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Home: Articles: Bipolar: The Family Psychoeducational Approach

The Family Psychoeducational Approach

Rationale for a Multigenerational Treatment Modality for the Major Affective Disorders

Demitri F. Papalos

Seymour Kety's classical study (Kety et al., 1968), which followed parents and their adopted and biological offspring in Denmark, provided evidence that schizophrenia has a hereditary component. He also provided a methodology that has since been used to study other psychiatric disorders, including manic-depressive illness. Twenty years ago, the idea of a genetic influence on complex human behavior was anathema to many, and the findings from Kety's studies were met with great resistance, not only from a large segment of the public, but from many behavioral scientists and psychiatrists who maintained that such behavioral disorders must be due primarily to environmental factors. The acceptance of genetics as an important factor in mental illness has come slowly. In retrospect, it is not difficult to ask how anyone could have doubted the mounting evidence. Yet, while the implications of the emerging genetic data largely substantiate the importance of a genetically transmitted vulnerability for mood disorders and schizophrenia, they also point to the importance of environmental factors.

Major affective disorders are familial illnesses. The biological relatives of both unipolar and bipolar patients are at far greater risk than the general population for developing affective illness. Familial is, of course, not synonymous with genetic, but several lines of evidence converge on attributing a major portion of this increased familial incidence to genetic factors (Bertelsen, Harvald, & Hauge, 1977; Mendlewicz & Rainer, 1977). The similar rates of mood disorders in every race, culture, and geographic location has bolstered the idea that these conditions have a genetic basis (Boyd & Weissman, 1981). Over the past half-century, numerous twin adoptions, and family studies all suggested that genetic factors were important in the etiology of mood disorders. Twin studies support the general case for a genetic factor but fail to tease apart the interactions between heredity and environment (Bertelson et al., 1977). Although adoption studies attempt more clearly to separate the influence of nature versus nurture and again attest to a genetic factor, they also indicate that the disorder is not wholly genetic (Mendlewicz & Rainer, 1977). Approximately a third of identical twins reared apart are not concordant for the disorder, suggesting that environmental factors also interact in some way with the genetic trait.

The most compelling evidence for genetic influence on a particular illness, short of finding the mutant allele, is to establish linkage to a known genetic marker-two traits segregating together in families because the genes that determine the two traits are located near one another on a chromosome. Unfortunately, as will be described in this book, obtaining evidence for linkage to known markers is handicapped by the complexities of psychiatric disorders. The simple Mendelian models-autosomal dominant, X-linked dominant, and recessive- must be modified to account for nongenetic factors. Confounding factors, such as age-related penetrance, variable presentations of illness within the same families, and lack of consensus diagnoses, have thus far precluded the development of a working genetic model (Faraone, Kreman, & Tsuang, 1990) (also see Chapters 2 and 5).

THE GENERATIONAL IMPACT OF MOOD DISORDERS

When a parent is affected with a mood disorder, there is strong evidence of a markedly increased risk of childhood disorders in their offspring (Beardslee, Bemporad, Keller, & Klerman, 1983; Beardslee, Keller, & Klerman, 1985). Children who have at least one parent with an affective disorder have a significantly increased rate of depression and other psychopathology when compared with children whose parents have no history of affective illness (Akiskal et al., 1985; Weissman et al., 1987; Weissman, Warner, Wickramaratne, & Prusoff, 1988). In a study of the offspring of parents with manic- depressive illness which used direct interviews with children, Decina and colleagues (1983) found an increased frequency of major and minor affective disorders in children of bipolar parents as compared with normal controls. Hammen, Burge, Burney, and Adrian (1990) reported on offspring from four groups of mothers, including unipolar, bipolar, medically ill, and normal mothers. This study found that the children in the two affective disorder parent groups had very high rates of diagnoses (82% unipolar, 72% bipolar). Offspring of the medical group had lower (43%) but nonetheless moderate rates compared with children in the normal group (22%). It is apparent from offspring research, both cross-sectional and longitudinal, that when a parent is ill, the children are likely to also manifest some psychiatric disorder. Thus mood disorders are not illnesses that affect just individuals; they are also familial illnesses that may have lifelong consequences across multiple generations.

Many family studies not only have found higher rates of bipolar disorder among relatives of bipolar probands, but also increased rates of major depression and other forms of affective illness (Perris, 1966; Tsuang & Faraone, 1990). Wender et al. (1986), investigating the contribution of genetic and environmental factors to the etiology of mood disorders, found an eight-fold increase in unipolar depression and a 15-fold increase in suicide among the biological relatives of index cases with unipolar depression. This study demonstrated a significant genetic contribution to unipolar depression and suicide. Studies have shown that more than 25% of patients with unipolar affective disorder have a parent or first-degree relative with an affective disorder. Taken together, these findings are compelling justification for clinical interventions that undertake to evaluate and treat the family.

