The brain has evolved from the brain stem structures that link the brain to the spinal cord all the way up to the cerebral cortex. As we go up the brain stem, processing gets more complex. In fact, it is the very top, the cerebral cortex, that differentiates our brains from those of all other animals. The cerebral cortex enables such complex processes as decision making, language, and perception. Even so, all of the structures below the cerebral cortex are essential for normal behavior and mental processing. This will become clearer as we discuss each structure’s role in this complex, interactive system we call the brain.

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Between the spinal cord and the cortex, there are two sets of brain structures—the central core and the limbic system. The brain stem and structures near the brain stem (cerebellum, thalamus, and basal ganglia) can be thought of as the central core of the brain. Surrounding the top border of the brain stem are the limbic system structures—the hypothalamus, hippocampus, and amygdala. Our discussion will start with the central core structures going up the brain stem to the limbic system structures.

The central core. Figure 2.6 shows the central core brain structures. The brain stem spans from the spinal cord up to the thalamus. The first brain stem structure is the medulla, which links the spinal cord to the brain. The medulla is involved in regulating essential body functions such as heartbeat, breathing, blood pressure, digestion, and swallowing. This is why damage to the medulla can result in death. A drug overdose that suppresses proper functioning of the medulla can also lead to death. Just above the medulla, where the brain stem bulges, sits the pons. Along with the medulla, the pons serves as a passageway for neural signals to and from higher areas in the brain. The pons (Latin for “bridge”) functions as a bridge between the cerebellum and the rest of the brain and is involved in sleep and dreaming.

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The reticular formation, a network of neurons running up the center of the brain stem and into the thalamus, is involved in controlling our different levels of arousal and awareness. This function was demonstrated by Moruzzi and Magoun (1949) in research with cats. When they stimulated a sleeping cat’s reticular formation, the cat awoke and entered a very alert state. When they severed the connections of the reticular formation with higher brain structures, however, the cat went into a coma from which it could never be awakened. The reticular formation also plays a role in attention by deciding which incoming sensory information enters our conscious awareness.

The cerebellum is involved in the coordination of our movements, our sense of balance, and motor learning. Cerebellum means “little brain” in Latin, and it looks like two minihemispheres attached to the rear of the brain stem. The cerebellum has roughly the same surface area (if unfolded) as a single cerebral hemisphere does (Bower & Parsons, 2007), but it is composed of smaller neurons so it takes up far less space. Only making up about 10% of the brain’s weight (Rilling & Insel, 1998), it has more neurons, an estimated 70 billion (Azevedo et al., 2009), than the rest of the brain combined. This is because the great majority of cerebellar neurons are granule neurons, which are very small and can be densely packed into a smaller space. The cerebellum coordinates all of our movements, such as walking, running, and dancing. Damage to the cerebellum will lead to very unsteady, unbalanced movement. Alcohol depresses the functioning of the cerebellum, leading to the uncoordinated movements typical of someone who is drunk. This is why some of the tests for being drunk involve coordinated movement. In addition, the cerebellum is the location of motor learning, such as how to ride a bicycle or to type. There is also some emerging evidence indicating that the cerebellum not only coordinates movement but may also play a role in integrating and coordinating sensory input and in mental functions such as planning (Bower & Parsons, 2007). Lastly, recovery from cerebellar damage, and even from removal of the cerebellum at a young age, is relatively good. Why this is so remains unanswered.

The thalamus, located at the top of the brain stem, serves as a relay station for incoming sensory information. As such, it sends each type of sensory information (visual, auditory, taste, or touch) to the appropriate location in the cerebral cortex. The only type of sensory information that does not pass through the thalamus is olfactory (smell) information. Smell information goes directly from the receptors in our nose to the cortex. The basal ganglia are on the outer sides of the thalamus and are concerned mainly with the initiation and execution of physical movements. Like the cerebellum, the basal ganglia are affected by alcohol, and so make the movements required by tests for drunken driving difficult to execute. The basal ganglia are actually a group of various interacting brain regions. As we discussed earlier in this chapter, abnormally low dopamine activity in one region of the basal ganglia results in Parkinson’s disease. Another disease that involves difficulty in controlling movements is Huntington’s chorea, which stems from problems in another region of the ganglia in which there are GABA and acetylcholine deficits.

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All of the various central core structures are summarized in Table 2.3 along with some of their major functions.

The limbic system. Surrounding the top border (or limbus in Latin) of the brain stem is the limbic system, which is made up of the hypothalamus, the amygdala, and the hippocampus. These limbic structures play an important role in our survival, memory, and emotions. Figure 2.7 shows the three parts of the limbic system. The hypothalamus is a very tiny structure, weighing about half an ounce, which is named after its location—below the thalamus (hypo means “below” in Greek). The hypothalamus controls the pituitary gland (and so directs activity in the endocrine glandular system) and the autonomic nervous system to maintain the body’s internal environment, such as regulating body temperature. It also plays a major role in regulating basic drives such as eating, drinking, and having sex. Thus, this tiny structure plays a huge role in both our behavior and our survival.

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The hippocampus is involved in the formation of memories. Hippocampus may seem like a rather strange name, but like many parts of the brain, it was given a name that matched its visual appearance. The hippocampus looks somewhat like a seahorse, and hippocampus means “seahorse” in Greek. Recall the case study of H. M. that we discussed in Chapter 1. H. M. had his left and right hippocampal structures removed for medical reasons and as a result suffered severe memory deficits (Corkin, 1984). Subsequent research on H. M. and other people with amnesia has shown the hippocampus to be critical for the formation of certain types of new memories (Cohen & Eichenbaum, 1993), which we will discuss in Chapter 5.

The hippocampus has also been found to have the capacity to generate new neurons, a process called neurogenesis (Gage, 2003; Kempermann & Gage, 1999). The research group most responsible for demonstrating neurogenesis in humans was led by Fred Gage. Given that brain-imaging techniques cannot detect neuronal growth and that ethics prohibit neurosurgery to detect such growth in humans, Gage and his colleagues developed a very clever way to demonstrate that such growth exists. BrdU is a traceable substance that has been used in cancer treatment to track how rapidly the disease is spreading. BrdU is integrated into the DNA of cells preparing to divide. Hence it becomes part of the DNA of the new cells and all future descendants of the original dividing cells. Thus, BrdU functions as a marker for new cells. Because BrdU cannot be administered to healthy people, Gage and his colleagues examined postmortem hippocampal tissue of cancer patients who had been injected with BrdU before their deaths, and new noncancerous cells with BrdU were found (Eriksson et al., 1998; van Praag et al, 2002). Although the purposes of neurogenesis in the hippocampus of humans are not yet clear, some research suggests that it may play a key role in depression (Jacobs, van Praag, & Gage, 2000a, 2000b). We will consider this hypothesis in Chapter 10, Abnormal Psychology.

