Broca Aphasia Results from a Large Lesion in the Left Frontal Lobe
Broca aphasia is a disorder of speech production that includes impairments of grammatical processing. Patients have labored and slow speech, articulation is impaired, and the melodic intonation of normal speech is lacking (Table 60–2). Yet patients sometimes have considerable success at verbal communication even when they are difficult to understand because their selection of certain types of words, especially nouns, is often correct. By contrast, verbs as well as grammatical words such as prepositions and conjunctions are poorly selected or can be missing altogether. Another major sign of Broca aphasia is a defect in the ability to repeat complex sentences spoken by the examiner. In general, patients with Broca aphasia give the impression that they comprehend the words and sentences they hear, but suitable tests reveal that comprehension is incomplete.
Table 60–2Examples of Spontaneous Speech Production and Repetition for the Primary Types ||Download (.pdf) Table 60–2 Examples of Spontaneous Speech Production and Repetition for the Primary Types
|Type of aphasia ||Spontaneous speech ||Repetition |
| ||Stimulus (Western Aphasia Battery picnic picture): What do you see in this picture? ||Stimulus: "The pastry cook was elated." |
|Broca ||"O, yea. Det's a boy an' a girl … an' … a … car … house … light po' (pole). Dog an' a … boat. 'N det's a … mm … a coffee, an' reading. Det's a mm … a … det's a boy … fishin.'" (Elapsed time: 1 min 30 s) ||"Elated." |
|Wernicke ||"Ah, yes, it's, ah … several things. It's a girl … uncurl … on a boat. A dog …' S is another dog … Uh-oh … long's … on a boat. The lady, it's a young lady. An' a man a They were eatin.' 'S be place there. This … a tree! A boat. No, this is a … It's a house. Over in here … a cake. An' it's, it's a lot of water. Ah, all right. I think I mentioned about that boat. I noticed a boat being there. I did mention that before … Several things down, different things down … a bat … a cake … you have a …" (Elapsed time: 1 min 20 s) ||"/I/ … no … In a fog." |
|Conduction ||"Kay. I see a guy readin' a book. See a women /ka … he … /pourin' drink or something.' An' they're sittin' under a tree. An' there's a … car behind that an' then there's a house behind th' car. An' on the other side, the guy's flyn' a /fait … fait/(kite) See a dog there an' a guy down on the bank. See a flag blowin' in the wind. Bunch of /hi … a … /trees in behind. An a sailboat on th' river, river … lake. 'N guess that's about all … 'Basket there." (Elapsed time: 1 min 5 s) ||"The baker was … What was that last word?" ("Let me repeat it: The pastry cook was elated.") "The baker-er was / vaskerin/ … uh …" |
|Global ||(Grunt) ||(No response) |
Because most patients with Broca aphasia give the impression of understanding conversational speech, the condition was initially thought to be a deficit of production only. But Broca aphasics only comprehend sentences whose meaning can be derived from the meaning of the words used. They have difficulty comprehending sentences with meanings that depend mostly on grammar. Broca aphasics can understand The apple that the girl ate was green but have trouble understanding The girl that the boy is chasing is tall. This is because the patients can understand the first sentence without recourse to grammatical rules—girls eat apples, but apples do not eat girls; apples can be green, but girls cannot. The patients have difficulty with the second sentence, however, because both girls and boys can be tall, and either can chase the other. To understand the second sentence it is necessary to analyze its grammatical structure, something that Broca aphasics have difficulty doing.
Broca aphasia results from damage to Broca's area (the inferior left frontal gyrus, which contains Brodmann's areas 44 and 45); surrounding frontal fields (the external aspect of Brodmann's area 6, and areas 8, 9, 10, and 46); the underlying white matter, insula, and basal ganglia (Figure 60–6); and a small portion of the anterior superior temporal gyrus. A small sector of the insula, an island of cortex buried deep inside the cerebral hemisphere, can also be included in the correlates of Broca's aphasia. This is because patients who have lesions in a small part of the left insula have difficulty pronouncing phonemes in their proper order. They usually produce combinations of sounds that are very close to the target word, suggesting that they have trouble coordinating the articulatory movements necessary for speech. They have no difficulty perceiving speech sounds or recognizing their own errors and no trouble in finding words.
Sites of lesions in Broca aphasia.
(Reproduced, with permission, from Hanna Damasio.)
