Individuals with post-stroke aphasia have long been observed to show relatively preserved musical and rhythm abilities in the presence of varied, and often profound, language impairments. Accordingly, speech-language pathologists frequently use rhythm-based strategies (e.g., tapping) to facilitate speech output in people with aphasia. However, there is little empirical work to support the clinical practice of using rhythm techniques. In this study, we investigated the neural bases of rhythm in aphasia by combining thorough behavioral rhythm assessments with structural brain imaging. Individuals with chronic, post-stroke aphasia (n = 33) and a matched neurotypical control group (n = 29) completed a rigorous battery of rhythm production and perception tasks. We found marked individual variability within the aphasia group, with about one third of individuals showing impaired rhythm processing, while the remaining two-thirds performed within the control range. Using lesion-symptom mapping, we found that individual variability in tapping performance was associated with damage to a left temporoparietal area, extending into white matter specifically in the arcuate fasciculus. That is, individuals who struggled with tapping tended to have damage to this region. Tapping was also associated with language production scores, but not motor speech, in the aphasia group. These findings, which systematically link rhythm, language, and the brain, have the potential to be translated into clinical practice for understanding which patients may benefit the most from rhythm-based treatments. Our study in a population with focal brain injury complements evolutionary work highlighting the importance of the left temporoparietal region and underlying white matter for beat synchronization.

After a stroke, individuals with aphasia often recover to a certain extent over time. This recovery process may be dependent on the health of surviving brain regions. Leukoaraiosis (white matter hyperintensities on MRI reflecting cerebral small vessel disease) is one indication of compromised brain health and is associated with cognitive and motor impairment. Previous studies have suggested that leukoaraiosis may be a clinically relevant predictor of aphasia outcomes and recovery, although findings have been inconsistent. We investigated the relationship between leukoaraiosis and aphasia in the first year after stroke. We recruited 267 patients with acute left hemispheric stroke and coincident fluid attenuated inversion recovery MRI. Patients were evaluated for aphasia within 5 days of stroke, and 174 patients presented with aphasia acutely. Of these, 84 patients were evaluated at ∼3 months post-stroke or later to assess longer-term speech and language outcomes. Multivariable regression models were fit to the data to identify any relationships between leukoaraiosis and initial aphasia severity, extent of recovery, or longer-term aphasia severity. We found that leukoaraiosis was present to varying degrees in 90% of patients. However, leukoaraiosis did not predict initial aphasia severity, aphasia recovery, or longer-term aphasia severity. The lack of any relationship between leukoaraiosis severity and aphasia recovery may reflect the anatomical distribution of cerebral small vessel disease, which is largely medial to the white matter pathways that are critical for speech and language function.