Bipolar Affective Disorder (BPAD) is a severe psychiatric mood disorder.  Patients who suffer from the disorder oscillate between manic and depressive episodes as well as periods of mood normalcy.  Persons in manic episodes may experience euphoria, mood expansiveness, irritability, mood lability, anxiety, or panic.  Often, they experience racing thoughts, and their thoughts contain ideas of grandiosity, delusions, and even hallucinations.  The depressive phase shares classification criteria with Major Depressive Disorder, and primary symptoms are a depressed mood, anhedonia, changes in sleeping and eating habits, and decreased energy.  BPAD is diagnosed using the criteria in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) as well by as a complete history, physical and pertinent laboratory testing to rule out organic pathology.  Pharmacotherapy includes lithium, a well known mood stabilizer, as well as anti-epileptics with mood stabilizing properties such as valproate, carbamazepine, and lamotrogine, and atypical antipsychotics such as olanzapine and risperidone.  Comprehensive treatment can be achieved using a combination of various medications along with psychotherapy, family therapy, and patient education.

Introduction

 The following case introduces a 51 year old Caucasian female with a past psychiatric history significant for a fall down concrete stairs seven years ago which caused her to lose consciousness.  Since that time, she has suffered from subsequent new onset depression with auditory and visual hallucinations of a “devil face that tells me to kill myself” with one attempted suicide by overdose three years ago.  Her past medical history is significant for hypertension for seven years and hypothyroidism and headaches for one year.  Upon admission to the psychiatric unit at Abington Memorial Hospital, she reported feeling “down and depressed” with crying spells and having hallucinations of a “monster face that is back again and wants me– he controls me.”  She reported feeling suicidal and had planned to commit suicide either by stabbing herself or by taking pills.  These symptoms had been worsening since December but she had tried to “fight them off.”  She was voluntarily admitted to the hospital when she was no longer able to fight off the suicidal ideations.  Also, since December, she complains of worsening memory, difficulty concentrating, dizziness, hypersomnia, and hyperphagia.  She reports a lifelong history of social phobia that has significantly worsened in the past year to the point where she does not attend social activities, and when she is among people, she gets “sweaty” and her “heart starts pumping.”

 She had been previously treated for depression shortly after her fall seven years ago.  Recently, she had been labeled with schizophrenia due to her psychotic symptoms.  Past medication trials included valproic acid (Depakote), paroxetine (Paxil), risperidone (Risperdal), bupropion (Wellbutrin), clonazepam (Klonopin), buspirone (Buspar), and sertraline (Zoloft).  Upon admission, she was taking venlafaxine (Effexor), diazepam (Valium), temazepam (Restoril), Levothyroid, and Hyzaar.

 Her initial mental status examination revealed a well developed, overweight, Caucasian female dressed in a hospital gown who was overly animated and dramatic, verbose, and child-like.  Her speech was fluent, mildly pressured, and loud.  She reported her mood as depressed though her affect was bright.  She was alert and oriented to person, place, and time. Her immediate memory and recall were intact but remote memory was poor.  She was able to simply abstract proverbs but was unable to complexly abstract.  Her thought content was positive for hallucinations.

 At the time of the initial evaluation, she was started on olanzapine (Zyprexa) 2.5mg at bedtime. The differential diagnosis included bipolar affective disorder with psychotic features and organic mood disorder secondary to head trauma.  During her hospitalization at AMH, she underwent an MRI of the brain, neuropsychiatric testing, and a neurology consult to rule out organic pathology.  Laboratory work included thyroid function testing, B12 and folate to rule out anemia, RPR to rule out neurosyphilis, and serum Ceruloplasmin to rule out Wilson’s disease.  A sleep study was ordered by neurology to rule out obstructive sleep apnea as a cause of her hypersomnia.

 All laboratory work was negative, and MRI of the brain and sleep study were determined to be normal.   Neuropsycologic testing performed by Dr. H. revealed that her expressive and perceptive language skills were intact but attention and concentration were limited.  There was no ideational or construction apraxia.  Gnostic functions and stereognosis were intact.  The exam was significant for orbitofrontal signs, and diffuse heterogeneous findings in the frontal cortex as were demonstrated by disinhibition and lack of impulse control.  She also showed impaired perceptual motor integrative skills, decreased cortical inhibition, and affective instability.  Diagnosis per Dr. H. was Organic Mood Disorder secondary to closed head trauma.

