Language SS Buckingham and HW Buckingham, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA ã 2015 Elsevier Inc. All rights reserved.
Glossary Agrammatic A term characterizing agrammatism, a condition of impoverished, telegraphic sentence structure where content words (nouns, verbs, adjectives, and adverbs) are retained and grammatical markers are absent or misused. Anomia A language impairment characterized by difficulty with word retrieval. Aphasia An acquired multi-modality impairment of language comprehension and/or formulation caused by focal damage to the language region(s) of the brain while leaving general intelligence intact. Apraxia of speech A central motor planning disorder that impairs articulatory positioning and sequencing for volitional speech despite intact sensory-motor control.
The Neurolinguistics of Aphasia Numerous neurological impairments (including seizures, tumors, and hemorrhages) can cause the acquired disorder of central language processing known as aphasia; the most common of these in adults is focal, ischemic stroke (Davis, 2014). Many modern imaging techniques, including magnetic resonance imaging (MRI), positron-emission tomography (PET), diffusion imaging, perfusion imaging, and magnetoencephalography (among others), have been used productively to study stroke and its impact on the language-processing regions of the brain. Stroke can cause fluent aphasias with symptom profiles that include anomia, numerous semantic and phonemic paraphasias, paragrammatic comprehension and production of morphosyntax, and verbal repetition skills that vary from excellent to impossible. Auditory comprehension of language may range from severely impaired to very good for different fluent syndromes (Davis, 2014; pertaining to grammar and syntax, word comprehension, naming, and disorders of language). Lesions associated with these aphasias are generally located either in the thalamus or in posterior cortical regions of the inferior parietal lobe (BA 40), the angular gyrus (BA 39), the inferior temporal gyrus (BA 37), the middle temporal gyrus (MTG and BA 21), or Wernicke’s area (BA 22), part of the superior temporal gyrus (STG; Helm-Estabrooks, Albert, & Nicholas, 2014). Stroke can also cause nonfluent aphasias with symptom profiles that include anomia, few semantic and phonemic paraphasias, a grammatical comprehension and production of morphosyntax, and verbal repetition skills ranging from excellent to extremely poor. Although impaired, auditory comprehension of language will usually be better than its verbal expression in all but the most severe of nonfluent syndromes. Lesion sites associated with these aphasias include regions of the anterior language cortex (e.g., the inferior–posterior frontal gyrus (IFG) region known as Broca’s area (Brodmann areas 44
Brain Mapping: An Encyclopedic Reference
Morphosyntax A combined term referring to morphology, knowledge of the internal structure of words, and syntax, knowledge of how words may be sequenced into phrases and sentences. Paragrammatic A term characterizing paragrammatism, a condition of impaired selection of content words (nouns, verbs, adjectives, and adverbs) within sentences otherwise having intact grammatical structure. Paraphasia A word (semantic) or sound (phonemic) substitution commonly associated with aphasia. Phonology The sound system of a language. Pragmatics The social usage system of a language. Semantics The meaning system of a language. Syntax The sentence structure system of a language.
and 45)) or the anterior or posterior capsular–putaminal regions of the basal ganglia (Helm-Estabrooks et al., 2014). Although Brodmann areas 44 (pars opercularis) and 45 (pars triangularis) are often referred to collectively, evidence from volumetric MRI studies (cf., Foundas, Eure, Luevano, & Weinberger, 1998) suggests that there may be a greater linguistic role for lexical retrieval, syntax, and semantics and a greater leftward (hemispheric) functional asymmetry for area 45 than for area 44 in both right- and left-handed individuals. In contrast to area 45, area 44 appears to have a greater role in speech fluency and articulation than in language processing, with a functional hemispheric localization pattern that is contralateral to handedness. The pattern of stronger left than right lateralization for frontal linguistic functions suggests that better recovery of language may be seen in individuals for whom leftward ‘relateralization’ of language function occurs after injury as opposed to poorer recovery in individuals who show either a persistently equal or rightward pattern of activation instead (Tecchio et al., 2006; Thomas, Altenmuller, Marckmann, Kahrs, & Dichgans, 1997). Although discrete regions of the language cortex are important with regard to aphasia, it should be understood that the neural systems that support language processing in humans are widely distributed, massively interconnected, and functionally redundant to a significant degree (Kiran, 2012; Mesulam, 1990). This architecture can be both a strength and a weakness of the system in that widely distributed functions, such as word finding, can be protected by the richness of their associative networks and yet become impaired with lesions to any number of brain sites (Kertesz, 1991). It can mean that a lesion in a given brain region can yield a panoply of diverse language symptoms, because the systems that mediate semantics, morphosyntax, and phonology are so interwoven. It can also mean, however, that improvements in one aspect of language processing may have a beneficial effect on associated others during the course of recovery.
