Three particular informational sources have played a key role in making sense of disparate symptoms:
The Driscoll Theory by Dr. Diana Driscoll. Although primarily focused on Ehlers-Danlos/POTS patients and the particular Intracranial Pressure Dysregulatory Disorder these patients often experience – Intracranial Hypotension – especially her observations about the carotid triangle, vagus tone, and cerebrospinal pooling/blockage due to “brain sag”.
Adrenal Fatigue Syndrome by endocrinologist Dr. Michael Lam, MD and Dorine Lam, RD, MS, MPH. A well written book describing endocrine system interactions as a result of long term, high level stress, how that system begins to become dysregulated, and the hormonal consequences thereof, as well as approaches in dealing them.
Multiple Research Papers that have documented the presence of hormonal receptors in the cells that produce CSF. In a word, many of these hormones become dysregulated in Adrenal Fatigue/Failure. Each in its unique way contributes to increases in blood pressure, CSF production – or, as in the case of aldosterone – is responsible for both. This means increased blood pressure & therefore increased Cerebrovascular Dynamics as well as increased CSF production. The perfect storm for development of elevated ICP, and if not controlled, an ICPDD in patients with predisposing factors. Some receptors are estrogen/progesterone sensitive, possibly explaining why patients are more commonly female. Further, looking back to Dr. Lam and Dorine Lam’s body of work, it will be interesting to compare the upswing in ICPDD diagnosis with the increase in estrogen-like compounds in everything from food supply to dental fillings.
All these fell in my lap within a two week period in December 2018 while I was hunkeringS down waiting for a shunt revision, and to my surprise, they did not lead me to what I was looking for: why I developed IIH.
Well, sort of.
They actually led me to a conclusion that I cannot emphasize enough, hence the big letters here:
“The Secondary Acquired Adult Onset form of the “disorder” known as IIH is actually a complex symptom of a dysregulated endocrine system, including “Adrenal Fatigue”, which is most commonly caused by chronic stress. Therefore, I name CHRONIC STRESS to be the main cause of altered/elevated ICP and the onset of ICPDDs, and the ultimate reason I developed an ICPDD.”
Shuntwhisperer’s Neuroendocrine Theory of IIH, Dec 2108
But wait, there’s more:
“Successful treatment of ICPDDs must necessarily involve endocrine function AND CAPACITY* before any ICPDD can be successfully treated. To treat only the ICPDD is treating only the symptom; without lifestyle/dietary changes and endocrine support can possibly condemn a patient to unnecessary prolongation of their ICPDD.”
Shuntwhisperer Neuroendocrine Theory of IIH Corollary #1 Jan 2019
And just when you didn’t think it could not get ANY better:
“Elevated ICPs cause deformation and damage to key portions of the brain controlling the endocrine regulation, especially the HPA Axis. The HPA axis must be well regulated to maintain ICP equilibrium. THEREFORE: TREATMENT OF ICPDDS WITHOUT TREATMENT OF ASSOCIATED ENDOCRINE DYSREGULATION WILL BE SUBOPTIMAL.”
Shuntwhisperer’s Neuroendocrine Theory of IIH Corollary #2 Jan 2019
In other words, endocrine dysregulation that leads to an ICPDD, left untreated, can cause the ICPDD to persist, and more corollaries are coming.
But don’t take my word for it.
Take an expert’s. I swear, I did not rip this off, but Dr. Lam’s book led me to the same conclusion:
“…My last post was in late 2018 regarding an epiphany I had been given regarding a theory about how a person develops acquired adult IIH. Of course, right at that point, the creaking, weak, bottom fell out from under me.
Note: I need to acknowledge something to a person who reached out to me for help. This person believed they were developing an infection of their shunt and were desperate. Due to my own recent challenges, I didn’t open that email until a week later, and then due to some strange glitch, lost it entirely. To that person, I am deeply sorry, and I pray you were able to avail yourself of the ER in time. FWIW, I just went through the same problem 7 weeks post-revision. I post my email contact, ShuntWhisperer@ShuntWhisperer.com to help answer questions if possible, but I am not a neurologist or neurosurgeon, and if anyone should find themselves in and emergency situation (infection of the shunt tract qualifies), get to your physician or ER first, then email me if you like. FWIW, I am making it a point to check my email every morning at the very least as long as I am able.
