Concepts of Brain and Behavior1. The brain has evolved as an organ that creates

a representation of the external world andproduces behavior in response to that world.

2. The neuron is the basic unit of anatomy, phys-iology, and cognition.

3. The synapse is the key site of neural commu-nication and learning.

4. Neural development depends on the influ-ences of both genes and experience.

5. Consciousness organizes the information that enters the brain, the knowledge that thebrain creates, and the behavior that the brainproduces.

6. Functions are both localized and distributedto specific regions of the brain.

7. Brain organization segregates sensory infor-mation that is used for action and for knowl-edge (such as object recognition).

8. Both symmetry and asymmetry exist in brainanatomy and function.

9. The nervous system operates by a juxtaposi-tion of excitation and inhibition.

10.Patterns of neural organization are plastic.11. Animals engage in behaviors for multiple reasons.

12.The study of brain–behavior relationships ismultidisciplinary.

13.Abnormalities in nervous system structure,biochemistry, or functioning lead to abnormalbehavior.

Disorders of Brain and BehaviorInvestigating the Neurobiology of Behavioral

DisordersIdentifying and Classifying Mental DisordersCauses of Abnormal Behavior

Neurobiology of Schizophreniaand Affective DisordersSchizophreniaAffective Disorders

Treatments of Brain andBehavioral DisordersNeurosurgical TreatmentsPharmacological TreatmentsBehavioral Treatments

Neuroscience in the 21st Century

574 ■

What Have We Learnedand What Is Its Value?

C H A P T E R

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F. Martinez/Photo Edit

Micrograph: Dr. Dennis Kunkel/Phototake

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W e have come a long way through 14 chapters.

We have met Fred, D. B., Roger, Donna, Alex

the parrot, and Kamala the elephant. We have

examined car engines, robots, and prehistoric flutes. We

have investigated puffins and sea bears, as well as butter-

flies and mussels. Each has provided a different lesson

about the organization and functioning of the brain. As we

reflect on the many topics we have covered, it is time to

ask two important questions: What basic concepts about

the brain does all this information suggest? And how can

we apply what we have learned to the solution of real-life

problems?

To answer these two questions, this chapter first re-

traces our journey through the brain to identify a number of

key concepts that summarize the major points of Chapters

1 through 14. Second, it examines ways in which our

knowledge about the brain might be used to alleviate some

behavioral disorders. To accomplish this second task, we

review the nature of behavioral disorders and how they are

related to the nervous system. We also discuss in some de-

tail two disorders—schizophrenia and depression—to

show how neurobiological information has suggested

some causes and treatments. Finally, we look to the future

of neuroscience in the twenty-first century.

■ 575

CONCEPTS OF BRAIN AND BEHAVIORUnderstanding the basic organization of the brain is only a beginning in understand-ing how this organ functions. The real task is learning how the brain produces behav-ior, including thought. In the writing of this book, our discussions of the brain andbehavior had to be packaged into separate chapters, each of which covered only a lim-ited amount of information. In fact, however, most of the themes we have introducedspan more than a single chapter. Our goal here is to sew those themes together to pro-duce a set of key concepts about brain function and its links to behavior.

1. The Brain Has Evolved as an Organ That Creates a Representation of the External World and Produces Behavior in Response to That World(Chapters 1, 2, 8–14).Most animals with a multicellular brain have a common problem. They must movearound in the world in order to eat and to reproduce. These movements, which arecontrolled by the nervous system, cannot be random. Rather, they must be made in re-sponse to the external world where food and mates are found. This external world isalso created by the nervous system through inputs from various sensory receptors. Ananimal’s perception of what the external world is like therefore depends on the com-plexity and organization of its nervous system.

Recall that different animals, such as dogs, bats, andchimpanzees, have developed different “views” of the exter-nal world. For a dog, the world is dominated by odors; for abat, it is largely a world of sounds; and for a chimpanzee,colors are in the forefront of perception. None of these rep-resentations of the external world is more “correct” than theothers. They are simply different perspectives on what is“out there” to be perceived. Each representation creates aunique picture that suits the behavioral repertoire of the animal species. The behavior of dogs is driven by smells,whether it is the smell of a strange dog, a potential mate, ora possible prey. The flight of bats is guided by auditory in-formation, as when bats use sound to locate insects to eat.And the behavior of chimpanzees is driven by color, the bestexample being the use of color to spot ripe fruit in trees.

Even though the world of a bat iscreated largely through sound,rather than sight, bats don’t seemto have much trouble gettingaround. This bat uses its acutesense of hearing and echolocationto ably navigate through this meshscreen. Its nervous system isdesigned to enable the bat tolocate insects and avoid obstaclesin the dark.

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The brains of these animals do something else as well: they create knowledgeabout the world. They keep track of where objects are, where food is found, where safesleeping places are located, and so on. As brains evolved into larger and larger organs,the amount of knowledge processed and stored grew so big that some mechanism fororganizing it was needed. One solution to the problem of categorizing information isto create some form of coding system, of which human language is the ultimate exam-ple. In essence, the earliest function of language may have been to organize the brain’sinformation. Language, in other words, evolved for the brain to talk to itself. Later, lan-guage also provided a way to share knowledge between brains. Given the achievementsof the human species in all these behavioral functions—representing the world andmoving around in it, as well as acquiring and organizing knowledge—it is clear thatour brain’s evolutionary development has been very successful indeed.

2. The Neuron Is the Basic Unit of Anatomy, Physiology, and Cognition(Chapters 1, 4–6, 13, 14).Nerve cells are remarkably similar in all species, no matter where they are found in thenervous system. These cells are the basic unit of information processing, of plasticity,and even of cognition. Drugs, for example, act at the level of individual neurons; andindividual neurons are what an animal’s experiences change. Individual neurons alsocommunicate with one another to generate sensory perceptions and to produce behav-iors. Differences between brains reflect differences in how individual neurons are dis-tributed, organized, and connected.

Although neurons are individual cells, each with a role in behavior, the number ofneurons performing similar functions has expanded exponentially as brains havegrown larger over the course of evolution. Consider a simple nervous system, such as

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The brain integrates and makes decisionsabout information at severalorganizational levels.

Source Inputs Integration

Molecularlevel

Outputs

N1 = neuron 1

N4

N5

N1

N2

N3 N6

N7

N8

Nucleilevel

AreaA

AreaB

AreaX

AreaY

AreaZArea

C

Brainlevel World Brain Behaviors

Brains process information on the level of signalling molecules from cells (neurons)…

1

The same kind of process occurs between groups of cells (nuclei) and larger areas of the brain.

These complex cellular interactions enable the brain to translate information from the world into behavior.

…and then sent to neurons that control an action such as movement.

3

…that are integrated at other neurons…

2

Review the structure of the neuron in the module on Neural Communica-tion on the CD.

that of the worm C. elegans, which consists of 302 neurons, each with a specific job. Ifone neuron dies or becomes dysfunctional, the entire system is affected. In contrast, thedeath of one neuron is not a problem in the human brain, which has 80 billion neurons.As brains have evolved to be larger and much harder to build to an exact blueprint, na-ture’s solution has been to create extra neurons that duplicate the function of other neu-rons. The strategy is to shed unused and unnecessary neurons, sculpting the brain to theorganism’s current needs and experiences. This strategy not only avoids dependence onthe survival of each individual neuron; it also allows great flexibility in adapting to spe-cific environmental conditions. The organism can put its energy into maintaining neu-rons that are required in its daily life, and allowing unneeded neurons to die does notresult in the loss of any essential mental or behavioral function.

3. The Synapse Is the Key Site of Neural Communication and Learning(Chapters 4–6, 13).The three basic parts of the neuron are the cell body, the dendrites, and the axon, in-cluding the axon terminal (Figure 15-1). The cell body acts as the factory of the neu-ron, producing the proteins and energy required for the cell’s operation. The dendrites,which are essentially extensions of the cell body’s surface, allow a neuron to collect in-formation from other cells, whereas the axon provides a pathway for passing along thatinformation. Although the dendrites and axon both handle messages, the business sitefor communication is the synapse (Figure 15-2). Synapses are most often between anaxon terminal of one cell and a dendrite, cell body, or axon of another cell. The pri-mary mode of communication across most synapses is chemical. The chemical eitheralters channels on the receiving (postsynaptic) neuron or initiates postsynaptic eventsthrough second messengers.

Synaptic activity can be influenced in several ways. The most direct route is eitherto increase or decrease the amount of chemical transmitter released into the synapticcleft or to enhance or attenuate that chemical’s action on its postsynaptic receptor. Thisis the primary route of action of most drugs. There are less direct routes, too. One ef-fect of repeated exposure to drugs is either to change characteristics of the postsynap-tic membrane (such as the number of receptor sites on it) or to alter the number ofsynapses. The number of synapses may be increased by adding new synapses to the ex-isting neurons, or the synaptic space may be increased by adding more dendritic mate-rial. Changes in receptors or in the number of synapses are likely involved in processes

WHAT HAVE WE LEARNED AND WHAT IS ITS VALUE? ■ 577

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Block of stone

Carving

Finished brain

Collectinginformation

Integratinginformation

Flow ofinformation

Sendinginformation

Axons fromother neurons

AxonCell body

End feet

Dendrites oftarget neuron

Dendrites

Nerve cells collect information,…

…and send it on to other neurons or organs.

…process it,…

Our brains are created with lots of extraneurons so that we can customize ourbrains to do exactly what we need themto do. The unneeded neurons can bediscarded, just like the residue frommaking a sculpture out of a block ofstone.

