Clinicians who work with patients suffering from bipolar disorder have known this for quite some time: medication alone, while helpful in controlling many of the acute symptoms of bipolar disorder, is not enough to help patients manage this complex illness.   Patients often feel overwhelmed by the diagnosis and need support to adjust to the realities of fluctuating mood states, which frequently result in interpersonal and occupational dysfunction.   For these and other reasons, psychotherapy is an important component of bipolar disorder treatment.

In recent years, multiple studies have been published which support this view, including randomized, controlled trials.  Taken together, they indicate that various psychotherapeutic approaches, such as individual and group CBT (cognitive behavioral therapy), family focused therapy, psychoeducation, and IPSRT (interpersonal and social rhythm therapy), can be helpful adjuncts in the management of bipolar disorder (1,2).   While these studies vary widely in terms of interventions given, patients selected and controls utilized, what they have in common is the idea that psychotherapy is effective as an “add-on,” to pharmacotherapy.  There is little, if any, indication that such treatments can be used as monotherapy in any phase of bipolar disorder.

This may be changing.

We happened to take notice of a small pilot study by Holly Swartz, M.D. and Ellen Frank, Ph.D. and their group in Pittsburgh (3).  Published in 2009, this study evaluates the effect of psychotherapy as monotherapy in patients with bipolar II depression.  Unmedicated individuals (n=17) meeting DSM-IV criteria for bipolar II depression received weekly IPSRT (interpersonal and social rhythm therapy) for 12 weeks.  After 12 weeks of acute treatment, individuals received an additional 8 weeks of follow-up treatment with continued IPSRT (with supplementary lamotrigine for IPSRT nonresponders).  By week 12, 41% (n=7) of the sample responded to IPSRT monotherapy; 53% (n=9) had responded by week 20 (by this time, one subject was receiving lamotrigine in addition to IPSRT while the other was receiving IPSRT alone).

While small and limited by the lack of a control group, this study is significant in that it demonstrates that psychotherapy – even without medication – can help those who suffer from bipolar II depression.  It puts psychotherapy back on the radar, not as a mere adjunct to treatment, but as THE treatment for this condition. 

Some caveats: the population consisted of bipolar II patients.  Thus, patients with a history of mania were excluded.   Mood stabilizing medication such as lithium, valproic acid, and neuroleptics remain the “gold standard” in managing acute mania.  However, bipolar depression is often resistant to medication treatment.  Antidepressants have been shown to cause worsening of mood cycling.  Not everyone can tolerate side effects.  This population, therefore, of depressed bipolar II patients, might be specifically amenable to psychotherapy as monotherapy. 

So what can we conclude from the results?  Obviously, more research is needed, but there are clues that psychotherapy, specifically IPSRT, can play an important role even in bipolar I patients taking medication.  Dr. Frank’s group in 2005 published a randomized trial of IPSRT vs. ICM (intensive clinical management), in which 175 patients were included (4).  This study showed that participants with bipolar I disorder assigned to IPSRT in the acute phase of treatment were able to stay in remission longer (during the maintenance phase) than those assigned to ICM.  This was especially true for individuals without serious medical illnesses or anxiety.

IPSRT is unique for multiple reasons:  it focuses on interpersonal relationships and how closely related these are to mood episodes.    A special emphasis is placed on how bipolar disorder has impacted one’s life, causing role transition, fractured relationships, career derailment and “grief for the lost self.”  In addition, sleep, wake, and social interactions are tracked closely.   Why?   Because of the “social zeitgeber hypothesis”: unstable or disrupted daily routines lead to circadian rhythm and mood instability (4,5).  This is certainly in keeping with our clinical observations that changes in sleep/wake patterns (i.e. pulling an all-nighter) and overstimulation can bring on a manic episode.

