Content uploaded by Nishanth Sadashiva
Author content
All content in this area was uploaded by Nishanth Sadashiva on Nov 16, 2016
Content may be subject to copyright.
Volume 8 Issue 1 January - March 2017
Journal of Neurosciences in Rural Practice • • • April-June • Volume 7Issue 22016 Pages 00-00
Spine
8 mm
Sadashiva N, Nandeesh BN, Shukla D, Bhat D,
Somanna S, Devi BI. Isolated sphenoid sinus lesions:
Experience with a few rare pathologies.
J Neurosci Rural Pract 2017;8:107-13.
107
© 2017 Journal of Neurosciences in Rural Practice | Published by Wolters Kluwer - Medknow
Introduction: The sphenoid sinus is often neglected because of its difcult access. The deep
position of the sphenoid sinus hinders early diagnosis of pathologies in that location. Delayed
diagnosis can cause serious complications due to proximity to many important structures.
Objectives: The aim of this study is to demonstrate different pathologies which can affect the
sphenoid sinus and elucidate the ndings. Methods: Cases of isolated sphenoid sinus lesions
encountered in the neurosurgical setting which had rare pathologies are discussed. Pathologies
such as Langerhans cell histiocytosis, solitary plasmacytoma, chordoma, pituitary adenoma,
leiomyosarcoma, fungal infection, and mucocele which appeared primarily in sphenoid sinus are
discussed along with their imaging features and pathological ndings. Conclusion: Multitude
of different pathologies can occur in sphenoid sinus. Detailed preoperative imaging is very
helpful, but transnasal biopsy and histological study are required often for denitive diagnosis.
The possible advantages of early diagnosis before spread of pathology for prognosis cannot be
overemphasized.
Keywords: Chordoma, Langerhans cell histiocytosis, leiomyosarcoma, mucocele,
pituitary adenoma, plasmacytoma, sphenoid sinus
Isolated Sphenoid Sinus Lesions: Experience with a Few Rare
Pathologies
Nishanth Sadashiva, B. N. Nandeesh1, Dhaval Shukla, Dhananjaya Bhat, Sampath Somanna, Bhagavatula Indira Devi
Address for correspondence: Dr. Dhaval Shukla,
Department of Neurosurgery, National Institute of Mental Health
and Neurosciences, Bengaluru ‑ 560 029, Karnataka, India.
E‑mail: neurodhaval@rediffmail.com
CaseIllustrations
• A 12‑year‑old male child had headache for 2 months and
diplopia for 15 days. Child had right 6th nerve paresis. CT
showed a well‑dened homogenously enhancing sphenoid
sinus lesion. Extending superiorly and on both sides.
MRI showed T1‑hypo‑isointemse, T2‑hyper‑isointense,
and heterogeneously enhancing mass in sphenoid sinus.
Patient underwent endoscopic transnasal decompression of
lesion. Lesion was grayish white granular with moderate
vascularity. Histopathology showed polymorphous cellular
lesion with multiple conglomerate conuent histiocytic cells,
with giant cells and mixed inammatory cells. Hemorrhage
and necrosis were noted. Histiocytes had a moderate amount
of cytoplasm with oval nucleus and central constriction
and groves. Immunohistochemistry (IHC) showed CD1a
positive with MIB‑1 labeling index of 10%–12% [Figure 1].
Diagnosis of Langerhans cell histiocytosis (LCH) was
made. Patient was conservatively managed, and the child is
asymptomatic at 18 months follow‑up
• A 43‑year‑old male had headache for 1 year, double vision
for 8 months, and diminution of vision in both eyes for
Introduction
As more and more intracranial lesions are approached
through the endoscopic transnasal route, neurosurgeons
nowadays come across a lot of lesions in the sphenoid sinus
with or without extension to intracranial cavity. We hereby
describe our experience with few of the lesions which were
in the sphenoid sinus. Isolated sphenoid sinus lesions are
uncommon, accounting for 1%–2.7% of all paranasal sinuses
lesions.[1] They usually present with nonspecic symptoms
and are inaccessible by physical examination. The clinical
presentation involves vague headaches and may be associated
with purulent rhinorrhea, retropharyngeal drip, nasal
obstruction, abnormal vision, and nerve decits.[2]
The sphenoid sinus is anatomically in close relationship with
the brain, meninges, optic nerve, internal carotid artery (ICA),
cavernous sinus, and cranial nerve (oculomotor, trochlear,
ophthalmic, and maxillary branches of the trigeminal nerve
and abducens).[3] Delayed diagnosis and treatment can result in
serious complications. Conventional radiographs do not allow
a good view of the sphenoid sinus due to its location in the
central skull base. Due its deep position, imaging technologies
such as computed tomography (CT), magnetic resonance
imaging (MRI), and endoscopic biopsy play a signicant role
in understanding different pathologies affecting this region.
