Signs of Aphasia

Antonio R. Damasio

This chapter discusses the clinical presentation of the aphasias, the major types, and the principal signs. A discussion of the neuroanatomy and neurophysiology of language (and, by extension, a discussion of the physiopathology of the aphasias) is outside the scope of this text. However, the comments on the clinical evidence presented here reflect a particular theoretical perspective on neuroanatomy, neurophysiology, and physiopathology, which has been documented elsewhere in detail (A. Damasio, 1989a, 1989b, 1989c; A. R. Damasio & Damasio, 1994; H. Damasio & Damasio, 1989).

It is important to note that when I refer to the LOCALIZATION VALUE or CORRELATE of a given sign, I do not mean to say that the correlated brain locus normally operates to produce whatever function a sign reports as missing. In the perspective outlined in the earlier articles, language, along with other complex cognitive processes, depends on the concerted operation of multicomponent, large-scale neural systems. The anatomical components are often widely dispersed and each acts as a partial contributor to a complicated process rather than as a single purveyor. In this view, Wernicke's area, a part of which is a component of a language system, does not accomplish anything as complicated as auditory comprehension, although its impairment leads to auditory comprehension defects (A. Damasio, 1992).

Aphasia

Aphasia is a disturbance of the complex process of comprehending and formulating verbal messages that results from newly acquired disease of the central nervous system (CNS).

The disease processes that cause aphasia are acquired (e.g., cerebral infarction, tumor, contusion) rather than congenital (e.g., genetic or environment-induced perinatal cerebral defect). The former befalls individuals previously capable of using language appropriately. The latter may produce developmental language defects in individuals whose ability to use language will never attain a normal level.

Although it is clear that all mental activity and communication stems from the activity of the CNS, reference to the CNS is important because aphasia is not the result of a peculiar utilization of language related to psychogenic or social deviations.

Throughout the chapter I refer to VERBAL COMMUNICATION and LANGUAGE almost interchangeably. Under the terms verbal and language I include both auditory-based words and the visuomotor-based signs of sign languages. On the other hand, language and speech are not interchangeable. The latter should be reserved for the act of “speaking a verbal message” independently of the process of formulating the message itself. In this definition, I use VERBAL MESSAGES to call attention to the fact that aphasia relates exclusively to a disturbance in the use of words and signs, as opposed, for example, to the use of gestures, facial expressions, or body expressions, which are also important components of social communication but are not language in the sense used here.

Aphasia can affect comprehension of the language the patient either hears spoken or sees written, or both. It can also affect the comprehension of visuomotor signs from a sign language. Aphasia can affect the formulation of oral language production, writing, or both. In users of a sign language it affects the ability to sign in a linguistically correct manner.

Aphasia often disturbs both reception and expression of language, in both visual (written) and auditory (spoken) modes. Yet, each of the several fundamental types of aphasia compromises one of these modes preponderantly. Indeed, in some instances (e.g., in PURE ALEXIA or in PURE WORD DEAFNESS), only one of these abilities suffers while all others remain unaffected. There is more about this particular question later in the chapter.

The emphasis on COMPREHENDING and FORMULATING is especially pertinent. Aphasics have trouble comprehending verbal messages, that is, deciphering their meaning as opposed to hearing or seeing those messages. Neither deafness (peripheral or central) nor blindness is the problem. A deaf or blind person cannot comprehend language in the modality of the perceptual impairment, but will comprehend the same verbal message normally when processed by an intact sensory channel, for example, tactile Braille reading in the blind. Aphasics also have trouble formulating verbal messages, for example, selecting the lexical and syntactical items necessary to convey meaning and deploying them in a relational framework such that meaning is indeed imparted on the receiver of the message. Yet an impediment of phonation that prevents speech production has nothing to do with formulation of verbal messages (people can still write what they cannot say), nor does the loss of one's hands interfere with language formulation (people may still say it if they have formulated it, and they may even write with a pen held between the teeth or the toes).

To characterize the nature of the disturbance, stating what aphasia is not becomes just as important as stating what it is. To begin with, aphasia is not a disturbance of articulation. Many patients suffer from speech disturbances due to acquired disease of the basal ganglia, of the brain stem or cerebellum, or even of the cerebral cortex, and yet few of those patients will have aphasia. Although their speech sounds are poorly formed or are inappropriately repeated, word selection and sentence structure are grammatically correct, appropriate to the intentions of their author, and understandable to the attentive listener. That is to say, such patients have a speech disturbance but it does not follow that they have a verbal language disturbance: Their language formulation is normal, their communication is linguistically correct, and thus they do not have aphasia.

Patients with mutism, who can be entirely silent, are not necessarily aphasic, although on occasion their absence of speech does conceal an aphasia. Often these patients fail to indicate any desire to communicate by gesture, mimicry, or writing. Consequently, little is known about what they do or do not comprehend, or about what they may or may not want to say (or think, for that matter). However, when most mutism patients awake from these peculiar states of apparent indifference, they resume language communication and show no evidence of aphasia. When probed about their abnormal behavior, these patients clearly relate a strange experience of avolition and diminished richness of thought content, but not of any problem with the actual composition of verbal communication. Most such patients have disease in areas of the brain that are different from those that produce the aphasias, for example, in the supplementary motor area or in the cingulate gyrus as opposed to the region surrounding the Sylvian fissure. A few have acute psychotic states and no macroscopically detectable brain disease, although they may suffer from profound changes in neurotransmitter systems innervating certain regions of the brain.

Also not aphasic are patients with aphonia that may result from diseases of the larynx and pharynx. They are mute, in the narrow sense of the word, and are suffering from an impediment in their phonatory apparatus that prevents them from speaking. They should be able to comprehend language (and indicate so by nodding or pointing responses), and they should be able to turn their thoughts into language by writing, in addition to being able to mouth words. The exception, other than for malingering, is a conversion reaction, the currently infrequent psychiatric diagnosis of HYSTERICAL APHONIA.

Finally, it should be noted that the language disorder experienced in altered states of awareness is not an aphasia. Any patient with a confusion-al state will produce disturbed language and fail to comprehend verbal communication. But such patients have a concomitant disorder of their thought processes that parallels the language disturbance. Unlike the patient with aphasia who struggles to turn properly organized meanings into language and fails (or tries, without success, to turn the message heard into internal meaning), patients with confusional states communicate their disordered thought processes verbally, with remarkable success. Confusional states are most commonly produced by metabolic disturbances or by substance intoxication, but they can also be the result of cerebral tumors (directly or indirectly affecting brain structures that sustain vigilance) or of trauma.

A picture of a patient with aphasia should begin to emerge:

1. An aphasic produces some speech, or even abundant speech, which does not conform to the grammatical rules of the language being used. The errors include omission of words, such as conjunctions or prepositions (functor words), erroneous choice of words (substitution of the intended word for another that may or may not be related in sound or meaning), and disturbances of the relationship among words in a sentence (e.g., as expressed in word order). The rule that aphasic patients always produce some speech may not be true during the first hours or days of onset of disease. But even during a phase of speechlessness, most aphasic patients attempt to communicate by gesture or facial expression.

2. An aphasic often has difficulty in comprehending a purely verbal command (i.e., a verbal message given through auditory or visual means, without accompanying gestures, facial expressions, or meaningful emotional...