Bipolar Disorder Managment and Treatment

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BIPOLAR DISORDERS are heterogeneous disorders defined by the classic domains of euphoria and depression. Over the past decade, there has been an increase in the estimated lifetime prevalence of these disorders. Recent population-based epidemiology studies suggest that up to 2% to 4% of the general population may have a bipolar disorder. These estimates represent a rapid trajectory of increase compared to estimates a decade ago.

Bipolar I disorder affects both genders equally, while other bipolar disorders (e.g. bipolar II, cyclothymia) may have a female preponderance. Bipolar conditions affect people from all socio-economic strata, with no known ethnic groups more often affected. Interestingly, both academic and popular press surmise that bipolar disorders and artistic creativity may be associated, although this relationship has understandably been very difficult to study rigorously.

PERSPECTIVE

The median age-of-onset for bipolar disorder is late adolescence to early adulthood. Despite decades of research, the precise etiology and ideal neurobiological model of bipolar disorder continue to elude us. The absence of a reliable animal model for bipolar disorders has greatly limited preclinical investigations of this complicated condition. What has emerged from the extant research is evidence that bipolar disorders, like most major mental disorders, are multifactorial phenotypes and cannot be explained by linear causality. Results from family, twin and adoption studies converge and suggest that bipolar disorders are presaged by genetic factors. It has been hypothesized that a single gene is unlikely to account for bipolar disorder and a polygenic model may be more appropriate. Observations from several lines of research have highlighted the high levels of early life adversity (e.g. abuse, neglect), chaotic family environments and high levels of negative 'expressed emotion' (e.g. critical, hostile communication patterns) in the anamnesis of people with these disorders. It has been further noted that these foregoing negative experiences may deleteriously affect the course and outcome of bipolar disorders. These individuals more often report early onset of illness, medical and psychiatric comorbidities, a continuous and/or rapid cycling course of illness, and poor response to treatment.

 
TABLE 1 Bipolar Spectrum

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Mania and major depression Hypomania and major depression

Cyclothymia

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Antidepressant-induced hypomania

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Major depression with a family history

of bipolar disorder

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Unipolar mania

Position Emission Tomography (PET) investigations assessing the brain metabolic correlates of bipolar disorder suggest that the symptoms of this disorder are mechanistically related to abnormalities in discrete neural network systems within the brain. Preclinical models of depression have established that environmental stressors (e.g. psychosocial adversity) may have the capacity to progressively disrupt the operating characteristics of these neural network systems, which may predispose and predict an adverse trajectory of illness. This may be due to abnormalities in cortisol secretion or other abnormal stress response systems. Delineation of a more comprehensive and integrated model of the pathophysiology of bipolar disorder will be buttressed in coming years by further developments in neuroimaging, genomics and molecular and cellular biology.

 
FIGURE 1 Recognizing Hypomania and Mania

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- Decreased need for sleep

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- Increased energy and/or motor agitation

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- Racing thoughts

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- Irritability often more common than classic euphoria or elation

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HYPOMANIA

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- Mild, less severe

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- Little to mild dysfunction

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- Little to mild lapses of judgment

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- Commonly responds to outpatient

management

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- Sleep regulation and/or benzodia-

zepines can sometimes terminate

episode

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MANIA

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- Severe

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- Severe dysfunction

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- Major lapses of judgment

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- Psychotic symptoms

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- Often requires inpatient treatment

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- Need for acute mood stabilizer and/or

neuroleptic treatment

FP Review Perspective

Diagnosing bipolar disorder requires extra awareness and suspicion. If you don't think of it, you can't diagnose it. Family physicians are increasingly skilled at diagnosing unipolar depression, but bipolar disorder fluctuates, so the longitudinal bipolar pattern may not be apparent at any single visit.

DIAGNOSIS

The Diagnostic Statistical Manual, fourth edition (DSM-IV) enumerates four bipolar subtypes. Integral to the bipolar disorders are biphasic mood instability that is distressing and/or impairing to the individual in any major sphere of functioning. To carefully differentiate the phenotypes of bipolar disorder, the clinician must be familiar with definitions of mania, hypomania and mixed states.

