From Wikipedia, the free encyclopedia

Attention is the cognitive process of selectively concentrating on one thing while ignoring other things. Examples include listening carefully to what someone is saying while ignoring other conversations in the room (e.g. the cocktail party problem, Cherry, 1953). Attention can also be split, as when a person drives a car and talks on a cell phone at the same time.

Attention is one of the most intensely studied topics within psychology and cognitive neuroscience. Of the many cognitive processes associated with the human mind (decision-making, memory, emotion, etc), attention is considered the most concrete because it is tied so closely to perception. As such, it is a gateway to the rest of cognition.

The most famous definition of attention was provided by one of the first major psychologists, William James:
"Everyone knows what attention is. It is the taking possession by the mind in clear and vivid form, of one out of what seem several simultaneously possible objects or trains of thought...It implies withdrawal from some things in order to deal effectively with others." (Principles of Psychology, 1890)
History of the study of attention

1850s to 1920s

In James' time, the only method available to study attention was introspection. Very little progress was made in quantifying the study of attention, though it was considered a major field of intellectual inquiry by such diverse authors as Sigmund Freud, Walter Benjamin, and Max Nordau. For example, one major debate in this period was whether it was possible to attend to two things at once (split attention). Some thinkers felt that they were unable to do so, and other thinkers felt that they could. Without experiments, it was impossible to settle the debate.

1920s to 1950s

From the 1920s to the 1950s, the field of attention was relatively inactive. The dominant psychological paradigm at the time was Behaviorism. This view was defined by an epistemology called Positivism, which does not permit assumptions about processes that cannot be observed directly (e.g. cognitive processes, gravitational forces in physics). Thus, the cognitive processes that govern attention were not considered legimitate objects of scientific study.

1950s to present

In the 1950s, psychologists renewed their interest in attention when the dominant epistomology shifted from Positivism to Realism during what has come to be known as the cognitive revolution (Harré, 2002). The cognitive revolution admitted unobservable cognitive processes like attention as legitimate objects of scientific study.

Cherry and Broadbent, among others, performed experiments on dichotic listening. In a typical experiment, subjects would listen to two streams of words in different ears of a set of headphones, and selectively attend to one stream. After the task, the experimenter would ask the subjects questions about the content of the unattended stream.

During this period, the major debate was between early-selection models and late-selection models. In the early selection models, attention shuts down processing in the unattended ear before the mind can analyze its semantic content. In the late selection models, the content in both ears is analyzed semantically, but the words in the unattended ear cannot access consciousness. This debate has still not been resolved.

In the 1960s, Anne Treisman began developing the highly influential Feature integration theory (first published under this in a paper with G. Gelade in 1980). According to this model, attention is responsible for binding different features into consciously experienced wholes. Although this model has received much criticism, it is still widely accepted or held up with modifications as in Jeremy Wolfe's visual search paradigm.

In the 1960s, Robert Wurtz at the NIH began recording electrical signals from the brains of macaque monkeys who were trained to perform attentional tasks. These experiments showed for the first time that there was a direct neural correlate of a mental process (namely, enhanced firing in the superior colliculus).

In the 1990s, neuroscientists began using fMRI to image the brain in attentive tasks. The results of these experiments have shown a broad agreement with the psychophysical and monkey literature.

Current research

Attention remains a major area of investigation within psychology and neuroscience. Many of the major debates of James' time remain unresolved. For example, although most scientists accept that attention can be split, strong proof has remained elusive. And there is still no widely-accepted definition of attention more concrete than that given in the James quote above. This lack of progress has led many observers to speculate that attention refers to many separate processes without a common mechanism.

Areas of active investigation involve determining the source of the signals that generate attention, the effects of these signals on the tuning properties of sensory neurons, and the relationship between attention and other cognitive processes like working memory. Some speculative research has even shown that flies may be able to attend (using a brain the size of a poppy seed) in much the same way neurologically as humans do.

Overt and covert attention

What we look at may not be what we attend to. It is possible to look in one direction but actually notice changes in another direction. Overt attention is the act of directing our eyes or ears towards a stimulus source. Covert attention is the act of mentally focusing on a particular stimulus. Covert attention is thought to be a neural process that enhances the signal from a particular part of the sensory panorama.

