 Well, welcome back to the ProScan Mentor case review. A younger radiologist and an older radiologist doing ortho-MR to try and help you raise the bar and get ready for your board preparation and your recredential examination. Today, we have a really special case for you. And I'll start out with the easy questions since I'm the older one. I need all the help I can get. This is a 49-year-old female with worsening pain and swelling in the ankle and foot. Since she took a vacation three to four months ago, actually, most of my vacations were like that, too. I usually needed a doctor after my vacation with six children. But let's go with the first question. What is the most salient MR finding? And I'm not even sure I have to really scroll these. I'd like you, the audience, to really just gaze on these two images, a fat-weighted image on the viewer's left, a water-weighted image on the viewer's right with excellent fat suppression. And the choices are picture, frame, pattern of oseous edema, subtaler and anterior tibiotailer joint effusion, periarticular soft tissue edema, deltoid ligament injury. Well, obviously, I haven't shown you the deltoid ligament yet, so maybe that's not a choice. Interstitial tear of the perineus brevis. Let's take a look at the perineus brevis for a moment and identify it. Here's the perineus brevis right there. Let's blow her up a little bit so we can see it a little better. We see it pretty well. And let's look at it sagittally. Here's the perineus brevis right there, going down to the base of the fifth. So let's go back to our midline section. And let's look at question number two. Two is, what is the most likely diagnosis given these imaging findings? A is reflex sympathetic dystrophy. B is overuse associated oseous edema. C is regional migratory osteoporosis. D is microtrabecular fracture. And E is inflammatory arthritis. So given the imaging findings, the most likely diagnosis is actually A, known more recently as complex regional pain syndrome, but previously known as reflex sympathetic dystrophy. And it's the most likely diagnosis due to the peripheral oseous edema that we see here in a picture frame kind of pattern, as we're pointing out here with the cursor. As you can see, it's subcortical, predominantly in location, and very high signal here. Overuse associated oseous edema is usually patchy, and it's going to be non-juxtararticular in distribution, unlike this. Regional migratory osteoporosis demonstrates diffuse type oseous edema, due to a rapidly increased function between two and 10 times their normal rate in response to noxious stimuli. Noxious stimuli may include microtrauma, such as a microscopic trabecular fracture due to stress or excessive loading of a mildly osteoporotic bone. Answer D is incorrect because a microtrabecular fracture is usually associated with a diffuser focal oseous edema, and RA, or inflammatory arthritis, RA being one of the most common. This isn't a typical appearance. RA is usually gonna show edema in the hands and feet, more in the carpal and tarsal bones, and adjacent to the PCP joints. And usually you're gonna see more other, or you're gonna see secondary findings such as more robustinovitis or soft tissue findings to suggest you along that diagnosis. Yeah, I mean, you're right. There really isn't any fuzzy gray material in the effusion. No. And then when you look at the bone, if it's an arthritis, the high signal should be next to the joint, and it is, but it also shouldn't be away from the joint, right? Because if there's no joint causing the inflammation, then why would it be inflamed in rheumatoid arthritis? And so the entire bone all the way around, both where it abuts another joint surface, and where it doesn't abut another joint surface, is often swollen and reflects sympathetic dystrophy. You know, in micro-trabecular fractures, it'd be highly unusual to fracture like every bone in the foot, although I have seen it with osteogenesis imperfect atarta, but this patient's a little old for that, and that would be a much less likely diagnosis. This picture frame appearance is absolutely critical for you to recognize, because the longer this patient sits with complex regional pain syndrome, the harder it is to treat. And the more lumbosacral blocks they have to have, the more aggressive treatment they have to have, and you know, we can talk a little bit about some of the newer treatments at the very end. Should we do another question? Sure. Let's see. The distinction between type one and type two, complex regional pain syndrome, CRPS is based on clinical presentation, co-existent vascular trauma, presence of motor deficit, osteoporosis, nerve injury. Let's go through the choices. A, A is false, both may present with chronic burning pain, pathologic changes in the bone and skin, excessive sweating, tissue swelling, and hypersensitivity to the touch. And when I say hypersensitivity, they cannot even have a sheet resting on their foot. And when you go to examine them, the first thing they say is, no, don't touch it, or don't take my shoe off. And you know immediately the diagnosis you have. B, co-existent vascular trauma, that's false. Vascular trauma is not part of the pathogenesis of CRPS. Even though some vasogenic components may contribute to it, it isn't actually trauma to the vessels that causes the disease. C is false. RSD is typically not associated with a motor deficit, although it may appear such, because the patients are in so much pain, they completely, they often completely stop moving their extremity. In fact, when they have it in the hand, they'll walk around with their hand next to their body to protect it. D is false. The osteoporosis is variably present with RSD, types one and two, and non-specific for all subtypes. And