By: for a period of 3 months for

By: Anthony SaraClass: UWP 104FProfessor William Sewell                           Case Presentation and Literary Review on Bipolar Disorder Case Presentation A 16-year-old, Caucasian female was initially presented to the psychologist’s office with presumed symptoms of ADHD. After questioning and medical history analysis, the patient was then diagnosed with OCD, anxiety, and depression. Symptoms included having the insatiable urge to balance all her actions out (e.g., any motion done by one side of the body had to be done the the other side), worrying excessively, sleep issues, irrational fears, excessive self-consciousness and self-doubt, fatigue, and difficulty concentrating. The patient has no known official family history of the listed disorders.

She first noticed these symptoms during class one year prior, as they started to impair her ability to perform in school and socially. After being put on medication for the anxiety and depression along with attending therapeutic sessions for a year and a half, the patient started to notice that she fluctuated daily (within 24 hours) between episodes of depression and episodes of hypomania Symptoms the patient felt for hypomania were elevated mood, overconfidence, and decreased need for sleep. Upon secondary presentation to a psychiatrist, the patient was diagnosed with bipolar II ultradian. The patient was then placed on 800 mg Lamotrigine (after a build up period of 5 weeks, increasing the dosage weekly), and is currently on 400mg after taking 800mg for four years as the patient stopped taking their medication for a period of 3 months for personal reasons. As the patient’s functioning was not too severely impaired during that period, and the drug requires that the user builds up to the proper dose to avoid undesired side-effects, the patient was then put on only 400mg. The patient was not diagnosed with BP earlier because of the severity of the anxiety symptoms that masked the fluctuating episodes of mania and depression. The patient’s mood was stabilized due to the medication, and the degree of the fluctuations also decreased.

Potential triggers for a depressive episode were usually daily stressors, thus the medication was effective. The durations of such episodes lasted between one or two hours, and longer if the patient could not go home to recover for a period of at least two hours. Manic episodes were triggered by any positive events during the day. The episode would cause the patient to be overly excited, and affected her ability to focus. The manic episodes also lasted between one to two hours.  Introduction Bipolar (BP) disorder is a mental disorder that causes a fluctuation between periods of depression and periods of elevated mood.The mood swings of BP are characterized by extreme shifts between mania and depression.

The periods of mania (elevated moods) are critical for the diagnosis of BP and can classified as either mania or hypomania, depending of whether psychosis is present or the severity. During such manic episodes, the individual feels less need to sleep and has little regard to consequences, along with feeling abnormally energetic or irritable and usually lasts for at least a week.1 The depressive phase is characterized by the symptoms of major depressive disorder: loss of interest or pleasure in everyday activities, feelings of emptiness, hopelessness, anxiety, worthlessness, guilt, changes in appetite, problems concentrating and making decisions, thoughts of or attempts of self-harm/suicide with self-harm occurring 30-40% of the time.2 There are three subtypes of BP, bipolar I (BPI) and bipolar II (BPII) and cyclothymia. In order to be diagnosed with BPI, the patient needs to have had at least have one manic episode and while it is common for there to be a depressive episode, it is not necessary for a diagnosis to be made. In order to diagnose a patient with BPII, they must have at least one episode of hypomania, accompanied by one or more episodes of major depression.3 Hypomania is distinguished from mania by the lack of psychotic symptoms, and lesser impact on functioning.4 Cyclothymia is diagnosed when the patient has a history of hypomanic episodes with episodes of depression that do not meet the minimum for major depressive episodes.

Best services for writing your paper according to Trustpilot

Premium Partner
From $18.00 per page
4,8 / 5
Writers Experience
Recommended Service
From $13.90 per page
4,6 / 5
Writers Experience
From $20.00 per page
4,5 / 5
Writers Experience
* All Partners were chosen among 50+ writing services by our Customer Satisfaction Team

5 There are instances, however, when the patient does not meet the criteria for any of the three subtypes. In such cases, the patient with diagnosed with other specified or unspecified BP. Other specified BP is used when the doctor decides that the most suitable explanation for why the minimum standard for full diagnosis was not met.6 Bipolar disorder has a median age of onset of about 25 years. Average lifetime prevalence of 0.