Figure 15-1

A neuron is made up of dendrites, whichcollect information from other cells; anaxon, which communicates thisinformation to other neurons, and a cellbody, which provides the energyrequired to keep the operation going.

such as learning and drug addiction. Indeed, synaptic change is required for virtuallyany behavioral change, whether the change is related to learning, to development andaging, or to recovery from brain injury. Because synaptic change is the key to behav-ioral change, it follows that factors that enhance or diminish synaptic change (such asneurotrophic factors, drugs, hormones, or experiences) will stimulate or retard behav-ioral change. Many new treatments for behavioral disorders are designed to maximizesynaptic change.

4. Neural Development Depends on the Influences of Both Genes and Experience (Chapters 7, 13).Development is not governed by a strict genetic code. Although developmental stagesare initiated by genetic instructions, the details of development are strongly influencedby experience (Figure 15-3). Experience does not just mean things that happen in theoutside world. It encompasses internal events, too, including the presence of hormonesand other chemicals, as well as disease and injury. Because experiential factors can in-fluence the messages that genes produce and because genes, in turn, can influence anorganism’s developmental environment, it is hard to determine the relative contribu-tions that genes and environment make to development. The complex interaction ofgenes and environment continues throughout life, influencing how we learn, behave,and think even into old age.

5. Consciousness Organizes the Information That Enters the Brain, theKnowledge That the Brain Creates, and the Behavior That the Brain Produces (Chapters 8, 14).Presumably, consciousness provides an adaptive advantage when a large amount of in-formation must be processed before we decide how to behave in a particular situation.But behaviors that depend on conscious processing are slower than those that are doneautomatically. As a result, conscious analysis is usually applied to tasks where speed is

578 ■ CHAPTER 15

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Figure 15-2

The synapse is the site wherecommunication happens betweenneurons. Most often, synapses occurbetween the axon terminal of one celland a dendrite, cell body, or axon ofanother cell.

Capillary

Muscle

Cell body AxonDendrites

Synapses occur between dendrites,…

…between axons and various other parts of the neuron,…

…and between axons and blood vessels and muscles.

Drugs, hormones,neurotrophic factors

Synaptic change

Behavioral change

not really critical, such as discriminating between the various colors of socks in adrawer. In contrast, movements that must be done rapidly, such as swinging a baseballbat at a ball (Figure 15-4), are usually done without conscious control. As you learned in the discussion of the ventral and dorsal streams of the visual system (Chap-ter 8), the distinction between conscious and unconscious processing is fundamentalto the difference between thinking about objects and moving in relation to objects.Very likely, the conscious processing of sensory information was enhanced by theemergence of language, which, as we said earlier, may have evolved in part to categorizeinformation.

6. Functions Are Both Localized and Distributed to Specific Regions of the Brain (Chapters 7–14).Sensory information, knowledge, and the control of movement are all represented atmultiple levels in the nervous system, beginning at the spinal cord and ending in theassociation cortex (Figure 15-5). These multiple levels of representation imply thatfunctions can be localized to specific regions in the brain. In fact, you have seen suchlocalization of function; the segregation of sensory and motor functions is just one ex-ample. Even though certain functions are relatively localized in the brain, there areparallel and distributed systems that participate in almost any complex behavior. Lo-calization, in other words, is a relative concept because the brain is also organized intofunctional networks. Parallel pathways take part even in what seem to be single func-tions, the clearest example being the visual control of movement versus the visualidentification of information.

A key issue in studying the brain is the extent to which functions can be thought toreside in specific locations. A fundamental difficulty in localizing functions beginswith the problem of defining what a function is. Consider motivation. In Chapter 11,we used the psychological construct of motivation as a shorthand way to describe theprocesses that initiate various behaviors. But motivated behavior ranges from basic

WHAT HAVE WE LEARNED AND WHAT IS ITS VALUE? ■ 579

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Figure 15-3

This experiment shows the jointcontributions of genetics and experienceto development. In early development, acat was deprived of vision in one eye.While the pattern of neuronal growth,determined by genetics, was normal, thecat’s cortical dominance columns areabnormal, showing the impact ofexperience.

Figure 15-4

Sometimes, processing happens soquickly that we cannot be aware of it.The ball coming out of the pitcher’s handwill be traveling too fast for MarkMcGwire to consciously see it, but hemay still be able to get a hit.

Cortical columnsfrom a normal cat

Cortical columns from a cat deprived of vision in one eye

Infant

Adolescent

Adult

L R L R L L R L R L

Cats develop cortical columns for ocular dominance.

Genetics determine the infant’s pattern of neuronal growth…

…but in normal cats, experience causes the development of discrete, equal-width columns.

A cat deprived of vision in one eye early in development develops columns of unequal size.

Mat

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Sto

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an /

Alls

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needs, such as maintaining a constant body temperature, to lusting after an abstractconcept, such as money. The neural systems underlying such disparate behaviors areclearly going to be segregated from each other. Even when we looked at sexual behav-ior, which seems to be a single function, we saw that there are two distinctly differentcomponents: wanting sex and engaging in sex. These two types of behaviors are orga-nized by different neural pathways. Apparently, the function that we call sexual behav-ior has many aspects, and these reside in widely separated areas of the brain.

A similar analysis may be applied to most other behaviors, a prime example beingmemory. Memories are often extremely rich in detail and may include sensory mater-ial, feelings, words, and much more. As we saw in Chapter 13, there are many types ofmemory processing, including the implicit–explicit distinction. Like sexual behavior,then, memory is not located in one place. Specific memory functions, such as facialmemory, may be located in discrete neural regions, but the behavior that we call mem-ory is distributed throughout vast areas of the brain.

One implication of the concept of localized and distributed functions is that dam-age to a small area of the brain produces focal symptoms, but it takes massive braindamage to destroy a function completely. For instance, a relatively small injury can de-stroy some aspect of memory, but it takes a very widespread injury to destroy all mem-ory capability. Thus, a brain-injured person may be amnesic for the explicit recall ofnew information, but he or she can still recall a lot of explicit information from thepast and may retain implicit recall of new information.

7. Brain Organization Segregates Sensory Information That Is Used for Action and for Knowledge (Such As Object Recognition) (Chapters 2, 8, 9, 10).The brain is organized around the law of Bell and Magendie, which states that there isa clear demarcation between the control of sensory and motor functions. For instance,in the spinal cord, the dorsal roots and their associated pathways are sensory in func-tion, whereas the ventral roots and their associated pathways are motor in function.Similarly, in the cortex, layer IV is the sensory layer, whereas layers V and VI are themotor layers.

580 ■ CHAPTER 15

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Rotate the brain and investigatebrain anatomy in the module on theCentral Nervous System on the CD.

Figure 15-5

Functions are localized in specific parts ofthe brain, but different aspects of afunction, such as memory, may belocalized in more than one area.

Basal ganglia

Cerebralcortex

Frontal lobe

Amygdala

Hippocampus

Specific areas of the cortex are part of circuits for motor activity, vision, memory, and other functions.

The basal ganglia are part of circuits for voluntary movement, and movement disorders such as Parkinson’s disease result from neural malfunction in that area.

Some memory and spatial functions are partially localized in the hippocampus…

…and other processes, such as emotion, include circuits that involve the amygdala.

A distinction between motor and sensory functions also exists in a more abstractsense. For example, we have emphasized the difference between vision for the purposeof moving to grasp objects and vision for the purpose of knowing about objects. It islikely that each sensory modality has a separate system for action and for knowledge.The action systems consist of the posterior parietal regions and the associated connec-tions to the frontal motor areas, whereas the knowledge systems consist of the anteriortemporal regions and the associated medial temporal and prefrontal regions. The dif-ference between these two systems becomes especially clear in the context of uncon-scious and conscious activity.

8. Both Symmetry and Asymmetry Exist in Brain Anatomy and Function(Chapters 8, 14).A logical extension of the concept of localization of function is the lateralization offunction to a single hemisphere. One reason functions are lateralized may be that it ismore efficient to have a single neural network controlling a complex behavior that de-pends on multiple sources of sensory input, knowledge, or both. For instance, it is hardto imagine language or birdsong being produced by a brain that has bilateral control ofthe sound-producing apparatus. After all, an organism cannot simultaneously maketwo different sounds, one produced by each hemisphere. A single control system there-fore makes more sense. This concept can easily be applied to other functions as well.For example, although we can move our limbs independently, many of our move-ments, such as eating or dressing, require limb cooperation. Control of such behaviorsclearly necessitates the integration of multiple sources of sensory input and multiplemovements. The nervous system has evolved lateralized networks to oversee thesefunctions.

It is tempting to overemphasize the asymmetrical organization of the brain, espe-cially the cerebral hemispheres (for an example of some of the brain’s asymmetry, seeFigure 15-6). In fact, however, both sides of the brain undertake many, perhaps most,brain functions. Both sides process sensory inputs from all the sensory domains, andboth sides produce movements of one side of the body. The brain, in other words, hasboth symmetrical and asymmetrical organization. Even a function like language,which we think of as lateralized, has both symmetrical and asymmetrical aspects. It isthe output apparatus for language that must be controlled unilaterally. There is no ob-vious reason why the receptive aspects of language must be unilaterally controlled,and, in fact, the right hemisphere does have receptive functions, especially for nouns.

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Investigate the sensory systems of the brain in the modules on the Central Nervous System and the Visual System on the CD.

Figure 15-6

Although the human brain looks as if itmight be identical on the right and theleft sides, closer inspection reveals that itis not. The brain’s functions, however, areboth symmetrical and asymmetrical.

