Governments and Psychiatric Beds

I read a paper yesterday (1) on psychiatric bed policy with a focus on OECD (Organisation for Economic Cooperation and Development) nations.  The OECD has extensive data collection on their member nations and one of the metrics they collect is the number of psychiatric beds per 100,000 inhabitants.  I have demonstrated some of this data before.  For the purpose of this post I downloaded it to create the two graphs above that were used in the paper. One of the authors main points was transinstitutionalization - in this case sending people with serious mental illnesses to jails rather than psychiatric hospitals.  They demonstrate the rough inverse correlation between psychiatric beds and the rate of incarceration.  Throughout my career available psychiatric beds has always been a problem.  It has been a favorite topic on this blog.  I was interested in whether or not this group of authors had anything new to say.

In their introductory section, they provide the back drop with the numbers.  The American state hospital psychiatric beds fell 97% from 558,922 in 1955 to 37,679 in 2016.  In Minnesota, the drop was about 98.5% from 11,449 in 1955 to 175 currently.  Using the OECD data, the average was about 99 beds per 100,000 population in 1998 to 71 per 100,000 in 2015.  Only Germany trended in the other direction by increasing the number of beds.

They do a fairly good job of analyzing the risks of the bed shortage.  They cite rehospitalizations, prolonged stay in emergency departments, pressure to discharge patients from inpatient setting, more frequent involuntary treatment, and associated staff burnout.  They make the argument that higher rates of suicide are noted in community treatment compared to hospitals where suicide is less likely.  They believe acute inpatient care is less available to the acutely suicidal patient and that may account for some increase in the suicide rate. Scandinavian registry studies are cited as providing some confirmatory data with one group of authors stating that the reduction in beds was the "most probable explanation for the rising mortality."  A similar study in Finland where more community resources were available and the beds were at OECD averages described fewer suicides.

Community treatment is typically cited as a reason for the bed reduction.  In the USA, rationing is more clearly the reason since the community resources are rarely developed to compensate for the bed loss.  It is also unstated that the two treatments are not equivalent.  They cite the UK as having extensive community resources that were not enough to overcome the drop in beds leading to higher rates of suicide, transfers out of the area where the patient lives, and involuntary treatment. From the graph, the UK has more beds than the OECD average.

The history of transinstitutionalization is briefly discussed.  The Penrose Hypothesis was developed by Lionel Penrose who pointed out the inverse relationship between mental hospital and prison populations in 1939.  Other authors like Harcourt look at historical data and note the same relationship but discuss it from the perspective of the institutionalized population.  At one point in his book Harcourt suggests that people in the military and in nursing homes may need to be counted as being institutionalized.  Inspection of the bar graphs at the top of this page does illustrate some clear trends but it also illustrates that the relationship is complex and not all of the variables have been studied.  They include a third graph of the Gini coefficient that I did not include.  The Gini coefficient is a measure of income disparity (approaching 0 means less disparity).  The 10/17 countries with Gini coefficients  > 0.3 had the lowest number of psychiatric beds. In other words, more income disparity translates to fewer psychiatric beds.

The statistics about the incarcerated mentally ill in the USA are reviewed and the numbers are significant.  Twenty percent of the incarcerated population or 350,000 people per day are estimated to have serious mental illness.

The problems that I have written about on this blog for years are highlighted including the declining length of stay and what the authors called revolving door admissions.  They point out that schizophrenia has the second highest readmission rate at 1 month compared with any other diagnosis (congestive heart failure is first).  The lengths of stay are not generally long enough to allow for adequate stabilization of severe psychiatric disorders and they provide the references.  I see this population of people as a steady state group that goes from jail to homelessness to a short stay in the hospital.  Substance use disorders are generally not addressed or treated in a cursory manner. 

The paper's strength is that they provide an estimate of what a reasonable number of psychiatric beds is for a given populations.  The Royal College of Psychiatrists established a standard that would give psychiatric patients the same access to high quality medical care as medical and surgical patients.  That includes 4 hour maximum time to wait for admission.  They also said that bed occupancy should not exceed 85% to allow for emergency admissions and the length of stay figure should be 2-4 weeks to allow for real improvement.  Using those parameters a US expert consensus group estimated that 50-60 publicly funded beds per 100,000 population were necessary. In case there is any difficulty reading the above graph, the point plotted was 25 beds per 100,000 US inhabitants - well below the estimated number.  In my home state of Minnesota, that number falls off the precipice to 3 publicly funded beds per 100,000!

A closing example is given of the situation in South Australia.  Hospital beds were closed to a level of 32 per 100,000.  Acute care occupancy exceeded 100%, emergency departments waits went up, acuity increased with increasing risk of the need for physical restraint, and the burden of care was often transferred to relatives and friends.  Reforms were enacted that led to an increase to 35 beds per 100,000 with associated 2 week lengths of stay and decreased rates of suicide.

This is an excellent paper for psychiatric societies and psychiatrists to read.  It documents the problems that we all see on a daily basis and provides some clear answers. The answer does not lie with continued or more perfect rationing.  Unfortunately the people who run these systems - largely bureaucrats in large state human services departments, the politicians who influence those bureaucrats, and administrators of most health care systems all see rationing as their only solution to the problem.  They are incentivized to ration and we (and our patients) are left picking up the pieces.

We finally have a paper that is making a stand against all of this rationing.     
     

George Dawson, MD, DFAPA




Supplementary 1: Data for the top graph was downloaded directly from the OECD and accessed today (July 12, 2018).

Supplementary 2: Data on incarceration rates was taken from the Prison Policy Initiative and accessed today (July 12, 2018).

For both graphs click on them for expanded and improved resolution.




References:

1:  Allison S, Bastiampillai T, Licinio J, Fuller DA, Bidargaddi N, Sharfstein SS. When should governments increase the supply of psychiatric beds? Mol Psychiatry. 2018 Apr;23(4):796-800. doi: 10.1038/mp.2017.139. Epub 2017 Jul 11. PubMed PMID: 28696434.

2:  Osby U, Correia N, Brandt L, Ekbom A, Sparén P. Mortality and causes of death in schizophrenia in Stockholm county, Sweden. Schizophr Res. 2000 Sep 29;45(1-2):21-8. PubMed PMID: 10978869.

3: Bernard E. Harcourt, "From the Asylum to the Prison: Rethinking the Incarceration Revolution," 84 Texas Law Review 1751 (2005). Link

4:  Royal College of Psychiatrists. The Commission to review the provision of acute inpatient psychiatric care for adults.  OLD PROBLEMS, NEW SOLUTIONS: Improving acute psychiatric care for adults in England.  February 2016.  Link  This is a detailed look at bed capacity including current estimates and what can be done to improve it.

