In order to clarify the mechanism of reference of pain following cordotomy (ROPC), the authors investigated ROPC in 66 patients undergoing percutaneous cervical cordotomy (PCC) and examined the features of ROPC and the correlation between the occurrence of ROPC and the pre-operative pain states, as well as the results of PCC. ROPC was observed in 7 patients. It occurred immediately after PCC in 6 of 7 patients and 6 h after PCC in 1 patient. The pain was referred horizontally and cranially from the region rendered totally or largely analgesic by PCC to the normally innervated region. The region to which the pain was referred was not fixed. The referred pain disappeared by rendering the region where referred pain was felt analgesic with additional PCC. There was no correlation between the occurrence of ROPC and pre-operative pain states, or the results of PCC. From these results we postulate that: (1) ROPC occurs via a subsidiary pathway consisting of ascending chains of short neurons connecting dorsal horn neurons longitudinally and latitudinally; (2) the subsidiary pathway is inhibited under normal conditions by feedback inhibition from second-order neurons and/or higher central neurons of the nociceptive pathway; and (3) ROPC results from the release of the feedback inhibition by cordotomy.
The present results indicate that new pain occurs frequently after unilateral cordotomy. Nonetheless, cordotomy may still be indicated for unilateral uncontrollable pain because new pain, when present, was weaker and more easily controlled than the original pain in nearly all cases. The authors speculate that new pain may represent a type of referred pain from the original painful area or may arise from sensitization of contralateral spinal nociceptive circuits due to metastasis or tumor infiltration, and that new pain is potentiated by the interruption of descending inhibitory pathways.
SUMMARY A case of musicogenic epilepsy or psychomotor seizures supervening whenever the patient hears a certain tune has been presented. The EEG features of the seizure are such as are often seen in psychomotor seizures. Auditory evoked response may be left out of consideration. There is no appreciable relationship between the disease and the life history of the patient. The attempt of our patient to cure herself by making use of conditioned reflex proved to be a failure. The patient is more liable to the disease when she is on the strain while hearing a tune. Our consideration of the mechanism of the disease has led to the presumptive conclusion that hyperacusis, conditioned reflexes and the impact of life history may be involved, and the fragility of the memory function of the temporal lobe underlie the genesis of the disease.
In an attempt to clarify the mechanisms of cytotoxicity mediated by CD4+ cytotoxic T lymphocytes (CTL), the expression of perforin and membrane-bound lymphotoxin (LT) (tumor necrosis factor-beta) in herpes simplex virus (HSV)-specific CD4+ human cytotoxic and noncytotoxic T- cell clones was examined. Three HSV-specific CD4+ human CTL clones that showed HLA-DR-restricted cytotoxicity and proliferative response were established. The cytotoxicity of these clones in 5-hour 51Cr release assays was found to be mediated by the directional target cell lysis and not by the release of cytotoxic soluble factors, ie, “innocent bystander” killing. Northern blot analysis showed that messenger RNAs for perforin and LT, which were both considered to be important mediators for cytotoxicity of CD8+ CTL and natural killer cells, were abundantly expressed in HSV-specific CD4+ CTL clones. Expression of perforin in the cytoplasm of CD4+ CTL clones was also detected by immunohistochemical staining using a monoclonal antibody against perforin. In addition, LT bound to the cell surface of CD4+ CTL clones was detected by flow cytometry. In contrast, little or no expression of perforin and LT was detected in three HSV-specific CD4+ noncytotoxic T- cell clones. Although the cytotoxicity mediated by lymphokine-activated killer cells was partly inhibited by addition of anti-LT antibody, it did not show any effect on the cytotoxicity of HSV-specific CD4+ CTL clones. In addition, it was found that cytotoxicity mediated by these CD4+ CTL clones was Ca2(+)-dependent. These data thus suggest that perforin and membrane-bound LT are both expressed in HSV-specific CD4+ CTL, although perforin might be the more important mediator in short- term culture.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.