Parietallobe

Temporallobe

Left hemisphere Right hemisphere

Sylvianfissure

The left Sylvian fissure is more horizontal,…

…and the right Sylvian fissure bends upward more.

As a result, the parietal lobe is larger on the left…

…and the temporal lobe is larger on the right.

9. The Nervous System Operates by a Juxtaposition of Excitation and Inhibition (Chapters 2–6, 8, 10, 11).An interplay of excitation and inhibition is one of the basic principles of nervous sys-tem organization that we listed in Chapter 2. As you have progressed through thisbook, you have seen that an interplay of excitation and inhibition occurs at many lev-els of nervous system function. At the level of the cell and its components, single neu-rons can be either excited or inhibited, and neurotransmitters can act to stimulate orinhibit synaptic activity (Figure 15-7, from Chapter 4). An example is how the activityof single neurons in the visual cortex can be excited or inhibited by stimulation in dif-ferent parts of the visual field, as shown in Figure 15-8 (from Chapter 8). Beyond thelevel of the cell, these dual processes continue to apply. For instance, systems in thereticular formation control sleep–waking cycles essentially balance the inhibition andactivation of forebrain systems (Chapter 12). Similarly, motor control includes the in-hibition of some movements while other movements are being activated (Chapter12), and many diseases can be thought of as disorders of excitatory and inhibitory sig-nals. Huntington’s disease, for example, is the loss of the ability to inhibit choreiform(convulsive) movements, whereas depression represents an inability to activate manykinds of behaviors. Some diseases are characterized by changes in both inhibition andexcitation. For instance, Parkinson’s disease features both an uncontrollable tremorand difficulty in initiating movement, and schizophrenia may feature both flattenedemotions and sensory hallucinations. The release of behaviors like tremor or halluci-nations reflects a loss of inhibition, whereas the absence of behaviors like movementor facial expression represents a loss of excitation. In all these ways, the activity ofneurons and neural systems may be viewed as a balance between the forces of inhibi-tion and those of excitation.

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Review the basics of excitationand inhibition in the module onNeural Communication on the CD.

Figure 15-7

Neurotransmitters can either excite orinhibit a postsynaptic neuron. Thephysiological effects of each—depolarization or hyperpolarization—areopposed. Researcher John C. Eccles usedthis experimental setup to demonstratethat stimulation of a neuron’s excitatorypathway produces a membranedepolarization called an EPSP (excitatorypostsynaptic potential). Stimulation ofthe inhibitory pathway produces amembrane hyperpolarization called anIPSP (inhibitory postsynaptic potential).

ON

OFF

Light strikescenter

Excitation

Inhibition

Light strikessurround

ON

OFF

Light stimulusin a part of thevisual field

Receptive fieldof a ganglion cell

Response of cell to stimulus at left

0 1 2 3Time (seconds)

0 1 2 3Time (seconds)

Figure 15-8

A single neuron in the visual cortex isreceptive to stimulation in part of thevisual field. A spot of light in the centercauses excitation, but when the lightshines elsewhere, the cell is inhibited.

Stimulate

Inhibitorypathway

Excitatorypathway

Stimulate

Oscilloscope

Motor neuron

SS

IPSPEPSP

Time (ms) Time (ms)

Excite Inhibit

Volta

ge (m

V)

10. Patterns of Neural Organization Are Plastic (Chapters 5, 13).The brain is plastic in two fundamental ways. First, although we tend to think of re-gions of the brain as having fixed functions, the brain has a capacity to adapt to differ-ent experiences by changing where specific functions are represented. For example,people with an amputated arm were found to have an increase in the representation ofthe face in the somatosensory cortex, as shown in Figure 15-9 (from Chapter 11). Inthe absence of the limb, the face becomes more sensitive. Second, the brain is also plas-tic in the sense that the connections among neurons in a given functional system areconstantly changing in response to experience. This type of plasticity is manifested inour capacity for learning and for subsequently recalling learned material (Chapter 13).

There are clearly some limits to the brain’s plasticity. Reorganization of sensoryrepresentations is constrained by the boundaries of the inputs. For example, the extentof somatosensory representation is limited by the inputs from the somatosensory thal-amus. Adjacent regions, which receive input from the motor or visual thalamic nuclei,cannot assume somatosensory functions because they are connected with different re-ceptors. Similarly, although neurons can grow new dendrites in response to experi-ences, there are limits to how much a given neuron can change and how manyconnections can be placed on it. Not only are there biophysical limits with respect tohow new connections affect membrane potentials; there are metabolic limits too. Neu-rons, after all, are not designed to have cell bodies a centimeter in diameter.

11. Animals Engage in Behaviors for Multiple Reasons (Chapters 11, 12).One of the most difficult questions to answer is why animals engage in behaviors, espe-cially why they perform particular behaviors at particular times. To address this ques-tion, we considered the story of Roger, who seemed to have strange, indiscriminatefood preferences. We also considered the housefly and learned that what appeared tobe purposeful behavior was really a response to stimuli coming from its feet andesophagus (Figure 15-10). In addition, we looked at why cats kill birds; we consideredthe annual cycle of polar bears; and we examined ideas about why we sleepand dream. We found it helpful to classify the many different kinds of ani-mal behaviors as either regulatory or nonregulatory. Regulatory behaviorsare those that maintain basic body functions, such as maintaining a con-stant body temperature or generating patterns of sleep and waking. Mostregulatory behaviors require very little brain and are largely controlled bythe hypothalamus and associated brainstem structures.

It is more difficult to say why we engage in our nonregulatory behav-iors. For example, we seek stimulation, finding an absence of sensory inputintolerable. We also seek mates, orienting much of our lives around this

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Figure 15-9

The brain is extraordinarily flexible. Aperson who has suffered an armamputation shows an increase in therepresentation of the face in thesomatosensory cortex. In effect, therepresentation of the missing hand istransferred onto the face. As a result,when the person’s face is lightly touched,as in this drawing, the person feels as ifhis or her hand is being touched.

Figure 15-10

A housefly tastes with its feet. Stretchreceptors in its foregut tell it when it isfull.

Ball ofthumb

Thumb

Index finger

(A) (B)

Amputee

Cotton swab

Pinkie finger

Foregut stretchreceptors

Taste receptors

Esophagus

Proboscis

behavior and activities associated with it. In addition, we make plans and organize ourbehaviors in time. Searching for the reasons for these behaviors led us to investigate theanatomical structures that control each of them.

Although we still do not know much about the reasons for many of our nonregu-latory behaviors, we can draw several conclusions. First, behavior is controlled by itsconsequences. These consequences may shape the behavior of a species or the behaviorof an individual organism. Behaviors that are adaptive and brains that are likely to en-gage in adaptive behaviors are selected in the course of evolution. We learned that catskill birds because there are neural circuits in the brainstem that control the killing be-haviors. Activation of these circuits is presumably rewarding, so, in a sense, animals en-gage in many behaviors because it feels good to do so. We learned, too, that animals donot need to actually engage in a rewarded behavior to experience this positive feeling.Electrical stimulation of the circuits appears to be just as rewarding (perhaps evenmore so) than actually using the circuits.

Second, as the brain has expanded in size throughout its evolution, structures in theforebrain have developed to control the activity of brainstem circuits. These develop-ments have probably occurred for two quite different reasons. One is to add complexityto the behaviors being controlled. A second is to ensure that engaging in rewarding be-haviors is safe. Sexual activity may feel good, but it will not last long if you are rat and acat is nearby! The principal forebrain structures involved in the initiation of motivatedbehaviors are the amygdala and the frontal lobe. Abnormality in these structures is re-lated to a variety of disorders, including schizophrenia and anxiety disorders.

A final conclusion we can draw about the reasons for nonregulatory behaviors isthat survival depends on maximizing contact with some environmental stimuli andminimizing contact with others. Reward is one mechanism for controlling this attrac-tion to certain stimuli and avoiding others. There are two independent features of re-ward: wanting and liking. Wanting is thought to be controlled by dopaminergicsystems, while liking is thought to be controlled by opiate–benzodiazepine systems.

12. The Study of Brain–Behavior Relationships Is Multidisciplinary(Chapters 1–14).Studying the link between the brain and behavior involves many methods, rangingfrom clinical observation to tools of molecular biology. Each method has advantagesand disadvantages. In this book, methods have been introduced in the context of spe-cific topics.

One way to summarize the methods of studying brain and behavior is to considerthem from the level of the whole organism to the molecular level, as shown in Table15-1. Behavioral studies by their very nature are investigations of the whole organism.Those conducted by Broca in the nineteenth century were in many ways the startingpoint of systematic studies of brain–behavior relationships. Later studies of this typeused groups of patients or laboratory animals with brain injuries. As the modern sci-ence of behavioral analysis developed, more elaborate measures were devised both toanalyze mental activity and to relate behavior to brain states. The development of mol-ecular biology has enabled the creation of strains of animals, usually mice, that have ei-ther a gene deleted (or inactivated) or a gene inserted. Currently, there is much interestin using this technology both to create animal models of human disorders and to gen-erate treatments for neurobehavioral disorders.

Over the past decade, the development of various brain-imaging techniques hasmade it possible for changes in brain activity to be measured without direct access tothe brain. Although these studies are still in their infancy, they have allowed new in-sights into the neural organization of cognitive processes. Recall, for example, the dis-sociation of linguistic and musical abilities both between and within hemispheres thatwe examined in Chapter 9.

