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Aphasia

  • Author: Howard S Kirshner, MD; Chief Editor: Jasvinder Chawla, MD, MBA  more...
 
Updated: Feb 19, 2016
 

Practice Essentials

Aphasia is an acquired disorder of language due to brain damage. It may occur secondary to brain injury or degeneration and involves the left cerebral hemisphere to a greater extent than the right.

Signs and symptoms

Aphasia develops abruptly in patients with a stroke or head injury. Patients with neurodegenerative diseases or mass lesions may develop aphasia insidiously.

People with aphasia may exhibit the following symptoms:

  • Difficulty using words and sentences (expressive aphasia)
  • Difficulty understanding others (receptive aphasia)
  • Difficulty with both using words and understanding (global aphasia)

Patients may also experience problems with spoken and written language. Typically, reading and writing are more impaired than talking or understanding.

See Clinical Presentation for more detail.

Diagnosis

Careful assessment of language function with an evaluation of neighborhood signs is important in the diagnosis of the localization and cause of aphasia. These signs include:

  • difficulties with vision, especially hemianopia
  • deficits of motor or sensory function
  • neurobehavioral deficits such as alexia, agraphia, acalculia, or apraxia

Bedside examination

Components of bedside language examination include assessments of spontaneous speech, naming, repetition, comprehension, reading, and writing. Although bedside examination can usually reveal the type of aphasia, formal cognitive testing by a neuropsychologist or speech/language therapist may be important to determine fine levels of dysfunction, to plan therapy, and to assess the patient's potential for recovery.

Imaging tests

Because aphasia is most often caused by stroke, neuroimaging is required to localize and diagnose the cause of aphasia. CT scanning and MRI are the mainstays of neuroimaging.

See Workup for more detail.

Management

The treatment of a patient with aphasia depends on the cause of the aphasia syndrome. Acute stroke treatment for the aphasic patient, such as intravenous tPA, intra-arterial interventional treatments, carotid endarterectomy and stenting, or even blood pressure manipulation may help to alleviate the deficit. Surgery for a subdural hematoma or brain tumor may be beneficial. In infections such as herpes simplex encephalitis, antiviral therapy may help the patient recover.

If brain damage is mild, a person may recover language skills without treatment. However, most people undergo speech and language therapy to rehabilitate their language skills and supplement their communication experiences. Speech and language therapy is the mainstay of care for patients with aphasia.

See Treatment and Medication for more detail.

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Background

Aphasia is an acquired disorder of language due to brain damage. Aphasia does not include (1) developmental disorders of language, often called dysphasia in the United States; (2) purely motor speech disorders, limited to articulation of speech via the oral-motor apparatus, referred to as stuttering, dysarthria, and apraxia of speech; or (3) disorders of language that are secondary to primary thought disorders, such as schizophrenia.

Encompassed under the term aphasia are selective, acquired disorders of reading (alexia) or writing (agraphia). Closely related to aphasia are the family of disorders called apraxias (disorders of learned or skilled movements), agnosias (disorders of recognition), acalculias (disorders of calculation ability), and more global neurobehavioral deficits such as dementia and delirium. Such related syndromes may coexist with aphasia or exist independently.

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Pathophysiology

Aphasia may occur secondary to brain injury or degeneration and involves the left cerebral hemisphere to a greater extent than the right. Language function lateralizes to the left hemisphere in 96-99% of right-handed people and 60% of left-handed people. Of the remaining left-handed people, about one half have mixed hemisphere language dominance, and about one half have right hemisphere dominance. Left-handed individuals may develop aphasia after a lesion of either hemisphere, but the syndromes from left hemisphere injury may be milder or more selective than those seen in right-handed people.

Most aphasias and related disorders are due to stroke, head injury, cerebral tumors, or degenerative diseases. The neuroanatomic substrate of language comprehension and production is complex, including auditory input and language decoding in the superior temporal lobe, analysis in the parietal lobe, and expression in the frontal lobe, descending via the corticobulbar tracts to the internal capsule and brainstem, with modulatory effects of the basal ganglia and the cerebellum.

Aphasia syndromes have been described based on patterns of abnormal language expression, repetition, and comprehension. These classical syndromes have been roughly correlated with specific left hemisphere locations, though clear overlaps and individual differences make the aphasia syndromes limited in specificity. Patients may lose the ability to produce speech, to comprehend speech, to repeat, and to hear and read words in many nuanced ways. Classical aphasia syndromes (see Aphasia syndromes in History) include global, Broca, Wernicke, and conduction aphasia, as well as transcortical motor, transcortical sensory, and transcortical mixed aphasia. Pure alexia and optic aphasia are often discussed with the classical aphasias.