Located just in front of the hippocampal structures are the amygdala left and right structures. Amygdala means “almond” in Greek, and these structures look like almonds. The amygdala plays a major role in regulating our emotional experiences, especially fear, anger, and aggression. It is also responsible for generating quick emotional responses directly, without cortical involvement (LeDoux, 2000). The first evidence for the amygdala’s role in emotional behavior was done on wild, rather violent rhesus monkeys (Klüver & Bucy, 1939). The monkeys’ amygdalas were surgically removed. The surgery transformed the monkeys into calm, tame animals, clearly changing their emotional behavior. Other research has indicated that the amygdala also provides the emotional element in our memories and guides our interpretation of the emotional expressions of others (LeDoux, 1996).

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All three structures in the limbic system are summarized in Table 2.4 along with some of their major functions.

All of the brain structures that we have discussed so far are important to our behavior and survival. The most important brain structure, however, is the cerebral cortex, the control and information-processing center for the nervous system. This is where perception, language, memory, decision making, and all other higher-level cognitive processing occur. The cerebral cortex physically envelops all of the other brain structures, except for the lowest parts of the brain stem and cerebellum. It is by far the largest part of the brain, accounting for about 80% of its total volume (Kolb & Whishaw, 2001). The cerebral cortex consists of layers of interconnected cells that make up the “bark” or covering of the brain’s two hemispheres, which are called cerebral hemispheres. The two hemispheres are separated on top by a deep gap but joined together farther down in the middle by the corpus callosum, a bridge of neurons that allows the two hemispheres to communicate.

The cerebral cortex is very crumpled in appearance with all sorts of bulges and gaps. This allows more cortical surface area to fit inside our rather small skull. If we were to unfold the cerebral cortex to check the amount of surface area, we would find the area to be about the size of four sheets of notebook paper or one newspaper page. Think about this. You couldn’t fit four sheets of paper into your pants pocket unless you crumpled them up. This is the same principle that applies to fitting the large surface area of the cerebral cortex into the small space within the skull. It is this large amount of surface area in the cerebral cortex that not only allows our complex cognitive processing but also differentiates our brains from those of all other animals. To see where different types of processing occur in the cerebral cortex, we need to learn the geography of the two hemispheres. This geography is rather simple in that the outer surface of each hemisphere is divided into four defined parts, called lobes, which we will discuss first.

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The four lobes. Figure 2.8 shows the four lobes in the left hemisphere. They are the same in the right hemisphere and are named after the specific bone area in the skull covering each of them. Two distinctive fissures (gaps) serve as boundary markers for three of the lobes. The central fissure (also called the fissure of Rolando) runs down the center of each hemisphere, and the lateral fissure (also called the Sylvian fissure) runs back along the side of each hemisphere. The four lobes are named for the four bones of the skull that overlie them. The frontal lobe is the area in front of the central fissure and above the lateral fissure, and the parietal lobe is the area located behind the central fissure and above the lateral fissure. The temporal lobe is located beneath the lateral fissure. The remaining lobe is the occipital lobe, which is located in the lower back of each hemisphere. Brynie (2009) explains how to find your occipital lobes. Run your hand up the back of your neck until you come to a bump and then place your palm on the bump. Your palm is squarely over the occipital lobes. The frontal lobes are the largest of the lobes. Their location is easy to remember because they are in the front of the hemispheres and directly behind the forehead. Now that we know these four areas, we can see what we have learned about what type of processing occurs in each of them. We begin with the well-defined areas for producing voluntary movement of different parts of the body, such as raising a hand or making a fist, and for processing various types of sensory input, such as touch, visual, and auditory information.

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The motor cortex. The motor cortex, the frontal lobe strip of cortex directly in front of the central fissure in each hemisphere, allows us to move different parts of our body. The two motor cortex strips are related to the body by contralateral control—each hemisphere controls the voluntary movement of the opposite side of the body. This means that the motor strip in the left hemisphere controls movement in the right side of the body, and the motor strip in the right hemisphere controls movement in the left side of the body. It is also interesting that the amount of space allocated to a specific body part in the motor cortex is not related to the actual size of the body part, but rather to the complexity and precision of movement of which that part is capable. Smaller parts that can make complex movements, such as our fingers, get a large amount of space, and larger parts, such as our torso, that cannot make complex movements do not get much space. Figure 2.9 illustrates this with what is called a homunculus (“little man” in Greek)—a body depiction with the size of each body part proportional to its amount of area in the motor cortex and not its actual size. Note that the body parts are arranged in a toe-to-head fashion spanning from the top of the motor strip to the bottom. It is as if the homunculus is hanging by its toes over the side of the hemisphere.

The somatosensory cortex. The somatosensory cortex, the parietal lobe strip of cortex directly behind the central fissure in each hemisphere, is where our body sensations of pressure, temperature, limb position, and pain are processed. Somato is Greek for body. Somatosensory, then, refers to the body senses. In addition to information about touch, the somatosensory cortex receives input about temperature and pain and information from the muscles and joints that allow us to monitor the positions of the various parts of the body. As in the motor cortex, there are contralateral relationships between the somatosensory strips and sides of the body. The somatosensory strip in the left hemisphere interprets the body sensory information for the right side of the body, and the strip in the right hemisphere interprets this information for the left side of the body. In addition, the amount of space within these strips is not allocated by the size of the body part. In the somatosensory cortex, it is allocated in accordance with the sensitivity of the body part—the more sensitive, the more space. For example, the lips and other parts of the face are more sensitive, so they have larger processing areas than body parts, such as our torso, that are not as sensitive. The homunculus for the somatosensory strip is given in Figure 2.9. Like the motor strip, the body is arranged from toe to head, starting at the top of the strip.

