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I enjoyed the Editorial by Jeremy Fairbank, Professor of Spinal Surgery in Oxford, about “Surgery for Neurogenic Claudication in Spinal Stenosis”. It was relevant to the paper by Moogen and colleagues who reported a randomised controlled trial comparing conventional decompressive surgery with an interspinous spacer. As Fairbanks points out, there was no difference in outcome between the two groups although the interspinous spacer led to much higher and earlier vision rates. This is hardly surprising as the X-Fix is a “quick fix, only flexing the motion segment involved and not affecting the underlying pathology”.
Fairbank added some information about degenerative spinal stenosis to his comments about the trial and there is one important point requiring clarification. Degenerative stenosis is not the result of disc degeneration but by the completely different pathology of osteoarthritis of the posterior facet joints. As the lining articular cartilage thins so load is taken by the subchondral bone which in turn hypertrophies and it is these hypertrophic facet joints that dig into the spinal canal. This in turn can compress the cauda equina both centrally and in the lateral recesses. The undercutting of these hypertrophic facet joints is the essential feature of the decompressive surgery.
Fairbank was quite right to point out that not all individuals undergoing this decomporessive surgery do benefit, rather about two-thirds, and this is generally because while the central canal is decompressed there is often residual lateral canal stenosis because the full depth of the offending facet joint is not adequately undercut.
The Japanese study about magnetic resonance imaging of the lumbar spine showing a surprisingly high rate of spinal stenosis (almost 80%) of participants is in no way surprising. Spinal stenosis is a clinical diagnosis, not an MRI one, rather the latter is to confirm the location and severity of the offending structures to aid surgical precision. It is extraordinary how a patient whose spinal canal on MRI is reduced to no more than a pin hole, or indeed a complete block, but can often have very little in the way of clinical features and this is because of the 4th dimension time as it takes years for facet joint hypertrophy to become clinically relevant if at all.
Fairbank, who has spent most of his life looking at back pain and spinal disorders in particular analysing outcomes, quite rightly states that these disorders have headed the list of the global burden of disease but they are close to the bottom of the list when it comes to research investment. He concludes by saying the spacer devices should become cheaper with time. As they confer no benefit compared with conventional surgery and create their own problems let’s hope they become extinct by then.
Re: Surgery for neurogenic claudication and spinal stenosis
I enjoyed the Editorial by Jeremy Fairbank, Professor of Spinal Surgery in Oxford, about “Surgery for Neurogenic Claudication in Spinal Stenosis”. It was relevant to the paper by Moogen and colleagues who reported a randomised controlled trial comparing conventional decompressive surgery with an interspinous spacer. As Fairbanks points out, there was no difference in outcome between the two groups although the interspinous spacer led to much higher and earlier vision rates. This is hardly surprising as the X-Fix is a “quick fix, only flexing the motion segment involved and not affecting the underlying pathology”.
Fairbank added some information about degenerative spinal stenosis to his comments about the trial and there is one important point requiring clarification. Degenerative stenosis is not the result of disc degeneration but by the completely different pathology of osteoarthritis of the posterior facet joints. As the lining articular cartilage thins so load is taken by the subchondral bone which in turn hypertrophies and it is these hypertrophic facet joints that dig into the spinal canal. This in turn can compress the cauda equina both centrally and in the lateral recesses. The undercutting of these hypertrophic facet joints is the essential feature of the decompressive surgery.
Fairbank was quite right to point out that not all individuals undergoing this decomporessive surgery do benefit, rather about two-thirds, and this is generally because while the central canal is decompressed there is often residual lateral canal stenosis because the full depth of the offending facet joint is not adequately undercut.
The Japanese study about magnetic resonance imaging of the lumbar spine showing a surprisingly high rate of spinal stenosis (almost 80%) of participants is in no way surprising. Spinal stenosis is a clinical diagnosis, not an MRI one, rather the latter is to confirm the location and severity of the offending structures to aid surgical precision. It is extraordinary how a patient whose spinal canal on MRI is reduced to no more than a pin hole, or indeed a complete block, but can often have very little in the way of clinical features and this is because of the 4th dimension time as it takes years for facet joint hypertrophy to become clinically relevant if at all.
Fairbank, who has spent most of his life looking at back pain and spinal disorders in particular analysing outcomes, quite rightly states that these disorders have headed the list of the global burden of disease but they are close to the bottom of the list when it comes to research investment. He concludes by saying the spacer devices should become cheaper with time. As they confer no benefit compared with conventional surgery and create their own problems let’s hope they become extinct by then.
Competing interests: No competing interests