Search This Blog

Wednesday, March 4, 2026

Aphasia

From Wikipedia, the free encyclopedia
Aphasia
Regions of the left hemisphere that can give rise to aphasia when damaged

Aphasia, also known as dysphasia, is an impairment in a person's ability to comprehend or formulate language because of dysfunction in specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine, but aphasia due to stroke is estimated to be 0.1–0.4% in developed countries. Aphasia can also be the result of brain tumors, epilepsy, autoimmune neurological diseases like multiple sclerosisinfection of the brain, or neurodegenerative diseases like dementias.

To be diagnosed with aphasia, a person's ability to produce and/or comprehend written and/or spoken language must be significantly impaired. In the case of progressive aphasia, this impairment progresses slowly with time.

The difficulties of people with aphasia can range from occasional trouble finding words, to losing the ability to speak, read, or write; intelligence, however, is unaffected. Expressive language and receptive language can both be affected as well. Aphasia also affects visual language such as sign language. In contrast, the use of formulaic expressions in everyday communication is often preserved. For example, while a person with aphasia, particularly expressive aphasia (Broca's aphasia), may not be able to ask a loved one when their birthday is, they may still be able to sing "Happy Birthday". One prevalent deficit in all aphasias is anomia, in which the affected individual has difficulty finding the correct word.

With aphasia, one or more modes of communication in the brain have been damaged and are therefore functioning incorrectly. Aphasia is not caused by damage to the brain resulting in motor or sensory deficits, thus producing abnormal speech — that is, aphasia is not related to the mechanics of speech, but rather the individual's language cognition. However, it is possible for a person to have both problems, e.g. in the case of a hemorrhage damaging a large area of the brain. An individual's language abilities incorporate the socially shared set of rules, as well as the thought processes that go behind communication (as it affects both verbal and nonverbal language). Aphasia is not a result of other peripheral motor or sensory difficulty, such as paralysis affecting the speech muscles, or a general hearing impairment.

Neurodevelopmental forms of auditory processing disorder (APD) are differentiable from aphasia in that aphasia is by definition caused by acquired brain injury, but acquired epileptic aphasia has been viewed as a form of APD.

Signs and symptoms

People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems, such as dysarthria or apraxia, and not primarily due to aphasia. Aphasia symptoms can vary based on the location of damage in the brain. Signs and symptoms may or may not be present in individuals with aphasia and may vary in severity and level of disruption to communication. Often those with aphasia may have a difficulty with naming objects, so they might use words such as thing or point at the objects. When asked to name a pencil they may say it is a "thing used to write".

  • Inability to comprehend language
  • Inability to pronounce, not due to muscle paralysis or weakness
  • Inability to form words
  • Inability to recall words (anomia)
  • Poor enunciation
  • Excessive creation and use of protologisms
  • Inability to repeat a phrase
  • Persistent repetition of one syllable, word, or phrase (stereotypies, recurrent/recurring utterances/speech automatism) also known as perseveration.
  • Paraphasia (substituting letters, syllables or words)
  • Agrammatism (inability to speak in a grammatically correct fashion)
  • speaking in incomplete sentences
  • Inability to read
  • Inability to write
  • Limited verbal output
  • Difficulty in naming
  • Speech disorder
  • Speaking gibberish
  • Inability to follow or understand simple requests

Given the previously stated signs and symptoms, the following behaviors are often seen in people with aphasia as a result of attempted compensation for incurred speech and language deficits:

  • Self-repairs: Further disruptions in fluent speech as a result of mis-attempts to repair erred speech production.
  • Struggle in non-fluent aphasias: A severe increase in expelled effort to speak after a life where talking and communicating was an ability that came so easily can cause visible frustration.
  • Preserved and automatic language: A behavior in which some language or language sequences that were used frequently prior to onset are still produced with more ease than other language post onset.

Subcortical

  • Subcortical aphasia's characteristics and symptoms depend upon the site and size of subcortical lesion. Possible sites of lesions include the thalamus, internal capsule, and basal ganglia.

Cognitive deficits

While aphasia has traditionally been described in terms of language deficits, there is increasing evidence that many people with aphasia commonly experience co-occurring non-linguistic cognitive deficits in areas such as attention, memory, executive functions and learning. By some accounts, cognitive deficits, such as attention and working memory constitute the underlying cause of language impairment in people with aphasia. Others suggest that cognitive deficits often co-occur, but are comparable to cognitive deficits in stroke patients without aphasia and reflect general brain dysfunction following injury. Whilst it has been shown that cognitive neural networks support language reorganisation after stroke, The degree to which deficits in attention and other cognitive domains underlie language deficits in aphasia is still unclear.

In particular, people with aphasia often demonstrate short-term and working memory deficits. These deficits can occur in both the verbal domain as well as the visuospatial domain. Furthermore, these deficits are often associated with performance on language specific tasks such as naming, lexical processing, and sentence comprehension, and discourse production. Other studies have found that most, but not all people with aphasia demonstrate performance deficits on tasks of attention, and their performance on these tasks correlate with language performance and cognitive ability in other domains. Even patients with mild aphasia, who score near the ceiling on tests of language often demonstrate slower response times and interference effects in non-verbal attention abilities.

In addition to deficits in short-term memory, working memory, and attention, people with aphasia can also demonstrate deficits in executive function. For instance, people with aphasia may demonstrate deficits in initiation, planning, self-monitoring, and cognitive flexibility. Other studies have found that people with aphasia demonstrate reduced speed and efficiency during completion of executive function assessments.

Regardless of their role in the underlying nature of aphasia, cognitive deficits have a clear role in the study and rehabilitation of aphasia. For instance, the severity of cognitive deficits in people with aphasia has been associated with lower quality of life, even more so than the severity of language deficits. Furthermore, cognitive deficits may influence the learning process of rehabilitation and language treatment outcomes in aphasia. Non-linguistic cognitive deficits have also been the target of interventions directed at improving language ability, though outcomes are not definitive. While some studies have demonstrated language improvement secondary to cognitively-focused treatment, others have found little evidence that the treatment of cognitive deficits in people with aphasia has an influence on language outcomes.

One important caveat in the measurement and treatment of cognitive deficits in people with aphasia is the degree to which assessments of cognition rely on language abilities for successful performance. Most studies have attempted to circumvent this challenge by utilizing non-verbal cognitive assessments to evaluate cognitive ability in people with aphasia. However, the degree to which these tasks are truly "non-verbal" and not mediated by language is unclear. For instance, Wall et al. found that language and non-linguistic performance was related, except when non-linguistic performance was measured by "real life" cognitive tasks.

Causes

Aphasia is most often caused by stroke, where about a quarter of patients who experience an acute stroke develop aphasia. However, any disease or damage to the parts of the brain that control language can cause aphasia. Some of these can include brain tumors, traumatic brain injury, epilepsy and progressive neurological disorders. In rare cases, aphasia may also result from herpesviral encephalitis. The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia. In acute disorders, such as head injury or stroke, aphasia usually develops quickly. When caused by brain tumor, infection, or dementia, it develops more slowly.

