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Setting up and running an evidence based clinical e-practice in the field of mental health is an exhilarating challenge!

In other fields of medicine, this may not be the case, but in the mental health world, evidence based practice is a relatively new development.

"Evidence-based practice" means we conduct our clinical practice based on evidence that we've acquired from clinical research. Similar to drug research, your doctor will usually prescribe medications that've been tested thoroughly through many trials, and have been proven to benefit your health condition. Once upon a time, your therapy could've been based on Dr. Ego’s clinical expertise, big name or great insights, but thankfully these days such practices are slowly becoming a nightmare of the past (although, drug companies still invest on armies of Dr. Egos “aka opinion leaders” to influence your local doctor’s prescription practices).

However, evidence-based practice is a fairly recent development in the field of mental health, and especially in the field of psychotherapy. The rise of behavioral therapy in the 60s, partly as a reaction to the psychoanalytic status quo, and later its marriage with cognitive therapy, have given us a remarkable new tradition of true evidence-based psychotherapeutic practice.

 

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  • How mood regulates food

One thing that determines our enjoyment in life is mood. Mood changes from day to day, moment to moment. We may be happy, energized, have optimistic feelings, take part in enjoyable activities, feel loving; but we may also feel unpleasant, moody, irritable, anxious, tired and even depressed. We've all come across these feelings and have experienced the enormous impact they have on our psychological and physical wellbeing. However, as people tend to favor positivity and happiness, we try to regulate our bad moods by engaging in certain activities and routines such as eating, exercising, smoking, drinking, socializing, playing games, watching TV, etc.

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I recently attended one of the lovely webinars hosted by the International Bipolar Foundation. The speaker Dr Nassir Ghaemi (Professor at Tufts university) presented his book, a First Rate Madness: Mood disorders and Crisis Leadership and discussed the issue of leadership and mood disorders.

According to his talk people with mood disorders and in general mentally abnormal people make better leaders especially at times of crisis. He gave examples of many American and European political leaders who achieved "greatness" and their psychohistory suggests also had a mental disorder - in most cases a bipolar disorder.

I have trouble digesting this argument, not for personal reasons, I also love my bipolar patients and wish to think and speak well of them, but for scientific reasons.

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Having an understanding and knowledge of the natural course of the disorder, helps to understand how effective different treatments are, and at the same time provide information that helps the design of prospective naturalistic studies that investigate syndromal outcome. This is especially the case in naturalistic studies when there is no control group available to compare differences in syndromal outcome.

Angst and Sellaro (2000), in a review of the natural course of bipolar disorder conclude with a pessimistic view that the prognosis for the majority of the patients remains poor. The valuable studies reviewed prior to the drug treatment era reported information on both the natural length/duration of episodes as well as the number of episodes a patient is going to experience over his life time. The duration of manic episodes was reported to be anything from a median of 4-6 months (Mendel, 1881, Wertham, 1929) or a higher mean of 6-8 months (Kraepelin, 1913, Panse, 1924). Given that the mean values can be distorted by patients who have a rapid cycling or a chronic course the median values are probably more representative in terms of understanding the typical number of episodes. Also two early studies (Rennie, 1942, Kinkelin, 1954) suggested that later manic episodes would tend to last longer.

Contemporary naturalistic studies that essentially report data from medicated patients report briefer episode durations. The data from the longest naturalistic follow up (1959-1985), the Zurich study (Angst and Preisig, 1995) reported a median length of both pure manic and depressive episodes of three months (mean= 4.3 months) with no gender differences. The intervals between the first three episodes have also been found to shorten but later there appears to be an irregular rhythm of about 0.4 episodes per year, which is however highly variable across patients (Angst and Sellaro, 2000) and of course nowadays different treatment modalities.

Lifetime outcome appears to be poor both in early and contemporary studies. In the longest follow up to date the Zurich study, out of 219 bipolar I patients with a median age of 68 years old at follow up, only 16% of patients had recovered, 52% still suffered from recurrent episodes, and 32% had become chronically ill or had passed away by committing suicide. This data primarily refers to bipolar I patients. The few studies of the bipolar II sub-type conclude that there are no differences in the life-time course between the two (Angst 1986; Coryell, Keller et al. 1989).

 

key references

Angst, J. & Sellaro, R. 2000. Historical perspectives and natural history of bipolar disorder. Biol Psychiatry, 48, 445-57.

Mendel, E. 1881. Die Manie. Eine Monographie, Vienna, Urban & Schwarzenberg.

Wertham, F. I. 1929. A group of benign chronic psychoses: Prolonged manic excitements. With a statistical study of age, duration and frequency in 2000 manic attacks. Am J Psychiatry, 17–78.

Angst, J. & Preisig, M. 1995. Course of a clinical cohort of unipolar, bipolar and schizoaffective patients. Results of a prospective study from 1959 to 1985. Schweiz Arch Neurol Psychiatr, 146, 5-16.

Rennie, T. 1942. Prognosis in manic-depressive psychoses. Am J Psychiatry, 801–814.

Kinkelin, M. 1954. Verlauf und Prognose des Manisch-Depressiven Irreseins. Schweiz Arch Neurol Neurochir Psychiatry, 100 –146.
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The treatment of bipolar disorder has from early been pharmacological, which remains the primary treatment modality especially for the acute phases of the illness, the depressive and manic episodes. For the majority of the patients, however, long-term pharmacotherapy is expected for prophylactic reasons even though the long-term results suggest high relapse rates even when medicated. This inability of drug treatments to keep people well in the long term and also the high rates of medication non-compliance in this population has made welcome a number of psychological therapies, all of which tend to work in combination with drug treatments.

