Authors: Campbell, William W.
Title: Pocket Guide and Toolkit to DeJong’s Neurologic Examination, 1st Edition
Copyright ©2008 Lippincott Williams & Wilkins
> Table of Contents > Section D – The Cranial Nerves > Chapter 8 – The Olfactory Nerve
Chapter 8
The Olfactory Nerve
The olfactory nerve is a
sensory nerve with but one function, smell. Only volatile substances
soluble in lipids or water are perceived as odors. In true anosmia
there is loss of ability to perceive or recognize not only scents but
also flavors, for much of what is interpreted as taste involves smell.
Flavor is a synthesis of sensations derived from the olfactory nerves,
taste buds, and other sensory end-organs. A patient with olfactory
impairment may complain of loss of taste rather than of smell. Patients
with unilateral anosmia may be unaware of any impairment. Olfaction is
a phylogenetically ancient sensation. In lower mammals where olfaction
is extremely important, the olfactory cortex constitutes a large part
of the cerebral hemispheres. In higher primates and man, the area of
the uncus and anterior hippocampal gyrus is likely the primary
olfactory cortex. The connections between the olfactory system,
hypothalamus, certain brainstem nuclei, and autonomic centers is
pertinent to the understanding of many visceral functions. Olfaction is
the only sensation not directly processed in the thalamus.
sensory nerve with but one function, smell. Only volatile substances
soluble in lipids or water are perceived as odors. In true anosmia
there is loss of ability to perceive or recognize not only scents but
also flavors, for much of what is interpreted as taste involves smell.
Flavor is a synthesis of sensations derived from the olfactory nerves,
taste buds, and other sensory end-organs. A patient with olfactory
impairment may complain of loss of taste rather than of smell. Patients
with unilateral anosmia may be unaware of any impairment. Olfaction is
a phylogenetically ancient sensation. In lower mammals where olfaction
is extremely important, the olfactory cortex constitutes a large part
of the cerebral hemispheres. In higher primates and man, the area of
the uncus and anterior hippocampal gyrus is likely the primary
olfactory cortex. The connections between the olfactory system,
hypothalamus, certain brainstem nuclei, and autonomic centers is
pertinent to the understanding of many visceral functions. Olfaction is
the only sensation not directly processed in the thalamus.
Important historical points to address in a patient with
a smell or taste disturbance include past head injury; smoking; recent
upper-respiratory infection; systemic illness; nutrition; and exposure
to toxins, medications, or illicit drugs. Changes in the flavor of
coffee may be particularly informative. Unilateral loss of smell is
more significant than bilateral, which may be caused by many
conditions, primarily conductive (Table 8.1).
Impairments due to anosmia are not trivial. The problem is not merely
that patients with disturbances of smell sensation miss out on some of
life’s pleasures; they may also miss olfactory danger signals, such as
spoiled food, smoke, and leaking gas. As with hearing, olfactory
deficits are sometimes divided into (a) conductive deficits, due to
processes interfering with the ability of odorants to contact the
olfactory epithelium, such as nasal
a smell or taste disturbance include past head injury; smoking; recent
upper-respiratory infection; systemic illness; nutrition; and exposure
to toxins, medications, or illicit drugs. Changes in the flavor of
coffee may be particularly informative. Unilateral loss of smell is
more significant than bilateral, which may be caused by many
conditions, primarily conductive (Table 8.1).
Impairments due to anosmia are not trivial. The problem is not merely
that patients with disturbances of smell sensation miss out on some of
life’s pleasures; they may also miss olfactory danger signals, such as
spoiled food, smoke, and leaking gas. As with hearing, olfactory
deficits are sometimes divided into (a) conductive deficits, due to
processes interfering with the ability of odorants to contact the
olfactory epithelium, such as nasal
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polyps; and (b) sensorineural or neurogenic deficits, due to dysfunction of the receptors or their central connections.
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TABLE 8.1 Some Causes of Persistent Loss of Smell
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Before evaluating smell, ensure that the nasal passages
are open. Most cases of impaired smell are due to intranasal
obstructions. Acute or chronic rhinitis and chronic sinusitis may
seriously interfere with olfaction. Smell is tested using nonirritating
stimuli. Avoid substances such as ammonia that may stimulate the
trigeminal nerve instead of the olfactory nerve, causing a response
that can be confused with olfaction. The nasal passages are richly
innervated by free nerve endings from the trigeminal system, which
respond to many substances. Some patients with impaired taste and smell
enjoy spicy food because of its stimulation of the trigeminal system.
are open. Most cases of impaired smell are due to intranasal
obstructions. Acute or chronic rhinitis and chronic sinusitis may
seriously interfere with olfaction. Smell is tested using nonirritating
stimuli. Avoid substances such as ammonia that may stimulate the
trigeminal nerve instead of the olfactory nerve, causing a response
that can be confused with olfaction. The nasal passages are richly
innervated by free nerve endings from the trigeminal system, which
respond to many substances. Some patients with impaired taste and smell
enjoy spicy food because of its stimulation of the trigeminal system.
