Keywords
magnetic resonance imaging - pituitary - sella turcica
Introduction
Sellar region is a complex area of the brain housing the master endocrine gland adorning
its bony throne, sella turcica, surrounded by an army of other important structures,
any of which can give rise to pathologies ranging from incidental to potentially fatal.
Most of these lesions present with hypopituitarism, visual disturbances, headache,
and projectile vomiting due to obstructive hydrocephalus, cognitive disturbance, or
failure to thrive. These symptoms are nonspecific, occurring due to mass effect on
parasellar structures rather than due to any particular lesion. So differentiating
among these lesions on the basis of clinical presentation alone is not always possible.
Nonetheless, the management of each of these lesions differs considerably. Radiological
assessment is of utmost importance in reaching a definitive diagnosis thereby aiding
in formulation of an appropriate management strategy. Magnetic resonance imaging (MRI)
is the imaging investigation of choice for sellar and parasellar pathologies owing
to its multiplanar capability, superior soft tissue contrast resolution, and lack
of ionizing radiation. It allows better demonstration of anatomy, localization and
characterization of lesions, as well as assessment of their relationship with surrounding
structures thereby helping to plan the surgical approach.
A Glimpse of Anatomy
Superior part of the basisphenoid houses pituitary gland in a midline concavity known
as the sella turcica bounded anteriorly by anterior clinoid processes arising from
lesser wing of sphenoid and posteriorly by dorsum sellae and posterior clinoid processes
forming the superior border of clivus. Bony sella is lined by meninges on all sides
leaving a small central opening (diaphragmatic hiatus) superiorly for transmitting
the pituitary stalk. Superior to sella lies the suprasellar cistern which contains
optic chiasm and pituitary stalk surrounded by the circle of Willis. Further superiorly
lies the hypothalamus extending from lamina terminalis anteriorly to mammillary bodies
posteriorly. Tuber cinereum is a part of hypothalamus located between the optic chiasm
and mammillary bodies from which the infundibular stalk extends inferiorly, gradually
tapering downwards. Superior to hypothalamus lies the third ventricle. Inferior to
sella lies the sphenoid sinus which may be partially or completely aerated. Lateral
to sella on either side lie dura-lined venous compartments known as cavernous sinuses
(CSs). Through the CSs course the internal carotid artery (ICA) (cavernous segment)
and VI cranial nerve (CN), while III, IV, V1, and V2 CNs lie within its lateral dural
wall.[1]
Imaging Technique
Precontrast T1- and T2-weighted spin echo images are first acquired in coronal and
sagittal planes using thin 3 mm slices, small field-of-view, and high-resolution matrix.
This is followed by the dynamic and routine postcontrast images and delayed scanning
after 30 to 60 minutes. A three-dimensional (3D) Fourier transformation gradient echo
or fast/turbo spin echo sequence may be used for dynamic study. After a bolus injection
of 0.05 to 1 mmol/kg intravenous gadolinium, six consecutive sets of three images
are obtained in the coronal plane every 10 seconds.
Furthermore, a variety of advanced MRI techniques have been developed including 3D
volumetric analysis of pituitary,[2] intraoperative MRI,[3] diffusion-weighted imaging (DWI),[4] MR spectroscopy (MRS),[5] and magnetization transfer ratio (MTR).[6]
Step-By-Step Approach
Sellar and parasellar pathologies may be classified according to etiology (normal
variants, congenital, neoplastic, inflammatory, vascular, traumatic, etc.). Of the
myriad lesions that can arise in sella and parasellar region, more than three-fourths
are from among the “Big Five”' which include—adenoma, meningioma, aneurysm in adults,
astrocytoma in children, and craniopharyngioma (CP) in both. All other lesions together
account for less than 25% of parasellar pathologies.[7]
The goal of imaging is to localize and characterize the lesions as well as to delineate
its entire extent, to aid in planning proper medical or surgical management. A step-by-step
approach is suggested for complete evaluation and narrowing the differentials.
-
Localize: Begin by localizing the epicenter of the lesion to one of the four anatomical
compartments, namely, intrasellar, suprasellar, parasellar, or infundibular stalk.