Lithium has been the most popular medication for the treatment of acute manic episodes and prophylaxis from further episodes (Schou, 1999). Anti-convulsant medications such as carbamazepine and sodium valproate (Bowden, Brugger et al. 1994) are also used in the treatment of acute mania, along with antipsychotic medications such as chloropromazine and olanzapine for more rapid amelioration of acute mania or maintenance treatment (Vieta and Goikolea, 2005). Anti-depressant medications are often used for the treatment of bipolar depression but usually in combination with mood stabilisers in order to avoid switches to hypomania or mania (Moller and Grunze, 2000). The anticonvulsant lamotrigine (Calabrese, Huffman et al. 2008) appears to be promising for bipolar depression without having the risk for hypomanic/manic switches. Similar medications are used for bipolar II disorders but there is an increasing concern that the pharmacological treatments for bipolar II disorders are not adequate. Nevertheless, quetiapine, an atypical antipsychotic medication (Keating and Robinson, 2007) was recently approved by the FDA as an effective treatment for bipolar II depression.

Currently there are approximately four psychosocial treatments for bipolar disorder with at least one randomised control trial to demonstrate their efficacy. These include Cognitive Behaviour therapy (Lam, Watkins et al. 2003), Interpersonal and Social Rhythm Therapy (Frank, Kupfer et al. 2005), Family-focused therapy (Miklowitz, George et al. 2003), and Group Psycho-education (Bauer and McBride 2003; Colom, Vieta et al. 2003). Despite differences in the treatment targets of each therapy, they all emphasise patient education, mood and routine monitoring and medication compliance.

 

key references

Schou, M. 1999. Perspectives on lithium treatment of bipolar disorder: action, efficacy, effect on suicidal behavior. Bipolar Disord, 1, 5-10.

Moller, H. J. & Grunze, H. 2000. Have some guidelines for the treatment of acute bipolar depression gone too far in the restriction of antidepressants? Eur Arch Psychiatry Clin Neurosci, 250, 57-68.

Keating, G. M. & Robinson, D. M. 2007. Quetiapine: a review of its use in the treatment of bipolar depression. Drugs, 67, 1077-95.

Lam, D. H., Watkins, E. R., Hayward, P., Bright, J., Wright, K., Kerr, N., Parr-Davis, G. & Sham, P. 2003. A randomized controlled study of cognitive therapy for relapse prevention for bipolar affective disorder: outcome of the first year. Arch Gen Psychiatry, 60, 145-52.
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Even though the aetiology of the majority of mental disorders is unknown, bipolar disorder from early on has been thought to have a genetic causation.

The largest twin study in bipolar disorder by McGuffin and colleagues (2003) reported data from 67 bipolar probands (30 monozygotic and 37 dizygotic twins). Monozygotic twins, who share the same genetic code with each other, were found to have significantly higher rates of bipolar disorder, than dizygotic twins, who have different genetic codes.

Monozygotic concordance, where both twins sharing the same genetic code also had bipolar disorder was significantly higher than dizygotic concordance (67% MZ vs. 19% DZ). The heritability estimate was calculated to be 85% (when both twins had bipolar) or even higher to 89% (when one twin had bipolar and the other twin had unipolar).

Of course the risk from first degree relatives, where there is considerable genetic variability, is significantly lower and estimated to be approximately 5-10%, and the risk from unrelated persons even lower at 0.5-1.5% (Craddock and Jones, 1999). McGuffin et al. (2003) also argue that in comparison to twin studies of other disorders, sample sizes of twin studies in bipolar disorder are still too small to completely rule out or exactly determine the role of environmental influences.

Despite the high genetic correlation between mania and depression (0.65), mania appears to be more heritable than depression, with a heritability rate equal to bipolar disorder (85%) in the MZ twins. The hunt for the single gene has now been abandoned as most research suggests that what is inherited is multiple genes of small effect size that interact with each other (Farmer et al., 2007).

Structural brain abnormalities in bipolar patients have also been reported. These briefly include white matter hyper-intensities and differences in the size of temporal lobes, amygdala, basal ganglia, and caudate (Bearden et al., 2001). Functional abnormalities reported include differences in the activation of prefrontal areas, the striatum, and the amygdala (Strakowski et al., 2005). These are all brain areas that suggest subsequent abnormalities in the regulation of mood but it is still unclear whether these are a cause or an effect of the disorder or even a result of the different pharmacological treatments patients have to go through.

 

key references

Craddock, N. & Jones, I. 1999. Genetics of bipolar disorder. J Med Genet, 36, 585-94.

Farmer, A., Elkin, A. & Mcguffin, P. 2007. The genetics of bipolar affective disorder. Curr Opin Psychiatry, 20, 8-12.

Bearden, C. E., Hoffman, K. M. & Cannon, T. D. 2001. The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review. Bipolar Disord, 3, 106-50; discussion 151-3.

Strakowski, S. M., Delbello, M. P. & Adler, C. M. 2005. The functional neuroanatomy of bipolar disorder: a review of neuroimaging findings. Mol Psychiatry, 10, 105-16.
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Patients with bipolar disorder have been found to be at a greater risk for both additional mental health conditions and physical illnesses. The most common co-occurring conditions appear to be anxiety and substance use disorders, and physical illnesses such as cardiovascular disease and obesity.

In particular the NCS-R study found that nearly all of bipolar I and bipolar II patients (97.7% - 95.8%) also met criteria for another lifetime DSM-IV disorder (Merikangas, Akiskal et al. 2007). Anxiety disorders were prevalent in at least 63.1% - 86.7% of patients with bipolar disorder, 56.1% - 71.2% at least one life time impulse control disorder and 35.5% - 60.3% at least one life time comorbid substance use disorder. Impulse control disorders are thought to be part of the obsessive-compulsive spectrum and include disorders such as intermittent explosive disorder, kleptomania, pyromania, gambling and trichotillomania. Of course these are problem behaviours that may occur or even be maintained during symptomatic phases of bipolar disorder, even during sub-syndromal phases that may not be severe enough to require immediate clinical attention. Interestingly enough sub-threshold bipolar disorders in the NCS-R had an almost equally high rate of axis I comorbidity (88.4%) and an examination of the sequence of each disorder revealed bipolar disorders would most likely be secondary. The rates for comorbidities of axis I disorders in Unipolar disorder (Kessler, Berglund et al. 2003) were high but not as high as in bipolar disorder. Fifty nine (59%) had at least a life time anxiety disorder, 31.9% an impulse control disorder, 24% a substance abuse disorder.

