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Aphasia

From Wikipedia, the free encyclopedia


Jump to: navigation, search For other uses, see Aphasia (disambiguation). Aphasia (pronounced /fe/ or pronounced /fezi/) is an acquired language disorder in which there is an impairment of any language modality. This may include difficulty in producing or comprehending spoken or written language. Traditionally, aphasia suggests the total impairment of language ability, and dysphasia a degree of impairment less than total. However, the term dysphasia is easily confused with dysphagia, a swallowing disorder, and thus aphasia has come to mean both partial and total language impairment in common use. Depending on the area and extent of brain 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. 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. 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.

[edit] Causes
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.[citation needed] Aphasia is also listed as a rare side effect of the fentanyl patch, an opioid used to control chronic pain.[1]

[edit] 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.

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) incompleted sentences inability to read inability to write limited verbal output difficulty in naming

[edit] Types
The following table summarizes some major characteristics of different types of aphasia: Types of aphasia Auditory comprehension Presentation

Repetition

Naming

Fluency

Wernicke's aphasia mildmod mildsevere 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. Transcortical sensory aphasia good modsevere poor fluent Similar deficits as in Wernicke's aphasia, but repetition ability remains intact. Conduction aphasia

poor poor relatively good fluent Conduction aphasia is caused by deficits in the connections between the speechcomprehension and speech-production areas. This might be 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. Repetition ability is poor. Nominal or Anomic aphasia mild modsevere 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 non-fluent, effortful, modsevere modsevere mild difficulty 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" 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 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 can be paralysis of the patient's right face and arm. Transcortical motor aphasia good mildsevere 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 can be paralysis of the patient's right face and arm. 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 can be paralysis of the patient's right face and arm. 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. 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 se

[edit] Acquired childhood aphasia


Acquired childhood aphasia (ACA) is a language impairment resulting from some kind of brain damage. This brain damage can have different causes, such as head trauma, tumors, cerebrovascular accidents, or seizure disorders. Most, but not all authors state that ACA is preceded by a period of normal language development.[2] Age of onset is usually defined as from infancy until but not including adolescence. ACA should be distinguished from developmental aphasia or developmental dysphasia, which is a primary delay or failure in language acquisition.[3] An important difference between ACA and developmental childhood aphasia is that in the latter there is no apparent neurological basis for the language deficit.[4] ACA is one of the more rare language problems in children and is notable because of its contribution to theories on language and the brain.[3] Because there are so few children with ACA, not much is known about what types of linguistic problems these children have. However, many authors report a marked decrease in the use of all expressive language. Children can just stop talking for a period of weeks or even years, and when they start to talk again, they need a lot of encouragement. Problems with language comprehension are less common in ACA, and don't last as long.[5]

[edit] Classification
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. [6]

[edit] Localizationist model

Cortex 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". The most prominent writers on this topic have been Harold 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 dissect 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 localizationist model are: Pure word deafness Conduction aphasia Apraxia of speech, which is now considered a separate disorder in itself. Transcortical motor aphasia Transcortical sensory aphasia

1. 2. 3. 4. 5.

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 perisylvian region of the brain.

[edit] Other ways to Classify Aphasia [edit] Fluent, non-fluent and "pure" aphasias
The different types of aphasia can be divided into three categories: fluent, non-fluent and "pure" aphasias.[7]

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 Nonfluent aphasias, also called expressive aphasias are difficulties in articulating, but in most cases there is relatively good auditory verbal comprehension. Examples of nonfluent aphasias are: Broca's aphasia, Transcortical motor aphasia, Global 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

[edit] Primary and secondary aphasia


Aphasia can be divided into primary and secondary aphasia.[8]

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.

[edit] 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.

[edit] 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.[9]

[edit] Famous sufferers


Maurice Ravel Vissarion Shebalin Jan Berry of Jan and Dean Sven Nykvist Ralph Waldo Emerson[10] Joseph Chaikin Antony Flew Bob Woodruff Kevin Ryder of The Kevin and Bean Show Toggle (Doonesbury character), Iraq war veteran injured by IED

[edit] Treatment
There is no one treatment proven to be effective for all types of aphasias. Melodic intonation therapy is often used to treat non-fluent aphasia and has proved to be very effective in some cases. http://en.wikipedia.org/wiki/Aphasia

Speech disorder
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Jump to: navigation, search This article needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (February 2008)

Speech disorders or speech impediments are a type of communication disorders where 'normal' speech is disrupted. This can mean stuttering, lisps, etc. Someone who is totally unable to speak due to a speech disorder is considered mute.

[edit] Classification
Classifying speech into normal and disordered is more problematic than it first seems. By a strict classification, only 5% to 10% of the population has a completely normal manner of speaking (with respect to all parameters) and healthy voice; all others suffer from one disorder or another.

Stuttering is quite common.[citation needed] Cluttering, a speech disorder that has similarities to stuttering. Dysprosody is the rarest neurological speech disorder. It is characterized by alterations in intensity, in the timing of utterance segments, and in rhythm, cadency, and intonation of words. The changes to the duration, the fundamental frequency, and the intensity of tonic and atonic syllables of the sentences spoken, deprive an individual's particular speech of its characteristics. The cause of dysprosody is usually associated with neurological pathologies such as brain vascular accidents, cranioencephalic traumatisms, and brain tumors.[1] Speech sound disorders involve difficulty in producing specific speech sounds (most often certain consonant, such as /s/ or /r/), and are subdivided into articulation disorders (also called phonetic disorders) and phonemic disorders. Articulation disorders are characterized by difficulty learning to physically produce sounds. Phonemic disorders are characterized by difficulty in learning the sound distinctions of a language, so that one sound may be used in place of many. However, it is not uncommon for a single person to have a mixed speech sound disorder with both phonemic and phonetic components. Voice disorders are impairments, often physical, that involve the function of the larynx or vocal resonance. Dysarthria is a weakness or paralysis of speech muscles caused by damage to the nerves and/or brain. Dysarthria is often caused by strokes, parkinsons disease, ALS, head or neck injuries, surgical accident, or cerebral palsy. Apraxia of speech may result from stroke or be developmental, and involves inconsistent production speech sounds and rearranging of sounds in a word ("potato" may become "topato" and next "totapo"). Production of words becomes more difficult with effort, but common phrases may sometimes be spoken spontaneously without effort. It is now considered unlikely the childhood apraxia of speech and acquired apraxia of speech are the same thing, though they share many characteristics.

There are three different levels of classification when determining the magnitude and type of a speech disorder and the proper treatment or therapy:[2]

1. Sounds the patient can produce 1. A: Phonemic- can be produced easily; used meaningfully and contrastively 2. B: Phonetic- produced only upon request; not used consistently, meaningfully, or contrastively; not used in connected speech 2. Stimulable sounds 1. A: Easily stimulable 2. B: Stimulable after demonstration and probing (i.e. with a tongue depressor) 3. Cannot produce the sound 1. A: Cannot be produced voluntarily 2. B: No production ever observed

[edit] Causes
In many cases the cause is unknown. However, there are various known causes of speech impediments, such as "hearing loss, neurological disorders, brain injury, mental retardation, drug abuse, physical impairments such as Cleft lip and palate, and vocal abuse or misuse."[3] Child abuse may also be a cause in some cases.[4]

[edit] Treatment
The examples and perspective in this article may not represent a worldwide view of the subject. Please improve this article and discuss the issue on the talk page. (December 2009) Many of these types of disorders can be treated by speech therapy, but others require medical attention by a doctor in phoniatrics. Other treatments include correction of organic conditions and psychotherapy[5]. In the United States, school-age children with a speech disorder are often placed in special education programs. More than 700,000 of the students served in the public schools special education programs in the 2000-2001 school year were categorized as having a speech or language impediment. This estimate does not include children who have speech/language problems secondary to other conditions such as deafness"[3].Many school districts provide the students with speech therapy during school hours, although extended day and summer services may be appropriate under certain circumstances. Patients will be treated in teams, depending on the type of disorder they have. A team can include; SLP's, specialists, family doctors, teachers,and parents/family members.

[edit] Social effects of speech disorders


Suffering from a speech disorder can have negative social effects, especially among young children. Those with a speech disorder can be targets of bullying because of their

disorder. The bullying can result in decreased self-esteem. Later in life, bullying is experienced less by a general population, as people become more understanding as they age.

[edit] Language disorders


Language disorders are usually considered distinct from speech disorders, even though they are often used synonymously. Speech disorders refer to problems in producing the sounds of speech or with the quality of voice, where language disorders are usually an impairment of either understanding words or being able to use words and does not have to do with speech production[6] http://en.wikipedia.org/wiki/Speech_disorder

Dysnomia (disorder)
From Wikipedia, the free encyclopedia
Jump to: navigation, search For other uses, see Dysnomia. Dysnomia is a difficulty or inability to retrieve the correct word from memory when it is needed. Dysnomia can affect speech skills, writing abilities, or both. Normal individuals will occasionally suffer problems recalling words. This only becomes a medical condition when the recall problems interfere with daily life. Doctors use neuropsychological tests to diagnose the condition.[1] Dysnomia can develop because of brain trauma or can be a learning disability. Dysnomia from strokes or head injuries will frequently reduce or disappear with time. The learning disability, however, cannot be cured. Patients can improve their life skills by using coping strategies.

