Current rheumatology reports · 2019
Descending Control Mechanisms and Chronic Pain.
СтатьяПоддержка NIH: внешняя программаОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Chen QiLiang, Heinricher Mary M
Аннотация
PURPOSE OF REVIEW: The goal of the review was to highlight recent advances in our understanding of descending pain-modulating systems and how these contribute to persistent pain states, with an emphasis on the current state of knowledge around "bottom-up" (sensory) and "top-down" (higher structures mediating cognitive and emotional processing) influences on pain-modulating circuits.
RECENT FINDINGS: The connectivity, physiology, and function of these systems have been characterized extensively over the last 30 years. The field is now beginning to ask how and when these systems are engaged to modulate pain. A recent focus is on the parabrachial complex, now recognized as the major relay of nociceptive information to pain-modulating circuits, and plasticity in this circuit and its connections to the RVM is marked in persistent inflammatory pain. Top-down influences from higher structures, including hypothalamus, amygdala, and medial prefrontal areas, are also considered. The challenge will be to tease out mechanisms through which a particular behavioral context engages distinct circuits to enhance or suppress pain, and to understand how these mechanisms contribute to chronic pain.
RECENT FINDINGS: The connectivity, physiology, and function of these systems have been characterized extensively over the last 30 years. The field is now beginning to ask how and when these systems are engaged to modulate pain. A recent focus is on the parabrachial complex, now recognized as the major relay of nociceptive information to pain-modulating circuits, and plasticity in this circuit and its connections to the RVM is marked in persistent inflammatory pain. Top-down influences from higher structures, including hypothalamus, amygdala, and medial prefrontal areas, are also considered. The challenge will be to tease out mechanisms through which a particular behavioral context engages distinct circuits to enhance or suppress pain, and to understand how these mechanisms contribute to chronic pain.