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Classification and external resources
ICD-10 F80.0-F80.2, R47.0
ICD-9 315.31, 784.3
DiseasesDB 4024
MedlinePlus 003204
eMedicine neuro/437 
MeSH D001037
Classification and external resources
ICD-10 F80.1, F80.2, R47.0
ICD-9 438.12, 784.5
Look up aphasia, aphemia in Wiktionary, the free dictionary.

Aphasia (from Greek, aphatos : 'speechless'), also known as rhymnasia, is a loss of the ability to produce and/or comprehend language, due to injury to brain areas specialized for these functions, such as Broca's area, which governs language production, or Wernicke's area, which governs the interpretation of language. It is not a result of deficits in sensory, intellectual, or psychiatric functioning,[1] nor due to muscle weakness or a cognitive disorder.

Dysphasia (pronounced /dɪsˈfeɪziə/) is a language disorder in which there is an impairment (but not loss) of speech and of comprehension of speech. The term dysphasia has been eclipsed by the modern usage of the term aphasia particularly in the field of speech and language pathology so as not to confuse with the swallowing disorder dysphagia.

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

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 centres of the brain, such as Broca's area. These areas are almost always located in the left hemisphere, and in most people this is where the ability to produce and comprehend language is found. However, in a very small number of people, language ability is found in the right hemisphere. In either case, damage to these language areas can be caused by a stroke, traumatic brain injury, or other 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.[citation needed]

[edit] Symptoms

Any of the following may be considered symptoms of aphasia:

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

[edit] Types

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

Type of aphasia Repetition Naming Auditory comprehension Fluency Presentation
Wernicke's aphasia mild–mod mild–severe defective fluent paraphasic Individuals with Wernicke's aphasia may speak in long sentences that have no meaning, add unnecessary words, and even create new "words" (neologisms). For example, someone with Wernicke's aphasia may say, "You know that smoodle pinkered and that I want to get him round and take care of him like you want before", meaning "The dog needs to go out so I will take him for a walk". They have poor auditory and reading comprehension, and fluent, but nonsensical, oral and written expression. Individuals with Wernicke's aphasia usually have great difficulty understanding the speech of both themselves and others and are therefore often unaware of their mistakes. They are also often unaware of their surroundings, and may present a risk to themselves and others around them.
Transcortical sensory aphasia good mod–severe poor fluent Similar deficits as in Wernicke's aphasia, but repetition ability remains intact.
Conduction aphasia poor poor relatively good fluent Conduction aphasia is caused by deficits in the connections between the speech-comprehension 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 sympthoms, 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 aphasia mild mod–severe mild fluent Anomic aphasia, is essentially a difficulty with naming. The patient may have difficulties naming certain words, linked by their grammatical type (e.g. difficulty naming verbs and not nouns) or by their semantic category (e.g. difficulty naming words relating to photography but nothing else) or a more general naming difficulty. Patients tend to produce grammatic, yet empty, speech. Auditory comprehension tends to be preserved.
Broca's aphasia mod–severe mod–severe mild difficulty non-fluent, effortful, slow Individuals with Broca's aphasia frequently speak short, meaningful phrases that are produced with great effort. Broca's aphasia is thus characterized as a nonfluent aphasia. Affected people often omit small words such as "is", "and", and "the". For example, a person with Broca's aphasia may say, "Walk dog" meaning, "I will take the dog for a walk". The same sentence could also mean "You take the dog for a walk", or "The dog walked out of the yard", depending on the circumstances. Individuals with Broca's aphasia are able to understand the speech of others to varying degrees. Because of this, they are often aware of their difficulties and can become easily frustrated by their speaking problems. It is associated with right hemiparesis, meaning that there 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.
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.

[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


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:
  1. Pure word deafness
  2. Conduction aphasia
  3. Apraxia of speech, which is now considered a separate disorder in itself.
  4. Transcortical motor aphasia
  5. Transcortical sensory aphasia
  • Anomia is another type of aphasia proposed under what is commonly known as the Boston-Neoclassical model, which is essentially a difficulty with naming. A final type of aphasia, global aphasia, results from damage to extensive portions of the language areas of the brain.