Suprasellar lesions may arise from diaphragma sellae, optic chiasma, hypothalamus,
or circle of Willis. Parasellar lesions arise from contents of CS—meninges, CNs, and
blood vessels. Infrasellar lesions arise from nasopharynx. Various skull base lesions
can involve the sella as well. Enlargement of the sella might suggest pituitary origin
of the lesion. However, this is not always the case, as in case of empty sella, the
sella turcica is enlarged but cerebrospinal fluid (CSF)-filled and pituitary itself
is compressed to the floor of sella. If the pituitary gland cannot be identified separately
from the lesion, then the pituitary itself is the site of origin.
-
Characterize: Look for intrinsic signal intensity of the lesion—solid/cystic/vascular,
areas of hemorrhage/necrosis/calcification, and enhancement pattern.
-
Extension: Look for margins of the lesion—well circumscribed/infiltrating and describe
relationships with surrounding structures.
Pituitary Adenoma
Pituitary adenoma is a benign neoplasm that arises from the adenohypophysis and is
the most common intrasellar pathology.[8] Pituitary adenomas can be classified into micro, macro, or giant when they measure
less than 1 cm, more than 1 cm, or more than 4 cm, respectively. Clinically, microadenomas
present with hypersecretory syndromes while macroadenomas cause symptoms due to mass
effect on adjacent structures.
Detection rate of pituitary microadenomas has increased manifold after introduction
of dynamic contrast-enhanced MRI.[9] The enhancement of normal pituitary gland begins from the stalk, followed by pituitary
tuft and finally there is centrifugal enhancement of the rest of the pituitary. Within
30 to 60 seconds, the entire gland shows homogenous enhancement followed by rapid
washout. On the contrary, microadenomas show slow and gradual uptake of contrast with
peak enhancement at 60 to 200 seconds that persists for a longer duration.[2] The maximum contrast difference between the normal pituitary tissue and microadenomas
is attained approximately 30 to 60 seconds after the bolus injection of the intravenous
contrast. Most microadenomas appear as relatively nonenhancing lesions within an intensely
enhancing pituitary gland.[9] Delayed scan (30–60 minutes after contrast injection) may demonstrate a reversal
of the image contrast obtained at 30 to 60 seconds on dynamic scanning. This is because
the contrast from the normal pituitary gland fades but diffuses into the microadenoma
which stands out as a hyperintense focus[10] ([Fig. 1]).
Fig. 1 Coronal T2-weighted image (T2WI) (A) and T1WI (B) of a patient presenting with amenorrhea and hyperprolactinemia show a right lateral
pituitary lesion causing focal contour bulge and deviation of stalk. Dynamic contrast-enhanced
coronal T1WI (C, D) show a pituitary microadenoma which enhances more slowly than the normal pituitary
gland.
Some microadenomas exhibit maximum lesion-to-gland contrast on unenhanced scans; however,
this image contrast begins to diminish the moment the contrast-enhancing agent arrives
in the pituitary gland. Some authors have even documented early enhancement in the
microadenomas, long before the anterior lobe, which is attributed to pituitary adenomas
having a direct arterial blood supply similar to that of posterior pituitary.[4]
A large heterogeneously enhancing sellar mass which cannot be identified separately
from pituitary is a macroadenoma. It can show areas of hemorrhage and cystic change
but usually no calcification ([Fig. 2]). SIPAP (S, suprasellar, I, infrasellar, P, right and left parasellar, A, anterior,
P, posterior) classification is a 6-figure number describing the extrasellar extension
of pituitary adenomas.[11]
Fig. 2 In a 28-year-old lady presenting with headache and visual disturbance, coronal magnetic
resonance (MR) images show a large lobulated “snowman” or “figure of 8” sellar and
suprasellar lesion. Pituitary cannot be identified separately from this lesion suggesting
macroadenoma. Areas of cystic degeneration are seen in the lesion superiorly toward
the left. Solid component appears isointense on both T2-weighted image (T2WI) (A, B) and T1WI (C, D) and shows heterogeneous avid enhancement on postcontrast images (E, F). Superiorly, the lesion is compressing the optic chiasma and reaching up to the
floor of third ventricle. Laterally, it shows cavernous sinus invasion, however, flow-void
of internal carotid artery (ICA) is normal. Coronal (G) and axial (H) MR angio images show no e/o ICA stenosis.
