Welcome; let’s get to work…

“Members of Support Groups for ICPDDs frequently refer to themselves as warriors, and they are no less.  I truly pray that this site becomes a “weapon” in that battle by disseminating information…”

Welcome to ShuntWhisperer.com.

It’s gonna be a bumpy ride.

I started this site after being treated with a VP shunt for an Intracranial Pressure Dysregulation Disorder (ICPDD).   For whatever reason, the result of the shunt treatment was nothing like what I expected it to be.

Nothing like what the neurosurgeon said it would be.  “Infection”, with a shrug of the shoulders, no big deal, when I asked what my risks would be.   Quite possibly what he believed.  Not at all what I got.

Imagine brutal HALO free-fall onto a demon’s roller coaster that dropped off the tracks in the middle of a triple loop into a bottomless pit without safety harnesses, and that’s an outline of what I endured for four months after the shunt.  And don’t get me wrong, there were some enormous positive outcomes as well, improvements in long term pain and fatigue as pressure on critical areas of my brain was relieved and I began to recover; it’s my opinion that it has kept me alive.  But: Holy Acid Trip, Batman, I wish I had been prepared for the beatdown I received so I could have faced it head on, KNOWN it might be coming, instead of being sucker-punched.  Sucker Punched, I believe, to everyone’s surprise, including my neurosurgeon, trying to help, frustrated at not knowing the WTF of why the treatment was going sideways.

I was a dentist for 25 years.  I performed a lot of complex surgeries, sedations, cut pieces from one part of a patient’s mouth and sewed/screwed/glued it to another.  I spent A LOT of time preparing my patients for their post-op experience before I ever laid a scalpel on them.  Well, that level of attention didn’t seem to apply here.  Turns out that ICPDDs are in their infancy in the practice of medicine, thus the information that could prepare a patient for a Lewis-Carrol-meets-Hunter-S.-Thompson-esque outcome doesn’t exist.   Most PCPs don’t know what “Intracranial Hypertension” is, much less how to treat it.  Even amongst NeuroDocs (neurosurgeons and neurologists), there is no consensus as to the cause of ICPDDs and how to treat them.  There is even a vocal group of doctors who deny they exist (I would love to let you guys spend a couple of days in my head…).

I went into the shunt surgery believing I would end up with the blessed relief I had gotten from my diagnostic lumbar puncture.  I actually did get a lot of relief from pain, fatigue, cognitive difficulties, and other symptoms ICPDD patient’s struggle with, but I also got the Bonus Symptoms associated with unstable intracranial pressures, Bonus Symptoms that nobody seemed to understand.

The purpose for ShuntWhisperer was initially just to tell that story.  I thought it might give somebody else a reference point, a warning, an explanation should they find themselves on the same path.  But then I was hit with “bitchslap #2”, sort of a Buyer’s Remorse:  it was revealed at my first postop with the Nurse Practiioner that there was essentially zero understanding of what was actually going on in a human skull,  no way to measure the oh-so-important ICPs without drilling a hole in my head and inserting a “bolt”: quite literally a bolt with a a pressure transducer in my skull.  In an Intensive Care Unit.  Then she told me there was no follow-up program for shunt patients, “just come back if you have a problem.

Nothing like treating a problem instead of preventing it.  Not to mention the loss of valuable data from a pool of patients that medicine admits  to having zero knowledge of/about/how/why that a follow up program, a simple questionnaire might provide.

At that point, the purpose for ShuntWhisperer.com changed.  I had become a member of support groups for patients with ICPDDs, and all I saw were patients just like me.  Confused, struggling, refusing to give up but without any support.  And some who where actually doing well.

After graduating from dental school in 1986, I did an optional residency in a hospital. It was worth 8 years of dental school.  Exposed to Medical disciplines including Emergency Medicine and Anesthesiology was priceless, but without a doubt the group I came to admire the most was Internal Medicine.  Physicians with intimate knowledge of human physiology who often collaborated on cases where the patient presented with a set of symptoms without a known cause.  These docs were brilliant and were not satisfied until they knew exactly what had landed a patient in the hospital, a knowledge used to treat the cause of the patient’s condition, not just the symptoms.

They became my role models.

Now, faced with what appeared to be a terrible lack of understanding of a condition for which I had just had a tube stuck into by brain to drain cerebrospinal fluid, I was literally terrified.  I swallowed it down and started paying attention to the particulars of my condition.

I began to see patterns; from patterns, theories.   Testing of theories.  My theories resulted in methods of managing symptoms.  That management led to more days of function, fewer days of feeling so horrible I could not get out of bed, watching my life dwindle away one day at a time with no explanation.

Then it happened:  Inexplicably, against all odds, my Trina was diagnosed with Intracranial Hypertension.

What are the odds?  A married couple with an extremely rare disorder?  Outside of a care facility, support group, or other instrument that brings ICPDD patients together, few of us know another person with an ICPDD…much less be married to one.  Why?  What is the commonality?

I know.

Odd, no physician has ever considered it odd yet.  Asked that question: why?

(pssstttt: we both had multiple, severe neck injuries that preceded the onset of symptoms).

At that point, when Trina was diagnosed, it was all bets off.  She had watched me go through hell with my shunt.  She was scared to death.  She had migraine headaches so bad that she couldn’t get out of bed.  And then, just then, at that point:

Our neurosurgeon moves.  To another hospital.  Another STATE.  He said he’d take our records, but it would be about 3 months before he could get us in, to treat my unstable shunt, to treat Trina.  And considering it took me 3 months to get a consult appointment with him and another 3 months to get treated, and that other neuros treating ICPDDs were few and far between, it seemed as if there was no choice.  To his credit, he did get us in quickly and started making plans, but three months of the psychological effects of a daily migraine that left her bedridden with ice packed around her head, the physical effects of the pressure on the centers of her brain that controlled her mood, memory, body temperature, functional capacity, the literal pressure that in combination with some of the most cruel and discompassionate dismissals of suffering by so-called “healers”, all came together on one morning in October, when with no warning, no good-bye, no note, nothing, not to mention being totally, completely out of “character” with the bright, beautiful Trina I knew and loved, she put a gun to her head and ended her own suffering,  a result of having to cope with this disorder and its symptoms for an absolutely inhumane period of time.  Make no mistake: the person that ended their life that October morning was not the Trina I new and loved; that person had been taken by the disorder.  I was doing everything I could do, firm in my belief that if we could just hang on until she could get treated, she would be better…

It’s the day after Christmas.  Just recalling that moment still freezes me up.  It was so unnecessary.  So preventable.  She was the person everyone looks for: the soul-mate, the one human being who really gets you.  And this disorder took her from me.

So now, the purpose of this site, my mission, my only purpose to keep going, is to help others struggling with these disorders.  To challenge doctors with my theories, right or wrong, but to at least get them TALKING TO EACH OTHER.  Hoping, praying that something here sparks something in somebody’s head that leads to an advance that wouldn’t otherwise come for 10 years.  Not for me; I don’t care if anyone remembers me.  For Trina, to remember her; for those suffering this disorder, in service to God.  In one of the creeds of the Knights Templar, the words:

”Non Nobis, Domine, Non Nobis, Sed Nomini Tuo Da Glorium”: Nothing for us, Lord, nothing for us but for the glory of thy name.

