The brain is divided into three main parts: cerebrum/diencephalon, cerebellum and brainstem. The cerebellum is involved in proprioceptive tasks. Proprioception involves knowing where our arms and legs are, and how they are situated in relation to the rest of our body. This gives us the ability to control our posture and to coordinate body movements. Conscious body movements begin in the cortex, but are coordinated in the cerebellum. For example, in order to pick up a heavy load with our left hand, we must lean to the right, extend our right hand, and numerous other body tasks that our cerebellum performs almost instantaneously for us. Lesions of the cerebellum can cause problems walking and standing, tremors, eye twitching (nystagmus), jerky movements, labored speech, a general inability to make controlled, coordinated limb movements, and problems initiating and terminating movements (Burt 1993:365).
The next major section of the brain is the brainstem, which comprises less than 5% of total brain weight, but controls most of what happens subconsciously in the body. It is the bridge for most of the information coming from the body to the rest of the brain. It houses several “nuclei" that are essential for perception of the external and internal world. Some functions of the brainstem are respiration, cardiovascular activity, sleep and unconscious awareness. One of the important systems in the brainstem is the reticular formation. Damage to this area induces, at worst, coma, or less severe damage may produce losses of motivation or arousal. Stimulation of this area produces states of alert wakefulness, and pathological stimulation produces the inability to fall asleep (rare and fatal). Damage in other areas of the brainstem could cause paralysis or sensory loss (since the tracts carrying motor output, or sensory input almost all cross in the brainstem). Finally, many of the nuclei in the brainstem house complex sensory-motor reflexes, such as the vestibular-ocular reflex. This reflex stabilizes a person’s eyes on a stationary target as the head, body, or environment moves (for example when reading a sign from a moving car, both the eyes and head must move in a coordinated fashion to keep the sign fixed on the retina).
The third section of the brain is the cerebrum. It is further subdivided into the basal ganglion, thalamus, limbic structures and cortex. The basal ganglion is mainly involved with coordinating conscious motor functions, and lesions here are associated with Parkinson’s disease and Huntington’s chorea. All sensory information passes through the thalamus, which does first-level processing information going to the cortex. Lesions here will cause sensory deprivation, or sometimes intractable, chronic pain (thalamic syndrome). Limbic structures are involved in such diverse activities as emotions, learning and memory. Finally, the cortex is involved in higher-level processing, which many people consider to be the focus of distinguishing humans from all other animals. Humans have the largest cortex compared to the rest of the brain of any other animal, while reptiles and other lower species have little or no cortex at all.
The cortex is the outer layer of the brain, seen as the pinkish-gray convoluted, gelatinous material in most pictures showing the surface of the brain. It can be separated into four sections: frontal, parietal, occipital and temporal (some people include portions of the limbic system as a fifth section here). These sections are found on both the left and right hemispheres, and form mirror images in the non-pathological brain. In fact, the entire brain, not just the cortex, forms a mirror image from the left to right side, and abnormalities of this similarity in images of the brain (by techniques such as PET, CAT or MRI scans) can be used to determine where damage has occurred in the brain. Both hemispheres have extensive interconnections between themselves, passing almost entirely through the corpus callosum. Cutting this structure results in what is known as the split-brain patient, where the left hemisphere is unable to communicate with the right, and vice-versa (discussed later in this chapter).
The temporal lobe contains Wernicke’s area, which is essential in understanding spoken and written language (see chapter two for discussions about lesions to this area; specifically “receptive" aphasia, cf. Broca’s area in frontal lobe). This part of the cortex is also important for recognition of visual stimuli. Unlike the occipital lobe, which is essential for the perception of visual stimuli, the temporal lobe is essential for recognition. Damage to the temporal lobe disrupts the ability to recognize seen objects, and faces (including one’s own face, if seen in a mirror). Other results of damage to this area are short-term memory loss, hallucinations, or seizures, each of which are common in temporal lobe epilepsy.
