A'thank you' to Eric Robertson from over at NPA Think Tank for mentioning this blog in a recent post by him. This also was cross posted on the Evidence in Motion blog. His post was a follow up to his earlier post calling for more PT's to blog.

As a side note, his post also included a link to a blog written by Mark Schwall which has great insight and is easy to read. Check it out here.

Labels: blogs, Healthcare, physical therapy

Iontophoresis is a means of administering an ionic medication transdermally using a low electrical current to "push" it along. There is research out there that show it actually occurs and that "long wear", ultra low current, iontophoresis may deliver the medication to a greater depth; but using a skin model (pig skin to be exact). However, the general consensus in the literature tends to be that it doesn't make much of difference in musculoskeletal pain. Anecdotally, though, I have found success when very selectively applying it to areas where the intended tissue is plausibly close to the surface such as the lateral epicondyle, MCL (in thinner pt's), and tendons of the hand. Unfortunately, this practice has not been supported by the literature.

This is clearly shown by the multitude of insurance companies that won't reimburse it's use due to "lack of efficacy" (yet they gladly pay for the cheaper ultrasound). Now there is a new study recently published in the American Journal of Sports Medicine by A. Burke Gurney, PT and Daniel C. Wascher, MD that was very cleverly done. Here is the abstract:

Absorption of Dexamethasone Sodium Phosphate in Human Connective Tissue Using Iontophoresis

Background: Iontophoresis ostensibly facilitates the delivery of medications through the skin to underlying tissues using a direct electrical current. Dexamethasone is the most commonly used medication with iontophoresis to treat a variety of connective tissue disorders.

Hypothesis: Iontophoresis will facilitate the absorption of dexamethasone into connective tissue compared with diffusion.

Study Design: Controlled laboratory study.

Methods: Twenty-nine adults undergoing anterior cruciate ligament reconstructive surgery using the semitendinosus/gracilis autograft were randomly assigned to either a true iontophoresis (TI) or sham iontophoresis (SI). In the TI group, a 40-mA/min dose of iontophoresis using a 0.4% (4 mg/mL) solution of dexamethasone was used targeting the semitendinosus tendon just before surgery. The SI group underwent the same treatment, but the machine was not turned on. Tissue was extracted within 4 hours of treatment and analyzed for dexamethasone. In addition, 2 control samples were sent to the laboratory for analysis.

Results: There was a statistically significant difference in dexamethasone concentrations between the groups (P = .0216). Of the 16 samples in the TI group, 8 had measurable amounts of dexamethasone, with an average concentration of 2.906 ng/g of tendon tissue. In the SI group, 1 of the 13 samples had measurable amounts of dexamethasone with an average concentration of 0.205 ng/g of tendon tissue. The control samples contained no dexamethasone.

Conclusion: Iontophoresis facilitates the transmission of dexamethasone to connective tissues in humans.

Clinical Relevance: Iontophoresis can deliver dexamethasone to connective tissues in humans.

Now, we next have to show that that dexamethasone has a significant impact on tissue inflammation, but this a step in a good direction for iontophoresis as used by physical therapists.

Labels: dexamethasone, EBM, evidence based medicine, iontophoresis, physical therapy

Patellofemoral pain (aka EMM, patellar chondromalacia, PFPS, anterior knee pain, etc) is a common diagnosis that I see in the clinic. The problem is, we are not exactly sure what causes it (or if there or many causes) and what is best for remedying it (strengthening, stretching, neuromuscular re-education, bracing, even spinal mobilizations). In the past, PFP was attributed to lateral patellar tracking caused by poor VMO strength/activation and tight lateral structures such as the IT Band. While it is still commonly believed that PFP is from excessive lateral patellar tracking, it is thought that this is caused by poor lower extremity pronation/valgus control by the hip musculature. Specifically the hip abductors and external rotators. This has been preliminarily supported by research that shows, in weight bearing, in those with PFP the femur tends to internally rotate under the patella rather the the patella being pulled laterally (Salsich, GB - JOSPT Sept 2007).

The following article done by Lori Bolgla, PT, PhD, ATC et al looked at hip strength and lower extremity kinematics in those with PFP vs. those with out. Here is the abstract:

Hip Strength and Hip and Knee Kinematics During Stair Descent in Females With and Without Patellofemoral Pain Syndrome

Lori A. Bolgla, Terry R. Malone, Brian R. Umberger, Timothy L. Uhl

STUDY DESIGN: Cross-sectional. OBJECTIVE: To determine if females presenting with patellofemoral pain syndrome (PFPS) from no discernable cause other than overuse demonstrate hip weakness and increased hip internal rotation, hip adduction, and knee valgus during stair descent. BACKGROUND: Historically, PFPS has been viewed exclusively as a knee problem. Recent findings have indicated an association between hip weakness and PFPS. Researchers have hypothesized that patients who demonstrate hip weakness would exhibit increased hip internal rotation, hip adduction, and knee valgus during functional activities. To date, researchers have not simultaneously examined hip and knee strength and kinematics in subjects with PFPS to make this determination. METHODS AND MEASURES: Eighteen females diagnosed with PFPS and 18 matched controls participated. Strength measures were taken for the hip external rotators and hip abductors. Hip and knee kinematics were collected as subjects completed a standardized stair-stepping task. Independent t tests were used to determine between-group differences in strength and kinematics during stair descent. RESULTS: Subjects with PFPS generated 24% less hip external rotator (P = .002) and 26% less hip abductor (P =. 006) torque. No between-group differences (P > .05) were found for average hip and knee transverse and frontal plane angles during stair descent. CONCLUSION: Subjects with PFPS had significant hip weakness but did not demonstrate altered hip and knee kinematics as previously theorized. Additional investigations are needed to better understand the association between hip weakness and PFPS etiology. LEVEL OF EVIDENCE: Symptom Prevalence, Level 4.

J Orthop Sports Phys Ther. 2008;38(1):12-18, published online 21 November 2007, doi:10.2519/jospt.2008.2462

I commend the authors for doing this study. Treatment in the clinic is dependent on clinical theories and basic science being "put to the test" in RTC with actual patients. It is important to note that hip muscle weakness was found in the symptomatic group; however, significantly altered lower extremity mechanics were not. An admitted limitation is that they only looked at stair stepping (a common pain provoking activity with those with PFP) and this specific activity may not have been challenging enough.

I treat most of my patients with PFP using hip strengthening, lower extremity stretching, and proprioceptive exercises in general. But this study reminds us that we were wrong before about the cause of PFP and most certainly could be wrong about the hip weakness leading to increased pronation/valgus theory most of us currently abide by.

Labels: EBM, evidence based medicine, patellofemoral pain, PFP

The most savage controversies are those about matters as to which there is no good evidence either way.
- Bertrand Russell

Labels: EBM, Evidence, physical therapy