
[Greek, from aphatos, speechless : a-, not; see a-1 + phatos, spoken, speakable (from phanai, to speak; see -phasia).]
aphasiac a·pha'si·ac' (-zē-ăk') n.For more information on aphasia, visit Britannica.com.
Impairment in the use of spoken or written language caused by injury to the brain which cannot be accounted for by paralysis or incoordination of the articulatory organs, impairment of hearing or vision, impaired level of consciousness, or impaired motivation to communicate. The language zone in the brain includes the portion of the frontal, temporal, and parietal lobes surrounding the sylvian fissure and structures deep to these areas. In right-handed persons, with few exceptions, only injury in the left cerebral hemisphere produces aphasia. Lateralization of language function is variable in left-handers, and they are at greater risk for becoming aphasic from a lesion in either hemisphere. See also Hemispheric laterality.
Distinctive recurring patterns of deficit are associated with particular lesion sites within the language zone. These patterns may entail selective impairment of articulation, ability to retrieve concept names, or syntactic organization. Other dissociations affect principally the auditory comprehension of speech, the repetition of speech, or the recognition of written words. The erroneous production of unintended words in speech (paraphasia), oral reading (paralexia), or writing (paragraphia) is a feature of some forms of aphasia.
Mixed forms of aphasia, caused by multiple lesions or lesions spanning anterior and posterior portions of the speech zone, are quite common, and massive destruction of the entire language area results in a global aphasia. Further, individual variations in behavioral manifestations of similar lesions have set limits on the strict assignment of function to structures within the language area.
Preadolescent children suffering aphasia after unilateral injury usually recover rapidly, presumably by virtue of the capacity of the right cerebral hemisphere early in life to acquire the language functions originally mediated by the left hemisphere. Capacity for recovery of function decreases during later adolescence and young adulthood.
Complete recovery in adults after a severe injury is much less common, and severe aphasia may persist unchanged for the duration of the person's life. Many patients are aided by remedial language training, while others continue severely impaired. See also Memory.
The disruption or total loss of the faculty of speech, often resulting from local damage to the left hemisphere of the brain. In ancient scepticism aphasia is the silence enjoined on us after we have suspended judgement on things.
Aphasia, a word proposed by Armand Trousseau to replace the term "aphemia," created by Paul Broca, refers to language disturbances that arise from specific cerebral lesions, most often in the cortex. Between 1861 and 1865, when the dispute ended concerning the question of determining whether the cerebral cortex operated as a unit or as a collection of separate elements, Paul Broca showed, through a series of anatomical and clinical observations, that the destruction of the left side of the base of the third circumvolution of the frontal lobe in a right-handed subject who until then was able to speak normally led to the loss of articulate language. The subject was unable to express himself using a sequence of words or phrases.
In 1874 Carl Wernicke extended the field of research by describing two other types of aphasia, all caused by a lesion in the left hemisphere: sensory aphasia from damage to the posterior areas of the second and third circumvolution of the cortex, and conduction aphasia, arising from the disconnection of the bundles connecting this region to the base of the third circumvolution of the frontal lobe. Afterwards, the disturbance identified by Broca would be known as "motor aphasia." Later Wernicke identified two other types of aphasia: "motor transcortical aphasia" and "sensory transcortical aphasia."
By the end of the nineteenth century, three separate approaches to the problem had been developed. Some researchers, such as Jean Martin Charcot and Joseph Grasset, increased the number of types of aphasia; others, like Alfred Vulpian, and later Pierre Marie, renewed the "unitarian" position; the third group, following the important work by Jules Déjerine, demonstrated through the use of clinical and anatomical arguments that the nature of the aphasia would change with the nature and location of the lesion. For example, frontal lesions seemed to primarily affect speech production, posterior lesions seemed to affect speech recognition, and the destruction of the cortex resulted in disturbances of internal language, which affected the subject's autonomy.
