The Recurring Question Of Antidepressants During Pregnancy

Over the course of my career, the question of whether  or not women should take antidepressants while pregnant has been a recurring question.  The point-counterpoint seems to depend on whether you are a psychiatrist treating women with severe forms of depression or not.  A lot of these studies seem to be driven by the fact that there is a registry somewhere for pregnant women who have had exposure to various medications.  Studies like this make headlines and are simplistically interpreted.  That is a much different perspective than a psychiatrist who is talking with a woman who has had severe postpartum depression and does not want to experience that again.  There is also the case of acute care psychiatrists who have assessed many women who had a significant change in their mood and mental state during or after a pregnancy and never recovered from that.  They became chronically mentally ill at that point and sustained all of the expected comorbidity.  The first few times I encountered that situation it was difficult to accept.  Nobody teaches that in medical school or residency training.  It seemed like a well kept secret.  Since then I have seen many women who developed a chronic mental illness that started as a severe mood change in or immediately after pregnancy.

The most recent question arose as a result of the study in reference 1, an analysis of the Quebec Pregnancy Cohort.  These same authors have an additional 9 references in Medline.  Full text is available for the current study.  The conclusion of these authors is that SSRI, SNRI, and TCA type antidepressants are associated with a significant increase in congential malformations - specifically as cardiac, musculoskeletal, craniofacial, digestive and respiratory defects.  The authors have a detailed flow diagram that details patient selection from the original cohort of 289,688 pregnancies between 1998-2009.  The flow diagram is a good illustration of how the original cohort was narrowed down to 18,487 pregnancies with either first trimester exposure to antidepressants (3,640) or no exposure (14, 847).  Subgroups for the antidepressant exposure include SSRIs (2,327), SNRIs (738), TCAs (382), and other (193).  The numbers and percentages of major malformations for each group were no exposure 1650/14,847 (11.1%), SSRI 279/2327 (12%), SNRI 91/738 (12.3%), and TCA 51/382 (13.4%).    Over the ten year course of the study the prevalence of antidepressant use doubled from 21 to 43 women per 1,000 pregnancies.  Doing some quick arithmetic on those numbers we find that 11.6% (421/3,640) of the antidepressant exposed pregnancies resulted in major congenital malformations.  Using the baseline rate of the unexposed pregnancies to calculate the expected number of major malformations results in 404/3,640 or a difference or 17 major malformations in the exposed group of 3,640 pregnancies.

What did the authors consider to be major malformations?  They used definitions of major congenital malformations according to conventions in two databases and they provided ICD-9 and ICD-10 diagnostic codes.  There were very few named diagnoses as far as I could tell.  There is some concern here because the literature on congenital malformations varies a bit in terms of the rate of birth defects and whether they are considered to be major or not.  Some of this was expressed in a NEJM editorial by Greene in 2007(2).  In commenting on two papers (3,4) on the subject of major congenital malformations associated with SSRIs in that edition he notes that  "A survey of the aggregate data now available — positive, negative, and equivocal — makes it clear that neither SSRIs as a group nor individual SSRIs are major teratogens on the order of thalidomide or isotretinoin."  He goes on to elaborate that there is a low risk with SSRIs but it is not zero and it is not clear cut.  That opinion is in contrast to some written since suggesting that the risk is high enough that no women should be exposed to SSRIs. 

One of the strengths of this study is that they used depressed and anxious mothers as the reference group to attempt to remove any confounders due to those conditions.  A variety of diagnostic codes were determined including 33 ICD9/10 codes for episodic mood disorders, 17 ICD9/10 codes for neurotic disorders, 19 ICD9/10 codes for depressed, anxious, and other cognitive disorders, 3 ICD9/10 codes for adjustment disorders, and 2 ICD9/10 codes for depression not otherwise specified.  Data on indications for antidepressant use were not available but the authors sought to limit indication bias by comparing only women selected for diagnoses of depression.  Women were selected with diagnoses of anxiety or depression who were treated with antidepressants one year before their pregnancy and several exclusion criteria such as exposure to more than one antidepressant or multiple births were applied.  Total psychiatric visits were viewed as a proxy measure for severity rather than confirmation of the diagnosis.        

