DOI:10.2214/AJR.04.1518
AJR 2005; 185:1487-1497
© American Roentgen Ray Society
MRI of Cranial Nerve Enhancement
Farhood Saremi1,
Mohammad Helmy1,
Sahar Farzin1,
Chi S. Zee2 and
John L. Go2
1 Department of Radiological Sciences, University of California, Irvine, 101 The
City Dr., Rte. 140, Orange, CA 92868.
2 Department of Radiology, Keck School of Medicine, University of Southern
California, Los Angeles, CA.
Received September 25, 2004;
accepted after revision March 7, 2005.
Address correspondence to F. Saremi
(fsaremi{at}uci.edu).
Abstract
OBJECTIVE. In this pictorial essay, we review the MR appearance of
cranial nerve enhancement in a variety of entities including neoplastic,
infectious, and idiopathic diseases.
CONCLUSION. MRI with contrast enhancement is a valuable tool for
detecting and characterizing disease of the cranial nerves. Abnormal cranial
nerve enhancement on MRI may sometimes be the first or only indication of an
underlying disease process.
Introduction
MRI is invaluable in characterizing disease of the cranial nerves.
Gadolinium administration increases the ability of MRI to detect such
abnormalities. We begin this pictorial essay with a description of the
histologic anatomy of the cranial nerves and patterns of normal cranial nerve
enhancement. After briefly discussing the pathophysiology, we review the MR
appearance of abnormal cranial nerve enhancement in various diseases ranging
from common neoplastic and infectious conditions to rare conditions such as
ophthalmoplegic migraine and idiopathic pachymeningitis. In some cases,
abnormal cranial nerve enhancement on MRI may be the only clue to the
underlying disease.
Anatomy and Pathophysiology
The cranial nerves are surrounded by a series of connective tissue sheaths
called endoneurium, perineurium, and epineurium. The blood-nerve barrier of
cranial nerves is maintained by the combined actions of tight junctions in the
endothelium of the endoneural capillaries and tight junctions in the inner
layers of the perineurium. Various insults disrupt the blood-nerve barrier,
allowing leakage and accumulation of contrast material with resultant
perineural enhancement. Such disruption may arise secondary to neoplasm,
autoimmune disease, inflammation, demyelination, ischemia, trauma, radiation,
and axonal degeneration, all resulting in abnormal cranial nerve enhancement
(Appendix 1).
Normal Cranial Nerve Enhancement
There are instances of normal cranial nerve enhancement. The geniculate,
tympanic, and mastoid segments of the facial nerve possess peri- and epineural
venous plexuses that may cause moderate enhancement by an increased vascular
pool of contrast material [1].
The intracanalicular-labyrinthine segment does not normally enhance. The
trigeminal ganglion and the proximal portions of its divisions are seen as
discrete nonenhancing structures surrounded by an enhancing perineural
vascular plexus. Enhancement of the trigeminal ganglion or its maxillary or
mandibular divisions is infrequently seen as evidenced by their avascular
appearance in cadaveric specimens
[2]. When such enhancement is
seen on MRI, it may be related to suboptimal imaging parameters, avid
enhancement of the perivascular plexus, or a combination of both.
Neoplasm
Neoplastic meningitis refers to the disseminated seeding of the
leptomeninges by malignant cells. This includes carcinomatous meningitis in
patients with solid tumors and lymphomatous and leukemic meningitis when
involvement is related to these underlying diseases. The most common cancers
to involve the leptomeninges are breast (5%), lung (9-25%), and melanoma (23%)
[3] (Figs.
1A,
1B,
1C,
1D, and
1E). MRI findings include pial
enhancement and nodularity, smooth or nodular cranial nerve enhancement,
hydrocephalus, and coexisting brain or bone metastases
[4]. Primary diffuse
leptomeningeal gliomatosis is a rare condition whereby a glioma arises from
heterotopic cell nests in the leptomeninges. Leptomeningeal dissemination is
an uncommon complication of gliomas and other primary intraaxial malignancies.
The presence of a single unexplained enhancing cranial nerve in a patient with
cancer raises the possibility of leptomeningeal dissemination.
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Fig. 1A —48-year-old woman with metastatic melanoma and meningeal
carcinomatosis. Contrast-enhanced axial (A, B, D, and E) and
coronal (C) T1-weighted images show enhancement and involvement of
multiple cranial nerves: oculomotor nerves (arrows, A);
trigeminal nerves (arrows, B); complex of seventh and eighth
cranial nerves (arrows, C); complex of ninth, tenth, and
eleventh cranial nerves (long arrows, D and E); and
hypoglossal nerves (short arrows, E).
