Receptive aphasia
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Template:DiseaseDisorder infobox
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Most recent articles on Receptive aphasia Most cited articles on Receptive aphasia |
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Media |
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Powerpoint slides on Receptive aphasia |
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Evidence Based Medicine |
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Cochrane Collaboration on Receptive aphasia |
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Clinical Trials |
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Ongoing Trials on Receptive aphasia at Clinical Trials.gov Trial results on Receptive aphasia Clinical Trials on Receptive aphasia at Google
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Guidelines / Policies / Govt |
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US National Guidelines Clearinghouse on Receptive aphasia NICE Guidance on Receptive aphasia
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Books |
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News |
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Commentary |
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Definitions |
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Patient Resources / Community |
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Patient resources on Receptive aphasia Discussion groups on Receptive aphasia Patient Handouts on Receptive aphasia Directions to Hospitals Treating Receptive aphasia Risk calculators and risk factors for Receptive aphasia
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Healthcare Provider Resources |
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Causes & Risk Factors for Receptive aphasia |
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Continuing Medical Education (CME) |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Receptive aphasia, or Wernicke’s aphasia, fluent aphasia, or sensory aphasia is a type of aphasia often (but not always) caused by neurological damage (stroke) to Wernicke’s area in the brain (Broddman area 22, in the posterior part of the superior temporal gyrus of the dominant hemisphere). This is not to be confused with Wernicke’s encephalopathy or Wernicke-Korsakoff syndrome. The aphasia was first described by Carl Wernicke and its understanding substantially advanced by Norman Geschwind. Patients with this type of aphasia are usually not aware of the errors they may be making while speaking, or that it may not be logical.
Wernicke's aphasia may present with other deficits such as dysarthria, and severity depends on the lesion present though usually without motor dysfunction. This leads to proper stringing of words together to form fluent speech even though it is often without meaning. Language expression deficits can be accompanied with memory deficits, impaired understanding of language along with impaired reading and writing.[1][2]
Historical Perspective
- Receptive aphasia was first discovered by Carl Wernicke, a German neuropathologist studying with Mynert in 1874. Wernicke published Der Aphasische Symptomencomplex. He described sensory aphasia as a distinct entity from motor aphasia (Brocas aphasia).
- Early in the 15th century the development of basic aphasia treatment started considering it as a form of memory impairment. However it was in the 18th century that Gall developed his language and speech localisation theory, and Broca, Hughlings, Jackson and Bastian noticed that recovery could be due to some sort of reorganization, meaning therapy could be beneficial. The First World War saw Goldstein, Luria and the Viennese phoniatricians Hermann Gutzmann (1865 – 1922) (the father of aphasia therapy’) and Emil Froeschels develop initial systematic treatments. Between the wars the focus turned to the New World and a more objective approach was developed based on identifiable behaviors. Following World War II, the theory of localisation returned, developing an approach based on the Boston School and stimulation methods of Wepman and Schuell. In the latter part of the 20th century new methods based on linguistics, psycholinguistics, modular cognitive models and psychosocial and social models were formed.[3]
Classification
- Aphasia can be broadly classified according into :
Pathophysiology
- The pathogenesis of receptive aphasia is characterized by damage to the Wernicke's area (left posterior temporal area of the brain) and loss of understanding of speech. The extent of damage typically guides the severity and prognosis of the resulting aphasia.
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Clinical Features
Damage to the Wernicke's area in the non-dominant hemisphere results in sensory dysprosody, in which the ability to perceive the pitch, rhythm, and emotional tone of speech is lost.
Speech is preserved, but language content is incorrect. This can range from the inclusion of a few inappropriate or nonexistent words to a torrent of jargon. Grammar, intonation, stress, syntax and rate are normal. Substitutions of one word for another (paraphasias, e.g. “telephone” for “television”) are common. In severe cases, this can be confused with the psychiatric signs of “pressure of speech” and “word salad.” Comprehension may be poor and repetition is also inadequate.
Example:
- I called my mother on the television and did not understand the door. It was too breakfast, but they came from far to near. My mother is not too old for me to be young.
Regarding speech and comprehension, people with Wernicke’s aphasia may:
- Sequence words together to make illogical sentences
- Form new words which may be senseless
- Be able to deliver words in a normal melodic line
- Articulate words
- Face hardship or add words while repeating phrases
- Interrupt others and speak too fast
- Have impaired reading and writing capacity
- Understand visual materials better than written or spoken words
- Preserve cognitive abilities different than those related with language
- Be oblivious of spoken mistakes, and subsequently rectify them. These mistakes include
- Jargon: Incoherent but structurally intact speech that may be composed of neologisms (invented words) or incoherently arranged known words.
- Neologisms: Newly coined word
- Paraphasias:
Patients who recover from Wernicke’s aphasia describe that they experienced others speech to be incomprehensible and, despite knowing they were speaking, did not recognize their own words or were able to stop themselves from speaking. The ability to understand and repeat songs is generally unaffected, as these are processed by the opposite hemisphere. "Melodic intonation therapy" had been attempted with aphasic patients as therapy to help them speak normally, but in 2003 this was found to be ineffective.[4]
Aphasia is different from a disease like Alzheimer’s, in which many of the brain’s functions diminish over time. Interestingly, patients were able to recite from memory, a key difference from Alzheimer's Dementia. The patient is still able to express obscenity, however typically they have no control or knowledge of their spoken obscenities.
