Mental Health

“Practical Tips for Managing the Agitated Patient: Avoiding Violence in the Clinical Setting”

ORIGINALLY PUBLISHED IN THE: Psychiatric Times, February 27, 2017

Drs Lofchy and Fage write a nice article on violent patients. They rightly note that, “The risk of violence in psychiatric practice is a frightening aspect of our work”. The problem is that few of the many articles like this ever talk about what to do when a punch is on it way, you are getting pushed, or worse, getting strangled.

These articles are great-up to the point of attack assuming that the end-game is pushing a personal panic alarm. However, there needs to be a discussion of what we should do if things get out of hand, if there is no alarm and if security is not around the corner. Actual martial arts self-defense training, which also necessarily entails some offensive practice as part of defense, is the only thing to do next because by definition, all the processes, structures, and verbal de-escalations are not part of the equation at this point. My opinion is that kung fu would be the best training to have, but the best type could be subject to discussion and opinion.

Drs. Lofchy and Fage are right, there is a danger, and psychiatry needs to get over the “political correctness” of the assumption we should never discuss that we should learn how to physically defend, control, neutralize, or even attack back as a defense. Psychiatrists are too cerebral, once a week they need to get into a martial arts gym and train.

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Mental Health

“Bereavement, Grief, and Depression: Clinical Update and Implications”

Originally published on February 20, 2017 in “Psychiatric Times”

The logic of some key points of this article on complex bereavement (PCBD) has some serious problems, and I beg the senior author Dr. Bui of Harvard to reply.

In the “Persistent Complex Bereavement Disorder” section the authors state that PCBD, “has been shown to be distinct from mood, anxiety, and other trauma-related disorders despite some symptom overlap”.

Then later in that section they state that, “…risk factors for PCBD are similar to those for other bereavement-related conditions including MDD and PTSD, which suggests that all of these conditions share some common pathophysiologic processes.”

Two sections later under the “MDD” section they then say, “…recent studies have found no substantial differences between bereavement-related depressive syndromes and non-bereavement related depressive syndromes in terms of clinical characteristics and treatment response…”, and that, “The bereavement exclusion was dropped in DSM-5, and the death of a loved one no longer precludes the diagnosis of MDD…”.

They want to say that PCBD is distinct from MDD, but wait, they can have the same pathophysiology and the same clinical characteristics and treatment response (and we now can bill insurance companies for PCBD). This is strange medical science logic, unless billing has become part of medical science. 

Even if there are some clinical and epidemiologic data suggesting some difference between PCBD and MDD, distinguishing psychiatric disorders that have SUBJECTIVE parameters as the endpoints of a study is in no way robust enough to say, “…it has been shown..” by any stretch of the imagination in these constructs that have similar pathophysiology and the same clinical characteristics and treatment response to be “distinct”.

To begin with, there are really no biologic anchor points to clearly objectify any psychiatric disorder from another in a population of patients and certainly there is no way to prove what an individual’s diagnostic label should be much less in these conditions the authors themselves note to be extremely similar. Diagnostic labels in psychiatry are really only road signs for the doctor and patient to use as a working model for treatment. These authors need more modesty and clarity of the financial upside of making DSM diagnoses.

Ok, a person in complicated grief can yearn intensely for the deceased, feel confusion about themselves, and be unable to trust others. Is this so different from the many persons’ therapists see who are persistently depressed after any intimate breakup?

I recommend a review of this article in the PT

I think the logic presented by Allen Frances is the most lucid regarding avoiding over-medicalizing.

Next, the authors note that Complicated grief treatment (CGT) has “shown efficacy…across 3 randomized controlled trials”, all authored by Shear, however, none of these trials were single-blind (=subject blind), or double-blind (thus no blind placebo).

See the most recent trial here:

This study had a “placebo”, but the term is misleading as a psychotherapy can not have a blind placebo group.

Do these Harvard authors wish to opine that a therapeutic modality in conditions with subjective endpoints can be show efficacy without a double-blind and blind placebo controlled study? Blind raters only record what unblinded subjects report.

Regarding disclosures, Dr. Bui has also worked with Dr. Shear, the author of the Complicated grief treatment trials noted in references 9-11 in the PT article on this study, and Director of the “Center for Complicated Grief”. The therapists of which bill clients for grief therapy and charge fees for workshops up to $600 per attendee (, so there is some motivation to have CGT show efficacy in a “clinical trial”.

Bui and Shear coauthors on:


In this article, while Bui notes “Although diagnostic criteria for CG have yet to be adequately validated, the SCI-CG may facilitate this process.” He then says, “The SCI-CG can now be used as a validated instrument in research and clinical practice.”

This means we can validate an instrument for a diagnosis where the diagnostic criteria are not validated?

This article requires rethinking, rewriting, and re-disclosing.