Members of Support Groups for ICPDDs frequently refer to themselves as warriors, and they are no less.  I truly pray that this site becomes a “weapon” in that battle by disseminating information and pushing for change an improvements.  Not to demean, not to blame; I can’t imagine the responsibilities of the neurosurgeons and neurologists who, in my altruistic sense, are wrestling with the problems of their patients.  I pray for them especially, and suggest that we all do as well.IMG_0023 (2) - Copy - Copy

I also ask that you remember one beautiful woman named Trina, my wife, who was taken by this disease, who I hope to see again someday, and who I hold up as an example of what I hope to help prevent.

 

The Shunt Whisperer

December 26, 2017

A Christmas Story: Barometers, Blood, and Swollen Brains…now with Pictures and Proof!!!

THE WEATHER AND MY IIH/ICPDD:

WHAT I KNOW…

 

The latest installment in my ongoing narrative of the effects that barometric pressure has on my condition, and presumably, others as well.  The reason I have time to do this today is, of course, a rapidly dropping barometer accompanying a strong weather front.  December 23, 2017. 

I was recently surprised during a visit with a new neurosurgeon to discover that he was not aware that changes in barometric pressure, or even weather, were issues for his ICPDD patients.  He seemed as knowledgeable as a physician could be about this new class of disorders, and he eagerly and actively accepted patients into his care.  Thus, when I brought up the issue of barometric pressure and its effects on my personal disorder, it surprised me when he related that changes in barometric pressure were not a problem for the patients he saw.

Thinking about it afterwards, I can see how that impression could be an honest error, although having conducted polls of members of various support groups I belong to, it seems that almost everyone knows there is something about weather that affects their ICPDD symptoms for better or worse.  Most seem to relate impending stormy weather with a change in their symptoms, usually for the worse*.    Based on the information that most ICPDD patient are given to work with, I’m sure some know that some days they are better or worse than others.  Another group may associate impending weather with a change, usually worsening in their symptoms.  Some have discussed changes in altitude, which translates into changes in barometric pressure, as affecting their symptoms.    Perhaps patients aren’t questioned about they notice any factors that trigger their symptoms.

Then there’s me, who is so tuned in to my disorder that the neurosurgeon asked the fair question “Do you think your attention and management to your symptoms is making them worse?”

Really, a very fair question, and I was impressed with this doc’s diagnostic thought processes.  My answer is “No; I only started managing my own symptoms to the degree I’m able after months of study of my own disorder.  Since starting to manage those symptoms based on my study, I have more “good” days, fewer days when I can’t get out of bed, and have been able to formulate theories about ICPDDs when unfortunately, consensus amongst medical professionals is rare  (note that I said “consensus”, or “agreement”; the docs I see are desperately trying to get a handle on ICPDDs.  The problem is that none of them suffer from one.  That’s where I’ trying to help.).

Is my attention to and management of my ICPDD symptoms making my condition worse?  Only if swimming to the surface and taking a breath when you realize you’re drowning makes your “drowning disorder” worse.

Disclaimer:  I don’t know that my ICPDD is the same as somebody elses.  Even if the cause is the same (I believe mine is Venous Outflow Insufficiency), it’s not likely that each patient shares exactly the same physiology.  BUT:  there are immutable laws of physiology that apply to everyone, and as such, probably bear consideration.  I don’t know if I’m 100% right, but I’m definitely onto something; I’m not trying to get credit for anything except maybe to get people talking instead of just telling us how much medicine doesn’t know about ICPDDs.  Remember this as you read the following:

BAROMETRIC PRESSURE/WEATHER:  For the purposes of this segment, we’ll consider them one and the same, as I know that barometric pressure changes accompanying changes in weather and changes in altitude definitely affect my symptoms in a predictable manner.  Short version:  increases in barometric pressure cause and increase in symptoms that I associate with increased ICPs.   Before I was treated with a VP shunt, high pressure systems made my head feel like it was going to explode.  Extremely low barometric pressures as seen in hurricanes and severe storm fronts very simply put me in bed, barely able to function.  My best days were overcast, but not rainy days.  After I was shunted, barometric pressure still affects me in the same manner, but my symptoms are different because of the shunt.  That last part took me three months to figure out, but it is fact.  A couple of stories:

The first one I love to tell.  I hate that my surgeon had stopped ICP monitoring during shunt placement, because I (and a lot of others) would love to have know what that monitoring might have told them.  The day I had my diagnostic Lumbar Puncture (LP), my opening pressure (OP) was only 17mm H2O; it took nearly an hour to drain 30 cc of CSF, whereupon my closing pressure (CP) was 16.  Most would look at the OP/LP values and say “That’s too low for a diagnosis of “IIH”.”   However, the truth is that the numbers currently used to designate “high” and “low” ICPs have not basis in science.**   I had great relief from my symptoms of pain, cognitive difficulties, etc.   Based on the positive response, my surgeon recommended that I might benefit from a shunt; on the day of that consultation, I was feeling very uncomfortable with increased symptoms I associated with increased ICPs.

Fast forward five weeks to March 23rd:  I was counting the days till the shunt; it seemed that the onset of unstable spring weather was making my ICPDD symptoms swing wildly, and I felt I was deteriorating exponentially.  On the morning of the shunt surgery, I was particularly uncomfortable, my head feeling as if it was going to explode.  “If this doesn’t work,” I told my neurosurgeon, “we’re going to have to scramble to find another solution.”   When I woke up in postop, I was groggy, but the sensation that my head was going to explode had seeming disappeared.  My surgeon came by to check on me and related that “I appeared to have had some pretty high pressures, because when (he) opened my dura for the proximal catheter of the shunt,  my CSF literally shot across the room.”.  Contrast that to the day of my LP, when I was actually pretty comfortable, despite feeling lousy after my angiogram.  Could what I emailed to my surgeon as “Post-Angiogram Blues” been a result of the procedure, or the fact that the day between the angiogram and the LP was a near record low pressure for the area, and the lowest in the months of February and March 2017?  Maybe a little of both?

Look for yourselves.  These are screenshots of barometric pressure for Charlottesville, Virginia, with dates of procedures shown:

BAROMETRIC PRESSURE GRAPH 2/1/2017 – 3/31/2017, COURTESY WWW.WUNDERGROUND.COM

Screenshot-2017-12-23 Weather History for Charlottesville, VA Weather Underground

 

BAROMETRIC PRESSURE GRAPH 2/16/2017, DAY OF DIAGNOSTIC LP – OPENING PRESSURE 17mm H2O,  CLOSING PRESSURE 16mm

Screenshot-2017-12-23 Weather History for Charlottesville, VA Weather Underground(2)

BAROMETRIC PRESSURE GRAPH 3/23/2017, DAY OF VP SHUNT PLACEMENT – “YOUR CSF SHOT ACROSS THE ROOM.”