While the evidence for a genetic contribution to the etiology of these disorders is beyond dispute, none of the studies indicates that genetic effects account for all the variation between ill and not ill individuals. Indeed, when viewed objectively, the genetic data also support substantial effects of environmental influences on the development of illness. Because of the increased risk in these families, the genetic vulnerability to develop affective illness is compounded by loss during childhood through parental illness, suicide, separation, divorce, or more subtle forms of emotional deprivation (Davenport, Adland, Gold, & Goodwin, 1979).

Studies that have examined the effects on children raised by affectively ill parents have found that deficits in maternal parenting increase the offspring's risk of developing impairments in mood regulation and social relations, as well as for other psychiatric conditions (Davenport, Zahn-Waxler, Adland, & Mayfield, 1983; Zahn-Waxler, Cummings, & McKnew, 1984; Hammen et al., 1987a,b). Kochanska and colleagues (1987) compared normal, unipolar, and bipolar depressed mothers to determine whether depressive cognitive schemas extend to the perception of one's own child. Compared with well mothers, women from the depressed groups were less satisfied with their children's social and emotional development, experienced more helplessness regarding their offspring, and were more likely to feel that outcomes of their child's development would be determined by uncontrollable factors. Hammen et al., (1987b), in one of the few high- risk studies to investigate the impact of the variable of chronic stress in association with maternal depression, found that chronic family stress and current maternal depressive symptoms were more predictive of children's behavioral dysfunction than was a history of maternal affective illness.

Recent findings from an examination of data derived from the Amish Study further support the role of nongenetic maternal influences on the development of mood disorders. Carter and colleagues (1992) found that the offspring of affectively ill mothers and affectively ill fathers were at similar high risk when the parental psychiatric disorder was severe, for example, bipolar I disorder. However, when the parental affective illness was less severe, the offspring of affected mothers were at greater risk for illness than the offspring of affected fathers. Since there is no difference in the rate of affective illness among all relatives of male and female probands in the Amish community, they conclude that the family environment influences the expression of the underlying genetic vulnerability.

In recent decades, there has been a progressive increase in lifetime rates of major depression in the general population (Klerman et al., 1985; Gershon et al., 1985, 1987b). The increase is especially marked in the late teen and early adult years. These newly reported findings from epidemiologic studies of cohorts born after 1940 have rather ominous public-health implications. It is anticipated that as the younger cohorts age in the coming decades, a lifetime hazard of a broad spectrum of affective disorders will be observed that is greatly in excess of that observed in the previous generations. These studies also identify a population at greatly increased risk: the families of patients with affective disorders (Klerman et al., 1985).

Gershon and colleagues (1987b) suggested that one explanation for their finding of increased risk to later generations could be an increase in affective disorders in U.S. metropolitan areas that is due to non- genetic factors. One possible explanation for an earlier age of onset of affective disorder would be exposure at an early age (during childhood) to a parent who is experiencing affective illness, and consequently altering the dynamics of the family rearing situation. Stancer and colleagues (1987) examined this possibility in a study that compared the morbidity risk for affective disorder in relatives of probands who had bipolar disorder or major depression. Their review of the relatives of younger-onset patients revealed that 28% of the 128 siblings and 28% of the 40 offspring had developed affective disorder. On the other hand, 26% of 90 siblings and only 19% of 59 offspring of probands had later onset developed affective disorder. Therefore, the effect of age of onset of the probands is demonstrated-the increase in risk to relatives of younger-onset patients is for offspring, not siblings. An earlier age of onset of affective illness (in general, before the age of 40) increases the risk for all types of mood disorders among relatives, regardless of sex of proband or relative (Rice et al., 1987; Tsuang & Faraone, 1990). Additionally, there appears to be a particularly strong hereditary component in adolescent-onset affective illness. For example, patients with adolescent-onset bipolar disorders are associated with a rate of mood disorders or any psychiatric illness in first-degree relatives of 33% and 58%, respectively (Strober & Carlson, 1982). In this study, adolescent-onset unipolar depression carried a lesser but likewise significant risk to first-degree relatives, 25% and 47% respectively. As many of the proband's siblings were quite young, and had not passed through the period of risk for illness, these rates of risk are likely to increase significantl y over time.

GENETIC FINDINGS-IMPLICATIONS FOR CLINICAL ASSESSMENT AND TREATMENT

The findings that inheritance patterns suggestive of greater genetic deviance (i.e., loaded, multigenerational, and bipolar 1-positive pedigrees) are predictive of bipolar outcome lend support to the idea that much can be foretold about the diagnosis and subsequent course of illness in juveniles from the degree of affective morbidity in their family pedigree. These findings have implications for researchers interested in the ascertainment of pedigrees for linkage studies, as well as for clinical diagnosis and for the development of preventive treatment approaches.