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Mental Health

Nonvalidated Pharmacogenetic Tests, Part I: Confessions of an Embarrassed Psychiatry Professor

Referenced article originally published October 26, 2016 in the Psychiatric Times:
Dr. de Leon
It is refreshing to read about a seasoned clinician backtracking on mistaken prior conclusions. I would opine to go further in limiting the need or utility of these tests.
For example, you want to do CYP2D6 and 2C19 before giving a tricyclic. What is the risk of giving someone 10mg BID of nortriptyline and increasing by 10mg BID every 2 weeks up to 40mg BID watching how the patient reacts vs the risk of delaying treatment and cost of the test? Poor metabolizers may easily tolerate titration to 20mg or 30mg BID and have a response after 6-8 weeks stopping the dose there anyway. If a rare patient will have trouble after a few 10mg BID doses they can just stop the medication. EVERY patient regardless of metabolic profile requires careful and slow titration of a tricyclic and should be advised to pause their drug dosing and contact their Dr if they have trouble. I really don’t see the risk-benefit ratio falling on the side of doing a costly test.
For CYP2C, Asians have a 3-4x increase number of poor metabolizers. Here in Japan, CYP is not tested, its start low and go slow with most every psychiatric drug. There seems to be little problem with this method as long as there is close follow up. Again, EVERY patient should be followed closely.
You also want to do HLA testing before giving CBZ to Asians, I assume to decrease the risk of SJS. The best approach is not to give CBZ to Asians, not do a test. Why not use oxcarbazepine if you need to? There are plenty of other drugs to use, even for seizure disorder treatment, then again your article was on “genetic tests in psychiatry” not neurology. CBZ isn’t used much in psychiatry in Japan nowadays. HLA testing isn’t done here either, though LFT and WBC should be tested a week into CBZ therapy regardless of HLA type.
Ok, maybe there is an exceptional case where we want to do a test, but it should be a rare case and tests are no substitute for careful and knowledgeable clinical monitoring. I vote that these tests stay in the research lab for pharmacology research, and in pharmaceutical company labs during drug development, not in clinical psychiatry.
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Mental Health

Counseling Tokyo Social Media

Tokyo Counseling Douglas Berger Social Media



Mental Health

Deconstructing and Reconstructing the “Goldwater Rule”

Original article published, October 07, 2016 by Ronald W. Pies, MD in The Psychiatric Times:

Thank you, Ron, for your thorough reply that I largely agree with.

First though, let’s be clear, your article was on psychiatric diagnosis in INDIVIDUALS not on the validity of the existence of psychiatric diagnoses in the population. You stated, “On occasion psychiatrists are asked for an opinion about an individual who is in the light of public attention or who has disclosed information about himself/herself through public media.”

You are also falling into a logic trap by noting that SOME medical or neurological problems have no specific marker, i.e., migraine. This is because there are also many like stroke or brain tumor that DO have an objectively measurable parameter such as seeing infarction, hemorrhage, or mass on a brain scan. Unfortunately there is NO psychiatric condition that has an objectively measurable parameter in an INDIVIDUAL in spite of some persons in a POPULATION who fit diagnostic criteria showing various DIFFERENT and subtle brain abnormalities. Brain scans can be said to have near 100% validity in physically proving that the condition specified because scan results match physical findings on direct examination of the brain seen in surgery or autopsy. This is what is meant by “clearly definable and objectively measurable”.

The first link you provide below by Aboraya states:

“The authors encourage clinicians to use as many validity criteria as possible to improve the validity of their diagnosis.”

They do not state or prove anywhere that a psychiatric diagnosis in an INDIVIDUAL is the same as having objective proof as in neurology (I would place Alzheimer’s in neurology not psychiatry for this discussion).

The paper by Levy only discusses that pursuit eye movement findings are commonly found in POPULATIONS of persons who fit criteria for schizophrenia (and in the CLINICALLY UNAFFECTED relatives of these persons). As they show in Fig 5 and in other places in the article, findings are trends in these groups with a standard error but they nowhere state that these tests can be used clinically as proof of diagnosis in an individual. It’s not the same as seeing a mass in one’s head CT which is clearly a mass: there is no trend or standard error, nearly all INDIVIDUAL cases are either yes or no.

Coincidentally, I was also the lead author on a published study of eye-movements in schizophrenia:

Berger D, Nezu S, Iga T, Hosaka T, Nakamura S: INFORMATION PROCESSING EFFECT ON SACCADIC REACTION TIME IN SCHIZOPHRENIA, Neuropsychiatry, Neuropsychology & Behavioral Neurology, (Journal Name Changed to: Cognitive and

Behavioral Neurology) 3:2, 80-97;1990.

Full paper here:

We found a strong trend for differences between normals and those diagnosed with schizophrenia in the small group we studied, but there was overlap and there were outliers. Thus, it is just interesting research data, it is not useful clinically for individual diagnosis, nor does it prove the validity of schizophrenia.

Now, evaluating public figures who are more likely to have personality issues, ADHD, mild forms of mood disorder etc. and not schizophrenia is even more problematic because there is less robust evidence of a consistent biologic finding in populations of these persons compared to schizophrenia, especially in personality disorders.

So while we would agree on Goldwater, I think you need to take it to the next level of uncertainty when it comes to labeling individuals, examined or not. Psychiatric diagnoses are helpful in clinical treatment, but are unproven constructs and never more than concepts that guide us in what to do, and for mental health workers and institutions to bill medical insurance companies.

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