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Definition

Aphasia is condition characterized by either partial or total loss of the ability to communicate verbally or using written words. A person with aphasia may have difficulty speaking, reading, writing, recognizing the names of objects, or understanding what other people have said. Aphasia is caused by a brain injury, as may occur during a traumatic accident or when the brain is deprived of oxygen during a stroke. It may also be caused by a brain tumor, a disease such as Alzheimer's, or an infection, like encephalitis. Aphasia may be temporary or permanent. Aphasia does not include speech impediments caused by loss of muscle control.

Description

To understand and use language effectively, an individual draws upon word memory—stored information on what certain words mean, how to put them together, and how and when to use them properly. For a majority of people, these and other language functions are located in the left side (hemisphere) of the brain. Damage to this side of the brain is most commonly linked to the development of aphasia. Interestingly, however, left-handed people appear to have language areas in both the left and right hemispheres of the brain and, as a result, may develop aphasia from damage to either side of the brain.

Stroke is the most common cause of aphasia in the United States. Approximately 500,000 individuals suffer strokes each year, and 20% of these individuals develop some type of aphasia. Other causes of brain damage include head injuries, brain tumors, and infection. About half of the people who show signs of aphasia have what is called temporary or transient aphasia and recover completely within a few days. An estimated one million Americans suffer from some form of permanent aphasia. As yet, no connection between aphasia and age, gender, or race has been found.

Aphasia is sometimes confused with other conditions that affect speech, such as dysarthria and apraxia. These condition affect the muscles used in speaking rather than language function itself. Dysarthria is a speech disturbance caused by lack of control over the muscles used in speaking, perhaps due to nerve damage. Speech apraxia is a speech disturbance in which language comprehension and muscle control are retained, but the memory of how to use the muscles to form words is not.

— Julia Barrett



 
 
Dictionary: a·pha·sia  (ə-fā'zhə) pronunciation
n.

Partial or total loss of the ability to articulate ideas or comprehend spoken or written language, resulting from damage to the brain caused by injury or disease.

[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.
aphasic a·pha'sic (-zĭk, -sĭk) adj. & n.
 

Definition

Aphasia is a communication disorder that occurs after language has been developed, usually in adulthood. Not simply a speech disorder, aphasia can affect the ability to comprehend the speech of others, as well as the ability to read and write. In most instances, intelligence per se is not affected.

Description

Aphasia has been known since the time of the ancient Greeks. However, it has been the focus of scientific study only since the mid-nineteenth century. Although aphasia can be caused by a head injury and neurologic conditions, its most common cause is stroke, a disruption of blood flow to the brain, which affects brain metabolism in localized areas of the brain. The onset of aphasia is usually abrupt, and occurs in individuals who have had no previous speech or language problems. Aphasia is at its most severe immediately after the event that causes it. Although its severity commonly diminishes over time through both natural, spontaneous recovery from brain damage and from clinical intervention, individuals who remain aphasic for two or three months after its onset are likely to have some residual aphasia for the rest of their lives. However, positive changes often continue to occur, largely with clinical intervention, for many years. The severity of aphasia is related to a number of factors, including the severity of the condition that brought it about, general overall health, age at onset, and numerous personal characteristics that relate to motivation.

Demographics

The National Aphasia Association estimates that approximately 25–40% of stroke survivors develop aphasia. There are approximately one million persons in the United States with aphasia, and roughly 100,000 new cases occur each year. There are more people with aphasia than with Parkinson's disease, cerebral palsy, or muscular dystrophy.

Causes and symptoms

Although aphasia occasionally results from damage to subcortical structures such as basal ganglia or the thalamus that has rich interconnections to the cerebral cortex, aphasia is most frequently caused by damage to the cerebral cortex of the brain's left hemisphere. This hemisphere plays a significant role in the processing of language skills. However, in about half of left-handed individuals (and a few right-handed persons), this pattern of dominance for language is reversed, making right-hemisphere damage the cause of aphasia in this small minority. Because the left side of the brain controls movement on the right side of the body (and vice versa), paralysis affecting the side of the body opposite the side of brain damage is a frequent co-existing problem. This condition is called hemiplegia and can affect walking, using one's arm, or both. If the arm used for writing is paralyzed, it poses an additional burden on the diminished writing abilities of some aphasic individuals. If paralysis affects the many muscles involved in speaking, such as the muscles of the tongue, this condition is called dysarthria. Dysarthria often co-occurs with aphasia.

