Aphasia and the Relationship of Language and Brain

Eleanor M. Saffran, PhD, Center for Cognitive Neuroscience, Department of Neurology, Temple University School of Medicine, Philadelphia, Pennsylvania.

Semin Neurol. 2000;20(4) 

Abstract

This article provides a brief history of the study of aphasia, along with current data on aphasic syndromes and their localization in the brain as well as information on testing procedures. A brief examination of language from a functional perspective is also provided, as it is difficult to understand the breakdown patterns without an appreciation for the complexities of language processing per se.

A Historical Perspective

Interest in the relationship of language and brain began with the emergence of a scientific mind set in the 19th century. The question was first posed by phrenologists -- practitioners of the pseudoscience that associated bony protrusions in the skull with the enlargement of brain tissue below and hence the development of particular capacities. Although most of the traits that interested phrenologists would strike us as fanciful today (e.g., parental love, conjugality), they did attempt to localize language. They assigned this function to the frontal poles of both hemispheres and assessed it by measuring the size of the bony protrusion below the eye.

The young French physician and anthropologist Paul Broca was skeptical of this approach. He believed that capacities were associated with particular convolutions of the cerebral hemispheres that were not linked in any direct way to bumps on the skull. Broca had the opportunity to examine the brain of a language-impaired patient, M. Leborgne, when it came to autopsy. The patient had been capable of very little speech although his comprehension appeared well preserved. Broca observed an area of damage in the left cerebral hemisphere, surrounding the third frontal convolution. After seeing a number of similar cases, Broca[1] postulated that this area of the brain was the locus for articulate speech. He also suggested that left hemisphere control of language production was associated with its control of the dominant right hand, and he proposed mirror image organization -- right hemisphere dominance -- in left-handers. Although Broca was correct in his first assumption, we now know that the left hemisphere is dominant for language in most left-handers (approximately 70%) as well as nearly all right-handers (on the order of 96%).[2]

Several years later, Carl Wernicke[3] made other important observations. He saw a patient whose comprehension was severely impaired; when the patient came to autopsy, the lesion was discovered in the posterior, superior left temporal lobe. On the basis of additional observations of similar patients, although not always backed up by anatomical data, Wernicke hypothesized that this area was the locus of storage of "auditory word images," which were necessary for the production as well as the comprehension of speech. The patients he saw exhibited anomalies in production along with their comprehension disorder: they frequently produced words that did not fit the context and generated combinations of speech sounds that did not qualify as words in their native language ("neologisms"). Wernicke assumed, further, that there was a fiber tract connecting this region with the area identified by Broca and that speech production was influenced by activity in Wernicke's area, as this left hemisphere brain region came to be known. He predicted that damage to the connecting tract would lead to a speech production disorder with preserved comprehension, as well as a disorder of repetition -- a prediction later verified. That syndrome was termed "conduction aphasia." Although it was earlier believed that this disorder arose from interruption of the arcuate fasciculus, the fiber tract that connects these two areas, it is now generally accepted that the syndrome can be produced by damage at a variety of locations including the supramarginal gyrus as well as by interruption of fiber tracts lying deep to sensory cortex in the parietal lobe.[2]

This approach to the relationship of brain function and behavior, which posits centers for specific processing operations along with connections between them, came to be known as "connectionism" (which should be distinguished from the present usage of the term, which refers to computational modeling). The connectionist approach to language was further elaborated by Carl Lichtheim,[4] who posited a concept center, diffusely represented in the brain, that served as the endpoint of language comprehension as well as the source of messages that were ultimately produced by the speaker. Lichtheim's diagram for the language system is reproduced in Figure 1. On the basis of this diagram, he postulated disorders that had not yet been described, such as transcortical sensory aphasia, in which the projection from Wernicke's area to the concept center is disrupted, resulting in impaired comprehension and production, with repetition preserved because of the patent connection between Wernicke's and Broca's areas.[5]

Figure 1.

