1. Learn to understand the neuroscience of Mental Health.
2. Identify the manifestations of mental illness.
3. Describe the etiology of mental illness including biological and psychosocial influences.
4. Identify treatment options including pharmacological therapies.
5. Identify cultural diversity, demographics and barriers to receiving treatment.
A vast body of research on mental health and, to an even greater extent, on mental illness constitutes the foundation of this Surgeon General’s report. To understand and better appreciate the content of the chapters that follow, readers outside the mental health field may desire some background information. Thus, this chapter furnishes a “primer” on topics that the report addresses.
The chapter begins with an overview of research under way today that is focused on the neuroscience of mental health. Modern integrative neuroscience offers a means of linking research on broad “systems level” aspects of brain function with the remarkably detailed tools and findings of molecular biology. The report begins with a discussion of the brain because it is central to what makes us human and provides an understanding of mental health and mental illness. All of human behavior is mediated by the brain. Consider, for example, a memory that most people have from childhood—that of learning to ride a bicycle with the help of a parent or friend. The fear of falling, the anxiety of lack of control, the reassurances of a loved one, and the final liberating experience of mastery and a newly extended universe create an unforgettable combination. For some, the memories are not good ones: falling and being chased by dogs have left marks of anxiety and fear that may last a lifetime. Science is revealing how the skill learning, emotional overtones, and memories of such experiences are put together physically in the brain. The brain and mind are two sides of the same coin. Mind is not possible without the remarkable physical complexity that is built into the brain, but, in addition, the physical complexity of the brain is useless without the sculpting that environment, experience, and thought itself provides. Thus the brain is now known to be physically shaped by contributions from our genes and our experience, working together. This strengthens the view that mental disorders are both caused and can be treated by biological and experiential processes, working together. This understanding has emerged from the breathtaking progress in modern neuroscience that has begun to integrate knowledge from biological and behavioral sciences.
An overview of mental illness follows the section on modern integrative brain science. The section highlights topics including symptoms, diagnosis, epidemiology (i.e., research having to do with the distribution and determinants of mental disorders in population groups, including various racial and ethnic minority groups), and cost, all of which are discussed in greater and more pointed detail in the chapters that follow. Etiology is the study of the origins and causes of disease, and that section reviews research that is seeking to define, with ever greater precision, the causes of mental disorders. As will be seen, etiology research examines fundamental biological, behavioral, and sociocultural processes, as well as a necessarily broad array of life events. The section on development of temperament reveals how mental health science has attempted over much of the past century to understand how biological, psychological, and sociocultural factors meld in health as well as in illness. The chapter then reviews research approaches to the prevention and treatment of mental disorders and provides an overview of mental health services and their delivery. Final sections cover the growing influence on the mental health field of the need for attention to cultural diversity, the importance of the consumer movement, and new optimism about recovery from mental illness—that is, the possibility of recovering one’s life.
The Neuroscience of Mental Health1
Complexity of the Brain I: Structural
As befits the organ of the mind, the human brain is the most complex structure ever investigated by our science. The brain contains approximately 100 billion nerve cells, or neurons, and many more supporting cells, or ganglia. In and of themselves, the number of cells in this 3-pound organ reveal little of its complexity. Yet most organs in the body are composed of only a handful of cell types; the brain, in contrast, has literally thousands of different kinds of neurons, each distinct in terms of its chemistry, shape, and connections (Figure 2-1 depicts the structural variety of neurons). To illustrate, one careful, recent investigation of a kind of interneuron that is a small local circuit neuron in the retina, called the amacrine cell, found no less than 23 identifiable types.
But this is only the beginning of the brain’s complexity.
The workings of the brain depend on the ability of nerve cells to communicate with each other. Communication occurs at small, specialized structures called synapses. The synapse typically has two parts. One is a specialized presynaptic structure on a terminal portion of the sending neuron that contains packets of signaling chemicals, or neurotransmitters. The second is a postsynaptic structure on the dendrites of the receiving neuron that has receptors for the neurotransmitter molecules.
The typical neuron has a cell body, which contains the genetic material, and much of the cell’s energy-producing machinery. Emanating from the cell body are dendrites, branches that are the most important receptive surface of the cell for communication. The dendrites of neurons can assume a great many shapes and sizes, all relevant to the way in which incoming messages are processed. The output of neurons is carried along what is usually a single branch called the axon. It is down this part of the neuron that signals are transmitted out to the next neuron. At its end, the axon may branch into many terminals. (Figure 2-2.)
The usual form of communication involves electrical signals that travel within neurons, giving rise to chemical signals that diffuse, or cross, synapses, which in turn give rise to new electrical signals in the postsynaptic neuron. Each neuron, on average, makes more than 1,000 synaptic connections with other neurons. One type of cell—a Purkinje cell—may make between 100,000 and 200,000 connections with other neurons. In aggregate, there may be between 100 trillion and a quadrillion synapses in the brain. These synapses are far from random. Within each region of the brain, there is an exquisite architecture consisting of layers and other anatomic substructures in which synaptic connections are formed. Ultimately, the pattern of synaptic connections gives rise to what are called circuits in the brain. At the integrative level, large- and small-scale circuits are the substrates of behavior and of mental life. One of the most awe-inspiring mysteries of brain science is how neuronal activity within circuits gives rise to behavior and, even, consciousness.
The complexity of the brain is such that a single neuron may be part of more than one circuit. The organization of circuits in the brain reveals that the brain is a massively parallel, distributed information processor. For example, the circuits involved in vision receive information from the retina. After initial processing, these circuits analyze information into different streams, so that there is one stream of information describing what the visual object is, and another stream is concerned with where the object is in space. The information stream having to do with the identity of the object is actually broken down into several more refined parallel streams. One, for example, analyzes shape while another analyzes color. Ultimately, the visual world is resynthesized with information about the tactile world, and the auditory world, with information from memory, and with emotional coloration. The massively parallel design is a great pattern recognizer and very tolerant of failure in individual elements. This is why a brain of neurons is still a better and longer-lasting information processor than a computer.
The specific connectivity of circuits is, to some degree, stereotyped, or set in expected patterns within the brain, leading to the notion that certain places in the brain are specialized for certain functions (Figure 2-3). Thus, the cerebral cortex, the mantle of neurons with its enormous surface area increased by outpouchings, called gyri, and indentations, called sulci, can be functionally subdivided. The back portion of the cerebral cortex (i.e., the occipital lobe), for example, is involved in the initial stages of visual processing. Just behind the central sulcus is the part of the cerebral cortex involved in the processing of tactile information (i.e., parietal lobe). Just in front of the central sulcus is a part of the cerebral cortex involved in motor behavior (frontal lobe). In the front of the brain is a region called the prefrontal cortex, which is involved with some of the highest integrated functions of the human being, including the ability to plan and to integrate cognitive and emotional streams of information.
Beneath the cortex are enormous numbers of axons sheathed in the insulating substance, myelin. This subcortical “white matter,” so named because of its appearance on freshly cut brain sections, surrounds deep aggregations of neurons, or “gray matter,” which, like the cortex, appears gray because of the presence of neuronal cell bodies. It is within this gray matter that the brain processes information. The white matter is akin to wiring that conveys information from one region to another. Gray matter regions include the basal ganglia, the part of the brain that is involved in the initiation of motion and thus profoundly affected in Parkinson’s disease, but that is also involved in the integration of motivational states and, thus, a substrate of addictive disorders. Other important gray matter structures in the brain include the amygdala and the hippocampus. The amygdala is involved in the assignment of emotional meaning to events and objects, and it appears to play a special role in aversive, or negative, emotions such as fear. The hippocampus includes, among its many functions, responsibility for initially encoding and consolidating explicit or episodic memories of persons, places, and things.
In summary, the organization of the brain at the cellular level involves many thousands of distinct kinds of neurons. At a higher integrative level, these neurons form circuits for information processing determined by their patterns of synaptic connections. The organization of these parallel distributed circuits results in the specialization of different geographic regions of the brain for different functions. It is important to state at this point, however, that, especially in younger individuals, damage to a particular brain region may yield adaptations that permit circuits spared the damage and, therefore, other regions of the brain, to pick up some of the functions that would otherwise have been lost.
Complexity of the Brain II: Neurochemical
Superimposed on this breathtaking structural complexity is the chemical complexity of the brain. As described above, electrical signals within neurons are converted at synapses into chemical signals which then elicit electrical signals on the other side of the synapse. These chemical signals are molecules called neurotransmitters. There are two major kinds of molecules that serve the function of neurotransmitters: small molecules, some quite well known, with names such as dopamine, serotonin, or norepinephrine, and larger molecules, which are essentially protein chains, called peptides. These include the endogenous opiates, Substance P, and corticotropin releasing factor (CRF), among others. All told, there appear to be more than 100 different neurotransmitters in the brain (Table 2-1 contains a selected list).
A neurotransmitter can elicit a biological effect in the postsynaptic neuron by binding to a protein called a neurotransmitter receptor. Its job is to pass the information contained in the neurotransmitter message from the synapse to the inside of the receiving cell. It appears that almost every known neurotransmitter has more than one different kind of receptor that can confer rather different signals on the receiving neuron. Dopamine has 5 known neurotransmitter receptors; serotonin has at least 14.
