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Is Rehab Really Necessary?

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And How to Find the Right Rehab, if it is Necessary

By Julie Myers, PsyD, MSCP

Licensed Psychologist, Master Addiction Counselor, MS Clinical Psychopharmacology

 http://www.DrJulieMyers.com

It is my opinion that most people with substance abuse or dependency issues can recover with outpatient treatment from a licensed mental health professional or with the support of self-help groups.  However, in some cases, a Residential Treatment Center (RTC) may be necessary.

A licensed mental health professional, such as a psychologist certified in addiction treatment, can formulate an individualized treatment program equal to or better than many programs offered by “rehabs”.   A psychologist can provide individualized care to help identify behaviors and emotions that drive substance-using behaviors and can treat any underlying mental health conditions that likely exist.  Competent professionals can formulate an integrated, comprehensive program, which can include psychotherapy and referrals to psychiatric care, self-help meetings, group therapy, sober living homes, and other alternative treatments modalities.  The notion that everyone with substance abuse problems needs residential treatment is as unreasonable as stating that everyone with depression needs hospitalization.

Although outpatient treatment is preferable and sufficient for most people, there are those who may need a higher-level of care than outpatient treatment can provide.  In particular, some people may need a more restrictive environment, where there is no access to drugs or alcohol.  Sometimes, when a person is actively using and can’t stop, a Residential Treatment Center can provide the respite that a person needs from their access to drugs or alcohol.  They may also be indicated for those with severe forms of co-occurring psychiatric disorders that have not been adequately stabilized.

However, RTCs can vary greatly in their quality and level of care.  Some offer comprehensive, “gold standard” care, with evidence-based practice from qualified treatment professionals.   Others may offer little more than restrictive use of substances.  So the question becomes, how does one choose a Residential Treatment Center?   It may be difficult to determine which is the best RTC for themselves or their loved-ones, because they may not know the right questions to ask, and because many RTCs may be vague about what their programs include.

It would be helpful to have a set of key questions that someone seeking treatment could ask of the RTC about their program.  Recently, Dr. Donald Meichenbaum shared a letter with me, which he drafted for those seeking residential care.  This letter can be sent to the Director of an RTC that a person is considering.   This letter asks questions about the RTC’s program, questions that can help the consumer make an informed decision about that facility.   I have reposted his letter on my website, which you can find at http://www.DrJulieMyers.com.   I believe that this letter can help guide the consumer to find a residential treatment center that is right for them, should they need that level of care.

To find a list of Residential Treatment Centers, you can go to the SAMHSA government website located at:  http://findtreatment.samhsa.gov/

Copyright (2013) Julie Myers, PysD:  Psychologist in San Diego.  All Rights Reserved.

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

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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

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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.

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Copyright (2011) Julie Myers, PsD

Written by Julie Myers, PsyD, MSCP

July 13, 2011 at 5:44 pm

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

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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

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

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

 by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego, California

Etiology

 The strong relationship between stress and BD generates speculation about the etiology of the disorder.  The exact nature of the relationship between the two is unclear (Simon, et al., 2004).  Anxiety in early life may represent a prodromal symptom, or they may both share the same biological or genetic origin.   Heritability rates of BD are between 40 (a narrow definition) and 97% (a broad-spectrum definition) (Correll, et al., 2007).

 Preston and colleagues (2002) summarize the etiological theories that have been proposed for BD.  Several of these relate directly to the role that stress may play in the treatment of the disorder.  The Deregulation Theory revolves around the homeostatic regulation of mood.  Over activity outside of the bounds of homeostasis leads to associated behavioral manifestations.  The Chaotic Attractor Theory hypothesizes that there is a biochemical deficit that leads to deregulation of the synthesis of neurotransmitters.  The mood state depends on the physiological or environmental conditions present.  It predicts a chaotic course of the illness.  The HPA Axis Theory associates the overactivation of the HPA axis in mixed state and depressive states.   The Kindling Theory hypothesizes that the buildup of subclinical biochemical changes in the limbic system.  Eventually there is a build-up of neuronal excitability until symptoms appear.  This theory explains the progressive nature of the disorder, resulting in more frequent and severe symptoms.  It is the Kindling Theory that is the most relevant to the interaction of stress disorders and BD.

 The Kindling hypothesis asserts that the first episode of a mood disorder “… is more likely to be associated with major psychosocial stressors than are episodes occurring later in the course of the illness” (Post, 1992, pp. 999-1000).  Post further hypothesized that sensitization to stressors and episodes became encoded at the level of gene expression.

