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Language: Aphasia 343

Language: Aphasia N F Dronkers, VA Northern California Health Care System, Martinez, CA, USA; University of California at Davis, Davis, CA, USA; and University of California at San Diego, La Jolla, CA, USA J V Baldo, VA Northern California Health Care System, Martinez, CA, USA ã 2009 Elsevier Ltd. All rights reserved.

Aphasia is an acquired impairment in language due to a brain injury. To be considered aphasic, the impairment must affect a range of language functions, including speech, comprehension, reading, and writing. Aphasia usually follows from injury to the left hemisphere of the brain. In stroke, it is usually due to a disruption of blood flow in the middle cerebral artery, which provides blood supply to the lateral surface of the cortex. Aphasia can also occur following a traumatic brain injury or may emerge gradually due to progressive, degenerative brain disease. Traditionally, aphasia has been classified using subtypes that are characterized by specific patterns of impairment in spoken fluency, comprehension, naming, and repetition. These aphasia subtypes include Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, global aphasia, anomic aphasia, and transcortical aphasia. This article reviews the behavioral characterization of these aphasia subtypes as well as discusses their anatomical basis.

Broca’s Aphasia Broca’s aphasia was first described by the French neurologist, Paul Broca, in the 1860s. He described a patient who could say very few words and repeatedly uttered the sound, ‘tan tan tan,’ when trying to speak. Despite his poor speech output, this patient understood much of what was said to him. A second patient soon followed who showed a similar dissociation of reduced speech fluency and relatively preserved comprehension. This form of aphasia came to be known as Broca’s aphasia, and it is sometimes referred to as motor aphasia or nonfluent aphasia. The following is a speech sample of a patient with Broca’s aphasia as he attempts to describe a drawing of a lakeside picnic from the Western Aphasia Battery (WAB): I see dog, boy, boy, sand, see book, people, boats, on boat . . . girl and man reading, man fishing . . .

Such telegraphic speech is typical of patients with Broca’s aphasia. Despite its halting nature, such speech often contains important content words so that the

main ideas are conveyed, but smaller functor words (e.g., ‘a’ and ‘the’) are omitted, resulting in agrammatic speech (e.g., “I see dog”). There is debate as to whether such agrammatic speech is due to the inability of these patients to use grammatical forms or whether it simply reflects a strategic choice due to a reduced processing capacity. One way in which this issue has been addressed has been to study agrammatic patients who speak different languages. In German, for example, it has been shown that patients with Broca’s aphasia do not commonly omit functor words such as ‘the’ (as American Broca’s aphasics might) because these words are critical to the meaning of the noun (whereas in English they are not). This cross-cultural difference would suggest that patients with Broca’s aphasia can produce grammatical forms if necessary to communicate content but simply omit what is not essential in order to simplify production demands. The most severe form of Broca’s aphasia manifests as recurring utterances, where a patient repeatedly utters a single word or phrase (such as Broca’s original patient). Interestingly, such patients can effectively use intonation to vary the pitch of such utterances and thus communicate in a limited fashion. This behavior illustrates the fact that patients with Broca’s aphasia, despite their severely reduced speech output, have relatively good awareness of their communication deficit. Comprehension in patients with Broca’s aphasia is relatively preserved, as long as sentences are not complex. For example, sentences such as ‘The boy was kissed by the girl’ may be misunderstood as ‘The boy kissed the girl,’ the latter being the more canonical construction in English. Repetition and naming are also disrupted in Broca’s aphasia due to the speech output disturbance. Similarly, reading and writing are affected; for example, patients often are unable to write complete phrases or sentences (parallel to their spoken output). Commonly accompanying Broca’s aphasia is apraxia of speech, a motor speech disorder characterized by a reduced ability to coordinate the articulators (lips, tongue, etc.) that results in groping and misarticulated speech. Another commonly coexisting motor speech disorder is dysarthria, which results in slurred and distorted speech due to muscular weakness. Although these motor speech disorders often accompany Broca’s aphasia, they can also occur in the other aphasias described later. Textbook descriptions of the neural correlates of Broca’s aphasia most commonly associate it with Broca’s area in the posterior, inferior frontal gyrus, as originally described by Broca. Current research

