M. Thérèse Southgate, MD, Section Editor

Diagnosis and Treatment of Aphasia Part I Martin L. Albert, MD,

IN

Nancy Helm-Estabrooks, ScD

1971, Norman Geschwind1

com-

plained that the problem of aphasia was largely neglected by clinicians, despite its common occurrence. During the past

15 years, in great measure due to Geschwind's creative inspiration, clinicians and researchers have devoted considerable energy to understanding brain-language relationships and to developing new therapies for aphasic patients. With advances in imaging technologies and development of the fields of behavioral neurology, neuropsychology, psycholinguistics, and speech pathology, great progress has been made. Aphasia is no longer a neglected subject, and many aphasic patients now can be successfully treated. Contemporary research attempts to elucidate cognitive and neurobiological mechanisms underlying aphasic symptoms and to apply this knowledge to the development of therapy programs directed at specific clusters of aphasic symptoms. This article highlights clinically relevant aspects of this research.

PREVALENCE OF APHASIA Approximately 85 000 new cases of aphasia occur in the United States each year from stroke alone.2 Head injury, another common cause of aphasia, is increasing in medical importance in our society. In 1974, 422 000 new cases of From the Departments of Neurology (Dr Albert) and Audiology and Speech Pathology (Dr Helm-Estabrooks), Aphasia Research Center, Boston University Medical School and Boston Veterans Administration Medical Center. Reprint requests to the Boston Veterans Administration Hospital, 150S Huntington Ave, Boston, MA 02130 (Dr Albert or Dr Helm-Estabrooks).

closed head injuries requiring hospitalization were reported,3 and in 1982 there were 1.4 million reported cases of trauma to the nervous system.4 As many as 20% of these patients have lin¬ guistic deficits and other disorders of communication even several years after the injury. In addition, language prob¬ lems are common in our aging popula¬ tion, even in healthy persons, but especially in elderly patients with

dementing illness." To our knowledge, no complete esti¬ mate of the prevalence of aphasia exists.

The clinical dimensions must be great, however, since problems of communica¬ tion are related to stroke, head injury, dementing illness, brain tumors, infec¬ tions, other neurological disorders, and normal aging. CLASSIFICATION OF APHASIA

Traditionally, aphasie syndromes

have been classified into two major groups, based on the apparently simple expressive-receptive dichotomy.8"12 Ac¬ cording to this schema, an aphasie pa¬ tient with difficulty producing words would have an "expressive" or "motor" aphasia, presumably due to a lesion in Broca's area in the dominant frontal lobe, while an aphasie with difficulty comprehending language would have a

"receptive" or "sensory" aphasia, pre¬ sumably due to a lesion in or near

Wernicke's area in the dominant tempo¬ ral lobe. The expressive-receptive dichotomy, in its simple form, is misleading. Poste¬ rior lesions can produce disorders of expression and anterior lesions can produce disorders of comprehension.

Indeed, as we shall see below, subcortical as well as cortical lesions can produce

aphasie symptoms.

In the 1960s and

1970s, Gesch¬

wind11314 proposed a modification of the

expressive-receptive dichotomy. He described aphasies as "fluent" (effort¬ lessly producing well-articulated, long

phrases, with normal grammar, melo¬ dy, and rhythm) and "nonfluent" (pro¬ ducing sparse speech that is uttered slowly with great effort and poor articu¬ lation). As a general rule, lesions an¬ terior to the fissure of Rolando produce nonfluent aphasias—hence the term an¬ terior aphasias; and lesions posterior to the fissure of Rolando produce fluent aphasias—hence the term posterior aphasias. The notion of "anterior" vs "posteri¬ or" aphasias is a clinicoanatomic concept based on cortical localization along an anteroposterior dimension, usually in the left hemisphere of most right¬ handers. With newer imaging tech-, niques, brain-behavior studies of the past 15

years have shown that sub-

cortical, and even right hemispheric an¬

atomic structures contribute to lan¬ guage function. A comprehensive and meaningful clinicoanatomic map of brain-language relationships, there¬ fore, would require an integration of contributions to language from the entire brain: left and right hemispheres and subcortical structures. No such map exists at present. In the continuing process leading toward elaboration of that map, a simplified, highly schematic theory divides the aphasias into cortical and subcortical forms. This is the classi¬ fication scheme we currently use.