Substantial damage to tissue anywhere within the region shown in blue (on the figure in the infobox above) can potentially result in aphasia. Aphasia can also sometimes be caused by damage to subcortical structures deep within the left hemisphere, including the thalamus, the internal and external capsules, and the caudate nucleus of the basal ganglia. The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms. A very small number of people can experience aphasia after damage to the right hemisphere only. It has been suggested that these individuals may have had an unusual brain organization prior to their illness or injury, with perhaps greater overall reliance on the right hemisphere for language skills than in the general population.

Primary progressive aphasia (PPA), while its name can be misleading, is actually a form of dementia that has some symptoms closely related to several forms of aphasia. It is characterized by a gradual loss in language functioning while other cognitive domains are mostly preserved, such as memory and personality. PPA usually initiates with sudden word-finding difficulties in an individual and progresses to a reduced ability to formulate grammatically correct sentences (syntax) and impaired comprehension. The etiology of PPA is not due to a stroke, traumatic brain injury (TBI), or infectious disease; it is still uncertain what initiates the onset of PPA in those affected by it.

Epilepsy can also include transient aphasia as a prodromal or episodic symptom. However, the repeated seizure activity within language regions may also lead to chronic, and progressive aphasia. Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain.

Diagnosis

Neuroimaging methods

Magnetic resonance imaging (MRI) and functional magnetic resonance imaging (fMRI) are the most common neuroimaging tools used in identifying aphasia and studying the extent of damage in the loss of language abilities. This is done by doing MRI scans and locating the extent of lesions or damage within brain tissue, particularly within areas of the left frontal and temporal regions- where a lot of language related areas lie. In fMRI studies a language related task is often completed and then the BOLD image is analyzed. If there are lower than normal BOLD responses that indicate a lessening of blood flow to the affected area and can show quantitatively that the cognitive task is not being completed.

There are limitations to the use of fMRI in aphasic patients particularly. Because a high percentage of aphasic patients develop it because of stroke there can be infarct present which is the total loss of blood flow. This can be due to the thinning of blood vessels or the complete blockage of it. This is important in fMRI as it relies on the BOLD response (the oxygen levels of the blood vessels), and this can create a false hyporesponse upon fMRI study. Due to the limitations of fMRI such as a lower spatial resolution, it can show that some areas of the brain are not active during a task when they in reality are. Additionally, with stroke being the cause of many cases of aphasia the extent of damage to brain tissue can be difficult to quantify therefore the effects of stroke brain damage on the functionality of the patient can vary.

Neural substrates of aphasia subtypes

MRI is often used to predict or confirm the subtype of aphasia present. Researchers compared three subtypes of aphasia — nonfluent-variant primary progressive aphasia (nfPPA), logopenic-variant primary progressive aphasia (lvPPA), and semantic-variant primary progressive aphasia (svPPA), with primary progressive aphasia (PPA) and Alzheimer's disease. This was done by analyzing the MRIs of patients with each of the subsets of PPA. Images which compare subtypes of aphasia as well as for finding the extent of lesions are generated by overlapping images of different participant's brains (if applicable) and isolating areas of lesions or damage using third-party software such as MRIcron. MRI has also been used to study the relationship between the type of aphasia developed and the age of the person with aphasia. It was found that patients with fluent aphasia are on average older than people with non-fluent aphasia. It was also found that among patients with lesions confined to the anterior portion of the brain an unexpected portion of them presented with fluent aphasia and were remarkably older than those with non-fluent aphasia. This effect was not found when the posterior portion of the brain was studied.

Associated conditions

In a study on the features associated with different disease trajectories in Alzheimer's disease (AD)-related primary progressive aphasia (PPA), it was found that metabolic patterns via PET SPM analysis can help predict progression of total loss of speech and functional autonomy in AD and PPA patients. This was done by comparing an MRI or CT image of the brain and presence of a radioactive biomarker with normal levels in patients without Alzheimer's Disease. Apraxia is another disorder often correlated with aphasia. This is due to a subset of apraxia which affects speech. Specifically, this subset affects the movement of muscles associated with speech production, apraxia and aphasia are often correlated due to the proximity of neural substrates associated with each of the disorders. Researchers concluded that there were 2 areas of lesion overlap between patients with apraxia and aphasia, the anterior temporal lobe and the left inferior parietal lobe.

Treatment and neuroimaging

Evidence for positive treatment outcomes can also be quantified using neuroimaging tools. The use of fMRI and an automatic classifier can help predict language recovery outcomes in stroke patients with 86% accuracy when coupled with age and language test scores. The stimuli tested were sentences both correct and incorrect and the subject had to press a button whenever the sentence was incorrect. The fMRI data collected focused on responses in regions of interest identified by healthy subjects.  Recovery from aphasia can also be quantified using diffusion tensor imaging. The accurate fasciculus (AF) connects the right and left superior temporal lobe, premotor regions/posterior inferior frontal gyrus. and the primary motor cortex. In a study which enrolled patients in a speech therapy program, an increase in AF fibers and volume was found in patients after 6-weeks in the program which correlated with long-term improvement in those patients. The results of the experiment are pictured in Figure 2. This implies that DTI can be used to quantify the improvement in patients after speech and language treatment programs are applied.

Classification

Aphasia is best thought of as a collection of different disorders, rather than a single problem. Each individual with aphasia will present with their own particular combination of language strengths and weaknesses. Consequently, it is a major challenge just to document the various difficulties that can occur in different people, let alone decide how they might best be treated. Most classifications of the aphasias tend to divide the various symptoms into broad classes. A common approach is to distinguish between the fluent aphasias (where speech remains fluent, but content may be lacking, and the person may have difficulties understanding others), and the nonfluent aphasias (where speech is very halting and effortful, and may consist of just one or two words at a time).

However, no such broad-based grouping has proven fully adequate, or reliable. There is wide variation among people even within the same broad grouping, and aphasias can be highly selective. For instance, people with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors. Unfortunately, assessments that characterize aphasia in these groupings have persisted. This is not helpful to people living with aphasia, and provides inaccurate descriptions of an individual pattern of difficulties.

There are typical difficulties with speech and language that come with normal aging as well. As we age, language can become more difficult to process, resulting in a slowing of verbal comprehension, reading abilities and more likely word finding difficulties. With each of these, though, unlike some aphasias, functionality within daily life remains intact.

