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Classification and external resources
ICD-10F80.0-F80.2, R47.0
ICD-9315.31, 784.3, 438.11
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Classification and external resources
ICD-10F80.0-F80.2, R47.0
ICD-9315.31, 784.3, 438.11
Classification and external resources
ICD-10F80.1, F80.2, R47.0
ICD-9438.12, 784.5

Aphasia (/əˈfʒə/, /əˈfziə/ or /ˈfziə/; from ancient Greek aphatos meaning[1] ἀφασία (ἄφατος, ἀ- + φημί), "speechlessness",[2] derived from phat meaning "spoken"[3]) is a disturbance of the comprehension and formulation of language caused by dysfunction in specific brain regions.[4][5] This class of language disorder ranges from having difficulty remembering words to losing the ability to speak, read, or write. This also affects visual language such as sign language.[5] Aphasia is usually linked to brain damage, most commonly caused by stroke. Brain damage linked to aphasia can also cause further brain diseases, including cancer, epilepsy and Alzheimer's disease.[6]

Acute aphasia disorders usually develop quickly as a result of head injury or stroke, and progressive forms of aphasia develop slowly from a brain tumor, infection, or dementia.[4][7][8] The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms. Aphasia types include expressive aphasia, receptive aphasia, conduction aphasia, anomic aphasia, global aphasia, primary progressive aphasias and many others. Medical evaluations for the disorder range from clinical screenings by a neurologist to extensive tests by a speech-language pathologist.[4][7] Most acute aphasia patients can recover some or most skills by working with a speech-language pathologist. This rehabilitation can take two or more years and is most effective when begun quickly. Only a small minority will recover without therapy, such as those suffering a transient ischemic attack. 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.[7]


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 do not exist. The neural organization of language is complicated; language is a comprehensive and complex behavior and it makes sense that it is not 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.[9]

Localizationist model[edit]


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. [10] 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".

  1. Auditory verbal agnosia (also known as Pure Word Deafness)
  2. Conduction aphasia
  3. Apraxia of speech (now considered a separate disorder in itself)
  4. Transcortical motor aphasia (also known as Adynamic aphasia and Extrasylvian motor aphasia)
  5. Transcortical sensory aphasia

Progressive aphasias[edit]

Primary progressive aphasia (PPA) is associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimer's disease, which is the gradual process of losing the ability to think. It is characterized by the gradual loss of the ability to name objects. People suffering from PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence.[15][16][17] There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA)[17][18]

Progressive Jargon Aphasia is a fluent or receptive aphasia in which the patient's speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the patient has problems with the selection of nouns. Either they will 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. As such, patients with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they cannot find with sounds. Substitutions commonly 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).

Fluent, non-fluent, and "pure" aphasias[edit]

The different types of aphasia can be divided into three categories: fluent, non-fluent, and "pure" aphasias.[19]

Primary and secondary cognitive processes[edit]

Aphasias can be divided into primary and secondary cognitive processes.

Cognitive neuropsychological model[edit]

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 with a specific function.[21] Hence, there is a module that recognises phonemes as they are spoken and a module that stores formulated phonemes before they are spoken. In the clinical setting, use of this model 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" [22]), 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.

Deaf aphasia[edit]

There have been many instances showing that there is a form of aphasia among deaf individuals. Sign language is, after all, a form of communication that has been shown to use the same areas of the brain as verbal forms of communication. Mirror neurons become activated when an animal is acting in a particular way or watching another individual act in the same manner. These mirror neurons are important in giving an individual the ability to mimic movements of hands. Broca's area of speech production has been shown to contain several of these mirror neurons resulting in significant similarities of brain activity between sign language and vocal speech communication. Facial communication is a significant portion of how animals interact with each other. Humans use facial movements to create, what other humans perceive, to be faces of emotions. While combining these facials movements with speech, a more full form of language is created and enable the species to interact with a much more complex and detailed form of communication. Sign language also uses these facial movements and emotions along with the primary hand movement way of communicating. These facial movement forms of communication come from the same areas of the brain. When dealing with damages to certain areas of the brain, vocal forms of communication are in jeopardy of severe aphasias. Since these same areas of the brain are being used for sign language, these same, at least very similar, forms of aphasia can show in the deaf community. Individuals can show a form of Wernicke's aphasia with sign language and they show deficits in their abilities in being able show any form of expressions. Broca's aphasia shows up in some patients, as well. These individuals find tremendous difficulty in being able to actually sign the words they are trying to express.[23]

Signs and symptoms[edit]

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


Acute aphasias

The following table summarizes some major characteristics of different acute aphasias:

Type of aphasiaRepetitionNamingAuditory comprehensionFluency
Receptive aphasiamild–modmild–severedefectivefluent paraphasic
Transcortical sensory aphasiagoodmod–severepoorfluent
Conduction aphasiapoorpoorrelatively goodfluent
Anomic aphasiamildmod–severemildfluent
Expressive aphasiamod–severemod–severemild difficultynon-fluent, effortful, slow
Transcortical motor aphasiagoodmild–severemildnon-fluent
Global aphasiapoorpoorpoornon-fluent
Mixed transcortical aphasiamoderatepoorpoornon-fluent

Subcortical aphasias


Aphasia usually results from lesions to the language-relevant areas of the frontal, temporal and parietal lobes of the brain, such as Broca's area, Wernicke's area, and the neural pathways between them. These areas are almost always located in the left hemisphere, and in most people this is where the ability to produce and comprehend language is found. However, in a very small number of people, language ability is found in the right hemisphere. In either case, damage to these language areas can be caused by a stroke, traumatic brain injury, or other brain injury.

Aphasia may also develop slowly, as in the case of a brain tumor or progressive neurological disease, e.g., Alzheimer's or Parkinson's disease. It may also be caused by a sudden hemorrhagic event within the brain. Certain chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia as a prodromal or episodic symptom.[25]

Aphasia can result from herpesviral encephalitis.[26] The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia.[27]

Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain.[28][29] Adverse side effects including chronic aphasia can be caused by cortico-steroids.[citation needed]


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 is no consistency on treatment methodology in literature, there is a strong indication that treatment in general has positive outcomes.[30]

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.[30]

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 that targets deficits with specific exercises[30]

Several treatment techniques include the following:

More recently, computer technology has been incorporated into treatment options. A key indication for good prognosis is treatment intensity. A minimum of two–three hours per week has been specified to produce positive results.[32] 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.[32]

Several examples of programs used are StepByStep, Lingraphica, Computer-Based Visual Communication (C-VIC), TouchSpeak (TS), and Sentence Shaper.[32]

Melodic intonation therapy is often used to treat non-fluent aphasia and has proved to be very effective in some cases.[33]


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.[34] During the second half of the 19th century, Aphasia was a major focus for scientists and philosophers who were working in the beginning stages in the field of psychology.[5]


Following are some precautions that should be taken to avoid aphasia:

Notable cases[edit]

See also[edit]


