It is well understood that a significant amount of patients in a vegetative or minimally-conscious state are covertly aware and capable of cognitive function despite an absence of motor function, but the mechanism behind this dissociation has yet to be uncovered.

Now, research published in JAMA Neurology provides evidence of a possible biomarker for the absence of intentional movement in covertly aware patients, and may provide a new target for restorative therapies.

Davinia Fernández-Espejo, PhD, of the University of Western Ontario, and colleagues used a novel analysis combining dynamic causal modeling (DCM) of functional MRI and diffusion tensor imaging to analyze the functional integrity of cerebral networks that support voluntary motor imagery and motor execution. They conducted a case-control study consisting of two patients with severe brain injury and 15 healthy controls.

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Imaging data from the controls revealed that motor execution was associated with excitatory coupling between the thalamus and primary motor cortex (Bayesian model selection; winning model Bayes factors >17), in contrast to mental imagery. A selective structural disruption in fibers connecting the two regions was observed in the patient who fulfilled all criteria for the vegetative state (fractional anisotropy, 0.294; P = .047), but not in the patient with similar clinical variables but who was capable of behavioral command following (fractional anisotropy, 0.413; P = .35).

The results indicate that specific damage to motor thalamocortical fibers could serve as a possible biomarker for the absence of intentional movement in covertly aware patients. They also emphasize the role of the thalamus in execution of intentional movement, in turn suggesting a target for restorative therapies for behaviorally non-responsive patients.

The research also provides evidence for the identification of these patients as a distinct category, as noted in a related editorial.


  1. Fernández-Espejo D et al. JAMA Neurol. 2015; doi:10.1001/jamaneurol.2015.2614.
  2. Schiff ND. JAMA Neurol. 2015; doi:10.1001/jamaneurol.2015.2899.