Boston classification

Major characteristics of different types of aphasia according to the Boston classification
Type of aphasia Speech repetition Naming Auditory comprehension Fluency
Expressive aphasia (Broca's aphasia) Moderate–severe Moderate–severe Mild difficulty Non-fluent, effortful, slow
Receptive aphasia (Wernicke's aphasia) Mild–severe Mild–severe Defective Fluent paraphasic
Conduction aphasia Poor Poor Relatively good Fluent
Mixed transcortical aphasia Moderate Poor Poor Non-fluent
Transcortical motor aphasia Good Mild–severe Mild Non-fluent
Transcortical sensory aphasia Good Moderate–severe Poor Fluent
Global aphasia Poor Poor Poor Non-fluent
Anomic aphasia Mild Moderate–severe Mild Fluent
  • Individuals with receptive aphasia (Wernicke's aphasia), also referred to as fluent aphasia, may speak in long sentences that have no meaning, add unnecessary words, and even create new "words" (neologisms). For example, someone with receptive aphasia may say, "delicious taco", meaning "The dog needs to go out so I will take him for a walk". They have poor auditory and reading comprehension, and fluent, but nonsensical, oral and written expression. Individuals with receptive aphasia usually have great difficulty understanding the speech of both themselves and others and are, therefore, often unaware of their mistakes. Receptive language deficits usually arise from lesions in the posterior portion of the left hemisphere at or near Wernicke's area. It is often the result of trauma to the temporal region of the brain, specifically damage to Wernicke's area. Trauma can be the result from an array of problems, however it is most commonly seen as a result of stroke
  • Individuals with expressive aphasia (Broca's aphasia) frequently speak short, meaningful phrases that are produced with great effort. It is thus characterized as a nonfluent aphasia. Affected people often omit small words such as "is", "and", and "the". For example, a person with expressive aphasia may say, "walk dog", which could mean "I will take the dog for a walk", "you take the dog for a walk" or even "the dog walked out of the yard." Individuals with expressive aphasia are able to understand the speech of others to varying degrees. Because of this, they are often aware of their difficulties and can become easily frustrated by their speaking problems. While Broca's aphasia may appear to be solely an issue with language production, evidence suggests that it may be rooted in an inability to process syntactical information. Individuals with expressive aphasia may have a speech automatism (also called recurring or recurrent utterance). These speech automatisms can be repeated lexical speech automatisms; e.g., modalisations ('I can't ..., I can't ...'), expletives/swearwords, numbers ('one two, one two') or non-lexical utterances made up of repeated, legal, but meaningless, consonant-vowel syllables (e.g.., /tan tan/, /bi bi/). In severe cases, the individual may be able to utter only the same speech automatism each time they attempt speech.
  • Individuals with anomic aphasia have difficulty with naming. People with this aphasia may have difficulties naming certain words, linked by their grammatical type (e.g., difficulty naming verbs and not nouns) or by their semantic category (e.g., difficulty naming words relating to photography, but nothing else) or a more general naming difficulty. People tend to produce grammatic, yet empty, speech. Auditory comprehension tends to be preserved. Anomic aphasia is the aphasial presentation of tumors in the language zone; it is the aphasial presentation of Alzheimer's disease. Anomic aphasia is the mildest form of aphasia, indicating a likely possibility for better recovery.
  • Individuals with transcortical sensory aphasia, in principle the most general and potentially among the most complex forms of aphasia, may have similar deficits as in receptive aphasia, but their repetition ability may remain intact.
  • Global aphasia is considered a severe impairment in many language aspects since it impacts expressive and receptive language, reading, and writing. Despite these many deficits, there is evidence that has shown individuals benefited from speech language therapy. Even though individuals with global aphasia will not become competent speakers, listeners, writers, or readers, goals can be created to improve the individual's quality of life. Individuals with global aphasia usually respond well to treatment that includes personally relevant information, which is also important to consider for therapy.
  • Individuals with conduction aphasia have deficits in the connections between the speech-comprehension and speech-production areas. This might be caused by damage to the arcuate fasciculus, the structure that transmits information between Wernicke's area and Broca's area. Similar symptoms, however, can be present after damage to the insula or to the auditory cortex. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Paraphasic errors include phonemic/literal or semantic/verbal. Repetition ability is poor. Conduction and transcortical aphasias are caused by damage to the white matter tracts. These aphasias spare the cortex of the language centers, but instead create a disconnection between them. Conduction aphasia is caused by damage to the arcuate fasciculus. The arcuate fasciculus is a white matter tract that connects Broca's and Wernicke's areas. People with conduction aphasia typically have good language comprehension, but poor speech repetition and mild difficulty with word retrieval and speech production. People with conduction aphasia are typically aware of their errors. Two forms of conduction aphasia have been described: reproduction conduction aphasia (repetition of a single relatively unfamiliar multisyllabic word) and repetition conduction aphasia (repetition of unconnected short familiar words.
  • Transcortical aphasias include transcortical motor aphasia, transcortical sensory aphasia, and mixed transcortical aphasia. People with transcortical motor aphasia typically have intact comprehension and awareness of their errors, but poor word finding and speech production. People with transcortical sensory and mixed transcortical aphasia have poor comprehension and unawareness of their errors. Despite poor comprehension and more severe deficits in some transcortical aphasias, small studies have indicated that full recovery is possible for all types of transcortical aphasia.

Classical-localizationist approaches

Cortex

Localizationist approaches aim to classify the aphasias according to their major presenting characteristics and the regions of the brain that most probably gave rise to them. Inspired by the early work of nineteenth-century neurologists Paul Broca and Carl Wernicke, these approaches identify two major subtypes of aphasia and several more minor subtypes:

  • Expressive aphasia (also known as "motor aphasia" or "Broca's aphasia"), which is characterized by halted, fragmented, effortful speech, but well-preserved comprehension relative to expression. Damage is typically in the anterior portion of the left hemisphere, most notably Broca's area. Individuals with Broca's aphasia often have right-sided weakness or paralysis of the arm and leg, because the left frontal lobe is also important for body movement, particularly on the right side.
  • Receptive aphasia (also known as "sensory aphasia" or "Wernicke's aphasia"), which is characterized by fluent speech, but marked difficulties understanding words and sentences. Although fluent, the speech may lack in key substantive words (nouns, verbs, adjectives), and may contain incorrect words or even nonsense words. This subtype has been associated with damage to the posterior left temporal cortex, most notably Wernicke's area. These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement.
  • Conduction aphasia, where speech remains fluent, and comprehension is preserved, but the person may have disproportionate difficulty repeating words or sentences. Damage typically involves the arcuate fasciculus and the left parietal region.
  • Transcortical motor aphasia and transcortical sensory aphasia, which are similar to Broca's and Wernicke's aphasia respectively, but the ability to repeat words and sentences is disproportionately preserved.

Recent classification schemes adopting this approach, such as the Boston-Neoclassical Model, also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Broca's aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernicke's aphasia, conduction aphasia and transcortical sensory aphasia). These schemes also identify several further aphasia subtypes, including: anomic aphasia, which is characterized by a selective difficulty finding the names for things; and global aphasia, where both expression and comprehension of speech are severely compromised.

Many localizationist approaches also recognize the existence of additional, more "pure" forms of language disorder that may affect only a single language skill. For example, in pure alexia, a person may be able to write, but not read, and in pure word deafness, they may be able to produce speech and to read, but not understand speech when it is spoken to them.

Cognitive neuropsychological approaches

Although localizationist approaches provide a useful way of classifying the different patterns of language difficulty into broad groups, one problem is that most individuals do not fit neatly into one category or another. Another problem is that the categories, particularly the major ones such as Broca's and Wernicke's aphasia, still remain quite broad and do not meaningfully reflect a person's difficulties. Consequently, even amongst those who meet the criteria for classification into a subtype, there can be enormous variability in the types of difficulties they experience.

