- Joined
- Apr 7, 2011
- Messages
- 5,313
- Reaction score
- 1,086
EDX, Imaging, exam? Give me your rationale and - 🙂 - be prepared to defend your position.
Definition: Loss of function of a nerve root. This can be complete or incomplete.
Weakness, sensory loss or changes, +/- pain.
Physical examination is all that is needed to call the diagnosis.
MRI and EMG can support or refute the diagnosis.
Pain is often present, but is radiculitis, or pain in a radicular pattern, but is not part of the definitive diagnosis as it is a purely subjective phenomenon.
Definition: Loss of function of a nerve root. This can be complete or incomplete.
Weakness, sensory loss or changes, +/- pain.
Physical examination is all that is needed to call the diagnosis.
MRI and EMG can support or refute the diagnosis.
Pain is often present, but is radiculitis, or pain in a radicular pattern, but is not part of the definitive diagnosis as it is a purely subjective phenomenon.
You really need an EMG. Most times it's not necessary but the most RELIABLE way is EMG from an academic standpoint
But, how sensitive is the needle EMG for radiculopathy?
A neurologist presented on exactly that a few years ago at ISIS and stated the accuracy was between 30 and 60% for radiculopathy. Major nerve sensory blocks are not detected reliably by EMG and neither is the causation of numbness. We continue to order these tests since it is the best test we have, even if not always accurate. But neither is MRI. Or physical exam. Or history.....sigh....
A neurologist presented on exactly that a few years ago at ISIS and stated the accuracy was between 30 and 60% for radiculopathy. Major nerve sensory blocks are not detected reliably by EMG and neither is the causation of numbness. We continue to order these tests since it is the best test we have, even if not always accurate. But neither is MRI. Or physical exam. Or history.....sigh....
A neurologist presented on exactly that a few years ago at ISIS and stated the accuracy was between 30 and 60% for radiculopathy. Major nerve sensory blocks are not detected reliably by EMG and neither is the causation of numbness. We continue to order these tests since it is the best test we have, even if not always accurate. But neither is MRI. Or physical exam. Or history.....sigh....
What else? I'll spell out where I'm going with this: What - if anything - can be done to make the needle EMG more SENSITIVE for radiculopathy?
I didn't realize this was a quiz 🙂. My guess is good history and examination.
Sorry for pimping. What I'm thinking about is direct nerve root stimulation. We use a variant of this in our practices - sans the stim - everyday. However, our needle positioning is much more accurate than what is described in the literature. I think this technique holds something for us and it warrants a direct comparison with needle EMG.
Aside from good technique, is there anything else that can be added to an EMG to make it more sensitive for radiculopathy? What I'm thinking about is mentioned in Dumitru and it's akin to something all of us - even those who don't perform EMGs - do routinely.
[/B]
are you serious?
Not really. Adding electrical root stimulation prior to a SNRB - trying to provoke a concordant motor paresthsia - is all I'm really talking about. It's not a far cry from what Alon Winnie used to advocate for with his addage: "No paresthsia, no anesthesia." I'm just trying to provide a little electrodiagnostic justification.
I used to do these early on with my TFESIs (we used to call them SNRBs). I brought along my hand-held stim and would zap the nerve looking for concordance. Not enough patients could say the feeling was concordant with their regular pain - most were vague "Yeah, it hurts!" Is that your regular pain? "It just hurts!"
My only comment remains, emgs are dumb and a waste for radics in the vast majority of the time for PAIN, which is what our field is. I bet when the reimbursement of emgs get low enough, it will stop being "an extension of the physical exam" which I believe to be complete bull**** in 96.8% of the time. We do what we know how to do, when it pays to do it.
My only comment remains, emgs are dumb and a waste for radics in the vast majority of the time for PAIN, which is what our field is. I bet when the reimbursement of emgs get low enough, it will stop being "an extension of the physical exam" which I believe to be complete bull**** in 96.8% of the time. We do what we know how to do, when it pays to do it.
