NeuroRehabilitation An IntenlllCipiinary Journal

ELSEVIER

NeuroRehabilitation 5 (1995) 103-113

Recovery in aphasia and language networks Andrew Kertesz Department of Clinical Neurological Sciences, St. Joseph's Health Centre, University of Western Ontario, London, Ontario N6A 4V2, Canada

accepted 16 December 1994

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_.-------------------Abstract

Recovery from aphasia is presented as a model of compensation after vascular or traumatic brain damage. Initial severity, time from onset, and etiology are the major prognostic factors. Initial severity is closely related to the size and location of the lesion. Asphasic syndromes reflect the deficit in various language networks. Lesion studies suggest that ipsilateral connected cortex plays a major role in compensation; contralateral contribution may occur in large lesions. Articulated language output network includes Broca's area, rolandic operculum, anterior insula, and the striatum. The comprehension network includes the superior posterior temporal gyrus and temporal operculum, the supramarginal gyrus and the angular gyrus.

Keywords: Recovery; Aphasia; Articulated language; Comprehension; Network model ----_._-------_._-_. ._----------_.

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Recovery from aphasia has served as a model for recovery of other cognitive functions, as language has been defined and quantitated extensively. Loss of language is particularly disabling to a patient. Rehabilitation of language function is a large portion of the general rehabilitation after stroke and trauma. Approximately 25% of stroke patients have significant aphasia [1]. Clinicians have recognized that aphasic syndromes are not stable and recovery takes place to a considerable extent. Wernicke [2] postulated that much of the recovery from aphasic symptoms is affected

by right hemisphere compensation; subsequently, Henschen [3] restated this principle which was named 'Henschen's principle'. Von Monakow [4] stated, 'the temporary nature is one of the most important characteristics of aphasia.' He based his diaschisis theory on observations with aphasics and on the analogy of spinal shock, well established by physiologists. Diaschisis means that acute brain damage deprives the surrounding, functionally connected areas from a trophic influence causing a severe deficit initially. As the surrounding areas recover by acquiring reinnervation from somewhere else or become active after

1. Introduction

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adapting to the state of partial de nervation, in either way, recovery takes place. Axonal sprouting, regrowth, and collateral sprouting are important processes of repair following brain damage and have been observed centrally, as well as in the peripheral nervous system. Recently, the area of brain tissue grafting and transplantation has been developed to promote local physiological, pharmacological and structural repair. Despite the demonstration of axonal regrowth in central autografts [5] and in cerebral tissue transplantation, particularly for Parkinson's disease [6], it is likely that recovery from lesions of any substantive size in the brain takes place not as a result of axonal regrowth, but mainly as a result of functional reorganization. This implies strengthening of certain connections based on biochemical changes and even microstructural alterations. The considerable neuroplasticity that allows recovery is a subject of great interest in recent biological and anatomical research. Reorganization may take place by functionally-connected tissue substituting for some of the functions lost by altering complex polysynaptic connections and physiological mechanisms [7]. This form of recovery in man is probably subject to retraining and pharmacotherapy. Particularly in the early stages of recovery, a substantial imbalance of neurotransmitters may occur, not only in damaged tissue but also in the surrounding or functionally connected areas which have suddenly become denervated [8]. Replacing neurotransmitters may provide a form of pharmacotherapy that goes beyond neuroprotection in the very brief time window following a stroke. Denervation hypersensitivity and the reversal of inhibitory chemical neurotransmitters may also contribute to recovery pharmacologically. However, the pharmacotherapy of recovery from stroke is not yet established, although it is an evolving area. Clinical observations and experiments suggested to previous investigators that 'silent' areas or structures not involved in the function that was lost, take over the function or account for the compensation. This was called 'vicariation' or 'vicarious functioning' by Fritsch and Hitzig [9] who observed the recovery of hemiplegia in dogs

