| Literature DB >> 12534245 |
Steven Laureys1, Sylvie Antoine, Melanie Boly, Sandra Elincx, Marie-Elisabeth Faymonville, Jacques Berré, Bernard Sadzot, Martine Ferring, Xavier De Tiège, Patrick van Bogaert, Isabelle Hansen, Pierre Damas, Nicolas Mavroudakis, Bernard Lambermont, Guy Del Fiore, Joël Aerts, Christian Degueldre, Christophe Phillips, George Franck, Jean-Louis Vincent, Maurice Lamy, André Luxen, Gustave Moonen, Serge Goldman, Pierre Maquet.
Abstract
Positron emission tomography (PET) techniques represent a useful tool to better understand the residual brain function in vegetative state patients. It has been shown that overall cerebral metabolic rates for glucose are massively reduced in this condition. However, the recovery of consciousness from vegetative state is not always associated with substantial changes in global metabolism. This finding led us to hypothesize that some vegetative patients are unconscious not just because of a global loss of neuronal function, but rather due to an altered activity in some critical brain regions and to the abolished functional connections between them. We used voxel-based Statistical Parametric Mapping (SPM) approaches to characterize the functional neuroanatomy of the vegetative state. The most dysfunctional brain regions were bilateral frontal and parieto-temporal associative cortices. Despite the metabolic impairment, external stimulation still induced a significant neuronal activation (i.e., change in blood flow) in vegetative patients as shown by both auditory click stimuli and noxious somatosensory stimuli. However, this activation was limited to primary cortices and dissociated from higher-order associative cortices, thought to be necessary for conscious perception. Finally, we demonstrated that vegetative patients have impaired functional connections between distant cortical areas and between the thalami and the cortex and, more importantly, that recovery of consciousness is paralleled by a restoration of this cortico-thalamo-cortical interaction.Entities:
Mesh:
Year: 2002 PMID: 12534245
Source DB: PubMed Journal: Acta Neurol Belg ISSN: 0300-9009 Impact factor: 2.396