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bibliography * The PainScience Bibliography contains plain language summaries of thousands of scientific papers and others sources, like a specialized blog. This page is about a single scientific paper in the bibliography, Näslund 2007.

Poor patellar blood flow in many cases of patellofemoral pain

updated
Näslund J, Waldén M, Lindberg LG. Decreased pulsatile blood flow in the patella in patellofemoral pain syndrome. Am J Sports Med. 2007 Oct;35(10):1668–73. PubMed #17567822.
Tags: anatomy, etiology, knee, patellar pain, overuse injury, fun, pro, leg, limbs, pain problems, arthritis, aging, injury, running, exercise, self-treatment, treatment

PainSci summary of Näslund 2007?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided at the bottom of the page, as often as possible. ★★★★☆?4-star ratings are for bigger/better studies and reviews published in more prestigious journals, with only quibbles. Ratings are a highly subjective opinion, and subject to revision at any time. If you think this paper has been incorrectly rated, please let me know.

A 2008 study (Näslund et al) of 22 patients showed that 19 of them had reduced blood flow while the knee is flexed, but no such sign could be detected in healthy people. The method used to measure blood flow (photoplethysmography) is new and therefore not exactly a sure thing, but there’s a good chance it works as advertised. Their data was a bit all over the map — big error bars! — but the averages were clear enough. This could explain the notorious “movie sign,” in which simply sitting with flexed knees makes them ache. If the results can be believed, it raises more questions than it answers: Is it cause or a symptom? Why would blood flow be reduced in the first place? Could this be why almost any kind of exercise tends to help — by normalizing blood flow? And since when can you squeeze blood out of living bones?

(Because living bones are surprisingly rubbery. The kneecap in particular is subjected to simply astonishing compression forces even in unloaded knee flexion. The squishableness of kneecaps in itself is a fun fact, but not especially surprising. The real curiosity here is: what’s the difference between the patients with knee pain and healthy controls? Why does knee bending impair circulation in some kneecaps and not others? How does that work?)

This item got my friend Dr. Rob Tarzwell of One-Minute Medical School curious about arterial supply to the patella. He writes: “It looks like normal anatomy involves a circulatory anastomosis. That’s where multiple arteries plug into a ring, and the ring then has feeders going to the patella. Presumably, this is to allow for redundancy of supply in the event of flexion of the knee closing off supply. Now, if the anatomy isn’t sufficiently redundant, then supply could become temporarily compromised. Variants of normal anatomy are legion.” In other words, not everyone’s arteries may be arranged optimally to cope with flexion, and some may fail to keep the blood flowing during flexion — which would explain these results, and potentially a lot of otherwise mysterious anterior knee pain. This is a fascinating, plausible hypothesis.

~ Paul Ingraham

original abstractAbstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

BACKGROUND: Anterior knee pain without clinical and radiologic abnormalities has primarily been explained from a purely structural view. A recently proposed biologic and homeostatic explanation questions the malalignment theory. No objective measurement of the pathophysiology responsible for changes in local homeostasis has been presented.

HYPOTHESIS: Flexing the knee joint interferes with the perfusion of the patellar bone in patellofemoral pain syndrome.

STUDY DESIGN: Case control study; Level of evidence, 4.

METHODS: Pulsatile blood flow in the patella was measured continuously and noninvasively using photoplethysmography. Measurements were made with the patient in a resting position with knee flexion of 20 degrees and after passive knee flexion to 90 degrees. In total, 22 patients with patellofemoral pain syndrome were examined bilaterally, and 33 subjects with healthy knees served as controls.

RESULTS: The pulsatile blood flow in the patient group decreased after passive knee flexion from 20 degrees to 90 degrees (systematic change in position, or relative position [RP] = -0.32; 95% confidence interval for RP, -0.48 to -0.17), while the response in the control group showed no distinct pattern (RP = 0.17; 95% confidence interval for RP, -0.05 to 0.31). The difference between the groups was significant (P = .0002). The median change in patients was -26% (interquartile range, 37).

CONCLUSIONS: Pulsatile patellar blood flow in patellofemoral pain syndrome patients is markedly reduced when the knee is being flexed, which supports the previous notion of an ischemic mechanism involved in the pathogenesis of this pain syndrome.

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