after removing the motor cortex. It implied a built-in redundancy in the central nervous system. It is more likely, however, that all compensatory structures have some role even though partial in the function in question prior to brain damage. CNS is organized as a dynamic network rather than as a permanently determined cluster of distinct centres and the extensive nature of functional plasticity makes reorganization plausible. Much of what we know about the reorganization of brain function in man comes from the functional analysis of deficits and their relationship to brain lesions. After stroke, trauma, or infection, human cognition is affected in a complex fashion. The longitudinal measurement and analysis of deficit is difficult. The reproducibility of observations is influenced by many biological and psychological factors. The main areas investigated are language, visuospatial cognition, praxis, attention and memory. The complexity of deficit analysis in cognition and in aphasia has been increasingly recognized, and some quantitation has been achieved by several advances in methodology. Aphasia tests have become better standardized and more specific for a language disordered population, and the methods of follow-up and the statistical evaluation of change have become more sophisticated [10-14]. Advances in cognitive psychology and linguistics also contributed to deficit analysis [15]. Development in neuroimaging, such as computerized tomography (CT) and magnetic resonance imaging (MRI), allows us to localize and quantitate lesions in patients who can be concomitantly examined in detail with neuropsychological tests. More recently, functional activation of cerebral metabolism and blood flow with positron emission tomography (PET) and functional MRI are contributing to issues of recovery and compensation of function. Prognostic factors, such as initial severity, time-from-onset, etiology, age, handedness, aphasia type, lesion size and location, and the effect of therapy have been extensively investigated. In our laboratory, we have contributed systematically to the study of these factors and recently have studied recovery in networks of language output and comprehension.

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2. Initial severity Initial severity .of aphasia is one of the most important factors in recovery. Early investigators considered initial severity to have a highly predictive value [16-22]. The severity of deficit at onset has a considerable effect on recovery rates, because mildly affected aphasics do not have much room for recovery (a 'ceiling effect') and severe aphasics often have more potential. Treated patients tend to be selected from the less severe groups and this may bias results. Unless initial severity is considered a major factor to be controlled, studies of treatment should not be considered reliable. There are various methods of controlling for initial severity, such as analysis of covariance or the change expressed as a percentage of initial severity. Each of these statistical methods have some limitations on either end of the severity scale. 3. Time from onset The time from onset of stroke or trauma when the patients are studied is also an important factor. When patients are entered into studies at various stages in their recovery curve, comparison becomes very difficult. In our studies, we took care to start our evaluation within the acute period, between 10 and 45 days after a stroke [22]. Since most of our patients were examined at exactly 14 days after post-onset, this provides a rather homogenous population. Only the more severely affected patients, who could not be examined at that time because of intercurrent medical illness or obtund at ion, were kept until the upper limit of the acute period. On subsequent follow-up examinations, a considerable amount of attrition of patients can be expected for various reasons. Therefore, studies examining patients' performance may suffer if the comparison is between segments of various recovery slopes, unless the slopes and the n-s at each intersect are statistically accounted for. 3. Etiology Etiology is a major factor that needs to be

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considered. Traumatic aphasia, for instance, recovers quickly unless it is related to penetrating head injury [23]. Persisting dysarthria is common in severe trauma and this often disrupts communication to such a degree that the extent of posttraumatic aphasia is difficult to determine. Penetrating head injury affects a different age group and there is a variability in the speed and path of the missiles and the associated concussion. Therefore, post-traumatic aphasia is often biologically different from the vascular type. There are many similarities, nonetheless, indicating that the recurring patterns of aphasic types are not necessarily related to the 'artifact' of the distribution of vascular lesions. A recent study, for instance, by Ludlow et al. [23] on Vietnam veterans, showed that the lesions that produce a persisting asyntactic or Broca's aphasia are large, involving the subcortical structures and the parietal area, in addition to Broca's area. This study on penetrating missile injuries reached very much the same conclusions that have been obtained studying stroke recovery. 4. Functions, symptoms or syndromes Psycho linguists argue for testing functions based on theoretical definitions. Symptom analysis on this basis leads to increasing fractionation and lessens the success rate of localization. Recent evidence from PET and MRI studies of functional activation indicates a considerable cortical spread of activation during linguistic processes. Seemingly elementary, yet cognitively complex, linguistic processes, such as naming, are impaired from multiple lesion sites providing converging evidence for widely distributed localization. On the other hand, syndromes are more likely to correlate with localizable lesions. The syndrome approach is clinically productive and more valid for rehabilitation, because it consists of a set of coherent symptoms reliably associated with certain lesion size and location. Our recovery studies described below are based on the structural aspects of recovery in two major language networks in the brain as measured by quantitative language testing and neuroimaging: (1) articulated speech or language output, and

