SPEECH REPRESENTATION IN VENTROLATERAL THALAMUS 1

Transcription

1 Brain (1971) 94, SPEECH REPRESENTATION IN VENTROLATERAL THALAMUS 1 BY GEORGE A. OJEMANN AND ARTHUR A. WARD, JR. {From the Department of Neurological Surgery, University of Washington, Seattle, Washington 98105) THE role of the thalamus in brain mechanisms underlying speech has been controversial. The classical formulation suggested that speech functions were mediated by the cortex and immediate subcortical connexions and did not involve thalamic structures (Head, 1926; Neilsen, 1946). This view has been recently reiterated by Geschwind (1967, 1970). However, a considerable body of data suggests a thalamic role in speech mechanisms. Such a role has been inferred from the anatomical connexions of the cortical areas subserving speech (Penfield and Roberts, 1959; Myers, 1967). Aphasia has been noted clinically after thalamic hemorrhages (Penfield and Roberts, 1959, p. 215; Fisher, 1961). Prolonged aphasia associated with histologically verified thalamic hasmorrhage has been recently reported by Ciemins (1970). Aphasia has been noted as a symptom with thalamic tumours (Smyth and Stern, 1938; Cheek and Taveras, 1966). Aphasia has been well documented after thalamotomy (Allan et al, 1966; Selby, 1967; Bell, 1968; Ojemann, Hoyenga and Ward, 1971) with histological confirmation that the lesions were confined to the thalamus (Samra et al, 1969). Finally, stimulation of thalamic electrodes during a test of object naming has evoked anomia (Ojemann, Fedio and Van Buren, 1968), a response which at the cortical level is evoked exclusively with the areas considered to subserve ideational speech functions (Penfield and Roberts, 1959). The present paper is an extension of this last type of study. In the previous study of Ojemann, Fedio and Van Buren (1968), thalamic electrode placement sampled mainly the pulvinar and inferior portions of the ventrolateral nucleus. The present study reports the effects on object naming of electrical stimulation in the more central and superior portions of the ventrolateral thalamic nucleus. Fig. 1 illustrates the different left thalamic electrode placements in these two studies. Together these two studies provide further evidence relating the lateral thalamus to speech functions, and suggest a discrete localization of the areas concerned with speech within the lateral thalamus. 'Part of a presentation to the Western Neurosurgical Society, Vancouver, B.C., October 7, 1970.

2 670 GEORGE A. OJEMANN AND ARTHUR A. WARD, JR. FIG. 1. Left thalamus: Location of electrodes. Parasagittal sections are on the left, horizontal sections on the right. The baseline in each case is the intercommissural line, with the anterior commissure indicated by the vertical mark at the left end of the baseline, and the posterior commissure (in its mean location) by the mark at the right end. The mark extending below the baseline is 1 cm from the anterior commissure. In the horizontal sections the intercommissural line projects in the mid-line of the brain. The mean location of the border of the thalamus in relation to the commissural references is shown in selected plains. (This data is derived from Van Buren, 1971.) The parasagittal sections show plains 10 mm (solid line) and 15 mm (dotted line) lateral to the mid-line; the horizontal sections show plains 5 mm (dotted) and 10 mm (solid) above the intercommissural line. The mean location of the anterior nucleus, intralaminar nucleus and centrum medianum nucleus are also shown on the horizontal sections. The projection on to these sections of electrodes in the left thalamus in the present study are indicated by the heavy lines, projection of the electrode shafts of the previous study of Ojemann, Fedio and Van Buren (1968) by the thinner lines. In both parasagittal and horizontal sections, the centres of most of these electrodes fall between the plains illustrated. Right thalamic electrodes in both studies are similarly located. METHOD The data on the effects of lateral thalamic stimulation on object naming contained in this report were obtained in the course of a study of the effects of stimulation on short-term verbal memory, which has been previously reported (Ojemann, Blick and Ward, 1971). The subjects for the two studies were the same: 25 patients undergoing stereotaxic thalamotomy for the treatment of dyskinesias. The patients suffered from Parkinson's disease, except one with dystonia. All were right handed. Since the short-term memory study a second patient has had electrodes inserted into both ventrolateral thalami on separate occasions. In both patients, right thalamotomy preceded left by at least six months. The remaining patients had electrodes inserted only in either the right or left thalamus. Thus this report contains data on 14 patients with left ventrolateral thalamic and 13 patients with right ventrolateral thalamic electrodes. Nine of these patients had had previous thalamotomies (6 contralateral, 2 bilateral, one ipsilateral) but none less than six months before. The patients' age range was 14 to 64. The testing procedure was the same as that described for the study on short-term verbal memory (Ojemann, Blick and Ward, 1971) and was carried out in the operating room. The patients had been premedicated with 25 ml. of promethazine hydrochloride three to four hours previously. The choice of the ventrolateral thalamic target, and the technique of inserting the electrode is a standard one which has been previously described and includes electrical stimulation via the electrode, to provide physiological confirmation of its location (Ward and Stern, 1963). Testing of object naming was carried out immediately after the first insertion of the electrode in the thalamus. The test has also been described in detail in the report on short-term verbal memory (Ojemann, Blick and Ward, 1971). It is an adaptation of a single item test of short-term verbal memory which consists of 60 consecutive trials. The portion of each trial relevant to the study of object naming is designated as the "presentation slide." This slide contains a line drawing of one of 60 common objects with the words "this is a" printed above the object. The names of the objects

