All right, good morning everybody. Welcome to this session on hydrocephalus and shunts. My name is Nathan Dargy. I am from Carolinas Rehabilitation, Atrium Health. And I'd like to thank Dr. Ivanhoe and Dr. Danenbaum, who's a neurosurgeon at UT, for joining us for this talk today. So my objectives for this talk will be to describe normal CSF dynamics along with risk factors and clinical diagnosis of hydrocephalus after acquired brain injury. And we'll also describe the incidence, prevalence, and pathophysiology of hydrocephalus after acquired brain injury. And I'll also discuss risk factors for the development of hydrocephalus. And my co-presenters will be talking about clinical considerations and neurosurgical considerations for hydrocephalus. So the CSF has many functions. And one of the most important functions that it provides a constant controlled environment for brain cells by providing protection, nourishment, and waste removal. It also provides hydromechanical protection of the CNS by primarily two mechanisms. It acts as a shock absorber, cushioning the brain against the skull. And the CSF also allows the brain and spinal cord to become buoyant, so effectively reducing the weight, which then lessens the force in traumatic injuries. CSF also assists in the removal of brain metabolism waste products through the glymphatic system, as we'll discuss. CSF is primarily produced by the ependymal cells in the choroid plexus of the ventricles and absorbed by the arachnoid granulations. Majority of the CSF is produced in the lateral ventricles. And it's primarily comprised or derived from blood plasma. But when we compare CSF to plasma, it's notably protein-free and has some different levels of electrolytes. So the pathway of CSF flow is as follows. We start in the lateral ventricles, where the CSF is produced by the choroid plexus. It travels through the intraventricular foramen into the third ventricle. And from the third ventricle, the CSF travels through the aqueduct of sylveus into the fourth ventricle. And from the fourth ventricle, it goes through the medial and lateral apertures, finally into the cisterns and the subarachnoid space where CSF is reabsorbed. So the original thinking was that CSF is, the flow of CSF is driven by pulsations of the choroid plexus. There's more recent work showing that CSF flow is more correlated with the respiratory rate and, to a lesser degree, heart rate as well, such that there's rostral movement of CSF during inhalation and caudal movement during deep exhalation. There's newer hypotheses that CSF flow is primarily driven by the glymphatic system, and we'll discuss that in a bit. Finally, CSF is drained by arachnoid granulations, and the arachnoid granulations and arachnoid villi project from the subarachnoid space into the venous sinus. And there's this constant pressure gradient of three to five millimeters of mercury between the subarachnoid space and the venous sinus, which essentially pulls the cerebral spinal fluid into the venous outflow system. And this system acts as a one-way valve so that CSF can enter the subarachnoid space, but blood cannot enter the ventricular system. So as I was talking about, the glymphatic system has an important role in CSF flow. CSF also acts as a clearance mechanism for extracellular solutes in the central nervous system through the glymphatic system. So in this diagram, you can see that in the subarachnoid space, the cerebral spinal fluid is traveling into the periarterial space, also known as the Virchow-Robin space. And it's driven into the brain parenchyma by this convective flow aquaporin channels and astrocyte end-feet sort of facilitate this process. This convective flow then goes into the perivenous space where it can be reabsorbed by a variety of different mechanisms. It's important to note that the glymphatic system can be injured or can be disturbed by neurologic injury, and that can lead to the development of hydrocephalus. Changes in CSF can also influence the intracranial pressure. So the Monroe-Kelley hypothesis states that changes in one of the brain, blood, or cerebrospinal fluid will result in a change in one or both of the other two. In a normal compensated system, if there was an increase in blood volume, then we would have a compensatory decrease in the CSF volume. In an uncompensated system, if there's excess CSF volume, there is no compensation of blood or brain tissue, and that could lead to an elevation in intracranial pressure, and subsequently, a reduction in the cerebral perfusion pressure. And we know that a variety of central nervous system disorders can affect the intracranial pressure. So I'm gonna talk a little bit about hydrocephalus, and my co-presenters will also go into detail about this. So hydrocephalus is defined as this dynamic imbalance between the formation and absorption of CSF, which essentially results in an accumulation of CSF and associated ventricular dilatation. And it can be communicating or non-communicating. And in communicating, there's CSF flow is able to go through the ventricular system, and in non-communicating, there's an obstruction along the ventricular pathway, which causes hydrocephalus. We know that hydrocephalus is one of the most common treatable neurosurgical complications after traumatic brain injury, and can have a profound impact on the patient's rehabilitation and outcome. And the incidence and prevalence of hydrocephalus after brain injury, the numbers sort of range between 0.7 to 45%, and that's kind of a broad range. It's because we don't really have any defined diagnostic criteria for hydrocephalus after brain injury. There have been some studies looking into this, however. Zhang et al. in 2021 reported that 38% of patients admitted to a freestanding rehabilitation facility with DOC were diagnosed with hydrocephalus requiring ventricular peritoneal shunt placement. There's a cohort of 140 patients with TBI at a rehabilitation center in Italy, and about 45% of those patients develop hydrocephalus based on radiographic diagnosis. And as Dr. Ivanhoe will mention, hydrocephalus is not just a radiographic diagnosis, it's additionally a clinical diagnosis. Hydrocephalus occurs in 50% of patients with intraventricular hemorrhage. And in a newer study by Castagnani et al., they found that 55% of patients with severe acquired brain injury due to non-traumatic etiologies were diagnosed with hydrocephalus compared to 35% for traumatic etiologies. Hydrocephalus can have a tremendous impact on outcomes in patients with traumatic brain injury. In a study by Kowalski et al. based at Craig Hospital, hydrocephalus predicted poor outcomes in patients with TBI during inpatient rehabilitation, including lower FIM scores on discharge and less FIM improvement, and longer durations of post-traumatic amnesia. And we know that for traumatic patients, the duration of post-traumatic amnesia is directly correlated with their long-term outcomes. Among 63% of patients who developed hydrocephalus after severe TBI in a study done in Denmark, 27% of patients were diagnosed during acute care, and 73 were actually diagnosed during inpatient rehabilitation. So this is an issue more commonly encountered by us physiatrists in inpatient rehab than it is in acute care. This is, again, to highlight that study from Denmark, which shows that 44.25% of patients with hydrocephalus were diagnosed within 1.6 weeks of their inpatient rehabilitation stay, 50% within 3.1 weeks, and 75% within 7.9 weeks of their rehabilitation. So the pathophysiology for the development of hydrocephalus. So typically, this is a normal pressure hydrocephalus that we see, and the reason why is because of Pascal's Law of Hydraulic System. The pressure in NPH is normal because the ventricles expand initially and continue to expand despite pressures not being elevated as described by the formula force equals pressure by area. So the force is increasing, the area is increasing, but the pressure remains the same. Elasticity and compliance of brain parenchyma may also be reduced in patients with normal pressure hydrocephalus because of the compression of the arterioles and brain parenchyma can lead to structural changes. And then, as we mentioned, alteration in CSF flow across the perivascular spaces and glymphatic system also may play a role in the development of hydrocephalus after brain injury. So what are the risk factors for development of hydrocephalus? Intracranial hemorrhage, especially subarachnoid hemorrhage and interventricular hemorrhage pose a significant risk factor for the development of hydrocephalus. Decompressive hemicraniectomy, as a lot of our severe brain injury patients get this, and while it's a life-saving procedure, it can also pose a risk factor for the development of hydrocephalus. In particular, studies have shown that the larger the craniotomy defect, the more superior the craniotomy edges are closer to the midline, and bilateral craniotomy defects are particular risk factors for the development of hydrocephalus. And additionally, extracranial herniation or the development of subdural hygromas after decompressive hemicraniectomy