Nocebo - Part 2

I have been waiting for this paper (1) to come out for the past 6 months.  I posted on the very interesting nocebo effect in antidepressant trials and why it was so interesting and in the process learned that the lead author - Seetal Dodd had a paper being reviewed on the nocebo effect in bipolar trials.  That paper finally came out and I had the pleasure of reading it and presenting it here.

As a brief refresher, the nocebo effect is an adverse drug experience or worsening based on taking placebo or inactive medication in a clinical trial.  At the clinical level, it can also be an unrealistic reaction to a medication based on  similar response.  Any researcher who has participated in clinical trials that all breaking the protocol and allow the subject to be informed about whether they were taking active drug or placebo has probably observed this effect.  Clinicians commonly see it as an improbable reaction to a medication or in some cases multiple medications.  It is an important phenomenon because it blurs the results of clinical trials by making it seem that there is less difference between placebo and the active drug being studied.  It also may lead to the rate of actual adverse events due to the study drug being underestimated.

For the purpose of this study the nocebo response is defined as any a treatment emergent adverse events (TEAE) or clinical worsening in people treated with a placebo. That involves collecting data on both TEAEs and rating mania and depression.

The data used in this study was from a randomized placebo controlled clinical trial of olanzapine monotherapy for bipolar disorder versus placebo and several comparators (haloperidol, valproate, olanzapine-fluoxetine combination [OFC]).  The trials occurred between 1996 and 2007.  There were a total of 9 studies and 7 were published.

Only data for the patients randomized to placebo (N = 1185/4680) were used for the purpose of this study and meta-analysis.  866/1185 or 68% experienced  (TEAE) and 4.6% discontinued the study due to a TEAE.  Typical rating scales for mania and depression were used to rate symptoms. TEAEs were significant ranging from 3% to 11.8% of the placebo treated group.  Headache, insomnia , somnolence, anxiety, nausea, diarrhea, irritability, and agitation all occurred in over 5% of the placebo treated patients.  Median time to report the TEAE was 16 days with the longest time of 37 days.

Apart from the TEAEs, a significant number of the placebo treated patients experienced clinical worsening as noted on the rating scales for depression (321 or 27%), mania (585 or 49%), or global function (278 or 23%).

The 806 patients reporting TEAEs reported a total of 1,119 nocebo events.

TEAEs were associated with not being treatment naive, being obese, being located in the US, and participating in an earlier study.  There were no significant difference based on gender or smoking status.

A major limitation of the study is that it is not possible to detect if clinical worsening is a nocebo effect or and the effect of worsening illness.

In their discussion the authors point out that the evidence is that the nocebo effect is significant in clinical trials.  Of all of the possible correlates they studied they di not find any that were useful to predict who might be a nocebo responder.   They discussed some psychological theories and in a couple of additional papers discuss the putative neurobiological underpinnings of both the placebo and nocebo effect.  Certainly any effect that leads to 4.5% or placebo treated patients discontinuing the study is significant.  Until the nocebo effect is better characterized we probably do not have an adequate estimate of the side effect profiles.  The authors describe is as similar to the placebo response as "an expected consequence of exposure to therapy."

The nocebo response may be less clear in looking at the therapeutic effects of medication.  I think it is good to remember that true nocebo/placebo effects are estimated on the placebo response.  In other words a 20% placebo response rate means that 20% of the actively treated group also responded to placebo.  Hence, if 68% of the placebo treated group experience TEAEs and 4.5% discontinue the study on that basis - what happened when those number are applied to the actively treated group?  It would generally mean less subject carried forward in an intent-to-treat analysis and and a more favorable side effect profile if the nocebo responders could be accurately identified. A good place to start to look for more accurate numbers and methods of identification may be in large scale medicine studies looking at an identifiable quantitative endpoint like blood pressure.  The nocebo effect is easier to sort out with a medication that has a clear effect on a more easily measured parameter.

Clinicians are left with estimating the likelihood of a TEAE or nocebo response based on the likelihood of a patient exhibiting a particular side effect.  A low likelihood of a particular presentation is fairly frequent in clinical practice and continuing the medication in those circumstances often comes down to clinical necessity.  As an example, the patient has a vague TEAE, but learns from the physician that there are no other medications that can be prescribed for the problem.

Nocebo responses are certainly out there.  Clinically we can be more specific until there is better research guidance on what to do about it.  I have had conversations with many people who were interested in the placebo response or why a particular pattern of responding to a therapeutic intervention may have been established.     



George Dawson, MD, DFAPA


References:

1: Dodd S, Walker AJ, Brnabic AJM, Hong N, Burns A, Berk M. Incidence and characteristics of the nocebo response from meta-analyses of the placebo arms of clinical trials of olanzapine for bipolar disorder. Bipolar Disord. 2018 Jun 21. doi: 10.1111/bdi.12662. [Epub ahead of print] PubMed PMID: 29926533.

Attributions:

Figure at the top is stock photo from Shutterstock per their licensing agreement by kasezo entitled:

Stock illustration ID: 284558927 conceptual 3d design of false pill.( placebo and nocebo effect.red and green colored version)

A Stress Test.... Free Associations

I was just starting to breathe a little heavier.  The nurse running the test has been talking to me - continuously for the last nine minutes.  She was bright, pleasant, a great conversationalist but more to the point - everything she said seemed highly relevant. From time to time she would ask how I was doing, check my blood pressure and tell me what my heart rate was.  Some time at about the 9 minute mark she said that I might need to break into a jog for the next level.  It was a 16% grade at 4.1 mph.  The treadmill tilted up and it was a smooth transition.  I was still walking at a fast pace.  "Your heart rate is 160 are you OK?"  I was feeling very good.  Still talking in full sentences and not feeling stressed at all.  My left knee was sore and I said: "My knee is sore and I don't want to break into a jog.  I will complete this stage and call it a day."

I did have room at the end and am fairly confident I could have knocked off the next stage.  I have done it many times in the past starting with a test at about ago 42.  There were a number of considerations holding me back.  The knee.  It was nothing big.  When you exercise a lot as an adult - episodic knee pain is all part of it.  Secondly, a history of paroxysmal atrial fibrillation.  I probably got it in the first place from running heart rates too high for my age.  I did not want to flip into another episode of atrial fibrillation.  Third, the target rate.  Before starting, the supervising nurse told me that the target heart rate for a guy my age was 140 bpm and I was over that with no signs of ischemia or more importantly a widening QRS interval (I take flecainide).  Fourth, I was just happy to be there.  Even though I have had 5 exercise stress tests over the last 25 years, the last one was at the Mayo Clinic about 10 years ago.  These things are a lot less certain with age. As I was on the treadmill, I kept thinking of a review I read in the Medical Clinics of North America many years ago: "40% of 85 year olds have significant coronary artery disease".  Of course those are the 85 year olds who survived to that age.