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Recovery from Aphasia Occurring across communication modalities, symptoms of aphasia arise from the inefficient processing of language due to neurological insult rather than due to the loss of language knowledge caused by injury (Porch, 1994, 2001). Recovery is defined functionally and is uneven in its progress; improvements are evident when the accuracy and speed of word (semantics), sound (phonology), and sentence structure (morphosyntax) comprehension and/or production are each increased relative to baseline levels poststroke. Recovery within broad language domains will vary considerably across individuals and will vary by the nature and difficulty of specific task demands within and across individuals. Better blood perfusion to crucial language zones yields better task performance as reported in the blood oxygenation level-dependent (BOLD) functional MRI (fMRI) studies conducted by Jarso et al. (2013). Hillis and Heidler (2002) had described aphasia recovery as progressing in three overlapping phases: (1) acute, lasting approximately 2 weeks postonset, characterized by efforts toward reperfusion of the ischemic penumbra and reduction of diaschisis (Cappa, 2000); (2) subacute, lasting up to 6 months postonset, characterized by considerable neural reorganization and continued reduction of diaschisis (Kiran, 2012); and (3) chronic, lasting for 9 months to years postonset, characterized by the establishment of new neural pathways to link language-processing areas that had become functionally disconnected as a result of stroke (cf., Christman & Boutsen, 2006; Kiran, 2012). Hillis and Heidler (2002) suggested that different treatment approaches are warranted at the three different stages of recovery, with family counseling and medical interventions to reduce brain hypoperfusion most appropriate in the acute phase; with direct, intensive rehabilitation most appropriate in the subacute phase; and with daily, intensive rehabilitation plus the learning of compensatory strategies most appropriate in the chronic phase of recovery. There are considerable evidences that, in the acute stage of recovery, reperfusion of tissue near infarcts in the left STG can lead to improvements in auditory comprehension (Hillis & Heidler, 2002) and semantic processing (Hillis et al., 2001); that reperfusion of left STG, MTG, fusiform, and IFG peri-infarct tissue can lead to improvements in naming (Hillis et al., 2006); and that reperfusion of IFG tissue can lead to improvements in the comprehension and production of sentences and reduction of speech apraxia (Davis et al., 2008), in individuals with acute aphasia. Saur et al. (2006) had shown that during this period, activation of the left-hemisphere language cortex is greatly reduced. During the subacute phase of recovery, activations of the left-hemisphere language cortex and homologous righthemisphere zones are significantly increased (Saur et al., 2006), and cortical metabolism begins to improve with the reduction of diaschisis and mitigation of hypoperfusion (Cappa et al., 1997). As Kiran (2012) noted, the degree of neural plasticity in peri-infarct tissue and the nature and scope of directed rehabilitation applied at this time will probably determine the degree to which diaschisis is reduced and improved function is observed. After the acute phase of recovery, continued hypoperfusion will lead to tissue loss.
During the chronic phase of recovery, most research has suggested that a variety of ipsilesional and contralateral brain areas are recruited for successful recovery of word retrieval and syntax (see Kiran, 2012 for review). Of particular importance for the improvement of both functions is an increase in lefthemisphere perilesional activity following rehabilitative training. It is interesting to note that Saur et al. (2006) reported both the expansion and the reduction of network participation in language-processing abilities during subacute and chronic phases of recovery, respectively. Although the role of the right hemisphere in aphasia recovery requires further study, it may be the case that recruitment of additional processing resources from (especially posterior) contralesional and distant ipsilesional sites helps to improve language access during the subacute phase of recovery. Successful recovery in the chronic stage, however, will likely require refinement and reduction of those larger circuits to those that are smaller and more local in order to promote processing that is not only accurate but also quick and efficient. Behavioral and instrumental rehabilitation approaches can assist this circuitry reduction process (Porch, 1994, 2001) by employing intensive, massed practice for achievement of speech–language goals. Research regarding the nature and extent of recovery that is possible in chronic aphasia is quite promising, with some studies investigating the use of techniques as varied as constraint-induced language therapy (Pulvermuller et al., 2001), repetitive transcranial magnetic stimulation to contralesional cortex (Naeser et al., 2012), or even a combination of both in individuals with aphasia (Naeser et al., 2012).