Increasingly, retrospective diagnostic surveys are finding that patients with an earlier onset of affective illness in adolescence, especially if the initial hospitalization was for mania, are far more likely to receive a diagnosis of schizophrenia (Joyce, 1984). Unfortunately, the misdiagnosis of psychotic forms of mood disorders is not at all uncommon within the general patient population (Pope & Lipinski, 1983). This is of great clinical significance, since prospective, longitudinal, and retrospective analyses of the course of illness indicate that early and effective intervention with appropriate somatic treatments may have a pronounced effect on long-term outcome and cycle frequency (Prien et al., 1984; Prien & Kupfer, 1986; Baastrup & Schou, 1967; Angst, Weis, Grof, Baastrup, & Schou, 1970; Post & Weiss, 1989). In addition, patients whose bipolar illness began during adolescence are reported to present with a predominance of psychotic symptomatology (Strober & Carlson, 1982). Since there is no established pattern of illness, the diagnosis of psychotic disorders in this age group is fraught with uncertainty. Clinicians who rely only on the acute presentation of symptoms are much more likely to misdiagnose these patients as schizophrenic. While it is not universally the case, these conditions tend to breed true. In support of this notion, Egeland (personal communication) has observed that in the 37 multigenerational bipolar pedigrees ascertained by the Amish Study, no first-degree relative in this sample of 404 individuals was diagnosed by the psychiatric board (blind to family history) as having schizophrenia. Therefore, a positive family history of affective disorders in first-degree relatives may be of great clinical significance in diagnostic deliberations in this age group, and provides further justification for the inclusion of the family in the diagnostic process. This is of practical importance for several reasons: when misdiagnosed, the patient is likely to be denied a trial on medication more suitable for affective disorders, and with inappropriate treatment, the likelihood of chronicity or relapsing affective episodes is much greater. The practical importance of determining predictors of bipolar illness during the period of adolescence is underscored by follow-up data that suggest that the onset of bipolar disorder in early adolescence may portend an especially malignant outcome with a high incidence of suicide and frequent, recurring mood swings, presumably because uncontrolled fluctuations in the affective state have concomitant long-term effects on personality development (Strober et al., 1988).

Given the fact that the vulnerability to develop an affective disorder is inherited and that these disorders frequently are not accurately identified, and often are undertreated even when correctly diagnosed, coupled with the public-health implications of the recent epidemiologic studies (Gershon et al., 1987b; Klerman et al., 1985), it is clear that the establishment of educational programs directed toward highrisk families will be of critical importance over the next several decades.

CURRENT TREATMENT STRATEGIES-DO THEY REFLECT THE CURRENT STATE OF KNOWLEDGE?

Major affective disorders continue to be the leading causes of psychiatric disability, loss of productivity, consumption of health resources, and human suffering (Baldessarini, 1983; Prien & Kupfer, 1986). While the great majority of major depressions are recurrent, alternate or mix with excited psychotic states, or may become chronic (Baldessarini & Tohen, 1988), historically, the recurrent nature of these illnesses has been underestimated by American psychiatric researchers and clinical practitioners (Goodwin, 1989). Thus the need to develop safe, effective, and efficient long-term treatments for these disorders is of extreme importance.

Within the past decade, the thrust of the community mental health movement at the national and local level has generated a treatment model for the major psychiatric disorders composed of two phases-a brief inpatient plan measured in weeks, followed by an extended period of aftercare in the community. The knowledge base that would help to develop a firm relationship between treatment methods and the prevention of relapse following an acute episode of depression or mania has only been thinly developed, particularly in the case of integrated treatment strategies that are shaped and guided by psychological, biological, and environmental factors. These factors have been poorly understood and rarely studied interactively.

While most studies of drug-treatment response have focused on the effect on acute episodes of illness, during the past five years, clinical and research interest in the affective disorders has expanded beyond the diagnosis and treatment of acute episodes to include consideration of long-term maintenance treatment aimed at prevention or reduction of the frequency and intensity of further attacks. This interest in preventive treatment has been largely stimulated by results from long- term drug trials with antidepressants and lithium primarily designed to examine the comparative effects of different pharmacological treatments (Schou, 1979; Kukopulos & Reginaldi, 1980; Keller, Lavori, Rice, Coryell, & Hirschfeld, 1986), as well as the mounting realization that these conditions are, in a large proportion of cases, recurrent (Zis & Goodwin, 1979; Kukopulos, Reginaldi, Laddomada et al., 1980; Goodwin, 1989).

Unfortunately, very few well-controlled studies have systematically evaluated the impact of these illnesses on long-term psychological and interpersonal function or considered their impact on the family. As a result, a number of core questions have remained unanswered as to the implementation of effective models of treatment following hospital discharge. What are the factors that contribute to relapse and rehospitalization? What role does the patient's and family's understanding of the nature and course of illness play in the patient's adherence to a maintenance treatment program? What is the effect of episodes of illness on other family members? These questions are particularly pressing in the case of the major affective disorders given the natural course of these illnesses, with such heavy family loading, propensity for relapse and recurrence, and clear attendant consequences for the subsequent generation at risk.