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Cortical Aphasias These are the common forms of corti¬ cal aphasia.21"0 Broca's Aphasia.—Patients with Broca's aphasia generally have nonfluent speech output and poor repetition but relative preservation of auditory comprehension. Nonfluent speech is slow, effortful, agrammatic, and often telegrammatic, that is, limited to con¬ tent words, eg, nouns and action verbs. Writing generally is comparable with speech output and reading comprehen¬ sion is usually similar to auditory com¬ prehension. A long-lasting Broca's aphasia often is associated with a rightsided hemiplegia, affecting the face and the right arm most severely. These pa¬ tients usually have large anterior le¬ sions affecting Broca's area but also ex¬ tending deep into adjacent subcortical structures.

Wernicke's Aphasia.—Patients who have Wernicke's aphasia have fluent speech output with poor comprehen¬ sion, poor naming, and poor repetition. Speech is well articulated, with phrases of normal length and melody. Output, however, may be contaminated by sub¬ stitutions of words or parts of words (paraphasias). Writing usually is com¬ parable with speech output, but reading may be somewhat better than auditory comprehension. Unlike patients with Broca's aphasia, those with Wernicke's aphasia rarely have a hemiplegia. Usu¬ ally these patients have lesions involv¬ ing the posterior third of the left superior temporal gyrus. Conduction Aphasia.—This type of aphasia is characterized by a prominent deficit in repetition relative to sponta¬ neous speech and oral and written

comprehension. Spontaneous speech, though essentially fluent, may be con¬ taminated by occasional word or letter substitutions and word-finding diffi¬ culty. Repetition, however, is markedly impaired, especially for multisyllabic words and for sentences. In all speech tasks, a high level of self-criticism may disrupt fluency. Writing is usually com¬ parable with the level of spontaneous speech. Significant hemiparesis is rare, but a right-sided hemianesthesia is not

The responsible lesion most commonly is found in the left angular and supramarginal gyrus regions and in immediately subjacent white matter. Transcortical Motor Aphasia.— Transcortical motor aphasia is charac¬ terized by a marked reduction in the amount and complexity of spontaneous speech despite retained ability to repeat sentences, read aloud, and name objects. Auditory and reading compre¬ hensions are relatively preserved. The relative sparing of repetition abilities, uncommon.

ease of articulation, dis¬ transcortical motor aphasia from Broca's aphasia. When cortical lesions produce this syndrome, they are most often anterior and superior to Broca's area. Subcortical lesions, how¬ ever, may produce a similar syndrome. Transcortical Sensory Aphasia.— This type of aphasia is characterized by impaired auditory comprehension de¬ spite preserved repetition and fluent

and

a

greater

tinguish

output. Spontaneous speech, although fluent, is often disrupted by word-find¬

ing pauses and occasional word or letter substitutions. Reading aloud is possible but reading comprehension is poor. Writing is usually worse than spontane¬ ous speech. Hemiparesis or prominent sensory abnormalities are not common. Lesions causing this syndrome are usu¬ ally posterior to Wernicke's area and often spare the angular and supramar-

ginal gyri.

