Some controversies have arisen regarding the necessity of the emergence of nociplastic pain as the third division of the sensory component of pain. Nociplastic pain is defined as pain that arises from (or is sustained by) altered nociception, despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain, by the International Association for the Study of Pain [1–5].

Nociception is a neural process of encoding noxious stimuli resulting in autonomic and behavioral consequence, such as elevated blood pressure, motor withdrawal reflex, or complex nocifensive behavior. However, all nociception cannot be pain. What brings an alteration of nociception in nociplastic pain? Central sensitization is offered as the common answer for the mechanism of nociplastic pain. It is the increased responsiveness of nociceptive neurons in the central nervous system to their normal or subnormal afferent input due to dysfunction of endogenous pain control systems [2]. The characteristics of central sensitization pain include allodynia, hyperalgesia, expansion of the receptive field, and prolonged pain after removal of a stimulus [6]. Sensitization is clinically expressed as hyperalgesia or allodynia [2].

How to recognize central sensitization in clinical practice? Central sensitization inventory is a useful tool to diagnose central sensitization by both patients themselves (25 subjective symptom items in 5 categories: total 100 points) and physicians (10 combined disorders) [6].

Nociplastic pain occurs without clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence of disease or lesion of the somatosensory system causing the pain [2]. Nociplastic pain, which has a vague origin, must present ① pain, ② evoked hypersensitivity in the region of the pain, ③ hypersensitivity to touch, pressure, movement, or heat/cold, and ④ presence of comorbidities. Possible nociplastic pain must include ① and ②; probable nociplastic pain has all 4 of the above items. The 8 specific comorbid disorders include restless leg syndrome, chronic fatigue syndrome, fibromyalgia, temporomandibular joint disorder, migraine or tension headache, irritable bowel syndrome, multiple chemical sensitizations, and neck injury (including whiplash injury); 2 nonspecific comorbid disorders are anxiety/pain panic and depression [6].

To be classified as probable rather than possible nociplastic pain, at least one of the 8 specific disorders should coexist. Otherwise, nonspecific emotional components of pain, anxiety, depression, or pain panic, should coexist. All patients with chronic pain have these emotional components of pain. At first, nociplastic pain was asserted as a third new category of the sensory components of pain in addition to nociceptive and neuropathic pain, even though clear evidence of tissue damage or disease/lesion cannot be found. However, it may include the emotional component of pain. Consequently, nociplastic pain may have both emotional and sensory components of pain. Therefore, those who argue that nociplastic pain is solely the third division of the sensory component of pain contradict themselves. Chronification of pain is generally contributed by the existence of severe tissue damage (nociceptive pain) and/or coexisting neuropathic pain.

Grading of neuropathic pain ranges from possible (relevant history and pain distribution), through probable (pain associated with sensory signs) to definite (confirmation by diagnostic tests). Definite neuropathic pain has all the above features of probable nociplastic pain from ① to ④, except hypersensitivity to special senses, such as sound, light, or odor [1]. Functional pain syndrome, focused on fibromyalgia, has pain and the presence of comorbidities without evoked hypersensitivity in the region of the pain or pain hypersensitivity to touch, pressure, movement, or heat/cold. Similarly, psychogenic pain has pain and comorbidities without allodynia. The difference between functional pain syndrome and psychogenic pain lies in presence or absence of clear evidence of a nociceptive source.

In conclusion, the category of nociplastic pain may be developed for better understanding unexplained chronic pain beyond tissue damage. However, even though an effort is made to find the developing mechanisms of nociplastic pain from supraspinal, spinal, or peripheral origins, they are not significantly different from previous central sensitization [6,7]. It is also vague to classify nociplastic pain as a third category of the sensory components of pain, next to nociceptive pain and neuropathic pain, or into a third category of pain, next to the sensory and emotional components of pain.