This is a continuation of my thoughts about this subject.
Statistical analysis is extremely important to understand cause & effect! A very strong factor in this issue has to do with the way the human mind interprets data; Daniel Kahneman, the Nobel laureate psychologist, is a great expert on this subject, and I strongly recommend a fantastic book of his called Thinking, Fast and Slow. I'd like to review his book in much more detail later, but as a start I will say that it clearly shows how the mind is loaded with powerful biases, which cause us to make rapid but erroneous impressions about cause & effect, largely because a statistical treatment of information is outside the capacity of the rapid reflexive intuition which dominates our moment-to-moment cognitions. And, of course, a lack of education about statistics and probability eliminates the possibility that the more rational part of our minds can overrule the reflexive, intuitive side. Much of Kahneman's work has to do with how the mind intrinsically attempts to make sense of statistical information -- often with incorrect conclusions. The implication here is that we must cooly calculate probabilities in order to interpret a body of data, and resist the urge to use "intuition," especially in a research study.
I do believe that a formal statistical treatment of data is much more common now in published research. But I am now going to argue for something that seems entirely contradictory to what I've just said above! I'll proceed by way of a fictitious example:
Suppose 1000 people are sampled, (the sample size being carefully chosen using a statistical calculation, to elicit a significant effect size if truly present with a small probability of this effect being due to chance), all of whom with a DSM diagnosis of major depressive disorder, all of whom with HAM-D scores between 25 and 30. And suppose they are divided into two groups of 500, matched for gender, demographics, severity, chronicity, etc. Then suppose one group is given a treatment such as psychotherapy or a medication, and the other group is given a placebo treatment. This could continue for 3 months, then the groups could be switched, so that every person in the study would at some point receive the active treatment and at another point the placebo.
This is a typical design for treatment studies, and I think it is very strong. If the result of the study is positive, this is very clear evidence that the active treatment is useful.
But suppose the result of the study is negative. What could this mean? Most of us would conclude that the active treatment is therefore not useful. --But I believe this is an incorrect conclusion!--
Suppose, yet again, that this is a study of people complaining of severe headaches, carefully controlled for matching severity and chronicity, etc. And suppose the treatment offered was neurosurgery or placebo. I think that the results-- carefully summarized by a statistical statement--would show that neurosurgery does not exceed placebo (in fact, I'll bet the neurosurgery group would do a lot worse!) for treatment of headache.
Yet -- in this group of 1000 people, it is possible that 1 or 2 of these headache sufferers was having a headache due to a surgically curable brain tumor, or a hematoma. These 1 or 2 patients would have a high chance of being cured by a surgical procedure, and some other therapy effective for most other headache sufferers (e.g. a tryptan for migraine, or an analgesic, or relaxation exercises, etc.) would have either no effect or would have a spurious benefit (relaxation might make the headache pain from a tumor temporarily better -- and ironically would delay a definitive cure!)
Likewise, in a psychiatric treatment study, it may be possible that subtypes exist (perhaps based on genotype or some other factor currently not well understood), which respond very well to specific therapies, despite the majority of people in the group sharing similar symptoms not responding well to these same therapies. For example, some individual depressed patients may have a unique characteristic (either biologically or psychologically) which might make them respond to a treatment that would have no useful effect for the majority.
With the most common statistical analyses done and presented in psychiatric and other medical research studies, there would usually be no way to detect this phenomenon: negative studies would influence practitioners to abandon the treatment strategy for the whole group.
How can this be remedied? I think the simplest method would be trivial: all research studies should include in the publication every single piece of data gathered! If there is a cohort of 1000 people, there should be a chart or a graph showing the symptom changes over time of every single individual. There would be a messy graph with 1000 lines on it (which is a reason this is not done, of course!) but there would be much less risk that an interesting outlier would be missed! If most of the thousand individuals had no change in symptoms, there would be a huge mass of flat lines across the middle of the chart. But if a few individuals had a total, remarkable cure of symptoms, these individuals would stand out prominently on such a chart. Ironically, in order to detect such phenomena, we would have to temporarily leave aside the statistical tools which we had intended to use, and "eyeball" the data. So intuition could still have a very important role to play in statistics & research!
After "eyeballing" the complete setof data from every individual, I do agree that this would have to lead to another formal hypothesis, which would subsequently have to be tested using a different study design, designed specifically to pick up such outliers, then a formal statistical calculation procedure would have to be used to evaluate whether the treatment would be effective for this group. (e.g. the tiny group of headache sufferers specifically with a mass evident on a CT brain scan could enter a neurosurgery treatment study, to clearly show whether the surgery is better than placebo for this group).
I suspect that in many psychiatric conditions, there are subtypes not currently known about or well-characterized by DSM categorization. Genome studies should be an interesting area in the future decades, to further subcategorize patients sharing identical symptoms, but who might respond very differently to specific treatment strategies.
In the meantime, though, I think it is important to recognize that a negative study, even if done with very good study design and statistical analysis, does not prove that the treatment in question is ineffective for EVERYONE with a particular symptom cluster. There might possibly be individuals who would respond well to such a treatment. We could know this possibility better if the COMPLETE set of data results for each individual patient were published with all research studies.
Another complaint I have about the statistics & research culture has to do with the term "significant." I believe that "significance" is a construct that contradicts the whole point of doing a careful statistical analysis, because it requires a pronouncement of some particular probability range being called "significant" and others "insignificant." Often times, a p value less than 0.05 is considered "significant". The trouble with this is that the p value speaks for itself, it does not require a human interpretive construct or threshold to call something "significant" or not. I believe that studies should simply report the p-value, and not call the results "significant" or not. This way, 2 studies which yield p values of 0.04 and 0.07 could be seen to show much more similar results than if you called the first study "significant" and the second "insignificant." There may be some instances in which a p-value less than 0.25 could still usefully guide a long-shot trial of therapy -- this p value would be very useful to know exactly, rather than simply reading that this was a "very insignificant" result. Similarly, other types of treatments might demand that the p value be less than 0.0001 in order to safely guide a decision. Having a research culture in which p<0.05="significant" dilutes the power and meaning of the analysis, in my opinion, and arbitrarily introduces a type of cultural judgment which is out of place for careful scientists.
Monday, February 13, 2012
Tuesday, February 7, 2012
How long does it take for psychotherapy to work?
There are various research articles done in the past which describe rates of change in psychotherapy patients, some studies for example describing a plateau after about 25 sessions or so. I find these studies very weak, because of the multitude of confounding factors: severity and chronicity are obvious variables, also the type of follow-up assessments done.
In the CBT literature, a typical trial of therapy is perhaps 16-20 sessions.
In light of our evolving knowledge of neuroplasticity, and our breadth of understanding about education & learning, it seems to me that the most important variable of all is the amount of focused, deliberate practice time spent in a therapeutic activity. Oddly, most psychotherapy studies--even CBT studies--do not look at how many hours of practice patients have done in-between therapy appointments. This would be like looking at the progress of music students based on how many lessons they get, without taking into account how much they practice during the week.
I have often compared psychological symptom change to the changes which occur, for example, with language learning or with learning a musical instrument.
So, I believe that a reasonable estimate of the amount of time required in psychotherapy depends on what one is trying to accomplish:
-Some types of therapeutic problems might be resolved with a few hours of work, or with a single feedback session with a therapist. This would be akin to a musician with some kind of technical problem who needs just some clear instruction about a few techniques or exercises to practice. Or it might be akin to a person who is already fluent in a foreign language, but needs a few tips from a local speaker about idioms, or perhaps some help with editing or grammar in a written text.
-Many more therapeutic problems could improve with perhaps 100 hours of work. This would be like learning to swim or skate competently if you have never done these activities before. Regular lessons ("therapy") would most likely speed up your rate of progress substantially. But most of those 100 hours would be practice on your own, unless you're okay with the progress taking place over a year or more. With the language analogy, think of how fluent you might become in a foreign language with 100 hours of focused, deliberate practice. For most of us, this would lead to an ability to have a very simple conversational exchange, perhaps to get around in the most basic way in another country.
-A much larger change is possible with 1000 hours of work: with music, one could become quite fluent but probably not an expert. With a foreign language, comfortable fluency would probably be possible, though probably still with an accent and a preference for the old language.
-With 5000-10000 hours of work (this is several hours per day over a decade or more) one could become an expert at a skill or a language in most cases.
In psychotherapy, another confound though is whether the times in-between "practice sessions" lead to a regression of learning. An educational analogy would be of practicing math exercises an hour per day with a good teacher, but then practicing another 8 hours a day with another teacher whose methods contradict the first. Often times, learning will still take place with this paradigm, but it might be much less efficient. Persistent mental habits, in the context of mental illnesses, can be akin to the "second teacher" in this metaphor, and unfortunately they do tend to plague people for many hours per day.
This reminds me of the evolving evidence about stroke rehabilitation & neuroplasticity: substantial brain change can happen in as short a time as 16 days--but it requires very strict inhibition or constraint of the pathways which obstruct rehabilitation. (note: 16 days of continuous "immersion" = 16*24 = 384 hours!) In stroke rehabilitation, the neuroplasticity effect is much more pronounced if the unaffected limb is restrained, compelling the brain to optimize improvement in function of the afflicted limb. Here is a recent reference showing rapid brain changes following limb immobilization: http://www.ncbi.nlm.nih.gov/pubmed/22249495
In conclusion, I believe that it is important to have a clear idea about how much time and deliberate, focused effort are needed to change psychological symptoms or problems through therapeutic activities. A little bit of meaningful change could happen with just a few hours of work. In most cases, 100 hours is needed simply to get started with a new skill. 1000 hours is needed to become fluent. And 5000-10000 hours is needed to master something. These times would be much longer still if the periods between practice sessions are regressive. In the case of addictions, eating disorders, self-harm, or OCD, for example, relapses or even fantasies about relapse will substantially prolong the time it takes for any therapeutic effort to help. Of course, it is the nature of these problems to have relapses, or fantasies about relapse--so one should let go of the temptation to feel guilty if there are relapses. But if one is struggling with an addictive problem of this sort, it may help to remind oneself that the brain can change very substantially if one can hold onto to quite a strict behavioural pattern for the hundreds or thousands of hours which are needed.
As a visual reminder of this process, start with an empty transparent bottle, which can hold 250-500 mLof liquid (1-2 cups), and which can be tightly sealed with a small cap. Add one drop of water every time you invest one hour of focused, deliberate therapeutic work. The amount of time you need to spend in therapy depends on your goal. If the goal is total mastery--then you must fill the entire bottle. If simple competence in a new skill is an adequate goal, then you must fill just the cap of the bottle. If there are activities in your day which contradict the therapeutic work, it would be like a little bit of water leaking out of your bottle. So you must also attend to repairing any "leaks." But every hour of your effort counts towards your growth.
In the CBT literature, a typical trial of therapy is perhaps 16-20 sessions.
In light of our evolving knowledge of neuroplasticity, and our breadth of understanding about education & learning, it seems to me that the most important variable of all is the amount of focused, deliberate practice time spent in a therapeutic activity. Oddly, most psychotherapy studies--even CBT studies--do not look at how many hours of practice patients have done in-between therapy appointments. This would be like looking at the progress of music students based on how many lessons they get, without taking into account how much they practice during the week.
I have often compared psychological symptom change to the changes which occur, for example, with language learning or with learning a musical instrument.
So, I believe that a reasonable estimate of the amount of time required in psychotherapy depends on what one is trying to accomplish:
-Some types of therapeutic problems might be resolved with a few hours of work, or with a single feedback session with a therapist. This would be akin to a musician with some kind of technical problem who needs just some clear instruction about a few techniques or exercises to practice. Or it might be akin to a person who is already fluent in a foreign language, but needs a few tips from a local speaker about idioms, or perhaps some help with editing or grammar in a written text.
-Many more therapeutic problems could improve with perhaps 100 hours of work. This would be like learning to swim or skate competently if you have never done these activities before. Regular lessons ("therapy") would most likely speed up your rate of progress substantially. But most of those 100 hours would be practice on your own, unless you're okay with the progress taking place over a year or more. With the language analogy, think of how fluent you might become in a foreign language with 100 hours of focused, deliberate practice. For most of us, this would lead to an ability to have a very simple conversational exchange, perhaps to get around in the most basic way in another country.
-A much larger change is possible with 1000 hours of work: with music, one could become quite fluent but probably not an expert. With a foreign language, comfortable fluency would probably be possible, though probably still with an accent and a preference for the old language.
-With 5000-10000 hours of work (this is several hours per day over a decade or more) one could become an expert at a skill or a language in most cases.
In psychotherapy, another confound though is whether the times in-between "practice sessions" lead to a regression of learning. An educational analogy would be of practicing math exercises an hour per day with a good teacher, but then practicing another 8 hours a day with another teacher whose methods contradict the first. Often times, learning will still take place with this paradigm, but it might be much less efficient. Persistent mental habits, in the context of mental illnesses, can be akin to the "second teacher" in this metaphor, and unfortunately they do tend to plague people for many hours per day.
This reminds me of the evolving evidence about stroke rehabilitation & neuroplasticity: substantial brain change can happen in as short a time as 16 days--but it requires very strict inhibition or constraint of the pathways which obstruct rehabilitation. (note: 16 days of continuous "immersion" = 16*24 = 384 hours!) In stroke rehabilitation, the neuroplasticity effect is much more pronounced if the unaffected limb is restrained, compelling the brain to optimize improvement in function of the afflicted limb. Here is a recent reference showing rapid brain changes following limb immobilization: http://www.ncbi.nlm.nih.gov/pubmed/22249495
In conclusion, I believe that it is important to have a clear idea about how much time and deliberate, focused effort are needed to change psychological symptoms or problems through therapeutic activities. A little bit of meaningful change could happen with just a few hours of work. In most cases, 100 hours is needed simply to get started with a new skill. 1000 hours is needed to become fluent. And 5000-10000 hours is needed to master something. These times would be much longer still if the periods between practice sessions are regressive. In the case of addictions, eating disorders, self-harm, or OCD, for example, relapses or even fantasies about relapse will substantially prolong the time it takes for any therapeutic effort to help. Of course, it is the nature of these problems to have relapses, or fantasies about relapse--so one should let go of the temptation to feel guilty if there are relapses. But if one is struggling with an addictive problem of this sort, it may help to remind oneself that the brain can change very substantially if one can hold onto to quite a strict behavioural pattern for the hundreds or thousands of hours which are needed.
As a visual reminder of this process, start with an empty transparent bottle, which can hold 250-500 mLof liquid (1-2 cups), and which can be tightly sealed with a small cap. Add one drop of water every time you invest one hour of focused, deliberate therapeutic work. The amount of time you need to spend in therapy depends on your goal. If the goal is total mastery--then you must fill the entire bottle. If simple competence in a new skill is an adequate goal, then you must fill just the cap of the bottle. If there are activities in your day which contradict the therapeutic work, it would be like a little bit of water leaking out of your bottle. So you must also attend to repairing any "leaks." But every hour of your effort counts towards your growth.
Monday, February 6, 2012
Scopolamine for Depression
Scopolamine is an acetylcholine-receptor blocker, which is usually used to treat or prevent motion sickness. Some recent studies show that it might be useful to treat depression. Here is some background, followed by a few references to research studies:
The old tricyclic antidepressants (such as amitriptyline) were shown over many years to work very well for many people. Unfortunately, they are laden with side-effect problems and a significant toxicity risk (they can be lethal in overdose). The side effects are due to various different pharmacologic effects, particularly the blockade of acetylcholine and histamine receptors. Newer antidepressants, such as those in the SSRI group, have very few such receptor blockade effects.
In some studies, however, the old tricyclics actually are superior to newer antidepressants, especially for severely ill hospitalized depression patients.
It is interesting to consider whether some of the receptor blockade effects which were previously considered just nuisances or side-effect problems, could actually be part of the antidepressant activity. Or, in some cases, drugs which primarily have receptor blockade side effects may actually be indirectly modulating various other neurotransmitter systems.
A clear precedent exists in this regard: clozapine is undoubtedly the most effective antipsychotic, but it is loaded with multiple side effects and receptor blockades. It may be --at least in part-- because of the receptor blockades, not in spite of them, that it works so well.