Language function can be parsed in several important ways other than assignment to the classical aphasia syndromes. A variety of types of evidence have noted that certain specific language functions (such as naming pictures) activate widespread neural networks involving many parts of both hemispheres of the brain. Producing, receiving, and interpreting speech requires specific and distinct cognitive processes such as phonologic decoding and encoding, orthographic decoding and encoding (for reading), lexical access, lexical-semantic representations of words, and semantic interpretation of language. Differentiation of these processes involves testing patients with different aphasia types and attempting to find double dissociations among groups of patients to determine the neurologic basis of specific cognitive processes.

The lesion method, the principal source of information about aphasia from autopsy studies in the 19th and early to mid 20th centuries and from brain imaging modalities since the 1970s, remains a useful source of information. However, it has been abetted by cortical stimulation studies, mainly in patients with epilepsy, and functional neuroimaging, such as fMRI and PET scanning often carried out during language testing in healthy individuals, to determine the language function of specific areas of the brain.

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Frequency

United States

Data on incidence of aphasia in the United States are limited. Aphasia occurs in a variety of cerebrovascular, traumatic, and degenerative conditions. Stroke is likely the most common cause of aphasia, and it has been estimated that about 20% of stroke patients develop aphasia. More than 700,000 strokes occur in the United States each year, and approximately 170,000 new cases of aphasia every year are related to stroke. The number of patients with language disorders secondary to traumatic brain injury, brain tumors, and other brain lesions such as arteriovenous malformations is not precisely known. Patients with neurodegenerative disorders such as Alzheimer disease and frontotemporal dementia frequently manifest language deficits. The prevalence of Alzheimer disease in the United States is approximately 5 million cases.

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Mortality/Morbidity

Aphasia is a condition, not a disease; therefore, it has no attributable mortality rate.

Race

No reliable data exist on the incidence of aphasia in different racial groups. Within disease entities, however, such differences are well known. In stroke, for example, African Americans have almost a 2-fold higher incidence as compared with whites. In addition, specific types of stroke, such as cerebral hemorrhage, lacunar infarctions, and intracranial artery stenoses, are known to be more common in African Americans than Caucasians. One might therefore surmise that poststroke aphasias would be more common in African Americans.

Sex

Not enough data are available to evaluate differences in the incidence and clinical features of aphasia in men and women. Some studies suggest a lower incidence of aphasia in women because they may have more bilaterality of language function. Differences may also exist in aphasia type, with more women than men developing Wernicke aphasia.

Age

Age may be an important factor in recovery. Some studies suggest that recovery from aphasia due to a stroke is less favorable in patients older than age 70 than in younger patients. However, at any age, recovery of various degrees can occur, even at times remote from the brain injury.

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Contributor Information and Disclosures
Author

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Jasvinder Chawla, MD, MBA Chief of Neurology, Hines Veterans Affairs Hospital; Professor of Neurology, Loyola University Medical Center

Jasvinder Chawla, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Joseph Quinn, MD, MD Assistant Professor, Department of Neurology, Portland VA Medical Center, Oregon Health Sciences University

Joseph Quinn, MD, MD is a member of the following medical societies: American Academy of Neurology, Society for Neuroscience, Society for Pediatric Radiology

Disclosure: Nothing to disclose.

References
  1. Reuters Health. Verbal training during rTMS may improve chronic aphasia. Medscape Medical News. November 25, 2014. [Full Text].

  2. Wang CP, Hsieh CY, Tsai PY, Wang CT, Lin FG, Chan RC. Efficacy of synchronous verbal training during repetitive transcranial magnetic stimulation in patients with chronic aphasia. Stroke. 2014 Dec. 45(12):3656-62. [Medline].

  3. Conroy P, Scowcroft J. Decreasing cues for a dynamic list of noun and verb naming targets: A case-series aphasia therapy study. Neuropsychol Rehabil. 2012 Jan 16. [Medline].

  4. Alexander MP, Naeser MA, Palumbo C. Broca's area aphasias: aphasia after lesions including the frontal operculum. Neurology. 1990 Feb. 40(2):353-62. [Medline].

  5. Kreisler A, Godefroy O, Delmaire C, et al. The anatomy of aphasia revisited. Neurology. 2000 Mar 14. 54(5):1117-23. [Medline].