Mania and hypomania have similar symptom profiles. They are distinguished on the grounds of the severity and duration of mood shifts. Manic episodes last a week or longer, while hypomania lasts four days or longer. Manias are further characterized by more severe presentations, such as the presence of psychosis, the need for hospitalization, or severe psychosocial impairment (see Figure 1).

Mixed states are a common complex and highly disquieting experience for patients. Mixed states are defined as a combination of both manic and depressive symptoms. Patients often appear highly agitated and dysphoric.

Bipolar I disorder is defined as recurrent episodes of mania and depression. For people with bipolar II disorder, the elated episodes are delimited to hypomania. Cyclothymia is often difficult to diagnose or misdiagnosed as tempestuous personality or other psychiatric morbidity. It is diagnosed longitudinally in a person who repeatedly experiences episodes of subthreshold depressive and hypomania symptoms; at no point, however, do these patients experience a full syndromal mania or depression (see Figure 2, page 3).

The longitudinal stability of bipolar disorder is well established; that is, a small percentage of people with bipolar II convert to bipolar I. The stability of cyclothymia is less well established, but it has been suggested that a substantial minority of people with cyclothymia may later manifest a typical bipolar I/II presentation. This is analogous to many patients with dysthymia disorder later manifesting a full-blown major depression.

The phenotype variants of bipolar disorder are often described conceptually along a 'bipolar spectrum' (see Table 1), but the official nosology of the DSM-IV delimits official recognition to bipolar I/II disorder. The notion of a bipolar spectrum, although heuristically useful, awaits empirical confirmation. Rapid cycling bipolar disorder, is a longitudinal specifier in bipolar disorder denoting a pattern of at least four or more affective episodes in the previous 12 months. It affects an estimated 15% to 20% of people with bipolar disorder (both bipolar I and II, although individuals with bipolar II may be more prone to rapid cycling). Rapid cycling is more often observed in females, and in some cases may be related to abnormalities of the hypothalamic-pituitary-thyroid axis, antidepressant exposure or life events such as pregnancy. For some patients, rapid cycling may be a phase of the disorder; for others, it could be an index presentation (particularly adolescent onset cases) or a continuous course of the illness, which unfortunately is very often recalcitrant to treatment.

Patient-centred surveys in bipolar disorder have repeatedly noted a long delay from the onset of symptoms to the correct establishment of the bipolar diagnosis (10 to 15 years) (visit Web site www.NDMDA.org). Up to two-thirds of patients with bipolar disorder are misdiagnosed (typically as depression and anxiety), despite high utilization of both primary and specialty health-care services (visits with three to four mental health-care providers), resulting in an unnecessary delay in correct treatment. Since the majority of excess unnatural death in bipolar illness (i.e. suicide) occurs in the first decade of the illness, misdiagnosis means that an important window of therapeutic opportunity is missed. Moreover, repeated episodes of the illness due to insufficient treatment may unnecessarily increase the risk of recurrence and progression of the illness.

Most individuals with bipolar disorder have comorbidity with other major psychiatric and medical conditions currently or sometime in their life. Comorbidity may also precede the onset of overt bipolar disorder by many years. For example, a history of externalizing behaviour disorders (Conduct Disorder, Attention Deficit Hyperactivity Disorder, Oppositional Defiant Disorder) or anxiety disorder may be present in childhood or adolescence. In aggregate, anxiety disorders and substance-use disorders are the most common psychiatric comorbidity. A myriad of medical disorders, including obesity and diabetes, are also over-represented in people with bipolar disorder. Moreover, these patients often smoke. Extensive research is underway to delineate the intrinsic variables that may account for the excess cardiovascular death in people with mood disorders.

The onset-age for bipolar disorder may affect its index presentation. Typical adult onset bipolar disorder often begins as depression and anxiety followed later by more typical manic symptoms. Geriatric onset mania should be carefully investigated for the presence of medical comorbidity and/or iatrogenic mania (i.e. medication-induced). Adolescent-onset bipolar disorder is frequently complicated by distressing behavioural pathology (such as substance abuse and personality disorder) and often highly irritable rapid cycling/mixed presentations, which obscure the underlying bipolar illness and represent powerful non-response predictions. A constellation of psychiatric disorders, characterized by impulsivity and affective liability should alert the clinician to the possibility of an underlying cryptic bipolar disorder (see Figure 4, page 4).

