How Localized Grounding, Combined with Conductive Skincare, Improves the Outcomes of the Traditional Skincare?

The main goals of acute and long-term skincare are the protection and improvement of skin health and integrity. Skincare involves several procedures that help maintain the skin's integrity, improve its appearance, and alleviate skin problems. Proper blood flow is in dire need for the skin to absorb vital ingredients. There are many conventional treatments to help increase blood flow and recently it was discovered that connecting the with the electrical charges of the Earth, or “Grounding” can promote healthy blood flow in the facial region. Additionally, such effects of grounding do not seem limited to the facial region but are rather systemic, essential and are often quickly observable. Grounding also seems to reduce secondary injury, collateral sprouting, and nerve sensitization. In grounded patients, an increase in blood flow was clearly seen when compared directly to ungrounded subjects. The results of documented studies explain that even short contact with the Earth helps to restore blood flow regulation suggesting enhanced skin tissue repair and improved skin appearance with possible implications for overall health.

Mechanisms Lead towards Improved Health: Massage with Earthing

Massage can alleviate the inflammatory process, help to accelerate recovery, and relieve pain resulting from muscular injuries. In this paper, we combine the idea of mechanotransduction (conversion of mechanical stimulus into electrochemical activity) using grounding in massage to investigate beneficial mechanisms. Grounding massage has been discovered to stabilize the physiology of the body, help reduce pain, inflammation, stress, enhance sleep, increase energy, and blood flow, and enhance well-being by connecting the body with the electrical charges of the Earth. Such effects are systemic and basic, and often quickly evolve. This process can reduce secondary injury, collateral sprouting, and nerve sensitization by modifying inflammatory signaling pathways, resulting in improved damage recovery and pain reduction or prevention. Research shows that grounding, when simultaneously combined with many CAM clinical practices, can offer great potential to improve their effectiveness. The paper aims to explain how massage therapy, combined with geographically and simultaneous earthing, causes a potentially beneficial and properly activated immunomodulatory pathway.

Chondroitinase ABC Promotes Axon Regeneration and Reduces Retrograde Apoptosis Signaling in Lamprey

Paralysis following spinal cord injury (SCI) is due to failure of axonal regeneration. It is believed that axon growth is inhibited by the presence of several types of inhibitory molecules in central nervous system (CNS), including the chondroitin sulfate proteoglycans (CSPGs). Many studies have shown that digestion of CSPGs with chondroitinase ABC (ChABC) can enhance axon growth and functional recovery after SCI. However, due to the complexity of the mammalian CNS, it is still unclear whether this involves true regeneration or only collateral sprouting by uninjured axons, whether it affects the expression of CSPG receptors such as protein tyrosine phosphatase sigma (PTPσ), and whether it influences retrograde neuronal apoptosis after SCI. In the present study, we assessed the roles of CSPGs in the regeneration of spinal-projecting axons from brainstem neurons, and in the process of retrograde neuronal apoptosis. Using the fluorochrome-labeled inhibitor of caspase activity (FLICA) method, apoptotic signaling was seen primarily in those large, individually identified reticulospinal (RS) neurons that are known to be “bad-regenerators.” Compared to uninjured controls, the number of all RS neurons showing polycaspase activity increased significantly at 2, 4, 8, and 11 weeks post-transection (post-TX). ChABC application to a fresh TX site reduced the number of polycaspase-positive RS neurons at 2 and 11 weeks post-TX, and also reduced the number of active caspase 3-positive RS neurons at 4 weeks post-TX, which confirmed the beneficial role of ChABC treatment in retrograde apoptotic signaling. ChABC treatment also greatly promoted axonal regeneration at 10 weeks post-TX. Correspondingly, PTPσ mRNA expression was reduced in the perikaryon. Previously, PTPσ mRNA expression was shown to correlate with neuronal apoptotic signaling at 2 and 10 weeks post-TX. In the present study, this correlation persisted after ChABC treatment, which suggests that PTPσ may be involved more generally in signaling axotomy-induced retrograde neuronal apoptosis. Moreover, ChABC treatment caused Akt activation (pAkt-308) to be greatly enhanced in brain post-TX, which was further confirmed in individually identified RS neurons. Thus, CSPG digestion not only enhances axon regeneration after SCI, but also inhibits retrograde RS neuronal apoptosis signaling, possibly by reducing PTPσ expression and enhancing Akt activation.

Age-related Changes in Motor Function (I). Mechanical and Neuromuscular Factors

This two-part narrative review aims to provide an insight into the age-related mechanical and neuromuscular factors contributing to: (1) decreased maximal muscle strength and power; (2) decreased force control; and (3) increased fatigability. Structural and functional changes from the macro-level of the muscle-tendon unit to the micro-level of the single muscle fibre have been reviewed and are described. At the muscle-tendon unit level, muscle volume, thickness and cross-sectional area, as well as pennation angle and fascicle length all decrease as part of the natural ageing process. These changes negatively affect muscle quality, muscle and tendon stiffness and Young’s modulus and account for impairment in motor performance. A progressive age-related alteration in neuromuscular function is also well-established, with reduction in number and firing rate of the motor unit, contractile velocity and specific tension of muscle fibres, and stability of neuromuscular junction. These could be the result of structural alterations in the: (i) motor neuron, with number reduced, size and collateral sprouting increased; (ii) neuromuscular junction, with decreased post-synaptic junctional fold and density of active zones and increased pre-synaptic branching and post-synaptic area; and (iii) muscle fibre, with decreased number and size and increased type I and co-expression of myosin heavy chain.

