1/5. Insights into the pathophysiology of neuropathic pain through functional brain imaging.We present here an example case of neuropathic pain with heat allodynia as a major symptom to illustrate how the functional imaging of pain may provide new insights into the pathophysiology of painful sensory disorders. Tissue injury of almost any kind, but especially peripheral or central neural tissue injury, can lead to long-lasting spinal and supraspinal re-organization that includes the forebrain. These forebrain changes may be adaptive and facilitate functional recovery, or they may be maladaptive, preventing or prolonging the painful condition, and interfering with treatment. In an experimental model of heat allodynia, we used functional brain imaging to show that: (1) the forebrain activity during heat allodynia is different from that during normal heat pain, and (2) during heat allodynia, specific cortical areas, specifically the dorsolateral prefrontal cortex, can attenuate specific components of the pain experience, such as affect, by reducing the functional connectivity of subcortical pathways. The forebrain of patients with chronic neuropathic pain may undergo pathologically induced changes that can impair the clinical response to all forms of treatment. Functional imaging, including PET, fMRI, and neurophysiological techniques, should help identify brain mechanisms that are critical targets for more effective and more specific treatments for chronic, neuropathic pain.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
2/5. sympathectomy does not abolish bradykinin-induced cutaneous hyperalgesia in man.bradykinin is an endogenous peptide that is thought to be a chemical mediator of the hyperalgesia following inflammation. In rat, bradykinin has been postulated to cause hyperalgesia to mechanical stimuli by releasing prostaglandin from sympathetic post-ganglionic terminals. The aim of this study was to determine whether bradykinin-induced cutaneous hyperalgesia in humans requires post-ganglionic sympathetic terminals. In humans, intradermal injection of bradykinin produces dramatic hyperalgesia to heat but not mechanical stimuli. Therefore, we measured the magnitude and duration of pain and hyperalgesia to heat stimuli following intradermal injection of bradykinin into the leg of a woman before and 6 months after an ipsilateral, surgical, lumbar sympathectomy. The pain and hyperalgesia to heat following bradykinin was found to be unaffected by the sympathectomy. These results suggest that the algesic effects of cutaneous bradykinin in human are independent of the sympathetic nervous system.- - - - - - - - - - ranking = 0.5015851543744keywords = nervous system (Clic here for more details about this article) |
3/5. motor cortex stimulation for central pain following a traumatic brain injury.Central pain can occur in any lesions along the central nervous system affecting the spinothalamocortical pathway. Although diverse etiologies have been reported to cause central pain, there are few reports on the occurrence and surgical treatment of central pain following a traumatic brain injury (TBI). This paper describes the occurrence of central pain following a severe TBI, in which the diagnosis of central pain was typically delayed due to the patient's decreased ability to express his pain for severe aphasia as a neurological sequela. The severe burning pain, deep pressure-like pain, and deep mechanical allodynia, which presented over the contralateral side to the TBI, were successfully relieved with motor cortex stimulation (MCS). The analgesic effect of stimulation was found to be long lasting and was still present at the 12-month follow up. As shown in this patient, the occurrence of central pain syndrome should be considered by physicians caring for TBI patients, and a comprehensive, systematic study will be needed to determine the prevalence of central pain after a TBI.- - - - - - - - - - ranking = 1.2680757348632keywords = nervous system, central nervous system, brain (Clic here for more details about this article) |
4/5. Eosinophilic meningitis: cause of a chronic pain syndrome.Three tourists developed eosinophilic meningitis after visiting the Fijian islands. Two had a severe and long lasting illness with chronic intractable pain. In one patient electrophysiological studies and MRI scan of the brain were abnormal and provided evidence of both radicular and cerebral parenchymal involvement by the most likely causative agent, angiostrongylus cantonensis.- - - - - - - - - - ranking = 0.1keywords = brain (Clic here for more details about this article) |
5/5. Response of chronic neuropathic pain syndromes to ketamine: a preliminary study.Hyperactivity of N-methyl-D-aspartate (NMDA) receptors may be one of the factors in the genesis of neuropathic pain. ketamine is an NMDA-blocking agent widely used in human medicine. ketamine (at 250 mcg/kg i.v. slow push) was administered to 6 patients for control of chronic neuropathic pain syndromes in double-blind placebo-controlled fashion. All 3 patients with peripheral nervous system (PNS) disease-related pain, and 2 of 3 patients with central pain and dysesthesia syndromes responded with a temporary decrease in the rating of ongoing pain. The allodynia, hyperalgesia and after-sensation present in 5 patients improved after the administration of ketamine. Dose-response estimation in 2 patients with PNS-related neuropathic pain revealed that ketamine was effective in dose-related fashion. Continuous subcutaneous infusion of ketamine administered to 1 patient with PNS-related neuropathic pain caused no additional improvement in pain control but caused intolerable cognitive and memory side effects. In contrast, side effects during single-dose injections were mild and well tolerated. ketamine affected the evoked pain and associated after-sensation in chronic neuropathic pain syndromes more than the ongoing constant pain.- - - - - - - - - - ranking = 0.5015851543744keywords = nervous system (Clic here for more details about this article) |