Language and Speech Disorders: Aphasia and Aphasic Syndromes

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Chapter 12A Language and Speech Disorders

Aphasia and Aphasic Syndromes

Language Disorders: Overview

The study of language disorders involves analysis of that most human of attributes, the ability to communicate through common symbols. Language has provided the foundation of human civilization and learning, and its study has been the province of philosophers as well as physicians. When language is disturbed by neurological disorders, analysis of the patterns of abnormality has practical usefulness in neurological diagnosis. Historically, language was the first higher cortical function to be correlated with specific sites of brain damage. It continues to serve as a model for the practical use of a cognitive function in localizing brain lesions and for understanding human cortical processes in general.


Aphasia is defined as a disorder of language acquired secondary to brain damage. This definition, adapted from Alexander and Benson (1997), separates aphasia from several related disorders. First, aphasia is distinguished from congenital or developmental language disorders, called dysphasias. (In contrast with British usage, in the United States the term dysphasia applies to developmental language disorders rather than partial or incomplete aphasia.)

Second, aphasia is a disorder of language rather than speech. Speech is the articulation and phonation of language sounds; language is a complex system of communication symbols and rules for their use. Aphasia is distinguished from motor speech disorders (the subject of Part B of this chapter), which include dysarthria, dysphonia (voice disorders), stuttering, and speech apraxia. Dysarthrias are disorders of articulation of single sounds; causes of these disorders may include mechanical disturbance of the tongue or larynx and neurological disorders such as dysfunction of the muscles, neuromuscular junction, cranial nerves, bulbar anterior horn cells, corticobulbar tracts, cerebellar connections, or basal ganglia. Apraxia of speech is a syndrome of misarticulation of phonemes, especially consonant sounds. Unlike dysarthria, in which certain phonemes are consistently distorted, apraxia of speech is characterized by inconsistent distortions and substitutions of phonemes. The disorder is called an apraxia because there is no primary motor deficit in articulation of individual phonemes. Clinically, speech-apraxic patients produce inconsistent articulatory errors, usually worse on the initial phonemes of a word and with polysyllabic utterances. Apraxia of speech, so defined, is commonly involved in speech production difficulty in the aphasias.

Third, aphasia is distinguished from disorders of thought. Thought involves the mental processing of images, memories, and perceptions, usually but not necessarily involving language symbols. Psychiatric disorders derange thought and alter the content of speech without affecting its linguistic structure. Schizophrenic patients, for example, may manifest bizarre and individualistic word choices, with loose associations and a loss of organization in discourse together with vague or unclear references and communication failures (Docherty et al., 1996). Elementary language and articulation, however, are intact. Abnormal language content in psychiatric disorders is therefore not considered to represent aphasia, because the disorder is more one of thought than of language. Language disorders associated with diffuse brain diseases such as encephalopathies and dementias do qualify as aphasias, but the involvement of other cognitive functions distinguishes them from aphasia secondary to focal brain lesions.

An understanding of language disorders requires an elementary review of linguistic components. Phonemes are the smallest meaning-carrying sounds; morphology is the use of appropriate word endings and connector words for tenses, possessives, and singular versus plural; semantics refers to word meanings; the lexicon is the internal dictionary; and syntax is the grammatical construction of phrases and sentences. Discourse refers to the use of these elements to create organized and logical expression of thoughts. Pragmatics refers to the proper use of speech and language in a conversational setting, including pausing while others are speaking, taking turns properly, and responding to questions. Specific language disorders affect one or more of these elements.

