AJR 2004; 182:289-295
© American Roentgen Ray Society
Imaging Manifestations of Neurosarcoidosis
J. Keith Smith1,
Maria Gisele Matheus and
Mauricio Castillo
1 All authors: Department of Radiology, University of North Carolina School of
Medicine, CB# 7510, Chapel Hill, NC 27599-7510.
Received June 5, 2003;
accepted after revision August 12, 2003.
Address correspondence to J. K. Smith.
Introduction
Sarcoidosis is an idiopathic systemic disease characterized histologically
by the formation of non-caseating granuloma. The disease affects all parts of
the body, especially the lungs and lymph nodes. In the head and spine, the
most typical imaging appearance is thickening and enhancement of the
leptomeninges, especially around the base of the brain, but sarcoidosis may
involve bone, dura mater, nerve roots, leptomeninges, and parenchyma,
individually or in combination
[1,
2]. We review the clinical and
imaging findings of central nervous system involvement by sarcoidosis.
Epidemiology
Sarcoidosis can affect patients of all ages and races but is most common in
the third and fourth decades. Incidence is estimated to be around 20 per
100,000 among Caucasians. African Americans and North European whites have the
highest disease incidence, and women are more frequently affected than men
[1–3].
The exact cause of sarcoidosis is unknown. Genetic factors confer increased
susceptibility, perhaps the major histocompatibility complex or complement
receptor gene [4]. Also,
granuloma formation is initiated by T lymphocytes responding to a specific but
unknown antigen. RNA and DNA from Mycobacterium
[5] and
Propionibacterium organisms
[6] have been detected in
sarcoidosis lesions, suggesting a possible cause.
Central nervous system involvement is common in postmortem series, with
about one fourth of patients with systemic disease showing histologic evidence
of central nervous system involvement. Symptomatic central nervous system
involvement in living patients is less common, found in only about 5% of cases
[3]. Imaging evidence of
central nervous system disease, however, is seen in about 10% of patients with
systemic disease. It is estimated that less than 1% of patients have isolated
central nervous system involvement, without systemic evidence of disease. In
cases with central nervous system involvement, however, the central nervous
system symptoms are frequently the presenting ones. For this reason, it is
important for the radiologist to recognize the imaging manifestations of
neurosarcoidosis. Unfortunately, the imaging manifestations of central nervous
system sarcoidosis are protean.
Clinical Presentation
Clinical symptoms of neurosarcoidosis depend on the site of granuloma
involvement and are nonspecific. Facial nerve paralysis (central or peripheral
type) and vision loss are common symptoms, as are headache, seizure, and signs
of meningeal irritation [2,
3]. Signs and symptoms easily
confused with those of multiple sclerosis such as weakness, paresis,
paresthesia, diplopia, and dysarthria are frequent. Less common are symptoms
of diabetes insipidus, such as intense thirst and polyuria, stemming from
involvement of the hypothalamus or pituitary gland. Hydrocephalus is another
uncommon clinical feature. Spinal cord involvement may present clinically with
lower extremity weakness and other nonspecific signs of myelopathy.
Diagnostic Tests
The diagnosis of definite neurosarcoidosis is confirmed by biopsy results
showing non-caseating granuloma, with an absence of organisms or other causes.
In many cases, biopsy is not possible or desirable because of the site of
involvement. A diagnosis of probable neurosarcoidosis can be based on clinical
or imaging evidence of lesions, with evidence of systemic sarcoidosis obtained
from a biopsy of another organ or positive results on a Kveim test
[2], which is performed by
intradermal injection of homogenized spleen or liver from a patient with known
sarcoidosis. The test result is positive if biopsy of the skin site 4–6
weeks later shows typical sarcoid granulomas. Although the Kveim test has high
sensitivity and specificity, limited availability of suitable safe test
material has limited its widespread use
[3]. In the absence of
histologic proof of systemic disease, the diagnosis can be supported by two or
more findings, such as typical chest radiograph or gallium scan findings or
elevated serum angiotensin-converting enzyme levels.
A whole-body gallium scan shows increased uptake related to central nervous
system disease in less than 5% of patients with this condition but may give
evidence of the presence of systemic disease in 45% of patients with central
nervous system involvement [2].
Gallium-67 citrate injected IV is taken up by sites of active sarcoidosis and
other inflammatory and neoplastic processes such as tuberculosis and lymphoma.