[edit] Overview
Word-recall problems become a medical condition when severe enough to interfere with a patient's daily life. Neuropsychological tests of dysnomic individuals show a significant difficulty recalling words or names. [2] As a long-term condition, dysnomia can be:

An inherited learning disability [3] A symptom of dementia, including Alzheimer's [4] A result of brain trauma, including accidents or stroke [5] A side-effect of certain drugs [6] A result of aging

Dysnomia can also describe a short-term problem in recalling words or names. In this case it is used as a symptom, not as a condition. Dysnomia can be a symptom of alcohol intoxication, low blood sugar, concussion, fluid/electrolyte imbalance, nutritional deficiencies, hyperthermia, hypothermia, hypoxemia, and other conditions and illnesses.

[edit] Symptoms
Dysnomia impairs an individual's ability to succeed in speech and writing tasks.

People who have dysnomia may replace a word with a synonym in an attempt to express their thoughts without using the word they are having difficulty retrieving [7] Dysnomics will take longer to complete tests or leave timed tests incomplete. Dysnomics may pause or appear to struggle when trying to recall words or names

[edit] Dysnomia vs. anomia


The difference between dysnomia and anomia is the level of function. This is indicated by the nature of the names, dys-nomia vs. a-nomia. Anomia, "renders a person completely unable to name familiar objects, almost as if he or she were suddenly required to converse in a foreign language". Dysnomia, on the other hand, is a lesser level of dysfunction, a severe form of the "tip-of-the-tongue" feeling where the brain cannot recall the desired word or name. [8] [9] Despite the difference, some sources interchange the terms. A review of available literature shows:

The two diagnoses have similar, but separate references in diagnostic codes Anomia is cited more frequently/studied more frequently, possibly because anomic patients are more likely to be hospitalized or institutionalized Dysnomia appears more common in reference to a learning disability In cases where the two terms are used in the same materials, dysnomia is sometimes mentioned as the primary [10], other references place anomia first [11], and other references list both and treat them as synonyms [12].

Despite the separate diagnostic codes, a search of online materials failed to reveal clear clinical criteria for when dysnomia shifts to anomia.

[edit] Dysnomia and expressive aphasia

Dysnomia is a type of expressive aphasia [13] [14]

[edit] Relationship to dyslexia


Some models of dyslexia identify it as being caused by dysnomia. This model "proposes that the deficit in verbal label retrieval creates a short-term memory deficit resulting in difficulty recalling word labels in reading." [15]

[edit] Testing methods


Doctors use neuropsychological tests to diagnose dysnomia and anomia. The tests can measure the condition's severity and identify/eliminate other neuropsychological conditions with similar symptoms. [16] Rapid Automatized Naming is a good example of these tests. Rapid Automatized Naming times how quickly the patient can name common objects or colors. A typical test would have the patient rapidly name five pictures of common objects or colors appearing repeatedly on a computer screen. The doctor compares the completion time against average times for the patient's age group. [17]

[edit] Treatment
Doctors recommend different treatments based on the cause of the dysnomia. Dysnomia caused by a brain trauma, including injury or stroke, is frequently treated by a speech pathologist using exercises to improve recall. (Examples: [18]) For brain trauma cases, doctors recommend that, "language therapy should begin as soon as possible and be tailored to the individual needs of the patient." [19] Treatment is more difficult when dysnomia is caused by developmental issues. Since the area of the brain dealing with word recall has not fully developed, there is currently no way to cause the development or speed its process. In children with dysnomia, the condition may lessen or disappear as the child grows. If a medication is causing dysnomia as a side effect, the prescribing doctor can offer alternatives. A published case study reported that antidepressants helped a dysnomic patient. [20] http://en.wikipedia.org/wiki/Dysnomia_%28disorder%29

Dysprosody

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Jump to: navigation, search Dysprosody is the rarest neurological speech disorder known. Prosody refers to the variations in melody, intonation, pauses, stresses, intensity, vocal quality and accents of speech.[1] As a result, prosody has a wide array of functions including expression on linguistic, attitudinal, pragmatic, affective and personal levels of speech.[2] Dysprosody, which is also known as pseudo-foreign dialect syndrome, refers to a disorder in which one or more of these prosodic functions are either compromised or eliminated completely.[3] People diagnosed with dysprosody most commonly experience difficulties in pitch or timing control.[2] Essentially, a person diagnosed with the disease can comprehend language and vocalize what he intends to say, however, he is not able to control the way in which the words come out of his mouth. Since dysprosody is the rarest neurological speech disorder discovered, not much is conclusively known or understood about the disorder. The most obvious expression of dysprosody is when a person starts speaking in an accent which is not their own. It is important to note, however, that speaking in a foreign accent is only one type of dysprosody, as the disease can also manifest itself in other ways, such as changes in pitch, volume, and rhythm of speech. It is still very unclear as to how damage to the brain causes the disruption of prosodic function. The only form of effective treatment developed for dysprosody is speech therapy.

[edit] History
The first documented occurrence of dysprosody was described by Pierre Marie, a French neurologist, in 1907. Marie described the case of a Frenchman who started speaking in an Alsatian accent after suffering from a cerebrovascular accident which caused right hemiplegia.[4] The next documented report of dysprosody occurred in 1919 by Arnold Pick, a German neurologist. He noticed a 29 year old Czechoslovakian had started speaking in a Polish accent following a stroke. Pick's patient also suffered from right hemiparesis, a lesser version of hemiplagia, and aphasia after the stroke. Pick noticed that not only was the accent altered, but the timing of the speech was slower, and the patient spoke with uncharacteristic grammatical mistakes. Pick later wanted to follow up on his research but was not able to since the patient had died with no autopsy performed.[5] The most well documented account of dysprosody was in 1943 by G. H. Monrad-Krohn. A woman, Astrid L., in Norway was hit with a shell fragment during an air raid in 1941 through her left frontal bone, leaving her brain exposed.[5] She was unconscious for four days and when she regained consciousness at the hospital, she was hemiplegic on her right side, was suffering from seizures, and was aphasic.[5] Initially she could only speak in monosyllables, yes and no, but then started to form sentences. When first starting to speak again, she also spoke with uncharacteristic grammatical errors, but over time they became much less pronounced and eventually she gained back full fluency of speech.

However, she sounded as though she was speaking her native Norwegian with a German accent. It was two years later that she was admitted to the Neurological University Clinic in Olso, Norway and seen by Dr. Monrad-Krohn. Krohn examined the patient and noted that there was no noticeable difference in her fluency, motor functions, sensory functions, or coordination. Upon examination of her skull, he found a large scar on the left frontotemporo-parietal region.[5] This was not as helpful as Krohn would have liked. Since the scar was so extensive, it was impossible for Krohn to pinpoint the exact region of the brain which was causing this altered speech. Krohn then ran tests on Astrid to assess her language comprehension. He found that in addition to her altered speech patterns, she had trouble finding the Norwegian words for trivial objects, such as light switch and match box. She also had to repeat the examiner's questions aloud before answering, had to say words out loud to herself before writing them down, and had difficulty comprehending written instructions.[5] Krohn could not understand how she had acquired a foreign accent; it could not be attributed to any known disorder or disease. For those who suffer from this type of dysprosody, it is interesting to note that sometimes the accents they speak are from countries to which the person has never been. This fact is very puzzling for neuroscientists since dialects and accents are considered to be an acquired behavior of learning pitches, intonations and stress patterns.[4] There have been another 21 cases documented up until 1978. Thirteen of those cases were documented at the Mayo Clinic while the others were documented at clinics and hospitals elsewhere.[4] There have been more recent occurrences of people who have developed accents after brain injuries, specifically strokes. In 1999, Judi Roberts suffered a stroke which paralyzed the right side of her body, leaving her unable to speak. Over time, her speech began to improve, eventually recovering full fluency, but she developed a British accent despite living in the US for all of her life.[6] In 2006, another report was documented of Linda Walker, a native of England, who developed a foreign accent after suffering from a stroke.[7]

[edit] Causes
Dysprosody is usually attributed to neurological damage, such as brain tumors, brain trauma, brain vascular damage, stroke and severe head injury. To better understand the causes of the disease, 25 cases of dysprosody diagnosed between 1907-1978 were examined more closely. It was found that the majority developed dysprosody after a cerebrovascular accident while another 6 cases developed after a head trauma. In that same study, 16 of the patients were female while 9 were male. However, there has been no conclusive evidence that gender affects the onset of dysprosody. There has been no evidence that ethnicity, age, or genetics has any impact on the development of dysprosody.[4] In another reported case in 2004, a patient presented with dysprosody under interesting circumstances. The patient underwent surgery to correct a Reinke's edema, which originates in the vocal folds of the larynx. After the surgery, however, she began

speaking in a foreign German accent. Neurological examinations were carried out on the patient through magnetic resonance imaging, but the results were completely normal. The only conclusion the doctors could make was that the surgery somehow changed the patient's vocal identification causing the new voice pattern. It was possible that the patient suffered a lack of oxygen to the brain during the surgery, which would have gone undetected by the resonance imaging, causing dysprosody.[8] Although most causes of dysprosody are due to neurological damage, this case study shows that there can be other causes which are not necessarily neurologically based.

