Rabies is an acute infection that occurs in the central nervous system caused by a virus from the Rhabdoviridae family and the Lyssavirus genus that can be transmitted by dogs, cats, monkeys, bats, civets, and wolves. The purpose of writing this literature review is to determine the definition, epidemiology, neuropathogenesis and the role of neurotransmitters, clinical features, diagnosis, and management of rabies. The method used in writing this journal is a literature review, using literature searching. Search the library using website-based search tools, namely Google and Google Scholar using the keywords Rabies, Human Rabies, and Neuropathogenesis of Human Rabies. Free full text English and Indonesian publications. The journals selected in this literature review are 12 journals published between 2015-2021. Rabies infection begins with the transfer of viral microorganisms into the bite wound through the saliva of an infected animal. Rabies virus receptors consist of nicotinic acetylcholine receptors, Neural cell adhesion molecules (NCAM), and Nerve Growth Factor (NGF). Virus replication occurs in skeletal muscle and spreads via motor or sensory nerves to the spinal cord and brain. The virus binds to the nicotinic acetylcholine receptor via the neuromuscular route. There are 3 neurotransmitters that play a role in the neuropathogenesis of rabies, namely acetylcholine, serotonin, and GABA.
Peripheral neuromas caused by trauma or injury and surgical procedures can cause traumatic neuropathic pain, functional impairment and psychological distress, which can lead to decreased quality of life. Traumatic neuropathic pain can cause the patient to feel a burning, stabbing, stinging and nauseating sensation. Based on studies, the incidence of neuropathic pain due to peripheral nerve injury varies from 2.8 to 5% in the population. Estimates of the incidence of chronic postoperative neuropathic pain vary depending on the type of surgery and surgical technique. Various techniques for the prevention and treatment of traumatic neuromas have been recommended, including massage therapy, electrical stimulation, lipofilling, methods of transposition of nerve endings into muscle, bone or vein, and confining the injured nerve with synthetic or biological materials. The challenge in the treatment of traumatic neuromas today is that patients are resistant to analgesics, so standardized treatment is needed. Conclusion : The current challenge in the treatment of traumatic neuromas is that patients are resistant to analgesics, so standardized treatment is needed.
Bell's palsy is the most common neurological disorder affecting the cranial nerves with an onset that is rapid and unilateral, and it is common cause of facial paralysis worldwide. Bell's palsy occurs due to compression or enlargement of the stylomastoid foramen and causes nerve obstruction or damage caused by trauma, infection, inflammation, autoimmune, ischemic. This article aims to review bell's palsy, specifically motor nerve alignment, surgical disorders and management of bell's palsy. Source searches were carried out on online portals for journal publications such as Google Scholar (scholar.google.com) and the National Centre for Biotechnology Information/NCBI (ncbi.nlm.nih.gov), with the keyword “Facial palcy, dan Bell’s palcy”. In the United States, the annual incidence of Bell's palsy is approximately 23 cases per 100,000 people. Permanent facial paralysis and non-transient functional deficits are the main indications for surgical reconstruction of facial nerve function. The indications for surgery depend on the severity of the nerve lesion, blunt trauma that causes nondegenerative neuropraxia does not require surgical reconstruction, whereas disorders leading to degenerative neurotmesis require surgery.
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