Patients are usually physically independent in the absence of other focal neurological deficits.
Luria's theory on Wernicke's aphasia
Luria proposed that this type of aphasia has three characteristics.[5]
- A deficit in the categorization of sounds. In order to understand what is said, one must be able to perceive subtle sounds of spoken language. For example, differentiating between bad and bed is simple for native English speakers. The Dutch language however, makes no difference between these vowels, and therefore the Dutch experience trouble with these sounds. This is exactly what patients with Wernicke’s aphasia experience even in their own dialect: they can't isolate notable sound characteristics and organize them into known arrangements.
- A defect in speech. A patient with Wernicke's aphasia can and may be able to speak a great deal, though confusing sound characteristics, producing “word salad”: separately comprehensible words that make no sense together.
- An impairment in writing. Those who cannot differentiate sounds cannot be predicted to write.
Differentiating Receptive aphasia from other diseases
- Receptive aphasia must be differentiated from other diseases that cause language deficits and memory impairment such as:
- Brocas Aphasia
- Global Aphasia
- Dementia
- Alzheimers
- Agraphia
Epidemiology and Demographics
- About 750,000 strokes occur each year in the USA.
- About 1 third (225,000) of strokes result in aphasia.
- There are at least 2,000,000 people in the USA with aphasia.
- There are at least 250,000 people in Great Britain with aphasia.
Age
- Aphasia after stroke is more common for older adults than younger adults (Ellis & Urban, 2016). Fifteen percent of individuals under the age of 65 experience aphasia after their first ischemic stroke; this percentage increases to 43% for individuals 85 years of age and older (Engelter et al., 2006).
Gender
- Receptive aphasia affects men and women equally, though some data suggests that differences may exist by type and severity of aphasia. For example, Wernicke’s aphasia and global aphasia occur more commonly in women, and Broca's aphasia occurs more commonly in men (Hier, Yoon, Mohr, & Price, 1994).
Race
- There is no racial predilection for Receptive Aphasia.
Risk Factors
Natural History, Complications and Prognosis
- The majority of patients with [disease name] remain asymptomatic for [duration/years].
- Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
- If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
- Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
- Prognosis is generally [excellent/good/poor], and the [1/5/10year mortality/survival rate] of patients with [disease name] is approximately [#%].
Diagnosis
Diagnostic Criteria
- The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
- [criterion 1]
- [criterion 2]
- [criterion 3]
- [criterion 4]
Symptoms
- [Disease name] is usually asymptomatic.
- Symptoms of [disease name] may include the following:
- [symptom 1]
- [symptom 2]
- [symptom 3]
- [symptom 4]
- [symptom 5]
- [symptom 6]
Physical Examination
- Patients with [disease name] usually appear [general appearance].
- Physical examination may be remarkable for:
- [finding 1]
- [finding 2]
- [finding 3]
- [finding 4]
- [finding 5]
- [finding 6]
Laboratory Findings
- There are no specific laboratory findings associated with [disease name].
- A [positive/negative] [test name] is diagnostic of [disease name].
- An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
- Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
Imaging Findings
- There are no [imaging study] findings associated with [disease name].
- [Imaging study 1] is the imaging modality of choice for [disease name].
- On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
- [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Treatment is mainly comprised of speech and language therapy, which is most effective when started as soon as possible post injury. The aim of treatment is to enable the patient to make best use of their remaining language function, improve language skill, and learn how to communicate in other possible ways so their wants and needs can be articulated and addressed.[6] It often involves group therapy.
However, treatment is particularly challenging due to the fact that patients with aphasia suffer from impaired comprehension, which limits their perception of their degree of impairment.
When the cause of aphasia is a stroke, recovery of language function peaks within two to six months, after which further progress is limited. However, efforts should still be made, as an improvement in aphasia has been recorded long after a stroke.
Family support and social support are crucial to a positive outcome. Treatment of post-stroke depression and post-stroke cognitive issues, as well as of other neurological disorders such as neglect, agnosia, and hemiparesis, should be worked on during rehabilitation to further improve patient outcome.
Prevention
- There are no primary preventive measures available for [disease name].
- Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
- Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
See also
References
- ↑ "Aphasia".
- ↑ "Aphasia".
- ↑ TY - BOOK AU - Code, Chris PY - 2008/10/10 SP - T1 - A Short History of the Past and Future of Aphasia Therapy DO - 10.13140/2.1.3036.3840 ER -
- ↑ Hébert, S. & Racette, A., Gagnon, L. & Peretz, I. (2003). Revisiting the dissociation between speaking and singing in aphasia. Brain, 126, 1838-1850. http://brain.oxfordjournals.org/cgi/reprint/126/8/1838
- ↑ Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003), pages 503-504. The whole paragraph on Luria's theory is written with help of this reference.
- ↑ "The neurophysiology of language: Insights from non-invasive brain stimulation in the healthy human brain". Brain and Language.