PHYSIOLOGICAL BASES OF BEHAVIOR: ATTENTION, MEMORY, THINKING, CONSCIOUSNESS.
Learning & memory
A characteristic of animals and particularly of humans is the ability to alter behavior on the basis of experience. Learning is acquisition of the information that makes this possible, and memory is the retention and storage of that information. The two are obviously closely related and should be considered together.
Forms
From a physiologic point of view, memory is appropriately divided into explicit and implicit forms. Explicit memory, which is also called declarative or recognition memory, is associated with consciousness—or at least awareness—and is dependent for its retention on the hippocampus and other parts of the medial temporal lobes of the brain. It is divided into the memory for events (episodic memory) and the memory for words, rules, and language, etc (semantic memory). Implicit memory does not involve awareness and is also called nondeclarative or reflexive memory. Its retention does not involve processing in the hippocampus, at least in most instances, and it includes, among other things, skills, habits, and conditioned reflexes. However, explicit memories initially required for activities such as riding a bicycle can become implicit once the task is thoroughly learned.
Explicit memory and many forms of implicit memory involve (1) short-term memory, which lasts seconds to hours, during which processing in the hippocampus and elsewhere lays down long-term changes in synaptic strength; and (2) long-term memory, which stores memories for years and sometimes for life. During short-term memory, the memory traces are subject to disruption by trauma and various drugs, whereas long-term memory traces are remarkably resistant to disruption. Working memory is a form of short-term memory that keeps information available, usually for very short periods, while the individual plans action based on it.
Implicit Memory
Implicit memory includes skills and habits which, once acquired, become unconscious and automatic. It also includes priming, which is facilitation of recognition of words or objects by prior exposure to them. An example is improved recall of a word when presented with the first few letters of it.
The other forms of implicit memory can be divided into nonassociative and associative forms. In nonassociative learning, the organism learns about a single stimulus. In associative learning, the organism learns about the relation of one stimulus to another.
Habituation & Sensitization
Habituation is a simple form of learning in which a neutral stimulus is repeated many times. The first time it is applied, it is novel and evokes a reaction (the orienting reflex or “what is it?” response). However, it evokes less and less electrical response as it is repeated. Eventually, the subject becomes habituated to the stimulus and ignores it. Sensitization is in a sense the opposite reaction. A repeated stimulus produces a greater response if it is coupled one or more times with an unpleasant or a pleasant stimulus. It is common knowledge that intensification of the arousal value of stimuli occurs in humans. The mother who sleeps through many kinds of noise but wakes promptly when her baby cries is an example.
Habituation is a classic example of nonassociative learning. A classic example of associative learning is a conditioned reflex.
Intercortical Transfer of Memory
If a cat or monkey is conditioned to respond to a visual stimulus with one eye covered and then tested with the blindfold transferred to the other eye, it performs the conditioned response. This is true even if the optic chiasm has been cut, making the visual input from each eye go only to the ipsilateral cortex. If, in addition to the optic chiasm, the anterior and posterior commissures and the corpus callosum are sectioned (“split-brain animal”), no memory transfer occurs. Partial callosal section experiments indicate that the memory transfer occurs in the anterior portion of the corpus callosum. Similar results have been obtained in humans in whom the corpus callosum is congenitally absent or in whom it has been sectioned surgically in an effort to control epileptic seizures. This demonstrates that the neural coding necessary for “remembering with one eye what has been learned with the other” has been transferred to the opposite cortex via the commissures. There is evidence for similar transfer of information acquired through other sensory pathways.
Molecular Basis of Memory
The key to memory is alteration in the strength of selected synaptic connections. In all but the simplest of cases, the alteration involves protein synthesis and activation of genes. This occurs during the change from short-term working memory to long-term memory. In animals, acquisition of long-term learned responses is prevented if, within 5 minutes after each training session, the animals are anesthetized, given electroshock, subjected to hypothermia, or given drugs, antibodies, or oligonucleotides that block the synthesis of proteins. If these interventions are performed 4 hours after the training sessions, there is no effect on acquisition.
