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13 Articles in Volume 18, Issue #6
Authorities’ Use of Big Data May Harm—or Help—Your Chances of Investigation
Gaps in the Pharmacist’s Pain Management Role
How can cyproheptadine manage complicated chronic pain cases?
Letters to the Editor: Trackable Pills; Buprenorphine; CRPS Diagnosis
Managing a New High-Dose Opioid Patient
Managing Opioid Use Disorder
Medication Selection for Comorbid Pain Management (Part 2)
Mobile Trackers and Digital Therapeutics
New Insights in Understanding Chronic, Central Pain
Nocebo Effects: How to Prevent them in Patients
Polarizing Topics in Chronic Pain
The Fight to End Peripheral Neuropathy
Urine Drug Monitoring

Letters to the Editor: Trackable Pills; Buprenorphine; CRPS Diagnosis

September 2018 PPM Letters to the Editor from practitioner peers and patients

Trackables & Safety Risks

Dear PPM,

I am writing to sound an alarm regarding your June 2018 Guest Editorial, “The Emergence of Trackable Pill Technology: Hype or Hope?” by Young, et al. As a lifelong intractable pain patient married to a web developer working in cybersecurity, I am in perhaps a better position than most to recognize the terror this technology would unleash if used routinely for chronic pain patients.

Technology companies will, of course, claim their data is secure. This is never the case with any smartphone app or any “smart” device connected to a web portal. Literally 100% of these systems can be hacked, and terms-of-use documents always include a legal disclaimer to that effect. Imagine that criminals have an easy way to read data from a hacked server to determine which people on the street are carrying pain medication. This is a lethal threat to the safety and lives of patients.

As much as these companies will swear their technology is different... that message is along the lines of what Equifax said before accidentally allowing hackers to access nearly 150 million social security numbers. Would you please consider writing another article, perhaps in consultation with a cybersecurity expert, to raise this concern publicly?

–Reese Tyrell

Dear Ms. Tyrell,

Your feedback is greatly appreciated. Notwithstanding the benefits that digital medicine offers, there will always be legitimate questions about potential privacy and safety compromises. To allay some of these concerns, we offer the following response based on our experience as pain management providers who have kept an objective open mind about adopting new digital technologies for optimizing care of patients.

Like most pain physicians and providers, we care dearly about preserving the sanctity of patient data and maintaining the highest level of privacy, accuracy and security for our patient population. For chronic pain patients, this is especially important since pharmacological management of persons in pain often carries societal, vocational, and even legal implications, and data on how these drugs are used is vital for appropriate decision-making. Accordingly, we have had an opportunity to thoroughly research the requisite cybersecurity and safety standards associated with digital medicine.

To properly address data security, including the rigorous safeguard of personal information, the manufacturers of such technology leverage a variety of security technologies and procedures to protect data from unauthorized use, access, or disclosure. While no means of Internet transmission or cyberstorage is absolutely secure, necessary protections and firewalls are universally deployed to protect the end-user: the patient.

Digital medicines, specifically, introduce no new risks associated with understanding who has a prescription for a pain medication. Pain medication prescriptions are already being tracked in pharmacy systems. If there is concern that patients’ data could be read by hackers to determine who in a community is taking pain medication, digital medicines are exceptionally secure, with high levels of encryption, and are likely much more secure than electronic medical records or pharmacy systems.

Patients can voluntarily choose whether or not they use digital medicines, and those who do will benefit from a more informed collaboration with their healthcare team that comes from using this unique technology.

Manufacturers are committed to protecting the privacy of personal information. Before selecting a digital-medicine strategy, physicians should consider the above criteria to assure that these requirements are successfully satisfied.

Digital medicines have the potential to optimize delivery and efficiency of care throughout the healthcare spectrum. For pain patients as well as their providers such technological breakthroughs hold much promise. By optimizing patient engagement, digital medicines combined with requisite cyber-safeguards represent innovation for pain sufferers, their caregivers and their healthcare providers.