We applaud Drs. Frank and Swartz for showing us that psychotherapy can have a powerful effect on a patient’s overall response to treatment.  IPSRT has lent itself well to clinical trials, as it follows a fairly structured and manualized format, and we look forward to larger, controlled studies of IPSRT as monotherapy in bipolar II depression.   A more challenging, but no less important, endeavor would be to examine the efficacy of psychodynamic psychotherapy in the treatment of bipolar disorder.   While manualized treatments (such as IPSRT or CBT, cognitive behavioral therapy) address key symptoms in bipolar disorder, we should not lose sight of the importance of understanding the meaning and overall implications of such symptoms in the context of a person’s life.

 

(1)  Jones S.  Psychotherapy of bipolar disorder: a review.  J Affective Disorders 2004; 80: 101-114.

(2)  Schottle D et. al.  Psychotherapy for bipolar disorder: a review of the most recent studies.  Curr Opin Psychiatry 2011; 24: 549-555.

(3)  Swartz H, E et. al.  Psychotherapy as monotherapy for the treatment of bipolar II depression: a proof of concept study.  Bipolar Disord 2009; 11: 89-94.

(4)  Frank E, Kupfer DJ et. al.  Two-year outcomes for interpersonal and social rhythm therapy in individuals with bipolar I disorder.  Arch Gen Psychiatry 2005; 62: 996-1004.

(5)  Frank E.  Treating bipolar disorder.  New York: The Guilford Press, 2005.

The single most important research study in the past year in the area of clinical therapeutics of bipolar disorder was conducted  by Geddes and colleagues at Oxford University in England[1].  Using a randomized open-label design (no placebo control group and subjects knew which medications they were receiving), the BALANCE study sorted 330 subjects with bipolar disorder type I into three treatment groups: lithium alone, valproate (Depakote) alone, or combination treatment with both lithium and valproate.  The outcome measures were time to recurrence of a major mood episode, either mania or depression.  The study design allowed for an extended, two year follow-up on these subjects.  This time frame allows for meaningful assessment of genuine prophylactic effects.  The results found that combination therapy was most effective, marginally more so that lithium alone, but significantly greater than valproate monotherapy.  The interpretation of the data supports the unique efficacy of lithium as the single-most effective mood stabilizer available.

In recognition of the singular importance of this study, the journal Bipolar Disorders devoted an issue for commentaries from major luminaries in the field including  Ross Baldessarini[2], Rasmus Licht[3], and S. Nassir Ghaemi[4] and others.  The commentary by Ghaemi, a researcher and analytic thinker whose work I respect enormously, was forthright, pointed, and compelling.  In this commentary, he challenges the pharmaceutically-inspired practice habits of American psychiatrists and their seduction by the next, newest, sexiest drug brought to market.  His writing deserves to be read by patients and clinicians alike.  I include portions of his commentary below:

                “Clinical conclusions about lithium”

“Clinicians can, and should, draw some conclusions, if we have the courage. We need to avoid being mugwumps, refusing to commit to using lithium out of vague fears, despite clear benefits that outweigh the real risks. With the results of BALANCE, in the setting of forty years of lithium research, it seems to me that one clinical conclusion is hard to avoid: Lithium is, by far, the first-line treatment for bipolar disorder. There should be very good reasons not to give lithium to the majority of patients with bipolar disorder as initial treatment. Patient preference, by itself, is not a good enough reason to avoid lithium; the hassles of being a doctor (checking blood levels, assessing kidney function long term) are not good enough reasons either. Patients need to be educated about the many benefits of lithium, including two other major areas, besides mood prophylaxis: mortality reduction, both by suicide and by cardiovascular death, and neuroprotective effects, especially probable reduction of dementia risk and potential protection against the cognitive impairment that is a long-term consequence of multiple mood episodes (1). The drawbacks of lithium are well known, though exaggerated: long-term chronic renal insufficiency, in the best prospective studies with decades of follow-up, is not more than 5% (8); other kidney effects, like decreased urinary concentration capacity, are more common but reversible and not medically dangerous; hypothyroidism is more common but treatable and reversible; nuisance side effects are less frequent than many believe; weight gain is less than with valproate and much less than most neuroleptics; cognitive side effects are problematic in some, but not most persons, and counteracted by long-term cognitive benefits; toxicity in overdose is a risk but this is the only drug that is proven to prevent suicide by a huge effect size (estimated to be nine-fold decreased risk) (1).