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You may be wondering how the homunculi for the motor and somatosensory strips were determined. They were the result of pre-surgical brain evaluations carried out by Canadian neurosurgeon Wilder Penfield who applied mild electrical stimulation via a single electrode to a patient’s brain before performing surgery for epilepsy (Buonomano, 2011; Seung, 2012). Because the brain itself does not have pain receptors, these surgeries could be performed in conscious patients with only local anesthesia applied to the scalp where incisions were to be made. After pulling back the scalp and opening the skull to expose the brain, Penfield applied electrical probes to different locations in the brains of more than 500 patients. By carrying out multiple stimulations and meticulously recording the patient’s response to each one, Penfield was able to identify the abnormal tissue causing the patient’s seizures and delineate those areas surrounding the tissue that he had to avoid damaging during the surgery. In using this technique to carry out pre-surgical brain evaluations of his patients, Penfield amassed a large body of stimulation data, which led to the first detailed large-scale functional map of the human cerebral cortex (Penfield & Boldrey, 1937; Penfield & Rasmussen, 1968). He found that when a particular area in the motor cortex was stimulated, a specific part of the patient’s body moved, and when a particular area in the somatosensory cortex was stimulated, the patient reported feeling a sensation in a specific body part. These data were used to create the homunculi for the two strips. Using fMRI images, researchers have replicated Penfield’s functional mappings for these two strips (Seung, 2012). The researchers observed which locations in the motor strip were activated by touching parts of a subject’s body and which locations in the somatosensory strip were activated when a subject moved parts of the body.

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The visual cortex and the auditory cortex. There are two other important areas for processing sensory information in Figure 2.8 that we haven’t discussed yet. These are the primary processing areas for our two major senses, seeing and hearing. The visual cortex is located in the occipital lobes at the back of the hemispheres, and the auditory cortex is in the temporal lobes. Figure 2.8 shows where they are located in the left hemisphere. They have the same locations in the right hemisphere. The size of the primary visual cortex varies between individuals over a threefold range in surface area and volume (Dougherty et al., 2003). The reasons for this variability are not known. Interestingly, Schwartzkopf, Song, and Rees (2011) found a strong negative correlation between the magnitude of two context illusions and the surface area of the primary visual cortex. Thus, the smaller your primary visual cortex, the more dramatic some visual illusions appear. The primary visual cortex and the primary auditory cortex are only the locations of the initial processing of visual and auditory information. These primary areas pass the results of their analyses on to areas in the other lobes to complete the brain’s interpretation of the incoming visual or auditory information. These secondary cortical processing areas are part of what is termed the association cortex—all the areas of the cerebral cortex, except for those devoted to primary sensory or motor processing.

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The four cerebral lobes and the type of sensory/motor processing that occurs in each lobe are summarized in Table 2.5.

Given the different locations of the visual cortex and the auditory cortex, you may think that seeing and hearing function entirely separately from each other. The reality, however, is that there is plenty of crosstalk between them. A good example of this interaction is the McGurk effect, which demonstrates that the brain integrates visual and auditory information when processing spoken language (McGurk & MacDonald, 1976). The McGurk effect arises out of conflicting auditory and visual information. A person’s lip movements influence what we hear. For example, if you listen to an audio track of a syllable (“ba”) spoken repeatedly while you watch a video clip of a person making the lip movements as if repeatedly saying another syllable (“ga”), you actually hear a third syllable “da,” the brain’s best guess after merging the information from the two senses. You will have a much better understanding of the McGurk effect if you experience it, and you can find several Web sites that allow you to do so just by doing an online search for the McGurk effect. The McGurk effect is a good example of how visual information can exert a strong influence on what we hear, but it is just one example of how our senses interact. There are many others, such as the smell of food influencing its taste. In interpreting the world, the brain blends the input from all of our senses.

It is important not to confuse sensory interaction in general and the McGurk effect, which all of us with normal sensory capabilities can experience, with synesthesia, a rare neurological condition in which otherwise normal people have cross-sensory experiences in which stimulation in one modality leads to automatic, involuntary experiences in another modality. For example, in synesthesia, sounds may evoke tastes, and colors may evoke smells. In addition, perception of a form (e.g., a number) may induce an unusual perception in the same modality (e.g., a color). Although grapheme-color synesthesia (seeing letters, words, and numbers in colors) and sound-color synesthesia (seeing sounds as colors) are the most common types of synesthesia (Brang & Ramachandran, 2011), there are many other types. The exact number is not known. Some people with synesthesia appear to use this union of the senses to inspire their art (Ramachandran & Blakeslee, 1998). For example, Russian artist Wassily Kandinsky said that when he saw colors, he also heard music, leading him to develop his style of abstract painting (Blakeslee & Blakeslee, 2008). It was as if he was capturing music on canvas. Synesthesia affects only 2% to 4% of the population and is believed to stem from some type of cross-wiring in the brain in which normally separate areas of the brain elicit activity in one another (Brang & Ramachandran, 2011). Although familial linkage analyses have shown a strong genetic component, the precise genes involved in synesthesia have not been identified, and why this sensory anomaly has remained in our gene pool remains a mystery. As Eagleman (2011, p. 80) points out in discussing the tiny genetic changes that cause synesthesia, “microscopic changes in brain wiring can lead to different realities,” demonstrating once again that reality is more subjective than most people realize.

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The association cortex. Most of the cortex (about 70%) is association cortex. This is where all the higher-level processing such as decision making, reasoning, perception, speech, and language occurs. These areas were named the association cortex because higher-level processing requires the association (integration) of various types of information. Scientists have studied the association cortex for over a century, but they are only beginning to understand the functions of some of the association areas (helped greatly by scanning technologies, such as PET scans and fMRI). For example, Sergent, Ohta, and MacDonald (1992) and Kanwisher, McDermott, and Chun (1997) used PET scans and fMRI, respectively, and found a small region on the underside of the temporal lobe near the intersection of the temporal and occipital lobes that responded most strongly to faces. Kanwisher and her colleagues named it the fusiform face area (FFA). Subsequent fMRI studies have confirmed the engagement of the FFA during a range of facial perception tasks (Tong, Nakayama, Moscovitch, Weinrib, and Kanwisher, 2000). The asymmetry of the FFA (it is much larger in the right hemisphere) leads to a right-hemisphere specialization for face recognition (Kanwisher, 2006; Kanwisher & Yovel, 2009). Hence, it is the right hemisphere that is mainly at work when we process faces.

