Probably the most studied area of cognition is the area of learning and memory. For most people their memories define who they are, who they want to be, and who they will be. Learning and memory are actually two ways of thinking about the same phenomenon, in that they both describe an outcome based on the ability of the brain to change its structure and its functioning as a consequence of experience. This chapter investigates the major processes in brain structures involved in the process of learning and memory.
Technically, learning is described as a change in brain structure in response to experience, and memory is associated with how these changes to the brain are subsequently stored, represented, and reactivated when needed. Someone unable to learn or remember her experience would find every single moment as an original experience.
Learning new material or changing material already learned requires important changes in the structure of the brain. For the most part, the plasticity of the brain, or the ability of the brain to change in response to experience, is driven by genetic programs. In some animals specific types of learning occur via genetic programs; however, animals can also learn from experience. Certain animals, such as certain types of birds, immediately learn to associate themselves with the first living object they see upon exiting their shells as hatchlings, and will identify with that animal. This process is called imprinting and has survival value, as typically the first thing these animals see is their mother. Imprinting has been taken advantage of by some working in the pet trade where breeders of exotic birds, such as parrots, make sure that they are present when the chicks hatch and then rear and feed the young bird by hand. When this is done, the developing parrot believes itself to be a person and makes a better pet.
Classical conditioning occurs in a number of contexts, such as feeling nervous before going to the dentist or flinching before an expected loud noise. Neuroimaging techniques have implicated right hemisphere activation, and especially right frontal cortex activation and cerebellar activation, as being associated with learning via classical conditioning.
Imprinting does not occur in people, but several types of learning have been identified. Some of the best-known early learning experiments with animals that were applied to human learning came from the Russian physiologist Ivan Pavlov, who was studying digestion in dogs. Pavlov noticed that dogs would salivate, a reflexive action in dogs when food is present, before they were presented with any food. He performed a series of experiments and learned that the dogs had associated the presence of the white laboratory coat worn by the laboratory assistants with a soon-to-be presented food object. This type of learning, where a reflexive action is associated with an environmental stimulus, has been termed classical conditioning. Conditioning is a term used in psychological learning research to imply a specific type of learning that involves the association of two or more stimuli. In the classical conditioning model, the learning takes place via the association of a particular reflexive action (i.e., salivating) with some environmental stimulus that normally would not elicit this response (i.e., a white lab coat).
It works like this: A stimulus that elicits the reflexive action, such as the presence of food leading to salivation (the food stimulus is called the unconditioned stimulus [UCS] and the reflexive action of salivation is termed the unconditioned response [UCR]), is paired with some stimulus that normally would not elicit the reflex, such as a white laboratory jacket (this new stimulus is termed the conditioned stimulus [CS]). Over time, the animal learns to associate the white laboratory jacket with the presence of food and salivates whenever he sees the lab coat (this new response to the lab coat is termed the conditioned response [CR]). Pavlov initially believed that the conditioned, or learned, response was identical to the original unconditioned response; however, the conditioned response is actually a bit weaker. In addition, later experiments indicated that classical conditioning cannot pair any unconditioned stimulus to an unconditioned response (for example, it would be nearly impossible to get dogs to learn to salivate to a severe electric shock). Pavlov, who won a Nobel Prize for his work, is considered one of the pioneers of learning and memory.
While classical conditioning was being studied in Europe, a different type of learning or conditioning was being studied in the United States. Pioneers Edward Thorndike and John Watson investigated what later came to be termed operant conditioning. Probably the best-known proponent of operant conditioning is the behavioral psychologist B. F. Skinner. Operant conditioning works on the assumption that a particular behavior will either increase or decrease in response to being reinforced or punished. A reinforcer is anything that increases the probability of repeating a behavior, whereas a punishment decreases the probability that the behavior will reoccur. For example, a pigeon can be taught to peck a lever in response to a red light if every time he does so, he is provided with a food pellet immediately afterward. Soon the presence of a red light will emit the pecking of a lever in the pigeon. In this type of learning, many different behaviors can be learned if reinforced. Skinner became interested in how scheduling patterns of reinforcement (or what many people would call rewards) affected learning acquisition and the stability of the newly learned behavior. He found that learning occurred more quickly if continually reinforced, but once learned, a behavior could be maintained longer (the behavior was stronger) if a variable schedule of reinforcement was used.
