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There is a critical need to diagnose and treat headache disorders in primary care settings. This is especially true for those who face systemic barriers to healthcare access due to racism or poverty. In order to target those at higher risk of disability associated with neurologic disease in our healthcare system, we embedded a specialized headache and neurology clinic within the Brigham and Women's Hospital Southern Jamaica Plain Community Health Center in Boston, MA. The goal was to create a sustainable, integrated clinic consistent with the CHC's racial justice mission, with an emphasis on equitable care, awareness of structural barriers to care, improved communication with primary care and inclusion of trainees as important members of a healthcare team. In its' first year, the clinic had over 400 patient visits, with a near-perfect rate of completion of consults. In addition to improved access to tertiary care headache services, successes have included improving continuity of care, cultivating a model of shared care with primary care practitioners and stimulating interest in headache medicine among staff and trainees. Challenges have included the use of staff time to complete prior authorizations, and the need to find or develop Spanish-language and culturally appropriate patient educational resources. By providing care within the patient's medical home, the headache specialist gains a deeper appreciation of a patient's social determinants of health and can readily access resources to navigate barriers. The personal and professional fulfillment that headache specialists may experience while doing this important work could help protect against burnout. Sustainability depends on ensuring equitable provider reimbursement; departmental and institutional support is essential. We believe this clinic can serve as a model for specialists throughout the United States who wish to improve the delivery of care to patient populations who face access barriers.
Learn More >Stigma is increasingly recognized as an important social feature of living with migraine.
Learn More >To establish a new rat model of craniofacial myalgia, and to clarify which central nervous system pathways are activated in the model.
Learn More >Perioperative neurocognitive disorders (PND) is a common complication that occurs among elderly patients in the perioperative course. Current clinical evidence has shown that isoflurane exposure could cause cognitive decline but the exact molecular mechanisms remain unclear. As both NMDARs-dependent synaptic plasticity and histone acetylation play vital roles in processing learning and memory, we postulated that these alternations might occur in the isoflurane-associated PND. Here, we found that isoflurane impaired fear memory in aged mice, decreased GluN2B-containing NMDA receptors phosphorylation and trafficking, as well as the expression of EphB2, a key regulator of synaptic localization of NMDA receptors. We also identified that isoflurane could increase the expression of HDAC2, which was significantly enriched at the ephb2 gene promoter and regulated the transcription of ephb2. Furthermore, we showed that Suberoylanilide hydroxamic acid (SAHA), a non-selective HDAC inhibitor or knocking-down HDAC2 rescued the cognitive dysfunction in isoflurane-treated aged mice via increasing acetylation of H3Ac, expression of EphB2 and promoting NMDA receptor trafficking. Collectively, our study highlighted the crucial role of histone posttranslational modifications for EphB2-GluN2B signals in isoflurane-associated PND and modulating HDAC2 might be a new therapeutic strategy for isoflurane-associated PND.
Learn More >Neuropathic pain(NP) is derived from the dysfunctions of nerve system. The current research is to explore the impact and mechanism of miR-19a-3p in neuropathic pain in rats.
Learn More >Glial cells, such as microglia and astrocytes, in the trigeminal spinal subnucleus caudalis (Vc) are activated after trigeminal nerve injury and interact with Vc neurons to contribute to orofacial neuropathic pain. Complement C1q released from microglia has been reported to activate astrocytes and causes orofacial mechanical allodynia. However, how C1q-induced phenotypic alterations in Vc astrocytes are involved in orofacial pain remains to be elucidated. Intracisternal administration of C1q caused mechanical allodynia in the whisker pad skin and concurrent significant upregulation of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 in the Vc. Immunohistochemical analyses clarified that C1q induces a significant increase in the cytokine interleukin (IL)-1β, predominantly in Vc astrocytes and partially in Vc microglia. The number of c-Fos-positive neurons in the Vc increased significantly in response to C1q. IL-1 receptor antagonist (IL-1Ra) was used to analyze the involvement of IL-1β in C1q-induced mechanical allodynia. Intracisternal administration of IL-1Ra ameliorated C1q-induced orofacial mechanical allodynia. The present findings suggest that IL-1β released from activated astrocytes and microglia in the Vc mediates C1q-induced orofacial pain.
Learn More >Considerable functional and structural alterations, or plasticity, in the central nervous system (CNS) are accompanied by numerous chronic pain syndromes. Sensitization of the peripheral (primary hyperalgesia) or central (secondary hyperalgesia) nervous system as unhelpful neuroplasticity may result in stimulus-induced pain (hyperalgesia and allodynia). Furthermore, nociception induces extensive plasticity in the peripheral and central neural systems in pathological disease states. Disease-induced plasticity at both structural and functional levels is evident as alterations in different molecules, synapses, cellular function and network activity. In the present article, we review plasticity-induced pain and pain-induced plasticity. Moreover, we will review the pain matrix. Furthermore, we will focus on recent developments of the CNS alterations in long-lasting pain in some clinical entities encountered in rehabilitation. These clinical entities comprise nonspecific low back pain, complex regional pain syndrome, postamputation phantom pain, fibromyalgia, and chronic pain after spinal cord injury. Moreover, we will review the clinical treatment for the inhibition of pathological pain.
Learn More >Discogenic low back pain (DLBP) is considered the most common type of chronic low back pain (CLBP). Sinuvertebral nerve block (SVNB) is a rapid and precise intervention performed under local anesthesia to treat DLBP induced CLBP. Thus, in this study, we aimed to explore the clinical efficacy of SVNB for DLBP.
Learn More >Percutaneous balloon compression (PBC) is a safe and effective method to treat trigeminal neuralgia. Despite it is known that intraoperative balloon volume is crucial in the prognosis of PBC patients and correlates with Meckel's cave (MC) size, it is a lack of objective and valid criteria for intraoperative balloon volume of PBC.
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