can be a risk factor for hydrocephalus. Meningitis can cause irritation in the subarachnoid space, and that can also lead to development of hydrocephalus. Patients who are older can also develop hydrocephalus, with age being a particular risk factor. In more severe injuries, with patients with longer durations of post-traumatic amnesia, lower Glasgow Coma scales correlate with the development of hydrocephalus. So subarachnoid hemorrhages, as I was talking about, is a risk factor for the development of hydrocephalus, and the reason why is because the subarachnoids, the blood that gets into the subarachnoid space causes inflammation and damage to the arachnoid granulations, and so therefore it impairs reabsorption of the CSF in the ventricular system. And chronically, these arachnoid granulations can undergo fibrosis, which continue the whole process of decreased reabsorption and the development of hydrocephalus. Decompressive hemicraniectomy is becoming an increasingly common neurosurgical procedure being performed in patients with traumatic brain injuries. And in the study done by Vidantam et al. in 2018, they demonstrated that the presence of interhemispheric subdural hygromas in younger age were actually particular risk factors associated with shunt-dependent hydrocephalus after decompressive hemicraniectomy. And the etiology of this may be multifactorial and may include impaired venous drainage in the sagittal sinus, disruption of CSF drainage due to the arachnoid adhesions, as I was mentioning, and also the potential loss of pulsatile intracranial CSF dynamics that occurs after decompressive hemicraniectomy. Subdural hygromas, or external hydrocephalus, may also be prone to develop after decompressive hemicraniectomy. And the formation of these subdural hygromas may occur because of a tear in the arachnoid membrane, and therefore there's a communication between the subarachnoid and the subdural spaces. And what happens is if the subdural hygroma becomes large, it can compress on the arteries in the periarterial space and effectively reduce the lymphatic flow and lead to the development of hydrocephalus. Eventually, the fluid that's trapped in the subdural space will tamponade the opening of the arachnoid membrane and the formation of the subdural hygroma will cease. So, in conclusion for this portion of the talk, hydrocephalus is one of the most common treatable neurosurgical complications after TBI and can impact the patient's rehabilitation and outcomes. CSF pressure dynamics are altered after brain injury and play a role in the development of hydrocephalus. And hydrocephalus is more likely to present in rehabilitation than it is in acute care. I'm gonna now hand it over to my mentor, Dr. Cindy Ivanhoe, who's gonna talk about clinical considerations in hydrocephalus. First of all, I wanna say that I am honored to be identified as his mentor. And I also wanna thank Dr. Dandenbaum for coming because hydrocephalus is sort of like a religion. People either believe in it or they don't. And then finally, I am going to credit and acknowledge and dedicate this course to the late Catherine Bonke. So my objectives are to discuss the impact of post-traumatic hydrocephalus on the rehabilitation and future outcomes of our patients, to consider a clinical context for suspecting normal pressure hydrocephalus, to address communication with patients, families, neurosurgeons regarding hydrocephalus in these patients, and then to discuss if there is value in intervening and when. So wet, wobbly, and weird, I told someone this morning, I was asked to take this out of a traumatic brain injury, out of the brain injury textbook because it was felt to be pejorative, yet I have medical students who are still being taught that patients are wet, wobbly, and weird. My career has been based in brain injury. Most of my patients, at some point, are wet, wobbly, and weird. So does this really help us make that diagnosis? Another thing that I have faced, particularly from insurance companies in different contexts as well, as well as from some neurosurgeons, obviously not the good Dr. Dandenbaum, it's not worth it, they'll still be disabled. So as you see some of my patient videos, you tell me if it's worth it. What happens after discharge from inpatient rehabilitation? And I have had the luxury or curse of following patients long-term, from inpatient to outpatient, and to beyond, to infinity and beyond. And so I get to watch what does and doesn't happen. So making the diagnosis, it's interesting how, it's normal pressure hydrocephalus, but I can't tell you how many times people say, well, their opening pressure wasn't elevated, or wasn't that elevated. But it's normal pressure hydrocephalus. When I was training during my fellowship, and shortly thereafter, we didn't bother with the tap test, because I was taught by a very famous in neurosurgical land neurosurgeon that it's a clinical diagnosis, Cindy, why bother? And that was Dr. Clifton, for those of you who may remember him. If there's a positive change during a tap test, that's helpful. If there isn't a positive change, that tells you nothing. It's like so many other things that we do in medicine, where it may or may not be sensitive enough to what those changes are. And if your patient got a really good night's sleep the night before a tap test, maybe they just got a really good night's sleep and they did better that day. And if a patient didn't do well, maybe they got a really bad night's sleep because they were getting up at five in the morning to be there for a tap test. So it depends what you find. So change may or may not be obvious. And I go through this with a lot of people at TIER where they want definitive criteria for making this diagnosis. And every patient is very different. Every patient will have very different capabilities before you do that tap test or during the tap test. And so a lot of what we look at may very well be very subjective. And again, it's not just about the scan. You have to have the suspicion in the first place and the scan may or may not be helpful. So clinical presentation. You know, I learned wet, wobbly, and weird. A lot of you probably learned wet, wobbly, and weird. But how does that really translate to what we are seeing in our patients? So there can be failure to progress or slow progression or improvement. Can you improve? Yes, with hydrocephalus. But do you improve as well as you can? Prolonged coma. Coma being used in many different ways or a prolonged vegetative state or prolonged disorders of consciousness. Whatever you're using or whatever your frame of reference. Patients are not emerging as they should. You can see increased posturing. Seizures, papilledema. You may or may not see that. Central sleep apnea. Something that we're finding more and more in our outpatients, particularly as patients get discharged so quickly. You can see a gradual deterioration. Impaired executive functioning. That represents the frontal lobes. So I'll show you a patient who barely has frontal lobes and who has still, I think, hydrocephalus. But Dr. Danenbaum and I are gonna talk about that. Psychomotor slowing. How quickly do they perform at whatever command or activity that they're supposed to do? Gait disturbance. Gait disturbance during a tap test is one of the few things that has been shown to be useful in terms of a tap test if a patient's gait improves. Whether it's the speed of ambulation or fewer falls or whatever. That has been predictive of a better shunt outcome. But a lot of my patients can't walk or ambulate in any way so I'm not sure how helpful that would be. Memory impairment, okay, they all have it to a variable degree. And then your clinical history is really important. You have to still be a clinician. You cannot just rely on a scan. These are the typical gait deviations that are described if you have an ambulatory patient. Reduced step height. Decreased counter rotation of the trunk. Poor balance, widened stance. And Parkinsonism, this is very important because a lot of patients have magnetic gait. It has to do with a frontal gait where they will often turn like a Parkinson's patient. You know, Parkinson's patients don't just pivot. They take multiple steps to make a turn. Behavioral presentations. Again, that frontal or executive dysfunction, psychomotor slowing. Decreased initiation, keep that in mind. Perseveration, confabulation. Again, we're talking largely about frontal lobe findings but remember, the brain does a lot of circuitry. Motor planning and apraxia. I'm gonna go through this quickly because I think that the patient videos will be more useful, hopefully they're gonna play. Motor and persistence. The ability to start an activity but then not continue. One of the easy ways to look at this is when you ask that patient to close their eyes and they shut their eyes but they can't keep them shut so they keep opening and shutting their eyes. CT findings versus MRI. Very often, increasingly difficult to explain to an insurance company why you might want both but there is that more sensitive periventricular edema that can be more helpful in