participants experienced being in the presence of another person in the asynchronous versus synchronous stimulation condition (p < 0.01) and experienced being touched by that invisible presence behind them (p < 0.01).
controlled synchrony contrast supports reported experiences, with subjective measurement and unresolved demand effects limiting inference
the FoP is an illusory own-body perception with well-defined characteristics that is associated with sensorimotor loss and caused by lesions in three distinct brain regions: temporoparietal, insular, and especially frontoparietal cortex.
small heterogeneous lesion series supports association, but only frontoparietal specificity survives comparison with matched controls
These data show that the illusion of feeling another person nearby is caused by misperceiving the source and identity of sensorimotor (tactile, proprioceptive, and motor) signals of one's own body.
robotic conflict manipulation does not independently identify source and identity attribution as the causal mechanism
only frontoparietal lesions (Brodmann area 7) were specifically associated with the FoP.
matched-control comparison supports regional specificity within a small heterogeneous series using data-derived regions
during the asynchronous (FoP-inducing) condition, participants judged a significantly higher number of people as being close to them (mean = 2.0) as compared to the synchronous condition (mean = 1.6; p < 0.01; Figure 3C).
reported condition means support the numerosity contrast without establishing that the task excludes suggestion
Derived from the full evaluation — not a separate score.
Strengths
Asynchronous robotic stimulation produces reported presence and touch-by-other experiences relative to synchronous stimulation, turning a largely clinical phenomenon into an experimentally manipulable experience.
↳ Robotically Induced FoP; Figure 3A
The lesion comparison uses patients matched for complex hallucinations, etiology, and sensorimotor deficits. It distinguishes frontoparietal specificity from the broader three-region overlap pattern.
↳ Neurology and the FoP; Figure 1
The sensorimotor interpretation is situated within body-illusion and efference-copy research. The discussion also acknowledges that heterogeneous lesion modalities require caution.
↳ Discussion, lesion limitations and efference-copy model
Limitations
The Summary attributes FoP causally to three regions even though only BA7 shows specificity against matched controls. Robotic induction demonstrates effects of conflict without independently establishing the proposed source-and-identity attribution mechanism.
↳ Summary; Neurology and the FoP; Discussion
The 12-patient series combines structural and functional lesion information and projects lesions onto one hemisphere. Regions tested against controls are derived from the FoP overlap map, limiting the independence of the localization evidence.
↳ Table 1; Neurology and the FoP; Figure 1
The task described as implicit still asks how many people participants feel nearby. This does not directly resolve expectation or demand effects as alternative explanations for the reported experience.
↳ Results, person numerosity task; Figure 3C
The main contribution is the connection between a clinical lesion-control comparison and an experimentally controllable presence experience in healthy participants. Synchronous controls and convergent self-location and numerosity outcomes support the laboratory result, but they do not uniquely establish the proposed neural attribution mechanism. The regional evidence is narrower than the Summary suggests: only frontoparietal lesions show specificity against matched controls. The discussion acknowledges that restriction and lesion heterogeneity, while the explicit numerosity question leaves demand effects unresolved. Practical relevance lies chiefly in further mechanistic research rather than a demonstrated clinical application.
Nabu’s assessment, alongside the field’s view.
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Sound3.3
Confidence mediumThe score reflects a meaningful advance from clinical descriptions and a single stimulation case to controlled robotic induction in healthy participants, alongside lesion-control comparisons. The small, selected clinical series and incomplete identification of the proposed mechanism limit the breadth of that advance.
Matched clinical controls, synchronous robotic controls, and multiple outcomes provide a coherent experimental strategy. The three-region causal conclusion exceeds the regional control comparison, and the behavioral experiments do not uniquely identify the proposed attribution mechanism.
The sequence from lesion observations to robotic induction and sensorimotor interpretation is followable. Definitive causal and neural-mechanistic wording materially overstates what that sequence establishes.
The discussion connects FoP with earlier clinical reports, body illusions, agency models, and schizophrenia research, while explicitly narrowing lesion specificity. Competing explanations receive limited comparison, and the schizophrenia connection remains analogical.
Caveats4 of 4 checks
One reported value does not reconcile, but the key claims do not rest on it.
Informed consent and conformity with the Declaration of Helsinki are declared. No supplied-text reporting or research-conduct concern is established.
Ethics approval: declared
38 of 38 checkable references verified
41 references in manuscript 3 have no canonical index record — counted, but not index-checkable 2 references confirmed by manual review
References not verified automatically are resolved manually within 24 hours.
No retraction or expression of concern found in Crossref (includes Retraction Watch).
Sources: Crossref (incl. Retraction Watch) ✓
Where this paper’s evidence sits on the path from initial observation to real-world use.
The robotic paradigm is a laboratory mechanism demonstration rather than a validated clinical tool. No operational implementation or clinical validation is reported.
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