It has been suggested that stroke associated loss of inhibitory neurons in the spinothalamic tract causes disinhibition of thalamic neurons, which generate ectopic nociceptive action potentials responsible for the pain experience. However, recent data suggests that pain is dependent on the peripheral afferent input and may be mediated by misinterpretation of sensory input. Pain after a stroke is a very difficult thing to categorize. There’s a lot of prevailing theories, and we talk about five or so distinct possibilities. It all has to do with deafferentation of the pathways from the periphery into the brain after a stroke. Essentially what happens is an imbalance between the signaling that occurs and because of this, the floodgate opens and people have this unopposed perception of pain that can occur in the area of the stroke. Typically, it’s thalamic but there are oftentimes what we call extrathalamic strokes that can cause pain as well. Central poststroke pain is a phenomenon that occurs in 8% to 10% of patients that have a stroke. It can occur in a variable time course, anywhere from immediately after a stroke to as far out as a year after a stroke. Oftentimes it occurs in the distribution of the sensory areas where the person had their stroke. It’s obviously a central phenomenon in the sense that it occurred in the brain. That way, those floodgates open and there’s an unopposed sensation of the spinothalamic tract to the thalamus and whatnot that causes a very difficult pain syndrome to control.