Suprasellar grading ranges from 0 to 4 where grade 0 adenoma does not bulge into suprasellar
space, grade 1 bulges into the suprasellar cistern, grade 2 reaches up to the optical
chiasma without displacing or stretching it, grade 3 when it displaces stretches the
optic chiasm causing mass effect on third ventricle, and grade 4 adenoma obliterates
one or both foramen of Monro resulting in hydrocephalus in lateral ventricles.
Infrasellar extension is graded from 0 to 2 where grade 0 refers to intact sellar
floor, grade 1 refers to extension into sphenoid sinus, and grade 2 refers to extension
beyond sphenoid sinus into nasopharynx inferiorly or ethmoid anteriorly.
For grading of parasellar extent of pituitary adenomas, Knosp–Steiner classification
is used where three parallel lines, namely the medial tangent, intercarotid line,
and lateral tangent drawn on cross-sections of intra- and supracavernous ICA, are
used to define grades 0 to 4. Grade 0, 1, and 2 represents tumor extension up to the
medial tangent, intercarotid line, and lateral tangent, respectively. Grade 3 corresponds
to extension lateral-to-lateral tangential line and is further classified into 3a
and 3b depending on whether it is superior or inferior to intracavernous ICA. Finally,
grade 4 represents total encasement of cavernous ICA.[12]
Bulging of the lateral wall of the CS and lack of normal enhancement of the venous
extrasellar spaces suggest CS invasion. Different anatomical classifications, based
on MRI findings, have been proposed to specify if the CS is invaded by a pituitary
tumor (PT). Some authors have suggested that an encasement of the ICA greater than
67% makes invasion certain while others suggested that an ICA remote from the sphenoid
carotid sulcus is highly suggestive of CS invasion.[5]
Anterior grading ranges from 0 to 1 depending on extension into anterior cranial fossa
with the landmark being an imaginary line drawn perpendicular to tuberculum sellae
on sagittal section.
Posterior grading ranges from 0 to 1 depending on extension into prepontine cistern
below the level of dorsum sellae on sagittal section.
Most of the pituitary adenomas are functioning tumors, majority being prolactinomas
while 25% are nonfunctioning tumors.[13] This differentiation is crucial for management as prolactinomas are managed medically
whereas nonfunctioning adenomas are treated by surgical excision. Magnetization transfer
imaging is a recent advancement in MRI wherein tissue contrast is determined by the
concentration of macromolecules and is quantified by MTR. In cases with hyperprolactinemia,
the MTR value of prolactin-secreting adenomas is remarkably higher than the MTR of
normal pituitary gland resulting in the high signal of prolactin-secreting adenomas
on MT images. On the other hand, nonfunctioning adenomas have lower MTR values compared
with normal pituitary gland accounting for their low signal on MTR images.[6]
Majority of pituitary adenomas are soft and hence easily resectable via minimally
invasive endoscopic transsphenoidal approach, whereas some macroadenomas are hard
due to increased fibrosis and are thus difficult to remove via endoscopic technique
necessitating more extensive surgery. Pierallini et al demonstrated that soft adenomas
have a low apparent diffusion coefficient (ADC) value of (0.663 ± 0.109) × 10−3 mm2/sec, whereas hard adenomas have a relatively high ADC value (1.363 ± 0.259) × 10−3 mm2/sec. Thus, preoperative knowledge of pituitary adenoma consistency may help the surgeon
in deciding a proper surgical technique.[14]
Pituitary Apoplexy
Owing to their meager blood supply, pituitary adenomas may undergo infarction and
hemorrhage and present acutely. This condition is referred to as pituitary apoplexy
and can occur spontaneously or following therapy. These hemorrhagic pituitary adenomas
need to be differentiated from Rathke cleft cysts (RCCs) as both of them appear bright
on T1-weighted image (T1WI) owing to extracellular methemoglobin and mucoid protein,
respectively. Adenomas are characterized by off-midline location, fluid-fluid level,
tilting of the pituitary stalk, T2 hypointense hemosiderin rim, and internal septations,
while RCCs are mostly located in the midline and often have a T2 hypointense mural
nodule. Apart from these, other differentials for parasellar masses displaying high
signal on T1WI are lipoma, dermoid, thrombosed aneurysm, and CP[15] ([Fig. 3]).
