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Cerebrospinal fluid outflow along lumbar nerves and possible relevance for pain research: case report and review.

Bechter K, Schmitz B - Croat. Med. J. (2014)

Bottom Line: CSF outflow at lumbar nerves was also documented by neuroradiology.It is plausible that CSF signaling serves for interaction with nerves along the PCOP, which could explain previously unknown pathomechanisms in pain generation.Experimental findings of tactile pain hypersensitivity within lumbosacral pain pathways could be explained by releasing of molecules, microparticles, or exosomes into the CSF by mast cells, which then move with CSF outflow along the PCOP and interact with nerves, initiating even retrograde synaptic stripping.

View Article: PubMed Central - PubMed

Affiliation: Karl Bechter, BKH Guenzburg / Ulm University, Psychiatry II, D-89312 Guenzburg, Germany, Karl.Bechter@bkh-guenzburg.de.

ABSTRACT
CSF outflow through the cribriform plate near the olfactory nerves and the outflow along brain and spinal nerves are together known as peripheral CSF outflow pathway (PCOP). It is still not clear whether the PCOP has pathogenetic relevance. Our previous clinical observations have indicated that CSF may interact with nerves along the PCOP and in this article we present our finding of CSF outflow demonstrated by myelography in a single patient. We also discuss unexplained experimental pain pathomechanisms against the background of the PCOP hypothesis. We observed that CSF flowed along lumbar nerves in distal direction at a speed of about 10 cm per hour on its way through the tissues, mainly muscles. Total CSF outflow volume at the lumbar site was remarkable. CSF outflow at lumbar nerves was also documented by neuroradiology. It is plausible that CSF signaling serves for interaction with nerves along the PCOP, which could explain previously unknown pathomechanisms in pain generation. Experimental findings of tactile pain hypersensitivity within lumbosacral pain pathways could be explained by releasing of molecules, microparticles, or exosomes into the CSF by mast cells, which then move with CSF outflow along the PCOP and interact with nerves, initiating even retrograde synaptic stripping.

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Lateral view of the spine with the needle inserted into the lumbar subarachnoid spaces. The water soluble contrast agent (15 mL Solutrast 250M) was just injected and distributed immediately throughout the lumbar subarachnoid space (in black). Time 15:48.
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Figure 1: Lateral view of the spine with the needle inserted into the lumbar subarachnoid spaces. The water soluble contrast agent (15 mL Solutrast 250M) was just injected and distributed immediately throughout the lumbar subarachnoid space (in black). Time 15:48.

Mentions: In a patient undergoing lumbar myelography we observed physiological CSF outflow at lower body nerves, near the injection site (Figure 1). The patient was examined for clinical reasons unrelated to this study. There was immediate distribution of the contrast medium throughout the neighboring SASs, at all the neighboring nerve roots (Figure 2), and down the respective peripheral nerves (Figure 3-5). The cause of this CSF outflow cannot be increased intrathecal pressure from injection since we observed a similar finding in many cases before. Also, this can be excluded on the basis of logical considerations since after injection of the contrast agent into the SAS the intrathecal pressure may at best increase for a few seconds, because injection was performed slowly and an equivalent volume of CSF was removed before injection. Apparently, the contrast agent (now dissolved in the CSF) follows the natural course of CSF outflow along the nerves. The pattern of distribution is not compatible with a diffuse distribution or absorption from the SAS into the neighboring tissues, but with the CSF outflow scenario as proposed by the PCOP hypothesis (6). Although our neuroradiological pictures do not allow us to exactly define the anatomical borders of the outflow pathway and determine whether these borders definitely represent the epineurium and perineurium, they support such assumption. We observed that CSF roughly began to distribute from the SASs into the neighboring psoas muscle following the course of the nerve through the tissues. The outflow velocity was about 50 mm per 30 minutes (Figure 4). In addition, CSF slightly and diffusely distributed into the tissues closely adjacent to the nerve at many sites along its outflow course (Figure 4,5). Such disappearance of contrast agent might be explained by diffusion through the natural borders, ie, nerve sheets, or alternatively may be produced by multiple small wind ups of the PCOP all along the nerve, ie, at multiple nerve muscle end plates. One should note that the anatomy of the wind up of the PCOP pathway has not yet been described in histological detail.