Some people cannot take lithium. But everyone should be offered it, most should try it, and a minority can then stop it if it is intolerable. If we take this approach, we find that many persons tolerate it, do well, and do not need the common current rigamarole of antidepressants plus neuroleptics, which leaves patients partially treated at best, and hardly treated at worst.

Lithium is unique because it actually treats an entire disease—manic-depressive illness. It is not merely a treatment for a symptom—like neuroleptics for mania or antidepressants for depression. Studies indicate that about one-third of patients get completely well long term with lithium monotherapy (10). This figure is not minor, and compares favorably with the long-term remission seen with antidepressants in major depressive disorder in the STAR*D study (11). BALANCE is another source of evidence for the notable benefit of lithium monotherapy in a substantial minority of persons with bipolar disorder. The makers of our DSM-IV nosology have assumed that all our pills are mere symptom treatments; they do not think our diagnoses reflect diseases in any meaningful way, and they do not believe that any of our treatments cure diseases. Hence, the claim that we should only make pragmatic judgments, compensating for the follies of practitioners and the manipulations of pharmaceutical companies. Lithium is their refutation, and BALANCE is a modern proof that, though they are hard to conduct and require a great deal of labor, we can clarify clinical controversies with rigorous studies. We researchers need to do the studies, perpend on their importance, teach clinicians to implement the results in practice, and educate our nosologist colleagues, especially now as DSM-5 is in process, as to what they mean.”

 

We listen in full agreement to this elegant and rigorous analysis.  Lithium really is the closest thing we have to a wonder drug.  It is our first choice for the great majority of bipolar patients that we treat in our practice.

 

1.            BALANCE investigators and collaborators, G.J., Goodwin GM et al, Lithium plus valproate combination therapy versus monotherapy for relapse prevention in bipolar I disorder (BALANCE): a randomised open-label trial. The Lancet, 2010. 375(9712): p. 385-395.

2.            Baldessarini, R.J., Commentary: The Bipolar Affective Disorder: Lithium/Anticonvulsant Evaluation (BALANCE) Study. Bipolar Disorders, 2010. 12(7): p. 669-672.

3.            Licht, R.W., A new BALANCE in bipolar I disorder. The Lancet, 2010. 375(9712): p. 350-352.

4.            Ghaemi, S.N., From BALANCE to DSM-5: taking lithium seriously. Bipolar Disorders, 2010. 12(7): p. 673-677.

 

In the past several years, two new studies have been published examining the efficacy (in pristine, experimental conditions; rigorous selection criteria, minimal comorbid conditions) and effectiveness (real world variability) of lamotrigine (Lamictal) in the treatment of acute bipolar depression [1, 2].  These and other studies were recently summarized in a review paper by Amann and colleagues in the Journal of Psychopharmacology[3].  Attempting to synthesize disparate findings, Amann concludes that “…the antidepressant effect of LTG in acute bipolar depression, if it exists, is small.” 

 

These data support our own clinical work with this anticonvulsant, where we consistently find its acute antidepressant effects quite limited.  In our practice, we now reserve lamotrigine for use with residual depressive symptoms, which either fail to respond to primary mood stabilizers or other antidepressant treatment, or that fail to clear with the remission of the depressive episode.  We are less pessimistic but still uncertain about lamotrigine’s efficacy in the long-term prevention of depressive episodes.

 

This emerging profile of lamotrigine as a marginal antidepressant stands in stark contrast to the fanfare announcing its arrival in the late 1990’s when it was viewed as the Holy Grail for the treatment and prevention of bipolar depression.  This recalibration parallels our growing recognition of the limited potential of standard antidepressants, in general, in the therapy of the depressed phase of this illness[4]. 

