The same language symptom might arise at different functional loci in people with aphasia. Therefore, it is plausible that different therapeutic interventions should be adopted to approach the same difficulties in different patients. Although this point of view is still widely accepted, recently the focus has shifted from the functional locus of a rehabilitative intervention to the mechanisms of action underlying the relearning process. We maintain that both aspects should be taken into account when programming a rehabilitative intervention; furthermore, investigating relearning mechanisms might shed new light on the functional architecture of the disrupted processes. Here, we investigated, in a single case study, whether classical conditioning was a suitable relearning paradigm for targeting word-finding difficulties in pure anomia, that is in a patient with an impairment in accessing intact output lexical representations from a spared semantic system. Using a word-repetition task on picture presentation, we contrasted a condition in which the stimulus onset asynchrony between word and picture stimuli was well suited to produce classical conditioning with a condition in which repetition training could not benefit from this learning mechanism. Only classical conditioning training exerted a significant, long-lasting effect on our patient's naming skill. Tentative implications of our results for the functional architecture of single-word processing are discussed.
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http://dx.doi.org/10.1111/jnp.12088 | DOI Listing |
Psychophysiology
January 2025
Department of Psychology, University of Bonn, Bonn, Germany.
Imaginal exposure is a standard procedure of cognitive behavioral therapy for the treatment of anxiety and panic disorders. It is often used when in vivo exposure is not possible, too stressful for patients, or would be too expensive. The Bio-Informational Theory implies that imaginal exposure is effective because of the perceptual proximity of mental imagery to real events, whereas empirical findings suggest that propositional thought of fear stimuli (i.
View Article and Find Full Text PDFFront Public Health
January 2025
Dipartimento di Scienze Cognitive, Psicologiche, Pedagogiche e Degli Studi Culturali, Università di Messina, Messina, Italy.
Religious beliefs can shape how people process fear. Yet the psychophysiological mechanisms underlying this phenomenon remain poorly understood. We investigated fear learning and extinction processes in a group of individuals who professed a belief in God, compared to non-believers.
View Article and Find Full Text PDFBehav Brain Res
March 2025
Department of Psychological and Brain Sciences, Indiana University, USA. Electronic address:
Exposure to extreme stress can negatively impact behavior and lead to prolonged fear sensitization. These processes can be studied in the lab using stress-enhanced fear learning (SEFL), where prior exposure to inescapable stress exacerbates later contextual fear conditioning. A common method to reduce conditional fear is through extinction, where a conditional stimulus once paired with an unconditional (US; e.
View Article and Find Full Text PDFLearn Mem
January 2025
Department of Psychology, Arizona State University, Tempe, Arizona 85287, USA
Chronic stress typically leads to deficits in fear extinction. However, when a delay occurs from the end of chronic stress and the start of fear conditioning (a "recovery"), rats show improved context-cue discrimination, compared to recently stressed rats or nonstressed rats. The infralimbic cortex (IL) is important for fear extinction and undergoes neuronal remodeling after chronic stress ends, which could drive improved context-cue discrimination.
View Article and Find Full Text PDFJ Pain
January 2025
Innovative Clinical Training, Trials & Healthcare Initiative, Zermatt CH-3920, Switzerland.
In order to disentangle the effects of drugs from placebo responses, several approaches have been used, such as a placebo run-in phase in which only placebo nonresponders, or poor responders, are considered for further randomization to either placebo or active treatment. This study is aimed at investigating the variability of placebo nonresponders obtained through the classical placebo run-in paradigm (group RUN) and through mismatch conditioning (group MIS), as done in our previous study. To do this, we simulated a real clinical trial in the laboratory, in which the placebo responders of both groups were discarded and the remaining nonresponders of both groups RUN and MIS were randomized to either continuing on placebo (groups RUN-P and MIS-P, respectively) or receiving topical 0.
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