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(2) comprehension or language input processes. Although writing and reading are integral to language, they are often dissociated in their impairment and deserve separate discussion. Articulated language output is an example of a complex cognitive function subserved by a network in the central nervous system. Speech output differs substantially, whether it is in response to questions (responsive speech), extemporaneous expression of ideas, descriptive speech, or repetition. Spoken language incorporates many subfunctions, which have been categorized by linguists as articulation, fluency, prosody, phonological processing, lexical retrieval, syntax and pragmatics, etc. Nevertheless, all, or most of the functional components tend to be involved to some extent in the clinical syndrome of Broca's aphasia, that can be reliably defined by standardized test scores [12] or by careful clinical description. The more standardized the description, the more reliable will be the localization. Many identifiable, even dissociable phenomena, such as agrammatism or dysprosody contribute to the syndrome, but none of these have as consistent localization as the whole syndrome. 5. Lesion size Lesion size and location have also been recognized as interrelated and complex factors. Until recently, clinicians relied on autopsy correlations but modern neuroimaging has provided an opportunity to study lesion characteristics in vivo. We found, in our first study of lesion size measured on computerized tomography (CT) and recovery from aphasia, that the larger the lesion the poorer the outcome; in other words, outcome correlated negatively with lesion size [24]. This has been known to clinicians since Hughlings Jackson suggested, in principle, the so-called 'mass effect' [25]. Recovery rates also showed a trend of negative correlation with lesion size with one exception. The recovery rate of comprehension was found to be correlated positively with lesion size. This can best be understood if we look at another study of ours in which the best recovered modality was found to be comprehension [26]. Patients with large lesions having global or severe Broca's aphasia, often show greater improvement in com-

prehension. Patients with smaller lesions, such as anomic aphasics, already have good comprehension, therefore they have less room for recovery (a ceiling effect). The large lesions with more recovery and small lesions with little change give rise to a consistently positive correlation unless the initial severity is covaried as was done in our subsequent studies [27]. 6. Lesion location There are certain structural limitations of recovery, allowing compensation to take place only in certain areas, such as the adjacent cortex, contralateral homologous cortex or hierarchically connected structure, such as the subcortical ganglia [25,28]. The issue of a primary, noncompensable cortex for language function similar to the primary motor or visual cortex has become an important question for research. The existence of such a primary language cortex is supported by the large number of permanently aphasic patients and the anatomical and physiological evidence for networks for language output and comprehension. The characteristics of such networks can be summarized as: (1) a single, complex function is represented at multiple sites, therefore lesions from multiple sites can produce a similar deficit, (2) each area may belong to several overlapping networks, therefore a lesion in a single area often produces multiple deficits, and (3) severe and lasting deficit of function occurs when all or most structural components of a network are involved. 7. Broca's aphasia Lesions producing Broca's aphasia have been described from Broca's area, although they often extend beyond the 'foot' of the inferior frontal convolution [29], the rolandic operculum [30], anterior insula, subcortical (capsulostriataI) area, and periventricular or centrum semiovale lesion. Involvement of only Broca's area is usually followed by good recovery [31]. Such lesions often produce a transient motor aphasia (also called 'cortical motor aphasia', 'pure motor aphasia', or 'verbal apraxia'). Pure motor aphasia, or verbal apraxia, has been associated with anterior subcor-