Sigmund Freud's work on aphasia, published in 1891, accepts the work of Paul Broca but questions Wernicke's research, which Freud criticizes for being excessively schematic and lacking in clinical observations. Freud did not question the relationship of language function with the brain but was cautious about hastily assigning specific locations to specific functions. Although he accepts that certain clinically based forms of aphasia—"verbal aphasia," "asymbolic aphasia," "agnosic aphasia"—can be used to localize the cortical lesion with certainty (which was later confirmed by neurosurgery during the First World War), he refused to extrapolate from pathology to physiology and deduced a cerebral concept of the normal operation of language, with a critical position that was far removed from the scientism that is often attributed to him in this field. In the descriptive sections of his work, Freud distinguished between the representation of words and the representation of things, and their links with auditory images, visual images, and the motor images at work in these phenomena.
Bibliography
Freud, Sigmund. (1891b [1953]), On aphasia (A critical study) (E. Stengel, Trans.). New York: International Universities Press.
Hécaen, H. and Lantéri-Laura, Georges. (1977).Évolution des connaissances et des doctrines sur les localisations cérébrales. Paris: Desclée de Brouwer.
——. (1989). Les fonctions du cerveau. Paris: Masson.
Lantéri-Laura, Geoerges. (1993). Histoire de la phrénologie. Paris: Presses Universitaires de France.
Further Reading
Miller, Laurence (1991). On aphasia at 100: the neuropsychodynamic legacy of Freud. Psychoanalytic Review, 78, 365-378.
Rizzuto, Anna-Marie. (1990). Origin of Freud's concept of object representation: "On Aphasia." International Journal of Psychoanalysis, 71, 241-248.
—GEORGES LANTÉRI-LAURA
1. The manner of breakdown
The different forms of breakdown can be classified in different ways, but most people nowadays consider just two major groups: non-fluent (or Broca's) and fluent (or Wernicke's), the names in parentheses being those of the neurologists who first described them. (See language: neuropsychology, for a fuller discussion.)2. The causes of breakdown
Aphasia is caused by damage to tissue within the brain. But whether injuries to different areas of the brain cause different types of disorder, and whether the same patterns of disorder occur in all individuals, is less certain. Each hemisphere of the brain not only controls movement and sensation of the opposite side of the body, but seems to specialize in particular mental functions. (See neuropsychology.) It is the left hemisphere that seems to be most closely concerned with language, although in left-handed people and those with a family history of left-handedness the association is not so strong. Moreover it is not inevitable. People whose left hemispheres are damaged in early infancy or childhood can 'learn to speak' perfectly adequately with their right. By and large, however, it is damage to the left hemisphere that most commonly causes aphasia, that to the anterior part causing non-fluent disorders, and that to the posterior part causing those of the fluent type. It is sometimes held, though, that in fluent aphasia there is also usually some damage to the right or non-dominant hemisphere as well as to the left.3. Recovery
The vast majority of aphasic people, especially in the younger age groups, recover a good deal of speech as time goes on; and a few of the more literary ones have written accounts of their experiences. Unfortunately these seldom contain information about how the faculties were regained, probably because such processes — like many other forms of learning and remembering — occur at a level that is not available to normal consciousness. Psychologists who have been able to watch and study these people have, however, identified several factors that seem to be involved, especially in non-fluent aphasia.— Moyra Williams
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A loss of power of expression through speech, writing, or signs of comprehension of spoken or written language resulting from disease or injury of the brain centers.

| Aphasia | |
|---|---|
| Classification and external resources | |
| ICD-10 | F80.0-F80.2, R47.0 |
| ICD-9 | 315.31, 784.3, 438.11 |
| DiseasesDB | 4024 |
| MedlinePlus | 003204 |
| eMedicine | neuro/437 |
| MeSH | D001037 |
| Dysphasia | |
|---|---|
| Classification and external resources | |
| ICD-10 | F80.1, F80.2, R47.0 |
| ICD-9 | 438.12, 784.5 |
Aphasia (
/əˈfeɪʒə/ or /əˈfeɪziə/, from ancient Greek ἀφασία (ἄφατος, ἀ- + φημί), "speechlessness"[1]) is an impairment of language ability. This class of language disorder ranges from having difficulty remembering words to being completely unable to speak, read, or write.
