CHAPTER 57
Depressive Disorders and Bipolar Disorder
Kristy Loewenstein, MS, RN-BC, PMHNP-BC • William Jacobowitz, MS, MPH, EdD, RN, PMHCNS-BC
Depressive disorders and bipolar disorder (BPD), formerly called manic-depressive disorder, are mood disorders characterized by symptoms observable in the person’s affect, mood, cognition, and behavior. Occurring for specified periods of time, mood disorders cause variable but significant problems in social and occupational functioning. They are prevalent in all age groups and are more commonly diagnosed in women. Women are 50% more likely than men to experience a mood disorder over their lifetime (NIMH, 2005). The majority of suicides occur in persons with serious depression.
Patients with mood disorders are frequently seen in primary care, often presenting with somatic symptoms that complicate the clinical picture. Substance abuse, medications, and serious stressors may be precipitating factors. Frequently, a family history of depression is reported.
Primary care providers, in a managed care environment, may be expected to treat depression rather than refer the patient to a psychiatrist. However, depressive illnesses are, at times, underdiagnosed, untreated, or undertreated in primary care settings. Patients hesitate to discuss symptoms because of embarrassment and fear, or thinking they are only there for physical problems. The provider may avoid asking about suicidal ideation despite recognition of depressed mood. Patients with chronic physical illnesses are not routinely asked about mood and other behaviors indicative of masked depression. Individuals with BPD often present in the primary care setting with a depressed mood, masking the presence of BPD. They have a substantially higher suicide rate than persons with other types of psychiatric disorders and 78% of primary care physicians have failed to detect or have misdiagnosed BPD (Sansone & Sansone, 2011).
Elderly patients are assumed to have dementia when there are memory or concentration difficulties. Unless the provider develops adequate rapport with the patient and views the patient holistically, a mood disorder may be mis-diagnosed as dementia. If the patient is irritable or hostile or shows poor judgment (symptoms of a mood disorder), there is the possibility that the provider may dismiss the patient as uncooperative. Adequate treatment and prevention of further episodes are essential. Collaborative relationships must be maintained with psychiatric services. Prompt referrals and emergency care are vital when symptoms require it. Strategies for prevention may include building healthy coping skills, early detection, and relapse prevention.
ANATOMY, PHYSIOLOGY, AND PATHOLOGY
There are numerous biological changes that occur in depression and BPD, and they have helped create a new understanding of these painful, often life-threatening disorders. Genetic factors, neuroendocrine, neurotransmission, structural, and functional brain changes are all important aspects of the pathology of depression. Physical illness, medication effects, electrolyte disturbances, and nutritional deficits play an important role as well. In addition, exposure to adverse life events has been consistently implicated in the pathophysiology of depression (Klengel & Binder, 2013).
GENETICS
Family studies have demonstrated that monozygotic twins have a rate of concordance (agreement) of 70% to 90% for unipolar (depression, only) and bipolar mood disorders compared with 16% to 35% in dizygotic twins (Sadock & Sadock, 2007). Family aggregation studies point to the increased risk of depression and BPD in first-degree relatives. A child who has one parent with a mood disorder has a 10% to 25% risk of a mood disorder, and if both parents are affected, this risk doubles (Sadock & Sadock, 2007).
NEUROBIOLOGICAL CHANGES
Neurobiological changes in mood disorders primarily involve dysfunction of the limbic system, the basal ganglia, and the hypothalamus. The limbic system, specifically the amygdala, modulates emotions, whereas the hippocampus is implicated in memory and concentration difficulties. Changes in the basal ganglia involve motor changes such as stooped posture, motor slowness, and cognitive impairment. Dysfunction of the hypothalamus involves three axes: the hypothalamic–pituitary–adrenal (HPA) axis, the hypothalamic–pituitary–thyroid axis, and the hypothalamic–pituitary–gonadal axis (Accortt, Freeman, & Allen, 2008). The monamine hypothesis of mood disorders is still a focus of research. Deficits in serotonin and/or norepinephrine are believed to play a part in mood disorders and are targeted by many modern antidepressant medications (Bear, Connors, & Paradiso, 2007; Sadock & Sadock, 2007).
Dysregulation of several neurotransmitter systems has been found in depression and BPD. Neurotransmitters are molecules that carry messages between neurons. They are chemical signals that are stored in and released from the synaptic vesicles within the terminal of the axon (Bear et al., 2007). The biogenic amines, particularly serotonin (5HT) and norepinephrine, interact and modulate a variety of functions, such as movement, mood, attention, emotional behavior, sleep, and visceral function.
