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  • abprops
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    Post count: 8

    Thanks again Dr Gorenman.

    I had various problems between 2009 and 2012 when the very successful investigative and corrective surgery proved the existence of the larger than expected defect in my dura and resolved the spinal cord compressions.

    Three emergency admissions. I suffered infrequent serious instantaneous pains which resulted in my having to use crutches and neoprene back braces for most of the day – extremity co-ordination, numbness and problems walking. In 2009 I was admitted to hospital on three separate occasions by para medics, as a suspect heart attack and was advised I should use the angina spray prescribed following the first admission at the slightest sign of problems – tightness around the chest – I was had two emergency admissions as a suspect stroke by two different GPs within a month before I stopped all forms of walking exercise in favour of cycling to rebuild the wasted muscles down the left side of my body.

    When my problems first became apparent in July 2008 and doctors claimed the problem was sciatica and lower back plain for which the policy was to do nothing and not allow any form of imaging, I requested that my prostate gland be checked as the instantaneous pains I infrequently suffered were somewhere in my lower body and most definitely not in my back.

    The GP was reluctant to refer me to urology and when he did informed them I had no urinarty problems but was certainly very concerned about prostate cancer. I had not even mentioned cancer and had thought the problem could be an enlarged prostate. Not unusual for a man in his mid 60s.

    The urologists appeared to do everything possible, finger tests, PSA tests, CT urograms, Ultrasounds and were very helpful and considerate. But despite my frequently passing of blood and blood clots, they declared my prostate gland to be small smooth and benign and advised there would be no more clinics following the last one in 2010.

    In 2012 after the very successful investigative and corrective surgery my recovery was excellent and I steadily improved my level of fitness, by walking as far as I wanted, at least 6 miles each day and regularly cycling distances between 12 and 60 miles.

    However I still suffered testicular discomfort, and the feeling that there was some form of urinary infection. Then I discovered there were some doubts about my prostate problem and indeed the urologists had recommended that my GP arrange another PSA test for April 2011. As that PSA test had not been arranged by May 2012, I asked for a PSA test. The result was another urology clinic during which a urologists finger again found my prostate gland to be small smooth and benign.

    But when I expressed my concern the urologist arranged another PSA test and assured me no more such tests would be missed as he would arrange the next 6 monthly test well in advance. And to reassure me would arrange another PSA test and a testicular ultrasound. The letter for the next clinic arrived but was soon followed by another informing me a transrectal ultrasound and biopsy was required.

    The biopsy was said to be to reassure me but within two weeks a cancer specialist nurse informed me a small number of low grade malignant cells had been found in a small area in the left side of my prostate. Early stage prostate cancer for which the policy was to continue the 6 monthly PSA tests.

    I demanded removal of my prostate gland without further delay. An MRI scan was done and an Oncologist informed me the malignant cells were spread throughout my prostate as the needle biopsy test was as unreliable as the PSA test. And in combination with my medical files the Oncologist diagnosed PROSTATITIS as having been the cause of my discomfort since 2008. The GPs having relied upon plastic stick dip tests rather than lab tests. And as my problem was inflammation rather than infection the prostatitis had not been diagnosed. The result was two courses of a specific anti-biotic before surgery.

    The Urologist/Surgeon was very confident that he could remove my small prostate gland with full nerve sparing and an excellent prognosis. Until he found the left side of my prostate gland were the urologist finger could not reach was in poor mushy condition. The left nerve bundle attached to my prostate gland had been compromised by the cancer and had to be removed with the prostate gland, 12 lymph nodes and a suitable margin of tissue to allow the lab to confirm the cancer had HOPEFULLY not spread further. The biopsy Gleason Score 3+3=6 was changed to 3+4=7 which would not have been known had I waited or had opted for radiotherapy.

    Now some 16 months folowing surgery and 6 months following surgery to repair the small hernia first diagnosed in 2009, my recovery is slow but steady. My PSA levels remain at the minimum possible level suggesting the cancer has not spread. Though I am now aware that a further 9 years of such tests will be necessary before the prostate cancer can be consider cured. If ever.