Systematic reviews of the epidemiological studies that reported data on bipolar disorder (Pini, de Queiroz et al. 2005) suggest rather equal rates and disorders again, with anxiety disorder to predominate the clinical picture. More specific studies have revealed a higher likelihood of obsessive-compulsive disorder in bipolar I disorder in comparison with unipolar disorder (Goodwin and Jamison, 2007) and panic disorder, and repeated panic attacks especially for the bipolar II sub-type (Angst, 1998).

Of course all the above findings lead to greater disability and overall burden than by simply having bipolar disorder alone, and also highlight the difficulty of having a pure bipolar sample for conducting any relapse or sub-syndromal study in this population. Comorbid conditions are also likely to contribute to the heterogeneity of sub-syndromal symptoms. Hence in order to take into account the role of comorbid conditions in sub-syndromal symptomatology, studies would either need large samples or careful screening at baseline and inclusion of patients free of major comorbidities.

In UK the annual cost of bipolar disorder has been estimated to be £2 billion or £6900 per person with bipolar disorder at the 1999/2000 rates (Das Gupta and Guest, 2002). The unemployment rate was 46% as opposed to 3% of the 1999/2000 general population unemployment rates. Of the bipolar patients who are employed the NCS-R study found out that “presenteeism” as opposed to “absenteeism” was more important in terms of employment costs. “Presenteeism” was operationalised as being at work and underperforming, which most likely is the result of untreated sub-syndromal symptoms, most likely depressive.

Although bipolar disorder does not directly lead to death, the mortality rates of people with bipolar disorder are alarmingly high. Recent studies have found an increased mortality risk of 2.3 times higher than the expected rate in the general population (Goodwin and Jamison, 2007). Earlier mortality studies that combined unipolar and bipolar samples had found a mortality risk of six times higher than the normal population and prior to drug treatments death from manic exhaustion has also been reported (Derby, 1933). The largest prospective follow up study (38 years) of bipolar and Unipolar patients to examine mortality rates (Zurich cohort), (Angst et al., 2002) reported a higher risk of death from cardiovascular disease, suicide, and accidents in the bipolar sample than the Unipolar group. However, the treated bipolar sample had lower risks of death both for suicide and cardiovascular disease than the untreated sample. Goodwin and Jamison (2007) discuss that with proper lithium treatment some studies suggest that the mortality rates of bipolar patients (mainly from suicide risk) becomes almost equal to that of the general population.

 

key references

Das Gupta, R. & Guest, J. F. 2002. Annual cost of bipolar disorder to UK society. Br J Psychiatry, 180, 227-33.

Derby, I. M. 1933. Manic-depressive ‘exhaustion’ deaths. Psychiatr., Q7, 435.

Angst, F., Stassen, H. H., Clayton, P. J. & Angst, J. 2002. Mortality of patients with mood disorders: follow-up over 34-38 years. J Affect Disord, 68, 167-81.
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The prevalence of bipolar disorder is estimated to be relatively small. The most recent, largest, and best designed epidemiological study to date, the National Comordibity Survey - Replication - NCS-R (Kessler, McGonagle et al. 1994), was based on a representative sample of approximately 9,282 participants across 48 US states that covered the entire US population. The study used lay interviewers who interviewed participants with a structured lay diagnostic interview (CIDI) using DMS-IV criteria and took part in two phases. The first phase examined the prevalence of primary disorders and the second phase examined correlates of these disorders such as work performance and comorbidity.

The study revealed a lifetime prevalence rate of 1.0% for bipolar I, 1.1% for bipolar –II, and 2.4% for bipolar threshold (defined as having a lifetime history of 2 sub-threshold hypomanic episodes). These results lead to an overall prevalence of bipolar disorder of 4.4% in the US population. Lifetime prevalence rates of major depressive disorder were a lot higher reaching 16.2%. However, the bipolar disorders were found to be much more persistent than major depressive disorders. Persistence in such epidemiologic studies is calculated by looking at the ratio of past 12 month prevalence to lifetime prevalence. BP-II had the highest persistence (73.2%), with BP-I (63.3%) following second, and BP sub-threshold third (59.5%). Major depressive disorder had the lowest (40.7%) but still high persistence. Therefore bipolar disorders may not be as prevalent as major depression but they appear more persistent and chronic.

Lifetime estimates of bipolar I disorder from previous population studies across the world and Europe appear to be remarkably consistent most converging between 0.82% (Waraich, Goldner et al. 2004; Pini, de Queiroz et al. 2005) and 1% rate (Pini, de Queiroz et al. 2005) for bipolar I disorder. As Pini’s et al., (2005) review of European studies suggests most epidemiological studies are too small and underpowered to detect differences between bipolar I and II and very few studies have taken into account bipolar II and bipolar spectrum disorders.

For bipolar I disorder there is an almost equal prevalence of the disorder across males and females unlike major depressive disorders where there is a higher female to male ratio. Due to the higher prevalence of major depressive disorder in women it is not surprising that there is a slightly higher prevalence of bipolar II disorders in women.

The NCS-R study reported a median age of onset of 18 for bipolar I, 20 for bipolar II, and 22 for sub-syndromal bipolar disorder. Given the nature of the study the estimation of the age of onset was based on retrospective self-report. Pini’s et al., (2005) review suggests that there is considerable variability in the epidemiological studies in the reported age of onset due to differences in methodology and sample composition. Studies that interview older community samples (18-65) appear to report later ages of onset similar to the NCS-R study. However, a large epidemiological study that used a younger sample (14 – 24 years old), the Early Development Stages of Psychopathology Study (EDSP), (Wittchen et al., 2003) revealed a much younger age of onset. Hypomania had a mean age of onset of 14.8 years, Mania 15.4 years, and Major depression 17.9 years. These findings are consistent with recent research on paediatric bipolar disorder (Biederman, 2006). Hypomania appears to come early in life, and thus mark the onset of at least a form of bipolar spectrum disorder, until the occurrence of a manic or a depressive episode, which would then mark the onset of a bipolar I or a bipolar II disorder respectively.