Why should we have these two disjoint mechanisms for directing spatial attention? There are studies that show that the two mechanisms may not be so disjoint. Work by the group of Rizzolatti have suggested that, though humans and primates can look in one direction but attend in another, there is underlying neural circuitry that links shifts in covert attention to plans to shift gaze. So, if we attend to the right hand corner of our eye, we `want' to move our eyes in that direction, and have to actively suppress the eye movement that is linked to this shift in attention.

The current view is that visual covert attention is a mechanism for quickly scanning the field of view for interesting locations. This shift in covert attention is linked to eye movement circuitry that sets up a slower saccade to that location.

Neural correlates of attention

Most experiments show that one neural correlate of attention is enhanced firing. Say a neuron has a certain response to a stimulus when the animal is not attending to that stimulus. When the animal attends to the stimulus, even if the physical characteristic of the stimulus remains the same the neurons response is enhanced. A strict criterion, in this paradigm of testing attention, is that the physical stimulus available to the subject must be the same, and only the mental state is allowed to change. In this manner, any differences in neuronal firing may be attributed to a mental state (attention) rather than differences in the stimulus itself.

In this context it is instructive, though slightly tangential, to mention the Necker cube illusion. This is a great example of the mental preception of a stimulus changing, even though the stimulus itself is unchanged. A recent neural study in monkeys claims to have found a neural correlate to the Necker cube illusion.

Human attention

What members of a species will pay attention to is a function of their evolutionary and cultural history. In the case of humans there are problems presented by ecosystem changes resulting from human mobility and cultural artifacts. Humans no longer live in the ecosystem they evolved in, but in an ecosystem of their own creation. To take a mundane example, humans are attracted to sweet food, an adaptive trait for hunting and gathering, not so adaptive for modern nutrition.

A more substantial problem is presented by the human propensity to focus on emergency situations to the exclusion of background phenomena which may be more significant. This can be seen in what is considered news, where a spectacular auto accident easily outweighs a report on particulate pollution; although only a few may have died in the accident, thousands may suffer and die due to smog-related illnesses.

Humans, like all animals, respond more readily to novel objects and fast changes. That is why predators evolve to blend with their surroundings and move very little while stalking prey. Novel objects and fast changes are most likely to carry new information, and may be profitable to analyze in greater detail, than old objects, already inspected and slow changes that do not affect us immediately.

An interesting way to demonstrate how culture biases our attention is to fill a box with various everyday odds and ends from different walks of life and different cultures. For instance the box may include incense sticks as well as a microchip. People are then allowed to look into the box for a short period like one minute, and then asked, after an interval of a few minutes, to write down what objects they saw. They don't have to explicitly name the objects, but can also describe them. It may be found that the majority of objects that a person remembers are the ones that are unusual to them. Novel objects tend to attract attention.

Attention-deficit hyperactivity disorder

PET scans measure the activity of various parts of the brain. The image on the left illustrates areas of activity in the brain of a person without ADHD while doing an assigned task. The image on the right illustrates the areas of activity of the brain of someone with ADHD when given that same task. There is some controversy over the meaning of the research by Dr. Alan Zametkin that produced these images; the statistical findings visually demonstrated here were found to be the result of sampling error. The adults in these studies were in most cases severely dysfunctional.

Attention-deficit/hyperactivity disorder (ADHD) is a mental disorder, usually diagnosed in childhood, which manifests itself with symptoms such as hyperactivity, forgetfulness, mood shifts, poor impulse control, and distractibility.[1] In neurological pathology, ADHD is currently considered to be a chronic syndrome for which no medical cure is available. Pediatric patients as well as adults may present with ADHD, which is believed to affect between 3-5% of the human population.

Much controversy surrounds the diagnosis of ADHD, such as over whether or not the diagnosis denotes a disability in its traditional sense or simply describes a personal or neurological property of an individual. Those who believe that ADHD is a traditional disability or disorder often debate over how it should be treated, if at all. According to a majority of medical research in the United States, as well as other countries, ADHD is today generally regarded to be a non-curable neurological disorder for which, however, a wide range of effective treatments are available. Methods of treatment usually involve some combination of medication, psychotherapy, and other techniques. Many patients are able to control their symptoms over time, even without the use of medication. Some individuals who meet the diagnostic criteria of ADHD, according to the guidelines of the Diagnostic and Statistical Manual of Mental Disorders, do not consider themselves to be mentally ill, as the manual suggests, and therefore may remain undiagnosed or, after a positive diagnosis, untreated.

