Comparison of the Analgesic Effects of Pulse Radiofrequency and Cryoablation in Rabbits with Mental Nerve Neuropathic Pain

Purpose: After mental nerve injury, several sensory disorders may occur. The alterations in sensation may differ from mild paresthesia to complete anesthesia, or neuropathic pain. Neuropathic pain is a difficult clinical condition to manage. The aim of this study was to compare the analgesic effects of pulsed radiofrequency (PRF) and cryoablation in an experimental mental nerve neuropathic pain model in rabbits. Materials and Methods: Fifteen rabbits were divided into three groups. One‑third to one‑half of the mental nerve was ligated with 4‑0 silk sutures. In Group 1, a nonconducting PRF electrode was placed on the mental nerve for 6 min, whereas the mental nerve was exposed to PRF in Group 2. In Group 3, the cryoablation was processed. The responses to thermal and mechanical stimuli were measured at the 1st, 2nd, 3rd, and 4th weeks. Results: There were no statistically significant differences among the groups for thermal withdrawal latency to heat stimulation in any weeks (P > 0.05). However, a significant difference was found between the groups (P < 0.05) in the 3rd and 4th weeks for mechanical withdrawal latency values. Conclusions: Both PRF and cryoablation therapies are successful in the treatment of experimentally induced mental nerve neuropathic pain in rabbits.Keywords: Cryoablation, mental nerve, neuropathic pain, pulse radiofrequenc

The Potential of Antiseizure Drugs and Agents that Act on Novel Molecular Targets as Antiepileptogenic Treatments

A major goal of contemporary epilepsy research is the identification of therapies to prevent the development of recurrent seizures in individuals at risk, including those with brain injuries, infections, or neoplasms; status epilepticus; cortical dysplasias; or genetic epilepsy susceptibility. In this review we consider the evidence largely from preclinical models for the antiepileptogenic activity of a diverse range of potential therapies, including some marketed antiseizure drugs, as well as agents that act by immune and inflammatory mechanisms; reduction of oxidative stress; activation of the mammalian target of rapamycin or peroxisome proliferator-activated receptors γ pathways; effects on factors related to thrombolysis, hematopoesis, and angiogenesis; inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reducatase; brain-derived neurotrophic factor signaling; and blockade of α2 adrenergic and cannabinoid receptors. Antiepileptogenesis refers to a therapy of which the beneficial action is to reduce seizure frequency or severity outlasting the treatment period. To date, clinical trials have failed to demonstrate that antiseizure drugs have such disease-modifying activity. However, studies in animal models with levetiracetam and ethosuximide are encouraging, and clinical trials with these agents are warranted. Other promising strategies are inhibition of interleukin 1β signaling by drugs such as VX-765; modulation of sphingosine 1-phosphate signaling by drugs such as fingolimod; activation of the mammalian target of rapamycin by drugs such as rapamycin; the hormone erythropoietin; and, paradoxically, drugs such as the α2 adrenergic receptor antagonist atipamezole and the CB1 cannabinoid antagonist SR141716A (rimonabant) with proexcitatory activity. These approaches could lead to a new paradigm in epilepsy drug therapy where treatment for a limited period prevents the occurrence of spontaneous seizures, thus avoiding lifelong commitment to symptomatic treatment. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s13311-014-0266-1) contains supplementary material, which is available to authorized users