What is Biofeedback?

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

 

Biofeedback is a therapeutic technique that uses technology/computers  to help you become more aware of the subtle changes that occur in your body. Once you are more aware of them, you can control them better.

How does Biofeedback work?

Many physiological processes in your body are hard to detect, but computerized monitoring allows you to notice them better. The monitored information is then “fed” back to you in an understandable form. By being able to see this information on a computer monitor, you can learn how to control the processes better.

Why would I care about controlling my physiological processes?

Most people know that we control our body by using our mind. For example, if we are agitated, we can use our brains to calm our body. But did you know that many nerves that control our behavior actually go from the body to the brain? If you can create a calm body, you can create a calm state-of-mind.

What will biofeedback help me with?

Biofeedback has been used for stress and anxiety disorders (including muscle tension and panic), TMJ, low back pain, chronic pain anywhere in the body, migraine headaches, breathing disorders, Raynaud’s Syndrome, IBS, hypertension and addiction (when you are calmer cravings tend to diminish). There are also many additional health benefits from biofeedback.

What physical processes does biofeedback monitor?

The most common physiological processes monitored are heart rate, respiration (breathing), sweating, peripheral temperature, blood pressure and muscle tension.

How does receiving feedback about physiological processes help me control them?

If you shot a basketball in the general direction of the basket, but could not see the basket itself, your shooting would not improve. When you set the goal of relaxing, and then get feedback about exactly what is happening in your body, you will get better at relaxing.

How fast does Biofeedback work?

As with any therapy, the results will vary depending on your condition. Although lasting results may take 10 sessions or more, some people see results in 3-4 sessions. As with learning any skill, how fast you improve will depend on how much you practice.

What is a typical biofeedback session like?

Your biofeedback therapist usually begins treatment with a comprehensive assessment of your physiological processes and your awareness of them. Then you will jointly design a biofeedback training program to improve your capacity for self-regulation, based on your needs and goals. Electrodes are “pasted” to you so that you can get feedback on the computer monitor. The paste is easily wiped off. The electrodes do not transmit any electricity to you. You therapist will guide you through the entire process. Near the end of each session you will discuss the progress made, and the next steps to take. If you rent or purchase small practice equipment and use it at home you will make faster progress.

 

This sounds like meditation.

You’re right! There are many similarities between meditation, yoga, self-hypnosis, and biofeedback. However, biofeedback can help you achieve awareness of physiological processes much more quickly than other techniques. If you already use other techniques, you can master them faster!

Reference: Julie Myers, Psy.D. is a licensed clinical psychologist in San Diego.  She is Board Certified in Biofeedback.

What’s Your Caffeine IQ?

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

 

Caffeine Facts

For most people, moderate caffeine (200 – 300 mg, or about 2-3 cups of coffee a day) aren’t harmful.  But heavy caffeine use (more than 500 mg) can cause insomnia, nervousness, restlessness, irritability, nausea or other gastrointestinal problems, fast or irregular heartbeat, muscle tremors, headaches, and anxiety.

Some people are more sensitive to caffeine than are others.  Even one cup of tea may prompt unwanted anxiety, restlessness, irritability, and sleep problems. Research suggests that men may be more susceptible to caffeine than women.

Caffeine can interfere with sleep.  Sleep loss is cumulative, and even small nightly decreases can add up and disturb your daytime alertness and performance.  Caffeine keeps you from falling asleep at night, increases the number of times you wake during the night, and interfere with deep, restful sleep. Try to avoid caffeinated beverages eight hours before bedtime.