I had other associations while I was walking and talking. I take a cardiac history on every person I talk with. Some are more detailed than others. I know a number of ways that stress tests can be failed. I know from talking with people what happens when your ECG suddenly shows signs of ischemia. Generally the next step is a Cardiologist spraying nitro into your mouth.  I also know that passing a stress test is a generally a good sign, but it is not a guarantee. Nothing in medicine is.  Too many people have told me about cardiac problems in the absence of a positive stress test, including an infarction in the absence of any occlusions.  Irrespective of the result, I would maintain humility and strive even more to avoid the trans fats that are quantitatively too low to make it on the food label.  And of course all of that bakery with thick frosting - the first display you encounter in any supermarket.           

I had the exercise stress test two weeks ago.  Four days earlier I was doing my usual dictation of an assessment in my office and as I stretched back - I experienced an intense sharp burning pain going down the left side of my sternum.  It lasted about 5- 10 seconds.  I have been having this pains for at least a year all over the chest, left shoulder and back.  At one point they were clearly musculoskeletal in origin and I could replicate them by certain movements or flexing certain muscles.  But then the discriminatory ability was gone.  All of the tricks I learned in medical school and residency about the  difference between musculoskeletal pain and true cardiac pain or angina did not apply.  One of the things they never teach you is that when you get old - all of the routine pains that you live with every day meld into vague pains all over your torso.  Was that chest pain or did it originate in my back, neck or shoulder?  Arthritic pain or pain from trying to do too many pull ups last night?  At some point I just decided to go in to see my internist to see if we could figure it out.

My internist has known me for 30 years.  Any chest pain in the early part of that period was immediately dismissed as musculoskeletal pain.  He knew I was a compulsive exercise fanatic and between the ages of 30 and 55 probably cycled 200 miles per week or the equivalent. In the winter, I would speedskate as much as possible.  My goal was to end the season by doing as many laps as possible in an hour on the John Rose Oval - one of the few refrigerated speedskating outdoor tracks in North America.  Doing that kind of exercise gets the heart rate up to very high levels.  During interval training up to 190+ beats per minute.  Whenever the subject came up during those years my internist would say: "You do a stress test every time you exercise".

That all changed at age 55.  I was out doing a warm up on the speed skating track.  I looked down at my heart rate monitor and it read 170 bpm.  One lap later it was chirping loudly and now it read 240 bpm.  I felt my carotid pulse and it was the irregularly irregular rhythm of atrial fibrillation.  That led to 2 hospital admissions, 2 cardioversions, 2 consultations with a sports cardiologist at the Mayo Clinic and 2 exercise stress tests on a bicycle at Mayo.  I ended up on flecainide  with the advice to consider an ablation procedure at some point in the future as long as the flecainide continued to work and "if the technology improves".  That is a direct quote from one of my electrophysiologists.

During the bicycle stress tests, I ran my heart rate up to 170 bpm and could have gone higher, but was concerned about triggering another episode of atrial fibrillation that would no longer respond to flecainide.  On echocardiography, I have features that are seen in some series of cyclists who do high levels of dynamic exercise - primarily an large left atrium and a slightly enlarged aortic root.  During dynamic exercise, there is a steady increase in blood pressure despite the fact that stroke volume peaks at about 120 bpm and main contributor after that point is heart rate and sympathetic nervous system output.  My adaptation was to try to keep my heart rate at 140 bpm or lower when exercising and lately 130 bpm.  It is good to know I can go higher even for brief periods of time.

So the coronary arteries may be OK, but that leaves paroxysmal afib and the enlarged aortic root/aorta.  We have only recently discovered the role of the layered extracellular matrix in aortic anatomy. Like most of these structures disruption of those layers can result in permanent weakness.  It is also known that high levels of dynamic exercise results in aortic enlargement.  I have not seen any outcome studies of those individuals - but it would be useful to find an expert. 

My next step is to see a Sports Cardiologist about the afib and aorta.  I anticipate that he or she will wonder about why there is an old man in the examination room trying to get as much performance as possible out of an aging cardiovascular system.  If that question comes up, the response is simple:

"I don't want to die on the side of the road from a blown aorta because I tried to race a 40 year old up a hill.  I need your most conservative estimate on how I can prevent that."

And so it goes......


George Dawson, MD, DFAPA


Supplemental:

Previous exercise stress test done on a bike at the Mayo Clinic in 2012 showed a similar result (possibly low BP and heart rate this time but I find that it is easy to over rev on a bike as opposed to a treadmill).


         

Package Insert For Epidiolex - Does It Suggest A Problem With Medical Cannabis?

Cannabidiol (C₂₁H₃₀O₂)

Epidiolex was approved by the FDA two weeks ago for Lennox-Gastaut syndrome or Dravet syndrome in patients 2 years of age and older.  Epidiolex is cannabidiol (abbreviated CBD) one of several compounds in the plant Cannabis sativa.   I had a previous post on this compound but that was before the package insert came out.  I like to study package inserts of all of the pharmaceuticals I encounter to prevent unexpected side effects, anticipate drug interactions, look at the current prescribing recommendations, and study all of the safety considerations.  Every drug has a section in that package insert about the pharmacokinetics, pharmacodynamics, and considerations in the case of hepatic or renal impairment.  In some cases there are very specific recommendations for dosing with metabolic impairment or potential drug-drug interactions.  The other interesting aspect in this case is that Epidiolex is considered the first botanical extract to be FDA approved and the first cannabis derived compound.  A significant part of the population considers cannabis to be a benign natural product with none of the usual pharmaceutical concern about organ toxicity and drug interactions.

Reading the actual package insert a few things jump out at me today.  The original indications are the same, but the logical question is whether this medication will be used for off labeling prescribing for other indications.  After hearing one of the top epileptologists  in state talk about the use of cannabinoids for epilepsy, there is also the question of whether the diagnosis is correct.  In that lecture he pointed out that a case example in the news media probably did not have the diagnosis and that the expert in the state who could make that diagnosis was not consulted.

The dosing of the drug is fairly robust going from 5 mg/kg/day up to 20 mg/kg/day.  For a 70 kg man that comes out to a max dose of 1400 mg/day putting it in the range of several other anticonvulsants from different classes.

There are warnings about hepatotoxicity.  Early in the document, it states that some patients will experience elevated liver function tests and in some cases with develop overt side effects leading to drug discontinuation.  Baseline screening is recommended with AST, ALT, and total bilirubin.  Patients with elevated baseline transaminases were more likely to experience further elevation of these tests than those subjects with no baseline elevation.  The Child Pugh classification of severity of liver disease is used as a metric with dose adjustments suggested for mild, moderate, and severe disease.