  6. Naeser MA, Helm-Estabrooks N, Haas G, et al. Relationship between lesion extent in 'Wernicke's area' on computed tomographic scan and predicting recovery of comprehension in Wernicke's aphasia. Arch Neurol. 1987 Jan. 44(1):73-82. [Medline].

  7. Hillis AE, Gold L, Kannan V, et al. Site of the ischemic penumbra as a predictor of potential for recovery of functions. Neurology. 2008 Jul 15. 71(3):184-9. [Medline].

  8. Caramazza A. Minding the facts: a comment on Thompson-Schill et al.'s "A neural basis for category and modality specificity of semantic knowledge". Neuropsychologia. 2000. 38(7):944-9. [Medline].

  9. Geschwind N. Disconnexion syndromes in animals and man. I. Brain. 1965 Jun. 88(2):237-94. [Medline].

  10. Damasio AR, Damasio H. The anatomic basis of pure alexia. Neurology. 1983 Dec. 33(12):1573-83. [Medline].

  11. Naeser MA, Alexander MP, Helm-Estabrooks N, et al. Aphasia with predominantly subcortical lesion sites: description of three capsular/putaminal aphasia syndromes. Arch Neurol. 1982 Jan. 39(1):2-14. [Medline].

  12. Fromm D, Holland AL, Swindell CS, et al. Various consequences of subcortical stroke. Prospective study of 16 consecutive cases. Arch Neurol. 1985 Oct. 42(10):943-50. [Medline].

  13. Alexander MP, Naeser MA, Palumbo CL. Correlations of subcortical CT lesion sites and aphasia profiles. Brain. 1987 Aug. 110 (Pt 4):961-91. [Medline].

  14. Weiller C, Willmes K, Reiche W, et al. The case of aphasia or neglect after striatocapsular infarction. Brain. 1993 Dec. 116 (Pt 6):1509-25. [Medline].

  15. Crosson B. Subcortical Functions in Language and Memory. New York, NY: Guilford; 1992.

  16. Dejerine J. Contribution a l'etude anatomo-pathologique et clinique des differentes varieties de cecite verbales. Memoires Societe Biologie. 1892. 4:61-90.

  17. Benton AL. The fiction of the Gerstmann syndrome. J Neurol Neurosurg Psychiatry. 1961. 24:961-991.

  18. Benton AL. Gerstmann's syndrome. Arch Neurol. 1992 May. 49(5):445-7. [Medline].

  19. Thompson CK, Cho S, Price C, Wieneke C, Bonakdarpour B, Rogalski E, et al. Semantic interference during object naming in agrammatic and logopenic primary progressive aphasia (PPA). Brain Lang. 2012 Jan 12. [Medline].

  20. Lidzba K, Staudt M, Zieske F, Schwilling E, Ackermann H. Prestroke/poststroke fMRI in aphasia: Perilesional hemodynamic activation and language recovery. Neurology. 2012 Jan 11. [Medline].

  21. Berthier ML, Green C, Lara JP, Higueras C, Barbancho MA, Dávila G, et al. Memantine and constraint-induced aphasia therapy in chronic poststroke aphasia. Ann Neurol. 2009 May. 65(5):577-85. [Medline].

  22. Alexander MP, Benson DF, Stuss DT. Frontal lobes and language. Brain Lang. 1989 Nov. 37(4):656-91. [Medline].

  23. Alexander MP, Hiltbrunner B, Fischer RS. Distributed anatomy of transcortical sensory aphasia. Arch Neurol. 1989 Aug. 46(8):885-92. [Medline].

  24. Anderson P. Famous Faces Give Insight to Primary Progressive Aphasia. Available at http://www.medscape.com/viewarticle/809445. Accessed: August 22, 2013.

  25. Appell J, Kertesz A, Fisman M. A study of language functioning in Alzheimer patients. Brain Lang. 1982 Sep. 17(1):73-91. [Medline].

  26. Auerbach SH, Allard T, Naeser M, et al. Pure word deafness. Analysis of a case with bilateral lesions and a defect at the prephonemic level. Brain. 1982 Jun. 105:271-300. [Medline].

  27. Bakar M, Kirshner HS, Wertz RT. Crossed aphasia. Functional brain imaging with PET or SPECT. Arch Neurol. 1996 Oct. 53(10):1026-32. [Medline].

  28. Benson DF, Ardila A. Aphasia. A clinical perspective. First ed. New York: Oxford University Press; 1996. 1: 1-441.

  29. Benton AL, Hamsher K De S, Varney NR, et al. Contributions to Neuropsychological Assessment. New York: Oxford University Press; 1983.

