Differential Effects of Semantic and Identity Priming in Patients with Left and Right Hemisphere Lesions

Abstract

Patients with single brain lesions in the anterior or posterior left and right hemispheres and a group of controls were studied in two priming experiments. The first experiment employed associative pairs (DOCTOR-NURSE) and the second employed identical pairs (NURSE-nurse). Short and long prime-target stimulus onset asynchronies (SOAs) (i.e., 250 and 1850 msec) were manipulated within block in both experiments. In the first experiment, patients with left hemisphere injury showed a deficient priming effect while patients with right hemisphere injury and controls showed a normal pattern. In contrast, all groups showed an identity priming effect in the second experiment. These results indicate that while entries in the mental lexicon are available for the groups of patients studied, the spread of activation to related concepts in this lexicon is disrupted in the left hemisphere-damaged group.

The neural substrates of memory systems impairment in Alzheimer's disease. A PET study of resting brain glucose utilization

“…In accordance with our hypothesis (based on the relevant neuropsychological literature, e.g. Keane et al, 1991;Henik et al, 1993) and the work of Perani et al (1993), semantic priming effects were significantly correlated with activity in the left temporoparietal association cortex (Tables 1 and 4 and Fig. 5).…”

“…Finally, a role for the left putamen and globus pallidus in priming effects has, to the best of our knowledge, never been reported before. Taken at a more global level, however, and in agreement with neuropsychological data (Henik et al, 1993) and visual halffield studies (for review, see Abernethy and Coney, 1996), our findings indicate that, in right-handed Alzheimer's disease subjects, semantic priming effects largely depend on a network of left hemisphere structures.…”

Localizing damage in the functional architecture: The distinction between implicit and explicit processing in deep dyslexia

“…Importantly, the results of semantic priming studies examining patients with focal lesions support hemispheric differences in the activation of semantic information (e.g., Blaxton & Bookheimer, 1993;Bushell, 1996;Copland, Chenery & Murdoch, 2002;Hagoort, 1997;Henik, Dronkers, Knight, & Osimani, 1993;Milberg & Blumstein, 1981). Most notable is the finding that, although patients with left hemisphere lesions showed relatively rapid activation for a broad range of semantic information, these patients exhibited a diminished ability to select among semantically related lexical competitors and inhibit less likely meanings at later temporal intervals: patients with left hemisphere lesions showed lexical access and spread of activation for strong associates at early temporal intervals.…”

“…Thus, deficient performance on the semantic judgment task for left hemisphere patients clearly reflects impaired explicit access. Considered within the context of priming effects for a broad range of semantic information at early temporal intervals (e.g., Blaxton & Bookheimer, 1993;Bushell, 1996;Copland et al, 2002;Hagoort, 1997;Henik et al, 1993;Milberg & Blumstein, 1981), which suggests intact lexical access at the implicit level, these results imply dissociation between implicit and explicit lexical access in patients with left hemisphere damage.…”

“…Preliminary support for dissociation in performance based on task demands is provided by priming studies with left hemisphere patients. Specifically, patients with left hemisphere lesions showed automatic activation for a broad range of semantic information, but diminished ability to select among semantically related lexical competitors and use contextual information to inhibit inappropriate meanings over time (e.g., Blaxton & Bookheimer, 1993;Bushell, 1996;Copland et al, 2002;Hagoort, 1997;Henik et al, 1993;Milberg & Blumstein, 1981). These results suggest that left hemisphere patients have spared implicit access to semantic information, but impaired lexical access at the explicit level due to disrupted selective and inhibitory processes.…”