ArticleParkinsonism & related disorders2024
Comparing classic-onset corticobasal syndrome to speech/language-onset corticobasal syndrome.
Article in Parkinsonism & related disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Progressive Cognitive Decline and Pyramidal Signs in a Patient With a Novel Homozygous c.395A>T; p.Lys132Met Mutation in CHCHD2.Clinical case reports · 2026Article
- White matter hyperintensities in the deep cerebral venous territory differ between subcortical and cortical 4-repeat tauopathies.Parkinsonism & related disorders · 2026Article
- Pathomechanisms of neuropsychiatric disturbances in atypical parkinsonian disorders: a current view.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- The Spectrum of Cognitive Impairment in Atypical Parkinsonism Syndromes: A Comprehensive Review of Current Understanding and Research.Diseases (Basel, Switzerland) · 2025Review
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Authors and funding
12 authors.
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Abstract
introductionPatients with classic-onset corticobasal syndrome (CBS) present with asymmetric limb apraxia and parkinsonism. We have, however, observed patients who initially present with speech and/or language (SL) problems and several years later develop CBS (i.e., SL-onset CBS). We aimed to compare clinical, neuroimaging and pathological characteristics of classic-onset CBS with SL-onset CBS.
methodsWe conducted a retrospective cohort study of 62 patients who met criteria for CBS (17 presented with classic-onset CBS and 45 had SL-onset CBS). We compared demographics, clinical characteristics, and grey and white matter volume loss with SPM12 between groups and assessed pathology and corticobasal degeneration (CBD) pathological lesion counts in patients who had died and undergone autopsy.
resultsMedian age at CBS diagnosis was 66.4 years in classic-onset CBS and 73.6 years in SL-onset CBS. Classic-onset CBS had higher frequencies of dystonia, myoclonus, and alien limb phenomenon, while SL-onset CBS had a higher frequency of vertical supranuclear gaze palsy. Both groups showed smaller frontoparietal volumes than controls, with SL-onset CBS having greater volume loss in the left supplementary motor area than classic-onset CBS. All three classic-onset CBS cases with autopsy (100 %) had CBD pathology while 8/21 of SL-onset CBS cases (38 %) had CBD. Pathological lesion burden (including astrocytic plaques) did not differ between classic-onset and SL-onset CBS.
conclusionClassic-onset and SL-onset CBS appear to be different syndromes, with the former being a more profuse motor syndrome. The more widespread volume loss in SL-onset CBS likely reflects longer disease course.
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