ArticleNeurology2023
Involvement of Thalamocortical Networks in Patients With Poststroke Thalamic Aphasia.
Article in Neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 28 citations in OpenAlex.
- Preventing slowing down of alpha rhythms in stroke patients through modulation of cortical excitatory-inhibitory balance: a randomized controlled trial.Journal of neuroengineering and rehabilitation · 2026Trial
- Thalamic aphasia as an uncommon manifestation of thalamic stroke due to artery of Percheron occlusion: Case report with literature review.Radiology case reports · 2026Article
- Object Naming After Thalamic Damage: Evidence From a Large-Scale, Chronic-Phase Study of Left Hemisphere Stroke Survivors.Neurobiology of language (Cambridge, Mass.) · 2026Article
- Spatial neglect after subcortical stroke may reflect cortico-cortical disconnection.Scientific reports · 2025Article
- Thalamic disconnection from prefrontal cognitive control networks contributes to thalamic aphasia.Brain communications · 2025Article
- Characteristics and prognosis of language impairment in subcortical aphasia of acute stroke patients.Frontiers in neurology · 2025Article
- Optic ataxia in patients with thalamic lesions.Brain communications · 2025Article
- Altered brain structural covariance networks of the thalamic subfields in right chronic capsular stroke.Frontiers in neuroscience · 2025Article
- Treadmill Exercise Enhances Post-Stroke Functional Recovery in Mice via the CX3CL1/CX3CR1 Signaling Pathway.Molecular neurobiology · 2025Article
- Fronto-thalamic networks and the left ventral thalamic nuclei play a key role in aphasia after thalamic stroke.Communications biology · 2024Article
- Article
- Conversational production and comprehension: fMRI-evidence reminiscent of but deviant from the classical Broca-Wernicke model.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
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9 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectiveTheories assume that thalamic stroke may cause aphasia because of dysfunction in connected cortical networks. This takes into account that brain functions are organized in distributed networks, and in turn, localized damage may result in a network disorder such as thalamic aphasia. With this study, we investigate whether the integration of the thalamus into specific thalamocortical networks underlies symptoms after thalamic stroke. We hypothesize that thalamic lesions in patients with language impairments are functionally connected to cortical networks for language and cognition.
methodsWe combined nonparametric lesion mapping methods in a retrospective cohort of patients with acute or subacute first-ever thalamic stroke. A relationship between lesion location and language impairments was assessed using nonparametric voxel-based lesion-symptom mapping. This method reveals regions more frequently damaged in patients with compared with those without a symptom of interest. To test whether these symptoms are linked to a common thalamocortical network, we additionally performed lesion-network-symptom mapping. This method uses normative connectome data from resting-state fMRI of healthy participants (n = 65) for functional connectivity analyses, with lesion sites serving as seeds. Resulting lesion-dependent network connectivity of patients with language impairments was compared with those with motor and sensory deficits as baseline.
resultsA total of 101 patients (mean [SD] age 64.1 [14.6] years, 57 left, 42 right, and 2 bilateral lesions) were included in the study. Voxel-based lesion-symptom mapping showed an association of language impairments with damage to left mediodorsal thalamic nucleus lesions. Lesion-network-symptom mapping revealed that language compared with sensory deficits were associated with higher normative lesion-dependent network connectivity to left frontotemporal language networks and bilateral prefrontal, insulo-opercular, midline cingular, and parietal domain-general networks. Lesions related to motor and sensory deficits showed higher lesion-dependent network connectivity within the sensorimotor network spanning prefrontal, precentral, and postcentral cortices. DISCUSSION: Thalamic aphasia relates to lesions in the left mediodorsal thalamic nucleus and to functionally connected left cortical language and bilateral cortical networks for cognitive control. This suggests that dysfunction in thalamocortical networks contributes to thalamic aphasia. We propose that inefficient integration between otherwise undamaged domain-general and language networks may cause thalamic aphasia.
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