CENTER ON BEHAVIORAL MEDICINE
ADDITIONAL MATERIALRELATED PAPERS
by the author to reproduce this paper:
Mood DisordersScott Bury
In the following paper, I will summarize currently accepted theories about the causes of Major Depressive Disorder (MDD), the assessment process used to determine the existence of a mood disorder, pharmacological, psychological and psychosocial interventions, and how I plan to use this newfound information. I will then cover the same ground for the Bipolar Spectrum disorders. A specific focus of this paper will be on the childhood presentations of these illnesses. In order to avoid repeating much of the excellent information contained in our course text (Preston & Johnson, 2006), I will primarily be referencing other interesting information gleaned from a variety of other sources.
Major Depressive Disorder
Child and adolescent MDD and dysthymic disorder (DD) are common, familial, and recurrent conditions that are associated with comorbid psychiatric conditions, and usually persist into adulthood (American Academy of Child and Adolescent Psychiatry [AACAP], 1998). Symptom expression varies greatly with developmental stage (to be described later), and can often be alleviated by early identification and persistent treatment. The prevalence of MDD is estimated to be approximately 2% in children and 6% in adolescents with a male/female ratio of 1:1 during childhood and 1:2 during adolescence (Costello, Mistillo, Erkanli, Keeler, & Angold, 2003). Lewisohn, Roberts, Seeley, Rohde, Gotlib, and Hops (1994) postulate that the prevalence increases during adolescence due to biological factors (hormonal changes from sexual maturation and brain development), environmental factors (increased social and academic expectations, increased chance of exposure to negative events or a longer history of enduring same), and psychological factors (increasing autonomy and abstract thinking). The previous authors go on to say that girls might carry more risk factors because of certain personality characteristics: a tendency for American girls to deal with problems in a more ruminative and self-focused style than boys, a tendency to worry more about body image, and because girls are more likely to be exposed to sexual abuse and experience more pressure to conform to restrictive social roles than boys. Of course, being aware of ethnic and cultural factors in the presenting complaints, and resisting stereotypes and expectations during assessment and treatment can reduce underdiagnosis and misdiagnosis. Acute or chronic stress in general is also known to be a contributing factor in triggering the onset of MDD in both genders, as are illnesses, substance use (including medications), heredity, and biochemical imbalances. A common saying is “psychology is biology,” meaning that every thought and memory has a physical component. Through chemical changes, the brain keeps track of everything that happens to a person, and the stronger the environmental influences and the more often thoughts and actions are repeated, the more indelible the imprinting on the brain (LeDoux, 1996). When a person’s brain is bathed with repetitive stress hormones and chemicals, measurable effects include a depletion of norepinephrine, among other things, and this is especially destructive if a person is genetically susceptible to developing a mood disorder. This is where psychotherapy, social work, and psychopharmacology can help.
According to Inaba and Cohen (2004), well over 100 different neurotransmitters have been discovered. They also report that researchers have discovered hundreds of different receptor types, each one with a unique molecular composition of proteins. These receptors are designed to receive a compatible neurotransmitter. If we took a look at one of the neurotransmitters most often associated with depression, serotonin, we would see it has at least fourteen types of serotonin receptor sites in the brain (5-HT1A, 5HT4…). Some of these are excitory, most are inhibitory, but each one causes a slightly different effect. Each nerve cell sends out only one type of neurotransmitter, but can have receptors for several different types of neurotransmitters. A serotonin receptor, for example, will not accommodate dopamine, but a single nerve cell can contain both dopamine and serotonin receptors. There are often multiple receptors on a dendrite, with anywhere from a few contacts to up to 150,000 contacts with other cell bodies. Before researching this paper, I always thought of a nerve cell as sort of a two dimensional highway going from point A to point B with few on and off-ramps. It has been interesting to discover that cells are much more three-dimensional, (I’ve seen pictures where they look like cotton balls) and that the release of one neurotransmitter usually triggers a cascade effect. A serotonin release in one neuron, for example, can actually result in dopamine release in the brain’s emotional center way on down the line.