3 SPEECH AND THALAMUS 671 are words of Thorndike and Lorge (1944) A or AA frequency. The patient's response to the slide consists of reading aloud "this is a" and then giving the name of the object. The slide was shown for four seconds. (In the initial 6 left and 5 right cases this period was three seconds, the length of stimulus trains three seconds, and the time occupied by the distraction, recall and recognition slide of each trial twelve seconds.) The remainder of each trial consists of distraction, recall and recognition slides (which occupy a 14 sec period), followed by the presentation slide of the next trial. The test was presented to the patient by 2 x 2 slides back-projected on to a screen which the patient viewed through a set of prisms while lying supine on the operating table. The total of 60 trials was divided into thirds by limitations of capacity of slide trays for the projector. The order of these thirds was randomly varied among patients. The patient was exposed to the entire series of slides on the night prior to operation and the instructions as to the nature of the tests reviewed immediately before testing. Stimulation was carried out using 4 second trains of biphasic square wave pulses with 2$ milliseconds total duration, 60 cycle per second delivered from a Nuclear Chicago No constant current stimulator. Stimuli were delivered in a monopolar fashion through the thalamic electrode which has a 1 x 5 mm exposed tip. Immediately after the first insertion of the electrode into the ventrolateral thalamus, the current threshold for sensory and motor responses was determined by brief application of stimulating current starting at low levels (1 to 2 milliamps (ma), measured between peaks of the biphasic pulse), and gradually increasing. Subsequent stimulation was carried out at current levels below the threshold for any reported sensation. No stimulation was carried out during the first four trials of the test. Subsequent trials were divided into blocks of six or seven trials each. Randomly distributed in each block were two trials with stimulation during the presentation slide, that is at the time of object naming. Stimulation of the first block was generally at a current level of 2 ma and this was increased by 1 to 2 ma increments until the thresholds for sensation were reached or the entire test sequence utilized. The patient carried out the test continuously except for the two breaks necessary to change slide trays. His verbal responses and impulses from both the automatic timer controlling projector and the stimulator were recorded on 2 channel magnetic tape. Performance in response to the presentation slide, that is during object naming, was recorded for trials both with and without stimulation. The following definitions were used in describing the different types of alterations in object naming observed. Anomia was defined as the inability to name the object correctly, but with demonstrated retained ability to speak, such as would be indicated by being able to say "this is a." Perseveration was defined as the repetition of part or all of a correct object name. Anarthria was defined as the inability to speak at all during the period that the presentation slide was on the screen. These were the only alterations in object naming observed in this qualitative analysis. Electrode location was determined by measuring the distance (after appropriate correction for magnification) from centre of electrode to the anterior and posterior commissures, intercommissural plane, and mid-line of the third ventricle, which was outlined by air on films taken immediately after the first insertion of the electrode into the thalamus. These measurements were then transferred to charts prepared by Dr. J. M. Van Buren (1971) which showed the mean location and range of variation of the borders of the thalamus and some intrathalamic structures about these reference landmarks. Fig. 1 is an example of such a chart with the location of the left thalamic electrodes considered in this study projected on horizontal and parasagittal sections showing the mean location of the border of the thalamus about the commissural references. RESULTS Control Observations The current threshold for reported sensation evoked by stimulation of the right ventrolateral (VL) thalamus was significantly lower than that on the left. A more

