Editing Vegetative state (section)

=== Diagnostic experiments ===
Researchers have begun to use functional neuroimaging studies to study implicit cognitive processing in patients with a clinical diagnosis of persistent vegetative state. Activations in response to sensory stimuli with [[positron emission tomography]] (PET), [[functional magnetic resonance imaging]] (fMRI), and [[electrophysiological]] methods can provide information on the presence, degree, and location of any residual brain function. However, use of these techniques in people with severe brain damage is methodologically, clinically, and theoretically complex and needs careful quantitative analysis and interpretation.

For example, PET studies have shown the identification of residual cognitive function in persistent vegetative state. That is, an external stimulation, such as a painful stimulus, still activates "primary" sensory cortices in these patients but these areas are functionally disconnected from "higher order" associative areas needed for awareness. These results show that parts of the [[Cerebral cortex|cortex]] are indeed still functioning in "vegetative" patients.<ref>{{cite journal | vauthors = Matsuda W, Matsumura A, Komatsu Y, Yanaka K, Nose T | title = Awakenings from persistent vegetative state: report of three cases with parkinsonism and brain stem lesions on MRI | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 74 | issue = 11 | pages = 1571–73 | date = November 2003 | pmid = 14617720 | pmc = 1738238 | doi = 10.1136/jnnp.74.11.1571 }}</ref>

In addition, other PET studies have revealed preserved and consistent responses in predicted regions of [[auditory cortex]] in response to intelligible speech stimuli. Moreover, a preliminary [[fMRI]] examination revealed partially intact responses to semantically ambiguous stimuli, which are known to tap higher aspects of speech comprehension.<ref>{{cite journal | vauthors = Boly M, Faymonville ME, Peigneux P, Lambermont B, Damas P, Del Fiore G, Degueldre C, Franck G, Luxen A, Lamy M, Moonen G, Maquet P, Laureys S | display-authors = 6 | title = Auditory processing in severely brain injured patients: differences between the minimally conscious state and the persistent vegetative state | journal = Archives of Neurology | volume = 61 | issue = 2 | pages = 233–38 | date = February 2004 | pmid = 14967772 | doi = 10.1001/archneur.61.2.233 | doi-access = free }}</ref>

Furthermore, several studies have used PET to assess the central processing of [[Poison|noxious]] [[somatosensory]] stimuli in patients in PVS. Noxious somatosensory stimulation activated [[midbrain]], contralateral [[thalamus]], and [[primary somatosensory cortex]] in each and every PVS patient, even in the absence of detectable cortical [[evoked potential]]s. Somatosensory stimulation of PVS patients, at intensities that elicited pain in controls, resulted in increased neuronal activity in primary somatosensory cortex, even if resting brain metabolism was severely impaired. However, this activation of primary cortex seems to be isolated and dissociated from higher-order associative cortices.<ref name="pmid12377148">{{cite journal | vauthors = Laureys S, Faymonville ME, Peigneux P, Damas P, Lambermont B, Del Fiore G, Degueldre C, Aerts J, Luxen A, Franck G, Lamy M, Moonen G, Maquet P | title = Cortical processing of noxious somatosensory stimuli in the persistent vegetative state | journal = NeuroImage | volume = 17 | issue = 2 | pages = 732–41 | date = October 2002 | pmid = 12377148 | doi = 10.1006/nimg.2002.1236 | s2cid = 16891079 }}</ref>

Also, there is evidence of partially functional cerebral regions in catastrophically injured brains. To study five patients in PVS with different behavioral features, researchers employed PET, MRI and [[magnetoencephalographic]] (MEG) responses to sensory stimulation. In three of the five patients, co-registered [[PET/MRI]] correlate areas of relatively preserved brain metabolism with isolated fragments of behavior. Two patients had had [[Hypoxia (medical)|anoxic]] injuries and demonstrated marked decreases in overall cerebral metabolism to 30–40% of normal. Two other patients with non-anoxic, multifocal brain injuries demonstrated several isolated brain regions with higher [[metabolic]] rates, that ranged up to 50–80% of normal. Nevertheless, their global metabolic rates remained <50% of normal. MEG recordings from three PVS patients provide clear evidence for the absence, abnormality or reduction of evoked responses. Despite major abnormalities, however, these data also provide evidence for localized residual activity at the [[Cerebral cortex|cortical]] level. Each patient partially preserved restricted sensory representations, as evidenced by slow evoked magnetic fields and gamma band activity. In two patients, these activations correlate with isolated behavioral patterns and metabolic activity. Remaining active regions identified in the three PVS patients with behavioral fragments appear to consist of segregated corticothalamic networks that retain connectivity and partial functional integrity. A single patient who sustained severe injury to the tegmental [[mesencephalon]] and paramedian [[thalamus]] showed widely preserved cortical metabolism, and a global average metabolic rate of 65% of normal. The relatively high preservation of cortical metabolism in this patient defines the first functional correlate of clinical–pathological reports associating permanent unconsciousness with structural damage to these regions. The specific patterns of preserved metabolic activity identified in these patients reflect novel evidence of the modular nature of individual functional networks that underlie conscious brain function. The variations in cerebral metabolism in chronic PVS patients indicate that some cerebral regions can retain partial function in catastrophically injured brains.<ref>{{cite journal | vauthors = Schiff ND, Ribary U, Moreno DR, Beattie B, Kronberg E, Blasberg R, Giacino J, McCagg C, Fins JJ, Llinás R, Plum F | display-authors = 6 | title = Residual cerebral activity and behavioural fragments can remain in the persistently vegetative brain | journal = Brain | volume = 125 | issue = Pt 6 | pages = 1210–34 | date = June 2002 | pmid = 12023311 | doi = 10.1093/brain/awf131 | doi-access = free }}</ref>