Multiple central nervous system mechanisms have been associated with depression besides neurotransmitters like serotonin and noradrenaline, such as the HP axis and other stress-related endocrine systems, intracellular messengers and neurotropic factors, and the prefrontal cortical neurocircuitry. (Drevets, Ongur, & Price, 1998). The DSM IV-TR (2000) points its pathophysiology finger at the dopamine, acetylcholine, and gamma-aminobutyric acid systems, alterations of several neuropeptides, hormonal disturbances, and alterations in cerebral blood flow and metabolism. The DSM also reminds us that none of these changes are present in all individuals with MDD, nor are any of the particular biological disturbances listed above specific to depression.
Fortunately, we do know that certain interventions are effective in treating MDD. But before I get into those, I want to stress the importance of making an accurate diagnosis. In my practice, the team calls this “front-loading the treatment and relationship.” I believe in the “pay now or pay later with interest” philosophy, and “taking the time it takes” to do it right by scheduling longer or more frequent sessions up front. I try to assure that the child has had a complete medical check-up prior to my first visit, and I get authorization to see the report or speak to the doctor. Then, I like to spend 2-3 hours in the initial interview, and meet twice weekly for the first two weeks.
The AACAP (1998) has outlined the considerable variations in the presentation of MDD across different developmental stages of childhood and adolescence. Young children usually show more anxiety symptoms, phobias, social withdrawal, somatic complaints, auditory hallucinations, irritability, temper tantrums, and behavioral problems. In middle and late childhood, children may begin to report anhedonia and the cognitive components of their dysphoric mood such as low self-esteem, guilt, and hopelessness. Adolescents manifest more sleep and appetite disturbances, delusions, suicidal ideation and attempts, and more impairment of functioning than younger children, but fewer neurovegetative symptoms and more irritability than adults with MDD. It is important to assess for symptom clusters that define the subtypes of depression (seasonal affective d/o, atypical symptoms, psychosis, or hypomania) in order to choose the correct course of treatment. Differential diagnosis includes looking for non-affective disorders with similar symptoms as MDD such as poor self-esteem, attentional problems, irritability, etc., including anxiety disorders, learning disabilities, disruptive disorders, adjustment disorder with depressed mood, bipolar disorder, and general medical conditions. Substance abuse should always be suspected, as this is very common in adolescents with mood disorders.
It is also important to continue to assess for comorbid diagnoses, as these are ultimately found in 40% - 90% of youth with MDD. MDD usually manifests after the onset of the other psychiatric disorder(s) (Birmaher, Ryan, Williamson, Brent, Kaufman, Dahl, Perel, & Nelson, 1996). The most frequent of these include ADHD, dysthymia (aka double depression), any one of the anxiety disorders, disruptive behavior disorders, or substance use disorders. Comorbid separation anxiety disorder and reactive attachment disorder are more often seen in younger children. In order to make a diagnosis of MDD with confidence, spending 4-7 hours conducting a comprehensive assessment is considered best practice (Graham 2000). Reassessments should occur at periodic intervals throughout the course of treatment to track an improving or worsening condition, and because diagnoses can change over time.
Various forms of individual psychotherapy has been found to effective in treating MDD and have been studied extensively, some of the most popular methods being cognitive-behavioral therapy, psychodynamic psychotherapy, and interpersonal psychotherapy. My favorite therapy tools are embedded in experiential therapy, a method I have found to be efficacious but which appears to have received positive, but minimal attention by researchers in the literature. I am currently working for an agency (Heal Therapy Inc) that specializes in equine-facilitated mental health. I work with kids and horses at an arena, conduct supplemental school and home visits, and take kids on outdoor “adventure” outings on a regular basis.