    But the obvious problems and symptoms relating to my CNS, PNS and ANS which resulted in uncomfortable sensations from my left breast, down the left side of my body across my abdomen, into my testicles and down my left leg, which the neurosurgeons claimed was due to the damage to nerves in and attached to my thoracic spinal cord, have reduced considerably. Though I have been informed it will take between 18 months and two years for the damage to nerves that were attached to my prostate gland, hence erectile dysfunction and improving urinary incontinence there are encouraging signs of improvement. The uncomfortable sensations in my testicles still occur but are less frequent and do not last for long. The uncomfortable sensations in my lower abdomen are rarely noticeable and becoming less so. Even the sensations in my left leg are very much reduced and often unnoticeable. My main problem being muscle spasticity if I do not do regular stretching exercises. But that was pointed out following the investigative and corrective surgery and is also very much under control, though it became a problem following the hernia operation until the wound healed.

    I am still in the process of gaining physical fitness but that is steadily improving and I will continue to do what I can to achieve similar levels to that when I was 6 years younger. People including doctors are often surprised when they meet me for the first time and do not believe I am over 60. But next month I will be 70 and I have every intention of living for another 30 years if not longer. As I intend making the best of my excellent index linked pension for as long as possible.

    I hope the above makes it clear that my symptoms were not just NAUSEA. Though the neurosurgeons had informed what they described as Dyasthesia or The Syndrome were the cause of my symptoms and nothing could be done to relieve that Dyasthesia or The Syndrome and they strongly advised against further surgery but would not explain why. Apart from the neurosurgeons who offered investigative and corrective surgery which they advised was the only way to prove the existence of a permanently open defect in my dura. As indeed is the conclusion in the extensive medical literature and case studies on pseudomeningoceles and CSF fistulas.

    If you can advise on any text books which definitely refer to compression of the spinal cord by a pseudomeningocele or CSF fistula that would be very helpful.

    I understand and accept your comments on NAUSEA being unusual as a sole symptom of such compression and hope my explanation above explains NAUSEA is the symptom I refer to in connection with the pseudomeningocel.

    Thanks again.

    abprops
    Member
    Post count: 8

    Thanks again Dr Corenman.

    Yes I was pleased to find confirmation in a text book as you suggested.

    And as you describe my symptoms were described by a Neurologist as subtle. During consultations I was able to demonstrate my ability to perform various Yoga poses. As the neurologist noted in his report I was able to stand on either leg with the other tucked up into my perineum. Indeed I had demonstrated the same when doctors claimed my initial symptoms were sciatica in 2008. But the PT assessment they arranged cause nausea when the PT insisted I bend over backwards to release what she described as my stiff lower back. Three months latter an MRI scan found the schwannoma tumour the radiologists reported to be flattening my spinal cord and pressing the cord and the T9 nerve root against the far side and left of my spinal canal.

    My problem was the nausea which resulted if I walked more than 1/2 mile. Though I was able to cycle steadily increasing distances as my fitness improved. Providing I did not walk far when I reached my destination. Hence the conclusion the problem was due to the pumping action of my walking gait forcing CSF through a one-way valve resulting in the increased pressure in the cyst compressing my spinal cord. Pressure which dissipated when I lay down as when in the MRI scanner.

    I have asked for help searching the medical text books for similar descriptions as in Spinal Disorders: Medical & Surgical Management by J D Barieson and H Gordon Deen, Cambridge Uni Press Page 25. And the two references you provided.

    If you or anyone else can provide references to text books which definitely confirm spinal cord compression due to the difference in CSF pressure between that inside the dura and a pseudomeningocel with a permanent connection and one-way valve that would be very helpful.

    Can you confirm that the two references you provided definitely confirm such a condition?

    Just to make it clear the MRI imaging show both sides of my dura being compressed against my spinal cord over the combined length of the T9 to T10 vertebrae with a slight overlap at either end as noted in the associated radiologists reports. Though the radiologists reported no evidence of spinal cord compression. When I was in the MRI scanner and had been asked to hold my breath and not move. Quite a different situation from when I was walking.

    abprops
    Member
    Post count: 8

    Thanks again Dr Corenman.

    I have only been able to have a look at the index list for the two publications so far. And I don’t at this time want to outlay the money to purchase copies, as there is no mention of ball-valves and compression of the spinal cord by a cyst in either index.

    However I have found Spinal Disorders: Medical & Surgical Management by J D Barieson & H Gordon Deen, Page 25. Under the Heading Abnormalities that can be congenital or Acquired sub heading Archnoid and perineural cysts. The following info is given:

    They can occur at any level in the spine but most occur in the THORACIC REGION, more so POSTERIORILY. They are typically intradural or EXTRAMEDULARY. Many are asymptomatic , BUT THEY CAN CAUSE LOCAL COMPRESSION WITH back pain, radicular pain AND OR MYELOPATHY. Presumably the cysts grow via a BALL-VALVE MECHANISM which TRAPS CSF WITHIN THE CYST. IF SYMPTOMATIC they may require SURGICAL REMOVAL.