The primary statistic used in this paper was the Odds Ratio (OR) or Adjusted Odds Ratio (aOR).  I have been skeptical of some applications of OR in the past.  There are also theoretical concerns as discussed in reference 2 below.  The authors present an excellent argument that the OR is widely used in epidemiological studies because it characterizes population variations in risk.  The weakness is that it has low accuracy as a classifying marker and it tends to overestimate relative risk when sample size is low.  A number of papers also point out that when large numbers of comparisons are done like calculating the OR and aOR for a large number of antidepressants it is likely that some of the findings will be explained by chance.  In this case they do the calculations by antidepressant, overall major congenital malformations and by individual body systems.  They conclude that only exposure to citalopram  [(aOR) 1.36, 95% CI 1.08 to 1.73]  in the first trimester increases the risk of major malformations but that there was a trend with other antidepressants (ADs) and that some ADs seemed to result in more system specific malformations.  Another methodological problem that can occur and affect comparisons is when the control group has an unexpectedly large number of malformations and this has happened in some of the research studies.

A much larger study of the problem was provided by the NICE consortium in the UK and their 923 page document on the subject (17).  The supplement of Forest plots alone for this document is an additional 313 pages long.  The authors of this document carefully selected studies of prenatal exposure to psychiatric medications and compiled fairly large studies.  They also showed the actual numbers of lesions in the exposed and unexposed groups by rates and the absolute differences in addition to the OR.  The NICE methodology was exhaustive and included very large number of patients across 6 major drug classes - antidepressants, antipsychotics, anticonvulsants, lithium, benzodiazepines, and stimulants.  The antidepressants studies listed sample sizes ranging from 50,257 to 2,548,463.  According to the authors there was no statistically increased risk in major congenital malformations with SSRIs even though the absolute risk difference was 12 more per 1,000.  There were some possible system specific risks with paroxetine and fluoxetine with a range of absolute risk difference of 3-9 more per 1,000.  In their guideline they translated this to a series of prescribing principles that could be applied to prescribing antidepressants in pregnancy (p 813).  These principles amount to a detailed informed consent discussion about potential risk during pregnancy and breastfeeding.  The document also contains the observation that up to 90% of women stop taking medication when they find out they are pregnant.  That often happens without consultation.

Attending meetings where psychiatrists are the presenters and focused on maternal health provides a much different perspective than pregnancy databases focused on congenital malformations.  In the past couple of years I was to attend three conferences, two of which occurred at the University of Wisconsin Annual Updates.  In all three of those conferences the maternal burden of anxiety and depression is the context and is generally presented first.  Katherine Wisner (11) presented in Madison last year.  Here arguments were based on the fact that psychiatric disorders are the most common chronic conditions of women of childbearing age and that the rate of treatment is very low: 25.5% of non-pregnant women and 14.3% of women who were pregnant in the past year.  She pointed out that medication free and disease free pregnancies are a myth.  Pregnant women get sick and sick women get pregnant.  About 14.5% of pregnant women have a new episode of depression and about 14.5% of women have an episode of postpartum depression.  Dr. Wisner is one of several authors who referenced Cohen's work (6) on the recurrence risk of depression in women who discontinued antidepressants  around the time of conception versus those who did not (68% versus 26%).  Click to enlarge this graphic.

JAMA. 2006 Feb 1;295(5):499-507 with permission

The presentation by Zachary Stowe (10) used the Cohen survival curve to illustrate recurrent depression with antidepressant discontinuation in pregnancy.  He also showed survival curves of treated versus untreated bipolar disorder by Viguera (16) showing that 90% of untreated pregnant bipolar patient relapse during the pregnancy out ot 12 weeks post partum compared to 40% of treated bipolar patients.  He also had two excellent slides on the acute maternal and neonatal consequences of a relapse to a mood disorder documenting numerous neonatal complications maternal complications including suicide.

