Accidents Will Happen: Traumatic Brain Injury and the Impact on Our Senses

Our Senses: An Immersive Experience - Rob DeSalle 2018

Accidents Will Happen: Traumatic Brain Injury and the Impact on Our Senses

“Maybe when I’d wrecked I had hit my head. Could that be it? Did I have a brain injury? Was I hallucinating? I didn’t believe that.” —A. B. Shepherd, author

All our senses require external agents to penetrate the outer shield that our bodies have evolved to keep harmful agents out. It turns out that these protections and mechanisms have also resulted in keeping many signals from the outer world out of our bodies and hence removed from our brains. But the evolutionary process has resulted in a broad diversity of ways that signals from the outer world get collected and transmitted to our brains so that we perceive the outer world more accurately. For example, skin provides protection from dust, dirt, microbes, and other environmental agents that could otherwise harm us, and our skin acts as a first responder to any physical interaction our bodies have with the outer world, such as air pressure or a bump into something. Ears collect and sift through the sound waves that continually bombard us. Our eyes collect, sort through, and transmit the information from light waves to which we are exposed.

All our perception of the outer world, then, starts somewhat in the same place—in cells that act as the first responders to environmental stimuli. Some senses, such as smell and taste, have relatively simple and uniform ways of doing this. Only one first-response mechanism is involved in these two senses, and that is a lock-and-key mechanism. The variety of things we can taste and smell are just variations on a theme for these two senses. Sight is rather like smell and taste in that the first responder is a cell component (a seven-domain membrane spanning protein that is part of a system) very similar to the cell components used in the first response of smell and taste, except the lock-and-key mechanism isn’t used. Instead, light hits a cell and pops out an associated molecule (retinal) from an opsin receptor embedded in the retinal cell, and this triggers the further biochemical reactions in the rods and cones of the retina. Touch is unique, and it has coopted several kinds of first responder cells, but again, once they are activated what goes on in these cells is just a variation on a theme involving action potential to the brain. Balance and hearing are also closely related to how the cells in these systems act as first responders. In both of these senses, the bending of small cilia or hairs is critical in starting the response. Even nociception (pain) and sensing temperature act on a first-responder cell whose end job is to transduce a signal (action potential) on to the nervous system.

Once the action potential gets initiated and is passed on from the cell, the nervous system reacts pretty much the same way for all of these senses. The main job of the peripheral nervous system is to get the electrical action potential to the brain. The highways of nerves for the senses are all different, and so the senses reach the brain through a variety of pathways. As illustrated in a few cases, the signals go to very different parts of the brain for the various senses. What happens in the brain is complex, and it is important to understand that the senses aren’t simply projected onto the brain by action potential. In fact, a signal from a single odorant will reach many parts of the brain, and the perception of that odorant is actually the combination of action potential going to varied parts of the brain where perception is assembled by thought processes. To tell the story of our senses thus far, I have used the senses of animals and strange human sensing.

Researchers have examined brain function and its impact on the senses in yet another way. The nature of specific brain injuries and how people behave as a result of such trauma or surgical operations can illustrate how clever and plastic our brains are when dealing with sensory input. The approach even has a special name: the clinico-anatomical correlation method. I have already mentioned Wilder Penfield’s open-brain surgery experiments. The examples in this chapter will illustrate how the mixture of information and sensory detritus is processed in the brain and becomes perception.

One never knows when an accident is going to happen. Railroad construction foreman Phineas Gage didn’t know when he awoke one September morning in 1848 in Vermont that later that day an explosives accident would cause a four-foot-long dynamite tamping rod to blast straight through his skull and out. The result of Gage’s accident on his personality is legendary at best and more than likely mythical. When he died, his skull was preserved and deposited in the Francis A. Countway Library of Medicine at Harvard. The archived skull of Gage allows contemporary neuroscientists the opportunity to analyze the connections in the brain that the tamping iron tore through to better understand the impact on the parts of the brain that might have been damaged.

And Franz Breundl, known to science as Mr. B., had no clue when he awoke on a May morning in 1926 in Germany that later that day he would be exposed to overwhelming amounts of carbon monoxide from the smelting apparatus he worked near. The next several months of his life consisted of going in and out of hospitals because of the incredibly bizarre symptoms he suffered as a result of the lack of oxygen to his brain. Mr. B. became a psychological celebrity because his short-term memory had been nearly obliterated by the accident.