The occipital lobe, as mentioned above, is essential for vision. Information gathered from the eyes (which, by the way, are considered part of the brain; so when one looks at the eyes, one is looking at a part of the person’s brain!) is transduced from light waves to electro-chemical impulses in the retina, which are then transported and sorted down the optic tract. There is a stop (synapse) at the thalamus, and from there back to the occipital lobes. Damage to any area from the retina back to (but not including) the occipital lobe will result in the patient noticing a blind spot, or being totally blind in large areas of vision. If the damage occurs in the occipital lobe itself, the blind portions may not be noticed unless tests are performed on the patient’s vision, even though large chunks of vision are missing. The easiest way to understand this is that if the damage occurs in an area that transports the retinal image to the occipital lobes, then the lobes suddenly stop receiving information, thus a problem is detected. However, if the damage (stroke, embolism, etc) occurs in the lobe itself, since the machinery that “sees" has disappeared, then the brain as a whole doesn’t notice a loss, since the neurons which would detect the loss are now dead or damaged.
Damage to the parietal lobes typically will cause attentional disorders. For example, if the right temporal lobe is damaged (remember that all information crosses to the opposite side of the body), the patient may “neglect" the left half of his body, and/or the left half of his environment. People with this disorder just seem to “ignore" everything on one particular side of their bodies. They may only eat the left half of their food, then believe there is nothing else left, until the plate is turned around. Then, after eating the left half of what is remaining, again, they believe they are through, until the plate is turned again, and the other half of the food again comes into awareness. Similarly, if asked to draw another person, or object, the patient will only draw half of the object, not only leave off the “neglected" half, but not even realizing there is any problem (Sacks 1985:77-8)! Another problem is body neglect. The patient may try to walk, only using the right side of his body, not understanding why he isn’t moving (he isn’t even aware he has a left side) (Burt 1993: 466; Kaplan 1994: 101).
Finally, the human frontal lobe seems to be the most unique area of the brain, in terms of mind. In addition to Wernicke’s area in the temporal lobe, Broca’s area in the frontal lobe is essential for language production (again, see chapter one for more details; damage here leads to “executive" aphasia--the inability to produce language, as opposed to “receptive" aphasia with Wernicke’s damage).
The prefrontal cortex is an area within the frontal cortex. It constitutes 29% of cortical area in humans, 17% in chimpanzees, 7% in dogs, and 3.5% in cats (Kaplan 1994:99). Neurons in this area respond to several different sensory inputs, and are highly responsive to behavioral input. This area is therefore “thought to integrate motivational events with complex sensory stimuli" (Gilman 1992:238). Seizures or other disorders of this area can cause intrusive “thoughts" as well as hallucinations, similar to those found in schizophrenia. Additionally, damage here can cause bizarre behaviors, including total losses of “social graces," concern for others, foresight, and increases in apathy. They will typically seem totally unconcerned with their illness, or their odd behaviors (for example, they may eat off of the floor, ignore all cleanliness, etc.). Along with this, there are severe personality changes, mostly seen with flattened affect (inability to express emotion). Finally, there is seen a loss of insight and foresight, leading to severe deficits in problem solving and the ability to make informed decisions (Burt 1993:467).
At the top-central portion of the brain lay the sensory and motor homunculi. The motor “strip" is on the frontal side of the central sulcus, and the sensory strip is on the parietal side. These two strips are the final processors of sensory information coming into the body, and of motor commands sent out to the body. Stimulation of similar areas on these strips on different patients produce effects on similar places on the body. Studies like this have led to the production of “maps" on these strips of the body, called homunculi (see Appendix A). Electrically stimulating one area of the motor area, for example, will lead to a movement in the corresponding body part; stimulation on the sensory side will cause a tingling perception (see section on Penfield, later in this chapter).
There are thousands of different chemicals in the brain that combine to give us the phenomenon we call neurophysiology. Neurotransmitters are the classical brain chemicals. They are the major chemicals by which one neuron communicates with another neuron They function typically to either excite or inhibit the firing of other neurons.
Take an hypothetical neuron A. This neuron responds to some stimuli, and becomes “activated." This neuron, in turn, sends an electrical charge down its axon, which, if the charge is strong enough, will cause the “bouton" at the end of the axon to release the neurotransmitter stored there (see Appendix A for diagram). For each neuron, there is only one neurotransmitter found in each bouton, though there may be several different neuropeptides that are co-released with the transmitter. The area of the brain in which the cell is found partially determines which transmitter is used. When these transmitters are released, they cross the “synapse" to act on specific receptors on the dendrites of neuron B. Neuron B, in turn, is either inhibited, or excited by this transmitter, depending on the transmitter, and the area of the brain. When neuron B is sufficiently excited by the information transmitted by the neighboring neurons to cell B’s dendrites, this cell in turn will fire its axon, which will then cause a release of transmitter to neuron C, and so forth. Neuron B will undoubtedly be receiving hundreds of signals from neighboring neurons, some excitatory, some inhibitory, and it is the “summation" of these excitations or inhibitions that will eventually cause the neuron to fire, once it reaches the critical electrical threshold. To add to the complexity of the system, neurons can also act back onto themselves, as well as on other neurons. This is the process by which all information is passed in the brain, and the totality of this process gives us complex behaviors, learning, thinking, creativity, and “mind."
