Aphasia

For other uses, see Aphasia (disambiguation).

Aphasia
Classification and external resources
ICD-10	F80.0-F80.2, R47.0
ICD-9	315.31, 784.3, 438.11
DiseasesDB	4024
MedlinePlus	003204
eMedicine	neuro/437
MeSH	D001037

Dysphasia
Classification and external resources
ICD-10	F80.1, F80.2, R47.0
ICD-9	438.12, 784.5

Aphasia ( /əˈfeɪʒə/ or /əˈfeɪziə/) is an impairment of language ability. This class of language disorder ranges from having difficulty remembering words to being completely unable to speak, read, or write.

Aphasia disorders usually develop quickly as a result of head injury or stroke, but can develop slowly from a brain tumor, infection, or dementia, or can be a learning disability such as dysnomia.^[1]

The area and extent of brain damage determine the type of aphasia and its symptoms. Aphasia types include Broca's aphasia, non-fluent aphasia, motor aphasia, expressive aphasia, receptive aphasia, global aphasia and many others (see Category:Aphasias).

Medical evaluations for the disorder range from clinical screenings by a neurologist to extensive tests by a language pathologist. ^[1]

Most aphasia patients can recover some or most skills by working with a speech and language therapist. This rehabilitation can take two or more years and is most effective when begun quickly. Only a small minority will recover without therapy, such as those suffering a mini-stroke. Patients with a learning-disorder aphasia such as dysnomia can learn coping skills, but cannot recover abilities that are congenitally limited.^[2]

Improvement varies widely, depending on the aphasia's cause, type, and severity. Recovery also depends on the patient's age, health, motivation, handedness, and educational level. ^[1]

Event Drawing Task

Findings of the Event Drawing Task showed that "conceptualisation problems may be an additional source of deficit in aphasia" ^[3]

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.^[4]

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 Dr. 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. Dronkers and Dr. Odile Plaisant scanned Broca's original patients' brains using a non-invasive MRI scanner to take a closer look. 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. Video clips showing patients with Broca-type aphasia can be found here.

• 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. A video clip with a patient exhibiting Wernicke's aphasia can be found here

• 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 in-depth studies available. The other five types of aphasia in the localizationist model are:

1. Pure word deafness
2. Conduction aphasia
3. Apraxia of speech (now considered a separate disorder in itself)
4. Transcortical motor aphasia
5. Transcortical sensory aphasia

• Anomia is another type of aphasia proposed under what is commonly known as the Boston-Neoclassical model, which is essentially a difficulty with naming. A final type of aphasia, global aphasia, results from damage to extensive portions of the perisylvian region of the brain. An individual with global aphasia will have difficulty understanding both spoken and written language and will also have difficulty speaking. This is a severe type of aphasia which makes it quite difficult when communicating with the individual.^[5]

Intention

The study seeks to thoroughly identify similarities and differences between the event drawing performance of two aphasic participants and a group of 12 non-brain-damaged controls. ^[3]

Other ways to classify aphasia

Aphasia can also be classified as

1. Receptive
2. Intermediate
3. Expressive

Receptive aphasias can be subdivided into

A - pure word deafness (patient can hear but not understand words)
B - alexia (patient can read but not understand words)
C - visual asymbolia (written words are disorganized and can not be recognized).

Intermediate - also called nominal amnestic aphasia.

Expressive aphasia also known as Broca's aphasia or cortical motor aphasia (patient has difficulty in putting his thoughts into words)

Fluent, non-fluent and "pure" aphasias

The different types of aphasia can be divided into three categories: fluent, non-fluent and "pure" aphasias.^[6]

• 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^[6]

• 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^[6]

• "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: Pure alexia, Agraphia, Pure word deafness^[6]

Primary and secondary aphasia

Aphasia can be divided into primary and secondary aphasia.

• 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. ^[7] Hence there is a module which recognises phonemes as they are spoken and a module which stores formulated phonemes before they are spoken. Use of this model clinically involves conducting a battery of assessments (usually from the PALPA, the "psycholinguistic assessment of language processing in adult acquired aphasia ... that can be tailored to the investigation of an individual patient's impaired and intact abilities" http://www.psypress.com/palpa-9780863771668, last visited 1/21/2011), 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.

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.^[8] 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.^[9] An important difference between ACA and developmental childhood aphasia is that in the latter there is no apparent neurological basis for the language deficit.^[10]

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.^[9] 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.^[11]

Signs and symptoms

People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems such as dysarthria or apraxia and not primarily due to aphasia.