Relevant Neuroanatomy

Language processes have a clear neuroanatomical basis. In simplest terms, the reception and processing of spoken language take place in the auditory system, beginning with the cochlea and proceeding through a series of way stations to the auditory cortex, the Heschl gyrus, in each superior temporal gyrus. Decoding sounds into linguistic information involves the posterior part of the left superior temporal gyrus, the Wernicke area or Brodmann area 22, which gives access to a network of cortical associations to assign word meanings. For both repetition and spontaneous speech, auditory information is transmitted to the Broca area in the posterior inferior frontal gyrus. This area of cortex “programs” the neurons in the adjacent motor cortex subserving the mouth and larynx, from which descending axons travel to the brainstem cranial nerve nuclei. The inferior parietal lobule, especially the supramarginal gyrus, also may be involved in phoneme processing in language comprehension and in phoneme production for repetition and speech (Hickok and Poeppel, 2000). These anatomical relationships are shown in Figs. 12A.1 and 12A.2. Reading requires perception of visual language stimuli by the occipital cortex, followed by processing into auditory language information via the heteromodal association cortex of the angular gyrus. Writing involves activation of motor neurons projecting to the arm and hand. A French study that used aphasia testing and magnetic resonance imaging (MRI) scans to evaluate 107 stroke patients confirmed the general themes of nearly 150 years of clinical aphasia research: that frontal lesions caused nonfluent aphasia, whereas posterior temporal lesions affected comprehension (Kreisler et al., 2000).

These pathways, and doubtless others, constitute the cortical circuitry for language comprehension and expression. In addition, other cortical centers involved in cognitive processes project into the primary language cortex, influencing the content of language. Finally, subcortical structures play increasingly recognized roles in language functions. The thalamus, a relay for the reticular activating system, appears to alert the language cortex, and lesions of the dominant thalamus frequently produce fluent aphasia. Nuclei of the basal ganglia involved in motor functions, especially the caudate nucleus and putamen, participate in expressive speech. No wonder, then, that language disorders are seen with a wide variety of brain lesions and are important in practical neurological diagnosis and localization.

In right-handed people, and in a majority of left-handers as well, clinical syndromes of aphasia result from left hemisphere lesions. Rarely, aphasia may result from a right hemisphere lesion in a right-handed patient, a phenomenon called crossed aphasia (Bakar et al., 1996). In left-handed persons, language disorders are usually similar to those of right-handed persons with similar lesions, but occasional cases manifest with atypical syndromes that suggest a right hemisphere capability for at least some language functions. For example, a patient with a large left frontotemporoparietal lesion may have preserved comprehension, suggesting right hemisphere language comprehension. For the same reason, recovery from aphasia may be better in some left-handed than in right-handed patients with left hemisphere strokes.

Diagnostic Features

Muteness, a total loss of speech, may represent severe aphasia (see Aphemia later in the chapter). Muteness also can be a sign of dysarthria, frontal lobe dysfunction with akinetic mutism, severe extrapyramidal system dysfunction (as in Parkinson disease), non-neurological disorders of the larynx and pharynx, or even psychiatric syndromes such as catatonia. Caution must therefore be taken in diagnosing the mute patient as aphasic. A good rule of thumb is that if the patient can write or type and the language form and content appear normal, the disorder is probably not aphasic in origin. If the patient cannot speak or write but makes apparent effort to vocalize, and if there is also evidence of deficient comprehension, aphasic muteness is likely. Associated signs of a left hemisphere injury, such as right hemiparesis, also aid in diagnosis. Finally, if the patient gradually begins to make sounds containing paraphasic errors, aphasia can be identified with confidence.

Hesitant speech is a feature of aphasia but also of motor speech disorders such as dysarthria or stuttering, and it may be a manifestation of a psychogenic disorder. A second rule of thumb is that if the utterances of a hesitant speaker can be transcribed into normal language, the patient is not aphasic. Hesitancy occurs in many aphasia syndromes for various reasons, including difficulty in speech initiation, imprecise articulation of phonemes, deficient syntax, and word-finding difficulty.

Anomia, or inability to produce a specific name, is generally a reliable indicator of language disorder, although it also may reflect memory loss. Anomia is manifested in aphasic speech by word-finding pauses and circumlocutions, or use of a phrase when a single word would suffice (e.g., “the thing you tell time with” for watch).

Paraphasic speech refers to the presence of errors in the patient’s speech output. Paraphasic errors are divided into literal or phonemic errors involving substitution of an incorrect sound (e.g., “shoon” for “spoon”) and verbal or semantic errors involving substitution of an incorrect word (e.g., “fork” for “spoon”). A related language symptom is perseveration, the inappropriate repetition of a previous response. Occasionally, aphasic utterances involve nonexistent word forms called neologisms. A pattern of paraphasic errors and neologisms that so contaminate speech that the meaning cannot be discerned is called jargon speech.

