The Human Brain Book

RITA CARTER AN ILLUSTRATED GUIDE TO ITS STRUCTURE, FUNCTION, AND DISORDERS THE HUMAN BR A I N BOOK (c) 2011 Dorlin...

Author: Rita Carter | Susan Aldridge | Martyn Page | Steve Parker

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RITA

CARTER

AN ILLUSTRATED GUIDE TO ITS STRUCTURE, FUNCTION, AND DISORDERS

THE

HUMAN BR A I N BOOK

(c) 2011 Dorling Kindersley. All Rights Reserved.


THE

HUMAN BRAIN BOOK

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Gall thought that personality could be read by feeling the contours of the skull. He theorized that various faculties were localized in the brain and that the strongest were correspondingly large, making the skull bulge measurably. It was hugely popular in nineteenth-century America and Europe—nearly every town had a phrenology institute. Although nonsense, Gall’s idea that brain functions are localized has turned out E=G:CDADCC

Spanish neurologist Dr. José Delgado invented a brain implant that could be remotely controlled by radio waves. He found that animal and human behavior could be controlled by pressing a button. In a famous experiment, conducted in 1964, Delgado faced a charging bull, bringing it to a halt at his feet by activating the implant in its brain. In another, he put a device in the brain of a chimp that was bullying its mate. He put the control in the cage where the victim chimp used it to “turn off” the bully’s 9:AC< IdYVnVYkVcXZY^bV\^c\hZZ VWdkZVaadlhcZjgVaVXi^kîn idWZbViX]ZYidbZciVa iVh`h#=dlZkZg!bjX]d[i]Z 86C69>6C WVh^XbVelVhZhiVWa^h]ZYWn EZcÒZaY]Va[VXZcijgnZVga^Zg# HI6BE

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AD7DIDBN The first lobotomies were performed in the 1890s, but they only took off in the 1930s when the Portuguese neurosurgeon Egas Moniz found that cutting the nerves from the frontal cortex to the thalamus relieved psychotic symptoms in some patients. Moniz’s work was picked up by US surgeon Walter Freeman, who invented the “ice pick lobotomy.” From 1936 until the 1950s, he advocated lobotomy to cure for a range of problems, and 40,000 to 50,000 patients were lobotomized. The operation was overused and is now thought abhorrent. However, in many cases it eased suffering: a follow-up of patients in the UK found 41 percent were “recovered” or “greatly improved,” 28 percent “minimally improved,” 25 percent had “no change,” 4 percent had died, and 2 percent were worse off. IG:E6C6I>DC

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In 1953, aged 27, “HM” underwent an operation in the US, to stem severe epilepsy. The surgeons, then unaware of the functions of the hippocampus, took out a large area of that part of his brain (see p.157). When he came round, he was unable to lay down new memories and remained so for the rest of his life. The tragic accident demonstrated the crucial role of the hippocampus in recall.

A series of ingenious experiments by US neuroscientist Benjamin Libet (see p.187) in the early 1980s demonstrated that what we think are conscious “decisions” to act are actually just recognition of what the unconscious brain is already doing. Libet’s experiments have profound philosophical implications because, on the face of it, the results suggest that we do not have a conscious choice about what we do, and therefore cannot consider ourselves to have free will.

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Neurobiologist Roger Sperry conducted the split-brain experiments (see p.198) on people whose brain hemispheres were surgically separated in the course of treatment for epilepsy. They showed that, under certain conditions, each hemisphere could hold different thoughts and intentions. This raised the profound question of whether a person has a GDK:9 single “self.” I=:CD7:AEG>O:>C&.-&

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The structure of the brain is well known, but until recently the way it created thoughts, emotions, and perceptions could only be guessed at. Imaging technology has now made it possible to look inside a living brain and see it at work. The brain works by generating tiny electrical charges. Functional imaging reveals which areas are most active. This may be done by measuring electrical activity directly (EEG), picking up magnetic fields created by electrical activity (MEG), or measuring metabolic side effects such as E:IH86CC:G EdhîgdcZb^hh^dcidbd\gVe]n alterations in glucose E:IhXVccZghYZiZXih^\cVah[gdb absorption (PET) and gVY^dVXi^kZbVg`Zgh^ci^hhjZhid blood flow (fMRI). h]dlVXi^kîn^ci]ZWgV^c#

The brain is composed of modules that are specialized to do specific things. Functional brain imaging is largely about identifying which ones are most concerned with doing what. This has allowed neuroscientists to build a detailed map of brain functions. We now know where perceptions, language, memory, emotion, and movement occur. By showing how various functions work together, imaging also gives us a glimpse into some of the most sophisticated aspects of human psychology. For example, observing a person’s brain making a decision, we see that apparently rational decisions are driven by the emotional brain. Imaging the brains of master chess players shows why expertise depends on practice. Watching the brain of a person seeing a frightened face shows that emotion is contagious.

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B68G:HDC6C8:>B6C< Magnetic resonance imaging (MRI) provides a better contrast between tissue types than CT. Instead of using X-rays, it uses a powerful magnetic field, which causes hydrogen atoms in the body to realign. The nuclei of the atoms produce a magnetic field that is “read” by the scanner and turned into a three-dimensional computerized image. The brain is scanned at a rapid rate (typically once every 2–3 seconds) to produce “slices” similar to those in CT scans. Increases in neural activity cause changes in the blood flow, which alter the amount of oxygen in the area, producing a change in the magnetic signal. Functional MRI (fMRI) involves showing differing levels of electrical activity in the brain, overlaid on the anatomical details.

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8DB7>C:9>B6C< Each type of imaging has its advantages. MRI is good on detail, for example, but is too slow to chart fast-moving events. EEG and MEG are fast but are not as good at pinpointing location. To get scans that show both fast processes and location, researchers use two or more methods to produce a combined image. Here (right), for example, high-resolution MRI, taking about 15 minutes to acquire, is combined with a low-resolution fMRI, which takes seconds to produce and shows the location of activity in the brain areas used in hearing language. The areas shift HIJ9N>C8:9IDhXVch]dlh i]Zhjg[VXZ[daYhd[i]ZWgV^c#>iVahdgZkZVah i]Zh`jaaWdcZhVcYi]ZidekZgiZWgVZ#

13



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starting to understand the function of some of these, but we are only at the very beginning of this journey of understanding. The captions that accompany the scans indicate the most likely function of various brain regions. But these regions often have many functions, and these functions depend upon interactions with other brain regions. Most structures in the brain are paired, with identical counterparts in the left and right hemispheres, so structures identified in one hemisphere are mirrored in the opposite one. The scans themselves have been colored, so that the cerebrum appears in red, the cerebellum in light blue, and the brainstem in green.

15


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THE BRAIN AND THE BODY


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L=6II=:7G6>C9D:H The brain receives a constant stream of information as electrical impulses from neurons in the sense organs. The first thing it does is determine whether the information warrants attention. If it is irrelevant or just confirmation that everything is staying the same, it is allowed to fade away and we are not conscious of it. But if it is novel or important, the brain amplifies the signals, causing them to be represented in various regions. If this activity is sustained for long enough, it will result in a conscious experience. In some I=:7G6>C6C97D9N I]ZWgV^cVcYhe^cVaXdgY cases, thoughts are taken one XdchiîjiZi]ZXZcigVa step further, and the brain cZgkdjhhnhiZb!l]^X] ^hi]ZWdYnÉhbV^cXdcigda instructs the body to act XZciZg!gZhedch^WaZ[dg on them, by sending signals XddgY^cVi^c\Vaad[i]Z egdXZhhZhVcYbdkZbZci to the muscles to make ^ci]ZWdYn# them contract.

=DLI=:7G6>C9D:H>I No one knows exactly how electrical activity turns into experience. That remains a famously hard problem, which has yet to be cracked (see p.177). However, much is now known about the brain processes that turn incoming information into the various components of subjective experience, such as thoughts or emotions. Much depends on where the information comes from. Each sense organ is specialized to deal with a different type of stimulus—the eyes are sensitive to light, the ears to sound waves, and so on. The sense organs respond to these stimuli in much the same way—they generate electrical signals, which are sent on for further processing. But the information from each organ is sent to a different part of the brain, and then processed along a different neural pathway. Where information is processed therefore determines what sort of experience it will generate. 68I>DCH 8ZgiV^cWgV^cVgZVhVgZheZX^VaôZYid egdYjXZWdYnbdkZbZci#7gV^chiZb bdYjaZhXdcigdaVjidbVi^X^ciZgcVa VXi^dch!hjX]Vhi]Zajc\VcYX]Zhi bdkZbZcihcZZYZY[dgWgZVi]^c\!i]Z WZVi^c\d[i]Z]ZVgi!VcYi]ZXdchig^Xi^dc dgYâVi^dcd[WaddYkZhhZahidXdcigda WaddYegZhhjgZ#>cXdchX^djhVXi^kî^Zh!i]Z eg^bVgnbdidgXdgiZmhZcYhbZhhV\Zhk^V i]ZXZgZWZaajbVcYWVhVa\Vc\a^Vidi]Z bjhXaZhd[i]Za^bWh!igjc`!VcY]ZVYid XgZViZ\gdhhbdkZbZcih#

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The average adult human brain weighs about 3 1/4lb (1.5kg). Its volume and shape are similar to those of an average-sized cauliflower, and the consistency of its tissues is similar to stiff jelly. The size of a person’s brain bears little relation to his or her intelligence, and every brain, whatever its weight and volume, has roughly the same number of neurons and synapses. After the age of 20 or so, brain mass decreases by about 1/32oz (1g) per year. The brain shrinks as neurons die off and are not replaced. This is generally no cause for concern because there are plenty of neurons left to carry out the brain’s functions.

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Glucose is the brain’s sole fuel, except under conditions of starvation, when it breaks down protein. The brain is by far the body’s hungriest organ. Although it accounts for just 2 percent of the body’s weight, it requires a staggering 20 percent of its total glucose supplies. This is obtained from dietary carbohydrate, which is transported to the brain via the bloodstream. It consumes roughly 4oz (120g) of glucose (about 420kcal) per day. Because the brain cannot store glucose, it must be readily available at all times via the blood supply. Without oxygen or glucose, the brain can last for only about 10 minutes before irreparable damage occurs. This is why prompt resuscitation is needed in cases of cardiac arrest.

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The brain has several defense mechanisms to protect it from damage. The bony skull acts as a box, containing the brain and buffering it against blows. The meninges are three layers of membranes that line the skull, enclosing the brain and providing extra layers of protection between the skull and the brain. Cerebrospinal fluid circulates within the brain, nourishing brain tissue and working as a shock absorber to reduce the impact of knocks.

Brain tissue floats in cerebrospinal fluid (CSF) within the skull. CSF absorbs shocks from blows to the brain. It is produced in a series of connected chambers within the brain known as the ventricles, and is renewed four to five times per day. It contains proteins and glucose to nourish brain cells, as well as white blood cells to protect against infection. It moves through the ventricles, propelled by the pulsation of the cerebral arteries.

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BRAIN ANATOMY


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The brain’s major parts can be classified or categorized in several ways. In all of these systems, the dominant part is the cerebrum, the large pinky-gray wrinkled structure that forms more than three-quarters of the brain’s total volume. The cerebrum is divided into left and right hemispheres, which are linked by a “bridge” of nerve fibers, the corpus callosum. The cerebrum, which includes the hippocampus and amygdala, is also known as the telencephalon. Together with the parts

it wraps around—the thalamus, hypothalamus, and associated parts, collectively known as the diencephalon—it comprises the major brain “division” known as the forebrain (prosencephalon). Below the forebrain is the midbrain (mesencephalon), a small division that includes groups of nerve-cell bodies known as nuclei, such as the basal ganglia. Below the midbrain is the hindbrain (rhombencephalon), with the pons as its uppermost part, and beneath it the cerebellum and the medulla, which tapers to merge with the spinal cord.

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A:;I6C9G>HE=:G:H An overhead view of the “exploded” brain shows how the two cerebral hemispheres can be neatly separated by cutting through the corpus callosum. Many other brain structures are symmetrically paired in this way, such as the thalamus, which is sometimes described as “two hen’s eggs sitting side by side.” The cerebellum at the lower rear of the brain is accommodated within a bowl-like cavity of the skull known as the posterior cranial fossa. The cranial nerves (numbered I to XII, see p.43) enter the brain directly rather than connecting to the spinal cord.

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The uppermost brain region, the cerebral cortex, is mostly involved in conscious sensations, abstract thought processes, reasoning, planning, working memory, and similar higher mental processes. The limbic areas (see pp.64-65) on the brain’s innermost sides, around the brainstem, deal largely with more emotional and instinctive behaviors and reactions, as well as long-term memory. The thalamus is a preprocessing and relay center, primarily for sensory information coming from lower in the brainstem, bound for the cerebral hemispheres above. Moving down the 8DGI>86A brainstem into the medulla are the so-called “vegetative” centers of the brain, which sustain life even A>B7>8 if the person has lost consciousness. A:HH8DCH8>DJH!BDG:6JIDB6I>8 I]ZWgV^cÉhkZgi^XVaodcVi^dcbdkZh[gdb]^\]"aZkZa bZciVaVXi^kîn^ci]ZXZgZWgVaXdgiZm\gVYjVaan i]gdj\]idbdgZWVh^XdgÆeg^bî^kZÇadlZg[jcXi^dch! ZheZX^Vaani]ZVjidcdb^XXZciZghd[i]ZbZYjaaV^c i]ZadlZgWgV^chiZbi]ViYZValî]kîVaWdYn [jcXi^dch!hjX]VhWgZVi]^c\VcY]ZVgiWZVi#

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I=:6HNBB:IG>86A7G6>C In recent years, new and more accurate scanning techniques, especially MRI (see p.13), have shown that on average, brains are not as symmetrical in their left–right structure as was once believed. The scanning computer can be programmed to exaggerate any subtle departures from an exact mirror image. For example, near the lateral sulcus (Sylvian fissure), the part of the temporal lobe for understanding speech is slightly ;GDCI G^\]iaViZgVa larger on the left than on the hjaXjh right. The lateral sulcus itself is also usually different in shape, being longer and less curved on the left than the right. This is partly due to a twisting effect known as Yakovlevian torque, which warps the right side of the brain forward.

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I=:=DAADL7G6>C The brain has an internal system of chambers (ventricles), which are filled with a liquid—cerebrospinal fluid (CSF)—produced by the ventricle linings. The upper two chambers are the left and right lateral ventricles, one in each cerebral hemisphere, with hornlike forward- and side-facing projections. Small openings connect them to the third ventricle in the midbrain, which in turn links to the fourth ventricle in the pons and medulla. CSF flows slowly and continuously through the ventricles, then out via small openings into the subarachnoid space around the brain and the spinal cord. K:CIG>8A:H IldaVg\ZaViZgVakZcig^XaZh Xdbbjc^XViZVadc\YjXih lî]i]Zi]^gYkZcig^XaZ nZaadl!jeeZgXZciZg!l]^X] a^ZhWZilZZcVcYWZadli]Zb#

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57


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I=:CJ8A:>D;I=:7G6>C >CI=:7G6>C!CJ8A:>6G:9>H8G:I:8DAA:8I>DCHD;I=:8:AA7D9>:HD; C:JGDCHC:GK:8:AAH#I=:>GC:GK:;>7:GHDG6MDCHHEG:69DJIL6G9 IDEGD?:8I!DGA>C@!IDK6G>DJHDI=:G7G6>CE6GIH#I=:7G6>C=6HBDG: I=6C(%H:IHD;CJ8A:>!BDHIANE6>G:9A:;I6C9G>6IJB I]^hb^Xgd\gVe]h]dlhi]ZcZgkZ caudate nuclei, globus XZaaWdY^ZhYVg`VcYcZgkZÒWZgh pallidus, subthalamic eVaZi]VibV`Zi]^hWgV^cgZ\^dc nuclei, and substantia add`higêZYdghig^ViZY# nigra. The putamen and caudate nuclei are together called the dorsal striatum because of the striped or striated appearance of their tissues. Together with the globus pallidus, or “pale sphere,” the putamen and caudate nuclei are known as the corpus striatum.