Another example of this effect, quite possibly, is related to what I call the "active placebo" literature (I have referred to it elsewhere on this blog: http://garthkroeker.blogspot.com/2009/03/active-placebos.html) The active placebos used in these studies usually had side effects due to acetylcholine blockade, and the active placebo groups usually improved quite a bit more than those with inert placebos. This suggests another interpretation of the "active placebo" effect: perhaps it is not simply the existence of side-effects that psychologically boosts a placebo effect here, it is that the side-effects themselves are due to a pharmacologic action that is actually of direct relevance to the treatment of depression.
Here are some studies looking at scopolamine infusions to treat depression:
http://www.ncbi.nlm.nih.gov/pubmed/17015814
This 2006 study from Archives of General Psychiatry showed that 4 mcg/kg IV infusions of scopolamine (given in 3 doses, every 3-5 days) led to a rapid reduction in depression symptoms (halving of the MADRS score), with a pronounced difference from placebo. Of particular note is that the cohort consisted mainly of chronically depressed patients with comorbidities and unsuccessful trials of other treatments. Surprisingly, there were few side effect problems, aside from a higher rate of the expected anticholinergic-induced dry mouth and dizziness.
http://www.ncbi.nlm.nih.gov/pubmed/20074703
This is a replication of the study mentioned above, published in Biological Psychiatry in 2010.
http://www.ncbi.nlm.nih.gov/pubmed/20736989
Another similar study, this time showing a greater effect in women; again a 4 mcg/kg infusion protocol was used.
http://www.ncbi.nlm.nih.gov/pubmed/20926947
evidence from an animal study that scopolamine --or acetylcholine blockade in general-- affects NMDA-related activity, in general antagonizing the effects of NMDA. This is consistent with a theory that scopolamine may work in a similar manner to the NMDA-blocker ketamine (which has been associated with rapid improvement in depression symptoms) but without nearly as much risk of dangerous medical or neuropsychiatric side-effects.
http://www.ncbi.nlm.nih.gov/pubmed/21306419
This article looks at the pharmacokinetics of infused scopolamine, and also gives a detailed account of side-effects. There are notable cognitive side-effects, such as reduced efficiency of short-term memory.
http://www.ncbi.nlm.nih.gov/pubmed/16719539
This study looks at dosing scopolamine as a patch. The patch is designed to give a rapidly absorbed loading dose, then a gradual release to maintain a fairly constant level over 3 days. My own estimation, based on reviewing this information, is that a scopolamine patch would roughly approximate the IV doses used in the depression treatment studies described above, though of course the serum levels would be more constant.
Transdermal scopolamine (patches) are available in Canada from pharmacists without a physician's prescription.
While this is an interesting--though far from proven-- treatment idea, it is very important to be aware of anticholinergic side effects, which at times could be physically and psychologically unpleasant. At worst, cognitive impairment or delirium could occur as a result of excessive cholinergic blockade. Therefore, any attempt to treat psychiatric symptoms using anticholinergics should be undertaken with close collaboration with a psychiatrist.
The old tricyclic antidepressants (such as amitriptyline) were shown over many years to work very well for many people. Unfortunately, they are laden with side-effect problems and a significant toxicity risk (they can be lethal in overdose). The side effects are due to various different pharmacologic effects, particularly the blockade of acetylcholine and histamine receptors. Newer antidepressants, such as those in the SSRI group, have very few such receptor blockade effects.
In some studies, however, the old tricyclics actually are superior to newer antidepressants, especially for severely ill hospitalized depression patients.
It is interesting to consider whether some of the receptor blockade effects which were previously considered just nuisances or side-effect problems, could actually be part of the antidepressant activity. Or, in some cases, drugs which primarily have receptor blockade side effects may actually be indirectly modulating various other neurotransmitter systems.
A clear precedent exists in this regard: clozapine is undoubtedly the most effective antipsychotic, but it is loaded with multiple side effects and receptor blockades. It may be --at least in part-- because of the receptor blockades, not in spite of them, that it works so well.
Another example of this effect, quite possibly, is related to what I call the "active placebo" literature (I have referred to it elsewhere on this blog: http://garthkroeker.blogspot.com/2009/03/active-placebos.html) The active placebos used in these studies usually had side effects due to acetylcholine blockade, and the active placebo groups usually improved quite a bit more than those with inert placebos. This suggests another interpretation of the "active placebo" effect: perhaps it is not simply the existence of side-effects that psychologically boosts a placebo effect here, it is that the side-effects themselves are due to a pharmacologic action that is actually of direct relevance to the treatment of depression.
Here are some studies looking at scopolamine infusions to treat depression:
http://www.ncbi.nlm.nih.gov/pubmed/17015814
This 2006 study from Archives of General Psychiatry showed that 4 mcg/kg IV infusions of scopolamine (given in 3 doses, every 3-5 days) led to a rapid reduction in depression symptoms (halving of the MADRS score), with a pronounced difference from placebo. Of particular note is that the cohort consisted mainly of chronically depressed patients with comorbidities and unsuccessful trials of other treatments. Surprisingly, there were few side effect problems, aside from a higher rate of the expected anticholinergic-induced dry mouth and dizziness.
http://www.ncbi.nlm.nih.gov/pubmed/20074703
This is a replication of the study mentioned above, published in Biological Psychiatry in 2010.
http://www.ncbi.nlm.nih.gov/pubmed/20736989
Another similar study, this time showing a greater effect in women; again a 4 mcg/kg infusion protocol was used.
http://www.ncbi.nlm.nih.gov/pubmed/20926947
evidence from an animal study that scopolamine --or acetylcholine blockade in general-- affects NMDA-related activity, in general antagonizing the effects of NMDA. This is consistent with a theory that scopolamine may work in a similar manner to the NMDA-blocker ketamine (which has been associated with rapid improvement in depression symptoms) but without nearly as much risk of dangerous medical or neuropsychiatric side-effects.
http://www.ncbi.nlm.nih.gov/pubmed/21306419
This article looks at the pharmacokinetics of infused scopolamine, and also gives a detailed account of side-effects. There are notable cognitive side-effects, such as reduced efficiency of short-term memory.
http://www.ncbi.nlm.nih.gov/pubmed/16719539
This study looks at dosing scopolamine as a patch. The patch is designed to give a rapidly absorbed loading dose, then a gradual release to maintain a fairly constant level over 3 days. My own estimation, based on reviewing this information, is that a scopolamine patch would roughly approximate the IV doses used in the depression treatment studies described above, though of course the serum levels would be more constant.
Transdermal scopolamine (patches) are available in Canada from pharmacists without a physician's prescription.
While this is an interesting--though far from proven-- treatment idea, it is very important to be aware of anticholinergic side effects, which at times could be physically and psychologically unpleasant. At worst, cognitive impairment or delirium could occur as a result of excessive cholinergic blockade. Therefore, any attempt to treat psychiatric symptoms using anticholinergics should be undertaken with close collaboration with a psychiatrist.
Thursday, December 22, 2011
Mental health issues in the workplace
A frequent source of unhappiness I see has to do with a psychologically unhealthy work environment. I am interested to survey the research literature on this subject, but for starters here are a few thoughts:
1) many businesses simply do not seem to value the idea of simply treating employees well. Instead, a short-sighted view is taken, of attempting to maximize the work output or efficiency of the workers, while minimizing costs. On a short term basis (perhaps confirmed by mathematical models composed by the recent business or commerce graduate who is now in a managerial position), this leads to more profit for the business with fewer expenses. On a longer-term basis, however, this pattern leads to poor morale, loss of good or talented employees, higher rates of absenteeism, lower productivity, lower worker loyalty, which in turn must undoubtedly be perceived or intuited by customers, all of which would severely dampen the prosperity of the business.
2) counter-examples exist, of particular businesses which treat employees very well, allowing them more autonomy, healthy scheduling, security, non-authoritarian leadership, even paid time to attend fitness activities, etc. I can think of a few examples like this in which the business and the employees are prospering together, with a very positive public image as well.
3) I have to wonder if the current educational system biases the business world to perpetuate these types of problems. University programs in commerce, economics, or business may have a variety of biases: a money or wealth-acquisition-oriented value system may be very frequent in students drawn to these areas. The programs themselves, I observe, may be dealing with subject matter that involves very interesting, complex, and subtle interactions between human motivations, emotions, and behaviours. Yet the programs tend to have very little instruction or requirement for students to study the obviously related fields of psychology, sociology, ethics, history, political science, etc. Unfortunately this may equip graduates, who may be involved in group leadership and policy-making decisions affecting thousands of people, with strong profit-optimization skills, but very little wisdom or education about human nature or a foundation in altruistic values.
4) In any case, I think many employer-employee interactions are like a dysfunctional family: the "parents" either too authoritarian or enmeshed, or too detached and uninvolved. Usually there are problems with communication. Unfortunately, it is usually very difficult for this type of "family" to come for group therapy: it seems more common for these types of group problems to become more entrenched with time.
The field of "corporate psychology" seems to address some of these issues. I will be interested to survey this literature in the coming months, and hopefully add to this post in a helpful way. Aside from therapeutic ideas to make beneficial changes in business group dynamics, I wonder if it could be a useful trend in the future to allow free economic forces to help things along: if one is considering being a customer or an investor in a business, how about checking out how happy the employees are? It would be a service to the community, in the name of public and individual mental health, to support businesses which provide a healthy community not only to the public, but to their own employees.
1) many businesses simply do not seem to value the idea of simply treating employees well. Instead, a short-sighted view is taken, of attempting to maximize the work output or efficiency of the workers, while minimizing costs. On a short term basis (perhaps confirmed by mathematical models composed by the recent business or commerce graduate who is now in a managerial position), this leads to more profit for the business with fewer expenses. On a longer-term basis, however, this pattern leads to poor morale, loss of good or talented employees, higher rates of absenteeism, lower productivity, lower worker loyalty, which in turn must undoubtedly be perceived or intuited by customers, all of which would severely dampen the prosperity of the business.
2) counter-examples exist, of particular businesses which treat employees very well, allowing them more autonomy, healthy scheduling, security, non-authoritarian leadership, even paid time to attend fitness activities, etc. I can think of a few examples like this in which the business and the employees are prospering together, with a very positive public image as well.
3) I have to wonder if the current educational system biases the business world to perpetuate these types of problems. University programs in commerce, economics, or business may have a variety of biases: a money or wealth-acquisition-oriented value system may be very frequent in students drawn to these areas. The programs themselves, I observe, may be dealing with subject matter that involves very interesting, complex, and subtle interactions between human motivations, emotions, and behaviours. Yet the programs tend to have very little instruction or requirement for students to study the obviously related fields of psychology, sociology, ethics, history, political science, etc. Unfortunately this may equip graduates, who may be involved in group leadership and policy-making decisions affecting thousands of people, with strong profit-optimization skills, but very little wisdom or education about human nature or a foundation in altruistic values.
4) In any case, I think many employer-employee interactions are like a dysfunctional family: the "parents" either too authoritarian or enmeshed, or too detached and uninvolved. Usually there are problems with communication. Unfortunately, it is usually very difficult for this type of "family" to come for group therapy: it seems more common for these types of group problems to become more entrenched with time.
The field of "corporate psychology" seems to address some of these issues. I will be interested to survey this literature in the coming months, and hopefully add to this post in a helpful way. Aside from therapeutic ideas to make beneficial changes in business group dynamics, I wonder if it could be a useful trend in the future to allow free economic forces to help things along: if one is considering being a customer or an investor in a business, how about checking out how happy the employees are? It would be a service to the community, in the name of public and individual mental health, to support businesses which provide a healthy community not only to the public, but to their own employees.
Antidepressants = Psychotherapy = Placebo ?
Jacques Barber et al. have recently published the results of a randomized, controlled study conducted between 2001 and 2007, comparing antidepressant therapy, short-term dynamic psychotherapy, and placebo in a 16-week course of treatment for 156 depressed adults. Here is a link to the abstract: http://www.ncbi.nlm.nih.gov/pubmed/22152401
The bottom line in the study was that there was no significant difference between antidepressants, psychotherapy, or placebo. Response rates were 31% for medication, 28% for psychotherapy, and 24% for placebo -- which has a low probability of being statistically different. Remission rates were 26% for medication, 22% for psychotherapy, and 20% for placebo.
Critics trying to explain these findings might attempt to argue that the psychotherapy or the medication regime was not sufficient, etc. -- but I do not see this to be true. The medications (venlafaxine or sertraline) were given at quite sufficient doses for good lengths of time. The psychotherapy was not CBT (which has a larger research evidence base) but there is little reason, in my opinion, to believe that the therapy style was inferior.
The authors attempt to do some secondary analyses looking for explanations, but their conclusions seem quite weak to me (e.g. regarding race or gender). The fact that they spin these conclusions into a prominently framed set of "clinical points" seems quite inappropriate to me -- this is a negative study, there are no "clinical points" to be found here, unless they recommend placebos and cessation of other therapies!
There are a number of issues from this study that I do find very important to discuss:
1) despite a massive amount of data showing that various therapies (e.g. antidepressants or psychotherapy) are effective for various problems, there are examples of carefully-conducted negative studies, such as this one. These results cannot simply be explained away as statistical aberration: there must be a reason why one group of people responds to a treatment, while another does not. Many of these reasons are poorly understood. It may be that the diagnostic category of "major depressive disorder" is inadequate, in that it correlates poorly on its own with treatment responsiveness.
2) the subjects in this study had a high degree of comorbidity (e.g. substance abuse problems, anxiety disorders, and axis II problems). While the severity and chronicity of depression was not found to actually correlate with treatment responsiveness, I suspect that the comorbidities would substantially affect response to a relatively short-term course of therapy.
3) the subjects in this study were socioeconomically disadvantaged; while the effect of SES was also not found to "influence the initial findings," I believe that low SES is not necessarily a direct negative influence upon mental health; rather it is an indirect factor which for many people increases the likelihood of some profound mental health negatives (e.g. unemployment, lack of meaningful or satisfying employment, lack of healthy or safe community, lack of availability to do healthy or meaningful leisure activities, not enough money to eat healthily, etc.). I believe that the environmental adversities need to be looked at very closely in a study of this type.
This leads to what I believe is an obvious explanation for the findings here: there is no therapy for depression that is likely to help unless ALL contributing factors (including obvious environmental contributing factors) are addressed. By way of analogy, I believe it is pointless to treat insomnia using a powerful sedative if a person is sleeping in a room which is continuously noisy, cold, and prone to break-ins by violent intruders. The environmental issues need to be addressed first! Another analogy I have often used is of trying to repair a water supply system for a city: it is a waste of effort to pipe in more water from rivers, or to dig a deeper reservoir, if the walls of the reservoir and the pipes are leaking or bursting because of structural defects. In order for a therapeutic strategy to work, the "leaks" have to be repaired first. For a person with anemia, it is not an appropriate strategy to simply give a blood transfusion: while a transfusion may be necessary, it will not be sufficient--and could even make matters worse-- if the underlying cause of blood loss is not addressed and treated.
In the case of medications or psychotherapy, I believe these can be very helpful, but only if environmental adversity is also remedied. In some instances, of course, relief of a psychiatric symptom could help a person to improve the environmental circumstances. But in most other cases, I think the issue is broader, and could be considered a political or social policy matter.
Another related issue is that I do not believe "depression" can be treated on its own without addressing all psychiatric and medical comorbidities at the same time. Ongoing substance abuse, in my opinion, is often a powerful enough factor--psychologically as well as neurophysiologically--to completely dominate and dissolve the positive influences of psychotherapy or effective medication. In this study, 30-40% of the cohort reported substance use problems.
As a final thought, I think the "5 axis" model of diagnosis in the DSM system deserves some affirmation; many times, however, we only pay attention to Axis I (diagnoses such as depression or schizophrenia, etc.) or Axis II (personality disorder). I think that studies such as this one highlight the necessity to look closely at Axes III (medical illnesses) and IV (social, community, financial, and relational problems). It is likely that issues on these latter two axes can prevent any resolution of problems on the first two.
The bottom line in the study was that there was no significant difference between antidepressants, psychotherapy, or placebo. Response rates were 31% for medication, 28% for psychotherapy, and 24% for placebo -- which has a low probability of being statistically different. Remission rates were 26% for medication, 22% for psychotherapy, and 20% for placebo.
Critics trying to explain these findings might attempt to argue that the psychotherapy or the medication regime was not sufficient, etc. -- but I do not see this to be true. The medications (venlafaxine or sertraline) were given at quite sufficient doses for good lengths of time. The psychotherapy was not CBT (which has a larger research evidence base) but there is little reason, in my opinion, to believe that the therapy style was inferior.