Since children often have trouble expressing thoughts and feelings, and can easily become irritable and uncooperative, picking the brains of collateral informants such as parents, teachers, and other sources is crucial to a proper diagnostic evaluation of a child. An effective therapeutic alliance with all available collateral contacts should be fostered very early in treatment, to maintain child and family involvement over the course of treatment. A critical component of early treatment for MDD is education of the client and family about the disorder and its treatment, to help everyone become informed partners in the treatment team (Beardslee, Salt, Versage, Gladstone, Wright, & Rothberg, 1997). Weissman, Warner, Wickramaratne, Moreau, and Olfson (1997) note that education increases patient and parent cooperation and decreases premature termination of treatment. It also allows the discussion of treatment to proceed with less parental self blame (“I’m a bad parent”) and blame of the child (“She’s just being manipulative”, or “He’s just lazy”). Furthermore, it appears that educating parents about their child’s depression helps them identify their own depressive (or other) symptoms and potential need for treatment. Education could include teachers, siblings, and friends, because the symptoms of depression usually affect each of them and would cover the following topics: signs and symptoms of depression, its impact on relationships, the role of medications and common misconceptions of same, the role of parents and teachers and family in recovery, impact on school attendance and functioning, and the importance of trying not to become unnecessarily stressed or angry (making things worse) by taking the child’s behaviors personally. Being or living with a child with MDD is hard work! Family therapy can be helpful in preserving and restoring relationships, family or individual group therapy (where available) is good at reducing isolation and providing a different kind of helpful empathy and support than one would typically get from the clinician. An increase in family problems might be a consequence of living with a depressed child, or they may have been a precipitating factor. If a child is upset because of abuse between parents, for example, the primary problem may not be treating the depression but dealing with domestic violence. I consider strong connections to the DV shelter, family resource centers, leaders of local support groups, and knowledge about parent friendly websites part of my multidisciplinary team.
Given the developmental and psychosocial context in which depression unfolds in childhood, pharmacotherapy can be an essential ingredient in recovery from MDD but is usually not sufficient by itself. While there is still a notable amount of “overlap” in the psychosocial techniques used to treat MDD, ADHD, bipolar, and other mental illnesses (alone or when comorbid with MDD), research has led to increasingly diagnosis-specific psychopharmacology, so it is important for clinicians to do their best to get the diagnosis right the first time. Professionals still disagree about whether psychotherapy, pharmacology, or a combination should be offered as a first-line treatment for children and adolescents with MDD. Just a few years ago, I considered myself firmly in the “medication as a last resort” camp. But personal experience and continued training has humbled my opinion about the power of a healthy environment (and my own inspired and evidence-based therapeutic interventions) to change everyone, and how bad biology has the power to take down or keep down even people in the most supportive of environments. I now know that through my own ignorance, I colluded with and allowed some of my clients to suffer needlessly during a course of minimally effective psychotherapy when what (I think) they actually needed was medication. My thinking is now more in line with Jacobson, Dobson, Truax, Addis, Koerner, and Gollan, et al (1996), who recommend that the choice of therapy should depend on several factors, including severity, number of prior episodes, chronicity, subtype, age of the client, family history of mental illness, contextual issues (family conflict, academic problems, exposure to negative life events), compliance with treatment, previous response to treatment, and the child and family’s motivation for treatment.
These days, when a mutually arrived at decision to initiate medications for MDD is decided upon (in the context of a solid therapeutic relationship), there are helpful algorithms available to steer the decision- making (Preston & Johnson 2006; Hughes, Emslie, & Crismon, 1999). SSRI monotherapy is the current recommended starting point because of their safety, side effects profile, ease of use, and suitability for long-term maintenance, but the presence of comorbidities may require alternate initial agents. According to AACAP practice parameters (2000), a child with MDD and ADHD, for example may benefit more from a TCA, bupropion, or venlafaxine than an SSRI. Emslie, Hughes, Crismon, Lopez, Pliszka, and Toprac, et al (2004) suggest starting with their ADHD algorithm and going with a stimulant first in these cases. SSRIs work by entering the reuptake pore and blocking it, so the neurotransmitter released stays longer in the synapse in order to have a greater effect on the postsynaptic neuron. In addition to the SSRIs, I found at least 9 more classes or subclasses of antidepressant choices (Inaba et al 2004; Lott et al n.d.), which I will briefly describe below.