I=:HJ7I=6A6B>8CJ8A:> 6C99JH As the name implies, each one of the paired subthalamic nuclei is situated beneath the thalamus. They are also immediately above the substantia nigra. Each nucleus is about the size and shape of a partly squashed pea and is almost surrounded by nerve fibers passing to, from, or around it. Most of the incoming (afferent) nerve fibers are from the globus pallidus, along with some from the cerebral cortex and the substantia nigra. The majority of the outgoing (efferent) nerve fibers carry signals to the globus pallidus and the substantia nigra. The globus pallidus and the putamen are sometimes termed the lentiform or lenticular nucleus.

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58

Most brain nuclei have multiple nerve connections, both inputs and outputs, and carry out wideranging functions. The C-shaped caudate nuclei above and to the side of the thalamus, and next to the lateral ventricle, have a head part, main body, and tapering tail. They are involved in motor (muscle) control and also in learning and memory. The rounded putamen, the outermost of the main basal ganglia, partly follows the shape of the caudate nucleus and is intricately linked anatomically to it. It, too, is heavily involved in motor control and movements, and in learning. The putamen has major nerve connections with the globus pallidus and substantia nigra. All of the basal ganglia work together as an integrated brain system to help ensure that physical movements are smooth and coordinated. Problems with one or more of the nuclei can lead to movement disorders such as tremors, tics, Parkinson’s disease (see p.226), Tourette syndrome (see p.235), and Huntington’s chorea (see p.226). The subthalamic nuclei also have roles in impulsive actions and movement intentions.

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I=:I=6A6BJH Paired, egg-shaped masses that sit side by side make up the thalamus. In a typical brain, each mass is about 11/4in (3cm) long and 1/2in (1.5cm) across. There are no direct nerve connections from one mass to the other—in fact, the fluid-filled chamber of the third ventricle lies between them. The thalamus is the major relay station for nerve signals coming from all the senses except smell. It screens, sorts, and preprocesses this continuing torrent of sensory information and sends it on to the cerebral cortex.

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Nerve impulses from the cochleas of the inner ears go mostly to the medial geniculate nuclei, which forward them on to the auditory cerebral cortex (Brodmann areas 40 and 41, see p.67).

Information from the retinas, about what the eyes see, arrives at the lateral geniculate nuclei. After processing, it passes to the primary visual cortex (area 17) and visual association cortex.

Working with the lateral geniculate nuclei, each much larger lateral nucleus (or pulvinar) sends accessory sensory information to several parts of the visual cortex (see pp.80-81).

Sensory information from the facial skin and interior of the mouth travels along the trigeminal nerve and the trigeminothalamic tract to the medial ventral posterior nuclei.

The thalamus has both incoming (afferent) and outgoing (efferent) nerve fibers. Many nerve fibers to the lateral anterior nuclei are afferent, from the premotor area of the cerebral cortex.

60

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I=:=NEDI=6A6BJH Not much larger than the end segment of the little finger, weighing just 5/32oz (4g), and comprising only 0.4 percent of total brain volume, the hypothalamus has many and varied vital roles—in conscious behavior, emotions and instincts, and automatic control of body systems and processes. It consists of more than a dozen paired nuclei (regions of interlinked nerve-cell bodies) clustered into the floor of the diencephalon and separated by the lateral ventricle. Its secretory cells make hormones (called releasing factors) that enter the bloodstream, and its neurosecretory cells produce hormonelike substances that travel along nerve axons down to the pituitary gland (see below). Dei^X X]^Vhb

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>CI:GC6AHIGJ8IJG: Within the brainstem are groupings of nervecell bodies known as nuclei (see pp.58–59) and numerous bundles of nerve fibers or axons, called nerve tracts. For example, the pontine nuclei of the front or ventral pons are involved in learning and remembering motor skills—they act as relay stations for nerve signals from the motor cortex, which are traveling to the cerebellum behind the pons (see panel, opposite).

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The brainstem includes almost all of the brain except for the highest parts, which make up the forebrain (cerebrum and diencephalon, see p.52). Its uppermost region is the midbrain comprising an upper “roof” or tectum incorporating the superior and inferior colliculi or bulges at the rear, and the tegmentum to the front. Below the midbrain is the hindbrain. At its front is the large bulge of the pons. Behind and below this is the medulla, which narrows to merge with the uppermost end of the body’s main nerve, the spinal cord. The cerebellum joins to the rear of the medulla by three pairs of stalks, known as the cerebellar peduncles.

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The brainstem is highly involved in mid- to low-order mental activities, for example, the almost “automatic” scanning movements of the eyes as we watch something pass by, rather than higher activities such as abstract thought. It is also the site of subconscious or autonomic control mechanisms, of which we are usually unaware. The medulla, in particular, houses groups of nuclei that are centers for respiratory (breathing), cardiac (heartbeat), and vasomotor (blood pressure) monitoring and control, as well as for vomiting, sneezing, swallowing, and coughing.

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The cerebellum has a similar layered microstructure to the cerebrum. The outer layer, or cerebellar cortex, is gray matter composed of nerve-cell bodies and their dendrite projections. Beneath this is a medullary area of white matter consisting largely of nerve fibers. Toward the center are collections of more nerve-cell bodies known as deep cerebellar nuclei. Nerve fibers run from these nuclei to the cerebral cortex high above. In a cross section at almost any angle through the cerebellum, the white matter between the cortex and deep nuclei forms a complex branching pattern known as the arbor vitae.

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8DBEDC:CIHD;I=:A>B7>8HNHI:B The limbic system includes the areas of the cortex and adjacent parts known as the limbic lobe (see opposite page), along with the amygdala, hypothalamus, thalamus, mamillary bodies, and other deeper, more central brain structures. The system is also “hardwired” into parts of the sensory system, especially the sense of smell. Nerve fibers link all of these parts intimately and also connect them to other areas of the brain, particularly the lower frontal cortex, with its roles in expectation, reward, and decision-making.

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Rounded bulges of the cortex are known as gyri; grooves are termed sulci when relatively shallow and fissures when deeper. The overall patterns of gyri and sulci are similar but rarely identical among normal brains—individual variations occur. They are also similar for the left and right of an individual’s brain, although there are minor asymmetries (see p.57).

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HIGJ8IJG:D;I=:8DGI:M The highly convoluted “sheet” of gray matter that constitutes the cerebral cortex varies in thickness from about 1/16 to 3/16in (2 to 5mm). Estimates of its cell numbers vary from 10 billion to more than 50 billion neurons and about five to ten times this number of glial (supporting) and other

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HJEEDGI8:AAH Less than 10 percent of the cells in the brain are neurons. Most of the rest are glial or support cells. They both provide physical support for the amazingly thin dendritic and axonal processes that wind their way around the network, and also supply nutritional support for the neurons in the form of sugars, raw materials for growth and maintenance, and other nutrients. There are several types of glial cells. Microglia destroy invading microbes and clear away debris from degenerating neurons. Oligodendrocytes manufacture myelin sheathing, a task performed in peripheral nerves by Schwann cells.

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HNC6EH:H Synapses are communication sites where neurons pass nerve impulses among themselves. The cells are not usually in actual physical contact, but are separated by an incredibly thin gap, called the synaptic cleft (see p.72–73). Microanatomically, synapses are divided into types according to the sites where the neurons almost touch. These sites include the soma, the dendrites, the axons, and tiny narrow projections called dendritic spines found on certain kinds of dendrites (see illustration, right). Axospinodendritic synapses form more than 50 percent of all synapses in the brain; axodendritic synapses constitute about 30 percent.

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6C6IDBND;6C>BEJAH: Nerve signals are composed of series of discrete impulses, also known as action potentials. A single impulse is caused by a traveling “wave” of chemical particles called ions, which have electrical charges and are mainly the minerals sodium, potassium, and chloride. In the brain, and throughout the body, most impulses in most neurons are of the same strength—about 100 millivolts (0.1 volt). They are also of the same duration—around one millisecond (1/1,000 of a second)—but travel at varying speeds. The information they convey depends on how frequently they pass in terms of impulses per second, where they came from, and where they are heading.

HE::9D;8DC9J8I>DC Impulses travel at widely differing rates, from 3 to more than 330ft/s (1–100m/s), depending on the type of nerve carrying them. They are fastest in myelinated axons. Here the impulse “jumps” rapidly between the myelin-coated sections from one gap (neurofibral node), to the next node.

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6II=:HNC6EH: The synaptic cleft separating the membranes of the sending presynaptic) cell and the receiving (postsynaptic) cell has a width of some 20nm (20 billionths of a meter). This is so narrow that the neurotransmitter molecules can pass across it extremely quickly by simple diffusion—moving from a region of higher concentration to one of lower concentration. Depending on the neurotransmitter, the time taken for the impulse to pass from the pre- to the postsynaptic membranes is typically less than 2ms (1/500 of a second). There is then a recovery delay or clearance time, as the concentrations of neurotransmitter subside, before the next impulse can be sent across. This may last several tenths of a second.

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THE SENSES


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B>M:9H:CH:H Sensory neurons respond to data from specific sense organs. Visual cortical neurons, for example, are most sensitive to signals from the eyes. But this specialization is not rigid. Visual neurons have been found to respond more strongly to weak light signals if accompanied by sound, suggesting that they are activated by data from the ears as well as the eyes. Other studies =:6G>CC< show that in people who are blind or deaf, some neurons that would normally process visual or auditory stimuli are “hijacked” by the other senses. Hence, blind people hear better A:;IH>9:D;7G6>C A:;IH>9:D;7G6>C and deaf people see better.

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Our brains are bombarded with sensory information, but only a fraction of it reaches consciousness. Most sensory signals fizzle out unnoticed. Especially “loud” or important data grabs our attention (see pp.180–81), and we become conscious of it. Sensations we are not conscious of may still guide our actions. For example, unconscious sensations relating to our body position allow us to move without thinking about it. Also, sights and sounds that we fail to notice may nevertheless influence our behavior.

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Æ<J:HH>CC< Sensations are triggered externally, by an occurrence that impacts on a sense organ, and internally, by memory or imagination. The former is known as “bottom-up,” and the latter as “top-down” processing (see p.85). The two combine to create our experience of reality. Each person’s experience of a given event is different. Physiological differences affect bottom-up processing. One person’s colorprocessing area in the brain may be highly sensitive, for example, so that colors are more vibrant than average. Also, an individual’s own memories, knowledge, and expectations affect top-down processing.

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The retina contains three layers of cells, each one connecting to the next via junctions between neurons (synapses), through which information (electrical impulses) can pass. The first two layers send signals to the visual cortex in the brain, but these cells do not respond directly to the light. The third layer, at the very back of the retina, bears light-sensitive (photoreceptive) cells—the rods and cones. Light must pass over the first two layers to these cells to trigger any neural activity. Rods, which make up 90 GD9H6C98DC:H percent of photoreceptors, 8ZaaineZVcYcjbWZg XVcY^[[Zg#HdbZ are responsible for vision eZdeaZ]VkZbdgZ in dim light. Cones detect gZY"hZch^c\XdcZh fine detail and color. aZ[ii]Vcdi]Zghide# 6bVXg^cZXZaa

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I=:;DK:6 The central part of the retina allows for far sharper vision than the periphery because it contains more cones (which pick up detail and color) than rods. Right in the center of the retina is the fovea, a tiny pitted area where cones are most densely packed. In addition to being more numerous, foveal cones can also pass on more detail, because almost every one has a dedicated signal-sending pathway to the brain. Light-sensitive ;DK:6AB6;>86I>DC cells elsewhere on the I]^hZaZXigdcb^Xgd\gVe]h]dlh i]ZeVgid[i]ZgZi^cVi]Vi\^kZh retina must share these means of output. h]VgeZhik^h^dc!i]Z[dkZVaeî#

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K>HJ6A6G:6H The visual cortex is divided into several functional areas, each of which specializes in a particular aspect of vision (see table, right). The process is similar to assemblyline production: raw material is checked in by V1, then sent on to other vision areas, which contribute shape, color, depth, and motion. These components are then combined to form a whole image. Because of the modular nature of vision, if one of the sight areas is damaged, a particular visual component may be lost K(V while the others remain intact. Cell death in the motion-detecting area, for K( example, may cause the world to be seen as a series of still snapshots. >

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The crisscrossed layout of the visual pathways (see p.78) causes the view seen by the eyes to be reversed, so it registers on the primary visual cortex (V1) as a mirror image. Signals from the left field of vision end up in the right hemisphere and vice versa. The information is passed between the two sides to give a shared view. In certain rare conditions, each side of the brain sees something different—the person appears to be in “two minds” (see p.11, p.199).

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The dorsal, or “where,” pathway carries signals triggered by a visual stimulus—for example, the light bouncing off a nearby object—from the visual cortex to the parietal cortex. Along the way, it passes through areas that calculate the object’s location in relation to the viewer and creates an action plan in relation to it. The dorsal path gathers information about motion and timing that is integrated into the action plan. All the information needed to, say, duck a flying object, is gathered along this path with no need for conscious thought.

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I=:ÆL=6IÇE6I=L6N The ventral, or “what,” pathway follows a route that takes it first through a series of visual processing areas, each of which adds a specific aspect of perception, such as shape, color, depth, and so on (see pp.86–87). The loosely formed representation then passes into the bottom edge of the temporal lobe, where it is matched or compared to visual memories in order to achieve recognition. Some information continues along this pathway to the frontal lobes, where it is assessed for meaning and significance. At this stage, it becomes a conscious perception.

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Damage to the ventral pathway results in one or another form of visual agnosia—the inability to recognize what one is seeing. Prosopagnosia, the inability to recognize faces (see panel, above), is one type of agnosia, but there are many others. Visual agnosia is generally divided into two categories: apperceptive and associative. The first type results from damage to the parts of the pathway in the occipital lobe and manifests itself as an inability to form a properly constructed perception. Hence a person with apperceptive agnosia cannot copy or draw an object, even though they may be able to see the parts of it quite cleatly. Associative agnosia is an inability to identify objects. The person sees the object and may be able to mime an appropriate action in relation to it—for example, using a fork to raise food to the mouth—yet be unable to say what it is.

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IDE"9DLC6C97DIIDB"JEEGD8:HH>C< Visual perception is momentary, partial, and fragmentary. “Bottomup” visual processing presets the brain with information about the whole field of vision, but “top-down” processes select which parts of the scene to make conscious. When we look at a picture, our eyes typically alight on a few thumbnail-size areas that we scan in sequence repeatedly. The rest of the image remains a blur unless we deliberately turn our attention to it. Eye-tracking studies (see left) show that the parts of a scene that we look at most closely are those that relate to other people. Although this visual selection is determined by “higher” brain functions—those involved in social concerns rather than, say, ducking a low branch—people are often unaware of what they are looking at. When asked, they may say they are looking at one thing when in fact their eyes have been resting on another.

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K>HJ6AE:G8:EI>DC One way of thinking about visual perception is to see it as the end product that emerges from a long and complicated assembly line. The construction process begins in earnest when information from the eyes—the raw material—reaches the primary visual cortex at the back of the brain. This is then sent along two main pathways (see pp.82–83), through a number of cortical and subcortical areas. Each of these responds by creating neural activity that generates various aspects of vision such as color, form, location, and movement. Eventually, the various elements are bound together and we become conscious of a meaningful sight.

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Hearing loss is common but total deafness is rare and usually results from a congenital problem. Mild or severe hearing loss can result from ear disease, injury, or degeneration of the hearing system with age. Hearing loss is either conductive (a fault in the transferral of sound from the outer to inner ear) or sensorineural (sometimes known as nerve deafness, involving damage to the auditory nerves, or to the sensory parts of the inner ear). Common hearing disorders include otitis media and otosclerosis. Otitis media mainly affects young children and is an inflammation of the middle ear caused by a bacterial infection. Otosclerosis occurs when there is abnormal bone growth on the stapes bone of the middle ear, which stops it from vibrating and conducting sound waves on to the inner ear.