 

Lichtheim's diagram of the language system. A, Wernicke's area; B, concept center; M, Broca's area; a --> A, auditory input to Wernicke's area; M --> m, motor output from Broca's area. A --> M, tract connecting Wernicke's and Broca's areas; A --> B, pathway essential for understanding spoken input; B --> M, pathway essential for meaningful verbal output. Lesions: at A, Wernicke's aphasia; at M, Broca's aphasia; a --> A, pure word deafness; M --> m, articulatory disorder (aphemia); A --> M, conduction aphasia; A --> B, transcortical sensory aphasia; B --> M, transcortical motor aphasia.

Although the connectionist approach appeared to be productive and was subsequently extended to reading disorders,[6] it was criticized by later investigators who adopted a holistic view of the function of the language area.[7,8] The holistic approach prevailed until connectionism was revived by the neurologist Norman Geschwind in the 1960s.[9,10] At around the same time, some speech pathologists and psychologists promoted the idea that the language area was not divisible and functioned as a whole.[11] Among neurologists, this view was subsequently promoted by Mesulam.[12] The controversy between the localizers and those who take a more holistic approach to language function persists to this day. The holistic camp takes the co-occurrence of symptoms -- for example, word-finding deficits and grammatical simplification in the production of patients with Alzheimer's disease -- to reflect common, overlapping storage and retrieval mechanisms for words and syntax.[13] An alternative view, favored by those who accept regions of specialization within the language system, is that one deficit is the cause of the other: in this case, that the word retrieval deficit limits the ability to construct complex utterances.[14]

With respect to the localization of functions, the early researchers were limited by the restriction to autopsy material. The advent of imaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI), as well as the new methods for functional imaging (positron emission tomography [PET] and functional magnetic resonance imaging [fMRI]), have vastly increased the scope of these investigations. More recent studies have demonstrated the variability[15] as well as the extent of the lesions that give rise to particular language disorders. For example, Broca localized the center for articulate language at the foot of the third frontal convolution, even though the lesion in his patient extended well beyond this area. It has been shown that a lesion restricted to Broca's area gives rise to a transient impairment of language production and that the full complement of symptoms associated with Broca's aphasia (articulation problem coupled with simplified sentence structure -- the pattern known as "agrammatism") is the result of more extensive damage to the frontal cortex.[16] There is evidence, moreover, that the articulation problem present in Broca's aphasia ("apraxia of speech") is associated with damage to a portion of the insula, a part of the cerebral cortex that is not visible from the brain's surface because of the growth of other parts of the frontal lobe.[17] It has also become apparent that the language area includes the zone now known as the perisylvian cortex (the cortical area above, below, and posterior to the sylvian fissure), which includes considerably more brain tissue than the areas identified by Broca and Wernicke. There is also evidence that certain types of language impairments result from damage out-side the boundaries of the perisylvian cortex, a matter we will consider below.

The Classical Syndromes and Attempts at Quantification

The connectionist schema elaborated by Lichtheim4 specified a number of different syndromes, to which additional ones have been added in recent years (e.g., global aphasia; anomia). The classical syndrome patterns are described in . Important terms to note include "paraphasia," which refers to errors in word production; these include "verbal paraphasias," which are substitutions of other words (e.g., "doctor" for nurse; "horse" for house), and "literal (or phonemic) paraphasias," which are sound substitutions (e.g., "doctin" for doctor; "ramonica" for harmonica). (Note that the latter qualify as neologisms, because they are not words in English.) "Conduite d'approche" refers to the tendency, most evident in conduction aphasics, to make repeated attempts at a word (e.g., for pretzel, "trep . . . tretzle . . . trethle . . . tredfles . . . ki")[18] that do not necessarily result in closer approximations to the target. These attempts indicate that the patient knows what the word should sound like and is dissatisfied with his or her efforts. Repeated attempts are less frequent in Wernicke's aphasia, in which patients appear less successful in monitoring their output. The term "agrammatism" refers to a speech pattern in which sentence structures are simplified and grammatical morphemes -- inflections such as the past tense marker, -ed, as well as freestanding elements such as articles, auxiliary verbs, and prepositions -- are frequently omitted. "Semantic reversibility" refers to sentences such as "The boy is kissed by the girl" or "The dog that the cat chased was black," in which either entity could conceivably be performing the action on the other. Whereas many patients have no difficulty understanding semantically constrained sentences, such as "The bone was eaten by the dog," they are impaired in understanding sentences in which the syntax must be used to determine which entity is the perpetrator and which the recipient of the action. "Paragrammatism" refers to structured production in which grammatical morphology is not entirely correct, often because one morpheme is substituted for another. To illustrate these points, and provide examples of the production of an agrammatic Broca's aphasic ( ) and a fluent Wernicke's aphasic ( ).

