BRAIN

AND

LANGUAGE

25, 257-292 (1985)

Subcortical

Functions in Language: A Working Model

BRUCE CROSSON

Veterans Administration Medical Center and Department of Psychiatry and Behavioral Sciences, University of Oklahoma Health Sciences Center, Oklahoma City

The current paper explains a model of subcortical language functions that focuses on dynamic interactions between the cortex, the thalamus, and the basal ganglia in the production of spoken language. The model was derived from (a) studies of subcortical lesions and language, (b) studies of subcortical stimulation and language, (c) knowledge regarding neural pathways between various cortical and subcortical structures, and (d) indications that preverbal monitoring of language occurs. In the current model, the thalamus plays roles in cortical arousal and activation and in preverbal semantic monitoring. The basal ganglia function to regulate the degree of excitation conveyed from the thalamus to the cortex and to time the release of formulated language for motor programming. Consistency with classical syndromes of aphasia and potential applications to other areas in the neurosciences are discussed. The current theory, unlike previous formulations, is specific enough that testable hypotheses can be derived. o 1985 Academic PXSS.
Inc.

Aphasia, difficulty in the production, use, or comprehension of language caused by brain dysfunction, has been studied for more than a century. Much of what is known about how brain mechanisms produce, understand, and use language comes from the study of aphasia and its concomitant brain lesions. In addition to the study of aphasia, however, other methods have been used to study brain-language relationships, such as response to electrical stimulation of brain nuclei and tracts or the study of language functions in persons having unimpaired brain functioning. This research has spawned many theories regarding how the brain produces language.
The author thanks Reg L. Warren, Ph.D. (Center for Communication Disorders, Braintree Hospital), and Oscar A. Parsons, Ph.D. (Department of Psychiatry and Behavioral Sciences, University of Oklahoma Health Sciences Center), for their helpful comments on this manuscript. Appreciation is also extended to Carroll W. Hughes, Ph.D. (Department of Psychiatry, University of Kansas College of Health Sciences), and John Rhoades, Ph.D. (Department of Psychology, University of New Mexico), for their critique of the theory. Send correspondence and requests for reprints to Bruce Crosson, Psychology Service (183), Veterans Administration Medical Center, 921 Northeast 13th St., Oklahoma City, OK 73104. 257 0093-934X185$3.00
Copyright 0 1985 by Academic Press, Inc. All rights of reproduction in any form reserved.

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Until recently, consensus regarding aphasia and language function was that the overwhelming majority of language functions were performed by the outer layers of the cerebral hemispheres, the cerebral cortex. Penfield and Roberts (1959) were among the first to challenge this view, suggesting that one structure deep within the dominant hemisphere, the thalamus, played a role in the integration of language functions. Today, there are numerous reports of aphasia after dominant thalamic lesion (hemorrhage, infarction, thalamectomy, etc.). The issue of thalamic aphasia has been a controversial subject; indeed, Luria (1977) rejected the idea that language changes with thalamic lesion were true aphasias. Even though some variability regarding symptoms reported exists between studies of language after dominant thalamic lesion, a core syndrome of thalamic aphasia nonetheless has emerged. This syndrome is discussed in some detail below. Further, a few earlier reports and more recent literature have indicated that even structures lying lateral to the thalamus, the basal ganglia, are implicated in language functions. At this point in time, studies of subcortical functions in language have used mainly inductive reasoning to explain these functions. In other words, investigators have sought to describe language phenomena after subcortical lesions, and from these observations, they have inferred certain mechanisms must exist. Exploration of subcortical participation in language has suffered to some degree because such theoretical explanations have not had the degree of specificity from which hypotheses can be deduced and subsequently tested in new cases. Thus, exploration of subcortical aphasias has not been approached from the standpoint of systematically testing hypotheses. For this reason, important phenomena may be overlooked or misunderstood. The thesis of this paper is that enough evidence is now available to construct a more detailed theory regarding the role of subcortical structures in language. The model postulated herein begins to explain the formulation, monitoring, and refinement of spoken language and the role of subcortical structures in this dynamic process. It has its roots to some degree both in the classical model (Geschwind, 1972) and the functional systems approach as broadly defined by Luria (1973). The reader may recognize certain components of this model as having been explored previously in the literature, but until now, no attempts have been made to integrate these different components into a comprehensive model of language production. It should be emphasized that the current work is a theory of spoken language formulation. The motor execution of language (i.e., speech) is not detailed in this paper. Further, language comprehension, the production and comprehension of written language, and the generation of the ideas expressed in language are not detailed in the current work. These concerns must await further development of the model. The following discussion is divided into four sections. Before discussing

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hypotheses regarding the role of subcortical mechanisms in language, some background information must be presented. The first section discusses the classical model of aphasia (language function), and a few pertinent studies which have forced some reconceptualization of this model. Because the literature relating cortical functions to language is so voluminous and because the emphasis is on the role of subcortical structures, the review of cortical studies must be selective. The purpose of the first section is to provide the background from which gross cortical functions can be posited. Only then can the relationship between cortical and subcortical mechanisms be explored. The second section is a synopsis of the literature on subcortical functions in language. Both the thalamus and the basal ganglia are reviewed; studies include both reports of language functions after lesion and reports of language functions during electrical stimulation. Some attention is also paid to neuroanatomical pathways; with the exception of studies like Damasio, Damasio, Rizzo, Varney, & Gersh (1982), this type of evidence has been only superficially considered. Inasmuch as the directionality of these pathways constrains the possible ways in which various language structures in the brain can interact, information about these pathways constitutes important evidence concerning the ways in which various structures interact to produce language. The theory itself is presented in the third section, integrating the available evidence concerning cortical, thalamic, and basal ganglia functions. Finally, the fourth section discusses implications and limitations of the current model.
THE CLASSICAL MODEL OF APHASIA

The classical model of aphasia was most succinctly stated by Geschwind (1972) and has been a basis for other influential works in aphasia (e.g., Goodglass & Kaplan, 1983). Basically, the classical model states that there is an area in the posterior portion of the inferior frontal gyrus, Brocas area, which is responsible for the motor programming of language. Damage to this area produces slow, awkward speech with impaired intonation, a severely limited variety of grammatical constructions, and severely limited vocabulary. Originally, comprehension of language was considered to be nearly normal in Brocas aphasia. The classical model also postulated an area in the posterior portion of the superior temporal gyrus, Wernickes area, responsible for the comprehension of spoken language. Damage to this area produces severe deficits in the comprehension of language. In contrast to Brocas aphasia, language output in Wernickes aphasia shows relatively preserved rate, rhythm, variety of grammatical constructions, and articulation. However, language output is remarkably devoid of content and contains substitutions of one word or sound for another, circumlocutions, and incomprehensible jargon. The classical model of aphasia also proposes an area in the inferior

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parietal lobe (angular gyrus) which is responsible for the association of spoken language symbols with information from other modalities, particularly the visual modality. Damage to this area might result in reading or writing difficulties because of an inability to associate spoken language symbols with their visual counterparts, or it might result in an inability to name objects (anomia) because of an inability to associate language symbols with characteristics in other modalities of the objects which the symbols represent. In the latter instance (anemic aphasia), language output contains circumlocutions and vague descriptions of intended concepts. In contrast to Wernickes aphasia, comprehension remains relatively intact in an anemic aphasia. The classical model also notes that Brocas and Wernickes areas are connected by a fiber bundle called the arcuate fasciculus. Damage to this tract leaves language output fluent because Brocas area is intact and language comprehension relatively normal because Wernickes area is intact. However, the patient has a disproportionate difficulty repeating heard language because Wernickes area cannot relay the auditory patterns to Brocaa area. This syndrome is referred to as the conduction aphasia. In the classical model, transcortical aphasias occur when Brocas and Wernickes areas and the connections between them are intact but isolated from other areas of the cortex by lesions in surrounding areas and tracts. Transcortical sensory aphasia demonstrates preserved repetition in the context of language output and comprehension which is otherwise like that of Wernickes aphasia. Transcortical motor aphasia shows relatively preserved repetition and comprehension in the context of extremely limited conversational speech with at least some nonfluent characteristics (Goodglass & Kaplan, 1983). The classical model of aphasia can be criticized on several counts. For example, the classical model does not acount for all aphasia syndromes. Whitaker (1984) noted that only about 60% of patients tested can be classified into the various classical syndromes by the Boston Diagnostic Aphasia Examination (Goodglass & Kaplan, 1983). It may well be that many symptom clusters can be understood better by looking at subcortical aphasias since these aphasias are different from cortical aphasias and since the classical model considers mainly cortical phenomena. This matter is discussed further below. A second criticism of the classical model is that it does not explain how language is formulated. Because of the deterioration of language output in Wernickes aphasia, it is obvious that the damaged mechanisms play some role in formulating language; however, this role is not clearly defined. If language output was merely formulated posteriorly and conveyed forward for motor programming via the arcuate fasciculus, then there should be no difference in language output between conduction aphasia and Wernickes aphasia. However, conduction aphasia demonstrates dis-