There is confusion in the literature about the Kindling Hypothesis, which may be generated primarily from the ambiguities surrounding poorly described ideas and terminology in early studies.  Specifically “do recurrent episodes become autonomous of stress, such that stress is no longer an etiological mechanism in the precipitation of recurrence? Or, do individuals become sensitized to stress, such that ever more minor forms of adversity are capable of precipitating recurrence? Most generally, if minor events increase in their frequency and impact in precipitating onsets of depression across recurrence, then this would support  sensitization. By contrast, if all forms of stress (major and minor) decrease in their frequency and impact in precipitating recurrences, then this would support autonomy and suggest that some other mechanism “ (Monroe & Harkness, 2005, p. 442). The disruptions of the social rhythms that cause bipolar episodes gives credence to the psychobiological hypothesis of the etiology of BD (Malkoff-Schwartz, Frank, Anderson, Hlastala, Luther, & Houck, 2000).

With either interpretation, studies have shown that stress in early life predicts earlier onset of the disorder.  They also agree on stress as being a precipitator to episodes in early life.  Childhood abuse, for example, was reported in nearly half of one study of veterans with BD (Brown, McBride, Bauer, & Willifor, 2005).  Abuse may cause a change in brain physiology, making  BD more difficult to treat, with more rapid cycling, anxiety, and panic disorder (Post, 1992) and  (Brown, McBride, Bauer, & Willifor, 2005).  But the confusion in interpretation lies in what occurs after the initial onset.

In the first interpretation, the person with BD experience life stressors, which may be severe.  These stressors precipitate a manic or depressive episode.  Although the person has reacted to the stressor, it has desensitized him/her to further episodes of stress.  In other words, it is not that the person no longer has bipolar episodes, but that these episodes are endogenous  in nature and come independent (or at least less dependent) of the stressors.  McPherson, Hervison, and Romans (1994) found life events precipitate bipolar episodes only for earlier episodes. In another study, stress levels predict relapse, although the number of previous levels did not affect the stress response, which showed that BD episodes were not increasingly independent of stressors.  However, it did show that personality traits, such as introversion and obsessionality, did affect the patient’s reactivity to stress (Swendsen, Hammen, Heller, & Gitlin, 1995).  There are a certain number of episodes that cannot be explained be stress events (Malkoff-Schwartz, Frank, Anderson, Hlastala, Luther, & Houck, 2000)

In the second interpretation of the Kindling Theory, earlier stressors actually sensitize the person with BD to stress events.  That is, once someone has had experienced stress preceding a bipolar episode, they become more sensitive to any future stress.  In this case, even minor stressors may precipitate an episode.  Hammen and Gitlin (1997), for example, found that stressors may precipitate BD episodes and more quickly, especially in those with more prior episodes.  This, they say, is “inconsistent” with the Kindling Hypothesis.  They confirmed the importance of stressful life events as a contributor to BD and showed that patients with prior history of episodes were more likely to have had a several stressors in the previous months.

Although the debate about the interpretation of the hypothesis has not been resolved, I believe that both interpretations may be valid. I have seen bipolar episodes that appear to be independent of life events or stressors and those triggered by very minor stressors.  A bipolar client may switch into hypomania quite rapidly, without noticeable triggers, as if it is just “time to switch.”  What most people, even the patient, would not discern as a stress may be enough to trigger an event.  The bipolar event may thus look as if it was spontaneous.  This would give credence to the idea that prior stress might serve as a sensitizers, such that even minor stresses create a bipolar event.  Reactivity may actually be a complex interaction between age, stress, onset, and new episodes (Hlastala, et al., 2000).

(to be continued)

– Julie Myers, PsyD

http://www.DrJulieMyers.com

 

Written by Julie Myers, PsyD, MSCP

June 27, 2011 at 5:09 pm

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

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The Relationship of Stress to the Expression and Treatment of Bipolar Disorder  (Part II)

by Julie Myers, PsyD, MSCP

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

 

The Comorbidity of Bipolar Disorder and Stress disorders

 Comorbidity is common in BD, further complicating the diagnosis.  In one study, a comorbid disorder was found in all of the samples, and in 59% the condition preceded the onset of BD symptoms (Kessler, Rubinow, Holmes, Abelson, & Ahao, 1997).  Common among the comorbid disorders are anxiety, substance abuse, ADHD, Oppositional-Defiant Disorder, Bulimia, Social Phobia, Panic Disorder, and Obsessive Compulsive Disorder  (Correll, et al., 2007) and (Perugi, Ghaemi, & Akiskal, 2006), many of which are stress related.  Personality disorders also occur at a higher rate than the general public, which may actually be an expression of phenotypic expression of a bipolar diathesis (Correll, et al., 2007).  BD has the highest prevalence of any psychiatric disorder for alcohol and other substance use disorders, with a lifetime comorbidity estimated from 17 – 61% (Vizzarri, et al., 2007).  In one large study of 500 bipolar patients, a lifetime substance use disorders was found in the entire sample (Simon, et al., 2004).     In many cases, it is unclear whether these co-occurring disorders are truly biologically distinct, or simply risk markers, prodromal states, overlapping  characteristics, or subtypes (Correll, et al., 2007).

