Receptive aphasia

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Receptive aphasia
BrocasAreaSmall.png
Broca's area and Wernicke's area
Classification and external resources
Specialty psychiatry
ICD-10 F80.2
ICD-9-CM 784.3
MeSH D001041

Receptive aphasia, also known as Wernicke's aphasia, fluent aphasia, or sensory aphasia, is a type of aphasia in which an individual is unable to understand language in its written or spoken form. Even though they can speak using grammar, syntax, rate, and intonation, they typically have difficulty expressing themselves meaningfully through speech. Wernicke's aphasia was named after Carl Wernicke who recognized this condition.[1] People with receptive aphasia are typically unaware of how they are speaking and do not realize their speech may lack meaning.[2] This is due to poor comprehension skills and the inability to understand their own speech because of overall self-monitoring deficits.[3] They typically remain unaware of even their most profound language deficits. When experienced with Broca's aphasia, the patient displays global aphasia.

Like many acquired language disorders, receptive aphasia can be experienced in many different ways and to many different degrees. While the typical case shows severely disturbed language comprehension, many individuals are still able to maintain conversations. Many may only experience difficulties with things such as accents and fast speech with the occasional speech error and can often carry out simple commands. Not all individuals show a complete loss of language comprehension. A common symptom of receptive aphasia is misinterpreting the meaning of words, gestures, pictures. For example, a patient with receptive aphasia may take the expression "it's raining cats and dogs" literally instead of figuratively.[2] What is described here is what is referred to as a "textbook" example with the typical, fully expressed symptoms.[4] Many diagnosed with Wernicke's aphasia have effortless speech and have difficulty with repetition in words and sentences. A person with Wernicke's aphasia may speak over others during conversation, which is "press of speech", and may not be aware that their message does not have a full meaning.[5]

Signs and symptoms[edit]

Wernicke's aphasia is characterized as impaired comprehension of incoming speech stimuli[6] (Ropper, Samuels & Klein, 2014). An aphasic patient’s speech output is fluent and has normal prosody. Patients with aphasia will produce an equal number of words in their spontaneous speech output compared to a normal speaker, but their speech contains several paraphasias, circumlocutions, and repetitions[7] (Andreetta & Marini, 2014, p. 715). When speaking, a patient will often produce jargon, or nonsense utterances (ASHA, 2016). Patients are unable to appropriately express their thoughts as well as lack the ability to decode meaning within the incoming speech stimuli[8] (Marsel, 2014). The damage is associated with the posterior portion of the left hemisphere of the brain.[citation needed]

Causes[edit]

Receptive aphasia is traditionally associated with neurological damage to Wernicke's area in the brain[9] (Brodmann area 22, in the posterior part of the superior temporal gyrus of the dominant hemisphere). Since Wernicke's area is responsible for "reading, thinking of what to write, and processing information", that is where we see many of the deficits associated with damage to this area.[10] However, the key deficits of receptive aphasia do not come from damage to Wernicke's area;[9] instead, most of the core difficulties are proposed to come from damage to the medial temporal lobe and underlying white matter. Receptive aphasia results from damage in the posterior one-third of the superior gyrus of the temporal lobe of the left hemisphere. Damage in this area not only destroys local language regions but also cuts off most of the occipital, temporal, and parietal regions from the core language region.[11] While Wernicke's area is the site of language recognition, perception, interpretations, and understanding, that does not mean that it is wholly responsible for the comprehension of semantic meaning. Attempts to localize "receptive" language modules are generally futile, given the full range of interpretations of "receptive functionality". As Dennis C. Tanner states, "Although there may be ... areas important in perceiving vowels and consonants, pinpointing the brain cells ... [for] understanding the implications of a Robert Frost poem is absurd." The reason for this is due to the many levels of semantic understanding—auditory perception, speech discrimination, denotative extraction, and dynamic symbolism. The process of full-depth semantic decoding has the capacity to engage virtually the whole brain. Therefore, it is more apt to think of Wernicke's area as an important conduit for a larger, all-encompassing process.[12]

Aphasia and the psycholinguistic models of language[edit]

Researchers use language deficits seen in the aphasic population to draw conclusions about the psycholinguistic models of language including message formation, lexical selection and morphosyntactic encoding. Cho-Reyes, Mack & Thomson (2016) discovered that patients with aphasia access syntactic representations, including thematic representations, during sentence production, similarly to the typically developing cohorts.  Also, because the participants showed lasting priming effects, the incorporation of structural priming within treatment is hypothesized to aid production of complex structured utterances[13] (Cho-Reyes, Mack & Thompson, 2016, p. 213).