potentially tipping a surgeon to intervene and then, he nods, and then I also tend to look at the shape of the frontal horns and we'll see if we see that. So potential complications of shunting. Obviously, any sort of device can have some issues related to it. I'm gonna let Dr. Dannenbaum address the subdural hematoma, hygroma issue. So this is Trey. Trey was injured by a drive-by shooting. He's a really good kid, still is, though his initiation's interesting. He is admitted to rehab. He has a large bifrontal cranial defect. He was originally, at the time of the shooting, taken to the county hospital. Good insurance and I met Trey as an outpatient several months out and he still had no follow-up because he was taken to the county hospital and not only was he taken to a county hospital, he was taken to a county hospital in the days of COVID. So he had poor initiation, but he's ambulatory. He shows up in my clinic months later and now he has trepanation, which I unfortunately could not find a really good picture of. So I sent him to my friend over here, Dr. Dannenbaum, who eventually did a really lovely cranioplasty. In 2020, he's seen again in outpatient clinic. A wait alert, appropriately interactive, answers questions without delay. He has some minimal slowed initiation, whether to engage a conversation or a movement, it takes a little bit of time to initiate. He is able to follow commands without difficulty, but one of the things is he does not eat. He just doesn't initiate eating and he has a G-tube. And somebody that ambulatory, continent, everything else you would think he would initiate eating, but he's not too aware. He needs, this is before his cranioplasty, and there have been insurance issues with getting the cranioplasty. He got a tap test after his cranioplasty. That's with his PT, she can't keep up with him. It's pretty funny. But during his tap test, he ate for about 24 hours. He initiated and he fed himself. He is currently, and this one was even read as hydrocephalus. How odd is that when both all of us, the neurosurgeon and radiology and I, all agree that there is hydrocephalus. So this is him during his tap test. You get the idea? How do I make it progress? And this is him, oh no, hold on. Why can't I get it to play? Guys, anybody? Nathan, you're younger. This is supposed to, he's supposed to, this one, yeah. Oh, there we go, okay. And this is him now trying to initiate a jumping jack. So what do you guys think clinical deterioration So that is him now and I want you to watch him put on a sock and I'm going to torture you. Sorry, Flora But think about what you're seeing is he wet is he wobbly Is he weird? What's that So You're watching my interpretation and I'm open to other ideas does anybody see apraxia Motor planning problems Perseveration Now let's think you're the single mom taking care of him at home and you've not you need to go to work Are you gonna wait for him to put his socks on or are you gonna put his socks on? So hopefully he's gonna see my friend I should Dan and BAM in the near future So now what why is he subtly worse is it that subtle it's a good question My question is we've been waiting For various reasons for about a year. Is that going to affect his outcome if we shunt him now? Where would you go from here and What would be his worst possible outcome because certainly, you know, no good deed goes unpunished, right? So those are considerations And we can talk about his mom's concerns as well. But so this is Greg That's his at first brain injury on the one side and Then we have him after his second brain injury where he fell 59 year old male to traumatic brain injuries increasing falls now His wife is distressed by his lack of behavior So you can put him on the couch and he'll be on the couch when she comes home from work there are funding considerations where She's concerned about You know, will he need more therapy? How much is it going to cost me to drive him to the surgeon? Things that in the grand scheme of life. I'm not so sure Our unreal are our realistic issues for her But you know that is her call to make patient is totally good with where he is She's not So he has marked and the synosia look like the worst I've seen he has delusions He's confabulatory and his initiation etc is totally disrupted so his delusion I had a telemedicine follow-up with them recently because it's the fourth or so time that she wants to talk to me about what would happen if she shuns him and The issue is not his correct He's kind of happy where he is could he be better potentially might he get a shunt and then Not be so so happy to just lie on the couch all day and then have we have other issues like hiding the car keys But I don't know what's gonna happen. And that's what she wants me to make the decision and all I can tell her is Here's what I think He needs I cannot tell you what will become of him if he gets a shunt But he's totally happy because he actually believes he went to work the other day and managed a million-dollar account. It's pretty funny anyway So he has severe impairments across attention Processing speed executive functioning motor speed expressive language learning and memory pretty much sums it up He has a marked lack of awareness This is from his neuropsych testing most recently about a couple months ago and compared to his prior evaluations He has declined Her big issue is his he going to become incontinent. I can't predict that So again considerations, he had a positive tap test his gait improved his speed improved his stride length improved But he's stable so far where he is So is this his issue or her issue and that's a sort of ethical PM and our discussion, you know about I Was trained to do whatever I can to help these patients that it's worth it But will I be helping him if I were to insist on the shunt because she needs to She actually needs to figure out what's going to work for her but she also wants somebody to blame quite frankly and I Can just give her the information as best as I have it right now His delusion Ali has horrible short-term memory and his mental processing a speed of processing is severely decreased. So Now what? Do we shunt him? Do we repeat a tap test? Do we do nothing? Do we continue his therapies and outpatient? I mean even I as a patient advocate kind of feel like at what point because there is no carryover She doesn't carry over and he doesn't carry over. I have counseled her a lot on Things like her therapy. I have counseled her a lot on setting up things within the home But can he be left alone according to the neuropsych reports no Wife wants him to make the decision. Does he sound like he can make this decision? She's really overwhelmed. So what do you guys want to do who wants to shunt him now? Who wants to repeat a tap test? I mean, quite frankly, that sounds great. We don't even do catheter intrathecal baclofen trials because the logistics are so difficult. So, I don't think I can coordinate that. It'll be another year and a half until I can coordinate that. So, what we're gonna do is repeat the TAP test and see how he does, and it's largely for her. And maybe one of the questions for Dr. Dannenbaum is gonna be kind of what he would think in this instance. So, not to put you on the spot, Mark, but I did. So, this is Todd. He had a severe fall. We don't really know why. That's something that has bothered me, but not many other people in the middle of the night. He had a bifrontal temporal contusion, subarachnoid hemorrhage, left temporal, oh, I spelled uncle wrong, herniation, and right occipital fracture, and his GCS was three. So, I found him when I was covering one Monday, and by this point, he had definite trepanation. So, his progress had gotten to a certain point, and then it's kind of stopped. And severe left neglect. He had bilateral lower extremity findings. He went from the edema to trepanation to hydrocephalus. So, he got his cranioplasty, and then he came back, and he was really good for about a week, a whole week. And then he became slower to progress. He started to lose ground, slower to respond. Left neglect was getting worse. And here he is now after his cranioplasty. Not kind of what you would have expected if you knew his history. Oops, all right, I don't know why I can't do this. Okay, never mind. So, this is Emmy, well known to both of us. Actually, may even to you, Nathan. May even be known to you. Emmy had a really bad brain injury several years ago. Lived in El Paso, not too long ago moved to Houston. No pressure to be closer to me. So, I really need to fix Emmy. He had, originally had hydrocephalus. He had a cranioplasty. Eventually, everything had to be taken out, including an intrathecal baclofen pump, because he had an infection. Eventually, he got a cranioplasty, went back to Houston. There was a discussion about whether or not to put a pump and a shunt back in. He got a pump, this is him with his sister. You can see, in the past, he was a DOC patient, formerly known as a severe brain injury patient, by the way, but they both were removed. He comes to me on a ton of oral meds now, not helping with his tone. He got a