Screenshot-2017-12-23 Weather History for Charlottesville, VA Weather Underground(1)

 

What these graphs show is that on the days of my Angiogram and LP, the area was experiencing a near record low barometric pressure.  I always associated an extremely low barometer with feelings of “weakness”, leaving me bedridden.  I’d further postulate that the this also explains the fact that it took nearly an hour to drain 30 cc of CSF, and that there was no significant difference in the Opening/Closing Pressures because…wait for it…

…ICPs are proportionally affected by barometric pressure.  This theory is given further merit by the fact that on the day of the shunt, I was experiencing possibly the worst high pressure symptoms I’d had to that point, and the fact that I hosed the OR with my CSF, under increased pressure due to increased barometric pressure.

Why?  It turns out that barometric pressure units are very significant compared to the units used to measure ICP.  One millibar, or hectopascal, is the equivalent of almost 10mm H2O.  Thus, the difference in barometric pressure of 28-30 mb between the days of my LP and Shunt translate into 280-300mm H2O.  Normally not a problem unless you suffer from and ICPDD; now, it seems to be a big problem.

I believe this is one of those physiologic commonalities we all share.  Interestingly, after I received my shunt, my symptoms changed.   Now, instead of the severe pressure, I had a feeling of “lightheadedness” that I now, thru bitter experience, associate with “overdrainage”, or excessive loss of CSF.  The problem now was that I felt that way 95% of the time.   When the barometer was low, I still felt drained, but when the barometer rose sharply to high levels, I had a paradoxical “sensation” of pressure in my head and at the base of my skull, but still had the overdrainage symptoms.  As it turns out, the barometer is still affecting me in the same manner, but because I have a shunt (“an extra hole for CSF to drain through”), my symptoms are different, but no less debilitating.

My shunt has been like trying to balance a marble on top the end of a sewing needle with the other end on a granite slab.  The tendency has been to require ever-increasing pressure settings on my shunt to achieve ever shorter periods of “stability”, until in early July, the whole business went sideways and the shunt could not be turned up further.  I’ve been managing my symptoms by managing my cerebral perfusion and Mean Arterial Pressures in response primarily to symptoms, and the nature of those symptoms always follow certain stimuli such as barometric pressure.  Now, I believe my shunt is causing CSF Hypo-tension in the following manner:

When blood flow to my brain (cerebral perfusion) is at the low end of the scale I use to measure it, I feel very lightheaded, sleepy, weak.  I know it’s due to lack of CSF because these are the same symptoms for which I was hospitalized in mid-June due to lowered a “neurologic wane/depressed state of consciousness”, symptoms that resolved with in 8 hours of turning the shunt up to its max setting.  Remember, CSF is made from blood, and the amount of CSF produced and absorbed depends on the amount of blood flowing into and out of the brain.  In my case, at low perfusion, I don’t make enough CSF to make up for both the normal losses of my venous outflow AND the seepage/leakage through my shunt.*** During these periods, the flexible components of my shunt are soft and shrunken as if there is not a lot of pressure in them.  I believe a more appropriate term for this condition is Shunt-Dependent Underperfusion as opposed to Overdrainage.IMG-6505

I have a right jugular vein that has been described as between 60 and 80% stenosed at the level of C2.  Venous drainage from the brain favors one side, usually the right, for reasons I don’t know.  At any rate, one of the main veins that drain my brain is badly narrowed.  I’ve discovered that if my cerebral perfusion exceeds a certain limit, I start todevelop sensations of pressure at the base of my skull and inside the right side of my head.  My right ear turns red and swells noticeably compared to the right side (see pic).  Most significantly, my shunt swells up; the catheters and antechamber become tight and enlarged, and at times the skin over the shunt is painful to touch.  Why?

Simple.  The pinched/narrowed jugular.  At a certain point, more blood can flow into my brain than can flow out.  I’ve discussed this as the “Cerebrovascular Theory of ICPDD”; blood backs up in the blood vessel of the brain, the vessels swell, displacing brain tissue and causing the brain itself to swell.  The only place the brain can swell towards is where there is CSF:  the ventricles inside the brain and the subarachnoid space surrounding it.  Because the area inside the skull is fixed, CSF is now pressurized, blood is now more pressurized, brain tissue swells and….

…in my current condition, CSF is forced out of my shunt under high pressures, accounting for the swelling of its components.  CSF is only made at ~.35cc/minute; my shunt drains at .5 cc/minute under “normal” ICP.  Now, however, I have higher ICP, greater flow out of the shunt in addition to CSF absorption by normal venous pathways, and I still have a CSF deficit.  This explains the feeling of pressure (due to cerebrovascular edema) as well as the “overdrained” feeling due to excessive CSF loss.  This is also referred to as secondary intracranial hypotension, or iatrogenic hypotension.

This all leads me to believe that my shunt is only treating a symptom of my disorder – CSF pressurized as a result of restricted blood flow out of my brain.  Maybe this is why my particular condition is so unstable.  I believe the cause is the narrowed jugular, and treatment of that narrowing with a stent, then assessing its impact on my stability with the possible need to intervene by adjustment, removal, or replacment of my shunt is the next course of action.  All I want for Christmas….

My first neurosurgeon told me he was confused by my symptoms.  The low LP values.  The apparently odd instability of my shunt treatment.  I’ve actually been told (paraphrasing) that I am the “unicorn” of ICPDD cases.  Here’s the thing: when I was in practice, I learned the most from the cases that fell outside of the normal curve.  Cases that didn’t turn out as anticipated despite following all the accepted procedures.  Those cases got under my skin, and I took it as a personal challenge to figure out what happened so I might be able to avoid putting a patient into the same situation in the future.  I always became a better doctor/dentist/surgeon for the effort.  That’s all I’m doing here.  It’s a peculiar blessing to have a particularly challenging form of a disorder shared by others AND have the modicum of knowledge necessary to at least draw basic conclusions from observing my own condition in as scientific a fashion as possible.  At first it was solely to tell the story of my treatment so that others might not be as…”surprised”…if they experienced the challenging outcomes I’ve had.  Then, when my wife Trina was diagnosed (hello…rare condition…a married couple both have it…what are the odds, and more importantly, what is the reason?   I believe I know….), I changed mission to find out how to alleviate her suffering and hopefully prevent her from going through what I did, possibly prevent her from getting a shunt.   Tragically, help did not come fast enough.  Now, having lost my career and my wife/best friend, soul mate to this…disorder…my teeth are sunk in and I will not let go until somebody somewhere listens and for the sake of everyone suffering and ICPDD and being told “medicine doesn’t know why….”.  I’m grateful for everything that has been done for me up to this point, but as it turns out, it seems that the a combination of the misfortune of having a New and Exciting Medical Disorder along with the fortune of having a neurosurgeon in the right place at the right time who was at least willing to try this shunt (which I admit likely saved my life despite its unstable nature)  has left me with a polar opposite bag of blessings, losses and opportunities.  I miss my Leloo; Christmas will never be the same again; but as long as I have a story to tell, I’ll continue to Whisper in the hopes that the right person/people listen….