1. TCAs (imipramine, desipramine) are thought to block reabsorbtion of serotonin and norepinephrine by the sending neuron, which forces the synthesis of more receptor sites for these neurochemicals. Although TCAs are not recommended as first line treatment for youth with depressive disorders because of the lack of efficacy and potential side effects, it is important to keep in mind that what is universally true for a large group of people is rarely universally true for individual members of that group - some individuals will respond better to TCAs than other medications. 2. MAOIs (phenelzine, isocarboxazid) work by blocking the enzyme monoamine oxidase that metabolizes the neurotransmitters norepinephrine and serotonin, which increases their availability. These are also used infrequently in children because of the need for close supervision to prevent several serious, potentially fatal side effects. 3. NDRIs (bupropion and bupropion SR) are norepinephrine/dopamine reuptake inhibitors. 4. SNRIs (venlafaxine XR, duloxetine) are serotonin/norepinephrine reuptake inhibitors. 5. SARIs (nefazodone, trazodone) are serotonin modulators, a serotonin-2 antagonist, and reuptake inhibitor. 6. Remeron is a NASSA, a noradrenergic and specific serotonin antagonist that also modulates norepinephrine. 7. Buspirone is a partial 5HT-1 (serotonin receptor) agonist; it blocks the transmission of excess serotonin and mimics serotonin, so it can substitute for low levels of this neurotransmitter. 8. Heterocyclics include amoxapine and maprotiline. 9. Stimulants (amphetamines, methylphenidate) are occasionally used as antidepressants, and lastly, there are always other medications, probably with novel mechanisms of action that may have been, or are being used to augment antidepressants, that are being tried alone when patients have not responded favorably to the typical algorithm stages: SSRI, alternate SSRI, SSRI + augmentation, monotherapy with different class, another different class, etc., all the while checking for compliance, side effects, proper dosing, additional assessment information.
Despite those seductively neat and tidy practice parameters, algorithms, and guidelines, treating children with medications (and psychotherapy) is still just as much of an art as a science. “Correct” treatment is not (yet?) agreed upon. Children and their illnesses change as we treat them, and we practitioners, hopefully, continue become more skillful after each experience. “A tincture of time” (Lott & Koshes, n.d.) is an important ingredient to include with the use of any psychotropic medication. Adequate time must be given for biochemical changes to take place, which include therapeutic effects (which may go unnoticed by clients) and side effects (which seem to be immediately obvious to clients). Time is also required for common side effects to (hopefully) diminish, and for psychotherapy to have an effect on reducing psychosocial stressors. The risk of specific side effects of psychotropic medications are readily available, but a few are of particular concern in children and need special mention here. The number of people receiving outpatient treatment for depression has more than tripled since 1987, but during that same period, the number of clients receiving psychotherapy dropped about 15% (Inaba & Cohen, 2004). Are we returning to the traditional medical model? It is concerning that psychotherapy use seems to be trending downwards (I have noticed it has become more difficult to justify and receive continued 3rd party payments for necessary long term psychotherapy of children/families in which there is complicated MDD or Bipolar disorder [BPD]) at the same time that prescription drugs dispensed to children continues to increase, with a dramatic doubling of antidepressant use in teenagers reported from 1999 (1.8%) to 2000 (4%) (Benedetto, Zuvekas, Norquist, 2006). An interesting study of 40,639 children receiving mental health services (Harpaz-Rotem, 2006) reported no significant differences in the prescribing practices between PCPs and Psychiatrists in either the proportion of children who received psychotropic medication, the frequency of clinical contacts, or the dosages or types of medications prescribed. I have noticed that the well intentioned physicians and the one child-psychiatrist in my rural CA county always have overflowing waiting rooms, making adequate time for crucial supervision and follow-up difficult, more so when there isn’t also a therapist (safety net) also on-board. I find it interesting that the increase in SSRI prescriptions in 1999 came on the heels of the first reports of controlled trials of SSRIs in youths, which suggests that prescribing practices are strongly influenced by research findings (Benedetto, et al, 2006). It’s not hard to find research data on the efficacy and safety of psychotropics on the adult population, so why isn’t there more research being done on children? No doubt ethical concerns about drug effects on growth and development, potentially dangerous side effects, including the controversial suicide risk issue, and the risk of using placebos in clients with a known illness are holding back progress. Consequently, in child and adolescent psychiatry, changes in clinical practice have far outpaced the emergence of research data and clinical decisions are frequently not guided by a scientific knowledge base. Thus, nearly 80% of pediatric drug use is “off-label” (American Academy of Pediatrics, 1996). Ultimately, the philosophy I now convey to children and their families with severe mental illness is that I believe that the risk of not treating MDD aggressively with medication may far outreach the risk of side effects and may well be worth the potential risks. Of course, I will also convey a willingness to support and respect a family’s contrary opinions, as they have the ultimate responsibility for the management of their own illness.