The authors attempt to do some secondary analyses looking for explanations, but their conclusions seem quite weak to me (e.g. regarding race or gender). The fact that they spin these conclusions into a prominently framed set of "clinical points" seems quite inappropriate to me -- this is a negative study, there are no "clinical points" to be found here, unless they recommend placebos and cessation of other therapies!
There are a number of issues from this study that I do find very important to discuss:
1) despite a massive amount of data showing that various therapies (e.g. antidepressants or psychotherapy) are effective for various problems, there are examples of carefully-conducted negative studies, such as this one. These results cannot simply be explained away as statistical aberration: there must be a reason why one group of people responds to a treatment, while another does not. Many of these reasons are poorly understood. It may be that the diagnostic category of "major depressive disorder" is inadequate, in that it correlates poorly on its own with treatment responsiveness.
2) the subjects in this study had a high degree of comorbidity (e.g. substance abuse problems, anxiety disorders, and axis II problems). While the severity and chronicity of depression was not found to actually correlate with treatment responsiveness, I suspect that the comorbidities would substantially affect response to a relatively short-term course of therapy.
3) the subjects in this study were socioeconomically disadvantaged; while the effect of SES was also not found to "influence the initial findings," I believe that low SES is not necessarily a direct negative influence upon mental health; rather it is an indirect factor which for many people increases the likelihood of some profound mental health negatives (e.g. unemployment, lack of meaningful or satisfying employment, lack of healthy or safe community, lack of availability to do healthy or meaningful leisure activities, not enough money to eat healthily, etc.). I believe that the environmental adversities need to be looked at very closely in a study of this type.
This leads to what I believe is an obvious explanation for the findings here: there is no therapy for depression that is likely to help unless ALL contributing factors (including obvious environmental contributing factors) are addressed. By way of analogy, I believe it is pointless to treat insomnia using a powerful sedative if a person is sleeping in a room which is continuously noisy, cold, and prone to break-ins by violent intruders. The environmental issues need to be addressed first! Another analogy I have often used is of trying to repair a water supply system for a city: it is a waste of effort to pipe in more water from rivers, or to dig a deeper reservoir, if the walls of the reservoir and the pipes are leaking or bursting because of structural defects. In order for a therapeutic strategy to work, the "leaks" have to be repaired first. For a person with anemia, it is not an appropriate strategy to simply give a blood transfusion: while a transfusion may be necessary, it will not be sufficient--and could even make matters worse-- if the underlying cause of blood loss is not addressed and treated.
In the case of medications or psychotherapy, I believe these can be very helpful, but only if environmental adversity is also remedied. In some instances, of course, relief of a psychiatric symptom could help a person to improve the environmental circumstances. But in most other cases, I think the issue is broader, and could be considered a political or social policy matter.
Another related issue is that I do not believe "depression" can be treated on its own without addressing all psychiatric and medical comorbidities at the same time. Ongoing substance abuse, in my opinion, is often a powerful enough factor--psychologically as well as neurophysiologically--to completely dominate and dissolve the positive influences of psychotherapy or effective medication. In this study, 30-40% of the cohort reported substance use problems.
As a final thought, I think the "5 axis" model of diagnosis in the DSM system deserves some affirmation; many times, however, we only pay attention to Axis I (diagnoses such as depression or schizophrenia, etc.) or Axis II (personality disorder). I think that studies such as this one highlight the necessity to look closely at Axes III (medical illnesses) and IV (social, community, financial, and relational problems). It is likely that issues on these latter two axes can prevent any resolution of problems on the first two.
Saturday, December 10, 2011
Worksheets
Here's a good site that has many links to free therapy worksheets: http://therapyworksheets.blogspot.com/
Spending some focused time with a worksheet can be a healthy, useful, structured component of therapy or self-help. Worksheets can be especially useful if you want to build up healthy therapeutic habits, both in terms of inner reflection and external action, but find yourself in need of more clear structure to get started or to continue guiding you. I find this can be analogous to learning a subject at school, or a musical instrument, etc. : practicing is obviously important, but it can certainly help guide and discipline your practice efficiently to have a good textbook to work through.
Many thanks to the person who recommended this site to me!
Spending some focused time with a worksheet can be a healthy, useful, structured component of therapy or self-help. Worksheets can be especially useful if you want to build up healthy therapeutic habits, both in terms of inner reflection and external action, but find yourself in need of more clear structure to get started or to continue guiding you. I find this can be analogous to learning a subject at school, or a musical instrument, etc. : practicing is obviously important, but it can certainly help guide and discipline your practice efficiently to have a good textbook to work through.
Many thanks to the person who recommended this site to me!
Thursday, November 3, 2011
Piracetam
Piracetam is a so-called "nootropic" drug, a substance which supposedly helps improve cognitive functioning. It is available without prescription as a sort of supplement in many parts of the world. In Canada it is not illegal, but must be imported (such as by ordering over the internet from U.S. suppliers).
The mechanism of action is not clear. There is no obvious single receptor-mediated mechanism. There may be various effects on ion channels, cell membrane characteristics, etc. but of course such statements are quite vague.
It is quite clear that there are few side-effect problems or toxicity risks with this agent. Doses are typically 2-5 grams per day.
I became interested in this agent after encountering a case example of someone who reported quite a dramatic improvement in mood and overall functioning attributed to piracetam supplementation.
Here are the results of my survey through the research literature:
http://www.ncbi.nlm.nih.gov/pubmed/16007238 -- a 2005 review
http://www.ncbi.nlm.nih.gov/pubmed/1794001 -- a 1991 review looking specifically at its use in treating dementia; the data is really not impressive at all for dementia treatment.
http://www.ncbi.nlm.nih.gov/pubmed/11084917 -- a 2000 Japanese study affirming the effectiveness of piracetam combined with clonazepam for treating myoclonus (myoclonus is a neurological problem in which muscles are twitching involuntarily).
http://www.ncbi.nlm.nih.gov/pubmed/8914096 -- a 1996 study from Japan also showing benefit in treating myoclonus; there were also improvements in motivation, attention, sleep, and mood (possibly secondary to improvement in the movement disorder).
http://www.ncbi.nlm.nih.gov/pubmed/11346373 -- 2001 study from Archives of Neurology again affirming that piracetam is effective over 12 months of follow-up for treating myoclonic epilepsy.
http://www.ncbi.nlm.nih.gov/pubmed/10796585 -- this 2000 Cochrane review stated that the data on piracetam are inconclusive, with studies not being of good quality
http://www.ncbi.nlm.nih.gov/pubmed/10338110 - this 1999 article reviewed studies of piracetam for treating vertigo, concluding that it was useful for reducing frequency of recurrence, at doses of 2-5 grams per day.
http://www.ncbi.nlm.nih.gov/pubmed/17685739 -- this is a 2007 randomized placebo-controlled study from The Journal of Clinical Psychiatry, in which piracetam 4800 mg/d for 9 weeks led to substantial improvements in tardive dyskinesia, with large differences from placebo.
http://www.ncbi.nlm.nih.gov/pubmed/10338108 -- piracetam has some antiplatelet function, which could be used in managing or preventing recurrences of vascular disorders. This is a 1999 review of this subject.
http://www.ncbi.nlm.nih.gov/pubmed/8061686 -- this is a broad review of nootropics, published in 1994.
http://www.ncbi.nlm.nih.gov/pubmed/3305591 -- this 1987 study from The Journal of Clinical Psychopharmacology shows that children treated with piracetam may show improvements in dyslexia.
Doses were 3.3 grams daily x 36 weeks (dosed twice per day). However, as I look at the results, I see that there is a statistical difference, but the numbers really look very similar between placebo and piracetam. The placebo group improved substantially; the piracetam group improved only slightly more. For example, the raw scores in the Grey Oral Reading Test increased from 17.1 to 22.5 in the placebo group; in the piracetam group it increased from 14.8 to 22.9. It is true that the piracetam was well-tolerated, with minimal side-effect problems.
http://www.ncbi.nlm.nih.gov/pubmed/12394531
this is a 2002 study which attempted to show whether piracetam could prevent ECT-induced cognitive problems. The dose was 7.2 g/day for a 2-week loading phase, then 4.8 g daily for the remaining 2 weeks. They concluded that piracetam had no effect on cognition in this group; but the piracetam group did slightly better than the placebo group in terms of overall clinical improvement.
http://www.ncbi.nlm.nih.gov/pubmed/16878489
this 2006 study described anxiolytic effects of piracetam which were blocked by flumazenil (a benzodiazepine receptor blocker), suggesting that piracetam has some GABA-like activity.
http://www.ncbi.nlm.nih.gov/pubmed/12809069
a Hungarian study describing successful use of piracetam to treat alcohol withdrawal delirium
http://www.ncbi.nlm.nih.gov/pubmed/7906672
a 1993 Indian study showing that piracetam has anti-anxiety effects when administered on a longer-term basis in rats.
http://www.ncbi.nlm.nih.gov/pubmed/95599
a 1979 article from Journal of Affective Disorders describing anti-anxiety effects from piracetam similar to a benzodiazepine, but without sedation.
http://www.ncbi.nlm.nih.gov/pubmed/6415738
in this 1983 study, piracetam 2.4 g/day or 4.8 g/day was compared with placebo in treating 60 elderly psychiatric patients; the 2.4 g/day group showed increased socialization, altertness, and cooperation, and had some improvement on memory and IQ tests, compared to the placebo group.
http://www.ncbi.nlm.nih.gov/pubmed/360232
in this 1977 study, elderly psychiatric patients were given 2.4 g/day of piracetam or placebo, for 2 months. The piracetam group did not improve in any cognitive tests or mood symptom scores compared to placebo, but interestingly 52% of subjects in the piracetam group showed overall improvement (CGI) compared to only 25% in the placebo group.
http://www.ncbi.nlm.nih.gov/pubmed/11687079
a Cochrane review from 2001 concluding that there is evidence that piracetam may improve the course of aphasia after stroke; however, the evidence was found to be weak.
http://www.ncbi.nlm.nih.gov/pubmed/6128331
this 1982 study shows that 40 g of IV piracetam caused greater reduction than placebo in antipsychotic-induced Parkinsonian side-effects.
http://www.ncbi.nlm.nih.gov/pubmed/488520
a small 1979 study which showed that refractory depressed patients improved with the addition of 2.4 g piracetam.
http://www.ncbi.nlm.nih.gov/pubmed/10338106
a look at toxicity risk due to piracetam, when given in higher doses (12 g/day) for 12 weeks, to stroke patients. The paper concludes that there is no significant toxicity risk at this dose for this population.
In conclusion, piracetam appears to be clearly effective for a few uncommon conditions, such as myoclonus. There is possible effectiveness for some other problems such as tardive dyskinesia. The evidence for effectiveness as a "cognitive enhancer" appears to be quite shaky, but not absent.
I am particularly interested in some of the evidence which suggests that it could be useful as a safe, well-tolerated adjunct to treat depression or anxiety. Some of the studies quoted above appear to support this possibility. This theme also intersects with my recent thoughts about considering cognitive function in chronic mood, anxiety, ADHD, or personality disorders. A weakness in working memory capacity or executive functioning could substantially interfere with recovery from psychiatric illness; I suspect that a treatment which could specifically help with cognitive function could be a unique angle to augment treatments for these other psychiatric problems. (see my previous post, which discusses an association between rumination & working memory dysfunction: http://garthkroeker.blogspot.com/2011/08/chronic-pain-rumination.html). Here's another link about this: http://www.ncbi.nlm.nih.gov/pubmed/21742932)
I do think it would be worthwhile for research groups to consider doing some new, careful, large trials of piracetam as an augmentation for managing depression, anxiety disorders, etc.
The mechanism of action is not clear. There is no obvious single receptor-mediated mechanism. There may be various effects on ion channels, cell membrane characteristics, etc. but of course such statements are quite vague.
It is quite clear that there are few side-effect problems or toxicity risks with this agent. Doses are typically 2-5 grams per day.
I became interested in this agent after encountering a case example of someone who reported quite a dramatic improvement in mood and overall functioning attributed to piracetam supplementation.
Here are the results of my survey through the research literature:
http://www.ncbi.nlm.nih.gov/pubmed/16007238 -- a 2005 review
http://www.ncbi.nlm.nih.gov/pubmed/1794001 -- a 1991 review looking specifically at its use in treating dementia; the data is really not impressive at all for dementia treatment.
http://www.ncbi.nlm.nih.gov/pubmed/11084917 -- a 2000 Japanese study affirming the effectiveness of piracetam combined with clonazepam for treating myoclonus (myoclonus is a neurological problem in which muscles are twitching involuntarily).
http://www.ncbi.nlm.nih.gov/pubmed/8914096 -- a 1996 study from Japan also showing benefit in treating myoclonus; there were also improvements in motivation, attention, sleep, and mood (possibly secondary to improvement in the movement disorder).
http://www.ncbi.nlm.nih.gov/pubmed/11346373 -- 2001 study from Archives of Neurology again affirming that piracetam is effective over 12 months of follow-up for treating myoclonic epilepsy.
http://www.ncbi.nlm.nih.gov/pubmed/10796585 -- this 2000 Cochrane review stated that the data on piracetam are inconclusive, with studies not being of good quality
http://www.ncbi.nlm.nih.gov/pubmed/10338110 - this 1999 article reviewed studies of piracetam for treating vertigo, concluding that it was useful for reducing frequency of recurrence, at doses of 2-5 grams per day.
http://www.ncbi.nlm.nih.gov/pubmed/17685739 -- this is a 2007 randomized placebo-controlled study from The Journal of Clinical Psychiatry, in which piracetam 4800 mg/d for 9 weeks led to substantial improvements in tardive dyskinesia, with large differences from placebo.
http://www.ncbi.nlm.nih.gov/pubmed/10338108 -- piracetam has some antiplatelet function, which could be used in managing or preventing recurrences of vascular disorders. This is a 1999 review of this subject.
http://www.ncbi.nlm.nih.gov/pubmed/8061686 -- this is a broad review of nootropics, published in 1994.
http://www.ncbi.nlm.nih.gov/pubmed/3305591 -- this 1987 study from The Journal of Clinical Psychopharmacology shows that children treated with piracetam may show improvements in dyslexia.
Doses were 3.3 grams daily x 36 weeks (dosed twice per day). However, as I look at the results, I see that there is a statistical difference, but the numbers really look very similar between placebo and piracetam. The placebo group improved substantially; the piracetam group improved only slightly more. For example, the raw scores in the Grey Oral Reading Test increased from 17.1 to 22.5 in the placebo group; in the piracetam group it increased from 14.8 to 22.9. It is true that the piracetam was well-tolerated, with minimal side-effect problems.
http://www.ncbi.nlm.nih.gov/pubmed/12394531
this is a 2002 study which attempted to show whether piracetam could prevent ECT-induced cognitive problems. The dose was 7.2 g/day for a 2-week loading phase, then 4.8 g daily for the remaining 2 weeks. They concluded that piracetam had no effect on cognition in this group; but the piracetam group did slightly better than the placebo group in terms of overall clinical improvement.
http://www.ncbi.nlm.nih.gov/pubmed/16878489
this 2006 study described anxiolytic effects of piracetam which were blocked by flumazenil (a benzodiazepine receptor blocker), suggesting that piracetam has some GABA-like activity.
http://www.ncbi.nlm.nih.gov/pubmed/12809069
a Hungarian study describing successful use of piracetam to treat alcohol withdrawal delirium
http://www.ncbi.nlm.nih.gov/pubmed/7906672
a 1993 Indian study showing that piracetam has anti-anxiety effects when administered on a longer-term basis in rats.
http://www.ncbi.nlm.nih.gov/pubmed/95599
a 1979 article from Journal of Affective Disorders describing anti-anxiety effects from piracetam similar to a benzodiazepine, but without sedation.
http://www.ncbi.nlm.nih.gov/pubmed/6415738
in this 1983 study, piracetam 2.4 g/day or 4.8 g/day was compared with placebo in treating 60 elderly psychiatric patients; the 2.4 g/day group showed increased socialization, altertness, and cooperation, and had some improvement on memory and IQ tests, compared to the placebo group.
http://www.ncbi.nlm.nih.gov/pubmed/360232
in this 1977 study, elderly psychiatric patients were given 2.4 g/day of piracetam or placebo, for 2 months. The piracetam group did not improve in any cognitive tests or mood symptom scores compared to placebo, but interestingly 52% of subjects in the piracetam group showed overall improvement (CGI) compared to only 25% in the placebo group.
http://www.ncbi.nlm.nih.gov/pubmed/11687079
a Cochrane review from 2001 concluding that there is evidence that piracetam may improve the course of aphasia after stroke; however, the evidence was found to be weak.
http://www.ncbi.nlm.nih.gov/pubmed/6128331
this 1982 study shows that 40 g of IV piracetam caused greater reduction than placebo in antipsychotic-induced Parkinsonian side-effects.
http://www.ncbi.nlm.nih.gov/pubmed/488520
a small 1979 study which showed that refractory depressed patients improved with the addition of 2.4 g piracetam.
http://www.ncbi.nlm.nih.gov/pubmed/10338106
a look at toxicity risk due to piracetam, when given in higher doses (12 g/day) for 12 weeks, to stroke patients. The paper concludes that there is no significant toxicity risk at this dose for this population.
