(group i – without cavernous sinus invo lvement & group ii –with cavernous sinus...
TRANSCRIPT
A COMPARATIVE ANALYS
THE CLINICO-RADIOLOGICAL FEATURE
OUTCOME AND RECURRENCE
SUBGROUPS OF MEDIAL
(GROUP I – WITHOUT
GROUP II –WITH CAVERNOUS SINUS
Thesis submitted in partial fulfilment of the rules and regulations
for MCh (Neurosurgery) Degree of Sree Chitra
Tirunal Institute for Medical Sciences and Technology
Dr.
DEPARTMENT OF NEUROS
SREE CHITRA TIRUNAL
SCIENCES & TECHNOLOG
THIRUVANANTHAPURAM
A COMPARATIVE ANALYSIS OF
RADIOLOGICAL FEATURES, SURGICAL
COME AND RECURRENCE RATE OF TWO DIFFEREN
MEDIAL SPHENOID WING MENINGIOMAS
WITHOUT CAVERNOUS SINUS INVOLVEMENT &
WITH CAVERNOUS SINUS INVOLVEMENT)
Thesis submitted in partial fulfilment of the rules and regulations
for MCh (Neurosurgery) Degree of Sree Chitra
Tirunal Institute for Medical Sciences and Technology
By
Dr. Dipendra Kumar Pradhan
October 2013
DEPARTMENT OF NEUROSURGERY
SREE CHITRA TIRUNAL INSTITUTE FOR MEDICA
SCIENCES & TECHNOLOGY
THIRUVANANTHAPURAM, KERELA – 695011
S, SURGICAL
RATE OF TWO DIFFERENT
IOMAS-
LVEMENT &
Thesis submitted in partial fulfilment of the rules and regulations
Tirunal Institute for Medical Sciences and Technology
INSTITUTE FOR MEDICAL
“A comparative analysis of the
surgical outcome and recurrence rate of
subgroups of medial
without cavernous sinus involvement &
Group II –with cavernous sinus involvement
Submitted by
Programme :
Month & year of submission :
A comparative analysis of the clinico-radiological features,
ome and recurrence rate of two different
subgroups of medial sphenoid wing meningiomas (Group I
cavernous sinus involvement &
with cavernous sinus involvement).”
Submitted by : Dr. Dipendra Kumar Pradhan
Programme : MCh Neurosurgery
ubmission : October, 2013
radiological features,
two different
Group I –
Dipendra Kumar Pradhan
CERTIFICATE
This is to certify that the thesis entitled “A comparative analysis
of the clinico-radiological features, surgical outcome and recurrence
rate of two different subgroups of medial sphenoid wing meningiomas,
(Group I – without cavernous sinus involvement and Group II –with
cavernous sinus involvement) ” is a bonafide work of Dr. Dipendra
Kumar Pradhan and was conducted in the Department of
Neurosurgery, Sree Chitra Tirunal Institute for Medical Sciences &
Technology, Thiruvananthapuram (SCTIMST), under my guidance and
supervision.
Dr. Suresh Nair N.
Professor and Head
Department of Neurosurgery
SCTIMST, Thiruvananthapuram,
Kerala.
DECLARATION
This thesis titled “A comparative analysis of the clinico-
radiological features, surgical outcome and recurrence rate of two
different subgroups of medial sphenoid wing meningiomas (Group I –
without cavernous sinus involvement and Group II –with cavernous
sinus involvement) ”, is a consolidated report based on a bonafide study
of the period from January 2000 to December 2011, done by me under
the Department of Neurosurgery, Sree Chitra Tirunal Institute for
Medical Sciences & Technology, Thiruvananthapuram.
This thesis is submitted to SCTIMST in partial fulfillment of rules
and regulations of MCh Neurosurgery examination.
Dr. Dipendra Kumar Pradhan
Department of Neurosurgery,
SCTIMST, Thiruvananthapuram,
Kerala.
ACKNOWLEDGEMENT
I express my earnest gratitude to my esteemed teacher, Dr. Suresh Nair,
Professor and Head of the Department of Neurosurgery, whose guidance has
been invaluable and I am extremely grateful and indebted for his contributions
and suggestions during the entire work. To me he remains a mentor and a
source of inspiration throughout.
I owe a deep sense of gratitude to Dr. Girish Menon, Professor,
Department of Neurosurgery, SCTIMST, for his invaluable advice,
encouragement and guidance, without which this work would not have been
possible.
I express my gratitude to Dr. Mathew Abraham, Associate professor,
Department of Neurosurgery, SCTIMST, whose ever-available help and
guidance during the course of the study were invaluable.
I am deeply indebted to Dr. Easwer H. V, Dr. Krishna kumar. K, Dr.
Gopalakrishnan C.V., Dr. George Vilanilam, Dr. Jayanand Sudhir B, my
seniors and colleagues, and I thank them for their constant encouragement and
support.
I am thankful to Mr. Thampi N.G., Senior Medical records officer and Head,
Department of Medical Records, for his support in retrieving old medical
records during the entire study.
It is also my bounden duty to record my debt to the scholars and
authors whose works I have consulted for necessary materials in preparing
this dissertation.
Last but not the least, I owe a deep sense of gratitude to all my patients
without whom this work would not have been possible.
INDEX
Page No.
INTRODUCTION 1 - 3
REVIEW OF LITERATURE 4 - 34
AIM OF THE STUDY 35
MATERIALS AND METHODS 36 - 39
RESULTS 40 - 59
DISCUSSION 60 - 72
CONCLUSION 73
REFERENCES 74 - 88
PROFORMA
ABBREVIATIONS
ANNEXURE 1- Master chart for Group I & II
Introduction
1
INTRODUCTION
Meningiomas constitute approximately 13% to 19% of all primary
intracranial tumours and are the most common tumours of the sphenoid wing
in the anterior skull base, accounting for approximately 20% of supratentorial
meningiomas(1,2).
Cushing and Eisenhardt in 1938,(3) were the first to describe sphenoid
wing meningiomas in detail, distinguishing between globoid tumours with a
nodular shape and en plaque tumours. The globoid tumours were categorized
into 3 groups: 1) medial 2) middle and 3) lateral as per the anatomical
orientation of the lesser sphenoid wing —a medial third, representing the
medial posterior-to-anterior projecting segment most adjacent to the anterior
clinoid process; a middle third is the medial to lateral segment and the lateral
third is the anterior to posterior segment, joining with the temporal squamosa.
Meningiomas arising in the medial third of the sphenoid wing present
more challenges for neurosurgeons, given its proximity to the optic nerve, the
cranial nerves entering the superior orbital fissure and cavernous sinus and its
relation to internal carotid artery and its branches.
The middle and lateral third sphenoid wing meningiomas, as per the
present day concept, do not have distinct radiographic, microsurgical
characteristics or surgical outcome to warrant a separate grouping and are
Introduction
2
therefore clubbed into single entity, Stephen M. Russell et al(4). Their clinical
presentation and outcome of treatment is different from the medial group.
Till date, there are few studies analyzing and comparing the clinico-
radiological features, surgical outcomes and recurrences in patients
undergoing surgery for medial sphenoid wing meningiomas (SWM). This is
understandably so, due to rarity of this tumour location and also lack of
precise definition of this group of tumours. After Cushing and Eisenhardt in
1938,(3) Al-mefty(5) attempted to subclassify medial (clinoidal) sphenoid wing
meningiomas into three groups- Group I arising from dura proximal to
arachnoid ensheathment of supraclinoid ICA, Group II arising distal to
arachnoid ensheathment of ICA and Group III arising from optic foramen dura.
Group I and Group II had surgical relevance, as tumours in Group I had poor
arachnoid plane of dissection with the ICA, and therefore had increasing risk
of complications. Though, this concept has stood the test of time and being
followed by many, this theory is presently being challenged and refuted by
some comtemporary researchers(4,6,7,8). They have proposed that chronicity of
tumour compression, intrinsic tumour characteristics and invasiveness and
repeated surgery are the main determinants for poor dissection plane from
ICA.
Other important determinant for higher morbidity, mortality, and
recurrence rates observed in these medial group tumours compared with
meningiomas in other locations of sphenoid wing is the infiltration of
cavernous sinus which can be evaluated in pre operative imaging and also
Introduction
3
during surgery. Despite an improved orientation by understanding the
microsurgical anatomy and by advances in standard operative technique, the
surgical resection of cavernous sinus meningiomas remains a significant
challenge and is associated with high surgical morbidity (9,10,11,12,13,14,15). Unlike
in the past with aggressive approach to cavernous sinus
meningiomas (14,16,17,18,19), many authors have now confirmed the beneficial
outcome with subtotal excision and adjuvant radiotherapy (4,6,8,20).
We have also observed that, in this category of medial sphenoid wing
meningiomas, cavernous sinus infiltration is important determinant of surgical
morbidity like cranial nerve dysfunction involving the extraocular movements,
infarcts, poorer visual outcome and gross tumour residue and recurrence.
Recently, two authors viz. Makoto Nakamura et al.(6) in 2006 and Stephen M.
Russell et al.(4) have contributed to highlight the differences of medial SWM
between those with and without cavernous sinus infiltration.
Here, we also attempt to present our analysis of 72 cases of medial
SWM operated in our institute, in the period January 2000 to December 2011,
in the backdrop of cavernous sinus infiltration; with 43 cases in Group I
(without cavernous sinus infiltration) and 29 patients in Group II (with
cavernous sinus infiltration) .
Review of Literature
4
REVIEW OF LITERATURE
Historical Background
The first report detailing a successful craniotomy for the removal of an
intracranial meningioma appeared in The Lancet in 1881. In this article, Sir
William McEwen,(21) a Glasgow surgeon, reported on the operation he
performed on July 27, 1879, on a 14-year-old girl experiencing swelling at the
upper and inner portion of the left orbital cavity. Francesco Durante is known
for the successful removal of a left olfactory groove meningioma, performed
on June 1, 1884 (22,23). The neoplasms currently referred to as meningiomas
were referred to with a wide range of names in older medical literature,
depending on the source. Various descriptors included ‘fungoid tumours,
fungus of the dura mater, epithelioma, psammoma, dural sarcoma, dural
endothelioma, fibrosarcoma, angio endothelioma, arachnoidal fibroboastoma,
endotheliosis of the meninges, meningeal fibroblastoma , meningoblastoma ,
mestothelioma of the meninges and sarcoma of the dura’.(24)
Harvey Cushing is pre-eminent in the history of meningioma surgery.
Cushing proposed the term meningothelioma in an effort to describe these
tumours according to the tissue involved. Later, Cushing opted for the term
meningioma. In 1922, he reported on 85 cases of meningioma(25). Then, in
1938, Cushing and Eisenhardt published Meningiomas : Their Classification,
Regional Behaviour, Life History, and Surgical End Results, in which they
reported in detail the cases of 313 patients encountered between 1903 and
Review of Literature
5
1932 (3). In 1922 Cushing wrote: “There is today nothing in the whole realm of
surgery more gratifying than the successful removal of a meningioma with
subsequent perfect functional recovery.” (25)
Epidemiology
Incidence
Meningiomas constitute approximately 13%–19% of all primary
intracranial tumours(2) and accounting for approximately 20% of supratentorial
meningiomas(1,2,26). The distribution of intracranial meningioma’s is
approximately as follows: convexity (35%), parasagittal (20%), sphenoid ridge
(20%), intraventricular (5%), tuberculum sellae (3%), infratentorial (13%),
and others (4%)(1,2). The incidence of clinically significant meningiomas is
approximately 2.3/ 100,000 population, and about 5.5/100,000 population
when autopsy data are included(26). Age-specific incidence rates are given in
the graph below, revealing an increasing risk with age (27,28). The male:female
ratio ranges from 1:1.4 to 1:2.1, but it is widely accepted to be approximately
1:2 (1, 2).
0
5
10
15
20
age specific incidence of meningiomas
per 100,000 population
age specific incidence of
meningiomas per 100,000
population
Review of Literature
6
Sphenoid wing Meningioma
Anatomy of Sphenoid Bone (Os sphenoidale)
Ossification : Until the seventh or eighth month of fetal life the body of
the sphenoid consists of two parts, viz. Presphenoid in front of the
tuberculum sellae, with which the small wings are continuous and
postsphenoid, comprising the sella turcica and dorsum sellae, which are
associated with great wings, and pterygoid processes. The greater part of the
bone is ossified in cartilage. There are fourteen centers in all, six for the
presphenoid and eight for the postsphenoid.
The sphenoid bone (Fig. no. 1) is an unpaired bone situated in front of
the temporal bone and basilar part of the occipital bone. Its shape somewhat
resembles that of a butterfly or bat with its wings extended. It is divided into
the following parts:
• a median portion, known as the body of sphenoid bone, containing
the sella turcica which houses the pituitary gland
• two greater wings and two lesser wings
• Pterygoid processes of the sphenoides which project from it posteriorly
• Two sphenoidal conchae are situated at the anterior and posterior part of
the body.
Review of Literature
7
Figure no. 1- A sphenoid bone , superior view.
Lesser wing of sphenoid
The main features of the lesser wing are the optic canal, the anterior
clinoid process, and the superior orbital fissure.
Surfaces
Superior surface: is flat, and supports part of the frontal lobe of the brain.
Inferior surface: forms the back part of the roof of the orbit, and the upper
boundary of the superior orbital fissure.
Borders
The anterior border is serrated for articulation with the frontal bone.
The posterior border, smooth and rounded, is received into the lateral fissure
of the brain.
Review of Literature
8
Medial end of this border forms the anterior clinoid process, which
gives attachment to the tentorium cerebelli. It is sometimes joined to the
middle clinoid process by a spicule of bone, and when this occurs the
termination of the groove for the internal carotid artery is converted into a
foramen (carotico-clinoid).
The lesser wing is connected to the body by two roots. Between the
two roots is the optic foramen, for the transmission of the optic
nerve and ophthalmic artery.
Greater sphenoid wing
Cerebral surface
It forms part of the middle cranial fossa, It has a number of foramina in it:
• Foramen rotundum: transmits the maxillary nerve.
• Foramen ovale : transmits the mandibular nerve, the accessory meningeal
artery, and sometimes the lesser petrosal nerve.
• Sphenoidal emissary foramen: transmits a small vein from the cavernous
sinus.
• Foramen spinosum: transmits the middle meningeal vessels and
a recurrent branch from the mandibular nerve.
Lateral surface
The lateral surface is convex, and divided by a transverse ridge,
the infratemporal crest, into two portions:
• Superior temporal surface, forms a part of the temporal fossa, and gives
attachment to the temporalis.