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proportionate difficulty with repetition, and substitutions are mainly of one sound for another. In contrast, patients with Wemickes aphasia demonstrate difficulty in all language output with sound substitutions, word substitutions, neologisms, circumlocutions, and jargon (Goodglass & Kaplan, 1983). The classical model also does not explain why there should be two types of transcortical aphasia if Brocas area, Wernickes area, and the arcuate fasciculus are intact in both forms. The classical model has also been criticized as a schema for classification in aphasia research. Schwartz (1984) has noted that the classical syndromes have evolved into polytypic structures. In other words, no deficit is essential for classification into a particular syndrome, and some characteristics are included in several syndromes. This situation can lead to confusion and differences in classification criteria between studies. Caramazza (1984) has also criticized the classical classifications because the defining symptoms have not been specific enough. In other words, we should not consider just comprehension deficits, but specific types of comprehension deficits such as difficulty with syntactic comprehension. Further, recent research necessitates, at the very least, revision of many of the classical assumptions. Some of the more important findings have concerned the syndrome of Brocas aphasia. For instance, Mohr et al. (1978) studied their own cases and reviewed the literature concerning the relationship between Brocas area and Brocas aphasia. The authors concluded that cases of infarction had to extend considerably beyond Brocas area to produce Brocas aphasia. Casesof Brocas aphasia included damage to the frontal, parietal, and temporal opercula, the insula, and surrounding white matter. Infarcts limited to Brocas area might initially produce mutism, but mutism quickly evolves into rapidly improving dyspraxic and effortful articulation. Lasting language deficits, such as agrammatism, were not found with infarcts limited to Brocas area. Kertesz, Hat-lock, and Coates (1979) differed from the above authors in that they described Brocas aphasia acutely in lesions of Brocas area and in that they found language deficits lasting at least 3 months in five of six patients. However, Kertesz et al. supported the findings of Mohr et al. (1978) in that lesions producing a chronic Brocas aphasia did include the frontal, parietal, and temporal opercula, and the insula. Two further findings with respect to Brocas aphasia are important. Tonkonogy and Goodglass (1981) noted that symptoms of Brocas aphasia included word-finding difficulties and articulatory difficulties of the kind often associated with nonfluent aphasias. The authors found cases in which these functions could be separated, with differing anatomical locations. The articulatory difficulty, related to deficient motor programming, was placed in the Rolandic operculum, while they located word-finding functions in the posterior, inferior frontal gyrus. The second development showed that agrammatism in Brocas aphasia is not merely limited to

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language output. Recent research cited by Blumstein (1981) indicates that patients with Brocas aphasia show difficulty comprehending complex grammatical forms. The ability to self-monitor language was raised as early as 1972 by Goodglass and Kaplan. Goodglass and Kaplan suggested that the reason for deterioration of language in Wernickes aphasia is the breakdown in the internal monitoring of language output by damaged language comprehension mechanisms. Marshall and Tompkins (1982) studied self-correction behaviors in groups of aphasic patients which they broke down by classical categories of aphasia. The authors discussed the importance of their results in terms of their patients ability to monitor their own language. Although Marshall and Tompkins found no differences between groups of aphasic patients in the number of attempts to correct erroneous responses in a series of structured language tasks, they found that patients with Wernickes aphasia were the least successful in eventually correcting erroneous responses. These data supported the idea of Goodglass and Kaplan (1972) regarding poor self-monitoring skills in Wemickes aphasia. The observations of Kertesz et al. (1979) also generally supported a temporal lobe focus for Wernickes aphasia, though the lesion of one patient extended anteriorly. Finally, there is evidence from the cortical stimulation literature that language formulation and production are not limited to the more anterior zones associated with Brocas aphasia, even by Mohr et al. (1978). This holds true for both the phonological and the semantic aspects of language. Ojemann (1983) showed that there was a large overlap in cortical sites where stimulation interfered with the ability to discriminate speech sounds and where stimulation interfered with the ability to mimic sequences of orofacial movements. These sites were in the inferior posterior frontal, inferior parietal, and superior posterior temporal lobes. The author interpreted the data as indicating a link between motor speech and speech perception mechanisms. Not surprisingly, electrical stimulation evoked changes in naming from sites in the same areas. The one area showing naming changes in most patients was in the inferior frontal lobe immediately anterior to the motor cortex. This was the same area implicated in naming by Tonkonogy and Goodglass (1981). It was a little more surprising, however, that when patients were asked to name objects silently, electrographic potentials could be recorded concurrently from both frontal and temporoparietal sites (Ojemann, 1983). This suggests that both sites may be involved in word finding. The purpose of reviewing the literature described above primarily was to provide an understanding of issues which will assist in unravelling the role of subcortical structures in language. A consensus is emerging that the classical model of aphasia (e.g., Geschwind, 1972) can not account for many phenomena in aphasia and does not provide an adequate system

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for classifying aphasias, especially for research purposes. For these reasons, a new framework with greater explanatory power and heuristic value is needed. Thus, several inadequacies in the classical model are handled as follows. The controversy regarding the localization of Brocas aphasia is acknowledged, in this paper, primarily by using the terms anterior and temporoparietal to refer to language zones. The split between wordfinding and motor-programming functions in language suggested above is expanded upon. The participation of temporoparietal areas in monotoring language output is incorporated into the theory in a way which is consistent with evidence supporting the participation of these structures in language output. These themes are expanded upon later in the theoretical section of this paper.
STUDIES OF SUBCORTICAL LANGUAGE FUNCTIONS

As previously stated, understanding of the role of subcortical structures in language may explain phenomena which are unexplained by the classical model of aphasia; indeed, this is a major thesis of this paper. In this section, research regarding language functions of the thalamus and basal ganglia of the language-dominant hemisphere is reviewed. A relatively detailed knowledge of the anatomy of the basal ganglia and, especially, of the thalamus is necessary to read this paper. A detailed description of these structures is beyond the scope of this paper, but the unfamiliar reader may wish to refer to a more detailed neuroanatomy text, such as Carpenter and Sutin (1983) or Matzke and Foltz (1983). A pictorial representation of the thalamus and its major nuclei (Fig. 1)

MEDIAL

ANTERIOR

VENTRAL LATERAL

POSTERIOR NUCLEUS

MEDIAL

NUCLEUS

FIG. 1. The left thalamus, showing the major nuclei. (From A Synopsis of Neuroanatomy by H. A. Matzke and F. M. Foltz, 1983, New York: Oxford University Press. Copyright 1983 by Oxford University Press. Adapted by permission.)

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has been provided for reference during the discussion of thalamic structures. Most of the thalamic structures generally thought to be involved in language lie within the lateral nuclear complex. Evidence regarding the pulvinar, ventral anterior, and ventral lateral nuclei is discussed below. It should be noted that a few authors have implicated other thalamic structures in language, though their views are not necessarily shared by others. Ojemann (1983) speculated that the intralaminar nuclei might be involved in language as a part of the thalamocortical activating system. Brown (1979) implicated the dorsal medial nucleus as being involved with anterior language zones, and thereby responsible for nonfluent aphasias when they occur with thalamic lesion. In this paper, the term basal ganglia is used to refer to the caudate nucleus, putamen, and globus pallidus, collectively. A band of white matter, the anterior limb of the internal capsule, lies between the putamen and the caudate nucleus. As discussed below, all of these structures have been implicated in language. The following is a brief synopsis of evidence regarding subcortical mechanisms in language. This discussion is divided into three sections. The first section discusses thalamic mechanisms in language, and the second discusses mechanisms within the basal ganglia and internal capsule. The final section discusses pathways between the various cortical and subcortical structures implicated in language. This evidence subsequently is used to construct a model of language generation including both cortical and subcortical mechanisms. Studies of Language and the Thalamus Language has been studied both in cases of thalamic lesion and by electrical stimulation of thalamic nuclei. The issue of thalamic aphasia has been a controversial one with some authors questioning the existence of such a syndrome (e.g., Benson 1979; Luria, 1977). Nonetheless, an increasing number of scientists are beginning to accept and speculate about a role for the dominant thalamus in language. An in-depth review of this literature is beyond the scope of this paper; the reader interested in such detail may find Crosson (1984) helpful. A brief synopsis is offered below. Although there has been variability between studies of language functions after naturahy occurring vascular lesions of the thalamus, a core syndrome of thalamic aphasia has occurred. The features are (a) relatively fluent language with substitutions of one word for another and with spoken language sometimes deteriorating into incomprehensible jargon, (b) comprehension that is less impaired than the type of language output would normally indicate, and (c) relatively preserved repetition (e.g., Alexander & LoVerme, 1980; Cappa & Vignolo, 1979; Crosson, Parker, Warren, LaBreche, & Tully, 1983; Jenkyn, Alberti, & Peters, 1981; Mohr, Watters, 8z Duncan, 1975; Reynolds, Turner, Harris, Ojemann, & Davis, 1979).