 

key references

Wittchen, H. U., Mhlig, S. & Pezawas, L. 2003. Natural course and burden of bipolar disorders. Int J Neuropsychopharmacol, 6, 145-54.
Biederman, J. 2006. Pediatric Bipolar Disorder: The Promise of Psychopharmacotherapy. In: Akiskal, H. S. & Tohen, M. (eds.) Bipolar psychopharmacotherapy: Caring for the patient. Hoboken, NJ: John Wiley & Sons Inc.
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Two more disorders that are important to differentiate from but in some respects appear related to Bipolar disorder are Schizophrenia and Borderline Personality disorders.

The separation of manic depressive illness from schizophrenia was an important diagnostic task undertaken early on by Kraepelin (1896, 1919) who saw schizophrenia (“dementia praecox”) as a psychotic illness and a thought disorder, characterised by a steady downhill in cognition leading to chronic dementia, whereas manic depressive illness was seen as an episodic affective disorder with intermittent recovery. Although there is great heterogeneity in the symptom profiles of schizophrenia (or different schizophrenias), some of the primary symptoms of it such as delusions, hallucinations, disorganised behaviour (positive symptoms) and lack of insight can often appear in manic episodes to the extent that the two disorders may initially appear indistinguishable.

This is especially true if a cross-sectional approach is taken on the diagnosis without considering the history, content, and course of the symptoms even during the syndromal phases of each disorder. During manic episodes a key diagnostic feature is the mood congruence (or incongruence) of delusions as well as their content. Schizophrenic patients are more likely to have affect free or incongruent bizarre delusions, worse pre-morbid functioning prior to illness onset, and less insight throughout their illness. A factor analytic study of thought disorder (Solovay et al., 1987) that compared schizophrenic and manic patients found that combinatory and over-inclusive thinking was highly elevated in manic patients, whereas schizophrenics were more likely to have high levels of idiosyncratic, absurd, autistic, fluid and confused thinking.

Finally and perhaps most importantly during attempts to diagnose each disorder in remitted phases, the level of insight in bipolar patients appears to diminish only during manic phases of the illness (Ghaemi and Rosenquist, 2004), whereas in schizophrenia lack of insight is more chronic and trait-like. Also in bipolar disorder during subsyndromal phases the report of symptoms may be undermined mainly by social desirability biases rather than lack of insight as it would be in schizophrenia. Social desirability has been found to be high in bipolar patients (Neale, 1988) but no such reports exist in schizophrenia.

But most importantly the greatest challenge for diagnosing correctly bipolar disorder is brought up by Borderline personality disorder.

In many respects patients with Borderline personality disorder present a symptomatic picture that is not that different from bipolar disorder. They present both with depression and hypomanic symptoms and with extreme mood variability. Given that all personality disorders are also defined by the chronicity of particular problematic behaviours (easily misinterpreted as sub-syndromal symptoms), which are not usually severe enough to require acute treatment. In DSM-IV “Borderline personality disorder” is defined as “a pattern of instability in interpersonal relationships, self-image, and affects, and marked impulsivity”. However, many researchers have argued that borderline PD is a part of the bipolar spectrum and is closer to the bipolar II sub-type (Akiskal, 2004). Frank (2005, see p. 54) provides a thorough discussion on the similarities and differences between the two disorders. Symptoms that appear to be unique to borderline disorder are affective instability due to marked reactivity in mood, identity disturbance, chronic feelings of emptiness, dissociative states, frantic efforts to avoid real or imagined abandonment, recurrent suicidal threats, and self-mutilating behaviour. Even from this list of apparently unique borderline symptoms, “affective instability due to marked reactivity in mood”, and the fact that Borderline patients do not have full blown manic episodes (even if one decides to view this category as part of the bipolar spectrum), by diagnostic definition alone this group is not going to have either a history or a future of manic episodes.

 

key references

 

Kraepelin, E. 1913. Psychiatrie. Ein Lehrbuch fu ̈r Studierende und A ̈rzte, Leipzig Germany: Barth.

Kraepelin, E. 1919. Dementia Praecox and Paraphrenia.(1896) Translated by RM Barclay. Chicago: Chicago Medical Books.

Solovay, M. R., Shenton, M. E. & Holzman, P. S. 1987. Comparative studies of thought disorders. I. Mania and schizophrenia. Arch Gen Psychiatry, 44, 13-20.

Ghaemi, S. N. & Rosenquist, K. J. 2004. Is insight in mania state-dependent?: A meta-analysis. J Nerv Ment Dis, 192, 771-5.

Neale, J. M. 1988. Defensive functions of manic episodes. In: Oltmanns, T. F. & Maher, B. A. (eds.) Delusional beliefs. Oxford, England: John Wiley & Sons.

Akiskal, H. S. 2004. Demystifying borderline personality: critique of the concept and unorthodox reflections on its natural kinship with the bipolar spectrum. Acta Psychiatr Scand, 110, 401-7.

Frank, E. 2005. Treating bipolar disorder: A clinician's guide to interpersonal and social rhythm therapy, New York, NY, Guilford Press.

 

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Unipolar depressive disorder, from a diagnostic point of view, requires the presence of a single major depressive episode. According to DMS-IV and its diagnostic instruments, the key symptoms and duration are similar to the bipolar depressive episode. The primary unipolar disorders are also distinguished between a single episode or recurrent. The recurrent subtype has also been associated with bipolar disorder, especially when the depressive episodes are briefer than the usual two week period (Angst and Dobler-Mikola, 1985) specified in DSM-IV.

From a phenomenological point of view however research has shown interesting and consistent differences between unipolar and bipolar disorder. Leonhard (1957) early on discussed that his bipolar patients presented with more symptomatic variability from episode to episode than his unipolar patients who presented with more stereotyped symptom profiles.