Review of Literature
9
• Inferior temporal surface, enters into the formation of the infratemporal
fossa, and, together with the infratemporal crest, serves as an attachment
to the lateral pterygoid muscle
Orbital surface
The orbital surface of the great wing is smooth and quadrilateral in shape,
forms the posterior part of the lateral wall of the orbit.
Margin
• Its medial half forms the anterior boundary of the foramen lacerum, and
presents the posterior aperture of the pterygoid canal for the passage of
the corresponding nerve and artery.
• Its lateral half articulates, by means of a synchondrosis, with the petrous
portion of the temporal.
Cavernous sinus
The cavernous sinus (Fig.no. 2) is one of the dural venous sinuses, located on either
side of the pituitary fossa and body of the sphenoid bone between the endosteal and
visceral layers of the dura.
Figure no.2- cavernous sinus anatomy.
Review of Literature
10
Vascular connections
It receives blood from:
• Inferior ophthalmic vein
• Superficial middle cerebral vein
• Inferior cerebral veins
• Sphenoparietal sinus and occasionally
o central retinal vein
o frontal tributary of the middle meningeal vein
Drainage of the cavernous sinus is via:
• Superior petrosal sinus to the transverse sinus
• Inferior petrosal sinus directly to the jugular bulb
• Venous plexus on the internal carotid artery to the pterygoid plexus
• Emissary veins passing through sphenoidal foramen, foramen ovale,
foramen lacerum
• Facial vein through superior ophthalmic vein and angular vein or
pterygoid venous plexus or deep facial vein
• Superior sagittal sinus through middle cerebral vein and superior
anastomotic vein.
Depending on relative pressures, the superior ophthalmic veins either
drain into or drain the cavernous sinus. Additionally the cavernous sinuses
connect to each other via the intercavernous sinuses.
Review of Literature
11
Nerves
The cavernous sinus transmits multiple cranial nerves to the superior
orbital fissure, these are:
• In the lateral wall from superior to inferior:
o Oculomotor nerve (CN III)
o Trochlear nerve (CN IV)
o Trigeminal nerve (CN V) ophthalmic and maxillary divisions.
• Traversing the sinus lateral to the ICA
o Abducens nerve (CN VI)
Artery
The internal carotid artery enters the posterior inferior aspect of the
sinus, and bends upon itself as the carotid siphon (cavernous segment - C4).
Two branches arise from this segment: meningohypophyseal
trunk and inferolateral trunk. The artery is surrounded by a plexus of
sympathetic nerves from the superior cervical ganglion.
Classifications of sphenoid wing meningioma
Cushing and Eisenhardt
In 1938, Cushing and Eisenhardt(3) reported the first surgical
experience with meningiomas of the sphenoid ridge. They divided sphenoid
ridge meningiomas into four categories:
Review of Literature
12
1) Tumours of the deep or clinoidal third, 2) middle-ridge tumours, 3) en
plaque pterional tumours, and 4) global pterional tumours.
In this classification scheme the lesser sphenoid wing is divided into thirds,
with changes in the orientation of the wing roughly demarcating the
boundaries of these segments—
1) Medial third, which represents the medial posterior-to-anterior projecting
segment most adjacent to the anterior clinoid process
2) Middle third, which runs medial to lateral
3) Lateral third, which runs anterior to posterior, eventually joining with the
temporal squamosa.
Al-Mefty’s classification of clinoidal meningioma
Anatomical basis for classification
Al-Mefty(5) classified clinoidal meningiomas into three categories based
on the anatomic site of origin and degree of surgical difficulty. As the carotid
artery emerges from the cavernous sinus inferomedial to the anterior clinoid, it
enters the subdural space to be vested in the carotid cistern. The arachnoid
does not follow the internal carotid artery into the cavernous sinus space, nor
is it attached to the anterior clinoid process. A 1- mm or 2-mm segment of
naked internal carotid artery lies between the investment of the carotid cistern
and the dura of the cavernous sinus(29). This segment is not to be confused
with the extradural segment which lies between the two rings anchoring the
carotid artery as it exits the cavernous sinus space.(30)
Review of Literature
13
Group I
The meningioma's origin is proximal to the end of the carotid cistern,
inferior and medial to anterior clinoid process, the tumor enwraps the carotid
artery, directly adhering to the adventitia in the absence of an intervening
arachnoid membrane. This anatomic arrangement accounts for the surgeon’s
inability to dissect the tumour from the ICA and MCA branches. (Fig. no. 3)
Fig. no. 3- Artist's drawing of a Group I meningioma. The tumor encases the carotid artery
and its branches, with direct attachment to the adventitia. The optic nerve maintains an
arachnoid plane from the chiasmatic cistern.
Group II
Tumours of Group II originate from the superior and/ or lateral aspect
of the anterior clinoid above the segment of the carotid invested in the carotid
cistern. Thus, as the tumour grows, an arachnoid membrane of the carotid
cistern and distally of the sylvian cistern separates the tumour from the arterial
adventitia. (Fig. no.4)
Review of Literature
14
Fig. no 4 -Group II meningioma: An arachnoid membrane of the carotid cistern separates the
tumor from the adventitia, rendering dissection possible. The optic nerve maintains an
arachnoid membrane from the chiasmatic cistern.
Group III
Tumours in Group III originate at the optic foramen, extending into the
optic canal and the tip of the anterior clinoid process. The arachnoid
membrane investing the carotid artery is present. Because this tumor arises
proximal to the chiasmatic cistern, there may be no arachnoid investment
between the optic nerve and the tumour. (Fig. no. 5)
Figure no. 5- Group III meningioma: Artist's drawing showing the tumor originating in the
optic foramen. The tumor is small, separated from the carotid by the carotid cistern, but it
extends into the optic canal.
Review of Literature
15
Abdel– Aziz et al.(8) proposed classification of medial or clinoidal
meningiomas with respect to cavernous sinus involvement into 3 subtypes
(Fig. no. 6):
a) Clinoido-cavernous
b) Spheno-cavernous
c) Sphenoclinoido-cavernous meningiomas
Figure no.6 - Inner sphenoid wing and clinoidal meningiomas classified according to their
extension into the cavernous sinus. A, clinoido-cavernous, B, spheno-cavernous, and C,
spheno-clinoido-cavernous.(8)
Review of Literature
16
Makoto Nakamura et al. (6) classified sphenoid wing meningioma:
(Fig. no. 7)
I – Medial SWM without CS involvement
II – Medial SWM with CS involvement
III – Middle SWM
IV – Lateral SWM
Figure no. 7
Arterial supply to sphenoid wing meningioma
Meningiomas of the medial sphenoid ridge are usually fed by direct
(sometimes intracavernous) branches of the internal carotid, or the ascending
pharyngeal artery, and sometimes a recurrent branch of the ophthalmic artery
passing through the superior orbital fissure.
Review of Literature
17
Lateral tumours derive much of their blood supply from the superficial
temporal and middle meningeal arteries. Additional feeding vessels may
include the anterior meningeal and other branches of the ethmoidal arteries.
Clinical Presentation of Sphenoid wing meningioma
Clinical signs and symptoms reflect tumor location and growth pattern.
Tumours of the lateral sphenoid wing will often become relatively large before
the development of a focal deficit such as hemiparesis or aphasia. Tumours of
the medial sphenoid ridge commonly cause early and more specific
symptoms due to the proximity of the optic apparatus and cavernous sinus.
Patients with sphenoorbital meningiomas typically present with
exophthalmos, deterioration of visual acuity and field cuts, and diplopia.
Tumour growth in the cavernous sinus or superior orbital fissure may lead to
ocular palsies. Intraorbital tumor growth characteristically causes diplopia
due to restriction of ocular movements rather than oculomotor nerve paresis.
Involvement of the cavernous sinus will also sometimes result in sensory loss
in the distribution of the ophthalmic and eventually other division of the
trigeminal nerve.
Extracranial tumor growth and hyperostosis can cause cosmetic
disturbances. Seizures are relatively frequent. Uncinate fits and gustatory and
olfactory hallucinations point to the temporal lobe as their origin, as well as
complex-partial and generalized tonic-clonic seizures. Finally, the number of
patients with more or less asymptomatic meningiomas diagnosed during the
course of a workup (for headache or vertigo) is increasing.
Review of Literature
18
Risk factors
Ionizing radiation
At present, the primary environmental risk factor identified for
meningioma is exposure to ionizing radiation (IR) with risks from six fold to
tenfold. (33, 34,35,36) In one of the most well-known studies of ionizing radiation
and meningioma risk, children who were given radiation therapy for scalp
ringworm in Israel between 1948 and 1960 (the Tinea Capitis Cohort), were
observed to have a relative risk of almost 10 for meningioma.(37) Radiation
therapy for intra-cranial tumours has also been linked to meningioma risk.(35)
Hormones
An association between hormones and meningioma risk has been
suggested by a number of findings(38,39,40,41,42) including the increased
incidence of the disease in women versus men (2:1), the presence of
estrogen, progesterone, and androgen receptors on some meningiomas, an
association between breast cancer and meningiomas, and indications that
meningiomas change in size during the luteal phase of the menstrual cycle
and pregnancy and the regression of multiple meningiomas in a patient
following cessation of estrogen agonist therapy.(41, 42)
Review of Literature
19
Hormone Receptors
Estrogen
The prevalence and function of estrogen receptors in meningiomas
remains a controversial topic. Data from ‘Brigham and Women’s Hospital’
indicates that differences exist in the prevalence of estrogen receptor isoforms
alpha and beta, with 44% of meningiomas expressing ER-alpha mRNA and
68% expressing ER-beta mRNA.(43) These receptors have been more
extensively characterized for breast cancer but no such data exist for
meningioma response.(44)
Progesterone
The majority of meningiomas (40–100%) possess progesterone
receptors (PR). Hsu et al(40) observed that benign meningiomas were more
likely than malignant to be PR positive (96% versus 40%), with PR status
being inversely related to mitotic index and grade and therefore associated
with better prognosis.
Androgen
Approximately 50% of meningiomas have been noted to express
androgen receptors, with tumours from women exhibiting a higher rate than
tumours from men. Data suggest that androgen expression positivity rates
vary positively with stage(45). As for estrogen receptors and PR, little is known
regarding the usefulness of these receptors relative to clinical prediction and
treatment.
Review of Literature
20
Other receptors
Preferential immunoreactive staining for the sst2A subtype
somatostatin receptor has been shown in meningiomas. (46) The dopamine D1
(but not D2) receptor has also been demonstrated in meningiomas.
Meningiomas are also positive for prostaglandins, most notably prostaglandin
E2. (47) Several growth factors have been shown to stimulate meningiomas,
including epidermal growth factor, fibroblast growth factor, and PDGF.
Breast cancer and meningioma
Schoenberg and associates(48), were the first to suggest that the
concomitant occurrence of breast cancer and meningioma was higher than
could be expected from pure coincidence. A number of explanations have
been proposed for this association including common risk factors (age at
menopause or use of OCP) or shared genetic predisposition.
Head trauma
Since the time of Harvey Cushing, head trauma has been suggested
as a risk factor for meningioma, although the results across studies are not
consistent. Although several small case control studies from the early 1980s
report an increased risk of meningioma associated with head trauma for both
males (OR 1.9, P < 0.01) and females (OR 2.0, P <0.01), other studies report
no such association.(49,50)
Review of Literature
21
Cell phone use
At present, little evidence exists for an association between the two.
Newly reported data from the large Interphone study replicated earlier
negative findings even for the highest exposed groups (>10 years of heavy
exposure).[51] Of note, Swedish investigators of the Interphone study recently
reported a significant association between one type of benign brain tumor,
acoustic neuroma, and long-term cell phone use (OR 3.9; 95% CI, 1.6- 9.5)
[52].
Occupation/diet/allergy
An international case/control study found no association between diet
and meningioma.(53) Although a number of studies which examined the
relationship between glial brain tumours and allergic disease such as asthma
and eczema have found evidence for an association, little evidence has been
found for such an association for meningioma. (54,55) A study of innate immune
genes did not find strong evidence of risk imparted by variants in such
genes. (56)
Viruses
In work reported by Inoue (57), Inoue-Melnick virus (IMV), a DNA virus
linked to subacute myelo-opticoneuropathy, was isolated from six of seven
human meningioma-derived cell cultures but was not isolated from six other
brain tumor cell cultures. Of 26 patients with meningioma, 22 (84.6%) were
positive for the IMV antibody. Rachlin and Rosenblum stated that “although
Review of Literature
22
there is strong biochemical evidence associating DNA tumor viruses with
human meningiomas, the role of the virus in the development of the tumor
remains undefined.”(58)
Venous thrombosis
Sawaya and Ramo(59) demonstrated a higher rate of venous
thrombosis of the legs in patients with meningiomas than in those with
glioblastomas or brain metastasis. Using 125 I-fibrinogen leg scans, they
found that the incidence of thrombosis was 72% for meningioma patients,
60% for glioblastoma patients, and 20% for patients with brain metastasis.
Family history of meningioma
Malmer et al(60) and Hemminki et al(61) using data from the Swedish
and Norwegian Registry Databases, reveal an increased risk with increasing
numbers of affected first degree relatives with meningioma, indicating a
familial risk for meningioma tumours.
Molecular Genetics
Loss of heterozygosity at chromosome 22 with inactivation of the NF-2
gene, is the earliest and best characterized genetic change association with
meningiomas, (62) and is affected in the majority of NF-2–related tumours and
more than 50% of sporadic meningiomas. (63,64) DAL-1 on chromosome 18p,
have been found in the majority of atypical and malignant meningioma
specimens.(65) Deletions in chromosomes 1p ,10q and 14q appear to correlate
in several studies with a higher histologic grade and/or rate of recurrence. (66)
Review of Literature
23
Progression to atypical meningioma is associated with telomerase
activation,(67) and loss of progesterone receptor expression,(68) MIB-1 labeling
indices, VEGFR expression, quantitative staining of proliferating cell nuclear
antigen and expression of Janus tyrosine kinase and signal transducer and
activator of transcription proteins. (69,70,71)
Histopathology
The 2007 WHO classification of tumours of the CNS lists meningiomas
under the heading “Tumours of the meninges” and the subheading “Tumours
of meningothelial cells.” WHO recognizes three grades based on pathologic
criteria and the risk of recurrence and aggressive growth as follows: (72)
WHO Grade I WHO Grade II
Meningothelial meningioma Atypical meningioma
Fibrous (fibroblastic) meningioma Clear cell meningioma
Transitional (mixed) meningioma Chordoid meningioma
Psammomatous meningioma
Metaplastic meningioma WHO Grade III
Angiomatous meningioma Rhabdoid meningioma
Microcystic meningioma Papillary meningioma
Secretory meningioma Anaplastic (malignant)
Lymphoplasmacyte-rich meningioma
Review of Literature
24
Common histological variants are:
Meningothelial meningioma (Fig.no. 8)
Distinctive features of meningothelial meningiomas include intranuclear
cytoplasmic pseudo inclusions, in which an invaginated cytoplasmic remnant
occupies the interior of the nucleus and displaces the nuclear chromatin.