 

The Shunt Whisperer

December 23, 2017

 

ASTERISKY THINGS (Trina’s Humor):

*It is my belief based on observation and recordkeeping of my own ICPDD that ICP increases with increasing barometric pressure and vice versa.  For lack of any other explanation, I believe that increasing barometric pressure compresses skin against unyielding objects such as bone and cartilage, compressing blood vessels.  This blood is forced into the only structures where the atmospheric pressure changes do not affect their inner pressures.  Hard structures with hollow inner cavities filled with blood vessels.  The are the long bones, the teeth, and the skull.  Interestingly enough, the next time somebody complains about a joint hurting when weather is changing, you can impress them with this knowledge.

 

**The values currently used to decide if ICPs are “high” or “low” are arbitrary numbers plucked from 30 year old research papers.  There is no scientific evidence to support them; further, to say that a value of “24” is “normal” but “25” is “high” makes no sense in this system.  ICPs vary widely due to a number of factors, often with a few hours.  A patient’s symptoms are a far more important indicator of a disease process; ICP values are merely a snapshot of pressure for that patient, under the conditions observed, at that moment.

***The current generation of shunts are exquisitely manufactured examples of inefficient, analog devices that were originally intended for the treatment of true hydrocephalus in children.  They have no active control of valve mechanisms beyond simple springs or weights, and the ball valve design lends itself to “seepage” of fluid below specified “opening” values due to accumulations of proteins or brain cells that prevent the valve from closing fully.  When they do actually “open” at designated pressure setting, the valves don’t pop open, but rather creep open to “allow” CSF to flow based on the difference in pressure on either side of the valve – ranging from a slight seep to a full-on gush, again depending on pressure.  This process continues until pressure differentials are within specified limits again.   Further, at this time, there is no method of non-invasively measuring Intracranial Pressures, and thus determine if a shunt is functioning or not beyond patient symptoms.  While inclusion of electronics to monitor intracranial pressures is definitely possible, the challenge of using them in devices that must be subjected to MRI examination has yet to be overcome.  They are the best option available if regulation of CSF pressure is necessary.

IMG-5031

EMERGENCY RELIEF OPTIONS

…Everything here is based on the concept of reducing the demand for blood flow to the head beyond normal, and attempting to maximize the very tricky nature of how veins drain blood from our brain….

Reading about so many fellow ICPDD patients with terrible headaches, pain, when their pressures are high.  Questions about “How can I make this stop?!”.   Short of proper diagnosis and medical intervention, relief from symptoisms of high intracranial pressures may not be completely possible, but I know from personal experience that certain things help me enough to make things at least bearable.  I don’t know if they will help you or not, and as such, I’m opening this page up to comments so everyone can learn from everyone else.  This is the first time I’ve done this on ShuntWhisperer.   I pray it helps because I know the terrible toll that incessant pressure and pain can have on a human being.  One of my goals when I started this site was group data mining to help direct opinions and treatment of this disorder.   Achieving meaningful results through that goal start here.  I’m tired of seeing so many people suffer.  I’ll say up front, I don’t have a clue if this will help anyone else.  It may be the hardest I’ve worked on something that has little value, but I have to try.  This list is far from comprehensive and will be added to over time, but it’s a start.

These recommendations are based on conclusions I’ve arrived at through evaluation and tracking of my own personal condition.  I know that my pressure symptoms are directly related to how much blood is flowing to my brain.  Above a certain point*, the veins that drain blood from my brain can’t accommodate the amount of blood flowing in via arteries.   I have no idea if I have any CSF “imbalance”** aside from when it all drains out of my shunt when blood flow to my brain hits that critical mark.  Everything here is based on the concept of reducing the demand for blood flow to the head beyond normal, and attempting to maximize the very tricky nature of how veins drain blood from our brain.  And everyone, I’m not a doctor; I’m a patient just like you.   I’ve had a rough time after my shunt, but I’ve learned some things as a result.  I do this in service of God, praying that this information might make somebody else’s life easier.  Please don’t do anything here that your doctor has told you NOT to do.

 

Here we go:

EASY MEASURES

  1.   COOL YOUR HEAD/BODY  The brain does not like to be hot.  Heat, especially when combined with humidity, cause your body to demand more blood to run through the brain in order to carry away the heat.  Of course, heat taken from the brain is radiated away through the skin all over your body, so the more of “yourself” you can cool, the better.    Try these “easy” things first, based on where you what’s available
    1. COOL SHOWER/BATH:  Whichever you prefer, or is necessary depending on your equilibrium.  The water does not have to be cold, just cooler than your body.  Make sure to get your hair wet.   Refresh with cool water as needed.  It’s not rocket surgery.
    2. ICE TOWEL: soak two clean towels in water.  Wrap them separately in saran wrap.  Put one in the freezer and one in the refrigerator.  Wait for the towel in the freezer to get cold, maybe a little stiff, but not frozen hard.  Take it out and put the towel in the refrigerator in the freezer.   Wrap the towel you just took out of the freezer over your head, neck, and face.  Be careful that the towel is not so cold as to give you frostbite.  Leave it on for 15 minutes while reclining at about 45 degrees in a chair or against some pillows.  When that towel is no longer cool enough, rotate with the other one.  Of course, don’t leave them in the freezer long enough to turn to ice logs.
    3. FAN/WATER MIST:  Sit in front of a fan, again preferably reclined about 45 degrees. The bigger the fan, the better.  You’ll need a pump mister that puts out a fine mist.  Expose as much skin as modesty dictates, and spray your hair, face, and body with the water mist.  Let the fan evaporate the water from your skin.  Repeat as needed.  If you’re in a public place where stripping down and spraying yourself with water might be frowned upon, there are misting bottles with attached fans that you can use on your face/head/neck as privacy allows.
    4. EVAPORATIVE FABRIC HEADGEAR  I loved these thing last summer.  Go to Amazon, type in “Mission Multi-Cool”.  I have several.  I don’t necessarily endorse the mission brand; I have several of different brands, and they all seem to do what I need them to do: keep my head cool.  Get them wet, preferably with cool water, wmission scarfring them out, put them around your neck, pull them up over your face, or completely cover your head.  As the water evaporates from the fabric, an enormous amount of heat is carried away from your skin as well.  Carry a bottle of water to refresh them when they get dry.  I keep a few in the refrigerator to rotate as I use and launder them.  Even just keeping it around my neck helps, and when I can I pull it up over my face.  A must have in the ICPDD Warrior Kit

BOLDER STEPS

  1. CUT YOUR HAIR SHORT An extension of keeping your head cool.  During the summer, it was the consensus of many members of support groups for ICPDDs on Facebook that short hair helped some feel better.  Makes sense, long hair is an insulator and holds heat on your head.  I guess this decision requires weighing fashion sense with desire for comfort, and it’s a “semi-nuclear” option because you don’t know what degree of comfort you will get until you do it.  I’ve gone to a military “high and tight”, and I’ve got to say that it helps, especially when I’m using iced towels.
  2. AIR CONDITIONING AC removes humidity from the air in a room or home.  Dry air carries away moisture from your body more efficiently by allowing evaporation of sweat or the water you just spritzed on you.   I’d suggest that anyone with an ICPDD have air conditioning in at least one room,  especially the bedroom. 