Damage to the FFA has also been found to play a role in prosopagnosia (sometimes called face blindness), a condition that impacts a person’s ability to recognize faces including relatives, friends, and acquaintances or even oneself in a mirror (Greuter, 2007; Hadjikhani & de Gelder, 2002). Although a person with prosopagnosia cannot consciously recognize faces, some part of their brain does unconsciously distinguish familiar faces from unfamiliar ones because they show a higher skin conductance response to familiar faces (Tranel & Damasio, 1985). Sadly, prosopagnosia cannot be cured, but people with prosopagnosia learn other ways of recognizing people, such as memorizing people’s different speech patterns, their gaits, how they wear their hair, and so on. Surprisingly, prosopagnosia also occurs among people without brain damage and is highly heritable (Wilmer et al., 2010).

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During the nineteenth century and most of the twentieth century, however, brain scans obviously weren’t available, so scientists had to learn about the association areas by other methods. One major method was to study the behavior of people who had suffered brain damage in accidents and strokes, or had brain surgery for medical reasons. Their behavioral and mental processing deficits were then related to the particular cortical areas where damage or surgery had occurred. A railroad worker’s tragic accident in 1848 gave us some hints as to what type of processing occurs in our frontal lobes (Macmillan, 2000). Phineas Gage was taking a break from tamping some blasting powder into a rock with a metal tamping iron. He was distracted and the tamping iron slipped, generating some sparks that caused the powder to explode. The explosion caused the metal tamping iron, which was 3 feet 7 inches long, 1¼ inches in diameter, and 13½ pounds in weight, to fly through his left cheek and head, exiting through his left frontal lobe (Ratiu, Talos, Haker, Lieberman, & Everett, 2004; Van Horn et al., 2012). Before Ratiu et al.’s study, most researchers believed that both frontal lobes were damaged, but Ratiu et al. showed that the cerebral injury was limited to the left frontal lobe. Their computerized tomography scan of Gage’s skull clearly shows this, and Van Horn et al. later verified the damage was localized to the left frontal lobe.

Gage survived, but his personality appeared to be greatly changed. According to his doctor and friends, Gage was “no longer Gage” (Macmillan, 2000). He became very irresponsible, impulsive, and disorderly; had great difficulty making decisions and reasoning; and cursed regularly. This led neuroscientists to hypothesize that the frontal lobes played a major role in such behaviors. Subsequent collaborative evidence from similar cases and from studies using other techniques such as brain scans confirmed that this is the case (Klein & Kihlstrom, 1998). The frontal lobes play a major role in our planning, decision making, judgment, impulse control, and personality, especially its emotional aspects. Actually, the cortical area destroyed in Gage’s left frontal lobe (the prefrontal cortex just behind the forehead and in front of the primary motor cortex) was essentially the left portion of the cortex that was disconnected from the rest of the brain in the infamous lobotomies performed on hundreds of patients in mental hospitals in the middle part of the twentieth century. The frontal lobes may also be partially responsible for the bad decisions and risky behavior of teenagers, because frontal lobe development is not complete until the late teens and possibly even the early 20s (Sabbagh, 2006).

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What happened to Phineas Gage? While it has proved very difficult to fill in the exact details of Gage’s subsequent life, Fleischman (2002) provides a general account. Following his recovery, Phineas tried to return to his job as railroad foreman, but because of the “new” Gage’s vulgar, unreliable behavior, the railroad let him go. It appears that for a brief period of time he traveled around New England exhibiting himself along with the tamping iron, possibly ending up in P. T. Barnum’s American Museum sideshow in New York City. After this, because he got along very well with horses, he worked for a while in a livery stable in New Hampshire near his hometown. In 1852 he traveled, taking the tamping iron with him, to South America to care for horses and be a stagecoach driver in Chile. Because of health issues he returned in 1859 to California where his family had moved; and after recovering, he found work as a farmhand. In 1860 he began suffering epileptic seizures (likely due to slow changes in his brain tissue damaged in the railroad accident), and at that time, physicians could not control such seizures. These seizures killed him, 11½ years after the accident. The immediate cause of death was probably hypothermia created by the seizures (during which the body cannot control its internal temperature).

Macmillan and Lena (2010) provide a detailed argument that Gage seems to have made a surprisingly good psychosocial adaptation to his injury and that his mental changes were not as permanent as was once thought and that over time, he became a higher functioning, more socially adapted person. According to Macmillan and Lena, major factors in this rehabilitation were Gage’s highly structured employment and life over a period of nearly 8 years as a stagecoach driver in Chile and the social skills, responsibilities, and challenges entailed in this work. For example, driving a six-horse stagecoach team in which each horse was controlled separately by differing movements of the reins over steep and rough terrain clearly required complex sensory-motor/cognitive skills, and dealing with the non–English-speaking passengers in a foreign country clearly required social skills. With respect to Gage’s recovery, Kotowicz (2007) pointed out that a Harvard surgeon, Henry Bigelow, is the only person known to have observed Gage for an appreciable time (well over a year) after his accident and to have published his observations (Bigelow, 1850), and he reported Gage as fully recovered. Bigelow arranged to have Gage under his care and at his expense for purposes of observation for 8 to 9 weeks. Bigelow described Gage as having “quite recovered in his faculties of body and mind” and does not mention anything strange or unusual about his behavior (Macmillan, 2000). In addition, Macmillan and Lena found a statement from Dr. Henry Trevitt, a doctor who lived in Chile at the time Gage was there and knew Gage well. The doctor reported that Gage “was in the enjoyment of good health with no impairment whatever of his mental faculties (p. 648),” which strongly supports the argument that Gage made a good recovery. Given the long-term post-accident reports of Drs. Bigelow and Trevitt about Gage, Kotowicz argues that some of Gage’s short-term post-accident behavior is understandable in the context of his adjustment to his facial disfigurement, which obviously takes time. In addition, recently discovered photos of Gage, such as the one included here, are supportive of Macmillan and Lena’s recovery hypothesis in that they show Gage as a well-dressed man who appears confident and even handsome despite his facial disfigurement (Kean, 2014). Macmillan and Lena concluded that although they did not think that Gage recovered completely and became Gage again, “he seems to have come much closer to being so than is commonly believed” (p. 655). Such a recovery fits well with our current state of knowledge about neuroplasticity and the brain’s ability to heal itself. If you want to find out more about Phineas Gage, go to www.uakron.edu/gage/, a Web site devoted to him that was created by Malcolm Macmillan, the world’s leading authority on Gage.

