Shannon Delaney, MD
Neuropsychiatrist, Assistant Professor of Psychiatry
Director, Child and Adolescent Evaluation, Lyme & Tick-borne Disease Research Center
Columbia University Medical Center
Dr. Delaney is a neuropsychiatrist at Columbia University Irving Medical Center who is co-director with Dr. Fallon of the Cohen Center for Health and Recovery from Lyme and Tickborne Diseases. She completed her NIH-sponsored research fellowship at Columbia University in 2017. Her clinical research has focused on immune and infectious contributions to psychiatric disease, especially psychosis in children and young adults. She specializes in seeing children and adults with complex neuropsychiatric presentations, especially those with suspected Lyme disease or other tickborne diseases, as well as those with Pediatric Acute onset Neuropsychiatric Syndrome (PANS).
Interview with Dr. Shannon Delaney on Lyme and PANS
Anna Conkey: So thank you so much for taking the time to be here with me today Dr. Delaney. I really appreciate your time and your willingness to be interviewed. Can you please tell us about how you became interested in specializing in Lyme and then also about your interest in PANS?
Dr. Delaney: I’m a child and adolescent psychiatrist. We complete an adult residency in psychiatry and I did that at one of the Harvard programs in Boston. During my residency, and then later on during my fellowship, when I specialized in seeing kids in child psychiatry, we would all always encounter really complicated cases. Oftentimes in the hospital when we were serving the consultation liaison role, there’d be these chronic complicated sick medical cases. The doctors would do a multimillion dollar workup and nothing would come up positive. They didn’t know what to do with the patient, but the patient is in the hospital and sick, so they would call the psychiatrist. The patients were never fine seeing the psychiatrist because they felt as if their medical symptoms were being dismissed in some way. I was part of that psychiatry team all during my training, and it felt as if the psychiatry team or the attending psychiatrist would frequently have more of a psychoanalytical way they viewed the case. We would see somebody who was clearly very sick, and then they would sometimes attribute these symptoms to a psychological or somatic cause. I never agreed with that assessment, and it actually bothered me quite a bit that we’re giving some sort of psychiatric or psychological diagnosis to a situation that I felt was a very complicated medical scenario that science just didn’t have answers for. I just became very passionate about this because it wasn’t like a one off. It’s not like I saw one case and that’s it. We would encounter complicated cases like this all the time. I saw this in my adult residency, then I saw the same variation playing out from the child psychiatry perspective during my fellowship. That’s when I decided that I really needed to go into research to kind of better understand the questions and answers. Also, when I was an intern, this was the time when NMDA receptor antibody encephalitis was just being discovered in 2009, I think. There’s a case where most of those patients present initially with psychiatric symptoms, often psychosis. I thought it was really fascinating that we actually had a medical condition with a very specific neurobiology that was presenting with primarily psychiatric symptoms because like that’s kind of unknown in the psychiatric world. I started thinking there are probably a lot of patients out there with psychosis, who are hospitalized in mental institutions that have this underlying biological contributor to their psychiatric illness and they’re not getting appropriate treatment. It was really that happening while I was in my training, also encountering all these cases, that very, very much like got me going and made me passionate. At the same time, PANS/PANDAS was becoming more of a thing too.
I would say all of those things sort of steered me in the direction of doing more research. After I completed my clinical psychiatry fellowship, which was two years at Columbia Cornell, I stayed on at Columbia and did a research fellowship where I was really interested in psychosis and autoimmune and infectious origins of psychosis. I did a study where I recruited patients with psychosis. During that time, I needed a mentor and I found Dr. Brian Fallon, who was doing work with Lyme disease. As my mentor, I learned a lot about Lyme disease during that time. When I finished the fellowship, I got offered a job to stay on.
Anna Conkey: There is a great deal of controversy around Lyme–specifically chronic Lyme versus post-Lyme syndromes. What is happening research wise that will shed light on exactly what is happening in some of these very ill patients?
Dr. Delaney: Our center at Columbia–we’ve been a dedicated research center for a long time, and it’s just now that we’re kind of exploring into the clinical realm of things. We’re very excited because we’re just starting a new clinical trials network as well. Currently, we have a disulfiram trial where we recruit patients who have persistent symptoms related to Lyme disease. We’ll be starting a Vagus Nerve Stimulation study which will obviously help target theorized inflammation that may or may not be contributing to some of the symptoms and people who have persistent symptoms related to Lyme disease.
