I got my first shunt in March 2017.  It was miserable, not because there was a problem with the shunt itself, but because I had CSF leakage around the proximal catheter under my scalp.  This absolutely wrecked the ability of the shunt to regulate my ICP.  I transitioned rapidly to unstable Intracranial HYPOtension, which I found to be as equally miserable as Intracranial Hypotension in its own special ways.

Two years.

Finally, after tests and experiments, Dr. Kenneth Liu figured out I was leaking CSF around my shunt catheter.  The technical term is “external communicating hydrocephalus”; I just called it “Juice Box Head” after the way juice leaks around the straw of those drink boxes and pouches if you squeeze them too hard.

The following video is very tongue in cheek. It’s meant to be.  I needed short, sweet, not uber-technical, which I can do all too well.  Disclaimers:  the scale of the burr hole and “catheter” (IV tubing) are larger than the actual items.  The “Bone Plaster” I used is plumber’s putty.  The “thin titanium plate” is a piece of galvanized flashing.  This video was shot in on my dining room table where I was both “surgeon” and “camera operator” (hence, the shaky sections).  That said, it is an accurate representation of how Dr. Liu solved my leak.

Why am I showing this?  Because the difference between leak and no leak was immediately noticeable, and the magnitude of improvement was nothing short of miraculous (yes, I used the “M” word).  It has made all the difference in the world for me to have a shunt that actual controls my ICP without an unwanted leak that renders the shunt all but useless.  Big Statement:  I am fairly certain it is an issue for other shunt patients, or may become an issue for those who need a shunt.  I cannot emphasize the importance of attention to this simple process, nor the risk being taken by ignoring it.  I know of whence I speak on many levels…

Without further ado, the masterpiece.  Let it load, hit the full screen icon in the lower left hand corner, & turn it up – the audio worked out supernaturally well with this bit:


Opening Whisper:  2019 was a “rebuilding year”, as my neurological health recovered from 2 years of unstable Intracranial Hypotension.  The lack of posts on Shuntwhisperer has been due to my…invalidity.   I’ve been hammering away at this for over a month, and with the Great Coronavirus Pandemic in full swing, I am pushing this into publication, warts and all.  Please forgive any errors, sophomoric media, or broken links.  I will get around to corrections and improvements.  I believe the sentiment and subject matter make themselves obvious and cannot wait any longer…




In the Shuntwhisperer post “The Hole In My Head…”, I recounted my experience with a shunt complication known as Peritubal Leakage.  Peritubal leakage (aka “Juice Box Head”, as demonstrated in this brilliantly illustrative Spielberg-esque video) is the unwanted/unregulated leakage of cerebrospinal fluid between the outer surface of the proximal shunt catheter and the dural tissues pierced by the catheter.  This results in unintended and significant drainage of CSF from the larger subarachnoid space surrounding and supporting the brain, instead of intended shunt valve-controlled drainage from the ventricular reservoir of CSF inside the brain – the distinction of these different CSF reservoirs is very important.

CSF Reservoirs
Comparison of CSF volume of ventricles accessed by ventricular shunts vs. CSF volume of subarachnoid space subject to peritubal leakage

The result: lowered/unstable ICPs with associated neurophysiologic repercussions due to CSF overdrainage from the untargeted CSF reservoir around my brain.  I endured this condition for two years before Dr. Kenneth Liu diagnosed the problem.  In March 2019, he performed a revision surgery to “plug the leak”.  The improvement I have experienced has been so dramatic by orders of magnitude that I feel the need to share it with the Shuntwhisperer community, as well as the discipline of Neurologic Surgery.

An important observation:  the size of my ventricles never changed size despite signs of Intracranial Hypotension (see below under “…Consequences Of An External Communicating Hydrocephalus”).  This led to skepticism of my condition by neurologic physicians who view changes in ventricular size on MRI exams as an indicator of shunt function.  In hindsight, stable ventricle size would be an obvious finding since the CSF overdrainage I experienced was not from the CSF reservoir inside my ventricles and through my shunt, but rather from the larger CSF reservoior of the subarachnoid space around my brain through a leaking burr-hole.  Equally important is that my adjustable shunt valve had been set to its maximum of 200mm H2O as we “chased” my decline into unstable Intracranial Hypotension during the first 4 months postop.   Ironically, this action raised my ICP, making leakage around the proximal catheter the preferential route for drainage of CSF instead of the more resistant, higher pressure route of my shunt system.