Instead of categorizing every individual into a specific subtype, cognitive neuropsychological approaches aim to identify the key language skills or "modules" that are not functioning properly in each individual. A person could potentially have difficulty with just one module, or with a number of modules. This type of approach requires a framework or theory as to what skills/modules are needed to perform different kinds of language tasks. For example, the model of Max Coltheart identifies a module that recognizes phonemes as they are spoken, which is essential for any task involving recognition of words. Similarly, there is a module that stores phonemes that the person is planning to produce in speech, and this module is critical for any task involving the production of long words or long strings of speech. Once a theoretical framework has been established, the functioning of each module can then be assessed using a specific test or set of tests. In the clinical setting, use of this model usually involves conducting a battery of assessments, each of which tests one or a number of these modules. Once a diagnosis is reached as to the skills/modules where the most significant impairment lies, therapy can proceed to treat these skills.

Progressive aphasias

Primary progressive aphasia (PPA) is a neurodegenerative focal dementia that can be associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimer's disease, which is the gradual process of progressively losing the ability to think. Gradual loss of language function occurs in the context of relatively well-preserved memory, visual processing, and personality until the advanced stages. Symptoms usually begin with word-finding problems (naming) and progress to impaired grammar (syntax) and comprehension (sentence processing and semantics). The loss of language before the loss of memory differentiates PPA from typical dementias. People with PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence. There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA).

Progressive Jargon Aphasia is a fluent or receptive aphasia in which the person's speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the person has problems with the selection of nouns. Either they will replace the desired word with another that sounds or looks like the original one or has some other connection or they will replace it with sounds. As such, people with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they cannot find with sounds. Substitutions commonly involve picking another (actual) word starting with the same sound (e.g., clocktower – colander), picking another semantically related to the first (e.g., letter – scroll), or picking one phonetically similar to the intended one (e.g., lane – late).

Deaf aphasia

There have been many instances showing that there is a form of aphasia among deaf individuals. Sign languages are, after all, forms of language that have been shown to use the same areas of the brain as verbal forms of language. Mirror neurons become activated when an animal is acting in a particular way or watching another individual act in the same manner. These mirror neurons are important in giving an individual the ability to mimic movements of hands. Broca's area of speech production has been shown to contain several of these mirror neurons resulting in significant similarities of brain activity between sign language and vocal speech communication. People use facial movements to create, what other people perceive, to be faces of emotions. While combining these facial movements with speech, a more full form of language is created which enables the species to interact with a much more complex and detailed form of communication. Sign language also uses these facial movements and emotions along with the primary hand movement way of communicating. These facial movement forms of communication come from the same areas of the brain. When dealing with damages to certain areas of the brain, vocal forms of communication are in jeopardy of severe forms of aphasia. Since these same areas of the brain are being used for sign language, these same, at least very similar, forms of aphasia can show in the Deaf community. Individuals can show a form of Wernicke's aphasia with sign language and they show deficits in their abilities in being able to produce any form of expressions. Broca's aphasia shows up in some people, as well. These individuals find tremendous difficulty in being able to actually sign the linguistic concepts they are trying to express.

Severity

The severity of the type of aphasia varies depending on the size of the stroke. However, there is much variance between how often one type of severity occurs in certain types of aphasia. For instance, any type of aphasia can range from mild to profound. Regardless of the severity of aphasia, people can make improvements due to spontaneous recovery and treatment in the acute stages of recovery. Additionally, while most studies propose that the greatest outcomes occur in people with severe aphasia when treatment is provided in the acute stages of recovery, Robey (1998) also found that those with severe aphasia are capable of making strong language gains in the chronic stage of recovery as well. This finding implies that persons with aphasia have the potential to have functional outcomes regardless of how severe their aphasia may be. While there is no distinct pattern of the outcomes of aphasia based on severity alone, global aphasia typically makes functional language gains, but may be gradual since global aphasia affects many language areas.

Prevention

Aphasia is largely caused by unavoidable instances. However, some precautions can be taken to decrease risk for experiencing one of the two major causes of aphasia: stroke and traumatic brain injury (TBI). To decrease the probability of having an ischemic or hemorrhagic stroke, one should take the following precautions:

  • Exercising regularly
  • Eating a healthy diet, avoiding cholesterol in particular
  • Keeping alcohol consumption low and avoiding tobacco use
  • Controlling blood pressure
  • Going to the emergency room immediately if you begin to experience unilateral extremity (especially leg) swelling, warmth, redness, and/or tenderness as these are symptoms of a deep vein thrombosis which can lead to a stroke

To prevent aphasia due to traumatic injury, one should take precautionary measures when engaging in dangerous activities such as:

  • Wearing a helmet when operating a bicycle, motor cycle, ATV, or any other moving vehicle that could potentially be involved in an accident
  • Wearing a seatbelt when driving or riding in a car
  • Wearing proper protective gear when playing contact sports, especially American football, rugby, and hockey, or refraining from such activities
  • Minimizing anticoagulant use (including aspirin) if at all possible as they increase the risk of hemorrhage after a head injury

Additionally, one should always seek medical attention after sustaining head trauma due to a fall or accident. The sooner that one receives medical attention for a traumatic brain injury, the less likely one is to experience long-term or severe effects.

Management

Most acute cases of aphasia recover some or most skills by participating in speech and language therapy. Recovery and improvement can continue for years after the stroke. After the onset of aphasia, there is approximately a six-month period of spontaneous recovery; during this time, the brain is attempting to recover and repair the damaged neurons. Improvement varies widely, depending on the aphasia's cause, type, and severity. Recovery also depends on the person's age, health, motivation, handedness, and educational level.

Speech and language therapy that is higher intensity, higher dose or provided over a long duration of time leads to significantly better functional communication, but people might be more likely to drop out of high intensity treatment (up to 15 hours per week). A total of 20–50 hours of speech and language therapy is necessary for the best recovery. The most improvement happens when 2–5 hours of therapy is provided each week over 4–5 days. Recovery is further improved when besides the therapy people practice tasks at home. Speech and language therapy is also effective if it is delivered online through video or by a family member who has been trained by a professional therapist.

Recovery with therapy is also dependent on the recency of stroke and the age of the person. Receiving therapy within a month after the stroke leads to the greatest improvements. Three or six months after the stroke more therapy will be needed, but symptoms can still be improved. People with aphasia who are younger than 55 years are the most likely to improve, but people older than 75 years can still get better with therapy.

There is no one treatment proven to be effective for all types of aphasias. The reason that there is no universal treatment for aphasia is because of the nature of the disorder and the various ways it is presented. Aphasia is rarely exhibited identically, implying that treatment needs to be catered specifically to the individual. Studies have shown that, although there is no consistency on treatment methodology in literature, there is a strong indication that treatment, in general, has positive outcomes. Therapy for aphasia ranges from increasing functional communication to improving speech accuracy, depending on the person's severity, needs and support of family and friends. Group therapy allows individuals to work on their pragmatic and communication skills with other individuals with aphasia, which are skills that may not often be addressed in individual one-on-one therapy sessions. It can also help increase confidence and social skills in a comfortable setting.

Evidence does not support the use of transcranial direct current stimulation (tDCS) for improving aphasia after stroke. Moderate quality evidence does indicate naming performance improvements for nouns, but not verbs using tDCS.