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Fig. 1B —48-year-old woman with metastatic melanoma and meningeal
carcinomatosis. Contrast-enhanced axial (A, B, D, and E) and
coronal (C) T1-weighted images show enhancement and involvement of
multiple cranial nerves: oculomotor nerves (arrows, A);
trigeminal nerves (arrows, B); complex of seventh and eighth
cranial nerves (arrows, C); complex of ninth, tenth, and
eleventh cranial nerves (long arrows, D and E); and
hypoglossal nerves (short arrows, E).
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Fig. 1C —48-year-old woman with metastatic melanoma and meningeal
carcinomatosis. Contrast-enhanced axial (A, B, D, and E) and
coronal (C) T1-weighted images show enhancement and involvement of
multiple cranial nerves: oculomotor nerves (arrows, A);
trigeminal nerves (arrows, B); complex of seventh and eighth
cranial nerves (arrows, C); complex of ninth, tenth, and
eleventh cranial nerves (long arrows, D and E); and
hypoglossal nerves (short arrows, E).
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Fig. 1D —48-year-old woman with metastatic melanoma and meningeal
carcinomatosis. Contrast-enhanced axial (A, B, D, and E) and
coronal (C) T1-weighted images show enhancement and involvement of
multiple cranial nerves: oculomotor nerves (arrows, A);
trigeminal nerves (arrows, B); complex of seventh and eighth
cranial nerves (arrows, C); complex of ninth, tenth, and
eleventh cranial nerves (long arrows, D and E); and
hypoglossal nerves (short arrows, E).
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Fig. 1E —48-year-old woman with metastatic melanoma and meningeal
carcinomatosis. Contrast-enhanced axial (A, B, D, and E) and
coronal (C) T1-weighted images show enhancement and involvement of
multiple cranial nerves: oculomotor nerves (arrows, A);
trigeminal nerves (arrows, B); complex of seventh and eighth
cranial nerves (arrows, C); complex of ninth, tenth, and
eleventh cranial nerves (long arrows, D and E); and
hypoglossal nerves (short arrows, E).
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Perineural tumor extension, a form of metastatic disease, involves the
spread of primary mucosal or cutaneous tumors to noncontiguous regions along
nerve sheaths. Perineural tumor spread has been shown in perineural or
endoneural tissue planes along a path of least resistance. Retrograde spread
is significantly more common than antegrade spread. A series by Parker and
Harnsberger [5] found
perineural spread occurs most commonly with squamous cell carcinoma and
adenoid cystic carcinoma, with the facial nerve and second and third divisions
of the trigeminal nerve most frequently involved (Figs.
2A,
2B, and
2C). Other neoplastic and
aggressive infectious processes, such as acute lymphoblastic leukemia,
non-Hodgkin's lymphoma, malignant schwannoma, aspergillosis, mucormycosis, and
actinomycosis, also show perineural extension (Figs.
3A,
3B, and
3C). MRI findings of
perineural involvement include smooth thickening and enhancement of the nerve,
concentric expansion of the skull base foramina with obliteration of normal
fatty contents, enlargement of the cavernous sinus, and neuropathic muscular
atrophy [6].
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Fig. 2B —56-year-old woman after resection of adenoid cystic carcinoma
of right hard palate. Contrast-enhanced axial T1-weighted MR images reveal
infiltrating mass in right pterygopalatine fossa (short arrow,
B) and cavernous sinus (short arrow, C). Note abnormal
signal intensity in right masticator space (long arrows, B)
and right medial temporal lobe (long arrows, C).
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Fig. 2C —56-year-old woman after resection of adenoid cystic carcinoma
of right hard palate. Contrast-enhanced axial T1-weighted MR images reveal
infiltrating mass in right pterygopalatine fossa (short arrow,
B) and cavernous sinus (short arrow, C). Note abnormal
signal intensity in right masticator space (long arrows, B)
and right medial temporal lobe (long arrows, C).
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Fig. 3B —43-year-old man with acute lymphoblastic leukemia.
Contrast-enhanced axial T1-weighted images show antegrade perineural extension
along course of left spinal trigeminal tract and nuclei (arrow,
B) into preganglionic segment of left trigeminal nerve (arrow,
C).