in my experience, they do get osteoporosis, but they don't get it for a while. It can take as little as a month and as much as a year. But when they do get the osteoporosis, it can be unbelievably overwhelming. It can look like the bones are about to just crumble into a big pile of dust. E is true. CRPS is divided into type one, CRPS, RSD, and type two, CRPS or carzalgia. The distinction between the two is based on the absence of a documented nerve injury for carzalgia. Should we go with question number four? Sure. For all yours. Which is not a characteristic clinical future of complex regional pain syndrome? A, intense prolonged pain, B, vasomotor disturbances, C, delayed functional recovery, D, trophic changes, or E, hyperreflexia. The answer in that is hyperreflexia, E. All of the other four intense prolonged pain, vasomotor disturbances, delayed functional recovery, and trophic changes can be seen with a syndrome. And for those of you out there, there aren't clinicians, trophic changes include overgrowth of hair, the skin becomes very coarse. It often turns purple. So when you're in the later stages of disease, it's pretty obvious, but in the early stages it can be a very challenging diagnosis to make. Question five, which of the following statements with regard to radiologic features of RSD is true? RSD is usually a unilateral process. A, B, patchiosteopenia is an early radiographic finding of RSD. C, the subperiosteal bone is the region of greatest bone mineral loss in RSD. D, in patients with RSD, scintographic changes often precede radiographic abnormalities. And E, RSD may result in intraarticular erosions in joint space narrowing. Let's start out with A. A is false. RSD is a bilateral process, but it doesn't have to start at the same time. Although the patient's symptoms and imaging abnormalities will be much more pronounced on one side than the other, and rarely you can have a localized form affecting one joint or extremity, or one of several digits in the hand or even in the foot. They're personally seen, RSD, of the throat. The patient with a sore throat that responded to Neurontin immediately, which is one of the treatments for RSD. I've seen another one also affect the throat as a sore throat that responded to Lyrica. So this is a very bizarre, unusual disease. It can go anywhere. B is false. Once patchiosteopenia is present, the patient usually has already progressed to stage 2 RSD. They've had the disease for at least a month and usually several months. And that's unfortunate, because it makes the diagnosis that much harder to assess. C is false. The subperiosteal bone is the region of the greatest bone mineral loss. That is false. The endosteal bone is the region of the greatest bone mineral loss in RSD and results in the initially observed excavation and scalloping at the endosteal surfaces. As a result, there is uniform remodeling of the endosteum. There's widening of the medullary canal. And additional radiographic findings include metaphyseal, irregular resorption of the trabecular bone, resulting in patchiosteoporosis, subperiosteal, intracortical, endosteal bone resorption, and surface erosions of the subconvral and juxta articular bone. But hopefully, you're going to have an MR to assist you, which is going to show this window frame-like appearance of RSD, which conjures up diagnoses like Padgett's disease. But in Padgett's disease, it's the cortex that's involved, not the endosteal bone. So here, the edema is underneath the cortex, which is a very critical distinction. And clinically, they really don't resemble each other. D is true. Patients with RSD, the scintographic changes, precede the radiographic abnormalities. Three-phase scanning is often used with a vascular phase, an immediate static and a delayed static with Technetium-99M. The major problem being, if you are imaging young people, you are radiating some critical organ. So I personally like MR as the first test, but that's a personal choice and not necessarily an exam question answer. E is false. The erosions in the subconviral and juxta articular bones result in small periarticular erosions and intraarticular gaps. The RSD can be differentiated from other arthritis due to the absence of erosions and preservation of the joint space. So in rheumatoid, not only will you get erosions, you'll get thinning of the cartilage. You may get the gestion of the menisca. You may get giant pseudosists. The capsule becomes very elastic and distensible. That does not happen in RSD. So you should be able to make the distinction in the overwhelming majority of cases. And this is really a floored example of complex regional pain syndrome. Just to worry about the treatment, because I've lived this and seen it firsthand, the treatment is usually moving the extremity. In a child, if you move the extremity very vigorously, and sometimes you have to give them pain medication or an epidural to do so, you can usually eradicate it if you find it early. In adults, they often have to have a lumbar block. And that lumbar block is usually done anywhere from three to seven or eight times to beat this disease back. And it keeps working its way forward. There are some other treatments, including mirror therapy that they use for phantom pain syndrome. And they have even begun anesthetizing patients for 72 hours using ketamine to try and lower the autonomic nervous system. And then when they wake up, they have a lot less pain and they can move their extremity better. And they're in a twilight anesthesia. They're not completely out. So that concludes this super interesting and challenging case of RSD. Thanks a lot for joining me. Thank you. All right, I'm Steve Pomerance. This is Allison Garawi, two ortho radiologists doing OrthoMR. Hope you enjoyed it.