.  After reading the research and prescribing the medications over the years, I believe that it is clear that Lexapro is a more desirable medication;  it probably works faster with slightly fewer side effects.  Is it worth the money?  That depends on who is buying it and who it is being given to.  For my I will pay for Lexapro if the difference is only a copayment of 20 bucks.  If insurance won’t cover Lexapro, I will have them try Celexa first.  For me, Celexa is fine– but if I had a moderate to severe depression that was not getting better on Celexa, I would pay for Lexapro.  From my experiences with Medicare and my reading about the language of the bill being debated in Congress today, along with my understanding of Tom Daschl’s book and the comments off the current President of the US, I would be SHOCKED if Lexapro were available for people on any ‘public option’.  This is the type of savings that the administration seems to believe will make a difference in the price of health care.  I think it might help a little bit, but I think that many people will be angry when they gain ten pounds on Celexa and find that they cannot take Lexapro.  But they can always exercise– and then the problem is solved.  There is enough to argue about even if we take all of what I just said as fact– which is why everyone is arguing right now!

The difference between the two medications is difficult to understand… and yet very simple once you get the point.  Look at your two hands–  one is ‘right handed’ and the other is ‘left handed’.  Most medications consist of two ‘halves’, a right and left-handed form.  Your two hands are in many ways identical– the same tissue, the same genes, the same structure.  And yet they are different in that one is the mirror image of the other.  A batch of chemicals contains right and left handed molecules because chemical reactions produce a 50/50 mix of both right and left forms.  It is hard to separate them from each other, as they both act the same way in electrical fields and they both are the same size and shape– so you can’t just make some type of ‘filter’ that separates out just the active form. But when the chemicals are used in the body, they usually work at ‘receptors’, where they must ‘fit’ in order to cause something to happen.   And if you try to stick your right hand into a left glove, you have problems.  Same in the body;  one ‘half’ binds to the receptor and is effective, and the other half does not fit, and is inactive.  In other words, half of most of the medication you use does not do anything.

This is the case with Lexapro and Cexexa.  Celexa consists of both varieties of the molecule– the right and left forms.  But Lexapro is only the potent, active variety– the left-handed molecule.  When you are taking Celexa you are taking two chemicals that are mirror images of each other;  one of the chemicals binds to the proper site and blocks serotonin reuptake, and the other chemical is the mirror image of the active chemical, and probably doesn’t do much of anything.  If you take Lexapro, you are taking ONLY the active form.  So if you take 20 mg of Celexa, half of what you are taking– 10 mg– is Lexapro.

Both are 'Citalopram'; one half is 'Lexapro'

This would imply that a person could just take twice as much Celexa and get the same effect as Lexapro, right?  Maybe.  The problem is that some studies suggest that Lexapro is more than twice as potent as Celexa– that it is actually about 4 times as potent.  The only way that could be the case is if for some reason the inactive half is doing something bad– not just doing ‘nothing’, but maybe getting in the way of the active half.  The inactive half might also cause side effects that are not caused by the active half, explaining why some people find that Celexa causes them to gain weight or get sleepy, while Lexapro does neither.  What do I think?  I t hink that it is easy to get too tied up in the chemical issues.  Both medications are effective, with some minor differences between them.  I’ll stick with my earlier comments about it depending on who is taking/paying for the medications.  I think there are implications, though for ‘choice’ when it comes to health care.  I also recognize that if pharmaceutical companies cannot profit from their discoveries, then there will be fewer discoveries.  Most of the profits of pharmaceutical companies go right to where we should all want them to go– to research efforts for more effective, safer medications.  And if some team of scientists find a cure for something, they should benefit financially– just as Bill Gates became a billionaire for his work with computer operating systems.

I think I’ll leave it there before I say something controversial.  Lexapro or Citalopram– you get to decide.  Perhaps the bigger question– the one that is being debated in Congress right now– is SHOULD you get to decide?  I’m not taking a position on that question– but the people who are debating the health care reform should recognize– and admit– that THEY are taking a position on that question.