In conclusion, piracetam appears to be clearly effective for a few uncommon conditions, such as myoclonus. There is possible effectiveness for some other problems such as tardive dyskinesia. The evidence for effectiveness as a "cognitive enhancer" appears to be quite shaky, but not absent.
I am particularly interested in some of the evidence which suggests that it could be useful as a safe, well-tolerated adjunct to treat depression or anxiety. Some of the studies quoted above appear to support this possibility. This theme also intersects with my recent thoughts about considering cognitive function in chronic mood, anxiety, ADHD, or personality disorders. A weakness in working memory capacity or executive functioning could substantially interfere with recovery from psychiatric illness; I suspect that a treatment which could specifically help with cognitive function could be a unique angle to augment treatments for these other psychiatric problems. (see my previous post, which discusses an association between rumination & working memory dysfunction: http://garthkroeker.blogspot.com/2011/08/chronic-pain-rumination.html). Here's another link about this: http://www.ncbi.nlm.nih.gov/pubmed/21742932)
I do think it would be worthwhile for research groups to consider doing some new, careful, large trials of piracetam as an augmentation for managing depression, anxiety disorders, etc.
Wednesday, October 26, 2011
Therapeutic approaches to irritability
Irritability can be a challenging symptom, often present in a wide range of different clinical settings. Unipolar depression can present with irritable mood, as can the manic states of bipolar disorder. Irritability is also a common problem in borderline personality disorder, as well as in various other populations, such as in those with autism, dementias, brain injury, conduct or oppositional disorders, and addiction disorders. In some cases, arguably, irritability could be considered the primary problem for some people, which either exists on its own as a solitary symptom, or is the direct single cause of the person's other life problems (e.g. in relationships, employment, conflicts with the law, ability to work or study, etc.)
A variety of simple factors usually make irritability worse:
1) sleep problems. Insomnia or deliberate reduction of sleep hours will magnify irritability.
2) hunger. For some individuals especially, allowing a hungry state without eating healthily will magnify irritability.
In both cases above, a vicious cycle can arise, as greater irritability may prevent sleep or cause a further lack of appetite.
3) multiple environmental or medical irritants which are not improving: for example, crowding, noise, poor air quality, physical pains or discomforts
Therefore, in approaching irritability, it is essential to take steps to improve sleep, nutrition, pain, and environmental stimuli.
Further therapy for irritability should of course involve healthy lifestyle practices, such as exercise, relaxation, and meditative activity (if not formal "meditation" then something which accomplishes something similar, such as music listening or performance, biofeedback, hot baths, massage, etc.) Reduction of caffeine intake, etc. could be important to try. Developing healthy philosophical practices can be very useful; for example, some type of calm or peace-oriented religious or other community involvement may add to one`s ability to manage irritability, especially since there could be group-based support and healthy cultural activities.
Pharmacological treatment of irritability, if necessary, would depend on obvious underlying causes. In substance withdrawal states, for example, temporary appropriate sedation (e.g. with benzodiazepines, clonidine, or anticonvulsants such as gabapentin) could ease the irritability. In manic states, mood stabilizers, antipsychotics, and benzodiazepines which ease the manic symptoms, would be expected to ease the irritability. In major depression, an antidepressant of any sort, if it works for the individual, could dramatically improve the irritability. ADHD can be a cause of irritability, which--seemingly paradoxically--could improve with stimulant therapy.
In this post, I am particularly interested in looking at specific pharmacological treatments for idiopathic irritability, or irritability which has existed as a long-term emotional dynamic such as in those with borderline personality traits or disorder.
Here are a few pertinent links to abstracts in the research literature:
http://www.ncbi.nlm.nih.gov/pubmed/20010551
this 12 week randomized study shows modest benefits from divalproex to treat irritability in autistic children (ages 5-17)
http://www.ncbi.nlm.nih.gov/pubmed/18273430 gabapentin useful for borderline patients over a 6 month period
http://www.ncbi.nlm.nih.gov/pubmed/19283647 (this is a good article, but it's in German)-- review of anticonvulsant effectiveness in personality disorders. There is evidence in this paper to support trials of valproate, topiramate, and possibility also lamotrigine. They describe some data on carbamazepine as well. The level of evidence is such that I think these medications could be worth trying cautiously on an individual basis, particularly to target symptom domains such as irritability. However, I think expectations should be modest, due to there most likely being a lot of variability in an individual's response.
I am interested in the use of clonidine for irritability. This drug is effective for treating withdrawal states (including one of the most unbearable withdrawal states possible, from opiates), but has also been used for many years to treat ADHD. It can help with tic disorders as well, so could be a good choice for managing ADHD + tic comorbidity, a difficult problem often made worse by stimulants. Clonidine was originally developed as a treatment for high blood pressure. My main concern about clonidine is about how well its effects persist if taken continuously for more than a few months. Here is an article about treating borderline personality patients with clonidine:
http://www.ncbi.nlm.nih.gov/pubmed/19512980
Here's a study looking at treating children with conduct or oppositional problems with stimulants and/or clonidine: http://www.ncbi.nlm.nih.gov/pubmed/10660814
In conclusion, there are various options to try in the treatment of irritability from most causes. While the evidence base is limited, there is support for attempting a variety of different pharmacological treatments for idiopathic irritability, particularly anticonvulsant medications.
A variety of simple factors usually make irritability worse:
1) sleep problems. Insomnia or deliberate reduction of sleep hours will magnify irritability.
2) hunger. For some individuals especially, allowing a hungry state without eating healthily will magnify irritability.
In both cases above, a vicious cycle can arise, as greater irritability may prevent sleep or cause a further lack of appetite.
3) multiple environmental or medical irritants which are not improving: for example, crowding, noise, poor air quality, physical pains or discomforts
Therefore, in approaching irritability, it is essential to take steps to improve sleep, nutrition, pain, and environmental stimuli.
Further therapy for irritability should of course involve healthy lifestyle practices, such as exercise, relaxation, and meditative activity (if not formal "meditation" then something which accomplishes something similar, such as music listening or performance, biofeedback, hot baths, massage, etc.) Reduction of caffeine intake, etc. could be important to try. Developing healthy philosophical practices can be very useful; for example, some type of calm or peace-oriented religious or other community involvement may add to one`s ability to manage irritability, especially since there could be group-based support and healthy cultural activities.
Pharmacological treatment of irritability, if necessary, would depend on obvious underlying causes. In substance withdrawal states, for example, temporary appropriate sedation (e.g. with benzodiazepines, clonidine, or anticonvulsants such as gabapentin) could ease the irritability. In manic states, mood stabilizers, antipsychotics, and benzodiazepines which ease the manic symptoms, would be expected to ease the irritability. In major depression, an antidepressant of any sort, if it works for the individual, could dramatically improve the irritability. ADHD can be a cause of irritability, which--seemingly paradoxically--could improve with stimulant therapy.
In this post, I am particularly interested in looking at specific pharmacological treatments for idiopathic irritability, or irritability which has existed as a long-term emotional dynamic such as in those with borderline personality traits or disorder.
Here are a few pertinent links to abstracts in the research literature:
http://www.ncbi.nlm.nih.gov/pubmed/20010551
this 12 week randomized study shows modest benefits from divalproex to treat irritability in autistic children (ages 5-17)
http://www.ncbi.nlm.nih.gov/pubmed/18273430 gabapentin useful for borderline patients over a 6 month period
http://www.ncbi.nlm.nih.gov/pubmed/19283647 (this is a good article, but it's in German)-- review of anticonvulsant effectiveness in personality disorders. There is evidence in this paper to support trials of valproate, topiramate, and possibility also lamotrigine. They describe some data on carbamazepine as well. The level of evidence is such that I think these medications could be worth trying cautiously on an individual basis, particularly to target symptom domains such as irritability. However, I think expectations should be modest, due to there most likely being a lot of variability in an individual's response.
I am interested in the use of clonidine for irritability. This drug is effective for treating withdrawal states (including one of the most unbearable withdrawal states possible, from opiates), but has also been used for many years to treat ADHD. It can help with tic disorders as well, so could be a good choice for managing ADHD + tic comorbidity, a difficult problem often made worse by stimulants. Clonidine was originally developed as a treatment for high blood pressure. My main concern about clonidine is about how well its effects persist if taken continuously for more than a few months. Here is an article about treating borderline personality patients with clonidine:
http://www.ncbi.nlm.nih.gov/pubmed/19512980
Here's a study looking at treating children with conduct or oppositional problems with stimulants and/or clonidine: http://www.ncbi.nlm.nih.gov/pubmed/10660814
In conclusion, there are various options to try in the treatment of irritability from most causes. While the evidence base is limited, there is support for attempting a variety of different pharmacological treatments for idiopathic irritability, particularly anticonvulsant medications.
Monday, October 3, 2011
Parental behaviours associated with offspring personality traits
Johnson et al. have published an interesting article in the August 2011 edition of The Canadian Journal of Psychiatry (pp. 447-456) in which they describe a nice longitudinal study of 669 families, correlating parenting behaviour with future personality traits in the offspring.
To some degree, studies of this type might seem to be re-examinations of the obvious -- that is, children of friendly, gentle, stable, involved parents are more likely to be healthy and stable themselves. The thing is, much of this effect is arguably due to heredity rather than parenting. The genetic factors which influence temperament, mood, personality, etc. are likely to be present in both parents and children--the impact of parenting behaviours themselves are therefore likely to be overestimated.
A good method to tease out these factors would be to study families with adopted children, provided there is good data about psychological characteristics of the birth parents. In general studies of this sort have led to the surprising conclusion that genetic factors are quite a bit higher than expected, and parenting factors quite a bit lower.
But this particular study is quite good. It was longitudinal, following parents and offspring at various ages during the offspring's childhood years (ages 6, 14, and 16), then following up in the offspring's young adulthood years (ages 22 and 33). Most importantly, the study carefully assessed parental psychological traits and symptoms, which in my opinion would help control for inherited traits confounding the results.
This article has some problems with lack of clarity in the writing. It was not exactly clear when the interviews were done (particularly the data from when the children were 6 years old). Also, in the tables, various items (such as "high praise and encouragement" in Table 2) are listed twice, with different numbers! I'm surprised that the writers and editors didn't address these things before publication.
In any case, the results show that various positive parental behaviours led to substantially reduced risk of future psychological problems in the offspring ("reduced aggregate offspring personality disorder symptoms levels" and "elevated aggregate offspring personality resiliency"). Here are a few examples (some of these things may seem like obvious truths -- but it is important to be reminded about just how important these are):
1) speaking kindly to child
2) being calm, not reactive with child
3) attention and dedication to child
4) raised child without reliance on punishment
5) lots of time spent with child
6) shared enjoyable activities with child
7) high affection toward child
8) good communication with child
9) high praise and encouragement
A few findings might be surprising to some. For example, "encouragement of offspring autonomy" from fathers actually was associated with a higher risk of offspring psychological problems.
Studies about parenting may seem to have limited relevance to those of us who are not parents, or who are not currently being parented. But I believe these findings can be generalized: in a psychodynamic sense, all relationships have at least a partial "parental" quality to them. We all also have a "parenting role" with ourselves! This role, and the behaviours or stance we take in this role, are undoubtedly coloured by the type of parenting we have experienced in our childhoods.
Findings of this type encourage us to change our "self-parenting":
1) Speak kindly to self!
2) Be calm and not reactive to self!
3) Be attentive and dedicated with yourself!
4) Be with yourself without reliance on punishment!
5) Spend lots of time with yourself!
6) Share enjoyable activities with yourself!
7) Have high affection toward self!
8) Communicate well with self!
9) And give self praise and encouragement!
10) If you are accustomed to "encourage autonomy in yourself" a lot, maybe you can give this one a rest.
To some degree, studies of this type might seem to be re-examinations of the obvious -- that is, children of friendly, gentle, stable, involved parents are more likely to be healthy and stable themselves. The thing is, much of this effect is arguably due to heredity rather than parenting. The genetic factors which influence temperament, mood, personality, etc. are likely to be present in both parents and children--the impact of parenting behaviours themselves are therefore likely to be overestimated.
A good method to tease out these factors would be to study families with adopted children, provided there is good data about psychological characteristics of the birth parents. In general studies of this sort have led to the surprising conclusion that genetic factors are quite a bit higher than expected, and parenting factors quite a bit lower.
But this particular study is quite good. It was longitudinal, following parents and offspring at various ages during the offspring's childhood years (ages 6, 14, and 16), then following up in the offspring's young adulthood years (ages 22 and 33). Most importantly, the study carefully assessed parental psychological traits and symptoms, which in my opinion would help control for inherited traits confounding the results.
This article has some problems with lack of clarity in the writing. It was not exactly clear when the interviews were done (particularly the data from when the children were 6 years old). Also, in the tables, various items (such as "high praise and encouragement" in Table 2) are listed twice, with different numbers! I'm surprised that the writers and editors didn't address these things before publication.
In any case, the results show that various positive parental behaviours led to substantially reduced risk of future psychological problems in the offspring ("reduced aggregate offspring personality disorder symptoms levels" and "elevated aggregate offspring personality resiliency"). Here are a few examples (some of these things may seem like obvious truths -- but it is important to be reminded about just how important these are):
1) speaking kindly to child
2) being calm, not reactive with child
3) attention and dedication to child
4) raised child without reliance on punishment
5) lots of time spent with child
6) shared enjoyable activities with child
7) high affection toward child
8) good communication with child
9) high praise and encouragement
A few findings might be surprising to some. For example, "encouragement of offspring autonomy" from fathers actually was associated with a higher risk of offspring psychological problems.
Studies about parenting may seem to have limited relevance to those of us who are not parents, or who are not currently being parented. But I believe these findings can be generalized: in a psychodynamic sense, all relationships have at least a partial "parental" quality to them. We all also have a "parenting role" with ourselves! This role, and the behaviours or stance we take in this role, are undoubtedly coloured by the type of parenting we have experienced in our childhoods.
Findings of this type encourage us to change our "self-parenting":
1) Speak kindly to self!
2) Be calm and not reactive to self!
3) Be attentive and dedicated with yourself!
4) Be with yourself without reliance on punishment!
5) Spend lots of time with yourself!
6) Share enjoyable activities with yourself!
7) Have high affection toward self!
8) Communicate well with self!
9) And give self praise and encouragement!
10) If you are accustomed to "encourage autonomy in yourself" a lot, maybe you can give this one a rest.
Friday, September 30, 2011
Pregabalin for generalized anxiety
There have been a variety of studies in the literature showing that pregabalin is effective for treating generalized anxiety.
The latest of such studies I have seen is published by Mark Boschen in the September 2011 issue of The Canadian Journal of Psychiatry (p.558-565).
This article is a meta-analysis, and shows generally that pregabalin is effective compared to placebo, and has similar, if not greater, effectiveness than other medication options for treating generalized anxiety, such as SSRIs, venlafaxine, and benzodiazepines.
The most common doses have been in the 600 mg/day range, which I consider quite high, particularly since a reasonable dose range for pregabalin could be around 75-300 mg/day.
The "limitations" admitted by the author include issues about dosing, and the fact that Pfizer has funded every published randomized study quoted in the article.
I believe that pregabalin could be a very useful option to try, if a medication trial is being considered for generalized anxiety treatment (of course, the first lines of therapy for generalized anxiety are CBT, relaxation-oriented therapies, meditation, exercise, etc.--but for many people these approaches are not sufficiently helpful). Pregabalin has the advantage of having a quite different--and generally mild--side effect profile compared to other medications, and a what appears to be a fairly low (but I do not think zero) risk of addictiveness/dependence problems, particularly compared to benzodiazepines.
