Modern Life, Strokes, and the Senses: The Impact of Strokes and Other Brain Damage on Sensory Capacity

Our Senses: An Immersive Experience - Rob DeSalle 2018

Modern Life, Strokes, and the Senses: The Impact of Strokes and Other Brain Damage on Sensory Capacity

“I had a stroke in December of ’99, and it affected my left side—my fingering side.” —Johnny Gimble, Western swing fiddler

What specific kinds of physical damage can occur to the auditory and vestibular systems? When intense sound or air pressure from an explosion comes into the inner ear from the outer ear, it passes across the tympanic membrane, or eardrum. This structure is a thin sheath of skin separating the middle ear from the inner ear and is the first structure that collects sound waves from the outer world as the sound waves hit it and cause it to vibrate. Then the whole contraption of the inner ear starts cranking. Sometimes the intense pressure or strength of the sound waves can cause the thin sheath of skin to become perforated or tear. The effect on the eardrum is a lot like the effect on a snare drum that has been perforated by an overenthusiastic drummer (the late Keith Moon of the Who, who destroyed hundreds of drum kits, comes to mind): the vibrations no longer are true to sound. Another effect is on the stereocilia that line the inner ear and vibrate when affected by sound waves.

The bending of these tiny hairs triggers reactions inside the auditory neural cells, and the signals that these cells send to the brain are regulated via a neural loop in which feedback from the brain adjusts the information coming into the brain. Just like a guitar too close to an amp, if the brain does not adjust the loop, feedback will occur and unwanted sounds will be amplified. The feedback is caused by self-oscillation of stereocilia, and such oscillations in the inner ear can result in tinnitus (Chapter 10). Explosions can break the hairs and kill the stereocilia cells, another way that the feedback can be disrupted in the inner ear and tinnitus can be produced. The receptor cells themselves can be damaged by extreme sound or pressure. Such damaged cells are specific for certain wavelengths and cannot regenerate, so if they are damaged or killed there is no recovering, and deafness to certain wavelengths of sound will ensue. In addition, the lack of function of these receptor cells disregulates the information coming into them, and this will cause tinnitus in addition to the lack of hearing at specific wavelengths. The sounds, in this case, are generated by the disregulation and don’t exist except in the head of the beholder.

Hearing can be harmed by insults from other wavelengths in addition to injuries as a result of explosions and concussive hits to the head. We have already discussed the loudest sports stadiums in the world (Chapter 7), but we all experience a lot of ambient noise in our daily lives. This is noise that our ancestors even 500 years ago did not have to confront. Some of the common sounds we hear every day that were nonexistent even 150, 100, or 50 years ago include blenders, coffee grinders, automobiles, televisions, sirens, and ringing phones. Other modern sounds are occupational, such as a plane taking off, a power drill or chainsaw being operated, the sounds in a loud factory, or a subway’s brakes screeching. There are recreational exposures to noise, including stock cars or the noise from a Who album as listened to through headphones. And speaking of the Who, incredibly loud concerts like theirs are a major source of entertainment for people. Within this rock group, exposure to their own music resulted in hearing loss of three of their four original members (Pete Townshend, Roger Daltrey, and John Entwistle; the fourth member, Keith Moon, died at the age of thirty-two of excess before it could be determined that he lost his hearing).

If all of these modern sounds we are exposed to lasted only a few seconds, then whether the sound caused traumatic hearing loss, temporary hearing loss, or could be assumed to be safe would depend only on the strength of the sound as measured in decibels. According to Boris Gourévitch and his colleagues, though, damage to hearing is caused not only by how loud a sound is but by how long one is exposed to it. To assess the impact of specific modern-day sounds on the sense of hearing one needs to compute what is called a Leq, or an equivalent sound level, for different sources of sound.


Figure 11.1. Typical sounds and Leq (equivalent sound level).