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Brain-stimulation studies began in the late 1800s, using both humans and labora-tory animals as subjects. The early studies of this type involved direct stimulation ofthe brain with tiny electric currents (Chapter 9); more recently, magnetic stimulationtechniques have been developed, which alter brain activity through the skull (Chapter14). We also saw that brain stimulation can be used to affect the behavior of a freelymoving animal (Chapter 11). Recall that animals will press a lever to deliver a mildelectric current to certain regions of the brain, especially the medial forebrain bundle.

Brain-recording studies aim to measure the ongoing activity of large areas of thebrain (as in EEG or MEG) or to monitor the activity of individual neurons. One im-portant finding of such studies is that brain waves are not so much correlated withmental events as with behavior. Another important discovery is that the behavior ofindividual neurons is related to perceptions (Chapter 14).

Finally, neuroscience has a rich history of studies in neuroanatomy that began atthe turn of the twentieth century with one of the greatest scientists of all time, SantiagoRamón y Cajal (see Chapter 3). Today, we have a vast arsenal of cytological and histo-logical methods. These allow us to characterize details not only of cell structure butalso of changes in synapses during periods of brain plasticity.

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Table 15-1 Summary of Methods of Studying Brain and Behavior

Technique Chapter in which an example is discussed

Behavioral studies

Clinical investigations of individual cases 11

Neurosurgical studies of patients at surgery 9

Neuropsychological analyses of groups of patients 14

Neuropsychological analyses of laboratory animals

Ethological studies of behavior 7

Cognitive psychology and psychophysics 14

Developmental studies 7

Behavior genetics 7

Brain imaging

Positron emission tomography (PET) 7

Functional magnetic resonance Imaging (fMRI) 14

Brain stimulation

Electrical stimulation 10

Transmagnetic stimulation 14

Brain recording

Electroencephalography 5

Magnetoencephalography 5

Event-related potentials 5

Long-term enhancement 5

Single-cell recording 8

Brain anatomy

Cytological measures (i.e., measuring cell morphology) 3

Histological measures (i.e., measuring cell characteristics) 3

Tracing neural connections 4

Synaptic measures 13

13. Abnormalities in Nervous System Structure, Biochemistry,or Functioning Lead to Abnormal Behavior (Chapters 1–14).We have encountered disorders of brain and behavior in every chapter of this book, es-pecially in the Focus on Disorders boxes. As summarized in Table 15-2, the variety ofabnormalities is wide, including genetic disorders (such as Huntington’s disease), de-velopmental disorders (such as autism), infectious diseases (such as meningitis), ner-vous system injuries (such as closed head injury), and degenerative conditions (such asAlzheimer’s disease). The unifying characteristic of all these disorders is the presenceof some underlying nervous system abnormality.

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Table 15-2 Summary of Discussions of Disorders in Chapters 1–14

Disorder Location Disorder Location

Addiction 6

Agenesis of the frontal lobe 11*

Agnosia 8

Alzheimer’s disease 13*

Amnesia 13

Androgen insensitivity syndrome 11*

Androgenital syndrome 11*

Anxiety disorders 11*

Aphasia 9

Anencephaly 7

Arteriovenous malformations 9*

Autism 10*

Bell’s palsy 2*

Brain tumors 3*

Carbon monoxide poisoning 8*

Cerebral aneurysm 9*

Cerebral palsy 7*

Closed head injury 1*

Contralateral neglect 14

Down syndrome 3

Demoic acid poisoning 6

Depression 6, 11*

Drug-induced psychosis 6*

Encephalitis 2*

Environmental deprivation 7*

Epilepsy 4, 9*

Fetal alcohol syndrome 6*

Fragile X syndrome 7

Frontal leucotomy 11

Hemianopia 8

Huntington’s chorea 3*

Hyperopia 8*

*Focus on Disorders

Insanity 1*

Insomnia 12

Learning disabilities 1*

Lou Gehrig’s disease 4*

Korsakoff’s syndrome 13*

Mania 15

Meningitis 2*

Mental retardation 7

Migraine 8*

Missile wound 1

Myasthenia gravis 4*

Myopia 8*

MPTP poisoning 5*

Multiple sclerosis 3*

Narcolepsy 12

Panic disorder 11*

Paraplegia 10*

Parkinson’s disease 5*

Phenylketonuria 15

Presbyopia 8*

Psychosis 6

Restless legs syndrome 12

Schizophrenia 6, 7*

Scotoma 8

Seasonal affective disorder 12*

Sleep apnea 12*

Split-brain syndrome 14

Spinal-cord injury 10

Stroke 2*

Synesthesia 14*

Tay-Sachs disease 3

Tourette’s syndrome 10

Nervous system abnormalities are of many types. They includethe congenital absence of neurons or glia, the presence of abnormalneurons or glia, the death of neurons or glia, and neurons or neuralconnections with unusual structures. Similarly, there may be abnor-malities in the biochemical organization or the operation of the ner-vous system. Such biochemical abnormalities include disorderedmembrane channels, low or high numbers of receptors, low or highamounts of different molecules (especially transmitters or hormones),and an improper balance of any of these. The long-term prospects fortreating behavioral disorders depend on the ability to correct thesevarious structural and biochemical abnormalities.

Although all behavioral disorders are ultimately related to thenervous system, environmental factors often contribute to them aswell. Many social and cultural factors affect how the brain operates to produce behav-iors, both normal and abnormal ones. The influence of environmental factors on be-havior is illustrated by the simple fact that we behave quite differently in the context ofa formal social gathering and in the company of our closest friends. However, we are along way from understanding exactly how environmental factors can influence brainactivity or produce pathological behaviors at specific times and places.

Treatments for behavioral disorders need not be direct biological interventions.Just as the brain can alter behavior, so behavior can alter the brain (Chapter 11).Therefore, treatments for behavioral disorders often focus on key environmental fac-tors that influence how a person acts. As behavior changes in response to these treat-ments, the brain is affected as well. An example is the treatment of generalized anxietydisorders, as illustrated by the case of G. B. in Chapter 11. Although G. B. required im-mediate treatment with antianxiety medication, the long-term treatment involved be-havioral therapy. His anxiety disorder was not simply a problem of abnormal brainactivity. It was also a problem of experiential and social factors that fundamentally al-tered his perception of the world. We return to this idea shortly.

In ReviewWe have identified 13 general concepts that are central to the study of the brain and howit produces thought and behavior. The selection of these concepts is somewhat arbitrary,and additional ones could have been included. For the student, however, the reason forextracting these concepts is just as important as their particular content. Our task is to startto synthesize a large body of information into an integrated theory of how the brain works.Perhaps the overriding message that emerges from this effort is that mental activity resultsfrom brain activity, and through research we can eventually understand how this processoccurs.

DISORDERS OF BRAIN AND BEHAVIORFor most of us, the origins and treatment of abnormal behavior are one of the mostfascinating topics in the study of the brain and behavior. Although we have encoun-tered disorders of the brain throughout the preceding 14 chapters, we have not system-atically discussed the neural basis of behavioral disorders. This is our next task. Welook first at the special challenges inherent in investigating the neurobiology of thesedisorders. We then examine how such disorders are classified and distributed in thepopulation. Finally, we look at the general causes of behavioral disorders.

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The neurons of patients with Alzheimer’sdisease degenerate as they experienceworsening symptoms, including memoryloss and personality change.

Normal adultpattern

EarlyAlzheimer’s

disease

AdvancedAlzheimer’s

disease

TerminalAlzheimer’s

disease

Investigating the Neurobiology of Behavioral DisordersThat a single brain abnormality can cause a behavioral disorder, explaining everythingabout that disorder and its treatment, is nicely illustrated by the condition calledphenylketonuria (PKU). Babies with PKU have elevated levels of the amino acidphenylalanine in their blood, as a result of a defect in the gene for phenylalanine hy-droxylase, an enzyme that breaks down phenylalanine. Left untreated, PKU causes se-vere mental retardation. Fortunately, PKU can easily be treated just by restricting thedietary intake of phenylalanine. If other behavioral disorders were as simple and wellunderstood as PKU is, research in neuroscience could quickly cure them.

Many disorders do not result from a single abnormality, however, and the causesof most disorders are still largely matters of conjecture. The major problem is that di-agnosis is based mainly on behavioral symptoms, and behavioral symptoms give fewclues to specific biochemical or structural causes. This problem can be seen in PKU.Table 15-3 lists what is known about PKU at different levels of analysis: genetic, bio-chemical, histological, neurological, behavioral, and social. The underlying problem inPKU becomes less apparent as we move down the table. In fact, it is not possible to pre-dict from information at the neurological, behavioral, or social levels what the specificbiochemical abnormality is. This difficulty has major implications for most behavioralillnesses, because the primary information available is at the neurological, behavioral,and social levels. For most diseases, and especially most psychiatric diseases, thepathology is unknown. For PKU, elevated phenylpyruric acid levels in the urine of asingle patient was the clue needed to understand the disorder. The task for the futurestudy of most behavioral disorders is to identify the biological markers that will lead tosimilar understandings.

Knowledge about behavioral disorders is also hampered by diagnostic challenges.By its very nature, most of the diagnostic information that is gathered is about a pa-tient’s behavior. This behavioral information comes from both patients and theirfamilies. Unfortunately, people are seldom objective observers of their own behavioror that of a loved one. We tend to be selective in noticing and reporting symptoms. Ifwe believe that someone has a memory problem, we often notice memory lapses that

we might ordinarily ignore. Furthermore, weare often not specific enough in identifyingsymptoms. Simply identifying a memoryproblem is not really helpful. We need toknow exactly what type of memory deficit isinvolved. Loss of memory for words, places,or habits implies a very different underlyingpathology.