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Perseveration and a lack of spontaneous speech are also common. The most notable exceptions to this pattern are individual cases presented by Brown (1979), Glosser, Kaplan, and LoVerme (1982), and McFarling, Rothi, and Heilman (1982). In particular, these three cases showed elements of nonfluent output ranging from muteness in the former to impairment of intonation and articulatory agility in the latter. Sometimes, nonfluent language has been reported with thalamic degeneration (e.g., Daniels, Chokroverty, & Barr-on, 1969; Shulman, 1957), but it has been difficult to separate language deficits from the dementia normally exhibited by these cases. Benson (1979) stated that aphasia after naturally occurring dominant thalamic lesion tends to remit rapidly. However, in 20 cases of vascular lesion reviewed by Crosson (1984) which were followed over time, 17 showed aphasia persisting from 2 months to as long as 4 years. Aphasia has also been reported after thalamotomies which target the ventral lateral nucleus for lesion. The reported incidence has ranged from 3% (Gillingham, Watson, Donaldson, & Naughton, 1960) to as high as 42% in lesions of the dominant ventral lateral nucleus (Selby, 1967). Although aphasia symptoms rarely have been reported in detail after thalamotomy, those studies that have detailed symptoms described language dysfunctions similar to those previously described for vascular lesion (Allen, Turner, & Gadea-Ciria, 1966; Bell, 1968; Darley, Brown, & Swenson, 1975; Samra et al., 1969). In general, thalamotomy studies have reported aphasia to remit rapidly when it occurs (Crosson, 1984). Most likely, this pattern of rapid remission indicates that the ventral lateral nucleus is not directly involved in language. This is consistent with the fact that the ventral lateral thalamus is primarily a motor nucleus, receiving inputs from the basal ganglia, the cerebellum, and the motor cortex, and sending outputs to the motor cortex. The language symptoms probably resulted from temporary disturbance of surrounding nuclei or pathways. Two studies have shown no significant language changes after dominant pulvinectomies which created cryogenic or electrocoagulation lesions using stereotactic techniques (Brown, 1979; Vilkki & Laitinen, 1976): Ordinarily, one would interpret these data as indicating that the pulvinar is not involved in language; however, there have been other data strongly implicating a portion of the pulvinar. Kameyama (1976/1977)found aphasia in lesions of the dominant ventral posterior lateral nucleus only when lesions extended into the pulvinar. Other autopsied cases which were not described as involving the entire dominant thalamus have demonstrated involvement of the pulvinar (Ciemans, 1970; Crosson, 1984; Mohr et al., 1975). Ojemann (1977) has reported greater density of naming errors during dominant pulvinar than dominant ventral lateral stimulation. In particular, his studies have implicated the anterior superior lateral pulvinar. Studies of retrograde degeneration of thalamic nuclei after cortical aphasias have shown involvement of the anterior lateral pulvinar (Van Buren,

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1975; Van Buren & Borke, 1969). Degeneration of this area of the pulvinar did not occur when language was preserved. The most likely explanation for the apparent discrepancy between pulvinectomy studies and other studies of the pulvinar is that pulvinectomies have not extended the lesion to the anterior superior lateral margin of the nucleus. Other studies (Schaltenbrand, 1965, 1975) have implicated the ventral anterior nucleus or surrounding structures, showing compulsary speech when this nucleus was stimulated. Subjects in these studies have not been able to inhibit speech during ventral anterior stimulation, even when they tried. McCarthy and Warrington (1984) have shown that there are at least partially separated semantic and phonological functions in language production. Although the issue of semantic versus other types of paraphasia has not often been addressed in thalamic aphasia, Alexander and LoVerme (1980), Cappa and Vignolo (1979) and Crosson et al. (1983) have described a predominance of semantic errors in the 13 cases of thalamic aphasia collectively described by these studies. All authors interpreted their data as suggesting a semantic role for the thalamus in language. Indeed, Crosson (1981) has speculated that the symptoms of thalamic aphasia described above are exactly what one would expect if a mechanism for semantic monitoring were selectively damaged. Other theories have emphasized that the thalamus might be involved at a deeper level of language processing or formulation (e.g., Brown, 1975;Riklan & Levita, 1%5), that the thalamus might be involved in activating cortical language mechanisms (e.g., Horenstein, Chung, & Brenner, 1978; Luria, 1977; McFarling et al., 1982; Riklan & Cooper, 1975), that the thalamus might regulate access to stores of language information (e.g., Botez & Barbeau, 1971; Reynolds et al., 1979), or that the thalamus might be involved in some combination of such activities (e.g., Cooper et al., 1968; Samra et al., 1969). In summary, a syndrome of thalamic aphasia does appear to accompany dominant thalamic lesions. This syndrome is characterized by fluent but paraphasic language which sometimes degenerates into jargon. Language comprehension is usually less impaired than this type of output normally would indicate, and repetition is minimally impaired or normal. Cases of nonfluent language after dominant thalamic lesion are rare but do exist; however, a paucity of spontaneous language is frequently seen. Perseveration in speech is also common. This pattern has been seen in naturally occurring vascular lesion and thalamotomy. Although aphasia often has often remitted rapidly after thalamotomy, it has persisted more often than not in reported cases of vascular lesions of the thalamus. Stimulation data, lesion data, and retrograde degeneration studies implicated the anterior superior lateral pulvinar in language; this area probably was spared in pulvinectomies, where no language changes occurred. Transient language symptoms after ventral lateral thalamotomy probably resulted from temporary disturbance of surrounding tracts or structures rather than direct involvement of this motor nucleus in language. One series

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of stimulation studies producing compulsary language implicated the dominant ventral anterior nucleus. Studies of Language and the Basal Ganglia and Internal Capsule Language functions of the basal ganglia have been studied both in cases of basal ganglia lesion and by electrical stimulation of the basal ganglia. In naturally occurring vascular lesions, the internal capsule is frequently involved along with the basal ganglia; therefore, these structures are considered together. Although the functions have not been as extensively studied as the thalamus, increasing attention has been paid to their language functions. Indeed, one recent study (Wallesch et al., 1983) indicates that lesions of the basal ganglia in the language-dominant hemisphere may have longer lasting severe effects on language than lesions of the dominant thalamus. A synopsis of this literature is offered below. Lesions in the area of the internal capsule and putamen in the languagedominant hemisphere have resulted in both fluent and nonfluent language output. Naeser et al. (1982) found that lesions extending from this region anteriorly and ventrally to include the periventricular white matter deep to Brocas area generally produced language output with many nonfluent characteristics and lesser impairments of comprehension and repetition. When lesions extended posteriorly across the auditory radiations, speech was fluent and comprehension poor. Alexander and LoVerme (1980) generally described fluent language in 6 lesions with a putaminal focus (extent of capsular involvement was not detailed). Brunner, Kornhuber, Seemuller, Suger, and Wallesch (1982) described Brocas aphasia with transcortical features in one or two of their cases of lesions in the putamen and surrounding structures. Later in this paper, some import is placed on connections in the anterior limb of the internal capsule in the language-dominant hemisphere. Again, both fluent and nonfluent language output can be found with lesions in the anterior limb. Of 15 subcortical lesion cases in the literature which involve part of the anterior limb (Aram, Rose, Rekate, & Whitaker, 1983; Damasio et al., 1982; Naeser et al., 1982), 11 have nonfluent characteristics and 4 were reported as fluent. Again, the Naeser et al. data indicated that language was more likely to be nonfluent when lesions of the anterior limb extended further ventrally and laterally. In naturally occurring subcortical vascular lesions producing aphasia, the globus pallidus of the language-dominant hemisphere has seldom been mentioned. Patterns of vascular supply indicate a probability of involvement of the anterior pallidum when the anterior putamen has a vascular lesion (Carpenter & &tin, 1983). One case involving the posterior globus pallidus, posterior medial putamen, and other structures in an 1l-year-old child showed dysarthria (i.e., difficulties in the motor execution of speech) but no language symptoms (Aram et al., 1983). In the subcortical aphasias of Damasio et al. (1982), lesions extended

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into the caudate head or body in four cases. Language was nonfluent in three and fluent in one, and one case with such a lesion had normal language. All cases but the latter with normal language also had lesions in the anterior limb of the internal capsule. Data from Brunner et al. (1982) showed that aphasia was likely to .be more severe and more persistent if lesions of Brocas area extended to the caudate head. Language demonstrated nonfluent characteristics in such cases. In the early stages of stereotactic surgery for Parkinsonism, lesions were created in the globus pallidus instead of the ventral lateral thalamus. Svennilson, Torvik, Lowe, and Leksell(l960) described aphasia in some patients after creating lesions in the dominant globus pallidus. The target was in the lateral medial segment of the nucleus. Objectively, wordfinding difficulty and paraphasia were noted, though more detailed descriptions of language were not available. Subjectively, one patient described the difficulties as a lack of coordination between thought and speech. Other studies reported similar findings for lesions involving both the globus pallidus and ventral lateral thalamus (Cooper, 1958; Hermann, Turner, Gillingham, & Gaze, 1966). A few electrical stimulation studies have provided information about the basal ganglia. Hermann et al. (1966) demonstrated the arrest of ongoing speech with electrical stimulation in the globus pallidus as well as in thalamic nuclei. This effect may be related to the aphasias resultant from lesions in these structures; this possibility is explored at greater length below. The work of Van Buren (1963, 1966) has provided evidence of involvement of the caudate head in language. This investigator found arrest of ongoing speech when he stimulated frontocaudate pathways near the caudate head of the dominant hemisphere. Further, when stimulation was moved into the caudate head itself, ongoing speech was not only interrupted, but there was also inappropriate spontaneous speech. Such inappropriate speech was not observed during stimulation of the ventral lateral nucleus of the thalamus, the internal capsule, or globus pallidus. The importance of this distinction in response between the frontocaudate pathways and the caudate head is discussed further below. To summarize, language symptoms from lesions in the basal ganglia and internal capsule do not cohere into a single syndrome as well as symptoms accompanying dominant thalamic lesion. Data from Damasio et al. (1982) and Van Buren (1963, 1966) indicated that small differences in location within these structures and tracts may produce dramatic differences in language after lesion or during electrical stimulation. The putamen, globus pallidus, and anterior limb of the internal capsule have all been implicated. Lesions in the anterior limb of the internal capsule tend to produce nonfluent language output, especially if they extend ventrally and anteriorly. Stimulation of the frontocaudate pathways produced interruptions of ongoing language while stimulation of the caudate