Pediatric Bipolar Disorder (PBD)
There is ongoing debate in the field over whether PBD or juvenile bipolar disorder, as it is sometimes called, is best classified as bipolar disorder, or if it should be referred to as something other than the illness that is classically described in adults (McClellan, 2005). There is no question that children who are explosive, dysregulated, and emotionally labile suffer significant impairment, but are their symptoms better explained by another disorder such as PTSD, a disruptive behavior disorder, anxiety disorder, pervasive developmental disorder, emerging borderline personality disorder, or substance abuse disorder? In my experience, differential diagnosis of PBD has been frustrating and quite a challenge. The above disorders, and others, are frequently comorbid with PBD, but I believe PBD is most likely the same animal as adult BD, as evidenced by family history studies (Faraone, Glatt, & Tsuang, 2003) and psychopharmacogenetic research (Ikeda & Kato 2003) both showing a strong genetic component. The same medications used to treat adult BD are also often effective in children with PBD. There is other evidence to support the theory that bipolar disorder has biological causes.
Studies of the biological dysfunction involved in bipolar disorder suggest that the brain structures involved in this disorder are those considered part of the affective circuitry in the brain (Mayberg, 1997) They include the dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC), and the amygdala. The DLPFC is believed to be related to problem solving. The OFC and amygdala work in close concert to modulate affective response. Functional neuroimaging studies have demonstrated reduced activation of the DLPFC and OFC and activation abnormalities in the amygdala in adults with BD (Drevets, 2002, as cited in Chang, Karchemskiy, Barnea-Goraly, Garett, and Simeonova et al, 2005). Chang et al (2005) also reported that children and adolescents with BD have significantly smaller amygdala than healthy controls, possibly representing a genetically determined core neurobiological feature of BD. Furthermore, these researchers found relatively increased amygdalar gray matter in patients with significant past exposure to mood stabilizers, providing further understanding of how these medications may work to stabilize mood and improve problem-solving in BD. It also supports the idea that medications such as Lithium and VPA offer neuroprotection and that chronic administration of these medications might lead to biological benefits that could outweigh adverse side-effects. Other imaging studies implicate the mediodorsal thalamus, ventral palladium, striatum, and cerebellum. Lesions in any region in this circuit could hypothetically result in a primary dysregulation of mood or a vulnerability to environmental stressors (Soars and Mann, 1997). I was unable to figure out if these studies were sponsored by the drug manufacturers, so I think it wise to interpret all research results recommending lifetime medication with a bit of healthy skepticism.
PBD can emerge on its own, in conjunction with another disorder, or it can be precipitated by a course of MDD. Follow-up studies of depressed children and adolescents have found that 20% - 40% develop bipolar disorder within 5 years after the onset of MDD (Geller & Luby 1997). Once the illness starts, episodes tend to recur and worsen without treatment. Studies show that after symptoms first appear, there is typically a 10-year lag until treatment begins (Burkhamer, 2004). Characteristics of MDD associated with the switch to bipolar I disorder include early onset, psychomotor retardation, psychotic features, family history of BD, family history of psychotic depression, heavy familial loading for mood d/o, and pharmacologically induced hypomania. Like MDD and other mental illnesses, PBD cannot yet be identified physiologically; therefore, the diagnosis must be made on the basis of symptoms, course, and risk factors, such as those listed above. The DSM IV-TR doesn’t have PBD criteria, and the adult criteria do not do a good job of describing the typical PBD child’s behaviors. Liebenluft (as cited in the 2006 AACAP practice parameters for the assessment and treatment of children and adolescents with bipolar disorder) noted that the term pediatric bipolar disorder is used differently by different investigators to describe what may be, in fact, diverse clinical populations. So he proposed subdividing juvenile mania into three phenotypes: narrow (classically defined DSM IV-TR mania), intermediate (well-demarcated periods of mania or hypomania lasting 1-2 days), and broad (chronic difficulties with irritability and hyperarousal). Such an approach acknowledges the potential differences in the disorder, and because this seems so logical, I can’t imagine the reason the field will not keep moving in this direction.