Michelle Wiersgalla (12) expanded the postpartum disorders to include anxiety and psychosis.  She pointed out that suicide accounts for 20% of the post partum deaths and that suicide was the second leading cause of death in post partum women.   Some sources have classified it as the leading cause of maternal death (13, 14).  Infanticide occurs at the rate of about  8/100,000 and is associated with post partum psychosis.

All of those presenters would seem to have made a strong case for treating mood and anxiety disorders in pregnancy.  And of course the sterile research statistics are nothing like stress of clinical practice when a patient suddenly is destabilized and becomes unpredictable to both their family and the treating physician.  There is also the stress of an unplanned pregnancy in a woman who is being treated for a psychiatric disorder and that speaks to one of Dr. Stowe's main point and that is to treat all women of childbearing age in your practice as being potentially pregnant and documenting method of contraception and advice adn planning on pregnancy given the medication that they are taking.

It seems to me that the recurring problem of antidepressant safety during pregnancy is driven by a large body of research with widely discrepant low frequency findings.  We are generally talking about rates that are in the single to low double digits out of a thousand.  I think the conclusions of that research are probably affected by who is doing it.  You can find people who are interested in "proving" that antidepressants are harmful on the one hand.  They are likely to write from that perspective and minimize or completely ignore the severity of the associated women's mental health problems and the fact that they can be clearly treated with antidepressants.  They also never mention the potentially severe outcomes associated with untreated postpartum depression that can be observed in acute care settings.  On the other hand, there is research written from the perspective of treating women's mental health problems that (unexpectedly) will show less harm.  Clinicians - especially psychiatrists on the front lines who are often left advising women with unexpected pregnancies on what to do about their antidepressant treatment are stuck in the middle.  

A reasonable informed consent discussion with women of childbearing age begins by treating all women in this category as though they are potentially pregnancy or will be at some time. That includes a history of pregnancy and any associated changes in mood or anxiety.  It also includes a discussion of going from a no risk state for the fetus of not being pregnant while taking medications  to pregnancy while taking medication.  That includes plans for pregnancy and documenting the method of birth control.  With some high risk drugs - screening for pregnancy can be done.  If there is any concern about absolute minimization of risk pregnancy screening can be done and repeated if necessary.  In the case of planned pregnancies a window of 6-12 months prior to conception allows for a scheduled taper and discontinuation of the antidepressant medication.  The psychiatric evaluation can be valuable to determine the risk of relapse in these situations.  There are many patients who started taking antidepressants in acute situations where the stressor no longer applies.  There are many patients taking antidepressants for anxiety disorders who have never received psychotherapies for anxiety.  After these practical measures have been exhausted the decision comes down to whether or not there is an unplanned pregnancy and exposure or a situation where the discontinuation of the antidepressants would potentially be problematic.  In the cases I have been involved in, the women were also seeing high risk obstetric specialists and their pregnancies were closely monitored.    

As far as the actual drugs go, I do not think that paroxetine should be prescribed.  I am not basing that on anything in the pregnancy or congenital malformation literature.  I am basing it on my experience in psychiatry and the fact that in the first few years of its release - I determined it was a problematic drug in terms of drug interactions and discontinuation symptoms.  Why prescribe a problematic drug when there are plenty of other equivalent drugs?  I do not understand why anyone prescribes paroxetine these days.  That said, you can look at all of the data from the analyses of pregnancy registries and the difference in complication rates between drugs is so narrow and so small that the difference in changing to another drug with a lower odds ratio for congenital malformations probably makes little sense.  That does not mean that nobody will want to change and patient preference in this case requires a thorough and neutral discussion.



