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Brain mechanisms of pain affect and pain modulation   总被引:19,自引:0,他引:19  
Recent animal studies reveal ascending nociceptive and descending modulatory pathways that may contribute to the affective-motivational aspects of pain and play a critical role in the modulation of pain. In humans, a reliable pattern of cerebral activity occurs during the subjective experience of pain. Activity within the anterior cingulate cortex and possibly in other classical limbic structures, appears to be closely related to the subjective experience of pain unpleasantness and may reflect the regulation of endogenous mechanisms of pain modulation.  相似文献   

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Back pain     
Hamilton Hall 《CMAJ》1984,130(4):511-512
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Low-back pain     
C. Chan Gunn 《CMAJ》2013,185(4):325
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Muscle pain     
Victor D. Janzen 《CMAJ》1984,130(10):1380
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OBJECTIVES--(a) to determine the efficacy of papaveretum in treating pain when administered early to patients presenting with acute abdominal pain and (b) to assess its effect on subsequent diagnosis and management. DESIGN--Prospective, randomised, placebo controlled study. SETTING--Walsgrave Hospital, Coventry. SUBJECTS--100 consecutive patients with clinically significant abdominal pain who were admitted as emergencies to a surgical firm. INTERVENTIONS--Intramuscular injection of up to 20 mg papaveretum or an equivalent volume of saline. OUTCOME MEASURES--Pain and tenderness scores, assessment of patient comfort, accuracy of diagnosis, and management decisions. RESULTS--Median pain and tenderness scores were lower after papaveretum (pain score 8.3 in control group and 3.1 in treatment group, p < 0.0001; tenderness score 8.1 in control group and 5.1 in treatment group, p < 0.0001). Forty eight patients were deemed to be comfortable after papaveretum compared with nine after saline. Incorrect diagnoses and management decisions applied to two patients after papaveretum compared with nine patients after saline. CONCLUSION--Early administration of opiate analgesia to patients with acute abdominal pain can greatly reduce their pain. This does not interfere with diagnosis, which may even be facilitated despite a reduction in the severity of physical signs. These patients should not be denied effective treatment.  相似文献   

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Clinical presentation of osteoarthritis (OA) is dominated by pain during joint use and at rest. OA pain is caused by aberrant functioning of a pathologically altered nervous system with key mechanistic drivers from peripheral nerves and central pain pathways. This review focuses on symptomatic pain therapy exemplified by molecular targets that alter sensitization and hyperexcitability of the nervous system, for example, opioids and cannabinoids. We highlight opportunities for targeting inflammatory mediators and their key receptors (for example, prostanoids, kinins, cytokines and chemokines), ion channels (for example, NaV1.8, NaV1.7 and CaV2.2) and neurotrophins (for example, nerve growth factor), noting evidence that relates to their participation in OA etiology and treatment. Future neurological treatments of pain appear optimistic but will require the systematic evaluation of emerging opportunities.  相似文献   

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Brainstem-scalp discharge propagation was evaluated in 20 patients with chronic pain, of which 10 were ranked according to the frequency of involved systems making up the chronic pain syndrome. It is concluded that brainstem discharges alone were sufficient to generate the chronic pain syndrome.  相似文献   

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