Lately, I’ve been reading Oliver Sacks’s new-ish book Musicophilia. While it’s not quite the tour de force that The Man Who Mistook his Wife for a Hat was, it’s gotten me thinking once again about the neurology of consciousness, and after a few days’ contemplation (and a few years spent reading neurological books), I think I finally have a rough sketch for my own theory of how consciousness comes into existence. Of course, I’m not a neurologist. I don’t know the details of how all this works, and none of it is based on empirical evidence, but that’s the beauty of the Internet: you can talk about ideas abstractly. And, since that’s what I’m good at, that’s what I’m going to do. So, here goes: consciousness.
There are a few structures which are vital to conscious experience. These are:
- The thalamus
- The brainstem
- the prefrontal cortex (and the rest of the cerebral cortex as well)
The other structures are more involved in the contents of consciousness. They are the raw material that the conscious structures process. Here’s how it seems to me that consciousness happens:
- Sensory information enters via the brainstem.
- The brainstem preprocesses the information and sends it to the thalamus.
- The thalamus takes in the preprocessed sensory information and combines it with information about the state of the cortex itself.
- The thalamus relays this information to the relevant cortical structures. The prefrontal cortex may play a role here in organizing the arrival of the information, and perhaps in weighting it emotionally.
- The cortex processes the sensory information, and the prefrontal cortex reads the results and generates judgments based on emotional weighting from the limbic system. It may generate some of its own emotional reactions as well.
- The prefrontal cortex sends the interpreted brain state back to the thalamus. There may also be other loops between the thalamus and the other cortical regions.
- The processed mental state enters the thalamus, along with a new set of sensory information.
Of course, this says nothing about memory formation, which is very important for making sense of conscious awareness. It just so happens that I have a theory for how memories form as well.
- An emotional signal is sent by the amygdala (or some other part of the emotional system) to the hippocampus, which “reads” sensory information currently being process, thus forming connections between the disparate kinds of information.
- This association is stored in the temporal lobe. When the area where the memory structure is stored is activated, the temporal lobe re-activates the relevant structures (those whose particular activity patterns were linked by the hippocampus), and the remembered event is re-experienced.
I’m not really sure how a memory would be recalled in this model, though. I’d venture to guess that it’d have something to do with the prefrontal cortex sending a signal to the temporal lobe, in order to retrieve the memory for comparison to current events.
This little model (and I’ll say it again, I’m not a neurologist. Not even close, so think about this model in the spirit in which it was intended: as a useful idea, not as anything approaching a theory) does shed some useful light on certain kinds of mental illness and the effects caused by certain sorts of brain damage.
- Schizophrenia: It’s well known that in schizophrenia, the prefrontal cortex is not functioning as it should. Without a properly-functioning cortex, judgments based on memories and sensory information cannot be made properly, and sensory information does not get integrated properly. Also, the prefrontal cortex’s inhibitory connections are less functional as well, which would seem to explain not only the disorganized and unintegrated thought patterns associated with schizophrenia, but also the hallucinations, which could be the result of sensory information going to the wrong place or being integrated improperly. Or, perhaps, the hallucinations and delusions might have something to do with the fact that, without prefrontal cortical direction, the various cortical structures can no longer properly regulate their output.
- Anterograde amnesia: with damage to the hippocampus comes difficulty forming long-term memories. In this model, that would be because the structure which associates the various neural states with one another is either incapable of doing so, or else it is incapable of moving them into the temporal lobe for permanent storage.
- Thalamic coma: this may also apply to comas in general, as well as minimally-conscious states, but thsi model only really has something to say about thalamic comas. When the thalamus is damaged, not only can external sensory information not enter the cortex, but the cortical state itself is also prevented from being communicated to the cortex, so there is an absence of both sensation and cognition. The thalamus, however, is divided into two parts, one of which communicates primarily to the cortex, and the other of which is mostly responsible for preprocessing and relaying sensory information. If only the sensory-preprocessor (in the case of vision, this is the lateral geniculate nucleus) were to be damaged, the patient would still likely be able to achieve conscious awareness, but there would simply be no sensory information for them to process.
- Encephalitis lethargica: in patients with this disorder (which is, according to Oliver Sacks, an extreme form of parkinsonism), the patient is mostly functional, but they are unable to initiate much activity (if any). In this model, that would be because of damage or inactivity of the limbic system, which is crucial in communication emotional meaning to the prefrontal cortex. In patients with severe parkinsonism, there may be difficulty seeing the relevance of actions, and therefore, the actions are not generated. This can also occur with certain kind of brainstem and prefrontal lesions.
- Depression: in this disease, the prefrontal cortex is known to be less active. However, unlike in schizophrenia, its integrative functions must still be intact. However, its emotional functions become impaired, leading to difficulty forming memories (since the PFC cannot communicate the emotional necessity of remembering something to the hippocampus, and would likely have difficulty sending retrieval signals, too), lack of motivation (since the significance of actions would become unclear), and depressed mood or flat affect (since everything would have the same emotional significance).
I won’t go any further, for fear of over-inflating my ego and for starting to make claims that I have no hope of arguing for. But this, I think, is at least something to get people thinking. Of course, there are a billion things that I haven’t taken into account: the left versus right hemisphere functional disparity, the effects of neurotransmitters, and no doubt I’ve left out quite a few very important brain structures.