What is the most reliable way to determine a radiculopathy?

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101N

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EDX, Imaging, exam? Give me your rationale and - 🙂 - be prepared to defend your position.

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A diagnosis is 90% history and 10% examination, and EDX is an extension of the PE. Most of the time MRI confirms what we know on exam and eliminates some causes of said diagnosis.
 
I would not give history 90%. A lot of things can mimic radiculopathy. I would give the examination at least a 40% specially if it is thorough.

" The implications of symptoms and signs on electrodiagnostic findings were investigated by Lauder et al [4,5] for suspected cervical and lumbosacral radiculopathies. Even though physical examination findings were better for predicting who would have a radiculopathy, many patients with normal examination findings had abnormal EMG studies, indicating that clinicians should not curtail electrodiagnostic testing simply because the physical examination is normal. For lower limb symptoms, loss of a reflex or weakness dramatically increased the likelihood ofhaving a radiculopathy confirmed by EMG. Losing the Achilles reflex, for instance, resulted in an odds ratio of 8.4 (P\0.01)—in other words, eight times the likelihood of having a radiculopathy confirmed by EMG with this physical examination finding [4]. Similar findings were noted for upper limb symptoms—if a reflex was lost or weakness was noted, the likelihood of having a radiculopathy confirmed by EMG was many times greater [5]. Combinations of findings, particularly weakness with sensory loss or with reflex changes, resulted in a nine-fold greater likelihood of cervical radiculopathy and two- to three times-greater likelihood oflumbosacral radiculopathy "

[4] Lauder TD, Dillingham TR, Andary M, Kumar S, Pezzin LE, Stephens RT, et al. Predicting electrodiagnostic outcome in patients with upper limb symptoms: are the history and physical examination helpful? Arch Phys Med Rehabil 2000;81:436–41.

[5] Lauder TD, Dillingham TR, Andary M, Kumar S, Pezzin LE, Stephens RT, et al. Effect of history and exam in predicting electrodiagnostic outcome among patients with suspected lumbosacral radiculopathy. Am J Phys Med Rehabil 2000;79:60–8

http://www.med.nyu.edu/pmr/residenc...inics NA_sports med/radic EMG_PMR clinics.pdf
 
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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.
 
Agree with Steve. Pain is usually present in a dermatomal nature, but pain without other physical findings of weakness, hyporeflexia, numbness is by definition radicular pain and not a radiculopathy (Bogduk).
 
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.



agreed
 
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.

How can you tell the difference from an incomplete sciatic neuropathy from radic on exam? How about lumbosacral plexopathy from radic? L5 root avulsion from radic?

Answer? You can't. Not reliably. You really need an EMG. Most times it's not necessary but the most RELIABLE way is EMG from an academic standpoint
 
You really need an EMG. Most times it's not necessary but the most RELIABLE way is EMG from an academic standpoint

1+

No one mentioned 'conduction block' in their definitions, Boduk does. You need some measure of it.

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....
 
But, how sensitive is the needle EMG for radiculopathy?

Lumbosacral radiculopathy.
5 muscle screen without paraspinals: 68-88%
5 with paraspinals: 94-98%.
6 without parapsinals: 79-89%
6 with paraspinals: 98-100%

http://journals.lww.com/ajpmr/Abstract/2000/11000/Identifying_Lumbosacral_Radiculopathies__An.2.aspx

Cervical radiculopathy.
5 muscle screen without paraspinals has sensitivity of 84-92%
5 muscle screen with paraspinals: 90-98%
6 muscle screen without paraspinals: 89-94%
6 muscle screen with paraspinals: 94-98%

http://www.ncbi.nlm.nih.gov/pubmed/11212017
 
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....

Not sure where he got the 30-60% number. Never heard of it being so low. The lowest I have heard is
"In a prospective study of 100 patients with lumbosacral radiculopathy who underwent lumbar laminectomy, EMG precisely identified the involved root level 84% of the time"

From one of the classic studies.
Young A, Getty J, Jackson A, Kirwan E, Sullivan M, Parry CW. Variations in the pattern
of muscle innervation by the L5 and S1 nerve roots. Spine 1983;8:616–24
 
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....