 This patient displayed BPAD I with psychotic features as a direct result of her closed head injury with loss of consciousness.  She was treated accordingly with diazepam (Valium) 5mg three times a day, venlafaxine (Effexor) 75mg once a day, olanzapine (Zyprexa) 2.5 at bedtime,  Depakote ER 500mg at bedtime (which upon discharge was raised to 1000mg at bedtime), temazepam (Restoril) 15mg at bedtime, clonazepam (Klonopin) 0.5mg twice a day and 1mg at bedtime.

 After one week of in patient treatment, examination upon discharge showed improvement in affect, and the patient reported better moods and less hallucinating.  She felt that she had improved and that her medications were helping.  She no longer felt suicidal and showed future planning.  Discharge plans were to discharge home, continue medication regimen, continued medication monitoring with an outpatient psychiatrist, and outpatient psychotherapy and family therapy.

Discussion

 Bipolar Affective Disorder (BPAD) is a psychological disorder that has been documented in various accounts throughout history and fiction for thousands of years.¹  It is a common and recurrent disorder of extreme mood fluctuations that can result in cognitive and behavioral disturbances.  It is characterized primarily by the presence of mania and depression with periods of normal mood during the shift from one pole to the other.  Two main types of BPAD have been identified and are labeled as Bipolar I (BPAD I) and Bipolar II (BPAD II).  BPAD I is defined as episodes of full mania alternating with major depression.  Patients with BPAD II display major depressive episodes that alternate with hypomania.  The difference between the two is the severity of the manic phase.  A full manic episode lasts for longer than one week and must be severe enough to cause significant impairment or necessitate hospitalization.  Hypomania must last for at least four days, but does not cause significant impairment in social or occupational functioning or necessitate hospitalization.2  Subtypes of BPAD include BPAD with melancholic features, with psychotic features, rapid cycling BPAD, or mixed states.

 Commonly, comorbidities are seen in persons suffering from BPAD.  These include substance abuse, obsessive-compulsive disorder, panic disorder, social phobia, and impulse control disorders.^2,3  It can be a lethal disease as up to 25% of patients with BPAD attempt suicide.²  Because of the propensity of danger to self and others, BPAD must be treated aggressively and comorbidities must be taken into account during treatment.  Treatment should involve pharmacotherapy, psychotherapy, education, and addressing family and social issues.^3,4

Epidemiology and Etiology

 BPAD is thought to have a life time prevalence of 1-1.6% of adults in the general population.²  While the mean age of onset is 18, BPAD can occur at any point in the life span from childhood to middle age or beyond.  Men and women are both equally affected.³  Incidence is increased in first-degree relatives of people with BPAD, and genetic patterns suggest an autosomal dominance pattern on inheritance.⁴  Monozygotic twins show a 72% concordance rate while dizygotic twins have a concordance rate of 19% in same sex twins.5 BPAD also occurs more frequently in single and divorced individuals, but this may be because of the early onset of the disorder or its propensity to cause marital discord.¹  Lastly, BPAD occurs more frequently in people of higher socioeconomic status and in people who have not completed a college degree.²

 Experts agree that the specific etiology of BPAD is unknown.  However, recent research in neuroimaging studies has suggested that the thalamus, hypothalamus, amygdala, caudate, prefrontal cortex, and cerebellum may be involved in the pathophysiology.²  Also, BPAD I patients tend to show larger cerebral ventricles than do patients with major depressive disorder or control subjects.¹  Other findings of abnormal neurological functioning include neurochemical abnormalities of serotonin, norepinephrine, dopamine, acetylcholine, and second messenger pathways, dysregulation of the hypothalamic-pituitary-adrenal axis, and disruption in circadian rhythms.²   Research suggests that the limbic system plays a large role in emotions which implies that the limbic system may as well be involved due to the constricted range of emotions that a person in depression expresses.1  Alterations in sleep, appetite, and sexual behavior suggest hypothalamic dysfunction.¹  Changes in posture, motor retardation, and cognitive slowing that are seen in depressive states implicate the involvement of the basal ganglia.¹