Because it lacks specificity, other authors report limited utility of the
gallium scan [3].
Serum levels of angiotensin-converting enzyme can be elevated in patients
with pulmonary sarcoidosis. Angiotensin-converting enzyme is produced by the
epithelioid cells of granulomatous lesions and can therefore be elevated in a
number of disorders, including diabetes, silicosis, and cirrhosis
[3]. Patients with
neurosarcoidosis have been reported to have elevated serum
angiotensin-converting enzyme in 5–50% of cases
[7]. In a recent review, only
one patient of 12 with definite neurosarcoidosis had elevation of serum
angiotensin-converting enzyme levels, whereas one other of the 12 had elevated
cerebrospinal fluid angiotensin-converting enzyme levels
[2]. Other cerebrospinal fluid
abnormalities, also nonspecific, were common, including elevated protein
levels and lymphocytosis.
Imaging Findings
Sarcoidosis can involve any part of the nervous system and its coverings.
We concentrate on the types of involvement that might be seen on imaging of
the brain and spine. In both areas, sarcoidosis may involve the parenchyma of
the brain and spine, nerve roots, the leptomeninges, the dura mater, and the
surrounding bony structures. In most cases, the appearance of lesions is
nonspecific so that sarcoidosis is included in a broad differential diagnosis
[8].
Brain
Intraparenchymal lesions.—The most common parenchymal
abnormality described in some series is multiple nonenhancing periventricular
white matter lesions seen as high signal intensity on T2-weighted images
[2,
9]. These lesions may be
indistinguishable from those seen with vascular disease or multiple sclerosis.
Because this type of lesion is common in patients without sarcoidosis as well,
it is not clear that the lesions are always related to the sarcoidosis.
Enhancing parenchymal mass lesions (Fig.
1) are also commonly reported
[10]. These lesions may be
mistaken for primary or metastatic tumor or tumefactive demyelination.
Enhancing mass lesions are frequently associated with nearby leptomeningeal
involvement and are thought to represent spread of leptomeningeal disease
along the perivascular spaces in many cases
[11]. Mass lesions associated
with sarcoidosis may be dark on T2-weighted images
[10,
12], but very cellular
metastasis and lymphoma may also have this appearance. Central necrosis is
uncommon in sarcoidosis lesions. Patients with enhancing brain lesions
frequently present with seizures
[11].
View larger version (145K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 1. —T1-weighted parasagittal MRI of 31-year-old man with
neurosarcoidosis obtained after contrast administration shows enhancing lesion
(arrow) in brain parenchyma, arising from spread of sarcoidosis
granuloma along perivascular spaces.
|
|
Leptomeningeal involvement.—Leptomeningeal involvement is
perhaps the most typical manifestation of central nervous system sarcoidosis,
seen in about 40% of cases. This is usually seen as thickening and enhancement
of the leptomeninges on contrast-enhanced T1-weighted images
(Fig. 2). The enhancement may
be diffuse or nodular [7].
There may be spread along the perivascular spaces, causing the appearance of
intraparenchymal involvement. There is a predilection for the basilar
meninges. Leptomeningeal disease can be distinguished from dural disease by
involvement of the cortical sulci and perivascular spaces or the cisterns
around the base of the brain. This pattern of involvement is generally
indistinguishable from that seen with tuberculosis or lymphoma involving the
leptomeninges.
View larger version (149K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 2. —Leptomeningeal sarcoidosis of brain in 45-year-old woman.
T1-weighted axial image obtained after contrast administration shows
enhancement involving basilar cisterns, Sylvian fissures, and cortical sulci
(arrows).
|
|
Hypothalamus and pituitary involvement.— Leptomeningeal
involvement around the hypothalamus and pituitary infundibulum may be seen
with basilar leptomeningeal involvement or as an isolated finding
(Fig. 3). Again, this is seen
as thickening and enhancement on contrast-enhanced T1-weighted images. This
isolated involvement of the infundibulum mimics the appearance of
histiocytosis. Hypothalamic and infundibular involvement may present as
diabetes insipidus or amenorrhea
[13,
14]. Sarcoidosis of the
pituitary gland proper has been reported, with nonspecific imaging findings of
a cystic enhancing intrasellar mass extending into the suprasellar space
[15].
Cranial nerve involvement.—Cranial nerve involvement may
occur along with leptomeningeal involvement or as an isolated finding. There
is poor correlation between the imaging evidence of cranial nerve involvement
and clinical neuropathy, with some patients having clinical symptoms without
imaging findings and many having imaging findings without clinical symptoms.