Reducing Your Intake

Too abrupt a decrease in caffeine can cause withdrawal symptoms that include headaches, fatigue, irritability and nervousness. Fortunately, these symptoms resolve after a few days. Try these simple tips:

• Keep track of how much caffeine you use daily
• Cut back gradually to lessen withdrawal effects.
• Substitute decaffeinated beverages.  Try drinking half decaf.
• Lower the caffeine content by brewing tea for less time or drinking weaker coffee
• Read labels to check for caffeine content

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References

¹       Mayo Clinic Staff, MayoClinic.com, Nutrition and healthy eating. “Caffeine: How much is too much?” http://www.mayoclinic.com/health/caffeine/NU00600, March 5, 2010

Therapeutic alliance as a predictor of outcome in treatment of cocaine dependence: A Review

Therapeutic alliance as a predictor of outcome in treatment of cocaine dependence

by Barber, et al.

A Review by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego

There has been an increasing interest in outcome measures in therapy.  Although there is a school of thought that technique is the primary predictor of outcome, some therapists believe that it is the therapeutic alliance that is the major predictor of outcome.  The study by Barber, et al. examines outcome measures in drug treatment.

Substance abusers are often difficult to engage in treatment, yet the therapeutic alliance has rarely been studied.  This study is the first to examine the self-reports of the therapeutic alliance as a means to predict the outcome of cocaine treatment.  Because there is a high drop-out rate for cocaine dependence (50-80 % dropout within 3 months), the research also attempts to distinguish between intent-to-treat and completer samples to see if the alliance early in treatment predicts treatment outcome.

The study used a sample size of 252; many co-occurring disorders were excluded.  Clients were randomly assigned to three different treatment techniques:  Cognitive therapy (based on Aaron Beck), dynamic therapy (support-expressive therapy), and 12-step drug counseling.  A fourth treatment group was added later in the study, which used 12-step group drug counseling only.  In addition to the targeted technique, all treatment groups were mandated to attend group drug counseling 2 times per week for initial two weeks, then once per week for four months.  Therapists in the different treatment groups were not similarly trained; drug counselors had the least training.

Both patient and therapists completed two alliance scales, the Helping Alliance (Haq-II) and the California Psychotherapy Alliance Scales (CALPAS).  In addition, patients were administered measures of functioning.  Statistical analysis of the results looked at a number of different relationships, including the prediction of outcome from alliance given symptom improvement, completer sample, and the number of sessions.

The results did not find a strong relationship between the outcome measures and the therapeutic alliance.  The alliance didn’t predict drug outcome at six months, although at one month there was stronger correlation; the therapeutic alliance was a better predictor of outcome for depression scales.  Results also showed that the therapist’s rating of alliance was less predictive than patients.  Measures were similar across completer and intent-to treat samples.  The only strongly conclusive results were that the shorter the lag time between assessment and outcome measures and the longer clients remain in treatment, the better the outcome associations.   These results do not seem to be particularly surprising to me.  The authors state that a “good therapeutic alliance with the therapist, as viewed by the patient early in treatment, is important in predicting outcome when it is embedded in a long term relationship with that therapist.”

The authors state that there are several possible reasons for the weak predictive results, including the choice of the outcome and alliance variables, the nature of the patient population and/or disorder, and the restriction of range in the measures of alliance.  Although these seem likely influences on the results of the study, I found there to be several other possible explanations.

If a study is not well designed, all of the statistical analysis in the world will be meaningless.  In my own graduate-level econometrics classes, I was taught that when designing a study, the researcher must be careful not to examine too many variables, otherwise it becomes a study that is “hunting for” statistical significance, which biases and invalidates the results.  In my opinion, this study threw too many variables into the mix, both in the design of the study and in the statistical analysis.  A far more rigorous study would have chosen one or two associations to measure, then designed the groups with stricter protocol.

In my opinion, the addition of the fourth group-counseling treatment group invalidated the results, not only because of the late introduction of the treatment, but because of the cross-over between the different treatment samples in this group counseling.  Although the researchers attempted to make the treatment samples significantly different from one another, using different therapy methods and different therapist qualifications, for therapists and counselors who do not use 12-step methods, the mandatory attendance in a 12-step group treatment adjunct to therapy may harm the therapeutic alliance.  Cognitive therapists, in particular, may have little or no belief in the 12-step method.  From my understanding, when therapists do not believe in the methods being used, outcome is compromised.

