An Experimental Paradigm for the Prediction of Post-Operative Pain (PPOP)

Many women undergo cesarean delivery without problems, however some experience significant pain after cesarean section. Pain is associated with negative short-term and long-term effects on the mother. Prior to women undergoing surgery, can we predict who is at risk for developing significant postoperative pain and potentially prevent or minimize its negative consequences? These are the fundamental questions that a team from the University of Washington, Stanford University, the Catholic University in Brussels, Belgium, Santa Joana Women's Hospital in São Paulo, Brazil, and Rambam Medical Center in Israel is currently evaluating in an international research collaboration. The ultimate goal of this project is to provide optimal pain relief during and after cesarean section by offering individualized anesthetic care to women who appear to be more 'susceptible' to pain after surgery

Stimulation of the Sphenopalatine Ganglion Induces Reperfusion and Blood-Brain Barrier Protection in the Photothrombotic Stroke Model

The treatment of stroke remains a challenge. Animal studies showing that electrical stimulation of the sphenopalatine ganglion (SPG) exerts beneficial effects in the treatment of stroke have led to the initiation of clinical studies. However, the detailed effects of SPG stimulation on the injured brain are not known.The effect of acute SPG stimulation was studied by direct vascular imaging, fluorescent angiography and laser Doppler flowmetry in the sensory motor cortex of the anaesthetized rat. Focal cerebral ischemia was induced by the rose bengal (RB) photothrombosis method. In chronic experiments, SPG stimulation, starting 15 min or 24 h after photothrombosis, was given for 3 h per day on four consecutive days. Structural damage was assessed using histological and immunohistochemical methods. Cortical functions were assessed by quantitative analysis of epidural electro-corticographic (ECoG) activity continuously recorded in behaving animals.Stimulation induced intensity- and duration-dependent vasodilation and increased cerebral blood flow in both healthy and photothrombotic brains. In SPG-stimulated rats both blood brain-barrier (BBB) opening, pathological brain activity and lesion volume were attenuated compared to untreated stroke animals, with no apparent difference in the glial response surrounding the necrotic lesion.SPG-stimulation in rats induces vasodilation of cortical arterioles, partial reperfusion of the ischemic lesion, and normalization of brain functions with reduced BBB dysfunction and stroke volume. These findings support the potential therapeutic effect of SPG stimulation in focal cerebral ischemia even when applied 24 h after stroke onset and thus may extend the therapeutic window of currently administered stroke medications

The effect of acupuncture duration on analgesia and peripheral sensory thresholds

<p>Abstract</p> <p>Background</p> <p>Acupuncture provides a means of peripheral stimulation for pain relief. However, the detailed neuronal mechanisms by which acupuncture relieves pain are still poorly understood and information regarding optimal treatment settings is still inadequate. Previous studies with a short burst of unilateral electroacupuncture (EA) in the Tendinomuscular Meridians (TMM) treatment model for pain demonstrated a transient dermatomally correlated bilateral analgesic effect with corresponding peripheral modality-specific sensory threshold alterations. However, the impact of EA duration on the analgesic effect in this particular treatment model is unknown. To obtain mechanistically and clinically important information regarding EA analgesia, this current prospective cross-over study assesses the effects of EA duration on analgesia and thermal sensory thresholds in the TMM treatment model.</p> <p>Methods</p> <p>Baseline peripheral sensory thresholds were measured at pre-marked testing sites along the medial aspects (liver and spleen meridians) of bilateral lower extremities. A 5-second hot pain stimulation was delivered to the testing sites and the corresponding pain Visual Analog Scale (VAS) scores were recorded. Three different EA (5Hz) stimulation durations (5, 15 and 30 minutes) were randomly tested at least one week apart. At the last 10 seconds of each EA session, 5 seconds of subject specific HP stimulation was delivered to the testing sites. The corresponding pain and EA VAS scores of de qi sensation (tingling) during and after the EA were recorded. The measurements were repeated immediately, 30 and 60 minutes after the EA stimulation. A four-factor repeat measures ANOVA was used to assess the effect of stimulation duration, time, location (thigh vs. calf) and side (ipsilateral vs. contralateral) of EA on sensory thresholds and HP VAS scores.</p> <p>Results</p> <p>A significant (P < 0.01) main effect of time and location with warm, cold and hot pain thresholds at the four testing sites without any significant difference in duration effect was observed. Similar time and location effects were observed with HP VAS with the longer durations (15 and 30 minutes) of stimulation showed a slower onset, but a more sustainable bilateral analgesic benefit than the short stimulation duration (5 minutes). The 15-minute stimulation resulted in an earlier onset of analgesic effect than the 30-minute stimulation paradigm.</p> <p>Conclusion</p> <p>Longer durations of EA stimulation provide a more sustainable analgesic benefit to hot noxious stimulation than a shorter duration of stimulation. The increase of cold threshold with sustained warm threshold temperature elevation as observed in the longer durations of EA suggests that as the duration of EA lengthened, there is a gradual shifting from an initial predominantly spinally mediated analgesic effect to a supraspinally mediated modulatory mechanism of thermal pain. The 15-minute stimulation appeared to be the optimal setting for treating acute pain in the lower extremities.</p

Altered processing of sensory stimuli in patients with migraine

Migraine is a cyclic disorder, in which functional and morphological brain changes fluctuate over time, culminating periodically in an attack. In the migrainous brain, temporal processing of external stimuli and sequential recruitment of neuronal networks are often dysfunctional. These changes reflect complex CNS dysfunction patterns. Assessment of multimodal evoked potentials and nociceptive reflex responses can reveal altered patterns of the brain's electrophysiological activity, thereby aiding our understanding of the pathophysiology of migraine. In this Review, we summarize the most important findings on temporal processing of evoked and reflex responses in migraine. Considering these data, we propose that thalamocortical dysrhythmia may be responsible for the altered synchronicity in migraine. To test this hypothesis in future research, electrophysiological recordings should be combined with neuroimaging studies so that the temporal patterns of sensory processing in patients with migraine can be correlated with the accompanying anatomical and functional changes

Innocuous pressure sensation requires A-type afferents but not functional ΡΙΕΖΟ2 channels in humans.

The sensation of pressure allows us to feel sustained compression and body strain. While our understanding of cutaneous touch has grown significantly in recent years, how deep tissue sensations are detected remains less clear. Here, we use quantitative sensory evaluations of patients with rare sensory disorders, as well as nerve blocks in typical individuals, to probe the neural and genetic mechanisms for detecting non-painful pressure. We show that the ability to perceive innocuous pressures is lost when myelinated fiber function is experimentally blocked in healthy volunteers and that two patients lacking Aβ fibers are strikingly unable to feel innocuous pressures at all. We find that seven individuals with inherited mutations in the mechanoreceptor PIEZO2 gene, who have major deficits in touch and proprioception, are nearly as good at sensing pressure as healthy control subjects. Together, these data support a role for Aβ afferents in pressure sensation and suggest the existence of an unknown molecular pathway for its detection