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I=:H:CH:H>B6@>CCO6I>DC>CI=:7G6>CHI:B The brain locates the source of a sound—how far away it is, and in which direction—by sound localization. The input to each ear differs, as sound reaches the ear nearer to it about 1/1,500 second before the farther ear. Areas in the olivary nucleus of the brainstem compare the input from both ears (binaural input) and the delay, to find the source.

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Sounds start as vibrations entering the ears. In the inner ear, receptor cells in the cochlea transform these vibrations into electrical signals, which pass along the cochlear nerve to the medulla in the brainstem, and then to the inferior colliculus. The cochlear nerve fibers divide so that most of the input from each ear can go to both hemispheres. Processing at this stage enables the brain to determine the location of a sound. The signals reach the auditory cortex via the thalamus, where features such as frequency, intensity, quality, and meaning are perceived. The left auditory cortex is more concerned with the meaning and identification of sound; the right, with quality. HdjcYXgdhhZhid g^\]i]Zb^he]ZgZ Bdhih^\cVah[gdbaZ[i XdX]aZVigVkZaidg^\]i h^YZd[XdgiZm

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their sound source—a musical instrument—and how it is being played. Another important factor in music is timbre, or the “quality” of a sound. Timbre depends upon how many different frequencies of the note are heard at once; multiple frequencies or overtones (harmony) make a richer timbre. The auditory cortex responds to different qualities in music. The primary region responds to frequencies and the secondary area to harmony and rhythm, while the tertiary area adds higher levels of appreciation and integration.

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Sound consists of waves, or vibrations, whose characteristics are determind by the source of the sound. The main characteristics influencing our perception of sound are frequency (number of vibrations per second) and amplitude (the size of the waves’ “peaks” and “troughs”). Frequency influences pitch, and amplitude governs loudness. Irregular sound-wave patterns tend to be experienced as noise; in contrast, music produces regular patterns. Music is hard to define precisely, but the quality of IDC: musical notes depends upon

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E6I=L6ND;HDJC9 The ear is a complex, exquisitely designed instrument for the capture of sound and its transport to the brain. Once mechanical vibrations from sound sources reach the inner ear, they are transformed into electrical impulses that shoot along the cochlear nerve to the brainstem. Here, they follow complex pathways up to the thalamus before arriving at the auditory cortex. Processing in the brain allows perception of the meaning, direction, and volume of a sound.

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There is still much to be learned about the relationship between chemical structure and smell. Scientists have identified eight primary odors (rather like the three primary colors): camphorous, fishy, malty, minty, musky, spermatic, sweaty, and urinous. Smells are often produced by a combination of many different smell molecules, often from different categories. Comparisons of the structures of smell molecules within each category have shown some similarities—for example, minty smelling compounds often share a similar molecular structure. However, tiny differences in molecular structure can produce very different smells. Octanol, a fatty alcohol, smells like oranges, while octanoic acid, a saturated fatty acid that differs from octanol by only one oxygen atom, smells like sweat. HB:AA6C9BDA:8JA6GHIGJ8IJG:

Odors are initially registered by receptor cells in the nasal cavity. These send electrical impulses along dedicated pathways to the olfactory bulb (each nostril connects to one olfactory bulb). The olfactory bulb is part of the brain’s limbic system, the seat of our emotions, desires, and instincts, which is why smells can trigger strong emotional reactions. Once processed by the olfactory bulb, data is transmitted via three olfactory pathways to higher centers in the brain that process it in different ways. This process is called “orthonasal” smelling, in which smell data travels along pathways directly from the nose (see opposite). In “retronasal” smelling (see p.99), odors also have a flavor component that enters the olfactory pathways via the mouth.

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I=:A>JB The area within each nasal cavity that contains the olfactory receptor cells is known as the olfactory epithelium. A small amount of the air entering the nostrils will pass over the epithelium, which is covered in mucus. Smell molecules in the air dissolve in this mucus, bringing receptors into direct contact with the smell molecules. Three cell types are within the epithelium; in addition to the receptor cells, there are supporting cells, which produce a constant supply of mucus, and basal cells, which produce new receptor cells every few weeks. The larger the epithelium, the keener the sense of smell. Dogs, for example, have a considerably larger olfactory epithelium than humans.

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I=::KDAJI>DCD;HB:AA The smell brain, centered around the olfactory bulb in the limbic system, is of ancient origin, having evolved about 50 million years ago in fish. The sense of smell was overtaken in importance by the sense of vision when humans began to walk on two legs, although it is still dominant for many animals. But smell is an important aspect of survival for humans, shown in the fact that we take prompt action if we smell gas or smoke, for example. It also plays an important role in sexual selection, emotional responses, and forming preferences for food and drink. All of these factors were probably of key importance in the lives of our ancestors. 9>H<JHI L]ZcVWVYdYdg^hYZiZXiZY!hjX]Vh i]Vid[gdii^c\bZVi!î^hcVijgVaidWdi] [ZZaVcYZmegZhhY^h\jhi#6kd^YVcXZd[i]Z hdjgXZd[i]ZdYdg[daadlh!VcYî^hVabdhi ^bedhh^WaZidZVi[ddYi]VihbZaahWVY#

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HB:AAEG:;:G:C8:H Whether we find a smell nice, nasty, or neutral is very subjective and depends upon familiarity, intensity, and perception as pleasant or unpleasant. It is not clear if preferences are innate or learned, but much experimental evidence supports the latter possibility. Associative learning links pleasant smells to pleasant experiences, and vice versa. For example, people who fear the dentist do not like the clovelike smell of eugenol, which is used in dental cement; those without a fear of the dentist react positively or neutrally to this odor. HJ7?:8I>K:G:HEDCH:H I]ZY^hi^cXi^kZhbZaad[i]Z Yjg^Vc[gjî^heZgXZ^kZYWn hdbZVhgZkdai^c\Wjidi]Zgh ÒcYîZmigZbZaniZbei^c\#

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HI:G:DH8DE>86C97A>C9HB:AA It is generally believed that the human sense of smell has atrophied in relation to our other senses, but recent research shows that humans can still effectively track a scent. Using both nostrils to sample a smell, the human brain uses both sets of data to accurately pinpoint the location of the source of the odor. Therefore, as with vision and hearing, smell can be “stereoscopic,” relying on both nostrils for a full understanding of a scent. “Blind” smell refers to the ability of the brain to detect a smell without being consciously aware of it, which has been demonstrated in experiments using fMRI scans showing how olfactory areas are activated without the participant’s knowledge.

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An event is associated with input from all the senses, co-ordinated by the hippocampus. Reexperiencing any of the sight, smell, or sound inputs may trigger a memory of the event, but smell seems most strongly associated with memory. This may be because olfactory regions are linked to all emotional areas in the limbic system. Research shows that a memory of a visual image is likely to fade within days, but the memory of a smell may persist for up to a year or even decades. The hippocampus may not even be crucial for the link, because people who sustain damage to this region can still recall scents from their childhood, even though suffering from general memory loss.

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Animals emit compounds called pheromones that are used as communication signals and detected by an accessory olfactory system in the brain. Humans recognize each other in a similar way—for example, infants prefer the smell of their mother’s breast to that of other women. Research into the existence of pheromones in humans has found that women’s menstrual cycles can synchronize when one woman is exposed to odorless compounds (supposing that these are pheromones) emitted from the underarms of another woman. In animals, the accessory olfactory system is linked to the vomeronasal JH>C6AAN HdbZZhiViZV\ZcihXaV^bi]Vii]ZhbZaahd[WV`^c\WgZVY! region (VMO), an area in the nasal cavity that X^ccVbdc!VcYXd[[ZZXVc]ZaehZaaV]djhZWnZkd`^c\V responds to pheromones. The VMO’s existence \ddY[ZZa^c\^cediZci^VaejgX]VhZgh#:fjVaan!i]ZnVYk^hZ WVc^h]^c\eZih!hdi]ViVc^bVahbZaahYdcdiejid[[WjnZgh# in humans remains debatable.

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I=::KDAJI>DCD;I6HI: The sense of taste enables animals, including humans, to make the most of the variety of foods available to them. Many plants that look tempting are toxic, so genes that enable us to detect (and therefore avoid) these toxins have an obvious survival value. One such gene that has been identified affords taste sensitivity to phenylthiocarbamide (PTC), an organic compound that resembles many toxic compounds found in plants.

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I=:IDC<J: The tongue is the main sensory organ for taste detection. It is the body’s most flexible muscular organ, as revealed by its work in both nutrition and communication. It has three interior muscles and three pairs of muscles connecting it to the mouth and throat. Its surface is dotted with tiny, pimplelike structures called papillae. Other parts of the mouth, such as the palate, pharynx, and Ided[Ze^\adii^h epiglottis can also A^c\jVaidchâ detect taste stimuli. KV\jh cZgkZ

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Taste and smell are both chemical senses—receptors in the nose and mouth bind to incoming molecules, generating electrical signals to send to the brain. Both sets of signals pass along the cranial nerves. Smell-related (olfactory) signals travel from the nose to the olfactory bulb, then along the olfactory nerve to the olfactory cortex in the temporal lobe for processing (see also pp.94–95). The pathway of taste-related (gustatory) data travels from the mouth along branches of the trigeminal and glossopharyngeal nerves to the medulla, continues to the thalamus, then to primary gustatory areas of the cerebral cortex.

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When a sense receptor is activated, it sends information about touch stimuli as electrical impulses along a nerve fiber of the sensory nerve network to the nerve root on the spinal cord. The data enters the spinal cord and continues upward to the brain. The processing of sensory data is begun by nuclei in the upper (dorsal) column of the spinal cord. From the brainstem, sensory data enters the thalamus, where processing continues. The data then travels to the postcentral gyrus of the cerebral cortex, the location of the somatosensory cortex. Here, it is finally translated into a touch perception.

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HDB6IDH:CHDGN8DGI:M Touch sensations are turned into perceptions in the somatosensory cerebral cortex, which curls around the brain like a horseshoe. Data from the left side of the body ends on the right side of the brain, and vice versa. Each part of the cortex processes data from a different part of the body. It is possible to make a map of the cerebral cortex, dividing it into regions that correspond to distinct body parts. Such a map was first drawn by Wilder Penfield, a renowned Canadian neurosurgeon. Touch receptors are unevenly distributed across the body. For example, experiments show that the distance between touch receptors is far greater on the back than on the lips. The hands have the largest proportion of touch receptors in the body. 9ZgbVidbZ DcZd[i]gZZ gZ\^dchd[h`^c hZgkZYWn h^c\aZeV^gd[ he^cVacZgkZh

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The body has a natural opioid (pain relief) system that acts in much the same way as opiate drugs, such as heroin and morphine. Natural opioids, which include endorphins and encephalins, are produced by the thalamus and pituitary gland during stress and pain. These substances are also produced in situations associated with feeling a natural “high,” such as strenuous exercise and sexual activity. Nerve endings in the brain and throughout the body have special receptors on them that bind to opiate substances. The opiates then dampen the pain signals carried in those nerve endings, thus reducing pain.

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Stimulation of trigeminal nerves usually causes facial pain. It often affects only one side of the face and can be felt on the skin or in the mouth and teeth. It comes and goes unpredictably and its nature is variously described as stabbing, lacerating, like an electric shock, and shooting. It can range in severity from mild to excruciating. There are frequently “trigger points” on the skin, which, if touched, will bring on a violent pain spasm. People may experience pain daily for weeks and months, then it may disappear for months or even years.

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Pain usually arises when pain receptors are stimulated by heat, cold, vibration, overstretching, or by chemicals released from damaged cells. Specialized nerve fibers (see panel, above) transmit this information to the brain. However, certain types of pain are processed and experienced in different ways, for example the facial nerves connect directly to the cranial nerves (see below), whereas visceral pain, from internal organs such as the heart (see right), can be difficult to locate. Damage to the nervous system itself, such as a trapped nerve, is known as neuropathic pain (see bottom).

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Referred pain occurs when nerve fibers from areas of high sensory input (such as the skin) and nerve fibers from areas of low sensory input (such as internal organs) enter the spinal cord at the same location. Since the brain expects to be receiving the data from highsensory areas, it misinterprets the location of the pain. He^cVa XdgY

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C:JGDE6I=>8E6>C Pain that is caused by damage or malfunction in the nervous system itself rather than injury is known as neuropathic pain. A pain-transmitting nerve may be severed, or be stimulated so often that it gets into the “habit” of sending pain signals to the brain. Pain-registering neurons in the cortex can become sensitized so that they produce the experience of pain even when there is no external cause.

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Pain signals are transmitted to several areas of the cortex, where they activate neurons that monitor the state of the body. Two such areas are the somatosensory cortex, which lets the brain know which part of the body the pain stems from, and the insular cortex—the deep fold that divides the temporal and frontal lobes. The other cortical site associated with pain experience is the anterior (front) of the cingulate cortex (ACC), which lies in the groove between the hemispheres. The ACC seems to be particularly concerned with the emotional significance of pain and with determining how much attention an injury should command.

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6L=DA:"7G6>C6;;6>G Pain is so important to our survival that it may involve practically every part of the brain. Three main “pain areas” (see above) register and assess pain signals, and pinpoint the site of their source, but other areas also come into play. The supplementary motor area and motor cortex may plan and execute movement aimed at escaping the pain stimulus. Parts of the parietal cortex may direct attention to the threat, and several parts of the frontal cortex may be involved in working out the significance of the pain and what to do about it. BdidgXdgiZm

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Part of the role of higher brain areas is to modify pain. Nerve signals that travel from the brain into the body interrupt pain signals traveling up from the site of the injury before they reach the brain. This reduces the number of pain signals reaching the brain and, therefore, the amount of pain felt. Also, our thoughts, expectations, and emotions can all have a profound effect on the degree to which a person is “pained” by pain. People can affect pain consciously by directing attention away from it, or imagining that they are pain-free. An intensely imagined experience generates almost identical brain activity to the equivalent “real” experience, so an imagined state of physical ease may be achieved even as pain fibers in the body are being stimulated.

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A very few people—probably about one in 125 million—are born without the ability to feel pain. The condition is caused by a genetic disorder, congenital analgesia, that results in a lack of pain-sensitive nerve endings in the body. Some people with this condition are able to feel touch or pressure, which relies on different types of nerves. Although the idea of not feeling any pain may, at first, sound rather desirable, the effect is disastrous. Pain normally warns people that they are in danger and forces them to take action to protect themselves. Without it, physical perils are likely to be unnoticed or ignored, leading to lethal injuries and often to premature death.

107


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When the body’s water levels fall, salt concentration increases and blood volume decreases. Pressure receptors in the cardiovascular system and salt-concentration-sensitive cells in the hypothalamus detect these changes. In response, the pituitary gland releases antidiuretic hormone (ADH), which acts on the kidneys to retain water and produce less urine. The kidneys secrete the enzyme renin into the blood which, through a series of reactions, forms the hormone angiotensin II. This is detected by the subfornical organ, which is connected to the hypothalamus, which in turn activates more ADHproducing cells and creates the sensation of thirst, leading to drinking.

The suprachiasmatic nucleus (SCN) in the hypothalamus plays a key role in sleep–wake cycles. Light levels are sensed by the retina, and this information is relayed to the SCN, which then sends a signal to the pineal gland. This triggers the release of melatonin, the hormone that tells the body when to sleep. At this point, the brain becomes less alert and fatigue starts to take over. When melatonin levels fall in response to increased light, the waking part of the cycle begins.