Eminent British musician and musicologist Clive Wearing, another unfortunate psychological subject, woke up on a March day in 1986 feeling lethargic. He had no clue that he had contracted a Herpes simplex virus infection. Not long after the original diagnosis, his central nervous system became infected, and some neural tissue was destroyed. Wearing cannot form short-term memories as a result and has experienced amnesia for some of his stored memories.

And on the September day in 1953 that Henry Molaison (also known by the moniker H.M.) went into surgery at Hartford Hospital in Connecticut to have an epileptic condition corrected, he had no indication that he would wake up with no short-term memory. His neurosurgeon, William Beecher Scoville, had performed a bilateral medial temporal lobe resection, an operation designed to short-circuit the left and right sides of the brain to prevent epileptic seizures.


Figure 10.1. Phineas Gage, Louis Victor Leborgne, Henry Molaison, and Clive Wearing, along with the brain tracts of Gage, Leborgne, and Molaison as deduced in de Schotten and colleagues’ 2015 study. The only known photo of Leborgne is one of his pickled brain in a jar. After de Schotten et al. (2015).

Hundreds of cases like these four (fig. 10.1) have been documented and studied since brain anatomy became an interesting and important area of inquiry two hundred years ago. Almost two centuries of these cases have serendipitously added to the store of knowledge neuroscience has accumulated about brain structure and function. The French physicians and scientists in the 1800s were among the most skilled anatomists of their time. Their inquiries in the latter 1800s contributed much to what we know today about neuroanatomy. These French researchers also used patients with accidental (or, in some cases, self-inflicted) brain trauma to study the brain.

At a Paris scientific meeting in 1861, Ernest Aubertin, a Parisian physician, presented a paper describing an unfortunate suicide case. In addition to being a physician, Aubertin was also interested in brain function and language and the brain specifically. A Monsieur Cullerier, who had shot himself in the head, was rushed to the hospital where Aubertin was attending. This self-inflicted wound was terrible; part of Cullerier’s skull was destroyed and eventually removed by Aubertin, resulting in the brain being exposed. Apparently, Cullerier was conscious during the efforts Aubertin took to save his life, because he could speak. Aubertin then did what Wilder Penfield would do a century later: he placed a surgical spatula on a region of the brain he thought might be involved in language and speech. He asked Cullerier to speak while he applied pressure to this specific region of the brain with his spatula. As Aubertin described in his talk in Paris, Cullerier’s speech consisted then of “a word that had been commenced [being] cut in two.” When he released the pressure, the capacity to say words returned to Cullerier. Aubertin had manipulated a part of the brain that had something to do with speech. Unfortunately, Cullerier did not survive the day’s events.

A few days later, Paul Broca, another French physician who was at the talk, attended to a patient named Louis Victor Leborgne. Leborgne, who was also known as “Tan” (he used the syllable “tan” over and over when he tried to speak), had been in the hospital for most of his adult life as a result of several illnesses, one of which resulted in a loss of speech, known as speech aphasia. He was admitted to Broca’s care because he had contracted gangrene of the leg, a condition that Broca could not alleviate, and poor Leborgne died as a result of the infection. Broca, remembering Aubertin’s talk, wondered why Leborgne had lost the faculty of speech, so at autopsy, he dissected the brain of his unfortunate deceased patient. During dissection, Broca discovered that Leborgne’s brain had a lesion near the posterior end of one of the gyri on the left side of the brain called the inferior frontal gyrus. Two years later, Broca encountered another patient, one Monsieur Lelong, who had had a stroke that resulted in a speech aphasia similar to that experienced by Leborgne. This patient died soon after, and Broca was able to examine Lelong’s brain, too. By studying the brains of several more subjects with the same speech aphasia, Broca was able to pin down this area of the brain as one of great significance in the brain for speech, which now carries Broca’s name. About fifteen years later, after studying many patients with speech aphasia, the German physician Carl Wernicke was able to associate another region of the brain responsible for language apprehension. This area now carries Wernicke’s name (fig. 10.2).