Fig. 3 Known case of pituitary macroadenoma on treatment with bromocriptine presented to
emergency with sudden onset severe headache and visual disturbance. Coronal T2-weighted
image (T2WI) and T1WI show that the mass is very heterogeneous in signal intensity
with multiple hemorrhagic foci. Postcontrast sagittal (C) and coronal (D) images thin peripheral enhancement. These findings are consistent with pituitary
apoplexy. Necrotic hemorrhagic macroadenoma was found at surgery.
Meningioma
Parasellar meningiomas can arise from tuberculum sellae, planum sphenoidale, diaphragmatic
sellae, clinoid processes, sphenoid wing, CSs, or clivus. These tumors mostly occur
in middle-aged females. On imaging, they appear hyperdense on noncontrast computed
tomography (NCCT), iso- to hypointense on T1WI and T2WI, and show diffusion restriction
on DWI. On postcontrast scan, avid homogenous enhancement is seen with linear, gradually
tapering enhancement extending along dura, classically known as the “dural tail sign.”
Pituitary gland can be identified separately from the mass. Other ancillary signs
of extra-axial tumors are also seen, namely CSF cleft, displacement of subarachnoid
vessels, etc.[16] ([Fig. 4]). Another important sign is focal hyperostosis which is better appreciated on CT
scan. Meningiomas are highly vascular lesions. If diagnosis is certainly established
ahead of time, tumor embolization may be performed preoperatively that will substantially
reduce intraoperative hemorrhage.[17]
Fig. 4 In a 36-year-old lady presenting with headache and bitemporal hemianopsia, there
is e/o a well-defined extra-axial mass lesion seen in region of left cavernous sinus
which appears hypointense on T1-weighted image (T1WI) (A), hyperintense on T2WI (D), and shows blooming foci on gradient echo (GRE) (C) which appeared hypointense on filtered phase images consistent with intralesional
calcification. Medially, the sella is extending into sella and causing its expansion;
however, posterior pituitary bright spot is seen separately on sagittal T1WI (B). Compression of optic chiasm can also be appreciated (D). On postcontrast images, the lesion shows intense homogenous enhancement with dural
tail sign (E, F). The lesion is causing encasement of the cavernous segment of left internal carotid
artery (ICA) with mild luminal narrowing. On magnetic resonance (MR) spectroscopy,
alanine peak was seen at 1.4 parts per million (ppm) (not shown). These findings are
consistent with cavernous sinus/medial sphenoid wing meningioma.
Craniopharyngioma
CPs are the most frequently encountered nonglial neoplasms in pediatric population.
These are benign, locally invasive, and nonsecreting tumors that present with clinical
features related to mass effect on pituitary (hormone disturbances) or optic chiasma
(visual disturbances). Majority of them are centered in the suprasellar cistern while
only some of them are purely intrasellar. Rarely they may be infrasellar or intraventricular.
Pathologically, they have been classified into two types. Adamantinomatous CP, the
more common variant, is a lobulated mostly cystic partly solid tumor showing calcification
and occurs in children aged 5 to 15 years and adults aged 45 to 60 years. Papillary
CP, the less common variant that occurs in middle aged adults, is an encapsulated
almost entirely solid tumor that does not usually show calcification or cystic component
([Fig. 5]). On imaging, adamantinomatous CP appear hypodense on NCCT, hyperintense on T2/fluid-attenuated
inversion recovery (FLAIR), while on T1WI they can be either hypo- or hyperintense
depending on cyst contents. Lipid-lactate peak is seen on MRS owing to the cholesterol
content in the cystic component. Reduced cerebral blood volume is seen on MR perfusion
([Fig. 6]). Imaging differentials include RCC and suprasellar dermoid cyst. Enhancing solid
components help differentiate them from suprasellar dermoid cyst while RCC lacks both
calcification and solid enhancing components.[18]
Fig. 5 Coronal and sagittal postcontrast T1-weighted image (T1WI) of a 47-year-old lady
presenting with headache show a lobulated avidly enhancing predominantly solid suprasellar
mass invading the third ventricle likely suggestive of papillary craniopharyngioma.