The pharmacological induction of mania is not a uncommon initial presentation of bipolar disorder. Hypomania occurring only with antidepressant exposure may not permit a diagnosis of bipolar disorder. If a hypomanic episode is due to an antidepressant and has not occurred de novo, many patients will require prophylactic mood stabilizer therapy and/or go on to develop spontaneous hypomania (i.e. have a primary diagnosis of bipolar disorder), inviting the need for specific antibipolar therapy.

FP Review Diagnosis

Patients often present during a depressive phase with classic unipolar depression symptoms, symptoms disguised as multiple somatic complaints, unexplained physical symptoms or increased visits. The most common well-intentioned treatment error is using unopposed antidepressants. Antidepressants, particularly the older tricyclics, can push patients from being depressed to becoming manic.

Red flags suggesting bipolar versus unipolar depression include a family history of bipolar disorder, episodes of mood elevation and history of brief psychotic episodes. There is no sure-fire way to predict whether a presenting depression is part of a bipolar disorder; only over time may bipolar declare itself.

Patients less frequently present with mania or hypomania as they often feel 'great' in this phase and rarely seek medical attention. Instead, family members may complain of the individual's elevated moods or out-of-character behaviours.

Emergency department physicians see patients at their most disruptive manic phase. Intrusive, impulsive, loud and erratic behaviours can become concerning. Manic patients often engage in risk-taking behaviours. Increased spending, impulsive financial decisions, reckless driving, extreme sports, substance abuse and unsafe sex are common. Sequelae may bring patients in to family physicians to request STD testing, counselling regarding disrupted family or work relationships, disability forms, or post-injury suture or cast removal. Skilled clinicians look beyond the immediate concern and inquire about mania.

TREATMENT

The therapeutic objectives in treating patients with bipolar disorder are to suppress acute mania and acute depression and to offer prophylaxis. The available treatments for bipolar disorder vary in their spectrum of effectiveness and tolerability across these foregoing objectives (see Figure 5). No single psychopharmaceutical agent is capable of accomplishing all of these objectives in most patients. This therapeutic deficiency has invited the need for combination pharmacological regimens in most treated bipolar patients (see Figures 6 and 7, page 5). Once considered anathema, the rational combination of medications holds promise to both extend and synergize the spectrum of effectiveness of pharmacological treatment. This potential therapeutic asset is tempered by the well-known liabilities of combining agents together: increased cost, decreased compliance and drug interactions.

Treatment guidelines and regulatory agencies generally recognize four classes of neurotherapeutic agents with established or supposed efficacy in one or more of the symptomatic objectives in bipolar disorder: lithium, anticonvulsants, antipsychotics and antidepressants (see Table 3).

Lithium, isolated in 1817, remains the paradigmatic mood stabilizer. Lithium's efficacy in the various phases of this disorder is unequivocally established. Moreover, there are emerging provocative data that lithium may also bestow an antisuicide effect independent of its ability to abrogate psychopathology. Although we cannot exclude the possibility of a selection bias (i.e. people with lower suicide potential are more likely to adhere to therapy), the public health importance of this outcome measure is obvious. Lithium, however, is not a panacea. Naturalistic studies repeatedly have noted lower response rates (presumably secondary to enrolment of patients with mixed states, rapid cycling, comorbid conditions and other lithium non-response predictors). Predictors of acute nonresponse to lithium include:

- dysphoric mania

- rapid cycling

- comorbid medical disorder

- polarity sequence

- substance abuse

- negative family history

- frequent prior episodes.

Although conventional antipsychotics have been frequently employed in the treatment of bipolar mania (independent of psychosis), these agents are without proven anti-depressant or prophylactic efficacy. Moreover, patients often feel dysphoric on these agents and face significant risks for acute extrapyramidal syndromes (acute dystonia, akathisia) and tardive dyskinesia. The available first-line novel antipsychotics (NAPs) (i.e., risperidone, olanzapine and quetiapine) are pharmacologically and structurally heterogeneous agents. This similarity bestows enhanced depth and breadth of efficacy across various domains of psychopathology. Their disparate in vitro pharmacological profiles perhaps presage the differences between them in overall tolerability.