This study may be better used as a guide to setting up treatment protocols to assess therapeutic alliance than it is useful for the results of the study.  Significant changes that I would suggest are:  less lag-time between assessment of outcome and therapy, more clearly defined and independent treatment protocols, and fewer measurements of outcome.  Although the large sample size was a positive aspect, a smaller sample would not compromise the results.

– Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com

References:

Barber, J., L. Luborsky, P. Crits-Christoph, M. Thase, R. Weiss, A. Frank, L. Onken, R. Gallop (1999),  Therapeutic alliance as a predictor of outcome in treatment of cocaine dependence.  Psychotherapy Research 9(1), pp. 54-73.

Cocaine and its Negative Side Effects

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

 

As with other drugs, cocaine affects the nerve cells of the ventral segmental area, which extends into the nucleus accumbens, one of the reward centers of the brain.  Cocaine acts as a reuptake inhibitor of dopamine, whose increased presence creates the euphoria associated with cocaine.  The euphoric effects of cocaine are generally shorter acting than other drugs, lasting anywhere from a few minutes to a few hours, depending on the route of administration.  Because of its short duration, it is not uncommon for users to administer repeated doses (“binging”.)

In the short-term with small amounts, cocaine acts similarly to amphetamines, making the user feel euphoric, energetic, talkative, and mentally alert. It dilates pupils and increases vital signs such as temperature, heart rate, and blood pressure. With larger doses, the user can experience tremors, vertigo, and twitches.  A user may experience increasing irritability and restlessness.  Bizarre, erratic, and violent behaviors are associated with cocaine.  Chronic use can cause severe psychiatric symptoms, including anxiety, depression and psychosis.  Full-blown psychosis may result with paranoia, hallucinations, and delusions.

Medical complications associated with cocaine use include cardiovascular effects.  “Cocaine causes the blood vessels to thicken and constrict, reducing the flow of oxygen to the heart.  At the same time, cocaine causes the heart muscle to work harder, leading to heart attack or stroke, even in healthy people” (CAMH, 2007.)  It raises blood pressure, which can explode the weakened blood vessels in the brain.  It may also cause abdominal pain, nausea, and blurred vision.

As with other drugs, the route of administration can produce different adverse effects. Snorting cocaine can cause nasal effects, including loss of sense of smell, nosebleeds, problems with swallowing, hoarseness, and an even a perforated nasal septum.  Ingested cocaine can cause severe bowel gangrene, due to reduced blood flow. Smoking cocaine can cause “crack lung”, which includes severe chest pain and breathing problems.

When cocaine is mixed with alcohol, the two drugs are converted by the body to cocaethylene, a cocaine metabolite.  Cocaethylene appears to have more cardiovascular toxicity and hepatoxity than either drug alone.

Even though a user becomes tolerant to cocaine, they may not become sensitized to its anesthetic and convulsant effect, which may explain some cocaine deaths.  Overdose can cause seizures, heart failure, and arrest breathing. Withdrawal can include exhaustion, sleepiness or sleeplessness, hunger, irritability, depression.  Cocaine has a small index of tolerability.

 – Julie Myers, PsyD, MSCP    (www.DrJulieMyers.com)

The bulk of the information for this article was taken from NIDA (2004) and CAMH (2007.)  These resources offer a wealth of up-to-date information about the different drugs of abuse and are one of the first places to look for the most current information about any drug. I urge you to check out these resources for the latest information on addiction.

References:

CAMH (2007), Centre for Addiction and Mental Health, Do You Know… Cocaine

Castane, A., F. Berrendero, & R. Maldonado (2005), The role of the cannabinoid system in nicotine addiction Pharmacol Biochem Behav. 81(2), pp. 381-6.