Paul Broca also liked to save brains. Over his career he preserved and archived the brains of 292 men and 140 women for his research. His own brain was preserved and is famously described in Carl Sagan’s Broca’s Brain: Reflections on the Romance of Science. The preserved brains and the skulls of people with extreme trauma can be examined by modern brain imaging techniques. In a 2015 study by Michel Thiebaut de Schotten and colleagues, three of the very famous brains I discuss above were examined with computed tomography (CT) scans and magnetic resonance imaging (MRI). Both technologies have gained great popularity among neurobiologists over the past decade. The formalin-preserved brain of Leborgne was also visualized using MRI.


Figure 10.2. Location of Broca’s area and Wernicke’s area in the brain.

CT scans are produced by using a large number of independent X-ray images taken from different angles. The X-ray images are then reconstructed using computer technology to give an overall database that can produce cross-sectional images. The technology can therefore produce three-dimensional reconstructions of the object being scanned from the inside by a mathematical procedure called digital geometry processing. Phineas Gage’s skull was examined using this approach, and his long-vanished brain was reconstructed by using the CT scan and information from 129 healthy individuals’ real brains. The idea that Thiebaut de Schotten and his colleagues used is that the healthy individual brains and where they sit in the skull would tell them where in Gage’s brain the rod had blasted through. Specifically, these researchers could then reconstruct which of Gage’s neural pathways were obliterated by the accident.

H.M.’s brain was examined using MRI more than twenty years before his death, and these images were archived for future use in 1993. In addition, his brain was removed after his death in 2008. It was then that H.M. became known as Henry Molaison, because medical professionals do not use the name of living subjects in their publications or discussions. Molaison’s brain was preserved in gelatin and physically sectioned into 2,401 thin slices that were then preserved cryogenically for future research. Each section was subsequently photographically digitized so that the brain could be reconstructed in three dimensions. A web-based atlas of Molaison’s brain now exists and can be used as a frame of reference for science. Looking at the images and reconstruction is quite an experience, especially knowing what this person in life contributed to our knowledge of the brain. Take a look at it yourselves and perhaps you will be as impressed with H.M.’s brain as Carl Sagan was with Broca’s brain.


Magnetic resonance imaging (MRI) technology takes advantage of how atomic nuclei in molecules and cells placed in a strong magnetic field will absorb and emit radiofrequency energy. These radio waves are emitted because in the nuclei of each atom (such as hydrogen) there are protons that act like tiny magnets. In a normal tissue the nuclei are arranged randomly, but by changing the direction of magnetic fields around the nuclei, the protons in the nuclei will change directions, too, and align to the magnetic field. When the magnetic field is turned off, suddenly the protons return to their original orientation, and the amount and direction of change of the nuclei can be detected by release of energy. This energy has wavelengths on the order of 3,000 hertz up to 300,000,000 hertz (remember that the human hearing range is between 20 hertz and 20,000 hertz) and is the domain of radar waves. The energy released in the guise of radar waves is collected by a set of antennae placed around the object being imaged, and a computer takes the numerical data about the radar emitted and reconstructs the object. More hydrogen atoms (that is, the more water) in a specific kind of tissue or in a specific place in the object will give different wavelengths than an area with fewer hydrogen atoms. So, the image can be quite detailed and give information about an object such as the knee, hip, or brain without having to dissect the tissue or cut into the body.

The work of de Schotten and his colleagues illustrates that it is possible, with some effort, to reconstruct the brain lesions that afflicted Gage, Molaison, and Leborgne. In fact, their reconstructions were exquisitely precise. They used twenty-two landmark brain connections and were able to determine the degree of damage to each of these landmarks in the three brains. Although earlier work on Gage’s skull indicated extreme damage to the frontal to cortical regions of the brain, the 2015 analysis expanded this gross observation. Because the twenty-two landmarks used are focused on connections of different parts of the brain to others, the researchers could determine whether lesions other than the obvious large frontal and cortical ones existed. Among the several disrupted connections relevant to our examination of the senses, Gage’s frontal orbitopolar tract was about 35 percent destroyed. This tract is responsible for connecting the auditory, olfactory, visual, and taste inputs to memory. More than likely Gage’s memory of his versions of madeleines was wiped away by the injury he sustained. Molaison’s brain connections based on the twenty-two landmarks were the least disrupted of these three famous brains, and this can probably be attributed to the precision of the surgery he underwent that eventually caused his extreme lack of memory. From the surgical records and the MRI done in 1993, it is well known that Dr. Scoville removed several parts of the brain, including the medial temporal-polar cortex, the amygdaloid complex, the entorhinal complex, some of the dentate gyrus, the hippocampus, and other smaller parts of the limbic system. But de Schotten and colleagues’ work showed that Molaison’s surgery also affected six of the connections that the landmarks could detect. One of these connections is particularly important to the senses and involved the anterior commissure. This neural connection affects the olfactory response and indeed could have affected Molaison, because he had great difficulty discriminating smells after his operation. In two kinds of olfactory tests to identify common items, his accuracy was terrible. He could, however, identify the items by sight, which means that he had not lost the memory of what the things were; rather, as a result of the operation, he was simply terrible at smelling (fig. 10.3). For instance, when asked to identify a clove smell, Molaison answered “fresh woodwork” on the first test and “dead fish washed ashore” on the second.