REALLY BOLD STUFF

  1. SEEK HIGHER GROUND mountainsA temporary measure I employed in extreme situations. On several occasions this summer, weather conditions combined in a way that aggravate my ICPDD to the point of intolerablility .  Even indoors I was miserable.  Heat, Humidity, and High Barometeric Pressure were the evil triad for Trina and I.  As fortune would have it, my mother lives in the mountains 100 miles to the east at an elevation 1000 feet higher, so when weather made conditions in my head intolerable, we went to visit Mom.  Geography and elevation combined to reduce heat (approximately 10 degrees F per 1000 feet elevation) and barometric pressure (30-40 millibars, or mb. Note that this equates to 300-400 mm H2O…a very significant amount of pressure).  Unfortunately, Virginia summers make humidity almost pervasive in this area, so we could rarely escape that, but the change in elevation gave the most relief.  The downside is that my body would accomodate this new elevation after 2-3 days, so I would only do this when I was desperate.  There was also the fact that we had to eventually go back home, possibly back to the same conditions I had fled from.  Worse, after my body had accomodated to the higher latitude/lower pressure, returning to the opposite conditions was occasionally very unpleasant, but that few days of relief seemed to always give me a much needed break.

OXYGEN  Two things about this:  I’m just at the point of investigating this (see Sleep Therapy Section), AND you should talk to your doctor first about this.  The only way to find out if Oxygen Therapy will work is trying it.  Oxygen plays a major role in reducing cerebral perfusion, or blood flow to the brain.  Oxygen therapy is used to treat migraines, cluster headaches, and other headaches known to be caused by high blood flow to the brain.  Low oxygen tension in “thing” air at extreme altitudes is what triggers Acute Mountain Sickness, or Altitude Sickness, and its extreme and possibly lethal consequences, High Altitude Cerebral Edema (HACE) and High Altitude Pulmonary Edema (HAPE).  A current theory exists implicating ongoing elevated ICPs can continually trigger migraines one after another.  Oxygen is one of the most therapeutic drugs available, but needs to be used properly.  Some health conditions preclude use of concentrated oxygen, so checking with your physician is recommended.  Health Insurance may cover the cost of Oxygen Therapy; a visit to your doctor may save you a lot of cash.

Or Credit.

Or at least make a dent in that amazing “Deductible” your insurance plan has.

It is available in canisters from Amazon, convenient for use or trial purposes.  At $27.99/can, you’re paying for convenience.   As I said, I haven’t used these yet, but just hit “Buy It Now”, and I’ll get back to you in a couple of days.

Screenshot-2017-11-9 Amazon com oxygen

“OH-two”  can also be delivered by oxygen concentrator/generators, available in “portable” and “home” versions.  These devices compress atmospheric air, remove nitrogen, purify the gas, and deliver oxygen that is ~85-95% pure depending on flow and other factors.  These devices are expensive, but in the world of chronic pain that can be associated with ICPDD, they may prove to be literal lifesavers.  In literal 20/20 hindsight, I realize the one treatment I never tried for Trina was oxygen therapy, and that shoulda/coulda gnaws at me.

But, hey, I’m just a disabled dentist with a hole in my head.  What the heck do I know.

Only what I’ve learned from this incredibly disabling shunt that has both relieved a number of neuroendocrine disorders and a lot of fibro pain – at least until end of June when it and my personal physiology decided to part ways.

And that’s why we’re here.

Last thing, at least for today:

 

SLEEP THERAPY – NOT AN OPTION

snoring

           

The previous measures discussed so far are more aimed at relief of immediate symptoms.  Now we need to look at a very important interceptive/preventive measure that is aimed more at long term control of not only ICPDDs but other significant health issues as well: Sleep Disorders.  There is an intuitive link between Sleep Apnea and ICPDD, but the research at this point is limited and inconclusive.9,10

Doesn’t mean there isn’t a link, but if I had to guess…and in the end, ICPDD or no, Sleep Disorders carry their own serious issues.

I can’t emphasize this point enough.  If you have an ICPDD and have not had a Sleep Study to check for a Sleep Disorder, a critical part of your potential treatment may be overlooked.  There is a clear link between IIH and decreased levels of oxygen and increased of CO2 in the blood.  Our bodies can store a certain amount of oxygen in the tissues for use when the need is high.  There has even been some evidence that resolving sleep apnea can resolve symptoms associated with IIH10

During sleep, our bodies assume a lower level of activity.  Breathing, heart rate, blood pressure all drop.  So, to, do reserves of oxygen, especially in the presence of a sleep disorder that can range from light snoring to severe sleep apnea where breathing actually stops until CO2 levels build to the point that the patient wakes up, gasping for oxygen “rich” air – possibly several times a minute.

Proper diagnosis of a Sleep Disorder currently requires a “Sleep Study”, where you are taken from a familiar environment to a strange one, with a strange bed, have all sorts of wires and bands and sensors attached to you, cameras aimed at you, and told “go ahead and go to sleep”.  Home sleep studies are becoming more common; your doctor prescribes such a study, a monitor kit is mailed to you, you follow its directions at home, send the monitor back, and results return to your doctor.

However, if you have a smartphone and about $31.99, you can get a very accurate idea of any sleep disorder you have.  I need to warn you, it might scare the heck out of you.  Even if this has no effect on your ICPDD (not likely, IMHO), sleep disorders are also linked to increased blood pressure, stroke, type II diabetes, cardiovascular disease, weight gain, and other serious health disorders.  By the end of next week, you can do a self-diagnosis that you can take to your doctor.

I found this fingertip oxygen sensor on Amazon for $31.99   It records oxygen levels all night, and the results can be downloaded to a computer the next day.  It also has an alarm that can be set to go off if your blood oxygen level falls below a certain level.  My O2 level at rest is about 98%.  I set the alarm to go off at 89%; it woke me up 6 times that night.

Screenshot-2017-11-9 Amazon com CMS 50D+ Blue Finger Pulse Oximeter with USB and Sofware Sports Outdoors

As a reference, if I were supervising a sedation and the patient’s O2 level hit 94%, I would start to be alarmed.  89% is danger territory.

snorelab-record-your-snoring-logo-fit-wX-150Next tool is a phone app called SnoreLab.  It is designed specifically to record snoring, loudness, and duration.  You download and install it on your phone (last I knew it was a free app), perform the setup, hit “start” and place your phone face down next to you in bed.  Next morning you hit “stop”, and you’re presented with a graph showing when you snored, how loudly, and you have the ability to listen to see if you stop breathing…also called sleep apnea.  If you do, or if the oxygen monitor shows significant drops in oxygen levels during the night, you need to take this information to your doctor, continuing the monitoring process as many nights as you can until your appointment.

Based on the results of this oxygen monitor and SnoreLab, I recently purchased an adaptive CPAP machine.  Recent events have precluded me from putting it to use, but tonight, 11/9/2017, I’m going to start using it.   I’m also considering adding an oxygen generator.  I’ll let everyone know what the results are.  Regardless of my results, I strongly encourage anyone with and ICPDD who has not already had a sleep study to at least try this relatively inexpensive but potentially hugely important test to see if you possibly have an ICPDD.  If you do, run, do not walk to your physician with the handy printed results.  Let everyone know how what the result of any treatment is on your ICPDD via this group data mining, and maybe we can make some serious progress into treating this disorder.