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Fig. 3C —43-year-old man with acute lymphoblastic leukemia.
Contrast-enhanced axial T1-weighted images show antegrade perineural extension
along course of left spinal trigeminal tract and nuclei (arrow,
B) into preganglionic segment of left trigeminal nerve (arrow,
C).
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Fig. 4A —7-year-old girl with tuberculous meningitis.
Contrast-enhanced axial (A) and coronal (B) T1-weighted images
show abnormal peripheral enhancement of oculomotor nerves (long
arrows). In addition, there is leptomeningeal enhancement of anterior
surface of brainstem (short arrows, A).
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Fig. 4B —7-year-old girl with tuberculous meningitis.
Contrast-enhanced axial (A) and coronal (B) T1-weighted images
show abnormal peripheral enhancement of oculomotor nerves (long
arrows). In addition, there is leptomeningeal enhancement of anterior
surface of brainstem (short arrows, A).
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Fig. 5 —32-year-old man with cryptococcal meningitis and perioptic
neuritis. Contrast-enhanced axial T1-weighted image with fat suppression
reveals thickening and enhancement of perineural structures of left optic
nerve.
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Fig. 6A —61-year-old man with perineural spread of rhinocerebral
mucormycosis who presented for follow-up after right orbital exenteration.
Axial T2-weighted (A) and contrast-enhanced T1-weighted (B)
images show recurrence of infection with invasion of right cavernous sinus
(long arrows, A) and retrograde involvement of trigeminal
nerve along cavernous, ganglionic, and cisternal segments (arrows,
B). Abnormal signal within right pons indicates edema (short
arrow, A).
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Fig. 6B —61-year-old man with perineural spread of rhinocerebral
mucormycosis who presented for follow-up after right orbital exenteration.
Axial T2-weighted (A) and contrast-enhanced T1-weighted (B)
images show recurrence of infection with invasion of right cavernous sinus
(long arrows, A) and retrograde involvement of trigeminal
nerve along cavernous, ganglionic, and cisternal segments (arrows,
B). Abnormal signal within right pons indicates edema (short
arrow, A).
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Infection
Infectious meningitis results from viral, bacterial, fungal, or parasitic
infection. Leptomeningitis is the most common form of intracranial
tuberculosis, particularly in the pediatric population. Cranial nerve
involvement is seen in 17-70% of patients and occurs in the setting of diffuse
leptomeningeal tuberculosis. Impairment has been attributed to ischemia of the
nerve or entrapment of the nerve in basal exudates
[7] (Figs.
4A, and
4B).
Cryptococcus neoformans is the most common fungus to involve the
CNS. Cryptococcal meningitis is one of the typical pathologic manifestations
and can result in optic neuropathy in both immunocompetent and
immunocompromised patients (Fig.
5). Optic neuropathy is a rare complication of cryptococcal
meningitis and usually occurs in non-AIDS patients. Necrosis of the optic
nerves and infiltration of the meninges around the optic tracts, nerves, and
chiasm by cryptococcal organisms have been observed
[8].
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Fig. 7A —17-year-old boy with neuroschistosomiasis. Contrast-enhanced
T1-weighted images show range of involvement of CNS in schistosomiasis.
Sagittal image shows enhancing masses within chiasmatic-hypothalamic
(short arrow) and pineal (long arrow) regions.
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Fig. 7B —17-year-old boy with neuroschistosomiasis. Contrast-enhanced
T1-weighted images show range of involvement of CNS in schistosomiasis.
Coronal image shows thickened and enhancing trigeminal nerves
(arrows).
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Fig. 7C —17-year-old boy with neuroschistosomiasis. Contrast-enhanced
T1-weighted images show range of involvement of CNS in schistosomiasis. Axial
image reveals enhancing mass (arrow) in right cerebellopontine angle
with extension into internal auditory canal.
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Rhinocerebral mucormycosis is a potentially devastating fungal infection in
diabetic and immunocompromised patients. Sinonasal disease often progresses to
the orbit and cavernous sinus and may be complicated by vascular and
perineural invasion and local thrombotic infarction
[9] (Figs.
6A, and
6B).
Cranial neuroschistosomiasis occurs less commonly than the spinal variety
and may arise with any of the clinical forms of this parasitic infection. Eggs
within the CNS induce a cell-mediated periovular granulomatous reaction that
leads to signs and symptoms of increased intracranial pressure and focal
neurologic signs [10].