It is not just patients and their familieswho make diagnosis difficult. Behavioral in-formation about patients is also interpreted byevaluators who may be general physicians,psychiatrists, neurologists, psychologists, orsocial workers. Different evaluators have dif-ferent conceptual biases that shape and filterthe questions they ask and the informationthey gather. Consider the differences amongone evaluator who believes that most behav-ioral disorders are genetic in origin, anotherwho believes that most result from a virus,and a third who believes that many can be

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Phenylketonuria (PKU). A behavioraldisorder caused by elevated levels of theamino acid phenylalanine in the blood asa result of a defect in the gene for the enzyme phenylalanine hydroxylase; the major symptom is severe mental retardation.

Table 15-3 Phenylketonuria: A Behavioral Disorder for Which theNeurobiological Pathogenesis Is Known

Level of analysis Information known

Genetic Inborn error of metabolism; autosomal recessive defective gene

Biochemical pathogenesis Impairment in the hydroxylation of phenylalanine to tyrosine, causing elevated blood levels of phenylala-nine and its metabolites

Histological abnormality Decreased neuron size, dendritic length, and low-ered spine density; abnormal cortical lamination

Neurological findings Severe mental retardation, slow growth, abnormalEEG

Behavioral symptoms For 95 percent of patients, IQ below 50

Social disability Loss of meaningful, productive life; significant socialand economic cost

Treatment Restrict dietary intake of phenylalanine

Adapted from “Special Challenges in the Investigation of the Neurobiology of Mental Illness,” by G. R.Heninger, in The Neurobiology of Mental Illness (pp. 89–98), edited by D. S. Charney, E. J. Nestler, and B. S.Bunney, New York: Oxford, 1999.

traced to repressed sexual experiences during childhood. Each will make quite differ-ent types of observations and will give very different kinds of diagnostic tests. In prin-ciple, this diagnostic problem could apply equally well to nonbehavioral disorders, butthe diagnosis of nonbehavioral disorders is not so dependent on behavioral observa-tions made by an evaluator, with all the difficulties that entails.

Even if the problems of diagnosing behavioral disorders were solved, there wouldstill be major obstacles to investigating these disorders. For one thing, the organiza-tional complexity of the nervous system is far greater than that of other body systems.The brain has a wider variety of cell types than does any other organ, and the complexconnections among neurons add a whole new dimension to understanding normaland abnormal functioning. As our understanding of brain and behavior has pro-gressed, it has become apparent that there are multiple receptor systems that are usedfor many different functions. As George Heninger (1999) pointed out, there is as yet noclear demonstration of a single receptor system with a specific relation to a specific be-havior. For example, the neurotransmitter GABA affects some 30 percent of thesynapses in the brain. When GABA agonists are given to people, multiple effects on be-havior become apparent. In fact, it is difficult to administer enough of a benzodi-azepine to reduce anxiety to a “normal” level without producing sedative side effects aswell. Other receptor systems, such as those involving acetylcholine, NMDA, and sero-tonin, are equally diffuse, with little specificity between biochemistry and behavior.

Even when the patient has actual lesions of the nervous system, determining thecause of a behavioral disorder may still be difficult. For instance, MRI scans may showthat a person with multiple sclerosis has many nervous system lesions, yet the persondisplays very few symptoms. Similarly, only when the loss of dopamine neurons ex-ceeds something like 60 to 80 percent do we see clinical signs of Parkinson’s disease.This is not to suggest that most of our brain cells are not needed. It simply shows thatthe brain is capable of considerable plasticity and that when diseases are slow in pro-gressing, the brain has a remarkable capacity for adapting.

Just as obvious brain lesions do not always produce behavioral symptoms, so thepresence of behavioral symptoms is not always linked to obvious neuropathology. Forinstance, some people have notable behavioral problems after suffering a closed headinjury, yet no obvious signs of brain damage appear on an MRI scan. The pathologymay be subtle, such as a drop in dendritic spine density, or so diffuse that it is hard toidentify. Thus, given the current diagnostic methods for both behavioral disorders andneuropathology, identifying disorders and their causes is seldom an easy task.

One of the major avenues for investigating the causes of behavioral disorders is theuse of animal models. For example, rats with specific lesions of the nigrostriataldopamine system are used as a model of Parkinson’s disease. This model has led to sig-nificant advances in our understanding of how specific dopaminergic agonists andcholinergic antagonists act in the treatment of this disorder. One problem with the useof animal models, however, is the oversimplified view they provide of the neurobiol-ogy of behavioral abnormalities. The fact that a drug reduces symptoms does not nec-essarily mean that it is acting on a key biochemical aspect of the pathology. Aspirin canget rid of a headache, but that does not mean that the headache is caused by the recep-tors on which aspirin acts. Similarly, antipsychotic drugs block dopamine type-2 re-ceptors, but that does not mean that schizophrenia is caused by an abnormality inthese receptors. It is quite possible that schizophrenia results from a disturbance in glu-tamatergic systems and that, for some reason, dopamine antagonists are effective inrectifying the abnormality.

This is not to imply that animal models are unimportant. We have seen through-out this book that they are important. But modeling human disorders is a complextask, so caution is needed when you read news stories about studies using animal mod-els that point toward possible cures for human behavioral diseases.

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Identifying and Classifying Mental DisordersEpidemiology is the study of the distribution and causes of diseases in human popula-tions. A major contribution of epidemiological studies has been to help define and as-sess behavioral disorders, especially psychiatric disorders. The first set of criteria fordiagnoses in psychiatry was developed in 1972. Since that time, two parallel sets of cri-teria have been developed. One is the World Health Organization’s International Clas-sification of Disease (ICD-10 being the most recent version), and the other is theAmerican Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-IV being the most recent edition). The classification scheme used inDSM-IV is summarized in Table 15-4.

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DSM-IV. The fourth and most recent edition of the American Psychiatric Association’s classification of psychiatricdisorders, the Diagnostic and StatisticalManual of Mental Disorders.

Table 15-4 Summary of DSM-IV Classification of Abnormal Behaviors

Diagnostic category Core features and examples of specific disorders

Disorders usually first diagnosed in infancy, childhood, and adolescence

Delirium, dementia, 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

Eating disorders

Sexual disorders and gender identity disorder

Sleep disorders

Impulse-control disorders

Adjustment disorders

Other conditions that may be a focus of clinical attention

Adapted from Diagnostic and Statistical Manual of Mental Disorders (4th ed.), 1994, Washington, DC: American Psychiatric Association.

Tend to emerge and sometimes dissipate before adult life: pervasive developmentaldisorders (such as autism), learning disorders, attention-deficit hyperactivity disorder,conduct disorder, separation anxiety disorder

Dominated by impairment in cognitive functioning: Alzheimer’s disease, Huntington’sdisease

Caused primarily by a general medical disorder: mood disorder due to a general medicalcondition

Brought about by the use of substances that affect the central nervous system: alcoholuse disorders, opioid use disorders, amphetamine use disorders, cocaine use disorders,hallucinogen use disorders

Functioning deterioriates toward a state of psychosis, or loss of contact with reality

Severe disturbances of mood resulting in extreme and inappropriate sadness or elationfor extended periods of time: major depressive disorder, bipolar disorders

Anxiety: generalized anxiety disorder, phobias, panic disorder, obsessive-compulsivedisorder, acute stress disorder, posttraumatic stress disorder

Physical symptoms that apparently are caused primarily by psychological rather thanphysicological factors: conversion disorder, somatization disorder, hypochondriasis

Intentional production or feigning of physical or psychological symptoms

Significant changes in consciousness, memory, identity, or perception, without a clearphysical cause: dissociative amnesia, dissociative fugue, dissociative identity disorder(multiple personality disorder)

Abnormal patterns of eating that significantly impair functioning: anorexia nervosa,bulimia nervosa

Chronic disruption in sexual functioning, behavior, or preferences: sexual dysfunctions,paraphilias, gender identity disorder

Chronic sleep problems: primary insomnia, primary hypersomnia, sleep terror disorder,sleepwalking disorder

Chronic inability to resist impulses, drives, or temptations to perform certain acts thatare harmful to the self or others: pathological gambling, kleptomania, pyromania,intermittent explosive disorder

A maladaptive reaction to a clear stressor, such as divorce or business difficulties, thatfirst occurs within 3 months after the onset of the stressor

Conditions or problems that are worth noting because they cause significantimpairment, such as relational problems, problems related to abuse or neglect,medication-induced movement disorders, and psychophysiological disorders

Any classification of psychiatric disorders is to some extent arbitrary. These classi-fications unavoidably depend on prevailing cultural views. A good example is the clas-sification of what is considered abnormal sexual behavior. Until 1973, the DSM listedhomosexual behavior as pathological. Since then, the DSM has omitted this “disorder.”The revision reflects a change in cultural beliefs about how sexual abnormality shouldbe defined.

Recent large-scale surveys of our population have shown a surprisingly highprevalence of psychiatric disorders as currently defined by the DSM-IV. Figure 15-11summarizes the lifetime rates of psychiatric disorders among people in the UnitedStates. Nearly one-half of the sample had met the criteria for a psychiatric disorder atsome point in their lives. Of these, only a minority had received treatment of any kind,and an even smaller percentage had received treatment from a mental health specialist.Large-scale surveys of neurological disorders show a similar pattern of prevalence, assummarized in Table 15-5. Looking at Figure 15-11 and Table 15-5, we can only marvelthat most people are relatively normal most of the time.