[edit] Symptoms
Dysprosody is "characterized by alterations in intensity, in the timing of utterance segments, and in rhythm, cadency, and intonation of words."[8] These differences cause a person to lose the characteristics of their particular individual speech. While the individual's personality, sensory comprehension, motor skills, and intelligence all remain intact, their grammar as well as vocal emotional capacity can be affected. Prosodic control is essential to speech delivery because it establishes vocal identity since each individuals voice has unique characteristics. There are two types of dysprosody, linguistic and emotional, that each present with slightly different symptoms. It is possible that one can present with both forms of dysprosody.

[edit] Linguistic Dysprosody


Dysprosody works on a linguistic level in that it specifies the intent of ones speech. For example, prosody is responsible for verbal variations in interrogative versus declarative statements and serious versus sarcastic remarks. Linguistic dysprosody, in effect, alters an individuals vocal identity and impairs verbal communication.

[edit] Emotional Dysprosody


Emotional dysprosody deals with a person's ability to express emotions through their speech as well as their ability to understand emotion in someone else's speech. Whenever we speak, whether we realize it or not, there are nonverbal aspects of our speech that reveal information about our feelings and attitude. There has been strong evidence that dysprosody does affect the ability to express emotion, however the severity may vary depending on what part of the brain has been damaged. Studies have shown that the ability to express emotional information is dependent on motor, perceptual, and neurobehavioral functions all working together in a specific way.[9] A person suffering from dysprosody would not be able to accurately convey emotion vocally, such as through pitch or melody, or make any conclusion about another person's feeling through his speech.[10] Regardless of the inability to vocally express feeling through prosodic controls, emotions are still formed and felt by the individual. Since there are many different factors which contribute to emotional understanding of speech, it makes it much more complicated to understand.[10]

[edit] Related Symptoms


After experiencing brain injury, some people may begin speaking in an accent not native to their country of origin, as discussed in the preceding sections, but more common forms of dysprosody consist of alterations in vocal pitch, timing, rhythm, and control, not necessarily resulting in a foreign dialect.[5][11] In addition, there have been some cases in which seizures began to develop in patients also suffering from dysprosody,[4] but no decisive conclusions connecting dysprosody and seizure activity have been made. Dysprosody can last for differing durations, from a few months to years, although the reason seems to be unclear. There are several different types of dysprosody which have been classified. The most common types of dysprosody are associated with dysarthria and dyspraxia, which affect motor processing in speech. Among the most studied types are:

Flaccid dysarthria is characterized by for little control over pitch and voice volume, reduced speech rate, and impaired voice quality Hypokinetic dysarthria is characterized by harsh voice quality, monotone, reduced volume and breathiness Ataxic dysarthria is characterized by harsh voice quality, reduced speech rate, and poor volume and pitch control Verbal dyspraxia is characterized by monotone and poor volume control[12]

There can also be some emotional and mental side effects to dysprosody. Each individual has a distinct voice characterized by all the prosodic elements. Once a person loses control of the timing, pitch, melody, etc. of his speech, he can also feel a sense of loss of personal identity, which can sometimes lead to depression.[2]

[edit] Diagnosis
When studies of dysprosody first began, diagnosis involved an untrained ear determining impairments in the prosodic elements. However, over time and as dysprosody has been studied more closely, a more concrete method of diagnosis has been developed. One diagnosis technique is a rating scale, such as the Boston Diagnostic Aphasia Examination. The exam is a subjective rating system of volume (from loud to normal to soft), voice (from normal to whisper to hoarse), speech rate (from fast to normal to slow) and intonation which is rated on a scale from 1-7. One indicates no sentence intonation, four is given when sentence intonation is limited to abrupt pauses, and seven indicates normal intonation. There are also more involved diagnostic evaluations for which contain both productive and comprehensive parts. In the productive part, the patient is asked to say sentences with certain instructions. In the comprehension section, the patient is asked to listen to sentences being said and then answer questions about how they were stated. In order to determine linguistic dysprosody, a patient is asked to read sentences that can either be a statement or a question using both declarative and interrogative intonations. How the

patient uses prosodic contours to distinguish between asking a question and saying a statement is recorded. During the comprehension section of the evaluation, a clinician reads simple sentences with either a declarative or interrogative intonation and the patient is asked to identify whether the sentence is a question or a statement. Evaluation of these two parts can determine if the patient has linguistic dysprosody. Emotional dysprosody can be diagnosed by having a patient state a neutral sentence with different emotions, such as happy, sad, and angry. Patients with dysprosody will not be able to convey the emotions very well or differentiate their speech between the different emotions significantly. During the comprehension part, a clinician will say a sentence with specific emotional intonations and the patient must indicate the correct emotion.[10] These techniques ultimately allow for the diagnosis of dysprosody and the degree of its severity in the patient.

[edit] Dysprosody in the Brain


Since the discovery of dysprosody, scientists have been attempting to declare a particular area of the brain responsible for prosodic control. It was long believed that the right hemisphere of the brain was responsible for prosodic organization, ultimately leading to a grossly oversimplified hemispheric model.[13] This model argued that the organization of language, centered in the left hemisphere, parallels the organization of prosody in the right hemisphere.[3] Since its release, however, very few studies have given the model any substantial support. Scientists have attributed major control of the temporal aspects of prosody, including rhythm and timing, to the left hemisphere of the brain. On the other hand, pitch perception, such as singing and linguistics related to emotion, are believed to be organized in the right hemisphere. This belief led to the development of the Functional Lateralization hypothesis, stating that dysprosody can be caused by lesions in either the right or left hemispheres.[2] It further states that the left is responsible for acoustic and temporal aspects of prosody while the right is responsible for pitch and emotion.[2] This hypothesis, however, has also been a cause for concern as studies have shown that people with left hemispheric damage exhibit prosodic deficiencies associated with the right hemisphere as defined by the Functional Lateralization hypothesis and vice versa.[2] In addition, it has also been found that damage to the medulla, cerebellum, and basal ganglia may cause dysprosody.[2] These conclusions have led scientists to believe that prosodic organization in the brain is extremely complex and cannot be attributed to hemispheric divisions alone. Although not well understood as of yet, studies to identify prosodic organization in the brain continue, primarily through the examination of damaged brain areas in patients suffering from dysprosody and their resulting vocal deficiencies. In addition, dysprosody has been associated with several other diseases including Parkinson's Disease, Huntington's Disease, gelastic epilepsy (gelastic seizure), and behavioral disorders such as apathy, akinesia and aboulia. Understanding these disorders and the areas of the brain affected in each case is key in conducting further studies of dysprosody. Scientists are continuing to study these patients in the hope of creating more concrete connections between areas of brain damage and prosodic abnormalities, which

will hopefully someday lead to a full understanding of prosodic organization in the brain.
[14]

[edit] Parkinson's Disease and Dysprosody


Parkinson's disease, or sometimes referred to as PD, is a chronic neurodegenerative disorder that involves the loss of dopaminergic neurons in the brain. While common symptoms of PD are tremors, rigidity, bradykinesia, and postural instability, dysprosody is also a common issue in individuals diagnosed with PD.[15] A common characteristic feature of dysprosody in Parkinson's is monopitch, or an inability to vary pitch when speaking.[15] Several studies have been performed investigating the link between Parkinson's and dysprosody. They have concluded that PD patients tend to struggle with specific areas of prosody; Parkinson's patients are less able to produce the loudness, pitch, and rhythm patterns required for expressing certain emotions, such as anger.[16] In general, the voice modulations needed to express strong emotions are particularly difficult for PD patients. Because they generally have normal abilities to appreciate vocal or visual emotion presented to them, this inability to vocally express emotion has been linked to dysprosody and not the actual processing of emotions.[16] Abnormal pauses in speech are also a characteristic of Parkinsonian dysprosody, including both pauses in general speech and intra-word pauses. A decrease in speech rate can also be observed in Parkinson's patients.
[15]

