Conduction aphasia | |
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Other names | Associative aphasia |
Broca's area and Wernicke's area of the brain, which are also terms for different types of aphasia | |
Specialty | Neurology |
In neurology, conduction aphasia, also called associative aphasia, is an uncommon form of difficulty in speaking (aphasia). It is caused by damage to the parietal lobe of the brain. An acquired language disorder, it is characterised by intact auditory comprehension, coherent (yet paraphasic) speech production, but poor speech repetition. Affected people are fully capable of understanding what they are hearing, but fail to encode phonological information for production. This deficit is load-sensitive as the person shows significant difficulty repeating phrases, particularly as the phrases increase in length and complexity and as they stumble over words they are attempting to pronounce. [1] [2] People have frequent errors during spontaneous speech, such as substituting or transposing sounds. They are also aware of their errors and will show significant difficulty correcting them. [3]
For example:
Clinician: Now, I want you to say some words after me. Say 'boy'.
Aphasic: Boy.
Clinician: Home.
Aphasic: Home.
Clinician: Seventy-nine.
Aphasic: Ninety-seven. No ... sevinty-sine ... siventy-nice...
Clinician: Let's try another one. Say 'refrigerator'.
Aphasic: Frigilator ... no? how about ... frerigilator ... no frigaliterlater ... aahh! It's all mixed up! [4]
In 1970, Tim Shallice and Elizabeth Warrington were able to differentiate two variants of this constellation: the reproduction and the repetition type. These authors suggested an exclusive deficit of auditory-verbal short-term memory in repetition conduction aphasia whereas the other variant was assumed to reflect disrupted phonological encoding mechanism, affecting confrontation tasks such as repetition, reading and naming in a similar manner. [5]
Left-hemisphere damage involving auditory regions often result in speech deficits. Lesions in this area that damage the sensorimotor dorsal stream suggest that the sensory system aid in motor speech. Studies have suggested that conduction aphasia is a result of damage specifically to the left superior temporal gyrus and/or the left supramarginal gyrus. [6] The classical explanation for conduction aphasia is a disconnection between the brain areas responsible for speech comprehension (Wernicke's area) and that of speech production (Broca's area). This is due to specific damage to the arcuate fasciculus, a deep white matter tract. Aphasic people are still able to comprehend speech as the lesion does not disrupt the ventral stream pathway.
Conduction aphasics will show relatively well-preserved auditory comprehension, which may even be completely functional. All cases are individualized and unique to their own extent. Speech production will be fluent, grammatically, and syntactically correct. Intonation and articulation will also be maintained. Speech often contains some paraphasic errors: phonemes and syllables will be dropped or transposed (e.g., "snowball" → "snowall", "television" → "vellitision", "ninety-five percent" → "ninety-twenty percent"). The hallmark deficit of this disorder, however, is in repetition. Aphasic people will show an inability to repeat words or sentences when asked by an examiner. [7] [8] After saying a sentence to a person with conduction aphasia, he or she will be able to paraphrase the sentence accurately but will not be able to repeat it. This is possibly because their "motor speech error processing is disrupted by inaccurate forward predictions, or because detected errors are not translated into corrective commands due to damage to the auditory-motor interface". [9] [10] When prompted to repeat words, the person will be unable to do so, and produce many paraphasic errors. For example, when prompted with "bagger", a person may respond with, "gabber". [11] Recent summaries about the syndrome show similarities between defective speech and writing and their relatively good comprehension. The sudden speech of a conduction aphasic is fluent, yet it is lengthy and inadequately structured. Aphasic people have difficulty in finding words appropriate to context and in accurately pronouncing a word. Aphasic errors in naming, reading aloud, and repeating are recognized.
Individuals with conduction aphasia are able to express themselves fairly well, with some word finding and functional comprehension difficulty. [12] Although people with aphasia may be able to express themselves fairly well, they tend to have issues repeating phrases, especially phrases that are long and complex. [12] During an assessment of aphasia, the clinician usually examine the person's verbal fluency, comprehension, repetition, reading, writing, and naming. When asked to repeat something, the person will be unable to do so without significant difficulty, repeatedly attempting to self-correct (conduite d'approche).
