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14 Articles in Volume 21, Issue #5
Analgesics of the Future: Interleukin-17 Inhibitors for Treating Psoriatic Arthritis
Ask the PharmD: What evidence exists for metformin in treating rheumatoid arthritis pain?
Case Chat: Spasms vs. Spasticity and Muscle Relaxant Options
CDC Opioid Prescribing Guideline Updates Are in the Works: Will the Changes be Enough?
Chronic Pain Management in Marginalized Populations: How to Rebalance the Provider-Patient Relationship
Dantrolene: The Forgotten Molecule for Outpatient Spasticity
Forgotten Analgesics: The Drugs Pain Practitioners Need to Reconsider
Machine Learning Predicts Patient Response to Rheumatoid Arthritis Therapy
Perspective: Where Have All the Rheumatologists Gone?
Rheumatoid Arthritis and Bridge Therapy: Primary Care Considerations
Root Cause of Plantar Fasciitis: Three-Step Exercise Protocol
Shoulder Pain and Rotator Cuff Injuries: Emerging Treatments
Special Report: The Evolution of Rheumatoid Arthritis Treatment, from Gold to Gene Therapy
Transfer of Care: Barriers and Solutions in Chronic Pain Management

Case Chat: Spasms vs. Spasticity and Muscle Relaxant Options

Physiatrist and pain management specialist Steven P. Stanos, DO, on how to differentiate muscle spasms from spasticity and which therapies to pursue. The podcast includes a look at upper motor neuron presentations stemming from Multiple Sclerosis, post-stroke or spinal cord injuries, and lower motor neuron presentations, such as persistent muscle spasms localized to the cervical or lumbar region.

In this Case Chat, muscle spasms and spasticity are distinguished and experts discuss therapeutic options, from tizanadine to physical therapy and everything in between.

Featuring: Steven P. Stanos, DO, Medical Director of Swedish Health System Pain Medicine and Services in Seattle, Washington

Moderated by: PPM Co-Editors-at-Large Jeff Gudin, MD, and Jeffrey Fudin, PharmD, FCCP, FASHP, FFSMB

 

 

 

Listen to the full conversation (16 minutes) below or read the transcript.*

 

 

Muscle Spasms or Muscle Spasticity?

Dr. Gudin: At almost any pain center, patients describe painful muscle spasms. But we also see a unique and complex group of patients ­– those who have strokes, Multiple Sclerosis (MS), spinal cord injuries, etc. Could you give us an idea of the types of disorders that you see in your work, and how you differentiate between spasm and spasticity?

Dr. Stanos: These days, I see these patients more at a tertiary care level and they include patients with upper motor neuron conditions that would develop spasticity – that is, patients with stroke, spinal cord injury, and MS, essentially those types of patients that present with what we call velocity dependent tone, or increased tone, that can be in the upper or lower extremities.

The other group of patients that is probably more common on the pain side is the lower motor neuron patients who report muscle spasm. In these cases, it may be related to cervical or lumbar disc herniation with nerve root irritation and, then, at the lower motor neuron below the dorsal route ganglion they're getting muscle spasm. Unfortunately, there's some overlap in the physiology and some patients actually have a bit of both.

But I like to break it down into upper motor neuron disease patients with spasticity/velocity dependent and the lower motor neuron disease, which we more commonly see and which is more localized muscle spasm related to neck and low back pain.

Diagnostics for Upper or Lower Motor Neuron Disease

Dr Gudin: Before we get into treatment, where do you start from a diagnostic standpoint when someone comes in the office, say, with no obvious central nervous system injury but perhaps has rock-hard trapezius/cervical muscle spasm?

Dr. Stanos: The first thing, after you take a history, is performing a good physical exam right off the bat. With upper motor neuron lesions, you're going to see more brisk reflexes in the upper and lower limbs; besides the velocity dependent tone as you move the limb, you'll have an increased catch that's kind of an easy way to pick up even subtle spasticity in the limbs. For lower motor neuron, if we think it's more related to muscle pain/muscle spasm, those patients may have trigger points or muscle hypertrophy in the areas that they’re complaining about as well.

Your question reminds me of a patient that we had who had classic severe radiculopathy in his upper limb. He was a very active 38-year-old but his reflexes were really brisk – he was a little less on the side where he had his radiculopathy but, long story short, when we worked him up, he actually had MS plaques in his cervical thoracic cord, and this was actually his first presentation. So, you really want to do a good physical exam to rule those things out. (More on Multiple Sclerosis and differential diagnoses in PPM's new clinical primer.)

What we see in the clinic and what we should focus on is the myofascial assessment for muscle spasm where you can pick up a lot of these findings, such as whether a patient has trigger points or just a lot of muscle tenderness. They may have restricted or weak muscles in those areas and, many times, that's where they're going to complain about muscle spasm.

Dr. Gudin: You bring up a good point; I am always reminding fellows and residents to carry a reflex hammer. They're interested in pain and they know all about the latest spinal cord stimulator leads and generators but they don't carry a reflex hammer. As clinicians, we need to be able to do a complete physical examination on a patient to understand what’s happening. We know that pain is a neurological symptom and we need to understand the neurological basis.