Clinically, any cranial nerve can be affected, but the most common cranial
nerve deficit involves the facial nerve (VII), whereas radiographically the
optic nerves (II) are most commonly abnormal
[2,
11]. The optic nerve
involvement (Fig. 4A,
4B) may occur at the chiasm or
intraorbital portions of the optic nerves and may be bilateral or unilateral
[16]. The differential
diagnosis of isolated optic nerve involvement includes optic neuritis and
optic nerve glioma. The dural sheath of the optic nerve can also be involved,
mimicking an optic nerve meningioma
[2]. Sarcoidosis may involve
the orbital fat, muscles, lacrimal glands, or globe with a diffuse
infiltrative mass radiographically indistinguishable from orbital pseudotumor
[17,
18]. The imaging findings of
other cranial nerve involvement are enlargement of the cranial nerves with
enhancement on contrast-enhanced T1-weighted images
(Fig. 5). The cranial nerves
can also become involved via perineural spread of sarcoidosis from sinonasal
disease [19].
View larger version (155K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 4A. —Optic nerve sarcoidosis. Contrast-enhanced fat-saturated
T1-weighted axial image of 35-year-old woman shows enhancement of entire
visible portions of both optic nerves in orbit and optic canals
(arrowheads). Enhancement of extraocular muscles is normal
finding.
|
|
View larger version (161K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 4B. —Optic nerve sarcoidosis. Contrast-enhanced fat-saturated
T1-weighted coronal image of 26-year-old woman with rapid vision loss shows
enhancement and thickening of both optic nerves in prechiasmatic segment
(arrows).
|
|
View larger version (159K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 5. —Cranial nerve sarcoidosis in 43-year-old man with diffuse
sarcoidosis. Contrast-enhanced T1-weighted parasagittal image shows enhancing
lesion causing thickening and enhancement of cisternal segment of third
cranial nerve (arrowheads). Note enhancing suprasellar mass (m) and
diffuse leptomeningeal enhancement (arrows).
|
|
Hydrocephalus.—Hydrocephalus occurs in 5–12% of
patients with central nervous system involvement of sarcoidosis
[2,
7]. This may be a communicating
type, presumably due to altered cerebrospinal fluid resorption; associated
with dural or leptomeningeal involvement; or an obstructive type, due to
adhesions or loculations of the ventricular system caused by leptomeningeal or
pial involvement (Fig. 6A,
6B). Isolation of the fourth
ventricle (termed "trapped fourth ventricle") or other parts of
the ventricular system may occur
[20].
View larger version (131K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 6A. —Hydrocephalus associated with neurosarcoidosis in 31-year-old
man with neurosarcoidosis (same patient as in
Fig. 1). Contrast-enhanced
T1-weighted axial image shows enlargement of lateral ventricles and
enhancement in and adjacent to wall of left lateral ventricle.
|
|
View larger version (129K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 6B. —Hydrocephalus associated with neurosarcoidosis in 31-year-old
man with neurosarcoidosis (same patient as in
Fig. 1). Fluid-attenuated
inversion recovery MRI obtained at same level as A shows different
signal intensity in left and right lateral ventricles, presumably due to
elevated protein concentration within left lateral ventricle (L), which is
isolated from rest of ventricular system.
|
|
Dural involvement.—Dural involvement by sarcoidosis can
present as focal dural masses (Fig.
7A,
7B) or diffuse dural
thickening (Fig. 8). Lesions
typically enhance homogeneously on contrast-enhanced T1-weighted images. They
are commonly dark on T2-weighted images; this appearance can serve as a clue
to the diagnosis but still may be indistinguishable from calcified meningiomas
or very cellular dural metastases
[21,
22]. Other differential
considerations include lymphoma and idiopathic hypertrophic cranial
pachymeningitis. The latter can also be confused pathologically with
sarcoidosis because it is also a granulomatous process
[11].
View larger version (127K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 7B. —Focal masses in 31-year-old woman with dural sarcoidosis.
Fat-saturated T2-weighted axial image shows dural masses to be low signal
intensity (arrows), with some high signal of adjacent brain
parenchyma, most likely vasogenic edema.
|
|
Patients with dural involvement typically present with headaches or cranial
nerve compression. Dural involvement and leptomeningeal involvement are rarely
present together in the same region. Because of the arachnoid barrier cells, a
portion of the arachnoid mater forms a barrier to the spread of disease
through the arachnoid membrane
[11].