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I=:8:G:7:AAJB For the body to make any complex movement, the sequence and duration of each of its elements must be coordinated very precisely. This is controlled by the cerebellum, via a circuit that connects it to the motor cortex. It also modulates the signals that the motor cortex subsequently sends to the motor neurons. The cerebellum ensures that when one set of muscles initiates a movement, the opposing set acts as a brake, so that the body part in question arrives accurately at its target. Eg^bVgnbdidg XdgiZm GZYcjXaZjh EG:8>H:I>B>C< GZXZ^kZh I]ZXZgZWZaaVgX^gXjîh [ZZYWVX`[gdb ^cXajYZVhnhiZbi]Vi XZgZWZaajb bZVhjgZhi^bZ#>i[ZZYh îhXVaXjaVi^dchidi]Z eg^bVgnbdidgXdgiZm! l]^X]hZcYhi]Zh^\cVah idi]ZbjhXaZh# Edci^cZcjXaZjh @:N H>: M:8JI>CCC6G:6HG:HEDCH>7A:H:C9H>DC#HDB:D;I=:H:H>GHIIDI=:BDIDG8DGI:M!6C9I=:C DCL6G9I=GDJC6A8DG9#DI=:GHIG6K:A7NBDG:9>G:8IGDJI:H#BDK:B:CID88JGH L=:CI=:H>7:GH!86JH>CC6AIG68IH Action plans generated in the supplementary, premotor, and parietal cortices are forwarded to the motor cortex for execution. The motor cortex is made up of about one million neurons, which send long axons down the spinal cord. These are bundled together, along with axons that come directly from the somatosensory cortex, to form the lateral corticospinal tract. Just before entering the spinal cord, the nerves from each hemisphere of the brain separate and cross over, so the fibers from the left hemisphere of the cortex go down the right side of spinal cord, and vice versa. The rubrospinal tract originates from the red nucleus in the midbrain, and helps to produce fine movements.The vestibulospinal and reticulospinal tracts start lower down in the brainstem and help control balance and orientation. Eg^bVgnbdidgXdgiZm I]ZhiVgi^c\ed^ci[dgi]Z aViZgVaXdgi^Xdhe^cVaigVXi I]VaVbjh GZYcjXaZjh Edch GZi^XjaVg[dgbVi^dc KZhi^WjaVgcjXaZjh EngVb^YVaYZXjhhVi^dc AViZgVaXdgi^Xdehe^cVaigVXi WgVcX]ZhXgdhhdkZg]ZgZ He^cVaXdgY BdhicZgkZÒWZgh[gdb i]ZWgV^chncVehZdcid bdidgcZjgdch^ci]Z he^cVaXdgY

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The axons of the motor neurons, which receive signals from the spinal tracts, emerge from between the vertebrae and travel to the muscles. The nerve endings infiltrate the muscle fibers at neuromuscular junctions, and when they fire they release the neurotransmitter acetylcholine. This diffuses across the narrow “synaptic cleft” connecting the muscle to the nerve and binds to acetylcholine receptors in the muscle cell membrane, which, by a series of reactions, makes the specific muscle contract. Muscles required to carry out fine movements have correspondingly higher numbers of neurons than those required to perform gross movements.

Motor disorders can be divided into two principal groups: hyperkinesia (overactivity) and hypokinesia (too little movement). The former includes a wide range of motor disorders, from involuntary, slow shaking of various body parts to tics, which are uncontrollable, rapid, disjointed movements and/or sounds. Sudden, shocklike muscle contractions are symptoms of myoclonus, while quick, random, usually jerky limb movements are caused by chorea and ballism. Hyperkinesia disorders include: general slowness of movement (bradykinesia); “freezing” or inability to begin a movement or involuntary arrest of a movement; rigidity—an increase in muscle tension when a limb encounters force; and postural instability, which is the loss of ability to maintain an upright posture.

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G:68I>DCE6I=L6NH It takes up to 400 milliseconds (ms) for the brain to process incoming information to the stage where it may become conscious. It takes a similar length of time to prepare the body for action. So if we waited to be conscious of a sight or sound

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Professional tennis players can plan and initiate the complex moves required to return a fast service before they are consciously aware that the ball is on its way. Unlike novice players, they do not have to think consciously about each muscle movement because practice has turned the relevant action sequences into automated motor programs that are stored and run unconsciously. Familiarity with their opponents’ body language also allows them to make well-informed unconscious predictions about where the ball will land.

%bh6iiZci^dc The player’s brain prepares for action by focusing attention on his opponent. This prevents the brain from responding to irrelevant stimuli and amplifies information coming from the part of the visual field containing the target of attention. If the player is familiar with the opponent’s playing style, his brain will register the movements made by the opponent as he serves and compare them with previous observations to help predict where the ball will land. Attention to such cues may speed up reactions by 20–30 milliseconds. ;gdciVaadWZh

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L=6I6G:I=:N4 Mirror neurons were first discovered in the motor-planning area in the brains of macaques (a species of monkey) and subsequent brainimaging studies suggest that they exist in humans too. The human mirror system seems to be broader in scope than that of monkeys, in that mirror neurons exist not only in movement areas, but also in areas concerned with emotions, sensations, and even intentions. They provide people with immediate =DLI=:NL:G:9>H8DK:G:9 knowledge of what is going on B^ggdgcZjgdchlZgZY^hXdkZgZY^cV bdc`Znl]dhZWgV^clVhl^gZYjeidh]dl in another’s mind; this ability to l]^X]cZgkZXZaahaîjeVhîgZVX]ZYdjiid know what another person is \gVhe[ddY#L]ZcaVWdgVidgnhiV[[bVYZ i]ZhVbZbdkZbZcil]âZi]Zbdc`ZnhhVi feeling or doing is thought to be the basis of mimicry. VcYlViX]ZY!i]ZhVbZcZjgdchaîje#

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B>GGDG>CCI:CI>DCH Two movements may be identical, but may signal very different things in different contexts. Human mirror neurons seem to take this into account. When one person sees another picking up a cup in order to drink from it, a different set of neurons are activated from those that light up at the sight of a person making the identical movement but in a context that suggests they are clearing the cup away. Hence, the observer’s brain does not just generate a faint idea of what the other person is doing with their body, but also an echo of their intention in doing it. This allows us to get a glimpse of another individual’s plans and thought processes without consciously having to work it out. %#,

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EMOTIONS AND FEELINGS


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The amygdala “tastes” all stimuli and signals other areas to produce appropriate emotional reactions. It contains distinct regions called nuclei, which generate different kinds of responses to fear. The central nucleus generates the fear response of freezing, while the basal nucleus generates the fear response of flight. The nuclei are affected by sex hormones, and are therefore different in men and women. Activation of the amygdala can be modulated by the hypothalamus (see below).

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We have evolved a conscious emotional system, but we retain the primitive, automatic responses at the heart of emotion. A frightening sight or sound, for example, registers in the amygdala before we are even conscious of it. While the sensory information is sent to the cortex to be made conscious, the amygdala sends messages to the hypothalamus, which triggers changes that ready the body for flight, fight, or appeasement. This “quick and dirty” route allows us to take instant action to save ourselves. When we “start” at a loud noise, then relax on realizing that it is harmless, we are experiencing both stages— unconscious reaction and conscious response.

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8DCH8>DJH:BDI>DC :BDI>DCH6G:CI=:A>B7>8HNHI:B!L=>8=9D:HCDIHJEEDGI8DCH8>DJHC:HH >IH:A;#>CI:CH::BDI>DCH8G:6I:Æ@CD8@"DCÇ68I>K>IN>CI=:8DGI:M!:HE:8>6AAN>CI=: ;GDCI6AAD7:H!L=>8=L::ME:G>:C8:6H68DCH8>DJHÆ;::A>CB:H!6C :BDI>DC>H8A:6GANA>C@:9ID6C:ME:G>:C8:#6IDI=:GI>B:H!I=:86JH:>HCDID7K>DJH! 7JI7:>CDCB6@:H>I:6H>:GIDJC9:GHI6C9L=6I>H=6EE:C>CCDC Emotions are primarily unconscious physical reactions to threat or opportunity. The sight of a snake, for example, automatically prepares the body for flight. In humans, emotions are consciously experienced as powerful “feelings” that give our lives meaning and value. The unconscious physiological component of emotion is generated in deep brain areas as signals that are then sent to the body to prepare it for action. Some signals travel upward to activate cortical areas, and this activation produces the feeling of emotion. The type of emotion experienced depends on which parts of the cortical areas are activated.

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:BDI>DC8>G8J>IH Information from the environment, and from the rest of the body, is constantly “tasted” for emotional content. The main emotion “sensor” is the amygdala, which is particularly sensitive to threat and loss. The amygdala takes in information both directly from the sense organs and via the sensory cortices, and connects to the cortex and also to the hypothalamus, creating a circuit. When the amygdala is activated, it sends signals around this circuit. These trigger body changes as they pass through the hypothalamus, and create conscious recognition of the emotion as they pass through the frontal lobe. Positive emotions are passed along a slightly separate KZcigVaaViZgVa circuit, which takes in an area of the egZ[gdciVa brainstem that produces the moodXdgiZm lifting neurotransmitter dopamine. EGD8:HH>CDC

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Each emotion sparks a slightly different pattern of activity in certain brain areas. Hatred, for example, activates the amygdala (which responds to all negative emotion), the insula (which is associated with disgust and rejection), and also areas of the brain concerned with action and calculation.

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Things that we find emotionally moving grab our attention rapidly (see illustrations, right) compared with things that we do not. The sight of something that poses a threat, for example, is brought to conscious awareness faster than a nonemotional stimulus. This may be because the amygdala unconsciously picks up the threat and primes the conscious brain to “expect” an important perception. Good things also attract attention fast. Research shows that people react as quickly to an image of a smiling baby as they do to one of an angry face—both elicit quicker reactions than nonemotional stimuli.

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After about 350 milliseconds, the emotional meaning of a stimulus has been evaluated by the brain. Signals from the amygdala trigger a conscious response in the body, which in turn feeds back to areas such as the insula.

A little later, information comes in from the sensory cortices and association areas—such as the face-recognition area in the fusiform gyrus—providing more detailed input to emotion-inducing parts of the brain, such as the amygdala.

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An emotion is usually transient and arises in response to the thoughts, activities, and social situations of the day. Emotions act as cues that prompt adaptive behavior (see table, right). Moods, in contrast, may last for hours, days, or even months, in the case of some illnesses. Thus, the emotional state of distress, when extended over time, is called sadness; if it persists, unrelenting, for a period of weeks, it is referred to as depression (see p.231). Moods can be initiated very quickly by things that we are not even aware of. One study, for instance, found that flashing pictures of a disgusting nature for a split second—too fast to be seen consciously—made those who were subjected to them more sensitive to other stimuli of a similar nature afterwards. The feelings elicited by these unconscious stimuli were described by the volunteers as “moods” rather than emotions.

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9:H>G: Desire is a complex drive that strongly reflects personal preferences. It is made up of two different components—liking and wanting. Put simply, liking is linked to getting pleasure, while wanting is linked to an actual need for something. With some activities, such as eating, sleeping, and sexual activity, liking and wanting overlap, and the resulting desire has survival value. However, an individual with an addiction may want and “need” a drug, but not particularly like or enjoy it, so the resulting pleasure is tainted with destruction. Liking and wanting seem to use somewhat different brain circuits, although dopamine is the most important neurotransmitter in both cases. &#Hi^bjajhI]^hXVcdg^\^cViZ djih^YZi]ZWdYn![dgZmVbeaZ i]Zh^\]id[[ddY!dg[gdb lî]^c![dgZmVbeaZ[Vaa^c\ \ajXdhZaZkZah#

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EA:6HJG:"H::@>C8I>DC Addictive substances can activate the dopamine reward system, providing pleasure, even though the substances are not essential to survival. Chronic exposure to drugs leads to the suppression of reward circuits, increasing the amounts needed to get the same effect. The opiate system is involved in pain and anxiety relief. Heroin and morphine lock onto the opiate receptors, creating a sense of euphoria. The cholinergic circuits—where nicotine acts—are involved in memory and learning. Cocaine acts at the noradrenergic receptors, which are involved in stress responses and anxiety. 8JAIJG6A:MEDHJG: Hbd`^c\^hgZ\VgYZYVhV]^\]anhdX^Va VXi^kîn^cbVcnXjaijgZh#Egdadc\ZY ZmedhjgZidVYY^Xi^kZhjWhiVcXZhbVnaZVY id^cXgZVh^c\YZeZcYZcXZ!Ygj\"hZZ`^c\ WZ]Vk^dg!VcYlî]YgVlVaegdWaZbh#

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6CI>8>E6I>DC Learning and memory clearly play an important role in shaping desires and preferences. This leads to the possibility of anticipation, which is the expectation of a reward. Anticipation has been studied by researchers using a game of chance. In the anticipation phase, where participants were told they might win money, fMRI scans showed that cerebral blood flow in the amygdala and orbitofrontal cortex increased, indicating activity in the nucleus accumbens and the hypothalamus—all rich in dopamine receptors. The bigger the potential reward, the greater the brain activity. G:L6G96CI>8>E6I>DC I]^h[BG>hXVch]dlhVXi^kîn^ci]ZaZ[i^cigVeVg^ZiVa XdgiZm#6Xi^kîn^ci]ZVciZg^dgX^c\jaViZXdgiZmVcY ^cigVeVg^ZiVaXdgiZmh]dli]Vi\gZViZgViiZci^dc^h eV^YidViVh`l]ZcVeZghdc^hVci^XêVi^c\VgZlVgY#

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THE SOCIAL BRAIN


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:BE6I=N6C9HNBE6I=N “Feeling” for another person—experiencing a faint version of their sorrow or flinching when you see them hurt—seems to be largely instinctive. It depends partly on theory of mind (see pp.136–37), which ensures that we “know” what is likely to be going on in other people’s minds. Empathy goes a step further, in that it also involves “echoing” the emotions of another person. When a person is told a story about someone experiencing emotional trauma, the activated areas in the listener’s brain come into play when he or she is in such a situation. HNBE6I=:I>8HI6C8: 7Z^c\VWaZididejindjghZa[^cidhdbZdcZ ZahZÉhhîjVi^dc!idZmeZg^ZcXZVcZX]dd[ l]Vii]Zn[ZZa!VcYhnbeVi]ôZlî]i]Zb VeeZVghidWZVc^chi^cXi^kZ]jbVcigVî#

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A>HI:C>C< The sound of spoken words take a short time—about 150 milliseconds—to pass from the speaker’s mouth to the listener’s ear, for the ear to turn this stimulus into electrical signals, and for this to be processed as sound by the auditory cortex. Words are decoded in Wernicke’s area in the left hemisphere, but other areas are also at work to provide full comprehension, including parts of the right hemisphere concerned with tone, body language, and rhythm. If any of these areas are damaged, a person may be left with an incomplete understanding of what is being communicated.

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The speech process starts about a quarter of a second before words are actually uttered. This is when the brain starts to select the words that are to convey whatever the person wants to say. The words then have to be tuned into sounds, and are finally articulated. Most of this complicated activity occurs in specific language areas, which in most people are on the left side of the brain. However, in a minority of people they are situated in the right, or spread between both hemispheres. Right-hemisphere language dominance is more prevalent among left-handers (see p.195). 8GJ8>6AE6I=L6N

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A:6GC>CI: To learn how to read and write, a child has to translate the shapes of letters on the page into the sounds they make if they are spoken aloud. The word “cat,” for instance, must be broken down into its phonological components—“kuh,” “aah,” and “tuh”. Only when the word on the page is translated into the sound that is heard when the word is spoken, can the child match it to its meaning. Learning to write uses even more of the brain. In addition to the language areas concerned with comprehension, and the visual areas concerned with decoding text, writing involves integrating the activity in these areas with those concerned with manual dexterity, including the cerebellum, which is involved with intricate hand movements.