There are a few more problems that can result from the same brain injury that produces aphasia, and complicate its presentation. Most notable among them are the problems collectively called apraxia, which influences one's ability to program movement. Apraxic difficulties make voluntary movements difficult and hard to initiate. Apraxia of speech results in difficulty initiating speech and in making speech sounds consistently. It frequently co-occurs with both dysarthria and aphasia. Finally, sensory problems such as visual field deficits (specifically, hemianopsia) and changes in (or absence of) sensation in arms, legs, and tongue commonly occur with aphasia.

There are neurological disorders other than aphasia that also manifest difficulty with language. This makes it important to note what aphasia is not. Traumatic brain injury and dementias such as Alzheimer's disease are excellent examples. Although brain injury is a cause of aphasia, most head injuries produce widespread brain damage and result in other neuropsychological and cognitive disorders. These disorders often create language that is disturbed in output and form, but are typically the linguistic consequences of cognitive disturbances. In Alzheimer's disease, the situation is much the same. Language spoken by individuals with Alzheimer's reflect their cognitive problems, and, as such, differ from the language retrieval problems typically designated as aphasia. In short, if the damage that results in language problems is general and produces additional intellectual problems, then aphasia is a correct diagnosis. In the absence of other significant intellectual problems, then the language disorder is probably localized to the brain's language processing areas and is properly termed aphasia.

Finally, aphasia is not conventionally used to refer to the developmental language learning problems encountered by some atypically developing children. However, when children who have been previously developing language normally have a stroke or some other type of localized brain damage, then the aphasia diagnosis is appropriate.

Aphasia manifests different language symptoms and syndromes as a result of where in the language-dominant hemisphere the damage has occurred. The advent of neuroimaging has improved the ability to localize the area of brain damage. Nevertheless, the different general patterns of language strengths and weaknesses, as well as unexpected dissociations in language function, can explain how normal language is processed in the brain, as well as provide insights into intervention for aphasia.

Aphasic individuals almost uniformly have some difficulty in using the substantive words of their native language. Most experts in aphasia recognize that aphasia varies along two major dimensions: auditory comprehension ability and fluency of speech output. In reality, aphasic behaviors vary greatly from individual to individual, and fluctuate in a given individual as a result of fatigue and other factors. In addition, largely in relationship to lesion size, aphasias differ in overall severity.

Nonfluent aphasia

Frontal cortex is responsible for shaping, initiating, and producing behaviors. Individuals with nonfluent aphasia characteristically have brain damage affecting Broca's area of the cortex and the frontal brain areas surrounding it. These areas are responsible for formulating sound, word, and sentence patterns. Damage to the anterior speech areas results in slow, labored speech with limited output and prosody and difficulty in producing grammatical sentences. Because the motor cortex is closely adjacent, nonfluent Broca's aphasia, by far the most common nonfluent variant, is quite likely to co-occur with motor problems.

Several additional characteristics of nonfluent aphasia can be noted: in nonfluent aphasia verbs and prepositions are disproportionately affected; speech errors occur mostly at the level of speech sounds, producing sound transpositions and inconsistencies; auditory comprehension is only minimally affected; reading abilities parallel comprehension, writing problems parallel speech output, but are sometimes further complicated by hemiplegia; finally, there is an inability to repeat what someone else says.

Fluent aphasia

Fluent aphasias occur when damage occurs in the posterior language areas of the brain, where sensory stimuli from hearing, sight, and bodily sensation converge. In fluent aphasia, the prosody and flow of speech is maintained; one typically must listen closely to recognize that the speech is not normal. Because this posterior damage is located far from the motor areas in the frontal lobes, individuals with fluent aphasia seldom have co-existing difficulty with the mechanics of speech, arm use, or walking. There are three major variants of fluent aphasia, each thought to occur as a function of disruption to different posterior brain regions.

WERNICKE'S APHASIA Wernicke's aphasia results from temporal lobe damage, where auditory input to the brain is received. The essential characteristic is that individuals with this disorder have disproportionate difficulty in understanding spoken and written language. They also have problems comprehending and monitoring their own speech. They are often verbose, and frequently use inappropriate and even jargon words when they speak. Reading and writing are impaired in similar ways to auditory comprehension and speech output. Their comprehension difficulties preclude their being able to repeat others' words.