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Early brain researchers also analyzed the brains of deceased people, relating a person’s brain analysis to their behavior while living. Using this technique, two nineteenth-century researchers, Paul Broca and Karl Wernicke, studied people with aphasias—speech and language dysfunctions—and made some major discoveries about where speech and language abilities occur in the brain. By examining the brains of deceased persons who had lost their ability to speak fluently while alive, Paul Broca, a French brain researcher, identified an area in the left frontal lobe that is named after him, Broca’s area, which is responsible for fluent speech production (see Figure 2.10). Damage to Broca’s area leads to Broca’s aphasia—the inability to generate fluent speech while maintaining the ability to understand speech and read silently.

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Broca’s area is only in the left hemisphere in the majority of people, both right-handed and left-handed (unlike the sensory and motor processing areas that are in each hemisphere). This means that speech production seems to be a specialization of the left hemisphere (the comparable area in the right hemisphere is usually not used for speech production). So, what is this area in the right hemisphere used for? One possible answer that has been offered is singing and music. People with Broca’s area damage often retain these abilities (Besson, Faita, Peretz, Bonnel, & Requin, 1998). This means that singing and speaking seem to originate from different areas of the brain. What about Broca’s area in deaf people who use sign language? Will damage to Broca’s area impact their ability to use sign language? The answer is yes. Broca’s area seems important for both the production of speech and its complement in the deaf, sign language (Corina, 1998).

People with damage to Broca’s area do not have a problem understanding the speech of other people or reading silently, which means these skills must involve other areas. One of these areas is in the left temporal lobe and is named after its discoverer, Karl Wernicke, a German researcher. Wernicke’s area is responsible for the comprehension of speech and reading. Figure 2.10 shows exactly where this area is located. Damage to this area leads to Wernicke’s aphasia—incoherent speech and the inability to understand the speech of others and to read. Wernicke’s area functions as the understanding center for incoming speech and text. To sum up, Broca and Wernicke together discovered a double dissociation of speech production and comprehension. Damage to Broca’s area stops speech production but leaves speech comprehension intact, and damage to Wernicke’s area stops speech comprehension but spares speech production, though the speech is nonsensical.

Like Broca’s area, Wernicke’s area is only in the left temporal lobe of the majority of people (regardless of handedness). Many people have the misconception that these speech and language centers normally reside in the hemisphere opposite to a person’s handedness. This is only the case for a very small number of right-handers and some left-handers, however. Speech and language centers are located in the left hemisphere for about 95% of right-handers and 70% of left-handers (Springer & Deutsch, 1998).

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Broca and Wernicke examined the brains of deceased people who had speech and language dysfunctions in order to identify the speech and language centers in the brain. So perhaps this cortical localization technique could be used with highly intelligent people to identify the keys to their genius, the neural basis of intellect? What about the brain of acclaimed genius Albert Einstein? Was it studied after his death in 1955? The answer is a much qualified yes, because his brain was not studied in the careful, systematic manner that you would think it would be. The journey that Einstein’s brain took was indeed a bizarre odyssey (Abraham, 2001). With the exception of his brain and eyes, his body was cremated on the day of his death; but to this day no one seems to know where the ashes are (Lepore, 2001). The examining pathologist at Princeton Hospital where Einstein died, Dr. Thomas Harvey, removed the brain and took dozens of photographs of the whole and partially dissected brain before having it partitioned into 240 blocks of tissue, preparing a roadmap of the locations in the brain that yielded the dissected blocks, and sectioning and staining histological slides from the blocks.

Despite Harvey’s meticulous preservation of Einstein’s brain and the distribution of some brain sections to a few researchers, nothing had yet been published 23 years later when Harvey was interviewed in 1978 (Lepore, 2001). During this time period, Harvey kept most of the brain hidden away for his own personal research. He stored these remaining dissected and labeled brain pieces in glass jars of formaldehyde in a cider box in his office. Einstein’s brain usually accompanied him when he traveled. In fact, Dr. Harvey made a trip across America to visit Einstein’s granddaughter with some of the photographs and slides and some pieces of the brain floating in formaldehyde in a Tupperware bowl in a duffel bag in the trunk of a car (Paterniti, 2000).

Starting in the 1980s Harvey did dole out some more of the slides and photographs to researchers. This led to six peer-reviewed publications and a few speculative differences between Einstein’s brain and those of people with normal intelligence (Falk, Lepore, & Noe, 2012). For example, Diamond, Scheibel, Murphy, and Harvey (1985) found a higher glia to neuron ratio in the left parietal lobe, and Witelson, Kigar, and Harvey (1999) found that the gross anatomy of Einstein’s brain seemed within normal limits with the exception of his parietal lobes. These findings led to the hypothesis that Einstein’s unusual parietal lobes might have provided the neural basis for his visuospatial and mathematical skills, consistent with the finding of an enlarged parietal lobe in the preserved brain of Carl Gauss, one of the greatest mathematicians ever (Seung, 2012). In 2007 Harvey died, but fortunately Dr. Harvey’s Estate donated 14 of Harvey’s photographs of Einstein’s whole brain (last seen in 1955) along with some of the histological slides and the roadmap that identifies the brain locations that yielded the slides to the National Museum of Health and Medicine (Falk, Lepore, & Noe, 2012).

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Granted access to these materials, Falk et al. (2012) were able to describe the external gross neuroanatomy of Einstein’s entire cerebral cortex in comparison to 85 normal human brains. Many of the photographs show structures that were not visible in the photographs previously analyzed. Falk et al. found that Einstein’s brain was of unexceptional size but had very unusual morphology. The complexity and pattern of convolutions and folds in the prefrontal lobe, parietal lobe, visual cortex, and primary motor and somatosensory cortices gave these parts a much larger surface area than in normal brains. Falk et al. also speculated on the meaning of their findings. For example, the expanded prefrontal cortex may have contributed to the neurological substrates for some of Einstein’s remarkable abilities, and the unusual parietal lobes are consistent with the earlier hypothesis that they may have provided the neurological underpinnings for his visuospatial and mathematical abilities. But the long, strange journey for Einstein’s brain hasn’t ended. In 2012, digital preservations of some of the slides of Einstein’s brain became available to the general public as an iPad application. You have to wonder whether Einstein would have wanted images of his brain sold to nonscientists for $9.99.