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head produced inappropriate but fluent language. Lesions of Brocas area extending into the caudate nucleus tended to cause a longer lasting and more severe nonfluent aphasia. Both fluent and nonfluent language has been reported in putaminal lesions. Neuroanatomical Pathways between Cortical and Subcortical Structures Implicated in Language It is highly unlikely that the various cortical and subcortical structures involved in language operate in isolation from one another to produce the phenomena we know as language. It is more probable that these structures operate in an organized and coordinated fashion to produce and comprehend language. In order to understand how these structures function and how they are coordinated, then, it is necessary to understand how information flows between them. It follows that knowledge of the pathways connecting the various structures involved in language could shed some light on how they interact. Indeed, the possible ways in which the structures might interact is constrained by the direction in which information can flow between them. With the exception of Damasio et al. (1982), few authors have noted the importance of these connections in language. Connections between the centers most often implicated in language are discussed below. These centers include the inferior frontal, insular, and opercular cortex, the temporoparietal cortex, the ventral anterior nucleus of the thalamus, the ventral lateral nucleus of the thalamus, the pulvinar of the thalamus, the caudate nucleus, the putamen, and the globus pallidus. Readers desiring more detail should consult Carpenter and Sutin (1983) or Ingram (1976). The temporoparietal and anterior language zones of the cortex are connected by the arcuate fasciculus which transmits information both anteriorly and posteriorly. The caudate nucleus and putamen both receive input from most regions of the cortex, though the strength of representation of different cortical regions may vary between the two nuclei. Anteriorly, for example, the motor cortex projects primarily to the putamen, the premotor cortex projects to both nuclei, and the prefrontal cortex projects primarily to the caudate nucleus. Although there are these prolific connections from the cortex to the caudate nucleus and putamen, there are no fibers of any consequence which travel in the opposite direction, from the caudate and putamen to the cortex. The main outputs from the basal ganglia are channeled through the globus pallidus which receives fibers from both the caudate nucleus and the putamen (Carpenter & Sutin, 1983). Of the structures discussed in previous sections of this work, the globus pallidus projects to the ventral lateral and ventral anterior nuclei of the thalamus. The ventral lateral thalamus receives inputs from the globus pallidus, the cerebellum, and the motor cortex. This nucleus sends fibers

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to the motor cortex. This pattern of connections leads to the conclusion that the ventral lateral nucleus is primarily a motor nucleus. Thus, it is more likely to be involved in speech than language; thalamotomy studies support this conclusion since dysarthria is more common and more persistant after ventral lateral lesion than aphasia (e.g., Cooper et al., 1968). The ventral anterior nucleus receives input from the globus pallidus (anterior portions) and from the premotor and prefrontal cortex. Ingram (1976) described direct connections to the ventral anterior nucleus from the brainstem reticular formation, but Carpenter and Sutin (1983) emphasized input to the ventral anterior nucleus from the intralaminar thalamic nuclei which in turn receive fibers from the brainstem reticular formation. The ventral anterior nucleus sends outputs to the premotor and prefrontal cortex. The pulvinar has bidirectional connections with the temporoparietal cortex. There are indications of bidirectional connections of the pulvinar with the frontal cortex (Carpenter & Sutin, 1983). These connections between structures implicated in language tell us something about the way in which the structures may be organized in language functions. The cortical language centers may influence the caudate nucleus or putamen; however, due to an absence of direct connections, the caudate nucleus and putamen can have no direct influence on cortical language centers. Rather, any influence of the basal ganglia on cortical language centers must be mediated by thalamic centers. More specificially, influences from the basal ganglia upon the anterior cortical language centers must be mediated through the ventral anterior nucleus. Through direct or indirect inputs from the brainstem reticular formation, the ventral anterior nucleus may also transmit arousal or activation impulses to the anterior cortical language zones. Thalamic nuclei and cortical language centers, however, may have reciprocal influences by virtue of bidirectional connections. The ventral anterior nucleus may have reciprocal influences with the anterior cortical language zones. The pulvinar may have reciprocal influences with the temporoparietal cortex, and perhaps even the anterior language zones. When considered with lesion and stimulation data, the nature and direction of neuroanatomical pathways becomes an important piece of the puzzle of cortical-subcortical relationships in language. One key example should illustrate this point. In several subjects, Van Buren (1963, 1966) found that stimulation of the caudate head in the language-dominant hemisphere resulted in the interruption of ongoing language by the flow of irrelevant material into language. It is clear from the examination of neuroanatomical pathways that however stimulation of the caudate head influences the language cortex to produce irrelevant material must be mediated through the globus pallidus then the ventral anterior (or possibly the ventral lateral) nucleus because the basal ganglia have no direct output to the cortex. Van Buren further found that stimulation of front-

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ocaudate pathways interrupted ongoing language, but without the irrelevant language. The influence of frontocaudate pathways (lateral to the caudate head) on the actions of the language cortex must be mediated by the caudate head, globus pallidus, and ventral anterior nucleus, respectively. This theme is developed further below.
SUBCORTICAL FUNCTIONS IN LANGUAGE: THE MODEL

The data discussed above can be used to formulate a model of subcortical functions in language; however, a few simple premises which provide a framework for the model should be explained first. The first premise is that motor and sensory systems, in the broadest sense of the words, are to some degree separable in the human brain. Here, motor refers not only to motor execution but also to the plan and intent to act, and sensory refers not only to the reception of sensory information but also to the initial decoding of such information. In this sense, language is originally learned through both sensory and motor channels, and maturing language functions require increasingly complex interactions between motor and sensory systems. The second premise is that language is monitored by its speaker, not only externally through hearing oneself speak, but also internally before it is actually executed in speech. The breakdown of such monitoring is the most parsimonious explanation for the jargon of Wernickes aphasia (Goodglass & Kaplan, 1983). It has already been noted that patients with Wernickes aphasia are particularly ineffective in monitoring and correcting their own errors in spoken language (Marshall & Tompkins, 1982). The implication of the current premise is that this inefficiency applies to internal, preverbal monitoring as well. The third premise is that the motor and sensory systems involved in language interact in a complex way to produce spoken language. The production of fluent jargon which accompanies profound comprehension deficit in Wernickes aphasia is one indication of such an interaction. Evidence cited by Ojemann (1983) also supports this premise. The reader will remember that Ojemann reported that naming errors were evoked from stimulation of both anterior motor and posterior sensory sites and that silent naming produced simultaneous activity from both anterior motor and posterior sensory sites. The model of subcortical functions in language production is developed below. The purpose is to explain the involvement of the thalamus and basal ganglia in language, as has been indicated by recent data, to develop a theory of language production which is capable of explaining more known phenomena than the still popular classical theory, and to produce specific, testable hypotheses regarding subcortical functions in language. As in the above discussion of recent research, the development of the model addresses cortical, thalamic, and basal ganglia functions, respectively.

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Cortical Functions In the present model, language formulation is presumed to be a function of the more anterior language zones, which most likely include the posterior inferior frontal gyrus, the frontal operculum, the parietal operculum, the temporal operculum, and the insula. The term language formulation encompasses the conceptual, word-finding, and syntactic processes necessary for the encoding of language. The reader will recall that Tonkonogy and Goodglass (1981) found that the word-finding and motor-programming functions of these areas were separable. Extending the findings of Tonkonogy and Goodglass, language formulation (i.e., language encoding) is assumed to be partially separated from, but in close physical and temporal contiguity with, the motor programming of language. This extension from the narrower word-finding function to the broader language formulation function is justified by findings discussed above. First was that both agrammatism in verbal output and comprehension of complex syntax are associated with lesions in the more anterior language zones (Blumstein, 1981; Mohr et al., 1978). Syntactic as well as word-finding mechanisms are, of course, needed for language encoding. Second was that these same difficulties with syntax were found in Tonkonogy and Goodglass (1981) patient with word-finding but not articulatory problems. Finally, from an ontological standpoint, language formulation can be considered an extremely complex motor function, and as such, should be located in the anterior language zones in proximity with other such motor functions, not in the posterior cortical areas devoted to sensory function as some authors have suggested. In light of recent research regarding the comprehension of complex syntax (e.g., Blumstein, 1981), the function of the posterior temporoparietal cortex also must be described in a more circumscribed manner than in the classical model. Instead of assigning all comprehension functions to this region, the current model proposes that the decoding of language symbols is accomplished in this area. Such decoding may even extend to the level of the phrase or simple sentence, but the comprehension of complex syntax requires the participation of more anterior regions once the language symbols have been initially decoded. Observations of Luria (1973) are also relevant. He divided comprehension of language symbols into the discrimination of phonemes and the designation of semantic attributes. The latter can occur only after the phonological structure has been decoded. A further observation is that the semantic functions of the temporoparietal cortex are based, at least to some degree, on the association of language symbols with the characteristics of the objects they represent in other modalities (e.g., visual, tactile). For example, the word ball would be associated with a visual representation of a round object.