However -- the most obvious limitation of the literature findings is only mentioned briefly in passing by the author in the discussion: it is hard to make a good conclusion about a treatment for anxiety when the duration of follow-up is only 4-8 weeks! I believe that a study for this problem needs to extend for a year or more. First of all, many treatments for anxiety can be acutely helpful, but then wear off substantially over time. Arguably, having a beer every 4 hours could reduce GAD scores over a 4-week trial--but obviously this is not an acceptable long-term treatment! (not only would there be multiple physical harms caused by this over a period of many months or years, but there would be substantial tolerance to anxiety reduction effects, which might only become apparent over many months; furthermore,there would be new psychiatric symptoms induced over a period of months and beyond).
It is not clear from the literature whether the acute benefits over 4-8 weeks from pregabalin would persist over a year or more, whether there would be tolerance, whether there would be longer-term emergent physical or psychiatric side-effects, dependence phenomena, trouble with withdrawal or discontinuation, etc.
Research of this type could be used --spuriously--to justify giving GAD patients benzodiazepines on a routine basis as well, despite the frequent and obvious problem of tolerance, dependence, cognitive problems, etc. Most benzodiazepine studies are of similarly short duration, hence have very limited value to guide us for the long-term treatment decisions which are most important.
Yet, I do think that pregabalin is promising, and could be worth a cautious try, particularly if other approaches are not working well.
The latest of such studies I have seen is published by Mark Boschen in the September 2011 issue of The Canadian Journal of Psychiatry (p.558-565).
This article is a meta-analysis, and shows generally that pregabalin is effective compared to placebo, and has similar, if not greater, effectiveness than other medication options for treating generalized anxiety, such as SSRIs, venlafaxine, and benzodiazepines.
The most common doses have been in the 600 mg/day range, which I consider quite high, particularly since a reasonable dose range for pregabalin could be around 75-300 mg/day.
The "limitations" admitted by the author include issues about dosing, and the fact that Pfizer has funded every published randomized study quoted in the article.
I believe that pregabalin could be a very useful option to try, if a medication trial is being considered for generalized anxiety treatment (of course, the first lines of therapy for generalized anxiety are CBT, relaxation-oriented therapies, meditation, exercise, etc.--but for many people these approaches are not sufficiently helpful). Pregabalin has the advantage of having a quite different--and generally mild--side effect profile compared to other medications, and a what appears to be a fairly low (but I do not think zero) risk of addictiveness/dependence problems, particularly compared to benzodiazepines.
However -- the most obvious limitation of the literature findings is only mentioned briefly in passing by the author in the discussion: it is hard to make a good conclusion about a treatment for anxiety when the duration of follow-up is only 4-8 weeks! I believe that a study for this problem needs to extend for a year or more. First of all, many treatments for anxiety can be acutely helpful, but then wear off substantially over time. Arguably, having a beer every 4 hours could reduce GAD scores over a 4-week trial--but obviously this is not an acceptable long-term treatment! (not only would there be multiple physical harms caused by this over a period of many months or years, but there would be substantial tolerance to anxiety reduction effects, which might only become apparent over many months; furthermore,there would be new psychiatric symptoms induced over a period of months and beyond).
It is not clear from the literature whether the acute benefits over 4-8 weeks from pregabalin would persist over a year or more, whether there would be tolerance, whether there would be longer-term emergent physical or psychiatric side-effects, dependence phenomena, trouble with withdrawal or discontinuation, etc.
Research of this type could be used --spuriously--to justify giving GAD patients benzodiazepines on a routine basis as well, despite the frequent and obvious problem of tolerance, dependence, cognitive problems, etc. Most benzodiazepine studies are of similarly short duration, hence have very limited value to guide us for the long-term treatment decisions which are most important.
Yet, I do think that pregabalin is promising, and could be worth a cautious try, particularly if other approaches are not working well.
Thursday, September 29, 2011
Multi-dimensional nature of borderline personality symptom structure
Chmielewski et al. have published an article in the September 2011 edition of the Canadian Journal of Psychiatry in which they show that borderline personality is better described as having several separate symptom dimensions.
The benefit of having several dimensions instead of one could be illustrated by way of analogy: suppose we are talking about heart disease. One could simply describe all patients suffering a "heart attack" according to a single severity scale, perhaps including information of the amount of pain, degree of disability afterwards, etc. This scale could be quite useful, but it would obscure a great deal of information about the group, and reduce the efficiency of treatment. A multi-dimensional scale would instead look at several domains separately, such as perfusion abnormalities, rhythm abnormalities, and structural abnormalities. Abnormal perfusion might be treated specifically with bypass surgery, rhythm problems with a pacemaker, and structural problems with a valve replacement etc. Thus the management could become more meaningfully specific.
The authors of this paper about borderline personality show that a 3-factor model fit well to describe symptoms in borderline patients; a 1-dimensional model fit much more poorly. The 3 factors are "affective dysregulation," "behavioural dysregulation," and "disturbed relations." Affective dysregulation would refer to high intensity and lability of negative emotion, inappropriate anger, etc. Behavioural dysregulation would refer to self-injurious behaviour, excessive or out-of-control behaviours such as binge eating, or I might add any sort of chemical or behavioural addiction. Disturbed relations of course refers to interpersonal relationship problems. One could see that these three domains would each influence the others, but part of a theoretical model is to consider to what degree problems in each domain could be considered primary. (similarly, a blocked coronary artery would be a primary perfusion problem, but could in turn cause a secondary rhythm and structural problem in the heart).
A particularly relevant remark from the authors comes in the discussion: "...the current pattern of associations suggests that the glue that holds the BPD construct together may largely represent the general dysfunction or misery common across all forms of psychopathology and not just BPD." So, the authors are hinting that we could perhaps do away with the BPD construct altogether, without any loss of insight, and instead simply describe in succinct terms what the core symptoms are. This makes sense to me. I do believe that some of these core symptoms are extremely important to examine and address directly. "Affective dysregulation" would be almost automatically addressed in any therapy environment, and "relationship dysfunction" is perhaps the most frequent topic of discussion (and perhaps transferential work) done in therapy. But the "behavioural dysregulation"domain I think is not quite so well-addressed in much therapeutic work. I see this domain as the most common severe problem relatively more unique to those who fit into a "borderline personality" spectrum. It is my own view to consider this domain through a type of addiction-medicine lens, as a set of problems which are highly destructive and addictive behavioural habits, often engaged in to cope with other symptoms, but which become independent problems with time. This is similar to any other addiction; alcoholism, for example, may begin as alcohol consumption intended to calm nerves, deal with boredom, or to facilitate socialization, but in time becomes more and more a separate, self-contained behavioural and physiological addiction.
In my browsing through the literature as I was writing this post just now, I encountered a psychology master's thesis published online (by Edward Selby, M.Sc. 2007). Here's a link:
http://etd.lib.fsu.edu/theses/available/etd-07092007-164107/unrestricted/SelbyMastersThesisFinal.pdf
Selby makes the case well that negative emotional cascades leading to behavioural dyregulation are strongly fuelled by rumination. The events of behavioural dysregulation, such as self-injury, serve to distract one from the intense discomfort of rumination. Here is a quote from the conclusion:
"the findings of this study provide preliminary evidence for an
emotional cascade model of dysregulated behavior. In this model high levels of rumination may cause extremely intense states of negative affect, which result in dysregulated behaviors that distract from rumination and reduce that state of negative affect. This study specifically linked rumination to drinking to cope, binge-eating behaviors, reassurance seeking, and urgency, and it is likely that rumination is linked to a variety of other deregulated behaviors. "
Rumination, of course, is another phenomenon common to much "general dysfunction or misery." I am reminded how important it can be, as a practical therapeutic project with patients, to work on ways to move away from, or to let go of, rumination. (see my previous post on rumination: http://garthkroeker.blogspot.com/2011/08/chronic-pain-rumination.html)
The benefit of having several dimensions instead of one could be illustrated by way of analogy: suppose we are talking about heart disease. One could simply describe all patients suffering a "heart attack" according to a single severity scale, perhaps including information of the amount of pain, degree of disability afterwards, etc. This scale could be quite useful, but it would obscure a great deal of information about the group, and reduce the efficiency of treatment. A multi-dimensional scale would instead look at several domains separately, such as perfusion abnormalities, rhythm abnormalities, and structural abnormalities. Abnormal perfusion might be treated specifically with bypass surgery, rhythm problems with a pacemaker, and structural problems with a valve replacement etc. Thus the management could become more meaningfully specific.
The authors of this paper about borderline personality show that a 3-factor model fit well to describe symptoms in borderline patients; a 1-dimensional model fit much more poorly. The 3 factors are "affective dysregulation," "behavioural dysregulation," and "disturbed relations." Affective dysregulation would refer to high intensity and lability of negative emotion, inappropriate anger, etc. Behavioural dysregulation would refer to self-injurious behaviour, excessive or out-of-control behaviours such as binge eating, or I might add any sort of chemical or behavioural addiction. Disturbed relations of course refers to interpersonal relationship problems. One could see that these three domains would each influence the others, but part of a theoretical model is to consider to what degree problems in each domain could be considered primary. (similarly, a blocked coronary artery would be a primary perfusion problem, but could in turn cause a secondary rhythm and structural problem in the heart).
A particularly relevant remark from the authors comes in the discussion: "...the current pattern of associations suggests that the glue that holds the BPD construct together may largely represent the general dysfunction or misery common across all forms of psychopathology and not just BPD." So, the authors are hinting that we could perhaps do away with the BPD construct altogether, without any loss of insight, and instead simply describe in succinct terms what the core symptoms are. This makes sense to me. I do believe that some of these core symptoms are extremely important to examine and address directly. "Affective dysregulation" would be almost automatically addressed in any therapy environment, and "relationship dysfunction" is perhaps the most frequent topic of discussion (and perhaps transferential work) done in therapy. But the "behavioural dysregulation"domain I think is not quite so well-addressed in much therapeutic work. I see this domain as the most common severe problem relatively more unique to those who fit into a "borderline personality" spectrum. It is my own view to consider this domain through a type of addiction-medicine lens, as a set of problems which are highly destructive and addictive behavioural habits, often engaged in to cope with other symptoms, but which become independent problems with time. This is similar to any other addiction; alcoholism, for example, may begin as alcohol consumption intended to calm nerves, deal with boredom, or to facilitate socialization, but in time becomes more and more a separate, self-contained behavioural and physiological addiction.
In my browsing through the literature as I was writing this post just now, I encountered a psychology master's thesis published online (by Edward Selby, M.Sc. 2007). Here's a link:
http://etd.lib.fsu.edu/theses/available/etd-07092007-164107/unrestricted/SelbyMastersThesisFinal.pdf
Selby makes the case well that negative emotional cascades leading to behavioural dyregulation are strongly fuelled by rumination. The events of behavioural dysregulation, such as self-injury, serve to distract one from the intense discomfort of rumination. Here is a quote from the conclusion:
"the findings of this study provide preliminary evidence for an
emotional cascade model of dysregulated behavior. In this model high levels of rumination may cause extremely intense states of negative affect, which result in dysregulated behaviors that distract from rumination and reduce that state of negative affect. This study specifically linked rumination to drinking to cope, binge-eating behaviors, reassurance seeking, and urgency, and it is likely that rumination is linked to a variety of other deregulated behaviors. "
Rumination, of course, is another phenomenon common to much "general dysfunction or misery." I am reminded how important it can be, as a practical therapeutic project with patients, to work on ways to move away from, or to let go of, rumination. (see my previous post on rumination: http://garthkroeker.blogspot.com/2011/08/chronic-pain-rumination.html)
Thursday, August 18, 2011
"Anti-psychiatry"
I'm just bumping up this post, originally from July 2008, because there have been some new comments.
There are a lot of strong opinions out there about psychiatry.
Some people are concerned that the practice of psychiatry has caused harm, perhaps by "over-medicalizing" issues that should be considered matters of personal challenge, character, individual choice & responsibility, spirituality, or normal human experience. Other concerns are that psychiatry is overly influenced by large pharmaceutical companies, whose agenda is to earn larger profits by selling more medication. Critics holding these concerns often consider the results of research studies to be biased, since they have often been sponsored by drug companies.
I think these concerns need to be heard and respected. There are specific examples about some of the concerns having some validity to them. In the history of psychiatry, as in the history of all other human endeavour, mistakes have been made. Small mistakes and large mistakes. On a systemic level, I think some of the core theories about psychiatry over the past hundred years have been laden with huge inaccuracies, despite the many nuggets of wisdom contained within them (Freud's ideas are one example). Many times, attempts at treatment have not helped, or perhaps have reduced a symptom at a very great expense to other aspects of the patient's life. There have been trends and fashions in treatment, such as the widespread use of anxiolytic drugs in past decades--while only later do we discover that these treatments can cause entrenched problems with addiction.
Conversely, there are some testimonial accounts of individuals who have had long histories of conventional psychiatric therapies, who have gone on to thrive once leaving all of these behind (perhaps pursuing alternative or naturopathic medicine, or making some other lifestyle change).
I think it is important to step back and examine the evidence closely, with a critical eye (in future posts I will refer to some of the evidence). I hold that there is a vast body of evidence about psychiatry to look at. And the evidence shows that the treatments are truly helpful. The evidence also shows that the treatments are not perfect, and that typically 30% of people do not have a good response from a given psychiatric treatment. The evidence also shows that up to 30% of patients respond to "placebo treatments". These facts lead to several criticisms about psychiatric treatment: first, there are many (perhaps in the first group of 30%) who have tried "conventional psychiatry" and have found that it hasn't worked for them. Second, there are those who have tried "non-psychiatric" treatments, and found that these HAVE worked for them (perhaps these people are in the 30% "placebo" group). Both of these groups may have a tendency to criticize psychiatry; yet there is another 40% -- a group whose ailments have resolved as a direct result of their psychiatric treatments.
This has always reminded me a bit of other areas of medicine, such as cardiology or oncology: the treatments in these specialties can be remarkably curative for some, only palliative for others, and may not work at all for others still.
I do agree that we must never "over-medicalize" any human ailment. It is rare for a problem to be truly cured by a pill. Usually, for any human concern or challenge, any therapy that helps has to be accompanied by holistic changes in lifestyle & behaviour. For the cardiac patient, this means rehabilitative exercise, healthy diet, no smoking, etc. For the mind, just as for the heart, there are many lifestyle habits that are healthy, restorative, and protective against recurrent illness.
Yet, very often people are too ill to be able to institute the "healthy lifestyle habits". The cardiac patient may require medication to control blood pressure and angina before being able to safely or comfortably exercise. Similarly, there are medical treatments in psychiatry that can hopefully provide enough symptom relief to allow the patient to energetically change their life for the better.
I have observed that the "anti-psychiatry" group can be very vocal. I could understand that the individuals among this group could have good reasons to hold such strong, forceful opinions. But I don't want this site to be a forum to spend a lot of time on this debate, I would rather focus on my own beliefs about ways to manage the mind's symptoms in the healthiest possible ways.
There are a lot of strong opinions out there about psychiatry.
Some people are concerned that the practice of psychiatry has caused harm, perhaps by "over-medicalizing" issues that should be considered matters of personal challenge, character, individual choice & responsibility, spirituality, or normal human experience. Other concerns are that psychiatry is overly influenced by large pharmaceutical companies, whose agenda is to earn larger profits by selling more medication. Critics holding these concerns often consider the results of research studies to be biased, since they have often been sponsored by drug companies.
I think these concerns need to be heard and respected. There are specific examples about some of the concerns having some validity to them. In the history of psychiatry, as in the history of all other human endeavour, mistakes have been made. Small mistakes and large mistakes. On a systemic level, I think some of the core theories about psychiatry over the past hundred years have been laden with huge inaccuracies, despite the many nuggets of wisdom contained within them (Freud's ideas are one example). Many times, attempts at treatment have not helped, or perhaps have reduced a symptom at a very great expense to other aspects of the patient's life. There have been trends and fashions in treatment, such as the widespread use of anxiolytic drugs in past decades--while only later do we discover that these treatments can cause entrenched problems with addiction.
Conversely, there are some testimonial accounts of individuals who have had long histories of conventional psychiatric therapies, who have gone on to thrive once leaving all of these behind (perhaps pursuing alternative or naturopathic medicine, or making some other lifestyle change).