The aim of this study is to demonstrate different pathologies
which can affect the sphenoid sinus and elucidate the ndings.
Departments of Neurosurgery
and 1Neuropathology,
National Institute of Mental
Health and Neurosciences,
Bengaluru, Karnataka, India
ABSTRACT
Case Series
This is an open access arcle distributed under the terms of the Creave Commons
Aribuon-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak,
and build upon the work non-commercially, as long as the author is credited and the new
creaons are licensed under the idencal terms.
For reprints contact: reprints@medknow.com
Access this article online
Quick Response Code:
Website:
www.ruralneuropractice.com
DOI:
10.4103/0976-3147.193540
How to cite this article: Sadashiva N, Nandeesh BN, Shukla D, Bhat D,
Somanna S, Devi BI. Isolated sphenoid sinus lesions: Experience with
a few rare pathologies. J Neurosci Rural Pract 2017;8:107-13.
Sadashiva, et al.: Isolated sphenoid sinus lesions
108 Journal of Neurosciences in Rural Practice ¦ Volume 8 ¦ Issue 1 ¦ January - March 2017
1 month. He was on antiretroviral therapy for human
immunodeciency virus (HIV) infection since 3 years.
CD4 count was 320 cells/mm3. He was previously treated
for pulmonary tuberculosis 1 year back. The visual
acuity was 6/18 bilaterally with left lateral rectus palsy.
CT scan showed a sphenoid‑sellar lesion. MRI showed
well‑dened lobulated homogeneous lesion involving
the sphenoid sinus, sella, and clivus. The lesion was
homogeneously isointense to gray matter on T2‑weighted
image (T2WI) and hyperintense on T2‑weighted
image (T1WI) without any diffusion restriction. There
was no evidence of blooming on gradient images. Strong
homogeneous postcontrast enhancement was noted. The
lesion was seen invading bilateral cavernous sinuses.
Patient underwent endoscopic transnasal decompression
of the lesion. Histopathology showed cellular lesion with
monomorphic small to medium cells in sheets, inltrating
bone which was strongly positive for lambda light chain
and few cells for kappa chain, negative for cytokeratin,
chromogranin, and pituitary hormones [Figure 2]. Features
were suggestive of plasmacytoma. Systemic workup for
myeloma was negative. Patient underwent radiotherapy,
and MRI performed 1 year later showed no recurrence
• A 41‑year‑old male had headache and blurring of vision
for 1 year, which increased in last 10 days. There was
no perception of light in the left eye, and vision in the
right eye was 6/9. CT showed well‑dened sphenoid
sinus lesion with sellar and suprasellar extension. MRI
showed an expansile mass lesion arising from the
sphenoid sinus expanding the sinus uniformly. Pituitary
was seen separately and displaced superiorly. Lesion
showed hypointense signal on T1WI, hyperintense
on T2WI with scattered areas of microbleeds within.
Diffusion‑weighted imaging showed predominantly
facilitated diffusion. On postcontrast study, variegated
pattern of enhancement was seen within the lesion. Optic
nerves appeared to be compressed at the optic canal level
with superior displacement of the optic chiasm. Bilateral
ICA was splayed by the mass lesion without any luminal
narrowing. Patient underwent endoscopic transnasal
transsphenoidal decompression of soft suckable vascular
lesion inside sphenoid sinus. Histopathology showed a
cellular neoplasm with prominent myxoid stroma, small
epithelial‑like dispersed cells with eosinophilic cytoplasm
arranged in sheets, and trabeculae, interspersed with
characteristic vacuolated physaliphorous cells [Figure 3].
