The Declarative/Procedural Model of Pinker, Ullman and colleagues claims that the basal ganglia are part of a fronto-striatal procedural memory system which applies grammatical rules to combine morphemes (the smallest...The Declarative/Procedural Model of Pinker, Ullman and colleagues claims that the basal ganglia are part of a fronto-striatal procedural memory system which applies grammatical rules to combine morphemes (the smallest meaningful units in language) into complex words (e.g. talk-ed, talk-ing). We tested this claim b y investigating whether striatal damage or loss of its dopaminergic innervation is reliably associated with selective regular past tense deficits in patients wi th subcortical cerebrovascular damage, Parkinson’s disease or Huntington’s dis ease.We focused on past tense morphology since this allows us to contrast the re gular past tense (jump-jumped), which is rulebased,with the irregular past tens e (sleep-slept), which is not We used elicitation and priming tasks to test pat ients’ability to comprehend and produce inflected forms. We found no evidence o f a consistent association between striatal dysfunction and selective impairment of regular past tensemorphology, suggesting that the basal ganglia are not esse ntial for processing the regular past tense as a sequence of morphemes, either i n comprehension or production, in contrast to the claims of the Declarative/Proc edural Model. All patient groups showed normal activation of semantic and morpho logical representations in comprehension, despite difficulties suppressing seman tically appropriate alternatives when trying to inflect novel verbs. This is con sistent with previous reports that striatal dysfunction spares automatic activat ion of linguistic information, but disrupts later language processes that requir e inhibition of competing alternatives.展开更多
Objectives: The aetiology of the cognitive changes seen in Parkinson’s disease (PD) is multifactorial but it is likely that a significant contribution arises from the disruption of dopaminergic pathways. This study a...Objectives: The aetiology of the cognitive changes seen in Parkinson’s disease (PD) is multifactorial but it is likely that a significant contribution arises from the disruption of dopaminergic pathways. This study aimed to investigate the contribution of the dopaminergic system to performance on two executive tasks using 18F-6-fluorodopa positron emission tomography (F-dopa PET) in PD subjects with early cognitive changes. Methods: 16 non-demented, non-depressed PD subjects were evaluated with the Tower of London (TOL) spatial planning task, a verbal working memory task (VWMT) and 18F-dopa PET, all known to be affected in early PD. Statistical parametric mapping (SPM) localised brain regions in which 18F-dopa uptake covaried with performance scores. Frontal cortical resting glucose metabolism was assessed with 18F-fluoro-2-deoxy-D-glucose (18F-FDG) PET. Results: SPM localised significant covariation between right caudate 18F-dopa uptake (Ki) and TOL scores and between left anterior putamen Ki and VWMT performance. No significant covariation was found between task scores and F-dopa Ki values in either limbic or cortical regions. Frontal cortical glucose metabolism was preserved in all cases. Conclusions: These findings support a causative role of striatal dopaminergic depletion in the early impairment of executive functions seen in PD. They suggest that spatial and verbal executive tasks require integrity of the right and left striatum, respectively, and imply that the pattern of cognitive changes manifest by a patient with PD may reflect differential dopamine loss in the two striatal complexes.展开更多
文摘The Declarative/Procedural Model of Pinker, Ullman and colleagues claims that the basal ganglia are part of a fronto-striatal procedural memory system which applies grammatical rules to combine morphemes (the smallest meaningful units in language) into complex words (e.g. talk-ed, talk-ing). We tested this claim b y investigating whether striatal damage or loss of its dopaminergic innervation is reliably associated with selective regular past tense deficits in patients wi th subcortical cerebrovascular damage, Parkinson’s disease or Huntington’s dis ease.We focused on past tense morphology since this allows us to contrast the re gular past tense (jump-jumped), which is rulebased,with the irregular past tens e (sleep-slept), which is not We used elicitation and priming tasks to test pat ients’ability to comprehend and produce inflected forms. We found no evidence o f a consistent association between striatal dysfunction and selective impairment of regular past tensemorphology, suggesting that the basal ganglia are not esse ntial for processing the regular past tense as a sequence of morphemes, either i n comprehension or production, in contrast to the claims of the Declarative/Proc edural Model. All patient groups showed normal activation of semantic and morpho logical representations in comprehension, despite difficulties suppressing seman tically appropriate alternatives when trying to inflect novel verbs. This is con sistent with previous reports that striatal dysfunction spares automatic activat ion of linguistic information, but disrupts later language processes that requir e inhibition of competing alternatives.
文摘Objectives: The aetiology of the cognitive changes seen in Parkinson’s disease (PD) is multifactorial but it is likely that a significant contribution arises from the disruption of dopaminergic pathways. This study aimed to investigate the contribution of the dopaminergic system to performance on two executive tasks using 18F-6-fluorodopa positron emission tomography (F-dopa PET) in PD subjects with early cognitive changes. Methods: 16 non-demented, non-depressed PD subjects were evaluated with the Tower of London (TOL) spatial planning task, a verbal working memory task (VWMT) and 18F-dopa PET, all known to be affected in early PD. Statistical parametric mapping (SPM) localised brain regions in which 18F-dopa uptake covaried with performance scores. Frontal cortical resting glucose metabolism was assessed with 18F-fluoro-2-deoxy-D-glucose (18F-FDG) PET. Results: SPM localised significant covariation between right caudate 18F-dopa uptake (Ki) and TOL scores and between left anterior putamen Ki and VWMT performance. No significant covariation was found between task scores and F-dopa Ki values in either limbic or cortical regions. Frontal cortical glucose metabolism was preserved in all cases. Conclusions: These findings support a causative role of striatal dopaminergic depletion in the early impairment of executive functions seen in PD. They suggest that spatial and verbal executive tasks require integrity of the right and left striatum, respectively, and imply that the pattern of cognitive changes manifest by a patient with PD may reflect differential dopamine loss in the two striatal complexes.