6% for BPI (male predominated) and 0.4% for BPII (female predominated).7 In general, most patients diagnosed with BP experience several episodes, on average 0.4-0.7 times per year, each episode lasting 3-6 months.8 In addition to the three typical categories of BP mentioned above (BPI, BPII, and Cyclothymia), all three of the types of bipolar disorder mentioned above could atypically have an additional subcategorization; however, in order to discuss the atypical sub-types of BP, such as rapid-cycling BP, ultrarapid BP, and ultradian BP, we must first discuss the exact definition of a cycle and an episode, which are terms used interchangeably to discuss discrete time periods of mood disorders. Due to how rapidly a patient cycles through moods in these special cases, which pertain to our patient in the case report, differentiating between the three subtypes would not be possible without a proper definition for each.

For instance, if a patient cycled twice in a 24-hour period for an entire year (365 days), it would not be apparent if that implied a single episode that lasted for an entire year, or 730 episodes in that year (365×2=730), each lasting less than 24 hours.9 In order to address this, researcher Barbara Geller M.D,proposed the following definitions. “(1) Episodes will be defined by (a) the duration from onset to offset of a period of at least 2 weeks in length during which only one mood state persists or (b) the duration from onset to offset of a period of ultrarapid or ultradian cycling for at least 2 weeks.

(2) Cycles will be defined by mood switches occurring daily or every few days during an episode. Further research will be needed to elucidate potential differences between child and adult cycling patterns.”9 Now that a set definition for the terms episode and cycle have been established. The following with clarify the inherent differences between rapid cycling, ultrarapid cycling, and ultradian cycling. Rapid Cycling BP has episodes lasting weeks to months, with at least 4 episodes per year. Ultrarapid Cycling BP has episodes lasting days to weeks, with at least 4 episodes per year. Ultradian Cycling has episodes lasting several hours, with at least 1 episode per day, in at least 4 days of the week.

9 Hypothetical Causes of BP There are usually three causes for BP, genetic, environmental, and neurological. Though these vary between individuals affected, the exact mechanism is still unclear.10 Several GWAS studies indicated the same handful of single nucleotide polymorphisms, typically within the genes NCAN, CACNA1C, and ODZ4 and an average overall heritability of about 0.71.11,12,13 Other studies seem to suggest that advanced paternal age may be linked to an increased likelihood of BP in offspring.14 Environmental factors, which may interact with the genetic factors mentioned, play an important role in etiology.15 It is likely that traumatic life events and interpersonal relationships encourage recurring BP episodes.

16 Around 40% of adults with BP in a self-survey claimed have had traumatic or abusive experiences during childhood.17 BP or BP-like symptoms may occur as a result of an injury or a neurological condition like brain injury, HIV, multiple sclerosis, etc…18 Diagnosing BP            The key to diagnosing BP is determining whether the patient has hypomania or mania.  It should be noted, an irritable mood may hide repressed mania, and symptoms could be mistaken for schizophrenia. Diagnosis typically occurs during early adulthood, however onset can occur anytime during a person’s life.

19 The difficulty occurs when differentiating BP from unipolar depression, thus there is an average of 5-10 year delay in diagnosis after the symptoms begin.20 Diagnosis typically requires multiple different physician visits and personal, family, and friends reports of moods and behaviours, and often medical work-up in order to rule out medical causes are taken into account are taken into account when trying to make an accurate diagnosis.21 Several rating scales for BP are available, however the use of scales cannot replace a full clinical assessment but they do help systematize the collection of symptoms.22                        One of the obstacles in properly diagnosing BP is that there are several other mental disorders with similar symptoms such as major depressive disorder, schizophrenia, borderline personality disorder, and attention deficit hyperactivity disorder (ADHD).23 Despite not having any diagnostic tests for BP, imaging and blood tests could be carried out to exclude diseases with similar symptoms to that of BP such as Huntington’s disease, complex migraines, strokes, brain tumors etc… There are also seemingly non-neurologically related diseases that could trigger symptoms of BP.