Thirteen percent of patients had ALT elevations that were three times the upper limit of normal (ULN).  Less than 1% had transaminases that were 20 times the ULN and some patients were hospitalized.  In a third of the cases the transaminase elevation resolved without treatment.  In the other two thirds it resolved with discontinuation of the Epidiolex or the associated anticonvulsant (valproate).

Risk factors (associated drugs - clobazam, valproate), dose, and baseline transaminases) were discussed as well as monitoring.  Given the prevalence of the problem screening transaminases at 1 month, 3 months, and 6 months and as indicated after that.  More importantly - screening for the physical illness from drug induced liver disease ("explained nausea, vomiting, right upper quadrant abdominal pain, fatigue, anorexia, or jaundice and/or dark urine") can lead to further evaluation.  Three scenarios for discontinuing the Epidiolex are recommended:

1.  Transaminase levels greater than 3 times the ULN.

2.  Bilirubin levels greater than 2 times the ULN.

3.  Transaminase levels greater than 5 times the ULN. 

My read of the difference between 1 and 3 is that 1 can be a temporary measure but 3 should be permanent.  In my experience with valproate, I would definitely discontinue with these levels.  That is based on the well validated concern that valproate can cause significant hepatotoxicity. It is still possible that additional trials and post marketing surveillance will show that there is not long term concern with CBD.  In the trials transaminase elevation was the most frequent reason that the drug was discontinued (24% versus 3% on placebo).

Drug interactions noted that could be clinically significant. Epidiolex is metabolized by  CYP3A4 and CYP2C19 so that inhibitors of these enzymes can potentially increase the plasma levels.  Strong inhibitors of CYP3A4 include HIV antivirals, antifungals, and buprenorphine.  There are no strong CYP2C19 inhibitors.

Inducers of the same enzymes can lower Epidiolex levels and the standard inducers of those enzymes are carbamazepine, oxcarbazapine, phenytoin, HIV antivirals, prednisone and glucocorticoids, and St. John's Wort. 

Additional warnings about the use of the drug include somnolence and sedation (32%), suicidal ideation and behavior, hypersensitivity reactions, and the risk of withdrawing an anticonvulsant and need to do it gradually.   Regarding the suicidal ideation and behavior the only data presented was from a large (N=199) pooled analysis of clinical trials.  It is a standard warning on all anticonvulsant drugs and there was nothing specific to Epidiolex or CBD.

Clearly Epidiolex or CBD extracted and used at pharmaceutical doses may have some of the power of pharmaceuticals but also has the same significant side effects.  The side effect profile and drug interaction concerns are very similar to other pharmaceuticals that are used to treat epilepsy. This raises some interesting issues in states like Minnesota where high potency extracts of cannabis are being sold as medical cannabis and there is minimal medical supervision - primarily because there is scant evidence that cannabis extracts are medical treatments.  As I previously observed from the most recent report of the Minnesota medical cannabis program, extracts are being sold in this state that result in the ingestion of 12.2 - 1,439.2 mg/day of CBD.  The middle to high end of that range is clearly in the dose range for Epidiolex and the extracts are not prescribed or monitored by physicians - at least there is no requirement for that to happen.  Looking at all of the available data it is clear that the person taking 1,439.2 mg/day is an outlier and the next cluster of patients is at the 100-200 mg/day range. 

In Minnesota, a medical provider certifies a patient as having a condition that qualifies them for medical cannabis. In the case of this report it is chronic pain.  That patient goes to a medical cannabis dispensary and discusses what they want with a pharmacist.  In the case of high CBD products, as far as I know there is no recommended screening, monitoring, or patient education.  Just based on what I read in the current Epidiolex package insert, if the CBD content of the medical cannabis is in a similar dose range that is the equivalent of taking a new pharmaceutical and making it an over the counter drug.  The neurologists prescribing Epidiolex have good guidance on what needs to be monitored and are undoubtedly very familiar with the compound.  Other physicians including psychiatrists need an awareness of the pharmacology of CBD - especially if the dose is in the range suggested by this package insert.

If it was needed, this seems like further evidence that the miracle of medical cannabis has affected the judgment of many who seem to consider it a benign natural product. It turns out in this case, it can have a therapeutic effect on specific seizures at a significant dose for conditions that did not have many good options.  That treatment comes with clear risks.  The risk is reduced since all of the patients treated for the indicated seizure disorders are being followed by neurologists who specialize in the polypharmacy necessary to treat complex seizure disorders.  That includes monitoring potential drug interactions and toxic effects.  Can we say the same thing for people obtaining it through the medical cannabis program or being prescribed the drug off label?

Medical cannabis needs to be taken as seriously for the side effects as it does for the purported benefits.


George Dawson, MD, DFAPA


Reference:

Full Prescribing Information for Epidiolex. FDA approved package insert.


Supplementary 1:

Any FDA package insert is available online by Googling:  "[Drug name] FDA Package Insert"   The PDF of that drug insert will pop up and you will have access to same the full prescribing information that any physician has.

Supplementary 2:

In Minnesota, there are two companies that are the exclusive providers of non-smokable medical cannabis products Leafline Labs and Minnesota Medical Solutions.  Actual THC and CBD content is available on the web sites of both companies.

Leafline Labs has a vaporization product, a sublingual spray, an oral suspension, and a topical preparation.  The highest concentration of CBD in the oral solution is 20 mg/ml.  Epidiolex is 100 mg/ml.

Minnesota Medical Solutions has similar delivery forms and their oral products are capsules and solutions in both 47.5 mg CBD or 100 mg per milliliter CBD.  The latter is the same as prescription strength Epidiolex.