NIDA (2004), NIDA Research Report – Cocaine Abuse and Addiction: NIH Publication No. 99-4342..

NIDA (2006), Research Report – Tobacco Addiction: NIH Publication No. 06-4342.1346417

Picciolo, M., D. Gigante, & A. Nunziata (2005), Nicotine addiction and current therapy of smoking cessation Clin Ter. 156(4), pp.159-71.

The Relationship of Stress to the Expression and Treatment of Bipolar Disorder – Part V

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

Treatment (cont.)

Psychoeducation is universally accepted as an integral part of the psychosocial treatment protocol and includes learning aspects of healthy habits, behavioral changes, symptom management, and adherence (Colom & Vieta, 2006). Colom and colleagues (2003) designed a 21-session program, which educates patients about all aspects of their illness, such as treatment, symptoms, drug use, life style and stress management.  Other common goals of psychosocial treatment include decreasing denial, challenging assumption, monitoring moods, managing environmental triggers, relapse prevention and enhancing social and occupational functioning (Miklowitz, 2006).

Cognitive behavioral techniques are useful, since bipolar patients have distinct attributional styles and cognitive distortions.   Research linking stress and lowered social support to bipolar episodes suggest treatment target stress reduction, improvement of relationships, and altering perceptions, and treatment that addresses these psychosocial vulnerabilities may help alter the course of Bipolar I disorder (Cohen, Hammen, Henry, & Daley, 2004).   Patients are then taught to plan for potential events and learn new ways of resolving interpersonal difficulties.  This approach has shown great promise for the treatment of BD (Colom & Vieta, 2006).  Combination CBT and medication has shown to delay relapse, improve symptoms, and sometimes increase social functioning (Miklowitz, 2006).

Interpersonal Social Rhythm Therapy revolves around the notion that sleep-wake cycles are primary to symptoms and disruption of the cycles can act as a stressor.  Social rhythms, such as exercise and personal habit routines, social stimulation, and work, affect the sleep cycle (Miklowitz, 2006).  Social routines may actually entrain circadian rhythms; disruption may cause bipolar episodes, suggesting that minimization of stressful and social rhythm disruptions may prevent episodes (Malkoff-Schwartz, Frank, Anderson, Hlastala, Luther, & Houck, 2000). The client is encouraged to track mood, sleep, and events that lead to a disruption of the social-rhythm, such as a lost night of sleep.   Bipolar manic episodes may be more sensitive to social rhythm disruption and life events, as compared to other types of bipolar and unipolar episodes (Malkoff-Schwartz, Frank, Anderson, Hlastala, Luther, & Houck, 2000

Other treatment modalities are available.  Family-focused therapy focuses on family interactions and use of family members as allies in the treatment process (Miklowitz, 2006).  Skill training is used to reduce negative expression of emotion, which result in stress.  Group therapy is also used, which help patients learn to feel accepted and learn self-care strategies from one another.

I am personally interested in the use of biofeedback and neurofeedback to treat BD. Although there is no real “hard” evidence about its effectiveness with BD, largely due to the difficulty in replicating treatment in controlled experiments, anecdotal information from such people as Siegfried Othmer (one of the “fathers” of neurofeedback) convince me that the possibility for treating BD with neurofeedback are just beginning to emerge.   The use of biofeedback techniques for stress management in those with BD are useful, but must be administered with care.   Over-activation of the parasympathetic or sympathetic nervous system may induce a bipolar event.