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Dyslexia is a language-development disorder with a genetic basis. It may affect 5 percent of the population, and is most obvious when a language such as English, has a complex mapping system between speech sounds and letters of the alphabet. One explanation for dyslexia, known as the phonological deficit hypothesis, is that dyslexics cannot analyze and remember the sounds contained in words. This slows down the learning of spoken language and makes it very difficult to map sounds to their corresponding letters of the alphabet when learning to read. =DL9NHA:M>8H 9>;;:G 9nhaZm^XhY^[[Zg bdhian^ci]ZWgV^c VgZV^cl]^X]ldgYh VgZigVchaViZY[gdb k^hjVahnbWdah^cid hdjcYhh]dlc^c \gZZcdci]^h[BG> hXVc#GZhZVgX]]Vh [djcYi]ViYnhaZm^Xh ]VkZbdgZ\gVn bViiZg^ci]^hVgZV i]VccdcYnhaZm^Xh! Wjii]Zh^\c^ÒXVcXZ d[i]^hÒcY^c\^hcdi [jaanjcYZghiddY#

There is no cure for dyslexia, but dyslexics can improve reading skills through compensatory learning, using the help of specialist teachers to find ways to remember spellings. While reading is likely to remain slow and spelling error-prone, audio books, spell-checkers, and voice-recognition programs can help circumvent the problems of dyslexia.

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L=6I>HB:BDGN4 A memory may be the ability to recall a poem or recognize a face on demand; a vague vision of some long past event; the skill required to ride a bike; or the knowledge that your car keys are on the table. What all these phenomena have in common is that they involve learning, and total or partial reconstruction of a past experience. Learning is a process in which neurons that fire together to produce a particular experience are altered so that they have a tendency to fire together again. The subsequent combined firing of the neurons reconstructs the original experience, producing a “recollection” of it. The act of recollecting makes the neurons involved even more likely to fire again in the future, so repeatedly reconstructing an event makes it increasingly easy to recall.

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I=:6C6IDBND;B:BDGN Only experiences giving rise to unusually prolonged and/or intense neural activity become encoded as memories. It takes up to two years to consolidate the changes that create a long-term memory (see sequence below) but, once encoded, that memory may remain available for life. Long-term memories include events from a person’s life (episodic memories) and impersonal facts (semantic memories). Together, these are termed “declarative memories,” since they can be recalled consciously (“declared”). Procedural (body) memories and implicit (unconscious) memories may also be stored long-term.

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A lot of humor arises from the juxtaposition of apparently unconnected ideas, which is similar to the process underlying creativity. Studies looking at how humorous interplay between coworkers affects workplace innovation suggest that keeping workers laughing may “jump-start” their creative faculties, perhaps because humor forces people to attend to “distractions,” making them more open to new information. Brain-imaging studies have shown that humor stimulates the brain’s “reward” circuit and elevates circulating levels of dopamine, which is linked to motivation and pleasurable anticipation.

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7:A>:K>CHH::>C< Most people have some kind of belief system, which forms a framework for their experience. Some were taught their beliefs, while others arrived at them by examining their experience and working out their own interpretation. Once a belief system has been formed, it acts both as an explanation for what has happened in the past and also a “working hypothesis” that is projected onto the world. For example, if a person believes that the world is governed by a benign supernatural being, they will “see” events such as coincidences or strokes of good fortune as evidence of this, while a person with a materialist belief system would interpret them merely as chance happenings. People who are quick to see meaningful connections between, for example, random events are more inclined than others to have a magical or superstitious belief system. =DANID6HI EZdeaZlî]ViZcYZcXnidlVgYbV\^XVai]^c`^c\VgZ fj^X`ZgidhZZeViiZgcha^`Zi]ZÆ[VXZÇ^ci]^he^ZXZd[ idVhi#I]ZnVgZVahdbdgZa^`ZanidhZZhjX]i]^c\hVh ÆbZVc^c\[jaÇÅeZg]VehZkZcVhh^\ch[gdbCDC>CI=:7G6>C Religious practice is largely determined by cultural factors. However, studies of identical twins who have been brought up separately suggest that the likelihood of a person experiencing a religious conversion or spiritual transcendence may be due more to genes than to upbringing. Spiritual transcendence shares some features with other “weird” experiences, such as out-ofbody experiences, auras, and “the sensed presence” (see opposite page). These are associated with flurries of unusually high activity in the temporal lobes. The areas involved in intense religious experiences seem to be more widespread, however. For example, a study of nuns from a meditative order showed that, as they recalled an intense religious experience, many different areas were activated. So there does not seem to be a single “God-spot.”

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High natural levels of the neurotransmitter dopamine may explain why some people are unusually quick to pick out patterns. Believers are known to be more likely than sceptics to see a word or face in nonsense images, and sceptics more likely to miss real faces or words that are partly hidden by visual “noise.” One study found that sceptics’ tendency to see hidden patterns increased when they were given L-dopa, a drug that increases dopamine levels. H8G6B7A:9;68:HHIJ9N 7Za^ZkZghVgZbdgZa^`Zani]Vc hXZei^XhidhZZÆgZVaÇ[VXZhl]Zc egZhZciZYlî]VgVe^YhZfjZcXZ d[ÆhXgVbWaZYÇ[VXZh#HXZei^Xh! WnXdcigVhi!VgZbdgZa^`Zanid [VâidhediÆgZVaÇ[VXZhb^mZY^c lî]i]ZhXgVbWaZYdcZh#

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I=:=6JCI:97G6>C Apparently “supernatural” experiences may be due to disturbances in various parts of the brain. Tiny seizures in the temporal lobes are thought to be responsible for many of the emotional effects reported in such events, such as feelings of ecstasy or intense fear. Temporallobe disturbance is also associated with the sense of an invisible presence that often accompanies perceiving ghosts. Distortions of space and embodiment, such as the illusion of looking down at oneself, known as an “out-of-body” experience, are linked to reduced activity in the parietal lobes, which normally maintain a relatively stable sense of space and time. Hallucinations may result from faulty visual or auditory processing or failure to interpret sights and sounds normally. L=>I:A69N :meZXiVi^dc]VhV higdc\Z[[ZXidc l]ViVeZghdchZZh# BVcnÆ]Vjci^c\hÇ Vg^hZWZXVjhZ eZdeaZ]VkZWZZc aZYidZmeZXiidhZZ V\]dhi^cVXZgiV^c eaVXZ#6cnjcjhjVa hZchdgnZ[[ZXi^h i]Zc^ciZgegZiZYVh VheZXiZg#

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INE:HD;8DI>K:>AAJH>DC The brain has certain rules that it applies to incoming information in order to make sense of it quickly. If we hear a voice and at the same time see a mouth moving, for example, we assume the voice comes from the mouth. Like all such rules, though, this is only a best guess and can be wrong. Hence it leaves us open to the illusion of ventriloquy. Low-level illusions—those created in the early stages of perception—are unavoidable, but those that arise due to higher-level cognition are less robust. It is impossible not to see the after-image that occurs when you have been looking at a bright light, for example, because this is created by low-level nerve activity, which

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>BEDH:9IG>6C<JDJH>AAJH>DCH Something strange happens when we look at ambiguous figures. The input to the brain stays the same, but what we see flips from one thing to another. This demonstrates that perception is an active process, driven by information that is already in our brains as well as information from the outside world. The switching occurs because the brain is searching for the most meaningful interpretation of the image. Normally, the brain settles quickly on a solution by using basic rules such as, “if one thing surrounds another, the surrounded shape is the object and the other thing is the ground.” Ambiguous figures confound such rules. For instance, in the vase illusion (left) it is impossible to see which shape is on top, so the brain tries one way of seeing it, then another. You see both images, but you can see never both of them simultaneously. H=6E:H=>;I:GH

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E6G69DM>AAJH>DCH It is possible to represent objects in two dimensions that cannot actually exist in the real, three-dimensional world. Paradox illusions are generated by such images, which are often dependent on the brain’s erroneous assumption that adjacent edges must join. Although impossible, the best examples are oddly convincing, and the conscious brain is teased and intrigued by them. As with ambiguous illusions, the brain tries first one interpretation and then another, but is unable to settle because none of the available views make sense. Brain-imaging scans show that impossible images are recognized by the brain very early in the process of perception, well before conscious recognition. Unlike the conscious brain, the unconscious part is not very concerned with such images, and spends less time trying to process them than it spends on “real” objects. I=:IG>76G I]ZEZcgdhZig^Vc\aZ! Vahd`cdlcVhi]Zig^WVg! ^hVeZgheZXi^kZYgVl^c\ i]ViXdbeg^hZhi]gZZ i]gZZ"Y^bZch^dcVa WVghi]ViVeeZVgid WZXdccZXiZY!Wji ^cgZVaînXdjaY cdiWZ#

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Consciousness has different modes, such as emotions, sensations, thoughts, and perceptions, which are all experienced at different levels of neural activity, focus, and concentration. The level of neural activity determines the intensity of consciousness. The direction of focus can be towards the outside world or the inner world (thinking about thoughts). Concentration can be loosely targeted, involving a range of objects or fixed, involving just one particular aspect. Consciousness also divides into three types of awareness: awareness in the moment—the brain registers and reacts to moment-by-moment events but does not encode them in memory; conscious awareness—events are registered and encoded in memory; and self-consciousness—events are registered and remembered, and the person is conscious of doing this.

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Different types of neuronal activity in the brain are associated with the emergence of conscious awareness. Neuronal activity in the cortex, and particularly in the frontal lobes, is associated with the arousal of conscious experience. It takes up to half a second for a stimulus to become conscious after it has first been registered in the brain. Initially, the neuronal activity triggered by the stimulus occurs in the “lower” areas of the brain, such as the amygdala and thalamus, and then in the “higher” brain, in the parts of the cortex that process sensations. The frontal cortex is activated usually only when an experience becomes conscious, suggesting that the involvement of this part of the brain may be an essential component of consciousness.

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G:FJ>G:B:CIHD;8DCH8>DJHC:HH Every state of conscious awareness has a specific pattern of brain activity associated with it. These are commonly referred to as the neural correlates of consciousness. For example, seeing a patch of yellow produces one pattern of brain activity, seeing grandmother, another. If the brain state changes from one pattern to another, so does the experience of consciousness. The processes relevant to consciousness are generally assumed to be found at the level of brain cells rather than at the level of individual molecules or atoms. It is likely that, for consciousness to arise, the factors listed below need to be present. Yet it is also possible that consciousness does arise at the far smaller atomic (quantum) level, and if so it may be subject to very different laws.

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If the brain registers an unexpected movement, a loud sound, or some other potentially significant stimulus, it directs the sense organs toward it—for example, by swiveling the eyes in the direction of a sudden movement. This happens automatically, in the lower regions of the brain, and it does not in itself create consciousness of the stimulus. However, attention also increases activity in the neurons that are concerned with the stimulus. If the stimulus is a person, for example, neural activity increases in the visual areas that monitor the place in space where the person is located; the face-recognition area; the amygdala; the temporalparietal areas, which work out their intentions; and the supplementary motor area, which works out what to do about them. If the neurons are excited beyond a certain point, consciousness “kicks in.” :ME:8I>C< IDH::

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Our normal waking state varies from through relaxed awareness, to sharply focused. The brain is capable of generating a much wider range of conscious experiences than this, though. Sometimes we slip outside the normal range spontaneously, when feverish or exhausted, for instance, or during or after an emotionally overwhelming event. We may also deliberately seek to get out of our normal state by engaging in rituals such as prolonged dancing, or through meditation, or by taking drugs.

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9>HHD8>6I>DC Dissociation refers to instances when elements of consciousness (the sensations, thoughts, and emotions of the moment) that are sometimes bound together as a whole are, instead, experienced separately or are cut out of conscious awareness. Many altered states fall into this category. Usually, dissociation is referred to as a mental or behavioral disorder, but some “normal” conscious states, such as daydreaming or concentrating, are dissociative. It is more accurate to look at these conscious states as a spectrum (see below), with highly unified or “bound” experience at one end and “fractured” consciousness at the other.

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I=:HA::E>CC No one is quite sure what it is about sleep that makes it so important. One theory is that it allows “down time” for the body to repair itself. Another is that it simply keeps the person out of danger for a period of time during each day, by keeping him or her still. A third is that the brain needs to switch off from the outside world in order to sort, process, and memorize information. Certainly, important memory functions do occur during sleep, but whether or not this is the primary purpose of sleep remains unclear. Sleep-wake cycles are controlled by neurotransmitters that act on different parts of the brain to induce sleep or waking up. Research also suggests that a chemical called adenosine builds up in the blood while we are awake and causes drowsiness; while we sleep, the chemical is gradually broken down.

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L6@>C99G:6BH Usually, when shifting from dreaming to waking, several changes occur together in the brain. The block on incoming stimuli is lifted, so external sensory inputs enter the brain again, which overrides and turns off the internally generated sensations that comprise dreams. The block on outgoing signals from the motor cortex is also lifted, so that it becomes possible to move again. Additionally, the frontal lobes are reactivated, shifting us back into a normal state of consciousness in which we know who and where we are, and can tell the difference between fantasy and reality. Lucid dreams occur when the frontal lobes “wake up” during sleep, but the block on incoming and outgoing signals continues. Because the frontal lobes are active, the dreamer is able to deduce that he or she is actually dreaming and experience events in a normal state of mind.

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HJ7?:8I>K:I>B: The passage of time as we experience it (known as subjective time) is not the same as the regular passage of time as measured by our clocks (objective time). The crucial difference is that subjective time can speed up and slow down, according to what we are experiencing. On a moment-by-moment scale, the rate at which time seems to pass is dictated by the rate of firing, or oscillation, of clusters of neurons. The faster they fire, the more events we register in any given second, giving us the impression that time lasts longer. Neuronal firing is controlled by neurotransmittersÅexcitatory ones speed it up, and inhibitory ones slow it down. Young people have more excitatory neurotransmitters and, therefore, are able to cope with faster external events. I=:7G6>C8AD8@ I]ZWgV^c]VhY^[[ZgZci ÆXadX`hÇ[dgY^[[ZgZcii^bZ hXVaZh#DcZ^h[dgbZYWn VYdeVb^cZ"\ZcZgViZY cZjgdcVaX^gXjîi]Vi gjchWZilZZci]Z hjWhiVci^Vc^\gV!i]Z WVhVa\Vc\a^V!VcY i]ZegZ[gdciVa XdgiZm#:VX]ÆXnXaZÇ d[i]ZXadX`XgZViZh Vh^c\aZÆeVX`ZiÇ d[hjW_ZXi^kZ i^bZ#

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E68@:IHD;I>B: The brain divides time into “packets” (a cycle of neural activity), each of which registers a single event. The size of the packet depends on how fast the relevant neurons are firing, but regardless of the size of the packet, the brain will only be able to take in one event from that packet. If two events happen, the brain will miss the second one. Some events will always appear blurred to us, such as the beating of a dragonfly’s wings, because several flaps occur in each packet.

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It takes on average half a second for the unconscious mind to process incoming sensory stimuli into conscious perceptions. Yet we are not aware of this time lagÅyou think you see things move as they move, and when you stub your toe you get the impression of knowing about it right away. This illusion of immediacy is created by an ingenious mechanism, which backdates conscious perceptions to the time when the stimulus first entered the brain. On the face of it, this seems impossible because cortical signals take the same “real” time to process to consciousness, but somehow we are tricked into thinking we feel things earlier. One way it might be explained is that consciousness consists of many parallel streams and that the brain =6A;6H:8DC9A6I: jumps from LZWZXdbZXdchX^djhd[ ZkZcihVgdjcYjhcZVgan one to another, ]Va[VhZXdcYV[iZgi]Zn revising them and dXXjg!WjilZYdcdi cdi^XZi]^hi^bZaV\# redrafting them.

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L=6I>HI=:H:A;4 We divide the world into that which is subjective and internal and that which is objective and external. The boundary between the two acts like a container, which holds the former and places the latter outside. This container is what we know as the “self”. Among other things, it includes our thoughts, intentions, and habits, as well as our actual bodies. Except in altered states (see p.182), all experiences we report include a sense of self, but most of the time the sense is unconscious. This “consciousness-with-self” is what we generally call “consciousness”. When the sense of self becomes conscious, we talk of being “self-conscious”. BdidgXdgiZm >ciZgVXi^c\lî] Zck^gdcbZci XdchiVcianXdcÒgbh WdjcYVg^Zhd[WdYn BZY^Va egZ[gdciVaXdgiZm :cVWaZhndjidWZ XdchX^djhd[ndjg dlcbZciVahiViZ VcY`cdlndjg dlcX]VgVXiZg

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Agency is our sense of control over our actions. We feel that our conscious thoughts dictate what we do, but this appears to be incorrect. A famous experiment by Benjamin Libet (see p.187) revealed that a person’s brain starts to plan and execute a movement unconsciously, before the person has consciously decided to do it. This is often interpreted to show that our sense of agency and of making “decisions” is illusory. The sense of agency we experience may actually have evolved primarily to give us early warning not of our own actions, but of the actions of others. Because we feel ourselves to be agents, we also intuit agency in others, and thus think we know their intentions and can predict what they will do.

