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.
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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)
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Excerpts From:
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
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