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Figure 15-11

The distribution of psychiatric disordersin the United States.Adapted from “Lifetime and 12-MonthPrevalence of DSM-III-R Psychiatric Disordersin the United States” by R. C., Kessler, K. A., McGonagle, S. Zhao, D. B., Nelson, M., Hughes, S., Eshleman, H., Wittchen, andK. S. Kendler, 1994, Archives of GeneralPsychiatry, 51, 8–19.

Table 15-5 Prevalence of the Major Neurological andCommunicative Disorders in the United States

Disorder Estimated number ofcases

Acute disorders (per year)

Trauma: head and spinal cord 500,000/yr

Stroke 400,000/yr

Infectious disorders ?

Chronic disorders (cumulative survivors)

Stroke 2,000,000+

Closed head injury 10,000,000+

Spinal cord injury 500,000

Epilepsy 2,000,000

Hearing and speech

Deafness 2,000,000

Partial deafness 11,600,000

Speech 8,400,000

Language 6,600,000

Movement disorders (e.g., Parkinson’s, 800,000

Huntington’s, Tourette’s)

Demyelinating diseases (MS, ALS) 200,000

Disorders of early life __________(e.g., cerebral palsy)

Neuromuscular disorders __________

Other neurological disorders 9,000,000(e.g., chronic pain, insomnia, neuro-AIDS)

Total chronic 49,700,000

Mooddisorders

Panicdisorder

Generalizedanxiety

Socialphobia

Agoraphobia

Anxietydisorders

Majordepression

Mania

Substancedependence

Alcohol

Otherdrugs

Psychosis

Anydisorder

Lifetime prevalence rate (%)

KEY

Percentage of men who will have this disorder in their lifetimes

Percentage of women who will have this disorder in their lifetimes

Percentage of the total population who will have this disorder in their lifetimes

500 10 20 30 40

Causes of Abnormal BehaviorLittle is known about the causes of psychiatric disorders. To date, no large-scale neuro-biological studies have been done of either postmortem pathology or biochemicalpathology in the population at large. Still, clues to the possible causes of these abnor-mal behaviors are found throughout the preceding 14 chapters. In each case, some ab-normality of the brain must be involved. The question is, What is that particular brainabnormality, and why does it occur?

Table 15-6 lists the most likely categories of causes underlying behavioral disorders.The most basic of these causes is a genetic error, such as those responsible for PKU andTay-Sachs disease. Genetic error is probably linked to some of the other proposedcauses, such as hormonal or developmental anomalies. Moreover, genes may be thesource not only of anatomical, chemical, or physiological defects, but also of suscepti-bility to other factors that may cause behavioral problems. For instance, a person mayhave a genetic predisposition to be vulnerable to stress or infection, which is the imme-diate cause of some abnormal condition. In other cases, no genetic predisposition isneeded, and abnormal behavior arises strictly for environmental reasons. The triggeringfactor may be poor nutrition or exposure to toxic substances, including naturally occur-ring toxins, manufactured chemicals, and infectious agents. Other disorders are un-doubtedly related to negative experiences. Such experiences range from developmentaldeprivation, such as the the extreme psychosocial neglect of Romanian orphans in the1980s and 1990s, to traumas in later life, such as those implicated in anxiety disorders.

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In ReviewNeurobiological investigations of behavioral disorders are based on the assumption thatthere ought to be a direct link between brain abnormalities and disorders in behavior. Inmost cases, however, this relationship is far from direct. We have seen that discrete bio-logical markers are difficult to identify, except in the most well-studied disorders.Surprisingly, we encounter instances of brain pathology without obvious clinical symp-toms and of clinical symptoms without obvious pathology. Epidemiological studies have

Table 15-6 Causes of Certain Behavioral Disorders

Cause Disorder (chapter in which it is discussed)

Genetic error Tay-Sachs disease (3)

Hormonal anomaly Androgenital syndrome (13)

Developmental anomaly Schizophrenia (7)

Infection Encephalitis (2)

Injury Closed head injury (1)

Natural environmental toxins Shellfish poisoning (4)

Manufactured toxins MPTP poisoning (5)

Poor nutrition Korsakoff’s disease (13)

Stress Anxiety disorders (11)

Negative experience Developmental delays among Romanian orphans (7)

been used to identify and classify behavioral disorders, but little is known about the rela-tionship between these disorders and specific biological pathologies. Still, it is possible toidentify the general causes of behavioral disorders. These causes range from genetic fac-tors to environmental ones, including injuries, toxins, and negative life experiences. It willbe some time, however, before a science of brain and behavior can fully explain the dis-ordered mind.

NEUROBIOLOGY OF SCHIZOPHRENIA AND AFFECTIVE DISORDERSSchizophrenia and affective disorders provide excellent examples of the challenge ofunderstanding the neurobiology of abnormal behavior. We have encountered both ofthese disorders several times in the preceding chapters. We revisit them here in an ef-fort to understand their causes. In doing so, we also touch on problems of diagnosis.

SchizophreniaIt has become clear over the past 20 years that diagnosing, classifying, and understand-ing schizophrenia is an evolving process that is far from complete. DSM-IV lists six di-agnostic symptoms of schizophrenia: (1) delusions, or beliefs that distort reality;(2) hallucinations, or distorted perceptions, such as hearing voices; (3) disorganizedspeech, such as incoherent statements or senselessly rhyming talk; (4) disorganized be-havior, or excessively agitated actions; (5) the opposite extreme, excessive immobility(called catatonic behavior); and (6) various “negative” symptoms, such as bluntedemotions or loss of interest and drive, all of which are characterized by the absence ofsome normal response.

One difficulty with the DSM-IV criteria for schizophrenia is that they are morehelpful in making clinical diagnoses than they are in relating schizophrenia to brainabnormalities. Timothy Crow addressed this problem by looking for some relationshipbetween brain abnormalities and specific schizophrenic symptoms. He proposed thatschizophrenia could be divided into two distinct syndromes, which he labeled type Iand type II (Crow, 1980, 1990). Type I schizophrenia is characterized predominantlyby “positive” symptoms, meaning those that involve behavioral excesses, such as hallu-cinations and agitated movements. This type of schizophrenia is also associated withacute onset, good prognosis, and a favorable response to neuroleptics. It likely is due toa dopaminergic dysfunction. Type II schizophrenia, in contrast, is characterized by“negative” symptoms, or those that entail behavioral deficits. It is associated withchronic affliction, poor prognosis, poor response to antipsychotic drugs, cognitive im-pairments, enlarged ventricles, and cortical atrophy, particularly in the frontal cortex.Crow’s analysis had a major impact on clinical thinking about schizophrenia, althoughone difficulty is that between 20 percent and 30 percent of schizophrenic patients showa pattern of mixed type I and type II symptoms. The type I and type II groupings mayactually represent points along a continuum of biological and behavioral manifesta-tions (Andreasen and Olson, 1982).

Another approach to investigating schizophrenia is to de-emphasize diagnostic cat-egories and to focus instead on individual psychotic symptoms. As Alan Breier (1999)stated, a growing number of brain-imaging studies suggest that some of these symp-toms may have a neuroanatomical basis. For example, researchers have found abnor-malities in the auditory regions of the temporal lobe and in Broca’s area among patientswith auditory hallucinations (McGuire et al., 1993). Similarly, structural abnormalities

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Schizophrenia. A behavioral disordercharacterized by delusions, hallucina-tions, disorganized speech, either agita-tion or immobility, and certain othersymptoms, such as blunted emotions.

in Wernicke’s area are often found among patients with thought disorders (Shenton etal., 1992). Another correlation is frequently seen between an abnormally low blood flowin the dorsolateral prefrontal cortex and deficits in executive functions, such as thosemeasured by the Wisconsin Card Sorting Test (for a review, see Berman and Wein-berger, 1999). Interestingly, when Daniel Weinberger and Barbara Lipska studied pairsof identical twins in which only one twin had been diagnosed as having schizophrenia,they found that the twin with schizophrenia always had a lower blood flow in the pre-frontal cortex while taking this card-sorting test, as shown in Figure 15-12 (Weinbergerand Lipska, 1995). Finally, schizophrenics have also been found to have abnormalities inthe hippocampus and the entorhinal cortex (Arnold et al., 1997), regions that are bothinvolved in various forms of memory. It is quite possible that deficits in verbal and spa-tial memory among people with schizophrenia turn out to be correlated with these me-dial temporal abnormalities.

A final way to approach brain–behavior relationships in schizophrenia is to con-sider neurochemical correlates. Although dopamine abnormalities are most com-monly mentioned, other chemical abnormalities have also been found. Table 15-7summarizes some of the major neurochemical changes associated with schizophre-nia. In particular, there are abnormalities in dopamine and dopamine receptors, glu-

tamate and glutamate receptors, and GABA and GABAbinding sites. Considerable variability exists among pa-tients in the extent of each of these abnormalities, how-ever. It is not yet known how these neurochemicalvariations might relate to the presence or absence ofspecific symptoms.

To sum up, schizophrenia is a complex disorder. It isassociated with both positive and negative symptoms,with abnormalities in brain structure and metabolism(especially in the prefrontal and temporal cortex), andwith abnormalities involving dopamine, glutamate, andGABA. Given the complexity of all these behavioral andneurobiological factors, it is not surprising that schizo-phrenia is so difficult to characterize and to treat.

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Han

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ersFigure 15-12

The left-hand photo is a PET scan of thebrain of a schizophrenic patient; theright-hand photo shows the brain of aperson without schizophrenia. Note theabnormally low blood flow in theprefrontal cortex at the top of the photoat left.

