Quantum Mechanical Aspects in the Pathophysiology of Neuropathic Pain.

Neuropathic pain is a challenging complaint for patients and clinicians since there are no effective agents available to get satisfactory outcomes even though the pharmacological agents target reasonable pathophysiological mechanisms. This may indicate that other aspects in these mechanisms should be unveiled to comprehend the pathogenesis of neuropathic pain and thus find more effective treatments. Therefore, in the present study, several mechanisms are chosen to be reconsidered in the pathophysiology of neuropathic pain from a quantum mechanical perspective. The mathematical model of the ions quantum tunneling model is used to provide quantum aspects in the pathophysiology of neuropathic pain. Three major pathophysiological mechanisms are revisited in the context of the quantum tunneling model. These include: (1) the depolarized membrane potential of neurons; (2) the cross-talk or the ephaptic coupling between the neurons; and (3) the spontaneous neuronal activity and the emergence of ectopic action potentials. We will show mathematically that the quantum tunneling model can predict the occurrence of neuronal membrane depolarization attributed to the quantum tunneling current of sodium ions. Moreover, the probability of inducing an ectopic action potential in the axons of neurons will be calculated and will be shown to be significant and influential. These ectopic action potentials are generated due to the formation of quantum synapses which are assumed to be the mechanism behind the ephaptic transmission. Furthermore, the spontaneous neuronal activity and the emergence of ectopic action potentials independently from any adjacent stimulated neurons are predicted to occur according to the quantum tunneling model. All these quantum mechanical aspects contribute to the overall hyperexcitability of the neurons and to the pathogenesis of neuropathic pain. Additionally, providing a new perspective in the pathophysiology of neuropathic pain may improve our understanding of how the neuropathic pain is generated and maintained and may offer new effective agents that can improve the overall clinical outcomes of the patients.

GABA Receptors Can Depolarize the Neuronal Membrane Potential via Quantum Tunneling of Chloride Ions: A Quantum Mathematical Study.

GABA (gamma-aminobutyric acid) receptors represent the major inhibitory receptors in the nervous system and their inhibitory effects are mediated by the influx of chloride ions that tends to hyperpolarize the resting membrane potential. However, GABA receptors can depolarize the resting membrane potential and thus can also show excitatory effects in neurons. The major mechanism behind this depolarization is mainly attributed to the accumulation of chloride ions in the intracellular compartment. This accumulation leads to increase in the intracellular chloride concentration and depolarize the Nernst potential of chloride ions. When the membrane potential is relatively hyperpolarized, this will result in a chloride efflux instead of influx trying to reach their depolarized equilibrium potential. Here, we propose different mechanism based on a major consequence of quantum mechanics, which is quantum tunneling. The quantum tunneling model of ions is applied on GABA receptors and their corresponding chloride ions to show how chloride ions can depolarize the resting membrane potential. The quantum model states that intracellular chloride ions have higher quantum tunneling probability than extracellular chloride ions. This is attributed to the discrepancy in the kinetic energy between them. At physiological parameters, the quantum tunneling is negligible to the degree that chloride ions cannot depolarize the membrane potential. Under certain conditions such as early neuronal development, gain-of-function mutations, stroke and trauma that can lower the energy barrier of the closed gate of GABA receptors, the quantum tunneling is enhanced so that the chloride ions can depolarize the resting membrane potential. The major unique feature of the quantum tunneling mechanism is that the net efflux of chloride ions is attained without the need for intracellular accumulation of chloride ions as long as the energy barrier of the gate is reduced but still higher than the kinetic energy of the chloride ion as a condition for quantum tunneling to take place.

Effect of Depth of Total Intravenous General Anesthesia on Intraoperative Electrically Evoked Compound Action Potentials in Cochlear Implantation Surgery.

PURPOSE: This study aims to compare the effect of the depth of total intravenous anesthesia (TIVA) on intraoperative electrically evoked compound action potential (e-ECAP) thresholds in cochlear implant operations. METHODS: Prospectively, a total of 39 patients aged between 1 and 48 years who were scheduled to undergo cochlear implantation surgeries were enrolled in this study. Every patient received both light and deep TIVA during the cochlear implant surgery. The e-ECAP thresholds were obtained during the light and deep TIVA. RESULTS: After comparing the e-ECAP means for each electrode (lead) between the light and deep anesthesia, no significant differences were detected between the light and deep anesthesia. CONCLUSION: The depth of TIVA may have no significant influence on the e-ECAP thresholds as there was no statistical difference between the light and deep anesthesia.

Intraoperative angioedema induced by angiotensin II receptor blocker: a case report.

BACKGROUND: Angiotensin II receptor blockers are a class of antihypertensive agent that is developed to exclude the adverse effects of angiotensin converting enzyme inhibitors. However, as angiotensin II receptor blockers have begun to be more widely prescribed, cases of angiotensin II receptor blocker-induced angioedema have been reported. Rare cases of angioedema following surgery in patients using angiotensin converting enzyme inhibitors have been published. CASE PRESENTATION: A 38-year-old man with past history of hypertension was admitted for an elective lumbosacral spine surgery. He had been taking Valsartan 160 mg a day for the past 4 years.At the end of the surgical procedure and turning the patient into supine position, we noticed severe swelling in the neck and the face with.an edematous tongue, floor of the mouth, glottis, and supraglottic areas. A diagnosis of drug induced angioedema was made and intravenous dexamethasone, diphenhydramine and ranitidine were given. The patient remained intubated and was transferred to the intensive care unit. The valsartan was suspected to be the precipitating factor for the angioedema and was therefore discontinued.The swelling started to regress after 2 h, and resolved completely by the third day. CONCLUSION: The precise mechanism of angiotensin II receptor blocker-induced angioedema is still unknown and should be thoroughly investigated. This report demonstrates a unique case of intraoperative angiotensin II receptor blocker-induced angioedema. Potential differential diagnoses of postoperative facial edema are discussed in detail, including the prolonged prone positioning for posterior spine surgery. Anesthesiologists should be aware of such rare, but potentially dangerous, perioperative adverse reaction that can occur with angiotensin II receptor blockers use.