Although categorized as antipsychotic, some NAPs appear to offer a direct antidepressant effect in individuals with schizophrenia, bipolar disorder and major depression. Over the past several years, psychiatrists have increasingly prescribed these agents as adjunctive and/or alternative strategies for patients with mood disorders. This prescribing pattern is supported by the Canadian Psychological Association's guidelines, which include NAPs as a proven option in treating refractory depression (visit Web site: www.canmat.org).

Several investigators have noted that adjunctive risperidone and olanzapine are effective in the treatment of adult bipolar mania (see Figures 8 and 9, page 5). Neither risperidone nor olanzapine have been approved in Canada for treatement of bipolar disorder or in children. A single recent study has noted the enhanced efficacy of adjunctive quetiapine over mood stabilizer monotherapy in the treatment of adolescent bipolar mania. The symptomatic benefit offered by these NAPs exceeds the therapeutic effects of a mood stabilizer offered as monotherapy. Importantly, the antimanic efficacy observed was independent of the presence of psychosis. Both treatments were generally well tolerated. This is perhaps related to the dose of medication employed in bipolar disorder (i.e., risperidone 2 mg to 4 mg, olanzapine 10 mg to 15 mg). There was no evidence of significant extrapyramidal syndromes in either group, and dropouts due to adverse events were relatively few. The most common adverse events with risperidone were insomnia and headache, while for olanzapine they were somnolence, appetite stimulation and weight gain.

The optimal duration of adjunctive NAP therapy in bipolar disorder is not empirically established. Some guidelines and bipolar experts recommend dismantling the adjunctive NAP after resolution of the acute episode, or approximately one to two months after. In clinical practice, however, this is often not possible due to a myriad of factors, such as insufficient acute response on mood stabilizer monotherapy and immediate symptom breakthrough after NAP discontinuation. Several uncontrolled reports have noted that most patients with bipolar disorder receiving an antipsychotic remain on the agent for at least one year of followup. Available evidence suggests that when patients are maintained on NAP therapy for a mean duration of six to seven months, further accrual of symptomatic benefit is observed (see Figure 10, page 5).

 
FIGURE 4 Psychiatric presentations that might suggest an underlyingbipolar disorder

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- Substance abuse/dependence

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- Personality disorder (e.g. borderline)

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- Seasonal affective disorder

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- Post-partum psychosis

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- Mood disorder onset prior to age 25

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- Psychotic symptoms in adolescence

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- Depression in persons with loaded family for bipolar disorder

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- Pharmacologically induced hypomania

 
FIGURE 5 What is a mood stabilizer?

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AN EFFECTIVE MOOD STABILIZER

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- Has >1 primary therapeutic objective

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- efficacy in acute mania, acute depression

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- efficacy in prophylactic use

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- Can be administered during the acute,

continuation or maintenance phase

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- does not worsen an acute episode

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- does not increase affective switch

 
TABLE 3 Available Evidence for Treatments of Bipolar Disorder

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Lithium + + +

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Divalproex + +/- +/-

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Carbamazepine + +/- +/-

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Conventional Antipsychotics + -/? (in the absence of psychosis) -

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Atypical Antipsychotics

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Risperidone + +/- +/-

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Olanzapine + +/- +

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Quetiapine + +/- +/-

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Third-generation Anticonvulsants

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Lamotrigine - + + (prophylaxis of depression)

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Topiramate +/- +/- ?

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Gabapentin - +/- ?

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Antidepressants - (worsen mania) + ? (may induce rapid cycling)

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Legend:

+ = Double-Blind, placebo controlled trial (DBPT) evidence

+/- = Partial controlled/open-data

- = Inefficacy in replicated (DBPT)

? = Not adequately studied

 
FIGURE 14 Ten Leading Causes of Disability: Adjusted life years in theworld in 1990 for persons aged 15 to 44 years
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Promising data are beginning to emerge about the effectiveness of NAPs in the depressive phase of the illness. A recent study assessing the safety and efficacy of both open risperidone and olanzapine as adjunctive treatment in bipolar depression (bipolar I/II) concluded that both agents offered pronounced and sustained antidepressant effect (in the absence of psychosis). Both treatments were generally well tolerated, with no evidence of extrapyramidal syndromes, tardive dyskinesia or dropouts due to side-effects. There was, however, significant weight gain in both groups, with significant between-group differences.