 Comorbidity of BD with anxiety disorders is particularly high.  In one large study of 500 BD patients, the lifetime comorbidity with anxiety disorder occurred in over half the sample (Simon, et al., 2004); approximately 11-63% had panic disorder, 8-47% social anxiety disorder, 3-35% obsessive compulsive disorder, 7-39% posttraumatic stress disorder and 7-32% generalized anxiety disorder.   Overall anxiety comorbidity was higher in Bipolar I disorder than Bipolar II disorder. The presence of anxiety predicted a lower age of onset (about 16 as opposed 20 years old) and a shorter time in the euthymic state.  Presence of anxiety disorder also was associated with impaired function, poorer quality of life, decreased likelihood of recovery, greater prevalence of substance abuse, and greater likelihood of suicide attempt.    In my experience, those in hypomanic states have a high reactivity to stress, often engaging in activities to relieve stress, such as compulsive shopping, sexual activity, or risk-taking.  Substances are often used to “self-medicate.”

When chronic stress in family, romantic, and peer relationships is present, there is less improvement in mood symptoms in adolescents.  “The association between chronic stress in peer relationships and mania symptoms is likely a recursive one in which the most impaired youths generate the highest levels of peer-related stress, which further exacerbates their mood symptomatology”  (Kim, Miklowitz, Biuckians, & Mullen, 2007, p. 37).  Possibly, this may create a pattern of dysfunctional reactivity to stress.

In one case example, Bob is an 18 year old male, who expressed BD at the age of 5 after a family stress.  Although he did not receive a diagnosis of BD until the age of 12, his symptoms where characteristic of juvenile BD.   He had symptoms of obsessive compulsive disorder, social anxiety disorder, separation anxiety, and generalized anxiety disorder.  His mind was often occupied with ruminative “bad” thoughts.  He developed many compensatory behaviors to relieve his stress including a shut-down depressive state, psychomotor agitation and tics.  Bob manifested psychotic symptoms and suicidal ideation during times of heightened stress.  School, for example, was a continual source of stress from teachers and peers, resulting in poor performance and exacerbation of bipolar switching.  This further resulted in a deterioration of peer relationships, recursively leading to a greater number of bipolar episodes.

Copyright (2011):  Julie Myers, PsyD:   All rights reserved.

Written by Julie Myers, PsyD, MSCP

June 25, 2011 at 6:48 pm

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

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

 

by Julie Myers, PsyD, MSCP

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

It is generally agreed in the literature that stress affects the course and severity of Bipolar Disorder (BD.)  Stress, particularly in early life, appears to have lasting effect and marks for early onset, although the exact mechanism of this effect is poorly understood.  The relationship of stress to the onset of the disorder and its course has implications for the treatment and management of the disorder, and perhaps even its onset.  In this paper, I discuss the characteristics of BD and its co-occurrence with anxiety disorders, and the etiology and the treatment of BD in relationship to stress management techniques.  Case examples are presented.

 

The Nature of Bipolar Disorder

 Bipolar Disorder is a mood disorder, characterized by shifting states between mania or hypomania and depression.   The length of time that a person spends in either the up or the down phases are not fixed in length nor in severity, although those with Bipolar I Disorder have periods of mania, while those with Bipolar II Disorder only reach hypomania.  Periods may last from years to hours in rapid or ultra-rapid cycling BD.  In most cases, it is a progressive disorder, with the length of time spent in the depressive stage increasing with time.  Those with BD have other characteristics, such as delayed-sleep cycle and neurocognitive deficits (Correll, et al., 2007).

The DSM-IV (APA, 1994) characterizes those with mania as having pronounced and persistent moods of euphoria, grandiosity or elevated self-esteem, decreased need for sleep, rapid pressure speech, racing thoughts, distractibility, increased activity or psychomotor agitation, behavior that reflects expansiveness, and poor judgment.  Hypomania is the occurrence of a persistent elevated, irritable or expansive mood for at least four days, with the presence of three additional symptoms including “inflated self-esteem or grandiosity, decreased need for sleep, pressure of speech, flight of ideas, distractibility, increased involvement in goal-directed activities or psychomotor agitation, and excessive involvement in pleasurable activities that have a high potential for painful consequences (p. 335.)