Another cardinal symptom of aphasia is failure to comprehend the speech of others. Most aphasic patients also have difficulty with comprehension and production of written language (reading and writing). Fluent paraphasic speech usually makes an aphasic disorder obvious. The chief considerations in the differential diagnosis here include aphasia, psychosis, acute encephalopathy or delirium, and dementia. Aphasic patients usually do not appear confused and do not exhibit inappropriate behavior; they are not agitated and do not misuse objects, with occasional exceptions in acute syndromes of Wernicke or global aphasia. In contrast, most psychotic patients speak in an easily understood, grammatically appropriate manner, but their behavior and speech content are abnormal. Only rarely do schizophrenics speak in “clang association” or “word salad” speech. Sudden onset of fluent paraphasic speech in a middle-aged or elderly patient should always be suspected of representing a left hemisphere lesion with aphasia.

Patients with acute encephalopathy or delirium may manifest paraphasic speech and “higher” language deficits, such as the inability to write, but the grammatical expression of language is less disturbed than its content. These language symptoms, moreover, are less prominent than accompanying behavioral disturbances such as agitation, hallucinations, drowsiness, or excitement, and cognitive difficulties such as disorientation, memory loss, or delusional thinking.

Chronic encephalopathies, or dementias, pose a more difficult diagnostic problem because involvement of the language cortex produces readily detectable language deficits, especially involving naming, reading, and writing. These language disorders (see Language in Dementing Diseases later in this chapter) differ from aphasia secondary to focal lesions mainly by the involvement of other cognitive functions such as memory and visuospatial processes.

Bedside Language Examination

The first part of any bedside examination of language is observing the patient’s speech and comprehension during the clinical interview. A wealth of information about language function can be obtained if the examiner pays deliberate attention to the patient’s speech patterns and responses to questions. In particular, minor word-finding difficulty, occasional paraphasic errors, and higher-level deficits in discourse planning and in the pragmatics of communication—turn-taking in conversation and the use of humor and irony, for example—can be detected principally during the informal interview.

D. Frank Benson and Norman Geschwind popularized a bedside language examination of six parts, updated by Alexander and Benson (1997) (Box 12A.1). This examination provides useful localizing information about brain dysfunction and is well worth the few minutes it takes.

The first part of the examination is assessment of spontaneous speech. A speech sample may be elicited by asking the patient to describe the weather or the reason for coming to the doctor. If speech is sparse or absent, recitation of lists (e.g., counting or listing days of the week) may be helpful. The most important variable in spontaneous speech is fluency. Fluent speech flows rapidly and effortlessly; nonfluent speech is uttered in single words or short phrases, with frequent pauses and hesitations. Attention should first be paid to such elementary characteristics as initiation difficulty, articulation, phonation or voice volume, rate of speech, prosody or melodic intonation of speech, and phrase length. Second, the content of speech utterances should be analyzed in terms of the presence of word-finding pauses, circumlocutions, and errors such as literal and verbal paraphasias and neologisms.

Naming, the second part of the bedside examination, is tested by asking the patient to name objects, object parts, pictures, colors, or body parts to confrontation. A few items from each category should be tested because anomia can be specific to word classes. Proper names of persons are often affected severely. The examiner should ask questions to be sure the patient recognizes the items or people he or she cannot name.

Auditory comprehension is tested first by asking the patient to follow a series of commands of one, two, and three steps. An example of a one-step command is “Stick out your tongue”; a two-step command is “Hold up your left thumb and close your eyes.” Successful following of commands ensures adequate comprehension, at least at this simple level, but failure to follow commands does not automatically establish a loss of comprehension. The patient must hear the command, understand the language the examiner speaks, and possess the motor ability to execute it, including the absence of apraxia. Apraxia (see Chapter 10 for full discussion) is defined operationally as the inability to carry out a motor command despite normal comprehension and normal ability to carry out the motor act in another context, such as for imitation or with use of a real object. Because apraxia is difficult to exclude with confidence, it is advisable to test comprehension by tasks that do not require a motor act, such as yes/no questions, or by commands that require only a pointing response. The responses to nonsense questions (e.g., “Do you vomit every day?”) quickly establish whether the patient comprehends. Nonsense questions often produce surprising results because of the tendency of some aphasics to cover up comprehension difficulty with social chatter.

