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Aphasia is an acquired disorder of language subsequent to brain damage that affects auditory comprehension, reading, oral-expressive language, and writing. Early observations by Broca (1861a, 1861b) and Wernicke (1874) suggested that aphasia might be classified into a variety of syndromes, or types, based on differences in auditory comprehension and oral-expressive language behaviors. Moreover, different syndromes were believed to result from different sites of brain damage. Revisions of early classification systems yield a contemporary taxonomy that comprises seven syndromes: global, Broca's, transcortical motor, Wernicke's, transcortical sensory, conduction, and anomic (Benson, 1988; Kertesz, 1979). Classification is based on the aphasic person's auditory comprehension, oral-expressive fluency (phrase length and syntax), spoken repetition, and naming abilities. The seven syndromes can be divided into nonfluent, those with short phrase length and impaired morphosyntax (global, Broca's, and transcortical motor), and fluent, those with longer phrase length and apparent preservation of syntactic structures (Wernicke's, transcortical sensory, conduction, and anomic). An aphasic person's syndrome may be determined by informal examination or by administering a standardized test, for example, the Western Aphasia Battery (WAB) (Kertesz, 1982) or the Boston Diagnostic Aphasia Examination (BDAE) (Goodglass and Kaplan, 1983). The following describes each syndrome and the assumed site of lesion associated with each.
Global Aphasia
This nonfluent syndrome is associated with a large left hemisphere lesion that may involve the frontal, temporal, and parietal lobes, insula, and underlying white matter, including the arcuate fasciculus (Dronkers and Larsen, 2001). It is the most severe of all of the syndromes. Auditory comprehension is markedly reduced and may be limited to inconsistent comprehension of single words. Oral-expressive language is sparse, often limited to a recurring intelligible—“bees, bees, bees”—or unintelligible—“doobe, doobe, doobe”—stereotype. Other automatic expressions, including profanity and counting, may also be preserved. Globally aphasic patients are unable to repeat words, and no naming ability is present. Reading and writing abilities are essentially absent.
Broca's Aphasia
This nonfluent syndrome receives its name from the early reports by Paul Broca (1861a, 1861b). Classical localization of the lesion resulting in Broca's aphasia is damage in the left, inferior frontal gyrus—Broca's area (Brodmann's areas 44 and 45) (Damasio, 1992). However, both historical (Marie, 1906) and contemporary (Mohr, 1976; Dronkers et al., 1992) reports question the classical lesion localization. Patients have been described who have lesions in Broca's area without Broca's aphasia, and other patients have Broca's aphasia but their lesion does not involve Broca's area. Auditory comprehension is relatively good for single words and short sentences. However, comprehension of grammatically complex sentences is impaired. Their phrase length is short, and they produce halting, telegraphic, agrammatic speech that contains, primarily, content words. For example, describing how he spent the weekend, a patient with Broca's aphasia related, “Ah, frat, no Saturday, ah, frisk, no, fishing, son.” Repetition of words and sentences is poor. Naming ability is disrupted, and reading and writing show a range of impairment.
Transcortical Motor Aphasia
Lichtheim (1885) provided an early description of this nonfluent syndrome, and he observed that the site of lesion spared the perisylvian language region. Currently, it is believed that the lesion resulting in transcortical motor aphasia is smaller than that causing Broca's aphasia and is in the left anterior-superior frontal lobe (Alexander, Benson, and Stuss, 1989). With one exception, language behaviors are similar to those in Broca's aphasia: good auditory comprehension for short, noncomplex sentences; short, halting, agrammatic phrase production; disrupted naming ability; and impaired reading and writing. The exception is relatively preserved ability to repeat phrases and sentences. Essentially, patients with transcortical motor aphasia repeat much better than would be predicted from their disrupted, volitional productions.
Wernicke's Aphasia
This fluent syndrome received its name from the early report by Carl Wernicke (1874). The traditional belief is that Wernicke's aphasia results from a lesion in Wernicke's area (posterior Brodmann's area 22) in the left hemisphere auditory-association cortex (Damasio, 1992), with extension into Brodmann's areas 37, 39, and 40. However, Basso et al. (1985) have reported cases of Wernicke's aphasia resulting from exclusively anterior lesions, and Dronkers, Redfern, and Ludy (1995) have found Wernicke's aphasia in patients whose lesions also spared Wernicke's area. Spoken phrase length averages six or more words, and a semblance of syntax is present. However, the oral-expressive behavior includes phonological errors and jargon. One patient with Wernicke's aphasia described where he went to college, Washington and Lee University, by relating, “There was the old one, ah Frulich, and the young one, young hunter, ah, Frulich and young hunter or Brulan.” A salient sign in Wernicke's aphasia is impaired auditory comprehension. These patients understand little of what is said to them, and the deficit cannot be explained by reduced auditory acuity. In addition, verbal repetition and naming abilities are impaired, and there is a range of reading and writing deficits.
Transcortical Sensory Aphasia
This fluent syndrome may result from lesions surrounding Wernicke's area, posteriorly or inferiorly (Damasio, 1992). Oral-expressive language is similar to that seen in Wernicke's aphasia: longer phrase length and relatively good syntax. Auditory comprehension is impaired, similar to that in Wernicke's aphasia, and naming, reading, and writing deficits are present. The salient sign in transcortical sensory aphasia is preserved verbal repetition ability for words and, frequently, long and complex sentences. Essentially, transcortical sensory aphasia patients repeat better than one would predict based on their impaired auditory comprehension.
Conduction Aphasia
Wernicke (1874) described this fluent syndrome. Lesion localization has been controversial. Geschwind (1965) proposed that conduction aphasia results from a lesion in the arcuate fasciculus that disrupts connections between the posterior language comprehension area and the anterior motor speech area. Damasio (1992) suggested that conduction aphasia results from damage in the left hemisphere supramarginal gyrus (Brodmann's area 40), with or without extension to the white matter beneath the insula, or damage in the left primary auditory cortices (Brodmann's areas 41 and 42), the insula, and the underlying white matter. Dronkers et al. (1998) reported that all of their patients with conduction aphasia had a lesion that involved the posterior-superior temporal gyrus, often extending into the inferior parietal lobule. The salient sign in conduction aphasia is impaired ability to repeat phrases and sentences in the presence of relatively good auditory comprehension and oral-expressive abilities. Although auditory comprehension is relatively good, it is not perfect. And, while oral-expressive language is fluent (longer phrase length and a semblance of syntax), patients with conduction aphasia make numerous phonological errors and replace intended words with words that sound similar. Naming, reading, and writing abilities are disrupted to some extent.
Anomic Aphasia
This fluent syndrome is the least severe. Anomia—word-finding difficulty—is present in all aphasic syndromes; thus, localization of the lesion that results in anomic aphasia is not precise. It can be found subsequent to anterior or posterior lesions (Dronkers and Larsen, 2001), and Kreisler et al. (2000) report anomic aphasia resulting from a lesion in the thalamus; medial temporal area; or frontal cortex, insula, and anterior part of the temporal gyri. Patients with anomic aphasia display longer phrase length and preserved syntax; mild, if any, auditory comprehension deficits; good repetition ability; and mild reading and writing impairment. Frequently, the anomic patient will substitute synonyms for the intended words or replace the desired word with a generalization, for example, “thing” or “stuff.”
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