4 672 GEORGE A. OJEMANN AND ARTHUR A. WARD, JR. detailed analysis of this phenomenon is the subject of a separate report (Fedio, Van Buren and Ojemann, in preparation). In the context of the present study, this finding might seriously confound comparisons in the incidence of object naming errors by stimulation of right or left VL electrodes, particularly if object naming errors tend to be associated with large stimulating currents, since the magnitude of the stimulating current was limited by the threshold for reported sensation. This confusion can be avoided by excluding all trials with stimulation at current levels less than 5 ma as this was the smallest current at which any changes in object naming were observed, and all those with stimulating currents in excess of 12 ma. With these restrictions, data are available for 13 patients with left VL electrodes, and 12 with right. These two groups show no significant difference in maximum stimulating currents (mean: right 6-3 ma; left 8-1 ma), or in the number of trials with stimulation (mean: right 9-4; left 10-6). Nor are there any significant differences in location of electrodes (as measured by AP, lateral, or superior-inferior co-ordinants about the anterior commissure, intercommissural line, and mid-line references), or ages of the patients. Preoperative object-naming performance, and performance on trials without stimulation at the time of intra-operative testing also were similar for these patients with right or left VL electrodes. They found the object-naming test quite easy even in the operating room setting. 4 of the 12 patients with right VL electrodes made one or more anomic errors in object naming on an average of 23 trials without stimulation. The proportion of errors for those who made any under these control conditions varies from *04 to -10. None of these patients showed any alterations in object naming with stimulation. 4 of the 13 patients with left VL electrodes made anomic errors on an average of 26 trials without stimulation. In all cases only a single error was made, for a proportion of errors under these control conditions of 03 to -06. Two of these patients made one or more anomic errors during stimulation. Based on each of these patient's control performance, the binomial probability (Siegel, 1956) that the observed or larger frequency of errors during stimulation at and above the threshold current for errors would occur on a chance basis is less than -01. Thus it seems very unlikely that random errors account for any of the evoked anomic errors in object naming reported here. Perseveration and anarthria were not observed during control trials. Differences between Right and Left Ventrolateral Thalamus No changes in object naming were evoked in the 12 patients who had right ventrolateral thalamic (VL) electrodes, while 6 of the 13 patients with left VL electrodes showed one or more evoked alterations in object naming. This difference is significant at the 2-5 per cent level (Fisher's exact probability Siegel, 1956). Thus there appears to be lateralization of the effects of stimulation in the ventrolateral thalamus on object naming to the left side in these right-handed patients.

5 SPEECH AND THALAMUS 673 \ FIG. 2. Left thalamus: Anomia, Anarthria, No alterations in object naming. Format is similar to fig. 1, with parasagittal sections on left and horizontal on the right. The area enclosed by small dots represents the portion of ventrolateral thalamus sampled by the electrodes in the present study. The open circles represent the centres of electrodes from which no changes in object naming were evoked. The capital "A's" represent the centres of electrodes from which anomia was evoked in the present study, the small "a's" the centres of the electrode pairs from which anomia was evoked in the previous study of Ojemann, Fedio and Van Buren (1968). The capital "N" represents the centre of the electrode from which anarthria was evoked in the present study. Localization within the Left Lateral Thalamus Anomia. Anomia was defined as the inability to name the object correctly with retained ability to speak, usually shown by the patient being able to say "this is a" even though he could not correctly name the object. This alteration in object naming was evoked in 4 of the 13 patients with left ventrolateral (VL) thalamic electrodes, at a mean threshold of 8 ma (range 6 to 10 ma). Fig. 2 shows the locations of the electrodes from which anomia was evoked and also the locations of the electrodes in the 7 patients with left VL electrodes in whom no changes in object naming were evoked. The maximum stimulating current applied to those electrodes (mean 7-4 ma, range 5 to 12 ma) does not differ significantly from the average threshold for evoking anomia in the other 4 patients. Differences in current levels do not therefore seem to account for the failure to evoke anomia in some patients. Performance in trials without stimulation and the incidence of previous ipsilateral and contralateral thalamic lesions also does not differ between these two groups. On the other hand, the site of stimulation is important as three of the electrodes from which anomia was evoked were in the posterior inferior medial portion of the area of VL sampled, the fourth being in the anterior portion. Anomia was not evoked from electrodes in the lateral and superior portions of VL. The posterior inferior medial portion of VL where anomic responses were evoked is contiguous with the area where anomic responses were evoked from left pulvinar electrodes in the study of Ojemann, Fedio and Van Buren (1968), also illustrated in fig. 2. All 5 of the right-handed patients with electrodes in the left pulvinar demonstrated anomia, an incidence significantly higher than that found from all VL electrodes in the present study. The mean threshold for anomia from the pulvinar was 7-6 ma which is slightly lower than that observed from VL though not significantly so. In the previous study of Ojemann, Fedio and Van Buren, anomic