Neural Mechanisms of Aphasia Recovery Recovery from aphasia proceeds via processes of neurological and behavioral change although the precise neurophysiological mechanisms involved remain the subject of considerable study. Chollet and Weiller (2000) had proposed that four mechanisms account for the cerebral reorganization that makes recovery possible after stroke. These include spontaneous neural reorganization, recruitment of remote brain areas (including contralateral cerebral cortex), extension of specialized areas into neighboring cortex, and increased neurological activity in the lesioned cortex. With regard to the first of these, it is generally accepted that poor perfusion of perilesional brain tissue predicts poor recovery from aphasia, and vice versa, in the first weeks immediately following stroke. Hillis et al. (2008) and Reineck, Agarwal, and Hillis (2005) had described a diffusion–perfusion mismatch technique that compares the difference between the volume of perfusion abnormality on perfusion-weighted imaging and that that is found on diffusion-weighted imaging to infer the volume of salvageable brain tissue in infarcted regions after stroke. This value is used to identify those individuals who would benefit from reperfusion therapies and likely show positive recovery from aphasia in the near term. Other studies using BOLD fMRI and arterial spin-labeling perfusion MRI techniques have indicated that functional improvement and increased neural activation can exist even
INTRODUCTION TO CLINICAL BRAIN MAPPING | Language
in brain regions with poor perfusion and tissue loss (Kiran, 2012). Although differences in the temporal hemodynamics of the ipsilateral cortex in stroke patients might explain those apparently conflicting results, BOLD fMRI studies have generally shown that (1) there is a correspondence between improved language function and increased brain perfusion over time and (2) rehabilitation may contribute to both, especially in the acute stage of recovery. Cellular mechanisms of recovery associated with spontaneous neural reorganization in the ipsilesional hemisphere include an increase in dendritic spines, axonal sprouting, and neurogenesis in the cortex adjacent to the infarcted tissue (Kiran, 2012). Research in mice has indicated that there are neuroplastic changes in the peri-infarct cortex that facilitate neural recovery, including the 2–4-week poststroke proliferation of neuroblasts that might form mature neurons and including the proliferation of neuronal dendritic spines in association with rehabilitative exercise and improved blood flow to the peri-infarct cortex (Kiran, 2012). By extension, rehabilitative activities directed toward recovery of motor and language functions and implemented intensively during early phases of neuroplastic activity and system reorganization are likely to be maximally beneficial in reducing persisting symptoms of aphasia in humans. The question of the role of the contralateral hemisphere in long-term recovery from stroke is particularly interesting with regard to aphasia because it appears to be different for nonfluent versus fluent syndromes. Research with PET and electroencephalography has shown that there is increased activation of the right-hemisphere homologue areas following damage to left-hemisphere IFG and MTG zones, for example, those to which damage would cause nonfluent and fluent aphasias. This activation persists in successful recovery from fluent aphasia (Thomas et al., 1997; Weiller et al., 1995) but diminishes in successful recovery from nonfluent aphasia (Thomas et al., 1997). It appears that recovery of the ipsilesional left inferior frontal cortex (especially Brodmann area 45) is crucial for recovery from nonfluent aphasia (Foundas et al., 1998; Papathanasiou, Coppens, & Potegas, 2011). Recovery of the ipsilesional left posterior auditory association cortex is naturally also most desirable, although perhaps not crucial for recovery from fluent aphasia. Research conducted by Papanicolaou, Levin, and Eisenberg (1984), Papanicolaou, Moore, Deutsch, Levin, and Eisenberg (1987), and Papanicolaou, Moore, Levin, and Eisenberg (1988) showed that among individuals with fluent aphasia, those with improved but persistent partial auditory comprehension deficits demonstrated a greater right-hemisphere response to language stimuli than those whose auditory comprehension deficits had resolved. In the latter population, better auditory processing appeared to be associated with eventual recovery of the dominant language cortex. As noted in Christman and Boutsen (2006), it is not clear whether longlasting bitemporal activity in individuals with functional auditory-processing abilities represents (1) compensatory activation of latent language-capable neural circuits in the contralateral hemisphere, (2) recruitment of cognitive resources (such as attention and memory) to support language processing, or (3) contralateral disinhibition leading to maladaptive functional reorganization. In fact, it is not clear whether successful recovery should be understood as the return of normal language networks
or as the emergence of reorganized language networks, maladaptive or otherwise (Kiran, 2012; Tecchio et al., 2006). Continued research to address this question is needed.