ANOMIC APHASIA Most people, particularly as they grow older, have trouble with the names of persons and things; all aphasic persons experience these difficulties. But when brain damage occurs in the area of the posterior brain where information from temporal, parietal, and occipital lobes converge, this problem of naming is much more pervasive than for normal and aphasic speakers alike. Most anomic aphasic individuals have excellent auditory comprehension and read well. But for most of them, writing mirrors speech, and individuals with anomic aphasia can take advantage of words provided by others. Hence, their repetition ability is good. Although anomic aphasia is classified as a fluent syndrome, frequent stops, starts, and word searches typically make speech choppy in between runs of fluency.

CONDUCTION APHASIA Individuals with conduction aphasia are thought to have a discrete brain lesion that disrupts the pathways that underlie the cortex and connect the anterior and posterior speech regions. These individuals have good comprehension, as well as high awareness of the errors that they make. Placement of their brain damage also suggests that there should be little interference with speech production, reading, and writing. However, damage to the neural links between posterior and anterior speech areas makes it quite difficult for these individuals to correct the errors they hear themselves making. Conduction aphasia also affects the ability to repeat the speech of others or to take advantage of the cues others provide. The speech of individuals with this problem includes many inappropriate words, typically involving inappropriate sequences of sounds.

UNUSUAL APHASIA SYNDROMES There are a few other rare aphasic syndromes (called "transcortical aphasias") and unique dissociations in aphasic patterns. The above aphasias represent the most common distinctive syndromes. However, they are estimated to account for only approximately 40% of individuals with aphasia.

MIXED AND GLOBAL APHASIA The remaining majority, about 60% of aphasic individuals, have aphasias that result from brain lesions involving both the anterior and posterior speech areas. Their aphasias, thus, affect both speech production and comprehension. They frequently have reading and writing disorders as well. Individuals with mixed and global aphasia are also very likely to have hemiplegia and dysarthria, as well as a variety of sensation losses. Depending upon the severity of these symptoms, people with mild-to-moderate symptomatology of this type are said to have mixed aphasia; global aphasia describes individuals with extensive difficulties in all language skills.

Diagnosis

As an aid to accurate diagosis immediately following stroke, it is important to differentiate aphasia from cognitive disorders such as confusion and disorientation. To this end, brief, but general testing of the language functions (naming, comprehension, reading, writing, and repetition) can be incorporated into broader testing that might determine other cognitive functions. Evaluators must remember that language is the medium though which most of these other functions are observed. Therefore, language should be assessed first; if extensive aphasia is present, then only cautious interpretations of other cognitive functions may be given. At present, there are few available objective and standardized measures for testing during the acute phases of disorders such as stroke.

A number of standardized measures are available that provide an inventory of aphasic symptoms. These tests are useful in providing baseline and follow-up assessments to measure progress in treatment, as well as to guide the treatment itself. A fairly general feature of aphasia tests is that individuals without aphasic symptoms should perform with almost no errors on them. Tests are available to measure the extent and severity of language impairments as well as to provide information about functional skills and outcomes. Finally, there are assessments designed specifically to look at quality of life with aphasia.

Treatment team

Because of the various other problems in addition to language that affect most individuals with aphasia, a multidisciplinary team is used in rehabilitation centers for the management of aphasia. Team members, as well as speech-language pathologists, typically include physical and occupational therapists, clinical neuropsychologists, nurses, and social workers who are guided by physiatrists and neurologists. Once discharged from rehabilitation centers, aphasic individuals often continue their treatment by speech-language pathologists in settings such as speech and hearing clinics. Self-help groups and support via the Internet are available as well.

Treatment

Most individuals with aphasia are hospitalized for some period of time for treatment of the condition that has resulted in aphasia. Assessment of the extent and type of language disorder is made during that time, as assessment of the ability to swallow (dysphagia). Early medical intervention is important for lessening the long-term effects of stroke.

Recovery and rehabilitation

To date, no pharmacological treatments for aphasia have proven effective, although a number of drugs (dopaminergic, cholinergic, and neurotrophic) continue to be investigated, usually in conjunction with behavioral treatments for aphasia. Various behavioral treatment approaches for aphasia exist. They are usually characterized dichotomously as restorative (restitutive) or compensatory. The goal of restorative treatments is to reestablish disordered language skills. Goals for compensatory approaches are to develop and train alternative approaches to circumvent the language skills that have been affected by aphasia. Most clinicians use both approaches (often simultaneously) to aid in language recovery. Some examples of restorative approaches include practice of carefully selected syntactic structures, naming drills, or practice using self-selected communication needs such as using the telephone.