Serotonin is derived from the amino acid tryptophan. The source of brain tryptophan is the blood, and the source of blood tryptophan is the diet. Thus, nutritional deficiencies can quickly lead to serotonin depletion (Bear et al., 2007). Depletion of serotonin may precipitate depression, and some patients with suicidal ideation have low concentrations of serotonin in the cerebrospinal fluid and low-serotonin uptake sites on platelets (Sadock & Sadock, 2007).
Depletion of norepinephrine is shown in most, but not all, depressed persons. Norepinephrine, whose precursor is the dietary amino acid tyrosine, is produced in the locus ceruleus and projects through six noradrenergic tracts through various parts of the brain. Dopamine levels are believed to increase in mania and decrease in depression. Gamma-aminobutyric acid (GABA), an inhibitory amino acid neurotransmitter, and acetylcholine (ACTH) are also dysregulated in depression. Neuroendocrine changes in the HPA axis include consistent findings of elevated cortisol secretion from the adrenal glands associated with the stress response. Corticotrophin-releasing hormone (CRH) is regulated by the amygdala and hippocampus. Inappropriate activation of the amygdala activates the stress response and hippocampal activation suppresses CRH release. Glucocorticoid receptors in the hippocampus respond to HPA system activation and there is feedback regulation of the HPA axis, inhibiting CRH, ACTH, and cortisol release when circulating cortisol levels get too high. Hyperactive HPA systems have been posited to be a cause of depression (Bear et al., 2007). HPA axis abnormalities have been reported in depressed women, including those with postpartum depression (Accortt et al., 2008). Elevated-CRH levels in depression normalize after electroconvulsive therapy (ECT) and after treatment with selective serotonin reuptake inhibitor medications (SSRIs).
Growth hormone is inhibited by somatostatin, a hypo-thalamic neuropeptide, and CRH. Decreased cerebrospinal fluid levels of somatostatin have been reported in depression, and increased levels in mania (Sadock & Sadock, 2007). hypothalamic–pituitary–thyroid axis changes frequently occur with depression and BPD. In approximately 5% to 10% of people evaluated for depression, there is previously undetected thyroid dysfunction as evidenced by an elevated thyroid-stimulating hormone (TSH) level (Sadock & Sadock, 2007). Elevation of thyroxin, or T4, may be significant in severely depressed patients.
BIOLOGICAL RHYTHM CHANGES
Sleep alterations frequently occur in both depressive (insomnia and hypersomnia) and manic (insomnia) episodes. This reflects circadian rhythm dysregulation. Sleep problems may include many if not all of the following: delayed sleep onset, shortened rapid eye movement (REM) latency (the time before falling asleep and the first REM period), increased length of first REM period, increased frequency of eye movements during REM sleep, increased spontaneous awakenings, and increased core body temperature. Antidepressant medications, cognitive–behavioral therapy (CBT), and interpersonal social rhythm therapy (IPSRT) are helpful in resetting sleep circadian rhythms.
PHYSICAL ILLNESS AND DEPRESSIVE DISORDERS
Clinically significant depressive symptoms are detectable in 12% to 36% of patients with a concomitant nonpsychiatric medical condition, and an estimated 20% of patients in the primary care setting have depression (Katon, Wulsin, Spiegel, Pinkowish, & Georgi, 2005). Patients with depression have an 81% increased risk for cardiovascular disease onset. One study among depressed patients found multiple metabolic dysregulations (abdominal obesity and lipid disturbances) and inflammatory dysregulation contribute to the chronicity of depression and may be the driving force of the relationship between depression and metabolic syndrome (Penninx, Milaneschi, Lamers, & Vogelzangs, 2013). Depression speeds the onset of cardiovascular disease and diabetes, and increases the risk of mortality for cardiac disease. Depression also increases the onset of stroke and obesity morbidity (Katon et al., 2005; Penninx et al., 2013). Certain physical illnesses that involve the same brain structures that are altered in depression will cause symptoms of depression. For example, in Huntington’s disease there is a high rate of depression, based on the reduction of volume in the putamen and caudate nuclei. In cerebrovascular accidents that involve the frontal and temporal lobes, manic symptoms are more common with right-sided lesions, whereas depressive symptoms are more common with left-sided lesions.
PSYCHOLOGICAL THEORIES
Psychological theories of depression are represented in a number of classic texts in the published literature. The psychoanalytic explanation of depression is anger directed internally. Early attachment difficulties, based on the impact of separation and loss, may precipitate depression (Bowlby, 1980). Behavioral theory views vulnerability to depression as a lack of social support, causing loneliness and isolation (Skinner, 1953). Inadequate social skills that prevent positive reinforcement from others contribute to depression under this model (Lewinsohn, 1974). Cognitive theory proposes that depression is precipitated and maintained by negative thoughts and attitudes (Beck, 1976).