Facial Sensory Restoration After Trigeminal Sensory Rhizotomy by Collateral Sprouting From the Occipital Nerves

BACKGROUND AND IMPORTANCE Lesioning procedures are effective for trigeminal neuralgia (TN), but late pain recurrence associated with sensory recovery is common. We report a case of recurrence of type 1A TN and recovery of facial sensory function after trigeminal rhizotomy associated with collateral sprouting from upper cervical spinal nerves. CLINICAL PRESENTATION A 41-yr-old woman presented 2 yr after open left trigeminal sensory rhizotomy for TN with pain-free anesthesia in the entire left trigeminal nerve distribution. Over 18 mo, she developed gradual recovery of facial sensation migrating anteromedially from the occipital region, eventually extending to the midpupillary line across the distribution of all trigeminal nerve branches. She reported recurrence of her triggered lancinating TN pain isolated to the area of recovered sensation with no pain in anesthetic areas. Nerve ultrasound demonstrated enlargement of ipsilateral greater and lesser occipital nerves, and occipital nerve block restored facial anesthesia and resolved her pain, indicating that recovered facial sensation was provided exclusively by the upper cervical spinal nerves. She underwent C2/C3 ganglionectomy, and ganglia were observed to be hypertrophic. Postoperatively, trigeminal anesthesia was restored with complete resolution of pain that persisted at 12-mo follow-up. CONCLUSION This is the first documented case of a spinal nerve innervating a cranial dermatome by collateral sprouting after cranial nerve injury. The fact that typical TN pain can occur even when sensation is mediated by spinal nerves suggests that the disorder can be centrally mediated and late failure after lesioning procedures may result from maladaptive reinnervation.

Injury-free priming: induction of Primary Afferent Collateral Sprouting in uninjured sensory neurons in vivo primes them for enhanced axon outgrowth in vitro

Prior “conditioning” nerve lesions can prime DRG neurons for enhanced axon regeneration. Here, we tested the hypothesis that adult DRG neurons can be primed for axon elongation in vitro without axonal injury by prior induction of Primary Afferent Collateral Sprouting (PACS) in vivo. Thoracic cutaneous nerves (T9, T10, T12, T13 but not T11) were transected to create zones of denervated skin. Neurons from the uninjured T11 DRG underwent PACS within the skin, as demonstrated by the expansion of its zones responsive to pinch up to 14 days. At 7 or 14 days after induction of collateral sprouting, DRG neurons were dissociated and cultured for 18 hours in defined media lacking neurotrophins and growth factors. Neurons from the uninjured T11 DRG had longer mean neurite lengths than neurons from naïve DRG. A larger proportion of neurons from the uninjured T11 DRG showed an elongating or arborizing phenotype than neurons from naïve DRG. Transcriptomic analysis of the uninjured T11 DRG and denervated/reinnervated skin reveal regulation of receptor/ligand systems and regulators of growth during collateral sprouting. For example, the glial cell-derived neurotrophic family ligands Artemin and Persephin were upregulated in denervated skin after 7 and/or 14 days. We suggest that extracellular cues in denervated skin modify the intrinsic growth program of uninjured DRG neurons that enhances their ability to elongate or arborize even after explantation. Collectively, these data confirm that induction of collateral sprouting does not induce an injury response yet primes many of these uninjured neurons for in vitro axon growth.

Dynamic Quantitative Assessment of Motor Axon Sprouting after Direct Facial–Hypoglossal End-To-Side Neurorrhaphy in Rats

Background End-to-side (ETS) neurorrhaphy is a promising procedure for peripheral nerve repair, yet controversies regarding the efficacy of this repair in facial nerve anastomosis for facial paralysis still exist. Materials and Methods Thirty rats were divided into three groups: intact control group, direct facial–hypoglossal ETS neurorrhaphy, and end-to-end (ETE) neurorrhaphy. Nerve regeneration was assessed with vibrissae motor performance, electrophysiological tests, retrograde labeling, and histomorphological analysis at 4 and 8 months postoperatively. Results Both ETS and ETE neurorrhaphies resulted in axonal regeneration and functional recovery of the recipient nerve but did not reach the level of intact controls. Significantly higher numbers of myelinated axons and labeled neurons giving regenerating fibers were found in group ETE compared with group ETS at both time points, consistent with the functional and electrophysiological recovery. Group ETS showed significantly smaller fiber diameter and thinner myelin thickness than group ETE at 4 months, but the difference became nonsignificant at 8 months. ETS neurorrhaphy had a very slight effect on the donor nerve, as determined electrophysiologically and histomorphologically. Sparsely distributed double-labeled neurons and relatively large amounts of single-labeled neurons contributing to reinnervation were found through double retrograde neuronal labeling in group ETS. Further quantitative analysis of the percentage of double-labeled neurons showed a pronounced tendency to decline from 19.8% at 4 months to 6.0% at 8 months postoperatively. Conclusion Successful reinnervation after ETS neurorrhaphy could be achieved through both collateral sprouting and terminal sprouting, with the latter seeming to be the principal origin of motor nerve sprouting.