Aphasia

Not to be confused with Aphagia. 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/, /əˈfeɪziə/ or /eɪˈfeɪziə/; from Greek a- ("without") + phásis (φάσις, "speech")) is the name given to a collection of language disorders caused by damage to the brain.[1][2] The word aphasia comes from the word ἀφασία aphasia, in Ancient Greek, which means[3] "speechlessness",[4] derived from ἄφατος aphatos, "speechless"[5] from ἀ- a-, "not, un" and φημί phemi, "I speak". A requirement for a diagnosis of aphasia is that, prior to the illness or injury, the person's language skills were normal (for developmental language disorders, see specific language impairment). The difficulties of people with aphasia can range from occasional trouble finding words to losing the ability to speak, read, or write, but does not affect intelligence.[1] This also affects visual language such as sign language.[2] The term "aphasia" implies a problem with one or more functions that are essential and specific to language function. It is not usually used when the language problem is a result of a more peripheral motor or sensory difficulty, such as paralysis affecting the speech muscles or a general hearing impairment.

Causes

Aphasia is most commonly caused by stroke.[6] It can also be caused by other brain diseases, including cancer (brain tumor), epilepsy, and Alzheimer's disease, or by a head injury.[7] In rare cases, aphasia may also result from herpesviral encephalitis.[8] The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia.[9] In acute disorders, such as head injury or stroke, aphasia usually develops quickly. Aphasia usually develops more slowly from a brain tumor, infection, or dementia.[1][10][11]

Although all of the disease listed above are potential causes, aphasia will generally only result when there is substantial damage to the left hemisphere of the brain, either the cortex (outer layer) and/or the underlying white matter. Substantial damage to tissue anywhere within the region shown in blue on the figure below can potentially result in aphasia.[12] Aphasia can also sometimes be caused by damage to subcortical structures deep within the left hemisphere, including the thalamus, the internal and external capsules, and the caudate nucleus of the basal ganglia.[13][14] The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms.[1][10] A very small number of people can experience aphasia after damage to the right hemisphere only. It has been suggested that these individuals may have had an unusual brain organization prior to their illness or injury, with perhaps greater overall reliance on the right hemisphere for language skills than in the general population.[15][16]

Regions of the left hemisphere that can give rise to aphasia when damaged (schematic diagram based on findings of Henseler, Regenbrecht and Obrig, 2014). doi:10.1093/brain/awt374

Finally, certain chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia as a prodromal or episodic symptom.[17] Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain.[18][19]

Classification

Aphasia is best thought of as a collection of different disorders, rather than a single problem. Each individual with aphasia will present with their own particular combination of language strengths and weaknesses. Consequently, it is a major challenge just to document the various difficulties that can occur in different people, let alone decide how they might best be treated. Most classifications of the aphasias tend to divide the various symptoms into broad classes. A common approach is to distinguish between the fluent aphasias (where speech remains fluent, but content may be lacking, and the person may have difficulties understanding others), and the nonfluent aphasias ( where speech is very halting and effortful, and may consist of just one or two words at a time).

However, no such broad-based grouping has proven fully adequate. There is a huge variation among patients within the same broad grouping, 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.[20]

Classical-Localizationist approaches

Cortex

Localizationist approaches aim to classify the aphasias according to their major presenting characteristics and the regions of the brain that most probably gave rise to them.[21][22] Inspired by the early work of nineteenth century neurologists Paul Broca and Carl Wernicke, these approaches identify two major subtypes of aphasia and several more minor subtypes:

Recent classification schemes adopting this approach, such as the "Boston-Neoclassical Model" [21] also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Broca's aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernicke's aphasia, conduction aphasia and transcortical sensory aphasia). These schemes also identify several further aphasia subtypes, including: Anomic aphasia, which is characterized by a selective difficulty finding the names for things; and Global aphasia where both expression and comprehension of speech are severely compromised.