The Problem of Antidepressant Discontinuation

Antidepressant discontinuation is a useful topic to discuss for a number of reasons.  First, it is a legitimate problem for a number of people who want to stop the medication and find that they can't for one reason or another.  Secondly, some of the people are unable to stop because they have discontinuation or withdrawal symptoms from the antidepressants and for some people these symptoms are extremely distressing.  In other cases the people trying to stop get recurrent symptoms of anxiety, insomnia, and depression and have to resume the medication.  Thirdly, the solutions to the problem are poorly defined.  In the US, antidepressants are prescription medications and that should mean that they are prescribed for a clear indication and carefully monitored.  Those safeguards are not clearly present any more and even if they are having the indication and carefully monitoring the medication does not guarantee that the patient will not get severe side effects or problems with discontinuation.  On a population wide basis, prescribing antidepressants for only clear cut indications will mean that the minimum number of people are affected and that an antidepressant will be stopped at the earliest sign of problems.  All of the current trends in screening for depression, encouraging treatment by nonspecialists, and limiting the availability of non-pharmacological methods for treating psychiatric and emotional problems suggests that a major cultural change would be required to reverse those trends.    Fourth, because of these problems - the antidepressant issue is an informed consent issue to patients.  In addition to warnings about the usual side effects they also need to hear about the more serious side effects including serotonin syndrome, cardiovascular side effects, possible drug interactions and withdrawal and discontinuation symptoms.  Finally, it is not clear that liberal antidepressant creates more problems than it solves.  The best example I can think of to illustrate this fact is a paper I posted here in the past showing that there was a clear trend in decreased suicide in the elderly with increased antidepressant prescribing across the entire population of Denmark.  On  clinical basis I have had conversations with hundreds of people about stopping antidepressants and the results of many of those conversations is surprising.  Although the main FDA psychiatric indications for antidepressant prescribing are mood disorders, anxiety disorders, and obsessive compulsive disorder - it is common to find people who are taking them for other reasons. Extreme irritability and anger control is one.  Needing to have a "level mood" is another.  Taking antidepressants for menstrual and menopausal mood symptoms that do not meet diagnostic criteria for major mood and anxiety disorders is another. 

The two main considerations for antidepressant discontinuation are whether the person experiences recurrent symptoms of the primary problem or specific discontinuation or withdrawal symptoms or a combination of both. 

A few addition points about antidepressant withdrawal.  The first case in the medical literature was reported for tricyclic antidepressants in 1959 (1) and the first review in 1993 (2).  The symptoms were also described in the first edition of a major psychopharmacology text (2):

"There is no withdrawal problems with the TCAs of the type seen with narcotics, alcohol, or sedatives.  Instead, abrupt discontinuation of 150-300 mg/day or more of a tricyclic, especially after 3 or more months of treatment can induce autonomic rebound (ie, gastrointestinal disturbances, autonomic symptoms, anxiety, agitation, and disrupted sleep)."  p 276.

Gradual taper rather than abrupt discontinuation was recommended.  The issue of rebound from REM suppression and nightmares or intensification of dreaming was also discussed.

For the sake of brevity, I am going to discuss a recent trial of antidepressant discontinuation (4), what is wrong with that trial, and how to improve the state of affairs in the future.  For some reason, I could not find this study indexed by the National Library of Medicine.  Full text is accessible by the DOI number.

This is a study of an attempt to withdraw patients from antidepressants with success in doing that designed as the primary end point - further defined as no antidepressant use in 6 months and no depression or anxiety by a standard rating at 1 year follow up.  The patients were selected from 45 primary care practices across the Netherlands between February 2010 and March 2013.  The algorithm for patients selection in each stage with the resulting numbers are available in diagram form in the body of the paper.  Anyone not meeting criteria for maintenance anti-depressant or anxiolytic treatment were identified as possible candidates for the study.  Appropriate use of antidepressants for depression and anxiety was defined as a history of recurrent depression [≥3 episodes] and/or a recurrent psychiatric disorder with at least two relapses after antidepressant discontinuation.

6442 long-term antidepressant users were identified in these primary care settings.  2411 (37%) were eligible with that determination made by their primary care MD. 358/2411 (15%) consented to participate and 146 were included in this study.

The specific intervention is hard to get at in the description given.  For the intervention group a patient specific letter was sent to the general practitioner with the recommendation to taper the antidepressant. Antidepressant tapering instructions, antidepressant discontinuation symptoms, and the recommendation for slow tapering were all included.  The GP discussed this with the patient and then sent a response to the research team on whether or not the patient would comply with the recommendation.  Reasons for not complying were requested.  For the control group, patients continued their usual care and their GPs were unaware of their participation in the study.  In US studies this would be the treatment as usual group.

34/70 rejected the intervention citing fear of relapse or recurrence as the primary reason.  That is interesting giving the inclusion criteria.  Is it possible that disorder severity or anxiety or depressive subtypes were perceived as more severe by the patient than the recorded primary care diagnosis? None of those patients cited antidepressant discontinuation symptoms as a reason.

Only 4 (6%) patients in the intervention group and 6 (8%) patients in the control group were able to successfully stop antidepressants.  There was a slightly higher relapse rate in the intervention (18/70)   versus the control group (10/76).  No other variables other than duration of antidepressant (5.7 years versus 9.6 years) were significant in who could discontinue the antidepressant and who could not.

In their discussion the authors comment on a higher relapse rate in the intervention group that was not associated with antidepressant discontinuation.  They attribute it to anxiety about wanting to comply with the recommendation but not being motivated to do it.  I think that any anxiety about the recommendation is more likely due to the fact that the recommendation is coming from a source that is not their primary care physician.  Most people in primary care with longstanding relationships with their physicians are there for a reason.  Taking a recommendation in opposition to their GP would be highly problematic for many.  They cite several other reasons among them a poorly done meta-analysis of antidepressant trials suggesting a large placebo effect.  In fact, all of these meta-analyses are significantly flawed based on the included studies.  But more on how to sort that out below.   

I am going to avoid constructing my own antidepressant discontinuation checklist but plan on that in the next several days.  My extensive clinical experience and the literature lead me to the following conclusions:

1.  Expose only the subpopulation who needs antidepressants to them:

This is easier said than done because of the literature on under diagnosis of depression in primary care settings, the literature (and lack of evidence supported guidelines) on screening everyone for depression, the new collaborative care initiative encouraging the use of a checklist to diagnose and treat depression, and the massive bureaucratic interventions to encourage screening and treatment with medication.  Like opioids - primary care physicians were scapegoated for not recognizing and treating depression.  Now both of the primary care professional organizations have their own depression treatment guidelines and these physicians are criticized for overprescribing antidepressants.  Things might go a lot better if the politics was wrung out of medicine.

2.  Recognize that some patients have severe discontinuation effects: 

There is 60 years of literature on this topic, we have all seen it, and it should be a given.  It should be addressed even if there is not perfect research on how to help these people.  I have said it in the past and will say again - I have treated people with severe discontinuation symptoms and helped them stop the medication.  Some syndromes are much more complicated than others - like SSRI withdrawal that has an anticholinergic component.  As I have said in the past - I just don't prescribe some of these medications (paroxetine) and have not in decades.  I would never have prescribed venlafaxine again if they had not invented an extended release version and found it was very useful for people who can't tolerate any SSRIs - but that does not mean that there aren't people out there who don't get severe discontinuation symptoms because of venlafaxine XR.  All of this is an informed consent issue and you can't have that discussion seeing people very 10 minutes and handing them a prescription.

I will say that the majority of people that all psychiatrists treat routinely go on and off antidepressants without problems.  It is so commonplace that many health care companies have systems that send the physician a letter if the patient has not picked up their antidepressant prescription.  That is very common and typically because patients have reservations about starting the medication or how the appointment went.