I think it is important to step back and examine the evidence closely, with a critical eye (in future posts I will refer to some of the evidence). I hold that there is a vast body of evidence about psychiatry to look at. And the evidence shows that the treatments are truly helpful. The evidence also shows that the treatments are not perfect, and that typically 30% of people do not have a good response from a given psychiatric treatment. The evidence also shows that up to 30% of patients respond to "placebo treatments". These facts lead to several criticisms about psychiatric treatment: first, there are many (perhaps in the first group of 30%) who have tried "conventional psychiatry" and have found that it hasn't worked for them. Second, there are those who have tried "non-psychiatric" treatments, and found that these HAVE worked for them (perhaps these people are in the 30% "placebo" group). Both of these groups may have a tendency to criticize psychiatry; yet there is another 40% -- a group whose ailments have resolved as a direct result of their psychiatric treatments.
This has always reminded me a bit of other areas of medicine, such as cardiology or oncology: the treatments in these specialties can be remarkably curative for some, only palliative for others, and may not work at all for others still.
I do agree that we must never "over-medicalize" any human ailment. It is rare for a problem to be truly cured by a pill. Usually, for any human concern or challenge, any therapy that helps has to be accompanied by holistic changes in lifestyle & behaviour. For the cardiac patient, this means rehabilitative exercise, healthy diet, no smoking, etc. For the mind, just as for the heart, there are many lifestyle habits that are healthy, restorative, and protective against recurrent illness.
Yet, very often people are too ill to be able to institute the "healthy lifestyle habits". The cardiac patient may require medication to control blood pressure and angina before being able to safely or comfortably exercise. Similarly, there are medical treatments in psychiatry that can hopefully provide enough symptom relief to allow the patient to energetically change their life for the better.
I have observed that the "anti-psychiatry" group can be very vocal. I could understand that the individuals among this group could have good reasons to hold such strong, forceful opinions. But I don't want this site to be a forum to spend a lot of time on this debate, I would rather focus on my own beliefs about ways to manage the mind's symptoms in the healthiest possible ways.
Wednesday, August 10, 2011
Chronic Pain & Rumination
I was planning to write separate posts on chronic pain and on rumination; but I have found that these subjects are related to each other, so I thought I would combine them.
In this article, I am defining "rumination" as frequent, repetitive thoughts about symptoms or problems. Such recurrent thinking can consume so much time and energy, that little is left in the mind to permit quality of life. And the ruminations, while understandable in the context of troubling symptoms or problems, do not help to resolve the problems at all. Rumination can also refer to a gastrointestinal problem, which I am not discussing here.
Chronic physical pain obviously has a huge negative impact on quality of life. The presence of physical pain symptoms is a strong risk factor for suicide. (references: http://www.ncbi.nlm.nih.gov/pubmed/21668756 ; http://www.ncbi.nlm.nih.gov/pubmed/16420727 )
If physical pain and depression are combined, the severity of both problems is substantially elevated.
Treatment of chronic pain requires good comprehensive medical care. Investigation and treatment of underlying medical causes is obviously important. Coordinated involvement of a mutlidisciplinary team is ideal, though often lacking in many people's experience.
In the psychiatric realm, a variety of therapies can help:
1) mindfulness meditation. Jon Kabat-Zinn developed much of his work on mindfulness meditation with patients suffering from physical pain. In my opinion, meditation is extremely important, since it carries no risk, has a variety of possible and probable benefits, and is likely to help with both emotional and physical symptoms.
This study shows similar reductions in pain from a mindfulness program vs. a multidisciplinary pain program without a meditation focus:
http://www.ncbi.nlm.nih.gov/pubmed/21753729
This study shows improvements in various types of chronic pain conditions, with greater improvements in symptoms when subjects practiced more at home:
http://www.ncbi.nlm.nih.gov/pubmed/20004298
This study showed that mindfulness strategies probably work best for those who already have higher levels of mindfulness to begin with, as a type of character trait:
http://www.ncbi.nlm.nih.gov/pubmed/21254055
This study shows a slight advantage for a mindfulness meditation program to treat back pain:
http://www.ncbi.nlm.nih.gov/pubmed/17544212
An interesting study showing improvement in distressing intrusive thoughts and images following a meditation program. This shows that mindfulness exercises can substantially improve symptoms of rumination and even psychosis. In chronic pain, ruminations and intrusive thoughts about the pain itself are a very common feature, and an element of the vicious cycle of pain perpetuation and reduced quality of life. The study was of good quality, and the effect was quite substantial and robust:
http://www.ncbi.nlm.nih.gov/pubmed/19545481
Similarly, a study showing the mindfulness training specifically increases ability to "let go" (in this case, of OCD thoughts). "Letting go" of ruminations about pain is very helpful in managing chronic pain conditions:
http://www.ncbi.nlm.nih.gov/pubmed/18852623
Here's another study once again showing that mindfulness is specifically helpful to reduce rumination:
http://www.ncbi.nlm.nih.gov/pubmed/17291166
2) Cognitive-behavioural therapy
There is a significant research literature showing the effectiveness of CBT for managing pain conditions. Here are some research examples:
non-cardiac chest pain: http://www.ncbi.nlm.nih.gov/pubmed/21262413
chronic TMJ (jaw) pain: http://www.ncbi.nlm.nih.gov/pubmed/20655662
fibromyalgia: http://www.ncbi.nlm.nih.gov/pubmed/20521308
severe back pain: http://www.ncbi.nlm.nih.gov/pubmed/19967572
vulvodynia: http://www.ncbi.nlm.nih.gov/pubmed/19022580
back pain (here, active behavioural/physical therapy was necessary for optimal improvement in performance, as expected): http://www.ncbi.nlm.nih.gov/pubmed/16426449
chronic headaches: http://www.ncbi.nlm.nih.gov/pubmed/17690017
3) Medications
a) antidepressants:
Several antidepressant types could help with chronic pain: tricyclics such as amitriptyline have been used in this way for decades, with reasonable evidence-based support. Cymbalta (duloxetine) has been marketed for this, and is reasonable to try. However, venlafaxine (Effexor) is probably just as effective for pain symptoms.
There have been no studies comparing venlafaxine with duloxetine in pain patients; I suspect that there would be little difference. Currently, duloxetine is more expensive, so I do not believe it should be a first-line agent. SSRI antidepressants or bupropion appear not to be consistently helpful for treating physical pain.
Here`s an animal study showing a difference favoring a tricyclic over an SSRI or bupropion for pain management: http://www.ncbi.nlm.nih.gov/pubmed/20689938
Here`s a negative study on moclobemide for physical pain: http://www.ncbi.nlm.nih.gov/pubmed/7549169
This study shows equivalent benefits from amitriptyline and duloxetine, with over 50% of patients having good pain relief in diabetic neuropathy: http://www.ncbi.nlm.nih.gov/pubmed/21355098
This study shows benefits from duloxetine in fibromyalgia; again with over 50% of patients feeling much better, compared to about 30% with placebo: http://www.ncbi.nlm.nih.gov/pubmed/20843911
This study shows significant benefit in treating osteoarthritis pain with duloxetine; the pain relief was not related to any change in depression scores (which, in this population, were quite low and did not change very much with either duloxetine or placebo). I find this study quite significant, in that it is looking at a different variety of pain than most of the other research: http://www.ncbi.nlm.nih.gov/pubmed/19625125
This study shows relief attributable to duloxetine in depressed patients with idiopathic pain symptoms: http://www.ncbi.nlm.nih.gov/pubmed/18052564
Here, venlafaxine is shown to be an effective agent to prevent migraine headaches: http://www.ncbi.nlm.nih.gov/pubmed/15705120
Venlafaxine shown to be effective in treating functional chest pain:
http://www.ncbi.nlm.nih.gov/pubmed/20332772
A 2007 Cochrane review concluding that venlafaxine and tricyclics are effective for chronic pain:
http://www.ncbi.nlm.nih.gov/pubmed/17943857
b) anticonvulsants, e.g. gabapentin, pregabalin, carbamazapine, topiramate
A comparison of gabapentin, pregabalin, and amitriptyline in treating neuropathic cancer pain. All of these drugs clearly helped, with pregabalin probably the best. Aside from direct relief, these drugs resulted in lower doses of opiates being needed: http://www.ncbi.nlm.nih.gov/pubmed/21745832
A review of gabapentin treatment for neuropathic pain, affirming its usefulness, particularly at higher doses of 1800-3600 mg per day: http://www.ncbi.nlm.nih.gov/pubmed/12637113
This is a negative review article, showing that lamotrigine is unfortunately not likely to be useful in treating chronic pain: http://www.ncbi.nlm.nih.gov/pubmed/21328280
An interesting study showing that pregabalin can reduce postoperative morphine requirement acutely: http://www.ncbi.nlm.nih.gov/pubmed/21786524
This is an example, and a review article, part of the large literature showing that topiramate is an agent of choice to prevent or treat recurrent or chronic migraine. There is preliminary evidence at a case-report level that topiramate could help with other types of pain: http://www.ncbi.nlm.nih.gov/pubmed/19838625
c) opiates, such as codeine or morphine -- outside of the scope of this posting. These may have a role in managing non-malignant chronic pain, but supervision is needed from someone with experience prescribing opiates, a pain clinic, etc. Long-acting opiates such as methadone are being used more often in acute or chronic non-malignant pain conditions. Of course, there is a balance here between pain relief and addictive risk.
Here is a recent review, which basically affirms that the use of opiates for chronic non-cancer pain is an "iffy" practice, yet I do affirm that in some cases it may be necessary. In any case I think that experienced and specialized prescribers, such as those at a pain clinic, would be highly preferred:
http://www.ncbi.nlm.nih.gov/pubmed/21412367
d) Atypical opiate: tramadol. This is an interesting drug, for various reasons, including that it has antidepressant activity as well as being a physical analgesic. It is an opiate, but a significant portion of its analgesic properties come from non-opioid mechanisms, such as neurotransmitter reuptake inhibition. It does a potential for addictive problems, but the risk is clearly less than other opiates. For this reason, I think it is reasonable to think of using tramadol before using other opiates (such as codeine or morphine) in treating pain syndromes.
Chronic CNS effects of tramadol differ from those of morphine, supporting the evidence that tramadol has a smaller risk of inducing opiate dependence/addiction:
http://www.ncbi.nlm.nih.gov/pubmed/17401159
Tramadol can be identified subjectively as having opiate-like effects, but mainly at higher doses:
http://www.ncbi.nlm.nih.gov/pubmed/21467190
Here are animal studies using a mouse model of depression, suggesting effectiveness of tramadol.. However, I would want to see longer-term studies of this sort, as the acute beneficial action of any therapy does not necessarily prove that the benefits will last, in fact many acutely beneficial things can become harmful if used long-term (e.g. benzodiazepines):
http://www.ncbi.nlm.nih.gov/pubmed/9749830
http://www.ncbi.nlm.nih.gov/pubmed/12417248
An animal study suggesting that tramadol and anticonvulsants (in this case, specifically topiramate) can work synergestically (cooperatively) in relieving neuropathic pain: http://www.ncbi.nlm.nih.gov/pubmed/17532139
Treatment of refractory major depression with tramadol monotherapy: http://www.ncbi.nlm.nih.gov/pubmed/11305709
Rapid remission of ocd with tramadol:
http://www.ncbi.nlm.nih.gov/pubmed/10200754
http://www.ncbi.nlm.nih.gov/pubmed/9559288
Restless legs treatment with tramadol:
http://www.ncbi.nlm.nih.gov/pubmed/10221285
Treating catalepsy with tramadol:
http://www.ncbi.nlm.nih.gov/pubmed/14504345
Tramadol dependence : in general these articles show that tramadol dependence occurs, but is significantly less likely than with stronger opiates:
http://www.ncbi.nlm.nih.gov/pubmed/19827010
http://www.ncbi.nlm.nih.gov/pubmed/21467190
http://www.ncbi.nlm.nih.gov/pubmed/20589494
http://www.ncbi.nlm.nih.gov/pubmed/16716877
There is a risk of serotonin syndrome with tramadol, particularly if combined with other serotonergic drugs, such as SSRI antidepressants:
http://www.ncbi.nlm.nih.gov/pubmed/21147393
Other direct approaches to treat rumination:
Here is a study showing effectiveness using a modified form of cognitive therapy called competitive memory training. It basically involves teaching techniques to either accept, or become indifferent to, the themes of the rumination:
http://www.ncbi.nlm.nih.gov/pubmed/21784413
Here`s a similar recent study showing improved relief in chronic depression with a CBT style modified to target rumination:
http://www.ncbi.nlm.nih.gov/pubmed/21778171
An interesting study from the psychology literature which shows that rumination is associated with a type of cognitive deficit involving reduced ability to manage negative material in working memory. This suggests to me that cognitive exercises, ones which train working memory, could have a role in treating depression and rumination. Conversely, it suggests to me that practicing ways of "letting go" such as via CBT or meditation, could improve working memory (by freeing working memory space of irrelevant, ruminative, or intrusive negative material), and therefore improve intellectual functioning, academic performance, etc. http://www.ncbi.nlm.nih.gov/pubmed/21742932
Here's one of many articles discussing rumination as a risk factor for depressive relapse or chronicity. Clearly, tactics to help manage or prevent rumination are very important in both acute treatment and in prevention:
http://www.ncbi.nlm.nih.gov/pubmed/19899844
Another article discussing the role of rumination as a sort of emotional amplifier, which causes "impaired down-regulation of negative feelings" -- thus preventing the maintenance of positivity or relationship health after a stressor. Such a dynamic would be a recipe for life disappointments to consistently derail one's emotional life. Once again, practicing ways to manage rumination directly could therefore help with emotional resilience, and prevent a recurrent depressive cycle:
http://www.ncbi.nlm.nih.gov/pubmed/21432690
In summary, there are a variety of ways to treat or manage chronic pain and rumination. Rumination itself may be an important perpetuating factor in pain syndromes. Due to the presence of many symptoms in such syndromes, affecting both physical and emotional domains, it is important to have a cohesive, integrated treatment plan. There is a risk of having multiple sources of therapy, each of which targeting only part of the symptom complex, which potentially could complicate or confound efficient treatment efforts. In physical pain, emotional pain, or rumination, it can be extremely valuable to practice ways of "letting go."
In this article, I am defining "rumination" as frequent, repetitive thoughts about symptoms or problems. Such recurrent thinking can consume so much time and energy, that little is left in the mind to permit quality of life. And the ruminations, while understandable in the context of troubling symptoms or problems, do not help to resolve the problems at all. Rumination can also refer to a gastrointestinal problem, which I am not discussing here.
Chronic physical pain obviously has a huge negative impact on quality of life. The presence of physical pain symptoms is a strong risk factor for suicide. (references: http://www.ncbi.nlm.nih.gov/pubmed/21668756 ; http://www.ncbi.nlm.nih.gov/pubmed/16420727 )
If physical pain and depression are combined, the severity of both problems is substantially elevated.
Treatment of chronic pain requires good comprehensive medical care. Investigation and treatment of underlying medical causes is obviously important. Coordinated involvement of a mutlidisciplinary team is ideal, though often lacking in many people's experience.
In the psychiatric realm, a variety of therapies can help:
1) mindfulness meditation. Jon Kabat-Zinn developed much of his work on mindfulness meditation with patients suffering from physical pain. In my opinion, meditation is extremely important, since it carries no risk, has a variety of possible and probable benefits, and is likely to help with both emotional and physical symptoms.
