Pain has been defined as an unpleasant sensory and emotional experience associated with or resembling that associated with, actual or potential tissue damage. Williams et al. suggested that the definition of pain should include cognitive and emotional components, which indicates that the cognitive function of people with pain is getting increased attention. Actually, co-morbidity of pain and cognitive dysfunction is common. Cognitive dysfunction has been described as loss of intellectual functions such as memory, attention, psychomotor skills, brain processing speed and decision making. And cognitive dysfunction is commonly associated with pain experience.
Pain can be broadly divided into chronic pain (such as neuropathic pain) and acute pain (such as acute postoperative pain). Growing evidence indicates that patients with chronic pain often suffer from cognitive dysfunction, which aggravates the poor quality of life of chronic pain patients. In addition, patients with fragile brain function are prone to postoperative cognitive dysfunction (POCD), which may be related to acute postoperative pain. To understand the precise mechanisms of pain-cognition interactions, investigators have carried out extensive researches from different perspectives. Recent studies have shown that reduced BDNF levels in the VTA-to-DG projection contributed to chronic pain-related memory formation deficits. In addition, hippocampal glutamatergic synapses impairment mediated cognitive dysfunction in rats with neuropathic pain. Moreover, neuroinflammation, dysregulated neurochemistry, alterations in proteins and their signaling pathways have also been proved to be involved in pain-related cognitive dysfunction. Still, the precise mechanism of pain-related cognitive dysfunction is poorly understood.
This Research Topic aims to broaden our knowledge of the precise mechanism of pain-related cognitive dysfunction and provide a forum for investigators to share innovative therapies for pain-related cognitive dysfunction. We welcome studies using animal models and cell lines to address the molecular and cellular mechanisms of pain-related cognitive dysfunction.
We encourage submissions of original research articles and review papers addressing, but not limited to, the following subtopics:
- Interactions between the neural circuits of pain and cognitive dysfunction;
- The role of neuroinflammation in pain-related cognitive dysfunction;
- The precise molecular mechanisms of pain-related cognitive dysfunction;
- Neuropathological alteration in pain-related cognitive dysfunction;
- The precise mechanism, prevention and innovative treatment of POCD;
- The treatment of pain, pain-related cognitive dysfunction using new technologies and methods
Pain has been defined as an unpleasant sensory and emotional experience associated with or resembling that associated with, actual or potential tissue damage. Williams et al. suggested that the definition of pain should include cognitive and emotional components, which indicates that the cognitive function of people with pain is getting increased attention. Actually, co-morbidity of pain and cognitive dysfunction is common. Cognitive dysfunction has been described as loss of intellectual functions such as memory, attention, psychomotor skills, brain processing speed and decision making. And cognitive dysfunction is commonly associated with pain experience.
Pain can be broadly divided into chronic pain (such as neuropathic pain) and acute pain (such as acute postoperative pain). Growing evidence indicates that patients with chronic pain often suffer from cognitive dysfunction, which aggravates the poor quality of life of chronic pain patients. In addition, patients with fragile brain function are prone to postoperative cognitive dysfunction (POCD), which may be related to acute postoperative pain. To understand the precise mechanisms of pain-cognition interactions, investigators have carried out extensive researches from different perspectives. Recent studies have shown that reduced BDNF levels in the VTA-to-DG projection contributed to chronic pain-related memory formation deficits. In addition, hippocampal glutamatergic synapses impairment mediated cognitive dysfunction in rats with neuropathic pain. Moreover, neuroinflammation, dysregulated neurochemistry, alterations in proteins and their signaling pathways have also been proved to be involved in pain-related cognitive dysfunction. Still, the precise mechanism of pain-related cognitive dysfunction is poorly understood.
This Research Topic aims to broaden our knowledge of the precise mechanism of pain-related cognitive dysfunction and provide a forum for investigators to share innovative therapies for pain-related cognitive dysfunction. We welcome studies using animal models and cell lines to address the molecular and cellular mechanisms of pain-related cognitive dysfunction.
We encourage submissions of original research articles and review papers addressing, but not limited to, the following subtopics:
- Interactions between the neural circuits of pain and cognitive dysfunction;
- The role of neuroinflammation in pain-related cognitive dysfunction;
- The precise molecular mechanisms of pain-related cognitive dysfunction;
- Neuropathological alteration in pain-related cognitive dysfunction;
- The precise mechanism, prevention and innovative treatment of POCD;
- The treatment of pain, pain-related cognitive dysfunction using new technologies and methods