Clinical Presentation

 The manic phase of BPAD is often defined as experiencing a euphoric mood.  However, pooled data show that most patients experience depression, irritability, expansiveness, and mood lability as often as they do euphoria.²  Mania may be divided into three stages: stage I- mood is predominantly euphoric; stage II- mood becomes more irritable, dysphoric and depressed; and stage III- mood is characterized by anxiety, panic, and dysphoria.²  Mania often encompasses flight of ideas, grandiosity, decreased hours of sleep but still feeling rested, pressured speech, a disregard for danger, and engagement in high risk behaviors such as promiscuous sexual activity, spending sprees, violence, and substance abuse.^2,3  During the manic phase, patients may experience psychotic symptoms of delusions and hallucinations.  Delusions may be grandiose, religious, thought control, insertion, or withdrawal.2  Other manifestations of mania may include arbitrary decision making, tendency to place blame on others, impulsive behavior, desire for self-enhancement, loudness, hypersexuality, racing thoughts, and distractibility.^2,4

 Hypomania may be manifested by an elevated and/or expansive mood, enhanced self-confidence, increased productivity, low frustration tolerance, or irritability.^2,3  In fact, hypomanic symptoms may be identical to manic symptoms but are distinguished based on the presence of one of the following: psychosis during the episode, severity which warrants hospitalization, or a marked social role impairment.⁶

 The depressive phase of BPAD is indistinguishable from that of Major Depressive Disorder (MDD).  Patients in the depressive phase will suffer from depressed mood or anhedonia that lasts for more than two weeks.⁶  Other symptoms include changes in sleep (insomnia or hypersomnia), appetite (hyperphagia or anorexia), energy, cognition, and judgment.⁶  The patient may show a change of greater than 5% body weight when not dieting.²  Also, suicidal ideation is common in depression.  This may be manifested as an actual suicide attempt or thoughts of death with or without a plan. The patient may also have a negative self-image, guilt or shame that may reach delusional proportions, lack of productivity, or loss of libido.⁴

Mental Status Examination

 The bipolar patient may present either in mania or in depression.  Generally a depressed patient may show psychomotor agitation or retardation, stooped posture, and poor eye contact.¹  Speech may be monotone, decreased in rate or volume, or delayed in production.⁷  The patient may describe his or her mood as depressed, anxious, or irritable.  Affect is generally flat or constricted.⁷ Thought processes may display thought blocking.¹  Thought content may show poverty of content, delusions, hallucinations, or suicidal ideations.  Cognition is measured by orientation is usually intact though memory or concentration may be impaired.¹  Also, if depression is severe, level of consciousness may vary throughout the interview.⁷  Impulse control is usually determined by the degree to which a patient is suicidal or displays violence towards others.  A patient who is moderately depressed may actually be more impulsive and have a greater propensity to commit suicide than a more severely depressed patient because of the lesser degree of their fatigue or psychomotor retardation.¹  The patient’s insight into their condition is usually excessive.¹

 A patient experiencing mania is generally hyperactive, excited, and may demonstrate psychomotor agitation.  Mood may be described as euphoric or as irritated, angry, or hostile.  Affect may be labile.  Speech may be pressured or increased in rate or volume.  Thought processes may show flight of ideas, loose associations, word salad, clanging, rhyming, or neologisms.⁷  Thought content usually includes extreme self-confidence, grandiosity, delusions or hallucinations.¹   Orientation and memory are intact.¹  Impulse control and judgment are typically extremely poor, and insight is often limited.⁷

Diagnosis

 BPAD if often diagnosed during a manic phase, but if a careful history is taken, it can be diagnosed during the depressive phase as well by recognizing symptoms of mania or, more commonly, hypomania before the onset of the depressive phase.  The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) outlines criteria for diagnosis of a patient with BPAD I, BPAD II, and subtypes.  BPAD I is diagnosed when the patient meets both the criteria for a Major Depressive Episode (MDE) and mania. BPAD II is diagnosed when criteria for an MDE are met along with the criteria for hypomania.

 DSM-IV criteria for an MDE include experiencing five or more of the following symptoms during a 2 week period: depressed mood for most of the day nearly every day, anhedonia, significant weight loss (when not dieting) or weight gain, insomnia or hypersomnia, psychomotor retardation or agitation, fatigue, feelings of worthlessness or excessive guilt, diminished ability to think or concentrate, and recurrent thoughts of death.  These symptoms must cause significant distress or impairment in social or occupational functioning but cannot be due to the physiological effects of a substance or a general medical condition.⁸