Dopamine is one example of a neurotransmitter and is involved in movement disorders such as Parkinson’s Disease. Drugs that mimic dopamine can be introduced into the basal ganglion, and decrease the symptoms of Parkinson’s. Drugs that inhibit the production of dopamine (such as most antipsychotics) will cause movement disorders. Here we find two types of disorders which are affected (caused?) by dopamine disorders. Positive symptoms of schizophrenia (hallucinations, bizarre behaviors; as opposed to negative symptoms such as social withdrawal, depression, etc) are produced by excesses of dopamine, and certain disorders of movement are associated with decreases of dopamine. Thus treatment of either disorder must be carefully balanced, so as to not produce symptoms of the other.
Serotonin (5-HT) is another transmitter implicated in several mental disorders. One is the negative symptoms of schizophrenia. Likewise, decreases in 5-HT are also implicated in causing depression. Increases in 5-HT has been shown to cause anxiety and obsessive-compulsive behaviors and hallucinations. In fact, the drug LSD is a 5-HT agonist, meaning that LSD metabolites mimic the action of 5-HT, thus activating 5-HT receptors, causing hallucinations. Moreover, 5-HT is a precursor to the melatonin produced in the pineal gland, thus decreased in 5-HT will cause decreases in melatonin, which will in turn cause disturbances in the circadian rhythms and sleep-wake cycles, which may be one of the pathways in the etiology of depression (Leonard 1992:25-7).
Norepinephrine (NE) and epinephrine (adrenaline) are two other transmitters implicated in depression. Decreases in NE are correlated with increases in depression, and increases in NE tend to elevate mood, and can cause mania. Acetylcholine (ACh), which is decreased in Alzheimers patients, is implicated in dementia-related disorders. The cholinergic system (the structures in the brain that produce ACh) is the main system destroyed in Alzheimer’s (Leonard 1992:20).
A second case of brain trauma is Zazetsky, who was hit in the head by a bullet (Jones 1981:3ff). The bullet had injured the “temporo-parieto-occipital region of the brain," which led initially to a coma, then recovery of consciousness, but formation of much scar tissue in these areas. His frontal lobes were spared, so he was able to entirely comprehend his situation, which had dramatically changed since his accident.
Initially he was unable to perceive anything, his world had collapsed into fragments. His brain was incapable of constructing complete pictures while, to complicate matters even further, the right side of everything was nonexistent. . . . To make matters worse, his sense of his own body had changed. Not only was he unable to see the right side of his body, he was unaware that it even existed. . . . He found he had forgotten the names of common objects, and would repeatedly get lost even in rooms and towns with which he had previously been familiar. . . . Perhaps more horrendous than the other tragedies for Zazetsky was the realization he was now illiterate. Before his head injury he had been a fourth-year student at a polytechnic institute, but afterward he could read nothing.Several fascinating cases are discussed in Oliver Sacks’ book The Man Who Mistook His Wife for a Hat. The first case he mentions involves a brilliant music professor who suffered a stroke, and was thereafter unable to visually recognize objects. All of his other mental faculties were intact, and he was still able to teach and play music wonderfully, but he was unable to recognize objects such as the door, gloves, or even his wife, who in fact had become used to such odd behavior as when he “reached out his hand and took hold of his wife’s head, tried to lift it off, to put it on" as if he had mistaken her for his hat (Sacks 1985:11)!
Another example Sacks gives is of the phenomenon of “equalisation" (pp. 116ff). Here, the patient, a former research chemist, came in with a rapid personality change. Though she behaved in a fairly normal fashion, including making jokes and being high-spirited herself, she was apathetic to everything that went on around her. She could respond fluently and accurately in any discussion, and though she had no problems understanding syntactical meanings, the phrases themselves had no deeper meanings to her. Nothing at all bothered her. Nothing was significant or important, but everything was “equal." Sacks speaks of her as “de-souled." He also refers to his patients with severe memory loss as “de-souled."