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Finally, the temporoparietal language areas are connected to the anterior language areas by the arcuate fasciculus. A case described by Naeser and Hayward (1979) supports the role of this structure in conduction aphasia, where repetition is disproportionately impaired in comparison with other language functions. Evidence also suggests that this pathway is involved in conveying phonological information in language. For example, the most common type of substitution error in conduction aphasia is the substitution of one sound for another rather than the substitution of one word for another (Goodglass & Kaplan, 1983). McCarthy and Warrington (1984) also showed that repetition could be facilitated in conduction aphasia by repetition tasks which required active semantic processing. The authors concluded that a phonological processing mechanism was damaged in conduction aphasia and that improvement in the semantically loaded repetition tasks was due to the involvement of intact semantic mechanisms. Cortical mechanisms discussed above have been schematically represented in Fig. 2. To summarize the role of cortical centers, language formulation (including conceptual, word-finding, and syntactic processes) is performed in the anterior language zones. Language formulation is closely associated with, but separate from, motor programming. Decoding of complex grammar is also performed anteriorly. The phonological and semantic decoding of language symbols is performed by the temporoparietal cortex. Semantic monitoring relies heavily on the association of language symbols with information in other modalities. The arcuate fasciculus, connecting the anterior and temporoparietal language zones, is involved in phonological processing, which is discussed further below.

FIG. 2. Schematic drawing representing cortical language mechanisms and their interconnection. FOR = language formulator (anterior cortex), MP = motor programmer (anterior cortex); DEC = language decoder (temporoparietal cortex); AF = arcuate fasciculus.

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Thalamic Functions In 1981, Crosson presented a paper at the meeting of the American Psychological Association proposing that the thalamus, with its reciprocal connections to cortical language areas, provided one mechanism through which the temporoparietal area, involved in language decoding, monitored the encoding of language peformed by anterior mechanisms prior to the actual execution of encoded material in speech. In other words, corticothalamo-cortical pathways provide the mechanism through which the temporoparietal area checks the encoded language for semantic accuracy. The author had reasoned that if such a semantic feedback mechanism existed, damage to it would result in a syndrome where verbal output was more impaired than language comprehension because the decoding mechanism would be left intact while the mechanism for monitoring semantic accuracy would be damaged. As previously mentioned, this has indeed been the picture presented by most cases of thalamic aphasia (e.g., Alexander & LoVerme, 1980; Cappa & Vignolo, 1979; Crosson et al., 1983; Jenkyn et al., 1981; Mohr et al., 1975; Reynolds et al., 1979). The predominance of semantic paraphasias in thalamic aphasia (Alexander & LoVerme, 1980; Cappa & Vignolo, 1979; Crosson et al., 1983) also supports the idea of an interruption in semantic monitoring. Relatively intact repetition is explained by reliance on a separate system for the transmission of phonological linguistic information used to perform the act of repetition (McCarthy & Warrington, 1984). In order for preverbal semantic monitoring of language formulation to take place, semantic information must be conveyed from anterior language areas where language is formulated to temporoparietal areas where language is decoded and monitored. The most likely pathway for this transmission of semantic information is from the anterior language zones to the thalamus via the connections with the ventral anterior thalamus, from ventral anterior thalamus to the pulvinar (probably via the internal medullary lamina), and from the thalamus to the temporoparietal cortex through connections with the pulvinar. The work of Ojemann and his colleagues has shown that anomia in dominant ventral lateral stimulation was much more likely when electrodes were close to the internal medullary lamina and that perseveration of the same wrong word during dominant ventral lateral stimulation was much more common when electrodes were near the ventral anterior nucleus (Ojemann, 1975, 1977, 1983; Ojemann & Ward, 1971). These data can be seen as confirmation of the role of the internal medullary lamina and the ventral anterior nucleus in language. However, it should be noted that there is evidence of pathways from the pulvinar to the frontal lobes (Carpenter & Sutin, 1983), and conceivably, semantic information might flow between the anterior and posterior language areas

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primarily through the pulvinar. As stated above, electrical stimulation data (Ojemann, 1977), postmortem data (Ciemans, 1970; Crosson, 1984; Kameyama, 1976/1977; Mohr et al., 1975), and retrograde degeneration data (Van Buren, 1975; Van Buren & Borke, 1969) support the role of the pulvinar in language. Also, in order for monitoring to be effective when refinement of semantic content is necessary, the message must be conveyed from the temporoparietal monitoring mechanism to the language encoder in the anterior cortex to initiate refinement. This message would be conveyed through the pathways mentioned above, but in the opposite direction since the cortico-thalamo-cortical pathways mentioned were bidirectional. In order for anterior cortical mechanisms to produce language, it is also necessary that an optimal arousal level of these mechanisms be maintained. Since it receives afferents from the reticular formation (direct or indirect), thought to be involved in cortical arousal, and since it sends efferents to the frontal cortex, the ventral anterior nucleus of the dominant thalamus is the likely site to provide such excitatory influences. The function of the ventral anterior nucleus would be to selectively distribute excitatory influences from the reticular formation to frontal mechanisms for language production via the anterior limb of the internal capsule. Primarily in the dominant thalamus, electrical stimulation in and around the ventral anterior thalamus, as demonstrated by Schaltenbrand (1965, 1975), often elicited spoken language which had little relevance to ongoing events and could not be voluntarily inhibited. These phenomena are probably related to perseveration during naming from anterior ventral lateral stimulation (Ojemann, 1983), as discussed above. Recent studies (Aram et al., 1983; Damasio et al., 1982; Naeser et al., 1982) also indicated that destruction of the anterior limb of the internal capsule produces dysfluent but often grammatical language, particularly when lesions extend anteriorly and ventrally into this region. Connections between the ventral anterior nucleus and the anterior language zones of the cortex traverse this portion of the internal capsule, and the dysfluent language can be explained by the interruption of excitatory influences from the ventral anterior nucleus to the language formulation centers. The occasionally dysfluent cases of thalamic aphasia (Brown, 1979;Glosser et al., 1982; McFarling et al., 1982) and the frequent lack of spontaneous speech in thalamic aphasia may also be due to the interruption of excitatory influence from the thalamus to the cortex. The cortical and thalamic mechanisms for language mentioned up to this point in the development of the model have been schematically represented in Fig. 3. To summarize thalamic functions in language, bidirectional cortico-thalamo-cortical pathways are involved in semantic monitoring mechanisms. Internal semantic monitoring of language formulated by the anterior language zones is performed by the temporoparietal

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FIG. 3. Schematic drawing representing cortical language mechanisms, thalamic language mechanisms, and their interconnections. FOR = language formulator (anterior cortex); MP = motor programmer (anterior cortex); DEC = language decoder (temporoparietal cortex); AF = arcuate fasciculus; VA = ventral anterior thalamus; PUL = pulvinar (thalamus); IML = internal medullary lamina (thalamus); RF = reticular formation.

cortex prior to the execution of the language segments in speech. Such monitoring may result in the refinement of formulated language segments prior to their release for motor programming. Pathways through the thalamus (particularly the anterior superior lateral pulvinar) act as a conduit for semantic information and messagesto refine semantic content during this monitoring process. Excitatory impulses are also conveyed from the ventral anterior nucleus to the anterior language zones which provide the proper level of activation for language formulation. Two questions remain to be answered, however: First, how are language segments held in abeyance from execution while the semantic monitoring takes place? Second, how are the excitatory influences from the ventral anterior nucleus regulated? For the answers to these questions, we must turn our attention to the mechanisms of the basal ganglia.
Basal Ganglia

Of the structures involved in language, the least data exist on the basal ganglia. Nonetheless, key data do exist allowing the formulation of tentative hypotheses regarding their role in language. Not least among these data is the anatomical position of the basal ganglia relative to the cortex and the thalamus. As previously highlighted, the putamen and caudate nucleus receive input primarily from the cortex, but these structures do not send any output directly to the cortex. Most output from the basal ganglia is mediated through the globus pallidus which sends numerous fibers to the ventral anterior and ventral lateral nuclei of the thalamus. These thalamic nuclei then send outputs to the frontal and motor cortex, re-