George Dawson, MD, DFAPA


References:

 1: Bérard A, Zhao JP, Sheehy O. Antidepressant use during pregnancy and the risk of major congenital malformations in a cohort of depressed pregnant women: an updated analysis of the Quebec Pregnancy Cohort. BMJ Open. 2017 Jan 12;7(1):e013372. doi: 10.1136/bmjopen-2016-013372. PubMed PMID: 28082367

2: Greene MF. Teratogenicity of SSRIs--serious concern or much ado about little? N Engl J Med. 2007 Jun 28;356(26):2732-3. PubMed PMID: 17596609.

3: Alwan S, Reefhuis J, Rasmussen SA, et al. Use of selective serotonin-reuptake inhibitors in pregnancy and the risk of birth defects. N Engl J Med 2007;356:2684-2692

4: Louik C, Lin AE, Werler MM, Hernandez-Diaz S, Mitchell AA. First-trimester use of selective serotonin-reuptake inhibitors and the risk of birth defects. N Engl J Med 2007;356:2675-2683

5: Andrade C. Understanding relative risk, odds ratio, and related terms: as simple as it can get. J Clin Psychiatry. 2015 Jul;76(7):e857-61. doi: 10.4088/JCP.15f10150. PubMed PMID: 26231012.

6:  Pepe MS, Janes H, Longton G, Leisenring W, Newcomb P.  Limitations of the odds ratio in gauging the performance of a diagnostic, prognostic, or screening marker.  Am J Epidemiol (2004) 159 (9): 882-890 https://doi.org/10.1093/aje/kwh101

7: Davies HT, Crombie IK, Tavakoli M. When can odds ratios mislead? BMJ. 1998 Mar 28;316(7136):989-91. Review. PubMed PMID: 9550961.

8: Deeks J. When can odds ratios mislead? Odds ratios should be used only in case-control studies and logistic regression analyses. BMJ. 1998 Oct 24;317(7166):1155-6; author reply 1156-7. PubMed PMID: 9784470.

9: Bracken MB, Sinclair JC. When can odds ratios mislead? Avoidable systematic error in estimating treatment effects must not be tolerated. BMJ. 1998 Oct 24;317(7166):1156; author reply 1156-7. PubMed PMID: 9841055.

10: Zachary N. Stowe, MD  Treatment of Mood Disorders in Pregnancy and Lactation: Where Are We Now?  Presented at 2nd Annual Update And Advances In Psychiatry.  October 10-11, 2014; Madison, Wisconsin

11: Katherine Wisner, MD, MS.  Treating Depression During Pregnancy: Are We Asking the Right Questions?  Presented at 4th Annual Update And Advances In Psychiatry.  October 14-15, 2016; Madison, Wisconsin

12: Michelle Wiersgalla, MD.  Postpartum Mood and Anxiety Disorders.  Presented at the Minnesota Psychiatric Society.  October 1, 2016.

13: Oates M. Suicide: the leading cause of maternal death. Br J Psychiatry. 2003 Oct;183:279-81. PubMed PMID: 14519602.

14: Knight M, Nair M, Tuffnell D, Kenyon S, Shakespeare J, Brocklehurst P, Kurinczuk JJ (Eds.) on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care - Surveillance of maternal deaths in the UK 2012-14 and lessons learned to inform maternity care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009-14. Oxford: National Perinatal Epidemiology Unit, University of Oxford 2016.

"Maternal suicides have now been reclassified by the World Health Organisation as a direct cause of maternal death. The rate of maternal death by suicide remains unchanged since 2003 and maternal suicides are now the leading cause of direct maternal deaths occurring within a year after the end of pregnancy" p. 11.

15:  Cohen LS, Altshuler LL, Harlow BL, Nonacs R, Newport DJ, Viguera AC, Suri R,Burt VK, Hendrick V, Reminick AM, Loughead A, Vitonis AF, Stowe ZN. Relapse of major depression during pregnancy in women who maintain or discontinue antidepressant treatment. JAMA. 2006 Feb 1;295(5):499-507. Erratum in: JAMA. 2006 Jul 12;296(2):170. PubMed PMID: 16449615.