Table 2-1. Selected neurotransmitters important in psychopharmacology
Excitatory amino acid
Glutamate
Inhibitory amino acids
Gamma aminobutyric acid
Glycine
Monoamines and related neurotransmitters
Norepinephrine
Dopamine
Serotonin
Histamine
Acetylcholine (quarternary amine)
Purine
Adenosine
Neuropeptides
Opioids
Enkephalins
Beta-endorphin
Dynorphin
Tachykinin
Substance P
Hypothalamic-releasing factors
Corticotropin-releasing hormone
|
Although there are many kinds of receptors with many different signaling functions, we can divide most neurotransmitter receptors into two general classes. One class of neurotransmitter receptor is called a ligand-gated channel, where “ligand” simply means a molecule (i.e., a neurotransmitter) that binds to a receptor. When neurotransmitters interact with this kind of receptor, a pore within the receptor molecule itself is opened and positive or negative charges enter the cell. The entry of positive charge may activate additional ion channels that allow more positive charge to enter. At a certain threshold, this causes a cell to fire an action potential—an electrical event that leads ultimately to the release of neurotransmitter. By definition, therefore, receptors that admit positive charge are excitatory neurotransmitter receptors. The classic excitatory neurotransmitter receptors in the brain utilize the excitatory amino acids glutamate and, to a lesser degree, aspartate as neurotransmitters. Conversely, inhibitory neurotransmitters act by permitting negative charges into the cell, taking the cell farther away from firing. The classic inhibitory neurotransmitters in the brain are the amino acids gamma amino butyric acid, or GABA, and, to a lesser degree, glycine.
Most of the other neurotransmitters in the brain, such as dopamine, serotonin, and norepinephrine, and all of the many neuropeptides constitute the second major class. These are neither precisely excitatory nor inhibitory but rather act to produce complex biochemical changes in the receiving cell. Their receptors do not contain intrinsic ion pores but rather interact with signaling proteins, called“G proteins” found inside the cell membrane. These receptors thus are called G protein-linked receptors. The details are less important than understanding the general scheme. Stimulation of G protein-linked receptors alters the way in which receiving neurons can process subsequent signals from glutamate or GABA. To use a metaphor of a musical instrument, if glutamate, the excitatory neurotransmitter, is puffing wind into a flute or clarinet, it is the modulatory neurotransmitters such as dopamine or serotonin that might be seen as playing the keys and, thus, altering the melody via G protein-linked receptors.
The architecture of these systems drives home this point. The precise brain circuits that carry specific information about the world and that are involved in precise point-to-point communication within the brain use excitatory or inhibitory neurotransmission. Examples of such circuits, which are massively parallel, can be found in the visual and auditory cortex. Overlying this pattern of precise, rapid (timing in the range of milliseconds) neurotransmission are the modulatory systems in the brain that use norepinephrine, serotonin, and dopamine. In each case, the neurotransmitter in question is made by a very small number of nerve cells clustered in a limited number of areas in the brain. Of the hundred billion neurons in the brain, only about 500,000, for example, make dopamine—that is, for every 200,000 cells in the brain, only one makes dopamine. Even fewer make norepinephrine. The cell bodies of the dopamine neurons are clustered in a few brain regions, most importantly, regions deep in the brain, in the midbrain, called the substantia nigra, and the ventral tegmental area. Norepinephrine neurons are made in the nucleus locus coeruleus even farther down in the brain stem in a structure called the pons. Serotonin is made by a somewhat larger number of nuclei but, still, not by many cells. Nuclei called the raphe nuclei spread along the brain stem. While each of these neurotransmitters is made by a small number of neurons with clustered cell bodies, each sends its axons branching throughout the brain, so that in each case a very small number of neurons, which largely appear to fire in unison when excited, influence almost the entire brain. This is not the picture of systems that are communicating precise bits of information about the world but rather are intrinsic modulatory systems that act via other G protein-linked receptors to alter the overall responsiveness of the brain. These neurotransmitters are responsible for brain states such as degree of arousal, ability to pay attention, and for putting emotional color or significance on top of cold cognitive information provided by precise glutaminergic circuits. It is no wonder that these modulatory neurotransmitters and their receptors are critical targets of medications used to treat mental disorders—for example, the antidepressant and antipsychotic drugs—and also are the targets of drugs of abuse.
Complexity of the Brain III: Plasticity
The preceding paragraphs have illustrated the chemical and anatomic structure of the brain and, in so doing, provided some picture of its complexity as well as some picture of its function. The crowning complexity of the brain, however, is that it is not static. The brain is always changing. People learn so much and have so many distinct types of memory: conscious, episodic memory of the sort that is encoded initially in the hippocampus; memory of motor programs or procedures that are encoded in the striatum; emotional memories that can initiate physiologic and behaviorally adaptive repertoires encoded, for example, in the amygdala; and many other kinds. Every time a person learns something new, whether it is conscious or unconscious, that experience alters the structure of the brain. Thus, neurotransmission in itself not only contains current information but alters subsequent neurotransmission if it occurs with the right intensity and the right pattern. Experience that is salient enough to cause memory creates new synaptic connections, prunes away old ones, and strengthens or weakens existing ones. Similarly, experiences as diverse as stress, substance abuse, or disease can kill neurons, and current data suggest that new neurons continue to develop even in adult brains, where they help to incorporate new memories. The end result is that information is now routed over an altered circuit. Many of these changes are long-lived, even permanent. It is in this way that a person can look back 10 or 20 or 50 years and remember family, a home or school room, or friends. The general theme is that to really understand the kind of memory—indeed, any brain function—one must think at least at two levels: one, the level of molecular and cellular alterations that are responsible for remodeling synapses, and, two, the level of information content and behavior which circuits and synapses serve.
To summarize this section, scientists are truly beginning to learn about the structure and function of the brain. Its awe-inspiring complexity is fully consistent with the fact that it supports all behavior and mental life. Implied in the foregoing, is the fact that brains are built not only by genes—and again, it is the lion’s share of the 80,000 or so human genes that are involved in building a structure so complex as the brain. Genes are not by themselves the whole story. Brains are built and changed through life through the interaction of genes with environment, including experience. It is true that a set of genes might create repetitive multiples of one type of unit, yet the brain appears far more complex than that. It stands to reason that if 50,000 or 60,000 genes are involved in building a brain that may have 100 trillion or a quadrillion synapses, additional information is needed, and that information comes from the environment. It is this fundamental realization that is beginning to permit an understanding of how treatment of mental disorders works—whether in the form of a somatic intervention such as a medication, or a psychological “talk” therapy—by actually changing the brain.
Imaging the Brain
There are many exciting developments in brain science. Of great relevance to the study of mental function and mental illness is the ability to image the activity of the living human brain with technologies developed in recent decades, such as positron emission tomography scanning or functional magnetic resonance imaging. Such approaches can exploit surrogates of neuronal firing such as blood flow and blood oxygenation to provide maps of activity. As science learns more about brain circuitry and learns more from cognitive and affective neuroscience about how to activate and examine the function of particular brain circuits, differences between health and illness in the function of particular circuits certainly will become evident. We will be able to see the action of psychotropic drugs and, perhaps most exciting, we will be able to see the impact of that special kind of learning called psychotherapy, which works after all because it works on the brain.
Different brain chemicals, brain receptors, and brain structures will come up in the discussion of particular illnesses throughout this document. This section is meant to provide a panoramic, not a detailed, introduction and also to provide certain overarching lessons. When something is referred to as biological or brain-based, that is not shorthand for saying it is genetic and, thus, predetermined; similarly, references to “psychological” or even “social” phenomena do not exclude biological processes. The brain is the great integrator, bringing together genes and environment. The study of the brain requires reducing problems initially to bite-sized bits that will allow investigators to learn something, but ultimately, the agenda of neuroscience is not reductionist; the goal is to understand behavior, not to put blinders on and try to explain it away. As the foregoing discussion illustrates, the brain also is complex. Thus, having a disease that affects one or even many critical circuits does not overthrow, except in extreme cases, such as advanced Alzheimer’s disease, all aspects of a person. Typically, people retain their personality and, in most cases, their ability to take responsibility for themselves.
In retrospect, early biological models of the mind seem impoverished and deterministic—for example, models that held that “levels” of a neurotransmitter such as serotonin in the brain were the principal influence on whether one was depressed or aggressive. Neuroscience is far beyond that now, working to integrate information coming “bottom-up” from genes and molecules and cells, with information flowing “top-down” from interactions with the environment and experience to the internal workings of the mind and its neuronal circuits. Ultimately, however, the goal is not only human self-understanding. In knowing eventually precisely what goes wrong in what circuits and what synapses and with what chemical signals, the hope is to develop treatments with greater effectiveness and with fewer side effects. Indeed, as the following chapters indicate, the hope is for cures and ultimately for prevention. There is every reason to hope that as our science progresses, we will achieve those goals.
Overview of Mental Illness
Mental illness is a term rooted in history that refers collectively to all of the diagnosable mental disorders. Mental disorders are characterized by abnormalities in cognition, emotion or mood, or the highest integrative aspects of behavior, such as social interactions or planning of future activities. These mental functions are all mediated by the brain. It is, in fact, a core tenet of modern science that behavior and our subjective mental lives reflect the overall workings of the brain. Thus, symptoms related to behavior or our mental lives clearly reflect variations or abnormalities in brain function. On the more difficult side of the ledger are the terms disorder, disease, or illness. There can be no doubt that an individual with schizophrenia is seriously ill, but for other mental disorders such as depression or attention-deficit/hyperactivity disorder, the signs and symptoms exist on a continuum and there is no bright line separating health from illness, distress from disease. Moreover, the manifestations of mental disorders vary with age, gender, race, and culture. The thresholds of mental illness or disorder have, indeed, been set by convention, but the fact is that this gray zone is no different from any other area of medicine. Ten years ago a serum cholesterol of 200 was considered normal. Today, this same number alarms some physicians and may lead to treatment. Perhaps every adult in the United States has some atherosclerosis, but at what point does this move along a continuum from normal into the realm of illness? Ultimately, the dividing line has to do with severity of symptoms, duration, and functional impairment.