  1. ^ a b What Is Aphasia? What Causes Aphasia?
  2. ^ ἀφασία, Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus.
  3. ^ http://dictionary.reference.com/browse/aphasia
  4. ^ a b c "American Speech-Language-Hearing Association (ASHA):- Aphasia". 
  5. ^ a b c Damasio, A.R. (February 1992). "Aphasia.". N Engl J Med 326 (8): 531–9. doi:10.1056/NEJM199202203260806 . PMID 1732792. 
  6. ^ Carenotes, "General Information: Aphasia", Truven Health Analytics Inc., 2012(subscription required)
  7. ^ a b c "Aphasia". MedicineNet.com. Retrieved 2011-05-23. 
  8. ^ Budd, M.A.; Kortte, K.; Cloutman, L.; et al. (September 2010). "The nature of naming errors in primary progressive aphasia versus acute post-stroke aphasia". Neuropsychology 24 (5): 581–9. doi:10.1037/a0020287 . PMC 3085899. PMID 20804246. 
  9. ^ Kolb, Bryan; Whishaw, Ian Q. (2003). Fundamentals of human neuropsychology. [New York]: Worth. pp. 502, 505, 511. ISBN 0-7167-5300-6. OCLC 464808209. 
  10. ^ Kennison, Shelia (2013). Introduction to language development. Los Angeles: Sage. 
  11. ^ Dronkers NF, Plaisant O, Iba-Zizen MT, Cabanis EA (May 2007). "Paul Broca's historic cases: high resolution MR imaging of the brains of Leborgne and Lelong". Brain 130 (Pt 5): 1432–41. doi:10.1093/brain/awm042 . PMID 17405763. 
  12. ^ Masdeu, Joseph (June 2000). "Aphasia". Archives of Neurology 57 (6). 
  13. ^ Sarno, Martha Taylor (2007). Neurogenic disorders of speech and language.. In Thomas J Schmitz, Susan B. O'Sullivan,. "Neurogenic disorders of speech and language". Physical rehabilitation (5 ed.) (Philadelphia: F.A. Davis). ISBN 0-8036-1247-8. OCLC 70119705. 
  14. ^ a b Carlson, Neil (2007). Psychology the Science of Behaviour. Toronto: Pearson. p. 278. ISBN 978-0-205-64524-4. 
  15. ^ Mesulam MM (April 2001). "Primary progressive aphasia". Ann. Neurol. 49 (4): 425–32. doi:10.1002/ana.91 . PMID 11310619. 
  16. ^ Wilson SM, Henry ML, Besbris M, et al. (July 2010). "Connected speech production in three variants of primary progressive aphasia". Brain 133 (Pt 7): 2069–88. doi:10.1093/brain/awq129 . PMC 2892940. PMID 20542982. 
  17. ^ a b Harciarek M, Kertesz A (September 2011). "Primary progressive aphasias and their contribution to the contemporary knowledge about the brain-language relationship". Neuropsychol Rev 21 (3): 271–87. doi:10.1007/s11065-011-9175-9 . PMC 3158975. PMID 21809067. 
  18. ^ Gorno-Tempini ML, Hillis AE, Weintraub S, et al. (March 2011). "Classification of primary progressive aphasia and its variants". Neurology 76 (11): 1006–14. doi:10.1212/WNL.0b013e31821103e6 . PMC 3059138. PMID 21325651. 
  19. ^ 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. 
  20. ^ Rohrer JD, Knight WD, Warren JE, Fox NC, Rossor MN, Warren JD (January 2008). "Word-finding difficulty: a clinical analysis of the progressive aphasias". Brain 131 (Pt 1): 8–38. doi:10.1093/brain/awm251 . PMC 2373641. PMID 17947337. 
  21. ^ Luria's Areas of the Human Cortex Involved in Language Illustrated summary of Luria's book Traumatic Aphasia
  22. ^ Coltheart, Max; Kay, Janice; Lesser, Ruth (1992). PALPA psycholinguistic assessments of language processing in aphasia. Hillsdale, N.J: Lawrence Erlbaum Associates. ISBN 0-86377-166-1. 
  23. ^ Carlson, Neil (2013). Physiology of Behavior. New York: Pearson. pp. 494–496. 
  24. ^ Alexander, Michael P; Hillis, Argye E. (2008). "Aphasia". In Georg Goldenberg; Bruce L Miller; Michael J Aminoff; Francois Boller; D F Swaab. Handbook of Clinical Neurology 88 (1 ed.). pp. 287–310. doi:10.1016/S0072-9752(07)88014-6 . ISBN 9780444518972. OCLC 733092630. 
  25. ^ Quigg M, Fountain NB (March 1999). "Conduction aphasia elicited by stimulation of the left posterior superior temporal gyrus". J. Neurol. Neurosurg. Psychiatr. 66 (3): 393–6. doi:10.1136/jnnp.66.3.393 . PMC 1736266. PMID 10084542. 
  26. ^ Soares-Ishigaki, EC.; Cera, ML.; Pieri, A.; Ortiz, KZ. (2012). "Aphasia and herpes virus encephalitis: a case study". Sao Paulo Med J 130 (5): 336–41. doi:10.1590/S1516-31802012000500011 . PMID 23174874. 
  27. ^ Naudé, H; Pretorius, E. (03 Jun 2010). "Can herpes simplex virus encephalitis cause aphasia?". Early Child Development and Care 173 (6): 669–679. doi:10.1080/0300443032000088285 . Retrieved 2013-06-08. 
  28. ^ "Fentanyl Transdermal Official FDA information, side effects and uses". Drug Information Online. 
  29. ^ "FENTANYL TRANSDERMAL SYSTEM patch, extended release". DailyMed. Retrieved 2013-06-08. 
  30. ^ a b c d Schmitz, Thomas J.; O'Sullivan, Susan B. (2007). Physical rehabilitation. Philadelphia: F.A. Davis. ISBN 0-8036-1247-8. OCLC 70119705. 
  31. ^ Alexander, Michael P; Hillis, Argye E (2008). "Aphasia". In Georg Goldenberg; Bruce L Miller; Michael J Aminoff; Francois Boller; D F Swaab. Neuropsychology and Behavioral Neurology: Handbook of Clinical Neurology 88. Elsevier Health Sciences. pp. 287–310. ISBN 978-0-444-51897-2. OCLC 733092630. 
  32. ^ a b c van de Sandt-Koenderman WM (February 2011). "Aphasia rehabilitation and the role of computer technology: can we keep up with modern times?". Int J Speech Lang Pathol 13 (1): 21–7. doi:10.3109/17549507.2010.502973 . PMID 21329407. 
  33. ^ Norton A, Zipse L, Marchina S, Schlaug G (July 2009). "Melodic intonation therapy: shared insights on how it is done and why it might help". Ann. N. Y. Acad. Sci. 1169: 431–6. doi:10.1111/j.1749-6632.2009.04859.x . PMC 2780359. PMID 19673819. 
  34. ^ McCrory PR, Berkovic SF (December 2001). "Concussion: the history of clinical and pathophysiological concepts and misconceptions". Neurology 57 (12): 2283–9. doi:10.1212/WNL.57.12.2283 . PMID 11756611. 
  35. ^ 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[edit]