Next, we will consider the question of whether there are any hemispheric specializations other than speech, language, and face perception. To try to answer this question, researchers have examined patients who have had their corpus callosum, the cortical bridge between the two hemispheres, severed as a medical treatment for severe cases of epilepsy. William Van Wagenen performed the first split-brain surgery in 1940 (Gazzaniga, 2008). Not many people have had this surgery, and because of improved medications and other modes of treatment for epilepsy, it is done even more rarely now. The rationale behind this surgery was that the epileptic seizures would be lessened in severity if they were confined to only one hemisphere. Indeed, the surgery did provide this benefit. However, it also created a group of people (usually referred to as “split-brain” patients) in which the two hemispheres of the brain could not communicate, composing an ideal group for studying the question of hemispheric specialization. According to Gazzaniga (2008), there have only been 10 split-brain patients who have been well tested. First, we will discuss the general experimental procedure that has been used to study the hemispheric specialization question with these patients.

Studying the two hemispheres. To understand the experimental procedure for studying the two hemispheres, we first need to understand how the visual fields, the eyes, and the cerebral hemispheres are related. These relationships are shown in Figure 2.11. Our field of vision has two halves—the left visual field (what is to the left of center in our field of vision) and the right visual field (what is to the right of center in our field of vision). Light waves from the left visual field go to the right half of each eye, and those from the right visual field go the left half of each eye. Each visual field is processed by half of each eye. The right half of each eye connects with the right hemisphere, and the left half of each eye with the left hemisphere. This means that the eyes and the hemispheres, with respect to processing incoming visual information, are not contralaterally related. Rather, the visual information in half of each eye goes to each hemisphere. The visual information in the right halves goes to the right hemisphere, and the visual information in the left halves goes to the left hemisphere. Thus, information in the left visual field goes only to the right hemisphere, and information in the right visual field goes only to the left hemisphere. The following diagram should help you remember this processing sequence:

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This relationship between the visual fields and the hemispheres is important because it allows information that is presented briefly in one visual field to go to only one hemisphere. With split-brain patients, the information cannot be transferred to the other hemisphere because the corpus callosum connecting their two hemispheres has been severed. By examining how split-brain patients can identify the presented information (orally, visually, or by touch), researchers can study the hemispheric specialization question.

Recall that the speech and language centers (Broca’s and Wernicke’s areas) are only in the left hemisphere of the vast majority of people. This would mean that a split-brain patient should only be able to identify information orally when it is presented briefly in the right visual field (it is this field that feeds information to the left hemisphere). In fact, this is what has been found with split-brain patients. For example, if a picture of a spoon were flashed briefly in the left visual field, a split-brain patient would not be able to say that it was a spoon. But if we blindfolded the split-brain patient and asked her to identify the flashed object from a group of objects by touch with the left hand, the split-brain patient can do this (Gazzaniga, 1992). Remember that the somatosensory strip in the right hemisphere is connected to the left hand. However, even after identifying the spoon as the object presented, a split-brain patient would not be able to identify it orally if asked what was in her left hand. What would happen if the blindfolded split-brain patient were asked to move the object from her left hand to her right hand? She would now say that she was holding a spoon. The information that it was a spoon would be gathered through touch by her right hand and sent to the somatosensory strip in her left hemisphere, allowing her to transfer this information to the speech centers in the left hemisphere.

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Split-brain patients are also sometimes asked to identify the presented information by pointing with the appropriate hand (left hand for right hemisphere, right hand for left hemisphere). A clever use of this methodology involves simultaneously presenting different objects to each hemisphere. For example, an orange might be shown in the right visual field so it goes to the left hemisphere, and an apple in the left visual field so it goes to the right hemisphere. If then asked to use the left hand to identify what was presented, the split-brain patient would point to the apple; but if she had been asked to use the right hand, she would have pointed to the orange. In each case, the nonresponding hemisphere would be baffled by the other hemisphere’s response.

What we know about the left and right hemispheres. The two most prominent researchers on split-brain questions have been Roger Sperry and Michael Gazzaniga. Sperry led most of the early split-brain research and in 1981 won the Nobel Prize in Physiology or Medicine for his discoveries concerning the functional specializations of the cerebral hemispheres. Sperry’s student, Michael Gazzaniga, who conducted the first studies with human split-brain participants in the early 1960s at the California Institute of Technology under the guidance of Sperry and neurosurgeon Joseph Bogen (Gazzaniga, 2015; Gazzaniga, Bogen, & Sperry, 1962), has continued this line of inquiry for the past five decades (Gazzaniga, 2005, 2008). Now let’s see what these studies with split-brain participants have told us about hemispheric specialization.

We know that the speech and language centers are specialties of the left hemisphere. This is why the left hemisphere is sometimes referred to as the verbal hemisphere. This does not mean, however, that the right hemisphere has no verbal ability. It can’t produce speech, but it can understand simple verbal material. In addition, the left hemisphere is better at mathematical skills and logic, while the right is better at spatial perception, solving spatial problems (e.g., block design), and drawing. The right hemisphere is also better at face recognition. Due to the asymmetry in the fusiform face area, recognition of faces is faster when faces are presented in the left- than the right-visual field of both split-brain patients (Stone, Nisenson, Eliassen, & Gazzaniga, 1996) and normal people (Yovel, Tambini, & Brandman, 2008). In general, the left hemisphere is more analytic, analyzing wholes into their elements or pieces; the right hemisphere processes information in a more holistic fashion, combining pieces into wholes (Reuter-Lorenz & Miller, 1998). The right gets the big picture (the “forest”); the left focuses on the smaller details (the “trees”). This information-processing style difference between the two hemispheres is sometimes referred to as global versus local processing.

