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Guide Pain and Depression: An Antidisciplinary Patient-Centered Approach

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The default position is that the patient must fail, in many cases several times before treatment is funded. All of this financial gaming leaves the addicted patient out in the cold. That starts with inadequate to nonexistent detox to treatment that lacks the necessary intensity to be successful. It can also create a very negative and counterproductive attitude by the system of care to the patient with the problem.

I just completed a formal presentation this morning at about AM. It was in a big conference room at a plush hotel near the Mall of America. There was a little pressure because I was the lead off man in terms of the scheduled presentations. I walked into the venue early and got up on the stage. It was a black elevated platform about 25 feet square. It looked like it was built to be portable. There was a lectern with a fixed microphone.

The platform was positioned between two large 20 x 25 foot screens. In order to see the screens or use a laser pointer, I had to walk out from behind the lectern to bring me about 12 feet away from the back wall. I looked out over the audience filing into to 4 sections of tables and thought: "Not the most convenient set up - but I have done this before.

Labels: death anxiety , existentialism , neurosis , performance anxiety , PowerPoint , presentation anxiety , presentations. Sunday, June 15, The Denial of Plasticity. For the past couple of months, I have spent a lot of my free time working on a presentation on neurobiology. The presentation is the lead off in a series of lectures on addiction and the target audience is primary care physicians.

I have a lot of experience with this topic because I give a very similar lecture at least six times a year to physicians and other professionals who take a course on the treatment of addiction at the facility where I work. Incorporating some of the most recent data on these topics is always a challenge and I depend a lot on Nature , Science , and Neuron for the latest reviews, research and commentaries. In order to make it more relevant I ran across a collection of article in Frontiers in Psychiatry on the issue of whether or not addiction is a disease or not and it seems like a lot of that has to do with neurobiology.

Neurobiology has also become en vogue in many ways. There is a conference posted in my clinic entitled "The Neurobiology of Play Therapy". I thought I would post my observations of the implications of neurobiology in addiction and psychiatry. Labels: addiction , addiction as a disease , disease model , Frontiers in Psychiatry , medical model , organic-functional dichotomy , plasticity. The Department of Justice came out with a report this week on the way that psychiatric problems are being managed in the LA County Jail.

There were 15 deaths by suicide in 30 months and the conclusion was that several of those deaths were preventable. By previous agreement, the county had demonstrated compliance with suggested measures including the development of a robust electronic health record. Unfortunately there is no obviously available detailed report on the findings at this time, but I have requested it through their web site. The issue of psychiatric services being provided in county jails is a national scandal that hardly anyone seems to care about. In terms of awareness it is probably well below the issue of mass shootings by people with mental illnesses.

Why is that important?

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There are several issues that never seem to be mentioned in the press. The first and foremost is how psychiatric services have been excised from clinics and hospitals by managed care companies - especially complex psychiatric issues. Anyone who cannot be seen in a minutes brief discussion about medications usually gets the message that they need to get services elsewhere.

Their stays are often complicated by a lack of available legal and financial resources that increase their stay times in jail. The following table is based on data in Forbes magazine and corroborated by other sources describing the total populations in these facilities. LA County Jail. Harris County Jail Texas. Cook County Jail Chicago. Maricopa County Jail Arizona. Miami Dade County Jail. Orange County California. Labels: beds , humanistic care , incarceration , mental illness , mental illness in jails. People certainly know how to spin drug studies.

The debate over "old" versus "new" or typical versus atypical antipsychotics always seems to contain an element of marketing and somebody pushing an agenda. Reality in those analyses is always lacking and the spin on the issue of older antipsychotics haloperidol and fluphenazine versus the newer risperidone and paliperidone is problematic especially when the conclusion is that there is no reason to use newer second or third generation antipsychotics.

It also points out the difference between clinical experience and clinical trials. Clinical experience is often minimized as being "anecdotal" but at some point anecdotal becomes statistically significant. That has been my experience with typical or first generation antipsychotics and neurological side effects. In looking at the results of the drug trials it might be interesting to look at the agendas of various parties involved. Certainly the pharmaceutical manufacturers want their products to look as good as possible. But there are also clear agendas on the part of the investigators, even when the financial conflict of interest is eliminated.