ADHD is most commonly diagnosed in children. When diagnosed in adults, it is regarded as adult attention-deficit disorder (AADD). It is believed that anywhere between 30 to 70% of children diagnosed with ADHD retain the disorder as adults.

Symptoms

The symptoms of ADHD fall into the following two broad categories:
Inattention:
1. Failing to pay close attention to details or making careless mistakes when doing schoolwork or other activities
2. Trouble keeping attention focused during play or tasks
3. Appearing not to listen when spoken to
4. Failing to follow instructions or finish tasks
5. Avoiding tasks that require a high amount of mental effort and organization, such as school projects
6. Frequently losing items required to facilitate tasks or activities, such as school supplies
7. Excessive distractibility
8. Forgetfulness

Hyperactivity-impulsive behavior

1. Fidgeting with hands or feet or squirming in seat
2. Leaving seat often, even when inappropriate
3. Running or climbing at inappropriate times
4. Difficulty in quiet play
5. Frequently feeling restless
6. Excessive speech
7. Answering a question before the speaker has finished
8. Failing to await one's turn
9. Interrupting the activities of others at inappropriate times

A positive diagnosis is usually only made if the patient presents with at least six of the above symptoms. In addition, a positive diagnosis is made if six or more of these symptoms presented before the age of seven; the symptoms usually begin to appear between the ages of four and six. Symptoms must appear consistently in varied environments. (Ex: At home, school, and in public.)
Children who grow up with ADHD often continue to have symptoms as they grow into adulthood. Adults face some of their greatest challenges in the areas of self-control and self-motivation, as well as executive functioning (also known as working memory). If the patient is not treated appropriately, co-morbid conditions, such as depression and anxiety may present as well. If a patient presents with such conditions as well, the co-morbid condition is usually treated first.

Diagnosis

The Centers for Disease Control and Prevention (CDC) emphasize that a diagnosis of ADHD should only be made by trained health care providers, as many of the symptoms may also be part of other conditions, such as bodily illness or other physical disorders, such as hyperthyroidism. Further, it is not uncommon that physically and mentally nonpathological individuals exhibit at least some of the symptoms from time to time. Severity and pervasiveness of the symptoms leading to prominent functional impairment across different settings (school, work, social relationships) are major factors in a positive diagnosis.

Possible causes

Exactly what causes ADHD remains unknown. In 1998 NIH (US National Institutes of Health) called together most of the experts in this field. They issued a consensus statement. This is the next to last sentence of that report: [6] "Finally, after years of clinical research and experience with ADHD, our knowledge about the cause or causes of ADHD remains largely speculative. Consequently, we have no documented strategies for the prevention of ADHD." Similarly the Surgeon General states [7]the etiology of ADHD is unknown. Numerous theories and speculations exist on the subject. For example, research indicates that the frontal lobes, their connections to the basal ganglia, and the central aspects of the cerebellum (vermis) may be involved in this disorder, as may be a region in the middle or medial aspect of the frontal lobe, known as the anterior cingulate.[citation needed] The cerebellum, which is believed to play important roles in "short-term memory, attention, impulse control, emotion, higher cognition, [and] the ability to schedule and plan tasks,"[10] has been shown to be smaller in the brains of those who have ADHD. [11] It should be noted however, that non biological patterns of behavior can effect brain size. For example, learning Braille causes enlargement of the part of the motor cortex that controls finger movements. [12] After they have passed their licensing exam, London taxi drivers have been found to have a significantly enlarged hippocampus (a part of the brain that stores memories (in this case spatial-visual memories))compared to non-taxi drivers [13] Patients abused during their childhood with post traumatic stress disorder will have a flattened out hippocampus.[14] Professional musicians have brains that are different from non-musicians.[8] Monks who meditate show measurable differences in their prefrontal lobes.

The source of claimed differences in those with ADHD is not yet known, but a couple of theories have been presented.