Despite the existence of a gray zone between health and illness, science can study the mechanisms by which illness occurs. Indeed, understanding mood regulation and its abnormalities, for example, proceeds independently from any set of diagnostic clinical criteria. Family studies, molecular genetics strategies, epidemiology, and the tools of clinical investigation tailored to specific populations are being used to investigate the mechanisms of mental illness. Specific manifestations of mental illness will be covered in succeeding pages.
This overview of mental illness focuses on those features of the disease process that are most common and characteristic of these disorders. The chapters that follow will present specific details about major categories of mental disorders that occur across the life span. The purpose here is to provide a framework upon which subsequent discussions of specific disorders can rest. The section leads with a descriptive overview of the cardinal manifestations, signs, and symptoms of mental disorders. It then describes how mental disorders are diagnosed and classified and provides an overview of the epidemiology and societal burden of mental disorders.
Manifestations of Mental Illness
Persons suffering from any of the severe mental disorders present with a variety of symptoms that may include inappropriate anxiety, disturbances of thought and perception, dysregulation of mood, and cognitive dysfunction. Many of these symptoms may be relatively specific to a particular diagnosis or cultural influence. For example, disturbances of thought and perception (psychosis) are most commonly associated with schizophrenia. Similarly, severe disturbances in expression of affect and regulation of mood are most commonly seen in depression and bipolar disorder. However, it is not uncommon to see psychotic symptoms in patients diagnosed with mood disorders or to see mood-related symptoms in patients diagnosed with schizophrenia. Symptoms associated with mood, anxiety, thought process, or cognition may occur in any patient at some point during his or her illness.
Anxiety
Anxiety is one of the most readily accessible and easily understood of the major symptoms of mental disorders. Each of us encounters anxiety in many forms throughout the course of our routine activities. It may often take the concrete form of intense fear experienced in response to an immediately threatening experience such as narrowly avoiding a traffic accident. Experiences like this are typically accompanied by strong emotional responses of fear and dread as well as physical signs of anxiety such as rapid heart beat and perspiration. Some of the more common signs and symptoms of anxiety are listed in Table 2-2. Anxiety is aroused most intensely by immediate threats to one’s safety, but it also occurs commonly in response to dangers that are relatively remote or abstract. Intense anxiety may also result from situations that one can only vaguely imagine or anticipate.
Anxiety has evolved as a vitally important physiological response to dangerous situations that prepares one to evade or confront a threat in the environment. The appropriate regulation of anxiety is critical to the survival of virtually every higher organism in every environment. However, the mechanisms that regulate anxiety may break down in a wide variety of circumstances, leading to excessive or inappropriate expression of anxiety. Specific examples include phobias, panic attacks, and generalized anxiety. In phobias, high-level anxiety is aroused by specific situations or objects that may range from concrete entities such as snakes, to complex circumstances such as social interactions or public speaking. Panic attacks are brief and very intense episodes of anxiety that often occur without a precipitating event or stimulus. Generalized anxiety represents a more diffuse and nonspecific kind of anxiety that is most often experienced as excessive worrying, restlessness, and tension occurring with a chronic and sustained pattern. In each case, an anxiety disorder may be said to exist if the anxiety experienced is disproportionate to the circumstance, is difficult for the individual to control, or interferes with normal functioning.
In addition to these common manifestations of anxiety, obsessive-compulsive disorder and post-traumatic stress disorder are generally believed to be related to the anxiety disorders. The specific clinical features of these disorders will be described more fully in the following chapters; however, their relationship to anxiety warrants mention in the present context. In the case of obsessive-compulsive disorder, individuals experience a high level of anxiety that drives their obsessional thinking or compulsive behaviors. When such an individual fails to carry out a repetitive behavior such as hand washing or checking, there is an experience of severe anxiety. Thus while the outward manifestations of obsessive-compulsive disorder may seem to be related to other anxiety disorders, there appears to be a strong component of abnormal regulation of anxiety underlying this disorder. Post-traumatic stress disorder is produced by an intense and overwhelmingly fearful event that is often life-threatening in nature. The characteristic symptoms that result from such a traumatic event include the persistent reexperience of the event in dreams and memories, persistent avoidance of stimuli associated with the event, and increased arousal.
Table 2-2. Common signs of acute anxiety
| • Feelings of fear or dread |
| • Trembling, restlessness, and muscle tension |
| • Rapid heart rate |
| • Lightheadedness or dizziness |
| • Perspiration |
| • Cold hands/feet |
| • Shortness of breath |
Psychosis
Disturbances of perception and thought process fall into a broad category of symptoms referred to as psychosis. The threshold for determining whether thought is impaired varies somewhat with the cultural context. Like anxiety, psychotic symptoms may occur in a wide variety of mental disorders. They are most characteristically associated with schizophrenia, but psychotic symptoms can also occur in severe mood disorders.
One of the most common groups of symptoms that result from disordered processing and interpretation of sensory information are the hallucinations. Hallucinations are said to occur when an individual experiences a sensory impression that has no basis in reality. This impression could involve any of the sensory modalities. Thus hallucinations may be auditory, olfactory, gustatory, kinesthetic, tactile, or visual. For example, auditory hallucinations frequently involve the impression that one is hearing a voice. In each case, the sensory impression is falsely experienced as real.
A more complex group of symptoms resulting from disordered interpretation of information consists of delusions. A delusion is a false belief that an individual holds despite evidence to the contrary. A common example is paranoia, in which a person has delusional beliefs that others are trying to harm him or her. Attempts to persuade the person that these beliefs are unfounded typically fail and may even result in the further entrenchment of the beliefs.
Hallucinations and delusions are among the most commonly observed psychotic symptoms. A list of other symptoms seen in psychotic illnesses such as schizophrenia appears in Table 2-3. Symptoms of schizophrenia are divided into two broad classes: positive symptoms and negative symptoms. Positive symptoms generally involve the experience of something in consciousness that should not normally be present. For example, hallucinations and delusions represent perceptions or beliefs that should not normally be experienced. In addition to hallucinations and delusions, patients with psychotic disorders such as schizophrenia frequently have marked disturbances in the logical process of their thoughts. Specifically, psychotic thought processes are characteristically loose, disorganized, illogical, or bizarre. These disturbances in thought process frequently produce observable patterns of behavior that are also disorganized and bizarre. The severe disturbances of thought content and process that comprise the positive symptoms often are the most recognizable and striking features of psychotic disorders such as schizophrenia or manic depressive illness.
Table 2-3. Common manifestations of schizophrenia
|
Positive Symptoms
|
| • Hallucinations |
| • Delusions |
| • Disorganized thoughts and behaviors |
| • Loose or illogical thoughts |
| • Agitation |
|
Negative Symptoms
|
| • Flat or blunted affect |
| • Concrete thoughts |
| • Anhedonia (inability to experience pleasure) |
| • Poor motivation, spontaneity, and initiative |
However, in addition to positive symptoms, patients with schizophrenia and other psychoses have been noted to exhibit major deficits in motivation and spontaneity that are referred to as negative symptoms. While positive symptoms represent the presence of something not normally experienced, negative symptoms reflect the absence of thoughts and behaviors that would otherwise be expected. Concreteness of thought represents impairment in the ability to think abstractly. Blunting of affect refers to a general reduction in the ability to express emotion. Motivational failure and inability to initiate activities represent a major source of long-term disability in schizophrenia. Anhedonia reflects a deficit in the ability to experience pleasure and to react appropriately to pleasurable situations. Positive symptoms such as hallucinations are responsible for much of the acute distress associated with schizophrenia, but negative symptoms appear to be responsible for much of the chronic and long-term disability associated with the disorder.
The psychotic symptoms represent manifestations of disturbances in the flow, processing, and interpretation of information in the central nervous system. They seem to share an underlying commonality of mechanism, insofar as they tend to respond as a group to specific pharmacological interventions. However, much remains to be learned about the brain mechanisms that lead to psychosis.
Disturbances of Mood
Most of us have an immediate and intuitive understanding of the notion of mood. We readily comprehend what it means to feel sad or happy. These concepts are nonetheless very difficult to formulate in a scientifically precise and quantifiable way; the challenge is greater given the cultural differences that are associated with the expression of mood. In turn, disorders that impact on the regulation of mood are relatively difficult to define and to approach in a quantitative manner. Nevertheless, dysregulation of mood and the expression of mood, or affect, represent a major category among mental disorders.
Disturbances of mood characteristically manifest themselves as a sustained feeling of sadness or sustained elevation of mood. As with anxiety and psychosis, disturbances of mood may occur in a variety of patterns associated with different mental disorders. The disorder most closely associated with persistent sadness is major depression, while that associated with sustained elevation or fluctuation of mood is bipolar disorder. The most common signs of these mood disorders are listed in Table 2-4. Along with the prevailing feelings of sadness or elation, disorders of mood are associated with a host of related symptoms that include disturbances in appetite, sleep patterns, energy level, concentration, and memory.