There are a few things I can do that involve prescription medications,  but I am not exactly sure how to present that.  Those will require an entire page unto themselves.  There is controversy about how certain medications might affect ICPDD patients and possibly give emergency relief.  When I am comfortable presenting this, I will put it out there.  Until then,

 

The Shunt Whisperer    2015-05-24 12.05.52

Longing for Leloo

Nov. 9, 2017

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3707935/

http://www.acnr.co.uk/pdfs/Case%20reports/PapAJLcasestudy.pdf

10  http://jcsm.aasm.org/viewabstract.aspx?pid=28230

A Rosetta Patient Speaks: The Cerebrovascular Theory of Intracranial Hypertension

Cerebrovasular Theory of Intracranial Hypertension, Part 2:  Leading to The Danger Zone

It’s really simple.  Damage/squeeze (“stenosis”) the main veins that drain the brain and a situation is created where the damaged veins can’t drain blood OUT as fast as the heart pumps it IN.  Blood backs up, the brain swells, and pressurized CSF.  The only cause?  Dunno, but interesting that Diamox, a nasty drug used to “reduce CSF production”, is actually a diuretic used to treat blood pressure.  Looking at the huge torrent of blood that flows through the brain, comparing it to what amounts to a quiet pool of CSF that changes at a snails pace, CSF MADE from blood to begin with, and it begs the question:  why the focus on reducing precious CSF if the cause is actually damaged veins that can’t drain blood away adequately during periods of increased blood flow to the brain?  Here’s the long story:

 

During my “experiential residency” in the study of Intracranial Pressure Dysregulation Disorders, it has become apparent that certain areas of the brain appear to be more susceptible to increased CSF pressure.   However, I don’t believe that an imbalance in CSF production and absorption is the principal cause  of my particular ICPDD,  but rather a symptom, the result of an imbalance in the blood flowing into the brain vs. blood flowing out of the brain.  The tenets of my current Cerebrovascular Induced Intracranial Hypertension are a direct extension of Dr. Mark Wilson’s ’s publication “Monro-Kellie 2.0“, and my personal experience as patient with an Intracranial Pressure Dysregulation Disorder that my neurosurgeon tell me does not fit any of the criteria for currently recognized conditions such as IIH.  These tenets are as follow; facts are derived from “Brain Facts and Figures” (https://faculty.washington.edu/chudler/facts.html):

 

  • Two Fluid Postulate: The cranium contains two fluids, blood and cerebrospinal fluid, in approximately equal volumes, ~ 150 cc 1, in patients without ICPDD and “intact” ICP Autoregulation.
  • Static Nature of CSF: Cerebrospinal Fluid volume is assumed to be essentially constant for this discussion This does not dismiss the possibility that a net positive or negative CSF dynamic is not a contributory factor in ICPDD. However, CSF turnover only averages .35 cc/minute1, leading to the next tenet…
  • Blood vs. CSF: Cerebrovascular blood flow dynamics greatly outweigh CSF dynamics.  Blood flow into the brain is 15-20% of cardiac output, 750-1000 cc/minute1, meaning that CSF dynamics represent a mere .05% of the change in volume of fluid In the brain per minute.  This is a known fact apparently forgotten or ignored according to Dr. Wilson.
  • Cerebrovascular Network: Our brains demand a lion’s share of oxygen and nutrients, provided by blood flow.  These nutrients are distributed through a network of blood vessels.  In order to provide each cell of the brain with oxygen/nutrients, blood vessels must be in extremely close proximity to each cell.  The vascular network is extremely complex, and is estimated to comprise 100,000 miles of blood vessels, the majority of them only wide enough to allow blood cells to pass through single file, about 6um (micrometers): 6/1000s of a millimeter.  Main arteries and veins into/out of the brain can be as large as an inch, then branch out continually into ever smaller vessels to provide nutrients to each of the approximately 100 billion neurons in our brains.  All of this is accomplished with a mere 150 cc of blood fluid volume, which flows through this cerebrovascular network at 750-1000 cc per minute.
  • Volumetric Balance: to maintain equilibrium of the volume of blood in the brain, the total venous outflow capacity has to equal the total arterial inflow   ***This is the critical tenet of this theory: blood flowing into the brain MUST flow out at an equal rate****
  • Venous Outflow Insufficiency: The 800 lb Gorilla in your head: Understanding the previous tenets, the critical nature of sufficient venous outflow becomes apparent. Arteries and veins are vastly different in nature and function.  Arteries are thick walled, contain smooth muscle, and dilate/contract in response to our nervous system and biochemicals (hormones).  Veins are thin walled tubes of cells; their diameter is susceptible to posture, gravity, and the actual rate of flow through them (as per Bernoulli’s Principle).   Veins are susceptible to damage by trauma, posture, and anatomical factors including Body Mass Index.  When Venous Outflow is insufficient to match Arterial Inflow, there is a net increase in the VOLUME of blood in the brain.
  • Intracranial Contents, The Volumetric Paradox, and The Physical Nature of The Brain: The adult skull is approximately 1700 cc in volume; the brain occupies 1400 cc; blood, 150 cc; csf, 150 cc.  However, there is a paradox: the 1400 cc of brain volume also contains a majority of the 150 cc of blood within the skull.   The brain itself is mostly water, 77-78%, contained within the network of neurons that comprise the tangible portion of the brain.  These neurons are chiefly lipids (10-12%), proteins (8%), and 4-5% a combination of carbohydrates, “soluble organic substances”, and inorganic salts.  The consistency of the brain is about the same as firm tofu (http://www.human-memory.net/brain.html); slightly elastic, with a degree of resilience.  The brain “floats” in cerebrospinal fluid that not only surrounds it, but again, a paradox: approximately 2% of the brain’s volume is hollow “ventricles” (https://www.ncbi.nlm.nih.gov/pubmed/21120804), spaces where CSF is produced and distributed through the brain and then to the space around the brain and spinal cord (subarachnoid space).  Thus, the 1400 cc volume of the brain also contains about 28 cc of cerebrospinal fluid.  This is the basis for the Volumetric Paradox: 15%  human brain’s volume is comprised of blood and cerebrospinal fluid. 
  • The End Game: When Venous Outflow Insufficiency meets the Volumetric Paradox:  Tofu and Internal Pressure:   Our brains are soft, mildly resilient structures.  They require enormous amounts of oxygen and nutrients, delivered by arterial blood flow.  Blood depleted of nutrients and oxygen is then drained by veins.  Cerebrospinal fluid, a crucial but poorly understood component of this system, changes at a snail’s pace compared to blood flow, and thus for this discussion will be considered a static innocent bystander for what happens next:  Venous Outflow Insufficiency.   If, for some reason, the main veins that drain the brain (sorry, it’s been a looooonnnnnnngggggg week, I’m a little punchy, I just couldn’t help it) are unable to handle the arterial blood flowing into the brain, a serious cascade of pernicious events follow.  Blood begins to back up in the brain’s cerebrovascular network.  Pressure within the network increases. This pressure cause the blood vessels in the brain to become engorged and expand, similar to the way that the veins in your arm start to bulge when a tourniquet is applied in order to draw blood for testing.  The next part is my speculation, but under equal pressures, it seems that thin walled, passive veins enlarge more than thick walled arteries that contain active muscle.  All within the 100,000 mile network of the Cerebrovascular network.  As the vessels expand, pressure is exerted outward on the tofu-textured brain.  The brain matter itself is forced to expand into the only spaces available to it:  the outer subarachnoid space and the inner ventricles.  The cerebrospinal fluid, the innocent bystander, is now “bitch-slapped” around by this building pressure,  referred to as EOMAP, or “End Organ Mean Arterial Pressure”.  Newton’s 3rd Law of Physics states that every action is met with an equal and opposite reaction; in the case of Venous Outflow Insufficiency,  this means that as cerebrospinal fluid becomes pressurized by brain tissue expanding due to a backup of blood in the vessels of the brain, the CSF “pushes back”, trapping brain structure between the”Devil” of the engorged and expanding blood vessels and “The Deep Blue Sea” of the now-pressurized CSF both outside AND inside of our brains.  And….
  • Voila: Intracranial Hypertension. By definition.  Caused not by CSF, the equivalent of a small pool of still water, but rather by the sudden blockage of the torrential river of blood that flows through our brains.  There is much, much more to the dynamics of this process and how the negative process feeds upon itself, but this concept is already a recognized process in an extremely acute ICPDD, Acute Mountain Disease and its associated deadly consequence of HACE, High Altitude Cerebral Edema.  For the time being, understanding this process as a potential cause of ICPDDs including IIH, NPH, pick-your-alpahabetic-combination-of-Hs, is critical to understanding what happens as its result.  This will be explored in the next topic on ShuntWhisperer.com, “The Danger Zones.”

