Preliminary data has shown that overall cerebral metabolism is less than in those with conscious awareness (20–40% of normal[3]) and is slightly higher but comparable to those in vegetative states.

There were also more cortiocortical functional connectivity between the auditory cortex and a large network of temporal and prefrontal cortices in MCS than vegetative states.

The DTI maps showed that there was significant reduction of volume in the medial corpus callosum and other parts of the brain compared to normal subjects.

They also found markedly lower diffusion values in white matter and increased cerebral spinal fluid compartments.

Cortical injuries at this level provides a particular favorable environment for sprouting of new axons to occur in the intact areas of the cortex, which may explain some of the greater recovery rates in minimally conscious state patients.

These findings support the efforts to prospectively and longitudinally characterize neuroplasticity in both brain structure and function following severe injuries.

Utilizing DTI and other neuroimaging techniques may further shed light on the debates on long-distance cortical rewiring and may lead to better rehabilitation strategies.

[5] Some areas of the brain that are correlated with the subjective experience of pain were activated in MCS patients when noxious stimulation was present.

[6] A functional magnetic resonance imaging (fMRI) study found that minimally conscious state patients showed activation in auditory networks when they heard narratives with personally meaningful content to them, by a familiar voice.

One of the more common diagnostic errors involving disorders of consciousness is mistaking MCS for VS which may lead to serious repercussions related to clinical management.

fMRI scans showed preservation of a large-scale, bi-hemispheric cerebral language network, which indicates that possibility for further recovery may exist.

There were longer periods of eye opening and increased responses to command stimuli as well as higher scores on the JFK coma recovery scale (CRS).

The observed improvements in arousal level, motor control, and consistency of behavior could be a result of direct activation of frontal cortical and basal ganglia systems that were innervated by neurons within the thalamic association nuclei.

These neurons act as a key communication relay and form a pathway between the brainstem arousal systems and frontal lobe regions.

[12] In another case study of a 50-year-old woman who had symptoms consistent with MCS, administration of zolpidem, a sedative hypnotic drug improved the patient's condition significantly.

Without treatment, the patient showed signs of mutism, athetoid movements of the extremities, and complete dependence for all personal care.

Forty-five minutes after 5 to 10 mg of zolpidem was administered, the patient ceased the athetoid movements, regained speaking ability, and was able to self-feed.

PET scans showed that after zolpidem was administered, there was a marked increase in blood flow to areas of the brain adjacent to or distant from damaged tissues.

The fact that zolpidem is a sedative drug that induces sleep in normal people but causes arousal in a MCS patient is paradoxical.

In 1995, "Recommendations for Use of Uniform Nomenclature Pertinent to Patients With Severe Alterations in Consciousness" was published by the American Congress of Rehabilitation Medicine (ACRM).

By definition, patients who are unconscious or are minimally conscious are incapable of giving informed consent which is required for participation in clinical research.

[4] The right to die in patients with severe cognitive impairment has developed over time because of their grave neurological state and the perceived futility of continued treatment.

[16] Fears of therapeutic adventurism has led to a disproportionate view about the under-appreciation of potential benefits and an overstatement of risks[clarification needed].

Thus, recognizing this distortion is important in order to calculate the right balance between protecting vulnerable populations that cannot provide autonomous consent and potentially restorative clinical trials.