Bipolar Disorder | Manic Depression Treatment

Bipolar Disorder:
Manic Depression Diagnosis and Treatment | Sustain Your Stability!

Assessment & Treatment Options

Bipolar Disorder Distinctions: The article below was written as part of my academic training and coursework in clinical psychology. It was written to an audience of professors and doctoral candidates. As such, this paper may be of interest to anyone wishing to know more about the differential diagnosis and distinctions between Bipolar I and Bipolar II Disorders. Indications for psychiatric treatment and implications for counselors, therapists, and practicing clinical psychologists are discussed.

Differential Diagnosis
Bipolar I and Bipolar II Disorder

bipolar disorder hot and cold water faucets depicting manic depressive episodes

Not long ago, Bipolar II Disorder emerged as a separate diagnostic category of Major Mood Disorders and this differentiation has provoked a number of interesting questions and compelling debates among clinicians and researchers. The psychological literature reveals lots of discussion as to how Bipolar II Disorder is best distinguished from Bipolar I Disorder and from “unipolar” Major Depression. There is also ongoing research dialogue and disagreement regarding the true nature, prevalence, and severity of the disorder.

Important questions concerning issues of comorbidity or overlap with other diagnoses such as Axis II Personality Disorders or Substance Abuse Disorders are also apparent. Although Bipolar II Disorder is generally viewed as a mild form of classic “manic-depressive” illness, recent debates suggest that it could be a valid diagnostic category that is different from Bipolar I in genetic, biological, clinical, and pharmacological aspects (Gasto, Otero, Neito & Vallejo, 1997).

A substantial literature also delineates the most effective psychotherapeutic management and pharmacologic treatment of the Bipolar I and II Disorders. Each of these discussions is of interest to practicing psychologists and the following review is informed by the questions and debates mentioned above. The following discussion is intended to illustrate the clinical picture associated with Bipolar II Disorder and to highlight some critical “guide-posts” for student-practitioners of clinical psychology.

Through this investigation I am motivated to inform my theoretical orientation as a cognitive-behaviorist. Whenever relevant, this perspective shall be emphasized below.

An Historical Context

Bipolar II Disorder was officially recognized as a separate diagnostic category in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) in 1994 (APA, 1994). In DSM-III-R this general condition was classified as “Bipolar Disorder Not Otherwise Specified,” and in DSM-III this was it was classified as “Atypical Bipolar Disorder.” The occurrence of Bipolar Disorder appears to have been noted as far back as 1686 when Bonet introduced the term “maniacomelancholicus” to describe a group of extremely labile patients. In the 1850’s, Falret adopted the term “circular insanity” for the same kinds of patients, around the same time Baillarger used the term “double-form insanity” to describe the same general condition. In his classical description of the clinical states of depression, Kraepelin (1921) defined six depressive groups according to severity. The resulting groups were melancholia simplex, stupor, melancholia gravis, paranoid melancholia, fantastic melancholia, and delirious melancholia. It is not surprising that each of these authors extended descriptions that seem to emphasize the most salient and distinguishing feature of Bipolar Illness —Hypomania and the Manic Episode.

Clinical Picture:
Hypomania and the Manic Episode: Three Cardinal Symptoms

It is noteworthy that acute mania may be heralded by a period of prodromal hypomanic signs and symptoms or it may begin acutely, rapidly manifesting its full form. In acute mania, all of the characteristics of hypomania (defined below) are increased in severity. Thoughts become disconnected, speech may become loud or”forced,” and vocalizations are noted for distinctly “pressed” or “guttural” quality. Cognitive associations appear vague, loose and tangential; excessively florid and grandiose delusions may be present. The individual’s mood might be described as expansive or effusive; self-representations are routinely exalted and may appear grandly embellished.

Frequently, individuals manifesting a Manic Episode do not recognize that their mental-status is compromised. This is true of both Bipolar I and Bipolar II diagnoses. Hence, such individuals are typically resistant to treatment regardless of the bizarre and disorganized quality of their behavior. In acute Manic Episodes this frequently leads to severe psychosocial disruption, involuntary psychiatric hospitalization or legal detention.

Behavior typically appears urgent, erratic, poorly regulated and extremely eccentric. Irritability and extreme mood lability may be associated with a distinctly impoverished insight, while self-defeating or destructive actions are routinely observed in manic patients. Bech, (1992) explains: “A lack of normal critical sense is another hallmark of mania, patients are frequently over familiar, talking to complete strangers to whom they may make inappropriate sexual and personal comments. They may demand preferential treatment because they are so busy and important and are easily irritated when their unreasonable demands are not met.” (P. 17). If changes in consciousness, reality-contact, or psychotic features are present, they often floured and come to dominate the clinical picture. Delusions are frequently elaborate, strongly defended and grandiose in nature; visual and auditory hallucinations may occur. Mood is typically noted for extreme lability and may shift rapidly between anger and dysphoria. It is not uncommon that: “Symptoms may last moments, hours, or, more rarely days. Not uncommonly, the depressive symptoms and manic symptoms occur simultaneously (APA, 1994, p. 330).

Diagnostically, it is worth remembering that: “Regardless of the severity of the behavioral symptoms, a patient with psychotic symptoms (delusions or hallucinations) is always classified as experiencing a Manic Episode. The clinical picture of a Manic Episode can vary considerably but most often contains the three cardinal symptoms of mania: elevated mood, flight of ideas, and psychomotor overactivity.” (Rohland, Winokur & Cook, 1997, p. 262).

DSM-IV Criteria for Manic Episode

(Please note that the that the presence of even a single Manic Episode warrants the diagnosis of Bipolar I Disorder)

(Criterion A) involves a distinct period of abnormally and persistently elevated, expansive, or irritable mood, lasting at least 1 week (or any duration if hospitalization is necessary). In the interest of brevity, only the most salient diagnostic features shall be discussed here. The reader interested in differential diagnostic clarification, specifiers, and associated features might simultaneously confer with DSM-IV.

