Once a long time ago on a 10 hour drive between London, Ontario back to Montreal in my little red MGB I fell asleep driving at the wheel outside Toronto somewhere on the highway 401 near Bowmanville close to Lake Ontario. I awoke unable to interpret the visual scene before me. Tall grass was splitting away from the hood of my car, the sound was a ripping sound, as the bright green grass erupted like I was running into a large green curtain hanging from a clothesline. The high whine of a 18 wheeler truck caught my attention off to the left, above me. I then screamed out at the top of my lungs, “That truck is on the road, I’m driving in the ditch at 60 mph inside tall grass!” I was terrified of hitting something in the swoosh of parting vegetation like my body spearing into a swaying kelp field. I released my foot off the accelerator and gliding slowly started to turn toward the highway until suddenly I emerged out of the grass grabbing at the car into the moist night air. Another 18 wheeler went by with his air horns screaming at me as the car skidded through the loose gravel along the shoulder of the road until I was driving on the smooth tarmac. I was completely, uncontrollably, shaking, sweat running in currents across my face down my neck saturating my jersey back. My mind was racing, I was asleep when I woke up driving in the tall grass, the car had all on its own veered down into the ditch. I could have rolled the car or hit something and I would have never woken up. What got me was how my consciousness simply clicked off like hitting a switch, somewhere inside my brain.
Where is consciousness in our brain?
This a fundamental question, how does our brain state sense its surroundings or one’s self? Which brain centers are engaged as our aware switch is on? Anesthesia is a useful tool for studying consciousness since the level of awareness can be directly manipulated as someone emerges from anesthesia. Researchers in Finland and Sweden mainly working with the University of Turku have recently investigated this fundamental question of which brain centers are turning on as consciousness re-emerges from anesthesia. The authors reported their observations in the Journal of Neuroscience April 4, 2012 32(14):4935-4943 in: Returning from Oblivion: Imaging the Neural Core of Consciousness by Jaakko Langsjo, Michael Alkire, Kimmo Kaskinoro, Hiroki Hayama, Anu Maksimow, Kaike Kaisti, Serge Aalto, Riku Aantaa, Satu Jaaskelainen, Antti Revonsuo and Harry Scheinin. The limitations of a drug/anesthetic state is the confounding effects of the drug itself used for inducing the anesthetic unconscious state. The authors addressed these shortcomings by, “First, we used neuroimaging in conjunction with pattern analysis methodology to dissociate the state-related changes in consciousness from the global effects of anesthesia. Second, we eliminated the drug-dose change effect on consciousness by imaging a rapid return to consciousness from the unconscious state induced by the unique anesthetic agent dexmedetomidine, a selective 2-adrenergic agonist, which allows awakening during a constant dosing of the drug. Third, with neuroimaging we dissociated the drug-specific effects on consciousness by showing similar activation to arousal from anesthesia with two different drugs. ” The authors were looking for the elusive minimum of brain correlates involved with arousal into a conscious state. Instead of using functional magnetic imaging in such a short arousal time frame can be confounded in the multiple effects of behavioral sequenced transitions caused by the anesthesia, they opted for positron emission tomography to image actual brain activities associated with the varying, merging states of consciousness.
What is anesthesia? Here is the authors description, “General anesthesia is often defined as comprising pharmacologically induced unconsciousness with the loss of the ability to feel or experience anything. amnesia, loss of remembering, analgesia, loss of pain sensation, and immobility, by not moving in response to surgical stimulation.” A previous study one month before helped determine each individual volunteer’s calibration anesthetic concentration for loss of consciousnesses for this open, non randomized study. Then the specific anesthetic dexmedetomidine was compared with propofol, each given with target plasma concentrations infused until loss of consciousness was achieved, and actual blood plasma concentrations were measured using reversed-phase high performance liquid chromatography. Magnetic resonance imaging was used to generate the neuroanatomy of the brain maps. Positron emission tomography (PET) scanning injected radioactive water using brain blood flow analysis in condition related brain states employing the tracer kinetic modeling with the realigned, co-registered spatially normalized three dimensional brain space according to accepted protocols developed at the Montreal Neurological Institute. “Images were analyzed for overall patterns of condition-related regional cerebral blood flow changes using partial least squares software, ” which is according to the authors, “a muti-variate analysis technique to detect optimal co-variation between brain voxel values and the experimental design.” The authors main analysesconcerned to identify those brain areas that, “..changed their function with the changing state of consciousness, independent of the anesthetic drug effects were obtained with the dexmedetomidine group.” Their second concern were matched statistically for the scans testing changes in anesthetic drug levels. The third concern was to generalize the anesthetic effects across the other anesthetic agent, from the propofol group. The related condition, as mentioned before is the fourth concern of the authors, involving a combined anesthetic analysis of both the propofol and the dexmedetomidine rather than the drug specific effects on consciousness.
The specific statistical methods of each latent variable from the various partial least squares was determined providing the authors with evidence of the stability of their findings rather than if an effect exists by bootstrapping the reliability with calculated permutations of the standard error. Basically this technique gives a means to estimate the significance within the measured image voxels comparing regional cerebral blood flow rates without having to correct multiple comparisons, in the lingo of the imaging people, its robustness of permutations is termed ,’voxel saliences.’
Imaging of the return of consciousness event during constant concentration levels of dexmedetomidine revealed, ” The presence of a conscious state specifically related to activation in a number of brain areas including: the mid-line thalamus, hypothalamus, the locus coeruleus/parabrachial area of the brain stem, cerebellum and portions of the lateral orbital frontal and parietal lobes. The change in the state of consciousness and the ability to respond affected the parietal cortex when the volunteers on dexmedetomidine again changed from the conscious, but sedated condition, to the second tested unconscious episode showed the inferior parietal cortex was functionally connected withe the rostral anterior cingulate cortex and other frontal regions more in the conscious state compared with the unconscious state.” The arousal from propofol-induced unconsciousness showed even less neo0-cortical activation. The final combined analysis of drug-related suppression associated with anesthesia portion of their experiments revealed,”…suppressed regional brain activity in bilateral fronto-parietal regions, the precuneus/posterior cingulate, the anterior cingulate cortex in the medial pre-frontal cortex, the thalamus and in the brain stem. ”
In the authors discussion, they are answering my falling asleep, switch off question in terms of what is switched back on as the brain arises into consciousness. ” The structures that activated when consciousness resumed were the brain stem, the thalamus, the hypothalamus and the anterior cingulate cortex. These findings reveal a functional network that activates with restored consciousness to enable arousal, the subjective awareness of stimuli, and the behavioral expression of the contents of consciousness.”
So the arousal activations are in the oldest brain structures rather than being out in the more evolutionary later evolved cortex. What these authors have pointed their focus on is also how does the priming of the arousal network unite, and what are its real attributes? These arousal network structures need to be really better understood because in them is the clue for how to begin to understand the first brain response event of a serious concussion.