Specific treatment techniques include the following:

  • Copy and recall therapy (CART) – repetition and recall of targeted words within therapy may strengthen orthographic representations and improve single word reading, writing, and naming
  • Visual communication therapy (VIC) – the use of index cards with symbols to represent various components of speech
  • Visual action therapy (VAT) – typically treats individuals with global aphasia to train the use of hand gestures for specific items
  • Functional communication treatment (FCT) – focuses on improving activities specific to functional tasks, social interaction, and self-expression
  • Promoting aphasic's communicative effectiveness (PACE) – a means of encouraging normal interaction between people with aphasia and clinicians. In this kind of therapy, the focus is on pragmatic communication rather than treatment itself. People are asked to communicate a given message to their therapists by means of drawing, making hand gestures or even pointing to an object
  • Melodic intonation therapy (MIT) – aims to use the intact melodic/prosodic processing skills of the right hemisphere to help cue retrieval of words and expressive language
  • Centeredness Theory Interview (CTI) – Uses client centered goal formation into the nature of current patient interactions as well as future / desired interactions to improve subjective well-being, cognition and communication.
  • Other – i.e., drawing as a way of communicating, trained conversation partners

Semantic feature analysis (SFA) – a type of aphasia treatment that targets word-finding deficits is based on the theory that neural connections can be strengthened by using related words and phrases that are similar to the target word, to eventually activate the target word in the brain. SFA can be implemented in multiple forms such as verbally, written, using picture cards, etc. The SLP provides prompting questions to the individual with aphasia in order for the person to name the picture provided. Studies show that SFA is an effective intervention for improving confrontational naming.

Melodic intonation therapy is used to treat non-fluent aphasia and has proved to be effective in some cases. However, there is still no evidence from randomized controlled trials confirming the efficacy of MIT in chronic aphasia. MIT is used to help people with aphasia vocalize themselves through speech song, which is then transferred as a spoken word. Good candidates for this therapy include people who have had left hemisphere strokes, non-fluent aphasias such as Broca's, good auditory comprehension, poor repetition and articulation, and good emotional stability and memory. An alternative explanation is that the efficacy of MIT depends on neural circuits involved in the processing of rhythmicity and formulaic expressions (examples taken from the MIT manual: "I am fine," "how are you?" or "thank you"); while rhythmic features associated with melodic intonation may engage primarily left-hemisphere subcortical areas of the brain, the use of formulaic expressions is known to be supported by right-hemisphere cortical and bilateral subcortical neural networks.

Systematic reviews support the effectiveness and importance of partner training. According to the National Institute on Deafness and Other Communication Disorders (NIDCD), involving family with the treatment of an aphasic loved one is ideal for all involved, because while it will no doubt assist in their recovery, it will also make it easier for members of the family to learn how best to communicate with them.

When a person's speech is insufficient, different kinds of augmentative and alternative communication could be considered such as alphabet boards, pictorial communication books, specialized software for computers or apps for tablets or smartphones.

When addressing Wernicke's aphasia, according to Bakheit et al. (2007), the lack of awareness of the language impairments, a common characteristic of Wernicke's aphasia, may affect the rate and extent of therapy outcomes. Robey (1998) determined that at least 2 hours of treatment per week is recommended for making significant language gains. Spontaneous recovery may cause some language gains, but without speech-language therapy, the outcomes can be half as strong as those with therapy.

When addressing Broca's aphasia, better outcomes occur when the person participates in therapy, and treatment is more effective than no treatment for people in the acute period. Two or more hours of therapy per week in acute and post-acute stages produced the greatest results. High-intensity therapy was most effective, and low-intensity therapy was almost equivalent to no therapy.

People with global aphasia are sometimes referred to as having irreversible aphasic syndrome, often making limited gains in auditory comprehension, and recovering no functional language modality with therapy. With this said, people with global aphasia may retain gestural communication skills that may enable success when communicating with conversational partners within familiar conditions. Process-oriented treatment options are limited, and people may not become competent language users as readers, listeners, writers, or speakers no matter how extensive therapy is. However, people's daily routines and quality of life can be enhanced with reasonable and modest goals. After the first month, there is limited to no healing to language abilities of most people. There is a grim prognosis, leaving 83% who were globally aphasic after the first month that will remain globally aphasic at the first year. Some people are so severely impaired that their existing process-oriented treatment approaches offer no signs of progress, and therefore cannot justify the cost of therapy.

Perhaps due to the relative rareness of conduction aphasia, few studies have specifically studied the effectiveness of therapy for people with this type of aphasia. From the studies performed, results showed that therapy can help to improve specific language outcomes. One intervention that has had positive results is auditory repetition training. Kohn et al. (1990) reported that drilled auditory repetition training related to improvements in spontaneous speech, Francis et al. (2003) reported improvements in sentence comprehension, and Kalinyak-Fliszar et al. (2011) reported improvements in auditory-visual short-term memory.

Individualized service delivery

Intensity of treatment should be individualized based on the recency of stroke, therapy goals, and other specific characteristics such as age, size of lesion, overall health status, and motivation. Each individual reacts differently to treatment intensity and is able to tolerate treatment at different times post-stroke. Intensity of treatment after a stroke should be dependent on the person's motivation, stamina, and tolerance for therapy.

Outcomes

If the symptoms of aphasia last longer than two or three months after a stroke, a complete recovery is unlikely. However, it is important to note that some people continue to improve over a period of years and even decades. Improvement is a slow process that usually involves both helping the individual and family understand the nature of aphasia and learning compensatory strategies for communicating.

After a traumatic brain injury (TBI) or cerebrovascular accident (CVA), the brain undergoes several healing and re-organization processes, which may result in improved language function. This is referred to as spontaneous recovery. Spontaneous recovery is the natural recovery the brain makes without treatment, and the brain begins to reorganize and change in order to recover. There are several factors that contribute to a person's chance of recovery caused by stroke, including stroke size and location. Age, sex, and education have not been found to be very predictive. There is also research pointing to damage in the left hemisphere healing more effectively than the right.

Specific to aphasia, spontaneous recovery varies among affected people and may not look the same in everyone, making it difficult to predict recovery.

Though some cases of Wernicke's aphasia have shown greater improvements than more mild forms of aphasia, people with Wernicke's aphasia may not reach as high a level of speech abilities as those with mild forms of aphasia.

Prevalence

Aphasia affects about two million people in the U.S. and 250,000 people in Great Britain. Nearly 180,000 people acquire the disorder every year in the U.S., 170,000 due to stroke. Any person of any age can develop aphasia, given that it is often caused by a traumatic injury. However, people who are middle aged and older are the most likely to acquire aphasia, as the other etiologies are more likely at older ages. For example, approximately 75% of all strokes occur in individuals over the age of 65. Strokes account for most documented cases of aphasia: 25% to 40% of people who survive a stroke develop aphasia as a result of damage to the language-processing regions of the brain.

History

The first recorded case of aphasia is from an Egyptian papyrus, the Edwin Smith Papyrus, which details speech problems in a person with a traumatic brain injury to the temporal lobe.