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impairment. This form of aphasia came to be called Wernicke’s aphasia but is also referred to as sensory aphasia or fluent aphasia. Unlike Broca’s aphasia, Wernicke’s aphasia is considered a fluent aphasia because patients with Wernicke’s aphasia speak spontaneously with a normal to fast rate of speech, and their speech rhythm and prosody (melody) are normal. The following is a sample from a patient with Wernicke’s aphasia describing the picnic scene: The/goll//dz/George. It isn’t correct. He guess – he/ hamilz/in the the one guy who/stamilz/in the – oh I can’t say it. This girl who has her own rain. She can see this/goll/who has a ride. A picnic – he is/kain/a you see the mai tai.

Figure 1 Average lesion map of 36 stroke patients with chronic Broca’s aphasia showing the region of common overlap in the insula, rather than Broca’s area.

data, however, suggest that for a chronic, persisting Broca’s aphasia, the lesion is generally much larger, encompassing regions of inferior frontal and insular cortex, as well as deeper, white matter. Indeed, a recent three-dimensional magnetic resonance imaging (MRI) imaging study of Broca’s two original patients’ brains (Tan and Leborgne) revealed that the lesions of these historic cases actually extended quite medially, much deeper than Broca could have seen. Figure 1 shows an average lesion map of 36 stroke patients with chronic Broca’s aphasia (poststroke > 12 months) from our research database. The color bar indicates the degree of lesion overlap across patients, from 0% (dark blue) to 100% overlap (dark red). As can be seen, the region of common overlap in patients with Broca’s aphasia is in the insula (deep red), a region of neocortex that is buried beneath frontal and temporal cortices. We have previously shown this region to be critical for coordinating articulation, which is commonly impaired in patients with Broca’s aphasia.

Wernicke’s Aphasia Karl Wernicke was a German neurologist and psychiatrist born in 1848. In 1874, at the age of just 26 years, he published a major work on aphasia that described patients with an inverse pattern of deficits from that observed by Broca, namely patients with fluent speech and a marked comprehension

Although their speech may be fluent, patients with Wernicke’s aphasia are often unintelligible. This is in part due to the presence of numerous speech errors. Such errors sometimes take the form of literal paraphasias, which involve the swapping of sounds or syllables, or substituting one sound for another (e.g., saying ‘pyramos’ for ‘pyramid’). Sometimes, these errors are so distorted that the target word is unclear (e.g., ‘tiromon’). Such errors are referred to as neologisms. Patients with Wernicke’s aphasia also make semantic errors, substituting a related word for an intended target (e.g., ‘son’ for ‘brother’). Paraphasic errors occur during repetition and naming as well as spontaneous speech. Interestingly, despite the abundance of paraphasic errors in Wernicke’s speech, many aspects of syntactic structure remain intact. In addition to their paraphasic speech, patients with Wernicke’s aphasia also have significantly impaired comprehension. This deficit is apparent in all modalities (i.e., whether spoken or written language), although patients may show slightly improved comprehension with written material. Unlike patients with Broca’s aphasia who only have difficulty with more complex items, patients with Wernicke’s aphasia fail on a range of comprehension tasks from single word comprehension to sentence comprehension. Relative to patients with Broca’s aphasia, patients with Wernicke’s aphasia appear less aware of the severity of their language deficits. Patients with Wernicke’s aphasia are less likely to self-correct errors in their speech production. This may be due in part to their impaired comprehension, which extends to monitoring their own speech output. Wernicke’s aphasia has traditionally been associated with lesions in Wernicke’s area, which generally is defined as the left posterior, superior temporal gyrus. However, the exact boundaries of this area vary from textbook to textbook, presumably because the boundaries were never clearly defined. An overlay of 11 patients’ lesions from our center reveals that a

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Figure 2 Average lesion map of 11 stroke patients with chronic Wernicke’s aphasia. Lesions are centered in the middle temporal gyrus, rather than Wernicke’s area.

lesion centered in the middle temporal gyrus is critical for a chronic, persisting Wernicke’s aphasia (Figure 2). Other areas that are commonly affected include the posterior, superior temporal gyrus and inferior parietal cortex. These regions have been associated with auditory processing, lexical semantics, and verbal working memory.