    The above describes my situation following removal of the intradural schwannoma tumour. The Pseudomeningocele which first appeared on MRI imaging 6 months later as the pseudomeningocel expanded slowly due to the initially small defect in my dura. Possibly assisted by my attempts to regain fitness.

    The radiologist report on the second post surgical MRI scan 6 months later noted a slight enlargement of the pseudomeningocel as the effects of surgery on the surrounding tissue reduced. Which seems to confirm that the steady flow of CSF was causing the pseudomeningocele to increase in size and fill the cavity over the back of my spinal canal the neurosurgeon described as a space due to removal of bone and muscle during the laminectonmy to access my dura and remove the tumour. The slow leakage of CSF and growth of the pseudomeningocel being the reason for the delay of over 6 months before I became aware of the symptoms which started to appear within weeks of the first 6 monthly monitoring MRI scan.

    I have copies of several international medical publications and case studies which conclude that investigative and corrective surgery is the definitive requirement for the very rare symptomatic pseudomeningoceles. The symptomatic pseudomeningocel that was confirmed by investigative and corrective surgery, to be the cause of my debilitating symptoms three years after the intradural schwannoma tumour was removed. However the above is the first publication I have found which confirms that a cyst connected to a defect in the dura with a ball-valve can result in compression of the spinal cord.

    Thanks again for your help Dr Coreman. If you can provide any other references to cysts, ball-valves resulting in spinal cord compression I would be very grateful.

    abprops
    Member
    Post count: 8

    Thank you again Dr Coreman.

    How can I post copies of the pictures on this website?

    I could send them by e-mail but have been unable to do so using your contact section.

    Can you provide details of a text book with the explanations?

    abprops
    Member
    Post count: 8

    Thank you again Dr Coreman for yet another detailed explanation.
    /Users/morris/Pictures/2012-01-09-0007.JPG.pdf/Users/morris/Pictures/2012-01-09-0008.JPG.pdf
    I have included photographs taken during the investigative and corrective surgery on the symptomatic pseudomeningocele. One showing the view down through the drained pseudomeningocele and showing the dura. The second showing the larger than expected defect in the dura and the stitches used to close the dura following removal of the schwannoma tumour there years before. The original small defect having expanded considerably due to the regular flow of cerebrospinal fluid.

    The pseudomeningocle did indeed have a one way valve preventing back flow of cerebrospinal fluid. Resulting in a build up of pressure within the pseudomeningocel leading to compression of the spinal cord and nausea until that increased pressure dissipated.

    Can you point me towards published medical literature which describes the pressure phenomenon similar to spinal canal stenosis?

    The MRI imaging shows the pseudomeningocele extending over the combined length of the T9 to T10 vertebra compressing both sides of the dura against the spinal cord and against the anterior wall of the spinal canal. This compression leaving two small areas on either side of the spinal cord to allow cerebrospinal fluid to circulate or flow. The reduced volume of cerebrospinal flow would presumably have caused cerebrospinal fluid stasis. Would the stasis or pressure difference produced be the pressure phenomenon you referred to?

    abprops
    Member
    Post count: 8

    Thank you again Dr Corenman for yet another excellent explanation.

    The fluid filled mass I referred to is a pseudomeningocel. The defect in the dura did not heal but remained and expanded in size. Hence the pseudomeningocele was symptomatic. The defect being connected into the pseudomeningocele with a permanent connection and one way valve preventing back flow of cerebrospinal fluid.

    In this situation the images produced by a conventional MRI scan when the patient was not moving showed no evidence of compression of the spinal cord. Would the spine, spinal canal and the spinal cord not adopt different positions when the patient was standing and walking. Would the change in position resulting from the patient walking, bending etc, not result in compression of the spinal cord. Particularly as the patients walking gait forced cerebrospinal fluid out from the dura into the pseudomeningocele.

    Conventional MRI images at 6 monthly intervals over a period of three years showed the pseudomeningocel compressing both sides of the dura against the spinal cord and against the anterior wall of the spinal canal over the combined length of the T9 and T10 vertebra. The larger than expected defect in the dura was located following investigative and corrective surgery done three years after the laminectomy done to remove an intradural schwannoma tumour at T9.

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