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

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

Type of aphasia	Repetition	Naming	Auditory comprehension	Fluency	Presentation
Wernicke's aphasia	mild–mod	mild–severe	defective	fluent paraphasic	Individuals with Wernicke's aphasia may speak in long sentences that have no meaning, add unnecessary words, and even create new "words" (neologisms). For example, someone with Wernicke's aphasia may say, "You know that smoodle pinkered and that I want to get him round and take care of him like you want before", meaning "The dog needs to go out so I will take him for a walk". They have poor auditory and reading comprehension, and fluent, but nonsensical, oral and written expression. Individuals with Wernicke's aphasia usually have great difficulty understanding the speech of both themselves and others and are therefore often unaware of their mistakes.
Transcortical sensory aphasia	good	mod–severe	poor	fluent	Similar deficits as in Wernicke's aphasia, but repetition ability remains intact.
Conduction aphasia	poor	poor	relatively good	fluent	Conduction aphasia is caused by deficits in the connections between the speech-comprehension and speech-production areas. This might be caused by damage to the arcuate fasciculus, the structure that transmits information between Wernicke's area and Broca's area. Similar symptoms, however, can be present after damage to the insula or to the auditory cortex. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Repetition ability is poor.
Nominal or Anomic aphasia	mild	mod–severe	mild	fluent	Anomic aphasia is essentially a difficulty with naming. The patient may have difficulties naming certain words, linked by their grammatical type (e.g. difficulty naming verbs and not nouns) or by their semantic category (e.g. difficulty naming words relating to photography but nothing else) or a more general naming difficulty. Patients tend to produce grammatic, yet empty, speech. Auditory comprehension tends to be preserved.
Broca's aphasia	mod–severe	mod–severe	mild difficulty	non-fluent, effortful, slow	Individuals with Broca's aphasia frequently speak short, meaningful phrases that are produced with great effort. Broca's aphasia is thus characterized as a nonfluent aphasia. Affected people often omit small words such as "is", "and", and "the". For example, a person with Broca's aphasia may say, "Walk dog" 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	mild–severe	mild	non-fluent	Similar deficits as Broca's aphasia, except repetition ability remains intact. Auditory comprehension is generally fine for simple conversations, but declines rapidly for more complex conversations. It is associated with right hemiparesis, meaning that there 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.
Mixed transcortical 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 semantically related to the first (e.g. letter - scroll), or picking one phonetically similar to the intended one (e.g. lane - late).

Research on understanding the nature, causes and treatment of aphasia is typically categorized into different components of language including phonological processing, lexical-semantic processing, syntactic processing, orthographic processing. There are two associations dedicated to the study of aphasia, the Academy of Aphasia and Clinical Aphasiology.

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.^[12]

Treatment

There is no one treatment proven to be effective for all types of aphasias. The reason that there is no universal treatment for aphasia is because of the nature of the disorder and the various ways it is presented, as explained in the above sections. Aphasia is rarely exhibited identically, implying that treatment needs to be catered specifically to the individual. Studies have shown that although there isn't consistency on treatment methodology in literature, there is a strong indication that treatment in general has positive outcomes^[13].

A multi-disciplinary team, including doctors (often a physician is involved, but more likely a clinical neuropsychologist will head the treatment team), physiotherapist, occupational therapist, speech-language pathologist, and social worker, works together in treating aphasia. For the most part, treatment relies heavily on repetition and aims to address language performance by working on task-specific skills. The primary goal is to help the individual and those closest to them adjust to changes and limitations in communication^[13].

Treatment techniques mostly fall under two approaches:

1. Substitute Skill Model - an approach that uses an aid to help with spoken language, i.e. a writing board
2. Direct Treatment Model - an approach which targets deficits with specific exercises^[13]

Several treatment techniques include the following:

• Visual Communication Therapy (VIC) - the use of index cards with symbols to represent various components of speech
• Visual Action Therapy (VAT) - involves training individuals to assign specific gestures for certain objects
• Functional Communication Treatment (FCT) - focuses on improving activities specific to functional tasks, social interaction, and self-expression
• Promoting Aphasic's Communicative Effectiveness (PACE) - a means of encouraging normal interaction between patients and clinicians.
• Other - i.e. drawing as a way of communicating, trained conversation partners^[13]

More recently, computer technology has been incorporated into treatment options. A key indication for good prognosis is treatment intensity. A minimum of 2-3 hours per week has been specified to produce positive results^[14]. The main advantage of using computers is that it can greatly increase intensity of therapy. These programs consist of a large variety of exercises and can be done at home in addition to face-to-face treatment with a therapist. However, since aphasia presents differently among individuals, these programs must be dynamic and flexible in order to adapt to the variability in impairments. Another barrier is the capability of computer programs to imitate normal speech and keep up with the speed of regular conversation. Therefore, computer technology seems to be limited in a communicative setting, however is effective in producing improvements in communication training^[14].

Several examples of programs used are StepByStep, Linguagraphica, Computer-Based Visual Communication (C-VIC), TouchSpeak (TS), and Sentence Shaper^[14].

Melodic intonation therapy is often used to treat non-fluent aphasia and has proved to be very effective in some cases^[15].

