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Background
Functional popliteal artery entrapment syndrome (FPAES) is thought to be secondary to compression of the popliteal fossa, mainly the popliteal artery or neurovascular bundle, by a hypertrophied gastrocnemius, soleus, or plantaris muscle, usually during active plantarflexion. Botulinum toxin A (BTX-A) has been well demonstrated as a chemodenervation treatment for masseter hypertrophy as well as spasticity seen in prematurity and cerebral palsy. There are also documented cases of BTX-A used as treatment for thoracic outlet syndrome. A study by Schroeder et al. found that a single dose of BTX-A injected into the gastrocnemius muscle in healthy volunteers produced MRI and muscle biopsy changes 1 year later. This evidence supports the reported long-term efficacy (for one patient, up to 50 months) of a single or few BTX-A treatments for FPAES reported in the literature.

Educational Goals / Teaching Points
It is important for the radiologist to recognize the imaging findings of both anatomic and functional popliteal artery entrapment syndromes (FPAES) and be able to differentiate between these entities. With the advent of BTX-A treatments for , which are often given under ultrasound guidance, radiologists are in a unique position to be able to provide both a diagnostic evaluation and a therapeutic treatment for active patients seeking nonsurgical treatment options.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Diagnosis of FPAES is particularly challenging, as there are many symptoms that overlap with other known causes of exertional leg pain in athletes. Further complicating the picture is the high number of false positive results with the preferred imaging modalities. Multiple studies have demonstrated that 53 - 88% of healthy, asymptomatic volunteers have popliteal artery occlusion with active plantarflexion during evaluation with duplex sonography or MRI. The diagnostic workup for suspected FPAES often includes ankle-brachial indexes, duplex sonography, and MRI/MRA, with CTA and conventional angiography used more occasionally. There is some consensus that these imaging evaluations need to be done with provocative maneuvers or exercise in order to elucidate the patient's symptoms.

Conclusion
Standard surgical treatments for FPAES have reported outcomes of symptom resolution in 77% of patients, with up to a 27.5% failure rate when arterial reconstruction was performed. Currently, there are no prospective data regarding outcomes in patients with FPAES treated either surgically or with BTX-A. A randomized controlled trial to investigate the surgical outcomes versus the BTX-A outcomes would be beneficial. There is also a need for a prospective trial in order to standardize the BTX-A dose and number of treatments, as there is currently no consensus on a preferred treatment regimen. BTX-A is a promising therapeutic (and diagnostic) agent for FPAES. Prospective research with standardized treatment regimens is needed to further characterize long-term efficacy and compare outcomes with surgical intervention.