The human counterpart of this phenomenon is the loss of memory for the events immediately preceding brain concussion or electroshock therapy (retrograde amnesia). This amnesia encompasses longer periods than it does in experimental animals—sometimes many days—but remote memories remain intact.
The biochemical events involved in habituation and sensitization in Aplysia and other invertebrates have been worked out in considerable detail. Habituation is due to a decrease in Ca2+ in the sensory endings that mediate the response to a particular stimulus, and sensitization is due to prolongation of the action potential in these endings with a resultant increase in intracellular Ca2+ that facilitates release of neurotransmitter by exocytosis.
Classic conditioning also occurs in Aplysia, and in mammals, in the isolated spinal cord. In Aplysia, the US acts presynaptically on the endings of neurons activated by the CS. This leaves free Ca2+ in the cell, leading to a long-term change in the adenylyl cyclase molecule, so that when this enzyme is activated by the CS, more cAMP is produced. This in turn closes K+ channels and prolongs action potentials. The key point in this case is the temporal association, with the US coming soon after the CS.
In Aplysia, there are morphologic correlates to learning and memory. For example, 40% of the relevant sensory terminals normally contain active zones, whereas in habituated animals, 10% have active zones, and in sensitized animals, 65% have active zones. Long-term memory leads to activation of genes that produce increases in synaptic contacts.
Encoding Implicit Memory in Mammals
Without doubt, molecular events similar to those occurring in Aplysia underlie some aspects of implicit memory in mammals. However, events involving various parts of the CNS also contribute. Some investigators argue that the striatum is involved, and it is known that learning of some habit tasks is disrupted by lesions of the basal ganglia. There is other evidence that the cerebellum is involved. For example, the vestibulo- ocular reflex (VOR), the reflex that maintains visual fixation while the head is moving, can be adjusted to new eye positions, and this plasticity is abolished by lesions of the flocculus. In addition, conditioning of an eye blink reflex by using a puff of air on the eye as the US and a tone as the CS is prevented by lesions of the interpositus nucleus. In this case, it appears that impulses set up by the US act via the inferior olive and climbing fibers to the cerebellar cortex to alter the Purkinje cell response to the tone arriving via the pontine nuclei and mossy fibers. Climbing-fiber-mediated modification of mossy-fiber-driven Purkinje cell discharge is also responsible for plastic changes in the VOR and learned muscle movements.
Encoding Explicit Memory
Encoding explicit memories involves working memory in the frontal lobes and unique processing in the hippocampus.
Working Memory
As noted above, working memory keeps incoming information available for a short time while deciding what to do with it. It is that form of memory which permits us, for example, to look up a telephone number, then remember the number while we pick up the telephone and dial the number. It consists of what has been called a central executive located in the prefrontal cortex, and two “rehearsal systems,” a verbal system for retaining verbal memories, and a parallel visuospatial system for retaining visual and spatial aspects of objects. The executive steers information into these rehearsal systems.
Hippocampus & Medial Temporal Lobe
Working memory areas are connected to the hippocampus and the adjacent parahippocampal portions of the medial temporal cortex. In humans, bilateral destruction of the ventral hippocampus or Alzheimer’s disease and similar disease processes that destroy its CA1 neurons cause striking defects in short-term memory. So do bilateral lesions of the same area in monkeys. Humans with such destruction have intact working memory and remote memory. Their implicit memory processes are generally intact. They perform adequately in terms of conscious memory as long as they concentrate on what they are doing. However, if they are distracted for even a very short period, all memory of what they were doing and proposed to do is lost. They are thus capable of new learning and retain old prelesion memories, but they cannot form new long-term memories.
The hippocampus is closely associated with the overlying parahippocampal cortex in the medial frontal lobe. Memory processes have now been studied not only with fMRI but with measurement of evoked potentials (event-related potentials; ERPs) in epileptic patients with implanted electrodes. When subjects recall words, there is increased activity in their left frontal lobe and their left parahippocampal cortex, but when they recall pictures or scenes, there is activity in their right frontal lobe and the parahippocampal cortex on both sides.
