Articles: neuralgia.
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    Central poststroke pain is a neuropathic pain syndrome that can occur from pathology of the brain. The case presented is of a woman with multiple comorbidities who was found to have an acute infarct in the left middle and anterior cerebral artery territories. She began to complain of worsening diffuse right upper and lower extremity pain, and central poststroke pain was diagnosed. ⋯ The patient's morbid obesity inspired the use of an adjunct medication protocol of a prednisone taper for proper treatment. After starting this treatment regimen, the patient experienced significant pain relief with eventual resolution. A steroid-based treatment protocol was used successfully in the early stages of central poststroke pain with proper side effect management and may have prevented difficult treatment management in the outpatient setting. 
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    Journal of neurosurgery · Mar 2016 Motor cortex stimulation and neuropathic pain: how does motor cortex stimulation affect pain-signaling pathways?Neuropathic pain is often severe. Motor cortex stimulation (MCS) is used for alleviating neuropathic pain, but the mechanism of action is still unclear. This study aimed to understand the mechanism of action of MCS by investigating pain-signaling pathways, with the expectation that MCS would regulate both descending and ascending pathways. ⋯ This study demonstrated that MCS effectively attenuated neuropathic pain. MCS modulated ascending and descending pain pathways. It regulated neuropathic pain by affecting the striatum, periaqueductal gray, cerebellum, and thalamic area, which are thought to regulate the descending pathway. MCS also appeared to suppress activation of the VPL, which is part of the ascending pathway. 
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    Clinical studies show that chronic pain can spread to adjacent or even distant body regions in some patients. However, little is known about how this happens. In this study, we found that partial infraorbital nerve transection (p-IONX) in MRL/MPJ mice induced not only marked and long-lasting orofacial thermal hyperalgesia but also thermal hyperalgesia from day 3 postoperatively (PO) and tactile allodynia from day 7 PO in bilateral hind paws. ⋯ In addition, microglial activation after p-IONX transmitted caudally from the Vc in the medulla to lumber dorsal horn in a time-dependent manner. Inhibition of microglial activation by minocycline at early but not late stage after p-IONX postponed and attenuated pain sensitization in the hind paw. These results indicate that neuropathic pain after p-IONX in MRL/MPJ mice spreads from the orofacial region to distant somatic regions and that a rostral-caudal transmission of central sensitization in the spinal cord is involved in the spreading process of pain hypersensitivity.