Many localizationist approaches also recognize the existence of additional, more "pure" forms of language disorder that may affect only a single language skill.[23] For example, in Pure alexia, a person may be able to write but not read, and in Pure word deafness, they may be able to produce speech and to read, but not understand speech when it is spoken to them.

Cognitive neuropsychological approaches

Although localizationist approaches provide a useful way of classifying the different patterns of language difficulty into broad groups, one problem is that a sizeable number of individuals do not fit neatly into one category or another.[24][25] Another problem is that the categories, particularly the major ones such as Broca's and Wernicke's aphasia, still remain quite broad. Consequently, even amongst individuals who meet the criteria for classification into a subtype, there can be enormous variability in the types of difficulties they experience.

Instead of categorizing every individual into a specific subtype, cognitive neuropsychological approaches aim to identify the key language skills or "modules" that are not functioning properly in each individual. A person could potentially have difficulty with just one module, or with a number of modules. This type of approach requires a framework or theory as to what skills/modules are needed to perform different kinds of language tasks. For example, the model of Max Coltheart identifies a module that recognizes phonemes as they are spoken, which is essential for any task involving recognition of words. Similarly, there is a module that stores phonemes that the person is planning to produce in speech, and this module is critical for any task involving the production of long words or long strings of speech. One a theoretical framework has been established, the functioning of each module can then be assessed using a specific test or set of tests. In the clinical setting, use of this model usually involves conducting a battery of assessments,[26][27] each of which tests one or a number of these modules. Once a diagnosis is reached as to the skills/modules where the most significant impairment lies, therapy can proceed to treat these skills.

In practice, the cognitive neuropsychological approach can be unwieldy due to the wide variety of skills that can potentially be tested. Also, it is perhaps best suited to milder cases of aphasia: If the person has little expressive or receptive language ability, sometimes test performance can be difficult to interpret. In practice, clinicians will often use a blend of assessment approaches, which include broad subtyping based on a localizationist framework, and some finer exploration of specific language skills based on the cognitive neuropsychological framework.

Other forms of aphasia

Progressive aphasias

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 progressively 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.[28][29][30] There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA)[30][31]

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).

Deaf aphasia

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 which enables 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 forms of aphasia. 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 to produce 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 linguistic concepts they are trying to express.[32]

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. Aphasia symptoms can vary based on the location of damage in the brain. Signs and symptoms may or may not be present in individuals with aphasia and may vary in severity and level of disruption to communication.[33] Often those with aphasia will try to hide their inability to name objects by using words like thing. So when asked to name a pencil they may say it is a thing used to write.[34]

  • 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 (anomia)
  • poor enunciation
  • excessive creation and use of personal neologisms
  • inability to repeat a phrase
  • persistent repetition of one syllable, word, or phrase (stereotypies)
  • 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
  • speech disorder
  • Speaking gibberish
  • inability to follow or understand simple requests

Presentation

Acute aphasias

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

Type of aphasia Repetition Naming Auditory comprehension Fluency
Receptive aphasia mild–mod mild–severe defective fluent paraphasic
Transcortical sensory aphasia good mod–severe poor fluent
Conduction aphasia poor mild relatively good fluent
Anomic aphasia mild mod–severe mild fluent
Expressive aphasia mod–severe mod–severe mild difficulty non-fluent, effortful, slow
Transcortical motor aphasia good mild–severe relatively good non-fluent
Global aphasia poor poor poor non-fluent
Mixed transcortical aphasia moderate poor poor non-fluent

Subcortical aphasias

Management

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. After the onset of Aphasia, there is approximately a six-month period of spontaneous recovery. During this time, the brain is attempting to recover and repair the damaged neurons. Therapy for Aphasia during this time facilitates an even greater level of recovery than if no intervention was given at this time.[37] 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.[10]

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.[38] Therapy for aphasia ranges from increasing functional communication to improving speech accuracy, depending on the person's severity, needs and support of family and friends.[39]

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.[38]

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[38]

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.[42] 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.[42]