(Criterion B) Manic Episodes are characterized by a clustering of three or more of the following behavioral changes.

  1. Inflated self-esteem or grandiosity
  2. Decreased need for sleep
  3. More talkative than usual or pressure to keep talking
  4. Flight of ideas or subjective experience that thoughts are racing
  5. Distractibility
  6. Increase in goal-directed activities (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., spending sprees, sexual indiscretions, foolish business decisions)

(Criterion C) These symptoms must not meet the criteria for a Mixed Episode (cf. APA, 1994, p. 335).

(Criterion 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 hospitalization to prevent harm to self or others, or there are psychotic features

(Criterion E) The symptoms are not due to the direct physiological effects of substance or medical condition.

It is noteworthy that Bipolar I Disorder does not necessitate a history of major depression, while Bipolar II Disorder requires at least one Major Depressive Episode as well as the presence of Hypomanic Episodes. “The essential feature of Bipolar I is a clinical course that is characterized by the occurrence of one or more Manic Episodes” (APA, 1994, p. 350); while the essential feature of Bipolar II involves a clinical course “characterized by the occurrence of one or more Major Depressive Episodes accompanied by at least one Hypomanic Episode (APA, 1994, p. 359). Research has established that Bipolar I patients presenting with a single Manic Episode show a 90% probability of manifesting future episodes (APA, 1994). Regarding Bipolar I patients specified with “Single Manic Episode” it is noteworthy that: “Unipolar manic patients tend to be male, are responsive to lithium and on further history or follow-up are usually found to have at least subclinical depressions (Nurnburger & Greshon, 1992, p. 135).

Bipolar II Disorder: Hypomania and the Hypomanic Episode

Clinicians are reminded that the criteria for defining mania and hypomania are identical; these disturbances are simply differentiated in terms of the severity of functional impairment manifest by the individual. Astute clinicians will remember that the diagnosis of a formal Manic Episode requires a mood disturbance that is: “Sufficiently severe to cause marked impairment in occupational functioning or in usual social activities or relationships, or to necessitate hospitalization to prevent harm to self or others” (APA, 1994, p. 332). The mood disturbance manifest in the Hypomanic Episode associated with Bipolar II Disorder, “. . . is not severe enough to cause marked impairment in social or occupational functioning or require hospitalization” (p. 335).

DSM-IV Criteria for Hypomanic Episode

A. A distinct period during which there is an abnormally and persistently elevated, expansive, or irritable mood that lasts at least 4 days that is clearly different from the usual nondepressed mood.

B. During the period of mood disturbance, three or more of the following symptoms have existed (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 3 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., the person engages in unrestrained buying sprees, sexual indiscretions, or foolish business investments)

C. The episode is associated with an unequivocal change in functioning that is uncharacteristic of the person when not symptomatic.

D. The disturbance in mood and the change in functioning are observable by others.

E. The episode is not severe enough to cause marked impairment in social or occupational functioning, or to necessitate hospitalization, and there are no psychotic features.

F. 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: Hypomanic-like episodes that are clearly caused by somatic antidepressant treatment (e.g., medication, electroconvulsive therapy) should not count toward a diagnosis of Bipolar II Disorder)

Criterion “D” above requires that the “hypomanic” mood disturbance associated with Bipolar II Disorder be apparent or “observable” of to significant others, and this is presently highlighted as an important clinical guide-post for the assessment Bipolar II Disorder. Because both Bipolar I and II patients characteristically no not recognize their psychopathology, the involvement of significant others or family may be critical for an accurate evaluation. Manic Episodes must be distinguished from Hypomanic Episodes and this is critical clinical distinction. The difference between these episodes simply lies in the degree severity of functional impairment associated with the episode. Bipolar I Disorder is noteworthy for precipitating severe client dysfunction and psychiatric hospitalization without appropriate treatment. While the same is not true of Bipolar II Disorder, formal Hypomanic Episodes are clearly diagnostic and these are frequently worthy of clinical attention.

Given that the “Hypomanic Episode” (APA, 1994, P.335) represents the defining characteristic of Bipolar II Disorder, it is given ample description below. An episode typically begins suddenly, and shows a rapid escalation of symptoms within the course of a couple days. Episode duration varies from weeks to months, and may precede or follow a Major Depressive Episode.

The Hypomanic Episode is defined as: “A distinct period during which there is an abnormally and persistently elevated, expansive, or irritable mood that lasts at least 4 days” (cf. APA, 1994, p. 335). Such an “elevated and expansive mood” might be described as euphoric, high, unusually cheerful or effusive, and this may appear incongruent or unrealistic to familiar observers: “Although the person’s mood may have an infectious quality for the uninvolved observer, it is recognized as a distinct change from the usual self by those who know the person well” (APA, 1994, p. 336). The expansive quality of hypomanic mood disturbance may be characterized by uncharacteristic enthusiasm for interpersonal, social, or occupational interactions. Although such mood elevation is considered prototypical, the mood state may also be represented as irritable and labile with, extreme swings of euphoria or frustrated agitation. Inflated self esteem and uncritical self-confidence are characteristic of hypomanic persons rather than the marked grandiosity and diminished “reality-contact” that accompanies more delusional states in acute Manic Episodes. There is frequently a decreased need for sleep that may be readily apparent and annoying to significant others. The individual may refuses to sleep, or awaken before the customary time with an apparent overabundance of intrusive energy. The speech or the hypomanic person may be somewhat louder, and notably more rapid than usual. Cognitive associations typically remain intact and appear meaningful; however, hypomanic ideas and motivations may seem to others to be grandiose or frivolous distortions of the realities at hand. Formal “flight of ideas” is uncommon, however, and if present, last for only brief periods of time.

