Articles: neuralgia.
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Questions from patients about pain conditions and analgesic pharmacotherapy and responses from authors are presented to help educate patients and make them more effective self-advocates. This article is about postherpetic neuralgia (PHN), a devastating complication following reactivation of the varicella-zoster virus. The answer offers an explanation for why this pain occurs, and cites literature regarding its incidence and treatment.
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The present study investigated the impact of a spared nerve injury (SNI) on the daily performance of rats tested in two instrumental conditioning procedures: the progressive ratio (PR) schedule of food reinforcement to study motivation for an appetitive stimulus, and the 5-choice serial reaction time task (5-CSRTT), a test of attention and reaction time. Separate groups of male, Sprague-Dawley rats of age 8-10 months were trained to asymptotic performance in either task, before undergoing either SNI or sham surgery. After a recovery period of 3-4 days the animals were run 5 days/week for 3 months in either task. ⋯ This deficit emerged during the second month post-surgery and was characterized by slower response speed, reduced accuracy and increased trial omissions. Both SNI groups showed equivalent hypersensitivity to evoked sensory stimuli compared to controls. Since attention based deficits have been reported in individuals with clinical forms of neuropathic pain, the present studies suggest a novel approach to study this phenomena and a means to study the effect of treatments against this cognitive endpoint.
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Questions from patients about pain conditions and analgesic pharmacotherapy and responses from authors are presented to help educate patients and make them more effective self-advocates. This article provides information to patients regarding the treatment of neuropathic pain syndrome. It narrates how a doctor might explain neuropathic pain to a patient and particularly discusses the use of anticonvulsants.
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Clin. Exp. Pharmacol. Physiol. · Jun 2015
The ventral portion of the anterior pretectal nucleus controls descending mechanisms that initiate neuropathic pain in rats.
Stimulating the dorsal anterior pretectal nucleus (dAPtN) in rats is more effective than stimulating the ventral APtN (vAPtN) at reducing tail-flick latency, whereas stimulation of the vAPtN is more effective at reducing postoperative pain behaviour. This study examines whether a cell lesion caused by injecting N-methyl-D-aspartate into the dAPtN or vAPtN changes the withdrawal threshold of a rat hind paw during different phases of the tactile hypersensitivity induced by a chronic constriction injury (CCI) of the contralateral sciatic nerve. The number of Fos immunoreactive cells in the APtN was also evaluated. ⋯ The tactile hypersensitivity of the rats whose dAPtN was lesioned 2 days before or 5 days after CCI was not different from that of the control on the second and seventh days after the CCI. The number of Fos immunoreactive cells in the vAPtN and dAPtN increased 2 days after CCI, but did not differ from that in the control 7 days after CCI. We conclude that vAPtN and dAPtN cells are activated by nerve injury; the vAPtN exerts inhibitory control of the initial phase of neuropathic pain whereas the dAPtN does not appear to exert an inhibitory effect in neuropathic processing.
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IEEE Trans Biomed Eng · Jun 2015
Burst and Tonic Spinal Cord Stimulation Differentially Activate GABAergic Mechanisms to Attenuate Pain in a Rat Model of Cervical Radiculopathy.
Spinal cord stimulation (SCS) is widely used to treat neuropathic pain. Burst SCS, an alternative mode of stimulation, reduces neuropathic pain without paresthesia. However, the effects and mechanisms of burst SCS have not been compared to conventional tonic SCS in controlled investigations. This study compares the attenuation of spinal neuronal activity and tactile allodynia, and the role of γ-aminobutyric acid (GABA) signaling during burst or tonic SCS in a rat model of cervical radiculopathy. ⋯ Together, these studies suggest that burst SCS does not act via spinal GABAergic mechanisms, despite its attenuation of spinal hyperexcitability and allodynia similar to that of tonic SCS; understanding other potential spinal inhibitory mechanisms may lead to enhanced analgesia during burst stimulation.