 DSM-IV criteria for a manic episode include  experiencing an abnormally and persistently elevated, expansive, or irritable mood lasting for at least one week.  During that week, at least three of the following symptoms are present: inflated self-esteem or grandiosity, decreased need for sleep, pressured speech, or being more talkative than usual, flight of ideas or racing thoughts, distractibility, increase in goal-directed activity or psychomotor agitation, and excessive involvement in pleasurable activities with high potential for severe consequences.  The mood disturbance must be severe enough to cause impairment in occupational or social functioning, necessitate hospitalization, or have psychotic features.  Lastly, the symptoms must not be due to the physiological effects of a substance or a general medical condition.⁸

  Hypomania does not reach such significant proportions.  Hypomania can be diagnosed if the patient experiences at least three for at least four days.  It must neither cause significant impairment in occupational or social functioning nor necessitate hospitalization.  Lastly, it cannot have psychotic features.  Presence of any of these three features warrants promotion from hypomania to mania.⁶

 A mixed episode is diagnosed when the patient exhibits both mania and depression concurrently.  Mixed episodes are defined as full blown mania accompanied by depressive symptoms.6   The DSM-IV criteria state that both the criteria for an MDE and mania must be met concurrently with the exception that depressive symptoms need to be present only for one week instead of two.8  Studies have estimated that up to 30% of manic patients present with mixed symptoms.²

 Other subtypes of BPAD are rapid cycling BPAD, melancholic BPAD, and BPAD with psychotic features.  Rapid cycling is defined as experiencing four or more mood episodes in one year.  These episodes do not have to alternate between depression and mania, however.  As defined by the DSM-IV, the episodes must meet criteria for a major depressive, manic, mixed, or hypomanic episode.  Each episode must be separated from the one prior by a partial or full remission for at least 2 months, or switch to the pole opposite the prior episode.8  Unfortunately, rapid cycling BPAD shows poorer outcome and worse response to treatment than do other types of BPAD.⁶

 BPAD with melancholic features is used to describe the depressive phase of the disorder and is specified when the patient meets the criteria for either BPAD I or BPAD II along with the following two criteria.  First, the patient must either experience anhedonia or lack appropriate reactivity to pleasurable stimuli.  Secondly, three or more of the following symptoms must be present: distinct quality of depressive symptoms, depression that is worse in the morning, early morning awakening, marked psychomotor retardation or agitation, significant weight loss or lost of appetite, or excessive or inappropriate guilt.⁸ If both criteria are met along with BPAD, then the patient is diagnosed with melancholic type bipolar disorder.

 BPAD I with psychotic features is diagnosed when the patient experiences psychotic symptoms (delusions or hallucinations) during an acute phase of either mania or depression.  The symptoms must not extend into periods of normal mood.  The psychotic symptoms should be defined as either mood congruent or mood incongruent.  Mood congruent symptoms are consistent with depressive themes of personal inadequacy, guilt, disease, death or nihilism.  Mood incongruent symptoms are inconsistent with the aforementioned themes and may be persecutory, thought insertion, thought broadcasting, or delusions of control.  The presence of psychotic symptoms mandates a diagnosis of BPAD I.⁸

Physical Exam and Laboratory Tests

  In a patient presenting for the first time with psychiatric symptoms, the examiner should carry out a complete history and physical examination including a detailed review of systems, basic screening tests and laboratory work.6   Regardless of the suspected psychiatric disorder, pertinent lab work includes complete blood count, hematocrit and hemoglobin, renal, liver and thyroid function, electrolytes, and blood glucose.¹  If abnormalities are found on the physical examination or if a cluster of symptoms suggest a general medical condition, good medical practice necessitates further investigation with the appropriate studies.  Basic lab work is also important prior to beginning pharmacotherapy in the patient diagnosed with BPAD as many of the medications can affect liver and kidney function.

Differential Diagnosis

 The diagnosis of BPAD may be made if the disorder is not due to a general medical condition or if the symptoms do not more appropriately meet the criteria of another psychiatric disorder.  When a patient presents with depressive symptoms, the differential followed is that of major depression.  Medical disorders that must be ruled out include hypothyroidism, endocrine abnormalities such as Addison’s disease or Cushing’s disease, infections such as AIDS, mononucleosis in adolescents, and pneumonia in the elderly, inflammatory conditions such as systemic lupus erythematosus, and vitamin deficiencies.1,6  Common neurological disorders that may present as depression are Parkinson’s disease, Multiple Sclerosis, dementia such as Alzheimer’s dementia, cerebrovascular disease, epilepsy, and tumors.¹  An accurate history must rule out substance abuse, and prescription medications must be carefully considered as causes of the depressed mood.  Common classes of medications causing depression include cardiac drugs, sedative/hypnotics, antipsychotics, antiepileptics, and antimicrobials.¹  The psychological differential for MDD is followed if there is no suggestion of prior mania, while the psychological differential for BPAD is followed if the patient’s history suggest previous manic episodes.