Vasculitis.—Histologically, a vasculitis-like pattern of
involvement of the intracranial vasculature has been reported, with
perivascular granulomatous infiltrate. This pattern may be related to
autoantibodies to vascular endothelial cells
[23,
24]. Nonenhancing white matter
lesions seen as areas of high T2 signal intensity on MRI have been attributed
to possible vascular involvement
[9]. Despite the clear reports
of histologic evidence of vascular involvement in central nervous system
sarcoidosis, it is rare that brain infarct is a presenting symptom of
neurosarcoidosis
[25–27].
Skull
Sarcoidosis lesions in the skull (Fig.
9A,
9B) are uncommon. They may be
seen in association with other bone disease or as an isolated abnormality. The
lesions show well-circumscribed nonsclerotic margins ("punched
out" appearance) and may show increased radiotracer uptake on nuclear
medicine bone scans. MRI may reveal some enhancing soft tissue in the lesion
[28,
29].
View larger version (93K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 9A. —Skull lesions of sarcoidosis. Axial CT image with bone window
settings in 46-year-old man with sarcoidosis shows well-circumscribed lytic
lesion involving inner and outer tables of calvarium, with sharp, nonsclerotic
margins (arrow).
|
|
View larger version (131K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 9B. —Skull lesions of sarcoidosis. Contrast-enhanced T1-weighted
coronal image in 38-year-old woman with diffuse sarcoidosis shows enhancing
lesion on patient's right that thins inner and outer tables of skull,
expanding diploic space (straight arrow). Second lesion on patient's
left involves only inner table (curved arrow).
|
|
Spine
Spinal neurosarcoidosis can cause an array of imaging findings, which
include intramedullary, intradural extramedullary, extradural, vertebral, and
disk space lesions.
Intramedullary spinal lesions.—Intramedullary sarcoidosis is
an uncommon manifestation of sarcoidosis, which often causes severe neurologic
sequelae. It occurs in less than 1% of sarcoidosis cases
[30]. Usually spinal cord
involvement is not an isolated or first manifestation of the disease. This
characteristic helps the radiologist presume the diagnosis and helps the
patients avoid spinal cord biopsy. From the imaging point of view,
intramedullary sarcoidosis is nonspecific with a broad differential diagnosis
including neoplasms, multiple sclerosis, and fungal infections.
Sarcoidosis spinal lesions usually appear as fusiform enlargements of the
spinal cord in the cervical or upper thoracic level
(Fig. 10). On MRI, the spinal
cord is enlarged with high signal intensity in T2-weighted images, low signal
intensity in T1-weighted images, and patchy enhancement after contrast
administration.
View larger version (88K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 10. —Spinal cord intramedullary sarcoidosis in 47-year-old man
with upper and lower extremity weakness. Contrast-enhanced sagittal
T1-weighted image shows enhancing lesion in spinal cord (arrows).
Note abnormal linear leptomeningeal enhancement (arrowheads).
|
|
Junger et al. [31] proposed
an MRI classification of intraspinal sarcoidosis in four stages correlating
with possible histologic stages of the disease: phase 1, early inflammation
showing linear leptomeningeal enhancement after gadolinium administration
along the spinal surface; phase 2, secondary centripetal spread of the
leptomeningeal inflammatory process through the Virchow-Robin spaces, showing
parenchymal involvement with faint enhancement and diffuse swelling; phase 3,
less prominent swelling and possible normal-sized spinal cord, associated with
focal or multiple enhancement; and phase 4, resolution of the inflammatory
process with normal size or atrophy of the spinal cord and no enhancement.
Phases 2 and 3 are the most frequent at clinical presentation. Other rare
findings such as calcifications, cyst formation, and extradural involvement
have also been described. Preoperative suggestion of intraspinal sarcoidosis
may alert the pathologist to look carefully for granulomas and giant cells
because sarcoidosis can mimic neoplasm and lead to frozen section
misinterpretation.
The correct diagnosis and early treatment with steroids can minimize
neurologic complications and decrease the disease morbidity rates in 42% of
the cases. MRI shows posttreatment changes or recurrence on follow-up after
steroid therapy. Koike et al.
[32] showed that the imaging
improvement of intraspinal lesions does not correlate well with clinical
improvement and depends on the degree of cord damage.