Differentials include germinoma in children; intraventricular meningioma and metastases
in adults.
Fig. 6 Magnetic resonance (MR) images of a 9-year-old boy presenting with headache and visual
disturbance show a lobulated suprasellar predominantly cystic mass lesion that is
hyperintense on T2-weighted image (T2WI) (A) and T1WI (B, C). Solid mural nodule and cyst wall show enhancement on postcontrast images (D). These findings are consistent with adamantinomatous craniopharyngioma. Enhancing
mural nodule helps differentiate them from Rathke cleft cyst. Noncommunicating hydrocephalus
is seen due to mass effect of the lesion.
Rathke Cleft Cyst
An incidentally detected cystic lesion in a middle-aged patient in suprasellar compartment
or intrasellar or both is usually a RCC. When large, it can cause symptoms due to
mass effect on pituitary (hypopituitarism) or optic chiasma (visual disturbance).
On imaging, they usually appear hypodense on NCCT, hyperintense on T2/FLAIR, while
on T1WI they can be either hypo- or hyperintense depending on contents. On postcontrast
scan, compressed pituitary is seen at the periphery of RCC as homogeneously enhancing
“claw sign.” Calcification is characteristically absent as opposed to CP which is
the other differential for a suprasellar cystic lesion[7] ([Fig. 7]).
Fig. 7 Rathke cleft cyst: 3.0-T sagittal T1-weighted image (T1WI) (A) and T2WI (B) of a 42-year-old lady presenting with headaches show a well-defined intrasellar
cystic lesion. Sagittal (C) and coronal (D) postcontrast T1WI show rim sign/claw sign of enhancing pituitary gland around the
nonenhancing cyst.
Suprasellar Dermoid Cyst
Intracranial dermoid cysts are extremely rare, accounting for only 0.5% of all primary
intracranial tumors and have a slight female predilection. On CT, it appears as a
well-defined suprasellar cystic lesion with fat and calcification. On T1-weighted
MRI, it shows fat-fluid level with hyperintense fat in its upper part and hypointense
fluid in its lower part. Isointense nonenhancing floating round structure may be seen
in its central part which has been referred to as Poke ball sign and is quite pathognomonic
for dermoid cyst.[19] Uncomplicated intracranial dermoids present with mass effect. These may be complicated
by rupture either spontaneous, traumatic, or iatrogenic. These patients have acute
presentation, and on imaging, T1 hyperintense droplets may be seen in sulcal spaces
and leptomeningeal enhancement is seen on postcontrast scan due to chemical meningitis.[20]
Pituitary Hyperplasia
Physiological variations in size of pituitary must be borne in mind. “Elster's rule”
is a handy guide for assessing height of pituitary vis-a-vis patient's age. It states
that the maximum upper limit for height in children is 6 mm, for men and postmenopausal
ladies it is 8 mm, for women of reproductive age the limit is 10 mm, while for pregnant
and lactating women, it is 12 mm. Anything exceeding this is pathological and shows
upward bulging contour of the gland. This may be caused by nonneoplastic hyperplasia
which mainly occurs as a response to end-organ failure, most commonly in cases of
hypothyroidism and is reversible with hormone replacement therapy. On imaging, hyperplastic
gland shows similar signal intensity as normal gland, appearing isointense to gray
matter on both T1WI and T2WI and shows homogenous postcontrast enhancement[1] ([Fig. 8]).
Fig. 8 Noncontrast (A) and contrast-enhanced (B) T1-weighted image (T1WI) of a prepubescent male with hypothyroidism show pathological
pituitary hyperplasia with an upwardly bulging gland that mimics macroadenoma; however,
it shows homogenous appearance on all pulse sequences with no discrete lesion. Reversal
to normal size was seen in repeat scan done weeks after initiation of thyroid hormone
replacement therapy. Physiologically, pituitary hyperplasia is seen in pregnancy and
at puberty.