 

This post, this topic, this site, is dedicated to the memory of my wife, Trina Haddix, who died as a result of complications related to an untreated ICPDD.  Her story will be told on TrinasPage.com in the coming weeks.  I miss you baby, I love you so much.  I will not let you be forgotten.

Let There Be No Doubt…

…about how serious Intracranial Hypertension and the group of related/associated conditions I refer 15482560-brain-pain-in-blackto as Intracranial Pressure Dysregulation Disorders (ICPDDs) are.

The toll they take on aa patient’s function and quality of life.

Or, if left untreated, the threat they pose to your life.

Ever heard the term that something “crushes your spirit”?  Guess what.  That is quite literally what ICPDDs can do.

I’m taking a brief moment from preparing the Celebration Ceremony for my wife Trina.  We were a couple that shared this rare disorder.  I know what happened to here.

In the name of trying to create a new sense of urgency in the medical community and remove any doubt that ICPDD patients need early, definitive, and meaningful intervention, I will be focusing in the near future on how elevated ICPs physically affect the brain as well as the potential results.

Trina died as a result of being afflicted with a rare disorder at a time when it is just being recognized by Medicine, when physicians who dared step in and treat her are few and far between, and resources are equally scarce.  Despite active promise of help, time just ran out for her.  Make no mistake: she was no quitter.  She was as tough as they come; she endured things that would have easily broken me.  The fact that it her condition ultimately took her from us is stark testimony to how seriously these conditons need to be viewed.

ICPDDs need to be seen in from a new point of view, and in Trina’s memory and honor, it is now my life’s work to answer this call and help all of us.  For now I mourn, but ShuntWhisperer.com is about to become very real.

May God Bless Us All.

 

ME AND THE BAROMETER, 2.0

“CSF is only one of the two fluids in the skull; blood is the other, and the volume AND FLOW of blood and its dynamics dwarf those of CSF”

noun | ba-rom-et-rick presh-shure|

1) the force exerted on an object by the weight of the column of air above it; affected by changes in weather patterns and altitude

2) the uncontrollable force of nature that can drive make blood shoot out of the eyeballs of a PERSON suffering an coping from an ICPSD

see also:  weather fronts, cold fronts, warm fronts, troughs, stationary fronts, Weather.com, weatheruderground.com, and the app “Barometer” on your iPhone ; )

The latest evolution in my understanding of how and why the barometer affects Intracranial Pressure after a doctor told me “(medicine) recognized that changes in barometric pressure affected (IPSCD) patients, but we don’t know why”.

Seriously.

Maybe they do and I’m on a fool’s errand, but in the off chance that one of the two people who read this get something useful from it, here, we go:
Before reading the long part, here are key points in the ongoing question of why changes in barometric pressure are affecting me, and I’m willing to bet apply to just about everyone else:

1) Intact adult skulls don’t expand
2) Our bodies expand and contract in response to changes in atmospheric pressure.
3) Increases in barometric pressure squeeze our bodies, pushing blood into the head
4) Blood vessels in the can head fill with blood if veins don’t drain it off
5) Swelling blood vessels push on brain matter
6) Brain matter expands into spaces filled with cerebrospinal fluid: around the  brain and the ventricles within
7) CSF becomes pressurized, and brain stuctures are compressed, causing pain, interfering with functions of the compressed structures (most notably but nowhere near the only function affected is vision), and if not relieved, deformity of the brain
8) In shunted patients, this swelling can cause flow of CSF out of the brain. Over a long term, this can lead to Slit Ventricle Syndrome.