Greetings to all.
It’s been a minute, to be sure…more like 4 months.
My last post was in late 2018 regarding an epiphany I had been given regarding a theory about how a person develops acquired adult IIH. Of course, right at that point, the creaking, weak, bottom fell out from under me.
I had to devote what little functional capacity I had to managing this new challenge; making new posts here was just not possible. February was a very, very, very (etc.) difficult month. Most days I felt like I a lone person in a dark void above a bottomless abyss, clinging by my fingernails to my spiritual, almost tangible touchstone, Jesus Christ. I can say with complete certainty He is the only reason I am still here to right this story.
The Lord works in His own way(s). In my case, Dr. Kenneth Liu of Penn State Neurological Services, the neurosurgeon who saved my life by placing my first VP Shunt two years ago, revised my shunt and repaired the inexplicably persistent hole/CSF leak associated with the craniotomy (surgically created hole in my head). I referenced this problem in the post “Juice Boxes and My Brain…Who Knew?). I can now say with a weird sense of satisfaction that I now have a metal plate in my head. A small one, but nonetheless, a metal plate.
This surgery resulted in an immediate, marked improvement, but still with instability, though not nearly as severe. There was still a small but noticeable CSF leak. At 5 weeks that last leak suddenly stopped, and it was as if my brain had suddenly been switched back “ON”. Most notable was that extreme sensitivity to certain triggers, especially barometric pressure, was either drastically reduced or eliminated altogether. Before the revision surgery, I could not stay at my new retreat in the mountains at a modest 2200’ elevation if the barometer dropped below 940 mb. I would become bedridden with fatigue, pain, and ‘brain fog’. I would be forced to leave the mountain for lower elevations, and I began to be able to predict at which turn in the road I would start to feel improvement. I would stay at a lower altitude for a week, and when I felt better, I returned, only to have the scenario play out over again within the next 7-10 days. Was this real, or was it some perverse trick of my psyche? I decided to find out, and with a prescription from Dr. Liu, I bought a home hyperbaric chamber. Expensive, but it was the only way I knew to answer the question about the effect of barometric pressure on my personal form of this disorder.
I’ll go into more detail about the chamber later; for now I’ll just say I ran a series of controlled experiments. The results were undeniable: climbing in the hyperbaric chamber and simply increasing the pressure inside to 30mb above local pressure reduced or eliminated by pain and feelings of fatigue. However, no matter how long I stayed in the chamber, once I exited, those symptoms returned in 1-6 hours depending on local conditions, so there was no doubt that this small change in barometric pressure was enough to drastically affect my well being.
I also noticed something else: when I got out of the chamber, I could feel my shunt flowing. If you have a shunt, you know what I mean. More importantly, I noticed that swelling developed along the shunt components under my scalp starting at the craniotomy and eventually proceeding back to behind my ear. I interpreted this as a CSF leak. The catheter that connects to the shunt valve is a surgical silicone; human tissue does not adhere to this material. I also discovered these catheters are further treated make them even more resistant to the adhesion of cells in order to prevent stray bits of protein and brain tissue from adhering to the inside of the catheter and eventually blocking it; this treatment is intended to prolong the life of the shunt. In my case, bone had failed to fill back in the craniotomy, leaving a path for CSF to leak between the outside of the catheter and the dura and along the catheter and shunt under my scalp. This resulted in overdrainage of CSF as it was drained not only from inside my brain as intended, but from outside the brain as well. This caused me to experience intracranial hypotension, and was a truly miserable test of my personal belief that a more appropriate term for this disorder is Intracranial Pressure Dsyregulatory Disorder (ICPDD).