Conduction Aphasia Conduction aphasia was first described by Wernicke to characterize patients with relatively preserved comprehension and paraphasic speech. Later, Wernicke added to the list of deficits a disorder of repetition. Clinically, patients with conduction aphasia present with fluent speech and relatively good comprehension, but their speech is somewhat paraphasic and their ability to repeat is greatly reduced. Reading and writing, as well as naming, are also affected to a moderate degree. A clinical sample of such a patient’s fluent spoken output describing the picnic scene follows: I see a bunch of people. There’s a tree and a car and a house and water and the pier. Guy’s fishing, and a couple o’ guys that are saying hi to the sail’s person. And a guy washing something next to a/hail/of sand and grass. A flag – is that a flag? And the wind and the pole and some more grass.

Despite such relatively fluent speech, patients with conduction aphasia exhibit significantly impaired

repetition. Patients may get the gist or general meaning of what is said (as evidenced by their relatively good comprehension), but they are impaired at repeating material verbatim. For example, in an attempt to repeat the sentence ‘The pastry cook was elated,’ one patient responded “Something about a happy baker.” This phenomenon suggests that patients with conduction aphasia are relying on a nonverbatim, semantic route since the phonological trace is no longer available. Dependence on this semantic route is also revealed by the fact that repetition is severely affected for nonsense words (e.g., ‘meppen’). Such words have no meaning and thus cannot give rise to a paraphrase or synonym, let alone reproduction of the same word. Although controversial, some researchers divide patients with conduction aphasia into two groups – reproduction and repetition conduction aphasia. These two groups reflect different parts of the complex repetition process. Repetition conduction aphasics are thought to primarily have a problem at the level of holding a memory trace – in other words, a deficit in verbal working memory. Reproduction conduction aphasics are thought to have their primary problem with the processing and production of phonological information. Researchers who maintain this division acknowledge that some patients diagnosed with conduction aphasia fall into both groups. Paraphasic errors in patients with conduction aphasia may take the form of phonemic substitutions (e.g., ‘free’ for ‘tree’) or semantic substitutions (e.g., ‘father’ for ‘brother’). However, they are more likely (than patients with Wernicke’s aphasia) to attempt to correct their errors. For instance, a patient with conduction aphasia was asked to name a line drawing of a cactus and responded by saying “gaktus, no, gaksus, gackone, no, cackus, little screwed up there, cack, cactus! cactus!” Traditional models of aphasia originally suggested that conduction aphasia should arise from lesions to the arcuate fasciculus, the white matter tract connecting Wernicke’s and Broca’s areas. Despite the fact that no data exist to support this model, most textbooks in psychology and neuroscience perpetuate this notion. Instead, patients with conduction aphasia most commonly have lesions centered in left posterior neocortex, most notably in inferior parietal cortex, not the arcuate fasciculus. Figure 3 shows a lesion overlay map of 13 patients with chronic conduction aphasia. As can be seen, the region of common overlap is centered in inferior parietal cortex. This region has been suggested to be critical for verbal working memory, which is consistent with the pattern of repetition deficits observed in this patient group.

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Figure 3 Average lesion map of 13 stroke patients with chronic conduction aphasia, showing a region of common overlap in the inferior parietal cortex.

Figure 4 Average lesion map of seven patients with chronic global aphasia; showing that lesion typically involves a large portion of the left hemisphere.

Global Aphasia Global aphasia is the most severe of all aphasia subtypes, with significant impairments across all aspects of language, namely impaired speech, comprehension, repetition, naming, reading, and writing. Patients with global aphasia may be able to utter automatic or stereotypic responses (e.g., “yes” and “no”) but do so unreliably. For example, one patient with global aphasia when asked to describe the picnic scene from the WAB was only able to utter “no . . . no . . . because” on one occasion and “yeah” on another occasion. Other patients with global aphasia are only able to produce overlearned or automatic phrases (e.g., “How are you?”). Patients with global aphasia also have significantly impaired comprehension. They often have difficulty responding to very simple yes/no questions (e.g., “Are you a man?”). Although the severe loss of speech and language makes it very difficult for patients with global aphasia to communicate, they are sometimes able to convey information by varying the intonation in their voice or by using simple gestures. Importantly, patients with global aphasia can be shown to perform normally on nonverbal tasks (e.g., picture matching), demonstrating that they are not suffering from confusion or dementia. As described previously, some patients with global aphasia have a preserved ability to utter automatic phrases or repetitive utterances. What is the brain