ME AND THE BAROMETER, PART 2
My understanding of why changes in the barometer affect me, and certainly other ICPSD patients, advanced last night after reading this article: “Monro-Kellie 2.0: The Dynamic Vascular and Venous Pathophysiological Components of Intracranial Pressure”  by Dr. Mark H. Wilson, a neurosurgeon practicing in London.  In coping with my ICPSD I had come to the obvious conclusion that ICPSD conditions (IIH, NPH, PTC) have at their root a failure of a patient’s physiology to maintain a fluid in/fluid out balance in the cranium. Currently, my personal condition is complicated by the fact that my shunt is turned up to its maximum pressure, but I still have symptoms of low ICP. Keeping the right amount of blood flowing to my head has become very important. I had been concentrating on the “fluid in” side of the ICPSD equation using by modifying the method medicine uses to manage ICP in head injuries. I take my blood pressure, calculate the mean arterial pressure (MAP), and multiply it by 0.2. This gives me a number I call the “Cerebral Perfusion Quotient 20”, or CPQ20, representing a very generous portion of cardiac output flowing to my brain; this is simplistic but served a purpose. Tracked over a couple of weeks and referenced with activities, barometric pressure, temperature, and humidity, I was able to determine identify a range where I was relatively comfortable and functional. I have identified certain activities and conditions that aggravate my low ICP, and take certain measures to manage it as best I could. It has helped me to a point to manage my ICP until I can have a shunt revision. I had a passing semblance of control until autumn in Virginia brought with it the wide swings (20+mb every 7-10 days) of barometric pressure normal for the season. The unstable weather has brought with it an instability in my ICPSD.
Barometric pressure changes are known to affect the symptoms of ICPSD patient. In research, I’ve also discovered that it is associated with aggravations of other central nervous system mediated disorders including seizure activity, multiple sclerosis, and dementia. Barometric pressure is literally the pressure that the air around our bodies exerts on every square inch of our skin . Barometric pressure change has always been an issue for me; but understanding why has been an ongoing challenge. I came to an initial part of the answer recently (“Why Barometric Pressure and Weather Affect Intracranial Pressure”). This was so surprisingly simple as to be elusive. In short, changes in barometric pressure cause our bodies to expand and contract; like a balloon in a pressure chamber, our bodies expand with lower pressure and contract with increasing pressure. This expansion/contraction literally changes the volume of our bodies and circulatory system. When the barometer rises, our bodies are squeezed, and blood is pushed into confined areas where air pressure does not directly affect, like the inside of the skull*.
Charting my CPQ20 numbers, I noticed that a drop in barometric pressure also meant a drop in my CPQ20 number. When that number falls below the comfort zone, I develop lightheadedness along with a sensation that my ears were being sucked into my head. My shunt system has several components that change in nature depending on my perception of my ICP. Pliable components of my shunt system, chiefly the domed silicone antechamber in front of the shunt body and the silicone catheter behind my ear became shrunken and limp; the antechamber would become pliable and easy to depress. Another shunt system indicator is the tantalum ball in the antisiphon/assist device behind my ear: at low pressures when I lightly tap the skin over the assist, the little ball rattles freely. These are indicators that there is little to no CSF flowing in the shunt. Contrast this to increases in barometric pressure and CPQ20 numbers above my comfort zone. The antechamber and catheters becomes swollen and very firm, and the tantalum ball doesn’t “rattle”; it might “tick” once, but seemed restrained by the pressure/flow of draining CSF.
I was still confused as to how I could have so much pressure in my shunt if I was “overdrained”, that is, have low ICP. Increases in barometric pressure inevitably lead to this peculiar condition; however, until I read Dr. Wilson’s article, I didn’t understand why. Now I believe I do, and strangely enough, being a dentist has given me a particular insight**.
The cranium is a fixed volume. Intact adult skulls don’t expand and contract. As such, maintaining ICP requires a precise balance of arterial blood flowing into the skull, production and absorption of cerebrospinal fluid, and venous drainage. In calculating my CPQ20, I was looking at blood flowing in. However, as Dr. Wilson points out in his article, CSF is produced and resorbed at low rate of .3-.5ml/minute, give or take. That dynamic is dwarfed by the 700 ml or more of arterial blood that is pumped to the brain every minute. It further occurs to me that the fact that CSF is produced from this arterial blood is important as well, but bottom line: if this blood isn’t drained out fast enough, blood accumulates in the brain.
And that led to this latest epiphany, such as it is in our grand medical cosmos.  It’s not an original notion, it turns out, but I still managed to claw my way their leaving a trail of CSF in my wake.
The human brain has been described as “incompressible” in the original Monro-Kellie Doctrine, referred to in Dr. Wilson’s publication, the first effort to explain the dynamics of fluids inside the skull associated with our brains. Brain tissue does have a degree of compressibility: it is seen in cases of hydrocephalus where the brain can be flattened into a thin layer against the skull as excessive CSF pressure. Pressure comes from the network blood vessels in and around the brain. In ICPSDs, blood enters the brain faster than it can be drained away, filling and expanding these vessels. When they expand in the skull, something has to give. In my case, I believe the expanding blood vessel cause the brain itself to expand in segments between the blood vessels. The only space available for the brain to expand “into” is the space occupied by cerebrospinal fluid: the subarachnoid space between the brain and the skull, and the ventricles, hollow cavities in the brain associated with the production, and circulation of cerebrospinal fluid. This pressurizes these spaces and the CSF contained within them. In a patient without an outlet for this fluid, such as a shunt, the end result is pain and damage to structures of the brain such as the optic nerves, the pituitary gland, and others. This is the same process behind hydrocephalus. In shunted patients like myself, it makes for a plausible explanation for why my shunt drains so heavily when the barometer spikes and my CPQ20 is above my comfort zone: a glut of blood is compressing the brain tissue, pushing CSF out of my shunt. When CPQ20 numbers are below the comfort zone, my shunt seems to barely drain owing to a lack of literal “pressure from blood” in the vessels in and around my brain. It explains how I can be living with a shunt that can’t be turned up high enough to maintain an appropriate ICP for me and still have sensations of pressure. And it is definitely related to changes in the barometer, whether weather related or altitude related. I’m writing this the morning after driving to visit my mother; her home is 1000 feet higher in altitude, and according to my iPhone barometer, 30 mb lower in pressure than where I live (interesting fact: one millibar is equivalent to 10mm H20. Average ICP in the adult population is 110mm water; a 30 mb change is the equivalent of 300 mm of water pressure change on my body. Hmmm.). I’ve noticed this phenomenon on other occasions when weather conditions at my home made my symptoms unbearable, but by relocating here, the symptoms usually abate. Barometric pressure is not the only factor I’ve identified: heat and humidity are two others, but will save discussions of those for another time.
ICPSD disorders are very focused on CSF and its management. Dr. Wilson bluntly points out an obvious fact of epic importance:  CSF is only one of the two fluids in the skull; blood is the other, and the volume AND FLOW of blood and its dynamics dwarf those of CSF++. Blood volume imbalance is likely one possible explanation for ICPSDs in some patients. Simply put, a failure of the body to balance of blood in/blood out of the cranium leads to pressure on the brain directly as blood vessels fill with blood and expand. Displaced tissues compress the ventricles of the brain and without intervention can lead to damage to the brain, its structures, and the functions of the body those structures control. In my case, pressure forces CSF through my shunt; however, the shunt has a limited drainage rate, and if ICP expels CSF at a rate greater than my shunt system can drain it into my abdomen, in manifests as symptoms of pressure in my head and signs of an engorged shunt system. This explains the paradoxical presence of high pressure symptoms I experience while living with a low ICP. At this point the only management method I have is to lower my barometric pressure, and the only way I can do that is to go to a location at a higher altitude/lower barometric pressure.
This is not the end of this mechanism either. Pressure in the abdomen and chest play a very significant role in not only possibly explaining the development of ICPSDs but their management as well. I’m going to put these related topics into a subcategory under “Topics” entitled “Factors of ICP”. Hopefully readers will find something that sheds light on their own conditions and management. Prayers and comfort to all.

*or the inside of bones/cartilage, giving an explanation of why joints ache when a storm is impending.
**Intact and undamaged teeth are also impervious to the direct effects of air pressure. Teeth also have an internal anatomical space filled with blood vessels and nerve tissue. This tissue can become damaged if it becomes inflamed and begins to swell. The swelling chokes the tiny blood vessels off, thereby causing the tissue to die from what amounts to self-strangulation, the dental equivalent of cerebral edema of the brain.

++Flow is dynamic; volume is fixed.  It’s not only how much blood is in the brain, it’s also how fast it flows in and out….

How I felt on the day I received my VP Shunt, when the barometer had hit a near record high for my area, 40 mb above mean.  My neurosurgeon told me my CSF literally shot across the room when he was placing the shunt.  Contrast this to the day I had my diagnostic lumbar puncture: my opening pressure was only 17cm, but after draining 30 ml of CSF, most of my symptoms and pain disappeared…

 

Bleeding from the eyes