A paradigm shift has occurred in the treatment of bipolar disorder. This illness is now seen as a chronic disorder that requires long-term treatment for most affected individuals. Long-term treatment raises the issue of long-term tolerability in patient psychoeducation and maintenance. A spectrum of weight gain exists with these agents (see Figure 11, page 5). Excess weight may increase predisposed patients' risks for obesity-related morbidity such as dyslipidemia and dysglycemia. Weight gain and disrupted glucose regulation may be further impacted by other medications frequently prescribed to bipolar patients (e.g. lithium, divalproex; see Figure 3, page 3). Patients treated with NAPs should be monitored for changes in weight, lipids and glucose.

Antiepileptic drugs (AEDs) are categorized as older generation (divalproex and carbamazepine) and new generation (lamotrigine, gabapentin, topiramate). Both divalproex and carbamazepine are effective in acute mania, with a paucity of evidence in the other two phases of the illness. They are often effective alone or in combination for many patients with non-response predictors (e.g. mixed states). The use of these medications is limited, however, by tolerability issues (e.g. weight gain, somnolence), the need for plasma level and haematological monitoring, and drug interactions.

Lamotrigine is established as an effective agent for acute bipolar depression and prophylaxis against the depressive phase of the disorder. This agent is similar to the other newer generation anti-epileptic drugs and does not require either plasma level or haematological monitoring. Lamotrigine is generally well tolerated with no weight gain or CNS impairment. However, its use is limited by the induction of a benign rash, which necessitates discontinuation in up to 10% of treated patients. In 0.1% of adult patients, the rash may progress to Stevens Johnson's syndrome. The risk of this serious cutaneous syndrome is higher in preadolescent subjects and when lamotrigine is combined with other agents that interfere with lamotrigine metabolism (i.e. divalproex).

Gabapentin has not been definitively established as a reliable treatment for any phase of bipolar disorder but has been effective in some anxiety and pain syndromes, which frequently accompany bipolar disorder.

Topiramate is currently under active investigation as a candidate treatment for bipolar disorder. In a recent controlled study comparing topiramate to an antidepressant in the treatment of mild bipolar depression, topiramate was found to be effective and well tolerated. Patients in this study lost a mean of 5.8 kg across eight weeks of treatment (see Figure 12).

The contemporary treatment of bipolar depression has followed pari passu the treatment of unipolar disorder. Somewhat remarkably, a dearth of evidence supports antidepressants as reliably effective in bipolar depression. Moreover, antidepressants may induce manic episodes or rapid cycling in predisposed individuals. Tricyclic antidepressants are generally avoided due to higher switch liability, while long half-life SSRIs such as fluoxetine are avoided because of their unfavourable elimination half-life. It is recommended that antidepressant use in bipolar patients be discontinued within two to three months of achieving remission. Some patients with this disorder will require longerterm antidepressant therapy, however.

FP Review Treatment

Multiple medications for bipolar disorder are becoming the norm. But getting patients to comply with psychiatric medications can be challenging. Patients may sense the family physician's discomfort or lack of conviction about bipolar treatment, resulting in decreased compliance and increased illness episodes.

It can be beneficial to ask the consulting psychiatrist to list a series of treatment steps to which you can refer, depending on the phase of illness.

A practical tool for managing bipolar disorder is the seizure disorder model. This validates bipolar as a 'real medical illness that's not all in your head.' It provides patients and family physicians with a precedent for using medications and prophylaxis. Keeping a life chart mood record alongside the cumulative patient profile is also helpful (see Figure 15).

Treating bipolar disorder requires a shift in thinking to classify it as a chronic, recurrent illness requiring long-term treatment, just like diabetes or hypertension. The foundation of medication management is using a mood stabilizer, such as lithium or valproic acid. Lithium has a narrow therapeutic window and requires monitoring of blood levels and kidney and thyroid functions. Valproate requires monitoring blood levels and hepatic enzymes.

A significant development is the use of novel antipsychotics (NAPs) as a mainstay in the treatment of bipolar disorder. Risperidone, olanzapine and quetiapine possess significant advantages over traditional antipsychotics with broader efficacy and less likelihood of extrapyramidal symptoms and tardive dyskinesia.