6 674 GEORGE A. OJEMANN AND ARTHUR A. WARD, JR. responses were also evoked from a single electrode in the anterior part of VL, as indicated in fig. 2. It will be noted that the location of that electrode is very close to the single electrode in anterior VL with evoked anomic responses in the present study. Anomic errors evoked from VL were of both the misnaming (63 per cent) and omission types. Misnamings were gross errors in the object named: "ace" for "church," "balloon" for "arm," with the incorrect name not necessarily the name of an object pictured elsewhere on the test. Anomic responses were reproduced in an average of 63 per cent of the trials with stimulation at or above the threshold for the first anomic error. Recall of objects where anomia occurred did not differ from recall of correctly named objects. The pulvinar electrodes of the previous study did not differ significantly from VL electrodes in any of these effects. Perseveration. Perseveration was denned as the continued repetition of the first syllable of the correct object name throughout the duration of stimulation. Two patients with left VL electrodes in the present study, and one patient from the previous study (Ojemann, Fedio and Van Buren, 1968) demonstrated this type of response during stimulation. Mean threshold for the response was 5\ ma. Fig. 3 FIG. 3. Left thalamus: Perseveration. Format is similar to fig. 1, with parasagittal sections on left and horizontal on right. Area enclosed by dotted line is the portion of ventrolateral thalamus sampled in the present study. Centres of electrodes from which perseverative responses were evoked in the present study are shown by "P", the single case with this type of response from the previous study of Ojemann, Fedio and Van Buren by "p". All of these electrode locations were measured in reference to the posterior commissure. shows the location of these responses in horizontal and sagittal planes. The three sites from which perseveration was evoked in the 58 patients in the combined studies are clustered together in the medial portion of the left ventrolateral thalamus. One of the two patients showing perseveration in the present study also showed anomia at a larger stimulating current, the only occasion in this study where a different alteration of object naming was evoked from the same electrode. The patient from the previous study who showed perseveration was left handed. Anarthria. Anarthria, that is the inability to speak during stimulation, was evoked in one patient of the present study with a lateral superior VL electrode at a threshold of 8 ma. The location of this electrode is indicated on fig. 2 by the letter "N."