Table 2-4. Common signs of mood disorders
|
Symptoms Commonly Associated With Depression
|
| • Persistent sadness or despair |
| • Insomnia (sometimes hypersomnia) |
| • Decreased appetite |
| • Psychomotor retardation |
| • Anhedonia (inability to experience pleasure) |
| • Irritability |
| • Apathy, poor motivation, social withdrawal |
| • Hopelessness |
| • Poor self-esteem, feelings of helplessness |
| • Suicidal ideation |
|
Symptoms Commonly Associated With Mania
|
| • Persistently elevated or euphoric mood |
| • Grandiosity (inappropriately high self-esteem) |
| • Psychomotor agitation |
| • Decreased sleep |
| • Racing thoughts and distractibility |
| • Poor judgment and impaired impulse control |
| • Rapid or pressured speech |
It is not known why diverse functions such as sleep and appetite should be altered in disorders of mood. However, depression and mania are typically associated with characteristic changes in these basic functions. Mood appears to represent a complex group of behaviors and responses that undergo precise and tightly controlled regulation. Higher organisms that must adapt to changing environments depend on optimal control of basic functions such as sleep, appetite, sex, and physical activity. This regulation must adapt to diurnal and seasonal changes in the environment. In addition, more complex behaviors such as exploration, aggression, and social interaction must also undergo a similar, perhaps closely linked, regulation. In humans, these complex behaviors and their regulation are believed to be associated with the expression of mood. A depressed mood appears to reflect a kind of global damping of these functions, while a manic state may result from an excessive activation of these same functions. The mechanisms underlying the diverse changes associated with the mood disorders are largely unknown, but their appearance as clusters in specific disorders along with their collective response to specific therapeutics suggests a common mechanistic basis.
Disturbances of Cognition
Cognitive function refers to the general ability to organize, process, and recall information. Cognitive tasks may be subdivided into a large number of more specific functions depending on the nature of the information remembered and the circumstances of its recall. In addition, there are many functions commonly associated with cognition such as the ability to execute complex sequences of tasks. Disturbances of cognitive function may occur in a variety of disorders. Progressive deterioration of cognitive function is referred to as dementia. Dementia may be caused by a number of specific conditions including Alzheimer’s disease (to be discussed in subsequent chapters). Impairment of cognitive function may also occur in other mental disorders such as depression. It is not uncommon to find profound disturbances of cognition in patients suffering from severe mood disturbances. More recently, cognitive deficits have been reported in schizophrenia and now have become a major new topic of research. Lastly, cognitive impairment frequently occurs in a host of chemical, metabolic, and infectious diseases that exert an impact on the brain.
The manifestations of cognitive impairment can vary across an extremely wide range, depending on severity. Short-term memory is one of the earliest functions to be affected and, as severity increases, retrieval of more remote memories becomes more difficult. Attention, concentration, and higher intellectual functions can be impaired as the underlying disease process progresses. Language difficulties range from mild word-finding problems to complete inability to comprehend or use language. Functional impairments associated with cognitive deficits can markedly interfere with the ability to perform activities of daily living such as dressing and bathing.
Other Symptoms
Anxiety, psychosis, mood disturbances, and cognitive impairments are among the most common and disabling manifestations of mental disorders. It is important, however, to appreciate that mental disorders leave no aspect of human experience untouched. It is beyond the scope of the present chapter to detail the full spectrum of presentations of mental disorders. Other common manifestations include, for example, somatic or other physical symptoms and impairment of impulse control. Many of these issues will be touched upon in subsequent chapters with reference to specific disorders.
Diagnosis of Mental Illness
The foregoing discussion has suggested that the manifestations of mental disorders fall into a number of distinct categories such as anxiety, psychosis, mood disturbance, and cognitive deficits. These categories are broad, heterogeneous, and somewhat overlapping. Moreover, any particular patient may manifest symptoms from more than one of these categories. This is not unexpected, given the highly complex interactions that take place among the neurobiological and behavioral substrates that produce these symptoms. Despite these confounding difficulties, a systematic approach to the classification and diagnosis of mental illness has been developed. Diagnosis is essential in all areas of health for shaping treatment and supportive care, establishing a prognosis, and preventing related disability. Diagnosis also serves as shorthand to enhance communication, research, surveillance, and reimbursement.
The diagnosis of mental disorders is often believed to be more difficult than diagnosis of somatic, or general medical, disorders, since there is no definitive lesion, laboratory test, or abnormality in brain tissue that can identify the illness. The diagnosis of mental disorders must rest with the patients’ reports of the intensity and duration of symptoms, signs from their mental status examination, and clinician observation of their behavior including functional impairment. These clues are grouped together by the clinician into recognizable patterns known as syndromes. When the syndrome meets all the criteria for a diagnosis, it constitutes a mental disorder. Most mental health conditions are referred to as disorders, rather than as diseases, because diagnosis rests on clinical criteria. The term “disease” generally is reserved for conditions with known pathology (detectable physical change). The term “disorder,” on the other hand, is reserved for clusters of symptoms and signs associated with distress and disability (i.e., impairment of functioning), yet whose pathology and etiology are unknown.
The standard manual used for diagnosis of mental disorders in the United States is the Diagnostic and Statistical Manual of Mental Disorders. Most recently revised in 1994, this manual now is in its fourth edition (American Psychiatric Association, 1994, hereinafter cited in this report as DSM-IV). The first edition was published in 1952 by the American Psychiatric Association; subsequent revisions, which were made on the basis of field trials, analysis of data sets, and systematic reviews of the research literature, have sought to gain greater objectivity, diagnostic precision, and reliability. DSM-IV organizes mental disorders into 16 major diagnostic classes listed in Table 2-5. For each disorder within a diagnostic class, DSM-IV enumerates specific criteria for making the diagnosis. DSM-IV also lists diagnostic “subtypes” for some disorders. A subtype is a subgroup within a diagnosis that confers greater specificity. DSM-IV is descriptive in its listing of symptoms and does not take a position about underlying causation.
Table 2-5. Major Diagnostic Classes of Mental Disorders (DSM-IV)
| Disorders usually first diagnosed in infancy, childhood, or adolescence |
| Delerium, dementia, and amnestic and other cognitive disorders |
| Mental disorders due to a general medical condition |
| Substance-related disorders |
| Schizophrenia and other psychotic disorders |
| Mood disorders |
| Anxiety disorders |
| Somatoform disorders |
| Factitious disorders |
| Dissociative disorders |
| Sexual and gender identity disorders |
| Eating disorders |
| Sleep disorders |
| Impulse-control disorders |
| Adjustment disorders |
| Personality disorders |
DSM-IV and its predecessors2 represent a unique approach to diagnosis by a professional field. No other sphere of health care has created such an extensive compendium of all of its disorders with explicit diagnostic criteria. The World Health Organization’s International Classification of Diseases (10th edition, 1992) is a valuable compendium of all diseases. Its mental health categories are expanded upon in DSM-IV. The International Classification of Diseases (ICD) is the official classification for mortality and morbidity statistics for all signatories to the U.N. Charter establishing the World Health Organization. ICD-9CM (9th edition, Clinical Modification, 1991) is still the official classification for the Health Care Financing Administration.
Knowledge about diagnosis continues to evolve. Evolution in the diagnosis of mental disorders generally reflects greater understanding of disorders as well as the influence of social norms. Years ago, for instance, addiction to tobacco was not viewed as a disorder, but today it falls under the category of “Substance-Related Disorders.” Although DSM-IV strives to cover all populations, it is not without limitations. The difficulties encountered in diagnosing mental disorders in children, older persons, and racial and ethnic minority groups are discussed later in this chapter and throughout this report. Diagnosis rests on clinician judgment about whether clients’ symptom patterns and impairments of functioning meet diagnostic criteria. Cultural differences in emotional expression and social behavior can be misinterpreted as “impaired” if clinicians are not sensitive to the cultural context and meaning of exhibited symptoms, a topic discussed later in this chapter in Overview of Cultural Diversity and Mental Health Services.
2 DSM-I (American Psychiatric Association, 1952), DSM-II (American Psychiatric Association, 1968), DSM-III (American Psychiatric Association, 1979), and DSM-III-R (American Psychiatric Association, 1987).
3 Although addictive disorders are included as mental disorders in the DSM classification system, the ECA and NCS distinguish between addictive disorders and (all other) mental disorders. Epidemiologic data in this report follow that convention.
4 The term “serious emotional disturbance” is used in a variety of Federal statutes in reference to children under the age of 18 with a diagnosable mental health problem that severely disrupts their ability to function socially, academically, and emotionally. The term does not signify any particular diagnosis; rather, it is a legal term that triggers a host of mandated services to meet the needs of these children.
Overview of Etiology
The precise causes (etiology) of most mental disorders are not known. But the key word in this statement is precise. The precise causes of most mental disorders—or, indeed, of mental health—may not be known, but the broad forces that shape them are known: these are biological, psychological, and social/cultural factors.
What is most important to reiterate is that the causes of health and disease are generally viewed as a product of the interplay or interaction between biological, psychological, and sociocultural factors. This is true for all health and illness, including mental health and mental illness. For instance, diabetes and schizophrenia alike are viewed as the result of interactions between biological, psychological, and sociocultural influences. With these disorders, a biological predisposition is necessary but not sufficient to explain their occurrence (Barondes, 1993). For other disorders, a psychological or sociocultural cause may be necessary, but again not sufficient.
As described in the section on modern neuroscience, the brain and behavior are inextricably linked by the plasticity of the nervous system. The brain is the organ of mental function; psychological phenomena have their origin in that complex organ. Psychological and sociocultural phenomena are represented in the brain through memories and learning, which involve structural changes in the neurons and neuronal circuits. Yet neuroscience does not intend to reduce all phenomena to neurotransmission or to reinterpret them in a new language of synapses, receptors, and circuits. Psychological and sociocultural events and phenomena continue to have meaning for mental health and mental illness.