EPIDEMIOLOGY
Depressive disorders and BPD are serious mental health problems that must be addressed in primary care. Depression affects 6.7% of the population in 12-month prevalence studies, and 30.4% of these cases are classified as severe. Women are 70% more likely than men and non-Hispanic Blacks are 40% less likely than non-Hispanic Whites to experience depression during their lifetime (NIMH, 2005; Reeves, 2011). Depression and BPD are found in all cultures. Cultural expressions of symptoms vary and should be considered during all aspects of care. True psychosis must be distinguished from culturally specific experiences. Treatment choices must be sensitive to the cultural needs of patients.
Increased rates of alcoholism are seen in depression. One study found that prior alcohol dependence in the patient increased the risk of current depression more than fourfold (Arnaout, Batchelder, Rosenthal, Hyler, & Hellerstein, 2008). The 12-month prevalence of persistent depressive disorder has been found to be 1.5% of the U.S. population, with 49.7% of these cases classified as severe (NIMH, 2005).
BPD disorder has a 12-month prevalence of 2.6% of the U.S. adult population, with 82.9% classified as severe. There is approximately equal gender distribution and no association with race or ethnic origin (NIMH, 2005). BPD usually starts in late adolescence or early adulthood. Studies estimate 0% to 3% prevalence among adolescence (NIMH, 2005).
DIAGNOSTIC CRITERIA
Screening, assessment, accurate diagnosis, adequate treatment, frequent follow-up, and referrals for psychotherapy and psychiatric evaluation (if needed) are critical for patients with symptoms of depression and BPD. Any patient with a history of depression or BPD needs to be assessed on a regular basis for treatment response, side effects, new symptoms, and recurrence of symptoms. Patients need encouragement to obtain and continue treatment. Providers need a thorough understanding of the diagnostic categories and the complexity and variability of depressive symptoms. The following is a list of diagnostic tools that can assist the primary care provider.
Diagnostic Tools for Depression
Altman Self-Rating Mania Scale (Altman, Hedeker, Peterson, & Davis, 1997; www.cqaimh.org/pdf/tool_asrm.pdf).
PROMIS Emotional Distress—Depression—Short Form (www.assessmentcenter.net/)
LEVEL 2—Somatic Symptom—Adult Patient (adapted from the Patient Health Questionnaire Physical Symptoms; www.phqscreeners.com/pdfs/04_PHQ-15/English.pdf)
PROMIS—Sleep Disturbance—Short Form (www.nihpromis.org/measures/SampleQuestions)
Severity Measure for Depression—Adult, Adapted from the Patient Health Questionnaire–9 (PHQ-9; www.cqaimh.org/pdf/tool_phq9.pdf)
A clinical history focusing on the patient’s history, including age, gender, family system, and cultural considerations, can also aid in the diagnosis of depression or BPD. The result of the screening tools, mental status exam, laboratory values, and physical examination will help determine the presence of depression or BPD. Medical illnesses and medications that may precipitate depression must also be evaluated (Tables 57.1 and 57.2).
SYMPTOMS—MAJOR DEPRESSIVE DISORDER
Major depressive disorder (MDD), or unipolar depression, is the most frequently diagnosed mood-related disorder. It signifies there have been at least one major depressive episode and no manic or hypomanic episodes. Symptoms have occurred every day for 2 weeks or longer. Significant distress or impairment in psychosocial or work functioning must be present. For a diagnosis of MDD to be made, substance use, medication, and medical conditions must be ruled out. A mood disturbance must be present with a number of alterations from normal mood (e.g., depressed mood with typical sadness, agitation and anger, irritability, dysphoria, numbing of feelings, or somatic preoccupation). Of equal importance is the loss of pleasure in activities that were previously enjoyed, such as hobbies, work, or sexual activity. One of these two symptoms (mood disturbance or loss of pleasure) must be present for a diagnosis of MDD.
General Medical Conditions Associated With Depression |
NEUROLOGIC Parkinson’s disease Huntington’s disease stroke Multiple sclerosis Sleep apnea Cerebral tumors Alzheimer’s disease | NUTRITIONAL Vitamin B12 deficiency Pernicious anemia |
CARDIOVASCULAR Coronary artery disease | |
INFECTIOUS Influenza Viral hepatitis General paresis Tertiary syphilis Tuberculosis Infectious mononucleosis Chronic fatigue syndrome | ENDOCRINE Cushing’s disease Addison’s disease Diabetes mellitus Hypo- and hyperthyroidism |
NEOPLASTIC Carcinoma of head of pancreas Oat cell carcinoma | |
COLLAGEN Systemic lupus erythematosus Scleroderma Rheumatoid arthritis |
|
Additional symptoms must also be present. Three neuro-vegetative symptoms are evaluated: sleep, appetite, and psychomotor activity. Sleep alteration may be present (insomnia or hypersomnia). Insomnia can take the form of difficulty falling asleep (initial insomnia), frequent waking without being able to fall back to sleep quickly (middle insomnia), or waking several hours earlier than usual (terminal insomnia). Hypersomnia means the person sleeps several more hours a day than is usual for that person. A key concern is whether the person feels rested after a night’s sleep. Psychomotor activity may be observed as either very sluggish, slow movements, or agitation and pacing. A significant increase or decrease in appetite and weight gain or loss, that is, 5% or more of body weight, is a pertinent finding. Another symptom to evaluate includes a feeling of fatigue or loss of energy, expressed as a loss of will.