Figure 2 illustrates typical locations for the lesions associated with these syndromes. It should be emphasized, however, that there is considerable variability in these lesion sites with respect to both the cortical tissue involved and the damage to white matter underlying the cortex.[15] Isolating a cortical area by interrupting the fiber tracts that project to it can produce functional consequences that are similar to those produced by damage to the cortical region itself. It should also be noted that the listing in and the lesion site examples in Figure 2 reflect some simplification of the actual syndrome complexes. For example, there are classifications that distinguish among subtypes of syndromes reflecting different lesion sites. In the case of transcortical motor aphasia,[19] two subtypes are proposed, one associated with the dorsolateral frontal lesion shown in Figure 2 and another that results from damage to the supplementary motor cortex in the left hemisphere, reflecting infarction of the anterior as opposed to the middle cerebral artery. They also suggest two loci for transcortical sensory aphasia, although the second type, reflecting damage to the angular gyrus of the parietal lobe, might be described by others as "anomic aphasia." No lesion sites for anomic aphasia are given in Figure 2 for the reason that this disorder can result from damage to a variety of loci within the left hemisphere15 and is often the residual symptom following recovery from a number of different types of aphasia. For additional information on lesion sites and variability in the symptomatology, see references 2 and 19.

Table 1.  Descriptions of Major Aphasic Syndromes

Syndrome Speech Naming Sentence
Production
Word
Comprehension
Sentence
Comprehension
Repetition
Global Aphasia Impaired Impaired Absent Impaired Impaired Impaired
Broca's Aphasia Nonfluent;
articulation
impaired
Impaired to
relatively
good; nouns
> verbs
Impaired,
agrammatic
Impaired to
relatively good
Impaired for
semantically
reversible
sentences
Impaired
Conduction
Aphasia
Fluent,
paraphasic;
conduite
d'approche
Variable, but
paraphasic
Well structured,
paraphasic
Good Variable; may be
impaired for
complex
sentences
Impaired
Wernicke's
Aphasia
Fluent but
paraphasic; may
be excessive
Impaired Structured but
empty
Impaired Impaired Impaired
Transcortical
Sensory
Fluent,
paraphasic
Impaired Structured but
empty
Impaired Impaired Preserved
Transcortical
Motor
Preserved but
sparse
Variable Variable Good Variable Preserved
Anomia Fluent but
hesitant due to
poor word
retrieval
Impaired Structured but
impaired by
word finding
difficulty
Variable Relatively good Preserve

Figure 2.

 

Lesion locations for the major aphasia syndromes.

There have been a number of attempts to develop quantitative descriptions of these syndromes based on data from batteries of aphasia tests. Currently, the most widely used are the Boston Diagnostic Examination for Aphasia (BDEA), developed by Goodglass and Kaplan,[18] and the Western Aphasia Battery, developed by Kertesz.[20] Two examples of syndrome patterns from the BDEA are illustrated in Figure 3. Although the tests offer rather strict guidelines for classifying patients, syndrome designations are applied rather broadly by practicing clinicians. Thus, for example, many utilize the term Broca's aphasia for nonfluent production patterns irrespective of whether the patient demonstrates the agrammatic speech characteristics specified in Figure 3. As a result, the variability tolerated under this label may render the syndrome designation too broad for the purpose of grouping patients for study.[21] There is also evidence that patients may shift from one syndrome to another as they recover; for example, some patients begin as Wernicke's aphasics and later, with some recovery of comprehension, are reclassified as conduction aphasics or anomics; others are initially diagnosed as global aphasics and subsequently qualify as Broca's aphasics. Although it is important to acknowledge shortcomings in applying these labels, it is nevertheless the case that the syndrome designations serve as a useful shorthand for the major deficit patterns exhibited by aphasic patients.