Just a quick comment tonight about an interesting report from the American Academy of Child and Adolescent Psychiatry 56th Annual Meeting– in Hawaii, of all places (gnashing my teeth in jealousy, but it should pass in a few minutes!).  As you may or may not know, my practice is split between classic psychiatry (med management and/or psychotherapy from a psychodynamic perspective), treatment of addictions (primarily opiate dependence), and treatment at the interface of chronic pain, psychiatry, and addiction.  Compared to the fatal nature of opiate dependence and the epidemic of cases locally and across the nation, I view pot-smoking as a relatively minor vice for most people.  I have met a number of people who seem to be able to smoke pot fairly regularly without significant harmful sequelae– although I would not be surprised if the pot use is costing something–  a reduction in marital intimacy or in one’s relationship with one’s children, for example.

On the other hand there are clearly people who have negative consequences from use of THC.   One thing that has always stood out, at least in patients I have followed, is that people who are depressed and who are regular pot smokers do not seem to benefit all that well from SSRI‘s– or from other treatments, for that matter.  I have assumed that the reason is more psychological than chemical– that since pot-smokers tend to be more sedentary, and tend to lack good coping skills other than smoking marijuana to deal with stress (whereas non-pot-smokers may deal with stress by exercising, meditating, or taking up a new hobby), they are simply harder to pull out of the ‘funk’ that depressed people are in.  But at the meeting in Hawaii, docs from the University of Pittsburgh School of Medicine reported partial data from a larger study that showed a reduced treatment response to antidepressants by patients using moderate amounts of alcohol or marijuana.

File this report in the ‘evidence backing up common sense’ drawer.  It was not a huge surprise, but it is always a good thing when the science is consistent with the general opinion on a topic.  This was not the case, as some of you may remember, when it came to breast implants and autoimmune conditions– and about a million other things that the media warns us about, that eventually turns out to be a bunch of baloney.  In the case of pot smoking and reduced response to antidepressants, seems that there isn’t much baloney going around.

JJ

Casual Cannabis, Alcohol Use Reduces Treatment Efficacy in Adolescents With Major Depression

Because of several highly-publicized deaths from combining Suboxone with benzodiazepines or ‘benzos,’ a class of sedative medications that includes Xanax and Valium, I am frequently asked about the safety of combining Suboxone with those medications.  The risk of life-threatening respiratory depression can be mitigated fairly easily, but that does not mean that benzos are safe or appropriate medications for people with or without addictions.  They are commonly-prescribed medications and there are a number of misconceptions among laypeople about their proper use, so they deserve a thorough discussion.  Most doctors with a bit of experience have learned to cringe every time a patient says the word ‘anxiety,’ knowing that in all likelihood they are about to be placed in a difficult position.  They will either do the right thing and disappoint their patient, or do the wrong thing and struggle with the consequences of their actions for months or years.

The problem is that the non-medical community sees SSRI’s as ‘antidepressants’, and believes that the proper treatments for anxiety disorders are sedatives like Valium or Xanax.  While the sedatives are appropriate for acute or short-term anxiety, chronic anxiety disorders are more appropriately treated using SSRI’s or SNRI’s.

Today I saw a new patient who asked for treatment of her addiction to pain medications.  When I asked about other psychiatric symptoms she said that she takes alprazolam and clonazepam for anxiety and panic attacks.  I explained that those medications are very dangerous for addicts and are intended for short-term use, and the primary treatments for anxiety disorders are SSRIs or SNRIs.  I asked her dose and wasn’t surprised to hear that her tolerance was quite high.  A milligram of alprazolam doesn’t even do anything, she said—intending to mean that the meds are no potent enough to worry about.  I of course took it the opposite way—she has taken benzos to the point that a very large dose has no effect due to her high tolerance.  She then said she also has ADD and takes Adderall (i.e. amphetamine).  I explained that it makes no sense to take both amphetamines and benzos, particularly a long acting benzo like clonazepam, which has a half-life of around 30 hours.  Benzos CAUSE deficient attention; that is how they work!  Worry consists of too much attention to a problem or a fear, and benzos prevent the brain from attending, attaching and remembering.  In fact, anesthesiologists and dentists use the short-acting benzodiazepine midazolam during uncomfortable procedures to block the patient’s memory.  Most adults have had the experience of watching the medication injected into the IV tubing, and next waking up to people saying ‘you’re OK—it’s all done.’  Don’t take a benzodiazepine if you are nervous about an exam the next day!  Beyond the amnesia it is simply a bad idea to take two polar-opposite medications as this patient is doing.  Stimulants cause wakefulness, attention, tight muscles, and anxiety.  Benzos cause drowsiness, amnesia, relaxation, and the inability to remember what you were supposed to worry about.  Instead of taking both, take neither.

