Suppression of Pain in the Late Phase of Chronic Trigeminal Neuropathic Pain Failed to Rescue the Decision-Making Deficits in Rats

Trigeminal neuropathic pain (TNP) led to vital cognitive functional deficits such as impaired decision-making abilities in a rat gambling task. Chronic TNP caused hypomyelination in the anterior cingulate cortex (ACC) associated with decreased synchronization between ACC spikes and basal lateral amygdala (BLA) theta oscillations. The aim of this study was to investigate the effect of pain suppression on cognitive impairment in the early or late phases of TNP. Blocking afferent signals with a tetrodotoxin (TTX)-ELVAX implanted immediately following nerve lesion suppressed the allodynia and rescued decision-making deficits. In contrast, the TTX used at a later phase could not suppress the allodynia nor rescue decision-making deficits. Intra-ACC administration of riluzole reduced the ACC neural sensitization but failed to restore ACC-BLA spike-field phase synchrony during the late stages of chronic neuropathic pain. Riluzole suppressed allodynia but failed to rescue the decision-making deficits during the late phase of TNP, suggesting that early pain relief is important for recovering from pain-related cognitive impairments. The functional disturbances in ACC neural circuitry may be relevant causes for the deficits in decision making in the chronic TNP state.

Ultrasound Guided Continuous Sciatic Nerve Block for Acute Herpetic Neuralgia

Herpes Zoster (HZ) is the reactivation of a well-known viral disease which manifests itself with painful skin lesions. An effective analgesic method during the acute phase of HZ can contribute to decrease the incidence of postherpetic neuralgia (PHN) by reducing neural sensitization. Sciatic nerve block (SNB) is useful in the management of distal lower extremity pain sustained by the sciatic nerve. We describe our experience with a continuous ultrasound guided subgluteus sciatic nerve block in a patient with herpetic neuralgia- (HN-) related refractory acute left leg pain.

Phantom Pain

This chapter discusses phantom pain, defined as an unpleasant or painful sensation in the distribution of the lost or deafferentiated body part. It is more commonly reported in the limbs but also has been reported in other body parts such as the tongue, teeth, nose, breast, part of the gastrointestinal tract, and the penis. The incidence varies from 42.2% to 78.8%. Perception of non-painful sensations from the amputated body part is known as phantom sensation. The severity and frequency of attacks slowly decrease with time during the first 6 months, after which they remain constant. Patients with significant preoperative pain, stump pain, and infection are at increased risk of developing phantom pain. The mechanism of origin is not known; it is thought to be due to peripheral nerve damage, which contributes to neural sensitization at peripheral, spinal, and supraspinal levels. Both chemical mediators and psychological factors are involved. Phantom pain improves with time and responds to conservative medical management, mirror therapy, and psychological counseling. A small percentage of cases are resistant to treatment and may require invasive neuromodulatory treatment options such as spinal cord stimulation and peripheral nerve stimulation.

Neural sensitization improves encoding fidelity in the primate retina

ABSTRACTAn animal’s motion through the environment can induce large and frequent fluctuations in light intensity on the retina. These fluctuations pose a major challenge to neural circuits tasked with encoding visual information, as they can cause cells to adapt and lose sensitivity. Here, we report that sensitization, a short-term plasticity mechanism, solves this difficult computational problem by maintaining neuronal sensitivity in the face of these fluctuations. The numerically dominant output pathway in the macaque monkey retina, the midget (parvocellular-projecting) pathway, undergoes sensitization under specific conditions, including simulated eye movements. Sensitization is present in the excitatory synaptic inputs from midget bipolar cells and is mediated by presynaptic disinhibition from wide-field amacrine cells. Direct physiological recordings and a computational model indicate that sensitization in the midget pathway supports accurate sensory encoding and prevents a loss of responsiveness during dynamic visual processing.

Exposure to Allergen Causes Changes in NTS Neural Activities after Intratracheal Capsaicin Application, in Endocannabinoid Levels and in the Glia Morphology of NTS

Allergen exposure may induce changes in the brainstem secondary neurons, with neural sensitization of the nucleus solitary tract (NTS), which in turn can be considered one of the causes of the airway hyperresponsiveness, a characteristic feature of asthma. We evaluated neurofunctional, morphological, and biochemical changes in the NTS of naive or sensitized rats. To evaluate the cell firing activity of NTS, in vivo electrophysiological experiments were performed before and after capsaicin challenge in sensitized or naive rats. Immunohistochemical studies, endocannabinoid, and palmitoylethanolamide quantification in the NTS were also performed. This study provides evidence that allergen sensitization in the NTS induced: (1) increase in the neural firing response to intratracheal capsaicin application, (2) increase of endocannabinoid anandamide and palmitoylethanolamide, a reduction of 2-arachidonoylglycerol levels in the NTS, (3) glial cell activation, and (4) prevention by a Group III metabotropic glutamate receptor activation of neural firing response to intratracheal application of capsaicin in both naïve and sensitized rats. Therefore, normalization of ovalbumin-induced NTS neural sensitization could open up the prospect of new treatments based on the recovery of specific brain nuclei function and for extensive studies on acute or long-term efficacy of selective mGlu ligand, in models of bronchial hyperreactivity.