During the second half of the 19th century, aphasia was a major focus for scientists and philosophers who were working in the beginning stages of the field of psychology. In medical research, speechlessness was described as an incorrect prognosis, and there was no assumption that underlying language complications existed. Broca and his colleagues were some of the first to write about aphasia, but Wernicke was the first credited to have written extensively about aphasia being a disorder that contained comprehension difficulties. Despite claims of who reported on aphasia first, it was F.J. Gall that gave the first full description of aphasia after studying wounds to the brain, as well as his observation of speech difficulties resulting from vascular lesions. A recent book on the entire history of aphasia is available (Reference: Tesak, J. & Code, C. (2008) Milestones in the History of Aphasia: Theories and Protagonists. Hove, East Sussex: Psychology Press).

Etymology

Aphasia is from Greek a- ("without", negative prefix) + phásis (φάσις, "speech").

The word aphasia comes from the word ἀφασία aphasia, in Ancient Greek, which means "speechlessness", derived from ἄφατος aphatos, "speechless" from á¼€- a-, "not, un" and φημί phemi, "I speak".

Further research

Research is currently being done using functional magnetic resonance imaging (fMRI) to witness the difference in how language is processed in normal brains vs aphasic brains. This will help researchers to understand exactly what the brain must go through in order to recover from Traumatic Brain Injury (TBI) and how different areas of the brain respond after such an injury.

Another intriguing approach being tested is that of drug therapy. Research is in progress that will hopefully uncover whether or not certain drugs might be used in addition to speech-language therapy in order to facilitate recovery of proper language function. It is possible that the best treatment for aphasia might involve combining drug treatment with therapy, instead of relying on one over the other.

One other method being researched as a potential therapeutic combination with speech-language therapy is brain stimulation. One particular method, Transcranial Magnetic Stimulation (TMS), alters brain activity in whatever area it happens to stimulate, which has recently led scientists to wonder if this shift in brain function caused by TMS might help people re-learn language. Another type of external brain stimulation is transcranial Direct Current Stimulation (tDCS), but existing research has not shown it to be useful for improving aphasia after a stroke.

Cognitive model

From Wikipedia, the free encyclopedia

A cognitive model is a representation of one or more cognitive processes in humans or other animals for the purposes of comprehension and prediction. There are many types of cognitive models, and they can range from box-and-arrow diagrams to a set of equations to software programs that interact with the same tools that humans use to complete tasks (e.g., computer mouse and keyboard). In terms of information processing, cognitive modeling is modeling of human perception, reasoning, memory and action.

Knowledge about the representation of cognitive processes in humans originated in Philosophy. It relies on two opposing philosophical approaches, internalism and externalism, which together explain the nature of the mind and its relation to the body and the external world. From the internalist's perspective, the modeling of human perception, reasoning, memory, and action is independent of the external world. Current academic literature generally categorizes Internalism's cognitive models into three groups of representations of cognitive processes in humans:

  • Box-and-Arrow models, these models identify the components involved in cognition;
  • Computational Models explain the "rules" that govern how information moves between the structures defined above;
  • Dynamical systems focus on how the system changes every instant.

Philosophical ideas of Professors Andy Clark and David Chalmers have developed an externalist approach to modelling cognition, based on the active role of the environment in driving cognitive processes: extended mind thesis. According to this approach, because external objects play a significant role in aiding cognitive processes, the mind and the environment act as a "coupled system" that can be seen as a complete cognitive system of its own. Externalism is represented by the Mother-fetus neurocognitive model, which explains cognitive development in part as a function of the environment.

Relationship to cognitive architectures

Cognitive models can be developed within or without a cognitive architecture, though the two are not always easily distinguishable. In contrast to cognitive architectures, cognitive models tend to be focused on a single cognitive phenomenon or process (e.g., list learning), how two or more processes interact (e.g., visual search and decision making), or making behavioral predictions for a specific task or tool (e.g., how instituting a new software package will affect productivity). Cognitive architectures tend to be focused on the structural properties of the modeled system, and help constrain the development of cognitive models within the architecture. Likewise, model development helps to inform limitations and shortcomings of the architecture. Some of the most popular architectures for cognitive modeling include ACT-R, Clarion, LIDA, and Soar.

History

Cognitive modeling historically developed within cognitive psychology/cognitive science (including human factors), and has received contributions from the fields of machine learning and artificial intelligence among others. However, long before the "Cognitive Revolution" of the 1960s, scientists already began approaching mathematical and mechanical models of the mind. The early contribution to the field was made in 1885. Ludwig Lichtheim proposed an idea (later expanded on by Carl Wernicke) arguably the first prerequisite of the "Box-and-Arrow" model, mapping language processing into specialized "boxes" for auditory recognition and speech production, connected by neural pathways (arrows). He established the Connectionist-Localist paradigm, which holds that complex functions such as language are not located in a single place but result from information flowing between specialized centers. In 1943, Professors McCulloch and Pitts created a mathematical model of a neuron as a set of logic gates to show how the brain could "compute" in their book "A logical calculus of the ideas immanent in nervous activity" published in 1943. In the same year, Kenneth Craik argued in "The Nature of Explanation" that the brain is a "calculating machine" building internal models of the world. Professors Richard Atkinson and Richard Shiffrin launched the "Box-and-Arrow" era in 1968 with the Atkinson-Shiffrin Multi-Store Model of Memory. This made the "Information-Processing" approach famous by drawing three distinct boxes for memory, describing flow between the sensory register (SR), short-term memory (STM), and long-term memory (LTM). In 1998, Professor van Gelder published the dynamical hypothesis in cognitive science. His dynamical model described how the system's state changes over time using several differential equations based on tracking data of the internal dynamics. The opposite, externalist view on the cognition development was put forward by Latvian professor Igor Val Danilov in his Mother-fetus neurocognitive model in 2024.

Box-and-arrow models

The Box-and-Arrow model represents the mind as a system of functional components (the "boxes") connected by pathways of information flow (the "arrows"). This group of models describes what the mind does without necessarily explaining how the neurons fire. The most influential applications of this model include:

Atkinson-Shiffrin Multi-Store Model (1968): A classic memory theory proposing that information flows through three distinct "boxes": Sensory Memory, Short-Term Memory, and Long-Term Memory.

Broadbent’s Filter Model (1958): One of the earliest "bottleneck" theories of selective attention, using a box-and-arrow diagram to show how sensory information is filtered before reaching higher-level processing.

Baddeley’s Working Memory Model (1974/2000): Refines the "short-term memory box" into a multi-component system including the Central Executive, Phonological Loop, and Visuospatial Sketchpad.

Norman and Shallice (1986) CS/SS Model: A model of cognitive control that uses "boxes" to represent Contention Scheduling (routine actions) and the Supervisory Attentional System (complex tasks).

Three major principles:

Modularity: the mind is composed of separate "modules."

Serial Processing (Directional Flow): information usually moves in a linear, step-by-step fashion.

Discrete Stages: each box completes its job in its entirety before passing the result to the next box. This is the opposite of the Dynamical Systems approach, which sees everything as a continuous, messy overlap.

Computational models

A computational model is a mathematical model in computational science that requires extensive computational resources to study the behavior of a complex system by computer simulation. Computational cognitive models examine cognition and cognitive functions by developing process-based computational models formulated as sets of mathematical equations or computer simulations. The system under study is often a complex nonlinear system for which simple, intuitive analytical solutions are not readily available. Rather than deriving a mathematical analytical solution to the problem, experimentation with the model is done by changing the parameters of the system in the computer, and studying the differences in the outcome of the experiments. Theories of operation of the model can be derived/deduced from these computational experiments. Examples of common computational models are weather forecasting models, earth simulator models, flight simulator models, molecular protein folding models, and neural network models.