Much of the research that is presented in the remainder of this report draws on theories and investigations that predate the more modern view of integrative neuroscience. It is still meaningful, however, to speak of the interaction of biological and psychological and sociocultural factors in health and illness. That is where the overview of etiology begins—with the biopsychosocial model of disease, followed by an explanation of important terms used in the study of etiology. Then, against the backdrop of the introductory section on brain and behavior, the following sections address biological and psychosocial influences on mental health and mental illness, a separation that reflects the distinctive research perspectives of past decades. The overview of etiology draws to a close with a discussion of the convergence of biological and psychosocial approaches in the study of mental health and mental illness.
Biopsychosocial Model of Disease
The modern view that many factors interact to produce disease may be attributed to the seminal work of George L. Engel, who in 1977 put forward the Biopsychosocial Model of Disease (Engel, 1977). Engel’s model is a framework, rather than a set of detailed hypotheses, for understanding health and disease. To many scientists, the model lacks sufficient specificity to make predictions about the given cause or causes of any one disorder. Scientists want to find out what specifically is the contribution of different factors (e.g., genes, parenting, culture, stressful events) and how they operate. But the purpose of the biopsychosocial model is to take a broad view, to assert that simply looking at biological factors alone—which had been the prevailing view of disease at the time Engel was writing—is not sufficient to explain health and illness.
According to Engel’s model, biopsychosocial factors are involved in the causes, manifestation, course, and outcome of health and disease, including mental disorders. The model certainly fits with common experience. Few people with a condition such as heart disease or diabetes, for instance, would dispute the role of stress in aggravating their condition. Research bears this out and reveals many other relationships between stress and disease (Cohen & Herbert, 1996; Baum & Posluszny, 1999).
One single factor in isolation—biological, psychological, or social—may weigh heavily or hardly at all, depending on the behavioral trait or mental disorder. That is, the relative importance or role of any one factor in causation often varies. For example, a personality trait like extroversion is linked strongly to genetic factors, according to identical twin studies (Plomin et al., 1994). Similarly, schizophrenia is linked strongly to genetic factors, also according to twin studies (see Chapter 4). But this does not mean that genetic factors completely preordain or fix the nature of the disorder and that psychological and social factors are unimportant. These social factors modify expression and outcome of disorders. Likewise, some mental disorders, such as post-traumatic stress disorder (PTSD), are clearly caused by exposure to an extremely stressful event, such as rape, combat, natural disaster, or concentration camp (Yehuda, 1999). Yet not everyone develops PTSD after such exposure. On average, about 9 percent do (Breslau et al., 1998), but estimates are higher for particular types of trauma. For women who are victims of crime, one study found the prevalence of PTSD in a representative sample of women to be 26 percent (Resnick et al., 1993). The likelihood of developing PTSD is related to pretrauma vulnerability (in the form of genetic, biological, and personality factors), magnitude of the stressful event, preparedness for the event, and the quality of care after the event (Shalev, 1996).
The relative roles of biological, psychological, or social factors also may vary across individuals and across stages of the life span. In some people, for example, depression arises primarily as a result of exposure to stressful life events, whereas in others the foremost cause of depression is genetic predisposition.
Understanding Correlation, Causation, and Consequences
Any discussion of the etiology of mental health and mental illness needs to distinguish three key terms: correlation, causation, and consequences. These terms are often confused. All too frequently a biological change in the brain (a lesion) is purported to be the“cause” of a mental disorder, based on finding an association between the lesion and a mental disorder. The fact is that any simple association—or correlation—cannot and does not, by itself, mean causation. The lesion could be a correlate, a cause of, or an effect of the mental disorder.
When researchers begin to tease apart etiology, they usually start by noticing correlations. A correlation is an association or linkage of two (or more) events. A correlation simply means that the events are linked in some way. Finding a correlation between stressful life events and depression would prompt more research on causation. Does stress cause depression? Does depression cause stress? Or are they both caused by an unidentified factor? These would be the questions guiding research. But, with correlational research, several steps are needed before causation can be established.
If a correlational study shows that a stressful event is associated with an increased probability for depression and that the stress usually precedes depression’s onset, then stress is called a “risk factor” for depression.5 Risk factors are biological, psychological, or sociocultural variables that increase the probability for developing a disorder and antedate its onset (Garmezy, 1983; Werner & Smith, 1992; Institute of Medicine [IOM], 1994a). For each mental disorder, there are likely to be multiple risk factors, which are woven together in a complex chain of causation (IOM, 1994a). Some risk factors may carry more weight than others, and the interaction of risk factors may be additive or synergistic.
Establishing causation of mental health and mental illness is extremely difficult, as explained in Chapter 1. Studies in the form of randomized, controlled experiments provide the strongest evidence of causation. The problem is that experimental research in humans may be logistically, ethically, or financially impossible. Correlational research in humans has thus provided much of what is known about the etiology of mental disorders. Yet correlational research is not as strong as experimental research in permitting inferences about causality. The establishment of a cause and effect relationship requires multiple studies and requires judgment about the weight of all the evidence. Multiple correlational studies can be used to support causality, when, for example, evaluating the effectiveness of clinical treatments (Chambless et al., 1996). But, when studying etiology, correlational studies are, if possible, best combined with evidence of biological plausibility (IOM, 1994b).6 This means that correlational findings should fit with biological, chemical, and physical findings about mechanisms of action relating to cause and effect.
Biological plausibility is often established in animal models of disease. That is why researchers seek animal models in which to study causation. In mental health research, there are some animal models—such as for anxiety and hyperactivity—but a major problem is the difficulty of finding animal models that simulate what is often uniquely human functioning. The search for animal models, however, is imperative.
Consequences are defined as the later outcomes of a disorder. For example, the most serious consequence of depression in older people is increased mortality from either suicide or medical illness (Frasure-Smith et al., 1993, 1995; Conwell, 1996; Penninx et al., 1998). The basis for this relationship is not fully known. The relationship between depression and suicide in adolescents is presented in Chapter 3.
Putting this all together, the biopsychosocial model holds that biological, psychological, or social factors may be causes, correlates, and/or consequences in relation to mental health and mental illness. A stressful life event, such as receiving the news of a diagnosis of cancer, offers a graphic example of a psychological event that causes immediate biological changes and later has psychological, biological, and social consequences. When a patient receives news of the cancer diagnosis, the brain’s sensory cortex simultaneously registers the information (a correlate) and sets in motion biological changes that cause the heart to pound faster. The patient may experience an almost immediate fear of death that may later escalate to anxiety or depression. This certainly has been established for breast cancer patients (Farragher, 1998). Anxiety and depression are, in this case, consequences of the cancer diagnosis,7 although the exact mechanisms are not understood. Being anxious or depressed may prompt further changes in behavior, such as social withdrawal. So there may be social consequences to the diagnosis as well. This example is designed to lay out some of the complexity of the biopsychosocial model applied to mental health and mental illness.
Biological Influences on Mental Health and Mental Illness
There are far-reaching biological and physical influences on mental health and mental illness. The major categories are genes, infections, physical trauma, nutrition, hormones, and toxins (e.g., lead). Examples have been noted throughout Chapter 1 and earlier in this chapter. This section focuses on the first two categories—genes and infections—for these are among the most exciting and intensive areas of research relating to biological influences on mental health and mental illness
The Genetics of Behavior and Mental Illness
That genes influence behavior, normal and abnormal, has long been established (Plomin et al., 1997). Genes influence behavior across the animal spectrum, from the lowly fruitfly all the way to humans. Sorting out which genes are involved and determining how they influence behavior present the greatest challenge. Research suggests that many mental disorders arise in part from defects not in single genes, but in multiple genes. However, none of the genes has yet been pinpointed for common mental disorders (National Institute of Mental Health [NIMH], 1998).
The human genome contains approximately 80,000 genes that occupy approximately 5 percent of the DNA sequences of the human genome. By the spring of 2000, the human genome project will have provided an initial rough draft version of the entire sequence of the human genome, and in the ensuing years, gaps in the sequence will be closed, errors will be corrected, and the precise boundaries of genes will be identified.
In parallel, clinical medicine is studying the aggregation of human disease in families. This effort includes the study of mental illness, most notably schizophrenia, bipolar disorder (manic depressive illness), early onset depression, autism, attention-deficit/hyperactivity disorder, anorexia nervosa, panic disorder, and a number of other mental disorders (NIMH, 1998). From studying how these disorders run in families, and from initial molecular analyses of the genomes of these families, we have learned that heredity—that is, genes—plays a role in the transmission of vulnerability of all the aforementioned disorders from generation to generation.
But we have also learned that the transmission of risk is not simple. Certain human diseases such as Huntington’s disease and cystic fibrosis result from the transmission of a mutation—that is, a deleteriously altered gene sequence—at one location in the human genome. In these diseases, a single mutation has everything to say about whether one will get the illness. The transmission of a trait due to a single gene in the human genome is called Mendelian transmission, after the Austrian monk, Gregor Mendel, who was the first to develop principles of modern genetics and who studied traits due to single genes. When a single gene determines the presence or absence of a disease or other trait, genes are rather easy to discover on the basis of modern methods. Indeed, for almost all Mendelian disorders across medicine that affect more than a few people, the genes already have been identified.
In contrast to Mendelian disorders, to our knowledge, all mental illnesses and all normal variants of behavior are genetically complex. What this means is that no single gene or even a combination of genes dictates whether someone will have an illness or a particular behavioral trait. Rather, mental illness appears to result from the interaction of multiple genes that confer risk, and this risk is converted into illness by the interaction of genes with environmental factors. The implications for science are, first, that no gene is equivalent to fate for mental illness. This gives us hope that modifiable environmental risk factors can eventually be identified and become targets for prevention efforts. In addition, we recognize that genes, while significant in their aggregate contribution to risk, may each contribute only a small increment, and, therefore, will be difficult to discover. As a result, however, of the Human Genome Project, we will know the sequence of each human gene and the common variants for each gene throughout the human race. With this information, combined with modern technologies, we will in the coming years identify genes that confer risk of specific mental illnesses.