Distractibility is often readily apparent to observing others, as evidenced by rapid changes in speech, interpersonal contact, or motor activity. An uncharacteristic increase in novel goal directed activity may involve planning and participation in multiple activities with unrealistic investment in idealized outcomes. Such activities are often quite creative and may actually appear functional at first glance. Efforts toward sociability may be markedly increased and there may be an apparent hypersexuality an associated increase in sex-seeking behavior. There may be a tendency toward impulsive activity such as spending sprees, reckless business ventures or other high-risk endeavors. However such activities are usually organized, without the bizarre quality manifest in fully Manic Episodes. Again, it is noteworthy that such responding typically does not result in the level of impairment that is characteristic and definitive of the Manic Episode.

The DSM-IV states that Hypomanic Episodes should not be confused with the several days of euthymia that may follow remission of a Major Depressive Episode. The presence of a Manic or Mixed Episode precludes the diagnosis of Bipolar II Disorder.
Although hypomanic symptoms must be severe enough to “cause clinically significant distress or impairment” in social, occupational or other important areas of functioning; “In some cases, “. . . the Hypomanic Episodes themselves do not cause impairment. Instead, the impairment may result from the Major Depressive Episodes of from a chronic pattern of unpredictable mood episodes and fluctuating unreliable interpersonal or occupational functioning” (APA, 1994, p. 359).

Vigilant assessors are encouraged to recognize that it is predictable for individuals with Bipolar II Disorder to show a distinct and quite baffling lack of insight. Even when their responding leads to threats of psychiatric hospitalization, arrest, or similar consequences, such clients may they may not acknowledge the functional impairment produced by their own behavior. Although others may be troubled by the individuals’ erratic and eccentric hypomanic behavior, it is probable that such clients will not view their mental status as problematic or pathological. The DSM-IV states: “Often individuals, particularly when in the midst of a Major Depressive Episode, do not recall periods of Hypomania without reminders from close friends or relatives. Information from other informants is often critical in establishing the diagnosis of Bipolar II Disorder” (APA, 1994, p. 359).

Psychologists are reminded that in DSM-IV, major changes in the diagnosis of Bipolar Disorder were specified with the refined definition of Bipolar II Disorder. Bipolar I Disorder is characterized by an occurrence of one or more Manic or Mixed Episodes, and Bipolar II is distinguished by the occurrence of one or more episodes that constitute a Major Depression, along with at least one episode that constitutes a Hypomanic Episode.

DSM-IV Diagnostic Criteria for Bipolar II Disorder

A. Presence (or history) of one or more Major Depressive Episodes
B. Presence (or history) of at least one Hypomanic Episode.
C. There has never been a Manic Episode
D. The mood symptoms in Criteria A and B are not better accounted for by Schizoaffective Disorder and are not superimposed on Schizophrenia, Schizophreniform Disorder, Delusional Disorder, or Psychotic Disorder Not Otherwise Specified.
E. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

(Most recent episode is specified Psychotic or Depressed)

DSM-IV Criteria for Bipolar I Disorder

A. Presence of only one Manic Episode and no past Major Depressive Episodes.
B. The Manic Episode is not better accounted for by Schizoaffective Disorder and is not superimposed on Schizophrenia, Schizophreniform Disorder, Delusional Disorder, or Psychotic Disorder Not Otherwise Specified

(Specify most recent episode: Single, Hypomanic, Manic,  Mixed or Depressed)

Note: The lifetime prevalence of Bipolar I Disorder in community samples has varied from 0.4% to 1.6%., while prevalence for Bipolar II Disorder has been estimated to be 0.5%. (APA, 1994).

DSM-IV Specifiers (DSM p. 361)

The following specifiers for Both Bipolar I and II disorders. These are used to indicate the nature of the current, or most recent, episode which may be either Hypomanic or Depressed. Episodes may be specified: Mild, moderate, severe without psychotic features, severe with psychotic features, in partial remission, in full remission, with catatonic features, with melancholic features, with atypical features, with postpartum onset, with seasonal pattern, with rapid cycling (APA, 1994, 361).

Suicidal Behavior

Completed suicide is most strongly associated with the presence of Major Depressive Episodes in Bipolar disorders. The literature indicates that: “Suicide is a significant risk, occurring in 10% to 15% of persons with Bipolar II Disorder” (APA, 1994, p.361). The Major Depressive Disorder associated with Bipolar Illness is also associated with a high mortality by suicide rate. Up to 15% of patients with chronic Major Depressive Disorder die by suicide (APA, 1994). Chiles and Stroshal (1995) report that patients that manifest the “Rapid-Cycling” specifier are noted for an elevated tendency for suicide. While this suicide rate has not been specifically defined, it should be considered by clinicians that manage the treatment of Bipolar II patients. Occupational failure, school failure, divorce and failed relationships are strongly associated with suicidality in Bipolar Disorders. Such events have been associated with suicidal behavior and such stressors must be acknowledged when assessing suicide risk.

DSM-IV Criteria for Mixed Episode in Bipolar I Disorder

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 tot cause marked impairment in occupational functioning or in usual social activities or relationships with others, or to necessitate hospitalization 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

Differential Diagnosis and Comorbidity Considerations
Comorbidity of Bipolar II Disorder with Personality Disorders:

One of the primary debates surrounding the diagnosis of Bipolar II Disorder concerns its comorbidity with personality disorders. In bipolar diagnoses, comorbidity with Personality Disorders has been reported at varying rates. Ucok, et al, (1998) indicate that epidemiological surveys using DSM-III criteria, have estimated the prevalence of overall personality disorders from 10% to 13% in outpatient clinical populations. In the 1980’s comorbidity rates between Bipolar I and Personality Disorders were reported at 4% to 12%, yet more recently such rates have been reported to be significantly higher at 47.7% (Ucok, 1998). One reason for such differences in reports of comorbidity rates may be due to the varying methodologies used for assessment of personality disorders and to changes in DSM-IV diagnostic nomenclature. Assessment methods vary from self-report measures, to structured interviews, and the need for more definitive research is apparent. One recent study indicates that: “It has been found that the majority of personality disorders associated with Bipolar II Disorder are from clusters B (histrionic, borderline, narcissistic, antisocial) in bipolars, and cluster C (avoidant, dependent, passive-aggressive, obsessive-compulsive) in unipolars” (Ucok, et al., 1998, p. 72). These authors report that 47.5% of bipolar I subjects in this study were noted for at least one Personality Disorder, as compared to a 15.5% in control subjects. Although the authors provide no statistic, it is noteworthy that suicide attempts were more frequent in patients with a history of Personality Disorder diagnoses. The authors also indicate that patients with Bipolar I Disorder in remission have personality traits that differ from those of normal controls. Unfortunately, the authors do not elaborate upon these differences; yet they conclude that: “These results suggest that the comorbidity of personality disorders with Bipolar Disorder predicts a poor treatment outcome” (p. 74).

Differential Diagnosis: Bipolar II Disorder and Personality Disorders

The discerning clinician will make clinical judgments carefully when diagnosis involves closely associated and potentially “comorbid” clinical pictures. This is especially true in differentiating diagnoses of Personality Disorders and Bipolar Disorders. The General Diagnostic Criteria for a Assessing Personality Disorders (APA, 1994, p. 633) specifically emphasizes “enduring patterns of behavior” as the definitive aspect of diagnostic decisions. Just the opposite is true in Bipolar II Disorder.

Vigilant assessors are aware that the “enduring patterns” associated with Personality Disorders may contradict the diagnosis of Bipolar II Disorder. Recall that “hypomania,” the essential feature of Bipolar II Disorder, must be associated with an: “… unequivocal change in functioning that is uncharacteristic of the person when not symptomatic (APA, 1994, p. 338). This nuance, alone, provides evaluating psychologists a critical and important clinical discernment. Having had person-to-person contact with the “euphoric—grandiose,” “enthusiastic” and “expansive quality of mood disturbance” described here as hypomanic; I will assure you this—given the above descriptors—you will recognize a Hypomanic Episode when you see it!

Recent research has revealed that only 5% to 15% of patients noted for Bipolar II Disorder develop a full-blown Manic Episode that ultimately warrants a diagnosis of Bipolar I Disorder (Vieta, et al, 1997). These authors indicate remarkable differences exist between Bipolar I and II patients. Their research showed that Bipolar II Disorder tended to be more severe in terms of episode frequency, however, symptom severity was found to be clearly greater in Bipolar I Disorder. The authors conclude: “Bipolar II Disorder could be described as a milder form of manic-depressive illness regarding symptom severity, but as a more malignant form concerning episode frequency” (p. 99).

Psychologists must also skillfully distinguish Bipolar II Disorder from episodes of Substance Induced Mood Disorder, Mood Disorder Due to a General Medical Condition, Dysthymic Disorder, Cyclothymic Disorder, Psychotic Disorder and Bipolar I Disorder (APA, 1994, pp. 361-362). The essential features of Manic and Hypomanic Episodes define the distinguishing attributes of Bipolar Disorders in all considerations of differential diagnosis.
Substance Induced Mood Disorder: (APA, 1994, p. 70)

Substance Induced Mood Disorders: Distinctions

Substance Induced Mood Disorder is distinguished from the Hypomanic Episode by the finding that a substance is judged to be etiologically related to the mood disturbance. Substance induced mood disorders may be induced by drugs of abuse, prescribed medications, or exposure to toxins. Bipolar Disorders are associated with a wide range of impulsive and self destructive behaviors and clinicians are advised to remain vigilant to the presence of substance abuse patterns in bipolar patients. Psychologists frequently do not have specialized training in the identification and treatment of substance related disorders. It has been reported that 90% of graduate psychology students have had no formal course work in the area of substance abuse (Margolis & Zweben, 1998). It is noteworthy that: “Many therapists today find themselves in the remarkable position of having no systematic understanding of how to identify, treat, or appropriately refer alcohol and drug problems, despite the fact that we are in the middle of an epidemic of chemical use of unprecedented proportions” (p.19). Furthermore, “Substance abuse disorders can and do mimic virtually every other psychiatric diagnosis” (p.10). Clearly, poor clinical discernment and not knowing the signs and symptoms of substance abuse disorders, can lead to misdiagnosis and legal vulnerabilities for those therapists who miss relevant signs and symptoms and incorrectly diagnose the problem.

Mood Disorders Due to a General Medical Condition (APA, 1994, p.370)

Medical conditions like hyperthyroidism, multiple sclerosis and brain tumor can lead to mood disturbances that mimic the symptoms of Manic, Mixed, and Hypomanic Episodes. Naturally, in determining whether the mood disturbance is due to a medical condition, the assessor must first substantiate the presence of the condition. The DSM-IV states: “Although there are no infallible guidelines for determining whether the relationship between the mood disturbance and the general medical condition is etiological, several considerations provide some guidance in this area” (p. 367). Temporal association between the onset of medical problems and the presence of mood symptoms may prove illuminating. Also the absence of indicators that are typical of the hypomanic mood disturbance may prove relevant (e.g., absence of family history, atypical age of onset).

Differential Diagnostic Considerations & Cyclothymic Disorder (p. 363)

The Manic and Hypomanic Episode must also be carefully evaluated in relation to the presence of the clinical picture in Cyclothymic Disorder (APA, 1994, 363). Considered as a Bipolar Mood Disorder, the essential feature of Cyclothymic Disorder involves: “A chronic, fluctuating mood disturbance involving numerous periods of hypomanic symptoms and numerous periods of depressive symptoms. The hypomanic symptoms are of insufficient number, severity, pervasiveness, or duration to meet full criteria for a Major Depressive, Manic or Hypomanic Episode (APA, 1994, p. 363). Clinicians might note that Studies have reported a lifetime prevalence of Cyclothymic Disorder from 0.4% to 1%. Prevalence in mood disorders in clinical populations have ranged from 3% to 5%. There is a 15% to 50% risk that persons diagnosed with Cyclothymic Disorder will subsequently develop Bipolar I or II Disorder (APA, 1994). There has also been speculation that Cyclothymia Bipolar II and Bipolar I Disorder exist on a continuum of related disorders (Akiskal, 1988), however, further research is necessary to substantiate such speculation.