 

1.            Calabrese, J.R., et al., Lamotrigine in the acute treatment of bipolar depression: results of five double-blind, placebo-controlled clinical trials. Bipolar Disorders, 2008. 10(2): p. 323-33.

2.            Geddes, J.R., J.R. Calabrese, and G.M. Goodwin, Lamotrigine for treatment of bipolar depression: independent meta-analysis and meta-regression of individual patient data from five randomised trials. British Journal of Psychiatry, 2009. 194(1): p. 4-9.

3.            Amann, B., et al., Lamotrigine: when and where does it act in affective disorders? A systematic review, in J Psychopharmacol OnlineFirst 2010. p. 1-6.

4.            Sachs, G.S., et al., Effectiveness of Adjunctive Antidepressant Treatment for Bipolar Depression, in NEJM 2007. p. 1711-1722.

 

May 13th, 2011

Evidence is building for the use of SAMe (S-adenosyl methionine) as adjunctive therapy in major depressive disorder. Just this past August, a landmark study by Papakostas, et al, demonstrated the superior efficacy of SAMe when combined with other antidepressant agents (e.g., fluoxetine, venlafaxine, duloxetine) over antidepressant monotherapy.¹ Although SAMe has been reported to induce mania in some case reports, there may be a potential role in treatment for bipolar depression as well.²

Previous to this double-blind, randomized controlled trial, SAMe had been shown to have similar efficacy to tricyclic antidepressants such as imipramine in small trials.³ Based on results from the most recent trial, in a group of patients with an incomplete response to conventional antidepressants, six would need to be treated to experience one response and seven would need to be treated to achieve one remission (also known as number needed to treat).¹ On the flip side, few adverse effects were reported. However, caution should be used because of the theoretical risk of serotonin syndrome.

In addition, the study results were only analyzed for patients who took the drug exactly as prescribed, which tends to favor the study medication and does not reflect real-life practice.¹ Caution is also warranted because exact percent improvements for each group were not reported and only 73 patients were included in the study. The study participants were only tracked for a period of six weeks, making long-term conclusions impossible.

Typical treatment doses are in the 400-1600 mg/day range.

Recommendation: Because SAMe is an affordable nutritional supplement with few side effects, it is a suitable option for patients with major depressive disorder and suboptimal response to standard antidepressant therapy. The jury is still out on a potential role in bipolar depression.

____________________

1. Papakostas GI, Mischoulon D, Shyu I, Alpert JE, Fava M. S-adenosyl methionine (SAMe) augmentation of serotonin reuptake inhibitors for antidepressant nonresponders with major depressive disorder: a double-blind, randomized clinical trial. Am J Psychiatry. 2010 Aug;167(8):942-8.

2. Nelson JC. S-adenosyl methionine (SAMe) augmentation in major depressive disorder. Am J Psychiatry. 2010 Aug;167(8):889-91.

3. Delle Chiaie R, Pancheri P, Scapicchio P. Efficacy and tolerability of oral and intramuscular S-adenosyl-L-methionine 1,4-butanedisulfonate (SAMe) in the treatment of major depression: comparison with imipramine in 2 multicenter studies. Am J Clin Nutr. 2002 Nov;76(5):1172S-6S.

One 8-week study showed possible response based on significant improvement in Montgomery-Asberg Depression Rating Scale scores in patients treated for acute bipolar depression when riluzole was added to other antidepressants.¹ However, the small, non-randomized, non-blinded nature of the trial limits the conclusions that can be drawn. Of note, there were no instances of mania or hypomania in this trial, indicating that riluzole may not have the mood destabilizing effects of many other antidepressants. Trials with larger sample sizes would be necessary to confirm this result.