Mood disorders affect one in five families. Of patients requiring acute psychiatric hospitalization, surveys have shown that clearly one- third to one-half have some form of affective disorder and are often underdiagnosed (Keisling, 1981). Treatment in most inpatient settings is brief and usually focuses on the management of acute symptoms. Once stabilized, patients are often discharged with little or no information about the nature of their condition and the implications for treatment. In a recent survey of 80 patients diagnosed with bipolar affective disorder (manic-depressive disease) admitted consecutively to the inpatient service of a municipal hospital in New York City (most with at least two previous psychiatric hospitalizations for mania or depression), over 90% of patients and 98% of the family members interviewed were unaware of their diagnosis (Papolos, unreported observations). An equal number did not know that they would be expected to continue on lithium for the rest of their lives.

Mental health professionals have often avoided detailed discussions of diagnosis, symptoms, and prognosis. Commonly held reasons for doing so include lack of diagnostic clarity, the ill effects of stigmatization, discomfort with imparting such information, and the potentially harmful effects of a distressed reaction on the part of the individual with the illness (Tsuang & Vandermey, 1980). The evidence from studies in general medical settings and lithium clinics suggests that by failing to educate the patient and family, physicians may inadvertently contribute to medication noncompliance that leads to relapse and rehospitalization (Jamison & Akiskal, 1983 ). It is important to note that psychiatrists can serve patients and their families beyond offering risk estimates: they can dispel myths surrounding the illness and increase the stability of the family environment by decreasing the family members' anxiety about the patient and increasing their self- confidence and knowledge about the disorder. Knowledge is empowering and can improve the family's capacity to react constructively to those who are affected. Psychoeducational approaches for various forms of psychiatric illness have resulted in significantly reduced relapse rates following acute episodes of illness and a markedly increased compliance with treatment (Anderson, Hogarty, & Reiss, 1986).

While the evidence to support the belief that the vulnerability to develop a major affective disorder is genetically transmitted and neurochemically expressed has been strengthened over the past decade, it has unfortunately been accompanied by a philosophy that drugs and other somatic therapies offer the best, and sometimes the only, choice for treatment. This view of what comprises adequate treatment is shortsighted. There is currently no evidence to support strict adherence to a purely psychotherapeutic or purely pharmacological treatment strategy. Indeed, there is some evidence to support the idea that pharmacological treatment alone is not sufficient to prevent relapse in a large percentage of cases (e.g., Rounsaville, Prusoff, & Weissman, 1980; Frank & Kupfer, 1986; Frank et al., 1990). Simply relegating these disorders to the realm of physiological disturbances that require medical treatment alone is a serious clinical oversight and a gross scientific presumption, similar to the earlier psychological oversimplifications and prejudices that compounded the difficulties that have inhibited the development of multidimensional treatment approaches.

MOOD DISORDERS-THE IMPACT ON THE FAMILY

The onset of a chronic, relapsing illness in a family is a major source of unremitting stress for every member of the family (Kreisman & Joy, 1974; Hendersen et al., 1979; Hinchcliffe et al., 1975, 1977). This is engendered not merely by concern about current symptoms and handicaps, but also by the fear of future exacerbations. Because the manic-depressive patient may experience periods of euthymia or " normality," there is a tendency to view the disorder in the patient as having a somewhat benign course. Effective prophylactic medication, which controls and attenuates acute mood swings, tends to minimize mental health professionals' awareness of continuing distress associated with the disorder for the patient and family (Jamison, Gerner, & Goodwin, 1979). The malignant quality of manic-depressive illness is insufficiently appreciated. The functional impairment found among many bipolar patients in follow-up studies, and the havoc and disruption reported in their occupational, family, and social lives, suggests that, in spite of adequate drug treatment, disturbing problems persist for many, impeding the optimal emotional growth and development of both the patient and family members. Despite their significant effect on symptoms, lithium and other somatic therapies by themselves have little impact on interpersonal problems that may have developed in the course of the illness (Rounsaville, Prusoff, & Weisman, 1980).