Of direct implication from the kindling hypothesis is the timing of intervention.  Intervention may be much more effective at the initial stages of expression than at later stages (Monroe & Harkness, 2005, p. 442).  By tackling the stressful life situations of those at risk early on, the course of the disorder may be changed.  How much of the developmental process is a reaction to life course and how much is an independent psychobiological process is as yet unknown, but begs for further investigation.  “The key implication of this study is that childhood adversity may be related to a more challenging presentation of bipolar disorder, with an earlier age at onset and greater vulnerability to experiencing recurrences of mood episodes in the face of even mild stress. Earlier onset and a more difficult course of bipolar disorder may have serious consequences for both the efficacy of treatment of bipolar disorder and for the functioning of bipolar individuals.  If childhood adversity is a trigger of earlier onset and sensitizes individuals to stress, preventing stress exposure in high risk families, or promoting coping capabilities in such youngsters might have positive consequences on the course of illness”  (Dienes, Hammen, Henry, Cohen, & Daley, 2006, p. 49).  Prevention of stress and early intervention may be critical in reducing the severity of the disorder in later life.

– Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com

References

Akiskal, H. (2006). The Scope of Bipolar Disorders. In H. Akiskal, & M. Tohen, Bipolar Psychopharmacotherapy (pp. 1-8). West Sussex, England: John Wiley & Sons Ltd.

Akiskal, H., Mendlowicz, M., Jean-Louis, G., Rapaport, M., Kelsoe, J., Gillin, J., et al. (2000). TEMPS-A: validation of a short version of a self-related instrument designed to measure variations in temperament. J. of Affective Disorders , 85 (1-2), 45-52.

Angst, J., & Gamma, A. (2002). Prevalence of bipolar disoders: traditional and novel approaches. Clinical Approaches in Bipolar Disorder , 1, 10-14.

APA. (1994). Diagnostic and Statistical Manual of mental Disorders, 4th Edition. Washington DC: American Psychiatric Association.

Berk, M., Malhi, G., Cahill, C., Carman, C., Hadzi-Pavlovic, D., Hawkins, M., et al. (2007). The Bipolar Depression Rating Scale (BDRS): its defvlopment, validation and utility. Bipolar Disorders , 9 (6), 571-579.

Brown, G., McBride, L., Bauer, j., & Willifor, W. (2005). Impact of childhood abuse on the course of bipolar disorder:A replication study in U.S. veterans B. J. of Affecgtive Disorders , 89, 57-67.

Brudick, K., Funke, B., Goldberg, J., Bates, J., Jaeger, J., Kucherlapati, R., et al. (2007). COMT genotype increases risk of bipolar I disorder and influences neurocontive performance. Bipolar Disorders , 9 (4), 370-376.

Cohen, A., Hammen, C., Henry, R., & Daley, S. (2004). Effects of stress and social suport on recurrence in bipolar disorder. J. of Affegtive Disorders , 82, 143-47.

Colom, F., & Vieta, E. (2006). The pivotal role of psychoeducation in the long-term treatment of bipolar disorder. In H. Akiskal, & M. Tohen, Bipolar Psycopharmacotherapy: Caring for the Patiens (pp. 331-345). West Sussex: John Wiley & Sons, Ltd.

Colom, F., Vieta, E., Sanchez-Moreno, J., Reinares, M., Martinez-Aran, A., Torrent, C., et al. (2003). Psychoeducatio efficacy in bipolar disorders beyond compliance enhancement. J Clin Psychiatry , 6, 294-298.

Correll, C., Penzner, J., Lencz, T., Auther, A., Smith, C., Malhotra, C., et al. (2007). Early identificaiton and high-risk strategies for bipolar disorder. Bipolar Disorders , 9 (4), 324-338.

DelBello, M., & Geller, B. (2001). Review of studies of child and adolescent offspring of bipolar parents. Bipolar Disorders , 3, 325-334.

Dienes, K., Hammen, C., Henry, R., Cohen, A., & Daley, S. (2006). The stress sensitization hypothesis: Understanding the course of bipolar disorder. Journal of affective Disorders , 95, 43-49.

Faraone, S., Lasky-Su, J., Glatt, S., Van Eerdewegh, P., & Tsuang, M. (2006). Early ongset bipolar disorer: Possible linkage to chromosome 9q34. Bipolar Disorder , 8, 144-151.