I took this information to Dr. Liu and ultimately the decision was made to revise the shunt and repair the craniotomy. Now that this unwanted leak has been stopped I have experienced increasingly stable improvement of my disorder, including greater functional capacity and dramatically reduced ‘fibro’ pain. I still have challenges from the effects of almost 2 years of wild swings in my ICP, including physical deconditioning. Spring weather patterns here have been brutal, with at least 4 “bomb-grade” storms (defined as a weather system with at least a 24 mb drop in barometric pressure in 24 hours) in the last month. Prior to the March surgery, these systems invariably laid me up for at least three days; now, their effects on my disorder are greatly diminished, and seem to be continuing to diminish with each passing day. Only one recent freak set of back-to-back storms really hit me hard, but in that case there was also a potentially serious late postop complication that I was fortunate to recognize and address before it got out of control.
All this preamble brings us to now. ShuntWhisperer started as merely a “this is my story, maybe it will help you” type of blog. Over the course of two years, I’ve learned more as I’ve continued research and experienced new challenges that while very difficult, contributed to a better understanding of my disorder. The structure of the original site was never intended to present this material of this depth in a coherent and orderly manner. I never expected it to be more than a few pages, but it has blossomed well beyond that. Thus I will be restructuring the site “on the run” as ShuntWhisperer 2.0. It is intended to be concise, presented in lay language to the degree possible, and accompanied by references to existing research, with a reference section for physicians. Please don’t expect a visually dazzling site; I simply don’t have the time to post anything but pertinent information. Also, the original ShuntWhisperer site and its contents will still be available, accessible from the new landing page.
SW 2.0 is still intended to be based on my personal experiences and research. I can’t claim anything I post applies to any other person with a disorder of altered intracranial pressure, although there are certain immutable laws of human physiology that lead me to suspect that is indeed the case; I just can’t make that claim. I’m not sponsored, I don’t get paid for this, and don’t care to receive any credit for any good that comes of what I post. I am doing this in Service to God in an attempt to help others, as well as in memory of my wife Trina. My contact email is Shuntwhisperer@shuntwhisperer.com for anyone who has a question, feedback, or suggestion.
As always, prayers to all for comfort, support, and a better quality of life.
April 26, 2019
Today’s storm and rain has passed; it’s a gorgeous spring day on the mountain, and I’m going to take a break to enjoy it, wishing Trina was with me.
“But ask the animals, and they will teach you, or the birds in the sky, and they will tell you; or speak to the earth, and it will teach you, or let the fish in the sea inform you. Which of all these does not know that the handoff the Lord has done this?”
*soft tissue tumors can also occupy space inside the skull and potentially raise ICP but are considered a separate causative mechanism from those that are considered in ICPDDs
The cause of these imbalances can be either genetic/developmental (primary) or related to trauma (secondary). They are closely interlinked and may both be present to a certain degree.
One example of CSF Imbalance would be non-communicating hydrocephalus. CSF is produced from arterial blood in small hollow areas of the brain called ventricles. Ventricles are normally interconnected with one another and the space around the brain. CSF circulates through these areas passively due to the pulsation of blood vessels and also likely movement of the body. If one or more of these ventricles does not communicate with the rest of the system, the CSF it produces accumulates and displaces the brain outward.
Another exmaple of CSF Imbalance illustrates the interrelationship between CSF and Blood dynamics: obstructed veins may not absorb enough CSF out of the skull to prevent a net accumulation of CSF, as well as leading to this example of:
Cerebrovascular Dynamic Imbalance: would be Chronic Cerebrovascular Venous Insufficiency, or CCVVI. In simple terms, damage or constriction (stenosis) of one or more of the veins that drains blood from the brain compromises the ability of blood to leave the brain. At a certain critical level of blood flow and pressure, blood begins to accumulate in the brain as it is pumped through arteries at a greater volume than it can drain. This accumulation of blood causes the thin-walled veins to swell, which in turn pushes on brain tissue. Brain tissue may become displaced as a result, being pushed into areas occupied by CSF. Since an intact skull is rigid and does not expand, the pressure of the CSF becomes pressurized (Newtons’s Third Law) while simultaneously trapping brain tissue between a vise of swelling veins. As focal areas of brain tissue that control specific physiologic functions become stressed, their functions become altered. This pressure on brain tissue is likely the cause of symptoms associated with IIH.