Table 15-7 Biochemical Changes Associated with Schizophrenia

Decreased dopamine metabolites in cerebrospinal fluid

Increased striatal D2 receptors

Decreased expression of D3 and D4 mRNA in specific cortical regions

Decreased cortical glutamate

Increased cortical glutamate receptors

Decreased glutamate uptake sites in cingulate cortex

Decreased mRNA for the synthesis of GABA in prefrontal cortex

Increased GAGAA-binding sites in cingulate cortex

Adapted from “The Neurochemistry of Schizophrenia,” by W. Byne, E. Kemegther, L. Jones, V. Harouthunian, and K. L. Davis, in The Neurobiology of Mental Illness, (p. 242),edited by D. S. Charney, E. J. Nestler, and B. S. Bunney, New York: Oxford, 1999.

Affective DisordersOver the past 50 years, researchers have debated whether affective disorders are psy-chological or biological in origin. It now seems likely that environmental factors suchas stress act on the brain to produce biological changes related to people’s moods andemotions. These changes are most likely to occur in those with genetic predispositionsfor them. Although the precise nature of these predispositions is not yet understood,several genes have now been implicated (Sanders et al., 1999).

DSM-IV identifies several categories of affective disorders, but the ones of princi-pal interest here are depression and mania. The main symptoms of clinical depressionare prolonged feelings of worthlessness and guilt, disruption of normal eating habits,sleep disturbances, a general slowing of behavior, and frequent thoughts of suicide.Mania, in contrast, is characterized by excessive euphoria, in which the person oftenformulates grandiose plans and behaves in an uncontrollably hyperactive way. Periodsof mania often change, sometimes abruptly, into states of depression and back again,in which case the condition is called bipolar disorder. Little is known about the neuro-biology of bipolar disorders, so our emphasis here will be on depression.

Clinical studies suggest that monoamine systems, particularly both the norepi-nephrine and the serotonin systems, have roles in depression. Many monoamine the-ories of depression have been proposed. To date, however, there is no unifying theorythat fully explains either the development of depression in otherwise normal peopleor the action of the antidepressant medications used to treat depression. For example,it has been known for more than 30 years that antidepressant drugs acutely increasethe synaptic levels of norepinephrine (NE) and serotonin (5-HT). This finding led tothe idea that depression results from decreased availability of one or both of thesetransmitters. However, lowering these transmitters in normal subjects does not pro-duce depression, and although antidepressant medications rapidly (within days) in-crease the level of NE and 5-HT, it takes weeks for them to start relieving depression.Various explanations for these results have been suggested, but none has been com-pletely satisfactory.

Ronald Duman (1999) reviewed evidence to suggest that antidepressant medica-tions act, at least in part, on signaling pathways, such as on cAMP, in the postsynapticcell. Furthermore, it appears that neurotrophic factors may affect the action of antide-pressants and that neurotrophic factors may underlie the neurobiology of depression.For example, it is known that brain-derived neurotrophic factor, or BDNF (see Chap-ter 13), is down-regulated by stress and up-regulated by antidepressant medication.Given that BDNF acts to enhance the growth and survival of cortical neurons andsynapses, BDNF dysfunction may adversely affect NE and 5-HT systems, through theloss of either neurons or synapses. Antidepressant medication may increase the releaseof BDNF through its actions on cAMP signal transduction. The key point here is thatthe cause is most likely not just a simple decrease in transmitter levels. Rather, explain-ing both the biochemical abnormalities involved in depression and the actions of anti-depressants is likely to be far more complex than it seemed 30 years ago.

It is unlikely that depression is related to a single brain structure, especially giventhat the NE and 5-HT systems are so diffusely distributed. Indeed, neuroimaging stud-ies have shown that depression is accompanied by an increase in blood flow and glu-cose metabolism in the orbital frontal cortex, the anterior cingulate cortex, and theamygdala. This elevated blood flow drops as the symptoms of depression remit when apatient takes antidepressant medication (Drevets et al., 1999). The involvement ofthese three structures should not be surprising, given the discussion in Chapter 11 oftheir role in emotional behavior.

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Depression. An affective disorder char-acterized by prolonged feelings of worth-lessness and guilt, disruption of normaleating habits, sleep disturbances, a gen-eral slowing of behavior, and frequentthoughts of suicide.

In ReviewAlthough significant progress has been made in understanding the neurobiology of schiz-ophrenia and depression, our knowledge of both of these behavioral disorders, as well asmost others, is best viewed as work in progress. Schizophrenia is correlated with abnor-malities in dopamine, GABA, and glutamate systems. Furthermore, there are structural ab-normalities and low blood-glucose utilization in both the prefrontal cortex and thetemporal cortex. In contrast, the monoamine systems are abnormal in depression, particu-larly in signal transduction in postsynaptic cells. And in depression, there are abnormallyhigh levels of blood flow and glucose utilization in the prefrontal and anterior cingulatecortex and in the amygdala.

TREATMENTS OF BRAIN AND BEHAVIORAL DISORDERSThe ultimate clinical problem for behavioral neuroscience is to apply its knowledge togenerate treatments that can restore a disordered brain (and mind) to order. This is adaunting challenge, because the first task is so difficult: learning the cause of a particu-lar behavioral disturbance. Few behavioral disorders have as simple a cause as PKUdoes. Most, like schizophrenia, are extremely complex. Still, it has been possible to de-velop a variety of more or less effective treatments for a range of behavioral disorders,as summarized in Table 15-8.

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Table 15-8 Summary of Treatments of Brain and Behavior

Treatment Chapter in which an example is discussed

Neurosurgical

Removal of abnormal tissue (e.g., epilepsy, tumor) 9

Repair of abnormality (e.g., 9arteriovenous malformations)

Damage dysfunctional area (e.g., Parkinson’s disease) 10

Implantation of stimulation electrode 10(e.g., Parkinson’s disease)

Transcranial magnetic stimulation 14

Implantation of embryonic cells or stem 13cells to regenerate lost tissue

Pharmacological

Drugs to alter neurochemistry 6

Neurotrophic factors 13

Antibiotic and/or antiviral agents (e.g., encephalitis) 2

Nutritional 11

Behavioral

Behavioral training (e.g., speech therapy, 13cognitive therapy)

Psychotherapy 15

These treatments can be classified into three general categories: neurosurgical,pharmacological, and behavioral. The categories range from very invasive (the skull isopened and some intervention is performed on the brain) to less invasive (a chemicalthat affects the brain is either ingested or injected) to noninvasive (experience is ma-nipulated, which in turn influences the brain). As you will see, each of these treatmentshas a specific objective.

Neurosurgical TreatmentsNeurosurgical treatments consist of surgical manipulations of the nervous system withthe goal of directly altering it. Historically, such treatments have been largely repara-tive, as when tumors are removed or arteriovenous malformations are corrected. Morerecently, however, the medical profession has begun to use neurosurgical approachesaimed at altering brain activity in order to alleviate some behavioral disorder. The ac-tivity is altered either by damaging some dysfunctional area of the brain or by stimu-lating dysfunctional areas with electrodes. The treatment of Parkinson’s disease is anexample of both these types of neurosurgery. In the first type, an electrode is placedinto the motor thalamus and an electric current is used to damage neurons that are re-sponsible for producing the tremor characteristic of Parkinson’s. In the second type oftreatment, an electrode fixed in place in the putamen is connected to an external elec-trical stimulator that can be activated to facilitate normal movements.

Another neurosurgical strategy is brand new. In Chapter 7, we saw that the brain de-velops in a fixed sequence: from cell division to cell differentiation to cell migration tosynaptogenesis. If a region of the brain is functioning abnormally or if it is diseased ordead, it should be possible to return this region to the embryonic state and regrow a nor-mal region. Although this technique has a science fiction ring to it, there is reason to be-lieve that it may someday be feasible. We saw in Chapter 11 that in laboratory rats, stemcells can be induced by neurotrophic factors to generate new cells that can migrate to thesite of an injury. This process may not be practical in a large brain such as the humanbrain, but the principle of using stem cells to generate new neurons still holds. Stem cellsmight be placed directly into a dysfunctional region and then supplied with differentgrowth factors that would be able to stimulate them to generate a functional region.

Where would the stem cells come from? During the 1980s, surgeons experi-mented with implanting fetal cells into adult brains, but this approach has had lim-ited success. Another idea comes from the discovery that multipotent stem cells inbone marrow appear to be capable of manufacturing neural stem cells. If this provesto be a practical way of generating neural stem cells, it should be possible to take bonemarrow cells from a person, place them in a special culture medium to generate thou-sands or millions of stem cells, and then place these stem cells into the damagedbrain. The challenge is to get the cells to differentiate appropriately and develop thecorrect connections. At present, this is still a formidable obstacle, but it is well withinthe realm of possibility.

Transplanting cells is today being seriously talked about as a treatment for disor-ders such as stroke. In fact, Douglas Kondziolka and his colleagues (2000) tried celltransplants with a sample of 12 stroke victims. They harvested progenitor cells from arare tumor known as a teratocarcinoma. The tumor cells were chemically altered to de-velop a neuronal phenotype, and then between 2 million and 6 million cells weretransplanted into regions around the stroke. The patients were followed for a year, andfor 6 of them PET scans showed an increase in metabolic activity in the areas that hadreceived the transplanted cells, indicating that the transplants were having some effecton the host brain. Behavioral analyses also showed some improvement in these pa-tients. This study is only the first of its type and the behavioral outcome was modest,but it does show that such a treatment may be feasible.

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The most recent development in the neurosurgical treatment of behavioral disor-ders is transcranial magnetic stimulation, or TMS (Chapter 14). Although not strictlyneurosurgical because it is not invasive, TMS works on a principle similar to that ofelectrical brain stimulation. That is, cerebral regions are activated by stimulation, al-though in TMS the stimulation is magnetic and is applied through the skull. To date,the only clinical applications of TMS have been in the treatment of depression, but thistechnique will probably become far more widely used in the coming decade (Post andWeiss, 1999).