This technique for quantifying the sounds we hear in everyday life is based on the decibels the sound makes and the average amount of time each noise is experienced during the day. Blenders and power drills are used in bursts, but power drills have higher Leqs than blenders because they are louder. Two minutes of sound from a blender has nowhere near the Leq level of a power drill sound for eight seconds. The Leq level of the blender run for five minutes is deemed safe, whereas the power drill on for five minutes is deemed threatening and can produce temporary hearing loss. Those noisy stadiums discussed in Chapter 7 are at a Leq level that is deemed traumatic, and if the sound at, for instance, Arrowhead Stadium during a Kansas City Chiefs’ game, is prolonged, it could produce permanent hearing loss. And those headphones the baggage handlers wear on the tarmac of any airport are not there for listening to music but rather to muffle the loudest everyday occupational noise that modern humans are exposed to—jet engines.

Noise in the workplace can be annoying at best and dangerous at worst. Most industry standards across the globe dictate that a decibel level of 80 for a full workday is acceptable and “assumed safe.” This would be equivalent to listening to cars on a busy freeway for the entire day about fifty feet from the road. Such levels of sound for that period of time should not cause damage to the sterocilia of the inner ear or to the auditory nerve pathways and hence are deemed safe. Indeed, when rats are exposed to sound levels equivalent to those that are at the industry standard, researchers do not see damage to the hairs in the inner ear. But Gourévitch and his colleagues have questioned our certainty that prolonged exposure to high decibel levels of sound are not harmful.

Some research on model animals suggests the opposite. Thirty days’ exposure of rats to sound sources at 70 decibels, well below a dangerous sound level, resulted in severe damage to the neural pathways of the primary auditory cortex. These rats could not discriminate between sounds close in frequency that unexposed rats could recognize. The findings indicate that the wiring of the auditory system is affected by noise at 80 decibels for extended periods of time. This rewiring is part of the plasticity that the brain has with respect to its neural connection.

Plasticity of the neural wiring of the brain is a well-known phenomenon, as is evidenced by stroke victims. Stroke causes tissue and nerve cell damage and subsequent loss of sensory, language, or motor capacity that the damaged parts of the brain control. However, because of the brain’s plasticity in rewiring neural connections, some stroke victims can regain motor and language capacity through therapy that exploits this ability. Conversely, with exposure to prolonged sound, the brain attempts to cope with the incoming information, and because of the plasticity with which the brain wires itself during challenges from the outer world, it does the best it can, which then causes the damage.

Why not take advantage of plasticity and use prolonged sound in a controlled way to retrain hearing in those people who have diminished capacity at this sense? In 2006, Arnaud Noreña and Jos Eggermont proposed just that: with the knowledge that prolonged sound exposure at high decibel levels can reorganize the cortical connection map for hearing, they hoped to put the principle to some good. They exposed cats to traumatic noise levels that result in hearing loss. After this exposure they separated the cats into groups, treating one with an enriched auditory environment and the other with a quiet environment. This approach is kind of like separating people into the club car and the quiet car on a train. Surprisingly, the group of cats exposed to the enriched environment had lower ranges of hearing loss than the cats in the “quiet car.”

Tinnitus, while prevalent in people with TBI (whether it be sports, military, or other injuries), is also found in others in populations who have not been injured. It is thought to affect about 15 percent of the human population and can be seriously disorienting and depressing to those who suffer from it. Researchers have looked for ways of alleviating or curing tinnitus and have concluded that perhaps the best therapy is psychotherapeutic counseling—a sort of mind-over-mind approach called psychoeducation. Since Noreña and Eggermont’s sound therapy suggestion in 2006, attempts to use similar approaches have been tried with some success. The best therapies may involve combinations—specifically, noise therapy combined with some other kind of brain stimulation. In rat model systems, targeting the vagus nerve appears to be an important component of this combined therapy. Stimulating this nerve, which is a huge player in neuromodulation, in combination with sound therapy can produce considerable improvements in the level of tinnitus. The vagus nerve stimulation triggers the plasticity of the cortex, and the sound is what the brain rewires on. The stimulation is accomplished by a process called transcranial magnetic stimulation (TMS). Briefly, this treatment involves the focused exposure of parts of the brain to magnetic fields. In this procedure, tones are repeated, interspersed with short pulses of TMS.