Psychotic Disorders and Differential Diagnosis (APA, 1994, p. 273)

Because Psychotic Disorders may share a number of presenting symptoms that are present in Manic Episodes, differential diagnosis can be difficult. Symptoms like grandiosity, irritability, agitation, or delusions are common in both conditions. The DSM-IV provides some guidelines for distinguishing these disorders. In contrast to Bipolar Disorders, Psychotic Disorders are all characterized by periods of psychotic symptoms that occur in the absence of prominent mood symptoms. Other clinical discernments include the accompanying symptom clusters, previous course of illness, and indicators like family history. Late stage onset (after 35 years) of delusions and hallucinations is uncharacteristic of formal psychotic disorders (APA, 1994) and such clinical findings suggest more careful evaluation to rule out bipolar illness, organic or substance induced causes.

Again, it is worth remembering that: “Regardless of the severity of the behavioral symptoms, a patient with psychotic symptoms (delusions or hallucinations) is always classified as experiencing a Manic Episode (Cook, 1997, 292). The DSM-IV states: “Because the psychotic features associated with Mood Disorders usually involve nonbizarre delusions without prominent hallucinations, the Delusional Disorder frequently has associated mood symptoms. The distinction depends on the temporal relationship between the mood disturbance and the delusions and on the severity of the mood symptoms. If delusions occur exclusively during mood episodes, the diagnosis is Mood Disorder with Psychotic Features. Although depressive symptoms are common in Delusional Disorder, they are usually mild, remit while the delusional symptoms persist, and do not warrant a separate Mood Disorder diagnosis” (APA, 1994, p.300). In the absence of clearly specified criterion that indicate formal Bipolar I Disorder or Psychotic Disorder, the diagnosis “Mood Disorder With Psychotic Features” or “Psychotic Disorder Not Otherwise Specified” may be applied (APA, 1994, 273). The diagnosis “Bipolar Disorder Not Otherwise Specified” is selected for disorders with bipolar features that do not meet criteria for any of the specific Bipolar Disorders, “. . . this includes symptoms about which there is inadequate or contradictory information” (p. 318).

Course of Symptoms and Etiology

Affective Disorders

Psychologists must consider the longitudinal nature of Bipolar Illness when following patients diagnosed with this disorder. A significant proportion of individuals with bipolar disorder show a course of illness characterized by chronic recurrences and such patients may benefit from treatment beyond the acute phase of the illness. It is estimated that over 50% of individuals who experience an initial episode of major depression and at least 80% of those who have an initial episode of mania will have one or more recurrences, often with serious psychosocial or economic consequences (APA, 1987). Approximately 15 to 30 percent of individuals with bipolar disorder do not fully recover from any given episode (Prien, 1992) and failure to adequately treat the progressive course of recurrence can have devastating effects on life functioning. A study sponsored by the United States Public Health Service (1979) indicates that, without adequate treatment and ongoing care, the average person experiencing the onset of bipolar disorder at the age of 24 can expect to lose about 9 years of life, 12 years of normal functioning and 14 years of diminished major life activity (e.g. occupational, scholastic, marital, child-raising).

Numerous controlled studies demonstrate the need for continuation of pharmacologic treatment in bipolar disorder and there is evidence from natural course of illness studies that the duration of episodes tends to lengthen slightly with each recurrence (Post, 1992). A frequently employed practice is to continue medication for approximately 6 months following initial control of symptoms and then gradually to reduce dosage while carefully monitoring the individual for signs of an emerging relapse. Clinicians should be aware that the signs of a manic or depressive phase may not be detected quickly enough to prevent a full-blown relapse, which can result in serious disruption for both the patient and the therapeutic alliance. In most cases involving lithium therapy, a relapse will not occur until the patient has been free of medication for two months or more (Post, 1992). Post (1992) reported that most clinicians who have published an opinion on the use of preventative drug interventions recommend that the patient should have two or three episodes before receiving preventative (continuous) drug therapy. This author also notes that: “There is general agreement that patients who have only a single episode, mild episodes or a lengthily interval between episodes (e.g. 5 years or more) should probably not be started on preventative drug treatment (p. 442).

Choice of Treatment: Bipolar I Disorder

Lithium is clearly the drug of choice for the treatment of Bipolar I Disorder and there is abundant evidence that lithium is significantly more effective than placebo in preventing both manic and depressive episodes. In placebo-controlled trials, the average failure rate for lithium is 33% and for placebo 81% (Post 1992). Generally, lithium treatment appears to be most effective with individuals who have a history of good inter-episode functioning and episodes uncomplicated by mixed manic and dysphoric features. Other positive predictors include a family history of Bipolar Illness and indications of positive response of first degree relatives to lithium treatment. Perhaps the most useful predictor of long-term lithium outcome is the initial response to lithium over the initial 6 months of therapy. Negative predictors of lithium response include a recent history of dysphoric mania or rapid/continuous cycling, a history of alcohol or drug abuse, and failure to comply with previous treatment efforts (Meyer & Deitsch, 1996).

The adequacy of lithium dosage for the individual patient is best determined by the blood-serum level achieved. Plasma lithium levels are determined by the size of the dose administered and the timing of subsequent dosages. The generally accepted therapeutic range for blood plasma levels is 0.8 – 1.2 (mmol/l) and this is to be determined 12 hours after the last dosage.

