The International Academy of Pain (IASP) has proposed a new concept of central pain, which considers pain caused by lesions or dysfunctions of the central nervous system as central pain (central pain). Anesthesia dolorosa occurs in pain of neuropathic origin in the head and face, commonly after surgical injury to the trigeminal nerve, the semilunar ganglion, or after a destructive nerve block for the treatment of trigeminal neuralgia. Areas of numbness due to injury produced by neurosurgery are also listed as central pain in the treatment of severe pain. Deafferentation pain (deafferentation pain) is similar, but is generally used in cases of spinal nerve injury. Etiology and pathogenesis of central pain 1. Etiology of central pain There are 10 causes of central pain as follows: (1) vascular injury of the cerebrospinal cord, which produces persistent pain after cerebrovascular injury. (2) Multiple sclerosis, i.e. multiple sclerosis or tumors of the cerebral bridge, medulla oblongata or spinal cord, producing central pain. (3) Lesions located at a level of the axon, the dorsal horn of the spinal cord to the cerebral cortex. (4) Traumatic brain injury. (5) Cavitation of the medulla oblongata, which often leads to central pain, but is not related to the slow rate of lesion onset. (6) Abscesses, tumors. (7) Myelitis caused by viruses and syphilis. (8) Epilepsy. (9) Parkinson’s disease. (10) Central pain after stroke, mostly lesions in the thalamus. (2) Pathogenesis of central pain (1) The disease process of central pain with lesions involving the spinal thalamic pathway, including indirect spinal reticular thalamic and spinal midbrain projections, is the same as the abnormal sensitivity of pain and temperature sensation. (2) The lesion does not involve the medial spinal thalamic pathway. (3) The lesion is located at some level of the axon, the dorsal horn of the spinal cord to the cerebral cortex. (4) A variety of disease processes may cause central pain, but it is highly variable, ranging from rare to common in most patients. (5) Central pain is concentrated in three thalamic areas, namely the posterior ventral area, the reticular area, the median nucleus, and the intraparenchymal area. The role of the cerebral cortex in central pain is unclear, and no specific studies have been reported. (6) Central pain due to spinal cord lesions with pain and sensory hypersensitivity is consistent with an increase in excitatory discharge from the posterior ventral thalamic area. This cellular activity is also present at other levels of the sensory pathways and in the cerebral cortex. As for the cellular mechanism of central pain it is not known, but this process involves excitatory amino acids, especially glutaminergic (qlutaminerqic)-containing NMDA receptors. Clinical features of central pain 1. Pain localization Central pain is difficult to localize, and this concept was usually emphasized in the past, mainly from the fact that central pain extends to most of the body, e.g., the entire right or left side of the body, or the lower half of the body. It may also involve only one hand or the radial or ulnar side of the hand or half of the face. Patients with widespread central pain have a relatively easy time describing the area of pain. Most central pain is widely distributed rather than scattered, and the location of the lesion determines the site of pain. Common sites of central pain Post-stroke central pain: entire half of the body, entire half of the body except the face, one upper extremity or (and) leg, one side of the face, the other upper and lower extremity, and the face. Multiple sclerosis: Lower half of the body, one or both legs, upper extremity and leg on one side, trigeminal neuralgia. Spinal cord injury: All of the body below the neck, the lower half of the body, one leg. Spinal cord cavitation: upper extremity and chest on one side, one arm, chest on one side, one leg plus one item on the face. Large lesions in the ventral posterior region of the thalamus or the posterior limb of the internal capsule, causing hemiplegia; injury to most of the spinal cord, causing bilateral pain; extensive somatosensory loss lesions involving areas innervated by the caudal segment of the lesion, which can cause central pain. Intramedullary cerebral vascular lesions, i.e., thrombosis of the inferior posterior cerebellar artery leading to Wallenberg syndrome, provoke bilateral central pain with pain in the head and face on the side of injury, and in the rest of the body on the contralateral side, due to injury to the ipsilateral trigeminal spinal tract branch and the contralateral spinal thalamic tract. Intraspinal lesions that invade the spinal thalamic tract cause pain on the contralateral side, for example, after severance of the anterolateral cord of the spinal cord. In spinal cord cavitation, pain may be limited to a portion of one side of the chest, but also extends to some areas of the upper extremities and lower body. Among the superficial pain, deep pain and mixed superficial and deep pain of central pain, skin hypersensitivity occurs at a high rate, so superficial pain is the majority. 2.Nature of pain The nature of central pain is not fixed, but can be of any nature, in other words, not always burning or tactile pain (disaethetic) in nature, but diverse and with great variation between patients in its nature. 3. intensity of the pain varies from low to very high. 4.Onset and temporal pattern Central pain appears immediately after having a lesion or is delayed for several years, up to 2-3 years, for example, most of the post-stroke pain occurs within 2-3 weeks after the stroke. Most spontaneous central pain, which is persistent, does not have pain-free intervals. It was reported that among 27 cases of post-stroke central pain, 23 cases were persistent, and 4 cases retained a continuous pain-free interval of up to a few hours per day. 5. Factors affecting central pain (1) Skin stimulation, body movement, visceral stimulation, nerve and mood changes can affect central pain. (2) Nociceptive hypersensitivity (allodynia), stimuli that do not produce pain under normal circumstances, such as touch, light pressure, warmth or slight cold and induce pain are common in patients with central pain. 6.Signs and symptoms of nerves Central pain is due to the disorder and lesion of somatosensory system, which is a physical sensory symptom, and abnormal somatosensory is the only symptom and sign. Central pain is not related to the abnormalities of muscle function, coordination, vision, hearing, vestibular function and higher cortical function. 7.Somatic sensory abnormalities The diagnostic basis for patients with central pain, and the symptoms that play a role in patients’ disorders, are quite important, mainly the following sensory abnormalities: (1) hyperalgesia (hypoaesthecia); (2) sensory hypersensitivity (hyperaesthesia); (3) sensory abnormalities (paraesthesia) and sensory retardation ( dysaesthesias); (4) numbness (numbness); (5) radiation, prolonged latency of response, post-sensory, and accumulation.