new pump, and he gets ongoing injections. He also had his vision assessed to see what part of that affects his posture, et cetera. At this point, he has a pump, bilateral AFOs, bilateral tendon lengthenings. And then, all of a sudden, this is how he looked after a shunt, about a couple weeks after the shunt. So, that's him in the ICU, probably about two, three weeks ago. You don't, first of all, posture for seven years, right? And the other thing is, something happened. And so, I had a conversation with the neurologist whose service was following him in the acute care setting. And what I got was, well, you know how it is with these severe TBI patients. We don't really know where their baseline is. And I go, he shouldn't be posturing. And then, I sent him this picture of ME 10 days before the presentation on the left. And I said, that's what you're looking for. You're looking for someone who can assist with transfers, who was engaging with his family. And he went, oh, that was the response. I can still hear him in my own head. Anyway, now there's a question about protein in the CSF. I'm not exactly sure. I think he may have just gotten better and returned to tier. So, my closing thoughts. When do you look for hydrocephalus? How many of you see patients acutely, or more acute rehab setting? How many of you follow those patients long-term? Good, because that's a nice trend to still see is happening. So, you know, you at least have that sense of who your patient is, and where they have been in their development. Is a tap necessary? Really kind of depends on your patient, your scan, and more importantly, your neurosurgeon's point of view. So, I had left for a year, and then come back to tier. And a lot of the physiatrists in brain injury thought you have to do a tap, that it's mandatory for the neurosurgeons. And so, that's a sort of bias in a different direction, right? How do you know when it's time? Well, we've talked a little bit. Some people have referenced an example I've given before, where I had a patient where the neurosurgeon, this was many years ago, thought, oh, I don't know if a shunt's really helpful. Why do you think that she needs one? And I went up to him and started picking the lint off his jacket, because that was all we could get that patient to do. I said, she's perseverating, and that's what it looks like. Do you expect that a tap will make the diagnosis? Do not expect that the tap will make the diagnosis. And is it worth the risk? Well, excuse me, tried to get through this. Is it worth the risk? Is it worth the risk? That's also an ethical discussion with the patient and family. Greg, the one whose wife wants me to make the decision, he says, whatever you think will make me better, and then promptly forgets the conversation, right? So, it comes down a little bit to the philosophy of care and your relationship with neurosurgery and your relationship with that family, about which risks they are or are not willing to accept. The impact of hydrocephalus and rehabilitation, I think Dr. Darji did a lovely job of showing some of the literature that supports that it does have a negative impact. And we have to watch for subtle. So, I have a handful of neurosurgeons who have faith in me about making that diagnosis, and then I have a few who, where I will get that usual, is it really worth it? I don't think it's worth the risk. But subtle matters, and hopefully we still at least have enough time with our patients to understand what it is we are looking for, because wet, wobbly, and weird doesn't really give us information. And you have to translate what it is you're seeing to what is potentially related to having hydrocephalus. Sometimes our patients have little to lose, especially the patients who are declining. And that's, again, where the discussion with patients and family, where that discussion is important. And sometimes there's a lot to gain. I have had one patient in my entire career who could tell me what it was like before he got shunted, which I thought was so exciting to me, but then I'm warped and a nerd. But he talked about, basically apraxia. He talked about wanting to say something and just not being able to start. He talked about having a really bad headache. And I try to get some patients now to tell me if they remember, but a lot of my patients are really severe, you can see that. They're not gonna necessarily be able to do that. And on that note, I will pass the baton. Thank you. Okie doke, well thank you for having me. My name is Mark Dannenbaum and I'm a neurosurgeon at UTHealth Houston. And it's a nice opportunity to be here to talk to you guys about hydrocephalus. Topic I was assigned was hydrocephalus and shunts in 20 minutes, neurosurgeon's perspective. So I'd like to thank Dr. Ivanhoe who invited me here. She's our self-professed shunt queen, I'm going to get that to play again, I'm not sure. One more time. So every Halloween she dresses up and you know is the shunt queen and there you see her in her Halloween gear so that it's coming up again, I imagine she'll don that outfit soon here. I'd also like to thank Monica Verdisco-Gutierrez who was with us at UTHealth and Memorial Hermann for a long time at TIER and about a year ago she was presenting at her first neurosurgery meeting we had our congress in Austin and there she is with myself and my partner Ryan Kitagawa who heads our trauma program and so I thought how fitting it is, this is my first PM&R presentation so we're sort of reciprocating there. So this is sort of the landscape of our place. What we have is we have this hospital which is the Memorial Hermann Texas Medical Center campus which houses our Level 1 Trauma Center and a Comprehensive Stroke Center and it's right next door to this building over here which is Ben Taub which is the only other Level 1 Trauma Center in the city of Houston for seven and a half million, we have two Level 1 Trauma Centers and they all right behind them immediately feed into this building which is TIER which is the rehab hospital so they get a lot of business particularly for stroke and for traumatic brain injury and that sort of ties into how I got involved with this racket is that we had a clinic of neurosurgical consultation in the TIER building so the patients didn't have to be transported, you know, the administration's kind of got to fighting each other and now they won't let us go there anymore but originally the idea was that we had Dr. Kitagawa who's the head of our trauma program and then the rest of us who take trauma call that also have a separate neurosurgical subspecialty, mine being cerebrovascular because obviously there's a lot of people over there with the stroke and subarachnoid hemorrhage related rehab and Carl Schmidt who's a director of our spine trauma program and Al Finoy who's our functional guide on pain pumps and you know things related to that. The one thing we all had in common though is we all took trauma call and we all dealt with a lot of people who had shunts. So this is the outline I was given, okay, I have 20 minutes to discuss CSF diversion as a treatment option for hydrocephalus, discuss how large craniectomies affect CSF dynamics and development of hydrocephalus, discuss shunt valve types and their function, complications after shunt placement, give a case example and talk about neurosurgical perspectives. That to me seems more like a weekend symposium. I'll do the best I can to get it done in 20 minutes. Alright, so CSF diversion, okay I have a whole extra 10 minutes, wow, I bet I can use it because my videos are not well edited. So CSF diversion is a treatment option for hydrocephalus. In short I break it down into temporary and permanent. So temporary we don't really use spinal tap as a treatment option but sometimes, you know, someone comes in with a small pseudomeningocele or something of that nature but generally speaking, you know, patient has a pseudomeningocele we use a lumbar drain for that. Someone has acute hydrocephalus we use an external ventricular drain, okay. Permanent is what you guys are more interested in hearing about because you're taking care of people for the long term and the workhorse of this talk is going to be about the ventricular peritoneal shunt. There is this concept of an endoscopic third ventricular endoscopy which I'll show you guys. It's a treatment for hydrocephalus. It doesn't involve leaving any hardware in. That works well in people in underdeveloped countries that have access to medical care or they don't have somewhere they can just go get shunt program every couple of weeks. But again, it's a fixed treatment. You can't modulate it. And then a lumboperitoneal shunt is something that we use most often times in pseudotumor and so I don't have a lot of applications for this in the rehab world and it's also not particularly practical because a lot of the people that you're making, that you're managing also have baclofen pumps in and things of that nature. So we don't see a lot of lumboperitoneal shunts in our rehab patient population. So if you haven't ever seen ventriculoscopy, I want to make sure you got a look at it. What we