Clinicians Are Advised:

Clinicians are advised that lithium is noted for a narrow therapeutic—toxic margin and practitioners must remain vigilant for signs and symptoms of toxicity. Prodromal symptoms of lithium intoxication include coarse tremor, sluggishness, nausea and vomiting. Plasma lithium levels exceeding 2.0 mmol/l are associated with increasingly severe symptoms including clouded consciousness, slurred speech, muscular hypertonia, epileptiphorm seizures. Levels approaching 4.0 mmol/l and above may lead to renal failure, coma and ultimately death. Obviously, appropriate precautions should be taken when suicidality is an issue.

Anticonvulsant medications like Carbamazpine (Tegretol) have received critical attention as a promising treatment for patients who do not respond adequately to lithium or are unable to tolerate lithium side-effects. Carbamazepine, like lithium has a therapeutic dose level that must be carefully monitored and it has been most widely used to treat “Rapid Cycling” in Bipolar Patients. Rapid cycling patients, those that show changes in mania to depression and back again over the course of hours or days, rather than months, seem to respond particularly well to carbamazepine (Meyer & Deitsch, 1996). Following the discovery or carbamazepine as an effective antimanic agent, similar medications like Valproic acid (Depcote) and clonazepam (Klonopin) have been found useful for bipolar patterns that have been resistant to other forms of treatment and this includes Bipolar II patients. Psychologists should note that clonazepam resembles a benzodiazepine in structure and, like the benzodiazepines it can have a pleasant sedative effect with a potential for abuse. Clorazepam also shows a synergistic effect with alcohol consumption, and since alcohol is commonly abused by bipolar patients, caution should be exercised even when substance abuse patterns are not apparent. A large body of research now suggests the utility of these anticonvulsant medications for treating patients that are unresponsive to lithium. Psychologists should note that Valproate has proven especially effective for persons presenting with rapid cycling and dysphoric mania (Prien, 1992).

Choice of Treatment:  Bipolar II Disorder

Presently, there is surprisingly little research on the long-term treatment of Bipolar II Disorder. One reason for this lack of conclusive research relates to issues of comorbidity and the scientific confusion that results from the presence of signs and symptoms of similar diagnostic categories. For example, research studies with depressed patients noted for a history of hypomania have been grouped with unipolar patients in therapeutic trials and such hypomanic patients have not been the focus of independent analysis. Another reason is that Hypomanic Episodes, the defining characteristic of Bipolar II Disorder, are sometimes overlooked or are unrecognized in the documentation of the psychiatric history for patients selected for therapeutic trials. Psychologists are reminded that the Diagnostic and Statistical Manual of Mental Disorders did not have a category for Bipolar II Disorder until the 1994 publication of DSM-IV;. In DSM-IIIR, the Bipolar II diagnosis appears to be more vaguely specified as “Bipolar Disorder Not Otherwise Specified” (APA, 1987).

The few long-term studies that have reported treatment-outcome for strictly Bipolar II samples suggest that lithium is an effective treatment (Prien, 1992). Kane (et al 1982) reported that lithium was more effective than imapramine and placebo in preventing recurrence of depression in patients that would now be considered to manifest Bipolar II . Lithium has been found to be more effective than placebo in reducing the frequency of Hypomanic Episodes but no more effective than placebo in preventing episodes of major depression (Dunner, et al, 1976). Peselow et al (1982) found lithium to be more effective with bipolar patients defined by the presence of hypomania than with unipolar patients; but found a relatively high recurrence rate for both groups (51% and 64% respectively). To highlight the confusion introduced by comorbidity, a third group consisting of cyclothymic patients showed a 69% rate of recurrence. Prien (1992) has reported that: “While lithium must be regarded as the treatment of choice for Bipolar II Disorder, its effectiveness is not nearly as well established as in Bipolar I Disorder” (Prien, 1992, p. 425).

One critical pharmacologic issue that clinical psychologists should remain aware of, involves a distinct precaution against the use of Tricyclic Antidepressants (TCA’s) in patients with an unknown or clinically unrecognized tendency toward mania and rapid cycling. Many researchers have cautioned against the use TCA’s because of the possibility of actually precipitating mania and rapid cycling. Researchers claim that: “The biggest problem in erroneously diagnosing a Bipolar II Disorder as a unipolar disorder is the risk of the patient receiving a TCA or other antidepressant capable of inducing rapid cycling or mania in susceptible patients” (Prien, 1992, p. 427).

Clinicians should note that carbamazipine or valproate (anticonvulsant agents) may prove to be useful alternatives to lithium for this population of Bipolar II patients who may be susceptible to induction of rapid-cycling mania by tricyclic medications (Fawcett, 1996). Because of the potentially serious consequences of an unexpected or poorly managed Manic Episode, psychologists must maintain exceptionally strong contact with both the patient and prescribing physician. Lithium therapy is the preferred treatment where there is suspicion or a latent or previously unrecognized Bipolar I Disorder or indicators of unusual risk of developing a Manic Episode (e g., rapid cycling, prior history). Risk factors for predicting increased risk of Manic Episodes include a family history of Bipolar Illness, young age at onset of depression, and a personal history of hypomania (APA, 1994).

As a general rule, the treatment of Bipolar Disorder is directed toward the dominant affective mode at the time of evaluation. Lithium is routinely used to alleviate severe mania, yet it is frequently only marginally effective with the depressive component of Bipolar Illness (Meyer & Deitsch, 1995). Again, when treatment involves pharmacologic interventions targeting the depressive features of Bipolar Illness, there is a clear caveat: “Administration of tricyclic antidepressants to an individual with bipolar disorder can induce a Manic Episode, or even rapid cycling” (p. 85).