Leborgne’s brain was the most affected by the lesion he sustained early in life. Included in the lesion was not only Broca’s area but also several neural tracts that connect it to Wernicke’s (fig. 10.1). Other parts of the brain were also affected. Much of the impact of Leborgne’s lesion to his behavior and his senses is not known, because Broca first attended to him as he was dying owing to gangrene of the leg. But given the extent of the lesion to his anterior commissure and to nearly every one of the twenty-two landmark connections on the left side of his brain, Leborgne’s life post-trauma must have been a nightmare with respect to his senses. To add insult to injury, in presenting their results, de Schotten and colleagues show photos of Gage sitting holding his famous tamping iron (the damage to his head is evident) and Molaison sitting with a wry smile on his face for his portrait, but poor Leborgne’s only lasting image is of his brain floating in a jar full of formalin.


Figure 10.3. H.M.’s smelling acuity. (Redrawn from Eichenborn et al. [1983].)

So how do neural connections we use from the information our senses gather integrate information from multiple sources to formulate our perception of the outer world? Much of the rest of the story about the senses involves multisensory integration, or crossmodal interactions. These interactions are important for fast, accurate, and sometimes lifesaving interpretation of sensory information (see Chapters 18 and 19).

These famous brains are only a few of the brains that have advanced our understanding of brain injury using the clinico-anatomical correlation method. One reason we have so much information on brain injury and its impact on our senses is that our brains are in the wrong place on our bodies. Evolving to have our brains balanced on our shoulders well away from the center of gravity is a cruel joke of nature. Our brains could not have been better placed for maximal damage when we lose our balance or fall. Actually, it is not so much that our brains were “placed” there, but rather that other things happened that demanded that our brains reside in our heads on our shoulders. Brains were less in the wrong place in our ancestors who did not walk upright and therefore kept their brains closer to a center of gravity nearer the ground. Our species’s evolution to upright locomotion dictated that our brains ended up in the worst place possible (other than in our feet, maybe) for keeping them from damage. And humans have figured out some innovative, imaginative, tragic, and downright stupid ways to put brains in situations to be injured. The fact that our brains are prone to injury means that our senses are also prone to disruption, and as we have seen, through examining brains of people with these injuries, we can learn a lot about how the senses and the brain work. We now turn to two of these kinds of injuries that are a scourge of modern life: concussion and battleground head trauma.

On a visit to the Ontario Science Centre in Toronto, I visited the Hockey Helmet Head Hit display in the Human Edge exhibit hall there. This hall is a wonderful example of integrating entertainment and science education in activities for children. The Hockey Helmet Head Hit contraption has a huge red hammer poised to slam into a crash-dummy head with a hockey helmet on it. Pull the hammer back to simulate collisions up to about 20 feet per second (12 miles per hour, or sprinting speed for a hockey player), and let it slam into the head. In addition to offering the thrill of swinging a huge hammer with levers and cranks, the exhibit uses the national pastime of Canada to make a point about how delicate our heads are. The foam head is mounted on another contraption that measures the concussive force delivered by the hammer. And if that weren’t enough, the exhibit allows you to choose where the head gets smacked—on the side or in the front. After whacking the crash dummy head a few times at different speeds, one realizes just how dangerous contact sports like hockey are, even with the proper protection. As I played with the contraption, I shuddered at the damage done to the brains of great players like Gordie Howe or Bobby Orr before the helmet era in the National Hockey League. There is no doubt that hits to the head at this speed and in the right place can cause concussive damage to the brain, and indeed, a lot of modern brain research has focused on concussion, how to diagnose it, and what it does to our senses.