A recent study of 14 patients with bipolar disorder given 100-200 mg of riluzole per day showed a relative decrease in glutamate in the brain, as demonstrated by imaging studies.² This suggests that imaging may play a role in determining response to therapy if further trials support the existing evidence.

Riluzole is being looked at with equal interest in the treatment of major depressive disorder. Another trial with a similar design that looked at response in treatment-resistant patients with major depression taking other antidepressants found a response in some.³ A third trial with high doses of 150-200 mg/day (ALS dose: 50 mg/day) found that riluzole could be effective—even when given without other antidepressants—over a 6-week period.⁴ However, as in the other two trials, this study was open-label and included fewer than 20 patients. Two randomized trials to be completed over the course of the next 2 years should provide additional evidence regarding the relative efficacy of riluzole in treating mood disorders.

From a safety perspective, the most pressing concern is that the medication may cause liver damage, especially in those already at risk or those who drink excessive amounts of alcohol. Coffee and other caffeinated drinks may increase the effect of riluzole, and smoking may speed its elimination from the body, making higher doses necessary. Riluzole also has to be taken 1 hour before or 2 hours after food, which may be inconvenient for many patients.

Recommendation: Based on preliminary study data, riluzole is a promising therapy that may provide an alternate treatment for bipolar depression and/or major depressive disorder, pending positive results in larger randomized, double-blind trails.

1. Zarate CA Jr, Quiroz JA, Singh JB, et al. An open-label trial of the glutamate-modulating agent riluzole in combination with lithium for the treatment of bipolar depression. Biol Psychiatry. 2005 Feb 15;57(4):430-432.

2. Brennan BP, Hudson JI, Jensen JE, et al. Rapid enhancement of glutamatergic neurotransmission in bipolar depression following treatment with riluzole. Neuropsychopharmacology. 2010 Feb;35(3):834-846.

3. Sanacora G, Kendell SF, Levin Y, et al. Preliminary evidence of riluzole efficacy in antidepressant-treated patients with residual depressive symptoms. Biol Psychiatry. 2007 Mar 15;61(6):822-825.

4. Zarate CA Jr, Payne JL, Quiroz J, et al. An open-label trial of riluzole in patients with treatment-resistant major depression. Am J Psychiatry. 2004 Jan;161(1):171-174.

Always looking for novel ways to treat bipolar disorder, researchers have turned to an old standby for Tylenol overdose: n-acetyl cysteine (NAC). Among other causes, mood disorders may be a result of oxidative or metabolic imbalances in the brain caused by low levels of the biochemical glutathoine. NAC works to restore these imbalances, which are possibly at the root bipolar depression, by working as an antioxidant.

While its absolute efficacy has not been proven, one randomized controlled trial showed statistically significant improvement in overall depressive symptoms in bipolar patients on long-term therapy with 1g of NAC taken twice daily in a capsule formulation.¹ This is a non-FDA approved version, which is only available as a nutritional supplement. Unlike the liquid and injection available by prescription, only a small percentage of the capsule formulation is active because it is broken down so quickly by the body.²

The study results also have to be interpreted with caution because the trial only involved 75 patients. Another limitation is that the time to next mood episode was the same regardless of whether the patient was taking NAC or placebo. On the positive side, the trial took place over a 24-week period and showed moderate improvement in symptoms. Despite the lack of published evidence, some U.S. psychiatrists are finding a useful place for NAC in clinical practice.

Although NAC is typically described as well tolerated, the side effects may be appreciable. Nausea, abdominal pain, vomiting, constipation, and diarrhea are common with oral treatment.

Recommendation: Because of its sparse efficacy data and at times noxious side effects, this nutritional supplement has a limited place in therapy.

1. Berk M, Copolov DL, Dean O, et al. N-acetyl cysteine for depressive symptoms in bipolar disorder: a double blind randomized placebo-controlled trial. Biol Psychiatry. 2008 Sep 15:64(6):468-475.