Medications Associated With Depressed Mood and Manic Symptoms |
DEPRESSED MOOD | MANIC SYMPTOMS |
Reserpine Propranolol Glucocorticoids Alcohol Physostigmine Sedative—hypnotics Amphetamine or cocaine withdrawal Benzodiazepines Neuroleptics Anti-inflammatories Anticonvulsants Antihypertensives Antineoplastics Antiparkinsonian drugs Stimulants Antihistamines Cimetidine Ranifidine Disulfiram Methysergide Antibiotics | Levodopa Amphetamines Bromide Bromocriptine Captopril Cimetidine Cocaine Corticosteroids Cyclosporine Disulfiram Hallucinogens Hydralazine Isoniazid Methylphenidate Metrizamide (following myelography) MAOIs Opiates and opioids Procarbazine Procyclidine TCAs Thyroid hormones |
MAOi, monoamine oxidase inhibitor; TCA, tricyclic antidepressant.
Feelings of worthlessness and guilt are common, sometimes manifested in psychotic delusions. Difficulty with concentration, thinking, or making decisions is distressing. A patient may forget to bathe or change clothes or complain of not being able to complete tasks. In the older person, memory loss may appear as dementia when in fact it is pseudodementia, which is a temporary loss of memory caused by depression. (Detailed criteria for major depressive episodes are available in the DSM-5).
Suicidality is an extremely serious symptom of MDD and must be assessed in anyone who has mood alteration. Hopelessness and thoughts of death without specific suicidal thoughts (e.g., “Death would be such a relief. Why go on?”) may be indicative of the presence of a suicide plan. More serious are suicidal thoughts or ideation (e.g., “I keep thinking that it is time to end it [my life].”), and a history of having actually attempted suicide further increases the risk of suicide. Asking the patient about suicidal thoughts will not cause the person to become suicidal. Frequency of thoughts, presence of a plan, methods, previous attempts, and history of suicide in the family are important assessment factors.
The types of depressive disorders include:
1. Disruptive mood dysregulation disorder
2. MDD (including major depressive episode)
3. Persistent depressive disorder (dysthymia)
4. Premenstrual dysphoric disorder
5. Substance/medication-induced depressive disorder
6. Depressive disorder due to another medical condition
7. Other specified depressive disorder
8. Unspecified depressive disorder (American Psychiatric Association [APA], 2013)
There are subtypes that delineate the severity and type of depression. These include mild, moderate, and severe (referring to the severity of impairment in functioning); psychosis with hallucinations or delusions; catatonic features; melancholic features; and atypical features.
The onset of depression in the peripartum/postpartum period (during the pregnancy or within 4 weeks of delivery) is a serious and potentially dangerous situation with respect to the safety of the mother and fetus/child. It can manifest with or without psychotic features. Women experiencing postpartum depression with psychotic features are 30% to 50% more likely to have a recurrence of the disorder with later deliveries (APA, 2013), and are at significant risk of causing harm to themselves and/or the child. Guilt is a major component of this type of depression.
Seasonal pattern delineation is made when there is a 2-year pattern of recurrence during the winter (or, more rarely, during the summer). Characteristics are weight gain, low energy, hypersomnia, and carbohydrate craving. Remission requires 2 months without symptoms.
The hallmarks of persistent depressive disorder include a depressed mood for most of the day, and for more days than not, as indicated by either subjective account or observation by others, and for a duration of at least 2 years. Two or more of the following symptoms must be present while depressed (APA, 2013).
Responses to a loss (e.g., bereavement, financial ruin, losses from a natural disaster, a serious medical illness or disability) may include the feelings of intense sadness, rumination about the loss, insomnia, poor appetite, and weight loss, which may resemble a depressive episode. Although such symptoms may be understandable, the presence of a major depressive episode in addition to the normal grieving responses should also be carefully considered (APA, 2013).
SYMPTOMS—BIPOLAR DISORDERS
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