Cerebrospinal fluid outflow along lumbar nerves and possible relevance for pain research: case report and review.

Bechter K, Schmitz B - Croat. Med. J. (2014)

Lateral view of the spine with the needle inserted into the lumbar subarachnoid spaces. The water soluble contrast agent (15 mL Solutrast 250M) was just injected and distributed immediately throughout the lumbar subarachnoid space (in black). Time 15:48.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4157386&req=5

Figure 1: Lateral view of the spine with the needle inserted into the lumbar subarachnoid spaces. The water soluble contrast agent (15 mL Solutrast 250M) was just injected and distributed immediately throughout the lumbar subarachnoid space (in black). Time 15:48.
Mentions: In a patient undergoing lumbar myelography we observed physiological CSF outflow at lower body nerves, near the injection site (Figure 1). The patient was examined for clinical reasons unrelated to this study. There was immediate distribution of the contrast medium throughout the neighboring SASs, at all the neighboring nerve roots (Figure 2), and down the respective peripheral nerves (Figure 3-5). The cause of this CSF outflow cannot be increased intrathecal pressure from injection since we observed a similar finding in many cases before. Also, this can be excluded on the basis of logical considerations since after injection of the contrast agent into the SAS the intrathecal pressure may at best increase for a few seconds, because injection was performed slowly and an equivalent volume of CSF was removed before injection. Apparently, the contrast agent (now dissolved in the CSF) follows the natural course of CSF outflow along the nerves. The pattern of distribution is not compatible with a diffuse distribution or absorption from the SAS into the neighboring tissues, but with the CSF outflow scenario as proposed by the PCOP hypothesis (6). Although our neuroradiological pictures do not allow us to exactly define the anatomical borders of the outflow pathway and determine whether these borders definitely represent the epineurium and perineurium, they support such assumption. We observed that CSF roughly began to distribute from the SASs into the neighboring psoas muscle following the course of the nerve through the tissues. The outflow velocity was about 50 mm per 30 minutes (Figure 4). In addition, CSF slightly and diffusely distributed into the tissues closely adjacent to the nerve at many sites along its outflow course (Figure 4,5). Such disappearance of contrast agent might be explained by diffusion through the natural borders, ie, nerve sheets, or alternatively may be produced by multiple small wind ups of the PCOP all along the nerve, ie, at multiple nerve muscle end plates. One should note that the anatomy of the wind up of the PCOP pathway has not yet been described in histological detail.

Bottom Line: CSF outflow at lumbar nerves was also documented by neuroradiology.It is plausible that CSF signaling serves for interaction with nerves along the PCOP, which could explain previously unknown pathomechanisms in pain generation.Experimental findings of tactile pain hypersensitivity within lumbosacral pain pathways could be explained by releasing of molecules, microparticles, or exosomes into the CSF by mast cells, which then move with CSF outflow along the PCOP and interact with nerves, initiating even retrograde synaptic stripping.

View Article: PubMed Central - PubMed

Affiliation: Karl Bechter, BKH Guenzburg / Ulm University, Psychiatry II, D-89312 Guenzburg, Germany, Karl.Bechter@bkh-guenzburg.de.

ABSTRACT
CSF outflow through the cribriform plate near the olfactory nerves and the outflow along brain and spinal nerves are together known as peripheral CSF outflow pathway (PCOP). It is still not clear whether the PCOP has pathogenetic relevance. Our previous clinical observations have indicated that CSF may interact with nerves along the PCOP and in this article we present our finding of CSF outflow demonstrated by myelography in a single patient. We also discuss unexplained experimental pain pathomechanisms against the background of the PCOP hypothesis. We observed that CSF flowed along lumbar nerves in distal direction at a speed of about 10 cm per hour on its way through the tissues, mainly muscles. Total CSF outflow volume at the lumbar site was remarkable. CSF outflow at lumbar nerves was also documented by neuroradiology. It is plausible that CSF signaling serves for interaction with nerves along the PCOP, which could explain previously unknown pathomechanisms in pain generation. Experimental findings of tactile pain hypersensitivity within lumbosacral pain pathways could be explained by releasing of molecules, microparticles, or exosomes into the CSF by mast cells, which then move with CSF outflow along the PCOP and interact with nerves, initiating even retrograde synaptic stripping.

Show MeSH
Related in: MedlinePlus