Introduction

The pathophysiology of different types of pain

Ongoing activation of peripheral nociceptors, with or without the presence of inflammatory mediators, results in ongoing peripheral sensitization. However, this is commonly supplemented by central sensitization. Clinical manifestations include ongoing peripheral mechanothermal hyperalgesia, and allodynia. Chronic inflammatory degenerative conditions (e.g. rheumatoid arthritis or degenerative osteoarthritis) can result in chronic pain.1Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006. p283.

The nervous system’s role in pain transmission

The sensation and interpretation of pain requires activation of brain regions associated with spatial discriminative and affective components of pain perception. This is clearly a potential (but not inevitable) consequence of activity of the primary afferent nociceptor and involves The sensation and interpretation of pain requires activation of brain regions associated with spatial discriminative and affective components of pain perception. This is clearly a potential (but not inevitable) consequence of activity of the primary afferent nociceptor and involvesThe sensation and interpretation of pain requires activation of brain regions associated with spatial discriminative and affective components of pain perception. This is clearly a potential (but not inevitable) consequence of activity of the primary afferent nociceptor and involves integration of the polysynaptic output from the primary afferent through multiple ascending pathways.2 Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006. p274

How is pain transmitted?

The polysynaptic, intraspinal pathway connects primary afferents to motor neurons. This basic pathway facilitates the withdrawal reflex. It can occur in the absence of pain perception, such as under anesthesia or following spinal cord injury. It is heavily modified by local and descending inhibitory influences. When descending controls are lost as in a complete spinal cord injury, the pathway can be activated by nonnociceptive afferents such that even innocuous stimuli will result in a flexor withdrawal response.3Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006. p274.

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