Another useful feature is the presence of so-called Orphan Annie's eye nucleii
with central clearing and peripheral margination of the chromatin.
Figure no. 8- A. Squash preparation of a meningothelial meningioma showing the typical
whorl formation. B. Meningothelial meningioma with typical intranuclear inclusions.
Fibrous (fibroblastic) meningioma
Uncommon in pure form, this meningioma variant consists of spindle
cells forming parallel, storiform and interlacing bundles in a collagen-rich
matrix. Whorl formation and psammoma bodies are infrequent.
Transitional (mixed) meningioma
Feature the coexistence of meningothelial and fibrous patterns as well
as transitions between these patterns.
Review of Literature
25
Atypical meningioma
A meningioma with increased mitotic activity (4 or more mitoses per 10
high-power), or three or more of the following histologic features: increased
cellularity, small cells with a high nuclear: cytoplasmic ratio, prominent
nucleoli, uninterrupted patternless or sheet-like growth, and foci of
‘spontaneous’ or ‘geographic’ necrosis. Atypical meningiomas often have
moderately high MIB-1 labelling indices.
Immunohistochemistry
The test for epithelial membrane antigen (EMA) is positive in 80% of
meningiomas. The results of S-100 staining are quite variable. Meningiomas
also express markers for fibroblasts (vimentin). Syncytial and transitional
meningiomas express E-cadherin. Another use of immunohistochemistry lies
in differentiating atypical meningiomas from similar but pathologically distinct
tumours, such as secretory meningioma from metastatic carcinoma. (71)
Radiology
Plain radiographs: reveal three characteristic findings in meningioma
patients, hyperostosis, increased vascular markings, and calcification.
CT scan: On non–contrast-enhanced CT, meningiomas are typically
isodense to slightly hyperdense compared with contiguous brain parenchyma.
Calcification may be seen. Meningiomas usually enhance homogeneously
and intensely and is usually broadly based against a bony structure or dural
Review of Literature
26
margin. A common bony manifestation is hyperostosis. The amount of edema
surrounding a meningioma is variable. The dura mater adjacent to the
attachment of a meningioma may enhance on CT or MRI after the
administration of a contrast agent, so-called dural tails. Histologically, in dural
tail, although only connective tissue and vascular tissue proliferation were
seen, in some cases meningioma cell nests were also identified. (73)
MRI: On T1-weighted MRI, 60% of meningiomas are isointense and 30% are
mildly hypointense compared with gray matter. On T2-weighted images, the
tumours are isointense (50%) or mildly to moderately hyperintense (40%).
Hyperintensity on T2-weighted images suggests higher water content,
denoting a meningothelial meningioma, a vascular meningioma, or an
aggressive meningioma. However, it is suggestive of an easily suckable tumor
during surgery. Meningiomas usually enhance intensely and uniformly after
the injection of gadolinium, with typical dural tail enhancement.
Angiography may be an adjunct in the preoperative assessment of some
meningiomas. It enables the surgeon to assess the vascularity and vascular
supply of the tumour, and the presence of tumour encroachment on vascular
structures. Angiography will also allow for a test occlusion of the carotid artery
if injury or sacrifice of this vessel is a possibility. Preoperative embolization is
used as an adjunct in some centers to reduce intraoperative blood loss, (74,75)
although in a comparative study no advantage of preoperative embolization
could be demonstrated. (74)
Review of Literature
27
Scintigraphy: Somatostatin receptor scintigraphy using 111In octreotide is
an extremely sensitive test for meningiomas. It can be used preoperatively
when the diagnosis is not straightforward. In the postoperative period,
somatostatin receptor scintigraphy can be helpful in differentiating contrast
uptake from residual tumour and that from nonspecific. (76)
Natural History
The authors of several studies have described the natural history of
meningiomas, and they based their findings on samples ranging from 17 to 70
tumours. Because of small sample sizes and the variety of the methods used
to measure the tumor growth, information regarding the tumor growth rate and
prognostic factors were inconclusive. One study from Cleveland Clinic ,
Ohio,(72) included 273 conservatively managed meningiomas in 244 patients.
Intracranial meningioma growth was observed in 44.0% by the linear diameter
measurement and in 74.0% by the volumetry within 4 years.
The following factors were found to be significant based on at least 2
methods of study: young age (≤ 60 years), lack of calcification, hyperintensity
on T2-weighted MR imaging, large size (> 25-mm diameter), and edema.
Patients with these positive factors may need to be observed more closely. (77)
Review of Literature
28
Treatment Options
Surgical Therapy and Recurrence
The only definitive cure for meningioma is complete surgical resection.
In 1957. Simpson(78) introduced a five-grade classification of the surgical
removal of meningiomas. (Table no. 1) In Simpson’s series of 265
meningiomas, 55 (21%) had recurrence. The rates of tumor recurrence
according to the extent of resection were: grade I, 9%; grade II, 19%; grade
III, 29%; grade IV, 44%. Other studies appearing subsequently, with at least
10 years’ follow-up, found similar recurrence rates. In one study, convexity
meningiomas undergone grade 0 resection showed no recurrence at mean
follow-up period 5 years and 8 months.(80)
In 1992, Kobayashi and associates(79) revised the Simpson grading
system from a microsurgical perspective by introducing a classification system
based on the extent of microscopic resection. (Table no. 2)
The anatomic location of a meningioma influences its rate of
recurrence. Highest recurrence rates (>20%) are with sphenoid wing
meningiomas, followed by those with parasagittal meningiomas (8% to 24%),
convexity and suprasellar meningiomas is 5% to 10% depending on the grade
of resection.(81)
Review of Literature
29
Table no. 1- Simpson Grading System
Grade Description
I Macroscopically complete tumor removal with excision of the
tumor’s dural attachment and any abnormal bone
II Macroscopically complete tumor removal with coagulation of its
dural attachment
III Macroscopically complete removal of the intradural tumor without
resection or coagulation of its dural attachment or extradural
extensions
IV Subtotal removal of the tumor
V Simple decompresssion of the tumor
(Adapted from Simpson D. The recurrence of intracranial meningiomas
after surgical treatment. J Neurol Neurosurg Psychiatry. 1957;20:22). (78)
Table no. 2- Modified Shinshu Grade or Okudera- Kobayashi Grade
Grade Description
I Complete microscopic removal of tumor and dural attachment with
any abnormal bone
II Complete microscopic removal of tumor with diathermy coagulation
of its dural attachment
IIIA Complete microscopic removal of intradural and extradural tumor
without resection or coagulation of its dural attachment
IIIB Complete microscopic removal of intradural tumor without
resection or coagulation of its dural attachment or of any extradural
extensions
IVA Intentional subtotal removal to preserve cranial nerves or blood
vessels with complete
microscopic removal of dural attachment
Review of Literature
30
IVB Partial removal, leaving tumor of <10% in volume
V Partial removal, leaving tumor of >10% in volume, or
decompression with or without biopsy.
Adapted from Kobayashi K, Okudera H, Tanaka Y. Surgical considerations on skull
base meningioma. Paper presented at the First International Skull Base Congress,
June 18, 1992, Hanover, Germany. (79)
Non surgical treatment
Nonsurgical therapies are used for recurrent or incompletely resected
meningiomas.
Radiation therapy/ Radiosurgery
Radiosurgery has proved to be an effective adjuvant therapy in
controlling growth of meningiomas and plays an important role in
meningiomas involving CS. Tumour growth control rate after Gamma knife of
CS meningiomas ranged from 91% to 96.5% at 5 years and 82% to 94% at 10
years(82,83,84,85,86,87). In terms of long-term control, however, the clinical
recurrence rate after 15 years with subtotal resection and radiation therapy is
75%, and the rate of complications is 56%.(87) Radiation induced complications
and the possibility of radiation-induced malignancy or tumor progression are
concerning issues. (88 -93) Guthrie and associates, (94) concluded that “while
surgical excision is the treatment of choice, radiation therapy should be
considered in following scenarios:
Review of Literature
31
(1) After surgery for a malignant meningioma,
(2) Following incomplete resection of a meningioma for which the risk of
resection of an eventual recurrence is judged to be excessive,
(3) For patients with multiple recurrent tumours for whom the surgeon judges
repeat surgery to be too risky, and
(4) As a sole therapy of a progressively symptomatic patient with a
meningioma judged by the surgeon to be inoperable.
Hormonal Therapy
The presence of hormonal receptors in meningiomas has prompted
research into hormonal manipulation as treatment. The oral progesterone
agonist megestrol acetate (Megace) was used in a small trial of nine patients
with no observed response. (95)
The SWOG completed a study of mifepristone for unresectable
meningiomas (198 total patients of whom 160 were evaluated).(96) The results
did not support a role for Mifepristone compared with placebo (median PFS
was 10 months in Mifeprisrone arm and 12 months in the placebo arm).
In addition, SWOG reported a Phase II trial of 21 patients with
meningioma treated with oral tamoxifen, an estrogen receptor antagonist (97).
One patient achieved a partial response, two patients had a minor response,
and six patients had stable disease for longer than 6 months.
Review of Literature
32
Biotherapy and Chemotherapy
Recombinant interferon-alpha has been found to inhibit the growth of
cultured human meningioma cell lines in vitro. (98,99) In the largest report, six
patients with recurrent unresectable and previously irradiated meningiomas
were treated. One patient had an objective response and four patients had
stable disease for longer than 6 months.
In a clinical trial with hydroxyurea by Schrell et al.(100) involving four
patients, another by Newton et al (101) involving 40 patients, and a third trial by
Mason et al (102) involving 20 patients suggested in vivo efficacy( > 80% with
stable disease for a median of 20 to 30 months).
A recent trial of chronic oral temozolomide for surgical and
radiotherapy refractory meningiomas failed to demonstrate activity in 16
patients (103) Trapidil, a drug with known antagonistic action against PDGF,
showed a dose-dependent inhibition of meningioma cell proliferation. (104)
In another small trial of 16 patients, those with recurrent meningiomas
shown to overexpress somatostatin receptors by octreotide scintigraphy were
treated with monthly long-acting somatostatin.(105) Thirty-one percent of
patients demonstrated a partial imaging-documented response, and 44%
achieved PFS at 6 months with minimal toxicity. Animal trials are being
conducted to assess the possible use of a growth hormone receptor
antagonist (pegvisomant) as a medical treatment for meningiomas.(106)
Review of Literature
33
Recurrence
Besides surgical grade of resection, as mentioned above, other factors
determining recurrence are pathology, cellular and molecular criteria,
hormonal receptor status and radiological imaging. Benign meningiomas
have recurrence rates of about 7–25%, atypical meningiomas of 29–52% of
cases and anaplastic meningiomas at rates of 50–94%. (107)
Pathological features associated with a significantly higher rate of
recurrence are invasion of the dura or brain infiltration, papillary or
hemangiopericytic pattern and lack of progesterone receptors. Cellular criteria
include the presence of mitoses (>20/10 high power fields), increased
cellularity, nuclear polymorphism, focal necrosis, high levels of expression of
VEGF and high MIB-1 labeling index. (40,68,69,71,81) Moller and Braendstrup,
(108) however, found that proliferating cell nuclear antigen and Ki-67 are of
minor value as predictors of the recurrence of benign meningiomas.
Multivariate analysis in Nakasu and coworkers (109) study of 101 patients
revealed that only the shape of the tumor was significant; “mushrooming” and
lobulated meningiomas were more likely to recur than round ones.
Surgical Outcome
Complications after surgery are related to lack of proper understanding
of the anatomy of medial sphenoid wing and its relation to the arteries, optic
nerve and cranial nerves in cavernous sinus and superior orbital fissure. The
Review of Literature
34
surgical morbidity/ mortality was higher in those with a radical and aggressive
resection, especially in cavernous sinus region (83,97,98). This has lead to
some authors in recent times (4,6,7,110,111,112) to follow a conservative strategy
with or without radiosurgery.
Summary of the outcome of surgery and the mortality rate of medial
sphenoid wing meningiomas in chronological order are given in table no.13
and discussed under relevant headings later on.
Aim of the Study
35
AIM OF THE STUDY
A comparative analysis of the clinico -radiological features, surgical
outcome and recurrence rate of two different subgroups of medial sphenoid
wing meningiomas (SWM), viz.
Group I – without cavernous sinus involvement and
Group II – with cavernous sinus involvement.
Materials and Methods
36
MATERIALS AND METHODS
A retrospective study was conducted from period of January 2000 to
December 2011 on sphenoid wing meningiomas operated in our Department
of Neurosurgery, Sree Chitra Tirunal Institute For Medical Science and
Technology, Trivandrum. Out of a total of 168 cases of sphenoid wing
meningiomas (SWM) operated, 72 cases were medial SWM (others included
17 cases of middle, 63 pterional, and 17 sphenoorbital meningiomas). We
further subclassified the 72 cases of medial SWM into two groups (Group I-
without cavernous sinus involvement and Group II – with cavernous sinus
involvement), from data obtained from pre operative radiological records and
operative findings.
Data collection
The list of patients having undergone surgery for SWM were obtained
from the operation theatre records, followed by study of individual files from
the medical records department. Clinical and radiological presentation, study
of operative notes for approaches and findings, and HPR were reviewed.
Follow up details were obtained by personally calling patients to our OPD and
assessing the present status, while few have been interviewed through
telephonic conversation.
Radiology
Preoperative evaluation of most of our patients included initial CT scan
with contrast and followed by MRI studies, T1 and T2-weighted sequences
Materials and Methods
37
with gadolinium contrast. Some patients operated on emergency basis or
during the first quarter of study period underwent only C T scan with contrast.
Digital Substraction Angiogram (DSA) of four cerebral vessels with cross
compression study were performed for most cases with encasement of ICA
(cavernous / supraclinoid). The purpose of doing DSA was to define the
arterial supply to the tumour bulk, nature of compression of ICA (narrowing,
obliteration, displacement) and adequacy of cross circulation to distal ICA
through alternate arterial territory. It also served to determine our
aggressiveness of tumour decompression around prominent vessels to avoid
inadvertent injury. Pre-operative embolization of feeders were not done in
any of our cases.
