There’s a number of treatment options that we tend to consider in patients who have central poststroke pain. The most efficacious treatment that we have is a simple medication and an old one: amitriptyline, a tricyclic antidepressant that’s been shown to be the most efficacious in patients with central poststroke pain, or at least it has the least number to treat and the greatest window for treatment. There are a lot of other options. Intrathecal baclofen can be very helpful, but those are really for patients who have spasticity after a stroke. Baclofen does have some neuropathic pain quality components to the medication, but it’s primarily an antispastic agent. We talk about carbamazepine. We talk about lamotrigine. We talk about other medications that are intravenous, like ketamine, lidocaine, even propofol. Those are really for recalcitrant patients, patients that you’ve tried a lot of different options and it’s still very hard to control. Interestingly, there are now interventional procedures. There are people who are getting deep brain stimulation, transcranial magnetic stimulation, and even caloric vestibular stimulation in the ear for patients who have that component to their pain syndrome. There is some degree of signaling in the periphery that is contributing to what we used to think is a central pain phenomenon. In a pilot study, eight patients ended up with the formal diagnosis of central poststroke pain. We wanted to know how much of that peripheral input is playing into what we would normally think is just a purely central phenomenon. We had these patients come in, and if they had arm pain, we would block the brachial plexus or some peripheral nerve in the distribution of the pain. If it was in the leg, we’d do a popliteal block, just numbing medicine lidocaine. We’d use an ultrasound to make sure that it was an appropriate spread. We wanted to categorize and see did they get any pain relief; because if this is a stroke in the brain, then theoretically they shouldn’t have any relief. Right? If the floodgate is open, they’re still having pain. It has nothing to do with the periphery. In every patient, their pain dropped significantly. It really changed the way we started to think about what we thought was a purely central phenomenon. When it comes to central poststroke pain, how much of the peripheral input or sensory afferent input is playing a role in what we thought was a normally purely central phenomenon.