The depressive state of BD is much like that of Major Depressive Disorder, although there is usually an increased need for sleep and psychomotor retardation rather than agitation.  Other signs include depressed mood, anhedonia, fatigue, feelings of worthless, guilt, thoughts of suicide, and executive functioning difficulties such as trouble concentrating.  Periods of mixed states or dysphoric mania also occur with BD. Symptoms of dysphoric mania include, marked irritability, severe agitation or anxiety, pessimism and unrelenting worry and despair, marked insomnia, and decreased need for sleep (APA, 1994).   In my experience, it is these mixed states that are the most troublesome, and they appear to be marked by severe stress reactivity.

Diagnosis is particularly difficult, because those with BD often do not recognize their hypomanic episodes as being abnormal and so do not report its presence; insight is state-dependent.  They may also loathe to give-up these hypomanic states. Patients usually present for help during the depressive stage (Perugi, Ghaemi, & Akiskal, 2006), and when in a depressive state, patients with BD have difficulty remembering their hypomanic states, feeling that they have always felt low. “Diagnosis may only be possible retrospectively utilizing histories from patients who have distorted recollections” (Stahl, 2005, p. 14.)     Because of these distorted recollections, it is important to have collaborating information from family members or close friends. The hypomania, which the client so often enjoys, is often more problematic to those close to the patient than to the patient themselves and may lead to dysfunctional family interactions and stress.  In my opinion, it is the client’s unwillingness to disclose these hypomanic states and the stressful events that trigger them that often leads to misdiagnosis.

(to be continued…….)

Copyright (2011) Julie Myers, PsyD:  All Rights Reserved

Making Changes in Recovery, Step-by-step

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Making Changes in Recovery, Step-by-Step

by Julie Myers, PsyD, MSCP

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

 

Have you ever wanted to make changes in your life, but felt so overwhelmed by the situation that you didn’t know where to start?  Sometimes it helps to break the change down, working through the situation step by step using pencil and paper.  (A useful worksheet can be found at http://www.smartrecovery.org/resources/library/Tools_and_Homework/Facilitators_Handout/Change_Plan_Worksheet.pdf).  First, think about why you want to make the change and then work through the steps you will need to get there. As you do this, you may find that the change you want to make really requires more than one significant change.

For example, let’s say you want to start exercising in the morning. As you work through the steps, you find that to do this, you will have to leave earlier in the morning, which means that you need to be more organized in the morning, which requires that you go to bed earlier, which means that you need to leave work earlier, which requires that you have lunch by noon.  Too many major changes means overwhelm!

Instead of becoming frustrated, break each of these steps into a different change plan, starting with the easiest change (such as having lunch earlier!)  By doing this, you will feel less overwhelmed, be more successful, and will feel better about your ability to make changes. With thoughtful forethought, you will be amazed at the changes you can make!

– Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com


The Diagnosis of Bipolar II Disorder

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The Diagnosis of Bipolar II Disorder

By Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego

Bipolar II Disorder  is a mood disorder, characterized by shifting states between hypomania and depression. Diagnosing Bipolar II Disorder is particularly difficult, because those with this disorder often do not recognize their hypomanic episodes as being abnormal and so do not report their presence. They may also loathe to give-up these hypomanic states. Patients usually present for help during the depressive stage (Perugi, Ghaemi, & Akiskal, 2006), and when in a depressive state, patients may have difficulty remembering their hypomanic states, feeling that they have always felt low; insight is state-dependent. “Diagnosis may only be possible retrospectively utilizing histories from patients who have distorted recollections” (Stahl, 2005, p. 14.)  Because of these distorted recollections, it is important to have collaborating information from family members or close friends.  The hypomania, which the client so often enjoys, is often more problematic to those close to the patient than to the patient themselves and may lead to dysfunctional family interactions and stress.

It may be the patient’s unwillingness to disclose these hypomanic states and the stressful events that trigger them that often leads to misdiagnosis. As a case example, Mr. Smith symptoms of depression had become so severe that he was no longer able to function. From the age of 30, he was treated intermittently for depression, acquiring a long medication history from many different psychiatrists, even one of the leading authority in psychopharmacology in the world, but he continued to cycle in and out of depression. It was not until he was persuaded, at the age of 57, to bring a close friend in with him to treatment that he was finally given a diagnosis of Bipolar Disorder II and received adequate treatment. It was Mr. Smiths’ unwillingness to share his hypomanic states, which were generally triggered by stressful events, which kept him from receiving a diagnosis of Bipolar II Disorder.

When assessing anyone with repeated periods of depression, it is extremely important to carefully consider the possibility of Bipolar II Disorder.  By creating an open and safe environment for the client to recount his/her history, periods of mood instability and hypomania are more likely to be revealed to the therapist. Mood-charts, which detail lifetime events and mood events, are particularly beneficial for use with those who either do not recognize their own hypomanic states or who may be unwilling to address them. Once properly diagnosed, someone with Bipolar II Disorder can be helped to manage their hypomanic and depressive states with various therapeutic methods.