Compensatory approaches include training conversational partners to modify their own language and communication skills in ways that make it easier for the aphasic individual to communicate, or teaching aphasic individuals to use a relatively intact language skill such as writing or drawing to substitute for talking. Computerized approaches to both restitutive and compensatory aphasia treatment are increasing. Many clinics offer both individual treatment and group treatment, with the latter offering increased psychosocial support. Many clinics also incorporate family support groups.

Clinical trials

Randomized control trials (RCTs) are rare for the behavioral realm of treatments. Aphasia is no exception. To date, only four RCTs have been completed, with three of the four addressing to the efficacy of treatment. A far greater number of phases I and II studies exist, and investigate the value of language intervention, particularly post stroke. The largest testimony comes from single-case designs and qualitative case studies that agree that treatment has a positive influence on outcome. Only one meta-analysis of significant scope has been completed (Robey, 1998).

Prognosis

The traditional view is that most of the language gains made by aphasic individuals will occur in the first six months following injury, except in persons with global aphasia, who may begin the recovery process later, but are shown to make gains through one year. Significantly, it must be noted that most traditional treatment techniques have been validated using aphasic patients whose period of spontaneous recovery has passed. Some people with aphasia may be able to return to work, although the communicative demands of many occupations may affect employment.

As of the late 1990s, research has begun to focus on recovery across the remainder of the lifespan, and it has become apparent that aphasic individuals continue to make progress, often for years after the precipitating event. The factors that explain very late recovery are not clear and will require scientific observation and study.

Special concerns

Despite the prevalence of aphasia, the disorder is neither well recognized nor well understood. Aphasia's psychosocial and vocational consequences are over-whelmingly devastating, but community understanding is at best limited. Similarly, despite substantial evidence concerning the effectiveness of intervention, skepticism about the value of treatment remains. As a consequence of both of these factors, many aphasic individuals and their families are not well informed about either the disorder or what might be done to alleviate it.

Additionally, although a significant and growing number of individuals in the United States is bilingual, there is a surprising lack of research concerning the effects of speaking more than one language on recovery from aphasia. Finally, current funding for only very limited treatment for aphasia is available via third-party reimbursement.

Resources

BOOKS

Davis, G. A. Aphasology: Disorders and Clinical Practice. Boston: Allyn and Bacon, 2000.

Goodglass, H. Understanding Aphasia. New York: Academic Press, 1993.

Hillis, A. E. The Handbook of Adult Language Disorders. New York: Psychology Press, 2002.

PERIODICALS

Robey, R. R. "A Meta-analysis of Clinical Outcomes in the Treatment of Aphasia." Journal of Speech and Hearing Research 41 (1998): 172–187.

ORGANIZATIONS

Aphasia Hope Foundation. 2436 West 137th St., Leawood, KS 66224. (913) 402-8306 or (866) 449-5894; Fax: (913) 402-8315. http://www.aphasiahope.org.

National Aphasia Association. 29 John Street, New York, NY 10038. (212) 267-2812 or (800) 922-4622. naa@aphasia.org. http://www.aphasia.org.


Audrey L. Holland, PhD


 

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.


 
(ə-fa′zhə)
n

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.

 

Defect in the expression and comprehension of words, caused by damage to the frontal and temporal lobes of the brain. It can result from head trauma, tumour, stroke, or infection. Symptoms vary with the brain area involved, and the ability to put words in a meaningful order may be lost. Speech therapy may be useful. In some cases, improvement may be due to assumption of some language functions by other areas of the brain.

For more information on aphasia, visit Britannica.com.

 

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.

 
(əfā'zhə) , language disturbance caused by a lesion of the brain, making an individual partially or totally impaired in his ability to speak, write, or comprehend the meaning of spoken or written words. It is distinguished from functional disorders such as stammering or stuttering, and from impaired speech due to physical defects in the organs used for speaking. Treatment consists of reeducation; the oral and lip-reading methods employed in the education of deaf and mute children have been found to be of assistance in therapy.


 
Psychoanalysis: Aphasia

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

 
Obscure Words: aphasia


inability to use or comprehend words
 
Word Tutor: aphasia
pronunciation

IN BRIEF: n. - Inability to use or understand language (spoken or written) because of a brain lesion.

Tutor's tip: "Aphagia" (inability to swallow) is worse than "aphasia" (inability to comprehend words), because you need to eat to survive.