Families of patients with depressive illnesses experience a wide range of difficulties (Keitner, Miller, Epstein, Bishop, & Fruzzetti, 1987; Coyne, 1976; Papolos & Papolos, 1992), yet few studies exist that have assessed the relationship of family functioning to course and outcome in patients with bipolar disorder or recurrent major depression. There is good reason to believe that factors other than compliance with medication, such as psychosocial stressors, affect the response to lithium salts, and, therefore, affect the subsequent clinical course and social adjustment in patients with recurrent mood disorders (Miklowitz, Goldstein, Nuachterlein, Snyder, & Mintz, 1988). Unfortunately, most studies that have attempted to identify environmental factors that influence the response to treatment have suffered from a number of methodological shortcomings, including small sample size, lack of control groups, diagnostically heterogeneous samples, assessments of only one family member, and lack of validated instruments to measure family functioning. A few studies are notable for their methodological rigor and testable conclusions (Miklowitz et al., 1988; Keitner et al., 1987). Miklowitz and colleagues applied methods that previously were effective in identifying psychosocial factors relevant to the course of other major psychiatric illnesses. This study used measures of family attitudes obtained from key relatives of recently hospitalized manic bipolar patients, including expressed emotion (EE) and interactional behaviors, affective style (AS), both of which have been found to predict relapse in schizophrenia (Vaughn, Snyder, Jones, Freeman, & Falloon, 1984). In this study, levels of intrafamilial EE and AS were found to predict the likelihood of patient relapse in bipolar disorder as well, and the predictive relationship observed was independent of patient medication, baseline symptoms, demographics, and illness history.

Although findings from several studies of combined individual psychotherapy and pharmacotherapy of unipolar depression (Rounsaville et al., 1980; Frank & Kupfer, 1986) suggest that poor response to treatment and a greater likelihood of relapse are associated with marital and family conflict, few reported studies have been conducted that include an assessment of the family's understanding of or response to the illness as a variable that may influence treatment outcome. Keitner and colleagues (1987), in a well-controlled study designed to address concerns regarding the relationship between family functioning and depressive disorders, found that depressive episodes were significantly shorter (4.1 months) in those families that improved in family functioning during follow-up than in those that did not (8.1 months) improve.

Reports from an ongoing study (Frank & Kupfer, 1986) of a combined treatment approach to patients with recurrent mood disorders suggest that the addition of psychotherapy, as well as an educational workshop offered to patients and their families, may reduce the risk of relapse to a rate below 10%. If replicated, this finding would be of great clinical significance, since patients with recurrent depression ordinarily experience a 40% rate of relapse within four to five months following recovery from an acute episode (Prien et al., 1984). Unfortunately, existing studies have tended to assess single dimensions of family health or pathology, and no well-controlled studies have investigated the effects of family psychoeducational models, while there is strong evidence from schizophrenia research to indicate a rather robust effect of family psychoeducational approaches in the prevention of relapse and costly rehospitalization in the treatment of that major psychiatric disorder (Anderson, Hogarty, & Reiss, 1986).

While only a handful of studies have examined the questions whose answers might inform the development of an integrated treatment approach, it is incumbent on clinicians and mental health administrators to formulate more rational multidimensional treatment strategies anchored by the cumulative data provided by genetic, family, and outcome studies. Although the involvement of the family in the treatment process departs from rigidly held tenets of the traditional one-on-one doctor-patient relationship and raises issues of patient confidentiality, it is nevertheless recommended that the education of high-risk families be a cornerstone of any such treatment paradigm. The view that these multigenerational, familial recurrent illnesses have profound effects on relationships within the family, that earlier onset in the parental generation predisposes to earlier onset in the subsequent generation and predicts a much higher risk of illness in first-degree relatives, and that juvenile-onset affective disorder frequently goes unrecognized and undertreated (Joyce, 1984) should provide the impetus. A multi-generational perspective would necessarily lead clinicians and designers of mental health services to view family education as a primary goal for mental health policy.

THE FAMILY PSYCHOEDUCATIONAL APPROACH: AN INTEGRATED TREATMENT MODALITY

A model program to educate patients and family members was developed at the Albert Einstein College of Medicine/Montefiore Medical Center (Papolos & Moltz, 1984). It is based on Drs. Carol Anderson, Gerald Hogarty, and Douglas Reiss' psychoeducational work with schizophrenic patients and their families in Baltimore and Pittsburgh. The approach is a practical one that goes far, in a short time, toward clearing up the myths surrounding the illness. It seeks to increase the stability of the family environment by decreasing the family members' anxiety about the patient and increasing their self-confidence and knowledge about the disorder. It improves the family's capacity to react constructively to the patient during episodes of illness and addresses the heritable nature of the condition. The approach typically requires five patient and family meetings.

Description of the Psychoeducational Approach

If the first of the five sessions takes place following an initial episode, or if the family has not been involved in previous episodes, it is often the case that each member has some theory about the disorder. The goal of the first meeting, then, is to understand the family members' theories. They are asked to entertain a medical hypothesis about the cause of the disorder and are given information that describes in a question-and-answer format the nature, symptoms, and course of major affective disorders (Papolos, 1987).