Everybody knows the old adage about how to eat an elephant. ICPDDs and their nuances certainly qualify, and the goal here is to present information in easily digestible bits. This is the first bite.
While the reason/reasons (“etiology” it doctor-speak) a person develops IIH/PTC/etc. remain unknown and controversial, the physiology of how the pressure develops is actually quite straightforward: ICPDDs reflect an increase in the pressure of fluid in and around the brain. Thus, they are a result of a disruption in the dynamics of the fluids in and around the brain. While CSF is most commonly discussed and treated, there is another fluid that actually rules everything, including CSF:
Blood is the 800 lb Gorilla of the brain. It is pumped into the brain primarily through the
carotid arteries at a rate of 750 to 1000 cc/minute when we are at rest; it courses through an estimated 100,000 miles of blood vessels delivering nutrients and oxygen to brain tissue. Depleted blood is drained via the venous sinuses, a network of veins around the brain, and eventually through the jugular veins back to the heart.
Blood enters the brain at an average pressure (“Mean Arterial Pressure”, or MAP) of 90mm Hg. It drains from the veins at a pressure of 15-20 mm Hg. Because the same amount of blood that flows into the brain has to flow out, and because venous pressure is lower than arterial pressure, the blood flow in veins must be higher to compensate (fluid dynamics, Bernoulli, a couple other Italian guys in there). Suffice it to say that veins have to be able to carry away ALL blood that is pumped into the brain. In addition to that important necessity, there are TWO factors of blood that must be considered in ICPDD: pressure (as expressed by MAP), and flow. For the sake
of simplicity we will use heart rate as an indicator of blood flow.
CSF is a plasma like fluid that is made from blood in an interconnected network of small hollow areas in the brain known as ventricles. It is produced at a very low
rate of ~0.35 cc/minute from arterial blood. Its rate of production is dependent on the am
ount of blood flowing into the brain. CSF circulates through the ventricles and around the brain; this circulation is slow, with pulsations from blood vessels and body movement being the primary motivators. It is primarily absorbed back into the blood circulation in the venous sinuses.
CSF is something of a Mystery Fluid. Aside from cushioning and supporting the brain, it is thought to play a role in delivering nutrients and cleansing dead cells from the outer surface of the brain. Deficiencies in CSF are associated with accumulations of these dead cells, known as plaques, which are themselves associated with dementias such as Alzheimers and Lewy Body. Anyone with an ICPDD can tell you that “overdrainage”, ie, not enough ICP and/or CSF makes them feel weak and lethargic. Again, suffice it to say that CSF is Very Important; otherwise, it would not be in our heads.
SUMMARY, PART ONE: THE TWO FLUID POSTULATE
The dynamics of blood and CSF lay the groundwork for understanding ICPDDs. ICP is a result of the interaction of these fluids inside the watertight, airtight, non-expandable skull. These facts lead to what I call the Two Fluid Postulate:
“There are only two fluids inside the skull: blood and cerebrospinal fluid (CSF). Both are present in approximately equal volumes, 150cc. Only one flows in and out of the brain: blood. CSF is made from blood that enters the brain and absorbed back into the veins that drain blood away from the brain. Intracranial pressure is the sum of the forces exerted within the skull by these two fluids. Changes in the balance of CSF production/absorption and/or blood flow into and out of the brain will necessarily affect ICP. Most critically, because the brain is encased in a rigid, non-expanding skull, ANY INCREASE IN ICP TRANSLATES INTO INCREASED PRESSURE DIRECTLY ON THE BRAIN.”
This is just a restatement of what is known as the Monro-Kellie Hypothesis from the 1890s by two Scottish physicians to explain what goes on inside the skull.
CSF, while the most often discussed fluid in ICPDDs, is not the only fluid in the brain. Blood, in fact, rules everything inside the skull, including CSF. Because the volume inside the skull is fixed, and because there practically zero extra space in the skull, any net accumulation of CSF OR Blood will cause increased ICPs, and those increased ICPs exert direct pressure on the brain itself.