Studies have also shown a progression of dysprosody in patients with PD over time. Abnormalities in speech rate, pauses, and variation range in speech become worse as the disease progresses.[15] It is important to note the degradation of prosody in PD over time is independent of motor control issues, and is thus separate from those aspects of the disease.[15] Studies have shown that normal treatment for PD can help with the dysprosody symptoms, however there is usually an improvement in pitch control only and not in the volume and emotional aspects of the disease. These treatments include medications such as L-DOPA as well as electrophysiological treatments.[17]

[edit] Treatments
The most effective course of treatment for dysprosody has been speech therapy. The first step in therapy is practice drills which consist of repeating phrases using different prosodic contours, such as pitch, timing, and intonation. Typically a clinician will say either syllables, words, phrases, or nonsensical sentences with certain prosodic contours, and the patient repeats them with the same prosodic contours. Once a patient is able to effectively complete this drill, they can start with more advanced forms of speech therapy. Upon completion of therapy, most people can identify prosodic cues in natural situations, such as normal conversation. Speech therapy has proven most effective for linguistic dysprosody because therapy for emotional dysprosody requires much more

effort and is not always successful. One way that people learn to cope with emotional dysprosody is to explicitly state their emotions, rather than relying on prosodic cues.[10] Over time, there have also been cases of people suffering from dysprosody gaining their native accent back with no course of treatment.[2] Since the part of the brain responsible for dysprosody has not definitely been discovered, nor has the mechanism for the brain processes which cause dysprosody been found, there has not been much treatment for the disease by means of medication.

[edit] Future Research


In the past decade research on dysprosody has begun to focus on its relationship to other, more common diseases such as Parkinson's disease. Scientists believe that studying the connections between dysprosody and these better understood conditions may help them pinpoint specific areas of the brain responsible for prosody.[2]

[edit] Conclusion
Dysprosody is an impairment in the prosodic elements such as rhythm, timing, melody, stress, pitch and intonation. It primarily results from neurological damage that can be caused by tumors, stroke, or severe head injury. There have been several hypotheses proposed discussing the area of the brain responsible for prosodic control, but since prosodic elements are so diverse, its organization in the brain is still unclear. There are different types of dysprosody including linguistic and emotional, which present different symptoms. The only course of treatment proven to be effective is speech therapy, although normal speech may naturally resume. Currently, there has been more research regarding dysprosody's link to other diseases, in particular Parkinson's disease, but also Huntington's disease, and gelastic epilepsy to name a few. http://en.wikipedia.org/wiki/Dysprosody

Aprosodia
From Wikipedia, the free encyclopedia
Jump to: navigation, search An Aprosodia is a neurological disease characterized by the inability of a person to properly convey and/or interpret emotional prosody. Prosody in language refers to the ranges of rhythm, pitch, stress, intonation, etc. These neurological deficits are the result of damage of some form to the non-dominant hemisphere areas of language production. The prevalence of aprosodias in individuals is currently unknown, as testing for aprosodia secondary to other brain injury is only a recent occurrence. However, this does

not alter the impact that aprosodia is able to have on the lives of those who have the condition, whether or not they are diagnosed with it. Through awareness, progress can be made in both the recognition and treatment of aprosodic individuals.

[edit] Causes
[edit] Localized Brain Damage
One cause of aprosodia is suffering brain trauma to one of several specific areas of the brain, resulting in the inability to properly process or convey emotional cues. This brain damage can occur in the form of ischemic damage from stroke[1], removal during surgery, brain lesions, or trauma such as a localized bullet wound. It is worth noting however, that this localization occurs over a range of areas that can vary from person to person and more research is required to further define these areas. Diagnostic confirmation of aprosodia using brain scanning techniques is a relatively recent occurrence, at least with respect to quantitative specificity.[2] As brain imaging techniques are refined to allow for greater temporal and spatial resolution, it is hoped that more will be able to be learned about aprosodias at a functional anatomical level.

[edit] Alcohol Abuse


An inability to process or exhibit emotions in a proper manner has been shown to exist in alcoholics and those who were exposed to alcohol while fetuses (FAexp). Initially, when detoxified alcoholics and FAexp individuals were tested for impairment in cognitive function, it was limited to testing the non-affective aspects of language, as those were the more easily recognized by a physician not trained in analyzing affective prosody. When tested using the aprosodia battery, it was found that detoxified alcoholics and FAexp individuals demonstrated significant impairment in their ability to detect affective prosody when used by others. The major factors which influence affective prosody in those impacted by alcohol use, from greatest to least impact, are: alcohol use by mother, age at onset of chronic abuse of alcohol, age at initial abuse, how chronic the abuse is, and the age when a person first becomes drunk.[3]

[edit] Aprosodia as a Symptom


Aprosodia has also been shown to appear secondary to several diseases such as multiple sclerosis or post traumatic stress disorder[4].It is likely that as time passes more diseases will be shown to exhibit aprosodia as a symptom. Aprosodia is a condition that was not often tested for in the presence of neurological deficits; however, as more becomes known about it, the aprosodia battery will likely be administered more frequently. For example, the first study testing for aprosodia in MS did not occur until 2009.[5] This is surprising given that changes in emotional affect would be expected to be noticed in patients exhibiting other changes in speech patterns. This is especially so given that the patients tested in these studies scored poorer than the controls by a statistically significant amount.

[edit] Brain Regions


Research into the perisylvan region of the right hemisphere has shown that there are similarly mapped analogues to the speech center in the left hemisphere. This is especially evident in those areas resembling Broca's area and Wernicke's area.[6]. The similarity of these regions has led scientists to view aprosodias in a similar manner to how some aphasias are viewed. Because the presence of an aphasia is often more pronounced in an individual than an aprosodia might be, apahsias have traditionally been more heavily studied. Because aphasias are rooted in deficiencies in language modalities rather than affective aspects of language, it has been easier to characterize the underlying impairment caused by brain damage (e.g. inability to choose the right word or inability to speak due to motor control). Combining aphasic research with right-left analogue mapping has allowed for researchers to produce hypotheses on the underlying process behind various aprosodias. Additionally, in studying the brain regions associated with aprosodia, brain imaging tests were performed to determine if aprosodia is both a lateralized and dominant function of the right hemisphere areas of language production. Aprosodia can be considered a dominant function of the right hemisphere because strong correlation was found between deficits in affective prosody and distribution of lesions in the cortices of those with right brain damage. No correlation was found between the distribution of cortical lesions in patients with left brain damage and the types of aphasic deficits pronounced in those patients. Aprosodia can be considered a lateralized function of the right hemisphere because of the differences in the ability of a patient to respond to affective prosodic information in those with left brain damage when compared to those with right brain damage. Patients with affective-prosodic deficits in the left hemisphere (dysprosodic patients) showed improvement in understanding and repeating prosodic information when other conveyed linguistic information was simplified, i.e. requiring the patient to mainly determine prosodic information contained in an interaction. This improvement in processing affective prosodic information under reduced linguistic processing demands did not occur for patients with right brain damage.[7]

[edit] Types
[edit] Motor
A motor aprosodia is characterized by the inability of a patient to produce or imitate emotional indicators, mainly through prosody or facial gestures. Those exhibiting only a motor aprosodia are still able to understand affective prosody when spoken by another, but are unable to respond in the same manner. This is believed to occur due to problems at the execution level of affective prosody. A patient may have an understanding of what emotion they wish to produce, but damage to the motor areas of the brain causes an impairment in the uttering of affective prosody.[7]

[edit] Sensory

Sensory aprosodia, also referred to as receptive aprosodia, is characterized by the inability of a patient to comprehend or repeat emotional gestures. A patient with receptive aprosodia also has difficulty identifying emotions presented. In extreme cases of sensory aprosodia, a patient may have difficulty discerning the changes in stress and intonation.[8]

[edit] Mixed
Mixed aprosodia is characterized by combinations of the other forms of aprosodia. It is often likely that an aprosodic individual will exhibit mixed aprosodia with varying degrees of intensity among the different aprosodias.

[edit] Expressive
Expressive aprosodia occurs when a patient is unable to properly produce the intended emotional cues to those around them, owing more from an inability to produce them at the cognitive than motor level.[2] It is believed that expressive aprosodia results from a lack of an emotional dictionary, much in the same way that patients with dominant hemisphere damage in the same area have a diminished ability to choose the right word.