Symbolic

A symbolic model is expressed in characters, usually non-numeric ones, that require translation before they can be used.

Subsymbolic

A cognitive model is subsymbolic if it is made by constituent entities that are not representations in their turn, e.g., pixels, sound images as perceived by the ear, signal samples; subsymbolic units in neural networks can be considered particular cases of this category.

Hybrid

Hybrid computers are computers that exhibit features of analog computers and digital computers. The digital component normally serves as the controller and provides logical operations, while the analog component normally serves as a solver of differential equations. See more details at hybrid intelligent system.

Dynamical systems

In the traditional computational approach, representations are viewed as static structures of discrete symbols. Cognition takes place by transforming static symbol structures in discrete, sequential steps. Sensory information is transformed into symbolic inputs, which produce symbolic outputs that get transformed into motor outputs. The entire system operates in an ongoing cycle.

What is missing from this traditional view is that human cognition happens continuously and in real time. Breaking down the processes into discrete time steps may not fully capture this behavior. An alternative approach is to define a system with (1) a state of the system at any given time, (2) a behavior, defined as the change over time in overall state, and (3) a state set or state space, representing the totality of overall states the system could be in. The system is distinguished by the fact that a change in any aspect of the system state depends on other aspects of the same or other system states.

A typical dynamical model is formalized by several differential equations that describe how the system's state changes over time. By doing so, the form of the space of possible trajectories and the internal and external forces that shape a specific trajectory that unfold over time, instead of the physical nature of the underlying mechanisms that manifest this dynamics, carry explanatory force. On this dynamical view, parametric inputs alter the system's intrinsic dynamics, rather than specifying an internal state that describes some external state of affairs.

Early dynamical systems

Associative memory

Early work in the application of dynamical systems to cognition can be found in the model of Hopfield networks. These networks were proposed as a model for associative memory. They represent the neural level of memory, modeling systems of around 30 neurons which can be in either an on or off state. By letting the network learn on its own, structure and computational properties naturally arise. Unlike previous models, “memories” can be formed and recalled by inputting a small portion of the entire memory. Time ordering of memories can also be encoded. The behavior of the system is modeled with vectors which can change values, representing different states of the system. This early model was a major step toward a dynamical systems view of human cognition, though many details had yet to be added and more phenomena accounted for.

Language acquisition

By taking into account the evolutionary development of the human nervous system and the similarity of the brain to other organs, Elman proposed that language and cognition should be treated as a dynamical system rather than a digital symbol processor. Neural networks of the type Elman implemented have come to be known as Elman networks. Instead of treating language as a collection of static lexical items and grammar rules that are learned and then used according to fixed rules, the dynamical systems view defines the lexicon as regions of state space within a dynamical system. Grammar is made up of attractors and repellers that constrain movement in the state space. This means that representations are sensitive to context, with mental representations viewed as trajectories through mental space instead of objects that are constructed and remain static. Elman networks were trained with simple sentences to represent grammar as a dynamical system. Once a basic grammar had been learned, the networks could then parse complex sentences by predicting which words would appear next according to the dynamical model.

Cognitive development

A classic developmental error has been investigated in the context of dynamical systems: The A-not-B error is proposed to be not a distinct error occurring at a specific age (8 to 10 months), but a feature of a dynamic learning process that is also present in older children. Children 2 years old were found to make an error similar to the A-not-B error when searching for toys hidden in a sandbox. After observing the toy being hidden in location A and repeatedly searching for it there, the 2-year-olds were shown a toy hidden in a new location B. When they looked for the toy, they searched in locations that were biased toward location A. This suggests that there is an ongoing representation of the toy's location that changes over time. The child's past behavior influences its model of locations of the sandbox, and so an account of behavior and learning must take into account how the system of the sandbox and the child's past actions is changing over time.

Locomotion

One proposed mechanism of a dynamical system comes from analysis of continuous-time recurrent neural networks (CTRNNs). By focusing on the output of the neural networks rather than their states and examining fully interconnected networks, three-neuron central pattern generator (CPG) can be used to represent systems such as leg movements during walking. This CPG contains three motor neurons to control the foot, backward swing, and forward swing effectors of the leg. Outputs of the network represent whether the foot is up or down and how much force is being applied to generate torque in the leg joint. One feature of this pattern is that neuron outputs are either off or on most of the time. Another feature is that the states are quasi-stable, meaning that they will eventually transition to other states. A simple pattern generator circuit like this is proposed to be a building block for a dynamical system. Sets of neurons that simultaneously transition from one quasi-stable state to another are defined as a dynamic module. These modules can in theory be combined to create larger circuits that comprise a complete dynamical system. However, the details of how this combination could occur are not fully worked out.

Modern dynamical systems

Behavioral dynamics

Modern formalizations of dynamical systems applied to the study of cognition vary. One such formalization, referred to as “behavioral dynamics”, treats the agent and the environment as a pair of coupled dynamical systems based on classical dynamical systems theory. In this formalization, the information from the environment informs the agent's behavior and the agent's actions modify the environment. In the specific case of perception-action cycles, the coupling of the environment and the agent is formalized by two functions. The first transforms the representation of the agents action into specific patterns of muscle activation that in turn produce forces in the environment. The second function transforms the information from the environment (i.e., patterns of stimulation at the agent's receptors that reflect the environment's current state) into a representation that is useful for controlling the agents actions. Other similar dynamical systems have been proposed (although not developed into a formal framework) in which the agent's nervous systems, the agent's body, and the environment are coupled together

Adaptive behaviors

Behavioral dynamics have been applied to locomotive behavior. Modeling locomotion with behavioral dynamics demonstrates that adaptive behaviors could arise from the interactions of an agent and the environment. According to this framework, adaptive behaviors can be captured by two levels of analysis. At the first level of perception and action, an agent and an environment can be conceptualized as a pair of dynamical systems coupled together by the forces the agent applies to the environment and by the structured information provided by the environment. Thus, behavioral dynamics emerge from the agent-environment interaction. At the second level of time evolution, behavior can be expressed as a dynamical system represented as a vector field. In this vector field, attractors reflect stable behavioral solutions, where as bifurcations reflect changes in behavior. In contrast to previous work on central pattern generators, this framework suggests that stable behavioral patterns are an emergent, self-organizing property of the agent-environment system rather than determined by the structure of either the agent or the environment.

Open dynamical systems

In an extension of classical dynamical systems theory, rather than coupling the environment's and the agent's dynamical systems to each other, an “open dynamical system” defines a “total system”, an “agent system”, and a mechanism to relate these two systems. The total system is a dynamical system that models an agent in an environment, whereas the agent system is a dynamical system that models an agent's intrinsic dynamics (i.e., the agent's dynamics in the absence of an environment). Importantly, the relation mechanism does not couple the two systems together, but rather continuously modifies the total system into the decoupled agent's total system. By distinguishing between total and agent systems, it is possible to investigate an agent's behavior when it is isolated from the environment and when it is embedded within an environment. This formalization can be seen as a generalization from the classical formalization, whereby the agent system can be viewed as the agent system in an open dynamical system, and the agent coupled to the environment and the environment can be viewed as the total system in an open dynamical system.