Conclusion Aphasia recovery is not an all-or-none phenomenon. Some language impairments will remit over time, while others may persist despite employment of best-practice rehabilitation strategies. A case in point is the typical persistence of anomia (Kertesz & Benson, 1970), the oft-studied impairment of word retrieval that is aphasia’s most salient, and often most intractable, symptom (Helm-Estabrooks et al., 2014), even in syndromes of mild severity (Goodglass & Wingfield, 1997; Laine & Martin, 2006). Semantic processing is interesting in that it is both robust and yet sensitive to neurological change; wordfinding difficulties (especially on confrontation naming tasks) not only characterize aphasia but also accompany cognition–communication disorders associated with nondominant hemisphere stroke (especially in generative naming tasks) and can be caused by conditions ranging from fatigue and depression (Fava, 2003), to normal aging (Goodglass & Wingfield, 1997), to incipient dementia (Bayles & Tomoeda, 2007). Aphasia recovery is an emergent phenomenon, a product of factors that are intrinsic and extrinsic to individuals and that contribute to language change over time. The classic recovery curve for aphasia has been described as one of the gradual inclinations and progressive decelerations over the first year postonset (Porch, 1994, 2001). The greatest improvement is usually seen in the first 3 months after injury (Kertesz, 1988), but the capacity for improvement is evident even in chronic stages of illness given sufficiently intense treatment stimulation (Pulvermuller et al., 2001). Individual variations in the nature and severity of aphasia symptoms, specific underlying etiology, and length of time postinsult, together with differences in the sizes, extents, and sites of lesion, age of onset, and the frequency/intensity, nature, and timing of treatments, all suggest that heterogeneity in aphasia recovery is to be expected. It is generally the case, however, that increases in aphasia severity, size and extent of neurological lesion, age at onset, and timeelapsed postonset are associated with reduced prognosis for successful recovery as is aphasia caused by ischemic stroke rather than hemorrhage (Basso, 1992, 2003; Davis, 2014). Factors such as gender, handedness, premorbid literacy, and motivation to seek treatment may influence the recovery of individuals to some extent but have not been shown to be major predictors of improvement within populations of people with aphasia (Basso, 1992, 2003; Davis, 2014). Among the aphasia subtypes, nonfluent global and fluent Wernicke’s types are often linked to poor outcomes, in part not only because auditory comprehension is compromised but also because the frontal IFG and temporal MTG brain regions frequently damaged in these aphasias are crucial processing zones and connectivity hubs for language expression and comprehension, respectively (Mesulam, 1990). Aphasias in these two regions can be severe, since damage may interrupt the extensive connectivity of these regions with those in the ipsilateral and contralateral cortices that might be vicariously recruited for language recovery (Kiran, 2012). In contrast, the
INTRODUCTION TO CLINICAL BRAIN MAPPING | Language
fluent anomic type of aphasia, having generally good auditory comprehension, verbal repetition, and morphosyntax, is usually characterized by better outcomes than global and Wernicke’s types. Despite frequently persistent word-finding difficulties, anomic aphasia is frequently the aphasia symptom profile toward which many other syndromes eventually evolve (Benson & Ardila, 1996; Simmons & Buckingham, 1992). The mechanisms for recovery from aphasia are not completely understood. Results from modern neurophysiological and behavioral research studies, however, point to the importance of limiting hypoperfusion and diaschisis in acute and subacute stages of recovery and providing intense, directed language rehabilitation during subacute and chronic phases of recovery. Mechanisms in the latter two phases frequently include the engagement of homologous contralateral regions of non-language-dominant cortex with the best recovery appearing to accompany a return to increased activation and efficient connectivity for language processing within the lesioned language-dominant hemisphere. Team-based research efforts should continue to identify those medical and behavioral rehabilitation procedures that can reduce aphasia severity; restore the accurate and prompt processing of semantics, syntax, and phonology for functional daily communication; provide the necessary psychosocial supports for individuals with aphasia and their families; and prevent the recurrence of ischemic stroke.