Operant reinforcers are used extensively in society: grades for school performance, medals and trophies for athletics, and money for labor. Money represents a special form of reinforcer called a token that has no intrinsic value in itself, but represents a means to procure other tangible rewards.
Some theorists did not believe that learning occurred only via reinforcement or punishment. One of these people was the cognitive psychologist Edward Tolman. Tolman allowed rats, who were neither hungry nor thirsty, to wander in a maze. This particular maze was in the shape of a T. At one end of the T, Tolman had placed water, and at the other end of the T he placed food. Since the rats were neither hungry nor thirsty, they had no motivation to go to either end of the T and simply explored the entire maze. Later, Tolman withheld food from half of the rats and water from the other half. When he rereleased them into the maze, the hungry rats went right to the food and the thirsty rats went right to the water, a finding that is inconsistent with what operant conditioning would predict. The rats learned without reinforcement. Tolman hypothesized that the rats had made cognitive maps of the maze and did not need to be reinforced to learn where the food and water were. Tolman’s study was followed with other research and would actually later develop into the field of cognitive psychology and cognitive neuroscience.
Albert Bandura performed another famous series of experiments that indicated that learning does not have to be directly reinforced. In these experiments, children watched a person being rewarded or reprimanded for beating up a clown doll (called a Bobo doll). When the children watched someone being rewarded for punching out the hapless doll, they themselves were later more likely to repeat that behavior, whereas children seeing someone punished or reprimanded for beating up the doll were significantly less likely to beat up Bobo. Bandura termed this form of learning “modeling,” in which the mere observation of seeing someone perform a task or behavior can lead to learning.
Of course there have been many modifications to these theories of learning, but learning can occur by any of these particular methods. Moreover, humans often learn for the sake of learning or for non-tangible rewards and other long-term potential reinforcers, as opposed to animal models where delays in reinforcement often lead to slower learning. While a certain amount of learning does occur via classical and operant conditioning in humans, there is a cognitive component that is associated with learning, and learning in humans often occurs via a combination of these previous methods.
The brain must somehow represent the learning process. Human and animal brains are plastic in that experience can directly lead to physiological changes in the brain, which can result in learning. In order for learning to be successful, there must be some structural change in the brain that occurs as a result of learning and allows the organism to store the memory of the newly learned material. If this were not the case, you would have to learn the same thing over and over again. There has been quite a deal of research investigating how the brain changes during learning. One of the most salient findings as a result of this research is the discovery of long-term potentiation in the brain.
Recall that most neurons communicate via a neurotransmitter sent across the synapse from the axon of a sending neuron to the dendrite of another neuron. The sending neuron is termed the presynaptic neuron and the receiving neuron is often termed the postsynaptic neuron. Learning at the cellular level would be dependent on an increase in the probability that a postsynaptic neuron would be activated in response to the neurotransmitters released from a presynaptic neuron. The more quickly this response takes place, the more learning is accomplished. Experimental studies have attempted to replicate this process by briefly applying high-frequency stimulation to presynaptic neurons and observing the response in the postsynaptic neuron. When this experiment is performed on the brains of rats and other animals, changes occur in the postsynaptic neuron that include the sprouting of new dendritic spines and a faster response to messages from the presynaptic neuron. When more presynaptic neurons that all synapse (connect) with the same postsynaptic neuron are stimulated, the effect is even stronger. This effect has been termed long-term potentiation (LTP).
LTP requires that inputs are excitatory. LTP occurs in the hippocampus and associated areas, such as the entorhinal and parahippocampal cortices, which use the major excitatory neurotransmitter glutamate. Typically many different inputs synapse on the neurons in these areas, and LTP is believed to occur in these areas when new memories are formed.
LTP has two characteristics: First, LTP can last for quite a long time after it is established (even several months after the initial stimulation), and secondly, it only occurs when the firing of the presynaptic neuron is followed by the firing of the postsynaptic neuron. The changes that occur as a result of this relationship between the presynaptic and postsynaptic neuron are further evidence of plasticity in the brain. Other findings indicate that LTP is most prominent in brain structures that are associated with learning and memory.
One of the most influential models of memory, proposed by Atkinson and Shiffrin in 1968, has been termed the modal model of memory. The following figure depicts this model:
Sensory Input
Sensory Memory
Short-Term Memory
Long-Term Memory
In this model, memory follows a linear process starting first with the sensory storage stage. This stage has a very brief duration (only a few seconds at most), a very large capacity, and has different representations for each sensory modality. For example, if you glance at the room around you and then close your eyes, there will be a very short period of time (less than a few seconds) where everything in your span of vision is stored in your visual sensory memory like a snapshot. The image will quickly dissipate.