The connections of the hippocampus to the diencephalon are also involved in memory. Some alcoholics with brain damage develop impairment of recent memory, and the memory loss correlates well with the presence of pathologic changes in the mamillary bodies, which have extensive efferent connections to the hippocampus via the fornix. The mamillary bodies project to the anterior thalamus via the mamillothalamic tract, and in monkeys, lesions of the thalamus cause loss of recent memory. From the thalamus, the fibers concerned with memory project to the prefrontal cortex and from there to the basal forebrain. From the basal forebrain, there is a diffuse cholinergic projection to all the neocortex, the amygdala, and the hippocampus from the nucleus basalis of Meynert. There is a severe loss of these fibers in Alzheimer’s disease (see below).
The amygdala is closely associated with the hippocampus and is concerned with encoding emotions related to memories. Amygdaloid lesions make animals less fearful. Iormal humans, events associated with strong emotions are remembered better than events without an emotional charge, but in patients with bilateral lesions of the amygdala, this difference is absent.
Confabulation is an interesting though poorly understood condition that sometimes occurs in individuals with lesions of the ventromedial portions of the frontal lobes. These individuals perform poorly on memory tests, but they spontaneously describe events that never occurred. This has been called “honest lying.”
New Brain Cells?
It is now established that the traditional view that brain cells are not added after birth is wrong; new neurons form from stem cells throughout life in two areas: the olfactory bulb and the hippocampus. Since the hippocampus is concerned with new memories, they could be related to new brain cells. There is now evidence that reduction in the number of new neurons formed reduces at least one form of hippocampal memory production. However, there is a great deal more to be done before the relation of new cells to memory processing can be considered established.
Long-Term Memory
While the encoding process for short-term explicit memory involves the hippocampus, long-term memories are stored in various parts of the neocortex. Apparently, the various parts of the memories—visual, olfactory, auditory, etc—are located in the cortical regions concerned with these functions, and the pieces are tied together by long-term changes in the strength of transmission at relevant synaptic junctions so that all the components are brought to consciousness when the memory is recalled.
Once long-term memories have been established, they can be recalled or accessed by a large number of different associations. For example, the memory of a vivid scene can be evoked not only by a similar scene but also by a sound or smell associated with the scene and by words such as “scene,” “vivid,” and “view.” Thus, there must be multiple routes or keys to each stored memory. Furthermore, many memories have an emotional component or “color”—ie, in simplest terms, memories can be pleasant or unpleasant.
Strangeness & Familiarity
It is interesting that stimulation of some parts of the temporal lobes in humans causes a change in interpretation of one’s surroundings. For example, when the stimulus is applied, the subject may feel strange in a familiar place or may feel that what is happening now has happened before. The occurrence of a sense of familiarity or a sense of strangeness in appropriate situations probably helps the normal individual adjust to the environment. In strange surroundings, one is alert and on guard, whereas in familiar surroundings, vigilance is relaxed. An inappropriate feeling of familiarity with new events or iew surroundings is known clinically as the deja vu phenomenon, from the French words meaning “already seen.” The phenomenon occurs from time to time in normal individuals, but it also may occur as an aura (a sensation immediately preceding a seizure) in patients with temporal lobe epilepsy.
In summary, there is still much to be learned about the encoding of explicit memory. However, according to current views, information from the senses is temporarily stored in various areas of the prefrontal cortex as working memory. It is also passed to the medial temporal lobe, and specifically to the parahippocampal gyrus. From there, it enters the hippocampus and is processed in a way that is not yet understood. At this time, the activity is vulnerable, as described above. Output from the hippocampus leaves via the subiculum and the entorhinal cortex and somehow binds together and strengthens circuits in many different neocortical areas, forming over time the stable remote memories that caow be triggered by many different cues.
Alzheimer’s Disease & Senile Dementia
Alzheimer’s disease is characterized by progressive loss of short-term memory followed by general loss of cognitive and other brain functions and, eventually, death. It was originally characterized in middle-aged people, and similar deterioration in elderly individuals is technically senile dementia of the Alzheimer type though it is frequently just called Alzheimer’s disease as well. Most cases are sporadic, but some are familial. The disease accounts for 50-60% of cases of senile dementia. Patients with Alzheimer’s disease eventually require around-the-clock care. Since 10-15% of the population over age 65 and almost 50% of the population over 85 have some degree of dementia, the condition is not only a serious medical problem but an economic load of increasing magnitude as the number of old people in populations of developed countries increases.