 The medical differential for mania includes hyperthyroidism, Addison’s disease, Cushing’s Disease, B12 deficiency, neurosyphilis, encehapalitis, and AIDS, as well as right frontotemporal or subcortical lesions.⁶ The psychological differential includes both BPAD I and II, cyclothymic disorder, schizophrenia, and schizoaffective disorder.¹  Differentiating between BPAD I and II can be done by following the above outlined DSM-IV criteria for each of the disorders.  The others require a brief discussion.

 Cyclothymia is defined as a period of at least two years of mood instability with both depression and hypomania with or without periods of normal mood.  Neither the depression or the hypomania can be severe enough to meet DSM-IV criteria for MDE or manic episodes.1 During at least some of the periods of depression, three depressive symptoms must be present, and three symptoms of elevated mood must be present during hypomania.  Mood instability is greater than what is seen in BPAD II.¹⁰

 Differentiating BPAD I with psychotic features from schizophrenia or schizoaffective disorder can pose a difficult task.  One must carefully determine exactly when psychotic symptoms are present and diagnose the patient based on when the patient displays the symptoms.  If the psychotic symptoms are limited to the mood episode, the BPAD with psychotic features can be diagnosed.  However, if psychotic symptoms persist significantly into periods of normal mood, then the patient is diagnosed with schizoaffective disorder.  DSM-IV delineates the diagnosis of schizoaffective disorder if the psychotic symptoms exist for two weeks during normal mood.6    BPAD I with psychotic features can also be differentiated based on the findings that elated mood and hyperactivity occur more often in BPAD than in schizophrenia.¹

Treatment

 Treatment of BPAD has four goals:  to treat acute mania, to treat acute depression, to prevent recurrent mania, and to prevent recurrent depression.⁹  Treatment, however, is difficult and challenging.  While pharmacotherapy is the mainstay of treatment, psychotherapy is usually indicated and often necessary.  Mono-drug therapy is often unsuccessful thereby necessitating combination therapy.  To further complicate treatment, different subtypes of BPAD respond differently to different regimens, and the depressive and manic phases differ in their response as well.  Therefore, control of the symptoms is difficult to achieve and is very sensitive to changes in both the drug levels and outside stressors endured by the patient.

 Drugs used currently in the treatment of BPAD include lithium, anticonvulsants such as valproate, carbamazepine, and lamotrogine, typical antipsychotics such as haloperidol, atypical antipsychotics such as olanzapine, risperidone, or clozapine, and antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs).

 Treatment for acute mania and mixed episodes is usually begun in the hospital as the patient is rarely safe in the community from their own indiscretions or suicidal ideations.⁴  Currently, the U.S. Food and Drug Administration has approved three medications for treatment of acute mania– lithium, valproate, and olanzapine.²   Since these drugs may take up to three or four weeks before results are seen, temporary measures may need to be taken including the short-term use of benzodiazepines and antipsychotics.²  Benzodiazepines may be needed initially to control severe psychomotor agitation.⁴  In severe mania with psychotic symptoms or severe psychomotor agitation, anticonvulsants or neuroleptics are superior to lithium in the first weeks of an episode.  After two weeks, lithium and the anticonvulsants seem to be more effective than neuroleptics.⁹ If medications cannot control agitation, electroconvulsive therapy may be needed.⁴ Long term use of typical neuroleptics is discouraged due to the high occurrence of extrapyramidal symptoms and tardive dyskinesia.

 Acute depression is a more difficult entity to treat than acute mania.  Pooled data showed that 36% of patients in depression who were given lithium displayed unequivocal response  while 79% had at least partial improvement in symptoms.²  However, many clinicians report poor response to lithium monotherapy.⁹  Carbamazepine showed only 32-46% response, and to date, there have been no controlled studies on valproate or other medications in their use for depression associated with BPAD.² Antidepressants are also used in treatment of the depressive phase, however, there needs to be great caution in their use as they have a tendency to induce mania.  Fluoxetine, paroxetine, and bupropion have been shown to reduce depressive symptoms when used in conjunction with mood stabilizers.  Theoretically, the risk of inducing mania should be reduced when SSRIs are used in combination with mood stabilizers.² In addition to these therapies, lamotrogine has recently been shown to be an effective treatment in depression associated with BPAD I, BPAD II, and rapid cycling.¹⁰

