Prefrontal and parietal cortex in human episodic memory: an interference study by repetitive transcranial magnetic stimulation

Rossi, Símone; Pasqualetti, Patrizio; Zito, Giancarlo; Vecchio, Fabrizio; Cappa, Stefano F.; Miniussi, Carlo; Babiloni, Claudio; Rossini, Paolo Maria · 2006 · OpenAlex-citations

DOI: 10.1111/j.1460-9568.2006.04600.x

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Summary

This study investigates whether parietal cortex (PC) activity is causally involved in human episodic memory, a question motivated by neuroimaging findings that consistently show PC activation during encoding and retrieval, despite uncertainty regarding its functional necessity. While the causal role of the prefrontal cortex (PFC) in memory is well-established, the specific contribution of the PC remains debated. The authors employed repetitive transcranial magnetic stimulation (rTMS) to induce reversible interference in the intraparietal sulcus, comparing these effects against a matched control group receiving rTMS on the dorsolateral PFC (DLPFC). The experimental design involved 42 healthy volunteers divided into groups receiving rTMS on either the PC or DLPFC during a standardized episodic memory task involving the encoding and retrieval of visual scenes. Event-related rTMS trains (20 Hz, 500 ms duration) were delivered coincident with the initial phases of stimulus presentation. The PC stimulation sites were targeted using neuronavigation based on individual MRI or Talairach coordinates. To assess intensity dependence, a subgroup received higher-intensity PC stimulation (120% of motor threshold). Additionally, a separate control experiment tested the effect of PC-rTMS on a purely visuospatial attention task to determine if stimulation impaired attention rather than memory specifically. The results demonstrated a clear dissociation between PFC and PC roles. In the DLPFC group, rTMS produced specific hemispheric interference consistent with the Hemispheric Encoding Retrieval Asymmetry (HERA) model: left DLPFC stimulation disrupted encoding, while right DLPFC stimulation disrupted retrieval. In contrast, PC-rTMS had negligible effects on memory performance. Neither standard intensity (90% motor threshold) nor higher intensity (120%) caused specific deficits in encoding or retrieval. High-intensity PC stimulation resulted only in non-specific performance declines across all conditions, likely due to distraction from stimulation noise. However, in the attention control task, right PC-rTMS significantly lengthened reaction times, indicating that the stimulation effectively disrupted visuospatial attention processes. The study concludes that, unlike the DLPFC, the intraparietal sulcus is not causally engaged in the encoding and retrieval of visual episodic memories. The authors suggest that parietal activations observed in functional imaging studies likely reflect the engagement of a widespread attentional network rather than direct memory processing. Because this network is distributed, interfering with a single parietal node is insufficient to disrupt memory performance, whereas disrupting the more specialized PFC nodes directly impairs memory functions. This finding clarifies the functional architecture of episodic memory, distinguishing between causal memory mechanisms and supportive attentional processes.

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• prospective memory interruptions