Anomic Aphasia.—Anomia is the in¬ ability to generate word names in con¬

frontational tasks and in spontaneous speech. As a symptom, it is common to all forms of aphasia. When anomia becomes the predominant feature in an aphasie disorder, the term anomic aphasia is used. Auditory and reading comprehension, reading aloud, and rep¬ etition are all relatively normal. Sponta¬ neous speech is fluent, though marked

by a severe word-finding difficulty. Any

the zone of language21 can produce anomia. Anomic aphasia is a common sequela of lesions in the sec¬ ond temporal gyrus and/or the angular gyrus and is often seen in patients in the recovery stages of Wernicke's aphasia. Global Aphasia.—In global or total aphasia, all aspects of speech and language are impaired. There is normal¬ ly an associated apraxia, hemiplegia, and hemianesthesia. Consequently, the ability to communicate through mean¬ ingful gestures is impaired, although facial expression and intonation pat¬ terns may often convey information. These patients may understand a sur¬ prising amount of personally relevant information in natural settings. Unlike many patients with bilateral cerebral damage, they often manage many of their activities of daily living and be¬ lesion in

or near

relatively independent. Usually a large lesion involving both anterior and posterior portions of the zone of lan¬ guage and extending deep into adjacent white matter is implicated. Subcortical Aphasias During the past 15 years, one major step forward in our understanding the neurological mechanisms of the apha¬ sias has been in our ability to describe syndromes of aphasia correlated with come

lesions located strictly in subcortical structures. The advent of computed to¬ mography (CT) has greatly enhanced our ability to identify small, subcortically localized lesions as causes of apha¬ sie syndromes.2236 The concept that subcortical struc¬ tures, in particular the thalamus, have a role to play in language is not new. Penfield and Roberts37 concluded that the thalamus functioned as an integra¬ tor of elements of language activity; Botez and collaborators38"40 asserted that the thalamus and periaqueductal gray matter served as the "starting mecha¬ nism" for speech. More recently, a series of studies of electrical stimulation of cortical and subcortical structures, especially by Ojemann and col¬ leagues,41^ confirms that subcortical structures serve fundamental roles in the organization of language.46,47 Until the past decade, most neurolo¬ gists believed that true aphasia could be caused only by cortical lesions in the zone of language. Although thalamotomies have been shown to produce lan¬ guage disorders, it was widely assumed that these language deficits were secondary effects of cortical dys¬ function.4850 Published case reports of the past ten years, however, have demonstrated convincingly that vascu¬ lar lesions limited to subcortical struc¬ tures

can

produce

dromes.22·23·25"27·32"34'61"56 No

true

aphasie

syn-

generally accepted classification

system for the subcortical aphasias has yet emerged. In broad terms, two major

forms of subcortical aphasia are recog¬ nized: thalamic aphasias and those due to lesions in the caudate and putamen (regions of the basal ganglia) and/or in adjacent internal capsules (especially the anterior limb). Many aphasiologists believe that each of these two major forms of subcortical aphasia subsumes several different syndromes, depending on specific lesion localization. Thalamic Aphasia.—This syndrome consists of generally fluent speech out¬ put, with occasional lapses into nonfluency, frequent word substitutions (paraphasias), and, often, abundant neologisms. Comprehension is only

mildly impaired, word-finding difficulty is mild to moderate, and repetition usu¬ ally is intact. Perseveration, especially the recurrent type,5,7 is common. Key nonlanguage features of this syndrome are fluctuating attention and perfor¬ mance, which may make language test¬ ing more difficult. The specific anatomic region implicated in this syndrome is the pulvinar.

Aphasia due to Lesions of Caudate, Putamen, and/or Anterior Limb of Internal

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Capsule.—Probably

several

syndromes will be identified within this A common core syndrome resembles transcortical motor aphasia: limited spontaneous speech, relatively intact repetition, mild anomia, and rela¬ tively good auditory comprehension. Depending on the extent and the precise location of the lesion, the syndrome may group.

include better or worse articulation, a greater or lesser degree of impairment of auditory comprehension, or stuttering.272931,3258 We have seen transient epi¬ sodes of mutism and syndromes resem¬ bling global aphasia with lesions in this area.

