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Salivary Gland Tumours
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
Facial weakness: Facial nerve injury is a significant morbidity. Risk of facial nerve damage is related to the extent of the disease, type of resection, and surgical experience. Neuropraxia usually recovers within 4–6 weeks, and more severe injuries, in 6–12 months. Risk of permanent facial palsy is 1–2%.
Nerve
Published in Manoj Ramachandran, Tom Nunn, Basic Orthopaedic Sciences, 2018
Mike Fox, Caroline Hing, Sam Heaton, Rolfe Birch
The degree of nerve injury affects the outcome. A neurapraxia comprises a transient concussion or crushing of the nerve. There is no Wallerian degeneration (see below), but instead there is a block to flow of nerve impulses, with consequent interruption of physical function. A neurapraxia has a favourable outcome, provided the source of the injury is removed. Axonotmesis and neuronotmesis have less favourable outcomes as they are degenerative lesions.
Benign Salivary Gland Tumours
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
The risk of temporary or permanent facial weakness must be carefully explained as it has a very significant impact on quality of life. The risk of facial nerve damage is related to the extent of the disease, the type of resection and the experience of the surgeon. Neuropraxia usually recovers within 4–6 weeks. More severe injuries cause some degree of degeneration and recovery may never be complete and take 6–12 months or even longer to take place. The risk of permanent facial palsy is in the region of 1–2%.20 There is a lack of clear data regarding more detail on facial nerve outcomes after parotid surgery, with grading data for example.
Current concepts review: peripheral neuropathies of the shoulder in the young athlete
Published in The Physician and Sportsmedicine, 2020
Tamara S. John, Felicity Fishman, Melinda S. Sharkey, Cordelia W. Carter
Peripheral neuropathies of the shoulder and upper extremity in the young athletic population – older children, adolescents and young adults – are uncommon, yet may result in significant pain and impairment. It is therefore important to understand the relevant anatomy, common injury mechanisms, characteristic clinical presentation, pertinent physical examination findings, diagnostic tools, treatment options and functional outcomes for these injuries. Furthermore, familiarity with standard terminology for nerve injuries is essential. Neuropraxia is the mildest nerve injury type, in which the nerve structure and its primary elements remain intact, but the myelin sheath is disrupted. The cause of a neurapraxia is typically a stretch mechanism and neurapraxias are often associated with complete functional recovery. Axonotmesis is a nerve injury in which the axon itself is disrupted in addition to its myelin sheath, although the endoneurial tubes and supportive tissues (perineurium, epineurium) remain intact. The mechanism of axonotmesis is typically a more severe stretch or crushing-type injury of the neural tissue. Finally, neurotmesis is the most severe form of nerve injury, in which there is complete nerve disruption. Neurotmetic injuries have the least potential for recovery. Fortunately, most sports-related peripheral neuropathies are either neurapraxic or axonotmetic in nature, rather than fully neurotmetic.
Great toe drop following knee ligament reconstruction: A case report
Published in Physiotherapy Theory and Practice, 2020
David A Boyce, Chantal Prewitt
Nerve injuries can be classified as neuropraxia, axonotmesis, and neurotmesis (Seddon, 1943). Neuropraxia injuries result in temporary interruption of nerve conduction without axonal injury and slowing or conduction blocks across nerve segments. EMG does not show signs of axonal loss, and recovery can take place days or weeks following injury. Axonotmesis injuries involve both myelin and axons, can result in sensory and motor NCS deficits distal to the site of injury, demonstrate signs of axonal loss (i.e., positive sharp waves and fibrillation potentials) in muscles distal to the site of injury, and based on the severity of the injury can regenerate. Neurotmesis injury is the most severe type, which results in total disruption or severance of the peripheral nerve. Neurotmesis injuries result in sensory and motor nerve deficits distal to the site of injury, demonstrate signs of axonal loss in muscles distal to the site of injury, and often require surgical repair.
Differential diagnosis of knee pain following a surgically induced lumbosacral plexus stretch injury. A case report
Published in Physiotherapy Theory and Practice, 2019
William R. VanWye, Harvey W. Wallmann, Elizabeth S. Norris, Karen E. Furgal
Interestingly, peripheral nerve, which is uniquely complex tissue, is the only soft tissue that does not follow the classic physiological phases of healing (Bélanger, 2015). Seddon classified peripheral nerve injury into 3 degrees of injury. The least severe is neurapraxia, followed by axonotmesis, and finally, the most severe form, neurotmesis (Burnett and Zager, 2004). Neurapraxia is a functional injury meaning there is focal demyelination, which is transient in nature. Axonotmesis and neurotmesis are not only functional, but also anatomical, which entails a disruption of nerve continuity (Burnett and Zager, 2004). A neurapraxia can range from 1 day to 3 months with full recovery expected. Axonotmesis has the most variability in recovery time and prognosis. Sunderland further divides axonotmesis into three classifications (i.e. Sunderland II–IV). In Sunderland II axonotmesis, the axon is injured, but the endoneurial tube is normal. This generally results in full recovery in 1–6 months. In Sunderland III axonotmesis, the endoneurial tube is injured; in this case, the recovery is less certain with partial return expected in 12–24 months. Lastly, with the Sunderland IV axonotmesis, only the epineurium is intact (i.e. the outer layer of the nerve) and recovery requires surgical intervention. Neurotmesis is a loss of nerve continuity, requiring surgical intervention with unpredictable recovery (Goubier and Teboul, 2015). Considering the patient’s steady progress and full recovery, the stretch injury appeared to be consistent with either a neurapraxia or Sunderland II axonotmesis.