  30. Benton AL, Hamsher KD. Multilingual Aphasia Examination. Iowa City, IA: AJA Associates; 1989.

  31. Bhogal SK, Teasell R, Speechley M. Intensity of aphasia therapy, impact on recovery. Stroke. 2003 Apr. 34(4):987-93. [Medline].

  32. Boatman D, Gordon B, Hart J, et al. Transcortical sensory aphasia: revisited and revised. Brain. 2000 Aug. 123 (Pt 8):1634-42. [Medline].

  33. Bookheimer S. Functional MRI of language: new approaches to understanding the cortical organization of semantic processing. Annu Rev Neurosci. 2002. 25:151-88. [Medline].

  34. Bowers D, Bauer RM, Heilman KM. The nonverbal affect lexicon: theoretical perspectives from neuropsychological studies of affect perception. Neuropsychology. 1993. 7:433-44.

  35. Broca P. Remarques sur le siege de la faculte du language articule, suivies d'une observation d'aphemie. Bull Soc Anat Paris. 1861. 2:330-57.

  36. Catani M, Jones DK, ffytche DH. Perisylvian language networks of the human brain. Ann Neurol. 2005 Jan. 57(1):8-16. [Medline].

  37. Catani M, Mesulam M. The arcuate fasciculus and the disconnection theme in language and aphasia: history and current state. Cortex. 2008 Sep. 44(8):953-61. [Medline].

  38. Cummings JL, Benson F, Hill MA, et al. Aphasia in dementia of the Alzheimer type. Neurology. 1985 Mar. 35(3):394-7. [Medline].

  39. Damasio AR. Aphasia. N Engl J Med. 1992 Feb 20. 326(8):531-9. [Medline].

  40. de Boissezon X, Peran P, de Boysson C, et al. Pharmacotherapy of aphasia: myth or reality?. Brain Lang. 2007 Jul. 102(1):114-25. [Medline].

  41. De Renzi E, Vignolo LA. The token test: A sensitive test to detect receptive disturbances in aphasics. Brain. 1962 Dec. 85:665-78. [Medline].

  42. DeWitt LD, Grek AJ, Buonanno FS, et al. MRI and the study of aphasia. Neurology. 1985 Jun. 35(6):861-5. [Medline].

  43. Freedman M, Alexander MP, Naeser MA. Anatomic basis of transcortical motor aphasia. Neurology. 1984 Apr. 34(4):409-17. [Medline].

  44. Freund CS. Uber optische Aphasie und Seelenblindheit. Archiv Psychiatrie Nervenkrankheiten. 1889. 20:276-97.

  45. Gefen T, Wieneke C, Martersteck A, Whitney K, Weintraub S, Mesulam MM, et al. Naming vs knowing faces in primary progressive aphasia: A tale of 2 hemispheres. Neurology. 2013 Aug 13. 81(7):658-64. [Medline].

  46. Goodglass H, Kaplan E. The Assessment of Aphasia and Related Disorders. Philadelphia, PA: Lea and Febiger; 1972.

  47. Goodglass H, Wingfield A, Hyde MR, et al. Category specific dissociations in naming and recognition by aphasic patients. Cortex. 1986 Mar. 22(1):87-102. [Medline].

  48. Hall DA, Anderson CA, Filley CM, et al. A French accent after corpus callosum infarct. Neurology. 2003 May 13. 60(9):1551-2. [Medline].

  49. Hillis AE. Aphasia: progress in the last quarter of a century. Neurology. 2007 Jul 10. 69(2):200-13. [Medline].

  50. Jacobs DH, Shuren J, Gold M, et al. Physostigmine pharmacotherapy for anomia. Neurocase. 1996. 2:83-92.

  51. Kaplan E, Goodglass H, Weintraub S. The Boston Naming Test. Philadelphia, PA: Lea and Febiger; 1978.

  52. Kertesz A. Western Aphasia Battery. London, Ontario: University of Western Ontario Press; 1980.

  53. Kertesz A, Sheppard A. The epidemiology of aphasic and cognitive impairment in stroke: age, sex, aphasia type and laterality differences. Brain. 1981 Mar. 104:117-28. [Medline].

  54. Kirshner HS. Behavioral neurology. Practical science of mind and brain. 1. 2. Boston. Butterworth Heinemann. 2002. 1-474.

  55. Kirshner HS. 1-532. Handbook of neurological speech and language disorders. First ed. New York: Marcel Dekker, Inc; 1995.

  56. Kirshner HS, Alexander M, Lorch MP, et al. Continuum: Disorders of speech and language. Baltimore MD: Lippincott Williams & Wilkins CONTINUUM.; 1999.