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tical, as well as opercular, inferior rolandic, and insular cortical lesions. Persisting Broca's aphasia is associated with large lesions that include not only Broca's area (posterior third of F3 and the frontal operculum), but also the inferior parietal and often the subcortical regions [27,29,31]. Persistent nonfluency has been associated with lesions extending to the rolandic cortical region and underlying white matter in previous studies [30,32-34]. The involvement of the central white matter is also important for the fluency deficit in the head injured population of Russell and Espir [35] and Ludlow et al. [23], and in stroke [36]. The centrum semiovale or periventricular white matter, that is involved in persistent cases of global or Broca's aphasia, often includes the pyramidal tract, thalamocortical somatosensory projections, striatocortical connections, callosal radiations, the subcallosal fasciculus [37], thalamocortical projections form the dorsomedial and ventrolateral nuclei [38], and the occipitofrontal fasciculus [39]. Lesion location was evaluated in Broca's aphasics who were divided at the median for poor and good recovery. The structures with significant involvement (more than 50%) were the inferior frontal gyrus, especially the pars opercularis and triangularis, and the insula in both groups. The difference between the persisting cases of Broca's aphasics and those who show good recovery was most prominent in the involvement of the precentral, postcentral, and supramarginal gyri in the cases of poor recovery. The subcortical regions showed significant differences in the involvement of the putamen and the caudate, which was twice as frequent in the persistent cases [27]. We have recently analyzed some selected biological features, such as lesion size and lesion location in the recovery of non-fluent aphasia in stroke. The target population consisted of all the non-fluent aphasics consecutively examined in our laboratory, in whom localization with CT or MRI was available. In a 10-year period, 71 right-handed stroke patients with single lesions, aged between 30-80, with non-fluent aphasia, were followed from the acute examination period between 10-45 days post-stroke to 12 months post-stroke with a standardized comprehensive aphasia test, the Western Aphasia Battery (WAB) [13]. Non-fluent

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aphasia was defined as having a fluency score of 4.0/10 or less, as well as a repetition score of 6.9/10 or less on the WAB. Broca's aphasia was further differentiated from global aphasia as having a comprehension score of 4.0/10 or above on the WAB. The lesion areas were digitized with an IBM computer using an area-from-contour algorithm [40]. Regions of Interest (ROn check-listing was carried out to determine the location of the lesions. ROI's were chosen for their physiological importance and anatomical distinctiveness, and were defined according to the CT Atlas of Matsui and Hirano [41], and a new set of templates for MRI based on a cadaver study with gadolinium-filled markers [42]. Outcome measures had a high negative correlation with lesion size throughout. Naming was an interesting exception, indicating possibly a ceiling-effect combined with the relative persistence of even moderate naming deficit. All of these patients were treated with a variable amount of language therapy; many of them for the duration of the study. Some of them participated in a formal study of language therapy [43]. There were several patterns, by which a vascular lesion could produce Broca's aphasia. The most common pattern involved the frontal opercular and central cortex, and the anterior insula, with or without significant subcortical involvement. These patients recovered quite well, with the exception of one who had central cortical, insular, and subcortical involvement. One patient with only an anterior insular lesion, which undercut the underlying white matter for Broca's area, showed moderate amount of recovery. Another patient with central and insular lesions, as well as one patient with central and subcortical lesions, showed poor recovery. This suggests a certain amount of variability in how the components of the network are affected producing different degrees of recovery. 8. Global aphasia Global aphasia is defined by the loss of speech output, and comprehension as well, usually associated with destruction of both the anterior and posterior language areas [44]. However in patients who are initially global, Wernicke's area may be