Acute aphasia disorders usually develop quickly as a result of head injury or stroke, and progressive forms of aphasia develop slowly from a brain tumor, infection, or dementia.[2][3] The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms. Aphasia types include expressive aphasia, receptive aphasia, conduction aphasia, anomic aphasia, global aphasia, primary progressive aphasias and many others (see Category:Aphasias). Medical evaluations for the disorder range from clinical screenings by a neurologist to extensive tests by a Speech-Language Pathologist.[2][4]
Most acute aphasia patients can recover some or most skills by working with a Speech-Language Pathologist. This rehabilitation can take two or more years and is most effective when begun quickly. Only a small minority will recover without therapy, such as those suffering a mini-stroke. Improvement varies widely, depending on the aphasia's cause, type, and severity. Recovery also depends on the patient's age, health, motivation, handedness, and educational level.[2]
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Classifying the different subtypes of aphasia is difficult and has led to disagreements among experts. The localizationist model is the original model, but modern anatomical techniques and analyses have shown that precise connections between brain regions and symptom classification don't exist. The neural organization of language is complicated; language is a comprehensive and complex behavior and it makes sense that it isn't the product of some small, circumscribed region of the brain.
No classification of patients in subtypes and groups of subtypes is adequate. Only about 60% of patients will fit in a classification scheme such as fluent/nonfluent/pure aphasias. There is a huge variation among patients with the same diagnosis, and aphasias can be highly selective. For instance, patients with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors.[5]
The localizationist model attempts to classify the aphasia by major characteristics and then link these to areas of the brain in which the damage has been caused. The initial two categories here were devised by early neurologists working in the field, namely Paul Broca and Carl Wernicke. Other researchers have added to the model, resulting in it often being referred to as the "Boston-Neoclassical Model".
Primary progressive aphasia (PPA) is 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 losing the ability to think. It is characterized by the gradual loss of the ability to name objects. People suffering from PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence.[11][12][13] There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA)[14]
Progressive Jargon Aphasia is a fluent or receptive aphasia in which the patient's speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the patient has problems with the selection of nouns. They will either 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. Accordingly, patients with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they can't find with sounds. Commonly, substitutions 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).
The different types of aphasia can be divided into three categories: fluent, non-fluent and "pure" aphasias.[15]
Aphasias can be divided into primary and secondary cognitive processes.
The cognitive neuropsychological model builds on cognitive neuropsychology. It assumes that language processing can be broken down into a number of modules, each of which has a specific function.[17] Hence there is a module which recognises phonemes as they are spoken and a module which stores formulated phonemes before they are spoken. Use of this model clinically involves conducting a battery of assessments (usually from the PALPA, the "psycholinguistic assessment of language processing in adult acquired aphasia ... that can be tailored to the investigation of an individual patient's impaired and intact abilities" [18]), each of which tests one or a number of these modules. Once a diagnosis is reached as to where the impairment lies, therapy can proceed to treat the individual module.
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.
Acute Aphasias
The following table summarizes some major characteristics of different acute of aphasia:
| Type of aphasia | Repetition | Naming | Auditory comprehension | Fluency |
|---|---|---|---|---|
| Receptive aphasia | mild–mod | mild–severe | defective | fluent paraphasic |
| Transcortical sensory aphasia | good | mod–severe | poor | fluent |
| Conduction aphasia | poor | poor | relatively good | fluent |
| Anomic aphasia | mild | mod–severe | mild | fluent |
| Expressive aphasia | mod–severe | mod–severe | mild difficulty | non-fluent, effortful, slow |
| Transcortical motor aphasia | good | mild–severe | mild | non-fluent |
| Global aphasia | poor | poor | poor | non-fluent |
| Mixed transcortical aphasia | moderate | poor | poor | non-fluent |
Subcortical aphasias
Aphasia usually results from lesions to the language-relevant areas of the frontal, temporal and parietal lobes of the brain, such as Broca's area, Wernicke's area, and the neural pathways between them. These areas are almost always located in the left hemisphere, and in most people this is where the ability to produce and comprehend language is found. However, in a very small number of people, language ability is found in the right hemisphere. In either case, damage to these language areas can be caused by a stroke, traumatic brain injury, or other brain injury.