Investigators with the view that schizophrenia is largely a disorder that can be adequately treated with an antipsychotic medication and that medication adherence is a big part of that treatment is certainly one interest. The idea that intramuscular injections is the best way to do this is another. I recall listening to some of these investigators talk about how this is good for the patient, not that painful and there why wouldn't a psychiatrist recommend an injectable medication as soon as it was shown that the medication was tolerated in the oral form.

They seem to suggest that the patient would actually want the injection. In my experience, nobody does. Who would want to take monthly painful intramuscular IM injections for the foreseeable future? I have seen people come to that conclusion, but they need to accumulate a significant amount of equally painful evidence related to missing oral doses of medication.

The argument about long acting injectables has take on a new dimension with the availability of long acting naltrexone Vivitrol injections. This medication is one approach to the treatment of opioid use disorders and it is very effective for some some people.

If opioids do not produce the expected euphoria there is no incentive to keep taking them. It also reduces the rate of accidental opioid overdose. Following detoxification, many people are taken off the medications that they were using in high doses. At the time of discharge, there is a real risk that many will attempt to go back to using the amount of opioids that they were using. If their tolerance is gone that creates the potential for opioid overdose and death.

The nature of addiction prevent many people from using substitution therapies like buprenorphine or methadone. Long acting naltrexone injections can be painful, but many people with opioid addiction realize it is their best chance to stop their ongoing addiction and avoid the complications of overdose including death. The neurological side effects of older antipsychotics are usually ignored or minimized in the debate of old versus new medications. They were the largest single side effect problem facing psychiatrists years ago.

I can recall the experience of stabilizing people with severe bipolar disorder on an antipsychotic medication and a mood stabilizer and by the time they came back to see me in clinic they had developed tardive dyskinesia or some other movement disorder like akathisia or drug induced Parkinson's syndrome. In the worst case scenario the movement disorder would not completely resolve with modification of the therapy or discontinuation of the antipsychotic medication.

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The treatment of tardive dyskinesia after it has developed is problematic. For anyone who continues to need the medication clozapine is the treatment of choice. Clozapine is highly regarded by experts treating schizophrenia because of its use in treatment resistant cases, protective effects against suicide, and use with movement disorders.

Those same experts often suggest that it is not used soon enough by front line clinicians, but it does have a unique set of liabilities in terms of metabolic and cardiac side effects and the need for white blood cell monitoring for the duration of use. Technically, the medication should not be dispensed to the patient unless their absolute neutrophil count is known at the exact days suggested in the protocol.

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Drug induced movement disorders can be much more than a cosmetic problem depending on your sensitivity to the medication. Although it rarely happens, I have treated patients with psychosis who had severe drug induced tardive syndromes that were identical to severe Parkinson's disease and who continued to have severe symptoms of psychosis. I would typically see patients with movement disorders because of my interest in the area, so I was seeing a large number of severe cases, but even rare cases of movement disorder related disability leave an impression. I have low threshold for discontinuing antipsychotic medication and would not use an antipsychotic medication when there is another option available.

The best case in point is the current practice of augmenting antidepressant medications with an atypical antipsychotic. I have used these augmentation strategies, but only after other options were exhausted and the patient was educated about the potential problems.

Even then, there is the risk that the pateint will not follow through with reporting the problems or stopping the medication does not have an effect on the movements.

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My read of this study is that the authors were sensitive to the issue of comparison studies between atypical antipsychotics and doses of the typical antipsychotic haloperidol that were designed to bias the neurological side effect results toward the newer medications. Haloperidol is a potent antipsychotic medication with significant neurological side effects even at low doses. In this study the authors chose perphenazine as the older antipsychotic medication because of its more moderate side effect profile.

Perphenazine also received special treatment in this study as indicated by the following 6 excerpts from the body of the paper: "Patients were initially randomly assigned to receive olanzapine, perphenazine, quetiapine, or risperidone under double-blind conditions and followed for up to 18 months or until treatment was discontinued for any reason phase 1.