In order to retain something from sensory memory, you must focus on it or pay attention to it. However, you can only focus on various aspects of sensory memory, and much information is lost in a short time. Attending to some event or stimulus from sensory storage allows you to transfer this information into the second mode, short-term memory, which has a very short duration (about thirty seconds or less) and a very limited capacity (five to nine items). This is demonstrated by the fact that if you try to remember the entire scene, you will only be able to focus on a very small portion of it at a time.
If you want to remember information for a longer period of time, you need to either practice or rehearse it. If you do this efficiently, it transfers into long-term memory, which according to this theory is essentially of unlimited duration and unlimited capacity.
Of course, the understanding that short-term memory is much more complicated than this model suggests resulted in the idea of working memory. Nonetheless, this Atkinson-Shiffrin model has endured over time with some adjustments (e.g., the replacement of short-term memory with a more complicated notion of working memory and the division of long-term memory into separate subtypes). This particular model has also led to the development of the idea of how a transfer from one particular stage to another memory stage occurs, and to the notion of being able to retrieve memories from long-term storage (which many equate with the process of memory). More current conceptualizations of this model include a reworking of the short-term memory component that includes both sensory storage and working memory.
Why do you always forget where your glasses are, but never forget how to read?
Forgetting where you put your keys or glasses are typically examples of poor encoding: Your attentional resources are divided, and you do not sufficiently encode your actions. Forgetting how to read is more difficult, as reading is a well-practiced procedural task. However, significant brain damage can lead to an acquired reading disability (alexia). Most reading disabilities represent learning disorders.
The modal model of memory has influenced the process model of how people learn and remember information. In this sequence of events, one is exposed to some environmental stimulation (sensory memory), pays attention to it (thus putting it in working memory, a process commonly called encoding), and then rehearses or practices it (thus transferring it into long-term storage, a process known as consolidation and storage). When one wishes to pull this memory from long-term storage, she engages in a process known as retrieval or recall. Long-term potentiation refers to the physical process involved in consolidation and storage of memories. However, all memories are not equal in long-term memory. The component of memory that most people identify as their real memory has been divided into several different types of memory processes.
The first major distinction that has been made in long-term memory is whether the memories in this type of storage are consciously accessible; whether there is a need for conscious recollection or recall when reproducing these memories (in other words, these memories would be part of the controlled processes in the dual process model of cognition). Memories that are consciously accessible have been termed declarative or explicit memory. Memories that are not consciously accessible have been termed non-declarative memory or implicit memory (this division would consist of automatic processes according to the dual process model of cognition). Declarative and non-declarative memory are also divided into several subdivisions.
Declarative memory can be further divided into memories for events that are personal (episodic memory) and memories for factual information (semantic memory). Personal events include your recall of when you graduate from high school, your first boyfriend or girlfriend, etc. Factual events include such things as who was the fifth president of the United States, what to use a screwdriver for, what the meaning of the word memory is, etc.
While there is quite a bit of supporting evidence for these different memory systems, there is also some overlap between them. In addition, the brain structures associated with the consolidation and retrieval of these particular memories differ depending on the type of memory involved. Declarative memories are formed in the hippocampal structures and sent to association areas.
Non-declarative memory has several different divisions: procedural memory (cognitive and motor skills), perceptual representations (systems for perceiving words, sounds, objects, etc.), conditioned responses (this can include both classical and operant), and non-associative learning. Non-associative learning consists of a number of processes, such as habituation, where one ignores the continual presence of a stimulus (not hearing background conversations when concentrating on something else), and sensitization, which is the opposite of habituation (becoming more sensitive to stimulation that is particularly relevant or threatening). While both declarative and non-declarative memory are important in functioning, traditionally researchers have focused on declarative memory, as it occupies such an important focus in the lives of most people and is much easier to study than forms of non-declarative memory.
Working memory requires the use of the prefrontal cortex and the hippocampus. Much of the information that enters and is used in working memory is disposable; it does not need to be saved over the long-term. The neurons in the areas of the prefrontal cortex maintain their firing rates, representing various sensory inputs so that you can use working memory to perform a specific task, such as ordering off a menu, dialing a phone number, following directions, etc. Some of this information may enter long-term memory depending on how relevant it is to you. Much of this information may require some form of additional processing, such as rehearsal, to transfer it into long-term memory. The process of transferring information from short-term, or working, memory into long-term memory requires the action of the hippocampus (although there are types of information that do not appear to be dependent on the hippocampus to enter long-term memory).