Neuroradiologists, please take note:  Hypotensive Ventricular changes only occur due to CSF pressure changes inside the ventricles; leakage from a CSF reservoir such as a leaking lumbar puncture or, as in this case, a leaking burr-hole, may not result in changes in ventricular size, making MRI evaluation of shunt function suspect if a CSF leak is present.  Re-examination of my MRI from July 2018 actually revealed changes in signal density of the cortex of my brain (parenchymal thickening) “consistent with chronic intracranial hypotension/subarachnoid hemorrhage”.

Before continuing further, I need to emphasize a very important point:

Nothing I have experienced is the result of incorrect diagnosis, improper treatment, or poor surgical technique.   It appears instead to be an unintended outcome of the current state of evolving ICPDD shunt treatment protocols.  It is my hope what follows will be taken in the spirit intended, for the benefit of patients and surgeons alike: the potentially significance of an understandably small detail in the larger picture that has more significant ramifications than currently believed.



Peritubal Leakage is significant due to its potential to interfere with maintenance of stable ICP. Unregulated CSF release out of the cranium independent of shunt management is known to exacerbate already dysregulated neurologic function and related symptoms.

“MRI Abnormalities” are dependent on the CSF reservoir affected. Leakage from extraventricular sources may not result in changes in ventricle size; chronic subarachoid leakage will cause changes in the MRI signal of the cortical (outer) layer of the brain. Graphic courtesy of Medscape.com

Peritubal Leakage itself appears to be an underappreciated/currently unrecognized potential complication of shunt placement surgery and does not appear in lists of “common” shunt complications, though symptoms associated with unstable ICP do appear; in my case, these symptoms were described as “normal”.  I now know otherwise and hope to impress upon all involved the severity of this preventable/treatable condition.  Peritubal Leakage is the result of a “perfect storm” of the wound physiology of the transdural silicone/polyurethane proximal catheter and subcutaneous shunt system components.  Researching “Peritubal Leakage” led to several articles mentioning it as a potential complication of ventricular shunts as a secondary result of distal catheter occlusion, but not as a primary complication related to delayed bone healing of the burr-hole craniotomy – mine “appears” to be the first reported case.   However, searching the term “Subgaleal CSF Leakage” results in a plethora of publications describing CSF leakage/accumulation beneath the scalp as a result of both cranial trauma and surgery.  Based on my research, observations, and personal experience, I believe Peritubal Subgaleal CSF Leakage from the subarachnoid space is a significant contributor to “common” shunt morbidities due to resulting suboptimal ICP management.  This unstable ICP  exacerbates already dysregulated neurologic  function as shown in the Medscape graphic above.  There is, however, a very bright spot: Peritubal Leakage is readily treatable, and more importantly, preventable using proven wound management techniques employing readily available materials in the neurological surgery suite.  Further, prevention of this complication is very low cost in terms of time and expense by making a simple modification to current shunt placement protocols.


The hallmark clinical sign of peritubal leakage I experienced was regular, periodic (over the course of several hours) visible and palpable swelling along the tract of my shunt system.  These episodes of swelling corresponded to increased relative ICP dynamics and were accompanied by tingling/itching of the scalp on the entire right side of my scalp. They persisted until ICP dynamic changed and CSF was resorbed into the tissues of the scalp.  Below are photos taken hours apart on the same day demonstrating this condition (hover cursor over photos for captions) :

The swelling  in the right photo is accumulation of CSF in the subgaleal layer of my scalp tissue originating from the burr hole where the proximal catheter of my shunt system enters my cranium..  The Subgaleal Layer is loose areolar connective tissue just above the bone of the external surface of the cranium, both binding the scalp to bone while allowing a degree of mobility of the overlying skin:

subgaleal space
Subgaleal Connective Tissue Layer and Space of the Scalp

As previously mentioned, there is scant information about Peritubal Leakage; however, much can be inferred from an accepted type of shunt employed in neonatal hydrocephalus patients known as a Subgaleal Shunt.  Subgaleal shunts relieve pathologic ICP without subjecting the neonate/infant to additional surgical stresses and growth considerations of draining CSF into the abdomen.  These shunts “simply” route a proximal catheter from an intracranial CSF reservoir into the subgaleal space before being ultimately absorbed by surrounding blood and lymphatic tissues of the scalp.  No shunt valves; tension of scalp tissues serve as the limiting factor of CSF drainage, along with direct taps of the shunt reservoir as needed.