7 SPEECH AND THALAMUS 675 DISCUSSION Alterations in object naming were evoked from the left but not from the right lateral thalamus. This lateralization of speech function at the thalamic level is similar to that which has been reported for the cortex, with alterations in the nonarticulatory components of speech confined to lesions in the left hemisphere at least in right-handed subjects (Penfield and Roberts, 1959). A similar lateralization of speech functions to the left thalamus was found in the previous study of the eifects of stimulation of pulvinar electrodes on object naming (Ojemann, Fedio and Van Buren, 1968). Aphasic disturbances have been often reported following left thalamic lesions (Allan et al, 1966; Bell, 1968; Samra et al, 1969; Ciemins, 1970; Ojemann, Hoyenga and Ward, 1971), but have generally not been reported with right thalamic lesions. 1 Within the left lateral thalamus there is some discrete localization of the sites where speech functions can be altered. Evidence from the effect of cortical stimulation suggests that certain changes in object naming are much more useful than others in localizing speech functions. Thus in Penfield and Roberts study (1959), what we have defined as "anomia," was evoked from only three cortical locations on the left side, the inferior frontal area of Broca, the region of the parieto-temporal junction (the Wernicke speech area), and the supplementary motor area. This type of response was not evoked either from the cortex on the right, or from the left motor strip. No other alteration in object naming was so discretely localized at the cortical level to those areas which are usually considered to subserve ideational speech function. What we have defined as "perseveration" in Penfield and Roberts study 2 was evoked from the same cortical sites as was anomia, and, in addition, was evoked from the left motor strip, and in a single instance from medial face of the right cerebral hemisphere. What we have defined as "anarthria," seems to be least useful in terms of localization. In Penfield and Roberts data, this type of response was evoked predominantly from the motor cortex and supplementary motor areas of both hemispheres as well as the frontal and to a much lesser extent, the parietotemporal speech areas on the left. In addition, this type of response seems very similar to the "arrest response" evoked by Guiot (Guiot et al, 1961) from either the ventrolateral thalamic nucleus, and by Van Buren (Van Buren, Li and Ojemann, 1966) from the frontal white matter and striatum of both cerebral hemispheres. It is also very difficult to separate anarthric responses from the type of performance which might be seen if stimulation interfered with consciousness. Thus anomia and perseveration are of value in localizing speech function within the left lateral thalamus, while anarthria probably is not. Fig. 4 summarizes the areas within the left lateral thalamus from which anomic and perseverative responses were evoked. Electrodes producing these responses 'Ojemann, Hoyenga and Ward (1971) noted a significant incidence of anomia acutely following right thalamotomy, but this was significantly less than that acutely following left thalamotomy. 2 In that study, perseveration, as defined here, is called "repetition."

8 676 GEORGE A. OJEMANN AND ARTHUR A. WARD, JR. FIG. 4. Left thalamus: Summary of speech representation. Format of this figure is the same as in fig. 1, with parasagittal sections of the thalamus 10 to 15 mm lateral to the mid-line on the left, and horizontal sections 5 to 10 mm above the intercommissural plane on the right. The area of ventrolateral thalamus sampled in the present study is enclosed by the dots as in figs. 2 and 3. The shaded areas enclose just those electrodes from which anomic and perseverative responses (as defined in this paper) were evoked in the present study and the previous study of Ojemann, Fedio and Van Buren (1968). The locations of the centrum medianum nucleus is indicated on the parasagittal sections, and location of the anterior, intralaminar and centrum medianum nuclear groups on the horizontal sections. are clustered in the medial central portion of the area of ventrolateral thalamus sampled. Those from which no alteration in object naming was evoked are scattered medially, superiorly, inferiorly and laterally around this area. The area from which anomia and perseveration were evoked is contiguous anteriorly and posteriorly with the areas from which anomic responses were evoked in right-handed patients in the previous study of Ojemann, Fedio and Van Buren (1968). Drs. P. Fedio and J. Van Buren (personal communication, 1971) have observed the effect on object naming of stimulation of a series of electrodes located immediately anterior to the shaded area of fig. 4. Anomia and perseveration have not been evoked in those cases. The failure to evoke anomia from electrodes in the region of VL in the study of Ojemann, Fedio and Van Buren (1968) may be partly a consequence of low stimulating currents applied to those electrodes, significantly below those applied to the VL electrodes in the present study. This difference in maximum current is due to the trajectories of the electrodes, the posterior trajectory from a parietal burr hole used in the previous study placing one contact of the bipolar stimulating pair centred in VL very near to Vpl the thalamic sensory relay nucleus, thus evoking sensory responses with small currents. The anatomic substrate for the sites within the ventrolateral thalamus from which these types of alterations in object naming were evoked is clearly not the posterior limb of the internal capsule. The variability in location of the border between the internal capsule and the ventrolateral thalamus in relation to the commissure reference points is very large (Van Buren and Maccubbin, 1962; Van Buren, 1971). Some of the most laterally placed electrodes that we have considered to be in VL (because they lie medial to the average location of this border) may have been in the capsule. Anomia and perseveration were not evoked from these electrodes.