A related question came to me by e-mail yesterday:

Hello, I found your website and see that you do phone consultations. I have been having anxiety problems and attacks for over a year. It has gotten worse and worse. I’ve been to the doctors in my area but no one wants to treat me for it…they just want to keep giving me Paxil, Zoloft, Prozac, Cymbalta and all these things I’ve tried and nothing seems to be helping me. I have anxiety attacks all the time where my heart beats out of my chest and I can’t breathe and go almost into this blackout stage. I have a lot of things that trigger it; one is my anxiousness all the time. I can’t focus, and any little dilemma sets me off. Everything is a crisis to me. And on top of that, I have the responsibility to take care of a 3 year old all by myself. I’m so scattered and anxious and upset all the time it is affecting me being a good mother. I cannot take it anymore and I am at the end of my rope. I don’t know what to do; no one will treat me with anything to calm me down along with the Paxil because of all the other people in this county that have abused it.. I DO NOT know what else to do. I have no one to talk to or turn to. It’s affecting my job, my personal life and my life in general. If you can’t help me maybe you know someone who will.

The person doesn’t come right out and say it, but her comments about needing to be calmed down and about abuse of the meds by others suggest that she is asking for a benzodiazepine.

Benzodiazepines include long-acting medications like clonazepam (Klonopin) and diazepam (Valium), intermediate-acting medications like lorazepam (Ativan) and alprazolam (Xanax), and the short-acting sleeping pills from my training years like triazolam (Halcion) and temazepam (Restoril). As an anesthesiologist I gave patients midazolam (Versed) more than any other medication.  All of these medications are appropriate in certain settings.  Most have a street value. Some have active metabolites that accumulate in the body over time.  All are sedating, all cause tolerance, and all have the potential to cause significant withdrawal symptoms.  The longer-acting medications will self-taper to some extent, but the intermediate-acting agents in particular have the potential to cause withdrawal syndromes that are severe, and even fatal.  The first patient I mentioned has been taking an anticonvulsant since presenting to the ER with a grand mal seizure while stopping Xanax ‘cold turkey.’

All of these medications have appropriate uses, almost always for short-term conditions.  When given long-term they cause problems.  In fact, from the top of my head I can think of 12 reasons to avoid prescribing benzos for ‘anxiety.’

Many anxious patients aren’t truly anxious.  When a patient complains of ‘anxiety’ he/she is often complaining of something else.  If I ask a patient to describe the symptoms without using the word ‘anxiety’, I often find that the patient is bored, restless, angry, depressed, overwhelmed, or appropriately frightened. Take a look at the second patient—the one who is ‘scattered,’ ‘at the end of her rope,’ and ‘caring for a 3-year-old boy all by herself,’ Do you really think she will be a ‘better mom’ if she is taking alprazolam or clonazepam? She is feeling overwhelmed, angry, tired, afraid, hopeless, depressed—feelings that when added together become ‘anxiety.’   Do we really want to give a person in this condition a medication that will make her sleepier, more forgetful, more scattered, and more disinhibited?

Even if we get it right, her relief will be short-lived due to tolerance.  Patients often escalate their dose at some point—no matter how many times they promise that they won’t.  Dose escalation is not the patient’s fault—it is simply what these meds do.  Once a pattern of dose escalation begins, it is difficult to control;   patients will call after two weeks reporting that they are out of alprazolam, and the doctor feels pressured to issue a refill to prevent withdrawal.