Embodied cognition

In the context of dynamical systems and embodied cognition, representations can be conceptualized as indicators or mediators. In the indicator view, internal states carry information about the existence of an object in the environment, where the state of a system during exposure to an object is the representation of that object. In the mediator view, internal states carry information about the environment which is used by the system in obtaining its goals. In this more complex account, the states of the system carries information that mediates between the information the agent takes in from the environment, and the force exerted on the environment by the agents behavior. The application of open dynamical systems have been discussed for four types of classical embodied cognition examples:

  1. Instances where the environment and agent must work together to achieve a goal, referred to as "intimacy". A classic example of intimacy is the behavior of simple agents working to achieve a goal (e.g., insects traversing the environment). The successful completion of the goal relies fully on the coupling of the agent to the environment.
  2. Instances where the use of external artifacts improves the performance of tasks relative to performance without these artifacts. The process is referred to as "offloading". A classic example of offloading is the behavior of Scrabble players; people are able to create more words when playing Scrabble if they have the tiles in front of them and are allowed to physically manipulate their arrangement. In this example, the Scrabble tiles allow the agent to offload working memory demands on to the tiles themselves.
  3. Instances where a functionally equivalent external artifact replaces functions that are normally performed internally by the agent, which is a special case of offloading. One famous example is that of human (specifically the agents Otto and Inga) navigation in a complex environment with or without assistance of an artifact.
  4. Instances where there is not a single agent. The individual agent is part of larger system that contains multiple agents and multiple artifacts. One famous example, formulated by Ed Hutchins in his book Cognition in the Wild, is that of navigating a naval ship.

The interpretations of these examples rely on the following logic: (1) the total system captures embodiment; (2) one or more agent systems capture the intrinsic dynamics of individual agents; (3) the complete behavior of an agent can be understood as a change to the agent's intrinsic dynamics in relation to its situation in the environment; and (4) the paths of an open dynamical system can be interpreted as representational processes. These embodied cognition examples show the importance of studying the emergent dynamics of an agent-environment systems, as well as the intrinsic dynamics of agent systems. Rather than being at odds with traditional cognitive science approaches, dynamical systems are a natural extension of these methods and should be studied in parallel rather than in competition.

Critique of dynamical systems

The onset of cognitive processes in a naive organism is a critical issue in the apodictic basis of the dynamical system approach. The critique of embodied cognition poses at least two arguments questioning its independence and self-sufficiency. First, the foundation of this dynamical system approach, the dynamical hypothesis in cognitive science, is based on a set of equations. This fact means that to describe each specific system, it is necessary to introduce data on its specific initial conditions: a specific dynamic system cannot be defined without primary data. Indeed, van Gelder's dynamical hypothesis in cognitive science regards the initial conditions. Even though a dynamical system tracks primary data less than it does internal dynamics, according to the hypothesis, it still needs external input of primary data. So, the dynamical system requires external data input to trigger it.

Second, in light of the above difficulty, embodied cognitivists introduced the notion of dynamically embodied information. It refers to the pairing of a stimulus with the particular symbol saved in the sensorimotor neuro-structures and processes that embody meaning (sense).

"Representational "vehicles" are temporally extended patterns of activity that can crisscross the brain-body-world boundaries, and the meanings or contents they embody are brought forth or enacted in the context of the system's structural coupling with its environment."

In a chaos of environmental stimuli, the link between specific stimuli and neural "patterns of activity" is unpredictable, owing to irrelevant stimuli that can be randomly associated with this embodied meaning. This bond is possible only when "the context of the system's structural coupling with its environment" has already been established, which is impossible for the naive organism in an unfamiliar environment. So, the evidence supporting embodiment abounds across the different sciences, yet the interpretation of results and their significance remains disputed, and researchers continue to look for appropriate ways to study and explain embodied cognition. The dynamical systems approach is not the only way to explain cognitive development in early-stage organisms.

Mother-fetus cognitive model

Research on child development inspired a different perspective on the representation of cognitive processes in humans. The mother-fetus neurocognitive model refers to a representation of neurophysiological processes within the biological system of this dyad that prepares the fetal nervous system for proper responses to stimuli at the onset of cognition. By describing cognitive development at earlier stages than other cognitive models (computational models and dynamical systems approaches), it addresses such gaps in our knowledge as the perception-stability problem, the binding problem, the excitatory-inputs problem, and the problem of morphogenesis.

The perception stability problem

Young organisms at the sensorimotor stage of development cannot capture the same picture of the environment as adults do because of their immature sensory systems. Since the similarity in perception of objects is unlikely to be achieved in these organisms, teaching through interpersonal dynamics is more limited.

The binding problem concerns the lack of knowledge about how organisms at the simple reflex stage of development overcome the threshold of environmental chaos in sensory stimuli. While young organisms need to combine objects, backgrounds, and abstract or emotional features into a single experience to build a surrounding reality, they cannot independently distinguish relevant sensory stimuli. Even the embodied dynamical system approach cannot get around the cue-to-noise problem. This ability requires categorizing the environment into objects that come into being through (and only after) perception and intentionality.

The excitatory inputs problem

According to the prevailing view in cognitive science, experience-dependent neuronal plasticity underlies cognitive development. Neuronal plasticity relies on the structural organization of excitatory inputs, which supports spike-timing-dependent plasticity, but this remains unknown. Specifically, the relationship between a specific sensory stimulus and the appropriate structural organization of excitatory inputs in specific neurons remains a problem for cognitive models.

The problem of morphogenesis

According to the received view in biology, cell actions during ontogenesis, including cell contact remodeling, cell migration, cell division, and cell extrusion, need control over cell mechanics. Collinet and Lecuit (2021) posed a question: "What forces or mechanisms at the cellular level manage four very general classes of tissue deformation, namely tissue folding and invagination, tissue flow and extension, tissue hollowing, and, finally, tissue branching"? "How are cell mechanics and associated cell behaviors robustly organized in space and time during tissue morphogenesis"? "What defines the time and length scales of the cell behaviors driving morphogenesis"? Notably, because the nervous system structures underlie everything that makes us human, the formation of neural tissues in a specific way is essential for shaping cognitive functions.

According to the mother-fetus neurocognitive model, the complex process of shaping the nervous system's determined structure requires a complete developmental program with a template for achieving the nervous system's final biological structure. Indeed, even processes of cell coupling that shape a nervous system during embryonic development challenge the naturalistic approach; how the nervous system grasps perception and shapes intentionality (independently, i.e., without any template) seems even more complicated. This model describes the physical interactions between two nervous systems that synchronize neuronal activity in perceiving environmental stimuli. Cognition and emotions develop through the association of affective cues with stimuli that activate neural pathways for simple reflexes, driven by non-local neuronal coupling in synchronized nervous systems. The emotion-reflex stimuli conjunction contributes to the further development of simple innate neuronal assemblies, shaping emotional neuronal patterns in statistical learning that are continuously connected to the neuronal pathways of reflexes.

Aphasia

From Wikipedia, the free encyclopedia https://en.wikipedia.org/wiki/Aphasia ...