Impression was chordoma. MRI at 3 months after surgery
showed small residue for which radiotherapy was given
• A 52‑year‑old male had headache for 5 years, and nasal
bleeding for 1 month. He is a known case of Parkinson’s
disease on treatment. Although his visual acuity was
normal, he had right temporal eld defect. MRI was
suggestive of primary sphenoid sinus lesion, with sellar
extension. Patient underwent transnasal decompression of
soft suckable vascular lesion. There was no bony defect
seen in the sellar oor [Figure 4]. Histopathology was
suggestive of ectopic pituitary adenoma. He underwent
radiotherapy for residual tumor. MRI performed at
7 months after surgery showed very small residual lesion,
which was managed conservatively
• A 53‑year‑old male had headache for 8 months,
decreased vision in the right eye, and numbness of face
for 1 month. Visual acuity was limited to perception of
light. MRI showed a sphenoid sinus lesion T1‑isointense,
T2‑hypointense, and well enhancing on contrast. CT scan
showed lesion extending till posterior nasal cavity with
bone erosion. Patient underwent endoscopic transnasal
Figure 1: (a) Magnetic resonance imaging T1‑weighted image sagittal view showing an
isointense mass lesion in the sphenoid sinus, (b) the lesion is enhancing on contrast on
gadolinium contrast sagittal view, and (c) coronal view. (d) Shows a microphotograph
with clusters of histiocytoid cells with a convoluted, indented nucleus admixed with
giant cells and mixed inammatory cells (H and E, ×400). Inset showing the tumor
cells positive for CD1a immunostain (×400) suggestive of Langerhans cell histiocytosis
ab
cd
Figure 2: (a) Showed a T1‑weighted sagittal view showing an isointense mass lesion
located in the sphenoid sinus with (b) showing postgadolinium contrast enhancement of
the lesion in T1‑weighted sagittal images and (c) coronal images. (d) Microphotograph
showing respiratory mucosa (*) with a submucosal cellular inltrating neoplasm (#) which
is inltrating the bone ($) as well (H and E, ×100). Inset shows the tumor composed of
plasmacytoid cells (H and E, ×200) suggestive of plasmacytoma
ab
cd
Sadashiva, et al.: Isolated sphenoid sinus lesions
109
Journal of Neurosciences in Rural Practice ¦ Volume 8 ¦ Issue 1 ¦ January - March 2017
decompression of lesion which was seen growing
predominantly posterior and inferior, occluding choana
superiorly till cranial base and nasal cavity. Lesion was
rm, moderately vascular with cartilaginous feel. Dura was
not involved. Histopathology of lesion showed variably
cellular lesion composed of fragments of interlacing and
whorled fascicles of spindle cells having oval at ended
nuclei and moderate eosinophilic cytoplasm. There
were signicant anisonucleosis and scattered mitosis
(2–3/10 hpf) and evidence of bone invasion. IHC showed
tumor cells to be strongly positive for vimentin and
smooth muscle actin, negative for desmin and S‑100.
MIB‑1 labeling was 8%–10% [Figure 5]. Features were
suggestive of leiomyosarcoma (LMS). Patient was referred
to oncologist for adjuvant therapy and is not available for
follow‑up
• A 48‑year‑old diabetic female had double vision for
2 days. She had isolated left 6th nerve paresis. MRI
showed a T1‑hyperintense, T2‑hypointense right‑sided
sphenoid sinus lesion, which was showing peripheral
contrast enhancement. Patient underwent transsphenoidal
biopsy. Histopathological examination revealed fungal ball
with admixture of broad aseptate fungi with thin septate
acute angled hyphae with chains of spores and conidia
indicative of Aspergillus. Some hyphae were pigmented.
There were no eosinophilic inltrate or Charcot‑Leyden
crystals [Figure 6]. Final impression was combined
zygomycosis and Aspergillus infection without any
host response. Patient was put on voriconazole and was
asymptomatic at 13 months follow‑up
• A 61‑year‑old male presented with progressive visual
deterioration in the left eye, and ptosis for 1 month. He
was previously operated for a mucocele about 5 years back.
Patient underwent transnasal resection of lesion [Figure 7].
Diagnosis was sphenoid sinus mucocele.
Discussion
The sphenoid sinus has often been neglected because of its
isolated location and difcult access. The deep position of
the sphenoid sinus prevents and hinders early diagnosis of
pathologies in that location.[4] Delayed diagnosis and treatment
can result in serious complications due to proximity of
different vital structures. Imaging technologies such as CT
and MRI along with the endoscopic surgical techniques have
revolutionized the treatment strategies for lesions involving
sphenoid sinus.
As more and more neurosurgical procedures are done through
endoscopic transsphenoidal route, there is an increase in the
number of sphenoid sinus lesions managed by neurosurgeons.