EMG is at least as much of a CYA as an MRI is.
a 30 yo male walks in with back and leg pain, doesn't want to sit because standing feels better, has sensory loss in L5 dermatome and pain shooting to the toes, you assume he has an HNP and radic. You don't need an MRI to treat it, but we do much of the time to CYA. Every so often, like I had twice in the past month, what looks like a simple radic turns out to be a god-awful tumor.
Similarly, hand surgeons don't need an EMG to tell them the pt has CTS. The EMG is a CYA to show the pt does have it, how bad it is, justifies the surgery and helps protect them against future disputes.
For radics, I estimate 50% or more are EMG negative due to be pre-ganglionic and not damaging motor axons. A surgeon who wants an EMG prior to back surgery is CYAing.
A pain doc should rarely order an EMG prior to TFESI. The main time I can see is borderline nerve root impingement on MRI and vague HX or PE that brings about the possibility of plexitis or sciatic lesion.
For radics, I estimate 50% or more are EMG negative due to be pre-ganglionic and not damaging motor axons.
My only comment remains, emgs are dumb and a waste for radics in the vast majority of the time for PAIN, which is what our field is.
I bet when the reimbursement of emgs get low enough, it will stop being "an extension of the physical exam" which I believe to be complete bull**** in 96.8% of the time. We do what we know how to do, when it pays to do it.
I would add..patients with radicular pain and opposite side findings on MRI. I see it quite often.
There was interesting talk on this exact same thing at ISIS this year, Lecturer on anatomy felt this was most likely caused by aberrant sinuvertebral nerves that referred pain to opposite side of pathology or even one to two levels above or below.
The SVN can't cause radicular pain. Hard to explain contrecoup sciatica anatomically.
This is what he presented at ISIS( Dr. Willard from New Zealand I believe)
The Sinuvertebral Nerves (SN), is a mixed nerve as well as it carries both autonomic fiber (sympathetic) and sensory (afferent) fiber. [note: the Autonomic Nervous System (ANS) The sensory portion of the sinuvertebral nerve, which has the capability to carry the feeling of PAIN to the brain, arises from the outer 1/3 of the posterior annulus fibrosus ( and PLL . It then splits and attaches to both the dorsal ramus and the grey ramus communicans, although this nerves anatomy and course seems to be quite anomalous. Of importance is the fact that if irritated, the nerve ending within the disc have the potential to generate both back pain and/or lower limb pain (Discogenic Pain). This lower limb pain-referral has been greatly studied by Ohnmeiss et al. and is quite an interesting phenomenon. Discogenic Sciatica is the term I have given this referred discogenic pain. It is believed that the sinuvertebral nerve-endings are 'sensitive' to the irritating effects of degenerated nucleus pulposus, which may be introduced into the outer region from a grade three annular tear. (see may pages on Annular Tears for more information.) Amazingly, the sinuvertebral nerve also innervates (connects to) the disc above and below! So, the sinuvertebral nerve of the L4 disc also innervates the L5 and L3 disc. This may help explain why a L4 disc herniation/annular tear may clinically present with some signs of L5 and/or L3 involvement/overlap as well.
Ohnmeiss DD, et al "Degree of disc disruption and lower extremity pain" Spine - 1997; 22(14):1600-1665
I think this was one of his references
Thanks for the reference. But I'm still not a believer. Leakage of PLA2, TNF, gluten, into the epidural space causing a radiculitis, yes. But irritation of an axial structure like SVN itself as a cause of sciatica, nope. The only time I can recall producing leg pain during discography is when there's a grade three tear and I can see contrast outlining a root.
That said, I've had quite a few patients with sciatic pain but no clear reason for it on imaging, exam, or EMG.
For radics, I estimate 50% or more are EMG negative due to be pre-ganglionic and not damaging motor axons.
[/B]
what about anxiety as a cause in those patients?