In Part 2, we will look at how the dynamics of blood and CSF become disrupted.
Communication over the internet can be challenging. Not like talking face to face; it’s easy to misunderstand what is being said, or why somebody is saying it. That said, I want to lead with this: ShuntWhisperer is just my story for about my ICPDD for whatever it’s worth. ICPDDs and their treatment are poorly understood, doctors do the best they can with what is available now. I think I’ve stumbled on to something…interesting… for no other reason than weird coincidence, and I don’t believe in coincidence. Maybe this story it will help somebody, maybe it will spark conversation or thought, but it is absolutely, positively not intended to point fingers or place blame. Despite the challenges of the last year, I would not change anything. I’m just trying to make the most of it for the possible benefit of anyone who finds my experience useful in their journey, both patient and doctor. I try to keep this as light as possible; any humor is just that, never intended to be irreverent. The fact is I’m still here to type this because of the efforts of my neurosurgeon and the Grace of God.
Now, we return to our irregularly unscheduled post:
Is it seriously this “simple”?
So, last year, after I received my shunt, I had a pretty wild ride to put things mildly. Despite all of it, I’m seriously grateful for everything. There seem to be so many unknowns in ICPDDs; all through my experience I’ve tried to learn as much as possible about what is going on in my head and pass that information along. It seems invaluable to me, and I pass it along not for my benefit, but in the hopes that it helps somebody else, and maybe fills in a small part of the overall puzzle.
My Biggest Issue: wild swings in my ICP, with a distinct trend towards overdrainage. The higher the shunt was adjusted, the worse it got. I never felt like I had enough CSF/ICP/MysteryFluid in my head. Ever.
Until November, when thing began to change…
I was using the Whisperer Method to monitor blood flow into my head. The numbers I got were deadly accurate both in how they related to my SOTD (Symptomology Of The Day). The Cerebral Perfusion Coefficient (a figure that gave me a relative idea of how much blood was flowing into my brain along with the static pressure in the blood vessels) numbers stayed within a fixed range. On the low end of the scale I considered myself “underperfused”, that is, not enough blood going into my brain to make enough CSF to keep up with normal losses along with…some other loss of CSF, someplace. I thought it might be through my shunt, but I don’t think so now. On the high side of the scale I felt like my head was going to burst, my shunt felt physically swollen, but perversely, I still felt as if I had no CSF in my head. The “no CSF” feeling is one that I was well accustomed to as it was the same set of overdrainage symptoms for which I was hospitalized in June 2017, 3 months after getting my shunt.
The Deadly Accuracy of the numbers and symptom correlation held up until the end of November, when I noticed numbers and symptoms starting to diverge a little. Then a bit more. This divergence continued up until Christmas day, the last “BAD” day I had according to the old pattern. Suddenly the numbers and symptoms no longer seemed to match. I had no answer.
From Christmas on, suddenly the wild instability rapidly diminished. Extremes of high and low ICPs became closer together. No more apparent swelling of my shunt which is
made largely of rigid materials incapable of expansion. It was as if either a blockage in my shunt had been cleared, or a leak in my head had been closed off. Curiouser (TheWhisperers Unabridged Dictionary), the Cerebral Perfusion Numbers started climbing to new highs, up to 20% higher, without the usual symptoms high ICP symptoms of feeling like my head was going to explode. January into March I actually felt pretty stable, still with bad days, but the best I had felt since getting the shunt. This left me scratching my head, and that’s where I found The Answer To It All.
I’ve never been accused of being the sharpest knife or having a full picnic basket, etc. A little slow at times. So, a few days ago, I’m rubbing my head where the shunt catheter goes into my skull. A slightly larger than dime sized hole created in my skull to allow the catheter to be poked into the hollow area in my brain. No jokes about how easy it should be to hit a hollow area in my brain, please. I’m delicate…
The skin over this hole, a.k.a. “craniotomy”, is slightly indented, normal for a surgical wound. What I noticed is that I no longer noticed it anymore, because it was no longer changingshape. All last year it changed contour with my ICP. Sometimes it was like it was being sucked/pressed into my skull, other times, it was almost as if it was being pushed out under conditions of high ICP. It had become a sign I used to make note of in recording what was going on with my disorder, but now it was no longer changing….