A number of recent articles and websites, including the Child and Adolescent Bipolar Foundation (http://www.bpkids.org) have outlined behaviors common to children currently diagnosed with PBD. They recommend to parents that they take their child in for an evaluation if 4 or more symptoms on the site’s PBD list have caused impairment in their child’s functioning for a week or more. Here is small sampling from the checklist: rapidly changing moods lasting a few hours to a few days (ultra rapid or ultradian cycling), explosive, lengthy, and often destructive rages, defiance of authority, suicidal ideation, separation anxiety, sleeping little, or alternately, sleeping too much, strong and frequent cravings for carbohydrates and sweets, potentially injurious dare-devil behaviors, and a grandiose belief in own abilities that defy logic. Because there is considerable overlap of these symptoms with other common childhood disorders, making a differential diagnosis or being astute enough to recognize secondary comorbid diagnoses is necessary. Burkhamer (2004) is one author who published a decision tree to aid this process. For example she states that ADHD children will carelessly break things, while the PBD child will break things on purpose. ADHD tantrums may be 10-20 minutes, while a PBD child’s may last from 45 minutes to 4 hours. Sensory and emotional overstimulation typically triggers ADHD children’s tantrums, while PBD children typically react to limit setting and the word “no.” This was a partial ADHD list. Similar lists are available to differentiate PBD from conduct disorder, ODD, Anxiety d/o, and more.
Mood stabilizers (prescribed out of a strong therapeutic alliance) are the cornerstone of the overall PBD treatment plan because psychotherapy may not be effective until mood stabilization occurs. An ideal mood stabilizer is any medication that would stabilize acute manic, mixed, and depressive symptoms without inducing the opposite mood symptoms, and will continue to work towards preventing symptomatic relapse.
The main drug used for the treatment of bipolar disorder over the last 30 years has been lithium. Some of the other standard medications that have come into use during this time include carbamazapine, valproic acid, divalproex, the olanzapine-fluoxetine combination (persons with BD should be protected from SSRI monotherapy), and lately risperidone, among others. Each of these medications is generally well tolerated and very effective in the treatment of PBD. However each has a very distinct side-effect profile that requires careful monitoring. As with MDD and other psychiatric disorders, algorhythms have been developed to assist the physician in choosing evidence-based medicine for adult clients presenting with manic, mixed, or bipolar depression criteria (Preston and Johnson, 2006, Sachs, 2006) and in the absence of age specific guidelines, these are also often applied in the management of the childhood presentation of the illness. The Sachs (2006) algorhythm for treating patients with acute mixed criteria, the most common childhood presentation, recommends: start with either a non-dopamine-blocking antimanic agent, a dopamine-blocking antimanic agent, or a combination of 2 antimanic agents, depending on patient history and unique presentation. If mania increases, a dopamine and one or two non-dopamine-blocking agents could be combined. If depression increases, a bimodal agent or SSRI could be added. I have noticed a change in verbiage used in the newer literature away from familiar phrases like “least restrictive” and “lowest effective dose” to terms such as “most effective treatment.” In spite of the fact that serious side effects will surely continue to be uncovered due to the increasing comfort in which physicians are prescribing off-label medicines, medication changes should still be initiated as systematically as possible, and ideally, only one medication at a time should be changed during a period in which other clinical variables are stable. ECT is not unheard of as a last resort for children and adolescents, because it is often effective when more conservative approaches have been unsuccessful (AACAP 2002).
Drugs that might be best to steer clear of with children with PBD, or with children in which PBD can not be ruled out, include the beta blockers (propranolol may increase depression), some alpha-adrenergic agonists (clonidine may increase depression if a child with PBD is misdiagnosed with ADHD and treated solely for ADHD), imipramine and desipramine (used to treat bedwetting but could contribute to mania or an aggressive state), Lamotrigine (can cause a dangerous rash progressing to Steven-Johnson’s syndrome), valproic acid in females (risk of polycystic ovary syndrome), and all OTC supplements (Gingko Biloba, St. John’s Wort, and any of the new “treatments” being promoted on consumer websites targeted to people with BPD), unless, of course when supervised by the physician treating the BPD.