2. Sjödin K, Nilsson E, Hallberg A, Tunek A. Metabolism of N-acetyl-L-cysteine: some structural requirements for the deacetylation and consequences for the oral bioavailability. Biochem. Pharmacol. 1989 Nov 15;38(22):3981-3985.

When it comes to mood disorders, American psychiatry, by and large, lacks rhythm. That is, it lacks an interest in research on circadian rhythms, the relevance of circadian neurobiology for understanding the pathophysiology of affective disorders, and in the application of such studies to generating new treatment techniques. Several European countries, in contrast, appear to feel this groove and have generated decades of clinical research in this area. So what gives?

For those of us interested in this area, the source of this rhythm agnosia, apathy and apraxia has been infinitely perplexing. Is it the absence of financial support from Pharma which limits research and clinical work in this area? Is it the absence of insurance reimbursement for therapies that are neither psychotherapeutic nor psychopharmacologic? Is it the lack of cross talk between basic scientists studying human timing and clinicians treating mood disorders? Or is it the lack of sexiness in the ultra low-tech nature of these treatments? Whatever the reason, and I’m sure there are many, this book is an initial attempt to help clinicians in this country understand and better use information about biological rhythms in our clinical work with affective illness.

Having set the stage, my capsule summary: A long-overdue, wonderful first step.

Chronotherapeutics for Affective Disorders is a neat, concise book which provides a very basic review of circadian neurobiology along with a how-to section that explains both the evidence for these treatments and a simple explanation of how they are to be conducted. As per my introduction, it is no surprise that two of the three authors of this little gem are European. Collectively, they represent leaders of the field and they have an unmistakable agenda to promote the use of circadian-modifying interventions.

Chronotherapies (from Greek Mythology, Chronos, for time) are any treatment that manipulates circadian rhythms for symptomatic benefit. While the focus of this book is on their use in the treatment of affective disorders, these strategies are also used for neurologic, sleep, and other conditions. The major forms of chronotherapy used today and the ones with the most empiric validation are sleep deprivation (rechristened Wake Therapy to avoid nasty connotations), light therapy, and sleep phase advance. Each is reviewed in clear and simple language that is enhanced by helpful diagrams and figures. Think Stephen Stahl-type clarity and exposition.

Always starting with the basics, the reader is carried from what is more common knowledge to more rarefied and detailed explanation. For example, information on the use of light therapy for seasonal affective disorder is leavened with practical guidance on what types of light to use, length and timing of administration, potential side-effects and non-seasonal mood indications and contraindications for this treatment. Similarly, though most of us know that keeping our depressed patients up for a full night can effect a rapid but transient remission, this book reviews a substantial body of literature on the use of various augmenting measures (concurrent use of lithium, SSRI antidepressants, sleep phase advance and/or bright light therapy), how these measures cement and preserve the initial antidepressant response, and thus makes the case that these wake therapy packages are some of the fastest, most effective and safest methods currently available. Making their survey complete, the authors include brief sections on dark therapy, melatonin and other chronobiotics, and chronotherapeutic strategies for children and the elderly. An appendix provides valuable diagnostic instruments used to rate and track rhythm-influenced mood disorders and circadian phase status.

Shortcomings? This is a very introductory primer. Those wanting more depth will not be satisfied with this book alone. If this shoe fits you, consider The Principles and Practice of Sleep Medicine, 4^th Edition; the sections on circadian rhythms provide a deeper foundation in the basic sciences.

In sum, this is a small work with a large agenda. It aims to educate mental health clinicians about the basics of circadian timing and how alterations in these intrinsic oscillations can contribute to mood disturbances. It then provides step by step guidance on how to use circadian-modifying strategies to treat depression, mania and mood instability. It’s not easy helping people develop a sense of rhythm. This book provides much-needed and elementary dance lessons for those who haven’t been able to appreciate the beat.