DSM-IV Specifiers Defining Most Recent Episode

The reader is directed to the DSM-IV for a full description of diagnostic “Specifiers Describing Most Recent Episode” (p. 375-391). These specifiers are frequently quite elaborate and the DSM describes them best!. The “Rapid-Cycling” specifier deserves special emphasis and this is discussed below.

DSM-IV Criteria for Rapid-Cycling Specifier

The specifier: “With Rapid Cycling,” is to be noted if the course of illness shows at least four episodes of a mood disturbance in the previous 12 months that meet criteria for a Major Depressive, Manic, or Hypomanic Episode (confer DSM-IV). This specifier can be applied to both Bipolar I and Bipolar II Disorders. DSM-IV notes that such episodes are to be demarcated either by partial of full remission for at least 2 months, otherwise switch to an alternative diagnosis is warranted and this will depend on the present episode and its polarity (e.g., Major Depressive Episode to Manic Episode).

From an ethical perspective, this is a very important specifier. It is important that psychologists maintain awareness that research on bipolar disorder and suicidality indicates a heightened risk of suicide when individuals are noted for rapid-cycling (Chiles and Stroshal, 1995). Rapid cycling has also been found to be resistant to lithium treatment (Bech, 1992). Discussing clinical indications for rapid-cycling patients, Meyer and Deitsch (1996) note: “Cycles become more frequent with time in most bipolars. Persons who show “rapid cycling” are difficult to treat, as they respond poorly to treatment and present a higher suicide risk and more negative prognosis. Unlike standard bipolars, rapid cyclers are more likely to have a depressive episode as a first manifestation. It is more common in women and may be associated with hormonal disruptions (especially in women), hyperthyroidism, or neurological trauma” (p. 85).

Astute Clinicians Remain Vigilant

Astute clinicians are advised to remain vigilant to the fact that that Bipolar Illness is episodic and typically recurrent, with a tendency toward faster and more severe recurrences as a function of course of the illness (Post, 1992). Because of this, bipolar disorder presents unique difficulties in psychotherapeutic and pharmacological treatment. Post (1992) has emphasized: “It behooves the physician and clinician to develop a systematic charting approach to mapping the course of illness, as this not only provides the best predictor of likely recurrences in the future, but is also of inestimable value in assessing the efficacy of prior treatment and thus in formulating novel treatment strategies for the future” (p. 387). Detailed methods for plotting the illness have been developed. Interested readers may explore these techniques (cf. Post, 1992).

Psychotherapeutic and Clinical Managemen

As previously mentioned, this investigation has been motivated to inform my psychological perspective from a cognitive-behavioral standpoint. Cognitive therapists must concede that an appropriate level of patient stability is necessary to support the efficacy of interventions driven my cognitive theories of psychotherapy. When Bipolar patients are clearly stable and motivated to seek psychotherapeutic resources, cognitive approaches appear perfectly appropriate to support desired clinical outcomes. However, clinicians must carefully consider the viability of cognitive “insight oriented” interventions when patients present with more acute symptomology. Psychologists working from a cognitive-behavioral framework will likely find that the acute bipolar patient’s mental status precludes traditional cognitive-based intervention and treatment strategies.

Foundational Cognitive Psychotherapists have stated this quite succinctly: “The cognitive model should probably be restricted to the so called reactive depressions, that is, those that are brought about by socially relevant events. We would postulate that although the negative cognitive processing is similar for all types of depression, the factors precipitating various disorders vary widely” (Haaga & Beck, 1992, p. 512). While the patient remains acute or unstable, restabilization becomes the clear clinical aim. Frequently this entails mobilizing not only the patient’s cooperation, but the assistance of families, friends and health professionals alike. Since cognitive interventions are clearly useful for mood management, anxiety reduction, and self regulation in the general practice of psychotherapy, these approaches can be reserved for more stable times.

The psychologist’s primary role is to promote continued stability through available resources. Because of its effective mood-stabilizing properties, lithium therapy is considered the treatment of choice for both Bipolar I and II disorders. In stabilization efforts, psychologists might find themselves assisting clients in monitoring of lithium blood levels. Routinely, this is necessary to avoid toxicity and assure appropriate therapeutic blood levels and positive response to this medication. Furthermore, psychologists must maintain appropriate precautions and maintain keen clinical vision because of the suicidality involved in bipolar disorders. As noted previously, rapid-cycling conditions deserve strident clinical attention because of the suicide potential correlated with this diagnostic specifier.

It seems evident that behavioral techniques may be particularly helpful in managing the clinical course of Bipolar Disorders. Interventions from the Behavioral Tradition might include contingency management techniques, assertiveness training, self-monitoring and the broad range of skills-development approaches that can be found in the relevant literature.

Clinicians are advised that bipolar individuals tend to manifest a wide spectrum of complications in clinical management, including non-compliance with taking medication, complications introduced by rapid cycling, substance abuse, and problems with diminished insight and impulse control as a function of the illness itself. Bipolar patients are typically noted for patterns of poorly regulated behavior that tend to defeat clinical efforts toward stability. Insight may become progressively compromised, and decision making can become impoverished to the extent that significant others and health care agencies must provide a large margin of support.

Because of this, psychologists are well advised to encourage strong family participation in the treatment of Bipolar Disorders. The bipolar individual’s family may share in the decision-making process and should understand the potential benefits and risks of the treatment program, as well as the likely consequences of receiving no treatment. Prien, (1992) notes that: “The support of family members, their attitude toward the illness and their capacity to recognize and report signs of an emerging episode are critical contributions to the success of preventive treatment programmes” (p.422). Cognitive-Behaviorally oriented psychologists may assist families through offering various psychoeducational and psychotherapeutic resources. Family members can themselves can benefit greatly from resources availed them by cognitive and behavioral psychology. From “rational-thinking” (Ellis, 1962) and “schema deactivation” (Beck, 1976); to “behavior-exchange” (Jacobsen, 1995) and “contingency-management” (Skinner, 1966) such clinical approaches can bolster supports for bipolar patients and families alike. Cognitive-behavioral interventions that assist families in interpreting and responding to their loved one’s illness are well advised for clinicians involved in the treatment of bipolar disorder.

