The Brain

by Gary L Wenk

  The temporal lobe also is devoted to understanding the meaning of information coming from your ears. This region is called the auditory cortex and it is organized just like the keyboard on a piano, with the high notes at one end of the temporal lobe and low notes at the other. Damage to the auditory cortex removes a person’s awareness of sound, but he can still respond reflexively to startling noises. This is because your response to unexpected or loud sounds is handled by a very primitive region of the brain that is not part of the normal auditory cortex. The region of temporal lobe that is dedicated to understanding language (either spoken or signed) is found only on the left side (for most people) of the brain and is called Wernicke’s area. Damage to this area causes a condition called aphasia. Patients injured in this area are unable to understand language in its written, spoken, or signed form. The language of patients who experience injury or stroke in this area has a normal rhythm, but it does not make sense. Patients who ultimately recover their language abilities report that when they were impaired they found the speech of others and themselves to be completely unintelligible. These patients do retain the ability to sing and to utter profanities; these abilities are believed to be processed by regions of cortex in the opposite hemisphere (usually the right hemisphere). The left hemisphere is often called the dominant hemisphere due to the presence of language in this half of the brain. The nondominant right hemisphere, however, also pays attention to language. The same regions in the right hemisphere may play a role in the simultaneous processing and resolution of lesser meanings of ambiguous words. When speaking English, we all struggle with the fact that some words in English have multiple meanings; it is the job of the right hemisphere’s temporal lobe to sort this out.

  What is a seizure?

  The circuitry and cellular architecture of the temporal lobe make it particularly vulnerable to generating patterns of neural activity that lead to seizures. A seizure occurs when neurons within a small brain region spontaneously fire off a series of electrical signals to neighboring neurons recruiting them into a self-sustaining pattern of recurrent and increasing activity that then spreads to other nearby brain regions. You might have witnessed the human version of this effect while sitting in a baseball or football stadium. A small group of people in the stands stood up and threw their hands skyward, thus inducing the people in a nearby section of the stadium to do the same. Slowly at first, then faster and involving more and more people, this wave of standing and waving fans crawls around the circular stadium until “the wave” becomes a self-sustaining rhythm of energy powered by the needs of people watching a ball game to do something to relieve the boredom of just sitting quietly. Brains behave in much the same way. Often, however, the original cause of the spontaneous activity is not completely understood; traumatic brain injury, fever, brain infections such as encephalitis and meningitis, stroke, brain tumors, and a variety of genetic syndromes may all contribute to the development of seizures. Neurons often behave as though they prefer to fire synchronously with each other rather than remain inactive. The problem is that the presence of seizure activity makes the normal functioning of the brain nearly impossible, just as participating in “the wave” during a ball game makes paying attention to the action on the field of play difficult. Once a seizure begins, it follows the natural behaviors of neurons; that is, it spreads to neighboring brain regions in just the same way that all neuronal information flows in the brain. As the seizure recruits more and more neurons, it spreads across the cortex as a wave of electrical disturbance crawling from one region to the next until the entire brain becomes engaged.

  Seizures always should be treated aggressively and never be allowed to occur repeatedly. Why? Because the increased neural activity in the brain that characterizes a seizure is very similar to the conditions that underlie the process of learning; ultimately, as seizures continue to occur, the brain will learn to produce more and more seizures. Usually, the neural pathways that are contributing to the seizures involve the neurotransmitter glutamate; the increased release of this amino acid in the brain leads to neuronal cell death. Therefore, repeat seizures must be avoided so that seizure incidence and cell death are reduced. The unique distributed locations of specific brain functions become evident by observing someone having a seizure. For example, the onset of a seizure originating within the temporal lobe is often associated with the function associated with that same temporal lobe region. Patients may report amnesia or the recall of a specific memory, an abnormal taste or smell, an extremely sad or happy unexplained emotion, or an auditory or visual hallucination. These are all temporal lobe processes being initiated by the uncontrolled activation of neurons that characterizes a seizure episode.

  Epilepsy is a common brain condition that has likely plagued humans for many millennia. As mentioned earlier, the temporal lobe is particularly vulnerable to generating seizures. A recent investigation discovered that the tendency to display extravagant religious behaviors correlated significantly with pathology within the right temporal lobe of patients with untreatable epilepsy. In fact, the medical literature is replete with reports of epilepsy patients who demonstrated elaborate religious delusions. Seizures can induce vivid hallucinations that often take on other-worldly or religious features. When auditory hallucinations occur, they usually involve a single voice at a time, speaking in the native language of the patient.

  What is a hallucination?