But let's talk now about treatments…from a physiatry standpoint, where do you start?

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Antispastics and Antispasmodics

Dr. Stanos: There's a lot we can do physically that is separate from medications to help decrease a spasm. You can do myofascial release – which may be guided by a physical therapist – to release trigger points. The key is understanding that those muscles are usually weak and inhibited, so even basic scapular strengthening exercises, say for the neck or the scapular spine, can really help increase even a small amount of muscle strength. If you increase muscle strength, a lot of times, that can decrease muscle spasm.

From a pharmacologic standpoint, if we base treatment on an upper motor neuron concern – for example, spasticity from MS or post-stroke pain, the most commonly used medications are baclofen even tizanidine – baclofen is a Gaba-b agonist whereas tizanidine is an alpha agonist – they may work at the muscle level to decrease spasm. I think of these as the antispasticity meds. There’s also botulinum toxin injections that would be probably done by a specialist.

On the antispasmodics for muscle spasm, there’s metaxalone, methocarbamol, and cyclobenzaprine. which is more of a tricyclic. It’s such a heterogeneous group of medications and mechanisms, I think that's a lot more complicated.

Going back to anti-spasticity medications, as a backup, maybe dantrolene as second- or third-line, which is kind of an oldie but a goodie but has some risks for adverse effects (see PPM’s recent review on dantrolene and other forgotten, underused analgesics).

 

Risks and Drug Interactions

Dr. Gudin: Medications like metaxalone and methocarbamol are touted to be less sedating but I don't find a whole lot of efficacy there. Cyclobenzaprine, which as Dr. Stanos mentioned, has a tricyclic backbone, appears to be more effective in my practice experience. But Dr. Fudin, what’s your pharmacist take on this?

Dr. Fudin: Well, it's complicated. First of all, you’re right that we have a marginal effect with a lot of these medications, particularly when we have to sort out whether we are dealing with upper motor neuron or lower motor neuron symptoms. Aside from that, most of these drugs work by affecting the central nervous system and you both brought up the fact that cyclobenzaprineis a tricyclic. That's interesting because if you look at a lot of these drugs, for example, tizanidine, which is essentially acting as an alpha agonist, and it looks lot like clonidine chemically. And if you look at dantrolene, it’s a lot hydantoin derivative; it’s a lot like, phenytoin or dilantin, which is something we don’t often think about.

Also, from a pharmacist perspective, we worry about drug interactions. A lot of these medications are affected by CYP1, or CYP3a4, so there's a large risk for drug interactions. And then there’s orphenadrine, which looks just like diphenhydramine, so I’m not so sure that orphenadrine might work any better than diphenhydramineand I wonder whether we’d get that effect from phenytoin. (More on optimizing pharmacotherapy and genetics.)

But the bottom line here is that almost all the drugs are central nervous system sedatives and so you could make the argument that if you gave a patient any sedating drug, it probably would work as well as a lot of drugs that we use already.

Dr. Stanos: You could throw benzodiazepines into the discussion as well, which we see a lot and which probably crosses into both groups (ie, antispastic and antispasmodic). In a pain clinic, there’s also the risk of potential opioid use among patients. Many times, we see patients come in who are already on two or three of these agents, and we need to spend time cleaning up their treatment regimens first. Sometimes, we underestimate, or we find that patients are not taking the right dose, or they’re taking more than we realize. So, we have to dig into that.

Dr. Fudin: As a pharmacist in the clinic, the first thing we want to do is start deprescribing. If you've got a patient on dantrolene, for example, or another drug that’s affected by CYP3a4 and they are on carbamazepine for trigeminal neuralgia or another condition, or maybe you want t to get them off carbamazepine and put them on oxcarbazepine so you don't have the induction…you really need to look at all the drugs first to make sure use or adherence is not the problem. Sometimes it’s not about giving drugs, but about taking drugs away.

 

The Go-To Muscle Relaxant for Spasms?

Dr. Gudin: One last question – let’s say a 50-year-old male, relatively healthy, presents with terrible low back spasms. There are no comorbidities and no upper motor neuron indications. What’s the muscle relaxant of choice?

Dr. Stanos: Tizanidine – of all of them, this medication may act potentially most at the muscle level (2 to 4 milligrams every 4 to 6 hours). I'd warn him about the potential for sedation and see if he got some relief. I’d also be thinking about PT for his scapular muscles and his low back muscles that are probably weak, and I may consider trigger point injections.

 

*Transcript edited for length and clarity.

Want more details on muscle relaxants? See PPM’s comprehensive Review of Skeletal Muscle Relaxants for Pain Management by Dr. Fudin and Mena Raouf, PharmD.

See also, our Case Chat on migraine with Charles Argoff, MD, and our Side Chat interview and audiocast series on evolving matters in pain management and pain practice leadership.

Last updated on: October 1, 2021
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