Genetic and Familial Considerations

Family studies, twin studies, and adoption studies all suggest that genetic factors are important in Bipolar Illness and genetic linkage studies have described associations between Bipolar Illness and genes localized in chromosomes X, 11, 18, and 21. However a specific mechanism of transmission has not been established conclusively (Rohland, et al, 1997). Clinicians should be aware the “No laboratory findings that are diagnostic of a Manic Episode have been identified” (APA, 1994, p. 330). However, laboratory research comparing manic subjects with controls, has found increased cortisol secretion, and an absence of dexamethasone, and polysomographic abnormalities. There is speculation that there may be abnormalities involving norepinephrine, serotioin, achetylcholine, dopamine, or gamma-aminobutyric acid neurotransmitter systems (APA, 1994).

Age of onset has proved significantly later in Bipolar I patients when compared to Bipolar II Disorder. Vieta, et al. (1997) found that the mean age of onset for Bipolar I was 31 years as compared to a 22 year old average age of onset for Bipolar II. These researchers argue that: “This finding could support the hypothesis that bipolar II disorder is a borderline illness between bipolar I and unipolar (Major) affective disorder, since the age of onset of bipolar II patients is intermediate between that for Bipolar I and unipolar disorder” (p. 100). The mean age of onset for Major Depressive Disorder is not specified in DSM-IV.

Bech, (1992) reported that there is some evidence from family studies for an increased prevalence of Bipolar II illness in relatives of Bipolar II patients, yet more recent research proved that such correlations to be insignificant (Vieta, et al., 1997). As mentioned previously, it has been demonstrated that Bipolar II Disorder tends to remain an enduring lifetime diagnosis with only 5% to 15% converting to Bipolar I Disorder because of the emergence of a formal Manic Episode (Vieta, et al, 1997). Noteworthy is the fact that: “There is no evidence that genetic vulnerability to rapid-cycling Bipolar Illness is different from the genetic vulnerability to bipolarity alone” (Nurunberger & Gershon, 1992, p. 134).

Racial-Ethnic and Gender Considerations

There have been no reports to date that support a differential incidence of bipolar disorders based on race or ethnicity (Rohland, Winokur, & Cook, 1997). However, clinicians are advised that cultural differences can affect the experience and communication of symptoms of both manic and depressive phases of such illness. Theorists indicate that: “In some cultures, depression may be experienced largely in somatic terms rather than subjective cognitive symptoms of sadness or guilt. Furthermore, cultures differ in their perception of the seriousness of certain emotions” (Rohland et al., 1997, p. 275).

Practitioners should be aware that there is a growing body of evidence that suggest that response to medications may be influenced by ethnicity. Several research studies, reviewed by Lin, Poland, & Lesser (1986) have suggested that Asian bipolar patients respond to lower lithium blood levels when compared to Caucasians. These authors report that cross-cultural considerations in the practice of psychopharmacology, suggest that ethnic variation in dosage requirements is most likely due to a complex interaction of cultural, environmental and genetic factors. These factors may include differential considerations of body weight and fat distribution, and differences in the enzyme systems that metabolize drugs may influence receptor mediated responses. Also, differences related to culturally related habits such diet and drug-alcohol use can also influence response to various medications. Presently there is a call for more research in this area.

Rohland et al. (1997) indicate that Bipolar I Disorder is equally common in men and women. This contrasts major depressive disorder which is more comment in women. It is interesting to note that gender, in patients with Bipolar Illness, appears to be related to the order of appearance of manic and major depressive episodes. Males are more likely to manifest mania as an initial episode, and females are more likely to present with a depressive episode. In a collaborative study of depression, the National Institute of Mental Health showed no difference in the number of manic or depressive episodes correlated with hospitalizations (Winokur et al., 1994). The age of onset of bipolar disorders shows no gender differences, yet psychologists should be aware that women that have their first episode of illness during a postpartum period following childbirth have an increased risk of developing subsequent episodes. Also, the premenstrual period may be associated with exacerbation of ongoing major depressive, manic, mixed or Hypomanic Episodes (Rohland et al., 1997).


Bipolar Illness is characterized by remissions and exacerbations, yet the majority of people with Bipolar I Disorder return to a full functional level between episodes. However, 20% to 30% of individuals with the disorder continue to display mood lability (typically depressive) or sociorelational and occupational difficulties between episodes. The lifetime prevalence of Bipolar I Disorder in community samples has varied from 0.4% to 1.6%., and it has been estimated that roughly 90% of individuals who have a single Manic Episode will have future episodes. Persons with Bipolar Illness may show only manias and no depressions, and it is also noteworthy that treatment, although effective in the resolution and prevention of symptoms of mania and depression, does not appear to alter the natural history of Bipolar Illness (Rohland, et al., 1997). Studies suggest that 5% to 15% of individuals presenting with formal hypomania as defined in Bipolar II Disorder will ultimately develop a Manic Episode, warranting a diagnostic change to Bipolar I Disorder (APA, 1994). Recent research results suggest that Bipolar II Disorder is less severe than Bipolar I with regard to symptom intensity and functional impairment, yet Bipolar II has been found to be more severe in regard to episode frequency ( Vieta, et al., 1997).

Astute student-practitioners of clinical psychology will attend closely to the aforementioned comorbidity issues and differential-diagnostic features when making clinical judgments as to the presence of Bipolar I and II Disorders. It is hoped that the above review illustrates the nature of the essential diagnostic features of Bipolar Illness—Hypomania and the Manic Episode. Such an understanding is foundational to discerning clinical perception, and such perception is necessary for the ethical practice of the profession.

Dr. Patrick J. Hart
Diagnosis and Treatment Options in Seattle

Dr. Patrick Hart