Distention of the scalp due to CSF forced out of intracranial spaces under ICP can be significant but are normal in this type of shunt system used in newborn infants.   However, for an adult patient with a VP shuntperiodic swelling along the shunt system tract constitutes a red flag of uncontrolled CSF leakage into the subgaleal space.  Swellings that persist for more than a day may be a sign of a subgaleal hematoma, a collection of blood beneath the scalp that could indicate bleeding inside the cranium which requires immediate medical attention.



Peritubal Leakage is the predictable result of shunt treatment based on the physiology of the surgical wound created in the cranium for introduction of the proximal catheter of ventriculoperitoneal/ventriculoatrial shunts.  This may also apply to lumbar shunts as well; however, I will restrict this post to VP/VA shunts and my understanding of currently accepted surgical procedures, very briefly summarized here:

  • Scalp flap incision and reflection:
  • Burr-hole/craniotomy: a surgically created bone wound performed for the purpose of exposing the dural lining of the brain to allow insertion of the proximal shunt catheter into a ventricular CSF reservoir inside the brain.  Creation of  the burr-hole must be performed with care to prevent pushing bone fragments into the cranium and/or tearing the dural tissue immediately beneath (Having performed many surgeries in nasal sinuses, I know from experience, this is delicate.  Think of removing the shell from a boiled egg without tearing the inner collagen membrane, a membrane that varies in consistency from tissue paper leather amongst various patients).  The diameter of the burr hole is approximately 15mm/0.6in.  (The average thickness of the adult human cranium is about 6.4mm/.25in; thus, the resulting bone wound in the cranium is ~2.5 wider than it is deep.  This is important in determining how the bone wound will heal without intervention as will be explained shortly.)
  • Placement of the proximal catheter through the dura, across the subdural space (containing CSF) around the brain, through the frontal lobe of the brain, targeting the Foramen of Monro at the base of the third ventricle inside of the brain. This is accomplished via real-time 3D guidance via Medtronic’s brilliant Stealth System, shown in this video:
  • The distal catheter is routed to its terminus equally brilliantly via subcutaneous tunneling, shunt valve(s) are connected with catheters, and the system checked for integrity, all very delicate tasks that require attention and time.
  • The scalp flap is repositioned and secured with sutures/staples.



This bone wound in the cranium is a small but very, very significant in terms of its size, shape, and presence/composition of the proximal catheter:

Intact cranium
Dural Bulge at Burr-hole
Removal of cranial bone results in lack of support of dura; CSF under ICP bulges dura outward
1317_CFS_Circulation(1) proximal catheter
Subarachnoid CSF Leakage
Unhealed Craniotomy
MRI demonstrating my CSF leak



Early wound physiology begins to demonstrate a potential problem with the transdural proximal catheter.  Shunt catheters are 4.0mm in diameter with 1.5mm inner lumen for CSF drainage.  They are made from a very flexible silicone or electrospun polyurethane-based material which are treated to prevent adhesion of clumps of cells to the inside of the catheter.  These adhesions can potentially obstruct the catheter resulting in shunt system failure.  The anti-adhesion quality of these components also prevents cells from adhering to its outer surface.  This means that neither collagen based dural tissue nor cranial bone adheres to the proximal catheter during healing. Examination of the transdural proximal catheter reveals that the collar of dural tissue around the catheter is no longer supported by bone;  as such, it cannot resist the outward pressure of CSF caused by ICP (Monro-Kellie Violation).   As a consequence, cerebrospinal fluid in the subdural space under sufficient intracranial pressure can displace the unsupported edges of the dural wound outward like an organic juice-box valve, allowing CSF to escape from the subdural reservoir and accumulate along the tract of the shunt system.  The visual analogy I prefer is how juice escapes around the straw of a juice box/pouch when squeezed, hence the moniker “Juice Box Head” to describe Peritubal Leakage.