Then, slowly, reality crept up on me. I like to blame the fact that I have a tube in my brain for all these issues of slow comprehension; rather convenient really. Never mind the fact I was slow before I got the shunt, but now I can point to it and say “See? I have a tube in my brain. I’m slow for a reason”, which sounds infinitely better than “I’ve always been slow.”
It was about the hole in my skull; a hole in bone. A dime-ish sized hole was made in my skull, exposing the dura underneath.
The dura is carefully opened, and a 3D guidance technique, a catheter over a needle, sort of like an IV catheter for the brain, was then inserted through the into the immense hollow area in my brain to drain CSF, after which the dura was sutured around the catheter and, my scalp repositioned and stapled shut. Joking aside, I have always appreciated the precision of this particular aspect of the procedure. I had employed guidance techniques generated from 3D scans to place dental implants with extreme precision; the shunt cath placement is another level of precision entirely.
I joke that placing a shunt is not unlike poking a straw into the foil hole of a juice box. No adult can put a straw in a juice box as well as a kid, who with a deft poke can stick that straw through the foil like a kung-fu master, creating an almost perfect hole to match the straw. Perfect enough to suck juice through the straw, but we all know what happens if you squeeze the box with the straw plugged: juice seeps out around the straw, and the ratio of juice-leakage-to-squeeze is directly dependent on the cost of the shirt that is being stained, and inversely dependent on the time since same shirt was laundered.
Doubling factor if dry cleaning is involved (see: Whisperer’s Laws of Life 301).
If I have failed in my wordsmithing to create a clear mental image of this condition in your head, let me invite you to get a juice box, a bag of Capri Sun, a Corona Beer Pouch
(see: Whisperer’s Intellectual Property Item 526), poke the straw through the foil (or get a child to do it for you, except for the Beer Pouch, of course), plug the end of the straw and squeeze the box/bag of juice. See where it leaks – between the foil and the straw, right where the straw goes through the foil. Except in my case, it was not juice, but CSF, leaking around the catheter where it penetrated the dura. There is no magic seal here, and if ICP exceeds the pressure/flow settings of the shunt system, here is a place where CSF can leak.
I’ve been crafting, honing, polishing this for 3 days now, and each time I think about it, I keep wondering how many other shunt patients this might be a factor for, with any type of shunt, VP or LP. The good news is there is a way to mitigate this leakage, or at least reduce the period of time it occurs through a simple surgical method to encourage faster growth of bone into the craniotomy.
As a dentist in my Previous Life, I was intimately familiar with the tissue of Bone. Drilled a lot of holes in bone, grafted a lot of bone, moved bone from one place to another, bone, bone, bone, all day long, bone. But, it paid the bills. I know about bone in the human body, how it reacts to injury, how it heals – or doesn’t. Without the fancy “bone bandage” known as a guided tissue membrane, bone may never fill in a defect completely, and if it does, it takes much longer. A hole in the skull heals from the sides in and from the bottom up, over top of the dura, which by the way makes a dandy guided tissue membrane, at least on the brain side. The issue here is the scalp tissue is a source of soft tissue that fills the hole in the skull well before bone has a chance.
Short story: I didn’t get the fancy bandage for whatever reason. I got a hole “stabbed” (actually carefully incised and then sutured, but for the sake of sensationalism…) in my dura (I wonder now if a child was brought into the operating room to do that part), a catheter inserted into my brain (with great care an precision), the latter hooked up to the shunt valve, and my scalp flopped back into place and stapled as the neurosurgeon asked the charge nurse if he still had time to make the late morning round of golf while the kid that poked the catheter into my brain sucked on a juice box under his surgical mask while sitting on a stool in the corner. In all seriousness, I can’t find a thing that says that shunt craniotomies should be grafted over; maybe they should be.