Examine each nostril separately while occluding the
other. With the patient’s eyes closed and one nostril occluded, bring
the test substance near the open one. Ask the patient to sniff and
indicate whether she smells something and, if so, to identify it.
Repeat for the other nostril and compare the two sides. The side that
might be abnormal should be examined first. Many substances can be used
to test smell (e.g., wintergreen, cloves, coffee, and cinnamon). At the
bedside or in the clinic one can use mouthwash, toothpaste, alcohol,
soap, and similar substances. Commercial scratch-and-sniff strips are
available.
other. With the patient’s eyes closed and one nostril occluded, bring
the test substance near the open one. Ask the patient to sniff and
indicate whether she smells something and, if so, to identify it.
Repeat for the other nostril and compare the two sides. The side that
might be abnormal should be examined first. Many substances can be used
to test smell (e.g., wintergreen, cloves, coffee, and cinnamon). At the
bedside or in the clinic one can use mouthwash, toothpaste, alcohol,
soap, and similar substances. Commercial scratch-and-sniff strips are
available.
The perception of odor is more important than accurate
identification. Perceiving the presence of an odor indicates continuity
of the olfactory pathways; identification of the odor indicates intact
cortical function as well. Since there is bilateral innervation, a
lesion central to the decussation of the olfactory pathways never
causes loss of smell, and a lesion of the olfactory cortex does not
produce anosmia. The appreciation of the presence of a smell, even
without recognition, excludes anosmia.
identification. Perceiving the presence of an odor indicates continuity
of the olfactory pathways; identification of the odor indicates intact
cortical function as well. Since there is bilateral innervation, a
lesion central to the decussation of the olfactory pathways never
causes loss of smell, and a lesion of the olfactory cortex does not
produce anosmia. The appreciation of the presence of a smell, even
without recognition, excludes anosmia.
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DISORDERS OF OLFACTORY FUNCTION
Loss of smell may occur in a variety of conditions (Table 8.1).
It may be congenital or acquired. The top four causes of anosmia are
upper-respiratory tract infection (URI), trauma, nasal and sinus
disease, and idiopathic. Persistent olfactory loss following a URI is
the most common etiology, accounting for 15% to 25% of cases. Some
definitions regarding disorders of smell are reviewed in Table 8.2.
It may be congenital or acquired. The top four causes of anosmia are
upper-respiratory tract infection (URI), trauma, nasal and sinus
disease, and idiopathic. Persistent olfactory loss following a URI is
the most common etiology, accounting for 15% to 25% of cases. Some
definitions regarding disorders of smell are reviewed in Table 8.2.
Few instances of disturbed smell are of neurologic
origin. Lesions involving the orbital surface of the brain may cause
unilateral anosmia. Meningiomas of the sphenoidal ridge or olfactory
groove and gliomas of the frontal lobe may damage the olfactory bulbs
or tracts. A typical clinical picture with sphenoidal ridge meningioma
consists of unilateral optic atrophy or papilledema and exophthalmos,
and ipsilateral anosmia. In meningiomas of the olfactory groove or
cribriform plate area, unilateral anosmia occurs early, progressing to
bilateral anosmia, often accompanied by optic neuropathy. Anosmia may
also occur with other frontal lobe tumors, and with parasellar and
pituitary lesions.
origin. Lesions involving the orbital surface of the brain may cause
unilateral anosmia. Meningiomas of the sphenoidal ridge or olfactory
groove and gliomas of the frontal lobe may damage the olfactory bulbs
or tracts. A typical clinical picture with sphenoidal ridge meningioma
consists of unilateral optic atrophy or papilledema and exophthalmos,
and ipsilateral anosmia. In meningiomas of the olfactory groove or
cribriform plate area, unilateral anosmia occurs early, progressing to
bilateral anosmia, often accompanied by optic neuropathy. Anosmia may
also occur with other frontal lobe tumors, and with parasellar and
pituitary lesions.