This information will be of the highest importance for several reasons. First, genes are the blueprints of cells. The products of genes, proteins, work together in pathways or in building cellular structures, so that finding variants within genes will suggest pathways that can be targets of opportunity for the development of new therapeutic interventions. Genes will also be important clues to what goes wrong in the brain when a disease occurs. For example, once we know that a certain gene is involved in risk of a particular mental illness such as schizophrenia or autism, we can ask at what time during the development of the brain that particular gene is active and in which cells and circuits the gene is expressed. This will give us clues to critical times for intervention in a disease process and information about what it is that goes wrong. Finally, genes will provide tools for those scientists who are searching for environmental risk factors. Information from genetics will tell us at what age environmental cofactors in risk must be active, and genes will help us identify homogeneous populations for studies of treatment and of prevention.
Heritability refers to how much genetics contributes to the variation of a disease or trait in a population at a given point in time (Plomin et al., 1997). Once a disorder is established as running in families, the next step is to determine its heritability (see below), then its mode of transmission, and, lastly, its location through genetic mapping (Lombroso et al., 1994).
One powerful method for estimating heritability is through twin studies.8 Twin studies often compare the frequency with which identical versus fraternal twins display a disorder. Since identical twins are from the same fertilized egg, they share the exact genetic inheritance. Fraternal twins are from separate eggs and thereby share only 50 percent of their genetic inheritance. If a disorder is heritable, identical twins should have a higher rate of concordance—the expression of the trait by both members of a twin pair—than fraternal twins. Such studies, however, do not furnish information about which or how many genes are involved. They just can be used to estimate heritability. For example, the heritability of bipolar disorder, according to the most rigorous twin study, is about 59 percent, although other estimates vary (NIMH, 1998). The heritability of schizophrenia is estimated, on the basis of twin studies, at a somewhat higher level (NIMH, 1998).
Even with a high level of heritability, however, it is essential to point out that environmental factors (e.g., psychosocial environment, nutrition, health care access) can play a significant role in the severity and course of a disorder.
Another point is that environmental factors may even protect against the disorder developing in the first place. Even with the relatively high heritability of schizophrenia, the median concordance rate among identical twins is 46 percent9 (NIMH, 1998), meaning that in over half of the cases, the second twin does not manifest schizophrenia even though he or she has the same genes as the affected twin. This implies that environmental factors exert a significant role in the onset of schizophrenia.
Infectious Influences
It has been known since the early part of the 20th century that infectious agents can penetrate into the brain where they can cause mental disorders. A highly common mental disorder of unknown etiology at the turn of the century, termed “general paresis,” turned out to be a late manifestation of syphilis. The sexually transmitted infectious agent—Treponema pallidum—first caused symptoms in reproductive organs and then, sometimes years later, migrated to the brain where it led to neurosyphilis. Neurosyphilis was manifest by neurological deterioration (including psychosis), paralysis, and later death. With the wide availability of penicillin after World War II, neurosyphilis was virtually eliminated (Barondes, 1993).
Neurosyphilis may be thought of as a disease of the past (at least in the developed world), but dementia associated with infection by the human immunodeficiency virus (HIV) is certainly not. HIV-associated dementia continues to encumber HIV-infected individuals worldwide. HIV infection penetrates into the brain, producing a range of progressive cognitive and behavioral impairments. Early symptoms include impaired memory and concentration, psychomotor slowing, and apathy. Later symptoms, usually appearing years after infection, include global impairments marked by mutism, incontinence, and paraplegia (Navia et al., 1986). The prevalence of HIV-associated dementia varies, with estimates ranging from 15 percent to 44 percent of patients with HIV infection (Grant et al., 1987; McArthur et al., 1993). The high end of this estimate includes patients with subtle neuropsychological abnormalities. What is remarkable about HIV-associated dementia is that it appears to be caused not by direct infection of neurons, but by infection of immune cells known as macrophages that enter the brain from the blood. The macrophages indirectly cause dysfunction and death in nearby neurons by releasing soluble toxins (Epstein & Gendelman, 1993).
Besides HIV-associated dementia and neurosyphilis, other mental disorders are caused by infectious agents. They include herpes simplex encephalitis, measles encephalomyelitis, rabies encephalitis, chronic meningitis, and subacute sclerosing panencephalitis (Kaplan & Sadock, 1998). More recently, research has uncovered an infectious etiology to one form of obsessive-compulsive disorder, as explained below.
PANDAS
In the late 1980s, it was discovered that some children with obsessive-compulsive disorder (OCD) experienced a sudden onset of symptoms soon after a streptococcal pharyngitis (Garvey et al., 1998). The symptoms were classic for OCD—concerns about contamination, spitting compulsions, and extremely excessive hoarding—but the abrupt onset was unusual. Further study of these children led to the identification of a new classification of OCD called PANDAS. This acronym stands for pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection. PANDAS are distinct from classic cases of OCD because of their episodic clinical course marked by sudden symptom exacerbation linked to streptococcal infection, among other unique features. The exacerbation of symptoms is correlated with a rise in levels of antibodies that the child produces to fight the strep infection. Consequently, researchers proposed that PANDAS are caused by antibodies against the strep infection that also manage to attack the basal ganglia region of the child’s brain (Garvey et al., 1998). In other words, the strep infection triggers the child’s immune system to develop antibodies, which, in turn, may attack the child’s brain, leading to obsessive and compulsive behaviors. Under this proposal, the strep infection does not directly induce the condition; rather, it may do so indirectly by triggering antibody formation. How the antibodies are so damaging to a discrete region of the child’s brain and how this attack ignites OCD-like symptoms are two of the fundamental questions guiding research.
Psychosocial Influences on Mental Health and Mental Illness
This chapter thus far has highlighted some of the psychosocial influences on mental health and mental illness. Stressful life events, affect (mood and level of arousal), personality, and gender are prominent psychological influences. Social influences include parents, socioeconomic status, racial, cultural, and religious background, and interpersonal relationships. These psychosocial influences, taken individually or together, are integrated into many chapters of this report in discussions of epidemiology, etiology, risk factors, barriers to treatment, and facilitators to recovery.
Since these psychosocial influences are familiar to the general reader, detailed description of each is beyond the scope of this section (with the exception of cultural influences, which are discussed in the Overview of Cultural Diversity and Mental Health Services section). Instead, this section summarizes the sweeping theories of individual behavior and personality that inspired a vast body of psychosocial research: psychodynamic theories, behaviorism, and social learning theories. The therapeutic strategies that arose from these theories, and modifications necessary to make them relevant to the changing demography of the U.S. population, are discussed in a later section, Overview of Treatment.
Psychodynamic Theories
Psychodynamic theories of personality assert that behavior is the product of underlying conflicts over which people often have scant awareness. Sigmund Freud (1856–1939) was the towering proponent of psychoanalytic theory, the first of the 20th-century psychodynamic theories. Many of Freud’s followers pioneered their own psychodynamic theories, but this section covers only psychoanalytic theory. A brief discussion of Freud’s work contributes to a historical perspective of mental health theory and treatment approaches.
Freud’s theory of psychoanalysis holds two major assumptions: (1) that much of mental life is unconscious (i.e., outside awareness), and (2) that past experiences, especially in early childhood, shape how a person feels and behaves throughout life (Brenner, 1978).
Freud’s structural model of personality divides the personality into three parts—the id, the ego, and the superego. The id is the unconscious part that is the cauldron of raw drives, such as for sex or aggression. The ego, which has conscious and unconscious elements, is the rational and reasonable part of personality. Its role is to maintain contact with the outside world in order to help keep the individual in touch with society. As such, the ego mediates between the conflicting tendencies of the id and the superego. The latter is a person’s conscience that develops early in life and is learned from parents, teachers, and others. Like the ego, the superego has conscious and unconscious elements (Brenner, 1978).
When all three parts of the personality are in dynamic equilibrium, the individual is thought to be mentally healthy. However, according to psychoanalytic theory, if the ego is unable to mediate between the id and the superego, an imbalance would occur in the form of psychological distress and symptoms of mental disorders. Psychoanalytic theory views symptoms as important only in terms of expression of underlying conflicts between the parts of personality. The theory holds that the conflicts must be understood by the individual with the aid of the psychoanalyst who would help the person unearth the secrets of the unconscious. This was the basis for psychoanalysis as a form of treatment, as explained later in this chapter.
Behaviorism and Social Learning Theory
Behaviorism (also called learning theory) posits that personality is the sum of an individual’s observable responses to the outside world (Feldman, 1997). As charted by J. B. Watson and B. F. Skinner in the early part of the 20th century, behaviorism stands at loggerheads with psychodynamic theories, which strive to understand underlying conflicts. Behaviorism rejects the existence of underlying conflicts and an unconscious. Rather, it focuses on observable, overt behaviors that are learned from the environment (Kazdin, 1996, 1997). Its application to treatment of mental problems, which is discussed later, is known as behavior modification.
Learning is seen as behavior change molded by experience. Learning is accomplished largely through either classical or operant conditioning. Classical conditioning is grounded in the research of Ivan Pavlov, a Russian physiologist. It explains why some people react to formerly neutral stimuli in their environment, stimuli that previously would not have elicited a reaction. Pavlov’s dogs, for example, learned to salivate merely at the sound of the bell, without any food in sight. Originally, the sound of the bell would not have elicited salvation. But by repeatedly pairing the sight of the food (which elicits salvation on its own) with the sound of the bell, Pavlov taught the dogs to salivate just to the sound of the bell by itself.