The most famous clinical case regarding the memory and the hippocampus is the case of HM. HM had both his temporal lobes removed due to intractable epilepsy, thus removing both hippocampi. Following his surgery, he scored relatively normal on IQ tests, but could not form any new memories. For instance, when his mother died, he could never encode this information. Years later, even after being told many times, if someone mentioned that his mother had died, he would break down and cry as if he were hearing this information for the first time. However, HM could learn some new procedural information like learning how to get to the lunchroom in the clinic he was in, even though he could never remember how he learned how to get there or having been there before.
The hippocampus is in the medial area of the temporal lobe and receives inputs from nearly every area of the cortex. The hippocampus is part of a larger system known as the limbic system that is important in processing emotions and in memory. The limbic system includes the amygdala, the orbitofrontal cortex, and the anterior cingulate cortex. The hippocampus has specialized, adjustable synaptic glutamate receptors known as NMDA receptors, named after their primary neurotransmitter (N-methyl-D-aspartate), which are able to define objects and collections of objects within particular contexts. The hippocampus is composed of a set of modifiable neurons that receive input from the cortex and represent what is going on in the current environment. For instance, the hippocampus right now is representing that you are reading this book, the phrases you are reading right now, where you are sitting or standing, and other events currently happening within this context. The hippocampus receives projections from various areas of the cortex that represent these particular aspects of your immediate experience. These hippocampal connections are strengthened via long-term potentiation in the cortex.
In addition, the connections between the hippocampus and the cortex are reciprocal. This allows the connections that have been activated in the hippocampus to be sent back to the cortex from the hippocampus. So if the process of forming a memory is involved in the actual representation of the experience itself in the cortex, then this experience is sent to the hippocampus and a re-creation of the experience is sent from the hippocampus back to the cortex where the memories become stored in the association areas. When a person continues to rehearse information, this activity reverberates back and forth between the cortex and the hippocampus, modifying the neurons in the cortex itself so that it can reproduce the activity that was originally associated with a person’s experience. It is believed that long-term memories that are developed in the hippocampus and sent to the cortex are stored or maintained in the same cortical areas that represented the initial experience. The hippocampus also interacts with the prefrontal cortex that houses working memory to maintain memories long enough for you to use them and transfer them back to the cortex.
Another aspect of transferring information into long-term memory was discovered by means of training rats how to navigate through mazes. It was determined that when the rats slept after the training sessions and entered REM sleep, their hippocampi continued to play back and forth the correct solutions to the mazes. This playback occurred several times during the night (this was determined by the patterns of activation in the rats’ hippocampi during REM sleep compared to the patterns of activation during running and learning the mazes). If the rats were prevented from entering REM sleep, they experienced difficulty consolidating the memories regarding learning the maze. Therefore, it is believed that if an activity is rehearsed enough, much of the consolidation from short-term, or working, memory into long-term memory takes place during REM sleep, although not all the evidence supports this.
Despite popular opinion, memory is not like a tape recorder. When you recall declarative memories, your brain must actually re-create them. This re-creation is subject to outside influences (context, suggestion, emotional states, etc.) and can alter the memory of past events. In psychology, it has been long known that outside influences can change the recollection of past events so as to distort them significantly.
One question that neuroscientists were concerned about was the contribution of the frontal lobes to the memory process. As mentioned previously, the frontal lobes send projections to the hippocampus, but the information from the frontal lobes may not consist of content information, such as the identity or meaning of something. It appears that the frontal lobe inputs add information regarding context and information about a particular event or environment, rather than just semantics. The hippocampal circuits also appear to be involved primarily in declarative memory and not in non-declarative memory. The famous amnestic patient HM discussed earlier was unable to form any new declarative memories; however, he still was able to learn procedural information (non-declarative memory) despite being unable to recall ever having performed these tasks before.
Procedural memories appear to be formed in the basal ganglia, stratum, and cerebellum. It may well be that certain types of classical conditioning are represented or formed in the cerebellum and in the limbic system.