Early changes in Alzheimer’s disease include atrophy of the hippocampus and entorhinal cortex, demonstrable by MRI up to 2 years before a definitive diagnosis can be made.
The cytopathologic hallmarks of the disease are intracellular neurofibrillary tangles, made up in part of hyperphosphorylated forms of the tau protein that normally binds to microtubules, and extracellular senile plaques, which have a core of β-amyloid peptides (Aβ) surrounded by altered nerve fibers and reactive glial cells. The ultimate cause of Alzheimer’s disease is unsettled. However, the Aβ peptides are products of a normal protein, amyloid precursor protein (APP), which projects from nerve cells. When this protein is hydrolyzed abnormally by the enzyme γ-secretase, which acts on the portion of the APP that crosses the cell membrane, two Aβ peptides are formed, one containing 40 amino acid residues and the other 42 residues. It is interesting in this regard that nonsteroidal anti-inflammatory drugs have been reputed to have beneficial effects in Alzheimer’s disease, though opinion on this point is not unanimous.
It is worth noting that selective degeneration with aging can occur in three different types of cells in the CNS, causing three different progressive, crippling, and eventually fatal diseases. Degeneration of the hippocampal neurons is associated with Alzheimer’s disease, as noted above; degeneration of the dopaminergic neurons in the substantia nigra is associated with Parkinson’s disease; and degeneration of the cholinergic motor neurons in the brain stem and spinal cord is associated with one form of amyotrophic lateral sclerosis (ALS). This last disease is often called Lou Gehrig’s disease because Gehrig, a famous American baseball player, died of it. All three diseases are mainly sporadic but have familial forms as well. Five percent of the cases of ALS are familial, and in 40% of these, there is a mutation in the gene for Cu/Zn superoxide dismutase (SOD-1) on chromosome 21. A defective SOD-1 gene could permit free radicals to accumulate and kill neurons.
FUNCTIONS OF THE NEOCORTEX
Memory and learning are functions of large parts of the brain, but the centers controlling some of the other “higher functions of the nervous system,” particularly the mechanisms related to language, are more or less localized to the neocortex. Speech and other intellectual functions are especially well developed in humans—the animal species in which the neocortical mantle is most highly developed.
Anatomic Considerations
There are three living species with brains larger than a human’s (the porpoise, the elephant, and the whale), but in humans, the ratio between brain weight and body weight far exceeds that of any of the other three species. From the comparative point of view, the most prominent gross feature of the human brain is the immense growth of the three major association areas: the frontal, in front of the premotor area; the parietal-temporal-occipital, between the somatesthetic and visual cortices, extending into the posterior portion of the temporal lobe; and the temporal, extending from the lower portion of the temporal lobe to the limbic system. The proportions of the various parts of the brain are similar in the brains of apes and humans, but the human brain is larger, so the absolute size of the association areas is greater. The association areas are part of the six-layered neocortical mantle of gray matter that spreads over the lateral surfaces of the cerebral hemispheres from the concentric allocortical and juxtallocortical rings around the hilum.
The neuronal connections within the neocortex form a complicated network. The descending axons of the larger cells in the pyramidal cell layer give off collaterals that feed back via associatioeurons to the dendrites of the cells from which they originate, laying the foundation for complex feedback control. The recurrent collaterals also connect to neighboring cells. The large, complex dendrites of the deep cells receive specific and nonspecific thalamic afferents, reticular afferents, and association fibers from other cortical areas. Specific thalamic afferents end in layer IV of the cortex.
