This sounds more like a legal question than a research question?

Research could be defined as"

The systematic investigation into and study of materials and sources in order to establish facts and reach new conclusions.

Can you help James?

Sorry, I'll take a pass on this one. I suggest you obtain an expert opinion.

No need to be sorry.  Both your answers are of interest.

"Could the spinal cord or dura resist forces exerted by increasing pressure within the peudomeningocele, which resulted in NAUSEA?"

I think the main (only?) cause of nausea is malfunction of the vestibular system in the inner ear, and a common but unrecognized cause of this is a pressure drop in the inner ear.   I do not think nausea ever occurs from high inner ear pressures, as during raised CSF pressure from any cause.   So I strongly suspect that low pressure in all or part of the CSF was a cause of nausea in your case.

Thank you Anthony your comments are valued.

However if you check the medical publications by the American Association of Nuerological surgeons (AANS) Publication Journal Neurosrug. Focus Volume 9 July 2000, Article .  You will find that Hawk MD and Kim MD in their publication Review of spinal pseudomeningoceles and cerebrospinal fluid fistulas Table 1 on page 3, listed NUSEA and Vomiting as one of the Signs and Symptoms associated with pseudomeningoceles.  References list 102 publications on the subject.

If you check the AANS publication journal Neurosurg. Focus Volume 15, December 2003 by Coutre MD and Branch MD.  Spinal pseudomeningoceles and cerebrospinal fluid fistulas  You will find they produced similar conclusions and refer to 65 publications on the subject. 

If you check the Asian Spine Journal, Asian Spine, September 2012; volume 6(3): page 157-162 by Tosun et. al.  Management of Persistent Cerebrospinal Fluid Leakage Following Thoraco-lumbar Surgery.  You will find that NAUSEA and VOMITING are noted as symptoms which result from a spinal pseudomeningocel. The publication refers to 26 publications on the subject.

If you check the Asian Journal of Neurosurgery. 2010 Jan-Jun; 5(1): page 54-59, Incidental Tears in Lumbar decompressive surgery: Incidence, causes, treatments, results.  You will find the symptoms listed include NAUSEA and VOMITING.

If you check Surgical Neurology International SNI: Spine, A review article on the diagnosis and treatment of cerebrospinal fluid fistulas and dural tears occurring during spinal surgery,  by Epstien, Surg Neurol Int 2013; 4:S301-17, 6 May 2013.  You will find similar conclusions with symptoms such as NAUSEA and vomiting.  This publication refers to 58 publications on the subject.

If you check The Indian Journal of Radiology and Imaging, NEURORADIOLOGY, Volume: 22 Issue: 2 Page: 108-115, 2012.  Long series segmented extra-arachnoid fluid collections: Role of dynamic CT myelogtaphy in diagnosis and treatment planning.   You will find that under the discussion section:  may present symptoms related to compressive myelopathy from the collection;  Usually considered to be an occult CSF leak through small defects in the meninges;  PULSATILE CSF dynamics; presence of an osmotic gradient between the subarnochnoiud space and CYST; valve-like mechanism between the fluid collection and subarachnoid space may play important roles in the enlargement of these spinal extra-arachnoid fluid collections; WITCH CAN OFTEN CAUSE CORD COMPRESSION and CORD SIGNAL CHANGE;  This included CSF cavity lesions (e.g, meningoceles, pseudomeningoceles) or root pathology (epidural cysts).  These conclusions are referenced to the 24 publications cited in this publication. 

Another publication which is relevant to the problems caused by pseudomeningocels compressing both sides of the dura against the spinal cord and displacing the annulus of cerebrospinal fluid which should surround damp the cord form body movements and protect the cord form damage due to contact with the vertebral bone or spinal canal is:

CEREBROSPINAL FLUID STASIS AND ITS CLINICAL SIGNIFICANCE.  Published by The US National Institute of Health publication NIH Public Access:  Altern Ther. Health Med. 2009 May-June; 15(3): 54-60.  PCID: PMC2842089 by Heaton and Glacey.  This publication cites 74 publications and also very relevant.  As it refers to reduced flow of CSF; CSF pulsations; CSF impeded by space occupying lesions, CSF stasis being detrimental to to health; pulsate flow of CSF in the spinal SAS; sacroiliac articular motions exerting a PUMPING ACTION  upon the CSF; CSF motions transmitted and co-ordinated by tensile forces in the spinal dura; affects upon autonomic balance; dural tension and decreased CSF flow being closely related to an overall pattern of structural and energetic dysfunction  in the axial skeleton and CENTRAL NERVOUS SYSTEM; adverse mechanical cord tension (AMTC); Strain of the spinal cord due to compression due to tension in the attachments between the dural sac and the bilaterally by the denticulate ligaments and superiorly and inferiorly to the bony surfaces of the spinal canal and bilaterally at multiple levels to connective tissue in the intravertebral foramen, with strain of the spinal dura between points of attachment resulting in strain of the spinal cord; CSF following the path of least resistance in the SAS, both anterior and posterior to the cord; flattening of the SAS likely to reduce CSF flow; anteroposterior flattening of the the cord possibly resulting in occlusion of the central canal due to adverse cord tension; CSF stasis resulting form loss of capacity due to cord tethering or chronic dural tension with CSF stasis resulting in a build-up of cerebral toxins and restriction of CSF circulation.  The beneficial affects of YOGA POSTURES resulting in spinal flexion, extension and inversion affecting CSF flow, with involuntary oscillations of the spine and or extremities enhancing CSF flow.  All of which would be affected by a pseudomeningocele compressing the posterior and anterior sides of the dural/meninges against the spinal cord and displacing all CSF over the combined length of the T9 & T10 vertebra to small areas to the left and right of the spinal canal.  The publication gives references to publications which relate to each of these effects.  

