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Neurophotonics for Peripheral Nerves
Published in Yu Chen, Babak Kateb, Neurophotonics and Brain Mapping, 2017
Ashfaq Ahmed, Yuqiang Bai, Jessica C. Ramella-Roman, Ranu Jung
Nerve fibers, both afferent and efferent, are grouped in fascicles surrounded by connective tissue in the peripheral nerve (Peters and Palay, 1991). The fascicular architecture changes with an increasing number of fascicles of smaller size from the proximal to the distal end of the nerve. These fascicles eventually give origin to branches that innervate distinct targets, either muscular or cutaneous. In addition to bundles of nerve fibers, the peripheral nerves are composed of three supportive sheaths: epineurium, perineurium, and endoneurium. The epineurium is the outermost layer, composed of loose connective tissue and carries blood vessels that supply the nerve. The perineurium surrounds each fascicle in the nerve. It consists of inner layers of flat perineurial cells and an outer layer of collagen fibers organized in longitudinal, circumferential, and oblique bundles. The perineurium is the main contributor to the tensile strength of the nerve, acts as a diffusion barrier, and maintains the endoneurial fluid pressure. The endoneurium is composed of fibroblasts, collagen and reticular fibers, and extracellular matrix, occupying the space between nerve fibers within the fascicle. The endoneurial collagen fibrils are packed around each nerve fiber to form the walls of the endoneurial tubules. Inside these tubules, axons are accompanied by Schwann cells, which either myelinate or just surround the axons (Peters and Palay, 1991).
Spinal Cord and Reflexes
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
In a manner exactly analogous to skeletal muscle (Figure 9.1), the individual nerve fibers of a peripheral nerve are surrounded by a thin layer of connective tissue, the endoneurium. Groups of nerve fibers are bundled together into fascicles that are surrounded in turn by another layer of connective tissue, the perineurium. The whole nerve is ensheathed by a layer of connective tissue, the epineurium. Blood vessels run between the fascicles.
Mechanism of peripheral nerve modulation and recent applications
Published in International Journal of Optomechatronics, 2021
Heejae Shin, Minseok Kang, Sanghoon Lee
The main structure of the PNS is a nerve that has an enclosed structure like a cable bundle in which neurons are gathered, playing the role of the passage for the electrochemical signals. As shown in Figure 1(a), a neuron consists of a cell body with the nucleus, a dendrite that receives nerve signals, generating an action potential when the signals exceed the threshold, and an axon that transmits the generated signals to an axon terminal to transfer the signal to another neuron. In some cases, this axon is covered with a myelin sheath, making the speed transmission is significantly faster compared to the unmyelinated neurons, which are covered with connective tissue called the endoneurium. In addition, the axon terminal forms a synapse with adjacent neurons, in which the electrical signal transmitted through the axon is converted into a chemical signal by releasing a molecule called a neurotransmitter that is a chemical messenger inhibiting or activating the neuron by influencing the receptor on the targeted neuron or organ. The aggregate of these nerve fibers is called a fascicle, and this fascicle is surrounded by connective tissue called the perineurium. Inside the fascicle, afferent fibers that send afferent (sensory) signals to the CNS and efferent fibers that send efferent (motor) signals from the CNS could be both located in a fascicle or a nerve which is called a mixed nerve fiber. The group of fascicles is called a nerve. A nerve is surrounded by epineurium, and it also consists of blood vessels that provide nutrients for the whole structure. (Figure 1(b)).[10]
Current devices used for the monitoring of injection pressure during peripheral nerve blocks
Published in Expert Review of Medical Devices, 2018
The risk of nerve injury during PNB may be reduced by the use of several monitors, such as ultrasound-guidance and nerve stimulation, although data supporting a definitive safety advantage with these technologies are lacking. Recently, an association between opening injection pressure (OIP) and subsequent nerve injury has been demonstrated in animal models [5–7]. These studies suggest that resistance to flow during the commencement of injection may indicate a needle tip location within a fascicle of the nerve, a condition that has long been known to result in axonal damage [8,9]. Cadaveric studies have confirmed a relationship between intraneural and/or intrafascicular needle tip placement and difficulty generating flow unless very high (>20 psi) pressures are used [10,11]. Taken together, these studies have led to the concept of prevention of nerve injury during PNBs through injection pressure monitoring. Those who advocate for its use have suggested a ‘safe’ limit for OIP of approximately 15–20 psi, based on the available animal and cadaveric data [5–7,10,11]. In addition to serving as a warning of intraneural/intrafascicular needle-tip placement, injection pressure monitoring has been shown to be able to predict needle-nerve contact in both interscalene and femoral nerve block models [12,13]; this may help to prevent inadvertent injection against a nerve structure or the injection into the epineurium via a needle that is partially lodged in the outer covering of the nerve. High injection pressures have also been demonstrated to increase the incidence of inadvertent epidural spread during both lumbar plexus block, and interscalene brachial plexus block [14,15].
Percutaneous cryoneurolysis for acute pain management: current status and future prospects
Published in Expert Review of Medical Devices, 2021
John J. Finneran IV, Brian M. Ilfeld
When nerve tissue is frozen, varying degrees of injury can be produced in a temperature dependent manner: When a nerve is frozen but the temperature does not drop below −20°C, neuropraxia occurs resulting in injury to the nerve not severe enough to cause degeneration of the axons. This generally induces a block lasting minutes to weeks [11].At temperatures between −20 and −100°C, axonal injury occurs and nerves undergo Wallerian degeneration. This phenomenon, eponymously named after Augustus Volney Waller, a British neurophysiologist, describes the process of axonal death distal to a site of injury occurring due to the fact that the nuclei and genetic information are contained in the proximal end of the cell. Importantly, at temperatures warmer than −100°C, the connective tissue surrounding the axon, consisting of endoneurium, perineurium, and epineurium, is not injured and remains intact. Axons can then regenerate at a rate of 1–2 mm per day along the surviving skeleton to reinnervate the tissue at the terminal nerve endings [12]. Thus, cryoneurolysis is successfully achieved at temperatures between −20 and −100°C [13,14]. Carbon dioxide and nitrous oxide, which respectively freeze to −55°C and −70°C via the Joule Thomson effect are the two most commonly used gases for cryoneurolysis. As the treated nerves regenerate at 1–2 mm per day, the duration of the induced block is variable, but proportional to the distance between the cryoneurolysis site and the terminal nerve branches responsible for the pain signals.When nerves are frozen to temperatures below −100°C, the connective tissues sheath around the nerve suffers irreversible injury (neurotmesis) and axons will not regenerate to reinnervate the tissue [11].