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Facial nerve—a clinical and anatomical review
Published in J. Belinha, R.M. Natal Jorge, J.C. Reis Campos, Mário A.P. Vaz, João Manuel, R.S. Tavares, Biodental Engineering V, 2019
Fernand Gentil, J.C. Reis Campos, Marco Parente, C.F. Santos, Bruno Areias, R.M. Natal Jorge
Facial palsy deserves a very special treatment, because it leads to great difficulties for patients to express themselves naturally, and to accept their disfigured face. This condition generates anguish, social networking and professional difficulties, requiring immediate medical treatment Facial palsy refers to the interruption of the motor information to the facial muscles. For the patient, the main complaints are related to the difficulty in closing the eyes, and when smiling. Other symptoms commonly referred include reductions or alterations in taste, dizziness, pain or discomfort, sinusitis, headache, numbness of the tongue, hypersensitivity to noises, dryness of the eye, and difficulty in chewing. Immediate care of the patient is important, since the wallerian degeneration occurs within 24–72 hours after the onset of paralysis (Myckatyn & Mackinnon 2004).
The neurotrophic factor rationale for using brief electrical stimulation to promote peripheral nerve regeneration in animal models and human patients
Published in Ze Zhang, Mahmoud Rouabhia, Simon E. Moulton, Conductive Polymers, 2018
Following peripheral nerve injury, the axons proximal to the injury remain in continuity with the neuronal cell bodies, while the axons that are disconnected undergo Wallerian degeneration (Fu and Gordon 1997). In the latter process, the distal axons lose their myelin sheaths as the Schwann cells revert from a myelinating phenotype to a growth permissive state, and the axons and myelin sheath progressively disintegrate. The Schwann cells initially ingest or phagocytose the myelin and axon debris prior to entry of macrophages into the nerve as the nerve–blood barrier becomes permeable along the length of the distal axons (Avellino et al. 1995; Beuche and Friede 1984; Gaudet et al. 2011; Hirata and Kawabuchi 2002). The latter cells become the prime cells responsible for the bulk of the removal of the debris, with the process taking at least 3 weeks to complete before the macrophages leave the distal nerve stump and the Schwann cells line the empty endoneurial tubes as the bands of Bungner (You et al. 1997). It is these bands that guide the regenerating axons, with the Schwann cells progressively reverting to the myelinating phenotype on contact with the axons (Arthur-Farraj et al. 2012; Lieberman 1971).
Metal bashing: iron deficiency and manganese overexposure impact on peripheral nerves
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Robyn M. Amos-Kroohs, Vanina Usach, Gonzalo Piñero, Charles V. Vorhees, Rocío Martinez Vivot, Paula A. Soto, Michael T. Williams, Patricia Setton-Avruj
Dysfunction of human DMT1 is associated with FeD anemia (Mims et al. 2005; Priwitzerova et al. 2005), Fe overload disorders (Hediger, Rolfs, and Goswami 2002; Rolfs et al. 2002), neurodegenerative diseases (Salazar et al. 2008; Zheng et al. 2009), cancer (Boult et al. 2008; Brookes et al. 2006) and inflammation (Gaudet, Popovich, and Ramer 2011; Martini et al. 2008). Martinez-Vivot et al. (2015) demonstrated a positive correlation between DMT1 protein expression and Fe levels and a negative correlation between DMT1 and MBP protein levels in a model of peripheral Wallerian degeneration. FeD constitutes a direct insult on peripheral myelin, while Wallerian degeneration indirectly affects myelin by interrupting SC-axon cross talk. However, both pathological scenarios induce a fall in MBP levels, which promote a rise in DMT1 to enhance Fe uptake for remyelination/regeneration. Interestingly, MnOE effects on MBP, Fe and DMT1 levels were most evident in the FeD rats, which may reflect heightened sensitivity to Mn-induced toxicity triggered by this common developmental nutritional deficiency.