Benzos turn manageable anxiety into an anxiety disorder.  Patients get a calming effect from the medication, but as the medication wears off the anxiety returns, including extra anxiety from a ‘rebound effect’—a miniature form of withdrawal.  Patients do not usually attribute that anxiety to rebound, but instead believe they have a horrible anxiety condition that appears as soon as the medication wears off.  When I worked in a maximum security prison for women in Wisconsin many inmates were taking benzos upon arrival; several months after the benzos were discontinued the most amazing thing happened:  the anxiety disorders went away!

A problem specific to addicts is that they don’t take sedative medications to achieve the ‘absence of anxiety,’ but rather they take them until they feel ‘relaxed.’  They are not seeking normalcy—they are seeking relaxation.  There is a difference between the two states; one is feeling normal without feeling excessive worry or panic; the other is feeling ‘relaxed,’ something other than feeling ‘normal.’  This doesn’t make addicts bad people; it is simply a consequence of the conditioning process during addiction.  Addicts are not aware that they are seeking a ‘fuzziness’ that non-addicts often find to be uncomfortable!

Again specific to addicts, benzos (like other medications that have an immediate psychotropic effect) direct the person’s attention inward.  An addict become obsessed with ‘how I feel;’ a goal in treatment is to get the addict out of his or her own head to experience life on life’s terms.  Benzodiazepines encourage the opposite effect, encouraging the addict to focus on internal feelings and sensations.

Addicts with one favored class of drugs, for example opiates, will often move to a different substance when the first drug of choice is removed, for example using Suboxone. This phenomenon is called ‘cross addiction.’

A final concern for addicts is that benzos help preserve the mistaken thought that the person cannot function without ‘taking something.’

Benzos impair driving and have the potential to impair a person working with dangerous machinery.  After all, patients get anxious at work too.  They also make a person appear intoxicated by causing slurred speech, forgetfulness, and sometimes ‘loopy behavior’, risking the person’s job and having other unforeseen consequences.  Some people have completely different personalities when disinhibited by benzos.

Benzos have been linked to fetal anomalies and early miscarriage.

They destroy sleep in the long run through tolerance and through rebound effects.  If the patient takes the benzo during the day, he/she will be trying to sleep just as the sedation is wearing off.  The alternative is to take the medication at bedtime, defeating the goal of finding relief for daytime anxiety.  If the person takes benzos both day and night, tolerance increases even more quickly.

I have already mentioned the need to taper off benzodiazepines and the risk of seizures and worse during withdrawal.

Benzodiazepines may calm a truly anxious patient, but they do not generally increase the patient’s function.  A person who can’t get out of bed becomes less likely to get out of bed.  Bills that are unpaid become even less likely to be paid.  Relationships do not generally improve when one partner is nodding off as the other talks about feelings.

I do prescribe benzodiazepines, usually for the short-term or while recommending they be taken no more than every other day.  Some patients do fine with them, but for others, benzos are a Pandora’s Box that should never be opened.  As a psychiatrist I often resent the treatment that led to the mess that I try my best to clean up— such as the case with the first patient I mentioned.  I think most doctors who read this will understand what I am saying, and many will have similar thoughts about benzodiazepines. Perhaps others will find the use of benzodiazepine much more beneficial than harmful. Comments anyone?

JJ

I wrote this introduction to readers of the Healthcare Professionals Network shortly after the tragic death of pop icon Michael Jackson. As I mulled over a topic and listened to the news reports, I realized that my professional experiences come together in such a fitting way in regard to his life and death that I had to make reference to the tragedy; I apologize for being opportunistic.

Was he happy?