Julie Myers, PsyD, MSCP

Licensed Psychologist, MS Clinical Psychopharmacology, Master Addiction Counselor, Board Certified Biofeedbachttp://www.DrJulieMyers.com.  

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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 Wiley & Sons, Ltd.

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

Brain, Behavior, and Drugs

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Brain, Behavior, and Drugs

By Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com

I.  The complex and adaptive brain

  1. Brain architecture:  gross anatomy, neurons
  2. How the brain communicates
  3. Adaptation and learning

II.  How drugs hijack the brain

  1. Pleasure and the reward center:  the dopamine connection
  2. What (or who) controls the reward center?:    bottom-up vs. Top-down
  3. Brain adaptation:   the change from use to abuse
  4. Binge, withdrawal, cravings, relapse, and the role of stress hormones
  5. Medication that can change the brain’s response

III:  Is addiction biology or just a bad habit?  The possibilities of change

I.  The Complex and Adaptive Brain

The brain is an extraordinarily complex organ.   Once thought to be essentially static after adulthood, we now know that the brain continues to adapt and change and even to grow new neurons.   This is important, as the formation and maintenance of addictive disorders depends not only on the environment, but on the molecular, genetic, and cellular adaptations of the brain.  Addiction to drugs follows a pattern of spiraling brain dysfunction, similar to that seen with gambling, compulsive exercise, binge eating, etc.  Let’s now look more closely at the structure of the brain itself in order to understand the way it processes information and how we become addicted.

A.  Brain architecture

Gross AnatomyThe brain lies nestled inside the protective skull, surrounded by the blood brain barrier, a filter that selects which chemicals/drugs to allow into the brain.  The largest part of the human brain is the cerebrum, and it is composed of four lobes (areas), each with their own specialization.   The outermost part of the cerebrum is the cerebral cortex, the part of the brain responsible for higher-order thinking.  The prefrontal cortex is in the front part of the cerebral cortex; it controls judgment, decision making, and emotional regulation.  Other structures of the brain important in addiction are the limbic system (made up of the hippocampus, and amygdala), ventral tegmental area (VTA), nucleus accumbens, and dorsal striatum.

NeuronsWithin the brain structures are clusters of neurons (nerve cells) called nuclei that govern specific brain processes.  They form routes that allow one part of the brain to communicate with another;  integrating, processing, interpreting, storing, and distributing information.  A neurons is made up of the cell body, axon, axon terminal, dendrites, and dendritic spines.  The neurons are separated by one another by a space called a synapse.

PICTURE

 

Within the axon terminal are small containers (vesicles) that store the brain chemical messengers called neurotransmitters.  Located on the dendrites are special proteins called receptors, which absorb the neurotransmitters into the cell.  Each receptor specializes in a particular chemical neurotransmitter.  The two most common neurotransmitters in the brain are glutamate and gamma-aminobutyric acid (GABA).  Drugs of abuse act on glutamate and GABA, but also on other neurotransmitters such as serotonin, norepinephrine, acetylcholine, and most importantly dopamine.

B. How the brain communicates

The brain does not act by a single process, but rather by millions of communication pathways made up of neurons and nuclei.  Neurons communication with one another via neurotransmission, which is carried out by the neurotransmitters   To better understand this communication, let’s first examine serotonin, a neurotransmitter important in the drug ecstasy.

Serotonin is synthesized within the neuron body and is stored in vesicles at the axon terminal.  When the neuron receives a signal to release serotonin, the vesicle moves to the interior membrane of the neuron (presynaptic membrane).  The vesicle fuses with the presynaptic membrane, releasing its contents into the synapse.  Once in the synapse, the serotonin travels to the dendritic spine of the receiving neuron, attaching to serotonin receptors.  It is then taken up into the cell by reuptake pumps, reducing the concentration of serotonin in the synapse.

In the receiving neuron, the serotonin may act to activate or inhibit enzymes, release ions, turn-on genes, or increase cyclic adenosine monophosphate (cAMP), which generates the neuronal electrical impulses that propagate communication through the nerve.  When an electrical impulse is generated, it travels down the axon toward the axon terminal, stimulating release of neurotransmitters from vesicles, which are then released to the next neuron to continue the communication pathway.  The electrical impulse transmission is very rapid, but transmission may also occur more slowly, particularly when hormones are stimulated for released by neurotransmitters.  As we will examine later, when drugs of abuse enter the brain, this delicate communication pattern is disrupted.