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spared. These patients tend to recover towards Broca's aphasia. Even 'Broca's area' cortex may not be destroyed, although it is usually disconnected from the rest of the language cortex by white matter involvement [36]. Occasionally white matter lesions may produce persistent global aphasia. There are also case reports of patients with initial global aphasia without hemiplegia who recover dramatically when they have posteriorfrontal and posterior-temporal lesions but sparing of the central structures [45,46]. We have also seen such a case, and the double lesions and the sparing of central cortex is illustrated in Fig. l. The classification of severely non-fluent aphasics influences the results of recovery studies. For instance, in the Boston Diagnostic Aphasia Examination (BDAE) [10], a large group of what others would classify as severe Broca's aphasics may be labelled, at times, as 'mixed anterior aphasics'. In the classification system of Aachen Aphasia Test (AAT) [14], many global aphasics would be reclassified as Broca's aphasics in other clinics. Some of these problems in taxonomy have been systematically studied in the comparison of aphasia batteries and how their scoring systems affect classification [47]. Global and Broca's aphasias, as defined by our taxonomy and methods of measurements, have similar spontaneous language characteristics. In our previous taxonomic studies [48], these were the two closest groups in the nearest neighbour-network analysis. The major difference between the two groups is in the extent of comprehension deficit. Since comprehension often recovers well, there are a great number of patients who change from global to Broca's aphasia during recovery (Syndromenwandeln) [49]. In our study, detailed analysis of the smallest lesions (less than 60 cc) that produce initial global aphasia indicated that the involvement of the centrum semi-ovale and some involvement of the anterior subcortical basal ganglia, mainly the striatum produced poor recovery. In two patients where only the centrum semi-ovale was involved moderate recovery was seen. Half of global aphasics had both Broca's (defined as the posterior third of the inferior frontal convolution) and Wernicke's (defined as the posterior superior temporal gyrus and the posterior temporal oper-

culum) areas involved, but a third of globals spared Wernicke's area and a few spared Broca's area. These patients had Broca's area completely undercut, but the cortex was not directly involved. 9. Transcortical motor aphasia

Transcortical motor aphasia is characterized by poor spontaneous speech but good repetition and comprehension. There is a variable naming deficit and the spontaneous writing is also poor. The localization of lesions is characteristically in the mesial frontal region or the supplementary speech area in the dominant hemisphere [50-54]. The importance of the supplementary motor areas on the left was recognized by Penfield and Roberts [55], who renamed it the 'supplementary speech area' because of the frequent speech arrest that was found during stimulation of this region. Cyto architecturally the supplementary motor cortex appears to represent a paralimbic extension of the limbic cortex [56]. This suggests a link between the limbic system and initiation of the motor mechanisms of speech. The lack of speech initiation is often considered to be a part of a general hypokinetic syndrome associated with frontal lobe lesions. The term 'adynamic aphasia' has also been used to describe this behaviour since Arnold Pick and Kleist. Recovery is usually excellent and these patients are only seen in acute units as a rule. Motor and premotor phonemic assembly and articulatory output mechanisms are elaborated by an extensive, yet definable, cortical/subcortical network. Partial damage to one or two components of the network is followed by good recovery. However, if all cortical and subcortical components of the network are impaired, the deficit is more severe and recovery is much less likely. There is converging evidence that the articulatory network for fluency involves the white matter connecting tracts between the components of the network, and lesion in the white matter alone can impair fluency in a persistent fashion. 10. Comprehension network

Language comprehension is a complex process that involves the analysis of the acoustic and

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phonological properties of input, as well as the recognition of syntactic and lexical elements [57]. This rapid parallel processing of input and matching it to linguistic' precepts is a dominantly left hemisphere function, although the right hemisphere has been shown to recognize words and syntax to a certain degree [58,59]. The auditory association cortex of the superior temporal gyrus region and the planum temporale located behind Heschl's gyrus performs the analysis and decoding of complex verbal stimuli (Wernicke's area). When the patient complains of not understanding speech, but hearing, reading, and speech output remain undisturbed, the diagnostic label of 'pure word deafness' is used. Although the condition is not always 'pure', good recovery is the rule. Auditory agnosia for nonverbal sounds and amusia is often associated, although these symptoms may be seen with right-sided lesions without the verbal component. In cortical deafness which is the result of bilateral temporal lesions, the patient appears clinically deaf with preserved primary hearing, but impaired central auditory processes, and the deficit is often more persisting. 11. Wernicke's aphasia Neologistic jargon output is distinctive and is associated with lesions of both the superior temporal and inferior parietal regions [60]. Wernicke's aphasia with semantic jargon is correlated with lesions that are somewhat smaller, inferior and more temporal than those with neologisms or phonemic paraphasia [61]. Other CT studies indicated that patients with semantic substitutions have lesions posterior to those with phonemic paraphasia [62]. Wernicke has postulated that the auditory association area plays a monitoring role in language output (presaging modern concepts of feedback and parallel processing), and that its damage results in paraphasic, faulty speech. Our studies of lesion location and size in recovery from Wernicke's aphasia suggest that ipsilateral connected structures, especially in the inferior parietal lobule, are the most likely to substitute after damage. The supramarginal and angular gyrus appear as the most likely compensating structures [63]. The evolution of Wernicke's aphasia is either in the direction from neologistic