Surgery
Perioperative Management and recent surgical technique used:
Antiepileptic prophylaxis of oral Phenytoin sodium 100 mg thrice daily
was started at least 1 week prior to surgery, else, loading dose of parentral
Phenytoin sodium 17mg/kg was administered. Those with allergy to Phenytoin
were started on alternate AED as per discussion with our Epileptologist. Pre
operative antibiotics of Ceftriazone 1gm and Amikacin 500mg were given in 2
doses at 12 and 2 hours prior to surgery. Intraoperative anti oedema
measures (i/v Mannitol, 1gm/kg, and hyperventilation) were carried out prior to
dural opening to make the brain lax, lumbar drainage of CSF was not done in
any of our cases.
Materials and Methods
38
Position - The patient was placed supine and head end elevated to promote
venous return. The head was rotated 30 to 40 degrees to the opposite side
and extended slightly to allow the brain to fall away from the cranial base
minimizing retraction. The head was fixed in position using the Mayfield head
clamp.
Craniotomy- Majority of patient underwent standard fronto- temporal
craniotomy, only three cases (1 in group I and 2 in group II) underwent FTOZ
during the mentioned period of study.
Extradural work- The steps included dissection of the pre temporal and
subfrontal dura away from the sphenoid wing. The dural fold at the level of the
meningio-orbital artery was cut to allow disconnection of the dura propria of
the temporal lobe from its attachment to the frontal dura. The dura propria of
temporal lobe was further mobilized by interdural dissection over the
cavernous sinus to complete the process of convexitization. This process of
exposing the anterior clinoid process itself lead to significant devascularization
of the tumor. Then, the anterior clinoidectomy was done with high speed
diamond drill and copious irrigation with saline. The optic canal was
decompressed by removing the optic strut and the optic roof as required. We
attempted to achieve maximum bony work extradurally in most of the cases.
Intradural exposure- The sylvian fissure was routinely opened from the level
of the limen insulae toward its proximal point to help visualize the MCA and
ICA. Once this was achieved, debulking of the tumor was started with
intermittent dissection of the tumor away from the adjacent brain and blood
Materials and Methods
39
vessels. The dura at the base of the skull and over the clinoid region was
totally removed. The dural defect was reconstructed with either fascia lata or
pericranium and was reinforced with fibrin glue. The clinoidal space was
obliterated with subcutaneous fat from thigh/abdomen.
Postoperative - All patients were cared for in a neuro ICU for 1 to 2 days
before returning to the ward. DVT prophylaxis was started with LMW heparin
from day 2, provided post operative CT scan showed satisfactory hemostasis,
for those with motor deficits, bedridden/immobile patient and obese females
beyond 3rd decade of life. In uneventful cases, patients were usually
discharged by 7 to 10 days. First follow up visit was at 6 weeks, then at
3months, 6 months and yearly thereafter.
Statistical Analysis
Data of both tumor groups were compared using the Chi Square test
with 1 degree of freedom (for comparison of percentages) and unpaired t test
for comparison of two mean values. A P value was calculated for each
comparison using two-tailed analysis with significance assumed at the 0.05
level.
Patient characteristics
Patients were divided into two groups
sinus involvement) and Group II (with cavernous sinus i
consisted of 43 patients and Group II of 29 patients
presentation in Group I was
38.4 years (range 28-51yr) with standard deviation of 8.9 and 8.3
respectively. Sex ratio was skewed towards females
Group I and 1.9:1 in Group
and 19/29 females in Group
Figure no.9
We also observed a
occurrence in both the groups
was the dominant hemisphere in
MEDIAL SPHENOID WING MENINGIOMAS
40
RESULTS
Patients were divided into two groups – Group I (without cavernous
sinus involvement) and Group II (with cavernous sinus involvement)
consisted of 43 patients and Group II of 29 patients. (Fig. no. 9) Mean age
I was 48.7 years (range 31–65yr) and Group II was
51yr) with standard deviation of 8.9 and 8.3
respectively. Sex ratio was skewed towards females, F: M ratio of 2.07: 1 in
Group I and 1.9:1 in Group II (or 29/43 females, 67.4%, affected in Group I
/29 females in Group II, 65.5%).
- Group I and Group II tumour distribution.
We also observed a predilection towards left side for tumour
groups (I & II, 58.1% and 55.2% respectively). L
misphere in all our patients. In Group I, 1 patient had
MEDIAL SPHENOID WING MENINGIOMAS
Group I (43 patients)
Group II (29 patients)
Results
cavernous
nvolvement). Group I
Mean age at
and Group II was
51yr) with standard deviation of 8.9 and 8.3,
M ratio of 2.07: 1 in
affected in Group I
for tumour
). Left side
1 patient had
Group I (43 patients)
Group II (29 patients)
Results
41
undergone initial surgery for same tumour at alternate centre and presented
to us with residue/recurrence, whereas, in Group II, there were 3 such
patients.
Clinical presentation
The most common presenting symptoms were headache (74.4% in
Group I and 89.7% in Group II, p =0.109), visual disturbances (58.1% in
Group I and 58.6% in Group II, p=0.968), seizures (16.3% in Group I and
20.7% in Group II, p= 0.633) and behavioural problems/ memory
disturbances. The symptoms presented to us at admission are tabulated in
Table no. 3. There was no preceding history of exposure to radiation or
trauma in any of the cases.
Group II patients were more likely to present with raised ICP
complications (9.3% in group I and 37.9% in group II, p = 0.003) and
dysphasia/apahasia (3 patients (10.3%) in group II and none in group I, p=
0.031). 3 patients were stuporous (GCS <8/15) at presentation in group II (2
had generalized seizures and were in post ictal state and 1 presented with
raised ICP and signs of herniation).
Results
42
TABLE no. 3 : Presenting complaints in Group I and II of medial
sphenoid wing meningiomas.
Clinical
presentation
GROUP 1,
n=43 (%)
GROUP 2,
n =29 (%)
Chi
square,
P- value
Headache 31 (74.4) 26 (89.7) 2.57 0.109
Raised ICP 4 (9.3) 11 (37.9) 8.61 0.003
Visual deterioration 25 (58.1) 17 (58.6) 0.00 0.968
Focal Seizures 4 (9.3) 1 (3.4) 0.92 0.338
Generalised
seizures
7 (16.3) 6 (20.7) 0.23 0.633
Stuporous
(GCS<8/15)
0 3 (10.3) 4.64 0.031
Proptosis 0 1 (3.4) 1.5 0.220
Hemiparesis 2 (4.7) 4 (13.8) 1.89 0.169
Dysphasia/aphasia 0 3 (10.3) 4.64 0.031
Behavioural
problems
8 (18.6) 5 (17.2) 0.02 0.883
Incidental 1 (2.3) 0 0.68 0.408
memory difficulties
(subjective)
10 (23.3) 4 (13.8) 0.99 0.320
Previous surgery
elsewhere
1 (2.3) 3 (10.3) 2.12 0.145
Neurocutaneous
markers
2 (4.7) 0 1.39 0.239
Results
43
Tumour characteristics
Tumour size was categorized into 3 sizes : <2cm, 2-4 cm and >4cm. Its
distribution is depicted in the graph below. (Fig no.10) Hyperostosis of
sphenoid wing and orbit were more common in Group II, 23/29 patients
(79.3%) compared to 23/43 patients (53.5%) in Group I, p= 0.025. Two
patients in group II showed erosion into the orbit and out of which, one
presented with proptosis. Three patients in group I (7%) and one patient in
group II (3.4%) had cystic component, p = 0.521. Tumour calcification was
noted in 5 patients (11.6%) and 2 patients (6.9%) in groups I and II,
respectively, p= 0.506.
Figure no. 10- Distribution of three categories of tumour sizes (<2cm, 2 -4 cm and
>4cm ), hyperostosis, cystic component and calcification in Group I and II medial
SWM.
0
10
20
30
40
50
60
70
80
90
Medial group I Medial group II
Tumour size <2cm
Tumour size 2-4 cm
Tumour size > 4cm
Column1
hyperostosis p=0.025
cystic
calcification
Results
44
Surgery
Gross total resection (Simpson Grade I + II) was achieved in 31
patients (72.1%) in Group I and 12 patients (41.2%) in Group II tumours
(Table no.4, Fig no. 11). To confirm the gross radicality of tumour resection in
each tumour groups, operative records findings and postoperative imaging
(CT scan with and without contrast) were analyzed in all cases. The rate of
subtotal excision or Simpson’s grade III/ IV excision was higher in group II,
58.8% vs 27.9 % in group I).
Figure no. 11- Distribution of Simpson’s Grades of tumour resection in Group I and II
medial SWM.
0
10
20
30
40
50
60
70
80
medial SWM group I medial SWM group II
SIMPSON I
SIMPSON II
SIMPSONIII
SIMPSON IV
Gross total
resection(Simpson's I + II)
Table no. 4 : Simpson’s Grades of tumour resection
Simpson
I
Simpson
II
Simpson III Simpson IV GTR
(I +II)
Group I 27.9% 44.2% 9.3% 18.6% 72.1%
Group II 6.8% 34.4% 31.2% 27.6% 41.2%
Rec. tumour 0 0 0 100% 0
Results
45
Figure no. 12- A 51 years old female with medial SWM (Group I) presented with
seizures and headache, a) MRI brain axial with gadolinium contrast, b) coronal
contrast, c) T2WI coronal d) Pre operative CT brain axial with contrast showing relative
sparing of cavernous sinus and was confirmed during surgery, e) & f) post surgery CT
with contrast showing no residue. Simpson’s grade I excision was done after
convexitization of dura.
a) b) c)
f) e) d)
Results
46
Figure no. 13- A 43 years old female with medial SWM (group II), presented with no
PL and 3rd
CN paresis in right eye. a), b) MRI brain T1W axial and coronal with
gadolinium contrast, c) CT brain axial contrast showing involvement of right cavernous
sinus with encasement of cavernous and supraclinoid ICA. d) &e) DSA with right ICA
injection showing opening of carotid siphon and upward displacement of M1 MCA and
genu with narrowing of supraclinoid ICA. f) post surgery CT brain showing residue
over cavernous region.
a) b) c)
f) e) d)
Results
47
The arachnoid plane of dissection from carotid vessels and
surrounding brain parenchyma was good in 55% of cases in either groups, but
poor in 44% of cases, rest of the cases had heterogenous/ patchy plane of
dissection. Encasement of the ICA and its branches, taken as encircling >270
degrees, was observed in 39.5% in Group I and 62% in Group II tumours,
significantly higher in Group II tumours (p= 0.029).
Optic canal was deroofed in 9 patients (20.9%) in group I and 5 patients
(17.2%) in group II , p=0.698. (Table no. 5)
Table no. 5- Intraoperative observations
Characteristics GROUP 1,
n=43 (%)
GROUP 2, n
=29 (%)
Chi
square
P-
value
Arachnoid plane with
ICA, MCA- Good
20 (55.6) 16 (55.2) 0.00 0.975
Poor 16 (44.4) 13 (44.8)
Intermediate 7 0
ICA encircled(> 270 deg) 17 (39.5) 18 (62) 4.74 0.029
MCA encasement na na
Orbital involvement 0 4 (13.8) 6.28 0.012
Optic canal deroofed 9 (20.9) 5 (17.2) 0.15 0.698
Results
48
Histology
Histological grading was done as per WHO classification of CNS
tumours 2007(72). It revealed that the most common subtype was
meningothelial and transitional types. Many specimens showed a mixed
picture or dual histopathological characteristics, mainly meningothelial and
transitional types. (Table no.6)
Table no. 6- Histopathological distribution.
Histology type Group I , n=43 (%) Gr II , n=29 (%)
Meningothelial 19 (44) 18 (62)
Fibroblastic 3 (7) 1 (3)
Transitional 22 (51) 20 (69)
Psammomatous 2 (5) 0
Angiomatous 4 (9) 0
Atypical 6 (14) 3 (10)
Rhabdoid 1 (2) 0
WHO grade I 35 (82) 26 (90)
WHO grade II 7 (16) 3 (10)
WHO grade III 1 (2) 0
WHO grade II tumours were seen in 7 cases (16%) in groups I and 3
cases (10%) in Group II. Group I consisted of 6 atypical type and 1 clear cell
histology. Group II had all 3 atypical meningiomas. WHO grade III
meningioma was seen in one patient of Group I (rhabdoid pathology).
Results
49
Visual outcomes
We defined a change in visual acuity (VA) as a worsening or
improvement of single line of Snellen acuity or from light-inspection to hand
movement, from hand-movement to figures-counting.
In group I, 16 (37.2%) patients presented with preoperative VA
impairment and 9 (20.9%) patients with visual field defect. This included 5
patients with no PL (perception of light) and 2 with HM (only perception of
hand movement) at presentation. 24 patients (56%) showed stable vision/
unchanged to pre operative status at time of discharge, 10 showed
improvement (23%) and 7 reported worsening (16%). Amongst the 7 reported
cases of worsening of vision, there were 2 new cases with no PL ( these were
the 2 cases with only HM before surgery) and 1 case of only PL.
In group II (29 patients), 11 (37.9%) presented with acuity loss and 6
(20.7%) presented with field defect. This included 4 patients with no PL and 1
with only HM at presentation. Visual acuity remained unchanged in 18 (62%),
2 (7%) showed improvement and 6 (21%) actually worsened after surgery
including 1 additional case with no PL (Table no. 7).
We want to highlight that, most of these above patients showed
improvement in vision subjectively and also by confrontation testing during
each subsequent follow up visits, though, we do not have formal visual acuity
and field charting for most of these patients. We have observed that, no
improvement occurred amongst those with no PL, either at presentation or
Results
50
after surgery. Comparing the visual outcome between these two groups, none
of the values were significant.
Table no. 7- Visual outcome in Group I and II.
Characteristics GROUP 1,
n=43 (%)
GROUP 2, n
=29 (%)
Chi square P- value
Pre surgery vision
Acuity loss 16 (37.2) 11 (37.9) 0.00 0.951
No PL 5 4
Only PL /HM 2 1
Visual Field defect 9 (20.9) 6 (20.7) 0.00 0.980
Post surgery vision-
Stable/unchanged 24 (56) 18 (62) 0.081 0.7762
improved 10 (23) 2 (7) 2.263 0.1325
worsened 7 (16)
(2 new
cases of no
PL + 1 with
only PL)
6 (21)
(1 new case
of no PL)
0.07 0.8691
Cranial nerves involvement
In Group I, one patient presented with partial ptosis (CN III), otherwise,
extraocular movements were normal in rest of the cases. But, new
postoperative CN III paresis was seen in 9 cases (20.9%), p = 0.012, and CN
VI paresis in 2 cases (4.7%) and Frozen eye on same side in 1 cases (2.3%)
(Table no. 8). In Group II, 4 (13.8 %) cases already presented with a CN III
deficit and 2 (6.9%) with CN VI paresis and 1 (3.4%) with CN V sensory
Results
51
deficit. 14 of 29 (48.3%) patients had a new or worsening postoperative CN
III paresis which was significant between the two groups, p = 0.015. In group
II, 4 (13.8%) cases had a new postoperative CN IV paresis and CN VI paresis
each.