The provision of information usually sparks a lively discussion among the family members and the psychiatrist in the second session. There are often emotional responses to the idea that the illness has a biological basis and is heritable. Questions about medication efficacy, side effects, and criteria for long-term maintenance are discussed also. In the meetings that follow, the patient is encouraged to describe his or her subjective experience of the symptoms and the limitations they impose, and the family members begin to pinpoint how they responded to the loss of the ill member during episodes of depression or mania. How did each person try to rouse the patient from his or her illness during episodes of depression? How did each family member attempt to set limits for the patient during episodes of mania? What feelings were aroused when the attempts failed?

During the fifth and final session, the therapist and the family review what has been learned: the nature, course, and treatment of the disorder; the effects on the relationship system; and the strategies developed to avoid the conflicts that arose as a consequence of the patient's change in behavior during an acute episode of illness. If all goes well, the conflict among family members is decreased, healthy coping skills are attained, and the family becomes more of a support for the patient.

The goals of the psychoeducational approach are as follows:

  • To enable the patient and family to accept the idea that the patient has a medical disorder that may be recurrent and that produces symptoms that affect mood, self-esteem, thinking, speech, activity, sleep, appetite, and social and sexual behavior.
  • To teach the patient and family to identify and label the specific symptoms that occur at the onset of an episode.
  • To facilitate the acknowledgment that the most recent and/or past episodes have had an impact on the way family members view the patient and to identify and describe any change in their attitudes toward the patient and in the pattern of their relationship with the patient during and after an episode of either mania or depression.
  • To examine the changes that occur in the usual caretaking roles during an acute episode.
  • To convey that major affective disorders are familial disorders and so may affect others in the family, and to provide information about studies that report the diagnostic difficulties frequently encountered with early-onset and first-time episodes.
  • To explain the potential advantages and risks of preventive treatment, as well as of no treatment, from the time the acute episode is brought under control.
  • To explain the importance of long-term monitoring, including laboratory tests, and to encourage the family to share in the decision to initiate maintenance treatment.
  • To teach the family to distinguish medication side effects from the symptoms of illness.

The following case illustrates a number of ways in which the psychoeducational approach worked for a patient and for her family members. It highlights the common finding of misdiagnosis as schizophrenia in adolescent-onset mania, and underscores the profound psychological impact of some of the common symptoms of mania when they are not viewed as occurring in the context of a medical disorder.

J.C. is a 27-year-old, single, white Catholic woman of Italian- American descent. At the age of 16, she had her first episode of hypomania, in which she became uncharacteristically and excessively sexual, propositioning family friends and passersby on the street. She also had symptoms of insomnia and pressured speech, and felt euphoric. This first episode ushered in a period of promiscuity and drug abuse.

Thinking that she was a "bad girl" who had disgraced the family, the patient's father reacted violently, and began to beat her for her sexual indiscretions. J.C. became more and more agitated and eventually required hospitalization. At the hospital, she was misdiagnosed as schizophrenic, treated with the antipsychotic drug, thioridazine and discharged several weeks after admission when her agitation had subsided.

The patient continued to suffer periodic exacerbations of her illness over the next six years. During the hypomanic episodes, her behavior bewildered the other members of her family since they assumed that she had received appropriate treatment and they did not attribute her excessive sexuality and argumentativeness to a medical disorder. Her father continued to lose his temper, to confine her to the home, and to beat her severely.

At the age of 22, following a second hospitalization, the diagnosis of bipolar affective disorder was established, and J.C. responded well to a trial of lithium. Her relationship with her parents eased somewhat, but they never fully understood the periodic nature of her disorder. The threat of physical violence loomed over the household, and yet the patient's parents feared that any confrontation or stress might trigger another episode.

Four years later, J.C.'s lithium level fell below the therapeutic range. She felt herself becoming ill and drove to the hospital, where she requested voluntary admission. She told the resident in the emergency room that she hadn't slept for a week and had racing thoughts and increased sexual feelings. Her speech was pressured and she was hypertalkative on admission. The dosage of lithium was increased and within a week she was free of symptoms.

The patient's psychiatrist felt that J.C. and her family could benefit from the psychoeducational approach and the social worker invited the family to participate in the five-session family therapy.

At the first family meeting, it became apparent that J.C. had a profound fear of her father as a consequence of the beatings she had suffered. Mr. C. expressed a desire to learn more about his daughter's illness, although initially he did not read the pamphlet on mood disorders that was given to him. When asked about his response to J.C.'s illness, he reported that he would typically stop talking to her when she appeared agitated, lest he set her off again. If the conversation became too heated, he used a hand gesture that prompted his wife and J.C. to stop talking. He felt that the only solution to the problem was to have his daughter move out of the house.

During the family sessions, Mr. C. reported how guilty he felt over the way he had treated his daughter. He admitted that the guilt and the outrage at his daughter's behavior left him feeling helpless. Mrs. C. appeared to be a quiet, passive mother and wife who possessed a greater tolerance of and sympathy for her daughter's behavior, but who would support her husband's viewpoint at all costs.

