With sad fondness, I post the email conversation I had with the late Dr. Behrendt.
When the EMMOSE idea occurred to me in 2013, I started exploring the literature, to find who had already started publishing. I found the late Gerald Edelman's book "The Remembered Present", which demonstrated that the hippocampus had the requisite 're-entrant' anatomy which would allow for buffering and binding of information into an experience.
But the only actual model that I could find belonged to Ralf-Peter Behrendt. He was a German-born psychiatrist, working in the UK, especially with aging and schizophrenic patients. In 2010, he published (what I think is) his first paper linking consciousness to the hippocampus. And in 2013, he published a working anatomical model, which is the first paper of his I found.
We began our conversation in 2013, and continued it until 2018, when I stopped hearing back from him. I was afraid I had said something wrong; offended him. It wasn't until 2021 that I found a death notice. I was always hoping to meet Ralf in person, and of course to interview him for the film. But also, I was sad because I felt I had lost a brother. We saw this problem the same way, and that connected us, across our differences.
We absolutely did have differences about our respective models, which will play out in the conversation below. We even both published journal responses to each other, which I'll attach at the end.
Those theoretical differences led me to feel I had to publish my paper, as well. There were elements (like the perception of mind and body) which I felt needed to be directly addressed. I hope that, despite some differences, Ralf's model and mine can be read as complementary literature. At least we agree on the pre-hippocampal story.
Of course, I am posting these emails without Ralf's permission, my apologies. But I don't think there's anything in here that would embarrass him in any way. I'm sure he would've been fine with this. If I'm wrong, then I owe you one, Ralf.
Hi Ralf,
Thank you for your reply.
I agree that a good deal of life probably happens without the person ever responding to the new memory simulation being created in the hippocampus. Driving mind is the most obvious example, since it happens during a dangerous activity, but I'm sure that there many stretches of daily life where inner and outer life are similarly divorced, from seconds to tens of minutes, if not more. Probably a great deal of assembly line factory work is done 'unconsciously'.
However, that's a tricky assertion to make in a paper, because I don't know where I'd get a citation for it.
I agree; it seems necessary that someone with complete bilateral hippocampal damage MUST have a different subjective experience, whether or not we're right about consciousness being an output of the hippocampus, just because the hippocampus (and previous memories) bring so much to the visual scene. However, finding some such statement in the literature is proving very difficult. Mostly the statements are along the lines of "other than memory, all cognitive function seems intact" or "his personality didn't seem to change much". Our most skeptical referee claimed that he had had plenty of experience with such patients, and they clearly had "subjective experience". I don't know what that referee was referring to, and so I have a hard time imagining how to convince him otherwise.
My current argument in the paper is: when it comes to immediate interaction with the world, our neocortex is not dealing with the hippocampal representation; rather, it's working from it's own representations, and then sending evidence of 'what happened' to the MTL for binding into memory, which is of course, what we remember as the interaction, even though the real (neocortex) interaction happened prior to the memory. It's only when we introspect or recall that we are specifically engaging the neocortex with the memory encode. That's my argument, but it's filled with assertion, and no reference.
In social life, I think we move quickly back and forth between the two representations, engaging in the conversation with the neocortex and then using the hippocampal simulation to ask one's self: how am I seen? did I say the right thing? what was that look on her face? how's he going to respond? etc.
In the case of anosognosia for hemiplegia (I'm guessing), the patient's neocortex is "aware" that one half the body is non-responsive, but the pathways which should get that information to the MTL are off-line, and so it never makes it to memory. When the doctor asks the patient to move, and then asks him if he did move, he is asking the patient to introspect upon a brand new memory, and that memory was created predictively, with the movement built in. However, it is only while consulting the MTL representation of self-and-body that the patient would try to move, because the rest of the time, it's abundantly clear that they can't move. Behavior arises from neocortex alone, but belief is based upon memory (flavored, of course, with semantic assumptive bias). That's the most reasonable explanation I can think of, but I certainly can't test it without access to such patients.
Same of course with hippocampal-damaged patients. If every speculation in a paper needs to be sourced, but no one has yet asked the questions experimentally, it makes it hard to get references.
As for HM, I read just the other day that small bits of his hippocampus were left in place, but they were isolated from their connections to other brain regions, so they were functionally moot.
I'm curious how you deal with HM viz. your "appetitive behaviors" paper. If the vmPFC is conditioned to the situation, as presented by the MTL, then what happens when there is no MTL? It seems like something must change, because the information flow has been cut.
Maybe that answer is in the last couple sentences of your most recent e-mail, about "it is bound to reduce the adaptability of behaviors...", etc. At the least, that gives a fair list of testable hypotheses, of probable subtle changes to look for, when testing this patient population. I hope we can get to the point where someone with access to these patients takes this theory seriously enough to test for these changes, because I haven't found any evidence that these tests have yet taken place. (And as I am learning about academic papers, nothing is considered worth listening to, unless someone else in a lab has said it first).
best,
matt faw