Most of the isolated post operative cases of CN III and CN VI deficit
showed improvement on long term follow up, but the 6 patients with frozen
eye (2 from group I and 4 from group II) remained status quo.
Table no. 8- Pre and Post surgery extraocular cranial nerves status.
Group 1, n=43
(%)
Group 2, n
=29 (%)
Chi square P value
Pre operative deficits
Cranial nerve 3rd 1 (2.3) 4 (13.8) 6.28 0.012
4th 0 0 - -
5th 0 1 (3.4) 1.50 0.220
6th 0 2 (6.9) 3.05 0.081
Post surgery
deficits (new/
worsening)
3rd 9 (20.9) 14 (48.3) 5.96 0.015
4th 1 (2.3) 4 (13.8) 1.89 0.169
5th Na Na na Na
6th 2 (4.7) 4 (13.8) 1.89 0.169
Frozen eye 1 (2.3) 4 (13.8) 1.89 0.169
Results
52
Residue and Recurrence Rate
All our patients underwent post surgery CT scan brain (plain and
contrast) on day 1. Residue present was descriptively noted, but volumetric
measurement was not done. In our present analysis, residue was seen in 8
(18.6%) cases in group I and 15 (51.7%) cases in group II.
Group I: Radiological residue in CT scan was seen in 8 (18.6%) cases
and recurrence with tumour growth was observed in 4 (9.3%) out of 8 cases.
The time to recurrence varied considerably ranging from 1 to 8 years.
Amongst these 4 cases, only 1 case underwent re- surgery for its recurrence
but then, the procedure was abandoned due to intraoperative cardiac event.
Patient was resuscitated and stabilized and later referred for RT.
Group II: Radiological residue in CT scan, on day 1, was found in 15
(51.7%) cases, (p =0.003). Increase in size of residue/recurrence was noted
in 8 (27.5%), 4 (13.8%) underwent repeat surgery. The time period to
recurrence ranged from 2 to 12 years but majority (6/8 cases) after 4th year.
The criteria for repeat surgery for recurrence were symptomatic patients and
significant increase in tumour size.
Following are the summary of 4 patients in group II subjected to repeat
surgery for recurrence:
Case 1, Female patient in 5th decade underwent repeat surgery after 12years
with Simpson’s grade IV excision. She was referred for SRS for residue but
patient refused. She is presently on 4th year of follow up after 2nd surgery
Results
53
with minimal increase in size of residue. She developed MCA stroke twice in
2007 and 2011 and is recovering.
Case 2, Patient presented with recurrence after 4 years and grade IV excision
done followed by RT. At last follow up, 8 years after 2nd surgery, there was
no recurrence.
Case 3, Patient presented with recurrence after 2 years and grade IV excision
done followed by RT. Patient is currently stable with small residue.
Case 4, Patient was earlier operated elsewhere and came with recurrence
after 2 years, underwent Grade I excision and is doing well.
Postoperative Radiotherapy
Post surgery radiotherapy (RT) were received by 5 patients in Group I
and 6 patients in Group II. Our policy for administering RT were, those cases
with gross tumour residue, recurrence with high risk of repeat surgery, WHO
grade II and III tumours and finally consenting patient.
In group I, 5 (11.6 %) cases underwent RT (4 cases of atypical
meningioma and 1 case of Rhabdoid histology). Remaining, 3 out of 8 cases
of WHO grade II pathology, refused to undergo any form of adjuvant therapy.
Though we had 8 residual Simpson’s grade IV excision cases in Group I,
initially, we followed up all these cases : 1 case showed resolution of tumour
in repeat imaging after 1 year, 4 showed increase in size/recurrence and 3
cases had a stable disease. Amongst the 4 recurrent cases in Group I, only 1
case underwent RT. (The fate of 5 irradiated patients in Group I were: 1 died
Results
54
due to medical reasons after over a year, 3 have shown no recurrence/
increase in size and 1 case in which surgery was abandoned due to
intraoperative MI has a stable residual tumour after RT).
In group II, 6 (20.7%) cases underwent RT- it included 2 out of 3
cases with atypical meningioma, the 3rd patient with atypical histopathology,
though planned for RT, developed cardiac arrest at 6 weeks of follow up and
died. Amongst the 15 (51.7%) cases of residual tumour in Group II, 8
(27.5%) showed increase in size, and out of which, 4 cases (13.8%)
underwent repeat surgery based on symptomatology . They all underwent
Simpson’s Grade IV excision and were subjected to RT post surgery. Those
not irradiated but with residual tumour i.e 11 (37.9%) cases were under
follow up and having stable tumour size.
All of 6 (20.7%) irradiated cases, in Group II, showed stable residual
tumour at last follow up, except one (who was earlier operated 3 times
outside our institute and received RT, he died after 6 months as a sequel of
ICA injury and massive infarct).
KPS and mortality
The clinical outcome was measured by Karnofsky Performance Score
(KPS). Group I - 43 cases were followed up for mean 3.95 years (range 1 to
11 years). At admission, mean KPS was 75.11 (range 40 to 90). The mean
score improved to 84.2 at the time of discharge, with KPS > 90 in 18 (41.8%)
cases . At last follow up, the calculated mean KPS was 90.7, with 33 (78.5%)
Results
55
cases having KPS >90. (Table no. 9). 5 (11.6%) cases presented with KPS
50-60 due to severe frontal lobe signs and raised ICP features. The latter
group of 5 cases showed marked improvement after surgery. There was 1
death at a follow up period of one year in group I. This case was a 57 years
old female patient who underwent Simpson’s grade II excision with atypical
meningioma. At the time of discharge, her KPS was 90 and was subjected to
RT. She died a year later due medical reasons (Table no. 9).
Table no. 9- Karnofsky Performance score (KPS) in GROUP I
(mean=3.95 years follow up).
KPS score Pre op. KPS,
no. (%)
Post op KPS at
discharge, no. (%)
KPS at last follow
up, no.42 (%)
100 0 1 (2.3) 12 (28.5)
90 4 (9.3) 17 (39.5) 21 (50)
80 20 (46.5) 24 (55.8) 9 (21.4)
70 14 (32.6) 1 (2.3) 0
60 4 (4.7) 0 0
50 1 (2.3) 0 0
40 0 0 0
10-30 O 0 0
Mean KPS 75.11 84.2 90.7
Group II - 29 cases were followed up for a mean of 4.7 years (range 1-
12 years). At admission, mean KPS was 67.2 ( range 10-30 to 80). 3 patients
presented with KPS 30- 40, amongst which 2 were in post ictal phase, and 1
with raised ICP with evidence of herniation. Amongst these 3 cases, one died
Results
56
on day 10th due to sequel of vascular injury, others improved and was
discharged with KPS of 60 to 70.
Two perioperative deaths were noted in group II- first case developed
right MCA territory infarct and succumbed to its sequel on the 10th post
operative day. Another case was recovering well after surgery, but
succumbed on the 5th day after surgery due to pulmonary embolism.
The mean KPS at discharge was 57.35, only 5 cases (17.2%) had >90
KPS at discharge. The mean KPS at last follow up was 84.54 and KPS
exceeding > 90 was noted in 15(68.1%) cases.
Table no. 10- Karnofsky Performance score in GROUP II (mean=4.7years
follow up).
KPS score Pre operative
KPS - no. (%)
Post op KPS at
discharge, no. (%)
KPS at last follow
up (no. 22 (%)
100 0 0 0
90 0 5 (17.2) 15 (68.1)
80 12 (41.3) 11 (37.9) 2 (9)
70 13 (44.8) 7 (24.1) 5 (22.7)
60 2 (6.8) 2 (6.9) 0
50 0 1 (3.7) 1 (left MCA stroke
after 5 years of
surgery)
40 1 (3.4) 1 (3.7) 0
10-30 2 (6.8) 0 0
Mean KPS 67.2 57.35 84.54
Results
57
Two deaths occurred at 6weeks and 6 months of follow up in group II.
The first patient died of cardiac arrest at 6 weeks and other patient
succumbed to sequel of right supraclinoidal ICA injury at 6 months.
Morbidity
Besides visual and cranial nerves involvement, arterial infarcts,
dysphasia / apahasia, meningitis and seizures were frequently observed
morbidities. List of other morbidites are given in the Table no. 11.
Group II patients experienced higher motor deficits due to infarct, 6
(20.7%) cases in group II versus 2 cases (4.7%) in group I, p= 0.014. The 2
cases in group I had small perforator infarct and its deficits improved with
time and physiotherapy. Amongst the 6 patients with infarct in group II, 1 had
ICA injury intraoperative, and 1 each with MCA and PCA territory infarct,
remaining 3 cases had small perforator infarct. Patient with MCA infract died
on 10th post operative day and one with ICA infract succumbed 6 months
later as a part of its sequel. 2 additional patients developed right MCA stroke
4 and 6 years post surgery in group II which was unrelated to surgery.
Post surgery meningitis was noted in 6 (20.7%) cases in group II and
none in group I, p=0.002. Seizures in 2 (4.7%) in group I vs 6 (20.7%) in
group II, p = 0.034. CSF rhinorrhoea was noted in 2 (4.7%) cases in group I
and 1 (3.4%) case in group II. The 2 cases in group I were treated
conservatively, whereas 1 case in group II underwent Theco- peritoneal
shunting.
Results
58
Table no. 11- Morbidity after surgery in group 1 and group 2
GROUP 1,
n=43 (%)
GROUP 2, n =29
(%)
Chi
square
P value
Hemiparesis (new/
worsening)
2 (4.7) 7 (24.1) 6.01 0.014
Infarct 2 (4.7)
(perforators)
6 (20.7) (1 ICA,
1MCA, 1PCA, 3
perforators)
4.51 0.034
CSF rhinorrrhoea 2 (4.7) 1 (3.4) 0.06 0.802
Seizures 2 (4.7) 6 (20.7) 4.51 0.034
Meningitis 0 6 (20.7) 9.71 0.002
DVT 1 (2.3) 1 (3.4) 0.08 0.776
SJS 1 (2.3) 0 0.68 0.408
Behavioural problem 1 (2.3) 4 (13.8) 3.52 0.060
Patient follow up
Follow-up data included clinical examinations and imaging (contrast-
enhanced MR images /CT scans) at 6weeks, 3 months, 6months and yearly
thereafter (Table no. 12).
Results
59
43 patients in group I were followed up for mean of 3.95 years (range 1 to 11
years) and 14 (32.5%) patients had >4 years of follow up. Out of 43 patients,
5 cases lost follow up, as given in table no. 12.
Out of 29 patients in group II, 2 died in perioperative period and 2 died
within one year period and the remaining were followed up for mean of 4.7
years ( range 1 to 12 years), 3 patients were lost to follow up.
Table no.12 – Patient follow up data given as frequency.
Group I (n=43) Group II (n=29)
Follow up
duration in
years
No. of
patient
No. lost
to follow
up
thereafter
Rec of
tumour
Death No of
patient
No. lost
to follow
up
thereafter
Rec of
tumour
Death
<1 years 3 1 0 3 1 1 2
>1-2 years 16 2 0 1 5 2 0
>2-4 years 10 0 0 6 0 1
>4-7 years 9 0 2 5 0 2
>7-10
years
3 2 1 6 0 2
>10 years 2 0 1 2 0 2
Discussion
60
DISCUSSION
Classification of Medial Sphenoid Wing Meningiomas
The initial classification on sphenoid wing meningiomas by Cushing
and Eisenhardt (3) has stood the test of time and remains mostly valid, but
now, numerous authors have sought a revision that incorporates information
and experiences gained from the contemporary use of multiplanar MRI
microsurgical technique and surgical outcome.
Then, almost after five decades, Al-Mefty (5) reported 24 patients with
clinoidal meningiomas, and subclassified the tumours into three groups: a)
medial ridge tumours with marked attachment to the carotid tree because of
no intervening arachnoid membrane, b) medial ridge tumours without marked
attachment to carotid tree secondary to an intervening arachnoid membrane
being present, and c) small tumours solely within the optic canal.
Recently, many of the contemporary authors like Kaye AH (121), Lee JH
(20), Samii M (122), Stephen M. Russell (4), Makoto Nakamura (6), have put forth
their reservations on the above Al-mefty’s classification(5) for the following
reasons. First, Group 3 tumours (optic canal meningiomas) do not involve the
carotid tree and, therefore, should not be included when evaluating medial
ridge (clinoidal) meningiomas. Secondly, these authors unanimously agree
that, amongst those tumours that are markedly attached to the intracranial
vessels without an apparent intervening arachnoid layer, not all originate
proximal to the carotid artery’s arachnoid ensheathment (i.e. Group 1 tumours
Discussion
61
in Almefty’s classification). They are of the view that, though in a small
minority of patients this is true, other factors like chronicity of tumour
compression, tumour consistency, invasiveness of the tumour, and cases with
a previous resection are probably more important determinants of resectability
and unfavourable plane of dessection. Even in Al-Mefty’s series (5), 4 out of
the 24 patients had previous resection.
In this study, we also agree with the above authors that, recurrence,
chronicity and intrinsic tumour behaviour are the deciding factors for
favourable arachnoid plane or interface with vessels which can be witnessed
only at the time of surgery. This is further proven by the fact that some
tumours show variable dissection plane even with the MCA vessels. In our
series, the main factors leading to subtotal tumor resection was CS
involvement and poor plane of dissection from major arteries especially in
recurrent cases (all underwent Simpson’s grade IV excision). Al-mefty’s grade
III tumours with optic foramen origin are of smaller size with predominantly
early visual disturbances. This particular group of tumour was excluded from
our present study.
Hereby, we classified the medial SWM according to pre and post
operative evidences of CS involvement. Stephen M. Russsell et al. (4) and
Nakamura et al. (6) have confirmed the clinical utility and treatment strategy of
this subdivision. Treatment for tumours without CS extension is gross total
removal, whereas, for tumours with CS extension, often, only the intradural
Discussion
62
tumour is removed with the residual part infiltrating the CS usually managed
conservatively or irradiated.