16:  Viguera AC, Whitfield T, Baldessarini RJ, Newport DJ, Stowe Z, Reminick A,Zurick A, Cohen LS. Risk of recurrence in women with bipolar disorder during pregnancy: prospective study of mood stabilizer discontinuation. Am J Psychiatry. 2007 Dec;164(12):1817-24; quiz 1923. PubMed PMID: 18056236.

17.  National Collaborating Centre for Mental Health.  Antenatal and Postnatal Mental Health Clinical Management and Service Guidance (Updated  Edition 2014). National Clinical Guideline Number 192.

Specific guidelines on treating depression in pregnancy for psychiatrists starts on about page 848 and continues.  A full gamut of treatment interventions in the context of clinical history and evaluation, patient preferences, and informed consent is presented.


antidepressants "congenital malformation"

antidepressants congenital malformation 

antidepressants pregnancy



Attribution:

The figure in the above post if from reference 15 - the figure is entitled:  "Figure. Kaplan-Meier Curves Illustrating the Time to Relapse by the 4 Medication Categories and Medication Reintroduction Categories" with permission from the American Medical Association, order number 4043410033700.  Thank you AMA.


Supplementary 1:

I tried to get permission to post survival curves from references 16.  The APA (of which I am a 32 year member) wanted to charge me $150 to repost a single 10 year old graphic that I have seen used in presentations.

Supplementary 2:

The graphics at the top are the actual fliers for the two conferences mentioned.  Other than two years of residency training, I have no affiliation with the University or Wisconsin Department of Psychiatry. 

University of Wisconsin 2nd Annual Update - Day 2

The second day of the conference was actually a half day that was as interesting as day 1.  The first speaker was Kenneth E. Towbin on Chronic Irritability and Pediatric Bipolar Disorder.  Dr. Towbin pointed out that all of the research discussed by him at the meeting was funded by the NIMH Intramural Research Program or the American taxpayers.  He briefly mentioned the advantages and disadvantages of working under those conditions including no usual conflicts of interest and working in an ivory tower with possible ascertainment bias.  The main focus of his discussion was to make a few points about the concept of bipolar disorder and how the overdiagnosis of this disorder came about.  The first point was that bipolar disorder is an episodic illness.  The word I like to use is phasic.  The second point sounds obvious to psychiatrists and that is that in order to make a diagnosis of bipolar disorder the patient has to have had an episode of mania or hypomania.

I am going to digress here a bit on my own before continuing the review of Dr. Towbin's work.  Much of what I do these days is correcting incorrect diagnoses of bipolar disorder.  When I try to reconstruct what happened patients will invariably tell me that they were given an "assessment" and told that they tested positive for bipolar disorder.  The assessment typically consists of a brief interview and then a battery of checklists and psychological tests.  Many are surprised when I tell them that the diagnosis really doesn't depend on any of those things.  It depends on whether or not they have had an episode of mania or hypomania and then I define those syndromes for them.  We try to reconstruct their history of mood disorders and whether or not they have ever had such an episode.   I also emphasize that these episodes have to occur when they are not using excessive amounts of alcohol or other intoxicants.  I ask them about the time before they developed a substance use problem and during their longest periods of sobriety.  In this day of overdiagnosis of Attention Deficit-Hyperactivity Disorder (ADHD) it is not uncommon to hear that a person who has developed a substance use problem using all of their Adderall in the first week or two.   When that is gone  they switch to alcohol for the second half of the month.  That combination can result in what appears to be a manic episode during the first week or two of the month followed by a 2-3 week depression.  That sequence of stimulant intoxication followed by stimulant withdrawal/alcohol intoxication followed by sustained alcohol intoxication is not bipolar disorder.