Figure 3A-B.

 

(A) Deficit pattern for Broca's aphasia. (B) Deficit pattern for Wernicke's aphasia. (Redrawn from Goodglass H, Kaplan E. The Assessment of Aphasia and Related Disorders. 2nd ed. Philadelphia: Lea & Febiger; 1983.)

Figure 3A-B.

 

(A) Deficit pattern for Broca's aphasia. (B) Deficit pattern for Wernicke's aphasia. (Redrawn from Goodglass H, Kaplan E. The Assessment of Aphasia and Related Disorders. 2nd ed. Philadelphia: Lea & Febiger; 1983.)

The standard aphasia examination involves tests of comprehension at the word and sentence level, word (e.g., picture naming) and sentence production, and repetition. Although the ability to repeat what others say has little function in adult life, this capacity is critical in differentiating certain of the aphasic syndromes from one another. For example, the symptoms of Wernicke's and transcortical sensory aphasia are similar except for the preservation of repetition in the latter. Reading and writing capacities are also examined, although they will not be considered in this article.

Language: A Functional Perspective

To appreciate the full range of symptoms exhibited by patients with language disorders, it is necessary to consider language from a functional perspective -- that is, the set of processes thought to account for the comprehension and production of language. The result of investigations within the subfield of psychology known as psycholinguistics, these processes are outlined in Figure 4. It is clear, for example, that there are specialized mechanisms for the perception of speech, which consists of brief stimuli that change rapidly in wavelength composition. Cutting off input to critical left temporal areas as a result of a left hemisphere lesion, or in some cases lesions in both hemispheres (the lesion on the right deprives the left hemisphere of transcallosal input), results in the disorder known as "pure word deafness," in which patients can hear but cannot understand speech; their native tongue, for example, sounds to them like a foreign language. Moreover, these patients have difficulty discriminating between speech sounds (between "pa" and "ba," for example), although they have little or no difficulty producing speech and understanding written language.[22]

Figure 4.

 

Language processing from a functional perspective.

Hearing speech adequately is not sufficient, however; words must be recognized as such and associated with their meanings. To examine the capacity for word recognition, psychologists use a task termed "lexical decision" in which the subject must determine whether a string of sounds (or letters, if visual presentation is used) is a real word or nonword. The retrieval of word meaning is often assessed by matching a word to a picture. The most sensitive way to construct such a test is to embed the correct picture among others that are related to the target word (e.g., if the word is "pear", the nonmatch drawings would depict other fruits). The reason for this is that patients sometimes retain some aspects of the meaning of a word (such as its semantic category) and therefore have difficulty distinguishing it from other category members, although they may perform very well if the choices come from other classes. But not all words are picturable; to examine knowledge of abstract words, subjects may be asked to match a word to one of several on the basis of meaning (e.g., freedom to liberty, justice, and knowledge). Sensitivity to verb meaning should also be tested; this can be done with pictures or by means of the word-matching paradigm described for abstract words.