Infundibulum
Normal infundibular stalk tapers craniocaudally, measuring 3.45 ± 0.56 mm at the level
of optic chiasm and 1.91 ± 0.4 mm at site of insertion in pituitary.[21] Its signal intensity on T1WI is usually less than that of optic chiasma and does
not normally enhance on postcontrast scan. Deviation of the stalk to one side does
not necessarily suggest an underlying disease process. Infundibular lesions are often
seen in children presenting with diabetes insipidus. Major differentials are Langerhans
cell histiocytosis (LCH) and germinoma. Even if the scan appears normal at initial
presentation, a repeat scan should be suggested after 3 to 6 months.[22]
Langerhans Cell Histiocytosis
Langerhans Cell Histiocytosis
In LCH, imaging shows a thick, enhancing nontapering stalk, often with absent posterior
pituitary bright spot (PPBS). Also, look out for the classical lytic bone lesions
with beveled edges[23] ([Fig. 9]).
Fig. 9 Precontrast T1-weighted image (T1WI) sagittal (A), coronal (B) and sagittal (C) postcontrast T1WI of a patient presenting with diabetes insipidus show absent posterior
pituitary bright spot (PPBS) and thick enhancing infundibulum, typical of Langerhans
cell histiocytosis (LCH). Coronal T2FS of right hip (D) of same patient showing skeletal involvement.
Germinoma
Germinomas appear as solid infiltrating masses often showing CSF dissemination. On
imaging, they are hyperdense on NCCT, iso- to mildly hyperintense on T1/T2WI, and
show homogenous avid postcontrast enhancement. Synchronous pineal lesion can also
be seen. Tumor markers like alpha-fetoprotein or human chorionic gonadotropin in serum
or CSF, if present, can help in confirming the diagnosis; however, their absence does
not exclude the diagnosis. They are very radiosensitive and amenable to treatment
by radiotherapy. Chemotherapy is added in cases with CSF spread. Follow-up MRI is
suggested for evaluation of treatment response. Germinomas are fluorodeoxyglucose
(FDG)-avid, thus 18-FDG positron emission tomography scan can be used to assist in
making the diagnosis or for posttreatment follow-up to look for residual or recurrent
tumor.[24]
Lymphocytic Hypophysitis
It usually affects peripartum women and presents with hypopituitarism or diabetes
insipidus. Major imaging differential is macroadenoma. Gutenberg et al have suggested
a clinicoradiological score to help differentiate the two, as their treatment is poles
apart. While macroadenoma has to be managed surgically, lymphocytic hypophysitis (LH)
is usually self-limiting and can be managed conservatively with anti-inflammatory
steroids and hormone replacement. Symmetrical enlargement of gland up to 6 mL, absent
PPBS, enlarged stalk, homogenous appearance, intense postcontrast enhancement, and
intact sellar floor are points favoring LH.[8]
Congenital Anomalies
Duplication of Pituitary Gland
Duplication of pituitary gland (DPG) is a very rare congenital anomaly with the most
recent review reporting 42 cases worldwide.[25]
It may be detected in some patients presenting with anosmia, precocious puberty, or
delayed onset of puberty. DPG is often associated with midline craniofacial anomalies
and together they constitute DPG-plus syndrome[26] ([Fig. 10]).
Fig. 10 Sagittal T2-weighted image (T2WI) (A) shows thickened floor of third ventricle from fusion of hypothalamus and an almost
inapparent sella. Coronal T2WI images of the same patient show two laterally displaced
pituitary glands (B) and duplicated pituitary stalks (C).
Ectopic Posterior Pituitary
Patients with ectopic undescended posterior pituitary often present with pituitary
dwarfism owing to growth hormone deficiency. Sagittal midline T1 images demonstrate
hypoplastic sella with an ectopically placed PPBS at the median eminence (floor of
third ventricle) ([Fig. 11]). On imaging they can be differentiated from hypothalamic lipoma by lack of fat
suppression. When ectopic PPBS is associated with hypoplastic or absent anterior pituitary
and infundibulum, it is referred to as pituitary stalk interruption syndrome. Numerous
other abnormalities may also be associated, like septo-optic dysplasia, vermian dysplasia,
Arnold-Chiari malformation, corpus callosum agenesis, holoprosencephaly, etc. Hence,
a careful screening of the entire neuraxis should be performed.[27]
Fig. 11 3.0-T sagittal (A) and coronal (B) T1-weighted image (T1WI) of a 4-year-old girl with panhypopituitarism show ectopic
posterior pituitary bright spot located along the undersurface of median eminence
of hypothalamus. The infundibular stalk is absent while sella turcica and adenohypophysis
are hypoplastic.