About three million adults and adolescents incur brain-related injuries every year while playing sports. Concussions are only one of eight ways to cause traumatic brain injury, or TBI, as a result of impact of the head with a moving or stationary object. Barry Jordan, chief medical officer of the New York State Athletic Commission and medical adviser to the National Football League (NFL), defines concussion as “a complex pathophysiological process that affects the brain and is induced by traumatic biomechanical forces.” Sports-related concussion is part of a growing yet underrecognized epidemic in Western countries where contact sports are played, such as American football or, for that matter, Aussie football, hockey, soccer, boxing, rugby, and even simulated martial arts. Many readers will be well aware of the symptoms of a concussion—dizziness, nausea, headache, and loss of memory. Not much is known about threshold of the impact and what concussion is. Even that 12-miles-per-hour hit to the crash-test-dummy head in the Ontario Science Centre might not cause concussion, despite the appearance that any brain inside of a head hit that hard would be damaged.

Because most injuries happen as a result of accidents, the details of many brain injuries are not known. This is why concussion research has focused so heavily on sports injuries. Nearly every concussion in the NFL in the past decade has been documented because of the popularity of American football on television. Researchers do know, by watching films and counting the number of concussions in NFL players and where the players were hit, that with professional players, the biggest damage comes from hits to the side of the head. For children playing football, hits to the top of the head cause the damage. This discrepancy is probably because as one learns more and more about how to play football, one simply does not lower the head readily to hit others, a lesson I learned the hard way as a high school freshman. My football concussion occurred on a kickoff where I wildly threw my body headfirst into the ball carrier. This event taught me to keep my head up and hit and tackle more with my center of gravity, which is with my shoulders and hips square on the target. Unlike the story I told earlier about lacking the athleticism for baseball, my football days ended when I realized I didn’t have enough meat on my bones to make hitting with my center of gravity effective. Oh, and by the way, if you are wondering if I ever boxed and got a concussion, yes, I did box—once. My ratio of delivering legal blows to low blows was so bad that the coach asked me to retire my gloves after my first practice. So, my concussions ended when I was in high school, but I can still remember them (at least parts of them), and they were not pleasant.


There are three ways to study traumatic brain injury (TBI). The first is to study those individuals who come in for treatment of brain injury. One important context for studying TBI is how the injury is incurred, and in many cases brought to the hospital, the precise nature of the injury is not known. The second approach is to use the crash dummy approach like the one in the Ontario Science Centre. The machine used there is not so cleverly named HIT (head impact telemetry). Most research is done this way, but some researchers use model organisms, usually rodents. One device called the FPI (fluid percussion injury) rapidly injects fluid into the skulls of the animals, simulating the role of fluid movement on the impact made during brain injury. Another machine called CCI (controlled cortical impact) uses a device like the one in the novel (and subsequent movie) No Country for Old Men that the character Anton Chigurh uses to dispatch his victims. The animal is secured in a stationary position, and a small rodlike apparatus that uses pneumatic pressure extends a piston in the rod that plunges into the skull and into the brain. The depth of the injury and the velocity of the rod can be tightly controlled by the researchers. Another device called the Feeney weight drop controls the dropping of a weight onto the skull of the target rodent. In a variation of the Feeney weight drop called the Marmarou weight drop, a small disk covers the head of the rodent to prevent skull breakage or fracture. The final research tool addresses the exposure of military personnel to explosive devices in the conflicts where they serve. Hence, some of these devices simulate blast injuries by actually setting off a blast with a rodent inside the device.

