Salvi moved to SUNY Buffalo in 1987. He had begun to consider a new theory, in which hyperactivity originated in the central nervous system rather than in the inner ear. He collaborated with Dr. Alan Lockwood, a neurologist at SUNY Buffalo. “Initially, we were going to do images of the brains of people who are normal and people with tinnitus,” Salvi recalled. “But when you are doing any sort of brain-imaging project what you have is all the other confounding variables”—such as age, gender, and head size. Shortly after Salvi’s arrival, he met with a group of local residents who had formed a tinnitus support group. One person, Salvi recalled, got up and said, “ ‘Dr. Salvi, I stick my tongue out and my tinnitus gets louder.’ I looked at the person, and my eyes started to wobble around in my head, and I thought, What’s going on with this person?” Then a second person got up and said, “When I clench my jaw, my tinnitus gets quieter.” Salvi told me, “A light bulb went off in my head. It seemed like what we should be doing with imaging studies was not comparing normal people to those with tinnitus but, rather, having these people come in and get scanned when their tinnitus was quiet, and then again while doing something like sticking out their tongue, which made it louder. In the same patient we can determine what part of the brain was changing.”

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The first PET-scan results were unexpected. Whereas a real sound will activate areas on both sides of the brain, “we found a big increase in activity in just one side of the brain,” Salvi told me. If the origins of tinnitus were in the ear, it would activate both sides of the brain; when only one side appeared active, it suggested that the tinnitus originated in the central nervous system. The brain became hyperactive in an effort to compensate for the reduced input, generating phantom sounds. This conclusion, which was published in the journal Neurology in 1998, began to change the way that researchers approached tinnitus. Still, there is no convincing explanation for why only one side of the brain shows activity in people with tinnitus, particularly since it doesn’t appear consistently on either the right or the left side.

Another oddity is a type of tinnitus called “gaze-evoked,” in which ringing in the ears is occasioned or worsened by moving one’s eyes to the right or left, or up or down. Case studies reported gaze-evoked tinnitus in patients who had had a tumor on the auditory nerve which was surgically removed. “The patient goes completely deaf in that ear, and then he starts hearing the phantom sound of tinnitus in the ear which is deaf,” Salvi explained. “The ear isn’t even connected to the brain anymore.” When patients with gaze-evoked tinnitus were given PET scans, some showed activity in the angular gyrus, an area of the brain near the auditory cortex; others had activity in the brain stem. “The bottom line was that you perceive tinnitus in your deaf ear but there is no nerve there, no input,” he went on. “So it has to come from various parts of the brain.”

Jean-Luc Puel, a professor of neuroscience in Montpellier, France, is not convinced that tinnitus always originates as a phantom sound in the brain. He has studied rats and guinea pigs that were treated with high doses of aspirin or exposed to noise trauma. Puel believes that glutamate, a neurotransmitter, is inappropriately processed in the cochlea, which causes abnormal impulses from the acoustic nerve, and that by infusing the animal’s ear with a drug that blocks the action of glutamate he can reduce the tinnitus. More broadly, Puel argues that the disorder may have multiple causes. “This conflict between peripheral and central origin of tinnitus is simplistic,” he said. “To have perception of tinnitus, which is subjective, you need a brain.” Puel allows that his view is contrarian, adding, “I like to arrive at scientific meetings and disturb people.” But he also believes that different causes of tinnitus may reflect differences in biology. “There is no one type of tinnitus,” he told me.

When I visited Salvi’s laboratories, Edward Lobarinas, a researcher, was conducting experiments on rats that had been subjected to acoustic trauma. Lobarinas showed me a Plexiglas platform with an embedded pressure sensor attached to a computer. On top of the Plexiglas was a metal mesh canopy. First, a normal rat that served as a control was caged under the canopy and the entire apparatus was placed inside an acoustic chamber, into which Lobarinas delivered a steady noise with a narrow frequency range. “It’s a continual sound in the background, a sort of sh-h-h,” he said. This was interrupted by a loud bang. “The animal startles,” he said, and this sent a measurement of the movement through the pressure sensor to the computer screen, which showed a sharp spike.

In the next step, the sudden bang was preceded by a silent gap in the noise. This time, the rat had a much smaller startle reflex, seen on the computer as a low peak. “When you have a silent gap before the loud noise, you’re less startled,” Lobarinas said. “It’s like when it’s dark and you’re in your room and a bogeyman jumps out at you. You have a maximum startle. But if, before the bogeyman jumps out, the door is slowly creaking open, you sort of know the bogeyman is going to come out, and that decreases your startle.”

When a rat with induced hearing loss underwent the same experiment, it had a robust startle reflex even when the loud noise was preceded by silence. “The rat has tinnitus,” Lobarinas said. “It can’t tell us, of course, but it has constant buzzing in the ear, and we know that although it hears, it doesn’t perceive the silent gap because of tinnitus. So its startle reflex is not attenuated. It doesn’t hear the door slowly creaking open, just the bogeyman.”

Total funding for tinnitus research in the United States has recently been little more than three million dollars. “People don’t realize how complicated tinnitus really is,” Salvi said. “It’s in the same league as epilepsy and many neurological disorders. But so little money is spent on it, so there is almost no scientific database you can build on.”

Perry Jefferies, now a forty-eight-year-old retired Army first sergeant, entered Iraq with the 4th Infantry Division in April, 2003, as part of the initial invasion of Operation Iraqi Freedom. “We moved from Kuwait to Baghdad,” he told me, when we spoke by phone, “and then went up to Tikrit, until we were posted at the Iran border.” Jefferies escorted and resupplied units moving into battle. After one firefight, as his convoy was evacuating an injured Iraqi soldier, U.S. helicopters fired missiles into enemy ammunition bunkers. “We were right there at the explosions,” he said. Later, as his convoy was resupplying a unit near the border with Iran, a massive explosion at a nearby Iraqi fort rocked his Humvee. “We think that looters set it off,” he said. “It fried the fort.”

Although hearing trauma was most intense in combat, Jefferies said, he had been exposed to repeated noise during his many years in the military. During basic training, while on the weapons range, “we only wore one earplug, so you could hear the instructor when he yelled at you.” While learning how to fire a .50-calibre gun from an armored personnel carrier, he recalled, “we had no hearing protection. Afterwards, blood was coming out of one of my ears.” He had ruptured his right eardrum. Even so, the close-range explosion at the fort was different from anything he had experienced before. “I felt like I was under water for a few minutes,” he said. Since that time, he has been afflicted with tinnitus. “It is a high, steady electronic tone,” he told me. “And my ears feel heavy and blocked.”