Whereas understanding the meaning of single words is essential to language comprehension, most messages are expressed as sentences, where structural considerations (grammar or syntax) are also important. To assess syntactic capacities, it is necessary to use sentences that are semantically reversible (e.g., "The girl is kissed by the boy") -- in other words, sentences in which either participant could conceivably be acting upon the other. If semantic constraints are present (as in "The book is read by the boy"), they may be utilized to construct the correct interpretation. Thus, Broca's aphasics appeared to have adequate sentence comprehension when they were tested with semantically constrained sentences; their difficulty with sentence-level materials did not emerge until they were tested with semantically reversible sentences.[23] It should be noted, however, that currently available aphasia batteries are not always sensitive to the reversibility factor. Other tasks used to examine syntactic capacities include judgments of grammaticality. Patients hear sentences that are either grammatical or contain some syntactic violation and are asked to judge whether the sentence represents "good" or "bad" English.[24] Interestingly, patients may perform well on the judgment task even though they are impaired in comprehending reversible sentences (this matter is discussed in more detail later). In addition, the information serially extracted from the sentence must be maintained in a short-term or working memory. Virtually all aphasic patients suffer from verbal short-term limitations (as measured, for example, by asking them to repeat digit strings; their performance tends to be well below the normal span of about seven.). One particular group with left posterior parietal lesions25 suffers from short-term memory limitations but little else, and many of these patients have sentence comprehension deficits similar to those described in Broca's aphasics.[26]

On the output side, production begins with an intention, initially encoded as a nonverbal message. The next task is to retrieve words that correspond to the message, which are first represented abstractly, as "lemmas" -- that is, not yet spelled out phonologically as sequences of sounds. The syntactic specifications of these words are also retrieved (i.e., whether they are nouns, verbs, adjectives, etc.; if verbs, the kinds of syntactic structures they require, and so forth). Then a sentence structure is specified (for example, whether the voice is active or passive, whether a relative clause is required). The sentence structure specifies the order in which the words are to appear. Then the words are retrieved, with their sound specifications, in the order dictated by the structure of the sentence. From this string of phonologically specified elements, a motor speech program is assembled and ultimately sent to the articulators. The manner in which this is accomplished is not yet clear. One possibility is that the speaker retrieves successive syllables from a syllabary that is acquired in learning to speak the language.[27] One virtue of this theory is that it constrains the speaker to the production of sound sequences that are present in the language; these sequences are seldom violated, even in the speech errors of normal speakers and aphasics. It should be noted that the motor speech program is specified not only for content words, such as nouns, verbs, and adjectives, but also for grammatical elements such as inflections on verbs, auxiliary verbs, relative pronouns, and prepositions. At least some of these elements must be inserted at a late stage of sentence production, as their form depends on context (e.g., use of "a" or "an," depending on whether the following word starts with a vowel or consonant). The grammatical features are an essential part of the prosodic (rhythmic) structure of the utterance, as they are pronounced together with the content words that follow or precede them (e.g., theboy istalking . . .). In English, these elements are often omitted by agrammatic speakers (see ); in other languages, where they cannot be deleted (as in Hebrew, where the vowels of a verb denote tense), they are prone to error because of the occurrence of substitutions.[28]

Table 2.  Speech Pattern of an Agrammatic Aphasic Telling the Story of Cinderella

Long ago Cinderella. One time many years ago two sisters and

one stepmother. Cinderella is washing clothes and mop floor.

One day big party in the castle. Two girls dresses is beautiful.

Cinderella is poor. Two sisters left. In the castle Cinderella is

. . . Godmother. Oh, what's wrong? No money. A little mouse.

Cinderella hurry. Queen. Magic wand. Mouses. Oh big men

now. Magic wand pumpkin then chariot. Cinderella dresses no

good. Cinderella. On my god beautiful now. Next time, twelve

o'clock, hex. Then Cinderella party. Many women at the party.

Prince is . . . no good. Oh, prince is . . . Cinderella. Dance

dance. Two hours. Dance dance dance. Twelve o'clock, oh my

god. Cinderella. What's wrong? I leave, I leave, I leave. One

shoe slip. Cinderella is twelve o'clock. Poor again. Tomorrow,

prince slipper. Village many houses. One house, knock, knock.

What's wrong. Prince is . . . One, two kids, OK, OK. First one

too small. Second was too big. Hey wait a minute, wait a

minute. Prince. You. What's wrong. Hey, slip it on. Oh. Does fit.

Godmother. Magic wand. New gown again. Then magic prince

and godmother went in the castle.