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The brain holds various “body maps” – internal representations of the physical self. The earliest, most basic map to emerge tells us where our body ends and the rest of the world begins. A more developed body “atlas” enables us to know our spatial location in the world. Normally, the >C;6CI7D9NB6EH 7VW^ZhegdWVWanYdcdiY^hi^c\j^h] internal maps and the body itself are WZilZZci]Z^gWdYnVcYZmiZgcVa closely matched, but it is possible for dW_ZXihjciâi]Z^gWdYnbVehhiVgiid them to be askew. If a person loses a iV`Z^c^c[dgbVi^dc[gdbi]ZldgaY# limb, for example, they may develop what is known as a phantom limbÅa feeling that they have a limb that, in fact, no longer exists (see p.102). People can also be tricked into “owning” a limb or even a body that is not actually theirs. K>GIJ6A7D9N KdajciZZghlZgZ\^kZc \d\\aZh!i]gdj\] l]^X]i]ZnXdjaYhZZ VXVbZgVk^Zld[i]Z^g dlcWVX`hîi^c\ ^c[gdcid[i]Zb# IdjX]^c\i]^hk^gijVa WVX`lî]VeZcaZY idgZedgihi]Vii]Zn XdjaYVXijVaan[ZZa i]^hhZchVi^dc!bV`^c\ i]Zb[ZZai]Zk^gijVa WdYnlVhi]Z^gdlc#

Out-of-body experiences (OBEs) occur when the internal representation of the body is out of kilter with the real body. This happens all the time in dreams, but when it happens during wakefulness it may be interpreted as a supernatural event. OBEs typically occur as you wake up, before the brain has properly reconnected with the external world (see p.171).

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THE INDIVIDUAL BRAIN


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A gene is a unit of hereditary information linked to one or more physical traits (such as eye color). Genes are made of DNA (see panel, below) and some genes achieve their effects by the production of proteins. Genes are like dimmer switches—they can turn their activity (expression) on, off, up, or down. In the brain, gene expression affects the levels of neurotransmitters, which, in turn, influences complex functions like personality, memory, and intelligence. However, neurotransmitters also affect gene expression. Environmental influences affect patterns of gene expression, so that brain function also depends upon factors such as diet, geographical surroundings, social networks, and even stress levels.

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A number of structural and functional differences have been found between male and female brains. Both the corpus callosum and the anterior commissure (a more primitive connection between the two hemispheres that links the unconscious areas) are larger in women than in men. This may be why women are more emotionally aware—the more emotional right side is better connected to the more analytical left side of the brain. It may also allow emotion to be incorporated more readily into thought and speech. When doing complex tasks, women use both sides of their brain, while men use the side more obviously suited to the task.

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Researchers have shown that culture influences the way the brain works. They carried out tests during fMRI scans on people raised in the US and people raised in East Asia, in which participants did puzzles involving lines in a square (see below). US culture is perceived to be focused upon the individual, while East Asian culture tends to be more focused on family and community. The brains of the US participants had to work harder when they were doing tasks involving context, while those of the East Asians worked harder when they had to judge individual lines. Brain activity lessened when participants undertook tasks related to their culture’s comfort zone. Participants were also asked how closely they identified with their culture, and the brains of those who identified most strongly had to work the hardest when doing tasks related to the “opposite” culture.

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E:GHDC6A>IN6C9I=:7G6>C Many different personality traits have been linked to specific patterns of activity in the brain, some of which are linked to the expression of certain genes or particular genetic mutations. For example, a person who produces more excitatory neurotransmitters is less likely to feel the need to seek thrills than someone who needs a lot of stimulation to experience the same level of excitement. E:GHDC6A>INB6G@:GH>CI=:7G6>C :migdkZgh^dc

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B6CNE:GHDC6A>I>:H4 Type tests like the Myers–Briggs (above) have been found to give different results according to the situation in which the person is tested. Trait tests allow for people to be different at different times, but still assume they have a “major” personality that is more real than others. Some evidence suggests, however, that practically everyone has more than one personality, and that many people have a large number of them. Memories that are available to a person in one situation may not be accessible in another. In extreme cases, this results in dissociative identity disorder (DID), but in normal 9G#?:@NAA6C9BG#=N9: people it merely shows up 9gVbVi^XeZghdcVaînX]Vc\Zh! as mood changes, memory hjX]VhVÆheaîeZghdcVaîn!Ç “glitches,” and the coming VgZVhiVeaZd[]dggdgÒabh VcY\]dhihidg^Zh#I]Zn and going of different skills, gZÓZXiVY^higjhid[eZdeaZ behaviors, and ways of l]dVeeZVgcdiid]VkZ hiVWaZeZghdcVaî^Zh# seeing the world.

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Brain scans have revealed some astonishing physical abnormalities, such as brains that are missing an entire hemisphere. The effect of losing half a brain would be catastrophic if it happened in later life. However, several cases have come to light in which brain growth has been severely restricted in infancy and yet the =6A;67G6>C person has gone on 9ZheîZ]Vk^c\dcZ to live a near normal h^YZd[]ZgWgV^c gZbdkZY!i]^h\^ga life with few, if any, aZVgcZYidWZÓjZci adverse symptoms. ^cildaVc\jV\Zh#

H>O:9D:HCÉIB6II:G Brains do not, generally, vary greatly in size, and there is little evidence to suggest that bigger brains produce greater intelligence. At one extreme, Irish writer Jonathan Swift (1667–1754) had a brain that, at the time of his death, weighed a relatively enormous 70oz (2,000g). In 1928, the Moscow Brain Research Institute started collecting and mapping the brains of famous Russians, including that of the physiologist Ivan Pavlov (1849–1936). His brain was at the other end of the size scale, weighing a mere 53 1/2 oz (1,517g).

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I=:I:GGD>HIÉH7G6>C Ulrike Meinhof (1934–76) was a member of the infamous Baader–Meinhof Gang, responsible for a number of killings, bombings, and kidnappings in Germany during the 1970s. She was captured and commited suicide in prison. After her death, studies suggested that brain damage resulting from an operation on a swollen blood vessel might have accounted for her violent behavior.

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Albert Einstein’s brain was removed after his death. Many years later, it was examined by Dr. Sandra Witelson and compared with other brains in a brain bank. It was found to be wider than normal, and part of a deep groove that normally runs through the parietal lobe was missing. The area affected is concerned with mathematics and spatial reasoning, and it is possible that the missing groove allowed neurons in that area to communicate more easily, giving him his extraordinary talent for describing the universe mathematically.

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199


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DEVELOPMENT AND AGING


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8DC8:EI>DCID7>GI= In the days following conception, the embryo is just a minute ball of cells. Development of the brain and nervous system starts at about three weeks, with differentiation of cells to form the neural plate along the back (dorsal) part of the embryo; this broadens and folds to form the liquid-filled neural tube, which will become the brain and spinal cord. The brain starts to develop at about four weeks as a tiny bulb at the upper end of the neural tube, while the lower part begins to form the spinal cord. The main sections of the brain, including the cerebral cortex, are visible within seven weeks. During the next several weeks, the brain continues @:N;DG:B7GND9:K:ADEB:CI to grow and develop. ;dgZWgV^c =^cYWgV^c EgdhZcXZe]Vadc

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7G6>CÄB68=>C:>CI:G;68:H When a person is thinking, the brain produces electrical signals. Scientists have discovered ways in which the electrical signals can be picked up by sensors and sent wirelessly to other electrical devices, making it possible for a person to move or alter objects by thought alone. Most research in this field is directed toward developing devices to help people with nervous-system injuries regain the use of paralyzed limbs. The technology has also been picked up by some computer-game manufacturers, who have produced games that can be played using thought power.

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:9:I:8I>DC Mind-reading is not limited to revealing what it is that a person is looking at. Brain-scanning studies have shown that, when a person is lying, the brain generates a different pattern of neural activity from when they telling the truth. This has been used to develop a “lie detector” that analyzes brain activity captured by fMRI. Although still in development, BZY^Va [gdciVa the technology is \ngjh claimed to have an accuracy rate of over 90 percent— significantly greater >c[Zg^dg than the accuracy rate [gdciVa A:;I=:B>HE=:G: \ngjh of polygraph tests.

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6GI>;>8>6A>CI:AA>CDC>8:N: People who have become blind as a consequence of eye conditions (as opposed to damage to areas of the brain associated with vision) may soon be able to see again thanks to the development of artificial eyes. A “bionic” eye prototype has been created, comprising a computer chip that sits in the back of the individual’s own eye socket, which is linked up to a tiny video camera built into a pair of glasses. Images captured by the camera are beamed to the chip, which translates them into electrical impulses and sends them on to the visual cortex via the optic nerve.

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The vagus nerve is a cranial nerve, traveling from the brainstem to various internal organs, that has an important role in mediating brain arousal. A number of different types of brain disorders, such as chronic epilepsy and severe depression, benefit from the effects of stimulating this nerve. A small disk with a tiny generator fueled by a lithium battery is surgically implanted in the chest, which sends regular, rhythmic pulses along a wire that is tethered to the left vagus nerve (the right vagus nerve runs directly to the heart). The frequency and intensity of the electrical pulses can be altered according to the severity of the condition.

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I=:7>DC>86GB A bionic arm that is operated by the power of thought alone is already in use, and future models, which are currently being developed, are likely to be more lifelike and increasingly dextrous. The current versions work by rerouting motor nerves from the brain that originally ran to the hand, and terminating them instead in electrodes, which communicate with computer-driven motors in the arm itself. Sensors feed a limited degree of sensory information back to the brain, so the user can determine both temperature and pressure.

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211


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DISEASES AND DISORDERS


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Many disorders that have conventionally been seen as discrete conditions are now being recognized as related. People with autism, for example, have a core problem with understanding other people’s mental processes. Around this core lies a constellation of symptoms grouped into three overlapping “suites” of behavior. These suites are conventionally seen as different types of problem, but their common relationship to the core deficit suggests that they share a genetic underpinning. Psychosis has a core that is characterized by over-interpretation of other minds. It too can be seen as the core of symptoms from overlapping suites.

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The pain tends to be constant, although it may throb, and it may occur in the forehead or more generally over the head. The pain may be accompanied IZch^dc by tightening of the neck muscles and ^ccZX` a feeling of pressure behind the eyes bjhXaZh and/or tightness around the head. Tension headaches are typically brought on by stress, which causes tension in the muscles of the neck and scalp. This, BJH8JA6GI:CH>DC in turn, is thought to stimulate pain EV^cgZXZeidgh^ci]ZbjhXaZhd[i]ZhXVae receptors in these areas, which send VcYcZX`VgZhi^bjaViZYWnbjhXjaVgiZch^dc! aZVY^c\idi]ZeV^cd[ViZch^dc]ZVYVX]Z# “pain impulses” to the sensory cortex.

During cluster headaches there are several attacks (typically one to four) a day, followed by an attack-free remission period. The cluster period usually lasts from a few weeks to a couple of months. A remission period may last for months or even years, although some people experience no significant remissions. The cause of cluster headaches is not known, although there is some evidence that abnormal nerve cell activity in the hypothalamus may be involved.

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A migraine headache usually occurs at the front or one side of the head, although the area of pain can move during an attack. Migraine is classified into two types: classical migraine and common migraine. In classical migraine, the headache is preceded by aura, a group of warning symptoms that includes: visual disturbances, such as flashing lights and other distortions; stiffness, tingling, or numbness; difficulty speaking; and poor coordination. In common migraine there is no aura. In both types there may be an early stage, known as prodrome, with features such as difficulty concentrating, mood changes, and fatigue or excessive energy. In common migraine, the prodrome is followed by the headache; in classical migraine, the prodrome is followed by aura, which is

then succeeded by the headache. The headache gets worse with movement, and it is accompanied by symptoms including nausea and/or vomiting, and increased sensitivity to sound, light, and sometimes smells. It is often followed by a postdrome stage, in which there may be fatigue, difficulty focusing, poor concentration, and persistence of increased sensitivity.

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The cause of chronic fatigue syndrome is not known. It can develop after a viral infection or a period of emotional stress, but in many cases there is no specific preceding factor. The principle symptom is persistent, overwhelming fatigue that lasts for at least several months. Other symptoms vary, but commonly include poor concentration, impaired short-term memory, muscle and joint pain, and feeling ill and/or extremely tired after even mild exertion. The

disorder is also often associated with depression or anxiety, but it is unclear whether these are a cause or a result of the condition. Chronic fatigue syndrome is usually diagnosed from the symptoms, although various tests and psychological assessments can be carried out to exclude other possible conditions. It is a long-term disorder, although there may be periods of remission and sometimes the disorder clears up spontaneously.

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minor injuries, particularly if the injury has caused unconsciousness, and this may cause confusion, dizziness, and blurred vision, which may last for several days. Postconcussive amnesia can also occur. Repeated concussions eventually cause detectable brain damage, which may result in punchdrunk syndrome, symptoms of which may include impaired cognitive abilities, progressive dementia, parkinsonism (see p.226), tremors, and epilepsy. Severe head injury may produce unconsciousness or coma, and usually brain damage, which in very severe cases may be fatal. In nonfatal cases, the effects of brain damage vary widely according to the severity and location of damage. The effects may include weakness, paralysis, problems with memory and/ or concentration, intellectual impairment, and even personality changes. Such effects can be long-term or permanent.

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Normally, neuronal activity in the brain occurs in a regulated way. However, during an epileptic seizure neurons start firing in an abnormal way, disrupting normal brain function. Although seizures are a defining symptom of epilepsy, they can occur without epilepsy being the cause. The mechanism underlying epileptic seizures is not known for certain, but it is thought to involve a chemical imbalance in the brain. Normally, the neurotransmitter gamma-aminobutyric acid (GABA) helps regulate brain activity by inhibiting neurons in the brain. When the level of GABA falls too low—which itself may be due to abnormal amounts of enzymes that regulate GABA levels—neurons are not inhibited and they send a flood of impulses through the brain, resulting in a seizure. Epilepsy can have a number of causes, although in many cases the

cause is unclear. A genetic factor may be involved in some cases. Other causes include head injury; birth trauma; an infection such as meningitis or encephalitis; a stroke; a brain tumor; and abuse of drugs or alcohol. Many people find that specific factors can trigger a seizure. These triggers include stress; lack of sleep; fever; flashing lights; and drugs such as cocaine, amphetamines, Ecstasy, and opiates. Some women who suffer from epilepsy are more likely to have a seizure before the start of a menstrual period.

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Broadly, epileptic seizures fall into two main types: generalized seizures and partial seizures (see table below). Seizures often start in one area of the brain, which might contain scar tissue or some structural abnormality, and then spread throughout the rest of the brain. Some people experience a warning sign (called an aura) before an epileptic seizure. These warning signs may include a strange smell or taste; a feeling of foreboding; déjà vu; and a sense of unreality. In most cases, seizures stop by themselves. Sometimes a seizure can persist or seizures follow on from each other without the person recovering in between. This is known as status epilepticus and is a medical emergency.


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Typically, the infection reaches the meninges through the bloodstream from elsewhere in the body, although it may occasionally result from direct infection of the meninges after an open head injury. It may occur as a complication of various other diseases, including Lyme disease, encephalitis, tuberculosis, and leptospirosis. Viral meningitis may be caused by viruses such as herpes simplex or chickenpox virus. It tends to be relatively mild and causes symptoms similar to those of flu.