Isolated sphenoid sinus lesions usually present with headache,
followed by ophthalmological and nasal symptoms.[5] Of these
lesions, 72% are inammatory, 16% are neoplastic, and about
12% are because of other causes such as cerebrospinal uid
leak and brous dysplasia.[6] Although CT is investigation
of choice, it is difcult to distinguish tumor from soft tissue
swelling and secretions. MRI is thought to be complementary,
but bony septae and malignant osseous lesions are poorly
distinguished. Cases seen in neurosurgery are commonly
evaluated by MRI. We presented imaging and histopathological
ndings of seven cases of isolated sphenoid sinus lesion
with different diagnosis. In the above‑illustrated cases, only
lesions involving the sphenoid sinus were included. Patients
were evaluated by objective ear, nose, and throat examination
Figure 4: (a) Shows a T2 weighted sagittal magnetic resonance imaging image with
a heterogeneously iso‑hyperintense mass located in the sphenoid sinus, (b) the lesion
is enhancing heterogeneously on postgadolinium contrast sagittal magnetic resonance
imaging and (c) axial magnetic resonance imaging. (d) Microphotograph showing the
neoplasm composed of closely packed acinar clusters of uniform round to polyhedral
neuroendocrine cells (H and E, ×400) suggestive of pituitary adenoma
ab
cd
Figure 3: (a) Shows a T2‑weighted sagittal magnetic resonance imaging with a
hyperintense mass lesion located in the sphenoid sinus which is enlarged. (b) Shows
the lesion in not enhancing on T1‑weighted postgadolinium contrast compared to
(c) axial T1‑weighted image with a iso‑hypointense mass located in the sphenoid sinus.
(d) Microphotograph showing a myxoid neoplasm with diffusely scattered polyhedral
cells having a vacuolated bubbly cytoplasm (Physaliphorous cells) in a highly myxoid
stroma (H and E, ×400) suggestive of chordoma
ab
cd
Sadashiva, et al.: Isolated sphenoid sinus lesions
110 Journal of Neurosciences in Rural Practice ¦ Volume 8 ¦ Issue 1 ¦ January - March 2017
followed by imaging using MRI and a few cases with a CT as
well. Isolated sphenoiditis due to infection is a common cause
of such lesions, and hence a course of antibiotics for 3 weeks
was given in cases where there was no suspicion about some
other lesion. Such lesions were not included. We now discuss
each pathological entity seen in sphenoid sinus.
LCH is a rare disorder with excessive proliferation of
pathologic Langerhans cells. It is mainly seen in children and
adolescents, but may occur in any age group.[7] It is commonly
found in males, with a ratio of 2.5:1. The etiology of LCH
is not well dened, and there is a lack of understanding with
inconsistencies in the literature.[8] LCH is seen as hyperintense
lesion on T2 and hypointense on T1‑weighted MRI. LCH
occurring in sphenoid sinus is very rare, and only a few
cases have been described, especially involving neighboring
structures.[9‑11] When involving only skull base, various
modalities such as direct radiotherapy, only biopsy, biopsy
and radiotherapy, or excision and radiotherapy have been
reported with comparable efcacy. Our reported case was a
child; hence he underwent decompression of lesion followed
by observation.
Plasmacytomas are localized plasma cell tumors which can
occur either in tissues (extramedullary) or in bones (solitary
bone plasmacytomas).[12] Intracranial plasmacytomas usually
present in the skull base and arise from the bones or from
the soft tissue of the nasal cavity and paranasal sinuses.[13]
Extramedullary plasmacytomas constitute approximately 3%
of all neoplasms originating from plasma cells. They generally
display a destructive course.[14] Till date, only twenty cases
of sphenoid sinus plasmacytomas have been reported.[14]
Our reported case was HIV positive leading to possibility
of fungal, which was ruled out by IHC. There was no
systemic involvement, and diagnosis of isolated sphenoid
plasmacytoma was conrmed. Although the outcome of
solitary plasmacytoma is variable, our patient was recurrence
free after adjuvant therapy at 12 months follow‑up.
Chordomas are midline tumors of the central nervous system,
which arise from remnants of the primitive notochord where
the heterotopic rests are usually situated extradurally within the
bones of the axial skeleton. They are equally distributed in the
skull base (32%), mobile spine (32.8%), and sacrum (29.2%),
and of all intracranial tumors, skull base account for only
0.1%–0.2% of all chordomas.[15] Although clival chordoma is a
well‑known entity, our case was unique as it was predominantly
intrasphenoidal leading to possibility of alternate diagnosis.
There are only a few cases where chordoma has been reported
to be arising predominantly from sphenoid sinus.[16‑19] Although
the role of radiotherapy is controversial, we still chose to treat
this patient for residual lesion.
Ectopic sphenoid sinus pituitary adenoma by denition is the
tumors centered within the sphenoid sinus and demonstrated,
by imaging studies or intraoperative examination, a normal
sella turcica without a concurrent pituitary adenoma.[20]
Ectopic pituitary adenomas are derived from embryologic
remnants along the path of migration of Rathke’s pouch,
and more than fty ectopic pituitary adenomas have been
reported.[21] Ectopic pituitary adenomas may be found in the
sphenoid sinus region, clivus, parapharyngeal space, nasal
cavity and nasopharynx, hypothalamus, third ventricle, and in
the suprasellar locations.[22] About two‑thirds are hormonally
active adenomas.[23] Our reported case was a nonfunctional
pituitary adenoma which was managed surgically and with
radiotherapy for the residual lesion.