I think you are talking about the elusive 'sensory-only' radiculopathy. Agreed that there is no test or good exam for this? EMG will not identify this....
 
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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....

1+

I would agree with your neurologist. I think that the sensitivity of EMG for radiculopathy - in spite of claims otherwise here - is closer to 50% than 80%. I think this is due in part to sampling errors inherent in the needle study. You can't study all of the muscle fascicles/motor units.

"The sensitivity for EMG is unimpressive, ranging from 49% to 92% in these studies. Electromyography is not a sensitive test, yet it likely has higher specificity."

http://www.med.nyu.edu/pmr/residenc...inics NA_sports med/radic EMG_PMR clinics.pdf

But there is more to this discussion. EMG is also relatively poor at determining the specific root level. Here it's more sensitive but given that it misses 20 to 50% of true positives to begin with, still not very impressive.

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?
 
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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?

Test 6 muscles + paraspinals, know your anatomy, sample the right muscles, not have a purely sensory radiculopathy and rule out other neuro/MSK conditions that mimic radiculopathies.
 
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.
 
I didn't realize this was a quiz 🙂. My guess is good history and examination.
 
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.

What would be more sensitive for determining the root level of a suspected radiculopathy: 1. Direct root stim with a stimulating needle while querying the patient for a concordant/discordant paresthesia, or 2. A traditional needle EMG? While subjectivity is introduced with the patient self-report during stimulation it still might be be more sensitive than EMG due to inter-rater reliability issues with EMGs alone.

There seems to be a pretty broad consensus in the literature that adding root stim to an EMG increases sensitivity for radiculopathy. What if we just do comparative root stims - C6 vs C7, L5 vs S1 - while querying the patient for 'concordance' during our TFESIs? This is something I have been thinking about - and doing - for a couple of years.

1.http://www.elsevierhealth.com.au/me...ter_6_Special_Nerve_Conduction_Techniques.pdf

2. Dynamic change of proximal conduction in demyelinating neuropathies: a cervical magnetic stimulation combined with maximum voluntary contraction.
Hitomi T, Kaji R, Murase N, Kohara N, Mezaki T, Nodera H, Kawamura T, Ikeda A, Shibasaki H. Clin Neurophysiol. 2007 Apr;118(4):741-50. Epub 2007 Feb 20.
PMID: 17317300 [PubMed - indexed for MEDLINE]
Related citations

3. Cervical nerve root stimulation. Part II: findings in primary demyelinating neuropathies and motor neuron disease. Vucic S, Black K, Siao Tick Chong P, Cros D.
Clin Neurophysiol. 2006 Feb;117(2):398-404. Epub 2006 Jan 3.
PMID: 16403674 [PubMed - indexed for MEDLINE]
Related citations

4.Cervical nerve root stimulation. Part I: technical aspects and normal data.
Vucic S, Cairns KD, Black KR, Chong PS, Cros D.
Clin Neurophysiol. 2006 Feb;117(2):392-7. Epub 2006 Jan 3.
PMID: 16403485 [PubMed - indexed for MEDLINE]
Related citations

5. Root stimulation improves the detection of acquired demyelinating polyneuropathies.
Menkes DL, Hood DC, Ballesteros RA, Williams DA.
Muscle Nerve. 1998 Mar;21(3):298-308.
PMID: 9486858 [PubMed - indexed for MEDLINE]
Related citations

6. Evaluation of cervical radiculopathy by cervical root stimulation.
Tsai CP, Huang CI, Wang V, Lin KP, Liao KK, Yen DJ, Wu ZA.
Electromyogr Clin Neurophysiol. 1994 Sep;34(6):363-6.
PMID: 8001478 [PubMed - indexed for MEDLINE]
Related citations

7. Spinal nerve stimulation in the diagnosis of lumbosacral radiculopathy.
Chang CW, Lien IN.
Am J Phys Med Rehabil. 1990 Dec;69(6):318-22.
PMID: 2176087 [PubMed - indexed for MEDLINE]
Related citations

8. Magnetic and electrical stimulation of cervical motor roots: technique, site and mechanisms of excitation. Schmid UD, Walker G, Hess CW, Schmid J.
J Neurol Neurosurg Psychiatry. 1990 Sep;53(9):770-7.
PMID: 2174077 [PubMed - indexed for MEDLINE] Free PMC Article
Related citations

9. Cervical root stimulation in the diagnosis of radiculopathy.
Berger AR, Busis NA, Logigian EL, Wierzbicka M, Shahani BT.
Neurology. 1987 Feb;37(2):329-32.
PMID: 3808317 [PubMed - indexed for MEDLINE]
Related citations
 
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.

aahh offcourse!! I briefly read about it just last month while preparing for my PM&R boards. Unfortunately I have never seen a direct nerve root stim being performed. Thank you for sharing the sources and the link.
 