Hereditary dopamine deficiency

Research suggests that ADHD arises from a combination of various genes, many of which have something to do with dopamine transporters. [15] Suspect genes include the 10-repeat allele of the DAT1 gene[16] and the 7-repeat allele of the DRD4 gene, [17] Other studies have documented an association between ADHD and the dopamine beta hydroxylase gene (DBH TaqI).[citation needed]
In addition, SPECT scans found people with ADHD to have reduced blood circulation, [18] and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. [19]

Metabolism

It has long been suggested that ADHD could be the result of a nutritional problem. Recent studies have begun to find metabolic differences in these children, indicating that an inability to handle certain elements of one's diet might contribute to the development of ADHD, or at least ADHD-like symptoms. For example, in 1990 the English chemist N.I. Ward showed that children with ADHD lose zinc when exposed to a food dye. Waring, McFadden, and others have shown that children with autism or ADHD are low in sulfation metabolism, in particular the enzyme Phenol Sulfotransferase-P. Some studies suggest that a lack of fatty acids, specifically omega-3 fatty acids can trigger the development of ADHD. Support for this theory comes from findings that breast-fed children are less likely to have ADHD than their bottlefed counterparts and until very recently, infant formula did not contain any omega-3 fatty acids at all. Time will tell whether or not this is coincidence or a true correlation.

External Factors

There is no compelling evidence that social factors, alone, can create ADHD. (However, see discussion of parental role in section below) The few environmental factors implicated fall in the realm of biohazards including alcohol, tobacco smoke, and lead poisoning. Allergies (including those to artificial additives)[20] as well as complications during pregnancy and birth-- including premature birth--might also play a role.

Smoking during pregnancy

It has been observed that women who smoke while pregnant are more likely to have children with ADHD.[21]. Nicotine is known to cause hypoxia (lack of oxygen) in the uterus, which may lead to brain damage in the unborn child. Smoking could therefore play a major role in the child's development of the disorder prior to birth.

Head injuries

Head injuries may cause a person to present with ADHD-like symptoms, possibly because of damage done to the patient's frontal lobes. Because symptoms were attributable to brain damage, earliest designations for ADHD was "Minimal Brain Damage".

Dopamine deficiency caused by sleep apnea

Another theory is that ADHD is caused by brief pauses in breathing (apnea) during infancy. In October 2004, Dr. Glenda Keating and Dr. Michael Decker of Emory University presented data at the Society for Neuroscience's annual meeting showing that repetitive drops in blood oxygen levels in newborn rats similar to that caused by apnea in some human infants is followed by a long-lasting reduction in dopamine levels, associated with ADHD. Apnea occurs in up to 85% of prematurely born human infants[22]. It remains to be seen whether or not these findings can be replicated in human babies.

Mainstream treatments

The first-line medication used to treat ADHD are mostly stimulants, which work by stimulating the areas of the brain responsible for focus, attention, and impulse control. The use of stimulants to treat a syndrome often characterized by hyperactivity is sometimes referred to as a paradoxical effect. But there is no real paradox in that stimulants activate brain inhibitory and self-organizing mechanisms permitting the individual to have greater self-regulation. The stimulants used include:
• Methylphenidate — Available in:
o Regular formulation, sold as Ritalin, Metadate, Focalin, or Methylin. Duration: 4–6 hours per dose. Usually taken morning, lunchtime, and in some cases, afternoon.
o Long acting formulation, sold as Ritalin SR, Metadate ER. Duration: 6–8 hours per dose. Usually taken twice daily.
o All-day formulation, sold as Ritalin LA, Metadate CD, Concerta (Methylphenidate Hydrochloride), Focalin XR. Duration: 10–12 hours per dose. Usually taken once a day.
• Amphetamines —
o Dextroamphetamine — Available in:
Regular formulation, sold as Dexedrine. Duration: 4–6 hours per dose. Usually taken 2–3 times daily.
Long-acting formulation, sold as Dexedrine Spansules. Duration: 8–12 hours per dose. Taken once a day.
o Adderall, a trade name for a mixture of dextroamphetamine and laevoamphetamine salts. — Available in:
Regular formulation, Adderall. Duration: 4–6 hours a dose.
Long-acting formulation, Adderall XR. Duration: 12 hours. Taken once a day.
o Methamphetamine — Available in:
Regular formulation, sold as Desoxyn by Ovation Pharmaceutical Company.
• Bupropion. A dopamine and norepinephrine reuptake inhibitor, marketed under the brand name Wellbutrin.
• Atomoxetine. A norepinephrine reuptake inhibitor (NRI) introduced in 2003, it is the newest class of drug used to treat ADHD, and the first non-stimulant medication to be used as a first-line treatment for ADHD. Available in:
o Once daily formulation, sold by Eli Lilly and Company as Strattera. This medicine doesn't have an exact duration. It is to be taken once or twice a day, depending on the individual, every day, and takes up to 6 weeks to begin working fully. If the intake schedule is interrupted, it may take a few weeks to begin working correctly again.
Second-line medications include:
• Benzphetamine — a less powerful stimulant. Research on the effectiveness of this drug is not yet complete.
• Provigil/Alertec/modafinil — Recently approved by FDA for the treatment of ADHD. Provides an alternative to traditional stimulants.
• Cylert/Pemoline — a stimulant used with great success until the late 1980s when it was discovered that this medication could cause liver damage. Although some physicians do continue to prescribe Cylert, it can no longer be considered a first-line medicine. In March 2005, the makers of Cylert announced that it would discontinue the medication's production.
• Clonidine — Initially developed as a treatment for high blood pressure, low doses in evenings and/or afternoons are sometimes used in conjunction with stimulants to help with sleep and because Clonidine sometimes helps moderate impulsive and oppositional behavior and may reduce tics.article
Because most of the medications used to treat ADHD are Schedule II under the U.S. DEA schedule system, and are considered powerful stimulants with a potential for diversion and abuse, there is controversy surrounding prescribing these drugs for children and adolescents. However, research studying ADHD sufferers who either receive treatment with stimulants or go untreated has indicated that those treated with stimulants are in fact much less likely to abuse any substance than ADHD sufferers who are not treated with stimulants.[25]