Mathematical analysis of this condition reveals that the area perimeter of the 4mm catheter is an order of magnitude larger in potential volume than its 1.5mm inner lumen.  The inner lumen of the proximal catheter has a fixed cross sectional area of 1.76mm2. The same catheter’s 4.0mm outer diameter surface area is 12.56mm2.  if the dural edge is displaced by CSF under the influence of ICP by 0.5mm, the total area for potential leakage around the periphery of the catheter nearly matches the internal lumen area where CSF drainage is intended to occur under the control of the shunt valve.  If the dural tissues yield at ICPs lower than the opening pressure of the shunt valve, CSF will preferentially leak around the proximal catheter from the subdural CSF reservoir instead of the intended ventricular reservoir.  This process is the basis for the development of unstable ICP as well as transition from Intracranial Hypertension to Intracranial Hypotension as I discovered.

Current standard neurologic surgery protocols focus on the demanding tasks of opening the patient’s cranium, placement of the shunt catheter through the brain into the desired ventricular CSF reservoir, and routing of the distal catheter to drain CSF into the desired body cavity.  There is no standard protocol to address the small but very significant bone wound created by the craniotomy – it is left to “heal on its own”, an oversight which I contend is in contravention to known wound physiology.  Bone defects heals very slowly, at a rate of 100-200 microns (um) per day.  New bone grows from the blood supply of existing living trabecular bone; thus, the circular craniotomy heals from the edges towards the center (seen in the video of serial CT/MRI scans of my craniotomy).  Using these facts, it can be seen that it would take this 15mm/15000um wound between 10 and 20 weeks to heal with bone.   The discipline of Orthopedics tells us that the time required for a bone wound to heal to 70% density is 16 weeks (Human Bone Sigma Healing).

However, bone is not the only tissue actively growing in a healing wound: soft tissue (proliferative collagen, aka “scar tissue”) can – and does- preferentially invade the volume of a wound previously occupied by bone at a rate of 1000-2500um (1-2mm) per day, 10 times faster than the slower growing bone (osteoid  tissue, which begins as a soft tissue that later becomes infused with calcium in a form known as hydroxylapatite.  Once non-bony soft tissue organizes in a wound, bone formation is precluded from that volume of the wound.  In the case of our circular craniotomy, this is aggravated by the invagination of the scalp flap into the craniotomy, creating a dimple into the wound volume which was occupied by cranial bone pre-surgically.  Further aggravating this undesirable condition are the dimensions of the burr-hole, or rather the ratio of its diameter to the thickness of the cranium: at ~2.5 times as wide as it is deep, even this small wound becomes subject to immutable laws of bone healing.  Its shallow, wide shape predisposes it to soft tissue invasion as well as invagination of the scalp tissue into a volume once occupied by bone.

The result is a transdural silicone catheter surrounded, at least in the early weeks of healing, by “loosely organized” dural collagen and soft/scar tissue.  There is no actual “seal” of dural tissues to the outside of the catheter because cells cannot adhere to the silicone/polyurethane catheter.  The integrity of the bony cranium is compromised by the craniotomy, and as I discovered, can lead to significant morbidity if intracranial pressures are sufficient to cause CSF to seep between the outside of the catheter and attached shunt system components.  This chain of surgically implanted shunt components creates a potential reservoir in the subperiosteal/subgaleal space, allowing CSF seeping around the proximal catheter to accumulate around the shunt system  outside of the cranium creating the aforementioned subgaleal hygroma.  Below is a a video of images and models taken from serial CT/MRI scans taken at postop, 3 months+++++++demonstrating this exact series of circumstances that caused my unstable shunt treatment: a transdural catheter, lack of bone to support the dural tissues at the outer perimeter of the catheter, and the late bone healing pattern of the burr-hole craniotomy



Peritubal Leakage caused me to transition from Intracranial Hypertension (intolerance of upper limits of my ICP physiology) to unstable Intracranial Hypotension.  Having experienced both ends of this spectrum, I can say each has its own unique “misery index”.  I can further testify as to how unstable Intracranial Hypotension limits functional capacity by orders of magnitude.  Here is a brief summary of the most severe symptoms I experienced:

  • Subgaleal Hygroma: Regular periodic swelling, both palpable and visible, along shunt tract beneath scalp with accompanying increases in barometric pressure AND/OR systemic blood pressure/heart rate dynamics. These episodes of swelling were accompanied by soreness and tingling of my scalp three to four inches around my shunt components, with occasional crepitus (crackling sensation of skin when touched due to fluid accumulation).
  • MRI/CT evidence of transition to Intracranial HYPOtension: these findings are NOT restricted to changes in ventricular size, and instead may be evidenced by changes in the signal of the outer cortex of the brain.  Shunt settings and individual patient physiologies may show different combinations of these findings, and subjective patient symptoms MUST be given credence when they seemingly conflict with objective test results.
  • Severe Intolerance to barometric pressure changes related to weather.***
  • Intolerance to prolonged (24-36h) of barometric pressure below 950 mb, with accompanying symptoms:
    1. Extreme fatigue, frequently requiring bed “rest”
    2. Increased fibromyalgia pain
    3. Cognitive challenges including impaired problem solving, depressed mood/labile emotions
    4. Aggravated level of tinnitus during periods of perceived low ICP, compared to pulsatile tinnitus during periods of perceived high ICP.
    5. Changes in vision out of right eye (my “migraine side”) from day to day manifesting as changes in near vision accommodation
    6. Over the course of two years, the development of apparent autonomic and neuroendocrine dysfunction manifesting as the Hyperadrenergic form of POTS as well as exercise intolerance/muscle wasting presumably related to HPA axis dysfunction (I show evidence of Empty/Partial Empty Sella Syndrome which developed only after the onset of Intracranial Hypertension).

This list is short and does not delve into further subcategories at this time, some of which are very significant.  As noted in the title, this is “Part One”.



Guided Tissue Regeneration (GTR) is a surgical process originating in Orthopedics research in 1959:

  • Hurley LA, Stinchfield FE, Bassett AL, Lyon WH (October 1959). “The role of soft tissues in osteogenesis. An experimental study of canine spine fusions”. The Journal of Bone and Joint Surgery. American Volume. 41-A: 1243–54. PMID13852565.

GTR is used extensively in orthopedics, oral surgery, and  neurologic surgery to exclude soft tissue from a bone wound, as well as enhance bone volumes in areas so desired.   In my dental practice, I personally employed GTR as part of oral surgical procedures to ensure adequate bone volume and quality in the desired location of dental implants, as well as to regrow bone lost due to disease, pathology, or trauma.  GTR is beginning to become a topic of discussion in neurologic surgery as well, and after my experience, I can say it cannot come fast enough.

GTR facilitates desired bone growth by a twofold approach.   First, a biocompatible/bioactive grafting material is placed into a bone wound.  The grafting material “holds space” into which new bone to heals after graft material is resorbed during normal healing, ultimately being replaced with the patient’s own bone.  In some cases, vital bone is grafted from one part of the patient’s body to the desired site, but the healing process is still the same, even with vascularized grafts.  Calcium sulfate, essentially medical grade bioenhanced plaster, is a popular, effective, and inexpensive option for this size defect.  Newer materials are becoming widely accepted that may prove even more effective and will be the topic of another post in this series.

The second part of GTR is a “bone bandage”: a biocompatible membrane placed over the graft site (in this case, the burr-hole craniotomy) which excludes unwanted soft tissue from the bone wound.  This “bone bandage” is known as a guided tissue membraneGuided tissue membranes need to be biocompatible and must persist in the surgical wound long enough for osteoid tissue to form, preferably a minimum of 8 weeks.  These membranes are made from various materials; a very short list includes PTFE (aka “Teflon”), cross linked bovine collagen, and titanium in the form of foil and thin plates.  Some membranes such as those made from collagen are dissolved by the body over time; others such as Teflon and titanium persist.  Each has its unique pros and cons depending on the application, and in this particular application, I personally see titanium plates as the clear choice: the combination of calcium sulfate and titanium offer immediate dural support from postop through burr-hole healing with bone. Examples of these readily available materials in a neurologic surgery suite are shown below:


In the revision surgery which has literally given me my life back, Dr. Kenneth Liu revised my original shunt with the goal of sealing the unhealed and leaking burr-hole.  This was performed March 2019, almost exactly 2 years to the day Dr. Liu had placed my original shunt.  He removed/debrided the soft tissue that had formed in my burr-hole (preventing bone healing) and created bleeding points at the periphery with the surgical equivalent of a Dremel tool (remember: new bone grows from the blood supply of existing bone).   A groove was created in the edge of the craniotomy for the proximal catheter to lie in. The burr-hole defect filled the resulting wound with bioactive calcium sulfate (bone “plaster”) and covered the craniotomy with a readily available stock round titanium bone plate that, when screwed into place, extended beyond the edges of the craniotomy.