NAPs have important metabolic effects. Risperidone has low likelihood of extrapyramidal symptoms but may elevate prolactin levels, with potential amenorrhea. Olanzapine also has low risk of extrapyramidal symptoms but can cause drowsiness, appetite increase and weight gain. Monitoring weight, lipids and glucose take on extra importance when patients are treated with olanzapine, as most psychiatrists defer this monitoring to the family physician.

Lamotrigine and topiramate are promising agents that are easier to use than older anticonvulsants with no need for lab monitoring. Topiramate has the popular side-effect of weight loss. Further research and experience will define the roles of these agents for family physicians.

PROGNOSIS

Unfortunately, bipolar disorder exhibits an episodic course of illness, with a recurrence in more than 90% of patients. It appears that in some predisposed individuals, episodes may further promote subsequent episodes, hinting at a progressive neurobiological process (see Figure 13). Most patients who do not experience a recurrence manifest significant threshold affective symptoms, which powerfully and prospectively predict psychosocial impairment. Many patients with this illness report persistent cognitive and psychosocial deficits. The suicide rate in the bipolar population is approximately 10% to 20% higher than the general population. According to the World Health Organization, bipolar disorder is currently the sixth leading cause of disability and premature death among people 18 to 44 years of age (see Figure 14).

Novel treatments for this complicated illness are beginning to emerge. Empirically established psychosocial interventions, which aim to proceed psychoeducation, compliance enhancement and coping skills, are under active investigation.

Although medications are sine qua non in the continuation management of this disorder, optimal treatment often requires an admixture of both medications and psychosocial interventions.

RESOURCES

[Symbol Not Transcribed] [filled square] NATIONAL DEPRESSIVE AND MANIC-DEPRESSIVE ASSOCIATION:

www.ndmda.org

[Symbol Not Transcribed] [filled square] CANADIAN PSYCHOLOGICAL ASSOCIATION:

www.cpa.ca

[Symbol Not Transcribed] [filled square] CANADIAN NETWORK FOR MOOD AND ANXIETY TREATMENTS:

www.CANMAT.com

[Symbol Not Transcribed] [filled square] NATIONAL INSTITUTE OF MENTAL HEALTH:

www.nimh.nih.gov

[Symbol Not Transcribed] [filled square] BIPOLAR DISORDERS PORTAL:

www.pendulum.org

[Symbol Not Transcribed] [filled square] BIPOLAR DISORDER: A GUIDE FOR PATIENTS AND FAMILIES

Mondimore MF. M.D. Johns Hopkins Press: 1999.

[Symbol Not Transcribed] [filled square] THE DEPRESSION WORKSHOP: A GUIDE FOR LIVING WITH DEPRESSION AND MANIC DEPRESSION

Copeland ME. New Harbinger Publications: 1992.

[Graph Not Transcribed]

1 Case Study: Presentation

A 31-YEAR-OLD SINGLE MALE ENGINEER WHO LIVES ALONE WAS HOSPITALIZED TWO YEARS AGO FOR AN INDEX MANIC EPISODE, AND HE IS CURRENTLY ON DIVALPROEX.

He has been compliant and tolerating medications, although he continues to manifest a mixture of affective and anxiety symptoms. Specifically he describes being depressed, anxious and frustrated, along with having increased energy. He is described as argumentative and garrulous at work. He has been able to keep working well, and his family has expressed no concern about his behaviour, safety or overall conduct. You enquire further and learn that he does not have any psychotic symptoms. You assess that he is not certifiably capable of treatment decisions and rule out any comorbidity such as surreptitious substance use.

TREATMENT

You choose to treat this patient with risperidone 2 mg. After two weeks he is 50% better but still has residual symptoms, so you increase the risperidone to 3 mg. The patient is now in remission.

You have evaluated him at baseline, evaluated thyroid (TSH), divalproex, LFT levels, lipids and fasting glucose. You monitor him with the NIMH-Life Chart Method for at least six months, then reevaluate.

2 Case Study: Presentation

 

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1. Has there ever been a period of time when you were not your

usual self and...

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...you felt so good or so hyper that other people thought you

were not your normal self or you were so hyper that you got into

trouble?

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...you were so irritable that you shouted at people or started

fights or arguments?

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...you felt much more self-confident than usual?

----------------------------------------------------------------------

...you got much less sleep than usual and found you didn't

really miss it?

----------------------------------------------------------------------

...you were much more talkative or spoke faster than usual?

