Mechanisms for loss of consciousness revealed

 In brain connectivity, brain injury, consciousness, Neurology, neurotransmitters, subcortical structures, unconscious processes

What happens when we lose consciousness? Are there shared neural mechanisms for deep sleep, anaesthesia, vegetative state and coma?

In 2003, I co-authored a paper (PDF) in Trends in Neuroscience (with Bernard Baars and Steven Laureys). Here, we suggested that there may be common neural mechanisms for loss of consciousness, in particular for vegetative state, coma, anaesthesia and deep sleep and, by extension, generalized epileptic seizures. In particular, we demonstrated common deactivations in fronto-parietal systems, supported by thalamocortical loops, and to some extent also temporal regions.

We also suggested that the brain changes seen in such conditions may impact on consciousness at more than one level. In particular, the parietal deactivation may signify a loss of self awareness, or selfhood. The prefrontal deactivation may in turn demonstrate a loss of voluntary action. As with any other psychological phenomena, I subscribe to the view that consciousness – this mongrel concept – is a common term for a whole hierarchy of processes from the earliest perceptual events to the latest post-behavioural experiences.

In this article, which has turned out to become increasingly cited, we also speculated that the underlying common mechanism may be a disrupted function of the thalamocortical system, or the thalamus alone. As is well known, the thalamus is a composite of nuclei that receives input from all the senses and disperses information throughout the cortex., A braun hub in the right meaning of the word. Disrupting the thalamus means disrupting widespread activation throughout the brain, and thus coordination across distance and between modules.

Now, in a paper in the renowned New England Journal of Medicine, authors Emery Brown, Ralph Lydic and (famous researcher) Nicholas Schiff explains some of the mechanisms in detail. And, suffice to say, this demonstrates that albeit there may be commonalities, the neural mechanisms for loss of consciousness differs significantly between the conditions, and even within the conditions. For example, three different anaesthetic drugs – Propofol, Dexmedetomidine and Opioids – work through quite different mechanisms, as displayed below:

Possible Neural-Circuit Mechanisms of Altered Arousal Induced by Anesthetic Agents.

Caption:

Panel A shows a GABAergic inhibitory interneuron (orange) synapsing on a pyramidal neuron (gray) receiving excitatory inputs from ascending arousal pathways. The monoaminergic pathways arise from the locus ceruleus, which releases norepinephrine; the raphe, which releases serotonin; the tuberomammillary nucleus, which releases histamine; and the ventral teg- mental area, which releases dopamine. The cholinergic pathways, which release acetylcholine, arise from the basal forebrain, the lateral dorsal tegmental nuclei, and the pedunculopontine tegmental nuclei. Lateral hypo- thalamic neurons release orexin. Propofol binds post- synaptically and enhances GABAergic inhibition, counter- acting arousal inputs to the pyramidal neuron, decreasing its excitatory activity, and contributing to unconscious- ness. Dexmedetomidine binds to α2 receptors on neu- rons from the locus ceruleus, inhibiting norepineph- rine release (dashed line) in the ventrolateral preoptic nucleus, as shown in Panel B. The disinhibited ventro- lateral preoptic nucleus reduces arousal by means of GABAA-mediated and galanin-mediated inhibition of the midbrain, hypothalamic, and pontine arousal nuclei. As shown in Panel C, opioids reduce arousal by inhibit- ing the release of acetylcholine from neurons projecting from the lateral dorsal and pedunculopontine tegmen- tal nuclei to the medial pontine reticular formation and to the thalamus, by binding to opioid receptors in the periaqueductal gray and rostral ventral medulla, and by binding presynaptically and postsynaptically to spinal cord opioid receptors at the synapses between periph- eral afferent neurons in the dorsal-root ganglion and projecting neurons.

While these authors work out the neural mechanisms of loss of consciousness in these different conditions, the next necessary step will be to develop ideas on how this relates to the symptomalogy of the conditions. In particular, we need to know about whether – to any extent – there are differences in mental functioning in these conditions, and in how they are reflected in similarities and differences in neural mechanisms. As always, new ground-breaking work, like the one by Schiff and colleagues, leaves open large explanatory holes that need to be mended.

-Thomas

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