See also: INTRODUCTION TO ACQUISITION METHODS: Anatomical MRI for Human Brain Morphometry; Basic Principles of Electroencephalography; Basic Principles of Magnetoencephalography; Contrast Agents in Functional Magnetic Resonance Imaging; Diffusion MRI; Echo-Planar Imaging; Evolution of Instrumentation for Functional Magnetic Resonance Imaging; fMRI at High Magnetic Field: Spatial Resolution Limits and Applications; Functional MRI Dynamics; Functional Near-Infrared Spectroscopy; High-Field Acquisition; HighSpeed, High-Resolution Acquisitions; Molecular fMRI; MRI and fMRI Optimizations and Applications; Myelin Imaging; Obtaining Quantitative Information from fMRI; Perfusion Imaging with Arterial Spin Labeling MRI; Positron Emission Tomography and Neuroreceptor Mapping In Vivo; Pulse Sequence Dependence of the fMRI Signal; Susceptibility-Weighted Imaging and Quantitative Susceptibility Mapping; Temporal Resolution and Spatial Resolution of fMRI; INTRODUCTION TO CLINICAL BRAIN MAPPING: Disorders of Language; Recovery and Rehabilitation Poststroke; INTRODUCTION TO SYSTEMS: Grammar and Syntax; Naming; Speech Sounds.
References Basso, A. (1992). Prognostic factors in aphasia. Aphasiology, 6(4), 337–348. Basso, A. (2003). Aphasia and its therapy. Oxford: Oxford University Press. Bayles, K. A., & Tomoeda, C. K. (2007). Cognitive-communication disorders of dementia. San Diego, CA: Plural Publishing. Benson, D. F., & Ardila, A. (1996). Aphasia: A clinical perspective. Oxford: Oxford University Press. Cappa, S. F. (2000). Recovery from aphasia: Why and how. Brain and Language, 71, 39–41. Cappa, S. F., Perani, D., Grassi, F., Bressi, S., Alberoni, M., Franceschi, M., et al. (1997). A PET follow-up study of recovery after stroke in acute aphasics. Brain and Language, 129(6), 1371–1384.
Chollet, F., & Weiller, C. (2000). Recovery of neurological function. In J. C. Mazziotta, A. W. Toga, & R. S.J Frakowiak (Eds.), Brain mapping: The disorders (pp. 587–597). San Diego: Academic Press. Christman, S. S., & Boutsen, F. R. (2006). Recovery of language after stroke or trauma in adults. In K. Brown (Ed.), The encyclopedia of language and linguistics (2nd ed., pp. 401–414). London: Elsevier Ltd. Davis, G. A. (2014). Aphasia and related cognitive-communicative disorders. Boston, MA: Pearson. Davis, C., Kleinman, J. T., Newhart, M., Gingis, L., Pawlak, M., & Hillis, A. E. (2008). Speech and language functions that require a functioning Broca’s area. Brain and Language, 105(1), 50–59. Fava, M. (2003). Symptoms of fatigue and cognitive/executive dysfunction in major depressive disorder before and after antidepressant treatment. Journal of Clinical Psychiatry, 64(Suppl. 14), 30–34. Foundas, A. L., Eure, K. F., Luevano, L. F., & Weinberger, D. R. (1998). MRI asymmetries of Broca’s area: The pars triangularis and pars opercularis. Brain and Language, 64(3), 282–296. Goodglass, H., & Wingfield, A. (Eds.). (1997). Anomia: Neuroanatomical and cognitive correlates. San Diego: Academic Press. Helm-Estabrooks, N., Albert, M. L., & Nicholas, M. (2014). Manual of aphasia and aphasia therapy (3rd ed.). Austin, TX: Pro-ed. Hillis, A. E., Barker, P. B., Beauchamp, N. J., Winters, B. D., Mirski, M., Wityk, R., et al. (2001). Restoring blood pressure reperfused Wernicke’s area and improved language. Neurology, 56(5), 670–672. Hillis, A. E., Gold, L., Kannan, V., Cloutman, L., Kleinman, J. T., Newhart, M., et al. (2008). Site of the ischemic penumbra as a predictor of potential for recovery of functions. Neurology, 71, 184–189. Hillis, A. E., & Heidler, J. (2002). Mechanisms of early aphasia recovery. Aphasiology, 16(9), 885–895. Hillis, A. E., Kleinman, J. T., Newhart, M., Heidler-Gary, J., Gottesman, R., Barker, P. B., et