Cavernous Sinus Involvement
The surgical management of patients with meningiomas involving the
CS has been continuously debated and remains controversial. More
aggressive and radical intracavernous tumor removal was proposed by
Sekhar et al., (16,17,18) De Monte et al.,(14) and Dolenc et al.,(19) along with the
encased ICA, with or without saphenous vein graft reconstruction.(16,18)
Surgical morbidity associated with aggressive resection of
meningiomas involving the CS remains high. (7,9,10,11,12,13,14,15,118) There are
several reasons for this high morbidity. First, disruption of the fine blood
supply of the ocular CNs may occur during dissection of CS meningiomas.
(123,124) Second, dissection of the meningioma from the CNs may be
impossible because of the poor arachnoidal plane and tumour infiltration of
the nerves. (125) Finally, meningiomas may infiltrate the adventitia of the C4
segment of the ICA. (126, 127)
DeMonte et al. (14) reported 41 patients with histologically benign
meningiomas involving the CS who underwent aggressive surgery. Although
total removal was achieved in 76% of cases, 10% experienced recurrence 5
years after surgery. Pre-existing CN deficits improved in only 14% of the
patients, remained unchanged in 80%, and worsened permanently in 6%.
Discussion
63
De Jesus et al. (15) evaluated the tumour recurrence and progression in
119 patients with meningiomas involving the CS. During a relatively short
mean follow-up period of 33.8 months, they found recurrences in 10% of
completely resected tumours and 15% of incompletely resected tumours. The
data on most common complications of CS surgery, i.e. impairment of
extraocular muscles or loss of trigeminal nerve function was not mentioned.
Abdel-Aziz et al.,(8) in 2004, reported 38 patients with large SWM
involving the CS. In 22 of 24 patients, total microscopic excision was achieved
in tumours that involved only the lateral compartment of the CS (modified
Hirsch Grades 0 and 1) (128). (Modified Hirsch grades are as follows: HG 0,
tumour touches and rests on the ICA without encasement; HG 1, tumour
partially encases the ICA; HG 2, tumour completely encases, without
narrowing the ICA; HG 3 tumour completely encases and narrows the ICA;
and HG 4, tumour completely encases and obliterates the ICA).(128)
All 14 of 38 patients who had tumours that encased the CS of the ICA
(Hirsch Grades 2–4) underwent incomplete resection. Among 38 patients,
mortality was 0%, late CN deficits remained in 6 (16%), late KPS exceeded 90
in 34 patients (90%) and 4 patients (10.5%) developed a recurrence or
regrowth. Of 20 patients who were treated with either linear accelerator-based
SRS or fractionated conformal RT, 11 had residual tumour with a moderate to
high proliferative index, 4 had atypical tumours and 1 had angioblastic
meningioma, 2 had regrowth, and 2 had recurrent tumours. In 18 (90%) of the
20 patients who underwent radiation, tumour size was reduced or controlled.
Discussion
64
We also agree with their conclusions that residual tumour in the medial
compartment (HG 2–4) may be managed by observation or radiotherapy,
depending on cellular atypia, proliferative index, patient’s age, and clinica
status.
In Nakamura et al. (6) analysis of medial SWM with CS involvement,
indeed showed a high recurrence rate of 27.5% after surgery. This difference
in recurrence could be due to less radical approach of authors considering
that only 14.5% underwent GTR, in addition, this study had a significantly
longer follow up period of 79.04 months. IIIrd CN paresis was the presenting
complaint in 19 patients (27.5%) and additional 6 patients (12%) developed
new IIIrd CN paresis. 10 (14.5%) presented with IVth CN paresis with 2 new
cases after surgery and 9 (13%) presented with VI th CN paresis with 2 new
cases after surgery. Also to note here is that, 6 (12%) patients in this cohort
showed IIIrd CN improvement, 2 showed IVth CN but none showed VIth CN
improvement after surgery.
In similar study by Stephen M Russell et al.,(4) 11 out of 35 patients with
CS involvement was followed for a mean of 12.8 years, out of which 10 cases
(90%) underwent grade III/IV excision. Recurrence was seen in 3 (9%) and
IIIrd CN deficit seen in 1 patient (9%). Conventional EBRT was used for 5
patients (3 with recurrence and other 2 who had undergone Grade IV
excision). After receiving radiation, no tumor progression occurred in these
five patients (average follow-up, 7.1 yr). None of the patients had atypical or
malignant meningiomas. Therefore, the authors concluded that GTR of medial
Discussion
65
ridge meningiomas invading the CS, which was present in 11 (31%) of their
patients, is not warranted.
In our analysis, 29 of 72 patients of medial SWM with CS involvement,
we could achieve a GTR of 41.2% through meticulous interdural dissection
and stripping off the outer layer of CS. Those infiltrating the CS with vessels
encasement was left untouched. Residue was noted in 15 (51.7%) and the
majority were followed up regularly in yearly basis. 6 (20.7%) cases showed
enlargement of residue and became symptomatic with time lag ranging from 2
to 12 years (majority after 4 years), out of which 4 underwent repeat surgery (
Simpson’s grade IV). EBRT was given to 6 patients in group II, which
included all 4 with recurrence and repeat surgery and 2 patients with atypical
histology. Except for one patient who died due to sequel of ICA injury and
infarct after 6 months, others have shown a stable residual tumour after RT.
We also experienced significantly higher post surgical CN deficits: 14
cases (48.3%) with new/worsening IIIrd CN paresis, 4 (13.8%) of IVth CN
and VIth CN paresis each. 4 cases (13.8%) developed unilateral complete
ophthalmoplegia (frozen eye), 2(6.9%) out of which had frozen eye as
presentation before surgery. Our cranial neuropathy was higher amongst
contemporary studies because of our initial attempt to remove tumour
completely. Michael E. Sughrue et al.,(129) reported partial IIIrd CN palsY in
approximately 20% of medial-third tumor cases. Abdel-Aziz and colleagues
(8) reported cranial neuropathies in 16% of their cases, and Langevin and
colleagues (130) noted diplopia in 15.8% of patients.
Discussion
66
In our view, a more aggressive approach to meningiomas involving the
CS will lead to more surgical morbidity. A multidisciplinary approach using
tailored surgical resection and salvage postoperative RT can maximize tumor
control and minimize patient morbidity.
Extent of resection and recurrence rate of Medial SWM
The rate of recurrence for medial SWM is regarded as one of the
highest for intracranial meningiomas. Mirimanoff et al.(131) reported a
recurrence rate or tumour progression in 34% at 5 years and 54% at 10 years
for medial SWM compared to 3% and 25% at 5 and 10 years for convexity
meningiomas.
Analyzing the recurrence among different tumour locations at the
cranial base, Mathiesen et al. (132) also observed the highest recurrence rate
among clinoidal/medial SWM, with 60 to 100% at 10 years and 72 to 100% at
25 years after surgery, depending on the Simpson grade of resection. Basso
and Carrizo(133) reported a recurrence rate of 26.92% among 26 inner third
meningiomas at 10 years after surgery. Nakamura et al.(6) reported recurrence
in 7.7% of Group I tumours and 27.5% of Group II tumours during a mean
follow-up period of 69.3 months (5.8 yr). Nakamura et al.(6) could achieve
92.3% GTR in group I and 14.5% in group II tumours.
In our study, recurrence with tumour progression was observed in 4
cases (9.3%) of group I and 8 cases (27.5%) of group II at a mean follow up
of 3.95 years and 4.7 years, respectively. Here, it is to note that, all the
Discussion
67
recurrences occurred in those with residual tumours after first surgery [i.e , 4
of 8 residual cases (50%)in Group I and 8 of 15 residual cases (53.3%) in
Group II]. We could achieve GTR of 72.1% in group I and 41.2 % in group II.
Our policy regarding adjuvant therapy in WHO grade I meningiomas
was to follow up with serial imaging yearly regardless of grade of resection.
Patients were subjected to RT only after recurrence with progression, repeat
surgery and WHO grade II- III tumours.
Stephen M Russell et al. (4) achieved only 9 % GTR in group II tumours,
yet, recurrence rate was significantly lower at 9% because they subjected
their patients with subtotal resection to early RT.
Thus, it is widely evident from various studies that RT/SRS in cases
with subtotal resection of CS involvement, confirms to better outcome.
Visual Outcome in Medial Sphenoid Wing Meningiomas
The past views regarding postoperative visual recovery in patients with
clinoidal meningiomas have been quite pessimistic. (5) Poor visual outcome
was previously attributed to an ischemic mechanism, and visual deficits were
considered mostly irreversible. (5,134) Only few data exists concerning visual
function after resection of these tumours.
Al-Mefty et al. (5) reported 24 of 28 patients with clinoidal meningiomas
who presented with visual disturbances. Visual impairment improved in only
six (25%) patients after tumour removal.
Discussion
68
Risi et al(118) in their report on 34 patients with meningiomas involving
the anterior clinoid process, 32% of 20 patients with preoperative visual
impairment had postoperative improvement in their vision. Benjamin V et
al.(135) reported in their series of 20 surgically treated medial SWM,
improvement of vision in 50% of patients who were not blind before surgery.
Lee et al. (20) have done an extensive study on visual outcome in
clinoidal meningiomas. They proposed at least three possible mechanisms of
preoperative optic nerve injury- ischemia, compression, and demyelination.
Favorable results were reported in a recent series of 15 patients who
underwent surgery of clinoidal meningiomas with use of a cranial base
technique consisting of extradural anterior clinoidectomy coupled with optic
canal unroofing and optic sheath opening. Six of eight (75%) patients with
preoperative visual impairment experienced a significant improvement with a
follow-up period ranging from 6 to 60 months (mean, 37.2 months).
Nakamura et a.l (6), in their series of 108 medial SWM with 39 in group
I and 69 in group II, noted immediate postoperative improvement of visual
function in 56%, and vision remaining unchanged in 44% with Group 1
tumours who were not blind before surgery. Outcome of visual function was
less favourable in Group 2 tumours with vision improvement in 30%, stable in
60% and worsening in 10% of patients. Only 10% of patients who underwent
surgical resection of a recurrent Group 2 tumour showed immediate visual
improvement. Nakamura et al.(6) have questioned the necessity for extradural
extensive cranial base approach in Lee et al.(20) series for a favourable visual
Discussion
69
outcome. Nakamura et al. used this extradural cranial base approach only for
those with intraosseous involvement. (6)
Stephen M Russell(4) reported that among the 30 patients with
preoperative visual loss, 22 patients (73%) improved, six (20%) were
unchanged, and two (7%) worsened. Here also, the authors were very
sceptical regarding extensive extradural cranial base approach and were
selective in their approach.
We have noted a similar pattern of preoperative visual acuity loss and
field defect before surgery, in either of the groups I and II. Approximately, 37%
presented with acuity loss and 20 % with field defect. Post surgery, in group I,
vision remained unchanged in 56 %, improved in 23% and worsened in 16 %.
Whereas, in group II, vision remained stable in 62%, improved in 7% and
worsened in 21%.
Our approach to this category of tumour was decided on individual
basis considering radiological, clinical, age and general condition of patient.
14.6% (4 patients) underwent FTOZ and rest were subjected to standard
fronto-temporal craniotomy with sphenoid ridge drilling with or without anterior
clinoidectomy. Optic canal was deroofed in 20.9% (9 patients) in group I and
17.2% (5 patients) in group II. It is to be highlighted here, that most of our
patients presented with poor visual acuity and larger size of tumour (tumour
size >2cm in 74.5% in group I and 68.8% in group II) which probably explains
our poor visual outcome.
Discussion
70
Morbidity and mortality
Cushing and Eisenhardt (3) noted that “the crux of the removal lies in
freeing the growth from its entanglement with the vessels at the carotid
bifurcation,” and he cautioned surgeons about the hazards of entering the
carotid field.
Aggressive resection of tumour invading the CS is associated with new
and permanent CN palsies, cavernous ICA injury, and CSF leak. These risks
outweigh the benefits of GTR.
Injury to the vessels of the anterior circulation has been the major
cause of operative morbidity and mortality in past surgical series. Bonnal et
al., 1980 (10), had a surgical mortality of 43% and Fohanno and Bitar in 1986
had 27% mortality(117). Since then, more recent reports have shown lower
rates of operative morbidity and mortality, as approach became more
conservative and better understanding of the anatomy. (20,118,119)
Lee et al. in 2001 (20), reported a 87% GTR with no mortality in 15
patients with global medial ridge tumours. Other peer reviewed series in
chronological event are given in the table no.13 and shows decreasing trend
of mortality.
We in our study of 72 patients, had no perioperative mortality in group I
tumours, 1 died a year later due to medical reasons. In Group II, we
experienced 2 cases of intraoperative injury to MCA and ICA each. One case
succumbed to its sequel at 10th day and other at 6 months. One more death
Discussion
71
occurred on the 5th post operative day due to pulmonary embolism. Literature
shows that efforts to remove adherent tumour from encased vessels in the
past had met with rates of vascular injury exceeding 20% (136). Our 2 cases of
major arterial injury accounted for 6.89%. Small vessel/ perforator infarct with
hemiparesis occurred in 2 cases (4.7%) in group I and 4 cases (13.55%) in
group II. These patients improved in long term and was independent for
activities of daily living.
The outcome in our patients was measured with Karnofsky’s
Performance Score (KPS) at the time of discharge and at last follow up
(ranging 1 to 12 years). In group I, mean KPS at discharge was 84.2 and at
last follow up 90.7. In group II, mean pre surgical KPS was 67.2, at discharge
57.35 (increased morbidity was due to infarct, meningitis, behavioural
problems, metabolic disturbances, etc) and mean KPS improved significantly
to 84.54 at last follow up.
We believe that aggressive GTR of medial SWM invading the
cavernous sinus is not warranted, especially in older patients. In summary, a
multidisciplinary approach using both pragmatic surgical resection and
salvage postoperative radiation treatment can maximize tumour control while
minimizing patient morbidity.
Discussion
72
Table no 13: Summary of studies of medial SWM in the peer-reviewed literature
Series (ref
no.)
No. of
patients
Size CS
involve
ment
%
F/U mortality GTR Improved
vision
Rec.