Repetition of words and phrases should be deliberately tested. Dysarthric patients and those with apraxia of speech (see Chapter 12B) have difficulty with rapid sequences of consonants, such as in “Methodist Episcopal,” whereas aphasic persons have special difficulty with grammatically complex sentences. The phrase “no ifs, ands, or buts” is especially challenging for aphasics. Often, aphasics can repeat familiar or “high-probability” phrases much better than unfamiliar ones.

Reading should be tested both aloud and for comprehension. The examiner should carry a few printed commands to facilitate a rapid comparison of auditory and reading comprehension. Of course, the examiner must have some idea of the patient’s premorbid reading ability.

Writing, the element of the bedside examination most often omitted, not only provides a further sample of expressive language but also allows an analysis of spelling, which is not possible with spoken language. A writing specimen may be the most sensitive indicator of mild aphasia, and it provides a permanent record for future comparison. Spontaneous writing, such as a sentence describing why the patient has come for examination, is especially sensitive for the detection of language difficulty. When spontaneous writing fails, writing to dictation and copying should be tested as well.

Finally, the neurologist combines the results of the bedside language examination with those of the rest of the mental status examination and of the neurological examination in general. These “associated signs” help classify the type of aphasia and localize the responsible brain lesion.

Aphasic Syndromes

Broca Aphasia

In 1861, the French physician Paul Broca described two patients, establishing the aphasia syndrome that now bears his name. The speech pattern is nonfluent; on bedside examination, the patient speaks hesitantly, often producing the principal meaning-containing nouns and verbs but omitting small grammatical words and morphemes. This pattern is called agrammatism or “telegraphic speech.” An example is “wife come hospital.” Patients with acute Broca aphasia may be mute or may produce only single words, often with dysarthria and apraxia of speech. They make many phonemic errors, inconsistent from utterance to utterance, with substitution of phonemes usually differing only slightly from the correct target (e.g., /p/ for /b/). Naming is deficient, but the patient often manifests a “tip-of-the-tongue” phenomenon, getting out the first letter or phoneme of the correct name. Paraphasic errors in naming more frequently are of literal than of verbal type. Auditory comprehension seems intact, but detailed testing usually reveals some deficiency, particularly in the comprehension of complex syntax. For example, for persons with Broca aphasia, sentences with embedded clauses involving prepositional relationships cause difficulty in comprehension as well as in expression (“The rug that Bill gave to Betty tripped the visitor”). A positron emission tomography (PET) study in normal persons (Caplan et al., 1998) showed activation of the Broca area in the frontal cortex during tests of syntactic comprehension; the Broca area thus appears to be involved in syntactical operations, both expressively and receptively. Repetition is hesitant in these patients, resembling their spontaneous speech. Reading often is impaired despite relatively preserved auditory comprehension. Benson termed this reading difficulty of Broca aphasics the “third alexia,” in contradistinction to the two classical types of alexia (see Aphasic Alexia later in the chapter). Patients with Broca aphasia may have difficulty with syntax in reading, just as in auditory comprehension and speech. Writing is virtually always deficient in Broca aphasics. Most patients have a right hemiparesis necessitating use of the nondominant left hand for writing, but this left-handed writing is far more abnormal than the awkward renditions of a normal right-handed person attempting to write left-handed. Many patients can scrawl only a few letters.

Associated neurological deficits of Broca aphasia include right hemiparesis, hemisensory loss, and apraxia of the oral apparatus and the nonparalyzed left limbs. Apraxia in response to motor commands is important to recognize because it may be mistaken for comprehension disturbance. As mentioned earlier, comprehension should also be tested by responses to yes/no questions or commands to point to an object. The common features of Broca aphasia are listed in Table 12A.1.