Dr. Liu also replaced my Sophysa Polaris shunt valve with a Meithke ProGav 2.0 valve, not because the Sophysa was suspected of being defective (Sophysa has an outstanding record of reliability), but because the newly available Meithke ProGav offered a greater degree of opening pressure adjustability, not to mention being much a much smaller size.   Dr. Liu’s Facebook page has this picture of what may be my actual valve, giving an idea of its size, the approximate equivalent about of three quarters stacked atop one another:

My ProGav
(My?) ProGav 2.0 Shunt Valve from Dr. Liu’s FB page

This valve is adjustable in “infinite” increments over its 0-200mm H2O pressure rating using external magnetic tools, is MRI resistant to 3T (I can vouch for both the Pro-Gav and Sophya valve’s resistance to MRI fields).  Further, the Pro-Gav’s low profile has significantly improved comfort as well as not being as visibly apprarent with my “high and tight” hair…style.

From the first moment I remember postoperatively after revision surgery, I could feel enormous improvement.  The best description I can offer is that I actually had a “normal” pressure in my head, as opposed to an “empty” sensation.  This has only improved in the last year.  Some of the improvements I notice are:

  • Barometric pressure sensitivity: prior to the revision, I was a puppet to the weather as well as altitude.   This problem was so severe that I could not live at my home located at a modest 2200 feet above sea level, nor could I tolerate barometric absolute pressures (station pressures***) below 950mb.  I was a geographic hostage, a medical gypsy forced to relocate to lower elevations/higher barometric pressure areas almost weekly for relief.  Low barometric pressures due to weather or altitude would cause me to experience extreme fatigue.  As mentioned in “The Hole In My Head…”, I consulted with Dr. Liu to procure a home hyperbaric chamber to prove to myself and to Dr. Liu that my extreme sensitivity to normally tolerable environmental changes was real.  Post-revision, I have been from sea level to as high as 4000+ feet without any noticeable deleterious effects.   At the time of this post, the current station pressure is 918mb, and aside from a predictable mild morning migraine, I’m functional, whereas prior to the revision, I would be confined to bed and very lethargic.
  • Immediate 99% reduction in Peritubal Leakage: my craniotomy is by now healed with my own bone beneath the titanium plate.  This bone does not adhere to the proximal catheter,  but it does provide enough added resistance to dural displacement and unwanted CSF leakage around the catheter that 99% of the time I cannot appreciate any CSF accumulation as evidenced by tactile/visual swelling along the shunt system.  I no longer experience any swelling along the shunt components,  which now feel as if my scalp has “vacuum formed” over them. Occasionally there is a very, very small accumulation of CSF along the catheter at the edge of the plate, but it is not visibly evident, only noticeable by telltale slight tingling of the adjacent inch or so of scalp – greatly reduced from pre-revision conditions.  Best of all I do not have the symptoms of Intracranial Hypotension that previously accompanied the degree of peritubal leakage previously demonstrated.
  • Slow but steady improvement in neurologic functions:
    1. Exercise intolerance: pre-revision, I was pathologically intolerant of any degree of exercise and was becoming severely deconditioned.  Stairs were becoming a problem.  Now, I tolerate reasonable amounts of physical activity and light exercise with normal recovery as opposed to the week of intolerable pain that previously resulted from any exertion.
    2. Pain Level: 90% improved, and not a moment too soon.  Fibromyalgia pain is linked to Intracranial Hypertension. I can say with absolute certainty that Intracranial Hypotension made my fibro pain as bad, if not worse, than Intracranial Hypertension.  Let me be clear, both were severe and varied only by levels of misery.
    3. Functional Capacity: I was essentially a low-functioning invalid pre-revision.    I am now able to live independently in a manner consistent with a 59 year-old male with an Intracranial Pressure Dysregulation Disorder.  I enjoy several hours of function a day, whereas pre-revision, I would be bedridden for 3-4 days at a time for every “good” day I had out of bed.  I’m somewhat ashamed to say that the lack of posting on Shuntwhisperer has partly been because I’ve been actually able to get out and have a life.
    4. Improved Cognitive Function: Goodbye, Brain Fog, memory lapses, and the inability to perform simple math in my head.
    5. Improved sleep – prior to revision, sleep had become increasingly poor, with frequent episodes of waking at night with my heart pounding out of my chest for no apparent reason. I believe I was experiencing episodes of breathing patterns similar to Cheyne-Stokes due to aggravation of low ICP at night.  I required CPAP and supplemental oxygen, but no longer need them.  Mornings no longer involve an hour of misery/agony that persisted until I consumed enough caffeine to raise my ICP; these episodes would stop at about the same time I could detect flow in my shunt system.  (note: shunt-assist related nocturnal overdrainage will be covered in a separate post)
    6. Improved emotional health: though I had learned to cope with the ups and downs that seemed to accompany swings in ICP, it was exhausting. This too has improved by orders of magnitude, and I rarely find myself forced to evaluate  seemingly irrational emotional states for validity.