Zolpidem, a drug with the trade name of Ambien, may provide short-lasting but effective improvement in symptoms of aphasia present in some survivors of stroke. The mechanism for improvement in these cases remains unexplained and is the focus of current research by several groups, to explain how a drug which acts as a hypnotic-sedative in people with normal brain function, can paradoxically increase speech ability in people recovering from severe brain injury. Use of zolpidem for this application remains experimental at this time, and is not officially approved by any pharmaceutical manufacturers of zolpidem or medical regulatory agencies worldwide.

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.^[16]

Notable cases

• Ralph Waldo Emerson^[17]
• Maurice Ravel
• Jan Berry of Jan and Dean
• Sven Nykvist
• Robert E. Lee
• Edwyn Collins
• Paul David Wilson
• Joseph Chaikin
• Ralph Klein

See also

• Aphasiology
• Speech disorder
• Dysnomia disorder
• Aprosodia
• Dysprosody
• Glossolalia
• Paragrammatism

References

1. ^ ^{a b c} "Aphasia". MedicineNet.com. http://www.medicinenet.com/aphasia/article.htm. Retrieved 2011-05-23. 
2. ^ "Aphasia: Treatments and drugs". Mayo Clinic. http://www.mayoclinic.com/health/aphasia/DS00685/DSECTION=treatments-and-drugs. Retrieved 2011-05-23. 
3. ^ ^{a b} Black, Maria. "Drawing as a Window to Event Conceptualisation: Evidence from Two People with Aphasia." Aphasiology 25.1 (2010). Taylor & Francis Online. University of Toronto Libraries, 20 July 2010. Web. 08 Oct. 2011. <http://www.tandfonline.com.myaccess.library.utoronto.ca/doi/full/10.1080/02687031003714459>.
4. ^ Kolb, Bryan; Whishaw, Ian Q. (2003). Fundamentals of human neuropsychology. [New York]: Worth. pp. 502, 505, 511. ISBN 0-7167-5300-6. OCLC 464808209. 
5. ^ Taylor Sarno, M. (2007). Neurogenic disorders of speech and language. In: O’Sullivan, S.B. & Schmitz, T.J. (2007). Physical Rehabilitation (5th ed.). Philadelphia (PA): F.A. Davis Company.
6. ^ ^{a b c d} Kolb, Bryan; Whishaw, Ian Q. (2003). Fundamentals of human neuropsychology. [New York]: Worth. pp. 502–504. ISBN 0-7167-5300-6. OCLC 464808209. 
7. ^ Luria's Areas of the Human Cortex Involved in Language Illustrated summary of Luria's book Traumatic Aphasia
8. ^ Murdoch, B. E. (1990). Acquired neurological speech/language disorders in childhood. Washington, DC: Taylor & Francis. ISBN 0-85066-490-X. OCLC 21976166. 
9. ^ ^{a b} Woods, Bryan T. (1995). "Acquired childhood aphasia". In Kirshner, Howard S.. Handbook of neurological speech and language disorders. New York: M. Dekker. ISBN 0-8247-9282-3. OCLC 31075598. 
10. ^ Paquier, P.F.; van Dongen (1998). "Is Acquired Childhood Aphasia Atypical?". In Basso, Anna; Coppens, Patrick; Lebrun, Yvan. Aphasia in atypical populations. Hillsdale, N.J: Lawrence Erlbaum Associates. ISBN 0-8058-1738-7. OCLC 37712996. 
11. ^ Baker, Lorian; Cantwell, Dennis P. (1987). Developmental speech and language disorders. New York: Guilford Press. ISBN 0-89862-400-2. OCLC 14520470. 
12. ^ "Fentanyl Transdermal Official FDA information, side effects and uses". Drug Information Online. http://www.drugs.com/pro/fentanyl-transdermal.html#A02A9CB6-35CF-4F01-A980-C3733E0F861A. 
13. ^ ^{a b c d} O’Sullivan, S. B., & Schmitz, T. J. (2007). Physical rehabilitation. (5th ed.). Philadelphia (PA): F. A. Davis Company.
14. ^ ^{a b c} Van De Sandt-Koenderman, W. M. E. (2011). Aphasia rehabilitation and the role of computer technology: Can we keep up with modern times? International Journal of Speech-Language Pathology, 13(1), 21-27.
15. ^ Norton, A., Zipse, L., Marchina, S., & Schlaug, G. (2009). Melodic intonation therapy: Shared insights on how it is done and why it might help. Annals of the New York Academy of Sciences, 1169, 431-436.
16. ^ McCrory PR, Berkovic SF (December 2001). "Concussion: the history of clinical and pathophysiological concepts and misconceptions". Neurology 57 (12): 2283–9. PMID 11756611. http://www.neurology.org/cgi/content/abstract/57/12/2283. 
17. ^ Richardson, Robert G. (1995). Emerson: the mind on fire: a biography. Berkeley: University of California Press. ISBN 0-520-08808-5. OCLC 31206668. 

External links

• Aphasia at the Open Directory Project
• Luria's Areas of the Human Cortex Involved in Language Illustrated summary of Luria's book Traumatic Aphasia