[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
  • "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] Cognitive neuropsychological model

The cognitive neuropsychological model builds on cognitive neuropsychology. It assumes that language processing can be broken down into a number of modules, each of which has a specific function. Hence there is a module which recognises phonemes as they are spoken and a module which stores formulated phonemes before they are spoken. Use of this model clinically involves conducting a battery of assessments (usually from the PALPA), each of which tests one or a number of these modules. Once a diagnosis is reached as to where the impairment lies, therapy can proceed to treat the individual module.

A few less common subtypes include:

A combination of subtypes is possible.

[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] 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

[edit] See also

[edit] Sources

[edit] Handbooks

  • Primary Progressive Aphasia (PPA) Handbook (Northwestern University)
  • Handbook of Speech-Language, Pathology, and Audiology
  • Reference manual for communicative sciences and disorders: speech and language

[edit] Bibliographic Databases

  • MLA International Bibliography
  • Linguistics Abstracts Online
  • Linguistics and Language Behavior Abstracts
  • Encyclopedia of the Human Brain
  • PsycINFO

[edit] Specialized Bibliographies

  • MD Consult
  • Psychology and Behavioral Sciences Collection
  • Health Reference Complete (Academic)

[edit] Academic references

  • R. Chapey (Ed.) (2001). Language Intervention Strategies in Aphasia and Related Neurogenic Communication Disorders (Fourth Edition). Philadelphia: Lippincott, Williams & Wilkins.
  • Goodglass, H. & Kaplan, E. (1972). Assessment of Aphasia and Related Disorders. Philadelphia: Lea and Febinger.
  • Kay, J., Lesser, R., & Coltheart, M. (1992). Psycholinguistic Assessments of Language Processing in Aphasia (PALPA). Hove: Erlbaum.
  • Spreen, O. & Risser, A.H. (2003). Assessment of Aphasia. New York: Oxford University Press.
  • Tesak, Jürgen. Milestones in the history of aphasia: theories and protagonists. Hove, New York. Psychology Press: 2008.
  • LaPointe, Leonard L. Aphasia and related neurogenic language disorders. New York: Thieme: 2005
  • Duchan, Judith Felson. Byng, Sally. Challenging Aphasia Therapies: Broadening the Discourse and Extending the Boundaries. Hove, New York. Psychology Press: 2004.
  • Papathanasiou, Ilias. De Bleser, Ria. The sciences of aphasia : from therapy to theory. Amsterdam/Boston. Pergamon: 2003

[edit] Personal experiences of aphasia

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

[edit] References

  1. ^ Brookshire, 1992; Goodglass 1993
  2. ^ B.E. Murdoch: Acquired Neurological Speech/Language Disorders in Childhood: Language Disorders in Childhood (1990)
  3. ^ a b B.T. Woods: Acquired Childhood Aphasia, in: H.S. Kirshner: Handbook of neurological speech and language disorders (1994).
  4. ^ P.F. Paquier & H.R. van Dongen: Is Acquired Childhood Aphasia Atypical? In: P. Coppens et al.: Aphasia in Atypical Populations (1998)
  5. ^ D.P: Cantwell: Developmental Speech and Language Disorders (1987)
  6. ^ Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003), page 502, 505, 511.
  7. ^ Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003), pages 502-504. The whole paragraph "fluent, non-fluent and pure aphasias" is written with help of this reference.
  8. ^ http://christofflab.psych.ubc.ca/psych260/docs/L12-Language.pdf
  9. ^ Paul R. McCrory and Samuel F. Berkovic (2001). Concussion: The history of clinical and pathophysiological concepts and misconceptions. Neurology, 57(12): 2283-2289. PMID 11756611.
  10. ^ Richardson, Robert D. Jr. Emerson: The Mind on Fire. Berkeley, California: University of California Press, 1995: 569. ISBN 0-520-08808-5.

[edit] External links

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