3.  Study the problem in a realistic setting: 

The study I discussed above was destined to fail. A more realistic study should reflect the clinical reality that every psychiatrist knows.  Instead of an intervention telling people when to stop, the intervention could look at all episodes of antidepressant discontinuation in a health care system.  Various strategies could be used and data on the reason for stopping and any discontinuation symptoms could be gathered in a systematic way.  There are several statistical models that can be applied to multiple episodes across fewer patients.

I would suggest that the intervention not be conducted by the physician who prescribed the original treatment because of the aforementioned conflict of interest.

As in antidepressant trials, the nocebo effect is significant and needs to be studied in discontinuation.  In other words, if a person is told that the antidepressant is being discontinued and they are given the exact same dose of the same antidepressant will they develop symptoms of discontinuation?  Will people being treated with placebo develop discontinuation symptoms?

There is also a lot to be said for an unblinded study of people who are motivated to just get off the antidepressants with a standard protocol. I would not mind conducting that study myself and also adding a component to see, if the success of people who are highly motivated to stop could be predicted.

4.  Despite the evidence-based crowd, the experts need to be heard: 

Like many other psychiatrists, I have seen severe antidepressant discontinuation symptoms, but have been able to get the patient off of the antidepressant.  The idea that there are people who cannot get off these medications and they need evidence to get off the medications is a circular argument.  The evidence is out there, and the experts should write a consensus statement.  That should be the basis for further trials and those trials should employ psychiatrists who know how to do this.  If there are that many people with the problem - it should be easy for any University department to recruit them and study them in detail in the hope that they can successfully get off the medication.

5.  The issue is important in everyday clinical practice:

The best illustration is changing antidepressants.  There are three methods, abrupt discontinuation and starting the new one, gradual taper and start, or taper with cross titration.  The majority of people I see can tell me if they have ever had discontinuation symptoms when they stopped or ran out of the antidepressant that we are changing. That turns out to be a good predictor of who can just stop the antidepressant and start a new one the next day.

That concludes my brief discussion of the problem and what I think can be done about it.  One thing is for sure - political discussions of this issue fail to advance getting the best care to the maximum number of people - whether that is a bitter discussion of how antidepressants are poison and nobody should take them to how they should be casually prescribed as part of a screening process.



George Dawson, MD, DFAPA



References:

1: Mann AM, MacPherson AS. Clinical experience with imipramine (G22355) in the treatment of depression. Can Psychiatr Assoc J. 1959 Jan;4(1):38-47. PubMed PMID: 13629473.

2:  Garner EM, Kelly MW, Thompson DF. Tricyclic antidepressant withdrawal syndrome. Ann Pharmacother. 1993 Sep;27(9):1068-72. Review. PubMed PMID: 8219442.

3:  Philip G. Janicak, John M. Davis, Sheldon H. Preskorn, Frank J. Ayd.  Principles and Practice of Psychopharmacotherapy.  Williams and Wilkens, Baltimore Maryland, 1993.

4:  Eveleigh R, Muskens E, Lucassen P, Verhaak P, Spijker J,  van Weel C,  Voshaar RO, Speckens A.   Withdrawal of unnecessary antidepressant medication: a randomised controlled trial in primary care.  BJGP Open 2018; 1 (4): bjgpopen17X101265.  DOI: 10.3399/bjgpopen17X10126


Supplementary:

Reviews of antidepressant discontinuation syndrome. Link


Polling Question:

I thought I would add a polling question to this post for any physicians out there treating depression.  One of the commonest encounters that I have had due to this blog have been people who claim:

1.  Severe antidepressant discontinuation/withdrawal.
2.  Associated long term conditions with withdrawal.
3.  A complete inability to stop antidepressants.
4.  Extraordinary measures needed to stop antidepressants - like breaking the capsule or grinding up the tablet and reducing the dose by 1 mg amounts.

I don't doubt #1 at all because I have seen it and treated it.  In the case of #2, the only medication I have seen this occur with was beta blockers - metoprolol  specifically.  In that case the patient was taking the medication for blood pressure control and developed severe panic attacks and associated tachycardia and insomnia trying to taper and discontinue the medication.  There was no previous history of anxiety.

I am interested in what physicians have directly observed in these areas.

They Don't Even Know What They Are Seeing.......

I was walking back from a meeting with a psychiatric colleague the other day.  There was the usual grousing about the practice environment and miscommunication and she made the following observation about why physicians and psychiatrists don't get the information they need.  She pointed out that in many cases the nonphysician  observers: "Don't even know what they are seeing."  If you are counting on people for observational data and that is true - that is a setup up for suboptimal care at the minimum and a catastrophe at the worst.

Take the case of a very basic measurement - blood pressure and pulse.  Anyone taking those measurements should be aware of the guidelines and whether or not the patient has a baseline abnormality, condition that can affect either, or medication effect that leads to changes in the vital signs.  They should also be aware of the limitations of measurement.  All of the automatic blood pressure machines in the world will not be able to assess and treat the patient unless the operators know what the numbers mean.  They also need to know that one of the problems with single operator and strictly machine operated approaches is that arrhythmias are problematic even if the blood pressure is fine.  There have been situations where I had to put together a continuing education course on blood pressure and pulse and the correct assessment of both.  That was a long time before the recent article on common mistakes made by medical students in these measurements.

If measurements that are considered routine and done hundreds of times a day are problematic what about observations that occur on the other end of the spectrum.  A common health care myth today is: "If I have a checklist and check off all of the boxes on that list that will lead me to some kind of diagnosis."   That is probably a minimization of the myth.  In the case of psychiatry, the myth is more: "If I convert a standard psychiatric assessment into a form (or a checklist) - the ultimate product of going through that list will basically be a psychiatric evaluation and diagnosis."  Systems of care who use this approach can deny these myths as much as they want but I see this happening every day. Organized psychiatry and the DSM approach to diagnostic criteria is partially responsible, although the manual does say that it can't be used by anybody.  It doesn't say who specifically should use it and it does not suggest (like Kendler) that it is an indexing approach.

Looking at the graphic at the top of the page illustrates why a form or a checklist does not suffice.  The observer/psychiatrist in the drawing is doing more than asking the subject a series of yes or no questions.  The psychiatrist is looking for patterns in symptoms (medical and psychiatric), what is happening in relationships with the person (including the relationship to the psychiatrist), and the person's conscious state - specifically whether there has been a departure from baseline.  There is often a balance between historical detail, phenomenology, the person's ability to describe what has happened and a plausible scenario based on probability estimates from the psychiatrist's previous experience.  Any psychiatrist who has been trained in many presentations of complex psychiatric illness is more likely to see those patterns than somebody who has not been.