Dr. Towbin went on to give his very interesting take on how some mistakes can be made from reading diagnostic criteria.  He focused initially on how there could be ambiguity in the DSM-IV-TR.  For example under the "A-Criteria" - how is the requirement of a one week episode of elevated mood determined?  Does it have to be every day or every hour?  Could it last for a short a period of time as an hour?  Under the "B-Criteria" - could some symptoms antedate mood symptoms and what does "present to a significant degree" mean?  I was familiar with Angst's work on following patients with various durations of mania and what the outcomes could be and had since incorporated a shorter period of time into my evaluations of mania.  The DSM-5 criteria sought to clear up these areas by stating that the mood symptoms had to be present most of the day and nearly every day and the symptoms had to represent a noticeable change from usual behavior.   After these discussions of the nature and importance of manic episodes he went on to look at some epidemiological data on the increasing rates of bipolar disorder in children (1, 2).  In the study by Moreno, et al the authors demonstrated a significant increase in office visits by adults and children.  Between the years of 1994 and 2002 the rates of visits increased 60% for adults and 4,000% for children, but the rates from that graphic increased from 0.01-0.4% in children and 0.3 to 0.5% in adults.  Between 1996 and 2004, the number of inpatient discharges with a principle diagnosis of bipolar disorder increased 296.4% in adolescents and 438.6% in children.

Towbin's explanation for the increase in bipolar disorder diagnoses in children was that a cultural change was advanced by two research groups.  That cultural change was operationalized by saying that episodes of illness were not required and the diagnosis could be applied to children with chronic illness.   That led to the idea that bipolar disorder in children is not the same as bipolar disorder in adults and that chronic irritability was synonymous with bipolar disorder.  Or as he put it another way: "If you were really angry you must have bipolar disorder."  The importance of bipolar disorder as an episodic illness was also emphasized in the area of "double counting symptoms."  As an example, could the psychomotor agitation and flight of ideas of bipolar disorder be the same thing as severe hyperactivity or distractibility of ADHD?  Only if bipolar disorder was not an episodic illness.

Dr. Towbin proceeded to discuss how the concept of Severe Mood Dysregualtion (SMD) was developed at the NIMH as an additional clinical phenotype that could be compared to bipolar disorder.  SMD was defined as chronic irritability, ADHD-like symptoms and significant impairment.  At about the same time he went on the one of my favorite topics - irritability.  I like it because it is used as a descriptor in many DSM diagnoses but never well defined.  Many people are surprised that it is listed as a symptoms in Generalized Anxiety Disorder (and in the criteria for 6 other DSM diagnoses and in the text for an additional 3 DSM disorders.)  He defined a two component model for irritability including a background of a grumpy, annoyed and irritable mood and a phasic component of briefer flashes of anger or explosive episodes.  That allowed for a clearer definition of SMD and the subsequents development of Disruptive Mood Dysregulation Disorder DMDD) diagnostic criteria.  He reviewed the evidence from longitudinal studies, family history studies and pathophysiology that SMD/DMDD is not the same as bipolar disorder.  Followed for a long enough period of time this population tends to develop depressions rather than bipolar disorder and have families with histories of bipolar disorder.  From a recent study by Sparks that he referenced: "Parental bipolar disorder increase the risk for multiple categories of childhood psychopathology and DMDD is no more on the bipolar spectrum than anxiety disorders, MDD, or ADHD." He went on to discuss treatment approaches to this population emphasizing the significant degree of disability the is usually not discussed in non-technical publications about this problem.