A best-practice treatment plan (AACAP 2006, APA 2002) would also include psychotherapeutic interventions. These can help patients with PBD and their families learn to cope with the illness, prevent or prolong the time until relapse, and improve medication adherence. Components could include: education about the illness (symptoms, course, treatment options, hereditability, potential impact of the illness on relationships, common precipitating factors to relapse), personalized information about the need for treatment compliance (a particular problem because of the lack of insight that often accompanies PBD), shared decision making in the development of a relapse prevention plan (including anticipating medication noncompliance, management of medication side effects, anticipating stressors for planning ahead and coping better), promotion of regular patterns of activity and sleep (Interpersonal and social rhythm psychotherapy [IPSRT] is based on evidence that disrupting biorhythms can trigger mood episodes), and careful and systematic tracking of symptoms to help everyone know if particular interventions are making a difference in suppressing or eradicating symptoms. Clinical tools commonly used for this purpose are forms, evaluations, contracts, and charts (Nierenberg, Ostacher, Borrelli, Iosifescu, & Perlis et al, 2006). I find that the routine use of forms of any kind in the therapy session often strain my rapport, so I try to minimize their use. It is also important to keep the scoring of data from becoming the end, rather than just another means of examination. Excessive reliance on numbers and evaluations can actually be an obstacle to understanding the people coming to see us.
Individual therapy. McClellan & Hamilton (2006) captured the essence of the magnitude of the expectation inherent in evidenced-based treatment when they wrote: Although requiring clinicians to use first those therapies with the highest level of empirical support seems like common sense, the implications are potentially daunting. Should every clinician be able to expertly administer all of the myriad different specific interventions? (apparently the CA Board of Behavioral Sciences thinks so as evidenced by the failure rates on the MFT exam) McClellan and Hamilton continue: the image of the clinician’s office filled with volumes of therapy manuals awaiting the right patient is often used as an argument for why proven manual-based treatment approaches are not feasible or pragmatic. I once was told by a supervisor “today’s best practice truths are tomorrow’s old wife’s tales.” But that does not mean we shouldn’t stop learning. I think it is possible to pick a special interest(s) and keep current in the literature, and continue to evolve into using empirically supported strategies rather than adhering solely to past training or theoretical beliefs.
Teachers also need psychoeducation and support. Attending the IEP with the family is a great way to advocate for the needs of the child, gain new assessment information, and help pull a team together to get more resources to the BP child, which ultimately support the child, parents, teacher, and the therapeutic process.
Family work is crucial, but describing the directions this could go in would be great topic for a future paper. It is important, for example, for parents/caregivers to be educated about the biological basis of their child’s emotional dysregulation. When parents can see some of their child’s outbursts as unintentional, they are more likely to let go of an ineffective or punitive parenting style and act in a compassionate manner towards their child in times of crisis. They need encouragement to bring balance back into the family, and this often means finding more opportunities for their own “self-care” such as support groups, recreation, or just taking short breaks away from their child. Many families need to grieve the loss of hopes and dreams of a “normal” family. One approach that is receiving lots of positive reviews in the literature these days is family- focused therapy, or FFT (Hirschfield 2005). This manual-based psychosocial program involves bringing all family members together for weekly psychoeducation, communication enhancement training, and problem-solving skills training, and it occurs adjunctively with pharmacotherapy. I have not seen the manual yet, but thanks to this class, I am now aware of it and plan to follow-up.<>In conclusion, I’ll close with the words of Sibley et al (2004): The treatment process should be a blending of an interaction between the client and the psychiatrist (and/or clinician) in psychotherapy, an interaction between the brain and the medication, and the two processes overseen by the therapeutic alliance.
Psychiatric Association. (2000). Diagnostic and
Statistical Manual of
Mental Disorders (Fourth Edition, Text
American Psychiatric Association (2002). Practice guideline for the treatment of patients with bipolar disorder (revision). American Journal of Psychiatry 159: 1-50.