got going on here is just we're on the left side of the head and it's 10 centimeters back and in the mid pupillary line we take a cannula just like this in my hand here and we go in about 6 centimeters. You go straight through brain. There's nothing magic about it. You pull the stylet out and you hope you see CSF. It's just like doing a spinal tap on someone's head and it's like we're putting a straw into a coconut or something of that nature. And I want to make sure we got CSF so I can go home because I don't want to have to come back to find out it's nthalamus. Okay, good. So we got CSF. So that's the start and then after it's done, it's tunneled and then it goes into a bag. And the reason I'm showing you guys EVD is you don't use it a lot in the rehab world, but that's our game. You know, we're talking about weaning an EVD, getting the CSF diversion device out of the patient so they can be shunt free. And we're focused on things like ICP, the flap tension, all those kind of things. But honestly, those really aren't considerations further downstream. And those are the things that Cindy was talking about. I'll get into that in a minute. This is a real acute decision. So just because someone had their EVD weaned and removed doesn't necessarily mean that six months later they aren't going to need to have some kind of more definitive management of their hydrocephalus. It just means that their acute hydrocephalus didn't require ongoing CSF diversion. They didn't need a shunt when they're in the hospital. Okay, this is a third ventricular ostomy. And these are always kind of fun just to look at because the anatomy is so gorgeous. We're inside the lateral ventricle and this is right in the columns of the fornix. Here's the choroid plexus. Here's the thalamus striate vein. And if you look through the foramen and monroe, we go down into the third ventricle. And let's see if I can get this to play. It's amazing. I got this thing edited this morning prior to this talk because it was too big to load in my talk. So we go, so this balloon, it's just a Fogarty balloon, it's going through the foramen and monroe and we punch a hole in the floor of the third ventricle. You can see the basilar artery right there and the two posterior cerebral arteries. These are the mammillary bodies. And so the bottom line is, is that once we have, once the balloon inflates and I rip this hole in the arachnoid, we create a fenestration between the third ventricle and the prepontine cistern. So it's a nice, it's a nice treatment strategy for patients that are in underdeveloped areas where they don't, they can't get to a neurosurgeon's office regularly for some sort of adjustment of their shunt. And if you're into the medical missionary work, Ben Worf was a guy up at Harvard that did a real pivotal study on this in Uganda or showed this was an alternative to VP shunting in underdeveloped countries. And it's fascinating work. It's one of the greatest humanitarian works in all of medicine, in my opinion, besides maybe vaccines. So really, really interesting if you want to read about that kind of stuff. So if we get this balloon to inflate, I'll show you guys the hole that we made here in the floor of the third ventricle. I said, full disclosure, I'm a terrible video editor and had to get this emergently edited. So this 20 minute long video could fit in this 20 minute talk. Here we go. I guess you got to be kind of careful doing this because I'm right up against the basilar artery and I don't want to tear something and have a screen full of blood, but at a certain point we should be able to see this. Okay, there we go. Okay. Now you can see that nice hole in the floor of the third ventricle. And we have a CSF diversion pathway without any hardware in the patient. Okay. So this question of how large craniectomies affect CSF dynamics and the development of hydrocephalus. I know Nathan talked about this a little bit, but the reality of it is, in my opinion, it's like when Bob Dole was asked, you know, boxers or briefs? I think the real answer is depends. And so, you know, the bottom line is that this is a large ischemic stroke from a patient that had a carotid terminus occlusion. And you can see this pale dusky brain that is, I mean, the whole hemisphere is decompressed. We're right on the sagittal sinus all the way kind of outlining the transverse sigmoid sinus. There is no bone in this hemisphere. This person did not require a shunt. Okay. And they had probably the biggest hemicraniectomy I've ever done. This is a grade five subarachnoid hemorrhage in a patient that had a temporal clot. You can see this horrible looking brain with all that, you know, stain from the subarachnoid hemorrhage. They had a lot of intraventricular hemorrhage and they had a lot of blood, you know, getting in those arachnoid granulations. They did require a shunt. I don't think that the craniectomy size has anything to do with it. I know there's some literature that's published on the topic. I don't think it's reliable. I think each patient and the pathology dictates rather than the craniectomy size. VP shunts, the real workhorse of my talk here. Okay. So we have three components and I just did a shunt on Thursday in anticipation of this talk. So we've got some fresh, fresh video here. But the components that we have is start off with, everyone can look up here for a second. This is our ventricular cannula and it's got a little stylet in it. And so this is actually what goes through brain parenchyma. And so I thought my, what I brought here is a better representation than what we have on the slide. But this is, you know, our proximal catheter here. And then there's a valve that goes along with it. And nowadays we're mainly using programmable valves because you can adjust according to patient's needs. And these patients are very dynamic. And so I, you know, once upon a time people use fixed pressure valves and I have a slide on that in a minute, but I don't think, I think it's more for historical purposes. Most neurosurgeons these days that are taking care of patients in this context are not using fixed pressure valves. And then there's a peritoneal catheter, which is this long piece of tubing here that goes, you know, from the valve in the head down into the peritoneum or the pleura or wherever you're putting it. Okay. So I like to use a stereotactic stylet that goes inside the catheter so that we can use image guidance. And that's one of the things that comes up when you're talking about the decision making as far as safety. It's certainly something that I've had to learn to use in people that have had aneurysms with stent assisted coiling where they're on dual anti-platelet. At the time they've had to have their catheter placed for a shunt. I don't want to be making multiple passes in those, those patients. So I think this is a real nice technological advantage to be able to use image guidance. So the way we do that is like this. We have this machine in the room. There's a lot of different manufacturers, stealth and brain lab and whatnot. They're all the same. None of them are any better than the other, but you have this camera that is linked to this reference on the patient's head. And when we do that, we can see where we are relative to the patient's imaging. So I think of it as like GPS for the brain. So this is the cartoon from the company. I'll show you real time image guidance on a case from Thursday. So the next step, obviously, you know, it's a neurosurgery talk. You got to talk about, you know, cracking the skull. So of course we drill a burr hole. And then from that burr hole, there's always going to be some sort of intermediate incision, unless you do an occipital approach. And most people prefer to go in a frontal approach because that's the safest real estate. Over Coker's Point, you know, your middle frontal gyrus, it's relatively benign as far as any neurological function there. So we tunnel from the frontal incision to this intermediate incision. And once we've done that, the next step is to take this long tunneling device here. We actually go down to the abdomen. In the case that I was doing here, I had the general surgeons helping out on the abdomen because this lady had had a prior colon resection and history of peritonitis. So I was worried about a lot of adhesions in her belly. But if they don't have a prominent abdominal history, I usually do the belly myself. So once we have tunneled down to the abdomen, the next step is to take this catheter that's connected to the valve and go from the frontal to the intermediate incision. And then we have this long string that will pull through this tunneling track to get it to go from the intermediate incision down to the belly. So that completes our track from head to abdomen. Now, this video, thank God it played, is the stereotactic cannulation of the ventricle. So I have that probe inside my ventricular catheter. And then what we're doing is, yes, we're looking at the patient's head to make sure that we're on the surface of the brain. But then we go up and using real-time image guidance, we can watch the catheter on the