Certain endocrine disorders such as Cushing’s disease, hypo/hyperthyroidism and infectious etiologies of mania which are similar to BP mania could be HIV, influenza, herpes encephalitis etc…24 Even certain vitamin deficiencies such as niacin deficiency, cobalamin (vitamin B12) deficiency,  and thiamine deficiency could lead to BP like symptoms.24  Fortunately, tests are done to rule out these possibilities before a BP diagnosis is made in order to prevent overdiagnosis.              Management of BP BP can be treated both pharmacologically and psychotherapeutically. Hospitalization is typically required with the destructive manic episodes of BPI, however, it is atypical for long term inpatient stays due to deinstitutionalization.25              Psychotherapeutic Management  Psychotherapy is directed at recognizing early symptoms, triggers, diminishing basic symptoms, and the rehearsal of techniques targeted at maintaining remission.26 Despite most studies focusing on BPI, psychoeducation, Cognitive Behavioural Therapy (CBT), and family focused therapy has shown to be the most effective at relapse prevention, with CBT  appears to be the optimum method for dealing with the depressive symptoms.

Unfortunately, these treatments are not as effective during the acute phase of the disorder.26     BP Medication Numerous medications are used to treat BP.16 The most effective medication for treating severe manic episodes, bipolar depression, and preventing relapses, is lithium (w103).27 Unlike Ketamine, which has had questionable utility since 2015, lithium reduces the risk of suicide and self-harm in individuals with BP.28 Medication for BP uses a variety of mood stabilizers, antipsychotics, antidepressants and a few other drugs.              Antidepressants             Though not used alone in treating BP and having no advantage over mood stabilizers, antidepressants like venlafaxine are sometimes used in conjunction with mood stabilizers. Antipsychotics are preferred over antidepressants to be used alongside mood stabilizers.29              Mood Stabilizers             Anticonvulsants lamotrigine, carbamazepine, and valproic acid alongside lithium are mood stabilizers used to treat BP.

Though these drugs are not effective at treating acute bipolar depression, they demonstrate great efficacy at treating long-term mood swings.29 Lithium is the prefered drug used as a mood stabilizer.16 Carbamazepine, with some evidence it has greater benefit in rapid-cycling bipolar disorder,  effectively treats manic episodes; however, it is less effective in preventing relapse than lithium or valproate.30 Lamotrigine has the most efficacy in treating more severe bipolar depression and has the added benefit of preventing relapses; however, the drug has limited effect in rapid-cycling BP.

               Antipsychotics             Antipsychotics are typically used as a short term treatment of BP, as opposed to the antidepressants and mood stabilizers mentioned above.16 Antipsychotics like Olanzapine have shown to be effective in preventing relapses.31             Overall Prognosis             BP is a lifelong condition which is considered a severe health problem globally due to the increased rates of premature mortality and disability.32 Even once a diagnosis is made, it is still rare for a patient to achieve a complete remission of all the symptoms, which typically become more severe over time.33             Compliance with medication is the most significant factor that can lower the degree, severity of relapses and have an overall positive effect on prognosis. Unfortunately, current BP medication has severe side effects that, on average, decreases compliance by 75%.34 The different types of BP also have different prognoses.

Rapid-cycling BP has the worst in terms of suicide and self-harm.35 Psychotic symptoms and early onset (before 25 years of age) are usually associated with worse outcomes, and often are unresponsive to medication like lithium.36 Intervention and early recognition in patients have demonstrated to improve prognosis in earlier stages and the patients are statistically more responsive to treatment.33 Later onset, after adolescence, has also shown to improve prognosis outcome for patients.37 Long Term Effects on Cognitive Functioning A decline in cognitive during a patient’s first episode is common, and occasionally the decline can begin slightly before. Permanent cognitive dysfunction is common after the first episode, especially after acute phases of the disorder, with average levels of impairment during remission. This is similar for both BPI and BPII, however patients with BPII demonstrate lower levels of impairment.38 The degree of cognitive impairment positively correlates with the number of episodes a patient has, thus an inevitable decline in patients over time is commonplace.