Complementary Specialization of the Hemispheres Versus “Cerebral Dominance”
One group of functions more or less localized to the neocortex in humans consists of those related to language, ie, to understanding the spoken and printed word and to expressing ideas in speech and writing. It is a well-established fact that human language functions depend more on one cerebral hemisphere than on the other. This hemisphere is concerned with categorization and symbolization and has often been called the dominant hemisphere. However, it is clear that the other hemisphere is not simply less developed or “nondominant”; instead, it is specialized in the area of spatiotemporal relations. It is this hemisphere that is concerned, for example, with the identification of objects by their form and the recognition of musical themes. It also plays a primary role in the recognition of faces. Consequently, the concept of “cerebral dominance” and a dominant and nondominant hemisphere has been replaced by a concept of complementary specialization of the hemispheres, one for sequential-analytic processes (the categorical hemisphere) and one for visuospatial relations (the representational hemisphere). The categorical hemisphere is concerned with language functions, but hemispheric specialization is also present in monkeys, so it antedates the evolution of language.
Lesions in the categorical hemisphere produce language disorders, whereas extensive lesions in the representational hemisphere do not. Instead, lesions in the representational hemisphere produce astereognosis—inability to identify objects by feeling them—and other agnosias. Agnosia is the general term used for the inability to recognize objects by a particular sensory modality even though the sensory modality itself is intact. Lesions producing these defects are generally in the parietal lobe. Especially when they are in the representational hemisphere, lesions of the inferior parietal lobule, a region in the posterior part of the parietal lobe that is close to the occipital lobe, cause unilateral inattention and neglect. Individuals with such lesions do not have any apparent primary visual, auditory, or somatesthetic defects, but they ignore stimuli from the contralateral portion of their bodies or the space around these portions. This leads to failure to care for half their bodies and, in extreme cases, to situations in which individuals shave half their faces, dress half their bodies, or read half of each page. This inability to put together a picture of visual space on one side is due to a shift in visual attention to the side of the brain lesion and can be improved if not totally corrected by wearing eyeglasses that contain prisms.
Hemispheric specialization extends to other parts of the cortex as well. Patients with lesions in the categorical hemisphere are disturbed about their disability and often depressed, whereas patients with lesions in the representational hemisphere are sometimes unconcerned and even euphoric. Other examples of specialization are mentioned elsewhere in this book.
Hemispheric specialization is related to handedness. Handedness appears to be genetically determined. In 96% of right-handed individuals, who constitute 91% of the human population, the left hemisphere is the dominant or categorical hemisphere, and in the remaining 4%, the right hemisphere is dominant. In approximately 15% of left-handed individuals, the right hemisphere is the categorical hemisphere and in 15%, there is no clear lateralization. However, in the remaining 70% of left-handers, the left hemisphere is the categorical hemisphere. It is interesting that learning disabilities such as dyslexia, an impaired ability to learn to read, are 12 times as common in left-handers as they are in right-handers, possibly because some fundamental abnormality in the left hemisphere led to a switch in handedness early in development. However, the spatial talents of left-handers may be well above average; a disproportionately large number of artists, musicians, and mathematicians are left-handed. For unknown reasons, left-handers have slightly but significantly shorter life spans than right-handers.
There are anatomic differences between the two hemispheres that may correlate with the functional differences. The planum temporale, an area of the superior temporal gyrus that is involved in language-related auditory processing, is regularly larger on the left side than the right. It is also larger on the left in the brain of chimpanzees, even though language is almost exclusively a human trait. Imaging studies show that other portions of the upper surface of the left temporal lobe are larger in right-handed individuals, and the right frontal lobe is normally thicker than the left and that the left occipital lobe is wider and protrudes across the midline. Portions of the upper surface of the left temporal lobe are regularly larger in right-handed individuals. There are also chemical differences between the two sides of the brain. For example, there is a higher concentration of dopa-mine in the nigrostriatal pathway on the left side in right-handed humans and a higher concentration on the right in left-handers. The physiologic significance of these differences is not known.
In patients with schizophrenia, MRI studies have demonstrated reduced volumes of gray matter on the left side in the anterior hippocampus, amygdala, parahippocampal gyrus, and posterior superior temporal gyrus. The degree of reduction in the left superior temporal gyrus correlates with the degree of disordered thinking in the disease. There are also apparent abnormalities of dopaminergic systems and cerebral blood flow in this disease.
