Guest guest Posted January 9, 2008 Report Share Posted January 9, 2008 Sinusitis - The Olfactory Nerve NIH Guide Volume 21 Number 42 10-20-1992 The olfactory nerve provides a direct anatomic conduit between the external chemical environment and the brain. This location puts the olfactory system at risk for damage from environmental toxicants and pathogens. These toxic agents comprise the major health hazard to human olfaction. However, the direct and indirect effects of these agents on the peripheral and central olfactory system are poorly understood. The purpose of this Program Announcement (PA) is to foster investigator-initiated research fundamental to understanding the impact of environmental toxicants and pathogens on the olfactory system. A broad range of studies extending from the molecular to the behavioral areas of basic and clinical research is applicable to this PA. The scope of these areas encompasses the transport of toxic substances into the brain through the olfactory nerve; olfactory mucosal defense mechanisms; neurogenesis; the relation of neurodegenerative diseases, such as Alzheimer's disease, to olfactory abnormalities induced by toxic agents; and the vulnerability of an aged olfactory system to toxic agents. ---- Assessing Cranial Nerves I 1. Cranial nerve function and neuroforamina # CRANIAL NERVE FUNCTION APERTURE I OlfactorySpecial sensory (olfaction) Cribriform plate II OpticSpecial sensory (vision) Optic canal III OculomotorMotor (superior inferior and medial rectus, inferior oblique) Visceral motor (parasympathetic: pupillary constrictor muscles) Superior orbital fissure IV TrochlearMotor (superior oblique) Superior orbital fissure V TrigeminalMotor (muscles of mastication) Sensory (head and neck, sinuses and meninges, tympanic membrane) V1: Superior orbital fissure V2: foramen rotundum V3: foramen ovale VI AbducensMotor (lateral rectus muscle). Superior orbital fissure CRANIAL NERVE IThe first two cranial nerves are actually projections of the telencephalon (olfactory nerve) and diencephalon (optic nerve), and may thus be affected by the same diseases which affect the brain. They subserve the special senses of smell and taste, respectively. From the olfactory epithelium in the superior aspect of the nasal vault, olfactory nerve fibers ascend into the cranium via perforations within the cribriform plate. Some of these fibers synapse at the mitral and tufted cells within the olfactory bulb, others pass directly through to the olfactory nerve. The nerve is situated within the olfactory groove, interposed between the gyrus rectus and the medial orbitofrontal gyrus. Just ventral to the anterior perforated substance, the olfactory nerve trifurcates into medial, intermediate and lateral striae. Most of the axons travel in the lateral olfactory stria to the uncus and the entorhinal cortex at the anterior aspect of the hippocampal gyrus. The medial fibers travel to the medial olfactory area, which is subjacent to the genu of the corpus callosum. These neurons interface with the limbic system, and are thought to mediate the emotional response to olfactory stimulation. The 3 olfactory areas are interconnected by the diagonal band of Broca. Pathology located anywhere along the olfactory pathway can affect this special sense (Table 2). Upper respiratory infections, usually viral in origin, are a fairly common cause of anosmia. An obstructed nasal cavity prevents access of aromatic molecules to the olfactory mucosa, causing anosmia. Both benign and malignant conditions such as polyposis and tumors may obstruct the nasal vault. In young patients, rhabdomyosarcoma must be considered if an aggressive mass is present. The incidence of esthesioneuroblastoma peaks in the second decade, with a second peak in older adults. In adolescent males, juvenile angiofibroma may result in complete obstruction of the superior nasal vault. Although this lesion is histologically benign, it frequently presents as a very large, vascular and aggressive mass.Other sinonasal tumors may produce similar symptoms. Finally, trauma may cause transection of the olfactory fibers which traverse the skull base at the level of the cribriform plate, resulting in acute post- traumatic anosmia. Alternatively, delayed post-traumatic anosmia may result from cicatrization, or scar formation, caused by dural tears at this location. Lesions such as gliomas or infection involving the medial temporal lobes may give rise to olfactory hallucinations and other symptoms, but they usually do not cause anosmia ***Inflammatory Upper respiratory infection (viral), sinusitis,*** mucocele, meningitis, polyposis Neoplasm Meningioma, sinonasal tumors, nasopharyngeal tumors, Trauma Direct nerve bundle injury, scar formation (delayed injury) ---- Excerpts HSV-1 brain infection by the olfactory nerve route and virus latency and reactivation may cause learning and behavioral deficiencies and violence in children and adults: A point of view Journal Virus Genes Publisher Springer Netherlands ISSN 0920-8569 (Print) 1572-994X (Online) Issue Volume 10, Number 3 / October, 1995 DOI 10.1007/BF01701811 Pages 217-226 Subject Collection Biomedical and Life Sciences SpringerLink Date Monday, June 13, 2005 HSV-1 brain infection by the olfactory nerve route and virus latency and reactivation may cause learning and behavioral deficiencies and violence in children and adults: A point of view Yechiel Becker1 (1) Department of Molecular Virology, Institute of Microbiology, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel Received: 5 February 1995 Accepted: 5 February 1995 Abstract Two recent studies provided new evidence on the latency of HSV-1 DNA in 15.5% of olfactory bulbs and in 72.5% of trigeminal nerves from