First of all, my heartfelt gratitude to Dr. Kenneth Liu, most recently practicing at Penn State/Hershey Neurologic Services, for his support and willingness to make this improvement possible.  Dr. Liu, sincere thanks.

It took nearly 18 months to deduce that I was experiencing Peritubal Leakage, another 6 months before it was able to be corrected.  I will summarize the experience in technical terms: pure, absolute hell.  The condition I was experiencing was an uncontrolled CSF leak via an unintentional, surgically created, external communicating hydrocephalus.  Reviewing how this leak likely occurs: the dural wound around the proximal catheter lacks the rigid support of the cranial bone removed during shunt placement surgery.  ICPs exceeding the ability of elastic dural tissues to seal against (not “to”) the proximal catheter allowed CSF to seep out from the subarachnoid space, around the outside of the catheter between the catheter wall and edges of the dura.   The leaked CSF pooled along and around the components of the shunt system (catheters, shunt valve, shunt assist valve), resulting in noticeable periodic swelling of the scalp as shown in photos/video.  At the time, the opening pressure of my system was 200 to 450mm H20*.   In my case, it is likely that peritubal leakage occurred at ICPs below the opening pressure of the shunt, creating an “overdrainage” scenario similar to a shunt system set at too low of an opening pressure.  However, CSF leakage likely occurred from the undesired subarachnoid reservoir of CSF around the brain.  This is a much larger CSF reservoir than the intended third/lateral ventricles and thus not as self-limiting nor regulated by the shunt valve(s).  The volume of CSF in the subarachnoid space directly affects brain buoyancy as well as neurologic function.  I exhibit borderline Chiari 1 imaging when lying flat; a reduction in brain buoyancy would theoretically aggravate impingement of my foramen magnum by my cerebellar tonsils.  Further evidence supporting this theory is that while I exhibited symptoms of Intracranial Hypotension, the size of my ventricles remained stable over 2 years, indicating the shunt system was not responsible for the “overdrainage” because unwanted CSF loss was not coming from the ventricular reservoir, but rather the larger subdural reservoir.

As mentioned previously, I have experienced improvement in neurologic and emotional health that are literally orders of magnitude better than when I was experiencing PT.  Some of those improvements happened immediately; some of them have taken months.  Dr. Liu had a term: “Angry Brain Syndrome”, describing dysfunctional neurologic health caused by pathologic ICP dynamics.  The term has proven to be very apt.  And, while I endured significant difficulty for two years, I am now enjoying dramatic and continuing improvement as a result.