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spectively. Thus, the basal ganglia are in a position to receive input from various parts of the cortex, and on the basis of these inputs, the basal ganglia can in turn influence outputs from the thalamus to the cortex. The current model proposes that the basal ganglia are involved in two mechanisms which influence language production by integrating inputs from the cortex and subsequently influencing thalamic mechanisms. First, the basal ganglia influence tone in the anterior cortical language areas by regulating the flow of excitatory impulses from the ventral anterior thalamus. If tonic cortical excitation is maintained at too high a level, extraneous material will enter into the encoding (language formulation) and motor-programming processes. If tone is too low, language formulation will be inefficient or not occur spontaneously at all. The second mechanism is a motor release mechanism which allows language segments to be released at the proper time, after semantic monitoring has taken place. These two mechanisms are detailed in the following paragraphs. The mechanism directly affecting tonic activation of the anterior language cortex by the ventral anterior nucleus of the thalamus is most likely located in the globus pallidus. Fluent language output was described after surgical lesions of the globus pallidus (Svennilson et al., 1960). Further, the arrest of ongoing language during stimulation of the globus pallidus was reported (Hermann et al., 1966). The most parsimonious explanation for these two pallidal phenomena is that the globus pallidus maintains an inhibitory influence over the ventral anterior thalamus in such a way as to regulate the amount of excitation conveyed to the anterior language cortex. Thus, lesion of the globus pallidus would create disinhibition of the ventral anterior thalamus, leading to overactivation of the anterior cortical language zones. This overactivation would in turn result in the programming of extraneous material in language, for example, the paraphasias noted by Svennilson et al. (1960). Stimulation of the globus pallidus, however, would excite inhibitory mechanisms resulting in the inhibition of the ventral anterior nucleus and the interruption of ongoing language, as noted by Hermann et al. (1966).* A complete understanding of the tonic mechanisms, though, is dependent upon the understanding of the response release mechanisms.
Precedents for such tonic and response release mechanisms exist elsewhere in the nervous system, for example, the tonic and phasic changes in sudomotor response as measured by skin conductance. 2 There are several possible explanations of stimulation data besides the excitation of processes (Crosson, 1984). However, it should be noted that there is ample precedent for the excitation of sensory and motor processes in subcortical stimulation. Ojemann (1976) discussed the importance of eliciting sensory or motor responses in his work, and Selby (1967) used the elicitation of motor responses to place electrodes in surgery for Parkinsons syndrome. Further, excitation explanations become much more probable when it can be shown that stimulation and lesion produce opposite effects.

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However, one digression is necessary before discussing the response release mechanisms. The reader might now ask the following question: If tonic control of the ventral anterior nucleus resides in the globus pallidus, then why does the literature on vascular lesion more frequently implicate the putamen than the globus pallidus? There are two possible answers. The first is that the inhibitory mechanism actually resides in the putamen, and its influence is only transmitted by the globus pallidus to the thalamus. The second possibility is that lesions of the putamen producing aphasia directly or indirectly involve the globus pallidus. The reader will recall that the globus pallidus is immediately adjacent and medial to the putamen. It is quite likely that the six cases of dominant putaminal hemorrhage discussed by Alexander and LoVerme (1980) at least transmitted pressure effects to the globus pallidus during the acute stages. In reported cases of infarction (e.g., Damasio et al., 1982; Naeser et al., 1982), it is rare for the putamen alone to be involved. In cases involving the anterior putamen, it is also likely that the anterior globus pallidus is involved because of overlap in circulation (Carpenter & Sutin, 1983). This portion of the globus pallidus receives input from the caudate nucleus. The importance of this latter fact is discussed shortly. The reader also will recall that Aram et al. (1983) also reported dysarthria but no aphasia in one case of lesion in the posterior portions of the dominant globus pallidus and putamen. Damasio et al. (1982) reported similar findings in one of their cases. The response release mechanisms of the basal ganglia are closely related to the tonic mechanisms. Actually, both tonic and response release mechanisms involve both the globus pallidus and the caudate nucleus, as explained below. The purpose of the response release mechanism is to allow a temporary increase in excitation from the ventral anterior thalamus to the anterior language cortex which is timed to allow the motor programming of semantically verified language for speech. This response release function is performed by the head of the caudate nucleus through its input from the anterior and posterior language cortex and its output to the globus pallidus. The response release mechanism works as follows. Activity in the caudate head exerts an inhibitory influence over the inhibitory mechanisms of the globus pallidus. Thus, when required, activity from the caudate head will temporarily inhibit pallidal inhibitory mechanisms, thereby releasing the ventral anterior nucleus from pallidal inhibition, which in turn increases excitation to anterior cortical mechanisms allowing the release of semantically verified language for motor programming. Normally (i.e., when a person is not speaking), the caudate inhibitory link is under inhibition from the decoding mechanisms in the temporoparietal cortex, leaving the pallidal inhibitory mechanisms active, and there is no temporary increase in excitation of the anterior language mechanisms. Once semantic

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verification of a verbal message (formulated anteriorly) has occurred, however, the temporoparietal structures release the caudate mechanism from inhibition. This action subsequently causes the caudate mechanism to inhibit the pallidal inhibitory mechanism, freeing the ventral anterior thalamus to excite anterior mechanisms to the level where motor programming is initiated, which eventually leads to verbal expression of the language segment. Once programming of the segment has been completed, the anterior cortical mechanisms terminate activity of the caudate mechanism through frontocaudate pathways, restoring the relationship between temporoparietal and caudate mechanisms to its normal state, i.e., inhibition of caudate by temporoparietal mechanisms. Two sets of evidence support this role for the caudate head in language. First, when Van Buren (1963, 1966) stimulated frontocaudate pathways near the caudate head, he usually produced the arrest of ongoing speech. This result would be predicted from the current model because stimulation in that area excites the frontocaudate pathway responsible for terminating motor programming and reestablishing temporoparietal inhibition of caudate mechanisms. Furthermore, Van Buren found that when stimulation was moved into the caudate head itself, ongoing speech was interrupted by the flow of irrelevant material into speech. Again, this result can be explained by the current model. Caudate stimulation at the wrong time during the alternating sequencesof excitation and inhibition would interrupt the organization of language sequences and allow irrelevant material into the encoding and programming processes because the result of stimulating caudate mechanisms is to free the excitatory mechanisms in the ventral anterior thalamus from pallidal inhibition. In the second set of supporting data, Brunner et al. (1982) found Brocas aphasia to be relatively permanent only when the caudate head was damaged in addition to anterior cortical mechanisms. This finding is also consistent with the present model because damage to the caudate would leave pallidal inhibition of ventral anterior excitatory influences active, and it would be difficult to release language for motor programming. The result, of course, would be nonfluent language. Thus, the present model provides a parsimonious explanation for phenomena noted with stimulation of frontocaudate pathways, with stimulation of the caudate head, and with lesions extending into the caudate head. The model is also consistent with research and conceptualizations regarding the basal ganglia. For example, Evarts (1979) noted that cells in the basal ganglia fire in advance of volitional movement. In the case of language, this activity could represent activation of the response release mechanism in the caudate head which inhibits pallidal inhibitory mechanisms, allowing temporary excitation of anterior cortical programming mechanisms by the ventral anterior thalamus. Caudate mechanisms also play a role in regulating cortical tone by influencing the inhibitory mechanism of the globus pallidus. For example,

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if excitation of frontal mechanisms occurs through pathways other than those discussed above (e.g., the limbic system), then it might be necessary to limit the amount of excitation conveyed through the ventral anterior nucleus. This would prevent the summation of limbic and thalamic induced excitation from causing an overactivation of anterior language mechanisms leading to the admission of irrelevant material into the encoding process. This type of adjustment for anterior excitation through other mechanisms is accomplished through frontocaudate then caudopallidal pathways. Although motor execution of language (i.e., speech) is not the topic of this paper, a few words should be said regarding the relationship of motor execution and the phonological aspects of spoken language. It has already been mentioned that the arcuate fasciculus is involved in the phonological aspects of language. In light of the above discussion, it is likely that this pathway is involved in phonological monitoring in a way similar to the mechanisms discussed for semantic monitoring. In other words, the temporoparietal structures responsible for phonemic discrimination would monitor the motor programming of language through the arcuate fasciculus, determining whether the motor program is associated with the desired phonological pattern. Most likely this phonological monitoring is closely associated with motor programming since the correct placement and timing of movements of the vocal structures determine whether the correct phonemes are produced (e.g., see Blumstein, 1981). The reader will remember that there is overlap in the frontal, temporal, and parietal sites where stimulation interfered with the ability to discriminate speech sounds and where stimulation interfered with the ability to mimic sequences of orofacial movements (Ojemann, 1983).The latter data indicate some relationship between anterior motor-programming mechanisms and posterior phonological decoding mechanisms in speech output. It is likely that the final execution of language in speech is released by mechanisms in the putamen and ventral lateral thalamus which parallel the language mechanisms in the caudate and ventral anterior thalamus discussed above. The smooth flow of conversational speech is dependent upon the simultaneous activity of the mechanisms described herein. While one segment of language is being executed in speech, the next segment is being programmed for motor execution, the ensuing segment is being verified for semantic content, and another segment is in the process of being formulated. In this way, the alternating excitation and inhibition of frontal motorprogramming and motor-execution mechanisms for language must be taking place in rapid succession to allow the smooth flow of language. In the child just learning language, it is likely that semantic verification takes place at a word for word (or even morpheme for morpheme) level. Efficiency in a more complex adult language probably requires that semantic verification takes place at a phrase level. This would require comprehension of simple grammar by temporoparietal mechanisms, though the more complex grammar would require anterior assistance for decoding.