[edit] Diagnosis
[edit] Emotional Batteries
Emotional Batteries consist of asking patients to read various sentences with specific emotional indicators. Their performance is subjectively analyzed by an expert to determine if they are aprosodic. The analysis is often performed by two experts independently, with one of the judges not being present during the interview in case the patient was still able to use facial cues.[9]

[edit] Assessment Questionnaire


Another method implemented to test for aprosodia involves having questionnaires filled out by those close to the patient. The doctors and nurses taking care of a patient are also requested to fill out a questionnaire if aprosodia is suspected. This diagnosis method occurs more as an indicator that the aprosodia battery should be administered rather than being used as a singular diagnosis tool. Implementation of the questionnaire is expected to become more widespread as aprosodia is revealed to be a side-effect of more diseases.
[9]

[edit] Aprosodia vs. Dysprosody


Brain imaging studies related to speech functions have yielded insights into the subtle difference between aprosodia and dysprosody. The major differences in these result from functions which are characterized as belonging mainly to the left or right hemisphere. Several of the functions have been described as dominant and lateralized functions of the

corresponding hemispheres, while some have been found to arise from communication between the two hemispheres.[7] While the ability to express or be receptive to affective prosody is similar in dysprosody and aprosodia, a significant difference in the characterization of them is dominant vs. non-dominant hemispherical damage.

[edit] Impact
The loss of ability to express and understand emotions is debilitating to those experiencing aprosodia. It has a large impact on their lives and affects their day-to-day interactions with others. While it is often overlooked, affective prosody is as integral to communication as the ability to form and understand correct words. Patients exhibiting extreme cases of aprosodia speak in a monotone fashion and are barely able or unable to distinguish changes in stress or intonation.

[edit] Treatment
Due to the rarity of reported aprosodia cases, only a few labs are currently researching treatment methods of aprosodia. The largest study of treatments for aprosodia consisted of only fourteen individuals, resulting in sample sizes too small to report statistical significance when comparing one treatment to another. However, the data gained from this study still yielded some results and is being used in the next iteration of aprosodia research.

[edit] Methods
The two main forms of treatment are cognition based and imitation based. Cognitive treatments attempt to rebuild the "emotional toolbox" of those with aprosodia. The basis for this treatment is the belief that there exists a defined set of emotional responses that can be chosen for a given scenario. Choosing the proper emotional response can very much be likened to choosing the proper word when describing an object, and this deficiency can be likened to Broca's Aphasia but for emotions. Imitative treatments attempt to help "kickstart" the motor systems involved in the production of both vocal and facial emotive gestures. The basis for this treatment is the belief that the pathways responsible for the motor elements of expressive prosody were damaged. It is hypothesized that the motor damage occurs at the level of planning as well as the level of execution.[10]

[edit] Progress
The methods of treatment are being evaluated and changed through several iterations to reach the most beneficial treatment for those with aprosodia. Although the biggest limitation on progress of aprosodia treatment is sample size, some significant data has been found to influence each subsequent phase of study. The Rosenbek lab at the University of Florida is currently in a new phase of treatment study based on combinations of the cognitive-linguistic and imitative therapies delivered in a randomized

fashion in an effort to gain more insight into what most prominently affects aprosodia treatment.[9] http://en.wikipedia.org/wiki/Aprosodia

Expressive aphasia
From Wikipedia, the free encyclopedia
Jump to: navigation, search Expressive aphasia, known as Broca's aphasia in clinical neuropsychology and agrammatic aphasia in cognitive neuropsychology, is caused by damage to or developmental issues in anterior regions of the brain, including (but not limited to) the left posterior inferior frontal gyrus known as Broca's area (Brodmann area 44 and Brodmann area 45).[1] Expressive aphasia is one subset of a larger family of disorders known collectively as aphasia. It is characterized by the loss of the ability to produce language (spoken or written).[1] Expressive aphasia differs from dysarthria, which is characterized by a patient's inability to properly move the muscles of the tongue and mouth to produce speech. Expressive aphasia contrasts with receptive aphasia, which is characterized by a patient's inability to comprehend language or speak with appropriately meaningful words[1].

[edit] Presentation
Sufferers of this form of aphasia exhibit the common problem of agrammatism. For them, speech is difficult to initiate, non-fluent, labored, and halting. Similarly, writing is difficult as well. Intonation and stress patterns are deficient. Language is reduced to disjointed words and sentence construction is poor, omitting function words and inflections (bound morphemes). A person with expressive aphasia might say "Son ... University ... Smart ... Boy ... Good ... Good ... " For example, in the following passage, a Broca's aphasic patient is trying to explain how he came to the hospital for dental surgery: Yes... ah... Monday... er... Dad and Peter H... (his own name), and Dad.... er... hospital... and ah... Wednesday... Wednesday, nine o'clock... and oh... Thursday... ten o'clock, ah doctors... two... an' doctors... and er... teeth... yah.[2] Severity of expressive aphasia varies among patients. In the most extreme cases, patients may be only able to produce a single word. The most famous case of this was Paul Broca's patient Leborgne, nicknamed "Tan", after the only syllable he could say. Even in such cases, over-learned and rote-learned speech patterns may be retained[3]for

instance, some patients can count from one to ten, but cannot produce the same numbers in ordinary conversation. While word comprehension is generally preserved, meaning interpretation dependent on syntax and phrase structure is substantially impaired. This can be demonstrated by using phrases with unusual structures. A typical Broca's aphasic patient will misinterpret "the dog is bitten by the man" by switching the subject and object.[4] Note this element is a problem with receptive language, not expressive language, and is one reason why the problem is referred to as agrammatic aphasia. Patients who recover go on to say that they knew what they wanted to say but could not express themselves. Residual deficits will often be seen.

[edit] Classification and Diagnosis


Expressive aphasia is also a classification of non-fluent aphasia, as opposed to fluent aphasia. Diagnosis is done on a case by case basis, as lesions often affect surrounding cortex and deficits are not well conserved between patients.

[edit] Causes
The most common cause of expressive aphasia is stroke. A stroke is caused by hypoperfusion (lack of oxygen) to an area of the brain, which is commonly caused by thrombosis or embolism. Some form of aphasia occurs in 34-38% of stroke patients.[5] Expressive aphasia occurs in approximately 12% of new cases of aphasia caused by stroke.[6] In most cases, expressive aphasia is caused by a stroke in Broca's area or the surrounding vicinity. However, cases of expressive aphasia have been seen in patients with strokes in other areas of the brain. Patients with classic symptoms of expressive aphasia generally have more acute brain lesions while patients with larger, widespread lesions exhibit a variety symptoms which may be classified as global aphasia or left unclassified.[5] Expressive aphasia can also be caused by trauma to the brain, tumor, cerebral hemorrhage[7], by extradural hematoma.[8] Understanding lateralization of brain function is important for understanding what areas of the brain cause expressive aphasia when damaged. In the past, it has been believed that the area for language production differs between left and right-handed individuals. If this were true, damage to the homologous region of Broca's area in the right hemisphere should cause aphasia in a left-handed individual. More recent studies have shown that even left-handed individuals typically have language functions only in the left hemisphere. However, left-handed individuals are more likely to have a dominance of language in the right hemisphere.[1]

[edit] Treatment

Currently, there is no standard treatment for expressive aphasia. Most aphasia therapy is individualized based on a patients condition and needs as assessed by a speech therapist. The majority of patients go through a period of spontaneous recovery following brain injury in which they regain a great deal of language function. In the months following injury or stroke, most patients receive traditional therapy for a few hours per day. Among other exercises, patients practice the repetition of words and phrases. Mechanisms are also taught in traditional therapy to compensate for lost language function such as drawing and using phrases which are easier to pronounce.[9] Emphasis is placed on establishing a basis for communication with family and caregivers in everyday life. The following treatments are currently being studied to determine the best possible method for treating aphasia.

[edit] Singing and Melodic Intonation Therapy


Melodic intonation therapy was inspired by the observation that individuals with nonfluent aphasia sometimes can sing words or phrases that they normally cannot speak. This phenomenon has been noticed for the past 250 years. In some studies patients were able to sing entire songs with provided text that they could not speak with normal intonation. [10] It is believed that this is due to the fact that singing capabilities are stored in the right hemisphere of the brain, which is likely to remain unaffected after a stroke in the left hemisphere.[11] The goal of melodic intonation therapy is to utilize singing to accesses the language-capable regions in the right hemisphere and use these regions to compensate for lost function in the left hemisphere. Because patients are better at singing phrases than speaking them, the natural musical component of speech is used to engage the patients ability to voice phrases. Melodic intonation therapy has been shown to work particularly well in patients with large lesions in the left hemisphere.[11] MIT therapy on average lasts for 1.5 hours per day for five days per week. At the lowest level of therapy, simple words and phrases (such as "water" and "I love you") are broken down into a series of high and low pitch syllables. With increased treatment, longer phrases are taught and less support is provided by the therapist. Patients are taught to say phrases using the natural melodic component of speaking and continuous voicing is emphasized.[11] The patient is also instructed to use their left hand to tap the syllables of the phrase while the phrases are spoken. Tapping further triggers the rhythmic component of speaking to utilize the right hemisphere.[11] The efficacy of melodic intonation therapy has been proven by studies that show that MIT can result in greater recovery when compared to non intonation therapy.[10] FMRI studies have proven that melodic intonation therapy uses both sides of the brain to recover lost function as apposed to traditional therapies that only utilize the left hemisphere. Furthermore, it has been seen that in MIT, individuals with small lesions in the left hemisphere seem to recover by activation of the left hemisphere perilesional cortex while in individuals with larger left-hemisphere lesions, there is a recruitment of the use of language-capable regions in the right hemisphere.[11]