 
Wikipedia: aphasia


Aphasia
Classification & external resources
ICD-10 F80.0-F80.2, R47.0
ICD-9 315.31, 784.3
DiseasesDB 4024
MedlinePlus 003204
eMedicine neuro/437 
MeSH D001037

Aphasia (or aphemia) is a loss of the ability to produce and/or comprehend language, due to injury to brain areas specialized for these functions. It is not a result of deficits in sensory, intellect, or psychiatric functioning. (Brookshire, 1992; Goodglass 1993) It is also not muscle weakness or a cognitive disorder.

Depending on the area and extent of the damage, someone suffering from aphasia may be able to speak but not write, or vice versa, or display any of a wide variety of other deficiencies in language comprehension and production, such as being able to sing but not speak. Aphasia may co-occur with speech disorders such as dysarthria or apraxia of speech, which also result from brain damage.

Causes

Usually, aphasias are a result of damage (lesions) to the language centres of the brain (like Broca's area). 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 head injury. Aphasia may also develop slowly, as in the case of a brain tumor or progressive neurological disease. It may also be caused by a sudden hemorrhagic event within the brain.

Prognosis

The prognosis of those with aphasia varies widely, and is dependent upon age of the patient, site and size of lesion, and type of aphasia.

Diagnosis

Aphasia can be assessed in a variety of ways, from quick clinical screening at the bedside to several-hour-long batteries of tasks that examine the key components of language and communication.

Symptoms

Any of the following can be considered symptoms of aphasia:

  • inability to comprehend language
  • inability to pronounce, not due to muscle paralysis or weakness
  • inability to speak spontaneously
  • inability to form words
  • inability to name objects
  • poor enunciation
  • excessive creation and use of personal neologisms
  • inability to repeat a phrase
  • persistent repetition of phrases
  • paraphasia (substituting letters, syllables or words)
  • agrammatism (inability to speak in a grammatically correct fashion)
  • dysprosody (alterations in inflexion, stress, and rhythm)
  • uncompleted sentences
  • inability to read
  • inability to write

Types of aphasia

The following table summarizes some major characteristics of different types of aphasia:

Type of aphasia Repetition Naming Auditory comprehension Fluency Presentation
Wernicke's aphasia mild–mod mild–severe defective fluent paraphasic Individuals with Wernicke's aphasia may speak in long sentences that have no meaning, add unnecessary words, and even create new "words" (neologisms). For example, someone with Wernicke's aphasia may say, "You know that smoodle pinkered and that I want to get him round and take care of him like you want before", 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 Wernicke's aphasia usually have great difficulty understanding the speech of both themselves and others and are therefore often unaware of their mistakes. They are also often unaware of their surroundings, and may present a risk to themselves and others around them.
Transcortical sensory aphasia good mod–severe poor fluent Similar deficits as in Wernicke's aphasia, but repetition ability remains intact.
Conduction aphasia poor poor relatively good fluent Caused by damage to the arcuate fasciculus, the structure that transmits information between Wernicke's area and Broca's area. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Repetition ability is poor.
Anomic aphasia mild mod–severe mild fluent Anomic aphasia, is essentially a difficulty with naming. The patient 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. Patients tend to produce grammatic, yet empty, speech. Auditory comprehension tends to be preserved.
Broca's aphasia mod–severe mod–severe mild difficulty non-fluent, effortful, slow Individuals with Broca's aphasia frequently speak short, meaningful phrases that are produced with great effort. Broca's aphasia is thus characterized as a nonfluent aphasia. Affected people often omit small words such as "is", "and", and "the". For example, a person with Broca's aphasia may say, "Walk dog" meaning, "I will take the dog for a walk". The same sentence could also mean "You take the dog for a walk", or "The dog walked out of the yard", depending on the circumstances. Individuals with Broca's 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. It is associated with right hemiparesis, meaning that there will be paralysis of the patient's right arm, leg, and face.
Transcortical motor aphasia good mild–severe mild non-fluent Similar deficits as Broca's aphasia, except repetition ability remains intact. Auditory comprehension is generally fine for simple conversations, but declines rapidly for more complex conversations. It is associated with right hemiparesis, meaning that there will be paralysis of the patient's right arm, leg, and face.
Global aphasia poor poor poor non-fluent Individuals with global aphasia have severe communication difficulties and will be extremely limited in their ability to speak or comprehend language. They may be totally nonverbal, and/or only use facial expressions and gestures to communicate. It is associated with right hemiparesis, meaning that there will be paralysis of the patient's right arm, leg, and face.
Transcortical mixed aphasia moderate poor poor non-fluent Similar deficits as in global aphasia, but repetition ability remains intact.
Subcortical aphasias Characteristics and symptoms depend upon the site and size of subcortical lesion. Possible sites of lesions include the thalamus, internal capsule, and basal ganglia.