Another example of plasticity in the brain concerns strokes. If you have had a stroke, or if you know a relative or friend who has had one, you know that the damage to motor and language skills can be devastating. Strokes are complex injuries to the brain and occur in more than a million Americans every year. They occur because neural cells in the brain are not self-sufficient entities. They need a blood supply to function, and this is where stroke comes in. There are two kinds of stroke, but both cause death to the neural cells and extreme damage to the neural tissue where the dysfunction of blood supply occurs.


Figure 11.2. Ischemic stroke and brain damage.

Ischemic stroke occurs when the blood supply to specific parts of the brain is decreased to a level below which the cells can survive (fig. 11.2). Such strokes are localized to areas of the brain where the blood flow is restricted. Blood clots in the brain, embolisms elsewhere in the body, and systemic shock can all cause ischemic stroke because all of these reduce the amount of blood flowing to different parts of the brain. Hemorrhagic stroke is caused when a blood vessel breaks and spills blood into the brain tissue. The burst blood vessels no longer supply blood to the parts of the brain where they are supposed to go, and the lack of blood results in stroke. Ischemic damage can be extreme, but the death of the affected cells is not certain. When the neural cells themselves are killed, they are said to be infarcted. Ischemic regions of the brain have the capacity to recover; infarcted regions do not. More specifically, the lack of blood supply in an ischemic stroke is localized into an area called the ischemic core. This core is usually a small patch of neural real estate around the damaged blood vessels. Leading from the ischemic core is a secondarily damaged area called the ischemic penumbra. This area is also damaged, but not to the same degree as the core.

Recognizing damaged regions of the brain from either kind of stroke requires using brain imaging techniques. The core is diagnosed with a technique called diffusion-weighted magnetic resonance imaging. This approach uses the basic MRI approach but weights the overall image on data that infer diffusion of water. In this way, the tissues that are diffusing blood can be detected, and this is where the ischemic core resides. The penumbra is identified using the perfusion-weighted MRI approach. This MRI technique involves administering a chemical called gandolium to the patient and then detecting the location of the chemical using MRI. Gandolium is a contrasting agent that can be used to identify areas of the brain where the weaker signal of the penumbra resides. A third region, called the benign oligemia, is also identifiable using these brain imaging techniques, but this region after a stroke is, as the name implies, not dangerous because there is little chance of further damage by infarction of the area. The ischemic and hemorrhagic strokes I have discussed so far cause lasting damage to regions of the brain, but there are also transient stroke events called ministrokes. These occur when there is a momentary or brief lapse in storage of blood to a specific part of the brain. The brief stoppage of blood supply to a particular region might result in a temporary and brief loss of the senses, motor skills, or even language. Resupply of blood to the region restores most if not all of the function in the neural real estate that was initially affected. Many of you may have heard of the rather gross term “brain fart” (it’s actually in the Oxford English Dictionary). The brain fart is simply a momentary and temporary lapse of brain function usually tied to loss of memory. Although it is not a precise medical term, I think that it is quite descriptive in the context of ministroke.

The symptoms of either of these strokes are similar and affect motor skills, sensory processing, and language most acutely. Both tinnitus and hearing loss are the results of some strokes that affect the auditory cortex of the brain. The auditory cortex is localized in the temporal lobe of the brain, so if a stroke affects this region, there is a high probability that hearing will be affected. As you might have guessed, the sense of balance, which uses information from that other sensory organ in your inner ear, can also be affected by stroke. In fact, loss of balance from stroke is as complex as balance itself is and isn’t necessarily because the information from the vestibular system gets jumbled. Balance is all about how we sense where our bodies are in space. Our vestibular system of the inner ear does a lot of that calculation for us. But how we sense our muscle movements and muscular tension are also parts of balance, and these are not processed through the vestibular system. Stroke damage to the motor system can result in jerky motion that affects balance. And in fact, stroke can cause loss of sensation on the side of the body opposite the damaged side of the brain, producing a kind of a bodywide neglect. Vision is also involved in balance and is affected heavily by stroke.