39 The progression of cognitive impairment can be lowered by early intervention, with treatment being beneficial in addressing the later, more acute, phases of the disease.33 Conclusion Like many psychiatric disorders, there is still a vast amount to learn about bipolar disorder. Modern science has taken humanity a long way in terms of better treatment, going from institutionalization of patients in asylums, to lobotomization of patients (a blunt, inhumane and archaic tool for “solving” mental disorders) , and to finally humanely treating patients with the appropriate medications and therapy. Hopefully soon, humanity will find medications and treatments with less side-effects and better overall prognosis for the patients affected with this debilitating illness.

              References Anderson IM, Haddad PM, Scott J. Bipolar disorder. Bmj. 2012;345(dec27 3).              doi:10.

1136/bmj.e8508.2. Novick DM, Swartz HA, Frank E. Suicide attempts in bipolar I and bipolar II disorder: a review and meta?analysis of the evidence. Bipolar Disorders. http://onlinelibrary.

Published January 24, 2010.3. Bassett D. Borderline personality disorder and bipolar affective disorder. Spectra or spectre? A review. Australian ; New Zealand Journal of Psychiatry. 2012;46(4):327-339.

doi:10.1177/0004867411435289.4. National Collaborating Centre for Mental Health (UK). BIPOLAR DISORDER AND ITS DIAGNOSIS.

National Center for Biotechnology Information. https://www.ncbi. Published January 1, 1970.

5. Peet M, Peters S. Drug-Induced Mania. SpringerLink. Published November 18, 2012.

6. Diagnostic and Statistical Manual of Mental Disorders: DSM-5. American Psychiatric Publishing; 2014.7. Merikangas PDKR. Prevalence and Correlates of Bipolar Spectrum Disorder in the World Mental Health Survey Initiative. Archives of General Psychiatry. Published March 7, 2011.8. Akiskal HS, Bourgeois ML, Angst J, Post R, Möller H-J, Hirschfeld R. Re-evaluating the prevalence of and diagnostic composition within the broad clinical spectrum of bipolar disorders. Journal of Affective Disorders. 2000;59.

doi:10.1016/s0165-0327(00)00203-2.9. Bauer M, Beaulieu S, Dunner DL, Lafer B, Kupka R. Rapid cycling bipolar disorder – diagnostic concepts. Bipolar Disorders.

x/abstract. Published January 10, 2008.10. Mitochondrial modulators for bipolar disorder: A pathophysiologically informed paradigm for new drug development. Australian ; New Zealand Journal of Psychiatry.

1177/0004867412449303.11. Craddock N, Sklar P. Genetics of bipolar disorder. The Lancet. 2013;381(9878):1654-1662.

doi:10.1016/s0140-6736(13)60855-7.12. Sullivan PF, Daly MJ, O’Donovan M.

Genetic Architectures of Psychiatric Disorders: The Emerging Picture and Its Implications. Nature reviews. Genetics. https://www.ncbi.nlm. Published August 2012.13. Edvardsen J, Torgersen S, Røysamb E, et al. Heritability of bipolar spectrum disorders. Unity or heterogeneity? Journal of Affective Disorders.

2008;106(3):229-240. doi:10.1016/j.jad.2007.

07.001.14. Frans EM, Sandin S, Reichenberg A, Lichtenstein P, Långström N, Hultman CM. Advancing Paternal Age and Bipolar Disorder. Archives of General Psychiatry. 2008;65(9):1034. doi:10.


Serretti A, Mandelli L. The genetics of bipolar disorder: genome ‘hot regions,’ genes, new potential candidates and future directions. Molecular Psychiatry. 2008;13(8):742-771. doi:10.1038/mp.

2008.29.16. Geddes JR, Miklowitz DJ. Treatment of bipolar disorder. The Lancet. 2013;381(9878):1672-1682.

doi:10.1016/s0140-6736(13)60857-0.17. Brietzke E, Sant’Anna MK, Jackowski A, et al. Impact of Childhood Stress on Psychopathology. Revista Brasileira de Psiquiatria.

2012;34(4):480-488. doi:10.1016/j.rbp.2012.04.009.

18. Daroff RB. Neurology in Clinical Practice. Saunders; 2012.19.

Comorbidity in Bipolar Disorder. Comorbidity in Bipolar Disorder | Psychiatric Times. Manji HK, Quiroz JA, Payne JL, et al. The underlying neurobiology of bipolar disorder.