Pharmacological TreatmentsTwo developments in the 1960s led to a pharmacological revolution in the treatment ofbehavioral disorders. First, it was discovered that a drug used to premedicate surgicalpatients had antipsychotic properties. This finding led to the development of phenoth-iazines as a treatment for schizophrenia, and over the next 40 years, these drugs be-came increasingly more selective and effective. Second, a new class of antianxiety drugswas invented, namely the anxiolytics, and medications such as Valium quickly becameamong the most widely prescribed drugs in the United States. The power of these twoclasses of drugs to change behavior led to a revolution in the pharmaceutical industry,a revolution that is just now reaping major rewards with the development of so-calledatypical drugs, such as Prozac, that hold promise to restore more normal behavior inpeople with a wide range of behavioral disorders.

The success of L-dopa has also been influential in fostering a pharmacological revo-lution. As we saw in Chapter 10, L-dopa provided the first treatment for a serious motordisorder, Parkinson’s disease. Its effectiveness led to general optimism that drugs mightbe developed that acted as “magic bullets” to right the chemical imbalances found inAlzheimer’s disease and other disorders. We now know that most behavioral disorderscannot be reduced to a single chemical abnormality, so pharmacological treatments willneed considerable refinement before they can be seen as a solution to all neurobiologi-cal dysfunctions. Nonetheless, for many people, drug treatments have provided relieffrom a host of mental and motor problems.

Pharmacological treatments have their down sides. These drugs often have signifi-cant side effects, and their long-term effects may create new problems. Consider a per-son who is suffering from depression and receives antidepressant medication.Although the drug may ease the depression, it may produce unwanted side effects, in-cluding decreased sexual desire, fatigue, and sleep disturbance. These last two effectsmay also interfere with cognitive functioning. Thus, although the medication is usefulfor getting the person out of the depressed state, it may produce other symptoms thatare themselves disturbing and may complicate the person’s recovery. Furthermore, incases in which the depression is related to life events, a drug does not provide a personwith the behavioral tools needed to cope with an adverse situation. As some psycholo-gists say, “A pill is not a skill.”

A second example of the negative side effects that drug treatments may have canbe seen in people being treated for schizophrenia with neuroleptics. These drugs actnot only on the mesolimbic dopamine system, which is likely to be functioning abnor-mally in the schizophrenic patient, but also on the nigrostriatal dopaminergic system,which controls movement. It is therefore common for patients who take neurolepticsfor a prolonged period to begin having motor disturbances, such as an inability to stopmoving the tongue, a symptom known as tardive dyskinesia. These movement disor-ders often persist long after the medication has been stopped. Taking drugs for behav-ioral disorders, then, does carry some risk. Rather than acting like “magic bullets,”these medications can sometimes act like “magic shotguns.”

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Behavioral TreatmentsIf one of your relatives or friends were to have a stroke and become aphasic, you wouldexpect the person to receive speech therapy, which is a form of behavioral treatmentfor an injured brain. The logic in speech therapy is that by practicing (or relearning)the basic components of speech and language, the patient should be able to regain atleast some of the lost function. The same logic can be applied to other types of behav-ioral disorders, whether they be motor or cognitive. Therapies for cognitive disordersresulting from brain injury or dysfunction aim to retrain people in the fundamentalcognitive processes that they have lost. Although this type of therapy appears as logicalas speech therapy after a stroke, the difficulty is that such therapy assumes that weknow what fundamental elements of cognitive activity are meaningful to the brain.Cognitive scientists are far from understanding these elements well enough to generateoptimal therapies. Still, neuropsychologists such as George Prigitano and CatherineMateer and their respective colleagues are developing neurocognitive programs thatare able to improve functional outcomes following closed head injury and stroke (Pri-gatano, 1986; Sohlberg & Mateer, 1989).

In addition to having disturbances in cognitive activities like language and mem-ory, people may have disturbances in emotional behaviors. In the 1920s, SigmundFreud developed the idea that talking about such emotional problems enabled peopleto have insights into their causes that could serve as treatments, too. These “talkingcures,” as well as other forms of psychological intervention, may be broadly catego-rized as psychotherapies.

Since Freud’s time, many ideas have been put forth about the best type of behav-ioral therapy for emotional disorders. This topic is well beyond the scope of this chap-ter. The key point here is that for many disorders, whether they are neurological orpsychiatric, medical treatments are ineffective unless people also receive some type ofpsychotherapy. Indeed, in many cases, the only effective treatment is behavioral therapy.

Consider an example. A 25-year-old woman had a closed head injury in an auto-mobile accident. She had a promising career as a musician, but after the accident shefound that she was unable to read music. Not surprisingly, she soon became depressed.Part of her therapy was a requirement that she confront her disabling cognitive loss.Only when she did so was she able to begin to recover from her intense depression. Formany people with cognitive impairments resulting from brain disease or injury, themost effective treatment for their state of depression or anxiety is to help them adjustby encouraging them to talk about their difficulties. In fact, group therapy, which pro-vides such encouragement, is standard treatment in brain-injury rehabilitation units.In this regard, Fred Linge, whose case history that opens Chapter 1 of this book, hasplayed a major role in establishing support groups for people with head trauma, whichserve as a form of group therapy.

You may be thinking that although behavioral therapies may be of some help intreating brain dysfunctions, the real solution must lie in altering the brain and its ac-tivities. This may be true, but remember a key fact: because every aspect of behavior isthe product of brain activity, it can be argued that behavioral therapies do act bychanging brain function. That is, not only does altering the brain change our behavior,but altering our behavior also changes the brain. If people can change the way that theythink and feel about themselves or some aspect of their lives, this change has occurredbecause “talking about their problems” has altered the way their brains function. In asense, then, behavioral therapies can be viewed as “biological interventions.” These in-terventions may sometimes be helped along by drug treatments that make the brainmore receptive to change through behavioral therapies. In this way, drug treatmentsand behavioral therapies may have synergistic effects, each helping the other to bemore effective.

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In ReviewTherapies for brain and behavioral disorders range from very invasive ones, like neuro-surgery to moderately invasive ones using drugs and other chemicals to noninvasive cog-nitive rehabilitation and other behavioral therapies. Today, none of these therapies iscompletely effective. But as more is learned about the details of brain–behavior relation-ships, we can anticipate improved recovery from a wide range of behavioral dysfunctionsthat affect a large portion of the population.

NEUROSCIENCE IN THE 21ST CENTURYIt is often said that most of what we know about brain function was discovered in the1990s, the so-called Decade of the Brain. There is some truth to this statement. At thebeginning of the 1900s, investigators like John Hughlings-Jackson were just starting todevelop a vague idea of how the brain is organized. It was not even known until the1950s that there were chemical synapses in the brain. With the research technology ofrecent years, however, many new insights have come to light. For instance, we havenow begun to understand the important process of how genes control neural activity.In addition, the development of new imaging techniques like fMRI and ERPs haveopened up the normal brain to cognitive neuroscientists, allowing them to investigatebrain activity in laboratory subjects. As we reflect on the study of brain and behaviorover the past century, we can only marvel at where it is now and how much potentialfor future discoveries lies just at our doorstep.

Studies of brain and behavior have also begun to capture the public imagination.Whereas such studies were unknown to the general public 20 years ago, today it is hardto pick up a major newspaper without seeing at least weekly accounts of new discover-ies and their possible applications. It seems likely that one day we will be able to stimu-late processes of repair not only in malfunctioning brains but in injured spinal cords aswell. These advances will come about through the efforts of neuroscientists to under-stand how the brain produces and organizes the mind and, ultimately, behavior. Alongthe way, we will learn how the brain stores and retrieves information, why we engage inthe behaviors we do, and how we are able to read the lines on this page and generateideas and thoughts. The coming decades will be exciting times for the study of brainand behavior. They offer an opportunity for us to broaden our understanding of whatmakes us human.

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KEY TERMS

depression, p. 595DSM-IV, p. 590

phenylketonuria (PKU),p. 588

schizophrenia, p. 593

REVIEW QUESTIONS1. What are the difficulties in developing a science of the neurobiology of abnormal

behavior?

2. What are the causes of abnormal behavior?

3. What are the treatments for abnormal behavior?

4. What are the methods of studying brain and behavior?

5. In what sense is behavioral therapy a biological intervention?

FOR FURTHER THOUGHT Prepare the outline of a lecture to explain to your parents (or grandparents) how thebrain works. Remember that you will not be able to assume any knowledge on theirpart. Your real task is to extract principles that they will understand.

RECOMMENDED READINGCharney, D. S., Nestler, E. J., & Bunney, B. S. (Eds.). (1999). The neurobiology of mental illness.

New York: Oxford. This is a serious book for those interested in the latest informationon the neurobiology of mental illness. Coverage includes the entire spectrum of mentaldisorders with thorough reference lists and clear discussions.

Sacks, O. (1998). The man who mistook his wife for a hat: And other clinical tales. New York:Touchstone. This is a collection of short essays that provide interesting reading aboutsome strange relationships between brain and behavior. Sacks is an excellent writer, andhis accounts are not only entertaining but thought provoking as well.

Barondes, S. M. (1993). Molecules and mental illness. New York: Scientific American Library.Like the other books in the Scientific American Library, this is a beautifully written andillustrated volume that is easily accessible. It provides a good general discussion of theneurobiology of mental disorders.

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