Note, then, that both language comprehension and production entail the retrieval of several different types of information that must also be integrated -- meanings, word forms, syntactic specifications for words, and all of these with syntactic structure that is derived from the perceived sentence or sequenced for the sentence to be uttered. One can imagine that these complex tasks require a good deal of integration across knowledge sources, which may explain why they frequently break down in patients with aphasia.

Open Questions: Where is Syntax?

The finding that agrammatic Broca's aphasics also had a problem in sentence comprehension gave rise to the hypothesis that they suffered from a "central syntactic deficit" -- in other words, that their knowledge of grammatical structure was compromised, affecting comprehension as well as production.[29] It was subsequently found, however, that not all of these aphasics suffered from a comprehension problem;[30] further, they performed relatively well in judging the grammaticality of sentences spoken to them.[24] The ability to perform the grammaticality judgment task clearly depends on the preservation of syntactic knowledge. There is also evidence that although the spontaneous production of these patients is restricted to simple sentence forms, there are ways of getting them to produce more complex utterances. One such task involves alternating sentence repetition with picture description, where the pictures have no overlap with the content of the sentences provided for repetition.[31] But the production of more complex sentences does not guarantee that these patients will use correct morphology. For example, after repeating a passive sentence (e.g., "The dog was pulled by the man") and being presented with a picture of a boy stung by a bee, a patient might say "The boy is stinging for the bee." Although this sentence has the same underlying syntactic structure as the passive, the verb is improperly inflected and the preposition is incorrect.[32]

The fact that these patients can judge grammaticality with reasonable accuracy suggests that the critical area for syntactic processing lies outside the region of damage that results in Broca's aphasia. Indeed, unpublished data from our laboratory indicate that Wernicke patients perform worse than Broca's aphasics on grammaticality judgment tasks. But if syntax is preserved, why do these patients have a comprehension problem, at least with respect to semantically reversible sentences? This difficulty is often exacerbated when the noun that precedes the verb is not the doer of the action (as, for example, in the case of the passive), probably because the agent generally precedes the verb in English sentences.[33] One possibility is that the patients extract syntactic structure from the sentences they hear but fail to integrate structural with other critical information -- such as the identities of the lexical items, their meanings, and knowledge of the thematic structure of the verb (i.e., the roles of the nouns in relation to the verb -- e.g., agent or recipient of the action -- and their relation to syntactic structure). Instead, they rely on semantic constraints and on strategies such as taking the preverbal noun to be the agent.

A possible account of the effect of damage to frontal language cortex is that this area serves to activate posterior language processing regions -- as is the case for other capacities, such as spatial processing carried out by parietal cortex under the influence of frontal activation.[34] Functional imaging studies in normal subjects have shown that activation of the frontal language area increases with syntactic complexity;[35,36] in addition, electrophysiological investigations reveal that left frontal activation is increased by the presence of grammatical violations.[37] One might expect demands on the syntactic processor to increase as a function of increasing complexity or grammatical error. It is interesting to note that Broca patients also have difficulty with certain grammaticality judgment tasks, in particular, those that entail linking particular word identities (and/or their meanings) to particular locations in the sentence. Thus, they proved to be insensitive to violations involving reflexive sentences (e.g., "The woman looked at himself in the mirror") in which the gender of the pronoun conflicts with that of the noun to which it refers.[24,38] This further suggests that the capacity to integrate the various types of information required for the understanding of sentences is limited in these patients. It may also be the case that frontal activation is critical for sentence production. One view of the sentence production deficit in Broca's aphasics is that it reflects a timing problem in which lexical items are retrieved too slowly to integrate with sentence structure.[39] Decreased activation of lexical capacities because of the loss of frontal activation might account for such a deficit. It should be noted, however, that many other explanations of these impairments have been proposed, ranging from short-term memory limitations40 to specific syntactic functions attributed to frontal language cortex.[41] The literature on this question is still mired in controversy.[42]