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Rarely, it may cause serious symptoms, such as weakness or paralysis, speech problems, visual impairment, seizures, and coma. Bacterial meningitis is less common than the viral form, but is more serious and can be fatal. It may be caused by various bacteria but is usually due to infection with meningococcal or pneumococcal bacteria. Symptoms may develop rapidly, over only a few hours, and include fever, stiff neck, severe headache, nausea, vomiting, abnormal sensitivity to light, confusion, and drowsiness, and sometimes seizures and loss of consciousness. In meningococcal meningitis, the bacteria may multiply in the blood, leading to a reddish purple rash that does not fade when pressed. If left untreated, bacterial meningitis can enter the cerebrospinal fluid, triggering an immune response that causes increased intracranial pressure, which in turn can cause brain damage.

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if the immune system is compromised, there is a greater risk of developing encephalitis. When

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A rare condition, encephalitis varies in severity from a mild, barely noticeable illness to one that can be life-threatening. Only certain viruses are able to gain access to the central nervous system and affect nerves, and therefore potentially cause encephalitis. These viruses include the herpes simplex virus (which also causes cold sores), chickenpox virus, and measles virus. Occasionally, the infection may also affect the meninges, causing meningitis. In most cases, the immune system deals with the viral infection before it can affect the brain. However,

compressed against the skull. Rarely, encephalitis is due to an autoimmune reaction, in which the immune system attacks the brain, leading to inflammation and brain damage. Mild encephalitis usually causes only a slight fever and headache. In more severe cases, there may also be nausea and vomiting; weakness, loss of coordination, or paralysis; abnormal sensitivity to light; loss or impairment of speech; memory loss; uncharacteristic behavior; stiff neck and back; drowsiness; confusion; seizures; and coma. In very severe cases, encephalitis can cause permanent brain damage and may even be fatal.

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A brain abscess can result from a bacterial or, more rarely, a fungal or parasitic infection. Fungal and parasitic infections are usually restricted to people whose immune systems have been impaired—for example, those with HIV/AIDS, people undergoing chemotherapy, or those taking immunosuppressants. A brain abscess can occur as a result of a penetrating head injury or an infection spreading from elsewhere in the body, such as from a dental abscess, middle-ear infection, sinusitis, or pneumonia. It can also result from injecting drugs using a nonsterile needle.

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Also called a “mini-stroke,” a transient ischemic attack (TIA) is most commonly caused by a blood clot that temporarily blocks an artery supplying blood to the brain. It can also occur due to excessive narrowing of an artery as a result of atherosclerosis (buildup of fatty deposits on the artery wall). There are numerous risk

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factors that contribute to the likelihood of a TIA, such as diabetes mellitus, previous heart attacks, high blood-fat levels, high blood pressure, and smoking. Symptoms usually develop suddenly and vary according to the part of the brain affected by the restricted blood flow, but they include visual disturbances or loss of vision in one eye, problems speaking or understanding speech, confusion, numbness, weakness or paralysis on one side of the body, loss of coordination, dizziness, and possibly brief unconsciousness. If symptoms last for more than 24 hours, the attack is classed as a stroke. Having had a TIA indicates increased risk of stroke. Treatment for TIA is aimed at preventing a stroke and includes endarterectomy (a procedure to remove the lining of an artery affected by atherosclerosis), anticoagulant drugs, or aspirin. It is also important to treat any risk factors, and stopping smoking is essential.

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and seizures. In severe cases, there may be unconsciousness and coma. The long-term outcome depends on the size and location of the hemorrhage. A severe subdural hemorrhage may be fatal. A subdural hemorrhage is usually diagnosed with a brain scan (CT or MRI). An X-ray may be taken if skull fracture is suspected. A small hemorrhage may not need treatment and can clear up on its own, but usually surgery is needed. HXVae H`jaa 9jgVbViZg 7addYXadi

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This type of hemorrhage is most commonly caused by rupture of a berry aneurysm or, rarely, is due to the rupture of an arteriovenous malformation. High blood pressure is a significant risk factor. Symptoms occur suddenly, without warning, and often develop rapidly (over minutes). Some people recover completely, some are left with residual disability, and some die. Arteries in the brain may constrict to reduce blood loss, which can reduce blood supply to part of the brain and cause a stroke.

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Primary brain tumors first develop in the brain itself and can be malignant or benign. They can arise in various types of brain cells and in any part of the brain, but primary tumors in adults are most common in the front two-thirds of the cerebral hemispheres. Secondary tumors result from the spread of malignant cancer (metastasis) from elsewhere in the body, most commonly the lungs, skin, kidney, breast,

or colon. Several secondary tumors can develop simultaneously and the cause of most tumors is not known. Rarely, some tumors may be associated with certain genetic conditions. A tumor compresses the surrounding brain tissue and raises pressure inside the skull. Symptoms therefore depend on the size and location of the tumor, but may include severe, persistent headaches; blurred vision or other sensory disturbances; speech problems;

dizziness; muscle weakness; poor coordination; impaired mental functioning; behavioral or personality changes; and seizures. If left untreated, a brain tumor may be fatal. Brain tumors are diagnosed through brain scans and neurological tests. Treatment may involve a surgical removal (if possible), radiation therapy, and/or chemotherapy. Drugs to reduce the brain swelling may also sometimes be given.

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blood protein called apoliprotein E are implicated. These genes result in a protein (beta amyloid) I=:BDHI8DBBDC86JH:D;9:B:CI>6!I=>H>H6 being deposited in the brain as plaques, which EGDK:9:K:8DC9>I>DC>CL=>8= leads to the death of neurons. Alzheimer’s EA6FJ:H86JH:96B6C# disease is also associated with reduced Alzheimer’s disease is rare before the age of 60, but levels in the brain of the neurotransmitter increasingly common thereafter. Most cases occur acetylcholine. Additionally, it is thought without an identifiable cause. Mutations in several that the disruption of the mechanism that genes are associated with this disorder, however, and controls the inflow of calcium ions into the genetic component is especially strong in the neurons may be involved, leading to relatively rare cases of early onset disease (symptoms excessive calcium in the neurons, which occurring before 60). In late-onset Alzheimer’s disease, prevents them from receiving impulses from mutations in genes responsible for the production of a other brain neurons. Symptoms may vary from one person to another, but typically Alzheimer’s progresses HI6B:GÉH9>H:6H: through three stages (see panel, left). Alzheimer’s disease is usually diagnosed I]ZhnbeidbhVcYegd\gZhh^dcd[6ao]Z^bZgÉhY^hZVhZkVgn[gdb eZghdcideZghdc#=dlZkZg!i]ZhnbeidbhWZXdbZ^cXgZVh^c\anhZkZgZ from the symptoms, although brain scans, Vhi]ZY^hZVhZegd\gZhhZhVcYaVg\ZgVgZVhd[i]ZWgV^cVgZYVbV\ZY! blood tests, and neuropsychological tests Vai]dj\]^chdbZXVhZhi]ZgZbVnWZeZg^dYh^cl]^X]i]ZeZghdc are also carried out. hZZbhid^begdkZ#B:GÉH

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difficulty swallowing; depression; apathy; and dementia, which usually takes the form of lack of concentration, memory problems, and personality and mood changes (including aggressive or antisocial behavior). The disease usually progresses slowly, eventually causing death some 10–30 years after symptoms first appear.

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The underlying cause of Huntington’s disease is a single abnormal gene that occurs when a group of DNA base pairs is repeated many times. The faulty gene generates an abnormal version of Huntingtin protein, which then builds up in nerve cells and leads to the degeneration of neurons in the basal ganglia and cerebral cortex.

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Multiple sclerosis (MS) is thought to be an autoimmune disease in which the body’s immune system destroys the cells that produce the myelin sheaths that surround and insulate neurons. Eventually hardened (sclerosed) plaques of scar tissue form over the demyelinated areas and the neurons themselves degenerate. The effect of these changes is to impair or block nerve

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Paralysis can affect areas ranging from a single small muscle to most of the major muscles of the body. It is classified by the areas of body affected. Hemiplegia is paralysis of one half of the body. Paraplegia is the paralysis of both legs and sometimes part of the trunk. Quadriplegia is paralysis of all four limbs and the trunk. Paralysis may also be classified as “flaccid” (causing floppiness) or “spastic” (causing rigidity). Paralysis can be caused by any injury or disorder that affects the motor cortex or the motor nerve pathways that run from the motor cortex via the spinal cord and peripheral nerves to the muscles. It may also result from a muscle disorder or myasthenia gravis (a disorder affecting the junction between nerves and muscles). The affected area sometimes feels numb.

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can also be a risk factor, if the father is over 50. Parents who already have a child with Down or who have abnormalities of their own chromosome 21 have a higher risk of having a baby with Down syndrome.

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One of the most common chromosomal abnormalities, Down syndrome is usually the result of an extra copy of chromosome 21; affected people therefore have 47 chromosomes in all of their body cells, rather than 46. It may also result when part of chromosome 21 breaks off and attaches to another chromosome, a process called translocation, so that cells have the normal number of chromosomes but chromosome 21 is abnormally sized. Very rarely, Down syndrome may be the result of mosaicism, in which some body cells have 47 chromosomes and some have 46. Exactly how these abnormalities produce the characteristic mental and physical features of Down is not known. In most cases there is no identifiable reason for the chromosomal abnormality, although maternal age is a risk factor—after the early 30s, the risk of having a child with Down increases significantly. Paternal age

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Hnbeidbh There is considerable variation in the severity of symptoms, but typically they include slow motor and language development and learning difficulties. Physical symptoms may include a small face with upward-sloping eyes; a flattened back of the head; a short neck; a large tongue; small hands with a single horizontal crease on the palm; and short stature. There is also increased risk of various disorders, such as heart disease (often associated with congenital heart problems), hearing problems, underactivity of the thyroid gland, narrowing of the intestines, leukemia, and respiratory-tract and ear infections. Adults are at increased risk of eye problems such as cataracts. In older people there is a heightened risk of Alzheimer’s disease. People with Down syndrome have lower than normal life expectancy, but some survive into old age.

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In many cases, depression occurs without an obvious cause. A number of factors may trigger it, such as a physical illness; hormonal disorders or the hormonal changes during pregnancy (prenatal depression) or after childbirth (postpartum depression); or distressing life events, such as a bereavement. It may also occur as a side effect of certain drugs, such as oral contraceptives. Depression is more common in women, it tends to run in families, and various genetic mutations are associated with this disorder. Various biological abnormalities have been found in the brains of depressed people, such as decreased levels of the neurotransmitter serotonin, raised levels of the enzyme monoamine oxidase, loss of cells from the hippocampus (an area of the brain involved in mood and memory), and abnormal patterns of neural activity in the amygdala and parts of the prefrontal cortex. However, the mechanisms by which such biological abnormalities may lead to depression are not known.

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The exact cause of bipolar disorder (sometimes called manic–depressive illness) is not known, although it is believed that it results from a combination of biochemical, genetic, and environmental factors. The levels of

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HnbeidbhVcYigZVibZci There is considerable variation among different people in the symptoms and in their severity. Most people experience several of the following: feeling unhappy most of the time; loss of interest and enjoyment in life; difficulty coping and making decisions; impaired concentration; persistent fatigue; agitation; changes in appetite and weight; disrupted sleeping patterns; loss of interest in sex; loss of self-confidence; irritability; and thoughts of, or attempts at, suicide. In some people, episodes of depression alternate with periods of extreme highs (manic episodes); this is known as bipolar disorder (see below). Usually depression is 7G6>C6G:6H treated with a talking therapy, I]ZW^dad\^XVaWVh^hd[ antidepressant drugs, or both. YZegZhh^dc^hcdi[jaan jcYZghiddYWjihZkZgVa Experimental treatment using VgZVhd[i]ZWgV^cVgZ deep brain stimulation i]dj\]iidWZ^ckdakZY! (where implanted electrodes ^cXajY^c\i]ZegZ[gdciVa stimulate areas of the brain) XdgiZm!]êedXVbejh! is also being studied. VcYVbn\YVaV#

certain neurotransmitters in the brain, such as norepinephrine, serotonin, and dopamine, may play a role. Bipolar disorder tends to run in families and has a strong genetic component. However, environmental factors, such as a major life event, may act as triggers.

Hnbeidbh Typically, symptoms of depression and mania alternate, with each episode lasting for an unpredictable period. Between mood swings, a person’s mood and behavior are often normal. Symptoms of a depressive episode may include feelings of hopelessness, disturbed sleep, changes in appetite and weight, fatigue, a loss of interest in life, and a loss of self-confidence; there may also be suicide attempts. Symptoms of a manic episode may include extreme optimism, increased energy levels, drive and activity, inflated self-esteem, racing thoughts, and risk-taking behavior.

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Temporary feelings of nervousness, apprehension, and even panic in stressful situations are normal and appropriate. However, when these anxiety reactions occur frequently in ordinary situations and disrupt normal activities, it is considered to be a disorder. In a few cases there may be an identifiable physical cause for persistent anxiety, such as a thyroid disorder or substance abuse, and sometimes generalized anxiety may develop after a stressful life event, such as a bereavement. In most cases the cause is not known, although a family history of an anxiety disorder increases the risk of developing one. The brain mechanisms underlying anxiety disorders are also unknown, although disruption of neurotransmitters in the frontal lobes or limbic system may be involved. Whatever the underlying cause, the effect is to disrupt the body’s normal control of its stress response —the “fight or flight” response. With anxiety disorders either the stress response fails to turn off or the stress response becomes activated at inappropriate times. There are several forms of anxiety disorder. The most common is generalized anxiety disorder, which is characterized by excessive, inappropriate worrying that lasts for at least six months. Another form of anxiety disorder is panic disorder, in which there are sudden, unexpected attacks of intense anxiety or fear.

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There are many different forms of phobia, but they can be categorized into two broad types: simple and complex. Simple phobias are fears of specific objects or situations, for example, spiders (arachnophobia) or enclosed spaces (claustrophobia). Complex phobias are more pervasive and involve several anxieties. For example, agoraphobia may involve fear of crowds and public places or of traveling in planes, buses, or other forms of public transportation; it also includes anxiety about being unable to escape to a safe place, usually home. Social phobia (also known as social anxiety disorder) is another complex phobia in which there is intense anxiety in social or performance situations (such as public speaking) because of fear of public embarrassment or humiliation.

8VjhZhVcYZ[[ZXih The causes of phobias are not known for certain, Some phobias tend to run in families, which may be a result of children learning a specific fear from their parents. In other cases, a phobia may develop in response to a traumatic event or situation. The main symptom of a phobia is an intense, uncontrollable anxiety when confronted by the feared object or situation. Merely anticipating an encounter with the feared object or situation can cause anxiety. In severe cases there may be symptoms of a panic attack,

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such as sweating, palpitations, breathing difficulty, and trembling, when the object or situation is actually encountered. There is also usually a strong desire to avoid the feared object or situation, often to the extent of taking extreme measures. These effects can severely limit normal everyday activities and sometimes a person with a phobia may try using drugs or alcohol in an attempt to reduce the anxiety.

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The external cause of post-traumatic stress disorder (PTSD) is the experience of trauma. In the brain itself, various abnormalities in areas involved in memory, the stress response, and the processing of emotions have '*

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been identified. The amygdala (involved in memory and emotion processing) is overactivated in response to memories of traumatic events whereas the prefrontal cortex is under-responsive to fearful stimuli, which may result in its failure to inhibit the amygdala and thereby inhibit traumatic memories. The thalamus may also be involved; some people have a genetic constitution that is associated with an enlarged thalamus, which may in turn lead to an exaggerated response to fearful memories and an increased susceptibility to PTSD.

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The symptoms of PTSD may develop immediately after a traumatic event or may not appear for months. They may include flashbacks or nightmares that trigger the same intense fear originally felt; emotional numbness; loss of enjoyment in usually pleasurable activities; memory problems; hypervigilance and an exaggerated startle response; sleeping problems; and irritability.