al. (2006). Restoring cerebral blood flow reveals neural regions critical for naming. The Journal of Neuroscience, 26(3), 8069–8073. Jarso, S., Li, M., Faria, A., Davis, C., Leigh, R., Sebastian, R., et al. (2013). Distinct mechanisms and timing of language recovery after stroke. Cognitive Neuropsychology, 30(7–8), 454–475. Kertesz, A. (1988). What do we learn from recovery after aphasia? Advances in Neurology, 47, 277–292. Kertesz, A. (1991). Language cortex. Aphasiology, 5(3), 207–234. Kertesz, A., & Benson, D. F. (1970). Neologistic jargon: A clinicopathological study. Cortex, 6, 362–368. Kiran, S. (2012). What is the nature of poststroke language recovery and reorganization? ISRN Neurology, 2012, 1–13. Laine, M., & Martin, N. (2006). Anomia: Theoretical and clinical aspects. New York: Psychology Press. Mesulam, M.-M. (1990). Large-scale neurocognitive networks and distribution processing for attention, language, and memory. Annals of Neurology, 28, 597–603. Naeser, M. A., Martin, P. I., Ho, M., Treglia, E., Kaplan, E., Bhashir, S., et al. (2012). Transcranial magnetic stimulation and aphasia rehabilitation. Archives of Physical Medicine and Rehabilitation, 93(Suppl. 1), S26–S34. Papanicolaou, A. C., Levin, H. S., & Eisenberg, H. M. (1984). Evoked potential correlates of recovery from aphasia after focal left hemisphere injury in adults. Neurosurgery, 14(4), 412–415. Papanicolaou, A. C., Moore, B. D., Deutsch, G., Levin, H. S., & Eisenberg, H. M. (1987). Evidence for right-hemisphere involvement in recovery from aphasia. Archives of Neurology, 45, 1025–1029. Papanicolaou, A. C., Moore, B. D., Levin, H. S., & Eisenberg, H. M. (1988). Evoked potential correlates of right hemisphere involvement in language recovery following stroke. Archives of Neurology, 4(5), 521–524. Papathanasiou, I., Coppens, P., & Potegas, C. (2011). Aphasia and related neurogenic communication disorders. Burlington, MA: Jones and Bartlett Learning. Porch, B. E. (1994). Treatment of aphasia subsequent to the Porch Index of Communicative Ability (PICA). In R. Chapey (Ed.), Language intervention strategies in adult aphasia (3rd ed., pp. 78–183). Baltimore: Williams & Wilkins. Porch, B. E. (2001). Treatment of aphasia subsequent to the Porch Index of Communicative Ability (PICA). In R. Chapey (Ed.), Language intervention strategies in adult aphasia (4th ed., pp. 663–674). Philadelphia: Lippincott, Williams & Wilkins. Pulvermuller, F., Neininger, B., Elbert, T., Mohr, B., Rockstroh, B., Koebbel, P., et al. (2001). Constraint-induced therapy of chronic aphasia after stroke. Stroke, 32(7), 1621–1626. Reineck, L. A., Agarwal, S., & Hillis, A. E. (2005). “Diffusion-clinical mismatch” is associated with potential for early recovery of aphasia. Neurology, 64(3), 828–833.
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Saur, D., Lange, R., Baumgaertner, A., Schraknepper, V., Willmes, K., Rijntjes, M., et al. (2006). Dynamics of language reorganization after stroke. Brain, 129(6), 1371–1384. Simmons, N., & Buckingham, H. W. (1992). Recovery in jargonaphasia. Aphasiology, 6(4), 403–414. Tecchio, F., Zappasodi, F., Tombini, M., Oliviero, A., Pasqualetti, P., Vernieri, F., et al. (2006). Brain plasticity in recovery from stroke: An MEG assessment. NeuroImage, 32(3), 1326–1334.
Thomas, C., Altenmuller, E., Marckmann, G., Kahrs, J., & Dichgans, J. (1997). Language processing in aphasia: Changes in lateralization patterns during recovery reflect cerebral plasticity in adults. Electroencephalography and Clinical Neurophysiology, 102(2), 86–97. Weiller, C., Isensee, C., Rijintjes, M., Huber, W., Mueller, S., Bier, D., et al. (1995). Recovery from Wernicke’s aphasia—A PET study. Annals of Neurology, 37, 723–732.