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The Facial Nerve
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Christopher Skilbeck, Samuel MacKeith
An injury that physically separates axons from their cell bodies triggers cellular events at the site of the lesion and in distant parts of the injured neurons and their target organs, which has a significant impact on outcome. Wallerian degeneration refers to the degeneration of a nerve distal to the site of injury. Peripherally, atrophy of chronically denervated muscles may preclude their reinnervation. Table 21.1 shows the Seddon and Sunderland classifications of nerve injury.
Peripheral Nerve Examination
Published in J. Terrence Jose Jerome, Clinical Examination of the Hand, 2022
Nikhil Agrawal, Chaitanya Mudgal
These tests are immensely helpful when evaluating if an ulnar nerve palsy is improving after repair or a first- or second-degree Sunderland injury. A first-degree Sunderland injury is one in which axonal continuity is preserved and there is only a temporary conduction block. No Wallerian degeneration occurs and therefor the nerve will recover. In a second-degree Sunderland injury, Wallerian degeneration does occur, however the nerve can recover without surgical intervention due to the intact endoneurium. In these cases, recovery should be monitored closely utilizing these two-point discrimination and Semmes–Weinstein monofilaments [5,10].
Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Lesions of the nerves are associated with characteristic degenerative changes of injured nerve cells.161 These changes are primary or secondary, depending on the initial integrity of the axon and its interaction with the myelin sheath and the Schwann cell. Severing the axon triggers the degeneration process of the myelin sheath which is completely and irreversibly destroyed so that regeneration cannot be accomplished. Demyelination also occurs both in the central and the peripheral nervous system as the result of a primary demyelinating disease or secondary degeneration. In degenerative processes the neuron and its myelinsheath undergo structural destruction. Characteristic changes take place in Wallerian degeneration peripheral to the point of damage. Other conditions also produce secondary demyelination, including metabolic disorders, cerebral edema, anoxia, a variety of neuron intoxications, and tract compression.
The expanding role of chronic pain interventions in multimodal perioperative pain management: a narrative review
Published in Postgraduate Medicine, 2022
Ying Ye, Rodney A. Gabriel, Edward R. Mariano
Cryoneurolysis, or cryoanalgesia, in which targeted nerves are temporarily ablated using low temperatures, is an established chronic pain procedure that has shown recent potential as an acute pain management modality in the perioperative setting. Using agents such as carbon dioxide or nitrous oxide, cryoneurolysis causes second-degree injury to the peripheral nerve and temporarily blocks nerve conduction with resulting analgesia. The nerves undergo reversible Wallerian degeneration followed by slow regeneration of the nerve[21]. Recent developments in percutaneous cryoneurolysis devices have allowed the application of this technique beyond chronic pain treatment[22]. In one case study, patients undergoing mastectomy procedures received ultrasound-guided percutaneous cryoneurolysis to the intercostal nerves; all three patients reported no pain or opioid use during the postoperative period[23]. Preoperative cryoneurolysis has also been effective in controlling postoperative pain in patients undergoing rotator cuff repair[24], TKA[24], and limb amputation[25]. Case reports also describe effective use of cryoneurolysis in the postoperative setting for refractory surgical pain [26] and phantom limb pain[25]. Experiences from these case reports suggest an increasing role of cryoneurolysis in acute pain management.
Potential Effects of Stem Cells Derived from the Peripheral Nerve and Adipose Tissue after the Nerve Crush Injury in Control and Obese Rats
Published in Journal of Investigative Surgery, 2022
Elif Kayhan Kustepe, Berrin Zuhal Altunkaynak, Işınsu Alkan, Elfide Gizem Kivrak, Alişan Yildiran, Stefano Geuna
The peripheral nerve damage is a fairly common problem. The nerve damaged by various reasons has mechanisms that can be self-renewed in the natural process. Peripheral nerve injuries are classified according to different severities. When the damage reaches a certain extent in peripheral nerve injuries, a degeneration process called Wallerian degeneration begins in the nerve. In this process, different changes are observed in the proximal and distal parts of the damaged area, and regeneration proceeds independently. The most important point in nerve regeneration is the physical connection and the nerve whose integrity is disrupted must be brought together physically [16]. Another important issue in this process is that regeneration is affected by body weight. In a study examining obesity and regeneration researchers reported that obesity may cause peripheral neuropathy and decreased cAMP in the median and tibial nerves and a reduction in amplitude of action potential [17]. Watcho et al. (2010) showed that high-fat diet caused pre-diabetic changes and neuropathy in obese rats [18]. However, there are few studies on this subject in the literature [10,18].
Regenerative replacement of neural cells for treatment of spinal cord injury
Published in Expert Opinion on Biological Therapy, 2021
William Brett McIntyre, Katarzyna Pieczonka, Mohamad Khazaei, Michael G. Fehlings
The compressive forces that accompany spinal cord insults are also responsible for oligodendrocyte necrosis and necroptosis within days of the injury, eventually contributing to myelin damage [10,11]. As the injury progresses, accumulation of cytotoxic factors in the microenvironment causes oligodendrocytes to undergo apoptosis in a similar manner to neurons. This ultimately eradicates the associated myelin sheath [11,12]. ROS in the microenvironment can react with the lipids in the cell membrane of myelinating oligodendrocytes and results in the oxidative degradation and peroxidation of lipids (reviewed by Plemel et al. [12]). The products of lipid peroxidation interact with membrane receptors and transcription factors/repressors to induce signaling for apoptosis. This can stimulate the activation of both the intrinsic and extrinsic apoptotic signaling pathways [13]. Moreover, disorganization of the nodes of Ranvier occurs through the diffusion of nodal, paranodal and juxtaparanodal ion channels within hours of the injury, and is found to persist at 6 weeks following injury, ultimately disrupting signal transduction [14,15]. The denuded axons that have lost their metabolic and protective support from the associated myelin sheath are also vulnerable to Wallerian degeneration, which degenerates the neurons that had otherwise been spared during the initial traumatic mechanical insult [16].