[edit] Constraint Induced Therapy

Constraint induced aphasia therapy (CIAT) is based on the same principles as constraintinduced movement therapy developed by Dr. Edward Taub at the University of Alabama at Birmingham.[9] Constraint induced therapy is based on the idea that a person with an impairment (physical or communicative) develops a "learned nonuse" by compensating for their lost function with other means such as using an unaffected limb by a paralyzed individual or drawing by a patient with aphasia.[12] In constraint induced movement therapy, the alternative limb is constrained with a glove or sling and the patient is forced to use their affected limb. In constraint induced aphasia therapy, the patient is not allowed to use other forms of communication such as drawing or body language and they are constrained to using only spoken word.[9] Two important principles of constraint induced aphasia therapy are that treatment is very intense with sessions lasting for up to 6 hours over the course of 10 days and that it focuses on developing everyday language ability.[9] Constraint induced therapy contrasts sharply with traditional therapy by the strong belief that mechanisms to compensate for lost language function should not be used unless absolutely necessary, even in everyday life.[9] It is believed that CIAT works by the mechanism of increased neuroplasticity. By constraining an individual to use only speech, it is believed that their brain can reestablish old neural pathways and recruit new neural pathways to compensate for lost function.[12] The greatest advantage of CIAT has been seen in its treatment of chronic aphasia (lasting over 1 year). Studies of CIAT have shown that further improvement is possible even after a patient has reached a "plateau" period of recovery.[9] It has also been proven that the benefits of CIAT are retained long term. However, improvements only seem to be made while a patient is undergoing intense therapy.[9]

[edit] Pharmacotherapy
In addition to active speech therapy, pharmaceuticals have also been considered as a useful treatment for expressive aphasia. This area of study is relatively new and much research continues to be conducted. The following drugs have been suggested for use in treating aphasia and their efficacy has been studied in control studies.

Bromocriptine acts on Catecholamine Systems[13] Piracetam acts on the GABA-Minergic system[13] Cholinergic drugs (Donepezil, Aniracetam, Bifemelane) acts on acetylcholine systems[13] Amphetaminic drugs (Dexamphetamine, Methylphenidate, Chlordiazepoxide)[13]

The most effect has been shown by piracetam and amphetamine which may increase cerebral plasticity and result in an increased capability to improve language function. It

has been seen that priacetam is most effective when treatment is began immediately following stroke. When used in chronic cases it has been much less efficient.[14] Bromocriptine has been shown by some studies to increase verbal fluency and word retrieval with therapy than with just therapy alone.[13] Furthermore, its use seems to be restricted to non-fluent aphasia.[14] Donepezil has shown a potential for helping chronic aphasia.[14] No study has established irrefutable evidence that any drug is an effective treatment for aphasia therapy.[13] Furthermore, no study has shown any drug to be specific for language recovery.[14] Comparison between the recovery of language function and other motor function using any drug has shown that improvement is due to a global increase plasticity of neural networks.[13] Pharmaceutical therapy remains an important area of study in aphasia treatment.

[edit] Transcranial magnetic stimulation


In transcranial magnetic stimulation (TMS), magnetic fields are used to create electrical currents in specified cortical regions. The procedure is a painless and noninvasive method of stimulating the cortex. TMS works by suppressing the inhibition process in certain areas of the brain.[15] By suppressing the inhibition of neurons by external factors, the targeted area of the brain may be reactivated and thereby recruited to compensate for lost function. Research has shown that patients can show increased object naming ability with regular transcranial magnetic stimulation than patients in therapy without TMS.[15] Furthermore, this improvement has been proven to be permanent and remains upon the completion of TMS therapy.[15] However, some patients fail to show any significant improvement from TMS which indicates the need for further research of this treatment.[16]

[edit] Mechanisms of recovery


Mechanisms for recovery differ from patient to patient. Some mechanisms for recovery occur spontaneously after damage to the brain while others are caused by the effects of language therapy.[14] FMRI studies have shown that recovery can be partially attributed to the activation of tissue around the damaged area and the recruitment of new neurons in these areas to compensate for the lost function. Recovery may also be caused in very acute lesions by a return of blood flow and function to damaged tissue that has not died around an injured area.[14] It has been stated by some researchers that the recruitment and recovery of neurons in the left hemisphere apposed to the recruitment of similar neurons in the right hemisphere is superior for long term recovery and continued rehabilitation.[17] It is thought that because the right hemisphere is not intended for full language function, using the right hemisphere as a mechanism of recovery is effectively a "dead-end" and can only lead to partial recovery.[16] Among all types of therapies it has been proven that one of the most important factors and best predictors for a successful outcome is the intensity of the therapy. By comparing

the length and intensity of various methods of therapies, it was proven that intensity was a better predictor of recovery than the method of therapy used.[18]

[edit] Prognosis
In most individuals with expressive aphasia, the majority of recovery is seen within the first year following a stroke or injury. The majority of this improvement is seen in the first four weeks in therapy following a stroke and slows thereafter.[5] When compared to patients with the most common types of aphasia, patients with expressive aphasia tend to show the most improvement within the first year. This may be due to an expressive aphasiac's awareness and greater insight of their impairment (unlike in receptive aphasia) which motivates them to progress in treatment.[5] Studies have also found that prognosis of expressive aphasia correlates strongly with the initial severity of impairment. Those with the greatest initial disability tend to show the greatest improvement among test groups.[6] Within the first year, the diagnosis of patients with expressive aphasia may change to anomic aphasia. Similarly, patients diagnosed with global aphasia may be rediagnosed with expressive aphasia upon improvement.[6] Typically, little improvement is seen after the first year following a stroke. However, it has been seen that continued recovery is possible years after a stroke with effective treatment using methods such as constraint induced aphasia therapy.[9] Depression, anxiety, and social withdrawal are all factors which have been proven to negatively affect a patient's chance of recovery.[19] Location and size of the brain lesion may also play a role in the prognosis of aphasia. It has been seen in receptive aphasia that larger lesions correlate to slower recovery.[20] It has also been seen that patients with aphasia caused by sub cortical lesions have a better chance of recovery than those with aphasia due to cortical stroke.[21]

[edit] History
Expressive aphasia was first identified by the French neurologist Paul Broca. By examining the brains of deceased individuals who acquired expressive aphasia in life, he concluded that language ability was localized in the ventroposterior region of the frontal lobe. One of the most important aspects of Paul Broca's discovery was the observation that the loss of proper speech in expressive aphasia was due to the brain's loss of ability to produce language as opposed to the mouth's loss of ability to produce words.[1] The discoveries of Paul Broca were made during the same period of time as the German Neurologist Carl Wernicke who was also studying brains of aphasiacs post-mortem and identified the region now known as Wernicke's area. Discoveries of both men contributed to the concept of localization which states that specific brain functions are all localized to a specific area of the brain. While both men made significant contributions to the field of aphasia, it was Carl Wernicke who realized the difference between patients with aphasia who could not produce language and those who could not comprehend language (the essential difference between expressive and receptive aphasia).[1]

http://en.wikipedia.org/wiki/Expressive_aphasia

How is aphasia diagnosed?


Aphasia is usually first recognized by the physician who treats the person for his or her brain injury. Frequently this is a neurologist. The physician typically performs tests that require the person to follow commands, answer questions, name objects, and carry on a conversation. If the physician suspects aphasia, the patient is often referred to a speechlanguage pathologist, who performs a comprehensive examination of the person's communication abilities. The examination includes the person's ability to speak, express ideas, converse socially, understand language, read, and write, as well as the ability to swallow and to use alternative and argumentative communication.

How is aphasia treated?


In some cases, a person will completely recover from aphasia without treatment. This type of spontaneous recovery usually occurs following a type of stroke in which blood flow to the brain is temporarily interrupted but quickly restored, called a transient ischemic attack. In these circumstances, language abilities may return in a few hours or a few days. For most cases, however, language recovery is not as quick or as complete. While many people with aphasia experience partial spontaneous recovery, in which some language abilities return a few days to a month after the brain injury, some amount of aphasia typically remains. In these instances, speech-language therapy is often helpful. Recovery usually continues over a two-year period. Many health professionals believe that the most effective treatment begins early in the recovery process. Some of the factors that influence the amount of improvement include the cause of the brain damage, the area of the brain that was damaged, the extent of the brain injury, and the age and health of the individual. Additional factors include motivation, handedness, and educational level. Aphasia therapy aims to improve a person's ability to communicate by helping him or her to use remaining language abilities, restore language abilities as much as possible, compensate for language problems, and learn other methods of communicating. Individual therapy focuses on the specific needs of the person, while group therapy offers the opportunity to use new communication skills in a small-group setting. Stroke clubs, regional support groups formed by people who have had a stroke, are available in most major cities. These clubs also offer the opportunity for people with aphasia to try new communication skills. In addition, stroke clubs can help a person and his or her family adjust to the life changes that accompany stroke and aphasia. Family involvement is often a crucial component of aphasia treatment so that family members can learn the best way to communicate with their loved one. Family members are encouraged to:

Simplify language by using short, uncomplicated sentences. Repeat the content words or write down key words to clarify meaning as needed. Maintain a natural conversational manner appropriate for an adult. Minimize distractions, such as a loud radio or TV, whenever possible. Include the person with aphasia in conversations. Ask for and value the opinion of the person with aphasia, especially regarding family matters. Encourage any type of communication, whether it is speech, gesture, pointing, or drawing. Avoid correcting the person's speech. Allow the person plenty of time to talk. Help the person become involved outside the home. Seek out support groups such as stroke clubs.

