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The neuroanatomy of asomatognosia and somatoparaphrenia
  1. Todd E Feinberg1,2,
  2. Annalena Venneri3,4,
  3. Anna Maria Simone4,
  4. Yan Fan5,
  5. Georg Northoff6
  1. 1Albert Einstein College of Medicine, Bronx, New York, USA
  2. 2Yarmon Neurobehavior and Alzheimer's Disease Center, Beth Israel Medical Center, New York, USA
  3. 3Clinical Neuroscience Centre, University of Hull, Hull, UK
  4. 4Department of Neuroscience, University of Modena and Reggio Emilia, Modena, Italy
  5. 5Department of Psychiatry, Otto-von-Gueircke University, Magdeburg, Germany
  6. 6University of Ottawa Institute of Mental Health Research, Ottawa, Canada
  1. Correspondence to Dr Todd E Feinberg, Yarmon Neurobehavior and Alzheimer's Disease Center, Beth Israel Medical Center, First Avenue at 16th Street, New York, NY 10003, USA; tfeinber{at}chpnet.org

Abstract

Objectives Asomatognosia is broadly defined as unawareness of ownership of one's arm, while somatoparaphrenia is a subtype in which patients also display delusional misidentification and confabulation. Studies differ with regard to the underlying neuroanatomy of these syndromes.

Methods Three groups of patients with right-hemisphere strokes and left hemiplegia were analysed: G1, asomatognosia+neglect; G2, non-asomatognosia+neglect; G3, hemiplegia only. The asomatognosic group was further subdivided into somatoparaphrenia (G1-SP: asomatognosia+delusions/confabulation) and simple asomatognosia (G1-SA; asomatognosia without delusions/confabulation).

Results Patients with all forms of asomatognosia (G1) had larger lesions than non-asomatognosic patients in all sectors. While patients with or without asomatognosia had significant temporoparietal involvement, we found that the subset of patients with somatoparaphrenia had the largest lesions overall, and somatoparaphrenia cases had significantly more frontal involvement than patients with simple asomatognosia. All patients with asomotognosia (G1-SP and G1-SA) had significant medial frontal damage, suggesting that this region may play a role in the development of asomatognosia in general. Somatoparaphrenia cases also had greater orbitofrontal damage than simple asomatognosia cases, suggesting that the orbitofrontal lesion was critical in the development of somatoparaphrenia.

Conclusions Asomatognosia results from large lesions involving multiple—including temporoparietal—sectors, but the addition of medial frontal involvement appears important. The addition of orbitofrontal dysfunction distinguishes somatoparaphrenia from simple asomatognosia. The data indicate roles for the right medial and orbitofrontal regions in confabulation and self-related systems.

  • Asomatognosia
  • somatoparaphrenia
  • frontal lobes
  • confabulation
  • ego boundaries
  • cognitive neuropsychology
  • neuroanatomy
  • neuropsychiatry

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Footnotes

  • Funding This study was supported in part by The Gerald J and Dorothy R Friedman New York Foundation for Medical Research (to TEF); MIUR, the Italian Ministry for Education, University and Research (to AV); The Hope of Depression Research Foundation (HDRF) and German Research Foundation with the SFB 779 (A6) (to GN).

  • Competing interests TEF has been on the speaker's bureau or participated in CME programmes sponsored by Esai/Pfizer, Novartis and Forest Pharmaceuticals. AV has received educational grant support, travel support and speaker's fees from Novartis Pharmaceuticals. AMS has received educational fellowships from Bayer and Serono Pharmaceuticals.

  • Ethics approval Ethics approval was provided by the Comitato Etico Provinciale di Modena.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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