IELTS Academic Reading Practice Test 375

On 13 September 1848 a young American called Phineas Gage was working near the town of Cavendish in Vermont, where a new railway line was being cut through rock. Gage, who was twenty-five, had charge of a gang of labourers, and his job included setting explosive charges in holes drilled into the stone. After a charge had been poured in, the powder was packed down with a long iron bar.

The bar, about a metre long and three centimetres thick, was driven upwards with great force. It entered Gage's face below the left cheekbone, passed behind his left eye and came out through the top of his skull, landing some twenty-five metres away. Gage was knocked over and lay still for a few moments. Then, to the astonishment of the men around him, he got up and spoke. He was able to walk, with some help, and sat upright in an ox cart on the journey back to the town.

A local doctor, John Martyn Harlow, attended him. The wound was foul, and infection set in; for several weeks Gage hovered between life and death, and Harlow later admitted that he had not expected him to survive. Yet the patient recovered, and within a couple of months he was walking about the town. He had lost the sight of his left eye, and the left side of his face was scarred and partly paralysed. His speech, however, was clear; he knew his own name and recognised the people he had worked with.

His friends, however, soon noticed a change. Harlow, who questioned them some years afterwards, recorded that the injured man had become unreliable, impatient and given to coarse language, and that he could no longer hold to a plan. Acquaintances are said to have remarked that he was no longer Gage. It is on testimony of this kind, rather than on any measurement, that the case has always rested. Harlow's informants were describing a man they had known well against one they found almost unrecognisable, and their account has been repeated in every textbook since.

Gage did not settle back into his old life. For a time he is said to have shown himself and the iron bar to paying audiences. He then took work driving stagecoaches, first in New Hampshire and later in Chile, where he spent several years. In 1859, in poor health, he moved to San Francisco, where his mother and sister had settled. He died there on 21 May 1860, after a series of convulsions, less than twelve years after the accident.

The skull was not buried with the rest of him. In 1867 Harlow, by then practising in Massachusetts, asked Gage's mother and sister for permission to exhume it, and later received the skull together with the iron bar. Both are held today at the Warren Anatomical Museum in Boston, and the skull has been examined repeatedly. It was Harlow's account of the change in his patient, published in 1868, that first suggested a link between the front of the brain and the qualities we call personality.

The suggestion was radical. At the time, many physicians still thought of the brain as an undifferentiated organ, and the popular theory of phrenology claimed to read character from the shape of the skull. A single patient, however striking, could not settle the question, and for a century Gage remained a curiosity: a story told at dinner rather than a piece of evidence. What changed was the arrival of brain imaging, which made it possible to ask where, exactly, the iron bar had gone.

In 1994 a team led by Hanna Damasio took computed tomography scans of the skull and used measurements of its interior to reconstruct the path of the bar. They concluded that both frontal lobes had been damaged, especially in their lower, central parts. Later reconstructions disagreed: one published in 2004 placed the injury in the left frontal lobe alone, and in 2012 a study led by Jack Van Horn combined new scans with maps of the brain's white-matter connections, the bundles of fibres that link one region to another. It suggested that the bar had also cut many of the long tracts joining the left frontal lobe to the rest of the brain.

Historians have meanwhile chipped away at the story itself. Malcolm Macmillan, who has studied the case for decades, points out how little direct evidence there is for a dramatic transformation, and how much depends on a handful of witnesses recalling events years later. Gage held down responsible jobs after his recovery, which sits awkwardly with the image of a man incapable of self-control. The change was probably real, but it was also, in all likelihood, less complete than the version that reaches schoolbooks.

None of this diminishes the case's importance. It is still taught to students of neuroscience, and it still illustrates something that laboratory work struggles to convey. The frontal lobes, which make up roughly a third of the human cortex, are involved in more than movement or sensation. Modern textbooks are more cautious than their predecessors, but the case has not lost its power to unsettle: a man's character altered by a rod of iron, in an age that had no way of photographing the living brain. What exactly the frontal lobes do, and how far their role can be described as control, remains a subject of argument.