  Studies of hallucinations have demonstrated that your experience of the world is not solely determined by the direct sensory inputs into your brain. When you perceive something but there is nothing there to perceive, you are hallucinating. When your brain completely misinterprets incoming sensory information, you are hallucinating. When your brain generates its own sensory inputs without any assistance from the normal sensory systems, you are hallucinating. Any sensory modality—visual, auditory, tactile, and gustatory or even a mixture of these, called cross-modal—can experience a severe misinterpretation of the neural signals bouncing around in the back half of your brain. This is why seizures can induce hallucinations; they are characterized by random neural activity that your brain attempts to interpret as something meaningful. No one is certain how hallucinations are initiated in the brain. People with schizophrenia or dementia frequently report auditory or visual hallucinations; the severity of the illness correlates with the presence of visual hallucinations in these patients. Some theories suggest that these hallucinations occur because schizophrenic patients lack the ability to distinguish self-generated from externally generated thoughts and sensory experiences. If you cannot tell the difference between what your brain is generating versus what is really happening, you also may lose the ability to predict the consequences of what you are about to perceive. This odd situation has an unusual consequence that is quite fascinating: if you cannot predict the consequences of your movements, you should, unlike everyone else, be able to tickle yourself. Astonishingly, schizophrenics can tickle themselves. This peculiar trait offers insight into which brain regions are not functioning normally in the brains of schizophrenics.

  In order to gain some insight into what it means to hallucinate, we might begin by examining what pharmacological hallucinogens do inside our brains. One of the best studied hallucinogenic drugs, and the topic of numerous bad movies from the 1960s, is lysergic acid diethylamide (LSD). Once ingested, LSD attaches itself to a variety of serotonin receptor proteins all over the brain. Serotonin is a neurotransmitter released by neurons that project their axons to every part of your brain. If you were able to insert a recording device into a serotonin neuron, you would discover that it has a regular, slow spontaneous level of activity that varies little while you are awake. When you fall asleep, the activity of these neurons slows. When you start to dream—or if, as we will see shortly, you ingest a hallucinogen—these neurons cease their activity completely. The effects of LSD on serotonin neurons may be the initial trigger that sets in motion a cascade of complex processes throughout the brai
n that is experienced as a hallucination. In truth, no one currently understands how LSD or any of the hallucinogens actually work, or just how serotonin factors into their hallucinatory effects. Confounding this uncertainty is the fact that some powerful hallucinogens, such as Salvinorin A, have no effect on serotonin function at all. Some stimulants, such as amphetamine and cocaine, produce sensory hallucinations via the activation of dopamine receptors; others, such as PCP or ketamine, act directly on glutamate receptors. Hallucinations sometimes occur in people who live normal healthy lives and are never aware that their peculiar sensory experience is not shared by everyone. This is called synesthesia.

  What is synesthesia?

  Imagine yourself as a newborn baby lying in a crib. Your brain’s serotonin neurons at this age are not fully functional and your serotonin receptors have not yet converted to an adult profile. Your sensory systems—eyes, ears, fingers, toes, and nose—are all working quite well, but due to the immature state of your serotonergic system, your brain does not correctly process all of the incoming sensory information. Thus, visual information is blended with auditory signals, smells are confused for colors, and touch produces a sound. Why does this happen? One theory is that normal serotonin function is required for the brain to accurately process sensory information in the cortex. If this neurotransmitter system is not working correctly, then sensory experiences become confounded with each other. This experience is called synesthesia. Some scientists theorize that when we are only a few days or months old synesthesia is a normal experience for the brain due to the immature state of brain chemistry and anatomy. Twenty years later, with a fully functioning mature serotonin system, consuming LSD induces a temporary synesthesia experience similar to the one you had in your crib as an infant. Why? The inhibited function of your serotonergic system that is induced by LSD, or possibly any hallucinogen, may reproduce the condition of synesthesia that was “normal” when you were a newborn. As a newborn, you found this condition to be frightening and you cried. After all, who wouldn’t? However, as an adult who has just ingested some LSD, you might, in the right setting, come to believe that the condition is a transcendently mystical experience. In fact, it is not mystical; it is a drug-induced replication of the conditions that originally existed in your infant brain prior to the maturation of a small group of neurons that release serotonin. Fortunately, due to your “infant amnesia,” you remember nothing of this bizarre experience. Keep this in mind next time you find yourself hovering over the crib of a crying frightened baby—you may be inducing some terrifying hallucinations for the child.

  Some people never grow out of this infant phase of constant hallucination. These people are synesthetes. Imaging studies have found that these individuals have abnormalities that are consistent with altered patterns of connectivity within various temporal lobe brain regions. Synesthesia has a strong genetic component; it runs in families and males get it about as often as females. However, not everyone who gets the variant gene shows the symptoms. The condition is currently considered a harmless alternative form of perception.

  What happens in the parietal lobe?

  Next, move your attention to the top of the back half of the brain, which is called the parietal lobe. The front part of this lobe is responsible for processing the sensations of touch and taste. The back half of the parietal lobe is one of the most recently evolved brain regions and has a very complex task: it is responsible for integrating the sensory information (primarily visual information for humans) coming into the brain from all over the body into a single “world view” that is unique for each person. The parietal lobe also receives information from the frontal lobe. For example, once your frontal lobes have decided to move your right arm, a copy of this decision is sent back to the parietal lobe; the parietal lobe uses this information to predict the sensory consequences of the impending movement. The parietal lobe always wants to know what you are going to do before you do it so that it can anticipate the arrival of the subsequent sensory experience. This is why you cannot tickle yourself; it is impossible to sneak up on a region of your body because your parietal lobe always knows what your hands are doing even before they do it.