Attention versus memory in prefrontal cortex

A widely accepted theory regarding the function of the prefrontal cortex is that it serves as a store of short-term memory. This idea was first formulated by Jacobsen, who reported in 1935 that damage to the primate prefrontal cortex caused short-term memory deficits. Karl Pribram and colleagues (1952) identified the part of the prefrontal cortex responsible for this deficit as area 46, also known as the dorsolateral prefrontal cortex (PFdl). More recently, Goldman-Rakic and colleagues (1993) evoked short-term memory loss in localized regions of space by temporary inactivation of portions of the PFdl. Once the concept of working memory (see also Working Memory Model) was established in contemporary neuroscience by Baddeley (1986), these neuropsychological findings contributed to the theory that the prefrontal cortex implements working memory and, in some extreme formulations, only working memory. In the 1990s this theory developed a wide following, and it became the predominant theory of PF function, especially for nonhuman primates. The concept of working memory used by proponents of this theory focused mostly on the short-term maintenance of information, and rather less on the manipulation or monitoring of such information or on the use of that information for decisions. Consistent with the idea that the prefrontal cortex functions predominantly in maintenance memory, delay-period activity in the PF has often been interpreted as a memory trace. (The phrase "delay-period activity" applies to neuronal activity that follows the transient presentation of an instruction cue and persists until a subsequent “go” or “trigger” signal.)

Binding problem
From Wikipedia, the free encyclopedia

"The binding problem is, basically, the problem of how the unity of conscious perception is brought about by the distributed activities of the central nervous system" (Revonsuo and Newman (1999)).

In its most general form it arises whenever information from distinct populations of neurons must be combined. Somehow the activity of specialised sets of neurons dealing with different aspects of perception are combined to form a unified perceptual experience. The binding problem also occurs in each modality of perception and different versions of the problem have been described in language production, visual perception, auditory perception, and other mental processes.

In the case of visual perception, the brains of humans and other animals process different aspects of perception by separating information about those aspects and processing them in distinct regions of the brain. For example, different areas in the visual cortex specialise in processing the different aspects of colour, motion, and shape. This type of modular coding yields ambiguity in many instances. For example, when humans view a scene containing a red circle and a green square, some neurons signal the presence of red, others signal the presence of green, still others the circle shape and square shape. Here, the binding problem is the issue of how the brain represents the pairing of color and shape.

The binding problem is also an issue in memory. How do we remember the associations among different elements of an event? How does the brain create and maintain those associations? Both the hippocampus and prefrontal cortex seem to be important for memory binding.

The binding problem is also closely related to the problem of the homunculus needed to explain who is watching the wonderfully integrated internal TV screen. The alternative to a ghost in the machine in this context is infinite regress.

The solution to the problem is often sought in the direction of the synchronisation of the firing of different neurons in the cortex. Engel and his coworkers (1992) have found that two different neurons with a different receptive field produce divergent correlograms according to wether the stimuli were binded together or not.