A review of several decades of studies by (Goodwin and Jamison, 2007, pp. 16-17), identified that overall Bipolar depression is characterised by higher levels of psychomotor retardation, tension/fearfulness, atypical features, depressive mixed states, symptomatic variability across episodes, lability within episodes, irritability, late insomnia and hypersomnia, fragmented REM sleep, and psychotic features. On the other hand unipolar depression tends to have higher levels of anxiety, somatic complaints, psychomotor agitation, early insomnia, appetite and weight loss. It is worth noting that the majority of the studies reporting these differences have been referring to syndromal unipolar and bipolar states. Of course there is nothing to suggest that the sub-syndromal picture is likely to be different but such data are yet lacking.

The individual symptoms that may be present during the “well” sub-syndromal phases of the disorder merit further study. Such symptoms may have different contributions to the functional burden documented by bipolar sub-syndromal states and also may have different weights in predicting relapse or time spent in syndromal states.

 

key references

Angst, J. & Dobler-Mikola, A. 1985. The Zurich Study--a prospective epidemiological study of depressive, neurotic and psychosomatic syndromes. IV. Recurrent and nonrecurrent brief depression. Eur Arch Psychiatry Neurol Sci, 234, 408-16.

Leonhard, K. 1957. [Pathogenesis of manic-depressive disease.]. Nervenarzt, 28, 271-2.

Goodwin, F. & Jamison, K. 2007. Manic-depressive illness: bipolar disorders and recurrent depression, Oxford University Press, USA.
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Although conceptually the distinction between unipolar and bipolar disorder was made in the 19th century by French and German physicians, it was not until the family studies of Angst (1966) and Perris (1966) that the first evidence that these are two different conditions was provided. The distinction came primarily from family studies that found that patients with bipolar disorder had a higher incidence of family relatives with bipolar disorder. Recent genetic studies have confirmed this finding and have highlighted the heritability of mania over depression, which has been estimated to be close to 85% (McGuffin, Rijsdijk et al. 2003).

However, whether the two conditions are separate or related remains an open debate. Some researchers argue that mania is a separate condition (Cuellar et al., 2005); (McGuffin, Rijsdijk et al. 2003) to depression, with the later being or not being comorbid with mania.

 

key references

Angst, J. 1966. [On the etiology and nosology of endogenous depressive psychoses. A genetic, sociologic and clinical study]. Monogr Gesamtgeb Neurol Psychiatr, 112, 1-118.

Perris, C. 1966. A study of bipolar (manic-depressive) and unipolar recurrent depressive psychoses. Introduction. Acta Psychiatr Scand Suppl, 194, 9-14.

Cuellar, A. K., Johnson, S. L. & Winters, R. 2005. Distinctions between bipolar and unipolar depression. Clin Psychol Rev, 25, 307-39.
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Based on the above episodes, the DSM-IV identifies only two primary bipolar sub-types / diagnoses. Bipolar I disorder, which is also considered the classic presentation of Bipolar illness, and Bipolar II disorder, often mistakenly considered a less severe presentation of the disorder. The different episodes serve as building blocks for reaching either a bipolar I or a bipolar II diagnosis.

A. Bipolar I Disorder

A diagnosis of bipolar I disorder requires the presence of only one manic episode, which is not due to the presence of a general medical condition (or any other underlying “organic cause”) or substance use. The manic episode should also be outside the context of a Schizo-Affective or a Schizophrenic disorder.

Nevertheless, psychotic symptoms similar to the ones observed in schizophrenia are often present during manic episodes (Keck et al., 2003). Patients with bipolar I disorder will often have severe major depressive episodes as well. However, their presence is not required for a diagnosis of Bipolar I disorder. Although there have been reported cases of unipolar mania (Abrams, Taylor et al. 1979; Perugi, Akiskal et al. 1998) this presentation is unusual and its diagnostic stability is weak. Most such cases are reported to have a depressive episode at some point in their lifetime or if the onset is later in life an “organic cause” is usually suspected (Moorhead and Young, 2003)

B. Bipolar II Disorder

Bipolar II disorder is defined by the presence of at least one hypomanic episode and at least one major depressive episode. Patients with a bipolar II diagnosis will primarily suffer with major depressive episodes. As a result of this presentation and also because of having the difficulty in differentiating a hypomanic episode from a return to a normal “well” period, cases of BPII are often misdiagnosed for unipolar depression (Ghaemi et al., 2001). An increase in the recent recognition of this problem has fuelled the development of screening measures for hypomanic states (Angst et al., 2005). Nevertheless our understanding and measurement of hypomanic states is still rather limited.

C. Other Sub-Types and Diagnostic challenges

The DMS-IV also provides other diagnostic categories based purely on the course of the disorder. These are called course specifiers. There is the Rapid Cycling specifier, which requires the presence of four or more bipolar episodes (MDE, Manic/Hypomanic, Mixed) in the past year, and the seasonal specifier in which episodes tend to occur at particular times of the year independently of any psychosocial stressors.

Finally, a milder and more common presentation of Bipolar disorder is defined in cyclothymia. Cyclothymia is diagnosed for people who experience hypomanic symptoms and depressive symptoms without meeting the diagnostic criteria for bipolar episodes for at least two years.

The above definitions determine what is known about the prevalence of the bipolar disorder in the community. Many of the proposed criteria particularly about the duration of Hypomanic episodes (four days is an ad-hoc time frame) have caused considerable debate among epidemiologists and diagnosticians (Benazzi, 2007a). Additional debates have arisen from DMS-IV’s requirement of the presence of A1 symptom criteria (elevated or irritable mood) in order to allow the evaluation of the presence of further symptoms. Researchers (Benazzi, 2007b) (Bauer et al., 1991) who have challenged this practice argue that in hypomanic or mixed states the primary symptom is an increase in activity levels accompanied either by a positive or negative mood rather than a simply elevated or irritable mood that the patient may deny or not consider pathological. These problems often lead to missed episodes or even misdiagnosis, usually one of unipolar disorder. They also highlight the need for frequent and structured symptom monitoring in bipolar disorder, both for research and treatment/outcome monitoring purposes, and during all phases of the disorder.