The Foster Kennedy syndrome consists of anosmia
accompanied by unilateral ipsilateral optic atrophy and contralateral
papilledema, classically due to a large tumor involving the
orbitofrontal region, such as an olfactory groove meningioma. The
anosmia and optic atrophy are due to direct compression; the
contralateral papilledema occurs late when intracranial pressure
increases. The atrophic optic disc cannot swell and the unusual picture
of optic atrophy in one eye and papilledema in the fellow eye develops.
This ophthalmologic picture, without the anosmia, is more often due to
anterior optic nerve ischemia, sometimes termed the pseudo-Foster
Kennedy syndrome. A mass causing asymmetric compression of both optic
nerves may cause a similar picture.
accompanied by unilateral ipsilateral optic atrophy and contralateral
papilledema, classically due to a large tumor involving the
orbitofrontal region, such as an olfactory groove meningioma. The
anosmia and optic atrophy are due to direct compression; the
contralateral papilledema occurs late when intracranial pressure
increases. The atrophic optic disc cannot swell and the unusual picture
of optic atrophy in one eye and papilledema in the fellow eye develops.
This ophthalmologic picture, without the anosmia, is more often due to
anterior optic nerve ischemia, sometimes termed the pseudo-Foster
Kennedy syndrome. A mass causing asymmetric compression of both optic
nerves may cause a similar picture.
Chronic intranasal cocaine use may cause anosmia.
Rarely, toxins such as cadmium or toluene may cause anosmia, usually
accompanied by other neurologic abnormalities. Disturbances of taste
and smell may result from deficiency of vitamin B12, B6,
or A, and from the effects of some drugs. Decreased sense of smell has
been often attributed to abnormalities in zinc metabolism. Anosmia may
accompany some degenerative dementias, especially Alzheimer disease.
Rarely, toxins such as cadmium or toluene may cause anosmia, usually
accompanied by other neurologic abnormalities. Disturbances of taste
and smell may result from deficiency of vitamin B12, B6,
or A, and from the effects of some drugs. Decreased sense of smell has
been often attributed to abnormalities in zinc metabolism. Anosmia may
accompany some degenerative dementias, especially Alzheimer disease.
Craniocerebral trauma may result in damage to the
olfactory nerves at the cribriform plate due to coup or contrecoup
forces. Anosmia complicates 5% to 20% of major head injuries, sometimes
in isolation and sometimes with other sequellae such as diabetes
insipidus and cerebrospinal fluid (CSF) rhinorrhea. The incidence of
anosmia may be as high as 80% in patients with CSF rhinorrhea.
olfactory nerves at the cribriform plate due to coup or contrecoup
forces. Anosmia complicates 5% to 20% of major head injuries, sometimes
in isolation and sometimes with other sequellae such as diabetes
insipidus and cerebrospinal fluid (CSF) rhinorrhea. The incidence of
anosmia may be as high as 80% in patients with CSF rhinorrhea.
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TABLE 8.2 Terms and Definitions Related to Olfactory Abnormalities
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Disorders of smell other than hyposmia or anosmia
occasionally occur. Hyperosmia is usually functional, but it can occur
with certain types of substance abuse and in migraine. Parosmia and
cacosmia are often due to psychiatric disease but occasionally follow
head trauma and may accompany conductive dysosmia. Olfactory
hallucinations are most often due to psychosis, but they can result
from a lesion of the central olfactory system, usually neoplastic or
vascular, or as a manifestation of seizure. So-called uncinate fits are
complex partial or temporal lobe seizures preceded by an olfactory or
gustatory aura, usually disagreeable, and often accompanied, as the
patient loses awareness, by smacking of the lips or chewing movements.
Such attacks are typically due to a seizure focus involving medial
temporal lobe structures. There is never objective loss of smell
interictally.
occasionally occur. Hyperosmia is usually functional, but it can occur
with certain types of substance abuse and in migraine. Parosmia and
cacosmia are often due to psychiatric disease but occasionally follow
head trauma and may accompany conductive dysosmia. Olfactory
hallucinations are most often due to psychosis, but they can result
from a lesion of the central olfactory system, usually neoplastic or
vascular, or as a manifestation of seizure. So-called uncinate fits are
complex partial or temporal lobe seizures preceded by an olfactory or
gustatory aura, usually disagreeable, and often accompanied, as the
patient loses awareness, by smacking of the lips or chewing movements.
Such attacks are typically due to a seizure focus involving medial
temporal lobe structures. There is never objective loss of smell
interictally.