I could continue but perhaps the above is sufficient to make my case.  And I can assure you Anthony that NUASEA is a very real result of spinal cord compression by a pseudomeningocele compressing both sides of the patients dura/meninges against nerves, neve fibres, nerve roots and blood vessels within the spinal cord.  I can also assure you that operative procedures to locate the defect in the patients dura, repair that defect and obliterate the space/cavity the neurosurgeon who excised the original intradural extramedulary schwannoma tumour three years previously explained to his colleague a neurologist in response to the neurologist requesting an explanation of the risks associated with operative procedures of the pseudomeiningocele were very sucessfuyl.  The space or cavity which that neurosurgeon who wrote informing a neurologist he had created by removal of bone and muscle during the laminectomy necessary to excise the intradural extramedulary schwannoma tiumour.  The cavity/space created by removal of bone and muscle the neurosurgeon said he had been unable to obliterate or fill, as there was no tissue nearby to allow him to do so.  And that neurosurgeon also explained to his colleague the neurologist that the option of harvesting muscle form other parts of the patients body and transporting that muscle into the space or cavity he had created was not to the neurosurgeons  point of view worth the risks involved.  However the specialist spinal neurosurgeon who performed the investigative and corrective surgery to eliminate the pseudopmenuingocele, three years latter did so without having to resort to such complicated plastic surgery.  And described what  he referred to as very routine and very necessary procedures developed for just that purpose.  NOTE which is very similar to the opinions expressed by most of the answers to my previous question by obviously highly qualified researchers. 

Thank you again Anthony and I look forward to any further comments from yourself or any other researchers.  As all comments are relevant to my present research and I am very appreciative of all such answeres. 

The point in question is not whether pseudomeniningoceles cause or are correlated with nausea and vomiting, but the mechanism involved.   I do not think it is necessary to invoke a new or unique physiological process.  Cases referenced above of CSF fistulas only support my position, since resulting bouts of CSF hypotension will lead to perilymph hypotension and endolymphatic hydrops, a very common cause fo N & V.  Any surgical procedure likely to stem a CSF leak should therefore stop the N & V.

Thank you Anthony

A very clear and precise answer.  My question attempts to encourage advice on what mechanisms would have caused the NAUSEA, if not the pseudomeningocele.  One possibility being the compression of the dura/meninges by the pseudomeningocel resulting in a restriction to the flow of CSF.  Hence my inclusion of CEREBROSPINAL FLUID STASIS AND ITS CLINICAL SIGNIFICANCE in my response to your initial answers. 

The second part of my question relates to suggestions by neurosurgeons who disputed the possibility that the pseudomeningocele was symptomatic as there was no visible sign of the pseudomeningocele on the patients back at the wound and the pseudomeningocele could not be palpated.  The claim being no compression of the spinal cord could result and there would be no symptoms resulting from the cyst.  

The content of the publication on CEREBROSPINAL FLUID STASIS AND ITS CLINICAL SIGNIFICANCE seems to me to support your conclusion that CSF hypotension was involved.  Would you agree?

The patient suffered increasing hearing loss in the left ear following the CSF leakage and formation of the pseudomeningocel.  The result was the provision of a hearing aid.  The left side of the body being most affected by the original tumour, resultant spinal cord dysfunction and the symptomatic pseudomeningocele.  

During the three years before the pseudomeningocel and the dural defect were located and repaired the patient was admitted twice as having suffered a suspect stroke.  Following which CT and MRI scans of head and brain found no problems other than fluid in the left mastoid bone.  No further strokes occurred after the patient was advised to restrict all walking exercise to the minimum possible for daily life, to reduce the pumping action of the walking gait.  The PULSATILE CSF dynamics; presence of an osmotic gradient between the subarnochnoiud space and CYST; valve-like mechanism between the fluid collection and subarachnoid space; and  Sacroiliac articular motions exerting a PUMPING ACTION upon the CSF.  Referred to in  The Indian Journal of Radiology and Imaging, NEURORADIOLOGY, Volume: 22 Issue: 2 Page: 108-115, 2012.

Your final statement:  Any surgical procedure likely to stem a CSF leak should therefore stop the N & V, being exactly what I was looking for Anthony.

Thanks again for your interest.  Any further comments would be appreciated.   

I don't want to get into technical details of various neurosurgical procedures, but it would be very useful if the cause of nausea & vomiting could be established.  I propose that post-operative N & V is due to reduced inner ear pressure. This can be simply tested in neurosurgical patients with N & V since definite predictions follow:

Thank You Anthony

Unfortunately such tests were not carried out between 2009 and 2012.  But Investigative and Corrective surgery in January 2012, located the larger than expected defect in the dura that had caused the pseudomeningocele to be symptomatic.  The hypothesis being that the pumping action of the patients walking gait had caused CSF to be forced out of the dura into the permanent connection and via a one-way-vale mechanism.  Hence the pseudomeningocele expanded slightly resulting in nausea until the pressure dissipated.  

The defect was repaired and the cavity or space created by removal of bone and muscle during the laminectomy was obliterated resulting in a full recover with no further nausea.  Though muscle spasticity due to spinal cord dysfunction continues but is under control.

Interestingly your thoughts on ear problems could have been very relevant.  An MRI scan of the patients head and brain following two emergency admissions as a suspect stroke found no problems other than fluid in the left mastoid bone.  And following increasing hearing problems  the patient was referred to ENT and fitted with a hearing aid for the left ear.