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Despite this finding, more patients discontinued perphenazine than other medications owing to extrapyramidal effects. On the time to medication discontinuation olanzapine was significantly better than perphenazine. There were no differences on what are admittedly crude secondary measures and on those measures and efficacy perphenazine appeared to be as good as questiapine, ziprasidone and risperidone.

The actual study results of CATIE were widely interpreted as older antipsychotics "being as good as" newer antipsychotics.


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The usual conspiracy theories about pharmaceutical companies making billions from new drugs that were "no better" than the old drugs was in play. Grist for the popular press with the subtext that the gullible or greedy psychiatrists have been duped again. Even a cursory reading of the CATIE excerpts should suggest that the researchers here attempted to compensate for the tendency of perphenazine to cause neurological side effects and even then they could not prevent it.

They clearly did not want anyone with tardive dyskinesia to take perphenazine. Having personally practiced during that time both of those statements make perfect sense to me. The people with no expertise and no experience can always come up with a sensational theory of headline for one reason or another. Nobody should doubt that newer antipsychotic agents are a significant therapeutic advance in terms of neurological side effects. As an expert, I cannot think of a reason why I would prescribe a first generation antipsychotic.

I still see some opinions about using chlorpromazine for sleep, or other psychiatric conditions. There are some first generation antipsychotics that should not be prescribed to human beings. Only their low frequency of use keeps the FDA from pulling them off the market. I digressed on the issue of neurological side effects because it is one of the main contentions of the Goff editorial on typical versus atypical long acting injections.

In the actual study by McEvoy, haloperidol at the low end of the dosing spectrum did lead to significantly more neurological side effects: "Treatment discontinuations due to neurologic adverse effects according to clinician judgment were as follows: 2 patients 1. The study also borrows some of the logic from the CATIE study in discussing neurological side effects:. How might statistical significance be relevant here? The other interesting aspect of the McEvoy paper is that it references randomized clinical trials showing that long acting injectable medications add nothing in terms of reducing the frequency of hospitalization.

That is a useful fact compared with some experts who claim otherwise. First, the medication focus is not that intense. The researcher stake an approach to prescribing that is about as rigorous as the average clinician. Average clinicians do check prolactin levels but usually only when there is an indication and that will typically call for a more intensive intervention to treat the side effect. Whenever I look at samples of hundreds of people, I know that the metabolism of the drug in that sample is not going to be uniform and that accounts for a lot of the neurological side effects.

Given the reasonable costs of therapeutic drug monitoring, it is curious that is never done in these trials. Unlike observation of prolactin levels, it could result in something actually being done like lowering the dose of a medication. Second, now that we have interventions to prevent complications should they be incorporated into the clinical trials? In the McEvoy study, should all of the patients have been coached on metabolic syndrome and strategies to prevent weight gain? Are we past the point where informed consent and the idea that we are observing the effect of a medication alone enough these days?

Should Human Subjects Committees start introducing that idea? After all the neurological side effects were treated with a medication. What about the metabolic side effects? The bottom line for me is that there is no reason for prescribing first generation antipsychotics, unless a person has been stable on them for years and is not experiencing side effects.

Comparisons for academic purposes are interesting, but they lead to misinterpretations by both the media and managed care entities.

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Psychopharmacology trials remain fairly primitive and they are a blunt instrument compared with clinical experience dealing with the neurological side effects of first generation antipsychotics. Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. N Engl J Med. Epub Sep Erratum in: N Engl J Med. Effectiveness of paliperidone palmitate vs haloperidol decanoate for maintenance treatment of schizophrenia: a randomized clinical trial. The neuropathology of schizophrenia. A critical review of the data and their interpretation.

Neuropathology of schizophrenia: a mini review. I would say - probably when you have personally treated thousands of patients more than are in any clinical trial you are reading about - across multiple settings. At that point, your clinical experience and the conclusions that you draw from it are probably more valid than PANNS, extrapyramidal side effects and CGI ratings.