Gottesman, I., & Gould, T. (2003). The endophenotype concept in psychiatiry: Etymology and strategic intentions. Am J Psychiatry , 160, 636-645.

Hammen, C., & Gitlin, M. (1997). Stress reactivity in bipolar patients and its relation to prior hisotry of disorder. Am J Psychiatry , 154, 856-857.

Hammen, C., & Gitlin, M. (1997). Stress reactivity in bipolar patients and its relation to prior history of disorder. Am J Psychiatry , 154 (6), 856-7.

Hillergers, M., Burger, H., Wals, M., Reichart, C. V., Nolen, W., & Ormel, J. (2004). Impact of stressful life events, familial loading and their interaction on the onset of mood disorders: Study in a high-risk cohort of adolescent offspring of parents with bipolar disorder. British J. of Psychiatry , 185, 97-101.

Hirschfeld, R., & Vornik, L. (2004). recognition and diagnosis of bipolar disorder. J of Clinical Psychiatry , 65 (Supp 15), 5-8.

Hlastala, S., Frank, E., Kowlaski, J., Sherril, J., Tu, X., Anderson, B., et al. (2000). Sressful life events, bipolar disorder, and teh “kinlding model”. J Abnormal Psychol , 109 (4), 777-86.

Kessler, R., Rubinow, D., Holmes, C., Abelson, J., & Ahao, S. (1997). The epidemiology of DSM-III-R bipolar I disorder in a gerneal population survey. Psychol Med (27), 1079-1089.

kilbourne, A., Rofey, D., McCarthy, F., Post, E., Welsh, D., & Blow, F. (2007). nutrition and exercise behavior amongh patients with bipolar disorer. Bipolar Disorders , 9 (5), 443-452.

Kim, E., Miklowitz, d., Biuckians, A., & Mullen, K. (2007). Life stress and the course of early-onset bipolar disorder. J of affective Disorders , 99, 37-44.

Koukopoulos, A. (2006). The Primacy of Mania. In H. Akiskal, & M. Tohen, Bipolar p2006sychopharmacotherapy: Caring for the patient (pp. 169-192). West Sussex, England: John Wiley & Sons, Ltd.

Kupka, R., Altshuler, L., Nolaen, W., Suppes, T., Luckenbaugh, D., Leverich, G., et al. (2007). Three times more days depressed than manic or hypomanic in both bipolar I and bipolar II disorder. Bipolar Disorders , 9 (5), 531-535.

Leahy, R. (. (2006). Contemporary Cognitive Therapy. New York: Guilford Press.

Malkoff-Schwartz, S., Frank, E., Anderson, B., Hlastala, S., Luther, J. S., & Houck, P. K. (2000). Social rhythm disruption and stressful life events in the onset of bipolar and unipolar episodess. Psychol Med , 30 (5), 1005-6.

Manji, H., & Lenox, R. (2000). The nature of bipolar disorder. J Clin Psychiatry , 61 (Supp 13), 42-57.

McPherson, H., Herbison, P., & Romans, S. (1994). Life eventws and relapse in established bipolar affective disorder. Br. J Psychiatry , 164 (3), 417.

Miklowitz, D. (2006). Psychosocial interventions in bipolar disorders: Rationale and effectivness. In H. Akiskal, & M. Tohen, Bipolar psychopharmacogtherapy: Caring for the Patient (pp. 313-332). West Sussex: John Wiley & Sons.

Monroe, S., & Harkness, K. (2005). Life stress, te “kindling” hypothesis, and the recurrence of depression: Considerations from a life stress perspesctive. Psychological Review , 112 (2), 417-445.

Newman, C., Leahy, R., Beck, A., Reilly-Harrington, N., & Gyulai, L. (2002). Bipolar disorder: A cognitive therapy approach. Washington, DC: American Psychological Association.