Most people believe that forgetting is bad; however, it may be more of an efficient use of memory capacity as opposed to a fault of the system. The availability to previously stored information needs to be prioritized in the system so that the most relevant information can be accessed easily. In addition, as any student will tell you, the ability to recognize information is easier than the ability to recall information (this is why students prefer multiple-choice over essay examinations). The amount of processing at the encoding stage that free recall requires is much greater than what is needed for recognition. Some researchers have proposed that recognition consists of two separate mechanisms: familiarity, where the item just feels familiar and is context-free, and recollection, where context is important and cues memory. These two mechanisms of recognition may also explain why it is easier to recognize things than to recall them.
The way that information is processed will also determine its availability to be retrieved. The levels-of-processing account theory proposes that information processed in a semantic fashion will be easier to retrieve than information processed in a perceptual fashion. Research has suggested that the frontal cortex may be important for selecting attributes that allow for easier and quicker retrieval of material based on studies using neuroimaging. The famous memory theorist, Endel Tulving, believed that material is more easily recalled if the context during retrieval is similar to the context during the initial coding of the material, a theory termed the encoding specificity hypothesis. This theory appears to have good empirical support. So students should study under the same or similar conditions under which they will have to recall material.
However, suppose you encoded something correctly and could recall the information at one time, but then forgot it. What explains that type of forgetting? One line of theories suggests that passive processes such as decay of the memory explain such instances. Other explanations are theories that tend to be more active, such as interference inhibition theories.
Proactive interference refers to difficulty learning new information because of interference from previously learned information, whereas retroactive interference occurs when someone has difficulty recalling previously learned information due to interference from newly learned information. The idea of a passive process that leads to the decay of memory traces has been hard to substantiate empirically; however, the active mechanisms have been supported in some of the literature. It appears that the ability to learn new information can sometimes be impeded by information already stored in the cortex, and recall of previously learned information can sometimes be interrupted by newly learned information.
Can a bump on the head restore memory?
While there are claims of this happening, this is most likely a myth, typically seen in films. Such an event has never been replicated experimentally to the author’s knowledge.
Experiments looking at directed forgetting suggest that memories can be inhibited voluntarily. In some very clever experiments, participants are given two lists of words to remember. Some of the participants are later told that the first list was a practice list (after learning it) and it is okay to forget words from the first list, while others are told to remember both lists. Surprisingly, the recall of the list that the participants are instructed not to remember is significantly worse. These experiments demonstrate that the presence of strategic forgetting does occur. It may well be that once you learn material, use it to serve a purpose, and then decide either unconsciously or consciously that you no longer need to remember it, it is forgotten.
Learning disabilities are categorized by domain. Dyslexia is a term that describes several different types of reading difficulties that are not related to intellectual, visual, or motor problems in the person. There are two basic types of dyslexia: an acquired form of dyslexia that is caused by brain damage to a person who was previously able to read well (the term for this is alexia), and developmental dyslexia, which surfaces when the child is learning to read (this is true dyslexia).
Developmental dyslexia is more common than acquired dyslexia, and the majority of research has focused on the causes of developmental dyslexia. As with nearly all disorders and all human traits, either behavioral or physical, there is a strong genetic component that contributes to acquiring dyslexia such that a person’s probability of displaying some type of developmental disorder increases as a function of the presence of the same disorder in his direct relatives. Developmental dyslexia has a heritability of about 50 percent, which is not unusually high and is consistent with many other behavioral traits and developmental issues.
The difficulty in identifying the neural substrates in the brains of individuals with dyslexia is that there have been a large number of identified differences in the brains of these individuals, and no single brain-related pathology appears to occur in all or most of the cases. Many individuals with developmental dyslexia also have other attentional or sensory deficits linked to visual brain circuits or auditory circuits, or they have motor deficits. The most accepted explanation for dyslexia is that this disorder somehow results from a deficit in the ability to represent and comprehend speech sounds (deficits with phonological processing). The exact brain mechanism responsible for this deficit is not yet understood.
Dyslexia is not the only type of learning disorder. There are a number of different types of developmental learning disorders that have been identified, including such disorders as math-related learning disorders, nonverbal learning disorders, and others. Like dyslexia, there appears to be a strong genetic component to these, and like dyslexia, there are many hypotheses as to the neural substrates that are disrupted in these disorders; however, at this time the exact neural mechanisms involved in these disorders have not been verified.