During the five sessions, the nature of J.C.'s periodic disorder was explained to the family. The psychiatrist clarified that J.C.'s hypersexual behavior was a symptom of the illness and not the volitional act of a "bad child." This led the family to the realization that she had been punished and shunned for behavior that was out of her control. Mr. C. apologized for the years of physical abuse, and the family elected to continue in twice-monthly family treatment to further work through their responses to J.C.'s illness.

When a relative experiences recurrent episodes of depression or mania, there is a disruptive and disorganizing effect on family life. The other members of the family are faced with the challenge of looking after and providing for the needs of their relative-often in an atmosphere of confusion, isolation, embarrassment, anger, and guilt. Before long, the individual needs of all the family members are ignored as each tries to grapple with the tension that accompanies these disorders. The following case points to the generational impact of these conditions, and the usefulness in framing the treatment process within the family group.

E.G. began to suffer serious periods of hypomania and depression during his college years. Despite these interruptions, he persevered, graduated from college, and found meaningful work. Although his episodes had been muted by drugs, he continued to have mood swings. These periodic episodes of hypomania and depression flew in the face of his attempts to establish himself independently of his parents and so he continued to live at home. He was encouraged by his parents after each setback, but he felt a growing sense of isolation and a loss of credibility in the aftermath of each episode. He was having a great deal of difficulty understanding and coping with his family's reaction to his illness. The patient's mother appeared nervous around him and was overly sensitive to any changes in his mood. His father, a physician, denied that his son's problems were really serious, and his younger brother, once his closest confidant, refused to be seen with him or to invite friends to their home.

E.G. and his family came for consultation initially with questions about the medical treatment-his expectation and that of his family was that he should no longer have mood swings. The fact that he continued to have brief periods of depression and hypomania was unacceptable and meant to them that something was wrong with the way in which his treatment was being managed. Moreover, he was having trouble with a lithium tremor. It was a source of embarrassment to his family and he was increasingly sensing that his mood and behavior were a focus of concern in the household. He felt under constant pressure to explain even minor changes in his moods.

Fearing that the least stress might set off another episode, the family had been living with a prolonged uncertainty and apprehensiveness. In such an atmosphere, E.G.'s behavior and natural expression of such emotions as joy, sadness, and anger came under close scrutiny, and even suspicion. The family, in the position of being an early-warning system of impending mood swings, had stepped into the role of prosecuting attorney: The patient was faced with seemingly endless questions and doubts and was asked to provide motives for almost every act. This was a corrosive atmosphere for everyone concerned. The patient's credibility and competence as a person were called into question by the often unspoken suspicions of his motives and emotions and the family was placed under a terrible strain.

The effect of these constant unspoken suspicions had robbed the patient of his sense of credibility, which eventually can become crippling to self-esteem. Paradoxically, this atmosphere of mistrust within such a family springs not from prejudice, but from a natural inclination to care about and to protect the person who is ill. But the quality of the caring can be derailed by fear, denial, and lack of knowledge. Constant sympathetic attempts to raise a person s spirits during a depression are often of no avail, and family members feel frustrated, and then resentful or angry and despairing as they sense that no matter what they do, it does not make a difference.

A number of things changed as a result of the family sessions. By learning more specifically about the nature of E.G.'s condition and the natural course of the illness, the family members were able to begin to work collaboratively rather than at cross-purposes. E.G.'s mother learned that her desire to protect her son from any further episodes by scrutinizing his every change in mood was creating an unbearable tension in the household, sapping her energy and needlessly alienating her son. She lessened the demands on E.G. and her own unrealistic expectations of what treatment could accomplish.

E.G.'s physician father at first had a great deal of difficulty with acknowledging the emotional impact of his son's condition. He had chosen to minimize and downplay his son's symptoms, saying that he thought it best to reassure him rather than to offer him sympathy. He initially spoke about the cost of psychiatric treatment and focused his anger on the discriminatory policies of his firm's insurance coverage. However, he was unwilling to rock the boat and to appeal a decision that limited reimbursement.

Not long into the family sessions, E.G.'s father acknowledged that he, too, had experienced numerous episodes of depression, but without seeking treatment; he had chosen to "tough it out." As he spoke in more depth about his own experiences with depression, he confided a secret that had been kept from his family for years. His own father had been diagnosed as manic-depressive and had committed suicide. E.G.'s father had been unable to face the idea that there was some association between his own depressions, the suicide of his father, and his son's condition. The anger he harbored toward his father and the shame that had forced him to conceal his own pain had surfaced in subtle and self-destructive ways. As a result of the family treatment, he came to realize that the denial of his illness had contributed to the double messages he communicated to his son - on the one hand, minimizing his symptoms, and on the other hand, expecting him to be able to control his mood swings voluntarily. Denial, fear, and shame had cast long shadows-from grandfather to father to son.