patient's imaging. So this is called frameless stereotaxis. This isn't that groundbreaking of a concept, but it's amazing how few people use this. I mean, it's like the industry standard for biopsies and tumors and whatnot. But I think it really has a lot of value in the shunt population as well, just as far as minimizing the number of passes, things of that nature. Because like I said, sometimes these people will be on dual antiplatelets, you know, and I've had a subarachnoid hemorrhage patient that I need to do. Or I always say, you've got to get them ready to go to tier, because right when they go back to tier, you can get put on all kinds of anticoagulation. So we don't want to have four or five passes, you know, because the rehab doctors are always worried about anticoagulation needs. So here, I'm sorry, the blue thing is that we're watching the catheter pass. And so we can actually see our target going down to the frame in a Monroe. And so while we've been passing the whole time, and then again, I pull the stylet out, I want to make sure I see CSF. And so now I'm in, and I have some sort of radiographic confirmation that I'm in. I still get a CT post-op because I want to make sure there's no, you know, tracked hemorrhage or anything of that nature. Or I want to make sure that the navigation wasn't off, the registration or something. But anyway, the long story short is that it's a very effective way to get the catheter in. And I really think it optimizes the safety. Some neurosurgeons will say, oh, those ventricles are so big, you can't miss. And yes, I mean, there's some truth to that. Bigger ventricles, like you're going to see in the rehab population, are easier to hit. And so you don't have to use stealth. But in my opinion, it really doesn't add any significant cost to the patient. I think it only adds safety. So I advocate using it when I can. And so here we're connecting the proximal catheter to the valve. And then we're just going to pull the slack out of the system here. I wish I could speed this up, I think you have to watch. Now I'm just tying a little tie there to make sure that that doesn't slip off because the proximal catheter doesn't come pre-connected to the valve in this system. I mean, you can get it that way, but I use what's called a non-unitized system, so we're tying it down. I think originally when I was preparing this talk, I thought I could advance the video a little bit, but I realized I don't have control of the mouse here, so we had to do some editing today here, so sorry you're watching a few of these steps that aren't critical to the presentation. Once we pull it through, I want you guys to see what goes on in the abdomen. So we actually pull down from the abdominal side. And so what I do after we've pulled it through is I take a syringe and make sure that I have 10 cc's of fluid out, because I want to verify, I guess I'm neurotic like that, that we actually are in. So if I have 10 cc's of CSF that I can pull from the distal tubing, there's no way that I'm just pulling the saline that's in the tubing, or it's not in the cistern or something, we know it's in. Okay, and at this point we tuck the valve underneath. And we're done. So that's how we complete the circuit from head to abdomen. And then like I said, I have the lap assist for the peritoneal catheter placement in this case. Alright. I think we'll get a quick shot of that. And then they threaded in their little laparoscopic port after we just verified that we have some good spontaneous distal runoff. Here they go. Whoops. Oh, this is just showing, we put a couple little screws to anchor it with a right angle connector that prevents it from migrating. So sometimes if you see a patient that has some cranial plating screws around a burr hole, they have a shunt and no craniotomy, that's why they have cranial plating screws there. Let's see. I'm trying to, I wish I could fast forward. Here we go. Yeah, so that's just showing the threading into the peritoneal cavity. So that's basically a 30 minute shunt and, you know, five minutes of edited slides. And you can see there's the liver and there's the, they're going to be coming out pretty soon with the distal tubing. They're still threading it. There we go. See, it's coming out and then they feed it all the way down into the pelvis. Okay. This is a list of all the different types of valves that I think you're going to see in most major hospitals. I think it's more of a historical thing to talk about these fixed pressure systems like the Medtronic Delta valve or the regular or the Hakeem. Because unless you have like a pediatric patient that had their shunt placed long before everyone was using programmable, you don't see these that much nowadays. However, in the Medtronic makes, sorry, Medtronic makes a Strata system and J&J makes this Kodman Hakeem. So when you hear Kodman Hakeem, that is the original programmable shunt. And all of these are good. There's no difference. And I personally use the Medtronic system, but we've used the Certis before and I've used the ProGav system from Escolap. They're all very good. I don't think it makes any difference. There's not a, I think a commercial advantage to one system over the other. All right. Quick note on complications. So I think you can break this down into two categories. Shunt not working, shunt working too well. So as far as shunt failure obstruction, obviously the most common thing that we're going to see is an inclusion in the proximal catheter. And it's usually from something like this, whether you have some sort of bio debris from prior intraventricular hemorrhage or just something like this, which is choroid plexus. I mean, it varies and, you know, the bottom line is, is that it doesn't really help guide you to your management. If we have someone who has obvious ventricular enlargement and they have symptoms, we explore them and we usually try to look at all the components. But you know, I mean, people do talk about these symptoms, you know, irritability, confusion, lethargy, headache. I mean, obviously those are just signs of elevated intracranial pressure. But when we explore someone, we find they have proximal malfunction. This is what we see. Sometimes we'll know it's proximal malfunction going in because we'll try to tap the shunt and pull CSF out. And if we don't get CSF out, it's an obvious proximal malfunction. We still explore the system and look at the distal aspect too. Distal malfunction, you know, we see a lot and it can happen for various reasons. I mean, we see a lot of people who have disconnected catheters in the neck because the cervical spine is mobile. And so that's obviously an area that needs to be looked at when you get a shuntogram or, you know, an x-ray series of the skull, cervical spine, chest x-ray, and abdomen, kind of looking at the outline of the tubing. But people can also get fluid collections around the catheter tip, these pseudocysts, where in essence they're draining functionally from their head down to the distal tubing, but they've lost their absorptive capacity in the peritoneum and they get this large fluid collection that just continues to build up with no systemic absorption of the CSF. So we see that in distal shunt malfunctions a lot. And usually what we just do is, in that case, we will externalize the shunt at the clavicle or something like that and try to drain the pseudocyst and go for an interval of time, hopefully being able to re-implant later and going back into the peritoneum, because that's definitely the best spot. Shunt infections, I think you guys know this pretty well, and I think it's, you know, staph epidermidis and staph aureus are the most common bugs you see. And I think the two-month rule, some say three, is pretty consistent across institutions. It's pretty unusual if someone has a fever eight months out and they've had a shunt to blame it on the shunt. So most neurosurgeons, I would say, that if you have someone that's getting a fever workup and you want to get CSF beyond the three-month window, we'll recommend an LP over a tap of the shunt, even though the shunt tap may be easier just because there's a concern every time you tap a shunt of infecting it. So over drainage, you guys probably see pictures like this a lot in your different institutions. So here's someone that, you know, they've had a hemicraniectomy and they had a shunt. I mean, we have people that have hydrocephalus and have bad swollen brains, and then as their swelling goes down, they develop this kind of soup bowl head like this, where, I mean, literally it's so sunken that, you know, a lot of people are concerned that this is an emergency circumstance. I guess it can be if they have neurological symptoms, and that's my definition. This is what I call trepanation syndrome. We get a lot of calls from our tier colleagues about people that are having some dwindling neurological status and they don't know if it's trepanation or not. I think we can all agree that this is a pretty good case of trepanation syndrome regardless of the clinical status. I think this needs to get treated. So this is obviously the patient on