Finally, a book devoted to the other bipolar disorder. Bravo! Gordon Parker, the Australian psychiatrist, researcher and head of the venerable Black Dog Institute in Sydney, deserves credit on this basis alone. But this is far from the only virtue of this monograph. Here we get a rich, quirky wonderful assemblage of opinion from the leading authorities on this prevalent and understudied form of manic depression. The combination of being the first publication out of the gate on this important area together with its quality, diversity and depth make this required reading for all clinicians and those patients and significant others thirsty for knowledge of this bipolar subtype. For this group, here’s the bottom line: Read this book!

First, the layout. Eschewing the standard APA format of blandly compiling the accumulated data in an area and striving for a deadening impartiality, Parker chooses an all together different and creative alternative. Rather than draining the lifeblood out of the subject, he makes room for the full cacophony of opinion, debate, agreement and conflict that constitutes the field of research at this time. He specifically includes authors with differing viewpoints and distinct emphases. Even better, he puts forth his own, unique outlook in living color, warts and all. The result is less a compilation than a real-time, streetfight amongst respected colleagues. very real portrait of how medicine exists and evolves.

The second delightful aspect of the book’s format is who and what Parker has chosen to include. Clinicians and patients are given voice alongside of the more typical research-weighted authorship. Chapters reviewing the data on atypical antipsychotics alternate with vivid, first person accounts of disturbed mood states. Clinical experts are given the chance to present compelling arguments based on their treatment experiences. Models of well-being are described from sufferer, physician and research perspectives. Omega 3 fatty acids receive their fair share of attention. And the psychotherapies get equal billing with other psychoactive interventions. Here again, the result is a blooming circus of opinion stretching out in multiple directions.

The book is divided into two main parts. The first section starts with one of the most vivid first-person accounts of this illness that I have ever read. It is followed by a concise but richly detailed history and evolution of ideas about this disorder and where it fits in relation to other psychopathology. The next twelve chapters present short reviews of various points pertaining to diagnosis and treatment. Clinical expert James Phelps reprises his fascinating argument to reverse the default diagnostic bias of affective disorders, making bipolarity the baseline standard and only identifying unipolar illness in the absence of evidence for cyclicity or mixity. Parker then suggests an isomeric model that differentiates bipolar I from bipolar II exclusively on the basis of psychotic symptoms. The reader then gets the chance to see radically different viewpoints on the role of antidepressants in this mood subtype authored by Parker and Joseph Goldberg. Overall, this first section is well-written and the editing gives it a smooth, coherent feel.

The second section, however, is outstanding. Taking the lead, Parker describes a multidimensional treatment package for bipolar type II that emphasizes antidepressants, psychoeducation and well-being plans. And he’s not just talking SSRI’s for bipolar depression; they’re his first line choice for mood-stabilizing agents as well! With this as the set-up, the next twelve chapters allow the leading experts in the field to wrestle with the editor’s contentions.  Among the best responses are those of Post, Ghaemi, Goldberg and Ketter who emphasize the intrinsic recurrence and mixity of bipolarity and the corresponding indication for mood stabilizers over antidepressants. It is here in the noisy and well-reasoned squabbling that the book’s strengths truly shine. Not content to serve up the standard pablum, Parker forces the reader to weigh alternatives, consider the evidence and decide where they stand.

Kudos to this Aussie who has the wherewithal to show our field in all its messy beauty.

One sentence opinion: A necessary but typically uninspiring review of an important subject.

Is there a need to devote a book specifically to the depressed phase of bipolar disorder? Absolutely. Should it present data from each of the important research areas on this subject? Of course. Does it need to do so in a formulaic and bland fashion? Judging from the products of the major psychiatric publishers, the unfortunate answer appears to be yes. With a few rare exceptions, such as the stellar Manic Depressive Illness by Goodwin and Jamison or A Mood Apart by Peter Whybrow, review books on psychiatric topics are all too often poorly written, uncreative amalgams of multi-authored chapters without a coherent editorial voice or viewpoint. The result is reading that becomes as dutiful as the writing.