Aneurysm
Parasellar mass caused by aneurysmal dilatation of vessels shows significant signal
heterogeneity with areas of T1 hyperintensity caused by subacute thrombus or flow-related
enhancement or areas of T2 hypointensity caused by intracellular deoxy, or methemoglobin,
calcification, or flow void. Although CPs may have significant heterogeneity, they
usually have a more geographic variability from a combination of cysts, cholesterol
laden lakes, and tumor tissue. Flow misregistration artifact is pathognomonic as it
is not seen in other sellar masses.[28]
These aneurysms may be classified as infradiaphragmatic or supradiaphragmatic, based
on their pattern of invasion into the sella and relationship to the diaphragma sellae.
Infradiaphragmatic intrasellar aneurysms typically originate from the cavernous or
clinoid segment of the ICA, project medially into the sella through the CS dura, tend
to be smaller, and are more likely to cause hypopituitarism and CN paresis. Supradiaphragmatic
intrasellar aneurysms typically originate from the ophthalmic segment of the ICA or
the anterior communicating artery, are usually larger, and typically present with
visual loss. It is absolutely essential to rule out a parasellar aneurysm by imaging
as attempted biopsy or resection can be disastrous. Cavernous ICA aneurysms that become
intrasellar carry a risk of subarachnoid hemorrhage and are best treated with endovascular
techniques. Supradiaphragmatic aneurysms that cause mass effect on the visual system
are likely to be preferentially treated via surgical clipping.[29]
Glioma
Glioma is the most common lesion arising from optic chiasma, commonly seen in children.
Their association with neurofibromatosis 1 is well known. On imaging, it is seen as
a homogeneously enhancing suprasellar mass lesion with no calcification, hemorrhage,
or cystic change. Often, hypothalamus and optic chiasma both are involved and it is
difficult to pinpoint the site of origin.[30]
Metastases
Metastatic lesions comprise nearly 1% of all tumors in the sellar-parasellar region.
Breast and lung cancer are the two most common primaries, followed by lymphoma and
prostate. Clinically, metastasis should be suspected in patients with sudden onset
and rapid progression of symptoms regardless of a known primary. The possible metastatic
pathways to the sella-parasellar region include leptomeningeal or hematogenous spread.
Posterior pituitary is the preferred site of metastasis owing to its direct arterial
supply and larger area of contact with the dura.[31]
Hypothalamic Hamartoma
They are benign nonneoplastic masses of gray matter heterotopia. Symptoms often begin
in infancy and are gradually progressive. These patients present with gelastic seizures,
visual problems, precocious puberty, and behavioral problems. Morphologically, these
lesions can be classified into sessile and pedunculated types. As they are composed
of gray matter, they have imaging appearances similar to that of the normal cortex
on all sequences. They do not enhance and do not grow[32] ([Fig. 12]).
Fig. 12 Child presenting with precocious puberty. Sagittal T2-weighted image (T2WI) (A), coronal (B) and sagittal (C) T1WI show a pedunculated hypothalamic hamartoma appearing isointense on T1WI and
iso- to slightly hyperintense on T2WI.
Conclusion
To summarize, the sellar-parasellar region has a complex anatomy and can give rise
to a wide spectrum of lesions that present diagnostic challenges. MRI with its multiplanar
capability and excellent contrast resolution is the modality of choice for evaluation
of these lesions as it not only helps in diagnostic differentiation but also provides
useful information about their relationship with adjacent vital structures thereby
aiding to plan appropriate treatment. Knowledge of the anatomy and proper planning
of the scan are essential for complete evaluation of sellar and parasellar pathologies.