 

C.  Adaptation and Learning

The brain is able to adjust to both internal and external stimuli by forming new neuronal connection and by decreasing or increasing receptors, neurotransmitters, dendrites, and hormones.  This ability to adapt (neuroplasticity) helps to explain not only how we become addicted, but how we may unlearn addiction.  It even gives some hope for the possibility of the brain repairing itself from structural damage caused by drugs.

The brain responds to stimuli by generating new neuronal pathways.  For example, if you practice hitting a baseball, you become more skilled as the brain grows new dendritic spines and synapses, transmitting the learned sequence most efficiently.  Neurotransmitters decrease or increase to support this new structure.  The more the pathways are used, the more efficient they become and the stronger the neuronal connections become;  the less they are used, the more the skill (or habit) fades.  Habits can form from any repetitive action that stimulates the brain, such as checking our e-mail or drinking coffee.  Habits, particularly using drugs of abuse, involve the body’s natural hedonic reward system, or reward center.

II.  How drugs hijack the brain

The brain maintains an internal equilibrium by adjusting its structure and function to maintain homeostasis  (maintenance of normal body equilibria).  Although highly adaptive, when drugs of abuse enter the system, homeostasis can be disrupted.   Depending on the quantity, route of administration, and length of time the drug is used, disruption may be profound.   Drugs may come to dominate – or hijack – normal brain function, particularly in the reward center of the brain.

A. Pleasure and the Reward Center

We are hedonistically programmed to seek pleasure.  When the neurotransmitter dopamine is released into the brain, we experience it as pleasure.  Many things release dopamine, including natural highs like exercise, socializing, and sex, as well as all drugs of abuse.  Dopamine plays a dominate role in the reward center, which is controlled by the mesolimbic dopamine pathway.  This pathway starts in the VTA and connects to the limbic system.  The prefrontal cortex, our decision making center, is also involved in this pathway.

PICTURE

The mesolimbic dopamine pathway mediates pleasure using an array of natural chemicals, including endorphins (like morphine), anandaminde (like cannabis), acetylcholine (like nicotine), and dopamine (like cocaine/amphetamines).  When released naturally from neurotransmitter processes, these chemicals help regulate our mood and behavior and bring us pleasure.  However, when drugs of abuse are introduced, they hijack this system, bypassing our body’s own neurotransmitters and directly stimulating an explosive and large release of dopamine.  Such a large and quick release of dopamine dwarfs our natural hedonistic drive to seek pleasure from more sustainable, but smaller sources of dopamine.

Although all drugs of abuse result in a release of dopamine, they may also affect other neurotransmitters.   Cocaine works by a fairly simple mechanism:  It blocks dopamine transporter pumps from taking dopamine up into the neuron, thus increasing dopamine in the synapse.   Opiates affect the reward system via dopamine indirectly:   Opiates bind to a receptor, causing dopamine to be released, which then affects a nearby neuron containing GABA, which inhibits dopamine release thus increasing dopamine release.  Ecstasy binds to the serotonin transporter first, preventing transport and reuptake, which then increased serotonin is in the synapse,  causing activation of serotonin and dopamine receptors.

B. What (or who) controls the Reward Center?

Control of the mesolimbic dopamine pathway occurs at two levels:   Bottom-up control (originating at the level of stimulation) and top-down control (originating from brain cortical regions)

Bottom-up control

The amygdala — the area of the brain involved with memory and emotion – is connected to the mesolimbic dopamine pathway.  When a potentially pleasurable activity or substance is received (e.g., drugs), the amygdala signals neurons in the VTA and the nucleus accumbens.  Dopamine is released, and the stimulus is interpreted as pleasurable;  it becomes a “reward”.   The structures involved with this pathway “learn” that pleasure is created when the drug is introduced into the system.  The amygdala stores the “memory” of the drug, as well as associations of that drug, e.g., paraphernalia.   The brain learned how to acquire fast and large quantities of dopamine.  This reward-learning can be so powerful that the brain can forget how to acquire pleasure through natural engagement in everyday activities.  In essence, normal learning is short-circuited.

When we learn that a particular stimuli (reward) gives pleasure, it positively reinforces the behavior that produced it.  Positive reinforcement occurs on a small scale for everyday things we enjoy, for example, if we enjoy someone’s company, we seek them out.  Our choice to engage in repeated, pleasurable behaviors usually has a direct relationship to the amount of dopamine released.  Depending on individual brain make-up, drugs of abuse can be an extreme form of positive reinforcement (as may some activities such as sex, gambling, and food), driving us toward more drug seeking behavior.