The term amnesia refers to a pathological loss of memory. Sometimes amnesia can be due to psychological stress or psychological trauma. Memory loss of some degree is a common effect of brain damage. This section will focus on brain damage as a result of traumatic brain injuries and surgical procedures. The progressive brain damage that occurs in certain neurological disorders, such as Alzheimer’s disease, and brain damage due to conditions such as stroke will be discussed in a different section of this book.
Global amnesia refers to memory loss that is general in nature. The person is unable to remember information that occurred prior to her injury, during her injury, and after her injury. Retrograde amnesia refers to memory loss for events occurring before the brain injury happened. Anterograde amnesia refers to memory loss or an inability to remember events that occurred after the occurrence of the brain injury. The presence of lasting global amnesia or severe retrograde amnesia in individuals with a traumatic brain injury is actually rare, unless the brain injury is severe and the brain damage is extensive.
Most often following an injury to the brain, there is a period of post-traumatic amnesia where the individual is confused, may have global memory issues, and will often not remember the events that took place surrounding the time of the injury. As the individual recovers, it is not unusual for memories that were present prior to the brain injury to return, although there may be a temporal gradient associated with these memories such that information closer in time to the actual occurrence of the brain injury is more difficult to remember than information further back in time. It is not unusual for individuals who have even mild brain injuries to be unable to recall the event that led to the brain damage or events occurring within a short time before or after their injury. Anterograde amnesia or difficulties forming new memories is more common in cases of traumatic brain injury than is lasting retrograde amnesia.
A concussion occurs when there is some type of mechanical force applied to the brain that results in any alteration of an individual’s thinking processes. For most people, the typical bump on the head does not result in a concussion; however, many people do experience some form of mild concussion at least once in their lifetime. The experience of having one or two mild concussions has not been shown to result in any significant long-term effects (after all, nature built in recovery mechanisms in all animals for these events). Having multiple mild, moderate, or severe concussions in succession can result in long-lasting effects, and this is why there have been changes instituted in many contact sports, such as football, to protect the participants from this possibility.
Traumatic brain injury (TBI) is a condition that can occur when a severe mechanical force results in damage to the brain. Two general categories of TBI exist: closed-head injury, where there is no penetration into the skull, and open-head injury, where some projectile penetrates the skull and enters the brain. In the latter, such as gunshot wounds or other penetrating injuries, the effects of the injury are typically focal, that is, the behavioral effects as a result of the brain injury are typically limited to those associated with the area of the brain that has been penetrated. These effects may be temporary or longer-lasting, depending on the severity of the injury and other variables related to recovery in the person.
Closed-head injuries can have temporary or long-lasting effects and, depending on the initial severity of the injury, can have focal effects or more generalized effects. Because the circuits in the brain that deal with encoding, storage, and retrieval are so extensive, it is not unusual for individuals with moderate or severe TBI to experience long-lasting difficulties with memory. When the mechanical force applied to the brain is significant, this may result in not only injuries at the site of the blow to the head, but also in more diffuse injuries throughout the brain. When an object strikes the skull, it can produce damage to the brain at the site of the impact (called a coup injury), and the resulting shockwaves that travel through the brain and push it against the opposite side of the skull can result in injury in that area as well (termed a countercoup injury). Severe forces applied to the skull can result in rotational injuries, tearing axons in the brain, and diffuse brain damage known as diffuse axonal injury, which can lead to severe, long-lasting effects. In these cases, there may not be an actual physical blow to the head, but damage can result from forces that occur, such as during a car accident or when being violently shaken or tossed about (like in shaken baby syndrome).
One issue regarding rehabilitation that does seem to have a good amount of empirical support is that having these patients exercise and remain active following their injury is related to quicker recovery times. Because no two people with TBIs have exactly the same injury, it is difficult to design empirical studies to compare the effectiveness of different cognitive rehabilitation methods.
The prognosis for individuals who have experienced some type of TBI varies depending on the severity of the TBI and on the length of any post-traumatic amnesia they may have incurred. Individuals with more severe TBIs and longer terms of post-traumatic amnesia typically are at risk for longer-lasting and more severe effects. In general, there is some recovery in most cases of TBI; however, many individuals display long-lasting or even permanent cognitive effects. There are certain medications and combinations of medications that have been demonstrated to aid in the recovery time of individuals who have cognitive deficits following a TBI. However, it appears that these medications are most effective when applied early in recovery and may not be as effective in the later stages of recovery.
The use of cognitive rehabilitation techniques in treating people with TBI is common, but there is still some question as to whether these methods offer any additional rehabilitative effects outside of normal recovery.