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jargon to conduction aphasia or to 'pure word deafness' and from both of these intermediate stages to anomic aphasia [12]. 12. Transcortical sensory aphasia Patients with transcortical sensory aphasia who have semantic jargon usually have far more posterior lesions, usually in the watershed area between the middle cerebral and posterior cerebral circulation [64]. These patients are distinguished by preserved repetition. Sometimes the term semantic aphasia is applied to patients with similar behaviour. Recovery is usually rapid unless the syndrome evolves from a more severe lesion initially producing Wernicke's aphasia. Mixed transcortical aphasia has features of both the motor and sensory symptoms and tends to have a poor prognosis with nonfiuency persisting and not all comprehension returning, depending on the etiology. It occurs relatively uncommonly and the recovery patterns have not been described extensively. In our laboratory, we had two persisting cases, one with stroke and another with posttraumatic syndrome. Word finding or word access, the retrieval of lexical items (often tested by naming) is a fundamental process in language, and anomia is a feature of most aphasic syndromes. The study of lexical access and semantic processing is a major scientific and clinical topic. Recent advances in this field include the study of modality-specific fields (verbal vs. visual) and the categorical specificity of recognition and retrieval of lexical items. Lexical retrieval is thought to be dependent on a widely distributed cortical network. Lesion studies and functional activation have suggested the role of left temporoparietal and temporo-occipital cortex, and functional activation have added the frontal lobe as having a role in semantic processing [65]. Considering the complex nature of semantic association, narrowly restricted localization of this function is not likely. This is already evidenced from the wide distribution of lesions that result in anomia or anomic apl).asia. Patients who only have anomic aphasia de novo, usually recover well. Mild word finding and naming difficulty are very common in acute stroke and can be seen transiently with subcortical anterior corti-

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cal and posterior cortical lesions and rapid recovery is the rule even before they are transferred to rehabilitation. 13. Right hemisphere substitution for language Jackson [66] considered the right hemisphere capable of automatic utterances and being responsible for the residual output in severe aphasia. The principle of contralateral homologous cortical substitution was based on large left hemisphere lesions with relatively good recovery where there was very little left hemisphere remaining to take over. More recently CAT scan studies made the same point [67-68]. In addition, in some patients who became aphasic with a single left hemisphere stroke, but recovered, a second, right hemisphere stroke produced a language deficit again [69-71]. These cases, however, may have represented bilateral language organization to begin with, rather than a commonly operating mechanism of functional transfer to the contralateral hemispheres. The idea of compensation through right hemisphere function, even after partial left hemisphere damage, was also supported by studies of sodium amytal given to aphasics who had recovered [72,73]. These studies indicated that even though the aphasic disturbance occurred from a left hemisphere lesion, it was the right hemispheric injection that increased the language disturbance, implying that the right hemisphere compensated for the previous deficit produced by the left-sided lesion. More recent studies of cerebral blood flow (CBF) also suggested right hemisphere compensation [74]. 14. Other biological variables The variation in recovery, that cannot entirely be explained by the extent and location of lesions, has been postulated to relate to differences in language laterality, handedness, and gender. Sub iran a's [75], Gloning's et al. [76], and Geschwind's [77] suggestions that left handers and right handers, with a family history of left handedness, recover better from aphasia because more bilateral language distribution is based on anecdotal evidence. However, when more exten-