Figure 6: (a) Shows a T2‑weighted sagittal magnetic resonance imaging with a
hypointense mass lesion located inside the sphenoid sinus. (b) The lesion is not
enhancing peripherally on postgadolinium T‑weighted images (c) and in coronal
images. (d) Microphotograph showing ulcerated mucosa with a colony of fungal hyphae
morphologically resembling Aspergillus (H and E, ×100) inset shows the fungal colony
with slender septate and branching hyphae (H and E, ×400)
ab
cd
Figure5: (a) Showing a T2‑weighted sagittal view with a heterogeneously iso‑hypointense
mass lesion located in the sphenoid sinus. (b) Shows heterogonous enhancement of lesion
after gadolinium administration, (c) lesion is isointense on plain T1‑weighted images.
(d) Microphotographs showing a cellular spindle cell tumor with interlacing fascicles;
inset (1) showing the increased MIB‑1 labeling and inset (2) showing positive staining for
smooth muscle actin. Vimentin positive but negative for S100, desmin, creatine kinase,
and CD99 suggestive of leiomyosarcoma
ab
cd
Sadashiva, et al.: Isolated sphenoid sinus lesions
111
Journal of Neurosciences in Rural Practice ¦ Volume 8 ¦ Issue 1 ¦ January - March 2017
LMS is a disease of the gastrointestinal and genitourinary
tracts. It has been associated with a history of irradiation,
retinoblastoma, chemotherapy, HIV, and AIDS. Approximately,
fty cases of primary sinonasal LMS have been reported so
far, but only one case is described where LMS originated in
sphenoid sinus.[24] LMS arises most frequently from smooth
muscle cells within the walls of blood vessels but may also
come from undifferentiated mesenchymal cells. Pathologically,
the tumors may range from extremely well differentiated
to anaplastic. Prognosis for primary LMS remains poor,
with overall 5‑ and 10‑year survival rates of 20% and 6%,
respectively.[25] Approximately 8%–56% of patients will develop
metastatic disease.[26] LMS of the nasal cavity and paranasal
sinuses has a more favorable clinical course, with small tumors
limited to the nasal cavity having the better prognosis.[27] Wide
local excision is treatment of choice. Tumor size at the time
of diagnosis and complete excision appear to be the most
signicant prognostic factors. Adjuvant chemotherapy with or
without radiation therapy is recommended.[24] We referred our
patient for adjuvant therapy to oncologist.
Fungal sinusitis is classied into allergic, chronic
noninvasive (fungus ball), chronic invasive, granulomatous
invasive, and acute fulminant invasive fungal sinusitis based
on histological features according to the diagnostic criteria
of deShazo et al.[28,29] The rarest occurrence of invasive
fungal sinusitis is seen in the sphenoid sinus.[30] Clinical
manifestations are dependent on the immune status of patients
given the ubiquitous nature of these organisms. The presence
of neurological ndings due to intracranial complication
should be investigated immediately. Although bone destruction
is one of the radiologic ndings of invasive fungal sinusitis,
mucor extension along the blood vessels can with intact bony
sinus walls.[31] MRI is superior modality of investigation when
intracranial symptoms are present as it reveals soft tissue
involvement.[32] Even though imaging can give a clue about
fungal sinusitis, the microbiological identication of fungus
is of paramount in the management of the infection[33] and
differentiation from allergic fungal rhinosinusitis. Advanced
invasive fungal infection of the sphenoid sinus carries
signicant mortality. Hence, early diagnosis and appropriate
treatment are crucial.[34] Although noninvasive fungal sphenoid
sinusitis rarely presents with serious complications. Diplopia
and transient vision loss have been reported in up to 3% of
cases.[30] Three most common fungal infections in the nasal
sinuses are the opportunistic genera of Aspergillus, Mucor, and
Candida, of which Aspergillus is the most prevalent and Mucor
is most invasive.[35] It is considered that surgical treatment
should aim more at radically removing the mycotic infected
lesion, rather than draining it though there is no signicant
difference in outcome even if drainage is done, especially
in invasive fungal sinusitis.[36] Postoperative progression
of disease even after antimycotic therapy may lead to fatal
outcomes.[37] Our reported case was of primary focal fungal
ball with combined zygomycosis and Aspergillus infection
without invasion, successfully treated with decompression
followed by antifungal therapy.
Mucocele is dened as the accumulation and retention
of mucoid secretion within a paranasal sinus, leading to
thinning and distension and erosion of one or several of
bony walls.[38] While primary mucoceles occur as retention
cysts of the mucous glands of sinus epithelium, secondary
mucoceles arise from the obstruction of the sinus ostium.