Cushing and
Eisenhardt,
1938 (3)
13 na 7 yr 15% 31% 8% 36%
Ugrumov et al.,
1979 (113)
17 na Na 23% 0% Na Na
Konovalov et
al., 1979 (114)
70 na Na 19% 85% Na Na
Ojemann, 1980
(115)
13 na 11.3yr 0% 0% 15% 31%
Bonnal et al.,
1980 (10)
7 na 1-8 yr 43% 29% 17% 25%
Pompili et al.,
1982 (116)
9 na 7yr 4% 50% 48% 12%
Fohanno and
Bitar, 1986
(117)
18 na na 27% Na Na 25%
Al-Mefty, 1990
(5)
24 na 38 4.8yr 8% 89% 8% 4%
Risi et al., 1994
(118)
34 na 1.9yr 6% 59% 32% 21%
Day, 2000
(119)
6 <5cm 3
months
0% 66% Na Na
Goel, 2000
(120)
60 85%
>3cm
0 na 5 70 25.5 na
Lee et al., 2001
(20)
14 3.7cm 13 3.1yr 0% 87% 75% 0%
Abdel-Aziz et
al., 2004 (8)
38 >3cm 100 8yr 0% 58% Na 11%
Nakumura et al
2006 (6)
108 na 64 6.59yr 0% Gr I
92.3%
Gr II
14.5%
56%
30%
7.7%
27.5%
Stephen M
Russell et al
2008 (4)
35 4.5cm 31.4 12.8 0% 69% 63% 9%
Behari, 2008
(110)
20 6.12 90 na 5 45% 15% na
Bassiouni,
2009 (111)
106 na 29 6.9
years
1.9 58 40.4 10.2
Our study
2012-13
72 >2cm
74.5%
Gr I no.
43
Gr II
no. 29
3.95yr,
4.7yr
0%
6.9%
Gr I
72.1%
Gr II
41.2%
23%
7%
9.3%
27.5%
Conclusion
73
CONCLUSION
The surgical treatment of medial SWM still remains a challenge for
neurosurgeons. The major determining factors for subtotal resection are the
CS infiltration, repeat surgery for recurrence and vascular encasement. Group
II tumours though can be managed aggressively, it may be associated with
increased morbidity like permanent cranial nerve deficits of extraocular
movements, infarct and poorer KPS.
It is also observed that, many residual tumours remain stable for many
years and some even reduce in size/ disappear, depending upon the tumour
grade and growth pattern and hence, can be closely followed up. SRS can be
offered as an adjuvant therapy in cases of subtotal resection in view of recent
literature with favourable results, though long term outcome data is awaited.
In Group I tumours, GTR should be ideally attempted in all cases with
acceptable results, therefore, it is important to accurately identify these two
subgroups for optimal treatment.
There are several limitations to our study in view of shorter follow up
period, smaller sample size and fewer cases in the SRT/SRS arm.
Nevertheless, this study attempts to highlight the importance of classifying
medial SWM into two subgroups with respect to cavernous sinus involvement,
as the surgical approach, complication rates, recurrence and prognosis is
different between the two subgroups.
References
74
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122. Samii M, Tatagiba M: Surgical management of clinoidal meningiomas.
Neurosurgery 48:1020, 2001
123. Knosp E, Müller G, Perneczky A: The blood supply of the cranial
nerves in the lateral wall of the cavernous sinus, in Dolenc VV (eds):
The Cavernous Sinus. Berlin, Springer-Verlag, 1987, pp 60–68.
124. Krisht A, Barnett DW, Barrow DL, Bonner G: The blood supply of the
intracavernous cranial nerves: An anatomic study. Neurosurgery
34:275– 279, 1994
125. Larsen JJ, van Loveren HR, Balko MG, Tew JM Jr: Evidence of
meningioma infiltration into cranial nerves: Clinical implications for
cavernous sinus meningiomas. J Neurosurg 83:596–599, 1995
126. Kotapka MJ, Kalia KK, Martinez AJ, Sekhar LN: Infiltration of the
carotid artery by cavernous sinus meningiomas. J Neurosurg 81:252–
255, 1994
127. Shaffrey ME, Dolenc VV, Lanzino GL, Wolcott WP, Shaffrey CI:
Invasion of the internal carotid artery by cavernous sinus meningiomas.
Surg Neurol 52:167–71, 1999.
128. Hirsch WL, Sekhar LN, Lanzino G, Pomonis S, Sen CN: Meningiomas
involving the cavernous sinus: Value of imaging for predicting surgical
complications. AJR Am J Roentgenol 160:1083–1088, 1993
129. Michael E. Sughrue, M.D Modern surgical outcomes following surgery
for sphenoid wing meningiomas, Clinical article; Journal of
Neurosurgery Jul 2013 / Vol. 119 / No. 1, Pages 86-93
130. Langevin CJ, Hanasono MM, Riina HA, Stieg PE, Spinelli HM: Lateral
transzygomatic approach to sphenoid wing meningiomas.
Neurosurgery 67 (2 Suppl Operative):377–384, 2010
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131. Mirimanoff RO, Dosoretz DE, Linggood RM, Ojemann RG, Martuza RL:
Meningioma: Analysis of recurrence and progression following
neurosurgical resection. J Neurosurg 62:18–24, 1985
132. Mathiesen T, Lindquist C, Kihlstrom L, Karlsson B: Recurrence of
cranial base meningiomas. Neurosurgery 39:2–7, 1996
133. Basso A, Carrizo A: Sphenoid ridge meningiomas, in Schmidek HH
(ed): Operative Neurosurgical Techniques: Indications, Methods, and
Results. Philadelphia, W.B. Saunders, 2000, pp 316–324
134. DeMonte F: Surgical treatment of anterior basal meningiomas. J
Neurooncol 29:239–248, 1996
135. Benjamin V, McCormack B: Surgical management of tuberculum sellae
and sphenoid ridge meningiomas, in Schmidek HH (ed): Operative
Neurosurgical Techniques: Indications, Methods, and Results.
Philadelphia, W.B. Saunders, 2000, pp 305–315
136. Kattner KA, Fukushima T: Management of vascular invasion during
radical resection of medial sphenoid wing meningiomas. Skull Base
11:99–104, 2001
Sree Chitra Tirunal Institute for Medical Sciences &
Technology
Proforma for patients with sphenoid wing meningiomas
A. GENERAL INFORMATION:
1.Name 2. age
3. Sex (Male/Female)
4. hospital no.
5. address
6. Contact no.
8.Date of admission 9. Date of discharge/death
B. PRESENTATION AND HISTORY:
1. Memory disturbances (recent /past)
2. Behavioural problems (yes/no)
3. Headache (yes/no)(mild, moderate, severe)
4. Raised ICP
5. Seizure (SPS, CPS, GTCS)
6. Focal deficit (motor/ sensory/cranial nerves)
7. Visual deficit (acuity, field/none)
8. Incidentally detected (yes/no)
10. Duration of symptoms……………………. 11. History of radiation exposure (yes/no)
12. History of trauma (yes/no) 13. Family history- (meningioma/others tumours)
14. Syndromic association
C. EXAMINATION :
1. neurocutaneous markers
2. motor deficits
3. Cranial nerves involvement (yes /no)
4. Visual deficit (acuity - ……………. / field defect- ……………………………………….)
D. IMAGING:
1. CT scan: 1a. NECT: hypodense/Isodense/Hyperdense/Mixed/ Calcification
1b.CECT: homogenous/ Heterogenous/ Non- enhancing
1c. Bone changes: Normal/ Hyperostosis/ Bone erosion
2. MRI : 2a. T1WI: Hypontense/isointense/ Hyperintense
2b. T2WI: Hypontense/ Isointense/Hyperintense
2c. contrast: Homogenous/ Heterogenous/ Cystic changes
3. MRS (if done) 4.DWI-
5.Size of lesion-…………………………………
7. DSA : a. Feeders- ECA/ICA/ both/none
b. ICA involvement- narrowing/irregularity/displacement/total occlusion
c. Cross circulation (good/poor)
E. LOCATION:
Medial (clinoidal)/ middle/ lateral (pterional)/ en-plaque
F.SURGERY / Date:
1. Simpson’s grade of excision : grade I / II/ III/ IV/ V
2. Craniotomy: frontotemporal/ FTOZ/FTZ
3. Drilling of sphenoid bone : extradural / intradural
4. Hyperostosis (clinoid/ lesser wing/greater wing/ convexity/ orbital roof/lateral wall)
5. Vascularity (intraoperative)- (mild/mod/high)
6. Plane of dissection (Arachnoid plane) of tumour (good/ patchy/ poor all around)
7. Vascular injury intraoperative (yes/no)
8. Intraoperative finding of major blood vessel (encasement/displaced)
9. Optic canal de-roofed (yes/no)
10. Intraoperative finding of Cavernous sinus involvement (yes/no)
G. COMPLICATIONS post operative: CLINICAL:
1. Motor weakness (improved/ static/ worsening)
2.Visual deficit (acuity: improved/ static/ worsening )
(field : improved/ static/ worsening)
3. cranial nerves involvement ( yes/no)
3a. 3rd
CN (partial/complete)
3b. 4th
CN
3c. 5th
CN (sensory/ motor)
3d. 6th
CN (unilateral/ bilateral) 3e. other cranial nerves
4. Behavioural problems (yes/no) 5. DVT/PE (yes/no)
6. Meningitis (yes/no) 7. CSF rhinorrhoea- (yes/no)
8. Seizures 9. Horner’s syndrome (yes/no)
H. RADIOLOGICAL COMPLICATION:
1. Infarct : none/ small (perforators)/ large arterial territory)
2. Hematoma: no mass effect/mass effect/none
3.Residue (yes/no)
4.Recurrence-(yes/no) 5.Time to recurrence-
I.HISTOPATHOLOGY
1. WHO Grade I/ Grade II/Grade III 2. Specify HPR-
J. ADJUVANT THERAPY
1.Radiotherapy- EBRT/ Conformal RT/ SRT/SRS
K. FOLLOW UP- Karnofsky Performance Score /vision
1. At discharge / 6 weeks /6 months / 1 year / 2 year / total duration
L. MORTALITY(yes/no)
1. perioperative/ follow up (time period)
M . RESURGERY : Yes/ No
ABBREVIATIONS
1) CNS - Central Nervous System
2) CN - Cranial nerve
3) CS - Cavernous sinus
4) CT - Computerised Tomogram
5) D/s - Discharge
6) EBRT - External Beam Radiotherapy
7) F/U - Follow Up.
8) GCS - Glassgow Coma Scale
9) GTR - Gross Total Resection
10) HM - Hand movement
11) HPR - Histopathological Report
12) HSE - Herpes Simplex Encephalitis
13) ICU - Intensive care unit
14) IFN α - Interferon α
15) ICA - Internal cerebral artery
16) KPS - Karnofsky performance score
17) MCA - Middle cerebral artery
18) MRI - Magnetic Resonance Imaging
19) MSWM - Medial sphenoid wing meningioma
20) OCP - Oral contraceptive pills
21) OR - Odds Ratio
22) PDGFR - Platelet growth derived Growth Factor Receptor
23) PFS - Progression free survival
24) PL - Perception of light
25) PR - Progesterone receptor
26) RT - Radiotherapy
27) SRS - Stereotactic radiosurgery
28) VEGFR - Vascular endothelial growth factor receptor
Na
me
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Be
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Me
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tor
de
ficit
pre
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pre
op
CN
de
ficits
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Siz
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KP
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KP
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La
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PS
F/ U
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ratio
n in
ye
ars
mo
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lity
Re
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Re
cu
rre
nce
Tim
e to
re
c. in
ye
ars
Re
su
rge
ry
rem
ark
s
Mohammed KP 44 m 293885 L 12 0 0 G 13/15 0 0 1 0 0 U none none 0 0 1 0 1 na 1 1 IV 0 1 0 perf H M,T 0 40 60 70 4 0 1 1 2 0 follow up
Nirmala A 36 f 290212 R 6 1 0 0 0 0 0 no PL 0 cnbt 3rd 3rd 0 0 1 1 1 1 1 1 IV 0 1 0 ICA H M,T 1 70 40 died 1 1 1 3x 4x ICA injury, death <6months
Saharban K 24 f 305468 L 12 1 0 0 0 0 0 PL 0 died 3rd 3rd 0 1 0 0 1 na 1 1 IV 1 1 1 0 Sz, DVT M,T 0 70 died 0 0 1 0 - - 0 died on 5th POD, PE
Lisamma Samuel 44 f 254850 L 12 1 1 G 0 0 0 no PL 0 U, no PL none none 0 0 1 0 1 1 1 1 IV 1 1 1 0 0 M 0 70 80 90 6 0 1 0 0 0 Improved, left eye no PL
Murugan M 26 m 257899 L 1 1 0 0 0 0 0 no PL 0 U ,no PL none none 0 1 0 0 1 na 1 1 IV 0 1 0 perf H T 0 70 70 S ,50 7 0 1 0 0 Left MCA infarct in dec 2010
Syamala T 42 f 286688 R 12 1 1 0 0 0 0 0 0 U none 3rd 0 1 0 0 1 1 1 1 I 1 1 1 0 0 T 0 70 80 90 4 0 0 0 0 follow up
Rajalakshmi R 51 f 344061 L 8 1 0 0 0 1 0 0 0 U none none 0 1 0 0 1 na 1 1 II 0 1 1 0 0 M,T 0 80 90 90 1 0 0 0 0 improved
Lalithambika T 43 f 336512 R 6 0 0 G 1 0 0 1 0 U none none 1 0 0 0 1 1 1 I 1 1 1 0 Sz, B T 0 70 80 90 2 0 0 0 0 0 psychiatry problem
Rajan V 42 m 342334 L 1 0 0 F 0 0 0 0 0 U none 3rd 0 1 0 0 1 1 1 1 IV 0 1 0 0 Sz atyp 1 80 80 90 1 0 1 0 0 0 post RT, small residue
Shylaja 36 f 236279 R 8 1 1 0 0 0 0 0 1 I none 3rd 1 0 0 0 0 1 1 FTOZ IV 0 1 0 perf H, B M,T 0 60 70 70 5 0 1 1 2 0 follow up
Lilly Prascal 47 f 9702888 R 12 0 0 0 0 0 0 no PL 0 U, no PL none none 0 1 0 0 1 1 1 1 I 0 0 1 0 0 M,F,T 0 80 80 S, 70 16 0 1 1 12 1 stroke in 2007, sept.2011, f/u
Manoj kG 33 m 283880 L 4 1 1 0 0 0 0 1 1 W, no PL none none 0 1 0 0 0 0 1 1 II 0 0 1 0 B M,T 0 70 70 80 4 0 0 0 0 follow up
Subaida ashraf 41 f 275341 L 3 1 0 0 0 0 0 1 0 W none none 1 0 0 0 1 1 1 II 0 0 1 0 MN M 0 70 80 90 4 0 1 0 0 follow up
Jyoti Das 26 f 303649 L 6 1 0 0 0 0 0 0 0 U frozen frozen 1 0 0 0 1 na 1 1 II 1 1 1 0 0 T 0 80 90 90 1 0 1 0 0 residue, referred for SRS , no F/U
Shiny Thomas 31 f 265844 R 24 1 0 0 0 0 0 1 1 W, I 6th none 0 1 0 1 1 na 1 1 I 0 0 1 0 0 M,T 0 80 90 90 5 0 0 0 0 0 seizures
Nadasha Ravi 50 m 320408 L 6 1 0 0 0 0 0 0 0 U none 3rd 0 1 0 0 1 1 1 1 II 0 1 1 0 0 M,T 0 80 80 90 2 0 0 0 0 0 improved
padmanabhan 45 m 317900 R 2 1 0 0 0 0 0 0 0 W none 3rd 0 1 0 0 0 1 1 FTOZ II 0 1 0 0 0 M,T 1 80 70 90 3 0 0 1 2 1 first SX in KMC , mangalore
Santhamma 58 f 218285 R 8 1 0 0 0 0 0 0 0 U none none 1 0 0 0 1 1 1 1 II 0 0 0 0 B M 0 80 80 90 9 0 0 0 0 0 improved
Stella D 42 f 214102 L 1 1 1 0 1 1 1 1 0 W 7th umn frozen 0 0 1 0 0 0 1 1 II 0 0 0 0 Sz, MN T 0 70 80 90 8 0 1 0 0 0 improved
Asokan Pillai B 43 m 206695 L 4 1 1 0 4/15 0 cnbt cnbt cnbt cnbt cnbt 0 0 1 0 1 1 II 0 1 0 PCA H M,T 0 30 60 90 10 0 0 0 0 0 improved, left Pca infarct Razeeda Jamal TA 31 f 197264 L 3 1 0 0 0 0 0 0 0 U none 3rd 1 0 0 0 1 1 1 1 II 0 0 1 0 CSF rhi M 0 80 80 90 10 0 0 0 0 0 improved, TP shunt for CSF rhin
Sudhakaran P 53 m 190741 L 1 1 1 0 0 0 0 0 W none 3rd 1 0 0 0 0 na 1 1 II 0 0 1 0 0 M 0 80 80 70 10 0 0 0 0 0 HSE in 2005, memory
Lalithaambika PU 44 f 181908 R 36 1 0 G 0 0 1 1 1 U none frozen 0 0 1 0 1 1 1 FTOZ IV 0 1 0 0 Sz, Mn T 1 70 80 70 12 0 1 1 4 1 F/U
Mary Bennet V 46 f 253000 L 3 1 1 0 0 0 0 0 0 U none none 1 0 0 0 0 na 1 1 II 0 0 1 0 0 M 1 80 90 90 7 0 0 1 2 1 residue stable
Geetha S 20 f 253635 R 3 1 1 G 0 0 0 1 1 W frozen frozen 0 1 0 0 1 na 1 1 IV 0 1 0 0 Sz atyp 1 70 70 90 1 0 1 1 0 no follow up
Nalini Kv 61 f 282120 R 12 1 0 0
mmse
11/30 1 1 0 cnbt cnbt U none none 0 1 0 0 1 0 1 1 II 0 0 0 0 MN T 0 60 70 90 5 0 1 0 0 improved
Karrupaiah 62 m 279117 R 1 1 0 0 1 0 1 1 0 U none 3rd 0 0 1 0 1 1 1 1 II 0 1 1 perf H, MN atyp 0 70 70 70 6wk 1 1 0 0 cardiac arrest at 6weeks
Chellamma R 41 f 269479 L 6 1 1 0
mmse
14/30 0 0 0 0 1 U none none 0 0 1 0 1 1 1 1 I 0 0 1 0 0 F 0 70 90 0 6wk 0 0 0 0 no follow up
Jayabal R 54 m 263858 R 3 1 1 F 5/15. 0 0 1 cnbt cnbt died cnbt died 0 0 1 0 1 na 1 1 II 0 1 0 MCA H M,T 0 30 died 0 0 1 1 0 0 0 died, right MCA infarct, POD 10th
MN - Meningitis U - Unchanged M - Meningiothelial meningioma Atyp - Atypical Meningioma G - Generalized seizure
Sz - Seizure I - Improved T - Transitional meningioma HM - Hand movement F - Focal seizure
B - Behavioural problem W - Worsened F - Fibroblastic Meningioma PL - Perception of light S - Stroke
H - Hemiparesis
Medial Sphenoid Wing Meningioma with cavernous sinus involvement (Group II) n = 29
Na
me
Ag
e
se
x
Ho
sp
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l n
o.