To illustrate some of these concepts I will describe several cases that are all what non-psychiatrists (nonphysicians and other physicians) called hysteria. Hysteria is an old word that dies hard.  The DSM equivalent is histrionic personality disorder.  The generic use of the term suggests a person who is overly emotional, dramatic and attention seeking but there are 8 diagnostic criteria that are unchanged between DSM-IV and DSM-5.  Many clinicians opt for the term Cluster B - a DSM-IV originated term that grouped personality disorders in groups according to some common diagnostic features.  The Cluster B group included individuals that often appear dramatic, emotional, or erratic.  Those personality disorder diagnoses include antisocial, histrionic, narcissistic, and borderline.

The rule-in criteria (significant impact on life circumstances and onset when you expect a personality disorder to occur) and the rule-out criteria (not due to another mental or physical disorder) are predictable for any causal reader of a DSM and could be included on any checklist or form.  How does all of that play out?  Well here are a few examples:

Hysterical patient #1:   A 30 year old woman presents for a therapy intake.  She is mumbling and laughing.  The therapist describes her as "odd and having an odd affect."  She alludes to some suicidal behavior in the past but is smiling and joking about it.  The therapist has the impression that she is manipulative and overly dramatic.  He contacts the clinic psychiatrist and says that she is histrionic but he is concerned about her suicide potential.  The psychiatrist sees her that day and makes a diagnosis of bipolar disorder-mixed type with psychotic features.  The patient is eventually stabilized on lithium and an atypical antipsychotic.

Hysterical patient #2:  A 25 year old woman is being treated on a general medicine ward for dehydration from a respiratory infection.  She suddenly gets tearful and agitated.  Family members visiting have to physically restrain her when when she tries to get out of bed.  She starts to make very loud high pitched vocalizations.  A psychiatrist is called to go in to assess hysteria and possibly sedate the patient.  The psychiatrist sees an agitated young woman who is not able to respond coherently to any examination questions.  Brief neurological examination suggests increased intracranial pressure is the problem and the patient requires immediate transfer to a neurological intensive care unit. 

Hysterical patient #3:  A 58 year old man is referred acutely from a therapist for acute panic attacks and "probable Cluster B" personality traits.  He has recently retired due to osteoarthritis of the knees.  He had no earlier history of panic attacks but the therapist thought that he was overly dramatic at the initial session 2 days earlier when he was unable to relax and breathe normally with behavioral techniques that are usually effective.  The psychiatrist gets a history of the patient needing to abort an exercise stress test two weeks earlier due to the arthritis and having  a prolonged period of immobility at home due to sore knees. During that time he developed acute shortness of breath.  The episodes of anxiety that he described were secondary to shortness of breath and not panic attacks.  The psychiatrist sends the patient to the emergency department where an acute pulmonary embolism is diagnosed and he is admitted to the ICU.     

These are just a few examples restricted to one collection of psychiatric symptoms that illustrates what my colleague was referring to.  The value of psychiatric training goes far beyond what is in the DSM and what checklists and templates can be extracted from it.  I have never really met a psychiatrist who was focused on the DSM probably because it is implicitly evident to us that it is an index more than a diagnostic manual. We are focused on what is not in the DSM and as far as I know that is not well documented in many places.  Those are the patterns associated with clinical practice and that should have been gleaned along the way with medical training.  The DSM doesn't tell you how a pulmonary embolism presents. It is possible that you night have never seen one. But in medical training I can guarantee that it was discussed somewhere along the line in the differential diagnosis of dyspnea.  I can guarantee that one of those attendings discussed the phenomenon of the healthy young adult immobilized by air travel who gets off at their destination and suddenly has an acute pulmonary embolism. All of those features and urgencies should be in a physicians conscious state when they are seeing the whole patient and not some DSM/checklist version of a patient.

This brief post also illustrates the biasing effects of language.  What  does "Cluster B" really mean?  Aren't people who are acutely medically (or psychiatrically) ill dramatic, emotional, or erratic?  Hysteria is an extremely biasing term that over the centuries has been applied selectively to women rather than men.   The examples above illustrate that point.  If you are seeing the world through DSM language and that is your only lens - you are by definition not seeing the whole patient.  The list of possible errors in that landscape is very large.

There are a number of constraints that will get  in the way of a trained psychiatrist trying to see the whole patient.  Inadequate time is one, but time frames vary significantly.  Diagnosing a life threatening medical problem upon seeing a patient may take a matter of minutes and is clearly the most important diagnosis.  Seeing a long series of new patients briefly to prescribe treatment will necessarily mean that certain features in the above diagram will be missed.  So-called measurement based care depending on a large number of checklists to "quantitate" affects or other psychiatric states makes the same mistake.  Collaborative care where a psychiatrist looks at these rating scales and recommends treatments makes the same mistake.

The best assurance that the critical aspects of care will not be missed is to be sitting across the room from someone who has been taught all of the critical aspects of care.  That process is complex and as far as I know has never been adequately described.  A first approximation is whether that person knows what they are seeing and how to respond.

George Dawson, MD, DFAPA     

Conscious States and Suicide.....

When I first starting writing this blog - I decided that I was not going to make the common mistake of using celebrity tragedies as a springboard for posts.  I have been very pleased with that decision.  Given recent events - it is evident that people who use that approach are speculating and either don't know enough of the details or make sweeping statements that they could have made without any specific reference to the person or their family.  It is also evident that in some cases, the potential for damage to the survivors is great and should be avoided at all costs.  The only rationale that I hear is they were celebrities and the people want to know.

I will comment on the mystery of suicide.  How is it that a highly accomplished person with ample resources and even supportive people and family in their life can make a decision to take their life?  The press has settled on a couple of unsatisfactory answers that flow from the risk analysis approach to suicide.  In other words, let's look at number of modifiable and unmodifiable correlates of suicide attempts and use those in an analysis of a specific death by suicide.  After the fact it is basically a fishing expedition trying to fit the pieces together in a way that there is a logical and linear story about how the incident unfolded.  If the person is famous enough there may not be a final judgment until the autopsy toxicology comes in many weeks later.  Even if a coherent story is constructed, the story may be debated for years on cable TV shows that have medical experts second guessing real time experts.

Serious and intractable disorders and impulsivity is a big part of the current media story.  I had somebody ask me today: "Is it true that people just make the decision and in 5 minutes they are dead?"  People tell me stories about Golden Gate Bridge jumpers who survived to tell about it and that is what they reported.  All of the stories are very linear - there is a precipitant and then depression with depressed moods and then an impulsive suicide attempt. 

