Language disturbances after non-thalamic subcortical stroke: a review of the literature

Bouvier, Liziane; Groulx, Bertrand; Martel‐Sauvageau, Vincent; Monetta, Laura

doi:10.1684/pnv.2017.0666

Cited by 7 publications

(6 citation statements)

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“…Remarkably, only in cases of CD caused by the interruption of subcortical acoustic radiations [ 20 , 25 ] or by a secondary auditory area [ 43 ], a marked improvement leading to functional oral communication was observed on the follow-up. This was consistent with the findings from other cortical deficits caused by interruptions of cortico-subcortical circuits, for instance in patients with subcortical aphasia [ 52 ]. In subcortical aphasia, recovering is in general better and faster [ 52 ].…”

Section: Discussionsupporting

confidence: 92%

“…This was consistent with the findings from other cortical deficits caused by interruptions of cortico-subcortical circuits, for instance in patients with subcortical aphasia [ 52 ]. In subcortical aphasia, recovering is in general better and faster [ 52 ]. This improvement is boosted by an increased intrahemispheric functional connectivity and decreased interhemispheric functional connectivity [ 53 ], a combination of mechanisms associated with better outcomes in patients recovering from stroke [ 54 ].…”

Section: Discussionsupporting

confidence: 92%

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Stroke-Associated Cortical Deafness: A Systematic Review of Clinical and Radiological Characteristics

et al. 2021

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Background: Stroke is the leading cause of cortical deafness (CD), the most severe form of central hearing impairment. CD remains poorly characterized and perhaps underdiagnosed. We perform a systematic review to describe the clinical and radiological features of stroke-associated CD. Methods: PubMed and the Web of Science databases were used to identify relevant publications up to 30 June 2021 using the MeSH terms: “deafness” and “stroke”, or “hearing loss” and “stroke” or “auditory agnosia” and “stroke”. Results: We found 46 cases, caused by bilateral lesions within the central auditory pathway, mostly located within or surrounding the superior temporal lobe gyri and/or the Heschl’s gyri (30/81%). In five (13.51%) patients, CD was caused by the subcortical hemispheric and in two (0.05%) in brainstem lesions. Sensorineural hearing loss was universal. Occasionally, a misdiagnosis by peripheral or psychiatric disorders occurred. A few (20%) had clinical improvement, with a regained oral conversation or evolution to pure word deafness (36.6%). A persistent inability of oral communication occurred in 43.3%. A full recovery of conversation was restricted to patients with subcortical lesions. Conclusions: Stroke-associated CD is rare, severe and results from combinations of cortical and subcortical lesions within the central auditory pathway. The recovery of functional hearing occurs, essentially, when caused by subcortical lesions.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 92%

Stroke-Associated Cortical Deafness: A Systematic Review of Clinical and Radiological Characteristics

et al. 2021

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“…While the basal ganglia have a long "tradition" in the evolution of sound communication in terrestric vertebrates, the involvement of the cerebellum seems to be phylogenetically linked to the development of human language in a more specific way (Ziegler and Ackermann, 2017). Apart from sensorimotor and timing functions, subcortical structures are also involved in cognitive tasks and higher-order language functions (Booth et al, 2007;Bouvier et al, 2017;Kang et al, 2017) Basal Ganglia…”

Section: Subcortical Circuitsmentioning

confidence: 99%

“…Apart from PD, also other disorders or lesions of the basal ganglia, may lead to symptoms of subcortical aphasia such as anomia, reduced word fluency, and poor speech comprehension. In general, these deficits show up in more complex and demanding language tasks at the discourse or syntax level, and they seem to be more severe in language production as compared to comprehension (Bouvier et al, 2017). However, the detailed pathomechanisms of subcortical language symptoms are difficult to assess, and in many cases additional cortical or white matter lesions cannot strictly be ruled out (Radanovic and Mansur, 2017).…”

