Yaakov Stern is a professor of clinical neuropsychology in the Departments of Neurology, Psychiatry, and Psychology at the Taub Institute for the Research on Alzheimer’s Disease and the Aging Brain, at Columbia University College of Physicians and Surgeons. Dr. Stern also directs the Cognitive Neuroscience Division of the Sergievsky Center and is the director of neuropsychology for the Memory Disorders Clinic at the New York State Psychiatric Institute.
Stern's research focuses on a concept called cognitive reserve, which accounts for the individual differences in task performance, specifically why some individuals show more cognitive deficit than others given the same degree of brain pathology from Alzheimer's disease or given the same amount of sleep deprivation. Stern also studies potential non-pharmacologic interventions that might improve cognition in normal aging processes.
Dr. Stern received his PhD in 1983 from the Experimental Cognition Program at City University of New York. He has served on the editorial board of the journals Neuropsychology; and Aging Neuropsychology and Cognition. He is currently on the editorial board of The Journal of Clinical and Experimental Neuropsychology and is associate editor of the Journal of the International Neuropsychological Society.
Question: What did your research reveal about how the brain copes with a lack of sleep?
Yaakov Stern: So the main idea – the main way we did this study was we image people in the scanner before and after 48 hours of sleep deprivation and one of the primary tasks we used was the one that I just described. I’ll say it again, that people saw one, three or six letters for a few seconds, they wait a set of seconds, a probe letter came up and they had to decide whether that was one of the letters that had been presented to them. so we gave them the exact same task pre and post and what we found behaviorally was that people were slower and sometimes, maybe 20% of the time, they didn’t respond within the time limit. And then we image them with FMRI while they were doing that and we could look during the stimulus phase or the retention phase or the probe phase. When they saw the letters, while they were retaining the letters, or when we asked them, was that one that you saw? What was going on in their brain.
The way that we approach looking at these data is a little different than other a labs. So what we do is, first of all, we’re interested in what changes from pre to post sleep deprivation. And we look at the brain as a whole rather than look at a particular area of the brain. We try to find a set of brain areas that are working together and we call that a network. It’s not a network like a neurophysiologist would. One neuron wired to another to another. But because it’s a set of areas that worked together, we call it a network. So we look at a brain network that reduced its activity from pre to post sleep deprivation.
And the other thing were interested in was could we find a network that – where that happened in every single person. And the thing that we were hoping for was if we found such a network that the people who did worse after sleep deprivation would show more of a loss in the use of that network than the others. And that’s what we identified. So we identified this brain network. So some of the areas that were – the areas I showed reduced activation were in the back of the head, some occipital areas and some parietal areas. Some of the areas that sort of maintained activation or sometimes increased with sleep deprivation **** sort of like a fulcrum this network, were towards the front of the head.
So we identified this network that the more it reduced it’s activation from pre to post sleep deprivation, those people who showed more of a reduction were the ones who did the worst.
So in a sense, we solved the first problem, we found something in the brain – that was going on in the brain that was associated with differential susceptibility to sleep deprivation. That was already quite in advance, nobody really had a handle on that. The truth is that it is very hard that if you just looked at someone or talked to them to predict whether they can handle sleep derivation very well or not. Not matter what they tell you.
Then what we tried to do was say, okay are we just seeing something on imaging or is it something that really has to do with people’s behavior. And that’s where we used the Transcranial Magnetic Stimulation. So the idea was that with TMS, depending on the – what you’re doing is giving these pulses of magnetism, pretty intense. You can focus what area of the brain you put it on, and depending on the frequency, you can either stimulate that area or inhibit function in that area. So we picked an area that showed reduction post sleep deprivation and we tried to stimulate it. And our hope was that if we stimulated that area, we could improve people’s performance. And we focused on the occipital and the parietal areas that seemed to show the most reduction. And what we found, which was surprising to me was that, first of all, the stimulation to the occipital area did help people respond a little faster compared to some other area that had nothing to do with the network. And the people who benefited most from that stimulation were the people who had showed the most reduction in the network, which is another confirmation that we were finding something interesting.
So I found that quite surprising. Now, it’s not a cure for sleep deprivation, it was only while we were stimulating and while they were performing that task. So to imagine, let’s say you could really bring that into real life, you’d have to imagine like a truck driver who is very sleepy having a magnetic stimulator on their head, so I don’t think that it is very practical. But it was an idea of showing that we have this brain network, maybe we could intervene in other ways. The kinds of things we thought about if we were to continue that line of research would be, maybe we could train people using feedback to actually using the kind of neuro biofeedback to actually use that network more effectively. So if they were feeling tired, maybe they could actually, by themselves, up regulate that network.
Then the final experiment that we did was even more dramatic. What we did is we did the exact same thing, we sleep deprived people for 48 hours, but twice a day during the two days of sleep deprivation, they did this memory task that I described and they got stimulation to that brain area while they were doing the memory task. And some people got that stimulation and some were in like a placebo group, they didn’t get it. And overall, we didn’t see a huge difference between this TMS treat – it was like a drug study really, but using TMS. We didn’t see a huge difference between the treated group and the untreated group, but on some very specific measures we did see some differential improvement in the TMS group. And why that’s interesting is that we were – the post testing wasn’t done while they were getting TMS, so there was a more long-term relationship. So perhaps getting that four sessions of stimulation actually helped these people regulate this network a little better.