RESEARCH ARTICLE


Disembodied Mind: Cortical Changes Following Brainstem Injury in Patients with Locked-in Syndrome



Francesca Pistoia1, 2, *, Riccardo Cornia3, Massimiliano Conson4, Olivia Gosseries5, Antonio Carolei1, Simona Sacco1, Carlo C. Quattrocchi6, Carlo A. Mallio6, Cristina Iani7, Debora Di Mambro8, Marco Sarà8
1 Neurological Institute, Department of Biotechnological and Applied Clinical Sciences, University of L’Aquila, L’Aquila, Italy
2 Don Carlo Gnocchi ONLUS Foundation, Milan, Italy
3 Department of Biomedical, Metabolic and Neurosciences, University of Modena and Reggio Emilia, Modena, Italy
4 Neuropsychology Laboratory, Department of Psychology, Second University of Naples, Naples, Italy
5 Coma Science Group, GIGA, University of Liege, Liege, Belgium
6 Departmental Faculty of Medicine and Surgery, Unit of Diagnostic Imaging, University Campus Bio-Medico of Rome, Rome, Italy
7 Department of Communication and Economy, University of Modena and Reggio Emilia, Modena, Italy
8 Post-Coma Rehabilitation Care Unit, San Raffaele Hospital, Cassino, Italy


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© Pistoia et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Neurological Institute, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, Italy; Tel/Fax: +39.0862.433552; Mobile: +39.348.0136406; E-mail: francesca.pistoia@univaq.it


Abstract

Locked-in syndrome (LIS) following ventral brainstem damage is the most severe form of motor disability. Patients are completely entrapped in an unresponsive body despite consciousness is preserved. Although the main feature of LIS is this extreme motor impairment, minor non-motor dysfunctions such as motor imagery defects and impaired emotional recognition have been reported suggesting an alteration of embodied cognition, defined as the effects that the body and its performances may have on cognitive domains. We investigated the presence of structural cortical changes in LIS, which may account for the reported cognitive dysfunctions. For this aim, magnetic resonance imaging scans were acquired in 11 patients with LIS (6 males and 5 females; mean age: 52.3±5.2SD years; mean time interval from injury to evaluation: 9±1.2SD months) and 44 healthy control subjects matching patients for age, sex and education. Freesurfer software was used to process data and to estimate cortical volumes in LIS patients as compared to healthy subjects. Results showed a selective cortical volume loss in patients involving the superior frontal gyrus, the pars opercularis and the insular cortex in the left hemisphere, and the superior and medium frontal gyrus, the pars opercularis, the insular cortex, and the superior parietal lobule in the right hemisphere. As these structures are typically associated with the mirror neuron system, which represents the neural substrate for embodied simulation processes, our results provide neuroanatomical support for potential disembodiment in LIS.

Key words: Cognition, locked-in syndrome, magnetic Resonance (MR) imaging, ventral brainstem damage.