  57. Kirshner HS, Casey PF, Henson J, et al. Behavioural features and lesion localization in Wernicke's aphasia. Aphasiology. 1989. 3:169-176.

  58. Kirshner HS, Hughes T, Fakhoury T, et al. Aphasia secondary to partial status epilepticus of the basal temporal language area. Neurology. 1995 Aug. 45(8):1616-8. [Medline].

  59. Kirshner HS, Kistler KH. Aphasia after right thalamic hemorrhage. Arch Neurol. 1982 Oct. 39(10):667-9. [Medline].

  60. Kirshner HS, Tanridag O, Thurman L, et al. Progressive aphasia without dementia: two cases with focal spongiform degeneration. Ann Neurol. 1987 Oct. 22(4):527-32. [Medline].

  61. Lazar RM, Antoniello D. Variability in recovery from aphasia. Curr Neurol Neurosci Rep. 2008 Nov. 8(6):497-502. [Medline].

  62. Love T, Swinney D, Walenski M, et al. How left inferior frontal cortex participates in syntactic processing: Evidence from aphasia. Brain Lang. 2008 Dec. 107(3):203-19. [Medline].

  63. Mariën P, Paghera B, De Deyn PP, et al. Adult crossed aphasia in dextrals revisited. Cortex. 2004 Feb. 40(1):41-74. [Medline].

  64. Martin PI, Naeser MA, Theoret H, et al. Transcranial magnetic stimulation as a complementary treatment for aphasia. Semin Speech Lang. 2004 May. 25(2):181-91. [Medline].

  65. Mega MS, Alexander MP. Subcortical aphasia: the core profile of capsulostriatal infarction. Neurology. 1994 Oct. 44(10):1824-9. [Medline].

  66. Mesulam MM. Primary progressive aphasia. Ann Neurol. 2001 Apr. 49(4):425-32. [Medline].

  67. Morris HH, Luders H, Lesser RP, et al. Transient neuropsychological abnormalities (including Gerstmann's syndrome) during cortical stimulation. Neurology. 1984 Jul. 34(7):877-83. [Medline].

  68. Nicholas M, Obler L, Albert M, et al. Lexical retrieval in healthy aging. Cortex. 1985 Dec. 21(4):595-606. [Medline].

  69. Nishio S, Takemura N, Ikai Y, et al. Sensory aphasia after closed head injury. J Clin Neurosci. 2004 May. 11(4):442-4. [Medline].

  70. Ojemann G, Ojemann J, Lettich E, et al. Cortical language localization in left, dominant hemisphere. An electrical stimulation mapping investigation in 117 patients. 1989. J Neurosurg. 2008 Feb. 108(2):411-21. [Medline].

  71. Price CJ, Wise RJ, Watson JD, et al. Brain activity during reading. The effects of exposure duration and task. Brain. 1994 Dec. 117 (Pt 6):1255-69. [Medline].

  72. Robey RR. A meta-analysis of clinical outcomes in the treatment of aphasia. J Speech Lang Hear Res. 1998 Feb. 41(1):172-87. [Medline].

  73. Schiff HB, Alexander MP, Naeser MA, et al. Aphemia. Clinical-anatomic correlations. Arch Neurol. 1983 Nov. 40(12):720-7. [Medline].

  74. Shuren JE, Hammond CS, Maher LM, et al. Attention and anosognosia: the case of a jargonaphasic patient with unawareness of language deficit. Neurology. 1995 Feb. 45(2):376-8. [Medline].

  75. Tanridag O, Kirshner HS. Language disorders in stroke syndromes of the dominant capsulostriatum-- a clinical review. Aphasiology. 1987. 1:107-117.

  76. Thompson C. Functional neuroimaging: applications for studying aphasia. LaPointe LL eds. Aphasia and related neurogenic language disorders. 3rd ed. New York: Thieme; 2005. 19-39.

  77. Thompson CK, den Ouden DB. Neuroimaging and recovery of language in aphasia. Curr Neurol Neurosci Rep. 2008 Nov. 8(6):475-83. [Medline].

  78. Wertz RT, Weiss DG, Aten JL, et al. Comparison of clinic, home, and deferred language treatment for aphasia. A Veterans Administration Cooperative Study. Arch Neurol. 1986 Jul. 43(7):653-8. [Medline].

  79. Yang ZH, Zhao XQ, Wang CX, et al. Neuroanatomic correlation of the post-stroke aphasias studied with imaging. Neurol Res. 2008 May. 30(4):356-60. [Medline].

 
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