  Imaging studies have revealed that the parietal lobe becomes active when we are envisioning the future, making moral decisions, or recalling autobiographical memories. The complexity and abstract nature of these tasks may explain why the parietal lobe evolved so recently in vertebrates. It is probably not surprising that the parietal lobe is a vital component of the default network involved with daydreaming. Of all the lobes in your brain the parietal lobe is probably the least understood. Recent studies indicate that the parietal lobe shows significant pathology during the early phases of Alzheimer’s disease, which likely contributes to some of the initial diagnostic symptoms such as confusion, delusion, disorientation, and difficulty thinking, understanding, and concentrating.

  Where is my cingulate gyrus and why should I care?

  Imagine the brain as a melon you are holding with both hands. Now slice the melon down the middle so that you are holding two identical halves in each hand. Each half is analogous to one brain hemisphere. Now look at the inner flat surface of one of those halves; you would be able to see another important brain region, the cingulate gyrus, running horizontally from the front to the back of the brain. This gyrus performs some quite interesting tasks. Studies using noninvasive scanning machines have discovered that the cingulate gyrus becomes active when we experience either social or physical pain, thus confirming what all of us have always known—words can cut like swords and produce true misery. This gyrus is also active while making decisions about your next behavior. The cingulate gyrus may help you decide whether your next behavior will be rewarded or punished. This brain region is part of a large group of regions, collectively called the limbic system, which was discussed in Chapter 2.

  The volume of the cingulate gyrus is greatly reduced in the brains of patients with bipolar disorder or major depressive disorder. It is currently unknown whether the shrinkage of this critical brain region precedes the onset of the symptoms of these illnesses or is a consequence of experiencing long-term depression. In addition to its potential role in depression, recent imaging studies have found that the anterior region of the cingulate gyrus is smaller in schizophrenic patients and that this change correlated with a lower level of social functioning and a higher degree of psychopathology. Whether this correlation is the source of these symptoms remains to be determined by future studies.

  A colleague once had a patient with a benign tumor growing between her two hemispheres; as the tumor grew in size, it began to push against the cingulate gyrus in both hemispheres of her brain. The tumor was discovered during an examination following a car accident when the patient complained that she developed some unusual symptoms. The most problematic symptom was that she lost the ability to control her sexual desires. This was most distressing to the patient because she was a cloistered nun. Fortunately, when the tumor was ultimately removed, the woman was once again able to control her urges and return to her chosen vocation.

  What is “the little brain” and what does it do?

  Long ago, anatomists saw what appeared to be an additional companion brain hanging off the back of the larger hemispheres and decided to call it the cerebellum, or “little brain.” It is a tennis-ball-sized structure, only about a tenth of the size of the brain that, surprisingly, contains almost 50% of all of the neurons in your head. It has a highly convoluted cortex with only three layers; the interior of the cerebellum contains lots of myelinated axons going to and from the brain and spinal cord. What does the cerebellum do? Once again the answer to this question comes from studies using noninvasive scanning machines and indwelling electrodes. The cerebellum plays a role in the control of certain types of memory and mood. We also know that the neurons within the cerebellum become active just prior to and during the contraction of the muscles of the body. When the cerebellum is damaged due to injury, stroke, or t
umors, the most common symptom is difficulty with movement and posture. People with cerebellar damage can move, but their movements are not smooth or well controlled. The cerebellum receives sensory information from your muscles and joints to inform you about the location of your body parts; this allows you to move correctly without paying attention to every movement. Patients with cerebellar damage usually find that they need to walk with their feet placed widely apart and, because they cannot tell where their limbs are located, they need to watch what their limbs are doing at all times.

  The ability of the cerebellum to perform complex well-learned movements smoothly also can be impaired by alcohol or marijuana intoxication; this is because the cerebellum contains specific receptor proteins that respond to both of these drugs. If you are ever stopped by a police officer on suspicion of driving drunk, you may be asked to touch your nose with your outstretched finger. Ordinarily this is quite an easy task to perform; however, it is not easy to perform when the cerebellum is bathed in alcohol. Alcohol distorts the pattern of neuronal activity, preventing you from moving your arm accurately to touch your nose. Alcohol also distorts the ability of your cerebellum to control the smooth coordination of the muscles of the eyes. When the police officer instructs you to follow his finger with your eyes, he is testing to determine whether alcohol has impaired the ability of your cerebellum to control the muscles of your eye. If your eyes begin to move involuntarily from side to side in a rapid swinging motion rather than staying fixed on the officer’s finger, you are displaying what is called nystagmus. Nystagmus can be induced by alcohol intoxication. Obviously, the little brain in the back is just as important as the big brain up front when it comes to our survival and the success of our species.