human corpses at forensic postmortems (1) and in 35% of 40 autopsied human brains (2). In the latter brains, latent HSV-1 DNA was found in the olfactory bulbs, amygdala, hippocampus, brain stem, and trigeminal ganglia. Although in these studies it is not known by which route HSV-1 entered the olfactory bulbs and brain, experimental studies in mice (3) revealed that injection of HSV-1 into the olfactory bulbs leads to virus migration into the brain amygdala and hippocampus via the olfactory nerve and locus coeruleus. If the olfactory ciliary nerve epithelium is the port of entry of HSV-1 into the olfactory bulbs and brain in humans as well, protection of the nose against HSV-1 infection may be needed to prevent virus latency in neurons in the amygdala and hippocampus (3). Infection of humans by HSV-1 was estimated to increase from 18.2% in the 0-20 year population group to 100% in persons older than 60 years (1), ***indicating that worldwide human populations at all ages are at risk of brain infection by the olfactory nerve route.*** In addition, both primary infection and reactivation of latent DNA in the brain may lead to damage of neurons in the brain involved in memory, learning, and behavior, as observed in infected, acyclovirtreated mice (3). The current introduction of a live apathogenic varicella-zoster virus (VZV) vaccine to immunize children against chickenpox (4) may suggest that the time is ripe for immunization of children and adults against HSV-1 infections, especially infections by the olfactory nerve route, to prevent potential brain damage. Key words HSV-1 - olfactory nerve - brain amygdala and hippocampus - infection of serotonergic neurons - behavior deficit in children - learning deficit in children - HSV-1 latency in brain - virus Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 24, 2008 Report Share Posted January 24, 2008 Sinusitis - The Olfactory Nerve Bacterial/Viral/Fungal Excerpt NIH Guide Volume 21 Number 42 10-20-1992 The olfactory nerve provides a direct anatomic conduit between the external chemical environment and the brain. This location puts the olfactory system at risk for damage from environmental toxicants and pathogens. These toxic agents comprise the major health hazard to human olfaction. However, the direct and indirect effects of these agents on the peripheral and central olfactory system are poorly understood. The purpose of this Program Announcement (PA) is to foster investigator-initiated research fundamental to understanding the impact of environmental toxicants and pathogens on the olfactory system. A broad range of studies extending from the molecular to the behavioral areas of basic and clinical research is applicable to this PA. The scope of these areas encompasses the transport of toxic substances into the brain through the olfactory nerve; olfactory mucosal defense mechanisms; neurogenesis; the relation of neurodegenerative diseases, such as Alzheimer's disease, to olfactory abnormalities induced by toxic agents; and the vulnerability of an aged olfactory system to toxic agents. --- Excerpts HSV-1 brain infection by the olfactory nerve route and virus latency and reactivation may cause learning and behavioral deficiencies and violence in children and adults: A point of view Journal Virus Genes Publisher Springer Netherlands ISSN 0920-8569 (Print) 1572-994X (Online) Issue Volume 10, Number 3 / October, 1995 DOI 10.1007/BF01701811 Pages 217-226 Subject Collection Biomedical and Life Sciences SpringerLink Date Monday, June 13, 2005 HSV-1 brain infection by the olfactory nerve route and virus latency and reactivation may cause learning and behavioral deficiencies and violence in children and adults: A point of view Yechiel Becker1 (1) Department of Molecular Virology, Institute of Microbiology, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel Received: 5 February 1995 Accepted: 5 February 1995 Abstract Two recent studies provided new evidence on the latency of HSV-1 DNA in 15.5% of olfactory bulbs and in 72.5% of trigeminal nerves from human corpses at forensic postmortems (1) and in 35% of 40 autopsied human brains (2). In the latter brains, latent HSV-1 DNA was found in the olfactory bulbs, amygdala, hippocampus, brain stem, and trigeminal ganglia. Although in these studies it is not known by which route HSV-1 entered the olfactory bulbs and brain, experimental studies in mice (3) revealed that injection of HSV-1 into the olfactory bulbs leads to virus migration into the brain amygdala and hippocampus via the olfactory nerve and locus coeruleus. If the olfactory ciliary nerve epithelium is the port of entry of HSV-1 into the olfactory bulbs and brain in humans as well, protection of the nose against HSV-1 infection may be needed to prevent virus latency in neurons in the amygdala and hippocampus (3). Infection of humans by HSV-1 was estimated to increase from 18.2% in the 0-20 year population group to 100% in persons older than 60 years (1), ***indicating that worldwide human populations at all ages are at risk of brain infection by the olfactory nerve route.*** In addition, both primary infection and reactivation of latent DNA in the brain may lead to damage of neurons in the brain involved in memory, learning, and behavior, as observed in infected, acyclovirtreated mice (3). The current introduction of a live apathogenic varicella-zoster virus (VZV) vaccine to immunize children against chickenpox (4) may suggest that the time is ripe for immunization of children and adults against HSV-1 infections, especially infections by the olfactory nerve route, to prevent potential brain damage. Quote Link to comment Share on other sites More sharing options...
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