–Mark A. Young, MD
& Lauren DiMartino

Buprenorphine Conversion Post-Surgery

Dear PPM,

Could you help to clarify the conversion of buprenorphine to alternate opioids? I am trying to determine the equivalent of buprenorphine 20 mg daily for a patient who is on suboxone at home but using oxycodone in-patient. Buprenorphine 9999 mcg is converting to 888 mg oxycodone (with no modification for incomplete tolerance). The patient has a history of chronic pain and remote Hx substance abuse for which she takes suboxone 8-2 mg sublingual film (2.5 once a day = 20 mg buprenorphine) at home. On admission, she was started on oxycodone 10 mg PO q4h prn acute pain related to prosthetic joint infection (taking ~50 mg daily for most of admission). She is now nearing discharge with the plan to resume suboxone on return home. Her oxycodone was reduced to 5 mg PO q8h over the past few days; this is c/o 10/10 pain from knee.


Dear B.B.,

Since buprenorphine is a partial agonist/antagonist, it is almost impossible to make an accurate conversion as doses increase beyond that which we see with Belbuca or Butrans. The dose of oxycodone your patient is currently receiving will not likely be up-taken to the opioid receptors because buprenorphine has such a strong binding affinity to those receptors. In fact, it is higher than naloxone. A good way to approach such a case in the future is to use IV buprenorphine for acute pain and add NSAIDs as long as there are no cardiac or renal risks.

My suggestion upon discharge, if she is able to take NSAIDs is to give the patient etodolac 400mg PO TID for at least 72 hours, and then make it PRN. If you (or someone else) is prescribing the suboxone off-label for pain, that dose can be increased. If it’s being prescribed by a certified clinician for OUD, that will not be an option for them, but a non-certified prescriber that is treating pain could increase the dose by giving another RX, after consulting with the MAR doc.

These two documents may also be helpful:

  • Buprenorphine and Surgery: What’s the Protocol? (Bettinger JJ, Fudin J, Argoff C, Pract Pain Manage, September 2017).
  • Opioids for Surgery or Acute Pain in Patients on Chronic Buprenorphine (Fudin J, Srivastava A, Atkinson TJ, Fudin HR, Medication Management of Chronic Pain: What you Need to Know, Trafford Publishing, 2017).

–Jeffrey Fudin, PharmD

A 70-Month Journey to CRPS Diagnosis

Dear PPM,

In December 2012, I had a freak accident/injury while sitting at my computer. I could not read the font on a document, so I leaned forward, goose-necking my head to bring my eyes closer to the monitor. I felt a pain in my right neck/shoulder, and instantly, my right arms/hands turned red, and felt like pins and needles. This was the start of my 70-month, 22-doctor journey to be diagnosed with complex regional pain syndrome (CRPS) in July 2018 based on my still “unexplained” lower arm/hand pain and symptoms.

Four months after my initial injury, I picked up a fork while eating, and my left arm/hand turned the same way (red, pins/needles). I now have learned that CRPS can travel to the opposite limb and effect it.

Since the injury, I have not had one day of pain relief. On several occasions, the arm/hand pain has become so great that I have wondered if I would feel better without them. I have limited driving ability, as my hands fall asleep at the wheel, and I lost my job as I am no longer able to keyboard for long periods of time.

Initial testing involved a dedicated cervical MRI, which revealed that I unknowingly had two cervical bone spurs, one of which had pushed against my spinal canal, pushing it into my spinal cord and leaving my lower arms and hands with partial paralysis.

My doctors all said that my arms/hand showed typical symptoms of a spinal cord injury, but there were also some unexplained symptoms (eg, frequent color changes, internal burning, sensitivity to touch, feeling ice cold at times). At one point, my doctors thought I might have Raynaud’s disease (I tested negative), and at another point, carpal tunnel syndrome. I never had corrective neck surgery as my cervical doctor thought it was too late, and another surgeon offered to remove the bone spurs/fusion, but warned me that the surgery was at the paraplegic level and I could wake up worse off.

Instead, I went through several weeks of physical therapy, which made my arm/hand pain/neck worse. I was prescribed five different pain relief medications over the years, most of which did little for my pain, but made me feel like a zombie. Tramadol was the only medication that helped me to function as best as I could.

I have undergone numerous imaging tests, injections, and minor surgeries, and worked with vascular specialists, neurologists, and more. Most recently, I tested negative for Thoracic Outlet Syndrome, and an angiogram showed sluggish blood flow through my hands. Finally, in July 2018, a triphasic bone scan showed positive results for CRPS. I am now seeking general information that may validate one can indeed develop CRPS acutely.