So what is the underlying etiology that’s leading to the person’s persistence? A lot of people in the infectious disease world don’t like to refer to it as chronic Lyme disease because imply that there’s an active infection to some degree. I would say, the jury’s out in terms of the science about what’s contributing to patients persistent symptoms. I don’t think anyone knows but I think that the general consensus is that it’s probably some combination of persistent infection, as well as a post-infectious immune dysregulation process that’s occurring, and I wish I could say we have blood tests that we could do to say “okay, you have 30% active infection and you have 70% immune dysregulation,” but we don’t have that science worked out at this point. In my opinion it’s a mix of both that’s going on. And I would support that by citing the difficulty with studying this in human beings that have persistent symptoms related to Lyme disease. I think that the primary problem in trying to better understand the science is that we do not have any diagnostic tests right now to determine if someone has active infection and that is a huge problem. I think that is the singular reason that contributes to the cause of the controversy because you don’t have a test that can indicate or prove an active infection. That means you have a whole group of patients that had evidence of having a particular infection and have a similar like constellation of symptoms, but how do you prove that that you are linked? Certainly, if you have people who are more clinically minded and use their clinical judgment, then they put those two together, but if you have others who have a more rigid research perspective, an “I don’t believe in anything until I can see the proof” kind of viewpoint then that’s very difficult because this is a land where we don’t have that objective evidence yet. The reason that I think that active infection is playing a big role in most patients is because if you look at a lot of the animal studies, they will give the animals they will expose them to Borrelia burgdorferi bacteria and then they will give them standard treatment, such as treatment that’s recommended for humans for like three weeks. Then, they will follow the animals down the road and see which animals develop persistent symptoms related to Lyme disease and then eventually they will sacrifice the animals and they will actually find evidence of the bacteria Borrelia burgdorferi in all different places throughout their body, even after they have received standard treatment. So, it’s clear and the only reason they can do that is because they’re sacrificing the animals and which they we can’t do with human beings. There is multitudinous evidence in the scientific literature when it comes to mice, monkeys, multiple different animal models showing evidence of persistent infection after standard treatment in all of these animals. So my perspective is why wouldn’t similar things be happening in the human being, especially when we’re seeing clinical symptoms suggestive of it?
Anna Conkey: It is widely known that roughly one third of individuals who have had a positive strep culture will not show positive serum antibody titers. Is the same true in Lyme? Is this one of the reasons for the controversy and ambiguity?
Dr. Delaney: So, what I indicated before is the biggest problem that we have is that there’s no test for active infection. The tests that we do have are poorly sensitive, so that means that we’re probably missing a lot of patients that from a clinical standpoint have had Lyme disease. The other problem is that there’s a lot of inter-lab variability. That’s the reason we send people’s blood to a few different labs just so we can kind of get the full picture. If you ask me, if you take one person and you did a very comprehensive testing for Lyme disease, I would say most of the people we see, for example, have a pretty strong sort of laboratory indication for Lyme disease. If we’re doing a very robust panel in terms of testing, is that how the average Lyme patient is treated and diagnosed? The answer is no. So, I think a lot of patients with Lyme disease out there get missed because they only get a Lyme ELISA done. And if it’s negative, it never gets reflexed to Western Blot. Then maybe their doctor will say no, you don’t have Lyme disease and never repeat the testing or maybe they won’t even do the testing in the first place. We just know that we can’t trust isolated singular tests from one particular lab. It’s not like one lab is necessarily superior either. We just see variability across the board.
Anna Conkey: What is the gold standard for testing for Lyme disease and other tickborne illnesses today?
Dr. Delaney: When people come to us, we want to do a comprehensive evaluation and we send their blood to a few different labs. What would I recommend if you only have one lab? I would do a Lyme C6 peptide ELISA test through Medical Diagnostics Lab and I would do their Western Blot. I think that that that combination is the most reliable from my clinical standpoint.
Anna Conkey: Can you tell us more about neuro-Lyme? How do you test for it? How common is it amongst individuals with Lyme? Must the CSF show Lyme on PCR testing or is there other criteria that is used?
Dr. Delaney: I would probably say that over 75% of the patients we see in our clinic are presenting with very prominent neurological and psychiatric symptoms. So, is that partly because we have a center that focuses on neuro psychiatric symptoms? Maybe, but we kind of see all-comers. I think that the neuropsychiatric manifestations of Lyme disease are completely underappreciated. Not enough people know about this phenomenon in terms of a spinal tap and the lumbar puncture and how helpful it is. Honestly, it’s a pretty low yield test. A lot of the people who present to us with kind of the classic symptoms of neurological Lyme disease, if we do a lumbar puncture on them, it can be often negative. We also often look at something called a Lyme index, which basically looks at the amount of antibody that the CSF–the spinal fluid–is producing compared to what is being the antibody amount that’s being produced in the blood. If that’s elevated, that indicates neurological Lyme disease. If the PCR is positive, that would also indicate neurological Lyme disease. I see people who come back positive, but honestly, we usually don’t even recommend it in the setting of sort of classic symptoms related to Lyme disease, because doesn’t really change the workup so much. If people are having frank neurological symptoms related to Lyme disease, and it’s very clear that this is Lyme disease from the clinical perspective then we would usually recommend IV antibiotics in that setting. Going through the process of a lumbar puncture, and then finally getting a negative result, even though they have the symptoms suggestive of it, it’s just, again, low yield. We sometimes do it if we have a complicated situation for whatever reason, if there is some question about whether or not this is Lyme disease, or they have other symptoms that make us wonder. For example, maybe we’re wondering is this MS versus neurological Lyme disease or some other neurological condition and we’re not as certain about the Lyme disease diagnosis. Then it can be helpful from a differential diagnosis perspective, but usually we don’t need it to be certain that this is Lyme disease.