When a person suffers a concussion, the biomechanical force that disrupts the normal positioning of the head results in rotational movements of the brain inside of the skull. The brain moves in relation to all of the bones in the head, except for structures of the face like the cartilage of the nose. The upper reticular formation of the brain is at the end of the brain stem near where the pons is in the brain stem. It is in a highly conserved part of the brain, is found in all vertebrates, and contains several nerve clusters called nuclei that carry extremely important information to and from the brain. The neural nuclei that course through this part of the brain receive impulses from, and feed to, many other brain regions. This brain architecture makes sense, because after all, this is an ancient part of the brain that mediates very basic physiological and motor control. Electrical impulses from the optic nerve travel first to this formation in the brain to be dispersed to other regions of the brain. Signals from the auditory system do the same, making their first stop in the brain smack in the middle of this cluster of neural tissue. In addition, impulses from the tactile, nociception, and temperature-sensing nerves also pass through this region. What happens is the biomechanical force introduces movement to the brain writ large, which is tethered on the spinal cord. This movement creates torque on the upper reticular formation, that then will incur injury. Often the brain responds by shutting down for a while (loss of consciousness). If that weren’t enough, the movement of the brain also results in contact of the brain with the interior of the skull as the brain reverberates from the force of the initial contact. This movement has been described as swirling, and it causes bumping of the brain against protrusions on the inside of the skull that normally do not make articulated contact with the brain.

Perhaps even more dangerous are the effects of brain trauma that occur after the initial injury. These secondary injuries are the result of bruising of the brain and damage to tissues of the brain where contact was made with the interior of the skull and to movement of the cerebrospinal fluid. The damage includes tissue bruising of the brain and deformation of the brain where impact with the inside of the skull occurs. Where deformation occurs, the cells there are prone to dying and their loss of function is expected. Blood vessels get sheared and cause the nerve cells they feed to become nonfunctional. The physical damage to glia and axons (two kinds of neural cells in the brain) causes a cessation of neural activity in those cells that are sheared. Although the primary traumatic brain injury event does not cause breakage of the axons, the impact to axonal structure results in extreme stretching of the axons to such limits that the electrochemistry gets messed up. The cells work overtime to overcome the problem and well up and eventually break. Technical advances like CT scans and MRIs cannot detect these kinds of lesions, so researchers use yet a third technical advance called diffusion tensor imaging (DTI) to visualize shearing of axons. This method is pretty spectacular, because it can map the position of specific neural tracts in the brain. It is a magnetic resonance technique, but unlike MRI, which maps overall activity in a brain area, DTI maps the specific tracts that course through the brain. The technique relies heavily on computer processing and is quite expensive. DTI, however, can detect these breaks in the axons as a result of injuries.


Imagine a soccer ball glued on the tip of the handle end of a golf club and placed inside a basketball where the inside surface of the basketball doesn’t touch the outside of the soccer ball. As long as there is no extreme motion of the golf club, the soccer ball inside the basketball makes little or no contact with the inside of the basketball. But if you jar the golf club hard enough, the soccer ball will bounce off of the sides of the inside of the basketball. I want to say it bounces like a pinball, but not really, because the brain’s movement is dampened by the way it is tethered on the spinal column and our bodies. The front of the brain hits the front of the inside of the skull, makes hard contact sometimes with the inside of the orbital ridges (those bones that encircle our eyes) of the skull, and then bounces off. The back of the brain then strikes the back of the inside of the skull. These are called coup and contrecoup injuries, respectively.

A lot of traumatic brain injury research occurs in a military context. From 2000 to 2011, more than 233,000 TBI cases were reported in American servicemen and women serving in the Middle East. Improvised explosive devices and other blasts caused the overwhelming majority of head injuries. Sadly, heads are incredibly vulnerable to injury with explosions and gunfire. These tragic injuries, added to millions of sports injuries, have made TBI a major source of study and information about how injury affects our sensing the outer world. Obviously, bruising the brain and traumatizing the major throughway of information from the sense collection organs like the eyes, ears, tongue, and nose to the brain will affect lots of neural functions generally and how we perceive the outer world specifically.

Nearly every sense is affected by TBI. It has been known for some time that smell is diminished as a result of concussion and more severe kinds of TBI. Trauma to the nose itself has an obvious impact on the sense of smell. The problems caused by TBI on the olfactory bulbs, the neural tracts from the bulbs to the rest of the brain, and the other parts of the brain involved in interpreting smell like the thalamus and amygdala also impact olfactory loss. Loss of olfactory perception is used right after particularly nasty collisions in sports to assess the possibility of TBI. But the degree to which olfactory loss can be used to diagnose concussion or other brain injury has been controversial. However, two studies conducted in 2015 on domestic TBI patients (one in Australia and one in Canada) suggest that between 50 and 66 percent of patients who are treated for TBI have olfactory dysfunction. Nearly half of these patients are extremely affected in their olfactory acuity. In the United States, servicemen who had suffered TBI in Afghanistan and Iraq as a result of explosions were studied for the impact of their injuries on olfactory acuity. The conclusion was that it was possible to correlate actual visible brain injury with olfactory dysfunction only 35 percent of the time. Part of the problem in pinning down the correlation of olfactory dysfunction and TBI involves the tests given to detect the dysfunction. An oddly named tool called Sniffin’ Sticks is one of the more popular tests used, but it might behave differently than, say, the University of Pennsylvania Smell Identification Test, or UPSIT.