The precise clinicoanatomic correla¬ tions have not been determined for these anteriorly located subcortical aphasias. Whether subcortical nuclear structures (putamen and caudate) or white-matter structures are responsi¬ ble for the aphasie syndromes is not yet resolved. In the largest study to date, a comprehensive review of their own 19 cases plus analysis of 58 cases from pub¬ lished reports, Alexander et al59 con¬ clude that subcortical white-matter pathways are the critical structures involved in the language disorders. NEUROPSYCHOLOGY AND NEUROLINGUISTICS

Neuropsychology is the study of underlying human behavior60-61; neurolinguistics focuses on neural mechanisms

neural mechanisms of language.62"84 While neurologists and neuroscientists have concentrated on defining clinical syndromes and describing clinicoanato¬ mic correlations, neuropsychologists have attempted to formulate descrip¬ tions of the mental processes that are involved in cognitive skills (language, memory, and so on) and neurolinguists have provided theories of language for testing in brain-damaged populations. In contemporary terminology, neurolo¬ gists study the "hardware" and neuro¬ psychologists and neurolinguists study the "software." Current theory in aphasia rejects the notion of a one-to-one correspondence between individual components of a

language system (phoneme, morpheme,

lexicon, semantics, syntax, etc) and specific regions of the brain. As pointed out by Marr,K among others, separate levels of

description are necessary for neurological and psychological aspects of cognition, and these different levels are only loosely coupled. We make

to

provide

no a

these fields

attempt, in this section,

comprehensive review of or their relationship to

we call the reader's attention to these important areas. The interaction of neurologists, psycholo-

aphasia; rather,

gists, and linguists in the study of apha¬ sia has had practical consequences for aphasie patients, such as the develop¬ ment of theory-based aphasia test bat¬ teries and new approaches to aphasia therapy. DIAGNOSTIC TECHNIQUES

Neurodiagnosis It is not an exaggeration to speak of a revolution in neurodiagnostic tech¬ niques in the past 15 years. Computed

tomography, magnetic resonance imag¬ ing (MRI), positron emission tomogra¬ phy, regional cerebral blood flow (CBF) studies, and newer techniques involv¬ ing electrical stimulation of the brain have transformed the clinical practice of neurology. Each of these techniques has been applied to the study of aphasia and each has helped to clarify, confirm, rec¬ tify, or expand our understanding of the anatomic basis of language. The development of noninvasive in vivo brain imaging techniques has made it possible to test neurolinguistic and neuropsychological theories directly and to develop aphasia therapy pro¬ grams that are theory driven. Newer imaging techniques have allowed us to understand more about the undamaged portions of the brain, as well as about the damaged portions. Our own approach to aphasia therapy (see later herein) emphasizes stimulation of healthy brain tissue. Theories of brain function, increased knowledge of brainlanguage relationships, and improved aphasia therapy programs have blos¬ somed in a healthy symbiosis. Each of the new diagnostic tech¬ niques provides a different neurobiological perspective on aphasia: anatomic, physiological, and metabolic. CT.—The theory that specific apha¬ sie syndromes might be correlated with specific anatomic lesion sites was based on a

handful of clinicoanatomic correla¬

tions86,87 and was much disputed.88"90 Ran¬ dom selection of cases (based on what¬ ever

brain samples were available in the

autopsy room) and unsystematic

mea¬

surement of

language behavior ren¬ dered suspect any theory based on such correlations. As neurolinguistic and neuropsychological theory developed, valid and reliable aphasia batteries were created. These aphasia tests were administered to large numbers of aphasie patients who were subjected to CT scans of the brain.28,91100 In general, CT scans have confirmed the traditional site of the lesion for the major cortical aphasie syndromes. Many exceptions exist, however, due to individual differences of age of onset, handedness, medical history, etiology,

and pattern of hemispheric asymmetry. Computed tomographic scanning of aphasies has clarified the nature of atyp¬ ical aphasias, created the new category of subcortical aphasia, and correlated lesion site with selective linguistic impairments. The study of correlations in vivo has directed attention to the issue of "time-post-onset" in diagnosis and description of aphasie syndromes.