Sphenoid mucocele comprises 1%–2% of all mucoceles.[39]
Less than 150 cases of sphenoid sinus mucoceles have been
described in the literature.[40,41] Headache is the most common
symptom, and visual disturbance is the second most common
symptom.[38] Usually, the cranial nerves involvement brings
the patient to the physician. Our reported patient had 2nd and
3rd nerve involvement which improved after surgery, but the
exact cause of recurrent mucocele could not be found out.
Other common pathologies such as meningocele/
meningoencephalocele,[42] osteomas,[43] lymphoma,[44]
metastasis,[45] other cancers,[46,47] and rare pathologies such
as inverted papillomas,[48] epidermoids,[49] melanoma,[50]
myxoma,[51] esthesioneuroblastoma,[52] trigeminal
schwannoma,[53] and many others have been described. The
sphenoid sinus may be the starting point for primary malignant
tumors of different histological types.[54] Although CT and
MRI can help suspect a malignancy, only transnasal biopsy
and histological study allow the diagnosis. The possible
advantages of early diagnosis before spread of pathology for
prognosis cannot be overemphasized.
Financial support and sponsorship
Nil.
Conicts of interest
There are no conicts of interest.
Figure 7: (a) Shows a T2‑weighted sagittal magnetic resonance imaging with a
hyperintense mass lesion in the sphenoid sinus with enlargement of sphenoid sinus.
(b) The lesion is hyperintense on plain T1‑weighted images and (c) not enhancing on
postgadolinium injection axial and (d) coronal images
ab
cd
Sadashiva, et al.: Isolated sphenoid sinus lesions
112 Journal of Neurosciences in Rural Practice ¦ Volume 8 ¦ Issue 1 ¦ January - March 2017
References
1. Wang ZM, Kanoh N, Dai CF, Kutler DI, Xu R, Chi FL, et al.
Isolated sphenoid sinus disease: An analysis of 122 cases. Ann
Otol Rhinol Laryngol 2002;111:323‑7.
2. Gilony D, Talmi YP, Bedrin L, Ben‑Shosan Y, Kronenberg J. The
clinical behavior of isolated sphenoid sinusitis. Otolaryngol Head
Neck Surg 2007;136:610‑5.
3. Mra Z, Roach JC, Brook AL. Infectious and neoplastic diseases
of the sphenoid sinus – A report of 10 cases. Rhinology
2002;40:34‑40.
4. Grillone GA, Kasznica P. Isolated sphenoid sinus disease.
Otolaryngol Clin North Am 2004;37:435‑51.
5. Lawson W, Reino AJ. Isolated sphenoid sinus disease:
An analysis of 132 cases. Laryngoscope 1997;107
(12 Pt 1):1590‑5.
6. Friedman A, Batra PS, Fakhri S, Citardi MJ, Lanza DC. Isolated
sphenoid sinus disease: Etiology and management. Otolaryngol
Head Neck Surg 2005;133:544‑50.
7. Huang WD, Yang XH, Wu ZP, Huang Q, Xiao JR, Yang MS,
et al. Langerhans cell histiocytosis of spine: A comparative
study of clinical, imaging features, and diagnosis in children,
adolescents, and adults. Spine J 2013;13:1108‑17.
8. Howarth DM, Gilchrist GS, Mullan BP, Wiseman GA,
Edmonson JH, Schomberg PJ. Langerhans cell histiocytosis:
Diagnosis, natural history, management, and outcome. Cancer
1999;85:2278‑90.
9. Krishna H, Behari S, Pal L, Chhabra AK, Banerji D,
Chhabra DK, et al. Solitary langerhans‑cell histiocytosis of
the clivus and sphenoid sinus with parasellar and petrous
extensions: Case report and a review of literature. Surg Neurol
2004;62:447‑54.
10. Stromberg JS, Wang AM, Huang TE, Vicini FA, Nowak PA.
Langerhans cell histiocytosis involving the sphenoid sinus
and superior orbital ssure. AJNR Am J Neuroradiol
1995;16 4 Suppl: 964‑7.
11. Yu G, Huang F, Kong L, Kong X, Zhang L, Xu Q. Langerhans
cell histiocytosis of the sphenoid sinus: A case report. Turk J
Pediatr 2010;52:548‑51.
12. Kashyap R, Kumar R, Kumar S. Cranial nerve palsy in multiple
myeloma and solitary plasmacytoma. Asia Pac J Clin Oncol
2010;6:251‑5.