Dear J.K.,

I am sorry to hear about your difficult circumstances. I suspect that your immediate and early symptoms were the result of the injury to your spinal cord, and that over the subsequent weeks, this morphed into CRPS. I am concerned about the potential for the bone spurs to be a source of ongoing neurologic irritation, and the risk of further injury. I certainly understand that there are also significant risks with surgery. Hopefully, you have received two to three consultations from top-notch, spine-specializing neurosurgeons.

Regarding the CRPS, there are many treatment options, which you need to discuss with a pain specialist that works in the area of the condition.

–Steven Richeimer, MD

Reader Response from Ryan Kain, DC: Could Sclerotomes Be the Missing Key to Better Pain Treatment?

This submission was written in response to the coverage in PPM’s April/May 2018 issue of a presentation made by Roger Fillingim, PhD, at the 2018 American Pain Society (APS) Scientific Summit on understanding pain mechanisms.

I was excited to see PPM’s Meeting Highlight of Dr. Fillingim’s APS 2018 presentation, “To Treat Pain Better, Underlying Mechanisms are Key,1 as the topic focused on something near and dear to my heart: treating the cause of pain when possible and not just the symptoms.

Several keys to understanding pain were discussed in the overview, including the process and events that may causally contribute to pain; genetic and psychological factors that may contribute to pain chronification; patient self-management; and comorbidities that can complicate the clinical picture. The example used is quite common: start with knee pain, end up with sleep apnea and significant risk for a cardiovascular event and death. However, I believe one important key, or actual causative mechanism, was missing from the discussion: scleratogenous pain or sclerotomes.

Understanding Pain Patterns and Sclerotomes

Let me be the first to admit I am not an anatomist or researcher. I am a clinician in the trenches with my patients, much like the rest of PPM’s readers. I work at a large rural federally qualified health center/tribal medical center, where I am fortunate to serve in a rotation for interested health profession students of all degrees. As part of my time with the students, I poll them on possible sources of pain, such as dermatomes and myotomes, but few of them have heard of sclerotomes or scleratogenous referred pain patterns. I believe this lack of familiarity contributes to the oft confusion between physical medicine practitioners and the rest of medicine when discussing diagnoses and treatment of some chronic pain.

The majority of my patients present with sclerotome pain, which in physical medicine we relate to joint pain—think facet syndrome—with associated embryological tissues (including the nerves, mechanoreceptors, ligaments, tendons, connective tissue, muscles, the disc at that level and vertebrae above and below) or the spinal segmental motor unit as we are taught to consider. The next most common mechanism of pain is discogenic pain with or without radiculopathy, with their associated dermatomes and myotomes. A common complicating factor in chronic pain is myofascial trigger points.

If you layer charts of these patterns of pain, you may notice a clear but imprecise overlap; the dermatome is the most precise, the sclerotome the least. The same is true for published evidence, with dermatomes well established and a relative paucity on sclerotomes. Perhaps most interesting is the primarily negative review by Ivanusic, et al,2 regarding the existence and evidence for sclerotomes which missed a significant study from Simmons3 on the myotomal and sclerotomal origin of referred pain as often being overlooked clinically. The few remaining studies searchable in PubMed focus on documenting the mechanism and clinical application instead of doubting its existence, with several studies published since Ivanusic pointed out the need for more research (Takahashi4 and Slipman5 being good examples). The original concept of scleratogenous referred pain dates as far back as 1914 (Dejerine). Many subsequent papers and clinical posters use Inman and Saunders6 as the defining study. Back in the real world, I see evidence of sclerotomes every day with my patients and this underlying concept is of tremendous help in finding the actual source of their pain and treating them effectively, along with the other keys mentioned by Fillingim.1

Differentiating Sclerotomes from Dermatomes

In talking with my colleagues, the most common problem with sclerotomes, aside from not knowing they existed, is confusing them with dermatomes. As is well known, dermatomes are interpreted as superficial skin sensation disturbances from an irritated or injured nerve. Sclerotomes are used to describe deep radiating pain that does not quite follow dermatomal patterns. The most important factor in differentiating the two is the depth of the sensation. A clinical clue to remember is that the dermatome indicates primary nerve involvement, while the sclerotome indicates joint injury.

