Neural Correlate of Consciousness (NCC) #1: The Left Medial Parabrachial Nuclei

My investigation found that the location of the brain most likely to be foundationally responsible for the generation of consciousness is the brainstem’s left-medial parabrachial nuclei (mPBN) of the pons, as both a starting point and sine qua non of its generation. The following will walk through the evidence of why I believe this to be the case, which follows on from Mark Solms’s hypothesis outlined in his book The Hidden Spring: A Journey to the Source of Consciousness. Here, he builds a strong case for consciousness arising from the brainstem’s Reticular Activating System (RAS) and Periaqueductal Grey (PAG).

In doing so, he presents many studies as converging evidence from disparate sources to make his argument about where in the brain consciousness ultimately arises from, and a few of these studies will be shared here.

Perhaps the most convincing (as well as heartwarming) of the cases regarding what region of the brain is minimally sufficient to facilitate the generation of consciousness, was the case of a 3-year-old girl born with a clinical condition called hydranencephaly. People with this condition are born without a cerebrum or forebrain, and only with a brainstem and cerebellum. If one were to adhere to the predictions made from cerebrum focused models of consciousness38 (such as Higher Order Theories (HOTs) Global Neuronal Workspace, Integrated Information Theory (IIT), and Re-entry and Predictive Processing theories), one would predict that this girl would not have any conscious experience at all. However, this does not seem to be the case. She responds very emotionally to stimuli that would be expected for any 3-year-old, such as “expressing pleasure through smiling and laughter, and aversion by fussing… crying… [with] their faces being animated by these emotional states”(fig. 3). Reference:
Merker, 2007.

As Solms puts it, “it’s not only that she’s awake, but there’s a reactive mind with feelings and content”40. This is very strong evidence that there’s still a sense of subjective experience occurring within these people, despite not having any forebrain at all. Decorticated rats and other mammals also retain the capacity for the usual behaviours that are indicative of the animal being conscious39.Arguments denying that there’s any sentience present within these decorticated cases would seem to only rely on solipsistic appeals40, or a reductive-anthropomorphized definition of consciousness as strictly being the higher-order cognitive self-awareness inherent to human beings.

Conscious experience can occur without the cerebrum; therefore, consciousness isn’t foundationally dependent on these higher cortical structures, and it must be generated much deeper in both our anatomical and phylogenetic brain: somewhere within the brainstem or the cerebellum. This finding simultaneously narrows down the search while falsifying any cerebrum based NCC’s, unless one chooses to deny that the above-mentioned girl – or any other such cases- are conscious.

Another way to find NCC’s is by finding what causes consciousness to switch off, such as the state of being comatose. Solms leverages lesion and coma studies to further narrow down what locations are ultimately necessary for the generation of consciousness; if they weren’t necessary, then a lesion to the affected area wouldn’t disrupt consciousness and it would continue on being generated elsewhere. Using such studies, he narrows it down to the brainstem’s RAS (whose functional operationality is used in the determination of “Brain Death” within medical contexts42), but highlights a region within the Pons called the Parabrachial Nuclei(PBN) – this specific region is the area of the brain stem where the smallest lesions “cause a total loss of consciousness”36,43,44. Critiques coming from cerebrum-based proprietors, such as Koch, claim that this region only enables consciousness but “are not content providers”45,however Solms rebukes this quite effectively by pointing out that hydranencephaly patients clearly demonstrate the ‘contents’ of affective qualia36.

Upon learning this, I became curious about the PBN – what exactly is so special about its component parts or networks that make it critically important to the generation of consciousness? Upon looking for a differentiating factor, I found that only lesions in the medial PBN sub-region (mPBN)cause coma, and this asymmetrically only applies to the left-side rather than the right46,47. This demonstrates that the mPBN is necessary as a sine qua non to the generation of consciousness. Further studies found that electrically stimulating this region’s glutamatergic neurons causes wakefulness from sleep, more essentially so when compared with other wakefulness related clusters in the brainstem48,49, while others found stimulation even caused emergence from anesthetic unconsciousness50,51. These studies provide evidence that these neurons are ‘sufficient’ for the generation of consciousness.

Upon investigating the neural morphology, there didn’t seem to be any unique characteristic differences within these types of neurons other than a relatively higher density of grey matter, indicating the abundance of dendritic connections52. What’s more interesting however was its associated network of connections: the PBN has been described by various neuroscience researchers as a “general alarm system” for pain and aversion, and a “major hub” for receiving inputs from all primary internal and external sensory systems53,54,55. Furthermore, photoactivation of a certain type of glutamatergic PBN neurons alongside giving mice a novel stimulus is enough to create a “fear memory” for the stimulus, and when these same neurons are chemically deactivated, the mice become “relativelyfearless”55; this demonstrates that these neurons are capable of at least generating the qualitative content of ‘fear’, rather than simply being responsible for ‘contentless arousal’.

Given the above evidence, I hypothesize that the reason this particular location of the left mPBN should be crucial to consciousness among all other regions of the brain, is due to it having a fundamental role in the modulation of arousal, serving a dual purpose of modulating both sleep/wake cycles and the arousal of homeostatic inputs into phenomenological experience. Lesions in this area likely cause coma because it disrupts the underlying mechanism primarily responsible for conscious arousal, debilitating both sleep and conscious wakefulness, as evident by the coma and anesthetic state being physiologically different to sleep itself56. In short, it serves as a ‘gate-keeper’ being chiefly responsible for modulating signals into phenomenological experience, and the existing research already supports it as being a strong contender for a clear NCC, in terms of locations in the brain. 

However, at this point in my investigation I was still unsatisfied as there didn’t seem to be an evident mechanism to explain how this ‘arousal into conscious experience’ actually occurs. I was looking for a physiological-based mechanism that could account for this generation; action potentials are constantly firing (in a standard Hodgkin’s and Huxley sense56)across the entire brain in other terminating locations and don’t necessarily generate consciousness. Therefore, while perhaps being necessary, action potential firings and terminating neuronal networks did not seem sufficient in themselves to explain how experience arises – there must be another factor.