Operant conditioning, a process described and coined by B. F. Skinner, is a form of learning in which a voluntary response is strengthened or attenuated, depending on its association with positive or negative consequences (Feldman, 1997). The strengthening of responses occurs by positive reinforcement, such as food, pleasurable activities, and attention from others. The attenuation or discontinuation of responses occurs by negative reinforcement in the form of removal of a pleasurable stimulus. Thus, human behavior is shaped in a trial and error way through positive and negative reinforcement, without any reference to inner conflicts or perceptions. What goes on inside the individual is irrelevant, for humans are equated with“black boxes.” Mental disorders represented maladaptive behaviors that were learned. They could be unlearned through behavior modification (behavior therapy) (Kazdin, 1996, 1997).
The movement beyond behaviorism was spearheaded by Albert Bandura (1969, 1977), the originator of social learning theory (also known as social cognitive theory). Social learning theory has its roots in behaviorism, but it departs in a significant way. While acknowledging classical and operant conditioning, social learning theory places far greater emphasis on a different type of learning, particularly observational learning. Observational learning occurs through selectively observing the behavior of another person, a model. When the behavior of the model is rewarded, children are more likely to imitate the behavior. For example, a child who observes another child receiving candy for a particular behavior is more likely to carry out similar behaviors. Social learning theory asserts that people’s cognitions—their views, perceptions, and expectations toward their environment—affect what they learn. Rather than being passively conditioned by the environment, as behaviorism proposed, humans take a more active role in deciding what to learn as a result of cognitive processing. Social learning theory gave rise to cognitive-behavioral therapy, a mode of treatment described later in this chapter and throughout this report.
The Integrative Science of Mental Illness and Health
Progress in understanding depression and schizophrenia offers exciting examples of how findings from different disciplines of the mental health field have many common threads (Andreasen, 1997). Despite the differences in terminology and methodology, the results from different disciplines have converged to paint a vivid picture of the nature of the fundamental defects and the regions of the brain that underlie these defects. Even in the case of depression and schizophrenia, there is much to be uncovered about etiology, yet the mental health field is seen as poised“to use the power of multiple disciplines.” The disciplines are urged to link together the study of the mind and the brain in the search for understanding mental health and mental illness (Andreasen, 1997).
This linkage already has been cemented between cognitive psychology, behavioral neurology, computer science, and neuroscience. These disciplines have knit together the field of “cognitive neuroscience” (Kosslyn & Shin, 1992). This new and joint discipline has carved out its own professional society, journals (Waldrop, 1993), and textbooks (Gazzaniga et al., 1998). There is movement toward integration of other disciplines within the field. To promote linkages between psychiatry and the neurosciences, neuroscientist Eric R. Kandel has furnished a novel approach. His essay,“A New Intellectual Framework for Psychiatry,” supplies a set of biological principles to forge a rapprochement—conceptual as well as practical—between the two disciplines (Kandel, 1998). Integrated approaches are seen as vital to tackle the monumental complexity of mental function.
5 Chapter 4 contains a fuller discussion of the relationship between stress and depression. In common parlance, stress refers either to the stressful event or to the individual’s response to the event. However, mental health professionals distinguish the two by referring to the external events as the “stressor” (or stressful life event) and to the individual’s response as the “stress response.”
6 Other types of information used to establish cause and effect relationships are the strength and consistency of the association, time sequence information, dose-response relationships, and disappearance of the effect when the cause is removed.
7 Anxiety and depression may in some cases be caused by hormonal changes related to the tumor itself.
8 Establishing that a disorder runs in families could suggest environmental and/or genetic influences because families share genes and environment. Comparing identical versus fraternal twins assumes that their shared environments are about equal, thereby providing insight about genetic influences. Such comparisons are further enhanced by studies of twins (identical vs. fraternal) separated at birth and adopted by different families.
9 The median concordance rate for identical twins is only 14 percent (NIMH, 1998).
Overview of Development, Temperament, and Risk Factors
How we come to be the way we are is through the process of development. Generally defined as the lifelong process of growth, maturation, and change, development is the product of the elaborate interplay of biological, psychological, and social influences. By studying development, researchers hope to uncover the origins of both mental health and mental illness.
This section elaborates and extends concepts introduced above regarding the fundamental workings of the brain at different developmental stages. It then proceeds to explain several seminal theories of development pioneered by Jean Piaget, Erik Erikson, and John Bowlby. Their theories cover cognitive development, personality development, and social development, respectively, although there is some overlap. Their major works, published in the 1950s and 1960s, were pivotal for the psychological and social sciences, galvanizing a huge body of theoretical and empirical research. However, with the advancements of science and the diversity of the population, these models may not apply to all groups without some adaptation for cultural context. The section concludes with a reminder that the brain is the “great synthesizer” of the many biological, psychological, and sociocultural phenomena that make us who we are.
Physical Development
Physical development of the nervous system provides the architecture for mental function (cognition, mood, and intentional behavior). As can be inferred from the discussion of brain complexity in the introductory section, nervous system development is arguably one of the most monumentally complicated developmental achievements. One hundred billion neurons must form elaborate and precise arrays of interconnections. Neurons begin the developmental process as undifferentiated cells, cells so seemingly anonymous that they are almost indistinguishable from other cells in an embryo. On the basis of genetic and epigenetic10 influences, the cells must first specialize, or differentiate, into neurons, migrate to their final position, and then send their growing axons (the branch of a neuron that transmits impulses) to project over long distances in order to form synapses with distant target cells (Kandel et al., 1995).
Most neurobiologists are astounded at the level of precision that neurons achieve in their interconnections. The process of nervous system development has been studied at increasingly complex levels—molecular, cellular, tissue, and behavioral levels. Yet, while researchers have charted many of the behavioral milestones of development because they are so amenable to observation and analysis, far less is known about molecular, cellular, and tissue interactions that underlie them.
Four overarching findings or organizing principles have been gleaned from decades of neuroscience research. The first finding is that the formation of connections between neurons and their target cells depends on axons growing along anatomical pathways that are studded with signaling molecules, much like landing lights illuminate the runway for a descending plane. The second finding is that an axon’s reaching the vicinity of, and locating, its correct target cell depends on diffusable chemical signals being transmitted from the target cell. The third finding is that if an axon does not reach its correct target, it is likely to die. This phenomenon, known as cell death, or apoptosis, is so common that it affects up to half of all developing neurons. The brain overproduces the number of cells it needs, from which it pares down to only the correct connections (Kandel et al., 1995). Finally, neuron activity is essential to strengthening the connections that are formed. In other words, stimulation from the environment—which is translated into neuron activity—is vital for the forging of normal neural development (Shatz, 1993; Kandel, 1995). This is a fundamental principle that is revisited later in this section. This principle helps to explain why, for example, babies who are deprived of a stimulating environment during their first year sometimes suffer irreparable developmental effects.
Behavior at birth consists of a repertoire of simple reflexes, that is, inborn neurological reactions that are involuntary in nature. Two examples are the sucking reflex and the rooting reflex,11 both of which are designed to ensure food intake. Over time, the infant displays an expanded repertoire of fine and gross motor skills (e.g., crawling, walking) that begin to unfold in the first few months and year of life. These include the cherished ability to smile, which helps to solidify a social bond with parents and caregivers. What begins as a child’s biological survival need for food—evidenced by such behaviors as rooting and sucking—can turn into a social, interpersonal experience with the caregiver, as in the smile of an infant at the sight of a nurturing parent. These burgeoning motor capabilities are the forerunners of more complex behavioral and mental functions, but the actual relationships between early and later abilities, and their molecular and cellular basis, are understood only in the most rudimentary terms.
Theories of Psychological Development
Theories of human development are grounded in the developmental perspective. The developmental perspective takes into account the biological, social, and psychological environment; their interaction; and their combined effect upon the individual throughout the life span. Developmentalist L. Breger (1974) proposes that the developmental perspective incorporates three key precepts:
- Behavioral maturation proceeds from the simple to the complex;
- Future behaviors, whether temporally near or distant, are a product of their antecedents (prior responses to the developmental environment); and
- The human response to a particular event or experience often depends on the developmental stage at which the experience occurs.
Each of these precepts is thought to apply to neurobiological development, as well as behavioral/psychosocial development. Moreover, each has implications for whether an individual experiences either healthful or unhealthful development that may lead to a mental disorder.
The three precepts are at the heart of each of the three major mainstream theories of developmental psychology that have guided research and increased our understanding of both normal and abnormal human development across the life span. The following paragraphs offer brief sketches of the developmental theories of Jean Piaget, Erik Erikson, and John Bowlby; again, these sketches are provided to afford the reader an historical perspective of research on psychological development.
Piaget: Cognitive Developmental Theory
Jean Piaget formulated one of the most influential theories of cognitive development (Inhelder & Piaget, 1958). Its focus was on cognitive (intellectual) development, that is, the processes by which children come to know and understand the world. Other aspects of human growth, both physical and emotional, are beyond the scope of his theory. Piaget posited that each step of cognitive development proceeds from the previous step in a fixed pattern, beginning at birth and ending in the teen years.
Piaget had a seminal influence on the discipline of cognitive psychology. Although empirical research has called into question some of the specifics of his theories, the broad outlines remain widely accepted.
Erik Erikson: Psychoanalytic Developmental Theory
The psychoanalytic theory of development is best exemplified in the work of Erik Erikson, a psychoanalyst who expanded upon Freud’s original theories of psychosexual development. One of Erikson’s pioneering contributions was that development unfolded throughout the life span, a view that has become widely embraced.