Classification of aphasia

Classifying the different subtypes of aphasia is difficult and has led to disagreements among experts. The locationist 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. [1]

The locationist model

Cortex
Enlarge
Cortex

The locationist 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". The most prominent writers on this topic have been Howard Goodglass and Edith Kaplan.

  • Individuals with Broca's aphasia (also termed expressive aphasia) were once thought to have ventral temporal damage though more recent work by Nina Dronkers using imaging and 'lesion analysis' has revealed that patients with Broca's Aphasia have lesions to the medial insular cortex. Broca missed these lesions because his studies did not disect the brains of diseased patients so only the more temporal damage was visible. Individuals with Broca's aphasia often have right-sided weakness or paralysis of the arm and leg because the frontal lobe is also important for body movement.
  • In contrast to Broca's aphasia, damage to the temporal lobe may result in a fluent aphasia that is called Wernicke's aphasia (also termed sensory aphasia). These individuals usually have no body weakness because their brain injury is not near the parts of the brain that control movement.
  • Working from Wernicke's model of aphasia, Ludwig Lichtheim proposed five other types of aphasia but these were not tested against real patients until modern imaging made more indepth studies available. The other five types of aphasia in the locationist model are:
  1. Pure word deafness
  2. Conduction aphasia
  3. Apraxia of speech, which is now considered a separate disorder in itself.
  4. Transcortical motor aphasia
  5. Transcortical sensory aphasia
  • Anomia is another type of aphasia proposed under what is commonly known as the Boston-Neoclassical model, which is essentially a difficulty with naming. A final type of aphasia, global aphasia, results from damage to extensive portions of the language areas of the brain.

Fluent, non-fluent and "pure" aphasias

The different types of aphasia can be divided into three categories: fluent, non-fluent and "pure" aphasias.[2]

  • Fluent aphasias, also called receptive aphasias, are impairments related mostly to the input or reception of language, with difficulties either in auditory verbal comprehension or in the repetition of words, phrases, or sentences spoken by others. Speech is easy and fluent, but there are difficulties related to the output of language as well, such as paraphasia. Examples of fluent aphasias are: Wernicke's aphasia, Transcortical sensory aphasia, Conduction aphasia, Anomic aphasia
  • "Pure" aphasias are selective impairments in reading, writing, or the recognition of words. These disorders may be quite selective. For example, a person is able to read but not write, or is able to write but not read. Examples of pure aphasias are: Alexia, Agraphia, Pure word deafness

The cognitive neuropsychological model

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. 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), 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.

A few less common subtypes include:

A combination of subtypes is possible.

Primary and secondary aphasia

Aphasia can be divided into primary and secondary aphasia.[3]

  • Primary aphasia is due to problems with language-processing mechanisms.
  • Secondary aphasia is the result of other problems, like memory impairments, attention disorders, or perceptual problems.

Famous individuals who suffer(ed) from aphasia

See also

Sources

Academic references

  • R. Chapey (Ed.) (2001). Language Intervention Strategies in Aphasia and Related Neurogenic Communication Disorders (Fourth Edition). Philadelphia: Lippincott, Williams & Wilkins.
  • Goodglass, H. & Kaplan, E. (1972). Assessment of Aphasia and Related Disorders. Philadelphia: Lea and Febinger.
  • Kay, J., Lesser, R., & Coltheart, M. (1992). Psycholinguistic Assessments of Language Processing in Aphasia (PALPA). Hove: Erlbaum.
  • Spreen, O. & Risser, A.H. (2003). Assessment of Aphasia. New York: Oxford University Press.

Personal experiences of aphasia

  • Hale, S (2003), The Man Who Lost His Language, Penguin.
  • Paul E. Berger and Stephanie Mensh, How to Conquer the World With One Hand...And an Attitude, 2nd Ed., ISBN 0-9668378-7-8
  • Cindy Greatrex (2005) Aphasia in the Deaf Community.
  • Dardick, Geeta (1991), Prisoner of Silence, Reader's Digest, June issue

References

  1. ^ Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003), page 502, 505, 511.
  2. ^ Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003), pages 502-504. The whole paragraph "fluent, non-fluent and pure aphasias" is written with help of this reference.
  3. ^ http://christofflab.psych.ubc.ca/psych260/docs/L12-Language.pdf

External links

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