These powerful forces can immobilize the most caring of families. And with a heritable illness such as manic-depression, far more than the genetic vulnerability can span the generations.

After learning about and accepting the biological basis of the condition and its heritability within his own family, E.G's father was, for the first time, able to seek treatment for himself and to empathize with his son's struggle. Previously, he had been shackled by a sense of shame and the fear that he would be viewed contemptuously in his work and social circles. Now, he felt empowered by his new perspective as to the medical basis of the condition.

Our experience in applying the family psychoeducational approach with over 400 families of diverse ethnic and social backgrounds has reified our view that these conditions must be seen within the larger context of the multigenerational family, and that family members can serve as potent allies in the prevention of relapse.

GENETIC COUNSELING: AN EXTENSION OF THE PSYCHOEDUCATIONAL APPROACH

Once families learn and accept that mood disorders are heritable, some become interested in exploring the degree of risk in more depth. Many professionals in the health sciences have long felt that psychiatric disorders are not a fit subject for genetic counseling because of their unknown etiology. If we are not sure what gene defects are involved in psychiatric disorders, how can we estimate risks with any certainty? Indeed, knowing that there is a genetic basis for a disease is no substitute for understanding how the genetic mechanism works. However, some physical diseases with etiologies no more certain than those of most psychiatric disorders are commonly the subjects of genetic counseling and education. Such problems make counseling more difficult, but they do not preclude it.

Psychiatrists have recourse to other practical means for estimating the risk of recurrence for ambiguously inherited disorders. Great advances have been made during recent years and ingenious methods have been developed for examining the interaction between heredity and environmental factors. At the simplest level, investigators have used the "proband method," in which an index case with a particular diagnosis (e.g., bipolar disorder) is identified, and rates of illness in members of the subject's family are compared with rates in some appropriate comparison group (e.g., relatives of individuals who have never been psychiatrically ill). Many such large-scale epidemiologic studies have resulted in pools of data that allow psychiatrists to make reasonably accurate empirical risk estimates.

Although the relative contribution of genetic factors is not precisely known, it is possible to determine the empirical risk for the development of illness in relatives of ill patients. In Chapter 8, Dr. Shalom Feinberg describes the experience in a homogeneous community, the Orthodox Jewish community, and underscores basic principles of genetic counseling derived from his clinical experience.

REFERENCES

Akiskal, H., Downs, J., Parri, J., Jordan, P., Watson, S., Dougherty, D., & Pruitt, D. B. (1985). Affective disorders in referred children and younger siblings of manic-depressives. Archives of General Psychiatry, 42, 996-1003.

Anderson, C. M., Hugarty, G. F., & Reiss, D. J. (1986). Family treatment of schizophrenic patients: A psychoeducational approach. Schizophrenia Bulletin, 490-582.

Angst, J., Weis, P., Grof, P., Baastrup, P. C., & Schou, M. (1970). Lithium prophylaxis in recurrent affective disorders. British Journal of Psychiatry, 116, 604-614

Baastrup, R C., & Schou, M. (1967). Lithium as a prophylactic agent. Its effectiveness against recurrent depressions and manic-depressive psychosis. Archives of General Psychiatry, 16, 162-172.

Baldessarini, R. J. (1983). Biomedical aspects of depression and its treatment. Washington, DC: American Psychiatric Press.

Baldessarini, R. J., & Tohen, M. (1988). Is there a long-term protective effect of mood-altering agents in unipolar depressive disorder? In Current trends. Berlin, Heidelberg: Springer-Verlago.

Beardslee, W. R., Bemporad, J., Keller, M. B., & Klerman, G. L. (1983). Children of parents with major affective disorders: A review. American Journal of Psychiatry, 140, 825-832.

Beardslee, W. R., Keller, M. B., & Klerman, G. L. (1985). Children ofparents with affective disorder. International Journal of Family Psychiatry, 6, 283-299.

Bertelsen, A., Harvald, B., & Hauge, M. (1977). Danish twin study of manic-depressive disorders. British Journal of Psychiatry, 130, 330- 351.

Boyd, J. H., & Weissman, M. M. (1981). Epidemiology of affective disorders: A reexamination and future directions. Archives of General Psychiatry, 38, 1039-1046.

Brody, G. H., & Forehand, R. (1986). Maternal perceptions of child maladjustment as a function of the combined influence of child behavior and maternal depression. Journal of Consulting Clinical Psychology, 54, 237-240.


© Demitri F. Papalos - Reprinted with permission of the author

 

Modified December 25, 2002

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The information at this web site is for consumers, family members and mental health workers to make informed decisions about the care and treatment of bipolar disorder, AKA manic depression. These pages are not a substitute for consultation with your counselor, therapist, doctor, or psychiatrist.

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