Bottom Line: March 2017 until I’m guessing November-ish 2017, I had a CSF leak that mucked up the attempts to control my ICP. Ironically, whenever the shunt was “turned up” to a higher pressure setting, it made the problem worse. Nothing sealed the dura to the tube. CSF seeped between the tube and the dura, under the surgical flap, finding its way under my scalp, along the tube and around the shunt body, and likely farther. In surgery the phenomenon is called tunneling, and the leakage of CSF around the catheter created what is known as a pseudomeningocele. Finally in November a stage of healing of the craniotomy was reached that mitigated significant leaks. The timing is right for the size of the hole. However, since to guided tissue membrane/Bone Bandage was used, there is also a good chance the hole isn’t filled with bone, but with a thick scar tissue that may eventually turn to bone. Whatever is in the hole, my head isn’t leaking from an unwanted place anymore.
Google the term “Intracranial Hypotension”(not “hypertension”) . It’s a real thing. Usually caused by an unwanted, unpredicted leak in the dura. I believe this was a large part of the reason for my “wild ride” I went on after my shunt last year. My concern now is who else may be suffering from it or may potentially suffer from it; possibly by posting this, a surgeon may be persuaded to add 10 minutes to the procedure and graft a VP shunt: I don’t know about LP shunts.
This theory also explains a new phenomenon: the return in the last six weeks of my pre-shunt symptoms that were associated with high ICPs, the reason I got the shunt in the first place. Not as bad yet, but getting there. Fibro pain coming back, other bad stuff, BUT: there is a clear silver lining. Regaining proper ICP balance may be as simple as turning my shunt down a notch. As I write this I’m awaiting a CT to check my meninges, and I’ll post the results here.
(edit to add 5/22/18: those symptoms are definitely back. Time to check in with the neurosurgeon.)
The silver lining here is that I’ve gotten this far and have avoided at least one procedure that would likely have made things worse. Early on last August when I was still having overdrainage symptoms despite having a shunt set at 200mm H2O PLUS a 250mm shunt assist, my neurosurgeon graciously offered to revise me to a higher pressure shunt valve. I declined that offer because my personal situation was not amenable to having the surgery at that time, and I believed I could hold on until another option became available. In retrospect, that higher pressure shunt would have likely made me worse. I consulted with other neurosurgeons for their opinions, but I was never satisfied with their explanations based on nothing better than “gut feeling” and the personal records I had kept. Now I believe I have that explanation, and I’m hopeful that a simple pressure adjustment in my shunt will restore some or all of the reduction in fibro pain, stop the return of the exercise intolerance which is again threatening to leave me bedridden for days after engaging in any physical exertion, and the sleep cycle disorders/insomnia which is back. It is also my hope that this story helps somebody else, or sparks a thought process somewhere in the minds of doctors wrestling with a disorder that has so many unknowns attached. I was told by one surgeon I was the “Unicorn” of this disorder (!); if so, at least now I know from whenst my horn grew…
Bottom Line: without a good seal, CSF can and does leak around shunt catheters. Pseudomeningoceles are a known postoperative possibility with shunts, but their frequency of occurrence is controversial. Secret or not, the answer may be a few added minutes to a shunt placement and a few hundred bucks for a bone bandage. The bandage keeps soft tissue from the skin flap out of the craniotomy, encouraging more rapid and predictable bone healing around the shunt catheter. Bone grafting material made from the patient’s own blood (Platelet Rich Fibrin), can be used to further seal the craniotomy before the bandage is placed and everything sewn/stapled shunt. This is just an opinion I toss out there as a Disabled Dentist With a Hole In My Head.
It is my fervent hope that this clicks with ShuntWhisperer fans (both of you), maybe some docs, and that maybe, just maybe, addressing this small issue will make the post treatment course of other ICPDD patients and VP shunt recipients in general better. As always, prayers to all. Questions can now be sent via email to firstname.lastname@example.org, and I am have setting a Twitter Feed specifically for ShuntWhisperer.
The Shunt Whisperer
May 19, 2018
Missing my wife in my life more and more every day: I love you, baby.