The frontal lobes are the regions of the brain that lie directly behind the forehead, and in humans they are larger, in proportion to the rest of the cortex, than in any other animal. They are not one structure, however. At their rear, against the furrow that runs across the top of the brain, lies the motor cortex; farther forward, above the eyes, is the prefrontal cortex, the part that expanded most in human evolution. It is this prefrontal region, and the question of what it does, that has caused most disagreement.

The rear strip of the frontal lobe, the motor cortex, is the best understood. Its task is to issue the commands that produce voluntary movement. Its organisation was mapped in the 1930s by the Canadian surgeon Wilder Penfield, who stimulated the exposed brains of patients during operations for epilepsy and noted which part of the body moved in response. Stimulating a patch only a few millimetres across might produce a twitch of one finger or a movement of the jaw. Penfield found a distorted map of the body, in which the hands and the lips, which require fine control, occupy disproportionately large areas. Damage to this strip causes weakness or paralysis on the opposite side of the body. The motor cortex does not act alone, however: it works with the cerebellum and with deep structures such as the basal ganglia, and the planning that precedes a movement appears to happen elsewhere.

Just in front of the motor strip, on the left side in most people, is a region named after the French physician Paul Broca. In 1861 Broca described a patient who had been unable to say more than a single syllable for many years but could understand what was said to him. After the man died, Broca found damage in this part of the frontal lobe. The discovery was one of the first firm links between a mental faculty and a particular piece of tissue, and it showed that the two hemispheres are not interchangeable: injury to the matching area on the right does not produce the same disability. The region is now known as Broca's area, and it is among the most reliably located language areas in the brain.

The prefrontal cortex has no such single job. It is needed for what psychologists call executive functions: holding information in mind while using it, switching between tasks, resisting distraction and planning a sequence of actions. In the 1990s the neuroscientist Earl Miller and his colleagues recorded the activity of individual neurons in the prefrontal cortex of monkeys trained to remember a visual cue. Some cells fired steadily throughout the delay, as though the animal were keeping the cue in mind. This persistent activity is widely treated as a neural basis for working memory. Patients with damage here often do badly on tests that require them to sort cards by one rule and then switch to another, although their intelligence and their memory for facts may be intact.

A different puzzle emerged from patients whose damage lay lower down, in the orbitofrontal region just above the eye sockets. In the 1990s a team led by Antoine Bechara and Antonio Damasio studied patients with injuries there whose lives had fallen apart: they lost jobs, squandered money and made choices that seemed obviously unwise. On standard tests of reasoning and memory, however, the same patients scored normally. When the team gave them a card game in which they had to learn which piles were profitable, they kept choosing badly. What they lacked was not intelligence but a bodily signal; healthy players developed a faint sense of unease before selecting from a losing pile, and the patients did not. Damasio proposed that such signals are an essential component of practical decision-making rather than a distortion of it.

The frontal lobes are also central to the suppression of impulses. A region called the anterior cingulate cortex, buried in the fold where the two hemispheres meet, becomes active when a person detects a conflict between competing responses or makes an error. It is also involved in the unpleasantness of pain. The prefrontal cortex matures far later than the rest of the brain. Imaging studies show that the bundles of white matter connecting it to other regions continue to thicken through adolescence, and that the cortex itself thins as unused connections are pruned away. This does not mean that adolescents cannot reason or tell right from wrong; the evidence suggests, rather, that they weigh risks differently, especially when friends are present.

How far these findings amount to an explanation of behaviour is disputed. Executive function is a label for a cluster of abilities that may have little in common, and the tests used to measure it are often poor predictors of how people manage their lives. Nor is the prefrontal cortex a single controller. Imaging shows it working as part of widely distributed networks, and the same area may be recruited for quite different tasks. Some researchers argue that its role is better described as the construction of models of the world than as command. What can be said with confidence is that the frontal lobes are not the seat of the self, as some nineteenth-century writers imagined. They are a set of specialised regions whose damage may leave a person's intelligence intact while altering the use to which it is put.