sive data are examined no difference could be observed [78]. Recent studies of anatomical asymmetry on CT scans, inspired by the demonstration of commonly larger planum temporale on the left by Geschwind and Levitsky [79], have correlated better outcomes with atypical or less asymmetry [80]. This is also based on the idea that this pattern may be associated with more right hemisphere language. We have studied the factor of anatomical asymmetry on CT, as measured by occipital width, frontal width and protuberance (pet alia), and could not confirm that atypical asymmetry played a role in recovery in any of the aphasic groups [27]. It could be that anatomical asymmetries relate more to handedness variables than language distribution, as suggested by some of our studies in normals [81]; therefore, we are not seeing an effect on language recovery. It has been suggested that women have more bilaterally distributed language [82]. However, when we looked at sex differences in recovery, we found none and no evidence to support better right hemisphere substitution by women [27]. 15. Metabolic and functional studies Cerebral blood flow (CBF)" and positron emission tomography (PET) studies of cerebral metabolism provide methodologies that add functional information to structural or lesion studies of recovery. Recent studies of cerebral blood flow with xenon 133 have also revealed a right-hemisphere hypometabolism in aphasic strokes, the extent of which has correlated with recovery to a modest degree [83]. Positron emission tomography (PET) studies of cerebral metabolism have shown a great deal of hypometabolism surrounding, but also remote from cerebral infarcts, thus suggesting that not only surrounding areas but also homologous areas in the contralateral hemisphere playa role in compensation [84]. However, one CBF study showed no significant change while clinical recovery occurred in severe aphasics [85]. Patients who improved more, showed more blood flow in the left hemisphere. This appears to be the consequence of the size of the lesion, which correlates with the CBF changes. Another CBF study showed better than 60% hemispheric flow

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in patients with good recovery [86]. We had experience with four aphasics whose distant hypometabolism in the ipsilateral cortex outside their CT lesion persisted, despite significant recovery. Recent studies have suggested improved CBF at distant (contralateral) hypometabolic sites [74,87]. More recent functional activation confirms the importance of the posterior temporal area in auditory perception of language, and the central and premotor cortex in articulation, in addition to some newly emphasized components to the language network, such as the mesial frontal and lateral frontal areas in word retrieval and semantic association [65]. The anterior cingulate gyrus appeared to be part of an anterior attentional system indicated by its activation while monitoring lists of words for semantic category [65]. Some of the continuing work with PET and 0 15 , and recent efforts on magnetic resonance functional activation promises to shed further light on these issues [74,88,89]. 16. Conclusion The size and location of lesions, time-fromonset, etiology and initial severity, are complex, interdependent factors in the recovery of language loss. Other biological factors, such as age, education, handedness, and sex play a less significant role when an adult stroke population is followed. Lesion size is undoubtedly a significant factor in the extent of recovery. An exception to the negative correlation between language recovery and lesion size is comprehension. In some patients, even with large lesions, the amount of comprehension recovery is considerable; while patients with small lesions demonstrate a relatively small degree of recovery. One of the unresolved issues remains whether ipsilateral, connected, adjacent, or distant, even contralateral, cortex playa role in compensation. The answer is probably all, but our studies of lesion location and recovery in Broca's and Wernicke's aphasia suggest that ipsilateral connected structures play the major role in restoration of function after damage. These are structures which are likely to be used normally in the language network, although for somewhat different functions at dif-

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ferent times. The functional participation by these structures implies neuroplasticity rather than a built-in redundancy when recovery from damage occurs. The cytoarchitectonic similarity and anatomical contiguity make some structures prime candidates for substitution. This structural network is capable of a considerable degree of compensation, producing various clinical patterns of deficit, but its complete destruction results in permanent loss in the majority of individuals. Exceptions to this rule are best explained by contralateral substitution. Functional activation and cortical stimulation provides convergent evidence of such networks. References [1]

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