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Infectious Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Susanna J. Dunachie, Hanif Esmail, Ruth Corrigan, Maria Dudareva
This is a chronic granulomatous disease caused by Mycobacterium leprae and spread by nasal secretions. It can affect many tissues, especially skin and nerves, and it develops slowly. Nerve damage causes motor and sensory loss, which lead to traumatic damage to tissues.
Peripheral Neuropathy
Published in Charles Theisler, Adjuvant Medical Care, 2023
Although there are multiple causes of neuropathy, diabetes and alcohol are the two most common causes. Up to one-half of people with diabetes have peripheral neuropathy. Disorders of peripheral nerves are also the most common neurological complications of systemic amyloidosis. Nutritional disorders such as thiamine deficiency, also known as “dry” beriberi, may cause peripheral neuropathy. Vitamin B12 (cyanocobalamin) deficiency causes neurologic disease, most commonly a combination of spinal cord disease and peripheral nerve disease (myeloneuropathy). Vitamin B6 (pyridoxine) deficiency from severe malabsorption or as a consequence of therapy with isoniazid, cycloserine, hydralazine, or penicillamine can cause peripheral neuropathy.1 Vasculitic neuropathy can also damage nerves. Other factors may further contribute to nerve damage such as injury, high blood pressure, high cholesterol, some drugs, metabolic problems, and smoking.2 Despite the different etiologies leading to neuropathic pain, increased neuronal excitability is thought to be the underlying mechanism for all forms of painful neuropathies.
Psychophysical Measurement of Human Oral Experience
Published in Alan R. Hirsch, Nutrition and Sensation, 2023
Derek J. Snyder, Linda M. Bartoshuk
If a taste or oral pain complaint becomes more intense following oral anesthesia, then it does not arise from normal stimulation of oral sensory receptors. Venous taste sensations and other dysgeusias may be caused by intake of certain therapeutic agents (Bradley 1973; Fetting, Wilcox, Sheidler, Enterline, Donehower, and Grochow 1985; Stephen, McCrossan, Mackenzie, Macfarlane, and Speirs 1980), so the patient’s use of medications and supplements should be reviewed. Another possibility is that the nerve innervating the region of sensory disturbance has sustained physical damage. If damage is peripheral to ganglion cell bodies, the resulting neuroma may produce a nerve-stimulation phantom; topical anesthesia exacerbates nerve-stimulation phantoms via central disinhibition (Bartoshuk, Kveton, Yanagisawa, and Catalanotto 1994). Conclusions involving nerve damage should be confirmed by further neurological examination.
The effect of pulsed radiofrequency application on nerve healing after sciatic nerve anastomosis in rats
Published in Ultrastructural Pathology, 2022
Uğur Ö. Bayır, Recep Aksu, Özlem Öz Gergin, Gozde Ozge Onder, Leman Sencar, Eray Günay, Arzu H. Yay, İbrahim Karaman, Cihangir Bicer, Sait Polat
Although pathophysiological mechanisms in peripheral nerve damage are understood, recently with the help of histological molecular-level variations and studies on nerve healing, peripheral nerve injuries appear as a critical clinical problem that significantly affects economic and social life. The main target in the treatment of nerve injury is to ensure the integrity and conduction of the nerve and the organ in which the nerve provides function as closest to its former state. After nerve injury, peripheral nerve regeneration is slower than other tissues and less than half of the patients, who undergo surgical nerve repair, have recovery of motor or sensory functions. In addition, although it is technically possible to reconstruct the nerve with surgical repair, it is not possible at the axonal level.15
Taste and acoustic reflex after recovery from facial muscle paralysis in patients with facial nerve palsy
Published in Acta Oto-Laryngologica, 2021
Teruyuki Sato, Nobuo Ohta, Youji Tareishi, Takechiyo Yamada
At 6 months after treatment, the number of subjects with normal AR was significantly smaller than the number of subjects with a normal taste. This demonstrates that it is more difficult for AR to recover than it is for taste. The reason for this surmised to lie in the thinness of the nerves in the ear: thin nerve fibers are said to be more resistant to compression and pathological invasion than thick nerve fibers [6,13]. In addition, recovery of nerve damage usually begins in thick nerves [13]. Because the nerve thickness is in the order of facial nerve main trunk > chorda tympani > nerve to stapedius [14], there is the possibility that recovery of the nerve to the stapedius is delayed. Since the stapedius muscle is a striated muscle, the possibility of muscle disuse with prolonged nerve palsy should also be considered. Therefore, since the disuse of the stapedius muscle has a small effect in the early stage of onset, the AR can be used as a prognostic factor for FMP, in which AR appears if nerve damage is weak. However, it is also affected by the disuse of the stapedius muscle in the late stage of onset. It also suggests that AR may not be expressed even if the FNP is restored. These will need to be considered more thoroughly in the future.
The therapeutic efficacy of dexpanthenol on sciatic nerve injury in a rat model
Published in British Journal of Neurosurgery, 2020
Mehmet Fatih Korkmaz, Hakan Parlakpinar, Mehmet Nuri Erdem, Mehmet Fethi Ceylan, Levent Ediz, Emine Samdanci, Ersoy Kekilli
Peripheral nerve damage may be the result of congenital, mechanical, thermal, chemical, or other causes. Nerve damage can lead to loss of sensation and muscle function, as well as painful neuropathy when not treated timely or using proper techniques. The amount and duration of the pressure created, together with the size of the area exposed, define the severity of the lesion. However, while reperfusion following nerve ischemia is an essence, many toxic substances may emerge through the mechanism known as the ‘oxygen paradox’. Necrosis, which develops after nerve ischemia of acquired or other causes and ischemia-reperfusion (I/R), can render the nerve completely dysfunctional. There is no consensus on the optimal method for the treatment of peripheral nerve damage.1 Non-steroidal anti-inflammatory agents, steroids, nerve growth factors, erythropoietin, thyroid hormone, growth hormone, adrenocorticotropic hormone, and insulin-like peptides are currently used in the treatment of experimentally-induced peripheral nerve damage.2–4