Although meningeal spread of infection involving cauda equina nerve roots has
been reported, rare instances of cranial nerve involvement may also be seen as
in our case (Figs. 7A,
7B, and
7C).
Cranial neuritis in Lyme disease may involve any of cranial nerves III
through VII, with the facial nerve most frequently affected and often
associated with cochleovestibular nerve abnormalities. The affected segments
appear thickened and enhance. Viral infections related to herpes simplex virus
type 1, cytomegalovirus, and Varicella zoster organisms also manifest
with cranial nerve involvement and show abnormal enhancement on MRI.
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Fig. 8A —32-year-old man with Bell's palsy. Contrast-enhanced axial
(A) and coronal (B and C) T1-weighted images show
abnormal enhancement of right facial nerve extending from distal
intracanalicular segment (arrows, A and B) to distal
mastoid segment (arrow, C).
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Fig. 8B —32-year-old man with Bell's palsy. Contrast-enhanced axial
(A) and coronal (B and C) T1-weighted images show
abnormal enhancement of right facial nerve extending from distal
intracanalicular segment (arrows, A and B) to distal
mastoid segment (arrow, C).
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Fig. 8C —32-year-old man with Bell's palsy. Contrast-enhanced axial
(A) and coronal (B and C) T1-weighted images show
abnormal enhancement of right facial nerve extending from distal
intracanalicular segment (arrows, A and B) to distal
mastoid segment (arrow, C).
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Postinfectious and Demyelinating Disorders
Bell's palsy is the most common cause of unilateral peripheral facial
neuropathy. In addition to normal enhancement of the facial nerve segments
discussed earlier, there is pathologic enhancement of the
intracanalicular-labyrinthine portion (Figs.
8A,
8B, and
8C). Martin-Duverneuil et al.
[11] suggest three criteria
for pathologic enhancement of the facial nerve: enhancement outside the facial
canal, extension of enhancement to cranial nerve VIII, and intense enhancement
of the labyrinthine and mastoid segments. In Ramsay Hunt syndrome, abnormal
facial nerve enhancement is accompanied by enhancement of the vestibular and
cochlear nerves as a result of extension of inflammation from cranial nerve
VII to the intracanalicular portions of these cranial nerve VIII
divisions.
Ophthalmoplegic migraine is a rare condition characterized by headache and
oculomotor nerve palsy lasting days to weeks. MRI findings include reversible
enhancement of the cisternal segment of the oculomotor nerve and focal
thickening at the exit of the nerve in the interpeduncular cistern (Figs.
9A,
9B, and
9C). Involvement of cranial
nerves IV, V1, and VI also occurs. Multiple cranial nerve
involvement is also present in a group of inflammatory demyelinating
polyneuropathies that include Guillain-Barré and variants, such as
Miller Fisher syndrome and polyneuritis cranialis.
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Fig. 9A —57-year-old man with ophthalmoplegic migraine. Unenhanced
axial (A) and enhanced axial (B) and coronal (C)
T1-weighted images reveal smooth enlargement and homogeneous enhancement of
cisternal segment of left oculomotor nerve (arrows).
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Fig. 9B —57-year-old man with ophthalmoplegic migraine. Unenhanced
axial (A) and enhanced axial (B) and coronal (C)
T1-weighted images reveal smooth enlargement and homogeneous enhancement of
cisternal segment of left oculomotor nerve (arrows).
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Fig. 9C —57-year-old man with ophthalmoplegic migraine. Unenhanced
axial (A) and enhanced axial (B) and coronal (C)
T1-weighted images reveal smooth enlargement and homogeneous enhancement of
cisternal segment of left oculomotor nerve (arrows).
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Granulomatosis
Intracranial neurosarcoidosis has a predilection for the basal
leptomeninges, and involvement of every cranial nerve has been described. MRI
shows a spectrum of CNS abnormalities including diffuse or nodular thickening
and abnormal enhancement of the leptomeninges in the basal cisterns and
hypothalamic regions [12]
(Figs. 10A, and
10B). Perineural spread has
also been reported in sarcoidosis
[13]. Clinical involvement and
imaging cranial nerve involvement frequently do not coincide, and clinical
resolution may not imply imaging resolution
[14].