A. Top: Three-dimensional MRI reconstruction of a lesion (an infarction) in the left frontal operculum (dark gray) in a patient with Broca aphasia. Bottom: Coronal MRI section of the same brain through the damaged area.
B. Top: Three-dimensional MRI overlap of lesions in 13 patients with Broca aphasia (red indicates that lesions in five or more patients share the same pixels). Bottom: Coronal MRI section of the same composite brain image through the damaged area.
The structures damaged in Broca aphasia are part of a neural network involved in both the assembly of phonemes into words and the assembly of words into sentences. The network is presumably specialized for relational aspects of language, which include the grammatical structure of sentences and the proper use of grammatical vocabulary and verbs. The other cortical components of the network are located in lateral areas of the left frontal cortex (Brodmann's areas 47, 46, 9), the left parietal cortex (areas 40, 39), and sensorimotor areas above the Sylvian fissure between Broca's and Wernicke's regions (lower sector of areas 3, 1, 2, and 4). The critical subcortical component is in the left basal ganglia (head of the caudate nucleus and putamen). When damage is restricted to Broca's area alone or to its subjacent white matter, the result is the condition of Broca's area aphasia, a milder version of true Broca aphasia from which many patients are able to recover.
Wernicke Aphasia Results from Damage to Left Posterior Temporal Lobe Structures
The speech of patients with Wernicke aphasia is effortless, melodic, and produced at a normal rate, and is thus quite unlike that of patients with true Broca aphasia. The content of the speech, however, is often unintelligible because of frequent errors in the choice of words and phonemes, the order of which determines the word (Table 60–2).
Patients with Wernicke aphasia often shift the order of individual sounds and sound clusters, and add or subtract them to a word in a manner that distorts the intended phonemic plan. These errors are called phonemic paraphasias (paraphasia refers to any substitution of an erroneous phoneme or entire word for the intended, correct one). When phoneme shifts occur frequently and in close temporal proximity, words become unintelligible. Even when individual sounds are normally produced, Wernicke aphasics have great difficulty selecting words that accurately represent their intended meaning (known as a verbal or semantic paraphasia). For example, a patient might say headman when he means president.
Wernicke aphasics have difficulty comprehending the sentences uttered by others. Although this deficit is suggested by the Wernicke-Geschwind model, Wernicke's area is no longer seen as the center of auditory comprehension. The modern view is that Wernicke's area is part of a system that associates speech sounds with concepts. This system includes, in addition to Wernicke's area, the many parts of the brain that subserve grammar, attention, and the knowledge that is the source of the meanings of the words in the sentences.
Wernicke aphasia is usually caused by damage to the posterior section of the left auditory association cortex (Brodmann's area 22), although in severe and persisting cases there is involvement of the middle temporal gyrus and deep white matter (Figure 60–7).
Sites of lesions in Wernicke aphasia.
A. Top: Three-dimensional MRI reconstruction of a lesion (an infarction) in the left posterior and superior temporal cortex (dark gray) in a patient with Wernicke aphasia. Bottom: Coronal MRI section of the same brain through the damaged area.
B. Top: Three-dimensional MRI overlap of lesions in 13 patients with Wernicke aphasia, obtained with the MAP-3 technique (red indicates that five or more lesions share the same pixels). Bottom: Coronal MRI section of the same composite brain image through the damaged area.
Conduction Aphasia Results from Damage to a Specific Sector of Posterior Language Areas
Patients with conduction aphasia comprehend simple sentences and produce intelligible speech. However, like Broca and Wernicke aphasias, they cannot repeat sentences verbatim, they cannot assemble phonemes effectively (and thus produce many phonemic paraphasias) and cannot easily name pictures and objects. Speech production and auditory comprehension are less compromised than in the two other major aphasias (Table 60–2).
Persistent conduction aphasia is caused by damage to the left superior temporal gyrus and the inferior parietal lobe (Brodmann's areas 39 and 40). The damage can extend to the left primary auditory cortex (Brodmann's areas 41 and 42), the insula, and the underlying white matter.
A recent study by Buchsbaum and colleagues points to a specific subterritory, area Spt located at the boundary of areas 39 and 40, as the region of maximal lesion overlap in cases of conduction aphasia. Area Spt exhibits both auditory and motor responses. In brief, no evidence supports Wernicke's idea that conduction aphasia is caused by a simple interruption or disconnection of the arcuate fasciculus alone. The damage does compromise white matter, as Wernicke predicted, and destroys feed-forward and feedback projections that interconnect areas of temporal, parietal, insular, and frontal cortex. This connectional system seems to be part of the network required to assemble phonemes into words and to coordinate speech articulation.
