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Bipolar Disorder

Child Psychiatrist Denver - DepressionBipolar Disorder, also known as Manic-Depressive Disorder, is a serious, lifelong illness. It is a disorder of the brain characterized by extreme changes in mood, energy, and behavior. It is most commonly characterized by marked changes in mood and energy level, switching between periods of elevated, euphoric mood and high energy and of depressed mood and low energy. Many experience periods of high energy combined with irritability or agitation, instead of euphoria. These periods of elevated mood are referred to as mania. Periods of low mood are referred to as depression. Typically, these periods can last for days to weeks. Occasionally, some may have rapidly changing moods, wherein their moods change in hours to days. This is referred to as rapid cycling. Rapid cycling is an indication of worsening of the disease and can be brought on by untreated or inconsistently treated Bipolar Disorder.

Mania in children can look somewhat different from mania in adults1,2. Often children will have a mix of euphoria and irritability, looking silly one moment and rageful the next1-4. Mania typically includes symptoms such as: expansive or irritable mood, explosive or destructive rages, defiance of authority, hyperactivity, agitation, decreased need for sleep, impulsivity, daredevil behavior, racing thoughts, poor judgment, pressured or rapid speech, precocious or hypersexual behavior, grandiose thoughts of self, and sometimes hallucinations or delusions.

Depression in children often includes: pervasive sadness with short periods (hours) of normal mood, crying spells, increased sleeping, agitation or irritability, lack of interest in normal or enjoyable activities, social withdrawal or isolation, low energy, slowed thinking and decreased concentration, decreased appetite, suicidal thoughts or thoughts about death, and acts of self-harm1-4.

Without treatment, Bipolar Disorder tends to worsen with time. Episodes of mood dysregulation become more severe, more frequent, and may occur without any precipitant. Prior to the availability of mood stabilizers, most people with Bipolar Disorder became progressively more severely ill. With consistent, long-term treatment with mood stabilizers, many with Bipolar Disorder live healthy productive lives with minimal difficulties. However, research and clinical experience consistently show that discontinuing mood stabilizer treatment sharply increases the morbidity and, possibly, mortality of this illness5-7. Studies have consistently shown that when mood stabilizer treatment is stopped, patients tend to rapidly become ill5. Sudden interruption of mood stabilizer treatment or inconsistent dosing is much more likely to precipitate a recurrence of illness. There is some evidence that gradual reduction in the mood stabilizer can decrease the risk of recurrence8.

The neurological underpinnings of Bipolar Disorder are only partially understood. Based on the phenomenon of progressively worsening mood swings without treatment or with intermittent treatment, the effectiveness of anti-seizure medications, and neuroimaging studies, it is believed by some scientists that Bipolar Disorder is very much like a seizure (a storm of abnormal electrical activity) in the parts of the brain that regulate emotions. All of the current mood stabilizers, except for lithium are anti-seizure medications. Lithium appears to work by slowing the speed of electrical transmission in brain cells, particularly ones that are over-active. Thus, one explanation for the worsening of Bipolar Disorder symptoms in untreated or intermittently treated patients is that a “kindling” process occurs in the vulnerable parts of the brain involved in regulating mood. Kindling occurs commonly in seizure disorders and means that when one seizure occurs, it alters the physiology of the affected brain cells, such that they become more vulnerable or more likely to undergo a seizure again. They become sensitized. This has been physiologically demonstrated in animal studies of seizures in all parts of the brain. Imaging studies demonstrate that the parts of the brain involved in emotion are overactive in patients with Bipolar Disorder9,10, which lends further validity to the theory. The imaging findings have included patchy increased perfusion of the frontal cortex (less pronounced in the orbitofrontal regions) and posterior parietal cortex combined with increased asymmetrical perfusion of the thalamus, head of the caudate nuclei and ventral lentiform nuclei9,10. Indeed, these imaging findings may serve as a possible endophenotypic pattern of Bipolar Disorder11 which can be visualized with SPECT brain imaging during the manic or euthymic states. Bipolar depression may be similar to unipolar depression in terms of decreased frontal cortex perfusion12, but it is possible the two can be distinguished by differences in the perfusion of the thalamus and basal ganglia in these two conditions. Perfusion, whether measured by SPECT of fMRI is increased in the thalamus in bipolar disorder9,10,12-14.