9 SPEECH AND THALAMUS 677 In addition, the low threshold motor responses, a characteristic of portions of the internal capsule lateral to VL (Bertrand et al., 1965) were not seen with stimulation causing anomia and perseveration. The study of Beck and Bignami (1968) on the degeneration associated with human ventrolateral thalamic lesions suggests two pathways likely to pass through the portion of VL from which we have evoked anomia and perseveration. In lesions involving the central, medial and posterior portion of VL, Beck and Bignami noted degeneration both in the anterior centrum medianum nucleus, which they attributed to damage to en passage fibres from that nucleus, and also changes in the genu of the capsule and the dorsomedial nucleus which suggested that projection from the dorsomedial nucleus to the prefrontal cortex had been severed. Either pathway may have been involved by stimulation producing anomia and perseveration, but the failure to evoke alteration in object naming from our most medial electrode, which has some chance of lying in the lateral dorsomedial nucleus, may be some evidence against participation of this nucleus in thalamic speech mechanisms. Thus the pattern of speech representation in the left lateral thalamus that emerges from the present study, complemented by that of Ojemann, Fedio and Van Buren (1968) includes pulvinar and en passage fibres related to the centrum medianum and dorsal medial nuclei. This is strikingly similar to the model for thalamic speech representation proposed by Penfield and Roberts (1959) who suggested that the centrum medianum and dorsal medial nuclear connexions were related to the frontal (Broca) cortical speech area, and the pulvinar to the parieto-temporal (Wernicke) cortical speech area {see Van Buren and Borke, 1969, for a discussion of these latter connexions). In this framework perseveration, at the thalamic level, appears to be related to the frontal-centrum medianum or frontal-dorsomedial circuitry. At the cortical level, perseveration in speech has been associated with lesions in one part of that circuit, the inferior frontal premotor cortex on the dominant side (Luria, 1969). There are, however, several major unresolved problems with the Penfield and Roberts model of thalamic speech representation. One is the lack of direct information on the roles of the centrum medianum and dorsal medial nucleus, as we have not yet had a therapeutic indication to place an electrode in these areas to examine speech function. Secondly, the course and termination of the en passage fibres from the centrum medianum nucleus is unknown. The model proposes connexions between the centrum medianum and Broca's area, but the only well described connexions are fibres from the precentral cortex to the centrum medianum (Kuyper, 1966; Mehler, 1966). The thalamic role in speech functions is often considered to be an integrative one. Penfield and Roberts (1959) felt that the thalamus provided interrelationships between the frontal and parieto-temporal speech areas. Evidence for thalamic integrative functions might include overlap of those areas of lateral thalamus that appear to be related to object naming, with areas related to other functions which are part of speech. Ojemann and Van Buren (1967) noted an evoked inhibition of respiration, with prolonged expiration, which had a significantly lower threshold from left than

10 678 GEORGE A. OJEMANN AND ARTHUR A. WARD, JR. right lateral thalamus. They suggested that this might represent the respiratory substratum needed for vocalization. The area of the ventrolateral thalamus from which this phenomenon was evoked corresponds very closely to that from which anomia and perseveration were evoked in the present study, that is to say from the medial central portions of VL, and not from the more lateral, or superior portions. Such an inhibition of respiration clearly does not account for the evoked changes in object naming, particularly with the high proportion of misnaming errors, but does suggest that the thalamus may indeed have an integrative function between respiratory mechanisms needed for vocalization and speech functions. Ojemann, Blick and Ward (1971) reported the effects of stimulation of many of the ventrolateral thalamic electrodes considered in this present study on a test of short-term verbal memory. Stimulation at the time of recall, at current levels less than those interfering with object naming, significantly disturbed recall performance, while stimulation at the time of the presentation of the material to be later recalled was associated with a decrease in recall errors compared to nonstimulation conditions. Ojemann and Fedio (1968) noted a similar evoked disturbance of retrieval of verbal material from short-term memory with stimulation of pulvinar electrodes at current levels below the threshold for changes in object naming. Thus there is an overlap between the sites from which changes in object naming and changes in short-term verbal memory can be evoked, but the short-term verbal memory changes do not show the discrete localization in VL (to medial-central portions) seen with the anomic and perseverative types of object-naming alterations. This overlap of speech and shortterm verbal memory functions at the thalamic level does not seem to be present in the left temporal-parietal cortical area where anomia can be evoked. There, short-term verbal memory was intact during stimulation at the time of input or retrieval, at current levels which consistently evoked anomia, in the one case where we have tested both functions during cortical stimulation (G. Ojemann, unpublished data). Verbal memory processes, of course, play a significant role in object naming in that the object name is stored in and must be retrieved from memory, though these processes most often involve long-term, rather than short-term memory. Our studies of the effects of stimulation of the lateral thalamus on object naming suggest that the left thalamus is involved in this type of speech function, especially the portions of pulvinar and medial central VL probably involved in circuits relating the pulvinar to the parieto-occipital cortical speech area, and the centrum medianum and/or dorsal medial nucleus to the frontal cortical speech areas. These findings support Penfield and Roberts' hypotheses concerning the role of thalamus in verbal behaviour. They also support the concept that these portions of the thalamus are indeed integrating centres, not only relating parieto-temporal and frontal speech areas, but also relating speech functions to the appropriate respiratory substrate and to verbal memory processes. The knowledge of localization of speech function within the lateral thalamus may be of value to those surgeons who still make lateral thalamic lesions for the treatment of dyskinesias, in that