Oquendo, M., Galfalvy, H., Russo, S., Ellis, S., Grunebaum, M., Burke, A., et al. (2004). Prospective study of clinical predictors of suicidal acts after a major depressive episode in patients with major depressive disorder or bipolar disorder. Am J Psychiatry , 161 (8), 1433-1441.

Parkikh, S., Velyvis, V., Yatham, L., Beaulieu, S., Cervantes, P., MacQueen, G., et al. (2007). Coping styles in proderomes of bipolar mania. Bipolar Disorders , 9 (6), 589-595.

Perugi, G., Ghaemi, N., & Akiskal, H. (2006). Diagnosis and clinical management approaches to bipolar depression, bipolar II and their comorbidities. In S. Hagop, & A. Tohen, Bipolar Psychopharmacotherapy: Caring for the Patient. John Wile & Sons, Ltd.

Post, R. (1992). Transduction of psychosocial stress into the neurobiology of recurrent affective disorder. Am J. Psychiatry , 149, 999-1010.

Post, R. (1992). Transduction of psychosocial stress into the neurobiology of recurrent affective disorder. Am j. Psychiatry .

Preston, J., & Johnson, J. (2004). Clinical psychopharmacology made rediculously simple. United States: MedMaster, Inc.

Preston, J., O’Neal, J., & Talaga, M. (2002). Handbook of clinical psychopharmacology for therapists. Canada: New Harbinger Publications, Inc.

Simon, N., Otto, M., & Wisneiewski, S. (2004). Anxiety disorder comorbidity in bipolar disorder patients: data from the first 500 participants in the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). Am J Psychiatry , 161, 2222-2229.

Simon, N., Otto, M., Wisniewski, S., Fossey, M., Sagduyu, K., Frank, E., et al. (2004). Anxiety disorder comorbidity in bipolar disorder patients: Data from the first 500 participants in the systematic treatment enhancement program for bipolar disorder (STEP-BD). Am J psychiatry , 161, 2222-2229.

Smith, Cornelius, V., Warnock, A., Tacchi, M., & Taylor, D. (2007). Pharmacological interventions for acute bipolar mania: a systematic review of randomized placebo-controlled trials. Bipolar Disorders , 9 (6), 551-560.

Smith, L., Cornelius, V., Warnock, A., Bell, A., & Young, A. (2007). Effectivenessof mood stabilizers and antipsychotics in the mainenanc e phase of bipolar diosrer: a systematic review of randomized controlled trials. Bipolar Disorders , 394-412.

Stahl, S. (2006). Bioplar vs. difficult to treat depression. Advances in Psychopharmacology Throughout the Life Span (pp. 83-107). San Diego: U. of CA, San Diego School of Medicine.

Stahl, S. (2006). Bipolar vs difficult to treat depression. Advances in Psychopharmacology Throughout the Life Span (pp. 83-107). San Diego, California: University of California, San Diego School of Medicine.

Stahl, S. (2005). Diagnosis and treatment of bipolar spectrum disorders. NEI Psychopharmacology Academy 2-Day Series (pp. 37-54). United States: Neurscience Education Institute.

Stahl, S. (2000). Essential psychopharmacology of depression and bipolar disorder. Cambridge, United Kingdom: Cambridge University Press.

Stahl, S. (2003). Essential Psychopharmacology: Neurosceintific Basis and Practical Applications. United States: Cambridge University Press.

Stahl, S. (2005). Essential Psychopharmacology: The Prescriber’s Guide. Canada: Cambridge University Press.

Stahl, S. (2005). Mechanisms of action of mood stabilizers and atypical antipsychotics. In S. Stahl, NEI Psychoparmacology Academy Workbook: Tratment Issues for Depressiona dn Bipolar Disorder (pp. 29-36). United States: Neuroscience Education Institute.

Stahl, S. (2005). The every-evolving bipolar spectrum: From bipolar mania to mixed mania and beyond. Distinguishing the Diagnosis and Tretments for Bipolar Mania, Mixed Mania, and Difficult-to-Treat Depression within the Bipolar Spectrum (pp. 7-26). San Diego: Neuroscience Education Institute.