However, aphasics recognize their errors and will repetitively try to correct them. Typically, an aphasic will make multiple attempts correcting errors until they are correct. This recognition is due to preserved auditory error detection mechanisms. [10] Errors frequently fit a pattern of incorrect approximations. These common errors typically occur in morphemes that a) share one or more similarly located phonemes but b) differ in at least one aspect that makes the substituted morpheme(s) semantically distinct. This repetitive effort to approximate the appropriate word or phrase is known as conduite d'approche. [8] Repetitive self correction is commonly used by Aphasic people of conduction aphasia. Due to their relatively preserved auditory comprehension, conduction aphasics are capable of accurately monitoring, and attempting to correct, their own errors in speech output. [13] For example, when prompted to repeat "Rosenkranz", a German-speaking aphasic may respond with, "rosenbrau... rosenbrauch... rosengrau... bro... grosenbrau... grossenlau, rosenkranz,... kranz... rosenkranz". [11]
Conduction aphasia is a mild language disability, and most people return to their normal lives. [11] [14] Broca's and Wernicke's aphasia are commonly caused by middle cerebral artery strokes. [15] Symptoms of conduction aphasia, as with other aphasias, can be transient, sometimes lasting only several hours or a few days. As aphasias and other language disorders are frequently due to stroke, their symptoms can change and evolve over time, or simply disappear. If the cause is a stroke, people can make a good recovery but may have persistent deficits. [16] This is because the healing in the brain after inflammation or hemorrhage, leads to decreased local impairment. Furthermore, the plasticity of the brain may allow the recruitment of new pathways to restore lost function. For example, the right hemisphere speech systems may learn to correct for left-hemisphere damage. However, chronic conduction aphasia is possible, without transformation to other aphasias. [11] These people show prolonged, profound deficits in repetition, frequent phonemic paraphasias, and repetitive self-correction during spontaneous speech.
Conduction aphasia is caused by damage to the parietal lobe of the brain, especially in regards to the area associated with the left-hemisphere dominant dorsal stream network. [17] [10] The arcuate fasciculus, which connects Broca's area and Wernicke's area (important for speech and language production and comprehension, respectively), is affected. [17] These two areas control speech and language in the brain. The arcuate fasciculus is a thick band of fiber that connects the two areas and carries messages between them. When this area is damaged, the person experiences damage to the auditory-motor integration system. This results in disruption to the delayed auditory feedback network, causing the individual to have difficulty correcting themselves on speech repetition tasks. [10] Additionally, recent evidence suggests that conduction aphasia can also be caused by lesions in the left superior temporal gyrus and/or the left supramarginal gyrus. [6]
Conduction aphasia can also be seen in cases of cortical damage without subcortical extensions. [18]
Recent research has pointed to multiple different explanations for conduction aphasia, which is based on newer models suggesting language is facilitated by "cortically based, anatomically distributed, modular networks."
Several standardized test batteries exist for diagnosing and classifying aphasias. These tests are capable of identifying conduction aphasia with relative accuracy. [8] The Boston Diagnostic Aphasia Examination (BDAE) and the Western Aphasia Battery (WAB) are two commonly used test batteries for diagnosing conduction aphasia. These examinations involve a set of tests, which include asking person to name pictures, read printed words, count aloud, and repeat words and non-words (such as shwazel). Neuro-imaging should also be used to look for a stroke, tumor, infection, or another pathology in the setting of conduction aphasia. This can be done through a CT or MRI or the brain; these are the first imaging modality of choice. [16]
Speech and language therapy are typically used as a treatment. There are no medical or surgical treatments. Treatment for Aphasia is generally individualized, focusing on specific language and communication improvements, and regular exercise with communication tasks. Regular therapy for conduction aphasics has been shown to result in steady improvement on the Western Aphasia Battery. The Western Aphasia Battery assesses neurological disorders to discern the degree and type of aphasia present. The test also discerns a person's strengths and weaknesses, which can be used to treat the person better. Therapists should customize their treatment for each patient. The main focus for during speech therapy for conduction aphasia person is to strengthen correct word usage and auditory comprehension. A major goal is to focus on repetition. [19]
In the late 19th century, Paul Broca studied person with expressive aphasia. These person had lesions in the anterior perisylvian region (now known as Broca's area), and produced halting and labored speech, lacking in function words and grammar.