The final speaker of the day was Zachary N. Stowe, MD.  His presentation was: Treatment of Mood Disorders in Pregnancy and Lactation: Where Are We Now?  He made two observations at the outset that probably captured the imagination of at least some of the crowd.  The first was that any psychiatrist who specialized in the neuropsychiatric disorders of pregnancy would be unchallenged in any community they decided to practice. The second was that every psychiatrist treating women should treat all women of child-bearing age as though were pregnant and therefore needed clear conversations about whether they are using contraception and what the permutations might be with respect to prescribed psychiatric medications.  The method of birth control should be documented.  In terms of safe use of medications in pregnancy he made the point that is is all based on post marketing surveillance and there is no safety data for using 2 medications at a time.

He reviewed the frequent scenario that clinicians face when a patient who is being treated becomes pregnant.  He used an excellent graphic showing how pharmacokinetics and the timing of human development combine to virtually assure that the fetus will probably be exposed at some critical stage of organogenesis and how that factors into the decision to continue, discontinue, or change pharmacotherapy.  He showed survival curve data from both treated and untreated major depression and bipolar disorder on the proportion of women remaining euthymic at and several weeks following delivery.  As expected the rates of recurrence of the mood disorders was high and significantly higher for bipolar disorder.

When discussing the risks of medication he mentioned the current FDA Pregnancy Categories and the fact that there will be a new system that looks at more of the clinical aspects of making these decisions.   The old system will remain in place for existing ratings meaning that for the forseeable future there will be two FDA systems looking at medication safety in pregnancy.  He looked at a number of maternal and neonatal outcome variables for pregnancies associated with maternal depression and maternal antidepressant use.  There was a significant overlap and he suggested that a psychiatric illness diathesis and all that encompasses in terms of cormorbid medical illnesses and activation of the maternal and fetal HPA axis was a possible explanation.  In other words there  would be non-optimal outcomes whether the depression is treated or not.  He went on to discuss detailed basic science research in this area as well as fairly detailed treatment recommendations.  From a clinical standpoint, he pointed out that psychiatrists are more likely to discontinue antidepressants in pregnant women than OB-GYN physicians and attributed that to the American College of Obstetricians and Gynecologists treatment guidelines for depression in pregnancy.

Dr. Stowe's presentation covered all modalities of treatment including electroconvulsive therapy, medications, psychotherapy and exercise.  He was a participant in a workshop I attended on treating depression with exercise.  I think the single most important fact that he discussed in terms of medication was the need to avoid valproate and consider it to be the last drug used in women of child bearing age because of its effects on the fetus and subsequent development of the child.  I recommend that any psychiatrist who has the opportunity to see Dr. Stowe and who treats women of childbearing age take advantage of that opportunity.

That ends my brief review of the UW conference this year in Madison.  I felt fortunate to have been actively involved in all of the clinical work that these clinicians and researchers discussed over a day and a half.  I thought of all of the patients I had seen who could have benefitted from seeing this basic and clinical science applied.  As I listened to the translational aspects of Dr. Stowe's work, I tried to think of all the women I had treated who developed a severe post-partum affective psychosis at some point in their lives and never recovered from that.  I appreciated the quality of a conference that puts all of that information out there and tries to bring everyone up to the same speed as the top researcher-clinicians out there.

If you think this approach might interest you - mark your calendar for next October 23 and 24 and I hope to see you there.  In the two years that I have attended, Art Walaszek, MD and Ned Kalin, MD have an excellent method of picking presenters who can cover both the clinical and basic science of important disorders and treatment modalities that psychiatrists need to be aware of.  That information is presented well and there is ample time for discussion.

George Dawson, MD, DFAPA

1: Moreno C, Laje G, Blanco C, Jiang H, Schmidt AB, Olfson M. National trends in the outpatient diagnosis and treatment of bipolar disorder in youth. Arch Gen Psychiatry. 2007 Sep;64(9):1032-9. PubMed PMID: 17768268.

2: Blader JC, Carlson GA. Increased rates of bipolar disorder diagnoses among U.S. child, adolescent, and adult inpatients, 1996-2004. Biol Psychiatry. 2007 Jul 15;62(2):107-14. Epub 2007 Feb 16. PubMed PMID: 17306773.