Aphasia may also develop slowly, as in the case of a brain tumor or progressive neurological disease, e.g., Alzheimer's or Parkinson's disease. It may also be caused by a sudden hemorrhagic event within the brain. Certain chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia as a prodromal or episodic symptom.[19]
Aphasia can result from Herpes Simplex virus (HSV) encephalitis. The (HSV) affects the frontal and temporal lobes, subcortical structures and the hippocampal tissue which can trigger aphasia. [20]
Aphasia is also listed as a rare side effect of the fentanyl patch, an opioid used to control chronic pain.[21]
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, as explained in the above sections. Aphasia is rarely exhibited identically, implying that treatment needs to be catered specifically to the individual. Studies have shown that although there isn't consistency on treatment methodology in literature, there is a strong indication that treatment in general has positive outcomes.[22]
A multi-disciplinary team, including doctors (often a physician is involved, but more likely a clinical neuropsychologist will head the treatment team), physiotherapist, occupational therapist, speech-language pathologist, and social worker, works together in treating aphasia. For the most part, treatment relies heavily on repetition and aims to address language performance by working on task-specific skills. The primary goal is to help the individual and those closest to them adjust to changes and limitations in communication.[22]
Treatment techniques mostly fall under two approaches:
Several treatment techniques include the following:
More recently, computer technology has been incorporated into treatment options. A key indication for good prognosis is treatment intensity. A minimum of 2–3 hours per week has been specified to produce positive results.[24] The main advantage of using computers is that it can greatly increase intensity of therapy. These programs consist of a large variety of exercises and can be done at home in addition to face-to-face treatment with a therapist. However, since aphasia presents differently among individuals, these programs must be dynamic and flexible in order to adapt to the variability in impairments. Another barrier is the capability of computer programs to imitate normal speech and keep up with the speed of regular conversation. Therefore, computer technology seems to be limited in a communicative setting, however is effective in producing improvements in communication training.[24]
Several examples of programs used are StepByStep, Linguagraphica, Computer-Based Visual Communication (C-VIC), TouchSpeak (TS), and Sentence Shaper.[24]
Melodic intonation therapy is often used to treat non-fluent aphasia and has proved to be very effective in some cases.[25]
Zolpidem, a drug with the trade name of Ambien, may provide short-lasting but effective improvement in symptoms of aphasia present in some survivors of stroke. The mechanism for improvement in these cases remains unexplained and is the focus of current research by several groups, to explain how a drug which acts as a hypnotic-sedative in people with normal brain function, can paradoxically increase speech ability in people recovering from severe brain injury. Use of zolpidem for this application remains experimental at this time, and is not officially approved by any pharmaceutical manufacturers of zolpidem or medical regulatory agencies worldwide.
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.[26]
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This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)
Nederlands (Dutch)
afasie (verlies van vermogen tot taalgebruik)
Français (French)
n. - aphasie
Deutsch (German)
n. - Aphasie, (Verlust der Sprechfähigkeit)
Ελληνική (Greek)
n. - (παθολ.) αφασία
Português (Portuguese)
n. - afasia (f) (Med.)
Русский (Russian)
афазия, потеря речи
中文(简体)(Chinese (Simplified))
失语症
中文(繁體)(Chinese (Traditional))
n. - 失語症
العربيه (Arabic)
(الاسم) الحبسه : فقدان القدره على الكلام نتيجه تعرض الدماغ لأذى نتيجه اصابه
עברית (Hebrew)
n. - אובדן היכולת לדבר או להבין דיבור, שכחת הלשון, אפזיה
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