11 SPEECH AND THALAMUS 679 it seems likely that avoidance of the areas concerned with speech will reduce the dysnomic complications sometimes associated with this procedure in the dominant hemisphere. SUMMARY The effect on object naming of electrical stimulation of the ventrolateral thalamus was studied in a series of patients undergoing stereotaxic procedures for treatment of dyskinesias. Stimulation of the left side evoked alterations in object naming, while stimulation of right did not, the difference being statistically significant. Within the left ventrolateral thalamus, anomia and perseveration were evoked from the medial central portion of that nucleus but not from areas superior, inferior, medial or lateral to those electrodes. Anteriorly and posteriorly the area within the ventrolateral thalamus from which anomia and perseveration were evoked was contiguous with the areas from which anomic responses were evoked in right-handed patients in a previous study of the effects of thalamic stimulation on object naming. These two studies together suggest that within the left lateral thalamus the anatomical substrate for speech includes pulvinar and en passage fibres related to the centrum medianum and dorsal medial thalamic nuclei. This finding supports the proposal of Penfield and Roberts (1959) concerning intrathalamic localization of speech function. The overlap of the sites within the lateral thalamus from which anomia and perseveration, respiratory inhibitions, and alterations in short-term verbal memory can be evoked supports the concept of the lateral thalamus as an integrating centre for various activities concerned with speech. ACKNOWLEDGMENTS Supported in part by USPHS grants NB and NB Drs. P. Fedio and J. Van Buren kindly reviewed the manuscript. Dr. K. Blick Hoyenga assisted in some of the testing. REFERENCES ALLAN, C. M., TURNER, J. W., and GADEA-QRIA, M. (1966) Investigation into speech disturbances following stereotaxic surgery for Parkinsonism. Br. J. Disorder Commun., 1, BECK, E., and BIGNAMI, A. (1968) Some neuro-anatomical observations in cases with stereotactic lesions for the relief of Parkinsonism. Brain, 91, BELL, D. S. (1968) Speech functions of the thalamus inferred from the effects of thalamotomy. Brain, 91, BERTRAND, G., BLUNDELL, J., and MUSELLA, R. (1965) Electrical exploration of the internal capsule and neighbouring structures during stereotaxic procedures. /. Neurosurg., 22, CHEEK, W. R., and TAVERAS, J. M. (1966) Thalamic tumors. /. Neurosurg., 24, CIEMINS, V. A. (1970) Localized thalamic hemorrhage. Neurology, Minneap., 20, FISHER, C. M. (1961) Clinical syndromes in cerebral hemorrhage. In: "Pathogenesis and Treatment of Cerebrovascular Disease." Edited by W. S. Fields. Springfield: Thomas, pp GESCHWIND, N. (1967) Discussion on cerebral connectionism and brain function. In: "Brain Mechanisms underlying Speech and Language." Edited by C. H. Millikan and F. L. Darley. New York: Grune and Stratton, pp (1970) The organization of language and the brain. Science, N. Y., 170, GUIOT, G., HERTZOG, E., RONDOT, P., and MOLINA, P. (1961) Arrest or acceleration of speech evoked by thalamic stimulation in the course of stereotaxic procedures for Parkinsonism. Brain, 84,

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