sid
e (
rig
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ratio
n o
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CN
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PS
F/ U
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ratio
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ye
ars
Mo
rta
lity
Re
sid
ue
Tim
e to
re
cu
rre
nce
Re
su
rge
ry
Re
ma
rks
Krishna Kutty Nair 62 m 291238 R 3 1 0 G 0 0 0 0 1 U none none 0 1 0 0 0 0 0 1 I 0 0 1 0 T 0 90 90 3 0 0 0 0 improved
Thankam TP 55 f 318095 R 3 1 0 0 0 0 0 0 0 U none none 1 0 0 1 0 0 0 1 II 0 0 0 0 F,T 0 90 100 1 0 0 0 0 improved
NisaruddinK 40 m 322083 L 4 1 0 F 0 0 0 0 0 U none none 0 1 0 0 0 0 0 1 I 0 0 1 0 M,T 0 80 90 2 0 0 0 0 improved
Ramu N 57 m 321938 L 12 0 0 0 0 0 0 no pl 0 U, no PL none 6th 0 0 1 0 0 1 0 1 III 0 1 0 0 F,T 0 80 100 2 0 1 0 0 follow up
Sajimon KK 36 m 274757 L 1 1 0 G 0 0 0 0 0 U none none 0 1 0 0 1 1 0 1 I 0 0 1 0 M,T 0 100 100 5 0 0 0 0 improved
Mohanan PI 40 m 233355 R 6 0 0 0 0 0 0 no PL 0 U, no PL none none 0 1 0 0 0 1 0 1 II 0 0 0 0 M 0 90 90 4 0 0 0 0 no PL
Fathima K 37 f 254342 R 2 1 0 0 0 0 0 0 0 U none none 0 1 0 0 0 0 0 1 II 0 0 0 0 P 0 90 90 2 0 0 0 0 lost follow up
Ponnama TC 51 f 249005 L 4 1 0 0 0 0 0 no PL 0 U, no PL none none 0 0 1 0 0 0 0 1 II 0 0 0 0 M 0 80 80 6 0 0 0 0 no PL
pennama Daniel 52 f 319920 R 3 1 1 0 1 1 0 1 0 W, only PL none none 0 1 0 0 0 0 0 1 III 0 1 0 0 M 0 80 80 1 0 0 0 0 follow up
Rema M 26 f 340066 L 6 1 0 0 0 0 0 no PL 0 U, no PL none none 0 1 0 0 0 1 0 1 II 0 0 0 0 M 0 80 80 1 0 0 0 0 folow up, no PL
Marykutty T 59 f 281587 L 3 0 0 0 0 0 0 1 1 I none none 1 0 0 0 0 0 0 1 II 0 1 0 0 T 0 80 90 2 0 0 0 0 improved
Omana G 42 f 239878 L 2 1 0 G 0 0 0 0 0 W none 3rd 1 0 0 0 0 1 0 1 II 0 1 0 0 Atyp 0 80 90 7 0 0 0 0 status quo,
Suma Jacob 39 f 236501 R 2 0 0 0 0 0 0 1 1 I none none 0 1 0 0 0 1 0 1 I 0 0 1 0 T 0 90 90 7 0 0 0 0 improved
Jessy Anith 41 f 337795 L 4 1 1 0 0 0 0 1 0 W none 3rd 0 1 0 0 1 1 0 FTOZ II 0 0 0 0 Atyp 0 80 90 1.6 0 0 0 0 improved
Jayalatha Satheesh 31 f 280128 R 6 1 0 G 0 0 0 1 0 U none none 0 1 0 0 0 0 0 1 II 0 0 0 0 M,T 0 90 100 4 0 0 0 0 improved
Ratha V 62 f 280675 L 1 0 0 G 0 0 0 0 0 U none none 0 1 0 0 1 1 0 1 I 1 0 1 0 M,T 0 90 100 1 0 0 0 0 lost follow up
Thulasi bai P 51 f 311013 R 12 1 0 G 0 0 0 0 0 U none 3,4,6CN 0 1 0 0 1 0 0 1 I 0 0 0 0 M,F 0 90 100 2 0 0 0 0 improved
Murugeswaran 44 m 310856 R 3 1 1 0 0 1 0 0 U 3rd I 0 1 0 0 1 0 0 1 I 0 0 1 0 A 0 90 90 2 0 0 0 0 improved
Badarnisha 57 f 307725 R 2 1 0 0 0 0 0 no PL 0 U, no PL none none 0 0 1 0 1 1 0 1 II 0 0 0 0 Atyp 1 90 90 0.5 1 0 0 no follow up, death < 1yr
Rosamma Mathai 48 f 357591 L 24 1 0 0 0 0 0 0 0 U none 3rd 1 0 0 0 1 0 0 0 I 1 0 1 CSF rhinor T 0 80 90 2 0 0 0 0 improved
Subhagan B 50 m 288998 L 6 1 0 0 1 1 0 1 1 W, HM none none 1 0 0 0 0 1 0 1 III 1 1 1 DVT M,T 0 80 100 4 0 0 0 0 left eye HM
Selvamam A 58 f 284317 R 12 1 0 0 0 1 1 0 0 U 7 umn none 0 0 1 0 1 1 0 1 II 0 0 1 0 M,T 0 80 100 4 0 0 0 0 improved
Naga Lakshmi 51 f 344700 L 2 1 0 0 0 0 0 0 0 U none none 0 1 0 0 1 1 0 1 II 0 0 1 0 T 0 90 90 1 0 0 0 0 improved
Mini Ninan 40 f 320481 L 12 1 0 0 0 0 0 0 1 W, noPL none none 0 1 0 1 0 0 1 II 0 1 1 0 M,A 0 80 80 3 0 0 0 0 no PL
Irulayee M 41 f 334054 L 18 1 0 0 1 0 0 0 0 U none 3rd 0 0 1 1 0 1 0 1 IV 0 1 0 seizures M,T 0 80 90 2 0 0 1yr 0 RT
Soosamma Jacob 48 f 335958 R 6 1 0 0 0 0 0 0 1 I none 3rd 1 0 0 0 0 1 0 1 II 0 0 0 motor T 0 70 90 2 0 0 0 0 improved
Mungeswaran 44 m 310856 R 3 1 1 0 1 1 0 0 0 U none none 0 1 0 1 1 0 0 1 IV 0 1 0 0 A 0 80 90 2 0 1 0 0 improved
Kamimozhi 31 f 313100 L 1 1 0 0 0 1 0 0 0 U none none 1 0 0 0 0 1 0 1 IV 0 0 0 0 M 0 90 100 3 0 1 0 0 status quo
Pareed T A 32 m 248512 L 6 0 0 G 1 1 0 0 0 W none 3rd 1 0 0 1 1 1 0 1 II 0 1 0 0 M,T 0 80 80 6 0 0 6yr 0 follow up
Muthuval K 57 f 191773 L 2 1 0 G 0 0 0 HM 0 I none 3rd 1 0 0 0 1 1 0 1 II 1 1 1 0 M 0 90 90 8 0 0 0 0 improved
Komalavathy KG 59 f 197951 L 6 1 0 F 1 1 0 0 0 I none none 0 1 0 0 1 1 0 1 I 0 0 1 CSF rhinor P 0 90 80 11 0 0 8yr 0 follow up
Kumaran M 54 m 261350 L 6 1 0 F 1 1 1 1 0 I none none 0 1 0 0 1 1 0 1 IV 1 1 0 0 M 0 80 80 5 0 1 1yr 0 follow up, seizures
Habeeba N 45 f 276100 L 2 1 0 0 0 0 0 0 0 W none none 1 0 0 0 0 0 0 1 IV 1 1 0 0 T 0 80 90 5 0 1 0 0 seizures
Sarasa K 44 f 186752 L 2 1 0 0 0 0 0 1 1 I none none 1 0 0 0 1 1 0 1 I 1 0 1 0 T 0 80 80 11 0 0 0 0 psychiatry problems
Sarojini KK 52 f 194512 R 6 1 0 0 0 0 0 HM 0 W, noPL none none 0 1 0 1 1 0 0 1 II 1 0 1 0 T 0 80 90 8 0 0 0 0 no follow up
Esthappan T 62 m 228499 R 3 1 0 0 0 0 0 1 1 I none none 0 1 0 0 1 1 0 1 II 1 1 1 0 Atyp 1 80 80 8 0 0 3yr 1 2nd sx abandoned due to MI
Ameer M 54 m 228184 L 12 0 0 0 1 1 0 0 0 U none none 0 1 0 0 1 1 0 1 II 0 0 1 0 T,A 0 80 100 6 0 0 0 0 first op in 1991, improved
Jolly Ponnachan 47 f 288091 R 4 1 1 0 0 0 0 0 0 U none none 0 0 1 0 1 1 0 1 I 0 0 0 0 Atyp 1 90 90 3 0 0 0 0 improved
Prabha Sreenivas 54 f 263775 L 3 1 0 0 0 0 0 0 0 U none none 0 1 0 0 0 1 0 1 II 0 0 0 0 Atyp 1 80 100 5 0 0 0 0 improved
Balakrishnan K 54 m 307520 L 4 0 0 F 0 0 0 0 0 U none 3rd 0 1 0 0 1 1 0 1 III 0 1 1 0 T 0 90 100 2 0 0 0 0 improved
Sumathi KP 43 f 306276 R 6 1 0 0 0 0 0 0 0 U none none 0 1 0 0 1 1 0 1 IV 0 1 0 0 R 1 80 90 3 0 1 0 0 no residue in repeat scan
Narayanaswamy 65 m 305320 R 24 0 0 0 0 0 0 0 1 U none none 0 1 0 0 0 0 0 1 IV 0 1 1 motor M,T 0 80 90 2 0 1 0 0 incidental, BPPV subsided
Latha P V 44 f 291947 L 3 1 0 0 0 0 0 1 0 U none none 0 1 0 0 1 1 0 1 IV 0 1 1 seizures M 0 80 90 4 0 1 0 0 follow up
U - Unchanged M - Meningiothelial meningioma Atyp - Atypical Meningioma G - Generalized seizure
I - Improved T - Transitional meningioma HM - Hand movement F - Focal seizure
W - Worsened F - Fibroblastic Meningioma PL - Perception of light
Medial Sphenoid Wing Meningioma without cavernous sinus involvement (Group I) n = 43