Other treatment approaches involve the use of computers to improve the language abilities of people with aphasia. Studies have shown that computer-assisted therapy can help people with aphasia retrieve certain parts of speech, such as the use of verbs. Computers can also provide an alternative system of communication for people with difficulty expressing language. Lastly, computers can help people who have problems perceiving the difference between phonemes (the sounds from which words are formed) by providing auditory discrimination exercises.

What research is being done for aphasia?


Scientists are attempting to reveal the underlying problems that cause certain symptoms of aphasia. The goal is to understand how injury to a particular part of the brain impairs a person's ability to convey and understand language. The results could be useful in treating various types of aphasia, since the treatment may change depending upon the cause of the language problem. Other research is attempting to understand the parts of the language process that contribute to sentence comprehension and production and how these parts may break down in aphasia. In this way, it may be possible to pinpoint where the breakdown occurs and help in the development of more focused treatment programs. Although different languages have many things in common when specific portions of the brain are injured, there are also differences. Scientists are trying to understand the common (or universal) symptoms of aphasia and the language-specific symptoms of the disorder. Other researchers are examining whether people with aphasia may still know their language but have difficulty accessing that knowledge. These studies may help with the development of tests and rehabilitation strategies that focus on specific characteristics of one language or multiple languages. Researchers are exploring drug therapy as an experimental approach to treating aphasia. Some studies are testing how drugs can be used in combination with speech therapy to improve recovery of various language functions.

Researchers are also looking at how treatment of other cognitive deficits involving attention and memory can improve communication abilities. To understand recovery processes in the brain, some researchers are using functional magnetic resonance imaging (fMRI) to better understand the human brain regions involved in speaking and understanding language. This type of research may improve understanding of how these areas reorganize after brain injury. The results could have implications for both the basic understanding of brain function and the diagnosis and treatment of neurological diseases. http://www.medicinenet.com/aphasia/page3.htm

Aphasia
From Wikinfo
Jump to: navigation, search Search for "Aphasia" on Wikipedia Wikimedia Commons Wiktionary Wikiquote Wikibooks Mediawiki Wikia Wikitravel Google Advanced Search Yahoo Advanced Search WorldCat Advanced Search Amazon Recent NY Times Older NY Times. For other uses, see Aphasia (disambiguation). Aphasia (pronounced /fe/ or pronounced /fezi/) is an acquired language disorder in which there is an impairment of any language modality. This may include difficulty in producing or comprehending spoken or written language. Traditionally, aphasia suggests the total impairment of language ability, and dysphasia a degree of impairment less than total. However, the term dysphasia is easily confused with dysphagia, a swallowing disorder, and thus aphasia has come to mean both partial and total language impairment in common use. Depending on the area and extent of brain 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. 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. 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.

Causes
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. Aphasia is also listed as a rare side effect of the fentanyl patch, an opioid used to control chronic pain.[1]

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.

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) incompleted sentences inability to read inability to write

Types
The following table summarizes some major characteristics of different types of aphasia: Type of aphasia Repetition Naming Auditory Fluency comprehension Presentation

Wernicke's aphasia

mildmod

mild severe

Transcortical sensory good aphasia

mod severe

Conduction aphasia

poor

poor

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 fluent defective dog needs to go out so I paraphasic 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. Similar deficits as in Wernicke's aphasia, but poor fluent repetition ability remains intact. Conduction aphasia is caused by deficits in the connections between the speech-comprehension and speech-production relatively good fluent areas. This might be damage to the arcuate fasciculus, the structure that transmits information between Wernicke's area and Broca's area. Similar

Nominal or Anomic aphasia

mild

mod severe

mild

Broca's aphasia

mod severe

mod severe

mild difficulty

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. Repetition ability is poor. 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 fluent 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. Individuals with Broca's aphasia frequently speak short, meaningful phrases that are produced with great effort. Broca's aphasia is thus characterized as a non-fluent, nonfluent aphasia. effortful, Affected people often slow omit small words such as "is", "and", and "the". For example, a person with Broca's aphasia may say, "Walk dog" which could mean "I will take the dog for a walk", "You take the dog for a walk" or

Transcortical good motor aphasia

mild severe

mild

Global aphasia

poor

poor

poor

even "The dog walked out of the yard". 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 can be paralysis of the patient's right face and arm. Similar deficits as Broca's aphasia, except repetition ability remains intact. Auditory comprehension is generally fine for simple conversations, but non-fluent declines rapidly for more complex conversations. It is associated with right hemiparesis, meaning that there can be paralysis of the patient's right face and arm. 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 non-fluent nonverbal, and/or only use facial expressions and gestures to communicate. It is associated with right hemiparesis, meaning that there can be paralysis of the patient's right face

Transcortical mixed moderate aphasia

poor

poor

Subcortical aphasias

and arm. Similar deficits as in global aphasia, but non-fluent repetition ability remains intact. Characteristics and symptoms depend upon the site and size of subcortical lesion. Possible sites of lesions include the thalamus, internal capsule, and basal ganglia.

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 se

Acquired childhood aphasia


Acquired childhood aphasia (ACA) is a language impairment resulting from some kind of brain damage. This brain damage can have different causes, such as head trauma, tumors, cerebrovascular accidents, or seizure disorders. Most, but not all authors state that ACA is preceded by a period of normal language development.[2] Age of onset is usually defined as from infancy until but not including adolescence. ACA should be distinguished from developmental aphasia or developmental dysphasia, which is a primary delay or failure in language acquisition.[3] An important difference between ACA and developmental childhood aphasia is that in the latter there is no apparent neurological basis for the language deficit.[4] ACA is one of the more rare language problems in children and is notable because of its contribution to theories on language and the brain.[3] Because there are so few children with ACA, not much is known about what types of linguistic problems these children have. However, many authors report a marked decrease in the use of all expressive language. Children can just stop talking for a period of weeks or even years, and when they start to talk again, they need a lot of encouragement. Problems with language comprehension are less common in ACA, and don't last as long.[5]

Classification

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. [6] 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". The most prominent writers on this topic have been Harold 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 dissect 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 localizationist model are: Pure word deafness Conduction aphasia Apraxia of speech, which is now considered a separate disorder in itself. Transcortical motor aphasia 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

1. 2. 3. 4. 5.

final type of aphasia, global aphasia, results from damage to extensive portions of the perisylvian region of the brain.

Other ways to Classify Aphasia Fluent, non-fluent and "pure" aphasias


The different types of aphasia can be divided into three categories: fluent, non-fluent and "pure" aphasias.[7]

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 Nonfluent aphasias, also called expressive aphasias are difficulties in articulating, but in most cases there is relatively good auditory verbal comprehension. Examples of nonfluent aphasias are: Broca's aphasia, Transcortical motor aphasia, Global 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

Primary and secondary aphasia


Aphasia can be divided into primary and secondary aphasia.[8]

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.

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.

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.[9]

Famous sufferers

Maurice Ravel Vissarion Shebalin Jan Berry of Jan and Dean Sven Nykvist Ralph Waldo Emerson[10] Joseph Chaikin Antony Flew Bob Woodruff Kevin Ryder of The Kevin and Bean Show Toggle (Doonesbury character), Iraq war veteran injured by IED

Treatment
There is no one treatment proven to be effective for all types of aphasias. Melodic intonation therapy is often used to treat non-fluent aphasia and has proved to be very effective in some cases. http://www.wikinfo.org/index.php/Aphasia

Aphasia Treatment in Stroke Importnat Information About Aphasia Treatment After Stroke
From Jose Vega M.D., Ph.D., former About.com Guide Updated: July 22, 2008 About.com Health's Disease and Condition content is reviewed by the Medical Review Board See More About: common aphasias

speech pathology aphasia therapy research

Photo A.D.A.M. Aphasia treatment is an extremely important aspect of life after a stroke which has affected someone's ability to speak. In general terms, aphasia is a disturbance in the production, processing, or understanding of language due to brain damage, most commonly from stroke. Although multiple forms of treatment exist for the different types of aphasia, only a few of them have been studied rigorously enough to have proven efficacy. As a result, most forms of aphasia treatment are based on theoretical grounds which await further testing to prove their benefits. However, based on their experience with patients, most speech pathologists and physicians attest to the benefits of aphasia therapy.

