Central and Deafferentation Pain
Central pain is defined as pain that is initiated by a primary lesion within the CNS. Central pain can occur in association with all types of CNS lesions related to a wide variety of pathological processes. However, the probability that a particular lesion will induce central pain is probably less dependent on the type of lesion than on its location in the CNS.[1,19] One of the classic examples of central pain is the syndrome of thalamic pain related to hemorrhage or infarction of the sensory thalamus.
Deafferentation pain denotes a type of pain that results from complete or partial interruption of afferent nerve impulses. This type of pain results from lesions that interrupt the spinothalamic pathways at any level of the nervous system. Deafferentation pain can be caused by lesions of either the CNS (such as thalamic pain, brainstem infarction with bulbar pain, and so on) or peripheral nervous system (such as peripheral nerve injury, trigeminal neuropathic pain, and the like). Patients with deafferentation pain usually display varying degrees of sensory loss characterized by disturbances in pain and temperature sensation. In addition to objective sensory loss, many patients also experience abnormal sensory phenomena such as allodynia, hyperalgesia, dysesthesias, and hyperpathia.
There are large differences in the incidence and prevalence of central pain among the various lesions and disorders that can lead to this problem. Because truly accurate epidemiological data are lacking, most figures represent estimates. Additionally, many patients have mixed neuropathic and nociceptive pain syndromes, and it is sometimes difficult to distinguish central pain from other potential sources in a given patient. The highest prevalence of central pain appears to occur after spinal cord injury and in patients with multiple sclerosis.[2] The percentage of patients with spinal cord injury and multiple sclerosis who experience central pain has been estimated to be 30 and 23%, respectively, and it has been estimated that more than 100,000 patients with these two conditions have some degree of central pain. Although the percentage of patients in whom pain develops after stroke is only approximately 1.5%, stroke itself is so prevalent that the actual number of patients in whom poststroke pain develops is quite large. Based on epidemiological figures for patients with spinal cord injury, multiple sclerosis, and stroke, Bonica[2] estimated the prevalence of central pain to be approximately 54 per 100,000 persons, meaning that approximately 130,000 individuals in the US with these conditions suffer some degree of central pain.
Central pain can take many forms, and the distribution of the pain may be quite variable. It can affect large body areas or occur in a very restricted focal pattern. The severity of the pain can range from trivial to excruciating, and even in patients in whom the intensity of the pain is relatively low there may be a great deal of suffering, largely because central pain is usually constant and its characteristics are often extremely irritating. Although central pain can begin immediately after a lesion of the CNS occurs, it is not unusual for it to be delayed in onset, sometimes not appearing for many months or even years after the sentinel event. Although some patients with central pain will have spontaneous remission after a period of time, for the majority, the pain regrettably persists indefinitely.[1]
Neurosurg Focus. 2006;21(6) © 2006 American Association of Neurological Surgeons
Cite this: Motor Cortex Stimulation for Intractable Pain - Medscape - Dec 01, 2006.
Comments