MRI.—Magnetic

resonance,

as

a

chemical phenomenon useful for sophis¬ ticated chemical analysis, has been available since 1946.1C1 Only since the early 1970s has MRI been used as a clinical tool.102103 Magnetic resonance imaging has been shown to be clearly superior to CT scanning in specific situ¬ ations: MRI is free from certain arti¬ facts of CT and provides better graywhite matter discrimination and better lesion delineation; with MRI, lesions can be visualized directly on coronal

planes.104 Magnetic

resonance

imaging

has not yet been used extensively in the study of aphasia, but it has great poten¬ tial. For example, a study by De Witt et al105 in 1985 suggests that aphasie syn¬ dromes with subcortical lesions may in¬ volve cortex as well. Positron Emission Tomography.— Positron emission tomography is a dynamic biochemical technique that provides in vivo measurements of the rates and anatomic distribution of spe¬ cific biochemical reactions.106"109 Positron emission tomography has been applied to the study of both cortical and subcor¬ tical aphasias.110"112 Depression of [18F]fluorodeoxyglucose metabolic activity is congruent with anatomic models of aphasia, although the areas of metabolic depression seen on positron emission tomography are larger than the areas of infarction seen on CT. Use of both struc¬ tural and metabolic brain mapping pro¬ vides more detailed information about the cerebral basis of specific linguistic behaviors. Regional CBF.—In healthy brain tissue, CBF is regulated by neuronal metabolism. Measurements of CBF thus provide an indirect measure of neu¬ ronal activity in brain regions in which the blood flow is gauged. " During the past 15 years, numerous studies have correlated linguistic and other cognitive behaviors with CBF.116"119 Beyond gen¬ eral confirmation of traditional models of aphasia, these studies have shown that many parts of the brain, in addition to the classic language areas of Broca and Wernicke, are activated during speech production and comprehension. Cerebral blood flow studies have been used to determine prognosis in recovery from aphasia120 and have, in particular, documented evidence of right hemi-

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spheric involvement in recovery from aphasia.121 This information, together with data from studies of language in normal subjects using the technique of CBF with single-photon emission CT,122 is already being used in development of new aphasia therapy programs. Electrical Stimulation Mapping.— Localization of cerebral function by of electrical stimulation of the brain is not a new technique. Penfield and collaborators37,123 published exten¬ sively on this topic in the 1950s and early 1960s; much of what is currently ac¬ cepted as the map of cortical localization of function derives from those studies. What is new is the attempt to study intrahemispheric localization of cogni¬ tive function by means of both cortical and subcortical electrical stimulation means

with the use of sophisticated neurolin¬ guistic and neuropsychologic tech¬ niques. Ojemann and coworkers,4146 Van Buren and Bourke,124 and Mateer126 have been especially influential in the

past 15 years. The

application of an electrical cur¬ a variety of excitatory and inhibitory effects, and interpretation of results has many limi¬ tations. Nonetheless, with due consid¬ eration to these precautions, we can draw certain conclusions. Linguistic behaviors seem to be discretely elicitable by stimulation of specific regions of the brain; within limits, there is con¬

rent to neural tissue has

vidual there seems to be a degree of cerebral flexibility regarding which brain areas may participate in a particu¬ lar language function. Thus, converging evidence from sev¬ eral of the newer neurodiagnostic tech¬ niques confirms a growing clinical impression that the brain has a greater plasticity and potential for recovery of language function than had previously been believed. This is part I of a two-part article. Part II will appear in the Feb 26 issue. This article was supported in part by the Veter¬ Administration Medical Research Service and National Institutes of Health Center grant NS 06209. This article is dedicated to the memory of Nor¬ man Geschwind, MD.

siderable individual variation among adults in the precise cerebral location responsible for a particular linguistic function. Furthermore, within any indi-

ans

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40. Botez MI, Barbeau A: Role of subcortical structures, and particularly of the thalamus, in the mechanisms of speech and language. Int J Neurol

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