Getting to the meaning of the regular past tense: evidence from neuropsychology.

Neuropsychological impairments of English past tense processing inform a key debate in cognitive neuroscience concerning the nature of mental mechanisms. Dual-route accounts claim that regular past tense comprehension deficits reflect a specific impairment of morphological decomposition (e.g., jump + ed), disrupting the automatic comprehension of word meaning accessed via the verb stem (e.g., jump). Single-mechanism accounts claim that the deficits reflect a general phonological impairment that affects perception of regular past tense offsets but which might preserve normal activation of verb semantics. We tested four patients with regular past tense deficits and matched controls, using a paired auditory semantic priming/lexical decision task with three conditions: uninflected verbs (hope/wish), regular past tense primes (blamed/accuse), and irregular past tense primes (shook/tremble). Both groups showed significant priming for verbs with simple morphophonology (uninflected verbs and irregular past tenses) but the patients showed no priming for verbs with complex morphophonology (regular past tenses) in contrast to controls. The findings suggest that the patients are delayed in activating the meaning of verbs if a regular past tense affix is appended, consistent with a dual-route account of their deficit.

The basal ganglia and rule-governed language use: evidence from vascular and degenerative conditions.

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 by investigating whether striatal damage or loss of its dopaminergic innervation is reliably associated with selective regular past tense deficits in patients with subcortical cerebrovascular damage, Parkinson's disease or Huntington's disease. We focused on past tense morphology since this allows us to contrast the regular past tense (jump-jumped), which is rule-based, with the irregular past tense (sleep-slept), which is not. We used elicitation and priming tasks to test patients' ability to comprehend and produce inflected forms. We found no evidence of a consistent association between striatal dysfunction and selective impairment of regular past tense morphology, suggesting that the basal ganglia are not essential for processing the regular past tense as a sequence of morphemes, either in comprehension or production, in contrast to the claims of the Declarative/Procedural Model. All patient groups showed normal activation of semantic and morphological representations in comprehension, despite difficulties suppressing semantically appropriate alternatives when trying to inflect novel verbs. This is consistent with previous reports that striatal dysfunction spares automatic activation of linguistic information, but disrupts later language processes that require inhibition of competing alternatives.