Along with structural priming, clients with aphasia perform semantic priming, but they require more time to complete language tasks such as the lexical decision task. This is largely due to the large onset competitor effect, meaning the inability to distinguish words with shared semantic onsets[14] (Yee, Blumstein & Sedivy, 2009). However, aphasic patients perform at chance levels for semantic judgment tasks. In comparison to normal patients, those with aphasia will increasingly fixate on words semantically related to the target. Therefore, they are able to access lexical entries and activate the lexical network but lack the ability to use such information within an offline task[15] (McNellis & Blumstein, 2001, p. 162). Semantic representations decline largely due to the blurring of category boundaries, reduced difference between basic terms, incapability to judge semantic relatedness and abnormal activation of semantic representations of nonwords. Further, aphasia is characterized by deficits in lexical retrieval through the presence of nonword errors[16] (Marshall, 2006, pg. 392). Nonword errors are typically substituted for content words and follow pauses. Many times, patients will not recognize their speech errors and continue communicating jargon with little to no self-monitoring of the speech output[16] (Marshall, 2006, p. 398).[7][13][14][15][8][6][16][17][18][19]

Diagnosis[edit]

Receptive aphasia can be difficult to diagnose as the symptoms can be mistaken as a confused state due to stroke or blunt force trauma. In order for receptive aphasia to be diagnosed a complete language examination, especially of the auditory system, must be done. There are various diagnostic tests and measures used to determine whether a patient should be diagnosed with receptive aphasia.[4]

Some examples of these assessments can be seen below:

  • Formal screening and bedside tests of aphasia are shorter examinations that determine the presence or absence of aphasia. Some examples of these tests are: the Bedside Evaluation Screening Test, Second Edition (BEST-2; Fitch-West & Sands, 1998); the Aphasia Screening Test (AST; Whurr, 1996); and the Quick Assessment for Aphasia (Tanner & Culbertson, 1999).[20]
  • Once a physician determines that aphasia is a possible diagnosis, more comprehensive evaluations are done to determine the type of aphasia. These assessments are standardized aphasia test batteries and include: the Boston Diagnostic Aphasia Examination (BDAE-3; Goodglass et al., 2000); the Porch Index of Communicative Abilities (PICA; Porch, 1981); and the Western Aphasia Battery (WAB; Kertesz, 1982).[20]
  • In order to diagnose a patient with receptive aphasia, auditory comprehension should be assessed thoroughly because it is one of the most affected areas. Auditory comprehension can be assessed using the Functional Auditory Comprehension Test (FACT; LaPointe & Horner, 1978), the Revised Token Test (McNeil & Prescott, 1978) and through real-life conversations with patients.[21]
  • In addition to the aforementioned tests, reading comprehension and written language can be used to indicate the presence of receptive aphasia, although there are limited standardized assessment devices in this area.[21]

During assessment, clinicians evaluate the patient's initial functioning and performance on the above tasks to form a baseline for treatment. This baseline can help them decide what type of treatment they can use and compare the patient's future progress with their initial abilities.[20]

Treatment[edit]

By analyzing language processing in aphasic patients, researchers have discovered the importance of a multilevel approach in assessment and treatment[7] (Andreeta & Marini, 2015, p. 719).

Word retrieval[edit]

Anomia is consistently seen in aphasia, so many treatment techniques aim to help patients with word finding problems. One example of a semantic approach is referred to as semantic feature analyses. The process includes naming the target object shown in the picture and producing words that are semantically related to the target. Through production of semantically similar features, participants develop more skilled in naming stimuli due to the increase in lexical activation[17] (Boyle, 2004, p. 240).