----------------------------------------------------------------------

...thoughts raced through your head or you couldn't slow your

mind down?

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...you were so easily distracted by things around you that you

had trouble concentrating or staying on track?

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...you had much more energy than usual?

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...you were much more active or did many more things than

usual?

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...you were much more social or outgoing than usual, for exam-

ple, you telephoned friends in the middle of the night?

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...you were much more interested in sex than usual?

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...you did things that were unusual for you or that other

people might have thought were excessive, foolish, or risky?

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...spending money got you or your family into trouble?

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2. If you checked YES to more than one of the above, have several of these ever

happened during the same period of time? Please circle one response only.

YES NO

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3. How much of a problem did any of these cause you, such as being unable

to work; having family, money or legal troubles; getting into arguments or

fights? Please circle one response only.

No problem Minor problem Moderate problem Serious problem

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A 26-YEAR-OLD MARRIED MOTHER OF A TWO-YEAR-OLD DAUGHTER WHO IS EMPLOYED FULL-TIME IN AN ADMINISTRATIVE POSITION WITH THE FEDERAL GOVERNMENT.

The patient has been enrolled in your practice for the last six years. She visits your office at least biweekly, with a similar frequency of phone calls which are usually for non-specific somatic complaints, stress and difficulty coping. Her explanatory model for her difficulties is that her husband is frequently distant and aloof. She describes the relationship as 'rocky,' yet curiously she brightens up when speaking about her husband and spontaneously identifies him as the primary support in her life.

HISTORY

While at undergraduate university, the patient overdosed on a small number of acetaminophen (less than 10) after breaking up with her boyfriend of one month.

After the birth of her daughter, she experienced post-partum depression and began a course of antidepressants. However, she discontinued the medication after two weeks because they made her feel more anxious and irritable.

Last year, the patient had a difficult time coping at work and was irritable and anxious, although she denied feeling depressed. She again considered an antidepressant but discontinued, complaining of worsening irritability, racing thoughts and anxiety.

Six months ago she presented again with an exacerbation of anxiety, irritability and yelling outbursts at her partner and decreased need for sleep. Her working diagnosis has been 'mixed anxiety and depression'. Over the past month, in the absence of any triggers she is complaining of a confluence of both typical and atypical depressed symptoms, anxiety, increased appetite and prominent fatigue.

DIAGNOSIS

The diagnostic possibilities for this patient include major depressive disorder, bipolar disorder, anxiety disorder, substance abuse, personality disorder/relationship difficulties, and medical disorder (e.g. thyroid).

Approximately 10% of women have postpartum depression, 50% have post-partum blues, and 0.1% have post-partum psychosis. To diagnose bipolar II disorder, it is often helpful to have third-party information and family history. The patient needs to endorse periods of hypomania and major depression.

The variables that increase the likelihood of bipolar disorder are early-age onset, mood, high recurrences, seasonal pattern, pharmacologically induced hypomanias, postpartum onset, hyperinsomnia, psychotic symptoms in a depressed person and positive family history.

A recently validated screening instrument (the Mood Disorders Questionnaire, see left) has shown to reliably diagnose bipolar disorder in mood disorder subjects.

TREATMENT

After diagnosing bipolar II disorder, you initiate divalproex. The patient is not pregnant, so you run CBC and liver function tests. If she is stable, you will monitor her at least two times per year. Anti-depressants should be avoided if she has an episode, as you don't want to promote further rapid cycling of the illness.

Despite decades of research, the precise etiology and ideal neurobiological model of bipolar disorder continue to elude us. The absence of a reliable animal model for bipolar disorders has greatly limited preclinical investigations of this complicated condition. What has emerged from the extant research is evidence that bipolar disorders, like most major mental disorders, are multifactorial phenotypes and cannot be explained by linear casuality.

Aparadigm shift has occurred in the treatment of bipolar disorder. This illness is now seen as a chronic disorder that requires long-term treatment for most affected individuals.

Healing Depression & Bipolar Disorder Without Drugs features Gracelyn Guyol’s own story and those of thirteen other people around the country who have cured their depression and bipolar disorder using only natural therapies. In-depth research and the expertise of alternative health-care professionals are included in this landmark guide for patients and caregivers seeking responsible, safe alternatives to psychiatric drugs.