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.




are you serious?
 
i appreciate the discussion, 101, but you are barking up the wrong tree with a bunch of anesthesiologists here.
 
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.
 
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!"
 
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!"

During fellowship we occasionally used a Stimuplex with caudals to verify we were in; it causes an anal wink when your in the caudal canal. I started using it for TFESIs a couple of years ago at the request of a local NS. I use a 4 & 3/4" Stimuplex needle and drop it through an 18g introducer for lumbar procedures. I'll stim both roots in question and query the patient as to which paresthesia feels more concordant. In my experience they usually identify one root that feels more familiar so I will anesthetize only that one. While it's not been verified in the literature my local NS's all want me to use it.

I've not had much complaint of pain with the procedure but the ventral ramus twitch is truly impressive as you increase the voltage. I think you can recruit a lot of fascicles with this technique. I've never used my EMG stimulator and attempted formally record a latency with a needle in a muscle. Unlike RF and Stimuplex needles, EMG needles aren't insulated.

I've used the same technique to get close to the C2 root and I can tell you that, in spite of what's written in the literature, there is motor component to that root. You get a capital extensor - and strap muscle - twitch.
 
Like many things in Dumitru's book , what you are talking about is uacademic.
It is not used in the real world but in academic EMG labs.( ie single fiber EMG).
He does not teach this technique or many others many listed in his EMG Bible, most of this is strictly mental Masturbation.
He is the 1st to admit this.

...I do have some insight as my wife was one of his residents and I was his Chief Resident.
 
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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.

Disagree. But, - maybe because I've been so convoluted in my presentation- you've managed to miss my whole thesis. All I'm saying that electrical nerve root stimulation, prior TFESI, should be compared against EMG to see which is more sensitive for diagnosing root level radiculopathy.

A few years ago there was a similar dialog on FAD vs straight discography. I'm just suggesting that we add a 'provocation' arm to TFESIs.
 
pain past the knee with a positive SLT... then confirmed by MRI.
 
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.
 
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.

I would add..patients with radicular pain and opposite side findings on MRI. I see it quite often.
 
For radics, I estimate 50% or more are EMG negative due to be pre-ganglionic and not damaging motor axons.

This or sampling error during the needle study. (Actually, since pretty much all of the root stim articles suggest that it - root stim - is
more sensitive than traditional needle EMG, it must be sampling errors.)
 
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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.

Agree!!

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.

Disagree. It is and always will be an extension of the physical examination regardless of the reimbursement.
 
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.
 
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.
 
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
 
SVN mediated radic makes a whole lot less sense than traction on the nerve on opposite side. Still doesn't explain why no pain on appropriate or expected side.
 
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.
 
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.


what about anxiety as a cause in those patients?
 
For radics, I estimate 50% or more are EMG negative due to be pre-ganglionic and not damaging motor axons.

Just occurred to me. Preganglionic only applies to sensory neurons. Every alpha motor neuron in the canal has it's cell body in the ventral horn so there are no pre-ganglionic radiculopathies.
 
[/B]

what about anxiety as a cause in those patients?

That's certainly possible. But you have to admit that it's a weird manifestation of anxiety.
 
Cervical radiculopathy: good screening (high sensitivity) tests are ULTT, Spurling's; good confirmation/diagnostic (high specificity) test is cervical distraction.

Wainner's clinical prediction rule for cervical radiculopathy (4 criteria): cervical rotation less than 60, positive spurling's, positive distraction, positive ULTT. If 4/4 the +LR is 30.3, -LR is .76.

Lumbar radiculopathy: sensitive test is SLR, specific test is Well leg raise.

Took this info from a book by Chad Cook, PT, PhD...hope it helps.
 
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