Computer rehabilitation[edit]

Four types of treatment methods utilize the computer to drive communication in the aphasia population. This includes stimulation, drill and practice, simulations, and tutorials[18] (Raymond, 2004, p. 255). Stimulation focuses on the maintenance of skills over a longer period of time, while drill exercises are categorized as a "teaching deep" process. So, drill and practice exercises attend to only a few stimuli and continue teaching until the participant achieves accurate productions. Then, simulations depict a structured environment with a given challenge and a list of possible solutions to choose from. Lastly, tutorials are informative and strive to provide caregivers the necessary information to create optimal communication for the client[18] (Raymond, 2004, p. 255).

Augmentative communication devices are an alternate treatment method for aphasia. Augmentative communication utilizes computers to aid communication through digitized speech, pictures, animation and/or text[18] (Raymond, 2004, p. 255).

Comprehension training[edit]

Comprehension deficits as well as issues of pressure of speech can be improved through comprehension training. Comprehension training confronts the issues of pressure of speech by redirecting patients attention to listening rather than speaking. In this training the clinician will give the patient short instructions with contextual cues (such as facial expressions and gestures) and remind the patient to stop speaking while listening to these instructions through the use of these cues.[21] The comprehension tasks used in this training involve listening to short, context-dependent instructions given by a clinician and initially responding by pointing to an object or picture. These tasks become gradually more difficult as therapy continues. The main goal of this therapy is to enhance patient's attention towards incoming information while simultaneously slowing and monitoring his or her own speech output.[20] Therapists using this contextual approach have found they can increase speech comprehension from 2% to 90%.[10]

Schuell's stimulation[edit]

Schuell's stimulation is a well-known treatment, and is the most effective treatment. This treatment involves introducing the patient to strong, controlled, and intensive auditory stimulation. This immersion into intensive auditory stimulation is believed to increase neuronal firing causing an increase in neural activation. This neural activation is used as a facilitator to increase brain reorganization and therefore recovery of language in the patient.[20]

Redistribution of brain activation allows uninjured parts of the brain, such as the frontal and right hemisphere to compensate for the injuries found in Wernicke's area. On comprehension tasks, the average person shows activation in Broca and Wernicke's areas in the left hemisphere of the brain with little activation in the right hemisphere. In contrast, a patient with receptive aphasia shows activation in the right hemisphere of the brain, providing evidence that neuroplasticity plays a role in recovery.[20][21][22]

Social approach[edit]

The social approach involves a collaborative effort on behalf of patients and clinicians to determine goals for therapy and also determining the most important functional outcomes that could improve the patient's everyday life. A conversational approach which is thought to provide opportunities for development and use of strategies to overcome barriers to communication.The main goals of this treatment are to improve the patient's conversational confidence and skills using conversational coaching, supported conversations, and partner training.[20]

  1. Conversational coaching involves aphasic patients and their speech language pathologists, who serve as a "coach" discussing strategies to approach various communicative scenarios. The "coach" will help the patient develop a script for a scenario (such as ordering food at a restaurant), and help the patient practice and perform the scenario in and out of the clinic while evaluating the outcome.
  2. Supported conversation also involves using a communicative partner who supports the patient's learning by providing contextual cues, slowing their own rate of speech, and increasing their message's redundancy to promote the patient's comprehension.
  3. Promoting Aphasics Communicative Effectiveness (PACE) encourages conversation outside the clinic.

Successful treatment incorporates these various treatment programs and approaches to facilitate patient's learning. In order to improve self-monitoring speech language pathologists will slow their own rate of speech, pausing between meaningful segments and encourage patients to do the same, slowing down their own speech, listening to themselves speak and monitoring their speech output.[20]

It is also important to include patient's families in treatment programs so they can have speaking partners where they communicate the most, at home. Clinicians can teach family members how to support one another and adjust their speaking patterns to further facilitate their loved one's treatment and rehabilitation.[20]

Luria's theory[edit]

Alexander Luria proposed that this type of aphasia has three characteristics.[23]

  1. A deficit in the categorization of sounds. In order to hear and understand what is said, one must be able to recognize the different sounds of spoken language. For example, hearing the difference between bad and bed is easy for native English speakers. The Dutch language, however, makes a much greater difference in pronunciation between these vowels, and therefore the Dutch have difficulties hearing the difference between them in English pronunciation. This problem is exactly what patients with Wernicke's aphasia have in their own language: they cannot isolate significant sound characteristics and classify them into known meaningful systems.
  2. A defect in speech. A patient with Wernicke's aphasia can and may speak a great deal, but he or she confuses sound characteristics, producing "word salad" in extreme cases: intelligible words that appear to be strung together randomly.
  3. An impairment in writing. A person who cannot discern sounds cannot be expected to write.