In another case, a young man had no memories of murdering his girlfriend, and neither hypnosis nor sodium amytal could evoke the memories. For years he stayed in a psychiatric hospital, not knowing if he were guilty, but accepting his punishment because he could not remember. Moreover, because his mental competencies were questioned at the time of the trial, he was not admitted into the courtroom when the details of the grisly murder were given. One day, out on a day pass, he was hit by a car and sustained a head injury, which caused him to be in a coma for two weeks. When he regained consciousness, he not only remembered the murder in detail (details that he could not have known unless he had committed the murder, since he was not in court during the trial), but the image he received was clear and irresistible, so he could not remove it from his thoughts. Eventually, with therapy and anti-convulsant drugs, he was able to keep the image of the girl’s murder out of his mind so he could function normally (pp. 161ff).
In fact, however, the person functions normally with only a few exceptions that can be found during artificial laboratory situations. These situations usually involve a barrier separating the patients right field of view from the left, then testing the person’s ability to make certain judgments, descriptions or performances based on what they see in either field (Rathus 1987:79; Jones 1981:70ff). In normal situations, however, the patient cannot be distinguished from any other person based on function, and the patients report little or no difference in their experience of their own mental states.
Another example of cases where odd results are reported are known as blindsight. In these cases, the patient claims to be blind, and certain optical tests seem to indicate blindness, yet he is able to respond to, and describe certain types of visual stimuli. This can occur with strokes in the occipital lobe, where the primary visual cortex involved with “seeing" is destroyed. Certain of these patients can “guess" correct shapes, or the incidence of light flashed in their eyes with much higher correlations than other types of blindness, “even as good as 100 percent correct under some conditions" (Dennett 1991:325)! Though they claim total blindness, they are apparently able to become aware of certain visual images. What is thought is happening here (though we don’t know for sure), is that the processing that occurs in the thalamus or elsewhere along the visual pathway, is enabling the person to be aware of what is seen, but those images are not able to reach “consciousness" or “mind" because of the damage to the cortex.
Karl Lashley did experiments on rats in the early part of this century to try to localize where memory is stored. Lashley trained his rats to perform various tasks, and would then systematically lesion different areas of the brain to see if they would remember how to do the tasks. What Lashley found greatly disappointed him: “To his surprise it was not possible to find a particular region corresponding to the ability to remember the way though a maze" (Hofstadter 1979:342). Further, studies and observations of humans, have been unable to locate a single place where most memories reside. Language is localized, but memories such as songs, pictures, etc., though they can be found in certain regions of the temporal cortex, this is not necessarily the only place they reside. For example, many forms of amnesia appear after destruction of different areas of the brain, but later those memories may return (remember that those areas that are destroyed, cannot “grow back"). The conclusion by many researchers is that memory is not stored in one place, but is “networked" throughout the entire brain.1
Finally, we will conclude the case studies with findings from the work of W. Penfield. During operations which attempt to remove epileptic parts of the brain, the patient usually must be awake, so the surgeon can know if the area is truly the focus of the seizure activity. With the skull opened and brain exposed, the suspected areas of the brain can be electrically stimulated, and if that stimulation causes a seizure, then they know that is the spot that needs to be removed. During this process, it is common for certain experiences to occur in the patient’s consciousness due to this electrical stimulation of the brain. Depending on the region stimulated, the patient may experience songs (as described above), smells, hallucinations, etc.
Penfield, during his studies, took this to a different level. He systematically stimulated areas of the brain in an attempt to localize the “self." He would stimulate an area, which might result in a movement of the hand, a memory, or other phenomenon, and would then ask the patient if he himself (the patient) caused it, or if it occurred without his control (in response to Penfield’s electrical stimulation). There was no area Penfield could discover which caused the patient to respond with “I did that" (Loder 1992:44). After this research, Penfield concluded that there is no “I" region in the brain, but that Cartesian dualism must be the only reasonable solution. This conclusion, however, is not held by the majority of the scientific community, and more reasonable solutions have been proposed to explain these observations.