Again the above diagnostic problems primarily plague the bipolar II sub-type and bipolar-spectrum cases. The severity of manic episodes present in bipolar I disorder has made it difficult for anyone to challenge their presence or deny their existence. Unlike other disorders, the diagnosis of what is considered the primary or classic presentation of bipolar disorder (Bipolar I) is a relatively easy task. The only requirement set out by the current diagnostic manuals is the presence of one manic episode. The diagnostic picture is complicated when one is trying to diagnose the disorder in milder bipolar-spectrum cases where a manic episode by definition is absent. This diagnostic problem is primarily a result of the difficulty we have in measuring and diagnosing hypomanic episodes as well as the difficulty of patients in reporting such states (Ghaemi et al., 2004), and also monitoring sub-syndromal presentations of these symptoms. However, all these problems and the obvious reliance on the course of the symptoms to derive a correct diagnosis make vital the use of prospective symptom severity and diagnostic assessments for continuous monitoring.

 

key references

Keck, P. E., Jr., Mcelroy, S. L., Havens, J. R., Altshuler, L. L., Nolen, W. A., Frye, M. A., Suppes, T., Denicoff, K. D., Kupka, R., Leverich, G. S., Rush, A. J. & Post, R. M. 2003. Psychosis in bipolar disorder: phenomenology and impact on morbidity and course of illness. Compr Psychiatry, 44, 263-9.

Moorhead, S. R. & Young, A. H. 2003. Evidence for a late onset bipolar-I disorder sub-group from 50 years. J Affect Disord, 73, 271-7.

Ghaemi, S. N., Ko, J. Y. & Goodwin, F. K. 2001. The bipolar spectrum and the antidepressant view of the world. J Psychiatr Pract, 7, 287-97.

Angst, J., Adolfsson, R., Benazzi, F., Gamma, A., Hantouche, E., Meyer, T. D., Skeppar, P., Vieta, E. & Scott, J. 2005. The HCL-32: towards a self-assessment tool for hypomanic symptoms in outpatients. J Affect Disord, 88, 217-33.

Benazzi, F. 2007a. Challenging DSM-IV criteria for hypomania: diagnosing based on number of no-priority symptoms. Eur Psychiatry, 22, 99-103.

Benazzi, F. 2007b. Is overactivity the core feature of hypomania in bipolar II disorder? Psychopathology, 40, 54-60.

Bauer, M. S., Crits-Christoph, P., Ball, W. A., Dewees, E., Mcallister, T., Alahi, P., Cacciola, J. & Whybrow, P. C. 1991. Independent assessment of manic and depressive symptoms by self-rating. Scale characteristics and implications for the study of mania. Arch Gen Psychiatry, 48, 807-12.

Ghaemi, S. N. & Rosenquist, K. J. 2004. Is insight in mania state-dependent?: A meta-analysis. J Nerv Ment Dis, 192, 771-5.
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Table 1.3: DSM-IV Criteria for a Mixed Episode

A. The criteria are met both for a Manic Episode and for a Major depressive episode (except for duration) nearly every day during at least a 1-week period

B. The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or in usual social activities or relationships with others, or to necessitate hospitalisation to prevent harm to self or others, or there are psychotic features

C. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication, or other treatment) or a general medical condition (e.g. hyperthyroidism)

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Table 1.2: DSM-IV Criteria for a Major Depressive Episode

A. Five (or more) of the following symptoms have been present during the same two-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure

1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g. feels sad or empty) or observation made by others (e.g. appears tearful)

2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly ever day (as indicated by either subjective account or observation made by others)

3. Significant weight loss when not dieting or weight gain (e.g. a change of more than 5% of body weight in a month), or decrease or increase in the appetite nearly every day

4. Insomnia or hypersomnia nearly every day

5. Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down)

6. Fatigue or loss of energy nearly every day

7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick)

8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others)

9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide

B. The symptoms do not meet criteria for a Mixed episode

C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning

D. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g. hypothyroidism)

E. The symptoms are not better accounted for by Bereavement, i.e., after the loss of a loved one, the symptoms persist for longer than two months or are characterised by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation

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Table 1.1: DSM-IV Criteria for a Manic / Hypomanic Episode

A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood, lasting at least one week (or any duration if hospitalisation is necessary)

B. During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree

1. Inflated self-esteem or grandiosity

2. Decreased need for sleep (e.g. feels rested after only three hours of sleep)

3. More talkative than usual or pressure to keep talking

4. Flight of ideas or subjective experience that thoughts are racing

5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli)

6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation

7. Excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g. engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments)

C. The symptoms do not meet criteria for a Mixed Episode

D. The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or in usual social activities or relationships with others, or to necessitate hospitalisation to prevent harm to self or other, or there are psychotic features

E. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication, or other treatment) or a general medical condition (e.g. hyperthyroidism)

Note: Manic-like episodes that are clearly caused by somatic antidepressant treatment (e.g., medication, electroconvulsive therapy, light therapy) should not count towards a diagnosis of Bipolar I disorder

1.3.1.2 Criteria for a Hypomanic Episode

Here it is more interesting to note the similarities and differences between the hypomanic episode and the manic one, rather than to reproduce the criteria. To start with the similarities, both a hypomanic and a manic episode share the same key diagnostic symptoms (A: elevated-expansive-irritable mood and B: 3 or 4 manic symptoms out of 7 identified). Also, similarly to the manic episode, the causation of the hypomanic episode cannot be due to substance use or a general medical condition.