W. R., Salt, P., Versage, E. M.,
V., Zuvekas, S. H., Norquist, G. S. (2006). National estimates of
antidepressant medication use among
B., Ryan, N. D., Williamson, D., Brent, D., Kaufman, J., Dahl, R.,
& Nelson, B. (1996). Childhood and adolescent depression: A review
last 10 years –
J (2004). Bipolar disorder in
children and adolescents: what it is and
how to provide intervention to clients and families.
Copyrighted workbook distributed in June of 20005 at a
Karchemskiy, A., Barnea-Goraly, N., Garrett, A., Simeonova,
Adolescent Bipolar Foundation. (n.d.) What are the symptoms of bipolar
in children? Retrieved
Costello, E. J., Mistillo, S. Erkanli, A., Keeler, G., & Angold, A. (2003). Prevalence and development of psychiatric disorders in childhood and adolescence. Archives of General Psychiatry 60: 837-844.
Drevets, W. C., Ongur, D., & Price, J. L. (1998). Reduced Glucose metabolism in the subgenual prefrontal cortex in unipolar depression. Molecular Psychiatry 3:190-1.
J., Hughes, C. W., Crismon, M. L., Lopez, M., Pliszka, S., Toprac, M.
Boemer, C. (2004). A feasibility study of the
Faraone, S. V., Glatt, S. J., Tsuang, M.T. (2003). The genetics of pediatric-onset bipolar disorder. Biological Psychiatry 36 (10) 1378-1387.
& Luby, J. (1997) Child and adolescent bipolar disorder: a review
last 10 years. Journal of the
Graham, P. (2000). Treatment interventions and findings from research: bridging the chasm in child psychiatry. British Journal of Psychiatry 176: 414-19.
Harpaz-Rotem (2006) Prescribing practices of psychiatrists and primary care physicians caring for children with mental illness. Child: Care, Health and Development 32(2): 225-237.
R. M., (2005). Guideline watch:
Practice guideline for the treatment
of patients with bipolar disorder, 2nd edition.
W., Emslie, G. J., Crismon, M. L. (1999). The Texas Children’s
Algorhythm Project: report of the Texas Consensus Conference Panel on
medication treatment of childhood major depressive disorder. Journal of
and Kato, T. (2003). Biological predictors of lithium response in
disorder. Psychiatry and Clinical
Retrieved from Medline on
& Cohen W. (2004) Uppers, Downers, All
Jacobson, N. S., Dobson, K. S., Truax, P. A., Addis, M. E., Koerner, K, Gollan, J. K., Gortner, E., Prince, S. E. (1996). A component analysis of cognitive-behavioral treatment of depression. J Consult Clinical Psychology 64:295-304.
E. (1996). The Emotional Brain.
P. M., Roberts, R.E., Seeley J.R., Rohde, P., Gotlib,
A. & Koshes, R. J. (n.d.). Psychopharmacology for
Mayberg, H., (1997). Limbic-cortical dysregulation: a proposed model of depression. Journal of Neuropsychiatry and Neuroscience 9: 471-81.
J. (2005). Commentary: treatment guidelines for child and adolescent
disorder. Journal of the
Institute of Mental Health (n.d.). Bipolar
disorder: Retrieved from the World Wide Web on
Nierenberg, A. A., Ostacher, M. J., Borrelli, D. J., Iosifescu, D. V., and Perlis, R. H., et al (2006). The integration of measurement and management for the treatment of bipolar disorder: a STEP-BD model of collaborative care in psychiatry. Journal of Clinical Psychiatry 67 (suppl 11): 3-7.
Sachs, G. S. (2006). Implementing evidence-based treatment of manic and mixed episodes. Journal of Clinical Psychiatry 67 (suppl 11): 12-17.
K. & Kramer, D. A. (2004). Reframing the SSRI issue. Journal of
Soares, J.C. and Mann, J. J. (1997). The anatomy of mood disorders – review of structural neuroimaging studies. Biological Psychiatry 41: 86-106.
Weissman, M. M., Warner, V., Wickramaratne, P., Moreau, D., & Olfson, M. (1997). Offspring of depressed parents – 10 years later. Archives of General Psychiatry 54: 932-940.