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The development of the model for language production is now complete, and the mechanisms mentioned in the model have been schematically represented in Fig. 4. To summarize this model of language production and the participation of the basal ganglia, anterior cortical mechanisms are responsible both for the formulation of language and the motor programming of language for speech. Prior to motor programming, temporoparietal mechanisms monitor semantic aspects of the language which has been encoded by anterior mechanisms. Prior to spoken execution, phonological aspects of language are monitored in conjunction with motor programming via the arcuate fasciculus. Semantic aspects are monitored through reciprocal connections between the anterior cortical and temporoparietal areas which pass through thalamic structures (the anterior superior lateral pulvinar, and possibly the ventral anterior nucleus and internal medullary lamina). When semantic errors are discovered during the monitoring process, information is carried back to the anterior language zones via the thalamic pathway, and a process of semantic refinement is initiated. Refinement of the phonological aspects of language, when necessary, is probably carried out via the arcuate fasciculus which can excite a phonological refinement process. Activation of anterior cortical language mechanisms for formulation of meaningful language is performed by the ventral anterior nucleus of the thalamus which regulates the flow of excitation from the reticular formation to the anterior language mechanisms. Inhibitory influences exercised by the globus pallidus over the ventral anterior nucleus determine how much excitation is allowed to pass to the anterior cortical mechanisms.

FIG. 4. Schematic drawing representing cortical language mechanisms, thalamic language mechanisms, basal ganglia language mechanisms, and their interconnections. FOR = language formulator (anterior cortex); MP = motor programmer (anterior cortex); DEC = language decoder (temporoparietal cortex); AF = arcuate fasciculus; VA = ventral anterior thalamus; PUL = pulvinar (thalamus); IML = internal medullary lamina (thalamus); RF = reticular formation; CA = caudate nucleus (basal ganglia); PUT = putamen (basal ganglia); GP = globus pallidus (basal ganglia).

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At a tonic level, it is necessary to limit the level of anterior cortical excitation to prevent the entrance of extraneous material into the encoding process, yet to allow enough excitation for the encoding process to occur at appropriate times. In the response release mechanism, control of excitation conveyed to anterior language mechanisms by the ventral anterior nucleus is also exercised by cortical mechanisms through the caudate nucleus which, in turn, inhibits pallidal inhibitory mechanisms. Normally, this caudate mechanism is under inhibition from temporoparietal mechanisms; however, once encoded language has been verified for semantic content, the temporoparietal mechanisms will release the caudate head from inhibition, This action then causes the caudate head to inhibit the mechanism in the globus pallidus which is responsible for limiting the flow of excitation from the ventral anterior thalamus to frontal language mechanisms. The result is a temporary increase in excitation of anterior mechanisms that initiates motor programming of the semantically verified language, eventually leading to expression of the language in speech. Once the motorprogramming process has been completed, impulses from the frontal mechanisms to the caudate reestablish the inhibitory control over the caudate by temporoparietal mechanisms until the next language segment has been semantically verified and is ready to be programmed. Frontocaudate connections also influence tonic activation of anterior language mechanisms to prevent over- or underactivation of these mechanisms by influences not directly associated with language, e.g., the limbic system. IMPLICATIONS AND LIMITATIONS OF THE CURRENT MODEL The viability of any theoretical model of brain functioning depends upon the amount of available data for which it can account and its degree of consistency with established principles. The phenomena of subcortical aphasia which the present theory explains, for the most part, have been discussed above. It also should be mentioned, however, that the theory is consistent with many theoretical discussions of thalamic mechanisms in language which are already in the literature. For example, one group of theorists has hypothesized that the role of the thalamus in language involves the arousal or activation of cortical language mechanisms (Luria, 1977; McFarling et al., 1982; Riklan & Cooper, 1973, and another group has proposed that the thalamus is involved in the integration of language (Botez & Barbeau, 1971; Ojemann et al., 1968; Penfield & Roberts, 1959; Schuell, Jenkins, & Jimenez-Pabon, 1965). A third group of theorists has proposed the role of the thalamus to involve both integration and activation facets (Cooper et al., 1968; Samra et al., 1969). Indeed, the present theory fits the latter category, weaving both integration and activation threads into a theory treating the generation of language as a dynamic process involving not only the thalamus and cortex, but also the basal ganglia and the reticular formation.

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The theory also should be consistent with phenomena related to cortical aphasias. For example, recent discoveries have indicated difficulties comprehending complex syntax (e.g., Blumstein, 1981) and apparent separation of word-finding and motor-programming problems (e.g., Tonkonogy & Goodglass, 1981) in nonfluent aphasias. These discoveries have been incorporated into the theory as explained above. The fluent jargon in Wernickes aphasia perhaps needs further elaboration. According to the current theory, there are two processes responsible for this jargon. First, as suggested by Goodglass and Kaplan (1983), is that preverbal semantic and phonological monitoring of verbal output has been lost because the area responsible for this monitoring is dysfunctional. The second process is that the normal temporoparietal inhibition of the caudate is lost. This loss of inhibition results in greater activity of caudate mechanisms which, in turn, frees the ventral anterior thalamus from inhibition by the pallidum. The result is not only the substitution of one word or sound for another, but also the flow of extraneous material into the encoding process. The empty language in anemic aphasia also can be explained with some elaboration upon the current model. Goodglass and Kaplan (1983) have pointed out that there is a lack of substantives in this fluent language, resulting in vagueness and circumlocution. Luria (1973) discussed evidence that this pattern in anemic (amnestic) aphasia can be caused by an inability to associate the auditory patterns of words with the visual attributes of the actual objects the words represent (though other causes might exist as well). The defect in this particular association process is a result of dysfunction in the left parieto-occipital area which links visual and auditory areas. This associative linkage most likely occurs in other modalities such as tactile and kinesthetic as well. Spreen, Benton, and Van Allen (1966) have shown dissociation between visual and tactile naming in some aphasic patients. In the current model, verification of semantic content in language would require the association of the auditory patterns of words with actual physical attributes of the objects themselves which are recognized in other modalities, such as the visual modality. In other words, monitoring semantic content depends extensively upon these associations between the auditory modality and other sensory modalities. When the mechanism for such associations is not operative during the monitoring process described above, then a messageis conveyed back to the language encoder, via thalamic pathways, that the language based upon such associations cannot be verified (i.e., must be incorrect), and a process of correcting semantic content is initiated. Even when the language encoder has selected semantically accurate information, it will not be released for motor programming if it involves associations in other modalities. The only language that can be verified, resulting in release for motor programming, is language based upon associations which occur exclusively within the auditory-

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verbal modality. Thus, the language system attempts to communicate using descriptions based entirely upon auditory associations which contain vague verbal approximations of the intended concepts. This accounts for the circumlocutions and the vagueness of speech in anemic aphasia caused by left parietal occipital lesion. The current model also accounts for the language output in the transcortical aphasias where repetition remains relatively intact. It has been argued that repetition is accomplished via intact decoding and motorprogramming mechanisms via functional pathways in the arcuate fasciculus. In the current model, this would mean that repetition is accomplished primarily through phonological mechanisms. In transcortical motor aphasia, verbal output is variable but often nonfluent. From the discussion of thalamic mechanisms above, this type of language could be created by lesions in the anterior limb of the internal capsule which interrupt the transmission of excitation from the ventral anterior thalamus to the frontal language mechanisms. The degree of agrammatism may depend upon whether lesions extend to the insula or nearby structures (Mohr et al., 1978). Repetition is preserved if dysfunction does not extend to the arcuate fasciculus. This implies that frontal motor-programming mechanisms for language can be activated by temporoparietal mechanisms via the arcuate fasciculus, but such activation can only initiate repetition. Activation of spontaneous, propositional language requires thalamic activation of the language formulation system. There is some support in the literature for this view. Many cases with lesions in the anterior limb of the internal capsule show relatively preserved repetition (and comprehension) with dysfluent language soon after the lesion occurs (Damasio et al., 1982; Naeser et al., 1982). Further, McCarthy and Warrington (1984) showed that adding a semantic component to a repetition task adversely affected performance in transcortical motor aphasia. This latter finding would be consistent with repetition accomplished by intact superficial phonological pathways (arcuate fasciculus), but interruption of deep semantic pathways (thalamic). Transcortical sensory aphasia results in fluent jargon, impaired comprehension, and relatively intact repetition. Again, unimpaired repetition implies intactness of the auditory phonological mechanisms in the temporoparietal cortex, the arcuate fasciculus, and the frontal motor programmer. The jargon would result from lesions in white matter underlying the dominant temporoparietal region. An interruption of the pathway between the temporoparietal area and the caudate would cause the flow of extraneous material into language encoding as explained above. Further, semantic monitoring would also be dysfunctional because of interruption of pathways between the pulvinar and temporoparietal cortex. Disturbed comprehension would imply disruption of semantic decoding. Though this model of aphasia does account for language output in the major cortical and subcortical syndromes, it has only briefly dealt with