But what really differentiates the two episodes or states from each other, is the severity, duration, and from a psychological point of view the experience of each patient. The DSM-IV sets four days as the minimum duration for a hypomanic episode and states that the mood has to be “clearly different from the usual non-depressed mood”. But the two most important criteria (D and E) that refer to functional impairment essentially summarise the major difference between a hypomanic and a manic episode. The hypomanic episode is associated with an “unequivocal change in functioning that is uncharacteristic of the person when not symptomatic” (criterion C of hypomanic episode) and “the episode is not severe enough to cause marked impairment in social or occupational functioning, or to necessitate hospitalisation, and there are no psychotic features” (criterion D).

The four-day duration for hypomania has been challenged clinically, and more recently empirically (Benazzi and Akiskal, 2006). More recent criteria proposed by Swiss researchers (“Zurich criteria”, Angst et al., 2003), discuss at least a two-day duration for hypomania. These criteria make the diagnosis of Bipolar disorder easier in cases with brief hypomanias, but also tend to inflate the diagnosis of Bipolar disorder, and the time spent in syndromal states and number of episodes, that are usually reported in prospective naturalist studies on Bipolar symptoms (Bauer, Grof et al. 2006).

Any diagnostic definitions that rely on duration and severity of symptom states, especially in a variable condition such as a Bipolar disorder, require continuous monitoring in order to be accurate, and make prospective designs with multiple measurements a necessity.

Two more episodes that are often present in Bipolar disorder are major depressive and mixed episodes. Their symptoms and diagnostic criteria are given below. According to the DSM-IV, the diagnostic criteria and symptoms of a major depressive episode are the same both in Bipolar and Unipolar disorders. Mixed episodes by definition can only be present in Bipolar disorder as they require the presence of both a depressive and a manic episode.

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1.3.1 Diagnostic (DSM-IV) Criteria for Bipolar Episodes

The Diagnostic and Statistical Manual of Mental Disorders by the American Psychiatric Association (DSM-IV) defines four Bipolar episodes (Mania / Hypomania / Depression / Mixed) with the following symptoms / criteria for each episode:

 

 

 

 

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Current diagnostic formulations of mental disorders describe the primary symptoms of each mental disorder without making direct references to the cause of the “illnesses”. There have been several debates on this practice of categorising and “lumping” mental disorders in this respect, primarily from psychologists and psychiatrists who are taking a dimensional or experimental view of these conditions (Bentall, 2006).

Interestingly, the very same discipline of psychiatric researchers investigating the biological and genetic causes of psychiatric disorder who are largely responsible for our current “nosological” standardisation, are now trying to redefine mental disorders given that the original categories do not appear to provide specific enough “phenotypes” for genetic investigations (Duffy and Grof, 2001)

Nevertheless, current clinical and research practice as it is reflected in the World Health Organisation and the American Psychiatric Association in their diagnostic manuals (ICD-10 and DSM-IV) recognise four different episodes that characterise Bipolar Disorder: Mania, Depression, Hypomania, and Mixed episode (Mania + Depression).

In order to meet the criteria for being present, each episode is characterised by a key number of basic symptoms. Additional criteria that refer to the duration, functional impairment and causal factors (aetiology) are laid out in order for a researcher or a clinician to be able to accurately diagnose the presence of an episode or else a syndromal state of Bipolar disorder.

 

key references

Bentall, R. 2006. Madness explained: Why we must reject the Kraepelinian paradigm and replace it with a [] complaint-orientated'approach to understanding mental illness. Medical hypotheses, 66, 220-233.

Duffy, A. & Grof, P. 2001. Psychiatric diagnoses in the context of genetic studies of bipolar disorder. Bipolar Disord, 3, 270-5.
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Presentations of Bipolar disorder were described by the ancient Greeks. It was observed and described not only by physicians like Hippocrates and Aretaeus, but also by philosophers and poets. Angst and Marneros (2001) review the historical evolution of the concept of bipolar disorder from ancient to present times.

The first physician to actually observe and describe in detail the features of Bipolar disorder is (Aretaeus, 150 AD) of Cappadocia in his two books ‘On the Aetiology and Symptomatology of Chronic Diseases’ and ‘The Treatment of Chronic Diseases’. Although like Hippocrates he emphasised the biological bases of mental illness, he also pointed out the role of psychological factors especially for depression. He distinguished between a biologically caused depression (melancholia) and a “reactive depression”. Apart from the hypotheses he made regarding the cause of the disorder, he also made interesting observations regarding the interplay between melancholia and mania, which highlight the mixture of bipolar symptoms.

‘‘ . . . I think that melancholia is the beginning and a part of mania . . . The development of a mania is really a worsening of the disease (melan-cholia) rather than a change into another disease. . . In most of them (melancholics) the sadness became better after various lengths of time and changed into happiness; the patients then developed a mania’’. Aretaeus of Cappadocia (150 AD)

Aretaeus observations of the two primary phases of bipolar disorder emphasised their development over time and the complex interplay of bipolar symptomatology. The emphasis on the variability of bipolar symptomatology as the primary feature of the disorder has continued to appear through out the academic literature on bipolar disorder.

Plato, on the other hand, observed and highlighted the role of psychological factors in mania. In his book “Phaedrus” he distinguished between two kinds of mania; one characterised by mental strain that arises from a bodily cause of origin (what would nowadays be considered dysphoric mania), and a second divine or inspired mania with Apollo being the source of “inspiration” (euphoric mania). Plato made further distinctions between psychogenic manias, which he called “inspirations”. These were the “prophetic inspiration”, the “erotic inspiration” (sent by the god of love, Eros), and “protreptic inspiration” (sent by the muses) that makes men sing. Such observations further set the ground for investigating different causal factors of bipolar symptoms and also contemporary knowledge with regards to the factor structure of mania (Cassidy et al., 2001).

Contemporary medical accounts of bipolar disorder by physicians in the 18th century continued to describe the longitudinal associations between melancholia and mania but did not see this as one single condition. According to (Angst and Marneros, 2001) it was the French psychiatrist Jean-Pierre Falret (1854) who recognised bipolar disorder as an entity on its own by calling it “folie circulaire”, and describing it as an entity that is “characterized by a continuous cycle of depression, mania and free intervals of varying length”, Jean-Pierre Falret (1854).