Several examples of programs used are StepByStep, Lingraphica, Computer-Based Visual Communication (C-VIC), TouchSpeak (TS), and Sentence Shaper.[42]

Melodic intonation therapy is often used to treat non-fluent aphasia and has proved to be very effective in some cases.[43] MIT is used to help people with aphasia vocalize themselves through speech song which is then transferred as a spoken word. Good candidates for this therapy include left hemisphere stroke patients, non-fluent aphasias such as Broca's, good auditory comprehension, poor repetition and articulation, and good emotional stability and memory.[44] It has been hypothesized that MIT is effective because prosody and singing is located within the right hemisphere; it is these right hemisphere language areas that are recruited for normal speech production.[45]

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.[46] 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.[2]

Prevention

Following are some precautions that should be taken to avoid aphasia, by decreasing the risk of stroke, the main cause of aphasia:

Notable cases

See also

References

  1. ↑ 1.0 1.1 1.2 1.3 "American Speech-Language-Hearing Association (ASHA):- Aphasia".
  2. ↑ 2.0 2.1 2.2 Damasio, A.R. (February 1992). "Aphasia.". N Engl J Med 326 (8): 531–9. doi:10.1056/NEJM199202203260806. PMID 1732792.
  3. ↑ 3.0 3.1 What Is Aphasia? What Causes Aphasia?
  4. ↑ ἀφασία, Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus.
  5. ↑ ἄφατος, Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus.
  6. ↑ Manasco, M.H. (2014). Introduction to Neurogenic Communication Disorders. Burlington: Jones & Bartlett Learning.
  7. ↑ Carenotes, "General Information: Aphasia", Truven Health Analytics Inc., 2012 (subscription required)
  8. ↑ 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.
  9. ↑ Naudé, H; Pretorius, E. (3 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.
  10. ↑ 10.0 10.1 10.2 "Aphasia". MedicineNet.com. Retrieved 2011-05-23.
  11. ↑ 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.
  12. ↑ Henseler, I; Regenbrecht, F; Obrig, H (March 2014). "Lesion correlates of patholinguistic profiles in chronic aphasia: comparisons of syndrome-, modality- and symptom-level assessment.". Brain : a journal of neurology 137 (Pt 3): 918–30. doi:10.1093/brain/awt374. PMID 24525451.
  13. ↑ Kuljic-Obradovic, DC (July 2003). "Subcortical aphasia: three different language disorder syndromes?". European journal of neurology : the official journal of the European Federation of Neurological Societies 10 (4): 445–8. doi:10.1046/j.1468-1331.2003.00604.x. PMID 12823499.
  14. ↑ Kreisler, A; Godefroy, O; Delmaire, C; Debachy, B; Leclercq, M; Pruvo, JP; Leys, D (14 March 2000). "The anatomy of aphasia revisited.". Neurology 54 (5): 1117–23. doi:10.1212/wnl.54.5.1117. PMID 10720284.
  15. ↑ Coppens, P; Hungerford, S; Yamaguchi, S; Yamadori, A (December 2002). "Crossed aphasia: an analysis of the symptoms, their frequency, and a comparison with left-hemisphere aphasia symptomatology.". Brain and Language 83 (3): 425–63. doi:10.1016/s0093-934x(02)00510-2. PMID 12468397.
  16. ↑ Mariën, P; Paghera, B; De Deyn, PP; Vignolo, LA (February 2004). "Adult crossed aphasia in dextrals revisited.". Cortex; a journal devoted to the study of the nervous system and behavior 40 (1): 41–74. doi:10.1016/s0010-9452(08)70920-1. PMID 15070002.
  17. ↑ 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.
  18. ↑ "Fentanyl Transdermal Official FDA information, side effects and uses". Drug Information Online.