For example: [20] [ failed verification ]
Clinician: What brought you to the hospital? Patient: yes ... ah ... Monday ... ah ... Dad ... Peter Hogan, and Dad ... ah ... hospital ... and ah ... Wednesday ... Wednesday ... nine o'clock and ah Thursday ... ten o'clock ... doctors two ... two ... an doctors and ... ah ... teeth ... yah ... and a doctor an girl ... and gums, an I.
Comprehension is generally preserved, although there can be deficits in interpretation of complex sentences. In an extreme example, one of his person could only produce a single syllable, "Tan".
Meanwhile, Carl Wernicke described person with receptive aphasia, who had damage to the left posterior superior temporal lobe, which he named "the area of word images". These person could speak fluently, but their speech lacked meaning. They had a severe deficit in auditory comprehension. For example, "Clinician: What brings you to the hospital? [20]
The two disorders (expressive and receptive aphasias) thus seemed complementary, and corresponded to two distinct anatomical locations.
Wernicke predicted the existence of conduction aphasia in his landmark 1874 monograph, Der Aphasische Symptomenkompleks: Eine Psychologische Studie auf Anatomischer Basis. [3] [21] [22] He was the first to distinguish the various aphasias in an anatomical framework, and proposed that a disconnection between the two speech systems (motor and sensory) would lead to a unique condition, distinct from both expressive and receptive aphasias, which he termed Leitungsaphasie. He did not explicitly predict the repetition deficit, but did note that, unlike those with Wernicke's aphasia, conduction aphasics would be able to comprehend speech properly, and intriguingly, would be able to hear and understand their own speech errors, leading to frustration and self-correction. [22] [23]
Wernicke was influenced by Theodor Meynert, his mentor, who postulated that aphasias were due to perisylvian lesions. Meynert also distinguished between the posterior and anterior language systems, leading Wernicke to localize the two regions. [21] Wernicke's research into the fiber pathways connecting the posterior and anterior regions lead him to theorize that damage to the fibers under the insula would lead to conduction aphasia. Ludwig Lichtheim expanded on Wernicke's work, although he labeled the disorder commissural aphasia, to distinguish between aphasias tied to processing centers. [24]
Sigmund Freud would argue in 1891 that the old framework was inaccurate; the entire perisylvian area, from the posterior to the anterior regions, were equivalent in facilitating speech function. In 1948 Kurt Goldstein postulated that spoken language was a central phenomenon, as opposed to a differentiated and disparate set of functionally distinct modules. To Freud and Goldstein, conduction aphasia was thus the result of a central, core language breakdown; Goldstein labeled the disorder central aphasia. [21]
Later work and examination of brain structures, however, implicated the arcuate fasciculus, a white matter bundle connecting the posterior temporoparietal junction with the frontal cortex. Norman Geschwind proposed that damage to this bundle caused conduction aphasia; the characteristic deficits in auditory repetition were due to failed transmission of information between the two language centers. [21] Studies showed that conduction aphasics had an intact 'inner voice', which discredited the central deficit model of Freud and Goldstein. [25] The Wernicke-–Lichtheim–Geschwind disconnection hypothesis thus became the prevailing explanation for conduction aphasia. However, recent reviews and research have cast doubt on the singular role of the arcuate fasciculus and the model of spoken language in general. [26]
In aphasia, a person may be unable to comprehend or unable to formulate language because of damage to specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine, but aphasia due to stroke is estimated to be 0.1–0.4% in the Global North. Aphasia can also be the result of brain tumors, epilepsy, autoimmune neurological diseases, brain infections, or neurodegenerative diseases.
