The function of the piriformis muscle is to externally rotate the hip when the hip is in extension and to abduct the hip when it is in flexion. In approximately 20 % of the population, the piriformis muscle belly is split and one or more parts of the sciatic nerve passes through the piriformis muscle [1]. Typically, when it passes through, it is the peroneal portion of the sciatic nerve that pierces the piriformis muscle. The sciatic nerve itself, as a single nerve, is the largest in the human body. Historically, piriformis syndrome has been an overused diagnosis as it has been conflated with a lumbosacral radiculopathy which epidemiologically is much more common. Because the L5, S1, and S2 nerve roots innervate the piriformis muscle, the piriformis muscle is often tight and in spasm in the presence of a lumbosacral radiculopathy. Further, because the L5 and S1 nerve roots are so commonly inflamed, and because these spinal nerves are the primary feeders of the sciatic nerve, the diagnosis of piriformis syndrome or “sciatica” is often given when in fact the L5 and/or S1 nerve roots are the actual cause. In fact, true piriformis syndrome involves irritation or inflammation of the piriformis muscle that may result in compression or inflammation of the sciatic nerve.

Consider the following patient: Samantha is a 34-year-old attorney who is an avid early morning runner. While training for a marathon, she developed right buttock pain radiating into her right posterior thigh. The pain is worse with running and better when she lies down. Sitting does not make the pain worse although sometimes she has increased pain with transitioning from sit to stand after she has been sitting for a while. She has some numbness in the right lateral lower leg after a long run. On exam, she has a negative straight leg raise. Her piriformis muscle is very tender and pressure reproduces sciatic symptoms into the right thigh. MRI of her lumbar spine is normal and electrodiagnostic tests are within normal limits.

Most spine specialists would agree that Samantha is likely suffering from piriformis syndrome. Piriformis syndrome is often suspected when a patient presents with Samantha’s symptoms and then on exam she is found to have significant tenderness in the piriformis muscle. However, if all the examining physicians knew Samantha’s history and the fact that her piriformis muscle was very tender and that palpation reproduced her symptoms, then a diagnosis of piriformis syndrome would still be premature and likely incorrect. An L5–S1 radiculopathy would present in the same way and the piriformis muscle would likely be just as tender because it may spasm in response to the nerve root inflammation. However, the fact that the dural root tension sign is negative (straight leg raise) is Samantha’s case further supports the diagnosis of piriformis syndrome. Still, a diagnosis at that point of the work-up would be premature. For Samantha, it is the fact that she has all of the above features and the fact that her lumbosacral MRI is normal and that the electrodiagnostic studies were normal that suggest the diagnosis piriformis syndrome.

If Samantha had a positive straight leg raise or an L5–S1 disc herniation or electrodiagnostic studies revealing an L5 and S1 radiculopathy, then that would have been the most likely diagnosis. Even with all of the above data points, it is still not definitive that Samantha has piriformis syndrome but it certainly appears that she does. In the end, piriformis syndrome remains a clinical diagnosis without a gold standard test.