Swendsen, J., Hammen, C., Heller, T., & Gitlin, M. (1995). Correleates of stress reactivity in patients with bipolar disorder. Am j Psychiatry , 152 (5), 795-7.

Vizzarri, J., Sbrana, A., Rucci, P., Ravani, L., Massei, G., Gonnelli, C., et al. (2007). The spectrum of subtance abuse in bipolar disorder: reasons for use, sensation seekinjg and substance sensitivity. Bipolar Disorders , 9 (3), 213-220.

Wong, G., & Lam, D. (1999). The development and validation of the coping inventory for prodromes of mania. J Affect Disorders , 53, 57-65.

Yurgelun-Todd, D., Silveri, M., Gruber, S., Rohan, M., & Pimentel, P. (2007). White matter abnormalities observed in bipolar disorder: a diffusion tensor imaging study. Bipolar Disorders , 9 (5), 504-512.

Copyright (2011) Julie Myers, PsD

The Relationship of Stress to the Expression and Treatment of Bipolar Disorder – Part IV

 

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

 

Treatment

The treatment of BD is complex.   Psychosocial treatments are necessary but rarely sufficient for controlling relapse or acute symptoms.  From my observations, the treatment of BD is as much of an art as it is a science, with different researchers and clinicians having different ideas as to what is the appropriate formulation.   Critically important is the assessment of suicide throughout the treatment.  Suicidal ideation and suicide completion is a very real possibility in those with BD, both in depressed and hypomanic or manic states.   Suicidal acts in those with BD may be a tendency to develop pessimistic response to major life stressors (Oquendo, et al., 2004).

 Comorbid anxiety disorders should be treated concurrently.  Treatment of anxiety disorders may lessen the severity of the BD symptoms and possibly increase pharmacological response (Simon, Otto, & Wisneiewski, 2004).  According to Simon and colleagues (2004), there is a growing awareness of the need to address comorbid anxiety disorders, which should be integrated into the treatment of high-risk bipolar patients and suicide prevention.  However, few specific anxiety-targeted interventions for BD have been developed.  As of 2004, there was no data showing anxiety treatment efficacy for clinical course of BD.   There is also little known about how anxiety increases suicidality, although it may be that BD patients with severe anxiety are less able to tolerate negative affect and less capable of calling upon social supports or cognitive strategies.

 Psychopharmacological treatment focuses on controlling current acute symptoms and maintenance to prevent relapse.  Mood-stabilizers are administered for reducing episodes, anti-psychotics generally for reducing symptoms of mania, hypomania, aggression, and irritability, and anti-depressants for depressive phases (although generally only after mood-stabilizers are use.)  Psychopharmacological treatment also usually involves treatment of the co-occurring disorders.  However, because there is such a strong co-occurrence of substance abuse problems in those with BD, many of the anxiolytics are used with caution.  Benzodiazepines, although very effective for many of the anxiety disorders, can generate rapid physical dependence and are subject to abuse.  Particularly important, according to some researchers, is the discontinuation of any stimulants, even coffee.

 A wide array of psychosocial interventions are available including psychoeducational, cognitive-behavioral, family therapy, social rhythm therapy and interpersonal psychotherapies.  All of these techniques help to teach self-monitoring, identification of early warning signs of relapse, and enhance coping mechanisms (Parkikh, et al., 2007).  Early warning signs are associated with life-stressors.  A number of studies have identified the coping mechanisms involved with prodromal states as being particularly important in controlling symptoms, including Parkikh, et al. (2007) and Koukopoulus (2006).  A self-report questionnaire called the Coping Inventory for Prodroms of Mania (CIPM) has been developed to assess coping styles in the manic and hypomanic state (Wong & Lam, 1999).

(continued)

– Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com