Psychiatrists are trained to recognize and treat all of the major disorders that are thought to increase risk for suicide including substance use disorders.  We are also trained to be optimistic about the treatment and consider these diagnoses to be modifiable - if they are treated correctly they will respond to treatment and improve thereby reducing risk for suicide.  Overall psychiatrists are successful in that approach as evidenced by reduced suicidal thinking and in some cases behavior that is directly observable in hospital units.  Self report by patients is another valuable metric that is rarely talked about.  Patients can at some point say: "I seriously contemplating suicide and had a plan to kill myself until I came here for treatment." or "During my last pregnancy - at one point I was going to kill myself.  I don't want that to happen again.  I want to have a plan this time to prevent that from happening."

From an epidemiological standpoint, psychiatrists in general treat people who are at much higher risk than the general population for suicide.  The CDC, just came out with data to show that the suicide rate in the USA from 2014 was 13 per 100,000.  Many of the disorders treated by psychiatrists have lifetime suicide rates of 10-15%.  In a cohort of 100 people with the disorder, 10-15 are expected to die by suicide over the course of their lifetime.  Suicides by people in active treatment by psychiatrists is rare relative to those numbers but they do happen.  They are more likely to happen during transitions between care settings like hospital discharges or when care is fragmented. They are more likely to happen when there are destabilizing factors in the person environment and easy access to highly lethal methods of suicide - like firearms.

Even in the case where a person has survived a potentially lethal suicide attempt it may be difficult to piece together what has happened.  Consider the following case.  John M. is interviewed in his hospital bed by a consult psychiatrist.  Three days earlier he shot himself through the left shoulder with a handgun and barely survived.  He has extensive damage to the structure of his left shoulder and it will be a while before his surgeons can advise him on whether to not it can be reconstructed.  It is clear that he has been depressed and somewhat paranoid for years.  The psychiatrist asks him about the injury.

JM:  "I guess I shot myself?"
PSY: "Can you tell me about the sequence of events?"
JM:  "Well - I was feeling very depressed.  I thought about calling my parents but they have done too much for me already.  I started to think that I was not worthy of their help anymore.  I feel worthless and like a burden to my family.  I knew they would miss me - but at some point you realize sure they will feel bad for awhile, but they will get over it in a while and the burden will be lifted.  At that point I thought I would get out my .44 and shoot myself in the chest..."
PSY: "Tell me exactly what you were thinking.."
JM:  "Like I said I felt hopeless and like I was a burden. At some point I realized that I was pointing the gun at myself.  I knew I did not want to shoot myself. I have a nephew and I wanted to see him again. And then the gun just went off.."
PSY: "The gun went off?  Don't you remember pulling the trigger? Were you holding the gun in your right hand or your left hand?"
JM:  "I am right handed.  I was holding it in my right hand and pointing it at the center of my chest."
PSY: "Do you remember what you thought when you pulled the trigger?"
JM:  "I don't remember pulling the trigger.... One minute I see my hand and wrist and the gun barrel and then it goes off and I am on the floor bleeding."

Further discussion of the incident does not provide any further degree of clarity.  The psychiatrist has to come up with a diagnosis and a formulation as well as a risk assessment of future suicide potential.  There are several diagnostic possibilities including mood disorders with or without psychotic features including substance induced mood disorders.  Alcohol, stimulants, and opioids can all  cause acute suicidal thinking during intoxication and withdrawal states.  The suicide assessment is basically a collection of risk factors that at the time of this interview may not be entirely relevant.  For example, the patient in this case did not have any suicidal thinking at all and was pleased that he had survived at the time of this interview.  Irrespective of all of those considerations there may be some psychiatrists who would be comfortable discharging the patient at that point.  I am not one of them. In this case I would opt for a more detailed assessment and period of observation and an attempt to restore the person to his baseline level of functioning.

In acute care psychiatry, we talk a lot about baseline and cannot always achieve it.  People my not be aware of the fact that they are not at baseline, insist they are fine, and want to go home even if they are at high risk.  People may not want to access help in the first place for the same reason.  We can only assess baseline very indirectly.  The best current way is an extended conversation with a person who knows them very well.  Is their social behavior and personality the way it should be? How do they differ from that.

This baseline that we refer to and assess only peripherally is critically important when it comes to suicide risk.  We are actually referring to the person's conscious state.  There are no ways to assess baseline conscious states.  All of our energy has been focused on extreme psychopathological states and the handful of criteria that are used to define them.  By way of contrasts the human brain is designed to generate billions of unique conscious states - no two are ever alike because these billions of states have all had unique life experience to think about.  There is no universal agreement -even among researchers about how to define conscious states - but discussing the contents of consciousness is a fairly universal approach. I typically ask students to imagine their own stream of consciousness and why it night be unique. But that is only part of what defines a unique conscious state.  Subjective experience is another.  Unique subjective experience is diametrically opposed to the usual methods in psychiatry of trying to index disorders based on a handful of common features.  A person's unique experience is much less likely to be recorded anywhere in today's era of rationed psychiatric care and poor documentation.  Conscious states are also subject to perturbations that are transient  based on internal and external conditions.  In the case of suicidal thoughts, in my thousands of interviews of people the most common reply I get is: "Yeah - I have had a few suicidal thoughts -hasn't everybody?"

In this era of inability to assess and essentially predict a person's conscious state it should not be surprising that we have only the most basic knowledge about the assessment and treatment of suicide potential.  We are generally using a very crude risk assessment and many of the variables may be unchanged for years.  It is not like an actuarial assessment for insurance purposes where the outcomes and statistics are not that dynamic.  In the case of suicide assessment, we don't know all of the variables, the number of variables is large, and we may not even know the person's baseline conscious state unless we have known them for years.  To further complicate matters - they may not be able to tell us about their baseline state until they have recovered it and recognize that they have changed.  The change we are interested in is going from a state that would never consider suicide to one that would.

 The media storm around recent events, will seem to provide a number of pat answers based on society, culture, pop psychology, and special interests.  They seem to ignore the fact that in any given society, these rates rise and fall.  The current rate was the same in 1950 and 1970.  Moreover American society is intermediate relative to the rest of the world when it comes to suicide rates. Some countries with more psychiatrists per capita have higher suicide rates.

On an individual level, suicidal thinking especially if it is combined with of other psychiatric  symptoms is a red flag.  It suggests that a person should try to obtain professional help.  There is no easy way to discuss the consciousness issue on more than a fragmentary basis at this point.  I do try to discuss it with people as a risk factor, but if they are in an altered state they may not be able to hear what I have to say.  The current practical approach is to listen carefully to people who know that person well and have their best interest in mind. 

A reasonable pathway to assessment and treatment is paying attention to any changes that a concerned third party may have noticed and if that person with the problem can't see it - get a neutral third party professional involved and give them all of the information.



George Dawson, MD, DFAPA