In spite of the fact that the exact anatomical correlates of conduction aphasia are being revised and that the mechanism of the defect now appears more complex than that proposed in the Wernicke-Geschwind model, it is interesting to note that Wernicke correctly predicted both the main signs of the syndrome and the approximate location of the correlated lesion. The general model still holds.
Global Aphasia Results from Widespread Damage to Several Language Centers
Global aphasics are almost completely unable to comprehend language or formulate and repeat sentences, thus combining features of Broca, Wernicke, and conduction aphasias. Speech is reduced to a few words at best. The same word might be used repeatedly, appropriately or not, in a vain attempt to communicate an idea. Nondeliberate ("automatic") speech may be preserved, however. This includes stock expletives (which are used appropriately and with normal phonemic, phonetic, and inflectional structures), routines such as counting or reciting the days of the week, and the ability to sing previously learned melodies and their lyrics. Auditory comprehension is limited to a small number of words and idiomatic expressions.
Classic global aphasia is accompanied by weakness in the right side of the face and paralysis of the right limbs. It involves damage in three regions: damage to the anterior language region and the basal ganglia and insula, leading to Broca aphasia; damage to the auditory areas of cortex, leading to conduction aphasia; and damage to the posterior language regions, producing Wernicke aphasia. Such widespread damage can only be caused by a stroke in the region supplied by the middle cerebral artery (Appendix C).
Transcortical Aphasias Result from Damage to Areas Near Broca's and Wernicke's Areas
The Wernicke-Geschwind model predicts that aphasias can be caused not only by damage to components of the language system but also to areas and pathways that connect those components to the rest of the brain. Patients with transcortical motor aphasia, such as Broca aphasics, speak nonfluently, but they can repeat sentences, even very long sentences.
Transcortical motor aphasia has been linked to damage to the left dorsolateral frontal area, a patch of association cortex anterior and superior to Broca's area, although there can be substantial damage to Broca's area itself. The left dorsolateral frontal cortex is involved in the allocation of attention and the maintenance of higher executive abilities, including the selection of words. For example, part of the left dorsolateral frontal cortex is activated in functional neuroimaging studies when subjects have to produce the names or actions associated with particular objects (eg, saying "kick" in response to "ball"), and damage to it leaves a patient unable to perform such a task, although they can produce words in ordinary conversation.
The aphasia can also be caused by damage to the left supplementary motor area, located high in the frontal lobe, directly in front of the primary motor cortex and buried mesially between the hemispheres. Electrical stimulation of the area in nonaphasic surgery patients causes the patients to make involuntary vocalizations or to be unable to speak, and functional neuroimaging studies have shown it to be activated in speech production. Thus the supplementary motor area appears to contribute to the initiation of speech, whereas the dorsolateral frontal regions contribute to ongoing control of speech, particularly when the task is difficult.
Transcortical sensory aphasics have fluent speech, impaired comprehension, and great trouble naming things. The aphasia differs from Wernicke aphasia in the same way that transcortical motor aphasia differs from Broca aphasia: Repetition is spared. In fact, patients with transcortical sensory aphasia might repeat and even make grammatical corrections in phrases and sentences they do not understand. The aphasia thus appears to be a deficit in semantic retrieval, without significant disruption of syntactic and phonological abilities.
Transcortical motor and sensory aphasias are believed to be caused by damage that spares the arcuate fasciculus. This would explain the sparing of repetition skills. Transcortical aphasias are thus the complement of conduction aphasia, behaviorally and anatomically. Transcortical sensory aphasia appears to be caused by damage to parts of the junction of the temporal, parietal, and occipital lobes, which connect the perisylvian language areas with the parts of the brain responsible for word meaning.
Finally, the growing attention given to degenerative brain conditions has permitted a characterization of the primary progressive aphasias (PPA). Their presentation tends to correspond to that of the classical aphasias. The main variants of PPA, as classified by Maria Luisa Gorno-Tempini and colleagues, are nonfluent/agrammatic, semantic, and logopenic.
