Restoring function to peripheral nerves with a gap is challenging, with <50% of patients undergoing nerve repair surgery recovering function. Sensory nerve grafts (autografts) are the clinical “gold standard” for bridging nerve gaps to restore sensory and motor function. They have significant limitations and restore meaningful function only across short gaps when repairs are performed soon after trauma and patients are young. When the value of any of these variables is large, the extent of recovery decreases precipitously, and when two or all are simultaneously large, there is little to no recovery. The extent of restored meaningful recovery has not increased in almost 70 years. Thus, novel techniques are needed that enhance both the extent of recovery and the percentage of patients who recover meaningful recovery. This paper reviews the limitations of autografts and other materials used to repair nerves. It also examines autologous platelet-rich plasma (PRP), a promising nerve gap repair technique that induces recovery in clinical settings where autografts are ineffective, including when the values of all three variables are simultaneously large.

About 0.5% of the US population (1.7 million) is living with a lost limb and this number is expected to double by 2050. This number is much higher in other parts of the world. Within days to weeks of an extremity amputation, up to 80% of these individuals develop neuropathic pain presenting as phantom limb pain (PLP). The level of PLP increases significantly by one year and remains chronic and severe for about 10% of individuals. PLP has a serious negative impact on individuals’ lives. Current pain treatment therapies, such pharmacological approaches provide limited to no pain relief, some other techniques applied to the central nervous system (CNS) and peripheral nervous system (PNS) reduce or block PLP, but none produces long-term pain suppression. Therefore, new drugs or novel analgesic methods must be developed that prevent PLP from developing, or if it develops, to reduce the level of pain. This paper examines the potential causes of PLP, and present techniques used to prevent the development of PLP, or if it develops, to reduce the level of pain. Finally it presents a novel technique being developed that eliminates/reduces chronic neuropathic pain and which may induce the long-term reduction/elimination of PLP.

For most adult vertebrates, glaucoma, trauma, and tumors close to retinal ganglion cells (RGCs) result in their neuron death and no possibility of vision reestablishment. For more distant traumas, RGCs survive, but their axons do not regenerate into the distal nerve stump due to regeneration-inhibiting factors and absence of regeneration-promoting factors. The annual clinical incidence of blindness in the United States is 1:28 (4%) for persons >40 years, with the total number of blind people approaching 1.6 million. Thus, failure of optic nerves to regenerate is a significant problem. However, following transection of the optic nerve of adult amphibians and fish, the RGCs survive and their axons regenerate through the distal optic nerve stump and reestablish appropriate functional retinotopic connections and fully functional vision. This is because they lack factors that inhibit axon regeneration and possess factors that promote regeneration. The axon regeneration in lower vertebrates has led to extensive studies by using them as models in studies that attempt to understand the mechanisms by which axon regeneration is promoted, so that these mechanisms might be applied to higher vertebrates for restoring vision. Although many techniques have been tested, their successes have varied greatly from the recovery of light and dark perceptions to partial restoration of the optomotor response, depth perception, and circadian photoentrainment, thus demonstrating the feasibility of reconstructing central circuitry for vision after optic nerve damage in mature mammals. Thus, further research is required to induce the restoration of vision in higher vertebrates. This paper examines the causes of vision loss and techniques that promote transected optic nerve axons to regenerate and reestablish functional vision, with a focus on approaches that may have clinical applicability.