Physiology of Language
Language is one of the fundamental bases of human intelligence and a key part of human culture. The primary brain areas concerned with language are arrayed along and near the sylvian fissure (lateral cerebral sulcus) of the categorical hemisphere. A region at the posterior end of the superior temporal gyrus called Wernicke’s area is concerned with comprehension of auditory and visual information. It projects via the arcuate fasciculus to Broca’s area (area 44) in the frontal lobe immediately in front of the inferior end of the motor cortex. Broca’s area processes the information received from Wernicke’s area into a detailed and coordinated pattern for vocalization and then projects the pattern via a speech articulation area in the insula to the motor cortex, which initiates the appropriate movements of the lips, tongue, and larynx to produce speech. The angular gyrus behind Wernicke’s area appears to process information from words that are read in such a way that they can be converted into the auditory forms of the words in Wernicke’s area.
It is interesting that in individuals who learn a second language in adulthood, fMRI reveals that the portion of Broca’s area concerned with it is adjacent to but separate from the area concerned with the native language. However, in children who learn two languages early in life, there is only a single area involved with both. It is well known, of course, that children acquire fluency in a second language more easily than adults.
Language Disorders
Aphasias are abnormalities of language functions that are not due to defects of vision or hearing or to motor paralysis. They are caused by lesions in the categorical hemisphere. The most common cause is embolism or thrombosis of a cerebral blood vessel. Many different classifications of the aphasias have been published, but a convenient classification divides them into fluent, nonfluent, and anomic aphasias. Ionfluent aphasia, the lesion is in Broca’s area. Speech is slow, and words are hard to come by. Patients with severe damage to this area are limited to two or three words with which to express the whole range of meaning and emotion. Sometimes the words retained are those which were being spoken at the time of the injury or vascular accident that caused the aphasia.
In one form of fluent aphasia, the lesion is in Wernicke’s area. In this condition, speech itself is normal and sometimes the patients talk excessively. However, what they say is full of jargon and neologisms that make little sense. The patient also fails to comprehend the meaning of spoken or written words, so other aspects of the use of language are compromised.
Another form of fluent aphasia is a condition in which patients can speak relatively well and have good auditory comprehension but cannot put parts of words together or conjure up words. This is called conduction aphasia because it was thought to be due to lesions of the arcuate fasciculus connecting Wernicke’s and Broca’s areas. However, it now appears that it is due to lesions in and around the auditory cortex (areas 40, 41, and 42).
When there is a lesion damaging the angular gyrus in the categorical hemisphere without affecting Wernicke’s or Broca’s areas, there is no difficulty with speech or the understanding of auditory information, but there is trouble understanding written language or pictures, because visual information is not processed and transmitted to Wernicke’s area. The result is a condition called anomic aphasia.
Dyslexia, which is a broad term applied to impaired ability to read, is frequently due to an inherited abnormality that affects 5% of the population. Its cause is unknown, though two pathogenic theories have been advanced. One is that there is reduced ability to recall speech sounds, so there is trouble translating them mentally into sound units (phonemes). Another is that there is a defect in the magnocellular portion of the visual system that slows processing and also leads to phonemic deficit. In any case, decreased blood flow in the angular gyrus in the categorical hemisphere is commonly seen.
More selective speech defects have now been described. For example, lesions limited to the left temporal pole (area 38) cause inability to retrieve names of places and persons but preserves the ability to retrieve commoouns, ie, the names of nonunique objects. The ability to retrieve verbs and adjectives is also intact.
The isolated lesions that cause the selective defects described above occur in some patients, but brain destruction is often more general. Consequently, more than one form of aphasia is often present. Frequently, the aphasia is general (global), involving both receptive and expressive functions. In this situation, speech is scant as well as nonfluent. Writing is abnormal in all aphasias in which speech is abnormal, but the neural circuits involved are not known. In addition, deaf subjects lose their ability to communicate in sign language if they develop a lesion in the categorical hemisphere.