Anna Conkey: Is there a difference between your patients who have had PANS triggered by Lyme versus strep or another pathogen? Is the course of the illness or the onset different depending on trigger?
Dr. Delaney: I will tell you that from a clinical perspective, I would say that oftentimes, the Lyme patients, in contrast to strictly just PANDAS patients, they can sometimes present with more of a smoldering course. It can be, but it’s not likely that they wake up on a Tuesday in November, and now they have all of these symptoms and on Monday, they were totally fine. It’s typically more of a smoldering course. It’s not to say that the intensity of the symptoms at various time points aren’t as severe. I think in some ways, they can be definitely as severe or more severe than strep or mycoplasma kind of patients, so very sick patients but not necessarily that abrupt of an onset all the time.
Anna Conkey: What is your view on the abrupt onset criteria used in PANS and PANDAS? Is it possible individuals with sub-acute onsets of symptoms may benefit from the same treatments shown to be helpful in those with abrupt onset of symptoms?
Dr. Delaney: I don’t have a strict PANDAS perspective. The vast majority of the kids that I see are kids that have had Lyme disease, or a PANS presentation. Most of them are not acute onset. Am I in agreement with a subacute sort of process being possible? 100% with Lyme because that’s what I see clinically. It does not happen overnight.
Anna Conkey: Can you tell us a little about your psychosis biomarker study?
Dr. Delaney: So I recruited around 50 patients for psychosis. I think, 38 healthy controls and around 20 patients with like prodromal psychosis and we looked at a lot of different antineuronal antibodies as well as IL-6 and vitamin D levels. Probably the biggest finding was nobody had any antibodies that were positive in the psychosis groups or any or the healthy control group either. So that was kind of my initial hypothesis. I was very interested in looking at the antineuronal antibodies in psychosis populations thinking then that this might be contributing to some of their symptoms. Obviously, I had a very small study, so that limits us somewhat, but what we did find is, I found in my psychosis group, there is IL-6, which is an inflammatory cytokine, which had been previously looked at from like a public health population. People with schizophrenia had been found to have elevated IL-6 levels compared to healthy controls, and that had been confirmed in numerous studies before mine, but the unique thing about our studies that I found that in the psychosis group, there was a really, really tight correlation between IL-6 levels and vitamin D levels, and it was an inverse correlation. So high IL-6 went with low vitamin D. The reason why that was interesting is we found that across the board even healthy controls, everybody was deficient in vitamin D. So it wasn’t as if only the patients with psychosis were deficient. Everybody was deficient in vitamin D. But that unique relationship between the high IL-6 and low vitamin D was only found in the psychosis group. That was the main finding.
Anna Conkey: As a neuropsychiatrist, how do you see the field of psychiatry shifting? Do you believe focus on the immune system and inflammation in psychiatric disorders will continue to increase?
Dr. Delaney: I think the field of neuropsychiatry is in its infancy in so many ways. From the vantage point of, infection, immunity and how they influence neuropsychiatric disease, I feel like we know such a small amount and there’s like such a large amount that is currently unknown at this point. I have to tell you that in my clinical experience, I see dramatic improvements in people when they are put on the right treatment course. What that is obviously differs for each person depending on what the diagnosis is, but for the sickest of the sick patients, I often see a combination of antibiotics and IVIG showing the most substantial gains and incredible improvement in neuropsychiatric symptoms. Sure, my opinion is just that alone is groundbreaking, because both of those things are not standard ways to treat psychiatric symptoms, but I see those things completely changing someone’s course of their psychiatric symptoms. There’s not enough people, there’s not enough knowledge, and not enough people who are working in this field doing both clinical and research together so we have a very limited understanding. There’s a lot to learn.
Anna Conkey: What advice would you give to patients and families suffering from these poorly understood and sometimes marginalized illnesses?
Dr. Delaney: I think it’s very important for parents to trust their own intuition. I think as a parent, it can be very difficult because I think the natural tendency or intuition is for a parent to have a good sense of their kid and have a good sense of what’s going on from a medical perspective, even if they don’t have any background in medicine. And what the common story is oftentimes is that the parents will sense that something’s wrong, but they don’t exactly know what’s going on. Then, maybe they’ll go to a pediatrician or some other doctor and the doctor will either do a test or not do a test and say, “no, there’s no reason to think that this is Lyme disease.” The parents, since they don’t have a background in medicine, they don’t necessarily think that they should be questioning the medical clinicians, so they may just kind of let it go and think that it isn’t really a problem. I’m a big advocate of telling parents and patients and everyone that, just because a medical clinician tells you that something is or isn’t, you don’t necessarily need to trust or completely believe that one opinion. There’s a lot of value in second opinions or third. I would advise them to go to somebody who has experience in the realm if they think it’s Lyme disease in treating Lyme disease or other tick borne illnesses, or if they think it’s a PANS/PANDAS presentation, somebody who has experience in that realm.
Anna Conkey: Great. Thank you so much for your time today Dr. Delaney. This is really helpful and I’m really grateful that you took the time to share your expertise with us today.
Dr. Delaney: Thank you for the opportunity.