See also[edit]

References[edit]

  1. ^ Wernicke's APHASIA. Caspari, Isabelle LaPointe, Leonard L. , (2005).Aphasia and related neurogenic language disorders (3rd ed.)., (pp. 142–154). New York, NY, US: Thieme New York, xix, 274 pp
  2. ^ a b ASHA: American Speech and Language Association http://www.asha.org/Practice-Portal/Clinical-Topics/Aphasia/Common-Classifications-of-Aphasia/[full citation needed]
  3. ^ "American Speech-Language Hearing Association". American Speech-Language Hearing Association Practice Portal. American Speech-Language Hearing Association. Retrieved December 1, 2016. 
  4. ^ a b Brown, Jason (1972). Aphasia, Apraxia, and Agnosia Clinical and Theoretical Aspects. Springfield, Illinois: Charles C Thomas Publisher. pp. 56–71. ISBN 0-398-02211-9. 
  5. ^ "Common Classifications of Aphasia". www.asha.org. Retrieved 2016-12-03. 
  6. ^ a b Ropper. Disorders of Speech and Language. New York: McGraw Hill. 
  7. ^ a b c Andreeta, S., & Marini, A. (2015). "The effect of lexical deficits on narrative disturbances in fluent aphasia". Aphasiology. 
  8. ^ a b Marsel (2014). Aphasia, Memory Loss and Other Focal Cerebral Disorders. New York: McGraw Hill. 
  9. ^ a b Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003) page 505
  10. ^ a b http://www.theaphasiacenter.com/2012/01/what-is-wernickes-aphasia/
  11. ^ Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003) page 506
  12. ^ Tanner, Dennis C. (2007). "A redefining Wernicke's area: receptive language and discourse semantics". Journal of Allied Health. 36 (2): 63–6. PMID 17633961. 
  13. ^ a b Cho-Reyes, S., Mack, J.E., & Thompson, C.K. (2016). "Grammatical encoding and learning in agrammatic aphasia: Evidence from structural priming". Journal of Memory and Language. 
  14. ^ a b Yee, E., Blumstein, S.E., & Sedivy, J.C. (2008). "Lexical-semantic activation in Broca's and Wernicke's aphasia: Evidence from eye movements". Journal of Cognitive Neuroscience. 
  15. ^ a b McNellis, M.G., & Blumstein,S.,E. (2001). "Self organizing dynamics of lexical access in normals and aphasics". Journal of Cognitive Neuroscience: 151–170. 
  16. ^ a b c Marshall, Jane (2006). "Jargon aphasia: What have we learned?". Aphasiology. 
  17. ^ a b Boyle, M (2004). "Semantic feature analysis treatment for anomia in two fluent aphasia syndromes". American Journal of Speech Language Pathology. 13: 236–249. 
  18. ^ a b c d Kent, Raymond (2004). The MIT Encyclopedia of Communication Disorders. Cambridge, Mass: Bradford Books. pp. 250–270. 
  19. ^ "Aphasia Treatment". American Speech and Hearing Association. 
  20. ^ a b c d e f g h i LaPointe, Leonard (2005). Aphasia and Related Neurogenic Language Disorders (Third ed.). Thieme. pp. 149–152. ISBN 1-58890-226-9. 
  21. ^ a b c d Vinson, Betsy (2012). Language Disorders Across the Lifespan. Clifton Park, NY: Delmar, Cengage Learning. pp. 572–576. ISBN 978-1-4354-9859-4. 
  22. ^ Code, Chris (1987). Language Aphasia and the Right Hemisphere. Great Britain: John Wiley & Sons Ltd. p. 110. ISBN 0471911585. 
  23. ^ Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003), pages 503-504. The whole paragraph on Luria's theory is written with help of this reference.

Further reading[edit]

  • Klein, Stephen B., and Thorne. Biological Psychology. New York: Worth, 2007. Print.
  • Saladin, Kenneth S. Anatomy & Physiology: the Unity of Form and Function. New York: McGraw-Hill Higher Education, 2010. Print.

External links[edit]