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Support for this general processing style difference between the hemispheres has been corroborated by research with brain-damaged patients using hierarchical stimuli developed by David Navon (1977). These hierarchical stimuli consist of a large letter (the global, holistic level) that is composed of smaller versions of another letter (the local or analytic level). See the example in Figure 2.12a in which the large letter H is composed of smaller As. Delis, Robertson, and Efron (1986) used such stimuli to study perceptual encoding in brain-damaged patients. The patients were asked to study the hierarchical stimulus and then redraw it from memory after a brief period of distraction. The patients with right hemisphere damage who were dependent on their left hemisphere often drew As unsystematically scattered about the page (see Figure 2.12b). They remembered the constituent elements of the original stimulus but not the overall pattern. In contrast, the patients with left hemisphere damage who were dependent on their right hemisphere often drew a large capital H but with no As (see Figure 2.12c). They remembered the global pattern but not the constituent elements. Thus, the right hemisphere specializes in synthesizing global, holistic patterns, whereas the left hemisphere specializes in analyzing the details of a stimulus. Fink et al. (1996) have also observed this hemispheric processing style difference in PET scan data when normal participants were attending to either the global or local level of Navon hierarchical figures.

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This processing difference along with all of the other specialization differences that have been observed in split-brain patients have led to the expressions “left-brained” and “right-brained” to refer to people who seem to excel at the skills normally attributed to left and right hemispheres, respectively. We must remember, however, that these differences in hemispheric performance are for people whose two hemispheres can no longer communicate. When normal people are performing a task, the two hemispheres are constantly interacting and sharing information. There is no forced separation of labor as in the split-brain patient. Each hemisphere contributes in a complementary, not exclusive, way. It may be the case that one hemisphere tends to play a larger role depending on what mental activity we are currently engaged in, but both hemispheres are involved (Corballis, 2007; Hellige, 1993; Jarrett, 2015; Nielsen, Zielinski, Ferguson, Lainhart, & Anderson, 2013). This is why it is not accurate to say someone is “left-brained” or “right-brained.” It is best not to make the distinction. Nearly all of us are “whole-brained.”

There are many questions left for neuroscientists to answer about the brain and its many functions, but the most intriguing questions concern human consciousness—What is consciousness and what underlies it? Probably the best way to think about consciousness is as a person’s subjective awareness of his inner thinking and feeling as well as his immediate surroundings. Thus, consciousness is both internal (one’s thoughts and feelings) and external (what’s going on in one’s environment).

Most brain (and bodily) functioning goes on without our conscious awareness. For example, you are presently recognizing the letters and words in this paragraph, but you are not consciously aware of the actual processing required to accomplish this recognition. You are only consciously aware of the results of the recognition process (the meaningful collection of words). Even if you wanted to, you couldn’t become consciously aware of this processing by the brain. Think about the billions of neurons communicating with one another within your brain and nervous system at this very moment. You cannot become aware of activity at this neuronal level of processing. Our consciousness is privy to only some of the results of this processing.

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We can describe waking consciousness as our tuning in to both our internal and external worlds, but questions about exactly what underlies it (how it is generated) or why it evolved remain open for debate. Dehaene (2014) and Kaku (2014) provide some interesting theorizing about answers to these questions. Similarly, we are still pondering the question of why we experience sleep—a natural, altered state of consciousness. We do, however, have some better answers to questions about what the brain is doing during sleep. Electrical recordings of brain activity during sleep allow us to measure different stages of sleep and to tell us when we are dreaming. So first we’ll examine the stages of sleep and how they are related to dreaming. Then, we will briefly discuss theories that have been proposed to explain why we sleep and why we dream.

The five stages of sleep. The various stages of sleep have been determined by monitoring the electrical activity in the brain using an electroencephalograph (EEG). Small electrodes are attached to the scalp and connected to recording equipment that produces a real-time graph of electrical activity in the cortex of the brain. In Figure 2.13, a sample EEG for the awake, relaxed state is shown along with sample EEGs for the five stages of sleep. As we slip into sleep and pass through the first four stages, our brain waves change, in general becoming progressively slower, larger, and more irregular, especially in Stages 3 and 4. Stage 1 sleep, which lasts about 5 minutes, is followed by about 20 minutes of Stage 2 sleep, which is characterized by periodic bursts of rapid activity called sleep spindles. Some researchers believe these spindles represent the activity of a mechanism that lessens the brain’s sensitivity to sensory input and thus keeps the person asleep. The fact that older people’s sleep contains fewer spindles and is interrupted by more awakenings during the night is consistent with this explanation.

Next are the two stages composed of slow-wave sleep—the brief, transitional sleep of Stage 3 and then the deep sleep of Stage 4. These two stages, especially Stage 4, are characterized by delta waves—large, slow brain waves. You are now completely asleep and this initial period of slow-wave sleep lasts for about 30 minutes. In deep sleep, the parasympathetic nervous system dominates. So, muscles relax, heart rate slows, blood pressure declines, and digestion is stimulated. Mysteriously, the brain is still monitoring environmental information, though it is outside our conscious awareness. If a sensory stimulus is important, such as a baby’s cry, or very strong, such as a slamming door or a breaking glass, it will break through the perceptual barrier created by sleep and awaken us.

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Near the end of your first period of deep sleep (about an hour after falling asleep), you return through Stages 3 and 2 and enter REM (rapid eye movement) sleep, the most fascinating stage of sleep. REM sleep is characterized by very rapid waves somewhat like those of Stage 1 sleep. However, you are still sound asleep. REM sleep is sometimes referred to as paradoxical sleep because the muscles are relaxed but other body systems and the brain are active, following a waking pattern. Heart rate rises, breathing is more rapid, eyes move back and forth rapidly under closed eyelids, and one’s genitals become aroused. The brain is also highly active; both oxygen consumption and cerebral blood flow increase. Strangely, given all of this internal activity, the muscles are relaxed, leaving the body essentially paralyzed except for occasional muscle twitching.

REM sleep indicates the beginning of dreaming; it is the stage during which most dreaming occurs. How do we know this? If people are awakened during Stages 1 through 4, they only occasionally report dreaming; but if awakened during REM sleep, people usually recall dreams that they were having. This is as true for people who say they dream as for those who say they rarely do so, which means that we all dream whether we realize it or not. This first bout of REM sleep typically lasts about 10 minutes and completes the first sleep cycle of the night. The cycle of stages, in which we move out of and back into REM sleep, repeats itself about every 90 minutes throughout the night. Deep sleep (Stages 3 and 4) gets briefer and eventually disappears, as Stage 2 and REM sleep periods get longer with each sleep cycle. Over the course of the night, you have four or five REM sleep periods, amounting to about 20% to 25% of your sleep time (Figure 2.14).