The clinico-anatomical correlation method has been used only sparingly on TBI patients in the context of olfaction. But the development of DTI technology may offer an important method for studying TBI and its impact on the neural tracts. Patients who have suffered frontal lobe injuries as a result of TBI often have olfactory and gustatory hallucinations that consist of really bad smells or tastes. These dysfunctions substantiate the well-known connection of these two senses with the frontal lobe of the brain. Taste is probably the least studied sense in the context of brain injury and concussion, but some readers who have had a concussion or who have bumped their head will probably remember a metallic taste in the mouth. This sensation is a taste hallucination called parageusia. The metallic taste most likely isn’t caused by a dysfunction of your taste receptors on your tongue or of connections to the brain involved in taste. Instead, the impact is most likely on your olfactory system in the brain, and it reverberates in the taste perceived by your brain. (There is a lesson here that we will return to when we delve into how the senses interact with one another in Chapter 11.) Complete loss of taste (ageusia) as a result of TBI would indicate some dysfunction in the sense of taste itself.

Another poorly studied sense in the context of TBI is touch. It is known, however, that TBI damage to the parietal lobe of the brain impairs the sense of touch. This damage will cause tingling of the skin and other touch-based sensations. The parietal lobe is where the impulses from our tactile organs (the many kinds of touch receptor cells in our skin) are processed.

The impact of TBI on vision has been studied in a cohort of servicemen injured by blasts. While the study shows that blasts result in all kinds of vision impairment, oculomotor dysfunction is quite common. This motor-driven phenomenon involves the movement of the eyes in proper vision and results in problems with focusing and with aspects of reading. Computerized tracking of eye movement by individuals affected by blast-induced TBI is being developed as a diagnostic tool and to assess improvement of the visual system in TBI injuries after therapy. Other symptoms of TBI on vision affect so-called higher-order functions, and these include sensitivity to light, reading deficits, and reaction time to sight events. The impact on reading is important because it suggests that the problem isn’t entirely related to motor skills. Some TBI subjects complain of losing their place while reading and of not retaining information from reading. These symptoms suggest problems with integration of the information from the eyes as a higher-order process.

Hearing loss in people who have had concussions is also documented and in some instances is used to diagnose brain damage. In the context of TBI and military personnel, it is not difficult to imagine the impact on the auditory and vestibular systems of being exposed to explosive devices. In one of the first systematic, comprehensive analyses of the impact of explosions on American servicemen, Sarah Theodoroff and her colleagues evaluated more than eight hundred publications for information on the impact of explosions on hearing in military personnel. Their results indicate that hearing loss is indeed an outcome of exposure to explosions. One interesting result is that tinnitus, a persistent sound in the ears when there is actually no source of sound, could not be disentangled from hearing loss in the study subjects.

Tinnitus can be divided into two major kinds of problems. The first is pulsative tinnitus, and this occurs when the heartbeat is amplified and can be heard by the person. All other tinnitus phenomena are classified as nonpulsative tinnitus. There are many causes of both kinds of tinnitus, and military personnel exposed to explosive blasts are affected by all of them. These include direct trauma to the inner ear—temporal bone fracture, labyrinthine concussion, disruption of the ossicular chain (hammer, anvil, and stirrup), barotrauma (change in air pressure), and noise trauma. In addition, trauma to the neck and the nervous system (such as the auditory nerve leading to the brain or the areas of the brain involved in processing auditory signals) will also result in tinnitus. As these examples of trauma to the brain show, injury can have a profound impact on our senses. Healthy brains lead to proper sensory perception, but there are other ways to injure or physically alter the brain that will also lead to sensory dysfunction.