the table getting ready to have his cranioplasty performed. This is another over drainage that we see, and this is pretty common too where, you know, a patient has a shunt in place and the ventricles are just little tiny, tiny, you know, you barely see the lateral ventricles here. The third ventricle almost doesn't exist, and, you know, we see this picture a lot in someone who has pseudotumor, but if you had someone that previously had large ventricles, I mean, this is a diagnostic picture for someone who's draining too much, especially if they have, you know, positional headaches. So in this case, if they have a programmable shunt, we can adjust it. It's a nice thing to do, not to have to change their valve out. And if this goes on and on and on, these people can get diplopia from, you know, lateral rectus palsies and things from brain sag, but pretty uncommon to get that advanced nowadays. This is something we see quite a bit of, and it's just the same problem, over drainage, but instead of, you know, getting slit ventricles, you get extra axial fluid collections, and this can be a real management challenge for us because the color of this extra axial fluid is the same as the ventricular fluid, and so it's that old dilemma, is this hygroma or is this chronic subdural hematoma? So honestly, for both of them, if the collection's large and it's continuing to enlarge, usually we start off with just trying to adjust the shunt. That's one of the reasons I think, particularly in older patients that have a thin cortical mantle up front, there's such a huge benefit to putting in a programmable valve, and in my practice, I start at the highest setting, meaning the least amount of CSF drainage, and oftentimes it'll drive my rehab colleagues crazy because they're ready to start draining more CSF in anticipation of benefit, but I think we have to reach that point of balance where we're not potentially over-shunting because at my hospital, where everything comes in, it gets dumped in from the community, we see everyone else's subdural where they started off at a higher setting and they're draining more CSF and they come in with a subdural right away, and oftentimes we see people come in with acute subdurals because they're being drained too rapidly. I think you can always gradually build up to get to that happy place, and that's why I always tell Cindy, it's like slow and steady wins the race, so I think that's the best way to get there. So this is just showing a patient that has a strata valve in, and this is 2.5 is the highest level. I'm just going to stop this video for a second. That's what a chronic subdural looks like, that motor oil-like blood. They can be under pretty high pressure, and that's obviously what we want to prevent. I mean, if someone has a big enough collection and we have to drain it, that's what burr holes look like, and that's chronic subdural blood. I prefer not to do this unless we have to, because usually just by turning the shunt up to one of the higher levels, you can minimize the amount of drainage that you have and those things will go away spontaneously. It's very rare we have to operate on these, but if someone has been turned up all the way and they're still not responding, then sometimes we'll ligate the shunt even, because even at the highest level, it's still draining somewhat, even though it's a minimal amount. This is kind of the final pathway, if you have someone who has a chronic subdural that's not getting any smaller, despite all of your other non-invasive maneuvers. Just a quick case example, I want to show a ventricular atrial shunt, and this is a poor guy. He's had a myelomeningocele at birth, he's had shunt-dependent hydrocephalus, and he had this situation in his abdomen where he'd had a perforation from one of his prior shunts, and he had an open abdomen that had to granulate in over 90 days in some sort of long-term acute care facility, so he's got a very hostile abdomen. He came to us with a V-pleural shunt, but he had this opacified hemithorax, so putting it back in his pleural on the contralateral side wasn't a real good idea, because he presented not only with shunt malfunction, he also presented respiratory distress. Our hands are kind of tied in these options, obviously he's got dysmorphic ventricles, but they were bigger than they had on a prior CT scan. In this option, I begged my laparoscopic colleagues, can't you find a little tunnel in there? What about the gallbladder, or something like that? Nope, we're out of options. So this was a case where we actually did a stick in the IJ, and we tunneled it into the patient's atrium. So this is a ventricular atrial shunt. This is a real kind of nightmare scenario. We usually only use that if the peritoneum can't be used. So I just want to make one quick point that peritoneum is always a preferred target. If we have to go into the pleura temporarily, we will, but it always has an expiration date. It doesn't last forever. And then, obviously, if you can't go in the peritoneum, and the pleura wears out, then my protocol is to revert to a VA shunt. Last slide here is neurosurgical perspectives on shunt decision making. Again, that's a weekend symposium, okay? I can't really get that done in a slide. But I think for practical purposes, in this audience, it's already been addressed. And I just want to say it, in the rehab population, there's a lot of stuff that we don't see. I mean, you know, I would see this scene when I was walking by the gym, and we used to have our neurosurgery clinic in-house it here. And we don't get involved in this phase of care, okay? And so if someone gets a spinal tap, and they're doing better with these guys, under this lady's direction, those are meaningful inputs to me that I normally don't get. I mean, you have to think about it. Most of your neurosurgical colleagues are going to be dealing with things like I mentioned, you know, what's their ICP when their EVD is clamped, you know? Does the flap tense up, you know, when they don't have a bone flap on, and all those kind of... They're very black and white type of things. And these type of considerations are a little bit like the practice I have that I work with our behavioral neurology clinic, where I'm their sort of go-to person for the NPH population. It's interesting, they're calling these symptoms NPH-like, because in that circumstance, it's non-traumatic, and they're all 70- and 80-year-olds that are presenting for cognitive evaluations. And they focus on the gait as the primary determinant, but they still are doing tap tests in the behavioral neurology world, and getting gait assessments. And so it's a little more rigid in that context, but in this context, some of these people can't walk, and they have more profound challenges. They have spasticity and whatnot. So I think I've really learned to rely on trust, and this isn't just like, you know, I'm trying to get a gold star from all you guys, because you're rehab docs, I'm the lone neurosurgeon in the room saying, yes, trust your rehab docs. But I really have learned a lot in this capacity, because we just don't get exposed to this. And I mean, you're going to find, believe it or not, you're going to find a lot of arrogant neurosurgeons out there that think they know everything. I know it's shocking for y'all to hear that. But the reality of it is, is that someone's going to think they got it all figured out. And Cindy's mentioned, Guy Clifton, who was this guy that had all these papers in the New England Journal of Medicine. He was my chair when I was a medical student at UT. But he would say, oh, no, we're not going to shunt this, too much trouble, no, I know better than you. And the reality of it is, is I'll submit this to you, I'm confident in my own skin. Most neurosurgeons don't know better than you in this context. They don't know what the hell they're looking at in this context. They don't know what these tasks are and whatnot. So if there is some functional gain, I submit to you, there is some value in trusting that if someone's had a tap test or whatever diagnostic modality you use, there is some benefit to offering that. And I mean, Cindy always sends me these pictures, look, look at this person you shunted, you know, here they are in the gym doing this, that, or the other. It is nice to be humbled in that capacity, you know. So I think I don't have any other PR slides here, unless y'all want to see the shunt queen video again. I think that's it. Okay. So thank you very much. Appreciate it. Thank you. Well, a VA shunt can last forever, I mean any shunt can last forever, I just want to make sure that's clear. I mentioned the V pleural shunts expire just because I think the absorptive capacity of the pleura is so limited, but you know we see kids that have had ventricular peritoneal shunts since infancy and they don't wear out. The VA shunt can stay in forever. There are some known complications, you know people can get turbulent blood flow and they can get a little emboli that go off to the kidneys and there's this condition called shunt nephritis, so that can be a rate limiting factor if they