The Classical Aphasias Have Not Implicated All Brain Areas Important for Language
The cortical sites damaged in the classical aphasias comprise only a portion of language-related areas in the brain. More recent research on aphasia has uncovered several other language-related regions in the cerebral cortex and in subcortical structures. For example, the anterior temporal and inferotemporal cortex have only recently become associated with language.
Damage to the left temporal cortex, in Brodmann's areas 21, 20, and 38, causes severe and pure naming defects—impairments of word retrieval without any accompanying grammatical, phonemic, or phonetic difficulty. When the damage is confined to the left temporal pole (Brodmann's area 38), the patient has difficulty recalling the names of unique places and persons but not names for common entities. When the lesions involve the mid temporal sector (areas 21 and 20), the patient has difficulty recalling both unique and common names. Finally, damage to the left posterior infero-temporal sector causes a deficit in recalling words for particular types of items—tools and utensils—but not words for natural things or unique entities. Recall of words for actions or spatial relationships is not compromised (Figure 60–8).
Regions of the brain other than Broca's and Wernicke's areas involved in language processing.
The study used functional magnetic resonance imaging (fMRI) to study patients with selected brain lesions.
A. The left anterior temporal pole is the region of maximal overlap of lesions associated with impaired naming of unique images, such as the face of a person.
B. The left anterolateral and posterolateral temporal regions as well as Broca's region are the sites of maximal overlap of lesions associated with impaired naming of nonunique animals.
C. The left motor cortex and left posterolateral temporal cortex are the sites of maximal overlap of lesions associated with deficits in naming of tools.
The left temporal cortex contains neural systems that hold the key to retrieving words denoting various categories of things ("tools," "eating utensils"), but not words denoting actions ("walking," "riding a bicycle"). These findings were obtained not only from studies of patients with brain lesions resulting from stroke, head injury, herpes encephalitis, and degenerative processes such as Alzheimer disease, but also from functional imaging studies of typical individuals and from electrical stimulation of these same temporal cortices during surgery.
Areas of frontal cortex in the mesial surface of the left hemisphere, which include the supplementary motor area and the anterior cingulate region (known as Brodmann's area 24), play an important role in the initiation and continuation of speech. Damage in these areas impairs the initiation of movement (akinesia) and causes mutism, a complete absence of speech. In aphasic patients the complete absence of speech is a rarity and is only seen during the very early stages of the condition. Patients with akinesia and mutism fail to communicate by words, gestures, or facial expression because the drive to communicate is impaired, not because the neural machinery of expression is damaged as in aphasia.
Damage to the left subcortical gray nuclei impairs grammatical processing in both speech and comprehension. The basal ganglia are closely interconnected with the frontal and parietal cortex and may have a role in assembling morphemes into words and words into sentences, just as they serve to assemble the components of complex movements into a smooth whole.
Certain brain lesions in adults can cause alexia, a disruption of the ability to read, or agraphia, a disruption of the ability to write (also known as word blindness). The two disorders may appear combined or separately, and they may or may not be associated with aphasia depending on the site of the causative lesion. Given the very recent emergence of writing (less than 5,000 years ago), and the even more recent emergence of near universal literacy (probably less than a century ago), it is unlikely that a special reading system evolved in the human brain in such a short period of evolutionary time. Therefore pure alexia without aphasia cannot be attributed to impairment of a special reading system in the brain, and is more likely to be caused by a disconnection between the visual and language systems.
Because vision is a bilateral brain process while language is lateralized, pure alexia requires a disruption in the transfer of visual information to the language areas of the left hemisphere. In 1892 the French neurologist Jules Dejerine studied an intelligent and highly articulate man who had recently lost the ability to read, even though he could spell, understand words spelled to him, copy written words, and recognize them after writing the individual letters. The patient could not see color in his right visual field, but his vision was otherwise intact in both visual fields.
Postmortem examination revealed damage in a region of the left occipital region that disrupted the transfer of visually related signals from both the left and right visual cortex to language areas in the left hemisphere. The postmortem also revealed some damage to the splenium, the posterior portion of the corpus callosum that interconnects left and right visual association cortices. This lesion is no longer believed to be involved in pure alexia, however. When the splenium is cut for surgical reasons without damaging visual cortices, patients can read words normally in the right visual field but not those in the left.
Functional imaging studies have shown that reading words and word-like shapes selectively activates extrastriate areas (secondary visual cortex) anterior to the primary visual cortex in the left hemisphere. This suggests that the processing of word shapes, like other complex visual qualities, requires that general region.