Our 20th century descriptive and diagnostic understanding of Bipolar disorder is primarily the end product of the work of German psychiatry, in particular Emil Kraepelin who made the distinction between manic depressive illness and schizophrenia (Kraepelin, 1919).

Kraepelin made the distinction based on his careful prospective observation of the symptoms course and the prognosis of the two disorders. He considered schizophrenia as an illness with a deteriorating course, in contrast to bipolar disorder that was characterised by an episodic course and overall a better prognosis. Kraepelin was also one of the first modern physicians to advance the method of Bipolar Life-Charting as he kept detailed graphical records/charts of his patients’ illness course.

Nevertheless, the clinical significance of sub-syndromal symptoms in bipolar disorder was first put forward by a non-organic psychoanalytically trained psychiatrist, Karl Abraham. Even though Karl Abraham (1911, 1924) is often considered the father of the manic-defence hypothesis, which was a psychoanalytic insight/hypothesis proposing that mania is a defence against depression, he should also be credited for his early observations on the presence of sub-syndromal symptoms during “free intervals”, what we nowadays call inter-episode periods.

In his 1924 monograph, “Manic Depressive states and the pre-genital of the libido”, he wrote: “For we find that the patient who is liable to periodic fits of depression and exaltation is not really perfectly well during his “free interval”. If we merely question such patients rather closely we learn that during long intervals of this kind they pass through depressive or hypo-manic states of mind from time to time” (p.423, 1924) Predictably, as an early psychoanalyst trained to observe personality functioning he even gave some insight into the differences in the characters of bipolar patients during these “free interval” periods.

“But what is specially interesting to the analyst is the fact that in all cycloid illnesses the patient is found to have an abnormal character-formation during his “free interval”; and that this character-formation coincides in a quite unmistakable way with that of the obsessional neurotic” (p. 423, 1924)

Of course given the nature of his psychoanalytic work and the fact that he based most of his theories on six case studies, Abraham did not attempt to make any links between his observation on sub-syndromal symptoms or the “abnormal” character formation during well periods and the course of the disorder.

 

key references

Angst, J. & Marneros, A. 2001. Bipolarity from ancient to modern times: conception, birth and rebirth. J Affect Disord, 67, 3-19.

Aretaeus 150 AD. On the Aetiology and Symptomatology of Chronic Diseases.

Cassidy, F., Pieper, C. F. & Carroll, B. J. 2001. Subtypes of mania determined by grade of membership analysis. Neuropsychopharmacology, 25, 373-83.

Kraepelin, E. 1919. Dementia Praecox and Paraphrenia.(1896) Translated by RM Barclay. Chicago: Chicago Medical Books.

Abraham, K. 1911. Notes on the psycho-analytical investigation and treatment of manic-depressive insanity and allied conditions. Selected Papers, 137-56.

Abraham, K. 1924. A short study of the development of the libido, viewed in the light of mental disorders. Selected Papers, 418-501.
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Bipolar disorder (also known as manic depressive illness) is a severe mental disorder, primarily characterised by extreme mood swings and episodes of depression and hypomania/mania. It has a highly recurrent course and a strong hereditary basis (Goodwin and Jamison, 2007). Despite effective pharmacological (Goodwin 2002; Keck and McElroy 2002) and more recently psychosocial treatments (Lam, Watkins et al. 2003; Miklowitz, George et al. 2003; Frank, Kupfer et al. 2005), once expressed the illness is characterised by a chronic course that will involve numerous bipolar episodes and equally persistent disabling sub-syndromal symptomatology (Judd et al., 2005). Depending on the diagnostic threshold used, severe presentations of it make it a relatively rare condition with approximately 1% prevalence rate. Nevertheless, milder forms of the disorder have been estimated to be highly prevalent (6.4%, Judd and Akiskal, 2003).

 

key references

Goodwin, F. & Jamison, K. 2007. Manic-depressive illness: bipolar disorders and recurrent depression, Oxford University Press, USA.

Lam, D. H., Watkins, E. R., Hayward, P., Bright, J., Wright, K., Kerr, N., Parr-Davis, G. & Sham, P. 2003. A randomized controlled study of cognitive therapy for relapse prevention for bipolar affective disorder: outcome of the first year. Arch Gen Psychiatry, 60, 145-52.

Frank, E. 2005. Treating bipolar disorder: A clinician's guide to interpersonal and social rhythm therapy, New York, NY, Guilford Press.

Judd, L. L., Akiskal, H. S., Schettler, P. J., Endicott, J., Leon, A. C., Solomon, D. A., Coryell, W., Maser, J. D. & Keller, M. B. 2005. Psychosocial disability in the course of bipolar I and II disorders: a prospective, comparative, longitudinal study. Arch Gen Psychiatry, 62, 1322-30.

Judd, L. L. & Akiskal, H. S. 2003. The prevalence and disability of bipolar spectrum disorders in the US population: re-analysis of the ECA database taking into account subthreshold cases. J Affect Disord, 73, 123-31.

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By VALERIE KILABERIA, BSC., MSC. BIPOLARLAB JUNIOR PSYCHOLOGIST

Even though the majority of research highlights the negative aspects of bipolar disorder, it is not uncommon to listen to patients who talk warmly about their experiences.

A new study conducted by Lobban, Taylor, Murray & Jones (2012) at the University of Lancaster, UK investigated the positive experiences of people who suffer from bipolar disorder. The participants reported that they experience many positive feelings, including intensified abilities, such as higher academic abilities; acute senses, perceptual sensitivity, focus and clarity of thought. They also reported feeling more creative and productive. The research indicated that a sub-group of people with bipolar disorder prefers to be with the condition as they experience invaluable feelings. Some of the participants work or worked in high professional positions and provided information concerning the times when it was incredibly easy for them to work hard. They felt that they could achieve high levels of productivity and were very ambitious.

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