Although aphasias are produced by lesions of the categorical hemisphere, lesions in the representational hemisphere also have effects. For example, they may impair the ability to tell a story or make a joke. They may also impair a subject’s ability to get the point of a joke and, more broadly, to comprehend the meaning of differences in inflection and the “color” of speech. This is one more example of the way the hemispheres are specialized rather than simply being dominant and nondominant.
Stuttering has been found to be associated with right cerebral dominance and widespread overactivity in the cerebral cortex and cerebellum. This includes increased activity of the supplementary motor area. Stimulation of part of this area has been reported to produce laughter, with the duration and intensity of the laughter proportionate to the intensity of the stimulus.
Recognition of Faces
An important part of the visual input goes to the inferior temporal lobe, where representations of objects, particularly faces, are stored. Faces are particularly important in distinguishing friends from foes and the emotional state of those seen. In humans, storage and recognition of faces is more strongly represented in the right inferior temporal lobe in right-handed individuals, though the left lobe is also active. Lesions in this area cause prosopagnosia, the inability to recognize faces. Patients with this abnormality can recognize forms and reproduce them. They can recognize people by their voices, and many of them show autonomic responses when they see familiar as opposed to unfamiliar faces. However, they cannot identify the familiar faces they see. The left hemisphere is also involved, but the role of the right hemisphere is primary. The presence of an autonomic response to a familiar face in the absence of recognition has been explained by postulating the existence of a separate dorsal pathway for processing information about faces that leads to recognition at only a subconscious level.
Localization of Other Functions
Use of fMRI and PET scanning combined with study of patients with strokes and head injuries has provided further insights—or at least glimpses—into the ways serial processing of sensory information produces cognition, reasoning, comprehension, and language. Analysis of the brain regions involved in arithmetic calculations has highlighted two areas. In the inferior portion of the left frontal lobe there is an area concerned with number facts and exact calculations. Frontal lobe lesions can cause acalculia, a selective impairment of mathematical ability. In the areas around the intraparietal sulci of the parietal lobes bilaterally, there are areas concerned with visuospatial representations of numbers and, presumably, finger counting.
Two right-sided subcortical structures play a role in accurate navigation in humans. One is the right hippocampus, which is concerned with learning where places are located, and the other is the right caudate nucleus, which facilitates movement to the places. Men have larger brains than women and are said to have superior spatial skills and ability to navigate. It has been suggested, partly in jest, that the greater brain weight of men is due to more neural components involved in getting from place to place and that this is why men resist asking directions when lost, whereas women do not hesitate to seek help.
Other defects seen in patients with localized cortical lesions include, for example, the inability to name animals, though the ability to name other living things and objects is intact. One patient with a left parietal lesion had difficulty with the second half but not the first half of words. Some patients with parieto-occipital lesions write only with consonants and omit vowels. The pattern that emerges from studies of this type is one of precise sequential processing of information in localized brain areas. Additional research of this type should greatly expand our understanding of the functions of the neocortex.
Experimental Neurosis
Animals can be conditioned to respond to one stimulus and not to another even when the two stimuli are very much alike. However, when the stimuli are so nearly identical that they cannot be distinguished, the animal becomes upset, whines, fails to cooperate, and tries to escape. Pavlov called these symptoms the experimental neurosis. One may quarrel about whether this reaction is a true neurosis in the psychiatric sense, but the term is convenient. If connections between the frontal lobes and the rest of the brain are cut, animals still fail to discriminate but their failure does not upset them.
Because of those results in animals, prefrontal lobotomy and various other procedures aimed at cutting the connections between the frontal lobes and deeper portions of the brain were at one time used in humans. In some mental patients, tensions resulting from real or imagined failures of performance and the tensions caused by delusions, compulsions, and phobias are so great as to be incapacitating. Lobotomy may reduce the tension. The delusions and other symptoms are still there, but they no longer bother the patient. A similar lack of concern over severe pain led to the use of lobotomy in treating patients with intractable pain. Unfortunately, this lack of concern often extends to other aspects of the environment, including relations with associates, social amenities, and even toilet habits. It is damage to the orbitofrontal cortex that appears to cause this lack of concern.