 BPAD with psychotic features has a poorer prognosis than does BPAD without psychotic features.  Antipsychotic medications, specifically olanzapine and risperidone have undergone controlled studies in BPAD, and olanzapine as monotherapy has been shown to be superior to placebo in the treatment of mania.¹⁰  In addition, both risperidone and haloperidol added to lithium or valproate have been shown to be statistically superior to the use of lithium or valproate as monotherapy.¹⁰ Because these drugs have shown mood stabilizing effect, they are potential alternatives for treatment of BPAD with psychotic features.²

 Long-term management has historically been achieved with lithium and effectively prevents relapse.4  Factors which predict a favorable response to lithium therapy include patients with a family history of BPAD and a previous episode sequence of mania-depression-euthymia.  Poorer response may be seen with rapid cycling, mixed episodes, episode sequence of depression-mania-euthymia, multiple prior episodes, and comorbid substance abuse.⁹ One theory of long-term maintenance using lithium is to maintain the drug at a lower serum concentration than is used acutely to stabilize mood, or (0.4 to 0.6 mEq/L versus 0.8-1.4 mEq/L).   However, while these patients experience less side effects from the lithium, they have been shown to be more likely to experience subsyndromal symptoms than those patients maintained on standard lithium serum concentration.  These subsyndromal symptoms put the patient at four times the risk for developing a full episode relapse.²  Therefore, controversy exists over the practice of maintaining lithium levels at low concentrations for long-term managment.

 Alternatively, carbamazepine or valproate can be used in montherapy or in combination with lithium to help achieve mood stabilization.⁴  Valproate has been shown to be as efficacious as lithium in control of acute mania, and in open-label studies, it has reduce the frequency and intensity of mood episodes over extended periods of time.⁹  It is the drug of choice in patients unable to tolerate lithium or in those for whom lithium was ineffective (e.g. rapid cycling or mixed states).⁹  It can reduce the frequency and intensity of recurrent episodes in both poles of the disorder and may benefit patients with rapid cycling, mixed states, neurological abnormalities or head trauma.⁹  Carbamazepine appears to be effective, either alone or in combination with lithium, for acute treatment of mixed states and in the treatment of organic affective disorder.  It also lessens aggression so it can be used in the suicidal patient.⁹  It has been shown to be superior to placebo in maintenance, but its effect was incomplete, and most patients taking it required additional treatment for breakthrough mood episodes.⁹

 While pharmacotherapy is the cornerstone of treatment for BPAD, the disorder usually causes continued disruptions of psychosocial and occupational function.  Therefore, even when there is improvement with drug therapy, long-term supportive psychotherapy is usually indicated.²   The goals of psychotherapy are to help patients learn to cope with the effects the disorder may have on self-perception and interpersonal relationships.⁹  Psychotherapy is also used to help patients understand the disorder, to help them understand the role that their temperament plays, and to help them deal with issues of control.⁹  Family therapy may be needed to help family members understand the disorder and cope with their feelings of guilt, anger, grief, and ambivalence.³

 Patient and family education is also a key to effective treatment.  Patients must be taught that certain behaviors, such as insufficient or irregular hours of sleep, substance abuse, or even modest social alcohol ingestion can trigger a mood episode.³  Patients should strive to maintain a regular daily schedule of meals, exercise, and sleeping and waking times.⁹  Patients as well as family members must be taught to recognize symptoms of relapse, for example, one night of unexplained sleep loss may be an early warning sign of mania.⁹  They need to be educated about the consequences of the episodes including sexually transmitted diseases, financial ruin, and even suicide.  Lastly, it is important to counsel the family on how to handle various situations that may arise and where to find help when an episode does occur.³

Conclusion

 Bipolar Affective Disorder, a psychiatric mood disorder, causes significant disruptions in psychosocial and occupational functions with the possibility of severe repercussions.⁴  Patients are faced with the reality that they will suffer from this disorder for their lifetime and that they may experience mood episodes at various times, some unexpected and severe.  However, the prognosis is not as bleak as it once was as studies are continually showing more and more drugs to be effective mood stabilizers and to be effective in both acute and long-term treatment of BPAD.  Medication management by an experienced and knowledgeable psychiatrist in combination with supportive psychotherapy, education, and support groups can give patients with BPAD hope for their future and effective lifelong management of their disease.

References:

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