Leptomeningeal and dural lesions.—Extramedullary intradural
lesions are usually represented by leptomeningeal sarcoidosis infiltration,
present in up to 60% of spinal cord lesions. Junger et al.
[31] proposed that this
infiltration might be a precursor of intraspinal lesions, as discussed
previously. The leptomeningeal involvement may be visualized on
contrast-enhanced T1-weighted MRI as thin linear leptomeningeal enhancement or
small nodules (Fig. 11).
Clinical manifestations are not well correlated with MRI findings.
Extramedullary sarcoid granulomatous masses
(Fig. 12) are rare (we found
seven reports in the English-language literature)
[33,
34]. The extramedullary
masslike lesions have a dural base and were described as involving the
cervical, thoracic, and lumbar spine without predilection. The lesions are
shown on MRI as hypointense or isointense signal on T1-weighted images,
hyperintense signal on T2-weighted images, and marked contrast enhancement
with a dural tail described in some reports. The characteristic low T2 signal
found in dural intracranial sarcoidosis was not described in spinal lesions.
Clinical manifestations are usually present at the time of diagnosis and
result from local nerve or spinal cord compression. Surgical resection is
usually necessary to alleviate the compression symptoms, followed by treatment
with steroids. The differential diagnosis for the imaging findings includes
meningioma, nerve sheath tumors, lymphoma, carcinomatous metastasis, chloroma,
hemangiopericytoma, and other granulomatous depositions.
View larger version (125K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 11. —51-year-old man with spinal leptomeningeal sarcoidosis.
Contrast-enhanced sagittal T1-weighted images show multiple nodular enhancing
lesions along surface of spinal cord and on spinal nerve roots
(arrows).
|
|
Bone involvement.—Osseous involvement in sarcoidosis is
reported in 1–13% of patients
[35–37].
The actual frequency is probably higher because most of the osseous lesions
are asymptomatic and patients are not screened routinely. Small tubular bones
of the hands and feet are most commonly involved. Less common skeletal
involvement includes the long tubular bones, skull, ribs, spine, and pelvis
[35].
Vertebral lesions are rare and usually occur in the lower thoracic and
upper lumbar spine. Clinical manifestations include pain, tenderness, and
neuralgia. The imaging findings are usually multiple well-defined lytic
lesions with sclerotic margins in the vertebral body. They may extend into the
pedicles and paraspinal region. Sclerotic lesions (mimicking blastic
metastasis), mixed lytic and sclerotic involvement, and disk involvement are
rare and are described in a few reports
[36,
37]. MRI shows multiple
lesions with low T1 signal, high T2 signal, and enhancement after contrast
administration or low T1 and T2 signal in sclerotic lesions
(Fig. 13). Bone scintigraphy
has potential utility to localize additional sites to biopsy and as a tool for
monitoring disease activity. The imaging findings are not specific enough to
make the diagnosis of sarcoidosis. In the absence of confirmed disease
elsewhere in the body, biopsy is usually necessary to rule out diseases
causing similar-appearing lesions such as metastasis, myeloma, lymphoma, and
tuberculosis [38].
View larger version (114K):
[in this window]
[in a new window]
[as a PowerPoint slide]
|
Fig. 13. —37-year-old man with spinal vertebral sarcoidosis.
Contrast-enhanced fat-saturated sagittal T1-weighted image shows multiple
enhancing lesions in bodies and spinous processes of lumbar vertebrae
(straight arrows). Note diffuse leptomeningeal disease with nodular
thickening and enhancement of lumbar nerve roots (curved arrows).
|
|
Treatment
There is no consensus on the best treatment or efficacy of treatment of
neurosarcoidosis. Treatment of symptomatic patients is usually begun with
high-dose corticosteroids. If the patient responds to treatment, steroid
dosage may be lowered for a maintenance period or even discontinued
[3]. Correlation between
symptom resolution and resolution of imaging finding is poor, especially with
spinal cord lesions [32].
There is a high rate of progression or recurrent symptoms and recurrent
imaging findings. Patients with enhancing brain lesions show worsening, no
change, or recurrence of symptoms with treatment in 75% of cases
[11]. Methotrexate has been
used as a second-line treatment, although the effectiveness has not been
clearly established [3].