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the complexities of comprehension. In particular, it is of interest that patients with subcortical aphasias often show some comprehension deficits, even though comprehension usually is less impaired than verbal output. There are several possible explanations for this phenomenon, and the reasons may vary from case to case. First, in order to participate in the understanding of complex grammatical structures, anterior language mechanisms must receive semantically decoded information from temporoparietal structures. In the current model, thalamic pathways act as a conduit for this semantic information; therefore, patients with thalamic aphasias should have difficulty understanding complex grammar. The case of Glosser et al. (1982) showed this pattern. Second, semantic information must also be conveyed from the decoder to other anterior mechanisms which are responsible for organizing responses to various commands and requests during testing. Again, this involves thalamic pathways. Third, the basal ganglia may also be involved in the motor programming of responses to commands or requests in a way similar to their involvement in the programming of responses to commands or requests in a way similar to their involvement in the programming of language. Thus, dysfunction in this area could create an inability to release programmed responses for execution or the admission of extraneous responses into response sequences. In other words, responses to comprehension tasks might be disrupted after the initial semantic decoding sequence. It is also possible that some subcortical lesions could prevent auditory information from reaching the language decoder in the left hemisphere. This could happen by interrupting the auditory radiations from medial geniculate to the primary auditory cortex and auditory input to the language decoder from the right hemisphere via the corpus callosum. Indeed, Naeser and her colleagues (1982)found disrupted comprehension in patients where lesions extended across the auditory radiations from the medial geniculate nucleus of the thalamus. Another mechanism through which the thalamus may be involved in comprehension is activation of the decoding mechanisms in the temporoparietal cortex. Luria (1973) ascribed activation of the posterior, sensory cortex to the frontal cortex. It may be through the thalamic participation in language described above that the specific activation of language decoding mechanisms is optimized. Finally, it has also been accepted that certain thalamic structures (i.e., the dorsomedial nucleus) may be involved in memory (McEntee, Biber, Perl, & Benson, 1976; Speedie & Heilman, 1983). To the extent that memory is involved in some comprehension tasks (e.g., four- or fivestage commands), dysfunction of those thalamic structures involved in memory might affect comprehension. It is possible that memory and language mechanisms both could be involved in some cases of thalamic lesions, particularly hemorrhage where pressure effects are likely. Another limitation of the theory as expressed herein is that it discusses

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motor programming but only briefly deals with motor execution. Since dysarthria is a good deal more common than aphasia after surgical lesions of the ventral lateral nucleus of the thalamus (Cooper et al., 1968;Hermann et al., 1966), it is likely that this structure is involved in the motor execution of speech. This also makes sense from the standpoint of atferents to the ventral lateral nucleus from both the cerebellum and the globus pallidus and efferents from the ventral lateral nucleus to the motor cortex (Carpenter & Sutin, 1983).It was hypothesized above that speech sequences may be released for execution after phonological verification by an impulse from the temporoparietal cortex to the putamen (i.e., similar to the release of language sequences for motor programming). Unlike prior theoretical discussions of subcortical aphasia, the present model does provide clear predictions regarding what happens to language after damage to various structures. For example, a lesion close to the caudate head might interrupt fibers from the temporoparietal area to the caudate. According to the model, this would prevent temporoparietal inhibition of caudate mechanisms which would lead to the flow of extraneous material into language. A lesion a few millimeters away inside the caudate head might damage the caudate mechanisms themselves, which inhibit the inhibitory mechanisms of the globus pallidus. The result would be a limitation of excitation conveyed to anterior mechanisms, producing dysfluent language. A lesion of the frontocaudate fibers would prevent the termination of motor programming when programming of a language segment is complete. The result would be perseveration of an initially programmed language segment. Yet, future verification of the theory will not be as easy as it might seem. Lesions varying just a few millimeters could damage different mechanisms which produce entirely the opposite results from one another. Damasio et al. (1982) discussed the possibility that small differences in basal ganglia/capsular lesions might account for differences in two of their patients, one fluent, the other nonfluent. Such small differences in location may also be reflected in the variability of symptoms seen in thalamic aphasia. For example, the differences discussed by Alexander and LoVerme (1980) or the unusual dysfluencies seen in the cases of Brown (1979), Glosser et al. (1982), or McFarling et al. (1982). Most neuroscientists would concede that current CT scans cannot distinguish small differences in location such as those discussed above. Thus, verification of some of the finer points of the current theory may await the development of higher resolution structural imaging than is now available, or careful postmortem verification when such rare opportunities are available. A final word should be said regarding the implications of this model of language production for other areas in the neurosciences. Obviously, certain specific roles have been hypothesized for the thalamus and basal ganglia. In 1979, Evarts pointed out that the basal ganglia play an as yet

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not understood role in translating thought into action. In the realm of language production, the current model takes a step toward such an understanding. The mechanisms postulated herein can be applied to other problems involving thought and movement. For example, if the mechanisms for tone and response release in language formulation and programming were extended to movement, there would be implications for syndromes involving the basal ganglia such as Parkinsons disease and Huntingtons disease. The disturbance of tonic mechanisms in movement is consistent with concepts of Parkinsons disease. Accompanying changes in mentation with this syndrome might be related to a decrease in tonic activation of frontal mechanisms. In Huntingtons disease, on the other hand, the choreiform movements, sometimes resembling fractions of voluntary movements, might be related to response release mechanisms and the random release of movements for programming. Accompanying changes in mentation with this syndrome might be related to disruption of response release mechanisms related to frontal function. Given the current hypotheses, it should be noted that these basal ganglia diseases (i.e., Parkinsons and Huntingtons diseases) do not normally manifest language deficits. It may be that the gradual onset present in most instances of these diseases gives the brain some time to reorganize vital communicative functions. For example, Hutton, Arsenina, Kotik, and Luria (1977) described a lack of language deficits in a case when most of the left (language-dominant) hemisphere was removed in three separate operations with some time intervening between operations. Nonetheless, a complete understanding of the role of the basal ganglia in language requires the understanding of why acute vascular lesions can produce lasting effects on language, but degenerative diseases of the basal ganglia do not. With recent dopaminergic hypotheses in schizophrenia (e.g., Meltzer & Stahl, 1976), it also is tempting to apply the concepts of the current theory to this disorder. Nigrostriatal pathways, of course, are one of the major dopaminergic pathways in the brain, and some theorists (e.g., Klawans, Goetz, & Westheimer, 1972) have implicated the basal ganglia in schizophrenia. Again, if the idea of tonic levels of excitation for frontal mechanisms is invoked and if present concepts are extended to forms of thought other than language generation and programming, tentative hypotheses can be generated. As applied to mechanisms for language generation and programming, mechanisms for tonic anterior cortical excitation are mediated through the thalamus and basal ganglia. An overactivation of frontal mechanisms associated with forms of thought other than language might account for some of the symptoms in schizophrenia, such as loose cognitive associations. However, one should remember that other mechanisms, such as the limbic system and nonspecific thalamocortical pathways related to the reticular formation, are thought

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to be involved in cortical arousal and activation. Indeed, the mesocortical system, a limbic pathway, is another major dopaminergic pathway in the brain. SUMMARY The current model proposes a system for the production of language involving both cortical and subcortical structures. The components of the system interact in a dynamic process which results in the production of language. Left anterior mechanisms are involved in language formulation and motor programming of language. Language symbols are decoded in the left temporoparietal cortex, though the understanding of complex grammatical structures is an anterior function. Prior to its execution in speech, encoded language is monitored by the temporoparietal cortex for semantic and phonological accuracy. Semantic monitoring of an anteriorly encoded language segment is accomplished by the temporoparietal cortex through cortico-thalamo-cortical pathways prior to the release of the segment for motor programming. Phonological monitoring of motor programs is accomplished by the temporoparietal cortex via the arcuate fasciculus. The ventral anterior thalamus conveys a regulated flow of excitatory impulses specifically to anterior language mechanisms. Structures of the basal ganglia are responsible for regulating this flow of excitatory impulses, thereby allowing the programming of language monitored for semantic accuracy and preventing the flow of extraneous material into the process of language encoding. Pallidal mechanisms inhibit the flow of excitation from the ventral anterior thalamus. These pallidal mechanisms are in turn under the inhibitory control of mechanisms in the caudate nucleus. Together, pallidal and caudate mechanisms are responsible for maintaining or changing the tonic level of anterior excitation by the ventral anterior thalamus. The appropriate level of tonic excitation allows for the encoding of language yet prevents the flow of extraneous material into the language-encoding process. Levels of tonic excitation can be modified via frontocaudate pathways. When it has been determined that encoded language is semantically accurate, temporoparietal mechanisms temporarily release caudate mechanisms from inhibition. Caudate mechanisms in turn inhibit pallidal inhibitory mechanisms which allows a temporary increase in excitation to flow from the ventral anterior thalamus to the anterior language mechanisms. This increase in excitation causes the motor programming of the encoded segment to begin, and when motor programming has been completed, temporoparietal inhibition of caudate mechanisms is reestablished through frontocaudate pathways. The smooth flow of conversational language depends upon rapid alterations in excitation and inhibition of motorprogramming mechanisms performed by the basal ganglia and ventral anterior nucleus and in the ability of the system simultaneously to perform

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the operations of motor programming, verification, and encoding on successive segments of language. The current model can account for language output in the various major aphasia syndromes: Brocas aphasia, Wemickes aphasia, conduction aphasia, anemic aphasia, the transcortical aphasias, and thalamic aphasia. Furthermore, the model can account for many symptom patterns which do not fit the classical aphasia theory. The model is supported by literature examining the influences of subcortical structures on language. Future revisions must make clear the process of comprehension, on the one hand, and the process of motor execution on the other. Postulates of this model may have broader implications for understanding the role of the basal ganglia and thalamus in movement and thought.
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