The reward pathway for a particular stimuli can become so strong and automatic, that even when the stimuli is not so rewarding – or when there may be dire consequences – we continue to seek the stimuli.  Cravings arise out of these automatic pathways; the stronger and more fixed the pathways, the stronger our desire to seek the drug (reward).  Memory of the drug is stored in the amygdala, and when it receives information about the drug or its associations, it activates the reward system, triggering the neurons in the nucleus accumbens to procure that drug to seek pleasure.  The more we have used the drug and derived pleasure from it, the stronger will be the drive to complete the reward cycle.

Top-down control

Luckily humans possess a thinking brain, allowing interpretation and interruption of the automatic bottom-up pathway.   At the top of the reward center is the prefrontal cortex, which regulates impulse, analysis, flexibility, and integration of emotions.  At this level of reward center control, we are able to consciously make decisions to use (or not use) quick, dopamine releasing drugs or activities.  The strength of our top-down control system to override the impulses of the bottom-up control depends on our experience, our genetics, our learning about the benefits and cost of our decisions, and our ability to self-regulate.  It is this top-down control that is ultimately at the core of drug abuse treatment, which relies on the strengthening of the top-down control system to interrupt and reclaim bottom-up control.

C.  Brain Adaptation:   The progression from use to abuse

The neuroplasticity of the brain contributes to the progression from casual drug use to addiction.  Drugs of abuse cause short and long-term adaptation in a predictable succession (Koob, 2010), starting with the (1) mesolimbic dopamine pathways, moving to the (2) ventral striatum, (3) ventral striatum/ dorsal striatum/thalamus  (4) dorsolateral frontal cortex/inferior frontal cortex/hippocampus system, and finally the (5) extended amygdala.  This neuroadaptation reprograms the systems that process reward, motivation, memory, habituation, decision making, inhibition, self-awareness, and stress reactions.   This reprogramming leads to dysregulation of the brain reward center, causing compulsive drug use and loss of control.

 

Short-term change

All drugs of abuse have an immediate action on neurotransmission, particularly dopamine.  The opiates mimic neurotransmitters, which mimic dopamine.  Benzodiazepines enhance the receiving cells response to dopamine.  Cocaine hijacks the dopamine receptors, so that dopamine is not taken out of the synapse, and marijuana mimics cannabinoid neurotransmitters.  Other drugs alter neurotransmission by interacting with or interfering with the neurotransmission signals.  The quantity of drug taken, the metabolic breakdown of the drug, and route that the drug is taken all affect the strength of the dopamine reward (the faster the administration, the strongest reward).  The dopamine release is more prolonged and unregulated than natural stimuli, and the reinforcing effects from such large increases in dopamine in the brain affect the reward threshold.

 

Long-term change: 

As drug use continues, long-term structural changes occur in the brain, some of which may be permanent.  Simple structural changes include the up-regulation or down-regulation of receptors.  Up regulation means that when the neurons is exposed to too little neurotransmitter, more receptors are created to “capture” neurotransmitters in the synapse.  Down-regulation refers to the process where the number of receptors is reduced when exposed to too much neurotransmitter (or drugs mimicking the neurotransmitter).

Down regulation is especially important when drug use is stopped.  When a drug is actively being used, a lot of dopamine is in the synapse;  receptors down-regulate to adapt to the abundant dopamine.  If the drug is then stopped, less dopamine is available but few receptors are present.  Since neurons can’t up-regulate instantaneously, withdrawal symptoms are felt because of the relative reduction in dopamine.

More serious structural changes occur when drug use results in neuron death or loss of function. Neuroimaging of the brain (such as CAT scans or MRI) shows that some drugs can cause loss of brain structure and function.  Such loss may be caused by over-excitation of the neuron, which leads to apoptosis (cell suicide), and direct toxicity to the cell or dendrite.   Sometimes the brain can regrow dendrites, reversing drug damage and allowing the brain to return to normal;  in some cases damage is irreversible.

Most important of the long term adaptations is the change in the mesolimbic dopamine pathway, caused by dopamine that is released in a more prolonged and unregulated manner than natural stimuli.  The brain no longer responds to lower, slower levels of dopamine.   In other words, there is a recalibration of dopamine-activating (reward) thresholds for natural reinforcers.  This low dopamine tone contributes to the lack of motivation often seen in those using drugs.

The ability to choose between small, immediate rewards and large, deferred rewards is made in the prefrontal cortex.  With drug use, adaptations occur in the regulation of cognitive and emotional processes, which results in the overvaluing of drugs and the undervaluing of natural reinforcers.  There are deficits in inhibitory control of drug responses and an overall underperforming of the prefrontal cortex leading to poor impulse control.   With chronic drug exposure, the neurons responsible for memory and conditioned learning undergo abnormal neuroadaptations.

Binge, withdrawal, cravings, relapse, and the role of stress hormones

Each stage of the addiction cycle – binge, withdrawal, and cravings – is controlled by discrete brain system (Koons, 2010).  These systems play a role in developing and maintaining an addiction and they also contribute to relapse.

