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 to be central pain. This definition centers on primary processes within the CNS rather than peripheral triggers of pain, and peripheral triggers of pain are not central pain, although they have a central mechanism. For example, often discussed as central pain, pseudothalamic pain caused by extra-thalamic injuries are sometimes also attributed to central pain, touch pain pain is also attributed to central pain. However, in most cases, only the central pain caused by thalamic lesions is listed as central pain. First, numbness pain occurs in the head and face neuropathic pain Commonly in the trigeminal nerve, semilunar ganglion after surgical injury or for the treatment of trigeminal neuralgia after destructive nerve block. Areas of numbness due to injury produced by neurosurgery are also listed as central pain when treating severe pain. A similar situation exists with deafferentation pain, but it is generally used in cases of spinal nerve injury. Second, the etiology and pathogenesis of central pain 1, the etiology of central pain The etiology of central pain has the following 10 kinds: (1) cerebral spinal cord vascular injury, cerebral vascular injury produces persistent pain, shooting hospital vomiting lesions. (2) Multiple sclerosis, i.e., multiple sclerosis or tumors of the cerebral pons, medulla oblongata, or spinal cord, producing central pain. (3) Lesions located at a level of the axons, the dorsal horn of the spinal cord to the cerebral cortex. (4) Traumatic brain injury. (5) Medullary cavernous disease, which often results in central pain but is not related to the rapidity with which the lesion occurs. (6) Abscesses and tumors. (7) Myelitis caused by viruses and syphilis. (8)Epilepsy. (9)Parkinson’s disease. (10) Post-stroke central pain, most of the lesions in the thalamus. (2) The pathogenesis of central pain (1) The disease process of central pain, with lesions involving the spinal thalamic pathway, including indirect spinal reticular thalamus and spinal midbrain projections, is the same as that of the sensitivity abnormalities of pain and temperature sensation. (2) The lesion does not involve the medial spinal thalamic tract. (3) The lesion is located at some level of the axon, the dorsal horn of the spinal cord to the cerebral cortex. (4) Various 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 regions, the retroventral, reticular, median and intralaminar nuclei. The role of the cerebral cortex in central pain is unclear and no specialized studies have been reported. (6) Central pain due to spinal cord lesions with pain and sensory hypersensitivity is consistent with increased excitatory discharge from the retroventral 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 clear, but the process involves excitatory amino acids, especially glutaminergic (qlutaminerqic)-containing NMDA receptors. Third, the clinical characteristics 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 a large part of the body, such as: 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. In patients with widespread central pain, it is relatively easy to describe the area of pain. Most central pain is widespread rather than scattered, and the location of the lesion determines the site of pain (see Table 1). Table 1 Common sites of central pain Post-stroke central pain: entire half of the body, entire half of the body except the face, one upper limb or (and) leg on one side, one side of the face, upper and lower limbs on the other side, and the face Multiple sclerosis: lower half of the body, one or both legs, one upper limb and leg on one side, trigeminal neuralgia Spinal cord injuries: all of the body from the neck down, lower half of the body, one leg Spinal cord cavernous disease: one upper limb and chest on one side, one arm, one side of the chest, one leg plus one item on the face Large lesions of the posterior ventral region of the thalamus or the posterior limb of the internal capsule, causing hemiplegia; injury to a large part of the spinal cord, causing bilateral pain; involvement of the area innervated by the caudal segments of the lesion, widespread somatosensory loss lesions, which may cause central pain. Intramedullary cerebrovascular lesions, i.e., thrombosis of the posterior inferior cerebellar artery leading to Wallenberg’s syndrome, provoke central pain on both sides, with pain in the head and face on the side of the injury, and in the rest of the body on the contralateral side, due to injury to the ipsilateral spinal tract branch of the trigeminal nerve and to the contralateral thalamus fasciculus of the spinal cord. Lesions within the spinal cord that invade the spinal thalamic tracts cause pain on the contralateral side, e.g., after severance of the anterolateral cord of the spinal cord. In spinal cord cavernous disease, the pain may be limited to a portion of the side of the chest and also extend to some areas of the upper and lower body. Among the superficial pain, deep pain, and mixed superficial and deep pain of central pain, the incidence of skin hypersensitivity is high, so superficial pain accounts for the majority. 2, the nature of pain The nature of central pain is not fixed, and can be of any nature, in other words, not always burning or tactile pain (disaethetic), but the diversity, and the variation between patients is also very large, the nature of its (see table 2). Table 2 The nature of pain in patients with central pain Burning pain* Shooting pain Padding pain Persistent vague pain* Squeezing pain Stabbing pain Cutting pain* Jumping pain Clipping pain Stabbing pain* Cutting pain Tearing pain Crushing pain Pulling pain Squeezing pain* Splitting pain Coldness Refers to the nature of the most common pain 3. The intensity of pain Ranges from low to very high. 4, onset and tense Central pain occurs immediately after the presence of a lesion or is delayed for several years, up to 2 to 3 years, e.g., the majority of post-stroke pain occurs within 2 to 3 weeks after a stroke. Most spontaneous central pain, is persistent and does not have pain-free intervals. It has been reported that of the 27 cases of post-stroke central pain, 23 cases were persistent, and 4 cases retained a continuous pain-free interval of at most a few hours per day. 5. Factors affecting central pain (1) Skin irritation, body movement, visceral irritation, and changes in nerves and mood can affect central pain. (2) Nociceptive hypersensitivity (allodynia), under normal circumstances do not produce pain stimuli, such as: touch, light pressure, warm, slightly cold and induced pain is common in patients with central pain. 6, nerve symptoms, signs and symptoms of central pain is due to somatosensory system of confusion, lesions, which is a body sensory symptoms, somatosensory abnormalities are the only symptoms and signs. Central pain is not related to abnormalities in muscle function, coordination, vision, hearing, vestibular function, or higher cortical function. 7, somatosensory abnormalities Scoop Spirits Central pain in patients with diagnostic basis, but also for patients with disorders play a role in the symptoms, is quite important, the main sensory abnormalities are as follows: ① hypoaesthesia (hypoaesthesia), ② sensory hypersensitivity (hyperaesthesia), ③ sensory anomalies (paraesthesia) and dullness of sensation (dysaesthesias), ④ numbness (paraesthesia) and dullness of sensation (dysaesthesias), and ④ numbness (paraesthesia). ), ④ numbness, ⑤ radiation, prolonged reaction latency, after-sensation, and accumulation.