Conclusion
Central nervous system involvement occurs in a significant proportion
(5–25%) of patients with systemic sarcoidosis. Patients with systemic
disease may initially present with neurologic symptoms, and rarely, disease
may be isolated to the central nervous system. The typical imaging feature is
thickening and enhancement of the leptomeninges, especially around the base of
the brain. Other imaging findings, such as enhancing or nonenhancing
parenchymal lesions and dural and bone lesions also occur in the head and
spine. There is a high rate of progression and recurrence after treatment so
that imaging follow-up is recommended.
References
- Pickuth D, Spielmann RP, Heywang-Kobrunner SH. Role of radiology in
the diagnosis of neurosarcoidosis. Eur Radiol2000; 10:941
–944[Medline]
- Zajicek JP, Scolding NJ, Foster O, et al. Central nervous system
sarcoidosis: diagnosis and management. Q J Med1999; 93:103
–117
- Johns CJ, Michele TM. The clinical management of sarcoidosis: a
50-year experience at the Johns Hopkins Hospital.
Medicine 1999;78:65
–111[Medline]
- Iannuzzi MC, Maliarik M, Rybicki BA. Nomination of a candidate
susceptibility gene in sarcoidosis: the complement receptor 1 gene.
Am J Respir Cell Mol Biol2002; 27:3
–7[Free Full Text]
- Mitchell IC, Turk JL. Detection of mycobacterial rRNA in
sarcoidosis with liquid-phase hybridization. Lancet1992; 139:1015
–1017
- Ishige I, Usui Y, Takemura T, Eishi Y. Quantitative PCR of
mycobacterial and propionibacterial DNA in lymph nodes of Japanese patients
with sarcoidosis. Lancet1999; 354:120
–123[Medline]
- Nowak DA, Widenka DC. Neurosarcoidosis: a review of its
intracranial manifestation. J Neurol2001; 248:363
–372[Medline]
- Hayes WS, Sherman JL, Stern BJ, Citrin CM, Pulaski PD. MR and CT
evaluation of intracranial sarcoidosis. AJR1987; 149:1043
–1049[Abstract/Free Full Text]
- Dumas JL, Valeyre D, Belin C, et al. Central nervous system
sarcoidosis: follow-up at MRI during steroid therapy.
Radiology2000; 214:411
–420[Abstract/Free Full Text]
- Urbach H, Kristof R, Zentner J, Brechtelsbauer D, Solymosi L, Wolf
HK. Sarcoidosis presenting as an intra- or extra-cranial mass: report of two
cases. Neuroradiology1997; 39:516
–519[Medline]
- Christofordis GA, Spickler EM, Reccio MV, Mehta BM. MR of CNS
sarcoidosis: correlation of imaging features to clinical symptoms and response
to treatment. AJNR1999; 20:655
–669[Abstract/Free Full Text]
- Vannemreddy PS, Nanda A, Reddy PK, Gonzales E. Primary cerebral
sarcoid granuloma: the importance of definitive diagnosis in the high-risk
patient population. Clin Neurol Neurosurg2002; 104:289
–292[Medline]
- Konrad D, Gartenmann M, Martin E, Schoenle EJ. Central diabetes
insipidus as the first manifestation of neurosarcoidosis in a 10-year-old
girl. Horm Res2000; 54:98
–100[Medline]
- Lipnick RN, Hung W, Pandian MR. Neurosarcoidosis presenting as
secondary amenorrhea in a teenager. J Adolesc Health1993; 14:464
–467[Medline]
- Sato N, Sze G, Kim JH. Cystic pituitary mass in neurosarcoidosis.
AJNR 1997;18:1182
–1185[Abstract]
- Leu NH, Chen CY, Wu CS, et al. Primary chiasmal sarcoid granuloma:
MRI. Neuroradiology1999; 41:440
–442[Medline]
- Peterson EA, Hymas DC, Pratt DV, Mortenson SW, Anderson RL, Mamalis
N. Sarcoidosis with orbital tumor outside the lacrimal gland: initial
manifestation in 2 elderly white women. Arch
Ophthalmol 1998;116:804
–806[Abstract/Free Full Text]
- Carmody RF, Mafee MF, Goodwin JA, Small K, Haery C. Orbital and
optic pathway sarcoidosis: MR findings. AJNR1994; 15:775
–783[Abstract]
- Mazziotti S, Gaeta M, Blandino A, Vinci S, Pandolfo I. Perinueral
spread in a case of sinonasal sarcoidosis: case report.