basis of these abilities, if much of the language network is damaged? There is evidence that these automatic and overlearned phrases are generated by regions within the intact right hemisphere of the brain. The right hemisphere is also capable of supporting intonation in speech, musical ability, and emotional expression. Again, these are abilities that are sometimes preserved in patients with global aphasia. As with the other aphasias, global aphasia is most commonly the result of a stroke in the middle cerebral artery that supplies blood to the lateral surface of the left hemisphere of the brain. Not surprisingly, lesions necessary for a persisting, chronic global aphasia are generally quite large and encompass large portions of the left peri-Sylvian region. Lesion overlays from seven patients with global aphasia are shown in Figure 4. This large lesion is responsible for the gross impairment in most aspects of speech and language since the entire language network is affected. Whereas other patients with smaller lesions may find ways of compensating for their language disabilities, patients with global aphasia have less brain reserve with which to do so.

Anomic Aphasia Anomic aphasia is the mildest of the aphasias, with relatively preserved speech and comprehension but difficulty in word finding. The persistent inability to

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find the correct word is known as anomia (literally, ‘without names’). Anomia is actually a symptom of all forms of aphasia, but patients whose primary language problem is word retrieval are diagnosed as having anomic aphasia. In other words, patients with anomic aphasia have relatively preserved speech fluency, repetition, comprehension, and grammatical speech but sometimes have difficulty with word finding. The following is a sample from a patient with anomic aphasia describing the picnic scene: I see a boy who is flying a kite. I see a girl who pouring . . . um . . . the soda an’ I see a girl who is listening her radios. I see a man who is reading a book. I see a man who is fishin’ an’ I see a dog who is waggin’ his tail. I see a boy waiting . . . wading in the water.

Unlike the previous aphasia samples, this patient describes the scene using complete sentences and provides a relatively good level of detail. There are a few minor errors and some groping for words (e.g., ‘soda’), but otherwise her speech is quite clear and communicative, typical of anomic aphasia. When searching for a word, some patients with anomic aphasia paraphrase using words that they can easily retrieve. For instance, a patient shown a drawing of a pair of tongs said “You pick up things with it.” Such circumlocutions demonstrate that patients with anomic aphasia have lost neither conceptual understanding nor the ability to build coherent sentences and phrases. Whereas circumlocutions may be a characteristic feature of the speech of some patients with anomic aphasia, the main characteristic displayed by other patients may be periods of slow and halting speech as they search for the correct word. For instance, when shown a picture, a patient might say, “It’s a, ummm, uhhh, a, a, a . . . I know what it is, it’s a . . . Aww hell, it’s there but I just can’t get it.” Such hesitancy may be so frequent that a patient may be incorrectly classified as having Broca’s aphasia. Not surprisingly, patients with anomic aphasia benefit greatly from cueing, such as providing the first sound of the target word. Low-frequency words are typically more difficult for a patient with anomic aphasia to retrieve and produce than frequently used words. It is very common for proper names to be more difficult to retrieve than common nouns, and common nouns are often more difficult to retrieve than adjectives or verbs. Thus, both the grammatical function of a word and its frequency can affect word retrieval in patients with anomic aphasia. Lesions associated with anomic aphasia are the least well defined because word finding is sensitive to damage throughout much of the peri-Sylvian region.

Figure 5 Average lesion map of 37 patients with chronic anomic aphasia, in which there was no single, common region of overlap.

As shown in Figure 5, there is no single, common region of overlap in this group of 37 patients with anomic aphasia but, rather, the lesions span a wide range of areas in the left hemisphere.

Transcortical Aphasias The transcortical aphasias are a group of aphasia syndromes that all have in common a relatively preserved ability to repeat, despite other significant language deficits. Transcortical motor aphasia is similar to Broca’s aphasia; that is, patients exhibit nonfluent speech and relatively good comprehension, but the ability to repeat is relatively preserved. Transcortical sensory aphasia is simil...