I am a psychiatrist with a psychodynamic approach to diagnosis and treatment. One goal in my work is to provide insight into maladaptive patterns in the way people go about their lives; one goal with the blog will be to take a look at the more obvious examples of psychodynamic principles as they play out in society. The unconscious mind lives in a fantasy world of ‘primary process thinking’ where constraints from time, money, and other ‘buzz-kills’ of mature thought wield no power. We each have our unconscious fantasies, often at conflict with the limitations imposed by adult reality. Michael Jackson was in many ways a man living in a ‘primary process’ world, a ‘Peter Pan’ who never had to mature and face the facts, too wealthy and famous for anyone to stand in his way and say ‘you can’t have a merry-go-round—Grow up!! I will add the important caveat that I never met him, never even met someone who met him, so this is all just a guess. But we do a lot of guessing in psychodynamic psychiatry, so the point is still worth discussing.

My second connection with the Michael Jackson story is that I have significant experience with opiate dependence, and the relationship between opiate dependence and the treatment of chronic pain. I expect (another educated guess) that opiates played a role in Mr. Jackson’s death. I know too well the world of desperate addicts who consciously or unconsciously manipulate others to keep drugs available and keep sickness at bay. And like many physicians who deal with chronic pain, I know the pressure one feels when a patient has paid money in order to receive respite, and complains of aches and pains from years of dancing, spinning, jumping, and kicking—a world that surely left Mr. Jackson with osteoarthritis and chronic pain. Michael Jackson, I would surmise (sounds better than ‘guess’), developed the misguided but common notion that narcotics were appropriate and helpful for such aches and pains, when in reality they are only a seductive pathway to misery and desperation, as tolerance demands higher and higher doses of the narcotics and dependence prevents going without the drugs for longer than a few increasingly-miserable hours.

But there is more. I am Board Certified in Anesthesiology (having taken the Boards back in the days of lifetime certification!) and I worked as an anesthesiologist and pain doc for almost ten years. I pushed a large amount of Diprivan (Propofol) ‘back in the day’, making me more of an expert than many of the TV docs who I heard refer to the milky induction agent as a ‘sleeping medicine’—kind of like calling Fort Knox a ‘piggy bank.’ And the final reason for my connection with Michael Jackson is perhaps the most significant reason: I know how to moon walk. This last point alone puts me in a very select group of physicians—and was, I would again guess, the reason I was given the opportunity to write this blog.

I cannot promise that every blog post will come together in such a fascinating way (just say it—oh puh-leaze!!), but my general approach will be to try to remind the field of psychiatry that even as we learn more about brain function, and even as we develop better medications to treat psychiatric illness, psychiatry will always be a field concerned with the mind. I have a PhD in neuroscience and was, in the 1980s, a ‘grind and bind’ guy; tearing up rat neural membranes, spinning them down, and measuring the binding qualities of various radio-labeled chemicals, so I know the temptation for seeing the brain as a mass of chemical and electrical signals. But no understanding of neurochemistry will come close to explaining the thoughts and emotions of Michael Jackson, particularly in his last days, when he wanted so badly to turn off his brain that he resorted to using an anesthetic induction agent to quiet his thoughts at the end of the day. I have to wonder: were there no nice thoughts to focus on, to help tolerate the nighttime awake? Diprivan hurts when it is injected, and patients often wince in pain as they drift off to sleep in the operating room. But apparently the alternative was even more painful… which brings us back to an interesting thought.

As I said earlier, we all have our unconscious, primary-process fantasies. Some of us fly; I used to have wonderful dreams of jumping so high that I was nearly flying, and in a primary-process world it never hurts to land. Some have fantasies of limitless riches, or perfect love. But a person who had perhaps the best opportunity to live in the world of fantasy—in a world where people only say ‘yes’, and where pet monkeys are only a phone call away—was unable to tolerate such an existence. Why would that be? There is surely an important lesson for all of us in the tragic story of the boy living in Neverland; an ‘aha experience,’ or a moral to the story. I won’t spend any more of our time musing about the answers, since my answers would surely be different than yours. But the fun thing about psychodynamic psychiatry is that there is always a lesson, a story, or an ‘aha experience’ there for the taking for all of us, if we look for it.

JJ