Use of epidurography in the perioperative and acute pain setting.

Ensuring proper placement of epidural catheters is critical to improving their reliability for pain control and maintaining confidence in their continued use. This article will seek to address the role of objective confirmation of successful epidural placement via either single view or continuous epidural contrast studies, each creating an 'epidurogram.' Furthermore, the pertinent anatomical corollaries of continuous fluoroscopy used frequently in chronic pain medicine, from which these techniques emerged, will be addressed.

Impact of a perioperative oral opioid substitution protocol during the nationwide intravenous opioid shortage: A single center, interrupted time series with segmented regression analysis.

Introduction: To mitigate the recent nationwide shortage of intravenous opioids, we developed a standardized perioperative oral opioid guideline anchored with appropriate use of nonopioid analgesia, neuraxial and loco-regional techniques. We hypothesize that adoption of this new guideline was associated with: 1) equivalent patient reported pain scores in the post-anesthesia care unit (PACU); and 2) equivalent total opioid use (oral and parenteral) during the perioperative period.

Methods: Cases performed from July 1, 2017 to May 31, 2019 were screened.

A review and survey of policies utilized for interventional pain procedures: a need for consensus.

Background: Other than the newly published anticoagulation guidelines, there are currently few recommendations to assist pain medicine physicians in determining the safety parameters to follow when performing interventional pain procedures. Little information exists regarding policies for oral intake, cumulative steroid dose limits, driving restrictions with and without sedation, and routine medication use for interventional procedures.

Methods: A 16-question survey was developed on common policies currently in use for interventional pain procedures.

Hyperexcitability of rat thalamocortical networks after exposure to general anesthesia during brain development.

Prevailing literature supports the idea that common general anesthetics (GAs) cause long-term cognitive changes and neurodegeneration in the developing mammalian brain, especially in the thalamus. However, the possible role of GAs in modifying ion channels that control neuronal excitability has not been taken into consideration. Here we show that rats exposed to GAs at postnatal day 7 display a lasting reduction in inhibitory synaptic transmission, an increase in excitatory synaptic transmission, and concomitant increase in the amplitude of T-type calcium currents (T-currents) in neurons of the nucleus reticularis thalami (nRT).

Reversal of neuropathic pain in diabetes by targeting glycosylation of Ca(V)3.2 T-type calcium channels.

It has been established that Ca(V)3.2 T-type voltage-gated calcium channels (T-channels) play a key role in the sensitized (hyperexcitable) state of nociceptive sensory neurons (nociceptors) in response to hyperglycemia associated with diabetes, which in turn can be a basis for painful symptoms of peripheral diabetic neuropathy (PDN). Unfortunately, current treatment for painful PDN has been limited by nonspecific systemic drugs with significant side effects or potential for abuse.

TTA-P2 is a potent and selective blocker of T-type calcium channels in rat sensory neurons and a novel antinociceptive agent.

Several agents that are preferential T-type calcium (T-channel) blockers have shown promise as being effective in alleviating acute and chronic pain, suggesting an urgent need to identify even more selective and potent T-channel antagonists. We used small, acutely dissociated dorsal root ganglion (DRG) cells of adult rats to study the in vitro effects of 3,5-dichloro-N-[1-(2,2-dimethyl-tetrahydro-pyran-4-ylmethyl)-4-fluoro-piperidin-4-ylmethyl]-benzamide (TTA-P2), a derivative of 4-aminomethyl-4-fluoropiperdine, on T currents, as well as other currents known to modulate pain transmission. We found that TTA-P2 potently and reversibly blocked DRG T currents with an IC(50) of 100 nM and stabilized channel in the inactive state, whereas high-voltage-activated calcium and sodium currents were 100- to 1000-fold less sensitive to channel blocking effects.

Free radical signalling underlies inhibition of CaV3.2 T-type calcium channels by nitrous oxide in the pain pathway.

Nitrous oxide (N2O, laughing gas) has been used as an anaesthetic and analgesic for almost two centuries, but its cellular targets remain unclear. Here, we present a molecular mechanism of nitrous oxide's selective inhibition of CaV3.2 low-voltage-activated (T-type) calcium channels in pain pathways.