Every few years a death in the ring renews the argument, and every time the argument runs the same course. Doctors point to the damage that repeated blows inflict on the brain; defenders of the sport reply that boxers choose their trade and that other sports are dangerous too; and the discussion ends, as it usually does, with a call for better medical supervision. My view is that this settlement is indefensible, although the conclusion I reach is not the one most campaigners would choose.

The medical objection is not merely that boxing can kill, though it can. A punch to the head sets the skull rotating suddenly, and the brain, which floats in fluid and has something like the consistency of soft butter, lags behind. The movement stretches and tears the fine fibres that carry messages between nerve cells. A single blow can cause concussion, and a torn vessel can produce a haemorrhage that compresses the brain and kills within hours. These immediate risks are well understood and, in professional boxing, reasonably well managed.

The slower damage is the more troubling. In 1928 an American pathologist, Harrison Martland, described a collection of symptoms among prizefighters — slurred speech, tremors, an unsteady walk — which came to be known as punch-drunk syndrome. Examinations of boxers' brains have since found clumps of a protein that also accumulates in other conditions caused by repeated blows to the head. Scarring and the loss of nerve cells are also found, particularly in regions concerned with mood and memory. The disorder now generally called chronic traumatic encephalopathy has been identified in men who died decades after their last fight, and at present it can be diagnosed only after death.

How large the risk is, however, is genuinely uncertain. Serious injuries in professional boxing are rare enough that no single study can estimate their frequency with much precision. Nor are the fighters whose brains reach the autopsy room a random sample: tissue is examined because somebody already suspected damage. Some analyses have found that professional boxers, as a group, do not die younger than other men of their age, a result that is surprising and needs explaining. It may reflect the fitness the sport demands, or the fact that the men who are seriously hurt tend to leave it. The evidence for a large increase in the risk of dementia is suggestive rather than conclusive.

Against this stands a principle that liberals rightly defend: adults may take risks with their own bodies, provided that they understand them. Mountaineers, jockeys and rugby forwards all accept dangers that would appal an insurance company, and no serious party proposes to ban their sports. Boxers are rarely coerced. Many speak of the discipline and self-respect that the gym gave them, and the sport has long offered a way out of poverty for young men with few other options.

Consent, however, is meaningful only where the risks are understood, and here the damage falls on the very organ that does the understanding. A fighter in the early stages of brain injury is the person least able to judge whether he should go on. Nor is the choice as free as it looks. The boxers most likely to be hurt are those with the least education and the fewest alternatives, while the money is earned by promoters and broadcasters who take none of the blows. The conditions of genuine consent — information, competence and freedom from pressure — are unusually hard to meet in this trade.

The case of children is clearer. Amateur boxing for schoolchildren and teenagers is defended as a way of teaching fitness and self-discipline, and much of that can be had without anybody being struck on the head. Governing bodies have changed the rules in recent years: the men's Olympic tournament has been fought without headguards since 2016, after studies suggested that the guards did not reduce the risk of concussion. Tinkering with equipment, though, is not the same as protecting a brain that is still developing. Whatever is decided for adults, a sport whose central aim is to strike an opponent's head seems an odd thing to teach the young.

A total ban, though, would be a mistake, and for a practical reason. Prohibition rarely abolishes a sport; it moves it beyond the reach of inspectors and doctors. Bouts would continue in unlicensed halls, with no doctor at the ringside and no ambulance outside. Every reform that has made boxing safer — shorter championship bouts, a doctor's authority to stop a fight, a period of suspension after a knockout — was achieved by regulating the sport.

My position, then, is this. Boxing in which the head is a target should be prohibited for anyone under eighteen. Claims that it builds character in the young should be treated with scepticism until their supporters produce evidence. For adults, the state should license the sport nationally instead of leaving it to the bodies that profit from it. It should require independent medical assessment before and after every bout, limit the number of rounds and the interval between fights, and pay for a register that follows fighters for decades. None of this will satisfy those who want boxing abolished, but it would reduce harm, which is the proper aim of medicine in public life.

The romantic defence of boxing — that it shows courage, that it is an art — has real force, and I would not want a world without it. What I object to is the pretence that the danger has been brought under control when nobody has counted the damaged brains.