Expressive aphasia is a type of aphasia characterized by partial loss of the ability to produce language, although comprehension generally remains intact. A person with expressive aphasia will exhibit effortful speech. Speech generally includes important content words but leaves out function words that have more grammatical significance than physical meaning, such as prepositions and articles. This is known as "telegraphic speech". The person's intended message may still be understood, but their sentence will not be grammatically correct. In very severe forms of expressive aphasia, a person may only speak using single word utterances. Typically, comprehension is mildly to moderately impaired in expressive aphasia due to difficulty understanding complex grammar.
In neuroscience and psychology, the term language center refers collectively to the areas of the brain which serve a particular function for speech processing and production. Language is a core system that gives humans the capacity to solve difficult problems and provides them with a unique type of social interaction. Language allows individuals to attribute symbols to specific concepts, and utilize them through sentences and phrases that follow proper grammatical rules. Finally, speech is the mechanism by which language is orally expressed.
Wernicke's aphasia, also known as receptive aphasia, sensory aphasia, fluent aphasia, or posterior aphasia, is a type of aphasia in which individuals have difficulty understanding written and spoken language. Patients with Wernicke's aphasia demonstrate fluent speech, which is characterized by typical speech rate, intact syntactic abilities and effortless speech output. Writing often reflects speech in that it tends to lack content or meaning. In most cases, motor deficits do not occur in individuals with Wernicke's aphasia. Therefore, they may produce a large amount of speech without much meaning. Individuals with Wernicke's aphasia often suffer of anosognosia – they are unaware of their errors in speech and do not realize their speech may lack meaning. They typically remain unaware of even their most profound language deficits.
Broca's area, or the Broca area, is a region in the frontal lobe of the dominant hemisphere, usually the left, of the brain with functions linked to speech production.
Aphasiology is the study of language impairment usually resulting from brain damage, due to neurovascular accident—hemorrhage, stroke—or associated with a variety of neurodegenerative diseases, including different types of dementia. These specific language deficits, termed aphasias, may be defined as impairments of language production or comprehension that cannot be attributed to trivial causes such as deafness or oral paralysis. A number of aphasias have been described, but two are best known: expressive aphasia and receptive aphasia.
Anomic aphasia is a mild, fluent type of aphasia where individuals have word retrieval failures and cannot express the words they want to say. By contrast, anomia is a deficit of expressive language, and a symptom of all forms of aphasia, but patients whose primary deficit is word retrieval are diagnosed with anomic aphasia. Individuals with aphasia who display anomia can often describe an object in detail and maybe even use hand gestures to demonstrate how the object is used, but cannot find the appropriate word to name the object. Patients with anomic aphasia have relatively preserved speech fluency, repetition, comprehension, and grammatical speech.
Wernicke's area, also called Wernicke's speech area, is one of the two parts of the cerebral cortex that are linked to speech, the other being Broca's area. It is involved in the comprehension of written and spoken language, in contrast to Broca's area, which is primarily involved in the production of language. It is traditionally thought to reside in Brodmann area 22, which is located in the superior temporal gyrus in the dominant cerebral hemisphere, which is the left hemisphere in about 95% of right-handed individuals and 70% of left-handed individuals.
CarlWernicke was a German physician, anatomist, psychiatrist and neuropathologist. He is known for his influential research into the pathological effects of specific forms of encephalopathy and also the study of receptive aphasia, both of which are commonly associated with Wernicke's name and referred to as Wernicke encephalopathy and Wernicke's aphasia, respectively. His research, along with that of Paul Broca, led to groundbreaking realizations of the localization of brain function, specifically in speech. As such, Wernicke's area has been named after the scientist.
Global aphasia is a severe form of nonfluent aphasia, caused by damage to the left side of the brain, that affects receptive and expressive language skills as well as auditory and visual comprehension. Acquired impairments of communicative abilities are present across all language modalities, impacting language production, comprehension, and repetition. Patients with global aphasia may be able to verbalize a few short utterances and use non-word neologisms, but their overall production ability is limited. Their ability to repeat words, utterances, or phrases is also affected. Due to the preservation of the right hemisphere, an individual with global aphasia may still be able to express themselves through facial expressions, gestures, and intonation. This type of aphasia often results from a large lesion of the left perisylvian cortex. The lesion is caused by an occlusion of the left middle cerebral artery and is associated with damage to Broca's area, Wernicke's area, and insular regions which are associated with aspects of language.
