Cycling steroids d/t tachyphylaxis

[dc2md]

What does everyone attribute the tachyphylaxis-like effect from repeat ESIs to?? Why do our patients get (for example) 6 months relief from the first one, then 3, then barely a week?? Does the epidural space/disc/spinal nerve (with all those crazy interleukins, prostaglandins, CGRP, etc) develop tolerance??

Has anyone tried to use a different steroid (like cycling opioids when tolerance develops)??

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[Tenesma]

i don't know if it is always a tolerance issue

sometimes i think it is more like the starving soul you rescue from a few years in the desert - the first sip of water tastes like honey from the gods... the next few sips after a few weeks out of the desert just aren't that miraculous-feeling/tasting anymore...

 

[dc2md]

HAHAHA. great analogy!!

 

[PMR 4 MSK]

Law of diminishing returns, as Tenesma suggests, is part of how I think of it. Also is the mechanism of pain. ESI should reduce inflammation from within the spinal canal, such as from HNP or whatever. 6 months later, is there still inflammation, or has it recurred? When they get less response from repeat injection, I often suggest that it is no longer an inflammatory problem, possibly more of just a space-occupying lesion.

 

[dc2md]

space-occupying lesion.

As in mechanical compression from hypertrophied facets + disc bulge?? But then our injections shouldn't help right? Flexion-distraction then maybe.

 

[PMR 4 MSK]

As in mechanical compression from hypertrophied facets + disc bulge?? But then our injections shouldn't help right? Flexion-distraction then maybe.

Narrow the neuroforamina with a facet osteophyte + disc/osteophyte complex, then rub the nerve root around in it for a while, I presume you'd get an inflammatory response. Knock that down a bit with steroid and you get pain relief. Wait a while and you still have mechanical irritation, but the inflammatory response, which may have had some protective effects, is blunted, but pain returns.

It's a very good question, that no one really knows the answer to.

 

[dc2md]

Can't we torture some poor mice by creating a minor mechanical compression on some spinal nerve root and seeing if it creates an inflammatory response. Then of course get out our tiny interventional tools with maybe a Tb needle and inject an equivalent dose of depo-medrol (and certainly some bupivicaine so they walk out of the laboratory happy). I say go for a ventral transforaminal approach (b/c who cares if we cause a spinal infarct). So many possibilities here. ;-) lol

 

[SSdoc33]

Can't we torture some poor mice by creating a minor mechanical compression on some spinal nerve root and seeing if it creates an inflammatory response. Then of course get out our tiny interventional tools with maybe a Tb needle and inject an equivalent dose of depo-medrol (and certainly some bupivicaine so they walk out of the laboratory happy). I say go for a ventral transforaminal approach (b/c who cares if we cause a spinal infarct). So many possibilities here. ;-) lol

THAT may be a use for ligament's 27g TFESI needle.....

 

[dc2md]

THAT may be a use for ligament's 27g TFESI needle.....

Exactly!! And the little mice will thank you for it too.