So-called patient management problems have been building up on us over the past 30 years. I first encountered them in the old Scientific American Medicine Text. To nonphysicans reading this they are basically hypothetical patient encounters that claim to be able to rate your responses to fragments of the entire patient story in such a way that it is a legitimate measure of your clinical acumen.

I am skeptical of that claim at best and hope to illustrate why. Consider a recent patient management problem for psychiatrists in the most recent issue of Focus, the continuing education journal of the American Psychiatric Association APA. I like Focus and consider it to be a first rate source of the usual didactic continuing medical education CME materials.

Read the article, recognize the concepts and take the CME test. This edition emphasized the recognition and appropriate treatment of Bipolar II Disorder and it provided an excellent summary of recent clinical trials and treatment recommendations. The patient management problem was similarly focused. It began with a brief descriptions of a young women with depression, low energy, and hypersomnia.

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It listed some of her past treatment experience and then listed for the consideration of the reader, several possible points in the differential diagnosis including depression and bipolar disorder, but also hypersomnia-NOS, obstructive sleep apnea, disorder and a substance abuse problem. I may not be the typical psychiatrist but after a few bits of information, I would not be speculating on a substance abuse problem and would not know what to make of a hypersomnia-NOS differential diagnosis. Like most experts, I have found that the best way to proceed is to move form one clump of data to the next and not go through and exhaustive checklist or series of parallel considerations.

The other property of expert diagnosticians is their pattern matching ability. Pattern matching consists of rapid recognition of diagnostic features based on past experience and matching them to those cases, treatments and outcomes. Pattern matching also leads to rapid rule outs based on incongruous features, like an allegedly manic patient with aphasia rather than a formal thought disorder. If I see a pattern that looks like it may be bipolar disorder, the feature that I immediately hone in on is whether or not the patient has ever had a manic episode.

That is true whether they tell me that they have a diagnosis of bipolar disorder or not. I am looking for a plausible description of a manic episode and the less cued that description the better. I have seen evaluations that in some cases say: "The patient does not meet criteria for bipolar disorder. I need to hear a pretty good description of a manic episode, before I start asking them about specific details.

I should have enough interview skills to get at that description. The description of that manic episode should also meet actual time criteria for mania. Not one hour or four hours but at least 4 days of a clear disturbance in mood. I recall reading a paper by Angst, one of Europe's foremost authorities on bipolar disorder when he proposed that time criteria based on close follow up of his research patients and I have been using it ever since.

In my experience practically all substance induced episodes of hypomania never meet the time criteria for a hypomanic episode. There is also the research observation that many depressed patient have brief episodes of hypomania, but do not meet criteria for bipolar disorder. I am really focused on this cluster of data. On the patient management problem, I would not get full credit for my thinking because I am only concerned about hypersomnia when I proceed to that clump of sleep related data and I am only concerned about substance use problems when I proceed to that clump of data.

The patient management problem seems more like a standardized reading comprehension test with the added element that you have to guess what the author is thinking. The differential diagnosis points are carried forward until additional history rules them out and only bipolar II depression remains. At that point the treatment options are considered, three for major depression an antidepressant that had been previously tried, an antidepressant combination, electroconvulsive therapy, and quetiapine and one for bipolar II depression.

The whole point of the previous review is that existing evidence points to the need to avoid antidepressants in acute treatment and that the existing relatively weak data favors quetiapine. The co-occurrence of pain and depression is well known but a detailed understanding of their phenomenology, interrelationship, and effective therapies remains speculative.

This book provides a synthetic approach to the evaluation and treatment of patients with chronic pain and depression that will generate therapeutic optimism and lead clinicians to improve quality of life and restore function. The recognition that depression is not just an affective disorder or demoralization is discussed in detail in the contributions: "Function, Disability, and Psychological Well-Being" and in "Structural Models of Comorbidity among Common Mental Disorders: Connections to Chronic Pain".

Other articles review the complex regional pain syndrome and the Gulf War syndrome. Further papers discuss issues relating to the use of opioids in the treatment of chronic pain.

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Categories: Psychology. ISBN Series: Advances in Psychosomatic Medicine.

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