General Principles
Several principles of therapy have been shown in small studies to improve the outcome of therapy.

Regardless of the type of therapy used, the outcome is better if the intensity of therapy is increased. In other words, a given number of hours of therapy will yield a much better outcome if they are given in a few sessions over a few days rather than in many sessions over many days. The effectiveness of aphasia therapy increases when therapists use multiple forms of sensory stimuli. For instance, auditory stimuli in the form of music, and visual stimuli in the form of pictures, drawings, are routinely used during aphasia therapy sessions. Gradual increases in the difficulty of language exercises practiced during a given therapy session improves the outcome.

Listed below are some well-known forms of aphasia treatments.

Cognitive Linguistic Therapy


This form of therapy emphasizes the emotional components of language. For example, some exercises require patients to interpret the characteristics of different emotional tones of voice. Others require them to describe the meaning of highly descriptive words or terms such as the word "happy." These exercises help patients practice comprehension skills while focusing on understanding the emotional components of language.

Programmed Simulation:
This type of therapy uses multiple sensory modalities, including pictures and music, introduced in a gradual progression from easy to difficult.

Stimulation-Fascilitation Therapy:
This form of aphasia therapy focuses mostly on the semantic and syntactic parts of language. The main stimulus used during therapy sessions is auditory stimulation. One of the main assumptions of this type of therapy is that improvements in language skills are best accomplished with repetition.

Group Therapy:
This type of therapy provides a social context for patients to practice the communication skills they have learned during individual therapy sessions, while getting important feedback from therapists and other aphasics. Family treatment strategies have a similar effect, while also facilitating the communications of aphasics with their loved ones.

PACE (Promoting Aphasic's Communicative Effectiveness):


This is one of the best-known forms of pragmatic therapy, a form of aphasia therapy that promotes improvements in communication by using conversation as a tool for learning. PACE therapy sessions typically involve an enacted conversation between the therapist and the patient. In order to stimulate spontaneous communication, this type of therapy uses drawings, pictures, and other visually-stimulating items which are used by the patient to generate ideas to be communicated during the conversation. The therapist and the patient take turns to convey their ideas. The difficulty of the materials used to generate conversation is increased in a gradual fashion. Patients are encouraged to use any means of communication during the session, which allows the therapist to discover communication skills that should be reinforced in the patient. The therapist communicates with the patient by imitating the means of communication with which the patient feels most comfortable.

Pharmacotherapy:
This is one of the most appealing forms of aphasia therapy although its efficacy has yet to be proven. The list of medications tried so far include piracetam, bifenalade, piribedil, bromocriptine, idebenone and dextran 40, donezepil, amphetamines and several antidepressants. Although the evidence is not very strong, it appears that at least donezepil, piribedil and amphetamines might have some degree of efficacy in aphasia treatment. The latter appears to be especially helpful at enhancing the benefits of traditional non-medication based therapy, as some studies have shown a better outcome of therapy when patients are given amphetamines before therapy sessions.

Transcranial Magnetic Stimulation (TMS):


Although this modality of treatment is seldom used, its efficacy is under intense investigation. TMS consists of aiming a magnet directly at a part of the brain which is thought to inhibit language recovery after stroke. By suppressing the function of that part of the brain, recovery is enhanced. The type of magnetic therapy that has been tried in aphasia rehabilitation is the "slow and repeated" version of TMS. A few small studies have had encouraging results, but a large, well-controlled study is still needed to ensure the efficacy of this form of treatment.
Sources: Jordan Lori and Hillis Argye; Disorders of speech and language: aphasia, apraxia and dysarthria; Current Opinion in Neurology 2006 19 (6): 580-585. Cicerone et al., Evidence-based cognitive rehabilitation: Updated Review of the literature from 1998 to 2002 Archives of Physical Medicine and Rehabilitation 2005 Vol 86; 1681-1692. Froma P Roth and Colleen K. Worthington treatment resource manual for speech and language pathology 2nd edition Delmar, Albany NY.

http://stroke.about.com/od/caregiverresources/a/Aphasiarx.htm

How is aphasia treated?


In some cases, a person will completely recover from aphasia without treatment. This type of spontaneous recovery usually occurs following a type of stroke in which blood flow to the brain is temporarily interrupted but quickly restored, called a transient ischemic attack. In these circumstances, language abilities may return in a few hours or a few days. For most cases, however, language recovery is not as quick or as complete. While many people with aphasia experience partial spontaneous recovery, in which some language abilities return a few days to a month after the brain injury, some amount of aphasia typically remains. In these instances, speech-language therapy is often helpful. Recovery usually continues over a two-year period. Many health professionals believe that the most effective treatment begins early in the recovery process. Some of the factors that influence the amount of improvement include the cause of the brain damage, the area of the brain that was damaged, the extent of the brain injury, and the age and health of the individual. Additional factors include motivation, handedness, and educational level. Aphasia therapy aims to improve a persons ability to communicate by helping him or her to use remaining language abilities, restore language abilities as much as possible, compensate for language problems, and learn other methods of communicating. Individual therapy focuses on the specific needs of the person, while group therapy offers the opportunity to use new communication skills in a small-group setting. Stroke clubs, regional support groups formed by people who have had a stroke, are available in most major cities. These clubs also offer the opportunity for people with aphasia to try new communication skills. In addition, stroke clubs can help a person and his or her family adjust to the life changes that accompany stroke and aphasia.

Family involvement is often a crucial component of aphasia treatment so that family members can learn the best way to communicate with their loved one. Family members are encouraged to:

Simplify language by using short, uncomplicated sentences. Repeat the content words or write down key words to clarify meaning as needed. Maintain a natural conversational manner appropriate for an adult. Minimize distractions, such as a loud radio or TV, whenever possible. Include the person with aphasia in conversations. Ask for and value the opinion of the person with aphasia, especially regarding family matters. Encourage any type of communication, whether it is speech, gesture, pointing, or drawing. Avoid correcting the persons speech. Allow the person plenty of time to talk. Help the person become involved outside the home. Seek out support groups such as stroke clubs.

Other treatment approaches involve the use of computers to improve the language abilities of people with aphasia. Studies have shown that computer-assisted therapy can help people with aphasia retrieve certain parts of speech, such as the use of verbs. Computers can also provide an alternative system of communication for people with difficulty expressing language. Lastly, computers can help people who have problems perceiving the difference between phonemes (the sounds from which words are formed) by providing auditory discrimination exercises. Top

What research is being done for aphasia?


Scientists are attempting to reveal the underlying problems that cause certain symptoms of aphasia. The goal is to understand how injury to a particular part of the brain impairs a persons ability to convey and understand language. The results could be useful in treating various types of aphasia, since the treatment may change depending upon the cause of the language problem. Other research is attempting to understand the parts of the language process that contribute to sentence comprehension and production and how these parts may break down in aphasia. In this way, it may be possible to pinpoint where the breakdown occurs and help in the development of more focused treatment programs. Although different languages have many things in common when specific portions of the brain are injured, there are also differences. Scientists are trying to understand the common (or universal) symptoms of aphasia and the language-specific symptoms of the disorder. Other researchers are examining whether people with aphasia may still know

their language but have difficulty accessing that knowledge. These studies may help with the development of tests and rehabilitation strategies that focus on specific characteristics of one language or multiple languages. Researchers are exploring drug therapy as an experimental approach to treating aphasia. Some studies are testing how drugs can be used in combination with speech therapy to improve recovery of various language functions. Researchers are also looking at how treatment of other cognitive deficits involving attention and memory can improve communication abilities. To understand recovery processes in the brain, some researchers are using functional magnetic resonance imaging (fMRI) to better understand the human brain regions involved in speaking and understanding language. This type of research may improve understanding of how these areas reorganize after brain injury. The results could have implications for both the basic understanding of brain function and the diagnosis and treatment of neurological diseases. http://www.nidcd.nih.gov/health/voice/aphasia.asp

Aphasia Treatment
In general, treatment strives to improve a person's ability to communicate. The most effective treatment begins early in the recovery process and is maintained consistently over time. Major factors that influence the amount of improvement include the cause of the brain damage, the area of the brain that was damaged, the extent of the injury, and the person's general health. Usually a speech-language pathologist works with other rehabilitation and medical professionals, such as physicians, nurses, neuropsychologists, occupational therapists, physical therapists, and social workers, as well as families, to provide a comprehensive evaluation and treatment plan for the person with aphasia. http://seniorhealth.about.com/library/stroke/blaphasia3.htm