Olfactory neuropathy in severe acute respiratory syndrome: report of A case.
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This case was a 27 years old female with severe acute respiratory syndrome (SARS). She suffered from typical symptoms of SARS. Although she got almost complete recovery from most symptoms after treatment, she noted acute onset complete anosmia 3 weeks after the onset of her first symptom. Her brain MRI examination did not show definite lesion except an incidental finding of left temporal epidermoid cyst. Her anosmia persisted for more than 2 years during following up. Peripheral neuropathy and myopathy have been reported as a concomitant problem during the convalescent stage of SARS, while the sequel of permanent ansomia in SARS was not reported before. Olfactory neuropathy, which rarely occurred in typical peripheral neuropathy, could be a special type of neuropathy induced by corona virus infection in SARS. Olfactory function test should be taken into routine check-up for patients with SARS. The pathophysiology and therapeutic strategy of this special type of permanent olfactory dysfunction deserve further investigation. (+info)
Response of matrix metalloproteinase-9 to olfactory nerve injury.
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Matrix metalloproteinases function in the remodeling of the extracellular matrix during growth and development as well as in injury and disease processes. We examined the role of matrix metalloproteinase-9 in a model of olfactory nerve injury in mice. We measured changes in matrix metalloproteinase-9 protein levels for up to 60 days following olfactory nerve transection. Matrix metalloproteinase-9 levels increased within hours after injury, peaked at day 1 and were elevated for approximately 2 weeks before returning to control levels over the 60-day time period. The increase in matrix metalloproteinase-9 was temporally associated with the degeneration of olfactory neurons that follows nerve transection and with increased gliosis. Our results demonstrate a temporal relationship between matrix metalloproteinase-9 elevation, degeneration of olfactory neurons and gliosis. (+info)
Development of guideline for rating the physical impairment of otolaryngologic field.
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Host strategies against virus entry via the olfactory system.
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In mammals, odorants are inhaled through the nose and inside the nasal cavity they trigger olfactory sensory neurons (OSN) that are located within the olfactory epithelium. OSN project their axons into glomerular structures of the olfactory bulb. There they synapse with dendrites of second-order neurons that project their axons to the olfactory cortex. Thus, olfaction is based on direct interaction of environmental matters with OSN. This poses the question of how neurotropic viruses are prevented from infecting OSN and entering the central nervous system. Recent evidence indicates that upon instillation of neurotropic virus OSN are readily infected. By axonal transport virus reaches the glomerular layer of the olfactory bulb where it is efficiently curbed by a type I IFN dependent mechanism. In this review local mechanisms limiting virus entry via the olfactory system and virus spread within the CNS are recapitulated in the context of anatomical properties of the olfactory system. (+info)