Ok. Now that that’s out of my system, let me return to some specifics about this book.

Despite my overall take on this work, several chapters rise above the tepid baseline. Ghaemi’s pleasure in challenging the prevailing nosology of mood disorders in American psychiatry is evident in the introductory chapter. It is fun and informative. Likewise, the sections on suicide, mood stabilizers and antidepressants show similar signs of life while conveying important information.

The rest of the book is a painful slog. Data is presented in dense and rote fashion. Too many of the references are dated, even for the 2006 publication date.

The chapter on neurobiology is the most disappointing. The emphasis is on neurotransmitter studies of bipolar illness, many dating back to the 1970’s. More recent research on 2^nd messenger systems, functional neuroimaging, and kindling are paid token attention in single paragraphs that feel like afterthoughts.

While this book is indeed, so much less than it could have been, it did have one significant stealth asset: at the time of it’s writing, it was the first work published specifically on bipolar depression. Readers interested in this subject are, fortunately, no longer constrained by this former exclusive status.

Though almost 5 years old, Treating Bipolar Disorder, by Ellen Frank is still one of the first and most frequent reading recommendations that I make for newly diagnosed patients. Written in plain, easy to understand English, this little gem asserts that affective relapse in bipolar disorder follows from disruptions in social and circadian rhythms. This theory led to the development of a disorder-specific therapy, Interpersonal Social Rhythm Therapy (IPSRT) whose case-based description is the mainstay of this book.

Frank starts with a review of existing theories and empirically-validated treatments of bipolar disorder, In so doing, both this book and her treatment model include a healthy serving of psychoeducational information about this illness. Given that this is one of the most potent and, perhaps, a common element of all psychotherapies for bipolar conditions, this inclusion makes good sense.

The model of IPSRT is presented next. In formulating this model, Frank essentially connects two different research areas into a single causal pathway of affective relapse: the association of interpersonal conflicts with unipolar depression and the literature emphasizing circadian disruption in affective relapse of bipolar disorder. Rather than viewing these as separate contributory factors, she proposes that changes in social routine lead to altered biological rhythms (especially sleep) which form the final common pathway to the onset of new mood episodes. Using this model of relapse, IPSRT intervenes both at the level of social discord and circadian disruption to stabilize disordered rhythms.

The remainder of the book details these two fundamental components of IPSRT.

Beginning with a history-taking that seeks to demonstrate the relationship between social and biological rhythm havoc and episode onset, Frank walks the reader through the treatment process and its different modules. The IP component identifies and then addresses the most salient relationship problems the individual is experiencing. The SRT module, however, is what’s new and most interesting here.

Using a standardized tool, the Social Rhythm Metric, patients are asked to note and record the time of a host of daily activities such as sleep onset, awakening, meals, when one leaves home, physical exercise, exposure to sunlight, level of socializing, etc With the initial data as a baseline, therapists and patients work together to increasingly standardize fluctuations in these behavioral indices. Research studies are presented documenting the effectiveness of this approach in reducing relapse in patients with Bipolar Disorder Type I.

This book is readable, engaging and encouraging. The IPSRT model gives patients a new perspective and sense of empowerment in confronting their illness. No longer a disease which strikes randomly and without warning, IPSRT provides patients with a strategy to monitor, anticipate and modify social and biobehavioral rhythms and thereby exert better control over their lives. Not a bad thing.

Postscript: An article from February, 2009, published in the Journal, Bipolar Disorders, by Holly Swartz, Ellen Frank and colleagues at the University of

Pittsburgh, examined the efficacy of IPSRT as a monotherapy for Bipolar II depression. Yes, monotherapy, meaning only IPSRT and no psychoactive medications. Though the study was small, had a high number of drop-outs and no control group, about 40% of the treatment cohort experienced significant improvement.  Is it possible that a subset of bipolar patients can be managed through biologically-stabilizing psychotherapeutic interventions alone??? Stay tuned.