In neuroanatomy, the arcuate fasciculus is a bundle of axons that generally connects Broca's area and Wernicke's area in the brain. It is an association fiber tract connecting caudal temporal lobe and inferior frontal lobe.
Transcortical sensory aphasia (TSA) is a kind of aphasia that involves damage to specific areas of the temporal lobe of the brain, resulting in symptoms such as poor auditory comprehension, relatively intact repetition, and fluent speech with semantic paraphasias present. TSA is a fluent aphasia similar to Wernicke's aphasia, with the exception of a strong ability to repeat words and phrases. The person may repeat questions rather than answer them ("echolalia").
In psycholinguistics, language processing refers to the way humans use words to communicate ideas and feelings, and how such communications are processed and understood. Language processing is considered to be a uniquely human ability that is not produced with the same grammatical understanding or systematicity in even human's closest primate relatives.
Brodmann area 22 is a Brodmann's area that is cytoarchitecturally located in the posterior superior temporal gyrus of the brain. In the left cerebral hemisphere, it is one portion of Wernicke's area. The left hemisphere BA22 helps with generation and understanding of individual words. On the right side of the brain, BA22 helps to discriminate pitch and sound intensity, both of which are necessary to perceive melody and prosody. Wernicke's area is active in processing language and consists of the left Brodmann area 22 and Brodmann area 40, the supramarginal gyrus.
Transcortical motor aphasia (TMoA), also known as commissural dysphasia or white matter dysphasia, results from damage in the anterior superior frontal lobe of the language-dominant hemisphere. This damage is typically due to cerebrovascular accident (CVA). TMoA is generally characterized by reduced speech output, which is a result of dysfunction of the affected region of the brain. The left hemisphere is usually responsible for performing language functions, although left-handed individuals have been shown to perform language functions using either their left or right hemisphere depending on the individual. The anterior frontal lobes of the language-dominant hemisphere are essential for initiating and maintaining speech. Because of this, individuals with TMoA often present with difficulty in speech maintenance and initiation.
Mixed transcortical aphasia is the least common of the three transcortical aphasias. This type of aphasia can also be referred to as "Isolation Aphasia". This type of aphasia is a result of damage that isolates the language areas from other brain regions. Broca's, Wernicke's, and the arcuate fasiculus are left intact; however, they are isolated from other brain regions.
Speech is the use of the human voice as a medium for language. Spoken language combines vowel and consonant sounds to form units of meaning like words, which belong to a language's lexicon. There are many different intentional speech acts, such as informing, declaring, asking, persuading, directing; acts may vary in various aspects like enunciation, intonation, loudness, and tempo to convey meaning. Individuals may also unintentionally communicate aspects of their social position through speech, such as sex, age, place of origin, physiological and mental condition, education, and experiences.
Paraphasia is a type of language output error commonly associated with aphasia and characterized by the production of unintended syllables, words, or phrases during the effort to speak. Paraphasic errors are most common in patients with fluent forms of aphasia, and come in three forms: phonemic or literal, neologistic, and verbal. Paraphasias can affect metrical information, segmental information, number of syllables, or both. Some paraphasias preserve the meter without segmentation, and some do the opposite. However, most paraphasias affect both partially.
Auditory agnosia is a form of agnosia that manifests itself primarily in the inability to recognize or differentiate between sounds. It is not a defect of the ear or "hearing", but rather a neurological inability of the brain to process sound meaning. While auditory agnosia impairs the understanding of sounds, other abilities such as reading, writing, and speaking are not hindered. It is caused by bilateral damage to the anterior superior temporal gyrus, which is part of the auditory pathway responsible for sound recognition, the auditory "what" pathway.
Disconnection syndrome is a general term for a collection of neurological symptoms caused – via lesions to associational or commissural nerve fibres – by damage to the white matter axons of communication pathways in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.