Freud postulated that development proceeded through a series of stages in which children seek pleasure or gratification from a particular body part (i.e., the oral, anal, and phallic stage). In contrast, Erikson’s theories of child development focus on the interrelationship between a developing child’s internal psychosexual development and his or her more external emotional development, emphasizing the interpersonal relationships that arise between the child and parents (Erikson, 1950).
Erikson conceived of the life course, from birth to old age, as a series of eight epigenetic stages that, as other developmental theories, proceed in a stepwise fashion, the next dependent upon how well the previous has been mastered: trust versus mistrust; autonomy versus shame and doubt; initiative versus guilt; industry versus inferiority; identity versus role diffusion; intimacy versus isolation; generativity versus stagnation; ego integrity versus despair.
Erikson portrayed each stage as a crisis or conflict that needed resolution, either at the time or at a subsequent stage. Each successive stage presents its own challenges but, at the same time, offers the opportunity for correction of unresolved challenges of previous stages. At each stage the tension was between the psychosocial and psychosexual—the outward-looking versus inward-looking perspectives. Psychopathology, in the form of a mental disorder, would arise if a stage was ultimately not mastered successfully.
Over the years, Erikson’s theory has had great heuristic value to guide theorists and practitioners in organizing their approach to mental health and mental illness. However, his theory does not readily lend itself to empirical scrutiny. His theory also has been criticized as reflecting the concerns of male European culture (where Erikson was born and trained before moving to the United States) rather than those of women and other cultures. The need for cultural sensitivity and competence is discussed later in this chapter.
John Bowlby: Attachment Theory of Development
Fifty years ago, a new conceptualization of the psychoanalytic approach to development came into the lexicon of human development theory. John Bowlby’s reinterpretation of Freudian development is grounded in both Darwinian evolutionary theory and animal ethology. The previous work of Konrad Lorenz and others, who explored the relationship between other animals and their caregivers, determined that the bonds of infant care and the attachment of young to their caregivers are seminal in the drive for survival. Similarly, Bowlby theorized that for humans, attachment to a caregiver had a biological basis in the need for survival (Bowlby, 1951). Moreover, he suggested that this attachment drive exists alongside the drive for nutrition and the sex drive, yet distinct and separate from them. Attachment is seen as the anchor that enables the developing child to explore the world.
With the comfort and security of a stable and routine attachment to the mother—or other primary caregiver—a child is able to organize other elements of development in a coherent way. In contrast, instability in the caregiving relationship—whether physical distance, erratic patterns of parental behavior, or even physical or emotional abuse—may interfere with the sense of trust and security, potentially giving rise to anxiety and psychological problems later in childhood or even decades later in life.
Nature and Nurture: The Ultimate Synthesis
For over a century, an intense debate among developmentalists and other scientists has pitted nature (genetic inheritance) against nurture (environment) as the engine of human development and behavior. Francis Galton, a 19th-century geneticist and cousin of Charles Darwin, declared that“there is no escape from the conclusion that nature prevails enormously over nurture” (cited in Plomin, 1996). As the debate raged, either nature or nurture gained ascendancy. During the 1940s and 1950s, for example, behaviorism held sway over American psychology with its argument that nurture was preeminent.
The pendulum now is coming to rest with the recognition that behavior is the product of both nature and nurture (Plomin, 1996). Each contributes to the development of mental health and mental illness. Nature and nurture are not necessarily independent forces but can interact with one another: nature can influence nurture, and nurture can influence nature (Plomin, 1996).
Studies comparing identical and fraternal twins have shed light on the contributions of nature and nurture. These studies show that for many behavioral traits, as well as mental disorders, there is a noticeable heritable component (see earlier discussion of heritability). Yet even with the most highly heritable traits or conditions, identical twins who share the same genetic endowment display marked differences. Identical twins, for example, are concordant for schizophrenia in 46 percent of pairs (NIMH, 1998), meaning that more than 50 percent of pairs are not concordant. Something yet unknown about the environment protects against the development of schizophrenia in genetically identical individuals (Plomin, 1996).
How do nature and nurture interact? This question cannot be directly answered by twin studies. Animal models have proven to be fertile ground for study of the mechanisms—at the molecular and cellular level—by which nature and nurture interact. As reviewed earlier, research in different animal models has established that the environment can alter the structure and function of the central nervous system (Baily & Kandel, 1993). This holds true not only during early development, but also into adulthood. Nurture influences nature, right down to detectable changes in the brain.
During development of the nervous system, each neuron forms myriad intricate synaptic connections with other neurons, the outcome of the interaction of genes and the environment described above. In this case, the environment is a very general term—it denotes the local extracellular environment surrounding the growing neuron, as well as what we traditionally think of as the environment (sensory environment, psychosocial environment, diet, etc.). When a neuron forms a synapse with its target cell, the pattern of activity, usually furnished by external environmental stimulation, strengthens or weakens the developing synapse. Only strengthened synaptic connections survive early development to form enduring connections, while weakened synaptic connections are eliminated (Shatz, 1993; Kandel et al., 1995). For example, kittens deprived of visual experience early in life sustain permanent disruption to synapses in parts of their visual cortex (Hubel & Wiesel, 1970).
Later in the course of development, established patterns of connections still can be altered by the environment—through learning. Studies in a variety of animal models have found that certain forms of learning lead to changes in the structure and function of neurons. With long-term memory—the long-term storage of learned information—these changes take the form of an enhanced number of synaptic connections and increased gene expression (Kandel et al., 1995). Increased gene expression appears to be for synthesis of new proteins needed for the structural changes occurring at the synapse (Bailey & Kandel, 1993).
Researchers continue to probe for changes in the brain associated with mental disorders. They have found, for instance, that repeated stress from the environment affects the hippocampus, an area of the brain located deep within the cerebral hemispheres. Research in animals has shown that repeated stress triggers atrophy of dendrites of certain types of neurons in a segment of the hippocampus (Sapolsky, 1996; McEwen, 1998). Similarly, imaging studies in humans suggest that stress-related disorders (e.g., post-traumatic stress disorder) induce possibly irreversible atrophy of the hippocampus (McEwen & Magarinos, 1997). Anxiety disorders also alter neuroendocrine systems (Sullivan et al., 1998). These are some of the tantalizing ways in which nurture influences nature.
The mental health field is far from a complete understanding of the biological, psychological, and sociocultural bases of development, but development clearly involves interplay among these influences. Understanding the process of development requires knowledge, ranging from the most fundamental level—that of gene expression and interactions between molecules and cells—all the way up to the highest levels of cognition, memory, emotion, and language. The challenge requires integration of concepts from many different disciplines. A fuller understanding of development is not only important in its own right, but it is expected to pave the way for our ultimate understanding of mental health and mental illness and how different factors shape their expression at different stages of the life span.
10 Epigenetic influences are those that arise from outside the genes and lead to emergent, as opposed to predetermined, properties.
11 Newborns turn their head towards things—typically the breast—that touch their cheek
Overview of Treatment
Introduction to Range of Treatments
Mental disorders are treatable, contrary to what many think.12 An armamentarium of efficacious treatments is available to ameliorate symptoms. In fact, for most mental disorders, there is generally not just one but a range of treatments of proven efficacy. Most treatments fall under two general categories, psychosocial and pharmacological.13 Moreover, the combination of the two—known as multimodal therapy—can sometimes be even more effective than each individually (see Chapter 3).
The evidence for treatment being more effective than placebo is overwhelming, as documented in the main chapters of this report (Chapters 3 through 5). The degree of effectiveness tends to vary, depending on the disorder and the target population (e.g., older adults with depression). What is optimal for one disorder and/or age group may not be optimal for another. Further, treatments generally need to be tailored to the client and to client preferences.
The inescapable point is that studies demonstrate conclusively that treatment is more effective than placebo. Placebo (an inactive form of treatment) in both pharmacological and psychotherapy studies has a powerful effect in its own right, as this section later explains. Placebo is more effective than no treatment. Therefore, to capitalize on the placebo response, people are encouraged to seek treatment, even if the treatment is not as optimal as that described in this report.
If treatment is so effective, then why are so few people receiving it? Studies reveal that less than one-third of adults with a diagnosable mental disorder, and even a smaller proportion of children, receive any mental health services in a given year. This section of the chapter strives to explain why by examining the types of barriers that prevent people from seeking help. But the chapter first covers some general points about psychological and pharmacological therapies. It also discusses why therapies that work so well in research settings do not work as well in practice.
Psychotherapy
Psychotherapy is a learning process in which mental health professionals seek to help individuals who have mental disorders and mental health problems. It is a process that is accomplished largely by the exchange of verbal communication, hence it often is referred to as “talk therapy.” Many of the theories undergirding each orientation to psychotherapy were summarized earlier in this chapter.
Participants in psychotherapy can vary in age from the very young to the very old, and problems can vary from mental health problems to disabling and catastrophic mental disorders. Although people often are seen individually, psychotherapy also can be done with couples, families, and groups. In each case, participants present their problems and then work with the psychotherapist to develop a more effective means of understanding and handling their problems. This report focuses on individual psychotherapy and also mentions couples therapy and various forms of family interventions, particularly psycho-educational approaches. Although not discussed in the report, group psychotherapy is effective for selected individuals with some mood disorders, anxiety disorders, schizophrenia, personality disorders, and for mental health problems seen in somatic illness (Yalom, 1995; Kanas, in press).
Estimates of the number of orientations to psychotherapy vary from a very small number to well over 400. The larger estimate generally refers to all the variations of the three major orientations, that is, psychodynamic, behavioral, and humanistic. Each orientation falls under the more general conceptual category of either action or reflection.
Psychodynamic