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Fig. 10A —58-year-old man with neurosarcoidosis. Contrast-enhanced
axial T1-weighted images show enhancement and involvement of cisternal
segments of right and left seventh and eighth cranial nerve complexes
(arrows, A) and root entry zones of preganglionic trigeminal
nerves (arrows, B).
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Fig. 10B —58-year-old man with neurosarcoidosis. Contrast-enhanced
axial T1-weighted images show enhancement and involvement of cisternal
segments of right and left seventh and eighth cranial nerve complexes
(arrows, A) and root entry zones of preganglionic trigeminal
nerves (arrows, B).
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Idiopathic hypertrophic cranial pachymeningitis is a rare disease
characterized by inflammation and fibrosis of the dura mater. It remains a
diagnosis of exclusion but may be the presenting manifestation of
granulomatous diseases such as sarcoidosis, Wegener's granulomatosis, or
tuberculosis. MRI shows focal or diffuse thickening and enhancement of the
dura that encase cranial nerves causing recurrent cranial neuropathies. The
oculomotor, abducens, and facial nerves are more frequently involved
[15].
Tolosa-Hunt syndrome consists of painful ophthalmoplegia related to a
granulomatous inflammatory process in the cavernous sinus. MRI findings are
nonspecific and include enhancement and abnormal soft tissue in the
ipsilateral cavernous sinus and orbital apex
[16] (Figs.
11A, and
11B).
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Fig. 11A —35-year-old woman with Tolosa-Hunt syndrome presenting with
painful ophthalmoplegia. Enhancement and enlargement of left cavernous sinus
are illustrated on contrast-enhanced coronal T1-weighted image
(arrow).
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Fig. 11B —35-year-old woman with Tolosa-Hunt syndrome presenting with
painful ophthalmoplegia. Extension of enhancing tissue into left orbital apex
(arrow) is seen on contrast-enhanced axial T1-weighted image.
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Postradiation Neuritis
Radiation-induced cranial nerve injury is an uncommon, usually delayed,
complication of radiation therapy or radiosurgery. Cranial nerve deficits may
be permanent or resolve spontaneously. Loss of the nerve-blood barrier due to
demyelination and ischemia, coagulation necrosis, or peripheral fibrosis
results in cranial nerve enhancement. Radiation-induced optic neuropathy
occurs months to years after exposure of the anterior visual pathways to
ionizing radiation. MRI shows smooth enlargement and enhancement of the optic
nerve and chiasm (Fig.
12).
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Fig. 12 —48-year-old woman with postradiation optic neuritis who
presented with loss of vision in left eye 8 months after radiation therapy.
Patient had previously undergone resection of adenoid cystic carcinoma of
right maxillary sinus. Contrast-enhanced axial T1-weighted image shows
enhancement of intracranial portion of left optic nerve (long arrow).
Note large enhancing tumor (short arrows) with internal hemorrhage in
right temporal lobe.
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Primary Nerve Tumors
Vestibular schwannomas are the most common cranial nerve schwannomas,
followed by trigeminal and facial schwannomas and then glossopharyngeal,
vagus, and spinal accessory nerve schwannomas (Figs.
13A, and
13B). Neurofibromatosis 2 is
characterized by bilateral vestibular schwannomas. Schwannomas of the other
cranial nerves occur more frequently in neurofibromatosis 2. Enhancing
hemangiomas, meningiomas, or metastases may mimic the appearance of early
schwannomas.
APPENDIX 1: Classification of Cranial Neuropathies
Neoplastic: Carcinoma, lymphoma, leukemia, glioma, myeloma
Infection: Tuberculosis, syphilis, leprosy, mycoplasma, Lyme
disease, viral infections, fungal infections, parasi infections
Postinfectious and demyelinating: Bell's palsy, Ramsay Hunt
syndrome, ophthalmoplegic migraine, Miller Fisher syndrome, polyneuritides,
multiple sclerosis
Granulomatosis: Sarcoidosis, idiopathic granulomatosis, vasculitis,
inflammatory granulomatosis
Angiopathic: Wegener's granulomatosis, Churg-Strauss syndrome,
Behçet's syndrome, diabetes
Idiopathic: Idiopathic pachymeningitis, Tolosa-Hunt syndrome
Physical or chemical: Radiation, trauma, surgery, toxins, drugs
Hereditary: Dejerine-Sottas disease, Krabbe's disease
Primary nerve tumors: Schwannoma, neurofibromatosis
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Abstract
Introduction