World Psychiatry. https://www.ncbi.nlm. Published October 2003.21.

Miklowitz DJ, Chang KD. Prevention of bipolar disorder in at-risk children: Theoretical assumptions and empirical foundations. Development and Psychopathology. 2008;20(03). doi:10.

1017/s0954579408000424.22. Phillips ML, Kupfer DJ. Bipolar disorder diagnosis: challenges and future directions. The Lancet. 2013;381(9878):1663-1671. doi:10.1016/s0140-6736(13)60989-7.

23. Picardi A. Rating scales in bipolar disorder. Current Opinion in Psychiatry.

2009;22(1):42-49. doi:10.1097/yco.0b013e328315a4d2.24. Berns GS, Nemeroff CB.

The neurobiology of bipolar disorder. American Journal of Medical Genetics. 2003;123C(1):76-84.


25. Fountoulakis KN, Kontis D, Gonda X, Yatham LN. A systematic review of the evidence on the treatment of rapid cycling bipolar disorder. Bipolar Disorders. 2013;15(2):115-137.


Scott J, Paykel E, Morriss R, et al. Cognitive–behavioural therapy for severe and recurrent bipolar disorders. The British Journal of Psychiatry.

Published April 1, 2006.27. Havens LL, Ghaemi SN. Existential despair and bipolar disorder: the therapeutic alliance as a mood stabilizer. American journal of psychotherapy.

Cipriani A, Hawton K, Stockton S, Geddes JR. Lithium in the prevention of suicide in mood disorders: updated systematic review and meta-analysis. Bmj. 2013;346(jun27 4). doi:10.1136/bmj.

f3646.29. Mccloud TL, Caddy C, Jochim J, et al. Ketamine and other glutamate receptor modulators for depression in bipolar disorder in adults.

Cochrane Database of Systematic Reviews. 2015. doi:10.


30. Post RM, Ketter TA, Uhde T, Ballenger JC. Thirty Years of Clinical Experience with Carbamazepine in the Treatment of Bipolar Illness.

CNS Drugs. 2007;21(1):47-71. doi:10.2165/00023210-200721010-00005.31. Vasudev K, Macritchie K, Geddes J, Watson S, Young AH.

Topiramate for acute affective episodes in bipolar disorder. Cochrane Database of Systematic Reviews. 2006. doi:10.1002/14651858.cd003384.pub2.32.

Benzodiazepines for Bipolar Disorder. WebMD. https://www.webmd.

com/bipolar-disorder/guide/bipolar-benzodiazepines.33. Montgomery P, Richardson AJ. Omega-3 fatty acids for bipolar disorder. Cochrane Database of Systematic Reviews. 2008. doi:10.

1002/14651858.cd005169.pub2.34. Muneer A. Staging Models in Bipolar Disorder: A Systematic Review of the Literature. Clinical Psychopharmacology and Neuroscience. 2016;14(2):117-130.


35. Muneer A. Treatment of the depressive phase of bipolar affective disorder: a review. JPMA. The Journal of the Pakistan Medical Association. https://www.

Published June 2013.36. Kennedy KP, Cullen KR, Deyoung CG, Klimes-Dougan B. The genetics of early-onset bipolar disorder: A systematic review.

Journal of Affective Disorders. 2015;184:1-12. doi:10.1016/j.jad.


37. Tsitsipa E, Fountoulakis KN. The neurocognitive functioning in bipolar disorder: a systematic review of data. Annals of General Psychiatry. 2015;14(1).

doi:10.1186/s12991-015-0081-z.38. Jann MW.

Diagnosis and Treatment of Bipolar Disorders in Adults: A Review of the Evidence on Pharmacologic Treatments. American Health ; Drug Benefits.

Published December 2014.39. Serafini G, Pompili M, Borgwardt S, et al. Brain changes in early-onset bipolar and unipolar depressive disorders: a systematic review in children and adolescents. European Child ; Adolescent Psychiatry. 2014;23(11):1023-1041. doi:10.1007/s00787-014-0614-z.


I'm Dora!

Would you like to get a custom essay? How about receiving a customized one?

Click here