13. Mancardi GL, Mandybur TI. Solitary intracranial plasmacytoma.
Cancer 1983;51:2226‑33.
14. Ozdemir S, Tarkan O, Tuncer U, Sürmelioglu O, Dogrusöz M,
Ergin M. A case of extramedullary plasmacytoma in the sphenoid
sinus with unilateral loss of vision. J Craniomaxillofac Surg
2013;41:140‑3.
15. McMaster ML, Goldstein AM, Bromley CM, Ishibe N,
Parry DM. Chordoma: Incidence and survival patterns in the
United States, 1973‑1995. Cancer Causes Control 2001;12:1‑11.
16. Intracranial chordoma arising from the sphenoid sinus. J Iowa
Med Soc 1967;57:911‑5.
17. Cheng C, She C, Zhang Q. Chordoma originated from sphenoid
sinus, encroach on sella, metasella and clivus: One case
report. Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
2014;28:207‑8.
18. Harrison DF. A case of primary chordoma of the sphenoidal
sinus. J Laryngol Otol 1961;75:429‑32.
19. Karnik P, Bhat N, Shah B. Chondroid chordoma of the sphenoid
sinus – A rare tumour. Online J Otolaryngol 2014;4:101‑14.
20. Thompson LD, Seethala RR, Müller S. Ectopic sphenoid sinus
pituitary adenoma (ESSPA) with normal anterior pituitary gland:
A clinicopathologic and immunophenotypic study of 32 cases
with a comprehensive review of the english literature. Head
Neck Pathol 2012;6:75‑100.
21. Brito LB, Tinoco P, Tinoco T, Ferreira FR, Carrara VL.
Right ectopic sphenoid sinus pituitary adenoma. Braz J
Otorhinolaryngol 2014;80:451‑2.
22. Hou L, Harshbarger T, Herrick MK, Tse V. Suprasellar
adrenocorticotropic hormone‑secreting ectopic pituitary adenoma:
Case report and literature review. Neurosurgery 2002;50:618‑25.
23. Collie RB, Collie MJ. Extracranial thyroid‑stimulating
hormone‑secreting ectopic pituitary adenoma of the nasopharynx.
Otolaryngol Head Neck Surg 2005;133:453‑4.
24. Ramakrishnan VR, Said S, Kingdom TT. Primary
leiomyosarcoma of the sphenoid sinus. Arch Otolaryngol Head
Neck Surg 2009;135:949‑52.
25. Ulrich CT, Feiz‑Erfan I, Spetzler RF, Isaacs JD, Hott JS,
Nakaji P, et al. Sinonasal leiomyosarcoma: Review of literature
and case report. Laryngoscope 2005;115:2242‑8.
26. Montgomery E, Goldblum JR, Fisher C. Leiomyosarcoma of
the head and neck: A clinicopathological study. Histopathology
2002;40:518‑25.
27. Huang HY, Antonescu CR. Sinonasal smooth muscle cell
tumors: A clinicopathologic and immunohistochemical analysis
of 12 cases with emphasis on the low‑grade end of the spectrum.
Arch Pathol Lab Med 2003;127:297‑304.
28. deShazo RD, O’Brien M, Chapin K, Soto‑Aguilar M, Gardner L,
Swain R. A new classication and diagnostic criteria for
invasive fungal sinusitis. Arch Otolaryngol Head Neck Surg
1997;123:1181‑8.
29. deShazo RD, Chapin K, Swain RE. Fungal sinusitis. N Engl J
Med 1997;337:254‑9.
30. Stewart TA, Carter CS, Seiberling K. Temporal lobe abscess in
a patient with isolated sphenoiditis. Allergy Rhinol (Providence)
2011;2:40‑2.
31. Aribandi M, McCoy VA, Bazan C 3rd. Imaging features
of invasive and noninvasive fungal sinusitis: A review.
Radiographics 2007;27:1283‑96.
32. Farboud A, Trinidade A, Shakeel M, Rajapaksa S, Hanif J.
Unilateral blindness secondary to acute sphenoid sinusitis.
B‑ENT 2011;7:47‑9.
33. Glass D, Amedee RG. Allergic fungal rhinosinusitis: A review.
Ochsner J 2011;11:271‑5.
34. Lee DH, Yoon TM, Lee JK, Joo YE, Park KH, Lim SC. Invasive
fungal sinusitis of the sphenoid sinus. Clin Exp Otorhinolaryngol
2014;7:181‑7.
35. Anselmo‑Lima WT, Lopes RP, Valera FC, Demarco RC. Invasive
fungal rhinosinusitis in immunocompromised patients. Rhinology
2004;42:141‑4.