AJNR 2001:22:1207
–1208[Abstract/Free Full Text]
- Hesselmann V, Wedekind C, Terstegge K, et al. An isolated fourth
ventricle in neurosarcoidosis: MRI findings. Eur
Radiol 2002;12[suppl]:S1
–S3
- Seltzer S, Mark AS, Atlas SW. CNS sarcoidosis: evaluation with
contrast-enhanced MRI. AJNR1991; 12:1227
–1233[Abstract]
- Larner AJ, Ball JA, Howard RS. Sarcoid tumor: continuing diagnostic
problems in the MRI era. J Neurol Neurosurg Psychiatry1999; 66:510
–512[Free Full Text]
- Thiel HJ, Korenke HD. Generalized sarcoidosis with brain and eye
participation [in German]. Ophthalmologica1975; 170:393
–404[Medline]
- Tsukada N, Yanagisawa N, Mochizuki I. Endothelial cell damage in
sarcoidosis and neurosarcoidosis: autoantibodies to endothelial cells.
Eur Neurol1995; 35:108
–112[Medline]
- Michotte A, Dequenne P, Jacobovitz D, Hildebrand J. Focal
neurological deficit with sudden onset as the first manifestation of
sarcoidosis: a case report with MRI follow-up. Eur
Neurol 1991;31:376
–379[Medline]
- Brown MM, Thompson AJ, Wedzicha JA, Swash M. Sarcoidosis presenting
with stroke. Stroke1989; 20:400
–405[Abstract/Free Full Text]
- Younger DS, Hays AP, Brust JC, Rowland LP. Granulomatous angiitis
of the brain: an inflammatory reaction of diverse etiology. Arch
Neurol 1988;45:514
–518[Abstract]
- Zimmerman R, Leeds NE. Calvarian and vertebral sarcoidosis.
Radiology1976; 119:384
–384[Abstract]
- Slart RM, de Jong JW, Haeck PW, Hoogenberg K. Lytic skull lesions
and symptomatic hypercalcaemia in bone marrow sarcoidosis. J Intern
Med 1999;246:117
–120[Medline]
- Hashmi M, Kyristsis AP. Diagnosis and treatment of intramedullary
spinal cord sarcoidosis. J Neurol1998; 245:178
–185[Medline]
- Junger SS, Stern BJ, Levine SR, Sipos E, Marti-Masso JF.
Intramedullary spinal sarcoidosis: clinical and magnetic resonance imaging
characteristics. Neurology1993; 43:333
–337[Abstract/Free Full Text]
- Koike H, Misu K, Yasui K, et al. Differential response to
corticosteroid therapy of MRI findings and clinical manifestations in spinal
cord sarcoidosis. J Neurol2000; 247:544
–549[Medline]
- Connor SEJ, Marshman L, Al-Sarraj S, et al. MRI of a spinal
intradural extramedullary sarcoid mass. Neuroradiology2001; 43:1079
–1083[Medline]
- Weissman MN, Lange R, Kelley C, Belgea K, Abel L. Intraspinal
epidural sarcoidosis: case report. Neurosurgery1996; 39:179
–181[Medline]
- Fisher AJ, Gilula LA, Kyriakos M, Holzaepfel CD. MR imaging changes
of lumbar vertebral sarcoidosis. AJR1999; 173:354
–356[Free Full Text]
- Jelinek JS, Mark AS, Barth WF. Sclerotic lesions of the cervical
spine in sarcoidosis. Skeletal Radiol1998; 27:702
–704[Medline]
- Kenney CM, Goldstein SJ. MRI of sarcoid spondylodiskitis.
J Comput Assist Tomogr 1992;16
: 660–662[Medline]
- Rua-Figueroa I, Gantes MA, Erausquin C, et al. Vertebral sarcoid:
clinical and imaging findings. Semin Arthritis Rheum2002; 31:346
–352[Medline]
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
J. S. Hahn, D. Pohl, M. Rensel, S. Rao, and for the International Pediatric MS Study Group
Differential diagnosis and evaluation in pediatric multiple sclerosis
Neurology,
April 17, 2007;
68(16_suppl_2):
S13 - S22.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Kobylecki and S. Shaunak
Refractory neurosarcoidosis responsive to infliximab
Practical Neurology,
April 1, 2007;
7(2):
112 - 115.
[Full Text]
[PDF]
|
|
|
Top
Introduction
Epidemiology