Sight is affected by stroke because most strokes occur near regions of the brain dedicated to processing visual information. Decreased vision and double vision are two major visual symptoms of a stroke. Decreased vision is the result of the stroke damaging the optic nervous system and has a high probability of occurring because of the long traverse of the optic nerves from the eyes to the back of the brain to the occipital lobe and on to the occipital cortex. The optic nerve system emanating from the eyes crosses at a point in the midbrain called the optic chiasma. If the region affected by stroke also affects the optic nerves before the chiasma, then any injury to the right (or left) side of the nerves would result in loss of vision processed from the right (or left) eye. On the other hand, if damage occurs after the chiasma (that is, toward the back of the brain past the chiasma), then the pattern is reversed. Damage to the right optic nerve would result in the lack of transmission of information from the left eye, and vice versa. Field of vision is severely affected in all of these cases. Damage to the optic nerves is not the only cause of loss of vision with stroke. The damage can also occur to motor regions of the brain, and double vision is a good example of this. The motor regions control muscles of the legs, the arms, and even the eyes. Double vision is caused by damage to the motor nerves that control eye movement. Because the muscles cannot tell the eyes to align themselves for stereovision, a cross-eyed result occurs and double vision ensues.

So far, I have discussed damage to the visual system that involves upsetting the transport of the primary visual information to the brain. Other damage can occur when nerves involved in the higher-order interpretation of visual information are damaged. A whole set of problems can arise in this higher-order processing category. We’ll talk about split brains in Chapter 12, but for now let’s discuss four major problems involved in how we react to visual cues and how we read and write using vision. We use our visual system intricately to read and write, and the lack of both the ability to read (alexia) and the ability to write (agraphia) are sometimes the result of stroke. Although localizing the regions of the brain damaged in agraphic and alexic people as a result of stroke have helped localize the regions involved in reading and writing, recent evidence suggests that both of these functions use a surprisingly large number of the brain’s regions. Consequently, MRI methods are being used to replace the clinico-anatomical correlation method for localizing brain regions involved in these two brain tasks.

Another result of stroke on visual higher-order processes is a phenomenon called neglect. Although individuals with neglect can see the entire visual field, their brains simply do not process that things are there. Neglect usually is a brain side phenomenon where stroke damage on the left side of the brain will result in the neglect of things in the right visual field. A related problem to neglect is agnosia, where the visual signals are processed all the way through higher processes but the afflicted person cannot recognize people or things he or she sees. The connection of the sufferer’s visual system to the parts of the brain where the visual information is interpreted is disrupted, and hence people afflicted in these brain regions are incapable of finishing the visual process of recognizing objects and people. Oddly enough, the perception of color does not seem to be badly affected by stroke. In fact, color is used in rehabilitation of some stroke victims who are alexic. One of the problems that alexia creates is the inability to recognize margins when reading. Colors are often placed at the beginning of lines of type to help recovering stroke victims figure out where margins and new lines are.

Smell and taste of stroke victims are also altered as a result of damage to regions of the brain where the information from taste and olfactory receptors are processed, but less is known about the impact on these two senses. In fact, the loss of olfaction and taste are not considered classic symptoms of stroke. Again, as in vision, both of these senses send impulses to the brain and are delivered to the brain along two sets of nerves specific for the two senses. Stroke can damage the nerves running to the brain and also can damage the higher processing of smells and tastes, or in other words mess up recognizing things as a result of smelling a madeleine. Losing taste might at first glance look like a sense that a stroke victim could dispense with. But loss of gustatory capacity has a huge impact on diet, and because eating has such a social context in modern life, loss of taste can have an impact on family-related activities around which meals are centered. In addition, stroke victims lose a lot of weight as a result of not enjoying food. Finally, whatever taste a stroke victim does perceive is best described as foul and unappetizing, sort of like the metallic taste that TBI victims experience when tasting foods. To compensate, stroke victims have been known to salt or sweeten their food heavily to mask the foul taste generated by damage to the brain. Increased salt and sugar intake, though, is not a particularly good strategy to stay healthy after a stroke.

Stroke and physical injury are not the only ways a brain’s real estate can be altered. In fetal development, anomalies can occur that range from anencephaly (lack of development of the entire brain) to spina bifida (incomplete closure of the backbone and membrane around the spinal column). Looking at the impact of these other kinds of brain structure problems can be quite illuminating with respect to our senses.