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The exact cause of OCD is not known, but it is generally thought to be due to a combination of factors and may have different causes in different people. OCD tends to run in families, so there may be a genetic link in some cases. It has also been associated with childhood infection with Streptococcus bacteria. Brain imaging studies have found evidence of abnormal physiological connections in the communication loop between the orbitofrontal cortex,

caudate nucleus, and thalamus involving the neurotransmitter serotonin. In addition, personality type may be a factor—perfectionists appear to be more susceptible to developing OCD.

Hnbeidbh Symptoms typically appear during the teenage or early adult years and may consist of obsessions, compulsions, or both. Obsessions are thoughts, feelings, or images that recur involuntary and

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provoke anxiety. For example, there may be an excessive fear of dirt that may be so powerful that the person fears leaving home in case he or she becomes contaminated. Compulsions are actions that a person feels compelled to carry out repeatedly in an effort to ward off anxiety, such as repeatedly checking things such as locks or doors. The person may recognize that the obsessions and/or compulsions are unreasonable but cannot control them.

with everyday life. With treatment most people recover, although symptoms may recur under stress.

9^V\cdh^hVcYdjiadd` To be diagnosed with OCD, the symptoms must cause anxiety, must be present on most days for at least two weeks, and must interfere significantly

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constantly checking one’s appearance in mirrors; frequently comparing one’s 7D9N9NHBDGE=>89>HDG9:G799>H6B:CI6A=:6AI=EGD7A:B>CL=>8=6E:GHDC appearance with that of others; often >H:M8:HH>K:AN8DC8:GC:967DJI6E:G8:>K:99:;:8I>C=>HDG=:G6EE:6G6C8: seeking reassurance about one’s 6C9I=>HEG:D88JE6I>DCL>I=7D9N>B6;>86CI9>HIG:HH# appearance; frequently touching the The cause of body dysmorphic disorder disorders, obsessive-compulsive disorder, perceived flaw; and picking the skin to is unclear, although it is thought to be and generalized anxiety disorder, although make it smooth. In addition, a person due to a combination of several factors, it is not clear whether there is a causative may feel anxious and self-conscious possibly including low levels of relationship with such disorders. around other people because of the serotonin. It may occur in combination Many people are dissatisfied with some perceived flaw and may avoid social with other disorders, such as eating aspect of their appearance, but people situations in which it might be with BDD are obsessed with one or more )* perceived flaws. Typical )% G^\]i signs of BDD include ]Zb^he]ZgZ (* refusing to be in (% photographs; trying 6Xi^kZVgZV to hide the “flaw” with ^caZ[i '* ]Zb^he]ZgZ clothing or makeup;

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A person with this disorder typically experiences several physical symptoms that persist for years. The symptoms are not generated intentionally and are often severe enough to interfere with everyday life, but no physical cause for them can be identified.

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noticed. In some cases, medical and surgical treatment may be sought to correct the perceived flaw.

9^V\cdh^h Body dysmorphic disorder is diagnosed by psychiatric evaluation. To be diagnosed with this disorder, preoccupations with appearance must cause considerable distress and interfere with everyday life.

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making frequent visits to the doctor to have tests. Even when the test results prove negative, people may remain convinced that they have a serious illness and often seek other medical opinions. In addition, the person may believe they have a particular disease after hearing about it; for example, after

234

In hypochondria (also known as hypochondriases) trivial symptoms assume unrealistic significance. The

symptoms are real, such as a cough or headache, but people with hypochondria are genuinely worried that they indicate a serious disease, such as lung cancer or a brain tumour. In mild forms, the person may simply worry constantly. In more severe cases, hypochondria can seriously disrupt everyday life, with the person


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hearing about Alzheimer’s disease, an instance of momentary forgetfulness might lead the person to believe they have that disease. Many people with hypochondria also have other mental health disorders, such as depression, obsessive–compulsive disorder, phobia, or generalized anxiety disorder.

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People with Munchausen’s syndrome are aware that they are fabricating symptoms, unlike those with hypochondria, who truly believe they are ill. They do not fake illness in order to receive tangible benefits (such as

financial gain). Instead, the motive seems to be to obtain investigation, treatment, and attention from medical personnel. People with the syndrome often have a good medical knowledge and create plausible symptoms and

explanations for their faked illness, which makes diagnosis of Munchausen’s syndrome very difficult. In addition to lying about symptoms, they may try to manipulate test results—for example, by adding blood to a urine sample—and may even inflict symptoms on themselves; they may injure themselves or ingest poisons, for instance. Typically, they attend many different hospitals, often repeatedly presenting the same symptoms.

In a related condition, known as Munchausen’s by proxy or fabricated and induced illness (FII), people may invent or induce symptoms in somebody else. This usually involves parents faking or inducing symptoms in their child. Diagnosis is difficult and involves carrying out various tests to exclude an underlying illness. If a genuine underlying cause is not found, a diagnosis is made from a psychiatric assessment.

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causative relationship to Tourette’s has not been established. Environmental factors may also play a role in the development of Tourette’s syndrome.

feature, but is comparatively rare. Other mental health problems, such as depression or anxiety disorders, may also develop. Typically, the symptoms first appear during childhood and get worse during the teenage years but then improve. However, in some cases the condition gets progressively worse and lasts throughout adulthood.

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The characteristic symptoms of Tourette’s syndrome are motor tics, such as blinking, facial twitches, shoulder shrugging, and head jerking, and vocal tics, such as grunting or repeating words. The involuntary utterances of swear words (coprolalia) is a well-known

For a positive diagnosis of Tourette’s, both motor and vocal tics must be present and they must not be due to another medical condition, medications, or other substances. They must occur several times a day on most days or intermittently for more than a year.

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In most cases, Tourette’s syndrome runs in families and genetic factors may be involved, although the relevant genes and the mode of inheritance have not been identified. In some cases, known as sporadic Tourette’s syndrome, there is no apparent inherited link. Various brain abnormalities have been implicated, including malfunctioning of the basal ganglia, thalamus, and frontal cortex, and abnormalities in the neurotransmitters serotonin, dopamine, and norepinephrine, although their

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Contrary to popular belief, schizophrenia is not a “split personality,” but rather a form of psychosis in which a person is not able to distinguish what is real from what is imagined. The cause of schizophrenia is not known, although it is believed to result from a combination of genetic and environmental factors. Schizophrenia runs in families, and a person who has a close family member with the disorder is at increased risk of developing it. However,

it is believed that genetic susceptibility alone is insufficient to cause schizophrenia and environmental factors are also necessary. Among the environmental factors that may be involved are exposure to infection or malnutrition before birth, stressful life events, and the use of marijuana. Excess dopamine levels may also be involved since all antipsychotic drugs block dopamine, and drugs that release dopamine can trigger schizophrenia. Various brain abnormalities have been identified in people with schizophrenia, including unusually low

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people with family members who have this disorder or schizophrenia. Socially isolated people tend to be more susceptible, and in some cases it may also be triggered by stress. There are several types of delusional disorder: jealous (the delusion that their partner is unfaithful); persecutory (a belief that somebody is hounding or trying to harm them); erotomanic (somebody—often a celebrity—is in love with them); grandiose (an inflated sense of worth, power, talent, or knowledge); somatic (the delusion that they have a physical defect or medical problem); and mixed (two or more of the other delusional types).

236

In delusional disorder, the delusions are “non-bizarre” (involving things that are within the realms of possibility). Apart from the delusion and behavior related to it, someone with the disorder often functions normally, although preoccupation with the delusion can disrupt everyday life. The cause of delusional disorder is not known, but it is more common in

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It is possible to become addicted to anything, but whatever the addiction is, the person cannot control it. An addiction may be to a substance or an activity. It is believed that addictive substances or activities affect the brain so that it reacts in the same way that it responds to pleasurable experiences, by increasing the release of the neurotransmitter dopamine. It is not

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The cause of personality disorders is not known but they are thought to be due to a combination of genetic and environmental influences. Factors that may

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increase the risk of developing a personality disorder include a family history of such a disorder or another mental illness; abuse during childhood; a dysfunctional family life during childhood; and having conduct disorder (see p.240) in childhood. There are many types of personality disorders (see panel, below), but in general they are all characterized by an inflexible way of thinking and behaving,

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irrespective of the situation. Symptoms tend to develop in adolescence or early adulthood and may vary in severity. Often a person with a personality disorder is not aware that the behavior and thought patterns are inappropriate, but may be aware of problems with personal, social, or work relationships, and these problems may cause distress. Specific symptoms depend on the type of personality disorder a person has.

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237


Anorexia nervosa is characterized by self-starvation and excessive weight loss. Its main features are an intense fear of being fat or gaining weight; a resistance to maintaining normal weight; and the denial of the seriousness of low body weight. It can be fatal. Bulimia nervosa is characterized by binge eating and then repeated compensatory actions to prevent weight gain, such as self-induced vomiting, laxative or diuretic use, excessive exercise, or fasting. It can result in life-threatening heart abnormalities due to an 7D9NB6HH>C9:M imbalance of electrolytes. 7dYnbVhh^cYZm7B> ^hVÒ\jgZi]Vi^cY^XViZh Binge-eating disorder is l]Zi]ZgVeZghdc^h similar to bulimia nervosa but lî]^cV]ZVai]nlZ^\]i without the compensatory gVc\Z#6Yjaihlî] actions to counter the binges, VcdgZm^VcZgkdhV]VkZ V7B>d[&,#*dgaZhh# which can lead to obesity.

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The causes of eating disorders are not clear, although a combination of biological, genetic, psychological, and social factors are thought to be involved. The effects of social and peer pressure to be thin may be a contributory factor. Anxiety about body image, low self-esteem, and depression may also be involved.

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birth or in the early years of life, and food allergies. There is no evidence that parenting problems cause ADHD, but they may influence its severity and a child’s coping strategies. Some brain abnormalities have been found in children with ADHD, including low dopamine levels. Drugs that increase dopamine levels

in the brain, such as Ritalin, may lessen symptoms. Symptoms usually appear during early childhood and may become worse when the child starts school. Due to the various ADHD-related problems, there may also be difficulty making friends, low self-esteem, anxiety, or depression.

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238

ADHD is characterized by persistent difficulty paying attention and/or hyperactivity. It is most common in children, but it may persist into adulthood. ADHD tends to run in families and in most cases genetic inheritance, probably involving many genes, is thought to be the most probable underlying cause. However, this genetic predisposition interacts with various other factors, such as exposure to certain toxins (such as nicotine and alcohol) before birth, brain damage before

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Often delays are first noticed by parents, but a delay may also be detected during routine developmental checks. If a problem is suspected, a full developmental assessment is done, and the child may be referred to a L6A@>C9:9 specialist. Treatment depends on the severity and type 7Z^c\VWaZidlVa`lî]dji]Zae^hdcZ of delay. It may include physical aids, such as glasses d[i]Z`ZnYZkZadebZciVabâZhidcZh# or hearing aids, therapies such as speech therapy, and Ine^XVaan!X]âYgZcbVcV\Zi]^hl]Zc possibly special educational help. WZilZZcVWdji&%VcY&.bdci]hdaY#

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There are differences in opinion about what the term “learning disability” encompasses but, in general, it applies to conditions in which there is developmental delay. However, learning difficulty may also refer to a specific difficulty, for example, in reading or writing. AZ[i^c[ZgdiZbedgVa XdgiZm

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Various factors put a child at increased risk of conduct disorder, including genetic factors, an unstable and/or violent family life, lack of supervision, abuse, and bullying. Learning disabilities (see above), attention deficit hyperactivity disorder (see p.238), and mental health problems such as depression also increase the risk. Children with conduct disorder also tend to have abnormal responses to reward and punishment.

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Down syndrome (see p.228) and fragile X syndrome (see below). Other factors include problems with brain development before or during birth, possibly due to exposure to toxins such as alcohol or drugs in the uterus, lack of oxygen, or premature or prolonged labor; and a head injury, malnutrition, or exposure to environmental toxins (such as lead) at a young age. If a learning disability is suspected, a developmental assessment will be carried out. Hearing, vision, and other medical and genetic tests will also be done to check for underlying physical causes of the learning difficulties.

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In some cases, a child may also engage in alcohol or drug abuse. Many children act in an antisocial or disruptive way from time to time, but in a child with conduct disorder the behavior occurs repeatedly over a period of several months or longer. As a result of such behavior, a child may find it difficult to make friends, have low self-esteem, and do poorly at school. A diagnosis is usually based on a psychiatric assessment of the child’s G:9J8:97G6>C68I>K>IN behavior patterns. 8]âYgZclî]XdcYjXi Treatment of conduct Y^hdgYZgiZcYidh]dl disorder, through talking gZYjXZYVXi^kîn^ci]Zg^\]i therapies such as dgWîd[gdciVaXdgiZmdgVc\Z^c cognitive-behavioral i]^h[BG>hXVcl]Zc gZlVgYZY[dgViVh`#I]^h therapy, can be difficult, but early treatment is more hjeedgihi]Z^YZVi]Vii]^h Y^hdgYZgVg^hZh[gdbVWcdgbVa likely to be effective. It is gZhedchZhidi]ZgZlVgYhVcY important that parents are ejc^h]bZcihi]VicdgbVaan involved in the treatment. h]VeZWZ]Vk^dg#

240

Symptoms vary from individual to individual, but they include aggressive behavior, physical cruelty, theft or persistent lying, deliberate destruction of property, and violations of rules, such as playing truant from school.

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Specific learning disabilities (see table, below) affect only one or a few areas of mental functioning and, in many cases, intelligence is not impared. People with learning disability may also have various associated conditions, such as ADHD (see p.238), autistic disorder (see opposite page), or epilepsy (see p.218).

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There are several types of autism spectrum disorders, but the main ones are autistic disorder (sometimes referred to as “classic” autism) and Asperger’s syndrome. Autistic disorder usually appears in early childhood, before the age of about three years. It produces problems in three main developmental areas: impaired social skills, impaired communication, and restricted behavior. Typically, such children fail to respond to their name or to other speech directed at them; avoid eye contact; resist physical contact; start talking late and speak with an abnormal tone or rhythm; show abnormal response to social cues, such as faces and voices; perform repetitive movements, such as rocking; develop specific routines and become disturbed when they are changed; and may be unusually sensitive to sound, light, and touch, but sometimes ignore sensory signals. About half of all children with autistic disorder have learning difficulties and some children develop seizures. However, some children with autism have a high ability in one area, such as rote memory or precocious reading, and, rarely a child may have an

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exceptional ability in a specific area (called savant syndrome), such as mathematics. Children with Asperger’s syndrome tend to have similar symptoms, but in a less severe form. Many children are of average or above average intelligence and develop speech and language skills at the normal time. However, they have

very narrow interests, find it difficult to interact socially with their peers, and are usually inflexible in their behavior and routines. There is no cure for autism spectrum disorders, and treatment is based on supportive education to help a child reach his or her potential.

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I:BEA:C DcZd[i]ZWZhi"`cdlclgîZghdcVji^hb!IZbeaZ See functional magnetic resonance

\gVnbViiZg The darker tissues of the brain, made up of densely packed cell bodies, as seen in the cortex.

244

tissue that carries signals around the limbic system from the hippocampus at one end, to the mammillary bodies at the other.

neurotransmitter in the brain.


^c[Zg^dgXdaa^Xja^ The principal midbrain nuclei of the auditory pathway. ^c]^WîdgncZjgdigVchbîiZg A type of neurotransmitter that stops neurons from firing; see also excitatory neurotransmitter.

B

BG> See magnetic resonance imaging.

bV\cZi^XgZhdcVcXZ^bV\^c\BG> A brain-imaging technique that provides highresolution pictures of brain structures.

bnZaZcXZe]Vadc See medulla.

^ciZaa^\ZcXZfjdi^Zci>F A score based on a range of tests that represents the relative intelligence of a person.

^ciZgcZjgdc A “bridging” neuron connecting afferent and efferent neurons.

êhâViZgVa On the same side of the body as that in which a condition occurs; see also contralateral. >F See intelligence quotient.

@ @dghV`d[[hncYgdbZ A brain disease that is associated with chronic alcoholism. The symptoms include delirium, insomnia, hallucinations, and a lasting amnesia.

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