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Han, et al. (2004). Fibrocartilaginous embolism--an uncommon cause of spinal cord infarction

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    Han, et al. (2004). Fibrocartilaginous embolism--an uncommon cause of spinal cord infarction

    • Han JJ, Massagli TL and Jaffe KM (2004). Fibrocartilaginous embolism--an uncommon cause of spinal cord infarction: a case report and review of the literature. Arch Phys Med Rehabil. 85: 153-7. Children's Hospital and Regional Medical Center and Department of Rehabilitation Medicine, University of Washington, Seattle, USA. Fibrocartilaginous embolism is a rare cause of spinal cord infarction. It is postulated that an acute vertical disk herniation of the nucleus pulposus material can lead to spinal cord infarction by a retrograde embolization to the central artery. An increased intradiskal pressure resulting from axial loading of the vertebral column with a concomitant Valsalva maneuver is thought to be the initiating event for the embolus. We present a previously healthy 16-year-old boy with sudden onset of back pain and progressive paraparesis within 36 hours after lifting exercises in a squat position. His clinical presentation and neuroimaging studies were consistent with spinal cord infarction resulting from a central artery embolus at the T8 spinal cord level. Laboratory investigation showed no evidence of infectious, autoimmune, inflammatory, or neoplastic causes. Although no histologic confirmation was obtained, lack of evidence for other plausible diagnoses in the setting of his clinical presentation and in the magnetic resonance imaging findings made fibrocartilaginous embolism myelopathy the most likely diagnosis. We postulated that some cases of transverse myelitis might actually be fibrocartilaginous embolism, making it a more prevalent cause of an acute myelopathy than commonly recognized. Relevant literature and current theories regarding the pathogenesis of fibrocartilaginous embolism myelopathy are reviewed.

    Anyone else out there had FCE?

    I was diagnosed with having had a FCE 12months ago. At the time I was assessed as having a T7 incomplete SCI.

    I am yet to meet anyone else who has experienced the same thing as me, although, the young man's experience in the article is similar to mine. Although my outcome, so far, has not been quite as good as his.

    I was in Royal North Shore Hospital for 3 weeks and was diagnosed there. At RNS they said there had been 15 cases in the past 10 years and a farmer in NSW had suffered from the same thing 2 years ago.

    When I went for my driving test in Canberra, they said they had had one man who had suffered a FCE a few years ago, also go for his driving test there.

    So, anyone else out there?


      Clinically suspected fibrocartilaginous embolism

      see also : Eur J Neurol. 2011 Feb;18(2):218-25. doi: 10.1111/j.1468-1331.2010.03200.x. Epub 2010 Sep 6.Clinically suspected fibrocartilaginous embolism: clinical characteristics, treatments, and outcomes.

      Mateen FJ1, Monrad PA, Hunderfund AN, Robertson CE, Sorenson EJ. (august 2010)

      This paper by researchers at the Mayo clinic suggests that FCE is far more common than previously thought.

      There is a collection of 30 or so medical scientific papers, case studies and other special factors should anyone want, the source can be provided.

      Alludes to 5.5% of incoming spinal syndrome patients at Mayo clinic having FCE......far larger than believed historically.

      There is a also a separate collectiuon of 30 or so papers, case studies and special factors relating to FCE reported on by by mil and auto industries. Contact me if you want the source.

      Last edited by SCI-Nurse; 29 Jan 2016, 8:22 PM.


        Has anyone had an FCE and survived?
        Actually I have had a number of these and have a lot of data any information on the matter including causation.


          If anyone want to read the article here it is:

          I also found these being helpful:


            Whiplash of the lower spine is a general way to describe a sudden shape change of the spine, meaning the natural S curve is suddenly altered to conform with some other object by collision or fall and so on. Sudden shape changes can rupture or puncture the discs particularly in the location of schmorl. nodes which exist on many peoples discs, thereby releasing the mucus purposes. into the spinal vasculature. The spine is then either in a state of decay or vulnerable to further sudden deterioration should a further aggravating event to the spine occur. The scale of forces involved to cause such injury is (very) substantial yet these forces can be encountered, survived and discarded as unrelated events to final spinal injury which may occur months or weeks later. The events then become dissociated due to the passage of time and the underlying cause becomes a mystery. In the case of upper spinal whiplash, the time delay to final injury is well understood and hospitals put in place precautionary periods and neck braces. Not so for the lower spine. This important phenomenon is only coming to light.


              Very insightful Ronnoco! Thank you and I can only agree that the phenomenon is only starting to be talked about!


                A person presents at A&E complaining of loss of power in limbs, numbness and urinary incotinence. Its, neural, Its spinal but what is the cause.

                A neurologist examines and carries out battery tests, nothing shows. The patients is asked to describe what happened in recent hours, particularly what happened at the time of onset or hours just before. The patient describes recent events and perhaps alludes to an event involving a trauma, minor trauma or nothing at all, all the time referring to the time period assumed to be relevant....e.g. in the last few days, even a week or more.

                But suppose the relevant trauma occured weeks or even months before, it is likely to be considered by the patient as irrelevant and by the examiner as outside the scope of relevance in terms of time. Who for example would associate or even be able to identify a spinal trauma months after occurance. But if somebody is questioned against a protocol then there is a chance. However in the case of upper spine whiplash following RTA, the patient is asked to take precautions, no exertion, neck brace and so on so as not to provoke the onset of a more serious condition while healing takes place. The timescale being some months. What precaution could be taken in the case of lower spinal whiplash or sudden shape change, these are no lifting, limited walking, no jogging, limited articulation of the spine, blood thinners, non operation of vibratory machinery, no sports that load the spine.

                The timescale between physical event and presentation could be 3 months or more. The weakening process could be thought of as a tire which clipped the sidewall against a kerb but did not burst, weeks later, perhaps in hot weather, perhaps following some rough road, the tear has increased and remaining tyre strength is lowered. In a soft tissue, obviously we are dealing with a living organic structure, the healing phases may weaken a lesion that resulted in a transient reduction in strength and perhaps porosity but not sufficient to allow rupture of the end plate.

                Our calculations, (a private group involving some neurologists and bio engineers), calculated the imposed rupture forces involved in specific trauma events, indicated that relatively 'benign' (although alarming and painful) physical traumas could result in very large forces to the spine. We also examined some ways in which blood flow might be restored which appeared to have good potential.

                We see the case of a young person who did a somersault or back flip that was followed some hours later by the onset of the symptoms of FCE, diagnosis is 'suspected' FCE.
                BUt this may be only the tip of the iceberg as the condition may have actually have been caused months before, development have been prevented with precautions. It is clear that there are certain morphologies vulnerable to the condition and this can be identified before the event, it is clear than certain occupations, ph?sical events and traumas may lead to the condition and it is likely that significant time delays can exist between trauma and onset of paralysis.

                The tragedy is that cause and event are not well linked by examination at the moment, whereas in RTA, the event has a clear starting point, nontheless this can improve just as whiplash treatment did. Moreover it is currently thought that there is no treatment that may restore the vasculature. True, nothing in hospitals now, but there are grounds for optimism for treatment

                Any person with an interest in working with is welcome to contact.