This study shows similar reductions in pain from a mindfulness program vs. a multidisciplinary pain program without a meditation focus:
http://www.ncbi.nlm.nih.gov/pubmed/21753729
This study shows improvements in various types of chronic pain conditions, with greater improvements in symptoms when subjects practiced more at home:
http://www.ncbi.nlm.nih.gov/pubmed/20004298
This study showed that mindfulness strategies probably work best for those who already have higher levels of mindfulness to begin with, as a type of character trait:
http://www.ncbi.nlm.nih.gov/pubmed/21254055
This study shows a slight advantage for a mindfulness meditation program to treat back pain:
http://www.ncbi.nlm.nih.gov/pubmed/17544212
An interesting study showing improvement in distressing intrusive thoughts and images following a meditation program. This shows that mindfulness exercises can substantially improve symptoms of rumination and even psychosis. In chronic pain, ruminations and intrusive thoughts about the pain itself are a very common feature, and an element of the vicious cycle of pain perpetuation and reduced quality of life. The study was of good quality, and the effect was quite substantial and robust:
http://www.ncbi.nlm.nih.gov/pubmed/19545481
Similarly, a study showing the mindfulness training specifically increases ability to "let go" (in this case, of OCD thoughts). "Letting go" of ruminations about pain is very helpful in managing chronic pain conditions:
http://www.ncbi.nlm.nih.gov/pubmed/18852623
Here's another study once again showing that mindfulness is specifically helpful to reduce rumination:
http://www.ncbi.nlm.nih.gov/pubmed/17291166
2) Cognitive-behavioural therapy
There is a significant research literature showing the effectiveness of CBT for managing pain conditions. Here are some research examples:
non-cardiac chest pain: http://www.ncbi.nlm.nih.gov/pubmed/21262413
chronic TMJ (jaw) pain: http://www.ncbi.nlm.nih.gov/pubmed/20655662
fibromyalgia: http://www.ncbi.nlm.nih.gov/pubmed/20521308
severe back pain: http://www.ncbi.nlm.nih.gov/pubmed/19967572
vulvodynia: http://www.ncbi.nlm.nih.gov/pubmed/19022580
back pain (here, active behavioural/physical therapy was necessary for optimal improvement in performance, as expected): http://www.ncbi.nlm.nih.gov/pubmed/16426449
chronic headaches: http://www.ncbi.nlm.nih.gov/pubmed/17690017
3) Medications
a) antidepressants:
Several antidepressant types could help with chronic pain: tricyclics such as amitriptyline have been used in this way for decades, with reasonable evidence-based support. Cymbalta (duloxetine) has been marketed for this, and is reasonable to try. However, venlafaxine (Effexor) is probably just as effective for pain symptoms.
There have been no studies comparing venlafaxine with duloxetine in pain patients; I suspect that there would be little difference. Currently, duloxetine is more expensive, so I do not believe it should be a first-line agent. SSRI antidepressants or bupropion appear not to be consistently helpful for treating physical pain.
Here`s an animal study showing a difference favoring a tricyclic over an SSRI or bupropion for pain management: http://www.ncbi.nlm.nih.gov/pubmed/20689938
Here`s a negative study on moclobemide for physical pain: http://www.ncbi.nlm.nih.gov/pubmed/7549169
This study shows equivalent benefits from amitriptyline and duloxetine, with over 50% of patients having good pain relief in diabetic neuropathy: http://www.ncbi.nlm.nih.gov/pubmed/21355098
This study shows benefits from duloxetine in fibromyalgia; again with over 50% of patients feeling much better, compared to about 30% with placebo: http://www.ncbi.nlm.nih.gov/pubmed/20843911
This study shows significant benefit in treating osteoarthritis pain with duloxetine; the pain relief was not related to any change in depression scores (which, in this population, were quite low and did not change very much with either duloxetine or placebo). I find this study quite significant, in that it is looking at a different variety of pain than most of the other research: http://www.ncbi.nlm.nih.gov/pubmed/19625125
This study shows relief attributable to duloxetine in depressed patients with idiopathic pain symptoms: http://www.ncbi.nlm.nih.gov/pubmed/18052564
Here, venlafaxine is shown to be an effective agent to prevent migraine headaches: http://www.ncbi.nlm.nih.gov/pubmed/15705120
Venlafaxine shown to be effective in treating functional chest pain:
http://www.ncbi.nlm.nih.gov/pubmed/20332772
A 2007 Cochrane review concluding that venlafaxine and tricyclics are effective for chronic pain:
http://www.ncbi.nlm.nih.gov/pubmed/17943857
b) anticonvulsants, e.g. gabapentin, pregabalin, carbamazapine, topiramate
A comparison of gabapentin, pregabalin, and amitriptyline in treating neuropathic cancer pain. All of these drugs clearly helped, with pregabalin probably the best. Aside from direct relief, these drugs resulted in lower doses of opiates being needed: http://www.ncbi.nlm.nih.gov/pubmed/21745832
A review of gabapentin treatment for neuropathic pain, affirming its usefulness, particularly at higher doses of 1800-3600 mg per day: http://www.ncbi.nlm.nih.gov/pubmed/12637113
This is a negative review article, showing that lamotrigine is unfortunately not likely to be useful in treating chronic pain: http://www.ncbi.nlm.nih.gov/pubmed/21328280
An interesting study showing that pregabalin can reduce postoperative morphine requirement acutely: http://www.ncbi.nlm.nih.gov/pubmed/21786524
This is an example, and a review article, part of the large literature showing that topiramate is an agent of choice to prevent or treat recurrent or chronic migraine. There is preliminary evidence at a case-report level that topiramate could help with other types of pain: http://www.ncbi.nlm.nih.gov/pubmed/19838625
c) opiates, such as codeine or morphine -- outside of the scope of this posting. These may have a role in managing non-malignant chronic pain, but supervision is needed from someone with experience prescribing opiates, a pain clinic, etc. Long-acting opiates such as methadone are being used more often in acute or chronic non-malignant pain conditions. Of course, there is a balance here between pain relief and addictive risk.
Here is a recent review, which basically affirms that the use of opiates for chronic non-cancer pain is an "iffy" practice, yet I do affirm that in some cases it may be necessary. In any case I think that experienced and specialized prescribers, such as those at a pain clinic, would be highly preferred:
http://www.ncbi.nlm.nih.gov/pubmed/21412367
d) Atypical opiate: tramadol. This is an interesting drug, for various reasons, including that it has antidepressant activity as well as being a physical analgesic. It is an opiate, but a significant portion of its analgesic properties come from non-opioid mechanisms, such as neurotransmitter reuptake inhibition. It does a potential for addictive problems, but the risk is clearly less than other opiates. For this reason, I think it is reasonable to think of using tramadol before using other opiates (such as codeine or morphine) in treating pain syndromes.
Chronic CNS effects of tramadol differ from those of morphine, supporting the evidence that tramadol has a smaller risk of inducing opiate dependence/addiction:
http://www.ncbi.nlm.nih.gov/pubmed/17401159
Tramadol can be identified subjectively as having opiate-like effects, but mainly at higher doses:
http://www.ncbi.nlm.nih.gov/pubmed/21467190
Here are animal studies using a mouse model of depression, suggesting effectiveness of tramadol.. However, I would want to see longer-term studies of this sort, as the acute beneficial action of any therapy does not necessarily prove that the benefits will last, in fact many acutely beneficial things can become harmful if used long-term (e.g. benzodiazepines):
http://www.ncbi.nlm.nih.gov/pubmed/9749830
http://www.ncbi.nlm.nih.gov/pubmed/12417248
An animal study suggesting that tramadol and anticonvulsants (in this case, specifically topiramate) can work synergestically (cooperatively) in relieving neuropathic pain: http://www.ncbi.nlm.nih.gov/pubmed/17532139
Treatment of refractory major depression with tramadol monotherapy: http://www.ncbi.nlm.nih.gov/pubmed/11305709
Rapid remission of ocd with tramadol:
http://www.ncbi.nlm.nih.gov/pubmed/10200754
http://www.ncbi.nlm.nih.gov/pubmed/9559288
Restless legs treatment with tramadol:
http://www.ncbi.nlm.nih.gov/pubmed/10221285
Treating catalepsy with tramadol:
http://www.ncbi.nlm.nih.gov/pubmed/14504345
Tramadol dependence : in general these articles show that tramadol dependence occurs, but is significantly less likely than with stronger opiates:
http://www.ncbi.nlm.nih.gov/pubmed/19827010
http://www.ncbi.nlm.nih.gov/pubmed/21467190
http://www.ncbi.nlm.nih.gov/pubmed/20589494
http://www.ncbi.nlm.nih.gov/pubmed/16716877
There is a risk of serotonin syndrome with tramadol, particularly if combined with other serotonergic drugs, such as SSRI antidepressants:
http://www.ncbi.nlm.nih.gov/pubmed/21147393
Other direct approaches to treat rumination:
Here is a study showing effectiveness using a modified form of cognitive therapy called competitive memory training. It basically involves teaching techniques to either accept, or become indifferent to, the themes of the rumination:
http://www.ncbi.nlm.nih.gov/pubmed/21784413
Here`s a similar recent study showing improved relief in chronic depression with a CBT style modified to target rumination:
http://www.ncbi.nlm.nih.gov/pubmed/21778171
An interesting study from the psychology literature which shows that rumination is associated with a type of cognitive deficit involving reduced ability to manage negative material in working memory. This suggests to me that cognitive exercises, ones which train working memory, could have a role in treating depression and rumination. Conversely, it suggests to me that practicing ways of "letting go" such as via CBT or meditation, could improve working memory (by freeing working memory space of irrelevant, ruminative, or intrusive negative material), and therefore improve intellectual functioning, academic performance, etc. http://www.ncbi.nlm.nih.gov/pubmed/21742932
Here's one of many articles discussing rumination as a risk factor for depressive relapse or chronicity. Clearly, tactics to help manage or prevent rumination are very important in both acute treatment and in prevention:
http://www.ncbi.nlm.nih.gov/pubmed/19899844
Another article discussing the role of rumination as a sort of emotional amplifier, which causes "impaired down-regulation of negative feelings" -- thus preventing the maintenance of positivity or relationship health after a stressor. Such a dynamic would be a recipe for life disappointments to consistently derail one's emotional life. Once again, practicing ways to manage rumination directly could therefore help with emotional resilience, and prevent a recurrent depressive cycle:
http://www.ncbi.nlm.nih.gov/pubmed/21432690
In summary, there are a variety of ways to treat or manage chronic pain and rumination. Rumination itself may be an important perpetuating factor in pain syndromes. Due to the presence of many symptoms in such syndromes, affecting both physical and emotional domains, it is important to have a cohesive, integrated treatment plan. There is a risk of having multiple sources of therapy, each of which targeting only part of the symptom complex, which potentially could complicate or confound efficient treatment efforts. In physical pain, emotional pain, or rumination, it can be extremely valuable to practice ways of "letting go."
Wednesday, July 27, 2011
Optimal Sleep Duration
The best study which examines the relationship between sleep duration and mortality risk was published in 2007 by Hublin et al in the journal Sleep. Here's a link to the abstract:
http://www.ncbi.nlm.nih.gov/pubmed/17969458
It is part of the Finnish twin study, which followed over 20 000 twins over a 22 year period. This is an extremely large cohort, and the study had very high response rates. The analysis was thoughtful and comprehensive.
They showed that mortality rates were lowest for those who sleep between 7 and 8 hours per day. For those sleeping less than 7 hours per day, or more than 8, the mortality rates were about 20-25% higher. The results were adjusted for the covariates of education, marital status, age, working status, BMI, social class, drinking behavior, physical activity, smoking, and life satisfaction. Interestingly, and unexpectedly, sleep quality was not shown to be associated with differences in mortality risk.
The argument could be made that average sleep duration has a non-causal association with lower mortality. That is, people who happen to be healthier in the first place are more likely to have average sleep length. But another part of this analysis suggests that this is more than a non-causal association: subjects who changed their sleep duration during the course of this 22 year follow-up also changed their mortality rate, after controlling for the measured confounding factors. I suppose it could still be true that some other mortality-increasing factor was the cause of the sleep duration change, and not the other way around.
In conclusion, this data supports the commonly held belief that 7-8 hours of sleep per night is a desirable goal. It may be that particular individuals have a different "set point" for optimal sleep, and for those individuals optimal health might result from more or less hours than this average. Yet I do not actually see firm evidence of this in the research I've seen.
A 2010 meta-analysis supports the same conclusion: http://www.ncbi.nlm.nih.gov/pubmed/20469800 but I think the authors understate their findings. In particular, while a lot of the data showing increased mortality in short sleepers defined short sleep to be under 7 hours, the authors state in their discussion that "consistently sleeping 6 to 8 h per night may therefore be optimal for health." I think there is a significant difference between 6 and 7 hours, particularly due to pressures in the culture where many people are sleeping only 6 hours because of a busy schedule, while really needing 7 or 8.
Knutson in 2007 published a good article showing that sleep deprivation causes impairments in glucose tolerance (similar to the changes which occur in the development of type II diabetes), and impairments in the hormones associated with appetite regulation: http://www.ncbi.nlm.nih.gov/pubmed/185162
Here's one of the articles in the literature showing that sleep deprivation leads to an increase in proinflammatory cytokines and abnormal immune activation: http://www.ncbi.nlm.nih.gov/pubmed/19240794
I think it is especially true that if one has signs or symptoms related to sleep duration (e.g. feeling sleepy in the daytime after sleeping only 6 hours per night) then this could be taken as strong evidence that sleep duration should be increased up to the average (7-8 hours), if circumstances permit.
Patterns of sleeping long hours (above average) could be approached similarly, but of course if the reason for the long sleeping duration is medical illness or medication effects, etc. it would not be healthy to force oneself into a shorter (average) sleep regimen.
http://www.ncbi.nlm.nih.gov/pubmed/17969458
It is part of the Finnish twin study, which followed over 20 000 twins over a 22 year period. This is an extremely large cohort, and the study had very high response rates. The analysis was thoughtful and comprehensive.
They showed that mortality rates were lowest for those who sleep between 7 and 8 hours per day. For those sleeping less than 7 hours per day, or more than 8, the mortality rates were about 20-25% higher. The results were adjusted for the covariates of education, marital status, age, working status, BMI, social class, drinking behavior, physical activity, smoking, and life satisfaction. Interestingly, and unexpectedly, sleep quality was not shown to be associated with differences in mortality risk.
The argument could be made that average sleep duration has a non-causal association with lower mortality. That is, people who happen to be healthier in the first place are more likely to have average sleep length. But another part of this analysis suggests that this is more than a non-causal association: subjects who changed their sleep duration during the course of this 22 year follow-up also changed their mortality rate, after controlling for the measured confounding factors. I suppose it could still be true that some other mortality-increasing factor was the cause of the sleep duration change, and not the other way around.
In conclusion, this data supports the commonly held belief that 7-8 hours of sleep per night is a desirable goal. It may be that particular individuals have a different "set point" for optimal sleep, and for those individuals optimal health might result from more or less hours than this average. Yet I do not actually see firm evidence of this in the research I've seen.
A 2010 meta-analysis supports the same conclusion: http://www.ncbi.nlm.nih.gov/pubmed/20469800 but I think the authors understate their findings. In particular, while a lot of the data showing increased mortality in short sleepers defined short sleep to be under 7 hours, the authors state in their discussion that "consistently sleeping 6 to 8 h per night may therefore be optimal for health." I think there is a significant difference between 6 and 7 hours, particularly due to pressures in the culture where many people are sleeping only 6 hours because of a busy schedule, while really needing 7 or 8.
Knutson in 2007 published a good article showing that sleep deprivation causes impairments in glucose tolerance (similar to the changes which occur in the development of type II diabetes), and impairments in the hormones associated with appetite regulation: http://www.ncbi.nlm.nih.gov/pubmed/185162
Here's one of the articles in the literature showing that sleep deprivation leads to an increase in proinflammatory cytokines and abnormal immune activation: http://www.ncbi.nlm.nih.gov/pubmed/19240794
I think it is especially true that if one has signs or symptoms related to sleep duration (e.g. feeling sleepy in the daytime after sleeping only 6 hours per night) then this could be taken as strong evidence that sleep duration should be increased up to the average (7-8 hours), if circumstances permit.
Patterns of sleeping long hours (above average) could be approached similarly, but of course if the reason for the long sleeping duration is medical illness or medication effects, etc. it would not be healthy to force oneself into a shorter (average) sleep regimen.
Monday, June 27, 2011
Somatoform Disorders & CFS : a discussion
Somatoform disorders could be considered clusters or syndromes of physical symptoms which have a psychological cause.
Here are some examples:
1) somatization disorder -- a syndrome of multiple physical symptoms--typically pain symptoms-- which have a psychological cause
2) conversion disorder -- typically there is a complaint of paralysis or loss of sensation (including blindness) despite an absence of neurological signs; the symptoms may be generated without conscious intent, but may be profoundly disabling. With modern examination techniques and tests, these symptoms are easily demonstrated to be of non-neurological origin.
3) somatic delusions, in the context of psychotic depression or schizophreniform disorders. These have a wide variety of manifestations, though are most commonly bizarre in nature. Arguably, cases of somatization or conversion could be treated as somatic delusions.