Section: Subcortical Circuitsmentioning

confidence: 99%

The Margins of the Language Network in the Brain

2020

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This review paper summarizes the various brain modules that are involved in speech and language communication in addition to a left-dominant "core" language network that, for the present purpose, has been restricted to elementary formal-linguistic and more or less disembodied functions such as abstract phonology, syntax, and very basic lexical functions. This left-dominant perisylvian language network comprises parts of inferior frontal gyrus, premotor cortex, and upper temporal lobe, and a temporoparietal interface. After introducing this network, first, the various roles of neighboring and functionally connected brain regions are discussed. As a second approach, entire additional networks were considered rather than single regions, mainly motivated by resting-state studies indicating more or less stable connectivity patterns within these networks. Thirdly, some examples are provided for language tasks with functional demands exceeding the operating domain of the core language network. The rationale behind this approach is to present some outline of how the brain produces and perceives language, accounting, first, for a bulk of clinical studies showing typical forms of aphasia in case of left-hemispheric lesions in the core language network and second, for widespread activation patterns beyond this network in various experimental studies with language tasks. Roughly, the brain resources that complement the core language system in a task-specific way can be described as a number of brain structures and networks that are related to (1) motor representations, (2) sensory-related representations, (3) non-verbal memory structures, (4) affective/emotional processing, (5) social cognition and theory of mind, (6) meaning in context, and (7) cognitive control. After taking into account all these aspects, first, it seems clear that natural language communication cannot really work without additional systems. Second, it also becomes evident that during language acquisition the core language network has to be built up from outside, that is, from various neuronal activations that are related to sensory input, motor imitation, nursing, pre-linguistic sound communication, and pre-linguistic pragmatics. Furthermore, it might be worth considering that also in cases of aphasia the language network might be restored by being trained from outside.

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“…The neural substrates of cortical aphasia are well-established (Plowman et al, 2012; Yassi et al, 2015). Subcortical aphasia, which occurs after strokes in the basal ganglia, thalamus, or deep white matter, is not as well characterized (Bouvier et al, 2017; Kang et al, 2017; Radanovic & Mansur, 2017). Subcortical aphasia lacks some of the clinical features of classic aphasia subtypes (Damasio et al, 1982), and the type and severity of language impairments after subcortical stroke varies widely (Bouvier et al, 2017; Caplan et al, 1990) — with no characteristic error pattern found among these patients generally (Kennedy & Murdoch, 1993).…”

Section: Introductionmentioning

confidence: 99%

The contribution of white matter pathology, hypoperfusion, lesion load, and stroke recurrence to language deficits following acute subcortical left hemisphere stroke

Sharif

Goldberg

Walker³

et al. 2022

Preprint

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Aphasia, the loss of language ability following damage to the brain, is among the most disabling and common consequences of stroke. Subcortical stroke, occurring in the basal ganglia, thalamus, and/or deep white matter can result in aphasia, often characterized by word fluency, motor speech output, or sentence generation impairments. The link between greater lesion volume and acute aphasia is well documented, but the independent contributions of lesion location, cortical hypoperfusion, prior stroke, and white matter degeneration (leukoaraiosis) remain unclear, particularly in subcortical aphasia. Thus, we aimed to disentangle the contributions of each factor on language impairments in left hemisphere acute subcortical stroke survivors. Eighty patients with acute left hemisphere subcortical stroke (less than 10 days post-onset) participated. We manually traced acute lesions on diffusion-weighted scans and prior lesions on T2-weighted scans. Leukoaraiosis was rated on T2-weighted scans using the Fazekas et al. (1987) scale. Fluid-attenuated inversion recovery (FLAIR) scans were evaluated for hyperintense vessels in each vascular territory, providing an indirect measure of hypoperfusion in lieu of perfusion-weighted imaging. Compared to subcortical stroke patients without aphasia, patients with aphasia had greater acute and total lesion volume, were older, and had significantly greater damage to the internal capsule (which did not survive controlling for total lesion volume). Patients with aphasia did not differ from non-aphasic patients by other demographic or stroke variables. Age was the only significant predictor of aphasia status in a logistic regression model. Further examination of three participants with severe language impairments suggests that their deficits result from impairment in domain-general, rather than linguistic, processes. Given the variability in language deficits and imaging markers associated with such deficits, it seems likely that subcortical aphasia is a heterogeneous clinical syndrome with distinct causes across individuals.

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Language disturbances after non-thalamic subcortical stroke: a review of the literature

Cited by 7 publications

References 0 publications

Stroke-Associated Cortical Deafness: A Systematic Review of Clinical and Radiological Characteristics

Stroke-Associated Cortical Deafness: A Systematic Review of Clinical and Radiological Characteristics

The Margins of the Language Network in the Brain

The contribution of white matter pathology, hypoperfusion, lesion load, and stroke recurrence to language deficits following acute subcortical left hemisphere stroke

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