Pointed Statement Alert: by now I’m certain I’m not the only one who has or will experience negative impact on already impaired neurologic health due to Peritubal Leakage.  I’ll stop short of saying  peritubal leakage is nearly universal, but current shunt surgery protocols as described make it potentially possible in every patient if the burr hole craniotomy is not addressed with Guided Tissue Regeneration.   I have spoken with two neurosurgeons about the following proposal and have been greeted with “we don’t see peritubal leakage as a problem”.  Respectfully, as the surgeon and not the patient, that statement carries little validity when viewed in the dichotomy of subjective findings and objective experience, especially when based on known wound physiology as I have described.  The impact on patient function of this issue is inarguably quite significant, thus I recommend that the belief that Peritubal Leakage is “not seen as a problem” needs to be revisited.

Based on my surgical training and experience, knowledge of bone wound physiology,  not to mention my “experienced based residency” as a shunt patient, I can say with absolute certainty  that peritubal leakage potential carries a significant negative impact on the stability of intracranial pressure dynamics, and by extension, neurologic health.  My condition was ultimately and dramatically improved by a second surgical intervention and the employment of a well-understood wound care process known as Guided Tissue Regeneration.  The magnitude of that improvement has been literally the difference between having a modicum of function vs. being bedridden and essentially nonfunctional every time the weather changed or I just went to my home at the “dizzying” altitude of 2200 feet.  As such, I propose that Guided Tissue Regeneration repair of burr-hole craniotomies be considered a standard practice in VP/VA shunt surgery at initial placement using bioactive calcium sulfate and titanium plating.  I further propose that patients exhibiting signs of subgaleal hygroma be evaluated for peritubal leakage through CT/MRI imaging of bone healing of the burr-hole craniotomy, signs and symptoms of Intracranial Hypotension, with due consideration given to GTR revision/valve revision in cases of poor/delayed bone healing of the initial burr-hole craniotomy.

The addition of this extra measure necessarily requires an evaluation of the cost, time, and risk/benefits of a GTR repair of a craniotomy, and from every standpoint, pros outweigh cons in every category.  First, flap design needs to consider adequate wound margin from the titanium plate covering the craniotomy.  Next, materials: standard armamentarium of the neurologic surgical suite reveals that integral materials and components, chiefly bioactive calcium sulfate (with metronidazole/rifampin added)** and “stock” circular thin screw retained solid (not mesh) titanium bone plates, similar to those shown above. Surgical time is estimated to be 15-20 minutes at most during initial implementation to create a groove at the distal edge of the burr-hole for the proximal catheter to lie in,  preventing its impingement by the edge of the bone plate, followed by placement of the calcium sulfate, and fixation of the bone plate, preferably before final set of the calcium sulfate graft**.  At this point, repositioning and closure of the flap would proceed as normal.  Scalp invagination and soft tissue migration into the burr-hole/craniotomy would be effectively precluded.  The patient’s healing physiology will dissolve the calcium sulfate and replace it with their own bone over 4-6 months.  Cost of the bone plate and calcium sulfate, while not inexpensive, are comparative pennies (less than $1000 billable) compared to the cost of shunt placement surgery ($75,000+ for the my first shunt, $28,000 for the revision).  I would go so far as to consider billing these items at cost due to the critical nature of their role in enhancing wound healing and mitigating unpredictable leakage and suboptimal patient experiences as a result; in reality, “billing at cost” is becoming an unfortunate standard not only in Medicare/Medicaid, but private insurance plans as well.  But, losses here can be made up on volume (sad but true medical humor).  The true cost savings of adding Guided Tissue Regeneration to shunt placement surgery is the incalculable cost of improved treatment outcomes and reduction in monetary and risk costs of revision surgeries to correct the previously unrecognized consequences of Peritubal Leakage.

There is no apparent predictor for the incidence and degree that peritubal leakage will occur in a shunt craniotomy, but known wound physiology supports its likelihood.   Improving the seal around the transdural proximal catheter by ensuring ideal bone regrowth with Guided Tissue Regeneration at the time of shunt placement makes good surgical sense and is ultimately in the best interest of patient and surgeon alike.   Guided Tissue Regeneration is a refined field that extends back 35 years; the process I have described of using bioactive calcium sulfate and a non-porous titanium plating is a GTR process that has stood the test of time.  Therefore, I propose that Guided Tissue Regeneration be considered a standard practice in VP/VA shunt surgery at the initial surgery.

**Check back for an upcoming post: “Platelet Rich Fibrin: beyond Calcium Sulfate”