  19. ↑ "FENTANYL TRANSDERMAL SYSTEM patch, extended release". DailyMed. Retrieved 2013-06-08.
  20. ↑ Kolb, Bryan; Whishaw, Ian Q. (2003). Fundamentals of human neuropsychology. [New York]: Worth. pp. 502, 505, 511. ISBN 0-7167-5300-6. OCLC 464808209.
  21. ↑ 21.0 21.1 Goodglass, H., Kaplan, E., & Barresi, B. (2001). The assessment of aphasia and related disorders. Lippincott Williams & Wilkins.
  22. ↑ Kertesz, A. (2006). Western Aphasia Battery-Revised (WAB-R). Austin, TX: Pro-Ed.
  23. ↑ Kolb, Bryan; Whishaw, Ian Q. (2003). Fundamentals of human neuropsychology. [New York]: Worth. pp. 502–504. ISBN 0-7167-5300-6. OCLC 464808209.
  24. ↑ Godefroy O., Dubois C., Debachy B., Leclerc M., Kreisler A. (2002). "Vascular aphasias: main characteristics of patients hospitalized in acute stroke units". Stroke 33: 702–705. doi:10.1161/hs0302.103653.
  25. ↑ Ross K.B., Wertz R.T. (2001). "Type and severity of aphasia during the first seven months poststroke". Journal of Medical Speech-Language Pathology 9: 31–53.
  26. ↑ 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.
  27. ↑ Porter, G., & Howard, D. (2004). CAT: comprehensive aphasia test. Psychology Press.
  28. ↑ Mesulam MM (April 2001). "Primary progressive aphasia". Ann. Neurol. 49 (4): 425–32. doi:10.1002/ana.91. PMID 11310619.
  29. ↑ 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.
  30. ↑ 30.0 30.1 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.
  31. ↑ 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.
  32. ↑ Carlson, Neil (2013). Physiology of Behavior. New York: Pearson. pp. 494–496.
  33. ↑ American Speech-Language-Hearing Association (1997-2014)
  34. ↑ Nolen-Hoeksema, S. (2014). Neurodevelopmental and Neurocognitive Disorders. In Abnormal Psychology (6th ed.). New York: McGraw-Hill.
  35. ↑ Manasco, Hunter (2014). Introduction to Neurogenic Communication Disorders. Jones & Bartlett Learning. p. 71.
  36. ↑ Alexander, Michael P; Hillis, Argye E. (2008). Georg Goldenberg; Bruce L Miller; Michael J Aminoff; Francois Boller; D F Swaab, ed. Aphasia. Handbook of Clinical Neurology 88 (1 ed.). pp. 287–310. doi:10.1016/S0072-9752(07)88014-6. ISBN 9780444518972. OCLC 733092630.
  37. ↑ Manasco, M. Hunter (2014). Introduction to Neurogenic Communication Disorders. Burlington, MA: Jones and Bartlett Learning. ISBN 978-1-4496-5244-9.
  38. ↑ 38.0 38.1 38.2 38.3 Schmitz, Thomas J.; O'Sullivan, Susan B. (2007). Physical rehabilitation. Philadelphia: F.A. Davis. ISBN 0-8036-1247-8. OCLC 70119705.
  39. ↑ http://www.asha.org/PRPSpecificTopic.aspx?folderid=8589934663&section=Treatment
  40. ↑ 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.
  41. ↑ Manasco, Hunter. "The Aphasias". Introduction to Neurogenic Communcation Disorders. p. 93.
  42. ↑ 42.0 42.1 42.2 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.
  43. ↑ 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.
  44. ↑ van der Meulen, I; van de Sandt-Koenderman, ME; Ribbers, GM (January 2012). "Melodic Intonation Therapy: present controversies and future opportunities.". Archives of physical medicine and rehabilitation 93 (1 Suppl): S46–52. doi:10.1016/j.apmr.2011.05.029. PMID 22202191.
  45. ↑ http://www.clinicaltrials.gov/ct2/show/NCT00903266
  46. ↑ 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.
  47. ↑ Richardson, Robert G. (1995). Emerson: the mind on fire: a biography. Berkeley: University of California Press. ISBN 0-520-08808-5. OCLC 31206668.

Sources

External links

Look up aphasia or aphemia in Wiktionary, the free dictionary.