Table 12A.1 Bedside Features of Broca Aphasia

Feature Syndrome
Spontaneous speech Nonfluent, mute or telegraphic, usually dysarthric
Naming Impaired  
Comprehension Intact (mild difficulty with complex grammatical phrases)
Repetition Impaired
Reading Often impaired (“third alexia”)
Writing Impaired (dysmorphic, dysgrammatical)
Associated signs Right hemiparesis
  Right hemisensory loss
  ± Apraxia of left limbs

An important clinical feature of Broca aphasia is its frequent association with depression (Robinson, 1997). Patients with Broca aphasia typically are aware of and frustrated by their deficits. At times they become withdrawn and refuse help or therapy. Usually the depression lifts with recovery from the deficit, but it may be a limiting factor in rehabilitation.

The lesions responsible for Broca aphasia usually include the traditional Broca area in the posterior part of the inferior frontal gyrus, along with damage to adjacent cortex and subcortical white matter. Most patients with lasting Broca aphasia, including Broca’s original cases, have much larger left frontoparietal lesions, including most of the territory of the upper division of the left middle cerebral artery. In such patients, the deficit typically evolves from global to Broca aphasia over weeks to months. Patients who manifest Broca aphasia immediately after their strokes, by contrast, have smaller lesions of the inferior frontal region, and their deficits generally resolve quickly. In computed tomography (CT) scan analyses at the Boston Veterans Administration Medical Center, lesions restricted to the lower precentral gyrus produced only dysarthria and mild expressive disturbance. Lesions involving the traditional Broca area (Brodmann areas 44 and 45) resulted in difficulty initiating speech, and lesions combining the Broca area, the lower precentral gyrus, and subcortical white matter yielded the full syndrome of Broca aphasia. In other studies at the center, damage to two subcortical white matter sites—the rostral subcallosal fasciculus deep to the Broca area and the periventricular white matter adjacent to the body of the left lateral ventricle—was required to cause permanent nonfluency. These concepts concerning the Broca area and its mainly temporary role in Broca aphasia have been confirmed by a recent MRI study, indicating that MRI lesions in the Broca area correlate with Broca or global aphasia in acute stroke, but not in the chronic period (Ochfeld et al., 2010). Fig. 12A.3 shows an MRI scan of the brain from a patient with Broca aphasia.

Wernicke Aphasia

Wernicke aphasia may be considered the opposite of Broca aphasia in that expressive speech is fluent, but comprehension is impaired. The speech pattern is effortless and sometimes even excessively fluent (“logorrhea”). A speaker of a foreign language would notice nothing amiss, but a listener who shares the patient’s language detects speech empty of meaning, containing verbal paraphasias, neologisms, and jargon productions. Neurolinguists refer to this pattern as paragrammatism. In milder cases, the intended meaning of an utterance may be discerned, but the sentence goes awry with paraphasic substitutions. Naming in Wernicke aphasia is deficient, often with bizarre, paraphasic substitutions for the correct name. Auditory comprehension is impaired, sometimes even for simple nonsense questions. Deficient semantics is the major cause of the comprehension disturbance in Wernicke aphasia, along with disturbed access to the internal lexicon. Repetition is impaired; whispering a phrase in the patient’s ear, as in a hearing test, may help cue the patient to attempt repetition. Reading comprehension is usually affected in a fashion similar to that observed for auditory comprehension, but occasionally patients show greater deficit in one modality than in the other. The discovery of spared reading ability in Wernicke aphasics is important in allowing these patients to communicate. In addition, neurolinguistic theories of reading must account for the access of visual language images to semantic interpretation, even in the absence of auditory comprehension. Writing also is impaired, but in a manner quite different from that of Broca aphasia. The patient usually has no hemiparesis and can grasp the pen and write easily. Written productions are even more abnormal than oral ones, however, in that spelling errors are also evident. Writing samples are especially useful in the detection of mild Wernicke aphasia.

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