Open Questions: The Nature of Semantic Organization

Although most of the classical syndromes reflect damage to the perisylvian language area, the lesions that produce the transcortical aphasias -- sensory and motor -- generally lie outside this region. Other disorders also result from damage to cortical structures outside the perisylvian cortex. Lesions that affect anterior inferior regions of the left temporal lobe (or both temporal lobes) are known to result in semantic deficits in which patients have difficulty finding words and understanding them and often exhibit impairments with pictured materials as well.[43] In most cases, these deficits do not result from the vascular etiologies that are the primary causes of the major aphasia syndromes. One source of semantic impairment is herpes simplex encephalitis, which has a predilection for anterior (and medial) temporal tissue; another is a form of progressive aphasia, which leaves the patient fluent but with severe word-finding and comprehension difficulty because of deterioration of structures in the left anterior temporal lobe (sometimes both lobes). The latter disorder has been termed semantic dementia,[44,45] reflecting the fact that other cognitive functions (e.g., recent memory, spatial processes) remain intact for some period of time. This area is also affected in Alzheimer's disease, where the semantic deficit is accompanied by other cognitive disturbances.[46]

Although the semantic disturbance is in some cases quite general, in other instances there is some selectivity in the impairment. For example, some cases (of both herpes encephalitis and semantic dementia) have been described in which abstract words are better preserved than concrete words.[47-49] This is a surprising finding, as normal subjects typically show a superiority for concrete words,[50] which is often exacerbated by left hemisphere brain damage.[51] One possible account of this pattern is that the anterior temporal lobe is the locus of convergence of information from sensory association areas on its way to hippocampus and surrounding structures; consider, for example, that this area lies anterior to brain regions responsible for visual object recognition.[52] Indeed, knowledge of the perceptual properties of objects -- critical aspects of meaning for concrete words -- appears deficient in patients who demonstrate the abstract superiority effect.[47] Other patients, including most of those who show abstract superiority,[49] demonstrate better preserved knowledge of man-made objects (e.g., tools and utensils) than living things (animals, fruits and vegetables as well as other types of food). Again, perceptual properties may be particularly important in distinguishing among objects in these categories. Consider, for example, the primary distinctions among animals such as tigers, lions and leopards, who share many features of behavior and habitat; we differentiate them primarily on the basis of the way they look. Although perceptual properties may be critical here, loss of this information is not the only source of specificity in semantic impairment. Other patients with left frontoparietal lesions are more impaired on artifacts than living things; they are also typically impaired on body parts.[53] Evidence suggests that this deficit reflects loss of information as to the manner in which objects are manipulated, which may reflect impairment of motor and sensory areas in the left hemisphere.[54]

These findings suggest that semantic information is broadly distributed in the brain and that meaning resides in other regions in addition to the classical language areas. This is to be expected, given continuity with non-verbal creatures, who also acquire knowledge of the world they inhabit. It is likely, of course, that the representations of an object across different regions (visual, auditory, tactile, and linguistic) are interconnected and that all parts of the representation are normally activated when a word or object is encountered.[55] In fact, functional imaging studies have shown that words and objects activate the same brain regions in semantic tasks56 but that there is also some selectivity, depending on the type of object that is tested. For example, left frontal cortex is activated when the materials are tools.[57-59] It also seems reasonable that in cases of brain damage, subregions may be disconnected from one another. Although it is reasonable to propose that semantic information is distributed in the brain, there is still considerable debate as to whether there is a unitary semantic system in humans60 or one that includes subregions specialized for particular types of information.[49,61]

Concluding Remarks

Studied for well over a century, the clinical manifestations of aphasia have been well described, and reasonably good data that localize the major syndrome types are available. Nevertheless, our knowledge of the relationships between language and brain remains incomplete. We lack an adequate understanding of how sentences are comprehended as well as how they are generated. The path from some sort of fairly abstract phonological representation of an utterance to its motor implementation is also poorly understood. And, there is still considerable debate about how the meanings of words and objects are represented. Although the study of brain-damaged individuals has contributed a great deal to our understanding of these and other questions, much remains to be done. Future research will no doubt entail collaboration between psycholinguists and clinical scientists on the various forms of language breakdown, and the implementation of functional imaging techniques in studies of brain-damaged as well as normal individuals.

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