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We spend on average about 2 hours a night dreaming, which works out to about 6 years of dreaming across our lifetime, given current life expectancies. We don’t remember many of our dreams, though. The dreams we do remember are usually from our last phase of REM sleep, right before we wake up. Many dreams are highly emotional and unpleasant. For example, people often dream of being attacked or pursued. This may be due to the fact that the frontal lobes (responsible for rational thought) are shut down during REM sleep, but the amygdala and the hippocampus, the limbic system structures responsible for emotion and memory, are active, creating the irrational imagery and emotional experiences of our dream world. Given the strong visual nature of dreams, what are the dreams of blind people like? Research indicates that people born blind or who go blind very early in life do not have visual dreams. Their dreams are just as emotional, but involve other sensations, especially sounds.

Why do we sleep and dream? We do not know why we sleep, but we know that we need sleep. You cannot cheat sleep; it will always overcome you. Inadequate sleep has a high cost. Sleep-deprived people have impaired concentration and a general bodily feeling of weakness and discomfort, and they may even hallucinate. Sleep deprivation also suppresses your immune system, lessening your ability to fight off infection and disease. Sleep-deprived people are also more vulnerable to accidents. For example, traffic accidents increase following the shortened sleep accompanying the 1-hour time change in the spring (Coren, 1993). All of this may help explain why people who typically sleep 7 or 8 hours outlive those who are chronically sleep deprived (Dement, 1999). College students are notorious for being sleep deprived, with as many as four out of five not getting adequate sleep. Beware of sleep deprivation and its negative effects. Sleep deprivation makes it more difficult to concentrate, study, and take exams. So, creating a large sleep debt will, in simple terms, “make you stupid” (Dement, 1999, p. 231).

We clearly need sleep. How much, however, varies greatly with individuals. On the average, though, we spend about a third of our lives sleeping. Why? Four possible answers have been proposed, and the actual answer probably involves all four. First, sleep seems to serve a restorative function by allowing the brain and body time to rest and recuperate from the daily wear and tear of our existence. For example, recent research has shown that during sleep the brain cleans itself of toxic metabolic byproducts (Xie et al., 2013). This finding that sleep ensures metabolic homeostasis also has implications for many neurological disorders, many of which, such as Alzheimer’s disorder, are associated with sleep disturbances. These disturbances would prevent the brain from cleaning itself, and toxic byproducts would build up and cause brain damage. Second, gene activity during sleep ramps up the production of myelin, which as you have learned, protects our brain’s circuitry and facilitates neuronal transmission (Bellisi et al., 2013). Thus, sleep fortifies the brain over the long term by leading to the production of myelin, the brain’s insulating material. Third, sleep helps us process what we learn. It allows the brain the opportunity to consolidate our day’s experiences into our memory banks for later retrieval and use. Indeed, there is research evidence that memory is often strengthened and enhanced following a period of sleep (Stickgold & Ellenbogen, 2009). REM sleep is especially important in relation to memory. Disruption of REM sleep (by being constantly awakened during this stage) following learning impairs our memory for this learning (DuJardin, Guerrien, & LeConte, 1990). Disruption of other sleep stages does not similarly impair memory. Fourth, sleep may have evolved as an adaptive process. It served a protective function for our ancestors, increasing their survival by keeping them safe from predators during the night and from the dangers of wandering around cliffs in the dark. Those who stayed in their caves and slept had a better chance of surviving and passing on their genes.

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So, sleep has clear advantages. But why do we dream? One answer is the critical role of REM sleep in learning—providing the opportunity for memory consolidation of new information (Stickgold, Hobson, Fosse, & Fosse, 2001). Other answers to the question of why we dream have also been proposed. About a hundred years ago, Sigmund Freud proposed that dreams were disguised outlets for the inner conflicts of our unconscious (Freud 1900/1953a). But given its lack of scientific support, the Freudian view has been rejected by most contemporary sleep researchers. There are many contemporary theories of why we dream, and all have their critics. One explanation that has received much attention is the activation-synthesis theory (Hobson, 2003; Hobson & McCarley, 1977; Hobson, Pace-Scott, & Stickgold, 2000). This physiological theory proposes that neurons in the pons fire spontaneously during REM sleep, sending random signals to various areas in the cortex and the emotional areas in the limbic system. The signals are random, but the brain tries to make sense of them and produce a meaningful interpretation. Thus, a dream is the brain’s synthesis of these signals. However, because the signals evoke random memories and visual images, the brain has a difficult time weaving a coherent story, often resulting in the bizarre and confusing nature of our dreams. This relates to a major criticism of the theory: dream content is more coherent, consistent over time, and concerned with waking problems and anxieties than the activation-synthesis theory would predict (Domhoff, 2003). Criticisms aside, this theory has led to a wide body of research on the neurological stuff that dreams are made of and thus greatly increased our knowledge of the physiological basis of dreaming.

In contrast to the activation-synthesis theory of dreaming, the neurocognitive theory of dreaming emphasizes the parallels between waking cognition and dreaming (Domhoff, 2011). Neurocognitive theory argues that explaining dreams as our subjective interpretations of random neural firing is too simple and that dreams are meaningful products of our cognitive abilities, with continuity between waking and dreaming cognition. Most dreams are about people and activities that are well-known to the dreamer and reflect our waking concerns, personality, emotions, and interests (Domhoff, 1996; Nir & Tononi, 2010). According to neurocognitive theory, the dreams of children younger than 9 or 10 years old are simpler and less emotional and bizarre than adult dreams. Why? Children’s dream development parallels the gradual development of advanced cognitive abilities, such as visual imagination. Once their cognitive abilities are more advanced, their dreams become more complex. In brief, dreams are a product of our normal cognitive processes, but they use self-generated sensory data during sleep rather than external sensory input as they do when we are awake.

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Although sleep researchers do not agree about why we dream, they do agree that REM sleep is essential. This is clearly demonstrated by the REM sleep rebound effect—a significant increase in the amount of REM sleep following deprivation of REM sleep. The fact that REM sleep and the rebound effect are observed in other mammals implies a definite biological need for this type of sleep. Exactly what that need is, however, remains an open question.