4) somatic manifestations of anxiety -- this is extremely familiar to us all: tremor, sweating, bowel problems, etc. can all occur as a direct obvious consequence of anxiety. At times this physical component becomes the dominant feature, leading to behaviours intended to relieve the physical complaint, leading in turn to worsened avoidance, withdrawal, and exacerbation of the underlying problem.
This whole subject requires a lot of care, in my opinion. I believe that somatization is very common, and exists in a wide range of extremity--from minor symptoms to syndromes that can be almost totally disabling--yet it is also true that undiagnosed medical ailments of non-psychological origin can often be misdiagnosed as psychosomatic or somatoform. Therefore, thorough physical medical assessment and care is needed as a multidisciplinary strategy to manage these problems. These types of problems do indeed tend to be handled poorly by the conventional medical system--either through excessive and harmful medical interventions (e.g. in Munchausen's Syndrome), or through the dismissive neglect of a frustrated caregiver.
I think it is fair to say--and an observation I certainly find consistently in my experience--that physical symptoms of any cause ALWAYS have a psychological component as well. Often times, the psychological component is simple and direct: recurrent migraine headaches, malignant chronic pain, recurrent seizures, etc. (among hundreds of different causes of physical symptoms) cause a disruption to daily life & function, and their unpredictable patterns can leave one in a nearly constant state of anxiety. It can be hard to plan activities, time for relationships, work schedules, etc. when symptoms may come at any moment. So there is obvious direct psychological stress. This stress understandably can cause a feedback loop which may exacerbate the underlying medical condition.
Other times, I believe that the psychological effects of medical conditions can be more subtle or indirect. Chronic conditions can come to have a lot of power to redefine one's sense of self, often in a way which pronounces one to be more disabled than the medical problems necessitate. Some types of symptom clusters may be sufficiently common as to allow a community of fellow sufferers to form. While this may permit the supportive care of a community, it may also consolidate or entrench the aspects of the phenomenon which have to do with identity. The relief that one may find in a group of people experiencing something similar may sometimes be so compelling that entrenched factitious beliefs about disability are deepened, at the expense of therapeutic growth.
Some currently unexplained diagnostic entities, such as chronic fatigue syndrome (CFS), may in some cases be examples of complex somatoform illness. I acknowledge that in other cases--perhaps even in the majority--there may well be some as yet unexplained physical pathology driving the symptoms. A physiologic disposition towards fatigue may cause a cascade of behavioural changes (including withdrawal from activities), leading to a further cascade of cognitions about illness, mood change (which can often present itself, for many people, in a further somatized set of symptoms), and perpetuating of underlying symptoms. The worldwide network of fellow sufferers may lead to perpetuation of symptoms, rather than relief, because the group consolidates some of the beliefs and identity formation which individuals may have about the condition, and also may agitate against what is seen as a dismissive or ineffectual medical system. The group dynamics may also foster the spread of various spurious alternative therapies, whose evidence base would often consist of glowing testimonial accounts rather than careful randomized data. Factitious therapies could sometimes be quite effective for factitious illnesses, since the therapeutic effort would permit the sufferer a psychological opportunity to move away from the illness symptoms, and attribute the improvement to something external, rather than to psychological change. Such is, in my opinion, the basis for most stories of so-called "faith healing" which have been around for millenia.
It is helpful to have observed extreme examples of somatoform illness. Case examples include individuals who have had recurrent factitious seizures (pseudoseizures), often leading to dangerous and harmfully inappropriate medical interventions. Many persons with a history of pseudoseizures also have neurologically-based epilepsy as well: somatized, factitious, or conversion symptoms often co-exist with their non-psychiatric counterparts. Other case examples include situations where individuals are delusionally convinced that they are paralyzed (due to a conversion disorder) causing them to have lived in a wheelchair for years. Such individuals often have networks of people in their lives who support them in their paralyzed role; such supporters often include physicians and other caregivers. Yet, it has been an amazing experience for me to witness cases of this type--cases where there has never been any objective sign of neurologic disease, but where the impact of the problem has been extreme; if a very careful neuropsychiatric evaluation is done, with strongly structured psychiatric and rehabilitative therapy, I have seen situations where a person experiencing paralysis is able to walk home after a hospital stay.
But cases like these are inevitably complex. If a person has lived in a certain way for years, the behaviours themselves, and the associated thoughts, become integrated into identity. If you live as a paralyzed person for many years, it will not be so easy to get up and walk, even if you are neurologically healthy. There are physical barriers, but obvious psychological and social ones as well.
I believe this is a theme which epitomizes our understanding of brain function: repeated behaviour entrenches neural pathways. If "illness behaviour" exists despite "no illness", the brain learns to function "as if" a physical injury were present. It is just like language learning--with immersive experience over a course of months or years, the brain will speak the new language with ever greater fluency. It is a difficult task for the brain to "unlearn" such experience.
But this suggests a therapeutic imperative: for all cases of this type, immersive physical rehabilitation is necessary. In every single case I have ever seen of severe conversion, for example, the cure required intensive, prolonged, structured involvement of physiotherapists, in addition to whatever medications (typically antidepressants and antipsychotics) and psychotherapeutic work the person needed.
I believe this theme crosses over into the realm of ALL chronic disease, regardless of cause. Management of chronic disability or chronic diseases is greatly assisted by physical rehabilitation. In the language of narrative therapy, if we consider the illness or symptom to be like a negative character in our lives, that character is constantly telling us to do less and less--part of the therapy to challenge this is to find a structured and safe manner in which to do more and more, or to optimize our fitness so that we can do the most despite the limitations imposed by the disease.
Another interesting modality of therapy for conversion, one which can illustrate very compellingly the existence of a structure of drives and defenses first suggested by Freud, is the so-called "amytal interview." In the version I have seen, a patient with a conversion syndrome (following informed consent, of course) is given a dose of ritalin (which allows more amytal to be given without loss of consciousness), followed by intravenous sodium amytal (a barbiturate), with the supervision of an anesthetist in a well-equipped medical setting. The dose is titrated just to the point before the patient loses consciousness. The effect of the medication is to cause disinhibition. In this condition, the psychological forces necessary to continue the conversion symptom are weakened, so for example a person describing paralysis of an arm can be guided to raise the paralyzed arm in the air, and flex it, etc. This event can be videotaped. When the effects of the drug wear off, the person may not remember the scene, but when presented with the video footage (of the non-paralyzed limb in action), the person's psychological defense of conversion will be substantially weakened. As a result, often times a strong emotional reaction takes place, usually the overt emotions or affects consistent with a severe underlying depression which had previously shown itself through "paralysis." In this way, "conversion" operates as a psychological defense, a way in which the brain deals emotionally or behaviourally with a painful symptom. These defenses can be vital ways to survive in the world, but sometimes--as in conversion disorders--the defense system goes awry, and becomes the core problem.
Here are some examples:
1) somatization disorder -- a syndrome of multiple physical symptoms--typically pain symptoms-- which have a psychological cause
2) conversion disorder -- typically there is a complaint of paralysis or loss of sensation (including blindness) despite an absence of neurological signs; the symptoms may be generated without conscious intent, but may be profoundly disabling. With modern examination techniques and tests, these symptoms are easily demonstrated to be of non-neurological origin.
3) somatic delusions, in the context of psychotic depression or schizophreniform disorders. These have a wide variety of manifestations, though are most commonly bizarre in nature. Arguably, cases of somatization or conversion could be treated as somatic delusions.
4) somatic manifestations of anxiety -- this is extremely familiar to us all: tremor, sweating, bowel problems, etc. can all occur as a direct obvious consequence of anxiety. At times this physical component becomes the dominant feature, leading to behaviours intended to relieve the physical complaint, leading in turn to worsened avoidance, withdrawal, and exacerbation of the underlying problem.
This whole subject requires a lot of care, in my opinion. I believe that somatization is very common, and exists in a wide range of extremity--from minor symptoms to syndromes that can be almost totally disabling--yet it is also true that undiagnosed medical ailments of non-psychological origin can often be misdiagnosed as psychosomatic or somatoform. Therefore, thorough physical medical assessment and care is needed as a multidisciplinary strategy to manage these problems. These types of problems do indeed tend to be handled poorly by the conventional medical system--either through excessive and harmful medical interventions (e.g. in Munchausen's Syndrome), or through the dismissive neglect of a frustrated caregiver.
I think it is fair to say--and an observation I certainly find consistently in my experience--that physical symptoms of any cause ALWAYS have a psychological component as well. Often times, the psychological component is simple and direct: recurrent migraine headaches, malignant chronic pain, recurrent seizures, etc. (among hundreds of different causes of physical symptoms) cause a disruption to daily life & function, and their unpredictable patterns can leave one in a nearly constant state of anxiety. It can be hard to plan activities, time for relationships, work schedules, etc. when symptoms may come at any moment. So there is obvious direct psychological stress. This stress understandably can cause a feedback loop which may exacerbate the underlying medical condition.
Other times, I believe that the psychological effects of medical conditions can be more subtle or indirect. Chronic conditions can come to have a lot of power to redefine one's sense of self, often in a way which pronounces one to be more disabled than the medical problems necessitate. Some types of symptom clusters may be sufficiently common as to allow a community of fellow sufferers to form. While this may permit the supportive care of a community, it may also consolidate or entrench the aspects of the phenomenon which have to do with identity. The relief that one may find in a group of people experiencing something similar may sometimes be so compelling that entrenched factitious beliefs about disability are deepened, at the expense of therapeutic growth.
Some currently unexplained diagnostic entities, such as chronic fatigue syndrome (CFS), may in some cases be examples of complex somatoform illness. I acknowledge that in other cases--perhaps even in the majority--there may well be some as yet unexplained physical pathology driving the symptoms. A physiologic disposition towards fatigue may cause a cascade of behavioural changes (including withdrawal from activities), leading to a further cascade of cognitions about illness, mood change (which can often present itself, for many people, in a further somatized set of symptoms), and perpetuating of underlying symptoms. The worldwide network of fellow sufferers may lead to perpetuation of symptoms, rather than relief, because the group consolidates some of the beliefs and identity formation which individuals may have about the condition, and also may agitate against what is seen as a dismissive or ineffectual medical system. The group dynamics may also foster the spread of various spurious alternative therapies, whose evidence base would often consist of glowing testimonial accounts rather than careful randomized data. Factitious therapies could sometimes be quite effective for factitious illnesses, since the therapeutic effort would permit the sufferer a psychological opportunity to move away from the illness symptoms, and attribute the improvement to something external, rather than to psychological change. Such is, in my opinion, the basis for most stories of so-called "faith healing" which have been around for millenia.
It is helpful to have observed extreme examples of somatoform illness. Case examples include individuals who have had recurrent factitious seizures (pseudoseizures), often leading to dangerous and harmfully inappropriate medical interventions. Many persons with a history of pseudoseizures also have neurologically-based epilepsy as well: somatized, factitious, or conversion symptoms often co-exist with their non-psychiatric counterparts. Other case examples include situations where individuals are delusionally convinced that they are paralyzed (due to a conversion disorder) causing them to have lived in a wheelchair for years. Such individuals often have networks of people in their lives who support them in their paralyzed role; such supporters often include physicians and other caregivers. Yet, it has been an amazing experience for me to witness cases of this type--cases where there has never been any objective sign of neurologic disease, but where the impact of the problem has been extreme; if a very careful neuropsychiatric evaluation is done, with strongly structured psychiatric and rehabilitative therapy, I have seen situations where a person experiencing paralysis is able to walk home after a hospital stay.
But cases like these are inevitably complex. If a person has lived in a certain way for years, the behaviours themselves, and the associated thoughts, become integrated into identity. If you live as a paralyzed person for many years, it will not be so easy to get up and walk, even if you are neurologically healthy. There are physical barriers, but obvious psychological and social ones as well.
I believe this is a theme which epitomizes our understanding of brain function: repeated behaviour entrenches neural pathways. If "illness behaviour" exists despite "no illness", the brain learns to function "as if" a physical injury were present. It is just like language learning--with immersive experience over a course of months or years, the brain will speak the new language with ever greater fluency. It is a difficult task for the brain to "unlearn" such experience.
But this suggests a therapeutic imperative: for all cases of this type, immersive physical rehabilitation is necessary. In every single case I have ever seen of severe conversion, for example, the cure required intensive, prolonged, structured involvement of physiotherapists, in addition to whatever medications (typically antidepressants and antipsychotics) and psychotherapeutic work the person needed.
I believe this theme crosses over into the realm of ALL chronic disease, regardless of cause. Management of chronic disability or chronic diseases is greatly assisted by physical rehabilitation. In the language of narrative therapy, if we consider the illness or symptom to be like a negative character in our lives, that character is constantly telling us to do less and less--part of the therapy to challenge this is to find a structured and safe manner in which to do more and more, or to optimize our fitness so that we can do the most despite the limitations imposed by the disease.
Another interesting modality of therapy for conversion, one which can illustrate very compellingly the existence of a structure of drives and defenses first suggested by Freud, is the so-called "amytal interview." In the version I have seen, a patient with a conversion syndrome (following informed consent, of course) is given a dose of ritalin (which allows more amytal to be given without loss of consciousness), followed by intravenous sodium amytal (a barbiturate), with the supervision of an anesthetist in a well-equipped medical setting. The dose is titrated just to the point before the patient loses consciousness. The effect of the medication is to cause disinhibition. In this condition, the psychological forces necessary to continue the conversion symptom are weakened, so for example a person describing paralysis of an arm can be guided to raise the paralyzed arm in the air, and flex it, etc. This event can be videotaped. When the effects of the drug wear off, the person may not remember the scene, but when presented with the video footage (of the non-paralyzed limb in action), the person's psychological defense of conversion will be substantially weakened. As a result, often times a strong emotional reaction takes place, usually the overt emotions or affects consistent with a severe underlying depression which had previously shown itself through "paralysis." In this way, "conversion" operates as a psychological defense, a way in which the brain deals emotionally or behaviourally with a painful symptom. These defenses can be vital ways to survive in the world, but sometimes--as in conversion disorders--the defense system goes awry, and becomes the core problem.
A negative study on vitamin d supplementation
http://www.ncbi.nlm.nih.gov/pubmed/21525520
this 2011 randomized, controlled, prospective study from the British Journal of Psychiatry shows that vitamin d supplementation did not improve well-being in a group of over 1000 elderly women compared to a similar-sized control group.
This is a good study, with negative results. I don't think it means that vitamin d is of no use, but rather that it cannot be assumed to have obvious positive effects for everyone. Some of the effects measured in other vitamin d studies may be the result of non-causative associations (e.g. those with various healthier habits and health paramaters may be more likely to have higher vitamin d levels, but the vitamin d is not the cause of this healthiness, it results from it)
However, the data on this issue continues to evolve. There is some good positive data on vitamin d as well, though not enough in terms of randomized, prospective studies. It will be important, for example, to look at whether vitamin d could obviously be an effective adjunct to other therapies for treating depression. Or whether vitamin d alone has little effect, unless combined with other positive factors.
Meanwhile, I still believe that the standard recommended daily dose of 400 IU for vitamin D is too low, and that 1000-2000 IU per day is better.
See my previous post on vitamin d, http://garthkroeker.blogspot.com/2009/02/vitamin-d-other-vitamins.html
this 2011 randomized, controlled, prospective study from the British Journal of Psychiatry shows that vitamin d supplementation did not improve well-being in a group of over 1000 elderly women compared to a similar-sized control group.
This is a good study, with negative results. I don't think it means that vitamin d is of no use, but rather that it cannot be assumed to have obvious positive effects for everyone. Some of the effects measured in other vitamin d studies may be the result of non-causative associations (e.g. those with various healthier habits and health paramaters may be more likely to have higher vitamin d levels, but the vitamin d is not the cause of this healthiness, it results from it)
However, the data on this issue continues to evolve. There is some good positive data on vitamin d as well, though not enough in terms of randomized, prospective studies. It will be important, for example, to look at whether vitamin d could obviously be an effective adjunct to other therapies for treating depression. Or whether vitamin d alone has little effect, unless combined with other positive factors.
Meanwhile, I still believe that the standard recommended daily dose of 400 IU for vitamin D is too low, and that 1000-2000 IU per day is better.
See my previous post on vitamin d, http://garthkroeker.blogspot.com/2009/02/vitamin-d-other-vitamins.html
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