get endocarditis, but we work extremely hard to make sure that we minimize those as far as all the things you can do to, antiseptic technique because everyone's really on edge when we do a VA shunt that you know someone's going to come back and they have something horrible like a vegetation that you gave them from your technique. If everything goes well, I mean the case example I just showed, I did that guy at 15 and he still, his shunt's in and working and so, but yeah I mean they can stay in indefinitely. This is the question to my PMNR colleagues. He listed a number of very useful clinical presentations. Do you see the... I always kind of ask the family and the nursing staff and everyone about variability in response and functionality. So family would come and say, at times I'm sure he's a little bit more aware of my presence, or she is, and then he goes down, his response reduces. I see that I always ask about it, and it's kind of long. I've been in this for 20 years now, and I find this variability of response a kind of useful link or functionality that sometimes you... Just the same. So I consider that the CSF pressure is not a sort of static process. It changes from time to time through 24 hours or with a position or lying up and down. And it has been helpful to sort of talk to folks like the neurosurgery and go and plead my case to them. One particular case I had a very sort of static, and I fought with the neurosurgery to put the shunt in. Eventually they did, and the woman got up three days later and left the rehab unit and went home. So I always find that it's my own experience. I don't know whether you have any experience with asking the family or the patients, the nursing staff, does the person change his functionality in 24 hours, sometime more aware of his surroundings at a time, maybe not. I have no basis or literature experience of that. I've searched about it quite a lot. I don't find it, but it's one of the anecdotes and sort of as I grew older and I become more sort of just wanted to whether you guys have any experience with that. Yeah, thank you for that question. I think it's always important to talk to families and get their perspective on whether they felt either a TAP test or a shunt was helpful for their patient. Because at the end of the day, they're the ones spending most of the time with the patients. I think after, you know, I think they try to do this at tier, but after a TAP test we try to do formalized therapy evaluations to assess whether the patient is really getting meaningful function after a TAP test. And there are a few cases that I remember where after a TAP test there was just sort of a remarkable difference between what they were doing before and after. They were not initiating before the TAP test and after the TAP test they were initiating, they were continent, all the things that you would think of in hydrocephalus were improved. So I think if you're able to get more eyes on the patient after a shunt and a hydrocephalus, you can really get more of an evaluation and more of a sense of how the patient has done. You just reminded me of more videos I should have used because I think I have a feeling I know which patient Nathan was talking about. We had one patient where she had a TAP and she went from doing nothing to on command shooting a Nerf gun. Is that who you're thinking about? Yeah. And that TAP test was done largely for the sake of the family. We already were pretty convinced and unfortunately for everyone involved in that case she hadn't come from his institution. So it made getting the logistics and the buy-in a little bit more difficult. But there's variability in how we all do during the course of the day anyway and if you're at a particularly lower level of interaction that can vary. The other thing I think I want to comment that we're not talking about here is a TAP test gives you a little bit of useful information, but it doesn't help you understand what the neuroplasticity may be over the next six months, year, going forward and that's something that unfortunately, I think people expect from a TAP test or even when they first get... You know the patient finally gets back from having a shunt. So I think that's, you know, hopefully what we're doing... Hopefully, you know, someday I don't find out this was totally misinformed, but hopefully what we're doing is just facilitating an opportunity for a better degree of recovery. So are there any other questions? Alright, well thank you all. Thank you, Nathan. Oh, go ahead, go ahead. It's a simple question for a freshly shunted patient, are there any rehab precautions that you would? You know, I think after 24 to 48 hours, I usually tell my rehab colleagues, go ahead, do anticoagulate, whatever you need to do. I'm certainly not worried about anything mechanical with the shunt. So, I mean, I think with the exception of just wound care, making sure that they're keeping the wound dry and there's not something where they're going to be, you know, exposed to, you know, hydrotherapy or something where they could potentially have the wound in a tub or something of that nature, but they're not very delicate. And there are people in the NFL that have shunts, so yeah, they can take some abuse. Is the stabilization off when they rehab? No, no. You can do whatever you want, in my opinion, from the positioning. If we do have someone with a shunt, is there something we should watch for that would make us want to re-image or call you guys about maybe adjusting the flow? Well, I think it's clinical judgment and it's a very broad question, but I mean, obviously, any altered mental status, for sure. Any signs of fever, you know, particularly in the first couple of months. I think those are definitely very legitimate neurosurgical consults. And that's more on the emergency side of things. From the standpoint of where, you know, the interaction, I mean, like, Cindy and I have a pretty good relationship as far as, you know, I call her in my clinic to talk about people that follow. I think it helps to have that, but not every institution, you know, that neurosurgeons are as involved. And I'm not trying to pat myself on the back, but my point is, is that if you don't have someone that you don't have as close a working relationship for whatever reason, you know, if you don't have constant coverage or whatever it is, I think the main thing you have to figure out is, you know, what is their trajectory from your judgment at rehab? And if you feel that, you know, they have plateaued and you feel that they shouldn't be plateauing, to me, that's the language that Cindy and her colleagues at TIER use to talk about why we should give more consideration to some additional adjustments. And that's where it's always a balancing act, because patients do get fixated that it's sort of a fountain of youth. If we just dial it, every dial we make, they will get better. And it's not quite like that. I think you have to hit that happy point, and you have to balance safety with optimizing their outcomes. And so I think that's the magic that no one knows. I don't know that, and Cindy doesn't know that, but we try to do the best job we can of getting them to their best rehab state by dialing the shunt, minimizing those complications of over-drainage and things of that nature. But I would say failure to progress. That's my semi-professional opinion about rehab doctoring to a rehab doctor, is, you know, if they're not progressing, I think it's a legitimate thing to ask your neurosurgeon about additional programming. But is there, like, if they had set it too high, is there something to watch for, like something's urgent? So usually when the valves are set high, they're not draining much. Oh, I'm sorry. Yeah. So if they're set too low, then, you know, you have these, for sure, positional headaches. I mean, someone, every time they get up, they have a headache. Yeah. I mean, that's pretty good for over-drainage. You know, like I mentioned, you know, cranial nerve palsies, particularly people that are non-verbal. And if you suddenly have bilateral six nerve palsies and you're like, what's this all about? That's a classic physical exam finding for someone who's over-draining. And so I think the other things, too, I mean it can be a real challenge because, again, a lot of these patients aren't good historians or they can't talk or whatever. So, you know, I think any unexplained irritability or mental status changes, you know, it's worth, you know, looking at and you can evaluate a lot of this stuff just with a CT scan and an x-ray just to determine what the shunt setting is. Perfect. Thank you. The other thing I'll add to that is before I call any neurosurgeon, I always make sure that there isn't a medical reason for a decline in that patient. I rule out as much as I can first. Yes. You often don't want to call neurosurgeons unnecessarily at my institution. All right. Thank you. Thank you. Anybody else?

ventriculoscopy

hydrocephalus

endoscope

blockages

cerebrospinal fluid flow

shunt placement

infection risk

recovery time

qualified neurosurgeon

shunt valves

complications