In the literature, a common hangup is the focus on innervation of bone by single nerve root, but scleratogenous referred pain is not just about the bone but also the embryologically-associated tissues; the pattern does not follow a dermatomal single-nerve root pattern. This is an example of the confusion between academia and the clinical realm: if it was a single nerve root then it would be a dermatome, not a sclerotome, so why are researchers expecting a single nerve root pattern? Different involvement results in a different pattern, albeit very similar. As Bove put it: “Because radicular pain symptoms are perceived in deep structures rather than on the skin, the diagnostic value [in this clinical presentation] of dermatomal charts is questioned. Clinicians are advised to be specific when questioning patients with radicular pain symptoms...”7

Sample Diagnoses

An example of how following a dermatomal diagnosis flow for a scleratogenous presentation leads to misdiagnosis and unnecessary treatment is C8. C8 dermatome and sclerotome very closely overlap, with addition of scapular pain with the sclerotome. With a typical ortho/neuro workup nothing is found remiss except reported pain with regards to the disc or nerve root. However from a scleratogenous viewpoint, segmental joint dysfunction is palpated and demonstrated with segmental lack of motion with tenderness at C7-T1 motor unit. So the diagnosis may be deemed sclerotomal “radiculopathy,” for which no ICD-10 diagnosis exists, so it is then labeled “C8 radiculopathy” without any actual findings to support nerve root radiculopathy. Thus, the confusion.

Another example of common sclerotomal pain is cervicogenic headaches or “tension” headaches. As reported by Meloche about Robert Maigne’s work, headaches actually can originate from segmental dysfunction at the upper cervical segmental motor units that radiate pain up into the scalp “along myotomal, dermatomal and sclerotomal” pathways.8 He states, “These findings are key elements for the diagnosis of painful intervertebral dysfunction. The recognition of these signs is changing our understanding of the role of the cervical spine in headaches…is very frequently found in chronic daily headaches.” My professional experience highly corroborates this statement.

A final example involves C5, 6, 7, and 8. All of these involve sclerotomes that includes neck and scapular pain. C7 and 8 sclerotomes radiate into medial arm along C8-T1 dermatome as well as C4-5 dermatome. C7 sclerotome also radiates into the anterior chest. C6 sclerotome radiates not along the arm but more focal at posterior elbow, and includes deep upper trap area more than the others (clearly, better mapping of sclerotomes is needed, but that’s a topic for another paper).

Determining the Right Treatment & Location

In a clinical presentation of “neck and shoulder pain” (ask the patient to point as it may be actual shoulder pain or the upper trap area) with lack of traditional ortho/neuro findings and no clear findings on imaging other than ambiguous degenerative disc or joint disease, it’s unclear whether to perform a block or an intra-articular injection. It is no wonder a significant number of injections fail, as many injections may be occurring at the wrong level. This is where physical medicine testing and palpation skills can make a difference, and where chiropractic can help to guide effective treatment. We know exactly where the pain is coming from in many cases, and very often it is scleratogenous. While physical medicine clinicians often have a good idea of what may be causing the pain, sometimes the injury is too chronic or too complicated by comorbidities to fully correct the issue. However, we can help to manage the dysfunction and pain as part of the integrative pain management healthcare team and, ideally, eliminate the label “non-specific low back pain.” Understanding sclerotomes may offer a step forward in this regard.

My point, other than to thank Dr. Fillingim for reminding us to think deeper and more broadly on what is causing or contributing to patients’ chronic pain, is to call out a very common source of pain seen in the physical medicine arena but widely unknown to the rest of the healthcare team. One cannot see scleratogenous pain on a standard EMG, x-ray, or MRI, which may be frustrating. However, this source of pain has been shown to respond fairly well to medial branch blocks or facet injections as a temporary fix or diagnostic aid.9-14

A detailed and specific history regarding location and type of pain is also crucial. In physical medicine, clinicians such as myself find sclerotomal pain as a very common underlying source of pain that often responds well to joint manipulative therapy when combined with exercise; we aim to directly treat the injury responsible for the pain, rather than treating the symptoms of inflammation or pain.

Of course, nothing works all the time for all patients. I urge others to consider sclerotomes when evaluating patients with chronic pain and to include a chiropractor in your healthcare team, when appropriate, to help diagnose the source of pain before finalizing a treatment plan. Might I also suggest Cavanaugh, et al.15 and Govind16 as further reading to perhaps add to the understanding of low back pain.

Last updated on: September 5, 2018
Continue Reading:
Letters to the Editor: 90 MME/day Ceiling; Ehlers-Danlos; Redefining Pain
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