Future therapies will capitalize on other findings in the neurosciences. One of the most exciting areas of research is in growth factors. Most of the disorders we currently know about are caused by deteriorations of certain brain regions, and we know that damage is irreparable because neurons in the CNS do not grow back. However, research has been done to discover what factors cause the initial growth and development of the neurons in the embryological and infant stages. These factors we now know are a class of chemicals called “growth factors." Different growth factors are present in different areas of the body and brain and their presence stimulates these cells to grow. The hope is that if we can discover which factors are important for the affected brain regions, we will be able to apply these growth factors to deteriorated and damaged areas so new neurons will replace the dead ones. Thus the tragedy of Alzheimer’s, in which we find the massive death of neurons in the cholinergic and noradrenergic systems, can possibly be reversed by the proper application of growth factors in these areas.
Another method already in use in certain studies, is transplantation of neural tissue from one brain to another. We see this in certain Parkinsonian patients where the nerves from aborted fetuses that produce dopamine are grafted into the Parkinsonian brain. These studies have had moderately good results in reversing the symptoms of this debilitating disorder.
A final exciting area of work is genetic engineering. We know we can transplant brain tissue from one area to another brain to alleviate disease. But it would be safer, and have fewer ethical problems, if we could take the person’s own neural tissue, clone it, grow it, and replace it back into the brain. Or even if we could just “engineer" cells to match the patient’s dying cells, and put them in the troubled regions. Moreover, could genetic engineering be useful in disorders such as Down’s Syndrome? Could the missing DNA be inserted into a virus, then that virus implanted into the Down’s child, which could then distribute that DNA to the brain, thus averting the symptoms seen in Down’s?
This could be true for any disease with a genetic component, such as Huntington’s Chorea, schizophrenia, alcoholism or Alzheimer’s. Could the “bad" DNA be replaced with genetically engineered “good" DNA? In fact, since all brain functions are dependent on either the production, metabolism and disposal of certain chemicals, as well as the presence of certain cells, and all of these can theoretically be replicated by genetic engineering, couldn’t it potentially possible to someday “cure" any problem in the brain with genetic engineering techniques?
Aiding in the development of each of these areas is computer modeling. Using the rapidly developing field of computer science, we have been able to model both individual neurons, and whole neural systems using computer simulations. There are hundreds if not thousands of different types of neurons in the brain. Some of these neuronal types have beenimulated by computer programs so thoroughly, that we can perform “virtual" experiments on the cell with different types of “virtual" chemicals or situations, and the “virtual" cell’s reaction will usually be very close if not exactly like the real neuron (Churchland 1992:403).
Similarly, whole systems, such as the vestibulo-ocular reflex, have been simulated by neural nets (the term for a class of computer programs that give output similar to real neuronal systems). Just like the individual neuronal models, these systems can be provided with data that would mimic stimulation in a human body in different situations. Already some questions we had about how the VOR works have been worked out using the computer models (Churchland 1992:371).
These computer methods, combined with the biological methods we already have, should rapidly propel our ability to control mental disorders and deviant behaviors in the next fifty years. This fact raises serious concerns about ethics and personhood. For example, there are some schizophrenics who do not want to be “cured." They have come to enjoy and respect the altered patterns of thinking their “disease" provides for them, and are willing to give up social standing for these thought patterns. Similarly, manics typically enjoy their mental states, which can cause improvements in production and certain social skills. Again, some of these particular patients would rather suffer the consequences of manic states rather than give up the manic states altogether.
Further, two immediate questions arise. In an epistemological sense, how do we “know" that the altered thought patterns of the schizophrenic aren’t closer to “reality" than ours? Certainly their behavior and logic don’t conform to our ideas about life and social standards, but in many respects, neither did Jesus’. Secondly, if the “person" resides in the make-up of the brain, and we go around engineering it, and re-growing parts of it, even transplanting it, then what does that do to the original person? Did God make that person a schizophrenic, or is schizophrenia merely a consequence of a fallen world? Then what about legal issues such as criminal reform? Who defines what must be altered in the person’s personality (should the political dissident be biologically reformed?), and what about responsibility for crimes (should mass-murderers no longer be punished, but only sent to the local hospital for a transplant?)? Further, what does attributing all behavior to the brain mean for spiritual accountability to God (“sin")? These and many other questions will be addressed in the last chapter.