The increased risk of childhood bipolar disorder is not trivial15,16. In a review article, Dr. Baldessarini of Harvard University summarized research showing the risk of recurrence of mood symptoms is 7 times greater with sudden decrease in mood stabilizer dose. When mood stabilizers are suddenly stopped, the risk is 17 times greater17. Moreover, with each episode of recurrence of symptoms, the patient’s responsiveness to retreatment may decrease17,18. Dr. Barbara Geller, a recognized expert on child Bipolar Disorder who is at Washington University in St. Louis, reported research showing that patients with childhood onset Bipolar Disorder are more likely to have rapid cycling and have a 25% risk of dying by suicide, if untreated19. Practice parameters prepared by the American Academy of Child and Adolescent Psychiatry emphasize the importance of daily consistent medication to reduce the risk of relapse20.

References

1)       Geller B, et al., Pharmacological and non-drug treatment of child bipolar I disorder during prospective eight-year follow-up. Bipolar Disord. 2010 Mar;12(2):164-71.

2)       Geller B, et al., Child bipolar I disorder: prospective continuity with adult bipolar I disorder; characteristics of second and third episodes; predictors of 8-year outcome. Arch Gen Psychiatry. 2008 Oct;65(10):1125-33.

3)       Brotman MA, et al., Prevalence, clinical correlates, and longitudinal course of severe mood dysregulation in children. Biol Psychiatry. 2006 Nov 1;60(9):991-7

4)       Geller B, et al., Four-year prospective outcome and natural history of mania in children with a prepubertal and early adolescent bipolar disorder phenotype. Arch Gen Psychiatry. 2004 May;61(5):459-67

5)       Baldessarini RJ, Tondo L, Hennen J. Effects of lithium treatment and its discontinuation on suicidal behavior in bipolar manic-depressive disorders. J Clin Psychiatry. 1999;60 Suppl 2:77-84

6)       Altshuler LL, et al., Antidepressant-induced mania and cycle acceleration: a controversy revisited. Am J Psychiatry. 1995 Aug;152(8):1130-8

7)       Kilzieh N, Akiskal HS. Rapid-cycling bipolar disorder. An overview of research and clinical experience. Psychiatr Clin North Am. 1999 Sep;22(3):585-607

8)       Baldessarini RJ, et. al., Reduced morbidity after gradual discontinuation of lithium treatment for bipolar I and II disorders: a replication study. Am J Psychiatry. 1997 Apr;154(4):551-3

9)       Mena I, Correa R, Nader A. Bipolar disorder complicated by Selfmutilation: neurofunctional changes demonstrated by Tc99mHMPAO NeuroSPECT. Alasbimn Journal 2007; 10: Article N° AJ38-1 http://www.alasbimnjournal.cl/;

10)   Mena I, Correa R, Nader A, Boehme V. Bipolar affective disorders: Assessment of functional brain changes by means of Tc99mHMPAO NeuroSPECT. Alasbimn Journal 2004; 6: Article N° AJ23-2).

11)   Hasler G, et al., Toward constructing an endophenotype strategy for bipolar disorders. Biol Psychiatry. 2006 Jul 15;60(2):93-105.

12)    (Price JL, Drevets WC. Neural circuits underlying the pathophysiology of mood disorders. Trends Cogn Sci. 2012 Jan;16(1):61-71).

13)   Mena I. Neurospect applications in Psychiatry. Alasbimn Journal 2009; 11: Article N° AJ45-1 http://www.alasbimnjournal.cl/

14)   Blumberg HP, et al., Frontostriatal abnormalities in adolescents with bipolar disorder: preliminary observations from functional MRI. Am J Psychiatry. 2003 Jul;160(7):1345-7.

15)   Faedda GL, et al., Pediatric-onset bipolar disorder: a neglected clinical and public health problem. Harv Rev Psychiatry. 1995 Nov-Dec;3(4):171-95.

16)   Leverich GS, et al., The poor prognosis of childhood-onset bipolar disorder. J Pediatr. 2007 May;150(5):485-90.

17)   Tondo L, Hennen J, Baldessarini RJ. Lower suicide risk with long-term lithium treatment in major affective illness: a meta-analysis. Acta Psychiatr Scand. 2001 Sep;104(3):163-72.

18)   Swann AC, et al., Differential effect of number of previous episodes of affective disorder on response to lithium or divalproex in acute mania. Am J Psychiatry. 1999 Aug;156(8):1264-6.

19)   Geller B, et al., Prepubertal and early adolescent bipolarity differentiate from ADHD by manic symptoms, grandiose delusions, ultra-rapid or ultradian cycling. J Affect Disord. 1998 Nov;51(2):81-91.

20)   McClellan J, Werry J. Practice parameters for the assessment and treatment of children and adolescents with bipolar disorder.AmericanAcademyof Child and Adolescent Psychiatry. J Am Acad Child Adolesc Psychiatry. 1997 Oct;36(10 Suppl):157S-76S