During the binging stage, the ventral tegmental area and the ventral striatum of the forebrain play dominate roles.  The acute reinforcing effects of drugs depends on immediate neurotransmitter release.  Impulsivity (the rapid, unplanned reactions to stimuli without regard for negative consequences) is the dominate behavior when a person first starts using drugs and is controlled by these brain areas.

With continued drug use, both compulsivity (repeated behavior in the face of adverse consequences) and impulsivity play roles in maintaining the addiction.  During the withdrawal stage, compulsivity changes from a behavior leading to positive reinforcement (i.e., the high of the drug use) to a behavior with negative reinforcement.  Negative reinforcement refers to the removal of an aversive stimulus, i.e., the removal of the negative emotional state that comes with withdrawal.   The negative emotional mood state is caused by decreased neurotransmitters:  Decreased dopamine and serotonin leading to dysphoria,  decreased opioid peptides causing pain, and decreased GABA, which results in anxiety and panic.  The extended amygdala, which plays an important role in pain and fear/stress processing, dominates the withdrawal stage.

Acute withdrawal is drug specific, but all drugs of abuse increase the stress response from release of stress hormones such as corticotropin releasing factor (CRF).  Dopamine is low in post-acute withdrawal, which increases sensitivity to environmental cues and decreases sensitivity to reward.   Changes in the prefrontal cortex follows, with impaired control of impulsivity.  The decrease in the reward system and the increase in stress sensitivity persist in post-acute withdrawal and play a role in relapse.

The preoccupation(cravings) stage is controlled by an variety of brain systems, including the prefrontal cortex, amygdala, and hippocampus.  Brain stress systems play a key role in the cravings stage, particularly from actions of CRF and norepinephrine in the extended amygdala.   Combined dopamine and glutamate neurotransmission in the dorsal striatum (involved with habit formation and action initiation) is involved when cravings, which are triggered by stimuli from external environmental cues and internal mood states of anxiety, irritability, and dysphoria.

Medication that can change the brain’s response

Research on ways to inhibit cue-conditioned dopamine and glutamate responses is a focus of current development of medication to treat addictions.   Treatments for binging and cravings include naltrexone (ReVia, Vivitrol), buprenorphine (Suboxone, Subutex), varenicline (Chantix), nicotine replacement, and methadone.  Treatments for negative mood state and cravings include methadone (Dolophine), buprenorphine (Suboxone, Subutex), varenicline (Chantix), nicotine replacement, acamprosate (Campral), and bupropion (Zyban).   There is optimism in the scientific community about the possibility that new drugs will be developed, which may help individuals gain and maintain control over addictive behaviors and substances.

III:  Is addiction biology or just a bad habit?  The possibilities of change

To what extent does genetics control the propensity to develop an addiction?   It has been shown that genetic factors, the environment, and the non-shared environment all had nearly equal influences on an individual’s risk of developing a drug use disorder (Tsaung, 1996).  There are also appear to be genetic and environmentalcharacteristics that make up a common vulnerabilityto abuse a range of illegal drugs (Tsuang, 1998).  That is, abuse of one drug is associated witha marked increase in the probability of abusing every othercategory of drug.  Also, drugs may “turn-on” genes to produce proteins, which cause changes in cell function or structure, which may lead to neuroadaptations.  Cocaine, for example, causes genes to produce the proteins necessary for new dendritic growth, and those who abuse alcohol are more likely to have different  dopamine receptor genes (Smith, 1992).

From scientific studies, we know that certain genetic factors may play a role in the development of an addiction;  some people may simply be more predisposed to developing an addiction.  We also know that in the development of addiction, there is a spiraling dysregulation of brain reward systems, producing short and long term changes in the brain.  Changes include both structural and functional changes in the brain, which reinforce the response to conditioned cues and maintain cravings, strengthened by the development of a stress sensitivity.   But does this mean that some of us are “programmed” to use drugs and that their use is predestined by genetics?  No.

We know that people do stop using drugs.   How do they do this if they are programmed to use the drug genetically or environmentally?  They change, because when stopping the drug becomes more important to them than continuing the drug, they can override and overcome the impulses generated by brain adaptations that maintain the abuse.   They are able to reengage the more sophisticated top-down control of the brain, overriding the bottom-up control of the more primitive parts of the brain.    Simply stated, we as humans are able to choose.

Julie Myers, PsyD, MSCP

Licensed Psychologist, MS Clinical Psychopharmacology, Master Addiction Counselor, Board Certified Biofeedbachttp://www.DrJulieMyers.com.  

Copyright 2011 Julie Myers, PsyD.  All Rights Reserved

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