36. Pinzer T, Reiss M, Bourquain H, Krishnan KG, Schackert G.
Primary aspergillosis of the sphenoid sinus with pituitary
invasion – A rare differential diagnosis of sellar lesions. Acta
Neurochir (Wien) 2006;148:1085‑90.
37. Streppel M, Bachmann G, Arnold G, Damm M, Stennert E.
Successful treatment of an invasive aspergillosis of the skull
base and paranasal sinuses with liposomal amphotericin B and
itraconazole. Ann Otol Rhinol Laryngol 1999;108:205‑7.
38. Kataria R, Gupta S, Chopra S, Bagaria H, Sinha VD. Mucocele
of the sphenoid sinus: A rare cause of reversible 3rd nerve palsy.
Ann Indian Acad Neurol 2012;15:158‑60.
39. Sethi DS, Lau DP, Chan C. Sphenoid sinus mucocoele
presenting with isolated oculomotor nerve palsy. J Laryngol Otol
1997;111:471‑3.
Sadashiva, et al.: Isolated sphenoid sinus lesions
113
Journal of Neurosciences in Rural Practice ¦ Volume 8 ¦ Issue 1 ¦ January - March 2017
40. Hssaine K, Belhoucha B, Rochdi Y, Nouri H, Aderdour L,
Raji A. Paranasal sinus mucoceles: About 32 cases. Rev Stomatol
Chir Maxillofac Chir Orale 2016;117:11‑4.
41. Liu X, Wang X, Wen J, Liu C, Cai Y, Feng Y, et al. Clinical
analysis of patients with sphenoid sinus mucocele and literature
review. Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
2015;29:1850‑2.
42. Melo NA, Borges BB, Magliarelli Filho PA, Godoy MD,
Pereira LV, Pinna Fde R, et al. Lateral sphenoid sinus recess
cerebrospinal uid leak: A case series. Eur Arch Otorhinolaryngol
2014;271:2587‑94.
43. Canevari FR, Giourgos G, Pistochini A. The endoscopic
transnasal paraseptal approach to a sphenoid sinus osteoma: Case
report and literature review. Ear Nose Throat J 2013;92:E7‑10.
44. Park YM, Cho JH, Cho JY, Huh JS, Ahn JY. Non‑Hodgkin’s
lymphoma of the sphenoid sinus presenting as isolated
oculomotor nerve palsy. World J Surg Oncol 2007;5:86.
45. Zhao L, Yan J, Li L, Wei J, Li L, Qian X, et al. Gastric
metastasis from sphenoid sinus melanoma: A case report. Oncol
Lett 2015;9:609‑13.
46. Colak A, Benli K, Dönmez T, Onol B. Papillary carcinoma
of the sphenoid sinus associated with sphenoid sinus abscess
presenting as cavernous sinus syndrome. A case report. J Clin
Neuroophthalmol 1990;10:18‑20.
47. Guerrier Y, Dejean Y, Galy G, Botella JP. Primary cancers
of sphenoidal sinus. J Fr Otorhinolaryngol Audiophonol Chir
Maxillofac 1968;17:45‑54.
48. Liu SC, Lee JC, Chen JJ, Lin YS. Isolated inverted papilloma of
the sphenoid sinus. J Chin Med Assoc 2010;73:503‑5.
49. Sani S, Smith A, Leppla DC, Ilangovan S, Glick R. Epidermoid
cyst of the sphenoid sinus with extension into the sella turcica
presenting as pituitary apoplexy: Case report. Surg Neurol
2005;63:394‑7.
50. Lynch SC, Lee AG, Graham SM, Kirby PA. Primary melanoma
of the sphenoid sinus presenting with a third cranial nerve palsy.
J Neuroophthalmol 2005;25:289‑92.
51. Moore BA, Wine T, Burkey BB, Amedee RG, Butcher RB 2nd.
Sphenoid sinus myxoma: Case report and literature review.
Ochsner J 2008;8:166‑71.
52. Akinfolarin J, Jazaerly T, Jones K, Abu‑Hamdan M, Lonardo F,
Folbe A, et al. Fine needle aspiration cytology of primary
sphenoid sinus esthesioneuroblastoma metastatic to the skin.
Avicenna J Med 2012;2:15‑8.
53. Gundamaneni SK, Singh M, Madhugiri VS,
Vadivel Rathakrishnan RK, Sasidharan GM. Trigeminal
schwannoma of the sphenoid sinus – Report of a rare entity. Br J
Neurosurg 2014;28:281‑3.
54. Darouassi Y, Chihani M, Touati MM, Nadour K, Ammar H,
Bouaity B. Adenocarcinoma of the sphenoid sinus. Pan Afr Med
J 2014;18:284.